SPLANCHNOPTOSIA (ATONIA GASTRICA).

    Factors. 1. Deranged respiration (due to thoracic splanchnoptosia). 2. Relaxed Abdominal wall. 3. Altered form of Abdominal cavity (Pendulous). 4. Elongation of visceral supports (mesenteries). 5. Gastro-duodenal Dilation (due to compression of the transverse duodenal segment by the superior mesenteric artery, vein and nerve).  Splanchnoptosia signifies abnormal distalward movement (sinking prolapse) of viscera.  Atonia gastrica signifies abdominal relaxation which is preceded by thoracic relaxation.  Splanchnoptosia is included in the diseases of the vasomotor nerve (sympathetic) because the chief and final effect lies in its domain.  It is true that the thoracic (diaphragm) and abdominal wall (supplied by spinal nerves) are the primary factors in maintaining and fixing the thoracic and abdominal organs in their normal physiologic position, that relaxation of the thoracic (diaphragm) and abdominal walls are the primary factors in splanchnoptosia, and that in treatment the thoracic (diaphragm) and abdominal walls (areas of respiration) are the primary factors for consideration.  However, the damaging effects on the life of the patient rests on the seven visceral tracts (supplied mainly by the sympathetic nerve) viz: - (l) Tractus Respiratorius, (2) Tractus nervosus, (3) Tractus vascularis, (4) Tractus lymphaticus, (5) Tractus intestinalis, (6) Tractus urinarius, (7) Tractus Genitalis (in the order enumerated).

Pathological Relations.

    The object of this essay is to demonstrate the relations of splanchnoptosia (atonia gastrica) - to pathologic conditions, as deranged innervation, circulation, respiration, secretion, absorption, muscularis.  Relaxation of tissue - muscle, elastic, connective - means elongation of the same.  A triumvirate of conditions in splanchnoptosia demand skilled consideration viz.: Anatomy, Physiology and Pathology of the thoracic and abdominal viscera.
    In the first place we wish to employ scientific nomenclature only.  Splanchnoptosia indicates the ptosis (falling) of the thoracic and abdominal viscera and is the general term we will adopt.  It is constantly accompanied by relaxation of the thoracic (diaphragm) and abdominal walls.  Gastroptosia signifies abdominal ptosis (not merely of the stomach).  Atonia Gastrica signifies abdominal relaxation (and should for accuracy) displace gastroptosia.  However, since in stomachoptosia (ptosis of the stomach only) there are other associated visceral ptoses, the terms gastroptosia and atonia gastric are equivalent terms for they both include visceral ptoses and relaxation of the abdominal walls.  Enteroptosia is ptosis of the abdominal viscera in general and may include those of the thoracic cavity.  I shall reserve for the term enteroptosia the signification of ptosis of the enteron (duodenum, jejunum, and ileum). Coloptosia means ptosis of the colon, and its anatomic segments can be designated by an adjective as coloptosia transverse.
    Dr. Achilles Rose of New York and Dr. Kossman of Berlin should be credited for an attempt to introduce scientific nomenclature in this subject.
 

Fig. 170.  A female splanchnoptotic, a multipara, ventral view of relaxed abdominal walls. Observe that the relaxed abdominal walls pass sufficiently distalward to conceal the genitals from view.  Note the marked distalward position of the umbilicus. There is a depression at the epigastrium. The abdomen is flattened (changed in form), pendulous.

    Splanchnoptosia though a single unit is a general disease of the thoracic and abdominal viscera accompanied by relaxation of the thoracic and abdominal muscular walls.  In short splanchnoptosia prevails wherever the nerves of respiration innervate.  In splanchnoptosia not only several viscera are simultaneously affected but also the thoracic and abdominal walls are relaxed.  From an erroneous and limited view of the founder of splanchnoptosia (Glenard) and the acceptation of the error by numerous followers the idea has prevailed that ptosis of single viscera occur and to them numerous pathologic symptoms have been attributed.  Hence a stately literature has arisen from nephroptosia, stomachoptosia, coloptosia (transverse), enteroptosia, etc., etc.    On this error of single visceral ptosis has been founded the irrational surgery of so-called visceral pexies. One viscus may be afflicted with greater degree of ptosis than another, however, splanchnoptosia is a general process affecting the thoracic and abdominal walls, the visceral mesenteries and visceral shelves.

Historical

    Though Aberle, Rollet, Rayer, and Oppoltzer presented views of splanchnoptosia, it is probable that J. B. Morgangni (Italian, 1682-1771) was among the first to describe splanchnoptosia anatomically.  However, it is my opinion that Rudolph Virchow (1821-1902), my honored teacher, deserves the credit of calling the attention of physicians to splanchnoptosia.  He did this practically in 1853 in the fifth volume of his archives by an article entitled "An Historical Critical and Exact Consideration of the Affections of the Abdominal Cavity." The great genius of Virchow is displayed in this extensive autopsic investigation, thirty-two years before Glenard stamped his views on the profession.  He called especial attention to dislocation of viscera by peritonitis and advocated that they were the starting points of various symptoms of dyspepsia and indigestion.  To Kussmaul we owe the first definite views of gastropsia.  The French following Glenard view splanchnoptosia as a congenital affection.  The Germans are opposed to this view and maintain that splanchnoptosia is an acquired disease as through pregnancy, peritonitis, method of dress, avocation, living and so forth.  Others view splanchnoptosia as a combined effect, congenital predisposition and post natal acquisition.  Among some authors, chiefly German, the view is entertained that splanchnoptosia is a reversion to embryonic condition i. e., the viscera gradually reverse their embryonic growth and developmental process.
 

Fig. 171.  A lateral view of a female splanchnoptotic, a multipara, showing relaxed abdominal walls and umbilicus in a distalward location.  The abdomen is pendulous.  An attitude of lordosis is assumed for balancing support.

    The year 1885 was an eventful one in the pathology and treatment of relaxed abdominal walls, and consequent splanchnoptosia.  This was the period in which Glenard's labors became known.  But Glenard was not the only one working on the subject of splanchnoptosis.  Czerney and Keher, of Heidelberg, were presenting cases of visceral ptosis in their clinics in 1884 and as a pupil I gained 1884 and as a pupil I gained some views on the subject.  However, during a whole year's study in Berlin in 1885, with distinguished surgeons, the subject was not once discussed.  Subsequently, in a year's course of study with noted German specialists, Professor Schroder showed many subjects of splanchnoptosis.  Dr. Landau, who wrote "Wander Niere" (wandering kidney) and "Wander Leber" (wandering liver), gave extensive courses and discussed relaxed abdominal walls and consequent splanchnoptosia, in an interesting manner.  In fact, among Germans the term "Hangebauch" (hanging belly) has been common for twenty-five years.  Dr. August Martin presented instructive views on the subject in his excellent gynecologic course to physicians.  During the past twenty years I have pursued the study of splanchnology among hundreds of gynecologic patients, both medical and surgical, and in the personal abdominal inspection of six hundred adult autopsies.  In this paper I will present essentials of the knowledge gained in that experience.
 

Fig. 172.  A female splanchnoptotic with the ventral abdominal walls removed, presenting the viscera in an advanced state of splanchnoptosia.  The diaphragm is exposed showing the vena cava (v), the aorta (a) and the oesophagus (cc) projecting through it.  A typical splanchnoptotic relation appears with the liver and the stomach (st).  In this subject the stomach is practically vertical.  The right and transverse colon are forced in the greater pelvis with the main enteronic loop.  The flexura coli sinistra (sp) is dragged distalward.  The notable phenomenon in this subject is the hypertrophy and distalward movement of the right hepatic lobe - it is at its present stage a typical Riedel lobe.  General Views of Splanchnoptosia from Embryology.

    The abdominal viscera are maintained in their normal physiologic position by: (a) nerves and vessels; (b) peritoneum; (c) ligaments; (d) visceral pressure; (e) ligaments; (f) visceral shelves; (g) abdominal walls (muscular and osseous).  The first idea of importance is that no organ is absolutely or immovably fixed but that each viscus is endowed with a certain degree of movement, hence, the irrational surgical fixation (pexies) of organs is obvious.  The mobility of organs is due to various factors as: (a), attitude (prone or erect); (b), respiration; (c), material within the tractus intestinalis (ingesta, gas); (d), material within the tractus urinarius (urine); (e), muscular movement of viscera (rhythm) and abdominal wall; (f), gestation (material within the tractus genitalis).  Hence the abdomen should be viewed as occupied with viscera capable of more or less mobility - that fixation of abdominal viscera is abnormal, as e. g., peritoneal bands and visceral pexies.
    The embryology of the abdominal viscera is an unending source of interest.  It is not a surprise that after noting the development and axial rotation of the tractus intestinalis the view should be entertained that splanchnoptosia is a reversion of development and axial rotation of the digestive tube, i. e., that the tractus intestinalis (and its appendages) has retraced its lines of development.  In the early embryo the tractus intestinalis is a straight tube extending from mouth to anus in the middle line of the body (with the liver, spleen and pancreas).  Gradually with the progress of months the coecum passes from left to right across the ventral surface of the enteron (duodenum) and ends at birth in the region of the right kidney.
    The liver gradually passes from the middle line to the right proximal quadrant of the abdomen ending in the adult in the right concavity of the diaphragm.  This process of hepatic development is not complete at birth for the large (pot) belly of the child is due to a large liver.  In typical splanchnoptosia the position of the abdominal organs stimulate those of the embryo and infant.      Seeking a clue for treatment from embryologic phenomena it would be that splanchnoptosia is a general visceral disease and that rational treatment should be applied to the abdominal walls - not to single viscera as visceral pexies.

Clinical Aspects.

    From a clinical view certain organs may appear of more significance in splanchnoptosia than others.  For example the general surgeon who does not investigate the subject of splanchnoptosia centers his observations in idol worship on the liver, kidney, uterus or stomach and with his cranium completely occupied with visceral pexies (heathen gods in physiology) initiates his campaign of pexies or visceral fixation by suturing one of those organs to the abdominal wall.  What has he accomplished?  He has produced one lesion (visceral fixation) in attempting to improve another (supposed excessive visceral mobility).  Generally the worst is visceral fixation because the fixation is unphysiologic, irrational and affects but a detached part, a segment of the general splanchnoptosia.  The therapeusis should be applied to the abdominal wall.
    The embryologic view demonstrates that the seven visceral tracts (respiratorius, intestinalis, circularis, lymphaticus, nervosus, urinarius and genitalis) are practically alike affected - splanchnoptosia is a unit though a general disease.  However, the symptoms of splanchnoptosia of some visceral tracts are not so manifest as that of others e. g., the tractus nervosus is practically manifest as that of the urinarious and intestinalis.  Embryology suggests that viscera of late development and distant fixation from the radix mesenterica (coeliac and superior mesenteric arteries) are prominent in splanchnoptosia as the liver, stomach, colon, genitals, kidney.  They are distantly removed from the solid anchorage of the radix mesenterica and their solid fixation is hence more limited by peritoneal bands to the abdominal wall.
    For example the liver is practically fixed to the diaphragm only.  Its fixation to the radix mesenterica is limited by the anchorage it may obtain from the arteria hepatica ensheathed with its fibrous tissue from the aorta and its encasement of plexiform nerve network from the abdominal brain.  It must be admitted, however, that the late mesenterial development or expanding of the base of mesenteries. the increased areas of peritoneal adhesions (non-pathologic) to the dorsal wall as occurs in the liver, colon, stomach enteron serves as valuable fixation for the viscera.  These acquired basal mesenterial expansions produce compact solidarity of organs re-enforcing the supporting strength of the radix mesenterica (vascular).

GENERAL PATHOGENESIS OF SPLANCHNOPTOSIA.

    The method of origin (aetiology) and development of splanchnoptosia is explained by different authors through different views.  The divergent views entertained depend on the assumed beginning base - whether splanchnoptosia be due to (a) congenital predisposition; (b) acquired defects from life's opposing forces; (c) reversion to embryologic conditions or (d) a combination of the three preceding factors.
    First, a congenital predisposition suggests a characteristic body form or congenital weakness or fragility of tissue which predisposes the individual in the conflict of life's resisting forces to splanchnoptosia.
    Second, acquired defects producing splanchnoptosia, attempts to explain rationally the varied factors as rapidly repeated gestations, sudden loss of fatty tissues, pathologic conditions of the abdominal wall, body form, the influence of visceral motion in respiration, the evil effect of living and dressing (constricting bands), as well as various industries and traumata.
    Third, reversion to embryonic conditions would practically be a constitutional predisposition and hence belong to congenital predisposition.
    Fourth, the view which includes the combined factors of each theory (congenital or acquired defects) of splanchnoptosia is the more rational, because the disease is generally - prevalent among all nations.

Anatomy and Physiology

    In the pathogenesis of splanchnoptosia two factors must be carefully investigated, viz.: Anatomy and physiology.  The anatomy must not only include the elements - connective tissue, muscle, elastic fiber and bone - but bodily form, attitude, avocation, modes of life.  The physiology must include all the consideration of visceral functions - respiration, gestation, circulation, absorption, secretion and rhythm.
    Glenard a physician at Lyons, France, who practiced at Vichy observed that splanchnoptosia was closely related to neurasthenia and nervous dyspepsia.  Glenard observed three groups of symptoms viz: (1) (atonia gastrica) abdominal relaxation or lack of tone in the abdominal wall which presented: (a) deformity of the abdominal wall; (b) flabbiness, relaxation of the abdominal wall; (c) ease with which the hypochondrium may be compressed. (2) Splanchnoptosia presented: (a) (gastroptosia) splashing sounds in the stomach; (b) epigastric pulsation; (c) nephroptosia; (d) coloptosia transversum. (3) Enteroptosia presented three signs: (a) a palpable contracted band of the transverse colon; (Glenard's corde transverse colique) (b) the coecum; (c) the sigmoid.
    Glenard found at Vichy resort 148 cases of splanchnoptosia in 1,310 subjects - 11%.  He practiced among a neurotic class of subjects.  Glenard believed that the starting point of splanchnoptosia is the sinking of the flexura coli hepatica due to relaxation of the liganientum flexura hepatica.  He considered that ptosis of single viscera could occur in four conditions, viz. : (a) neurosis; (b) hepatic disease; (c) dyspepsia; (d) general or conditional illness.  The three main symptoms of splanchnoptosia according to Glenard are colic, stenosis, nephroptosia and hepatic deformity.  Glenard studied 40 splanchnoptotic autopsies and concluded that when the suspensory ligaments of the stomach and intestines are relaxed accompanied by the distalward movements of these viscera, stenosis will occur, and the coecum alone will maintain its normal form as it has no suspensory ligament.  Glenard's belt test of splanchnoptosia consists in the physician standing behind the patient, elevating the abdomen with the hands, and if it affords relief the diagnosis is confirmed.  The characteristic symptoms are: sensations of weakness, abdominal discomfort, constipation.
Space forbids further views from Dr. Frantz Glenard, the founder of splanchnoptosia whose excellent book of 875 pages lies before me.  It was published in 1899 and entitled the author to the pathologic eponym " Glenard's disease.  " The title of the book is "Des Ptoses viscerales Diagnostic et nosographie (enteroptosie - Hepatisme)." It is a monument of industry which will be admired for all time.
    Through all the pathogenesis of splanchnoptosia neurosis is a constant accompaniment, inseparably connected.  In 1896 Stiller published an article in which he claims that there is a neurasthenic stigma (stigma neurasthenicum), the floating tenth rib (costa decima fluctuens).  Stiller believes that splanchnoptosia rests on embryologic defect (vitium primae formationis).  This should be known by the pathologic eponym "Stiller's costal stigma." This view is supported by finding nephroptosia in children.  Splanchnoptosia subsequent to parturition (puerperium) should be designated by the pathologic eponym "Landau's splanchnoptosia.  "
    Splanchnoptosia accompanying chlorosis should be designated by the pathologic eponym "Meinert's splanchnoptosia.  " Dr. Einhorn believes that constricting bands (corset) play a large role in the pathogenesis of splanchnoptosis.
 

Fig. 173.  Represents the abdominal and thoracic organs separated by the diaphragm. The pillars or crura of the diaphragm (AC and A C) are marked, demonstrating that inspiration drags (forces) the thoracic organs distalward.  Observe that the pericardium is solidly and firmly fixed to the diaphragm, hence in inspiration, when the diaphragm moves distalward, the heart, lungs, and great thoracic vessels must accompany it.

Keith's Theory.

    In the pathogenic theories of splanchnoptosia the latest most elaborate and comprehensive is that of Arthur Keith, in the Hunterian lectures of 1903, published in the London Lancet, March 7, and 14, 1903.  Mr. Keith claims in these most excellent and well studied lectures that splanchnoptosia is the result of a vitiated method of respiration.  Keith's investigations of splanchnoptosia were conducted on an anatomic base rather than a clinical one and include vast labors based on the solid ground of nature.  I wish here to acknowledge my indebtedness to Mr. Arthur Keith.
Additional Factors in Etiology.

    1.  Intra abdominal pressure.
    Factors which increase intra-abdominal pressure: 1, Gestation. 2, Food. 3, Fluid.    4, Meteorism.  5, Adispose deposits.  6, Ascites. 7. Tumors.  8, Pleurisy.  9, Feces. 10, Urine. 11, Gastro-duodenal dilatation. 12, Coughing. 13, Contracted pelvis. 14, Blood and lymph volume.
    2.  Relaxed abdominal walls.
This consists in elongation and separation of fascial and muscular fibres of the anterior abdominal walls, the thoracic and pelvic diaphragm.
    3.  Compression of the transverse segment of the duodenum by the superior mesenteric artery, vein and nerve.
    4.  Congenital defects in the nervous, muscular and visceral systems.
    5.  Defective food and excessive labor.
    6.  Lordosis or anterior curvature of the vertebral column enhances
splanchnoptosia.
    7.  With the progress of relaxed abdominal walls there is a disproportionate or abnormal relation established between the nervous and muscular systems, and coordination is defective and hence nourishment and function are also defective.  The trauma to the sympathetic nervous system produces excessive, deficient or disproportionate secretions and peristalsis in the viscera, hence nourishment is again defective.  With the advance of splanchnoptosia the blood and lymph vessels become stenosed. their mechanism disturbed, producing irregular circulation and hence nourishment is again defective.
    Splanchnoptosia is a kind of neurosis.  It is devitalizing of the sympathetic system in which vitality of the neuro-vascular visceral pedicle is impaired, it becoming elongated, stretched.  Perhaps the elastic tissue is degenerated.
    Notwithstanding the manifold theories and dreams of respected authors and the easily recognized original work of industrious investigators in splanchnoptosia I am still convinced that one of the great factors of splanchnoptosis is the waist or constricting band, not merely the corset, for a corset may be worn so loose that it practically does no damage.  During the past 15 years Dr. Lucy Waite and the author have dissected over 35 female bodies for practical topographical and applied anatomy of the abdominal and pelvic viscera.  We opened the cadaver and then with the two hands as a corset band or any form of waist band the body was compressed and the result on the abdominal viscera noted.  What will happen in tightening the waist band?  The answer is clearly evident in watching the progress of constricting the band.  First the right more mobile kidney moves medianward and ventralward, compressing the junction of the descending and transverse duodenal segments, ending in a position almost in the middle of the abdomen.  The kidney suffers the most movement dislocation of any abdominal organ.  The liver is compressed as is shown in autopsies in the corset liver, the gallbladder projects ventralward, allowing stagnation of bile and subsequent formation of hepatic calculi.  The daily effect of the waist or constricting band is diminutive, but continued from week to week, month to month, and year to year, its end results are enormous in changing and damaging structure and function.  It constricts the right colon, compromising cecal evacuation, the canalization of the ureter, renal and ovarian veins and inferior vena cava.  The nephroptosia elongates the renal vessels especially, the artery which is sheathed in a network of ganglia not only traumatizing them, but, by tugging and dragging on the abdominal brain, the trauma produces the stigmata of hysteria and other neuroses.

Peritoneal and Omental Adhesions.

    I wish here to direct the attention of the practitioner to a fertile field in the etiology of splanchnoptosia which in short is peritoneal and omental adhesions.  I have published numerous articles during the past decade advocating the evil influence of peritoneal adhesions on the abdominal viscera.  I am gratified to observe that several physicians as Robert T. Morris and several others are realizing the value of these views.  In hundreds of autopsies I have noted the structures of the genitals, appendix, gall-bladder and sigmoid apparently ruined by contracting peritoneal adhesions distorting the viscera into a shapeless mass.
    I have explained for years how these peritoneal adhesions induced by muscular trauma, created distorted physiology, ending in appendicitis, cholecystitis, sigmoiditis and salpingitis.  Peritoneal adhesions fix the viscera in a single mass so that the several viscera cannot glide on each other.  The solid visceral mass acts like a solid piston in the abdomen forcing the viscera distalward.  The omentum is frequently found extensively adherent to the pelvic viscera which drags the viscera in the proximal abdominal distalward at every respiration.  Peritoneal adhesions are extensively vicious factors in compromising visceral anatomy and physiology and abetting remarkably splanchnoptosia and other diseases.

General Views.

    If single viscera become markedly splanchnoptotic, prolapsed by accident, trauma, the general painful neurotic symptoms of splanchnoptosia are markedly absent.  The existence and results of splanchnoptosia are not fully explained.  The difficulty has its seat: (a), in the determining of the exact or normal position of viscera; (b), the exact forces which establish an organ in its position; (c), the views of the cause or origins of splanchnoptosia are so various as to obscure the picture; (d), the symptoms are so complex that splanchnoptosia appears like a conglomerate disease.  The confusion is due to the multiple points from which the disease has been established.  The history of splanchnoptosia is that of displacement of single organs.
    Glenard, though comprehending a limited field, combined them into a single disease, a unit which should now be termed splanchnoptosia because it involves the thoracic and abdominal viscera (as well as their respective enclosing walls).  Splanchnoptosia is a disproportion, a disturbed relation between cavity lumen (chest, abdomen) and contents (viscera) not only anatomically but physiologically, that is the functionating organs are working in a distorted, dislocated position hence experiencing a change of form and function.
    The thoracic and abdominal cavities should be viewed as one general lumen, simply divided by the diaphragm.  The vertebral column may be viewed as a mast maintaining its erectness by means of the erector spinae muscles.  The ribs, sail arms, receive support from the fixed mastoid process through the sterno-cleido mastoid muscle.  The viscera are anchored, fixed to the dorsal wall - the great mast.  The solid, visceral contents are confined, maintained to the mast by the circular, fibro-elastic muscular band - the thoracico-abdominal walls.
    The physiology of viscera must be credited with the greatest role in splanchnoptosia for during their maximum functions the weakest and most defective anatomy begins to yield - especially in the diaphragm (in inspiration), in the abdominal walls (in gestation, ingesta, gas, defecation); in the circulation, variation of the volume of arterial, venous and lymphatic fluids.  Intra-abdominal pressure is the contraction of the circular Libroelastic muscular abdominal wall plus atmospheric pressure.

Mechanism of Splanchnoptosia.

    We know that the extra-abdominal pressure is greater than the intra-abdominal pressure, for, on peritoneal section the atmosphere rushes in with an audible sound.  This view would oblige the visceral supports (mesenteries and ligaments) to assume the office of not only anchorage but that of fixation (and support).  Viscera are essentially supported by underlying ones (visceral shelves) like bricks in a wall.  Schwerdt estimates that the viscera mesenteries or ligaments support about one-eighth of the organ weight.  The fixation of the viscera to the (dorsal) abdominal wall and their share in the visceral support might be compared to a boat at anchorage.  The boat rests on the water, which represents the compact supporting visceral shelves (like bricks in a wall).  The anchor cable (mesenteries, ligaments) merely decides the limit or space range of the boat (in fact seldom becoming tensionized).  The banks of the water represent the abdominal wall.
    The principal support of the viscera are: (a), the compact underlying visceral shelves; (b), the abdominal wall; (c), the visceral supports (mesenteries, ligaments) perhaps suspending one-eighth of the weight of the viscera.  By placing a body erect and removing the ventral wall the viscera pass distalward, prolapse, sink, placing the visceral mesenteries and ligaments on tension.  The visceral mesenteries or ligaments might be compared to a string attaching a specimen in a fluid filled jar, to the cork.  The string support is limited, but without it the specimen would sink or rest on the floor of the jar.
 

Fig. 174.  This illustration demonstrates the dorsal fixation and location of the mesenteries of the abdominal viscera.  The dotted spaces surrounded by black lines are the bases or areas of mesenteric insertion. 1, Ligamentum triangulum sinistrum; 2, ligamentum suspensorium (teres) hepatis; 3.and 5, vena cava (distal) ; 4, arteria phrenica dextra; 16, omentum gastro-hepaticum; 15, ligamentum gastro-phreneum; 8, arteria coeliaca; 7, arteria gastrica; 12, arteria linealis; 1,% ar.teria hepatica; 14, spleen; 17, mesocolon transversum; 10, ligamentum casto-coelicum; 11, kidney; a, omentum gastro-splenici-im; 18, shows dot between blades of omentum majus; 19, adrenal bodies; 20, foramen winslowi; 22, arteria mesenterica superior; 23, arteria renalis dextra; 24, mesocolon sinistrum. (Insertion line of its two blades.)  25, duodenum transversum (covered by peritoneum) ; 26, mesocolon dextrum. (Insertion line of its right and left blade.) 27, ureter (shimmering through the peritoneum) ; 28, aorta; 29, mesenteron; 30, arteria mesenterica inferior; 31, arteria colica dextra; 32, arteria iliaca communis; 33, arteria iliaca externa; 34, arteria iliaca interna; 35, mesosigmoid. (Double blades.) 36, uterus; 37, urinaria vescicae; 38, ligamentum rotundum uteri; 39, ovarium; 40, oviductum (sinistrum).

    The abdominal viscera are located more distalward while in the erect attitude (1 inch)  than  the  prone  position.  The  more  solid  organs as liver, kidneys, uterus and foreign material occupied segments of the tractus intestinalis pass distalward with more facility while organs containing gas pass proximalward with more facility.  Abdominal organs are limited in motion through the mesenteries, ligaments and adjacent organs.  The abdominal wall exercises an opposition to the static pressure of viscera.  With increased contents (ingesta, fluids, gestation) the ventral abdominal wall yields.  If a body be hung by the head and the abdomen incised the viscera will prolapse.  In the resting upright attitude the abdominal wall offers but passive pressure opposition to the viscera.
    The reason for the slow progress in the knowledge of splanchnoptosia among medical men is: (a), the autopsic reports, for the past years, have been of limited practical value as regards splanchnoptosia.  The reason of this fact is that when the subject is in the prone but especially the dorsal position the organs assume chiefly their normal physiologic location.  The pathologist does not appear to have anything to report; (b), the clinician seldom witnesses an autopsy on a previously diagnosed splanchnoptotic.  Hence the autopsist and clinician have practically opposed each other - possessed no views in common - did not agree and also seldom met at an autopsy.  The pathologist in the morgue returned no evidence to aid the clinician on the living.  In the symptomatology heretofore a tendency has existed to attribute excessive symptoms to single splanchnoptotic organs, especially the genitals. kidneys, stomach and liver, and deficient symptoms to other organs as the colon, enteron, vascular system and nervous system.  Splanchnoptosia is a unit - a general disease.  Also excessive symptoms have been attributed to single organs in order to prepare the road for the irrational pexy.

ANATOMY AND PHYSIOLOGY OF SPLANCHNOPTOSIA.

ABDOMINAL WALLS.

    The abdominal walls consist of oblique, perpendicular and transverse muscular layers woven in a powerful fascial band.
    All abdominal muscles are fixed on bony parts, as the costal, iliac and pubic crests, as well as the vertebral column, while the diaphragm is inserted into the ribs and vertebral column with its vault fixed by the pericardium.  The abdominal wall is covered externally by skin and internally by peritoneum - both powerful and elastic membranes.  Certain weak, yielding muscular and fascial lines exist in the abdominal walls, viz.:
    1.  Musculi recti abdominales arise from the pubic crest and become inserted into the ribs and os sternum.  The two recti muscles which lie parallel to each other are the ones which preserve the delicate visceral poise.  Slight extra intra-abdominal pressure produces diastases of the muscles.  In splanchnoptosis, the recti show (a) diastases, (b) elongation, and (c) separation of the fibres, (d) extensive thinning and flattening, and (e) atrophy.
    2.  The fascial lines which yield in splanchnoptosia are (a) the linea alba, which I have noted three inches wide, the fascial fibres are elongated and separated, making the abdominal wall very thin and lax in the median line, (b) the lineae semilunaries which also become quite thin and lax, the fascial fibres elongate and separate, (c) the fibres of the linea transversae, inscriptiones tendinae or the abdominal ribs, which elongate and separate.
 

Fig. 175.  Represents the separation and elongation of the recti abdominales in splanchnoptosia.

    The physiologic action of the abdominal wall is a combined one, as the varied direction of its muscular fibres indicate.  We may indicate its physiologic action in certain directions. 1. The abdominal wall acts as a circular band, to fix and support the abdominal viscera as the neuro-vascular visceral pedicles are not intended for primary mechanical visceral support. 2. The abdominal wall is a highly elastic apparatus.  It distends and contracts fitting the abdominal contents.  The skin and peritoneum are exceedingly elastic.  Observe how the skin and peritoneum will return without a fold to the normal state after distention from gestation, ascites or tumors, etc. 3. The physical function of the abdominal wall is aided by its capacity of contraction and of extension in respiration, defecation, urination, expulsion of uterine contents; in laughing and coughing.  In short it is the function of the abdominal wall to contract and dilate during the volume changes of the abdominal contents, as well as the volume changes in the thorax. 4. The physiological function of the abdominal wall is to maintain a vigilant guard, a vigorous but delicate elastic regulation of abdominal visceral contents.  The elastic spanning of the abdominal walls maintains a delicate visceral poise.
 

Fig. 176.  The diaphragm. (Ventro-distal view.) This illustration presents the central tendon of the diaphragm with its important long right (RC) and short left (LC) crus.  The right diaphragmatic crus extends to the (IV) lumbar vertebra.  The crtira of the diaphragm have a fixed immobile spinal insertion and forcible drag the central tendon of the diaphragm with its attached percardium distalward at every inspiration.  In the physiology of the stronger inspiration and weaker expiration begins splanchnoptosia.  The inspiratory muscles from sheer force - and to the crura must be attributed the chief factor.

Etiology of Relaxation.

    Relaxed abdominal walls arise in various forms in different subjects.  Not all thin abdominal walls are relaxed, neither are all relaxed abdominal walls thin.  The elements, the  fascial,  elastic  and muscular fibres must be separated and elongated to constitute relaxed abdominal walls, which are best observed in the erect attitude.  The causes of relaxed abdominal walls lie in the elements of the wall itself, viz. : fascia, muscle, peritoneum, skin and elastic fibres.  The fine tonus of the wall, its delicate elasticity may be lost.  Its fascia and muscular fibres are separated and elongated.  It is flaccid and hangs excessively distalward and the unsupported viscera follow it.  There seems to be a limited life for the abdominal walls, as there is for the utero-ovarian vascular circle of the genitals.  For the abdominal walls begin, as a widely applicable rule, to relax at about 35, and continue to relax or atrophy to the end of life.  There can be no doubt that the elastic fibres elongate and separate, perhaps also atrophy, for the abdominal wall is not only relaxed but is thinned, attenuated.  It may be that at a time of malnutrition the abdominal walls become relaxed, never subsequently recovering their normal state.  Relaxed abdominal walls frequently follow continuous fevers, gestation, ascites or any factor which increases intra-abdominal pressure.  The most frequent supposed cause of relaxed abdominal wall is rapidly repeated gestation.  In every gestation physiologic dastasis of the musculi recti abdominales occur.  It is not infrequent to find the recti muscles three inches apart at the end of gestation.  But relaxed abdominal walls are not confined to women, as the testimony of the 450 recorded autopsies of men proved, there being frequent splanchnoptosia in these subjects.
    The pelvic, thoracic and abdominal viscera are liable to frequent dislocation.  In visceral inspection of 600 adult autopsies I found local peritoneal adhesions in over 80 per cent.  In other words, more adult subjects have dislocated viscera from peritoneal adhesions than normally situated ones.  The neuro-vascular visceral pedicle, the mesentery, becomes elongated and its root glides distalward on the dorsal abdominal wall.  The distalward dislocation of the dorsal attachments of the mesentery allows (a) elongation of the mesentery, (b) an excessive range of visceral motion, (c) the abdominal and the pelvic organs pass distalward and become impacted in the pelvis, (d) Splanchnoptosia compromises circulation and deranges absorption secretion, (e) disorders peristalsis, (f) traumatizes nerve periphery, (g) it impairs nourishment, (h) it produces especially indigestion, (i) it invites constipation.  Splanchnoptosia accompanies a defective nervous system of perhaps congenital origin.  As it increases every decade, after 35 years of age it is liable to cause stenosis or partial obstruction of the canals, tractus intestinalis from traction of one part and elongation of other parts of the mesenteries.  It compromises canalization.  The effects of splanchnoptosia (Glenard's disease, 1884), on individual abdominal organs, are varied and numerous.

Intestinal Tract.

    The tractus intestinalis is affected chiefly by: (a), compromising of circulation, blood and lymph supply, i. e., congestion and decongestion, (b) trauma of nerve centers, strands and nerve periphery, (c) complication from loss of peristalsis and atony of bowel muscle, (d) gastrointestinal catarrh and indigestion from excessive, deficient and disproportionate secretions, absorptions.  Also dragging on the abdominal brain, an independent nerve center producing nausea, neurosis, headache, reflexes, and deranges secretion and motion on other viscera. (e) Dilatation of the stomach and duodenum, caused by the superior mesenteric artery, vein and nerve, obstructing the duodenum at this point where they cross the transverse segment.  The stomach is especially liable to dilatation from the above causes, where the prolapse of the enteron (enteroptosia) is sufficiently advanced to allow the enteronic loops to pass distalward into the lesser pelvis and particularly when the subject lies on the back, for then the superior mesenteric artery, vein and nerve are put on a stretch and they constrict vigorously the transverse portion of the duodenum. (f) The enteronic loops being dislocated (enteroptosia) into the pelvis, peristalsis, absorption secretion, circulation and nerve periphery are compromised, followed by catarrh, constipation and indigestion. (g) The colon, especially the colon transversum, may lie in the lesser pelvis, producing similar compromising circumstances as in the enteron. (h) The appendages (liver, pancreas, and spleen) of the tractus intestinalis, in ptosis are compromised in circulation, secretion, absorption, peristalsis and nerve periphery.
 

Fig. 177.  The diaphragm. (Dorsal viem,.) This illustration presents the central tendon and the attached Pericardium wit], the powerful right and left crura.  During inspiration the diaphragmatic crura, immovably fixed by insertion in the spina column contract, drawing the tendon of the diaphragm, to which the pericardium is attached,  distalward.  Splanchnoptosia begin the respiratory organs, i. e., in the conquering  of the inspiratory muscles R. A. F., right acute fibres.

Genital Tract.

    In splanchnoptosia the genital tract suffers, especially in circulation and nerve periphery as well as secretion and absorption.  Uteroptosia may arise to such an excessive degree of mobility that the uterus may be forced proximal to the umbilicus and in any portion of the great pelvis.
 

Fig. 178.  Proximal view of the pelvic floor.  This illustration is drawn from my own dissection (by Dr. toms mimic or simulate Shoter) to present the diaphragms pelvis.

Fig. 179.  Distal view of the pelvic floor.  This cut is drawn by Dr. Sholer from my own dissection.  The proximal and distal fascia of the levator ani is removed as in previous fig.

Urinary Tract.

    The urinary tract suffers in splanchnoptosia, chiefly from dislocation of the kidney (right) nephroptosia.  From several hundred autopsic inspections and living abdominal sections, I can say that in many subjects the kidney (right) has extensive motion and is significant in gynecology, as its symptoms mimic or simulate genital disturbances.  In my practice 60 per cent of subjects possess a kidney range of 4 inches, 2 inches proximalward and 2 inches distalward.  Large numbers of subjects have a right kidney range of 3 inches, 1 1-2 inches proximalward and 1 1-2 inches distalward.  The mobility of the right kidney is of extreme importance in multipara have a movable kidney nephroptosia - proved by examination in the horizontal and erect positions.  The mobility of the right kidney is due to (a) the longer right renal artery, (b) the liver through the diaphragm forces the right kidney distalward, (c) muscular trauma of the diaphragm, quadratus lumborum and constricting waist bands, (d) absorption of pararenal fat, (e) the abdominal cavity of woman is funnelshaped, with the large end of the funnel distalward and hence the kidney receives less support distally than it does in man, (f) subinvolution attacks the "Wolfian body." (g) The erect attitude.  By continual relaxation of the abdominal walls its physiological and anatomic functions are impaired.  The physiological regulation and chief anatomic support of the viscera are unbalanced, and the delicate visceral poise is lost.  The abdominal viscera move distalward, become prolapsed following the relaxed abdominal walls.  The condition of relaxed abdominal walls is followed by splanchnoptosia.  Of the three great systems of the abdominal viscera, the tractus genitalis, tractus urinarius and the tractus intestinalis, the last suffers the most severely.  Relaxed abdominal walls are followed by dislocated viscera.  A viscus is dislocated when it is permanently out of position.  In general a dislocated viscus suffers from trauma of its nerve periphery and its blood, and lymph vascular system is compromised.  Splanchnoptotic organs become hypertrophied.  Also the nourishment of a dislocated viscus is defecive, irregular.  Dislocated or prolapsed viscera are the segments of vicious circles.  Relaxed abdominal walls are followed by partial hernia, especially in the pouches of the most yielding parts, as the linea alba, supraumbilical and the lineae semilunares or the various defective rings.
    In the following scheme are noted not only the great factors in splanchnoptosia, but other detailed factors:

The diaphragm.

    The diaphragm is a muscular barrier anchored like a buoy between the thoracic and abdominal viscera.  It rises and falls with the ebb and flow of respiration.  There is a visceral tide - a stronger inspiratory ebb and a weaker expiratory flow.
    It is a muscular dome for the abdominal viscera and a muscular floor for the thoracic viscera.  The viscera move to and fro with the diaphragm.  The average height of the diaphragm is on a level with the fifth costal cartilage and its general fluctuating range level is two inches.
    The variation in the level of the diaphragm represents the phases of a respiratory rhythm.  The distalward displacement of the diaphragm is an essential feature in splanchnoptosia.  For the liver, spleen, stomach and kidneys are firmly bound to its abdominal surface.  The diaphragm is supported in its position first: by the abdominal muscles forcing the abdominal viscera proximalward against its distal concavity; second, it is supported by the thoracic viscera; by fusion of the pericardium to its proximal surface, the heart, great thoracic blood-vessels, trachea and lungs which attach the proximal surface of.the diaphragm to the dorsal thoracic wall; third, the costal support is from the 6 lower ribs and spinal support from the I, II and III lumbar vertebrae.  Hence the abdominal, thoracic, costal and spinal supports are required for a normal position of the diaphragm.  A defect in any support (contraction or relaxation) of the diaphragm prepares the road for splanchnoptosia.
The crura of the diaphragm send strong fibers to the pericardium, (through the central tendon) roots of the lung (reflected pleurae), vena cava, the great thoracic vessels, connective tissues of the oesophagus and trachea - all diaphragm and thoracic viscera, being solidly and compactly bound together.  With each inspiration the crura of the diaphragm contract on their immobile spinal origin - and draw the thoracic viscera (and force the abdominal) distalward.  The vigorous contraction of the diaphragmatic crura (in inspiration) is the most important factor in producing incipient splanchnoptosia.  For reasons, not fully known, the (inspiratory) diaphragmatic supports of certain individuals yield and splanchnoptosia begins.  The yielding of the diaphragm supports occur first in the muscles of inspiration.  The diaphragm (especially the crura) during contraction (inspiration) forces the mediastinal contents - heart (pericardium), trachea and oesophagus distalwards, which elongates the mediastinal mesentery, composed of pleural reflections.  By viewing a patient laterally with the fluoroscope the heart may be observed to move proximalward and distalward during respiration.  The range of proximalward and distalward action of the heart (and consequently the diaphragm which is fixed to the pericardium) is considerable especially in subjects with abdominal type of respiration and in such the distalward movements of the heart is the greater.

 Influence of Diaphragm in Splanchnoptosia.

    When the diaphragmatic supports begin to yield the inspiratory distalward movements (displacements) of the thoracic viscera are a cause of incipient splanchnoptosia.  Since the pericardium is not only solidly attached to the diaphragm but is also solidly attached to the roots of the lung, thoracic vessels, oesophagus and trachea a movement of the diaphragm (induced chiefly by crural contractions) must be accompanied by movements of the thoracic viscera.  In short, the diaphragm is connected to the mediastinum, pericardium root of lung, thoracic vessels, oesophagus trachea, vagi and the respiratory expansion is gained chiefly by a distalward movement of the diaphragm accompanied by the thoracic viscera - lungs and heart.  It is when this distalward movement of the diaphragm (inspiration) becomes excessive (from relaxation of diaphragmatic supports) that splanchnoptosia begins. (We will at present not dispute that atonia gastrica abdominal relaxation develops concomitant as respiration includes the abdominal muscles.) The diaphragm is a digastric muscle with two origins viz.: (a) spinal origin (vertebral column - crura - and arcuate fibers; (b) ventral origin (from the 6 lower ribs) and by the contractions of its two bellies enhances thoracic space for inspiration, therefore its share in incipient splanchnoptosia is evident.  From the above evidence it is obvious that the distalward movements of the diaphragm (in respiration) will depend on the opposition offered by the abdominal viscera through the strength of the abdominal wall, as well as the mobility of the 6 lower ribs.  If the muscles of the abdominal wall offer normal resistance to the distalward movements of the abdominal viscera the diaphragm will be supported by the abdominal viscera (liver, spleen, pancreas, stomach, kidneys) and cannot descend.  However, if atonia gastrica (abdominal relaxation) exist the diaphragm shares in the thoracic and abdominal splanchnoptosia with consequent abdominal type of respiration.  If, however, the contraction of the diaphragm (crura) cannot force the abdominal viscera distalward the thoracic viscera must expand (in respiration) within the thorax with consequent thoracic type of respiration.  Splanchnoptotics experience abdominal types of respiration.
 

Fig. 180 represents a normal transverse segment of the abdominal wall.  About the umbilicus. 1, rectus; 2, skin; 3, fascia; 4, fascia; 5, external oblique; 7, transversalis; 8, peritoneum; 9, linea semilunaris ; 10, linea alba; 11, spinal muscles; 12, quadratus lumbarium; 13, psoas muscle; 15, vena cava, and 16, aorta.

Fig. 181 illustrates a transverse section of the abdomen, about the umbilicus of a splanchnoptotic.  The fascial and muscular fibres of the abdominal wall are elongated and separated, the primary factor in the splanchnoptosis, 1, rectus; 2, linea alba; 3, 5, linea semilunaris; 6, skin; 7, fascia; 8, external oblique; 9, internal oblique; 10, transversalis; 11, transversalis fascia; 12, the peritoneum; 13, vena cava; 14, aorta; 16, quadratus lumborum; 15, psoas; 17, vertebra; 18, spinal nucleus.

Spinal Segment.

    The spinal segment of the diaphragm has a constant function, i. e., its contraction (inspiration) forces both thoracic and abdominal viscera distalward.  The ventral segment of the diaphragm is otherwise for its action on the lower 6 ribs depends on the position of the ribs.  If the lower 6 ribs become misplaced the action of the diaphragmatic muscles become altered.  The abdominal type of respiration signifies that the pulmonary space is gained chiefly by the expansion of the distal end of the thorax.  The thoracic type of respiration signifies that the pulmonary space is  gained mainly by the expansion of the proximal end of the thorax. 1. It may be noted therefore that the fixation of the thoracic viscera is through: (a) the thoracic, diaphragmatic and abdominal muscles; (b) thoracic vessels; (c) the cesophagus; (d) the trachea; (e) the pericardium; (f) dorsal thoracic mesentery (reflected pluree); (g) the thoracic fascia; (h) vagi and phrenic nerves. 2. The motion of the thoracic viscera is noted through: (a) the expansion (inspiration) of the chest; (b) the movements of the diaphragm; (c) the motion of the abdominal wall.  The thoracic diaphragm is one of the most important respiratory muscles.  It is innervated by a single nerve (Phrenic) therefore it contracts, functionates, as a single muscle.  Diaphragma thoraces serves as a floor, a support for the thoracic viscera. its peripheral origin is from the sterum, ribs (lower 6), and lumbar vertebrae (I to III).  Its fibers are inserted in the central tendon.  Its special fixum punctum is the vertebral column.  Its punctum mobile is the centrum tendineum with the two apertures (vena cava and oesophagus.  The aortic aperture is practically immobile).  Diaphragma thoraces resembles diaphragms pelvis in physiology and anatomy.  Both have (a) a similar fixum punctum, (circular bony origin); (b) similar punctum mobile (central tendon); (c) both support superimposed viscera; (d) both have 3 apertures for visceral transmission; (e) both diaphragms are respiratory; (f) both muscles by constriction limit the apertures of visceral transmission; (g) both contract as a single muscle; (h) both share in splanchnoptosia.  They differ in that contraction of the pelvic diaphragm draws the 3 visceral apertures proximalward, and ventralward, while contraction of the thoracic diaphragm draws the visceral apertures distalward and dorsalward.  Distalward movement of the thoracic diaphragm in splanchnoptosia traumatizes, injures, stretches the phrenic and vagi nerves hence will derange respiration (inducing neurosis).
    Derangement of respiration is clinically evident among splanchnoptostics.

Fixation and Motion of the Thoracic Viscera.

    Splanchnoptosia begins in the deranged anatomy and physiology of the tractus respiratorius.  At every inspiration the crura of the diaphragm contracts on the pericardium (which is fixed to the diaphragm) which in turn drags on the great thoracic vessels which finally tugs on the mediastinal structures (oesophagus, trachea and pulmonic mesentery) carrying the thoracic viscera and forcing the abdominal viscera distalward.  The viscera are poised between the two great systems of inspiratory and expiratory muscles which are arrayed in rhythmic opposition during life.
    The victory of the inspiratory muscles over their opponent, the expiratory muscles, is the beginning of splanchnoptosia.
    Students should be taught that not only the muscles of the thoracic wall belong to respiration but also the abdominal muscles are an integral part.  The thoracic and abdominal muscles are a breathing apparatus.  Man's respiratory muscles extend from face to pelvic floor.
    The XII intercostals with the I and II lumbar nerves practically supply the muscles of respiration which extend from manubrium to symphysis pubis.
    A knowledge of the movements of the viscera during respiration indicates the method and location of their fixation within the thoracic and abdominal cavities.
    Any prominent deviation of the respiratory muscles is accompanied by deranged visceral movements resulting in splanchnoptosia, disordered anatomy and physiology.  We will devote a few remarks to the diaphragm in splanchnoptosia.

The Respiration in Splanchnoptosia (irregular).

    The prominent symptoms of the respiration in splanchnoptosia are shortness of breath, irregular long respiration, difficult breathing and asthmatic breathing with cardiac palpitation.  The relaxed abdominal muscles, the respiration muscles, have lost their power and perfect muscular relaxation is not possible.  Complete respiration is muscular relaxation and contraction.  In the erect attitude the dislocated liver drags on the diaphragm through its coronary ligaments, and through the vena cava.  Besides, the liver is in turn dragged on by the tractus intestinalis through its two ligaments attached to the liver, viz., ligamentum hepato-colicum and ligamentum hepato - cavoduodenale, resulting in disturbance of a respiratory organ - the diaphragm.  The irregular respirations - frequent symptom of relaxed abdominal walls and consequent splanchnoptosia - is another link in the viscious circle, because it imperfectly and irregularly oxidizes the blood, disturbing nutrition.

CONSIDERATION OF VISCERAL FIXATION IN SPLANCHNOPTOSIA.

Fixation and Movement of Abdominal Viscera.

    (a) Abdominal viscera fixed immovably in position (to radix mesenterica) not sharing in respiratory movements (duodeno-jejunal flexure and body of pancreas).  I examined the viscera of numerous quadrupeds, some 20 monkeys, apes, baboons (i. e., animals which sit or stand practically erect in life) and several hundred humans.  The testimony from the investigations is that the more the animal lives in the erect attitude the more firmly and extensively are the viscera fixed to the abdominal walls.  The extensive and firm fixation of abdominal viscera to the abdominal walls found in man (and erect apes) marks the final process developing in erect animals.  However firm and extensive the fixation of viscera to the abdominal wall, it plays a minor role in the prevention or cure of splanchnoptosia, in comparison with diaphragm and muscular abdominal walls.  I found marked relaxed abdominal walls and advanced splanchnoptosia in erect apes.  The method of abdominal visceral fixation may now be considered.
    Through the courtesy of Prof.  W.  A. Evans I was sufficiently fortunate to secure an autopsy on the orang recently dying in the Lincoln Park Zoologic department.  This human - like orang, a native of Borneo, was a female some 10 years of age and weighed 80 pounds.  The thoracic and abdominal viscera resembled those of man in relation (to peritoneum), form, fixation and motion.  The appendix was precisely typical of man, six inches in length, and was located in the pelvis (woman's appendix lies in the pelvis in 48 per cent of subjects).  The coecum rested on the psoas muscle, however, since the orang does not walk (but sits) the psoas had not produced sufficient trauma to cause pericoecal peritoneal adhesions.  The colon in all its segments resembles that of man in relation, form, fixation and motion.  The transverse colon measured 12 inches while the sigmoid flexure measured 13 inches in length.
    In one matter of degree (not of difference) the colon presented more numerous appendicae epiploicae than that of man.  The fixation of the viscera on the dorsal abdominal wall, the location of the mesenteries, and the radix mesenterica, the relation of pancreas, liver, duodenum, stomach and spleen were duplicates of homo.  The omentum majus resembling man's (except its blades had not completely coalesced) ceased at the flexura hepatica.  The tractus genitalis in relation (to peritoneum), form, fixation and location precisely resemble that of man.  In the orang the relation (to peritoneum and viscera) of the diaphragm, the most important respiratory apparatus, precisely resembles that of man in location, relation, fixation and motion.  The psoas muscle was relatively not so large as that of man because the orang does not walk (practically lives sitting).  In the orang especially, but also in the human-like apes, baboon, monkeys I found that their viscera were similarly developed and point for point was fixed in detail similar to those of man.  The method of visceral fixation in man is due to respiration and attitude.

Radix Mesenterica.

    The radix mesenterica or root of the mesentery consists of the coeliac axis and superior mesenteric artery encased by its fibro-muscular sheath (prolonged from the sheath of the aorta and diaphragmatic crura).  The root of the mesentery (major visceral arteries) arise from the aorta as it enters the abdominal cavity between the crura diaphragmatica and at the junction of the intercrural arch through which the aorta encased in its fibrous sheath enters the abdominal cavity may be termed the hilum of the peritoneum.  In a limited area located at the root of the mesentery only is the abdominal viscera immovably fixed in position.  The root of the mesentery is the solid immovable center around which the abdominal viscera play in the ebb and flow of respiration.
    From the root of the mesentery (coeliac and superior mesenteric arteries) radiate strong fibrous bands from the sheath of the aorta and fibro-muscular bands from the diaphragmatic crura, on the peripheral arterial. trunks toward the viscera (stomach, spleen, liver. pancreas and enteron) At the root of the mesentery is located the solar plexus, ganglion coeliacum (abdominal brain) which emits rich plexiform network of nerves along the fibrous sheaths of the arterial trunks to the viscera.  Numerous lymphatic vessels pass along the vascular sheath.  A considerable fibro-muscular band, muscle of Treitz (musculus suspensorius duodeni), (Wenzel Treitz, Bohemian, 1819-1874, Prof. Pathology in Prague) is emitted from the diaphragmatic crura (right or left) to terminate in the duodeno-jejunal flexure binding it solidly to the root of the mesentery.
 

Fig. 182.  This figure illustrates the viscera of a female orang from Borneo.  Its age was about ten years.  App., appendix, six inches long, lying on the pelvic floor; U., uterus; C. coecum; F.S., signoid flexure; Am., oviductal ampulla; Ov., ovary; St., stomach; G., gall bladder; L, liver; hook drawing the severed omentum majus proximalward.

    The dorsal surface of the corpus pancreaticus is solidly and firmly bound by strong fibrous tissue in the fork between the coeliac and superior mesenteric arteries.  Hence whatever form of splanchnoptosia may afflict other abdominal viscera the duodeno-jejunal flexure and the middle of the body of the pancreas remain fixed, immovably, in position.  The radix mesenterica, root of the mesentery, is immovably fixed in position and hence does not move in respiration.  The duodenal-jejunal flexure and body of the pancreas are firmly fixed to the root of the mesentery and hence do not share in respiratory movements of the viscera.
    All abdominal viscera (except those fixed to the root of the mesentery as the duodeno-jejunal flexure and body of the pancreas) - are fixed to the abdominal wall and therefore share in respiratory movements. (Remark: - From the above anatomic facts reports of extensive hernia do not record the pancreas or duodenum as having passed through the hernia ring into the hernial sac.)
 

Fig. 183.   The areas of peritoneum shown at 25 and 27, as well as at 34 and 11, also at 5, 8, 12, 14, are additional aids to support the viscera. They are practical extensions of the mesenterial bases. The granular areas are the mesenterial bores, while the intervening areas are where the peritoneum is fixed to the abdominal wall.

    (b)  Abdominal viscera fixed to the abdominal wall and sharing in respiration. (The only exception are the duodeno-jejunal flexure and pancreas.)  A brief reference to the fixation of individual viscera to the abdominal wall and their share in respiratory movements will now be made in order to comprehend the nature and anatomy of the vast domain of splanchnoptosia.

Fixation of Tractus Intestinalis.

    The degree of firmness and extent of fixation of the tractus intestinalis increases with the erect attitude.  The erect apes and man form the culmination of extensive fixation of abdominal viscera.  The erect attitude is responsible for splanchnoptosia.  From careful examination of the viscera of mammals, monkey and erect apes, it is evident to me that all these animals progress through precisely the same stages of visceral development and that visceral fixation is exactly the same, analogous in all - the chief change in all the visceral fixation is due to attitude (erect) and respiration.
In the fixation of abdominal viscera there must be held in view (a) the abdominal wall; (b) respiration and erect attitude; (c) the mesenteries - their basal organ and method of insertion on the abdominal wall.  The mesenteries are not for mechanic support but for the conduction of nerves, vessels and prevention of visceral entanglement.  The mesenteries separate the viscera into compartments which enables them to be supported with greater facility by means of visceral shelves. I. The primary visceral support except the abdominal wall is vascular: (a) coeliac axis; (b) the superior mesentery artery; (c) the inferior mesentery artery. II.  The secondary visceral support to the abdominal wall is peritoneal adhesions (cellular-non-pathologic).  In splanchnoptosia the base or insertion of the mesentery on the dorsal abdominal wall may glide distalward.  The basal fixation of the foetal mesentery is unlike that of the adult.  The base of the foetal mesentery contains the cells, which later multiply, spreading into the broad base of the adult mesentery that lends to erect man his extensive width of mesenteric adhesions.
    A few remarks should be made as regards the acquired mesenteric adhesions of erect man.

1. Mesogastric Adhesions.

    In quadrupeds like the cat the origin or root of the mesogastrium is at the coeliac artery, the radix mesenterica.  With the erect attitude the root of the mesogastrium becomes increasingly adherent to the dorsal abdominal wall in an oblique line.  From the coeliac axis, the mesogastric root, the adhesions spread leftward over the adrenal and kidney to the spleen which is attached to the mesogastrium.  In embryos and infants one can trace the development of the mesogastric adhesions from the single point, the radix mesenterica to the extensive adhesions of adult man.  The mesogastric adhesions or insertion on the dorsal wall aids in the fixation of the stomach.

2. Mesoduodenal Adhesions.

    The duodenal loop is early in the human embryo entirely free, nonadherent, and is still free in adult lower mammals.  Gradually in man the rightward movement of the liver draws the duodenal loop with it and the right side of the mesoduodenum loses its endothelium and its mesenterii membrana propria becomes adherent to the right dorsal wall and especially to the renal hilum.  In dissection and operations in the biliary passages the mesoduodenal adhesions are released with facility.  However, the mesoduodenal adhesions afford a strong support to the duodenum itself and also make of the duodenum a solid visceral shelf for the liver and stomach.  The mesoduodenal adhesions are especially solid dorsal to the line crossed by the colon (coecum) in its journey to the right iliac fossa.
The duodenum is the most fixed segment of the tractus intestinalis due to: (a)  the muscles of Treitz; (b) the extensive fixation of the mesoduodenum; (c) ligamentum hepato-duodenale; (d) biliary passages; (e) pancreas (the body of which is solidly fixed to the coeliac axis).  Observe the absence of the duodenum (and the pancreas) in hernial reports on account of their solid fixation to the immobile radix mesenterica.

3. Mesenteronic.Adhesions.

    The mesenteronic adhesions (of man) extend some six inches in an oblique line from the duodeno-jejunal flexure to the coecum.  Originally in features the mesenteron and mesocolon were in one line, and fan-shaped, being attached by its apex to the coeliac axis or radix mesenteria.  With development of the tractus intestinalis a rotation occurred on the radix mesenterica and the coceum journeyed to the right, crossing ventrally to the duodenum, forming extensive acquired fixations for the testinal tract.  The extent of the mesenteronic adhesions (which are on the right side) depends on the degree of distalward movement acquired by the coecum.  Frequently (9 per cent in man and 5 per cent in woman according to my 700 autopsies) toe journey of the coecum to the right iliac fossa becomes interrupted (nondescent of coecum) at any point distal to the liver.  In such a case the mesenteron (except the duodenum) and a corresponding pact of the transversum and right colon are suspended practically (without adhesions) by the radix mesenteria, i. e., the superior mesenteric artery (as it originates from the aorta about one-half inch from the coeliac axis).
    Not long before birth (man) the mesenteronic adhesions beginning at the transverse (or right) colic margin radiate distalward toward the right ilias fossa.  From dissection it will be observed that with normal mesenteronic adhesions, the chief enteronic support is practically the radix mesenteria, i. e., the arteria mesenterica superior.  This can be demonstrated with facility in the dead.  However, the mesenteronic adhesions lend solid support to the enteron aiding to a high degree to prevent enteroptosia.

4. Mesocolic.Adhesions.

    Acquired mesocolic adhesions in the erect attitude assume two directions, viz. : (a) those of the left colon; (b) those of the right colon.  Originally the mesocolon was located in the medium line.  With development of the foetus the left mesocolic blade becomes adherent to the lumbar wall especially the splenic flexure becomes fixed to the ventral surface of the left kidney and the left colon becomes fixed to the lumbar wall as far as the intersigmoid fossa.  This extensive peritoneal adhesion in the lumbar region added to the vascular support (inferior mesenteric artery) reinforces to a high degree the effective fixation of the left colon.  It also forms a peritoneal compartment for enteronic loops.

(b) Adhesions of the Right Colon.

    By peritoneal adhesions of the transverse colon, the hepatic flexure and right colon are fixed in position.  The coecum and appendix being projections from the original digestive tube possess no peritoneal adhesions to the abdominal wall.  In all erect apes examined as to the right colon I found the same exact condition of peritoneal adhesions as man except that in man the axial rotation of the tractus intestinalis was more advanced or complete ending with coecum in the right iliac fossa or in the lesser pelvis.  In man the peritoneal adhesions of the right colon are more extensive than that of the left colon (which seldom possesses a mesocolon).  The adhesions fixing the duodenum to the abdominal wall and the adhesions fixing the right colon to the abdominal wall are practically developed at the same time.  The adhesions of the right colon spreads over the mesoduodenum, duodenum, distal ventral face of the right kidney and right lumbar region.  The mesocolon being fixed to the immobile mesoduodenum lends strong support to the flexura colihepatica.  The transverse colon and hepatic flexure of the colon secure additional peritoneal fixation apparatus from the fact that as soon as the rotating coeci.,m comes in contact with the ballooned mesogastrium a fusion of the mesogastrium and mesocolon from base to viscera occur.  Finally the mesogastrium (or rather gastro-colic omentum) envelopes the entire proximal segment of the colon.
    On the left colon there is an important fixation apparatus known as the ligamentum costo-colicum (sinistrum) located on the ventral surface of the left kidney.  On the right colon there is a similar fixation apparatus ligamentum costo-colicum (dextrum) located at the distal pole of the right kidney.  This band prevents frequently the coecum from further distalward movements and also from falling into the lesser pelvis.  The liganientilm costo-colicum dextrum is an important fixation apparatus for the coectini (and appendix) and prevents frequently the coecum from being a resident in the lesser pelvis.  Not infrequently the ligamentum costo-colicum dextrum, together with the right colon, offers more or less support to the right kidney especially at its distal pole.  At birth, so far as I am able to report on some 60 infant autopsies, the coecum lies in general at the junction of the duodenum and kidney.
    The peritoneal adhesions of the right colon are formed while the child is learning to walk, i. e., by the end of 18 months.  The peritoneal adhesions of the tractus intestinalis (secondary visceral supports) to the dorsal wall of the abdomen reinforce to remarkable degree the strength of the primary visceral supports (arteria coeliaca, mesenterica superior et inferior).  The secondary visceral supports (acquired peritoneal adhesions form visceral shelves), the contact of the viscera, like bricks in a wall, form solid barriers for visceral support.  The mesenterial partitions among the viscera, producing peritonea] compartments aid in visceral support by distributing their force separately against the abdominal wall.

Respiration Movements of the Tractus Intestinalis.

    The transverse colon moves freely with respiration as it is a shelf for the sub-diaphragmatic viscera (stomach, liver and spleen).  The flexura coli dextra (lying ventral to the right kidney) and the flexura coli sinistra (lying ventral to the left kidney) move with the kidneys in respiration.  Since the transverse mesocolon acts as a visceral shelf it is markedly forced distalward during splanchnoptosia, especially in enteroptosia.  I have seen it lying on the pelvic floor and once 9 inches in an inguinal hernia, where as its average location is immediately proximal to the umbilicus.  The two colonic flexures in coloptosia produce vigorous traction in the kidneys.
    In the usual autopsy the enteron is found in a compartment formed by the mesocolonic square and closed ventrally by the omentum majus.  The transverse mesocolic shelf prevents the subdiaphragmatic viscera from exercising vigorous respiratory movements on the enteron.  Defective respiratory movements of the diaphragm will aid in forcing the enteron distalward, from the right and left lumbar regions, into the lesser pelvis.  In final advance states of enteroptosia, the transverse segment of the duodenum becomes obstructed by the traction, compression of the superior mesenteric artery, vein and nerve - a distant stage in splanchnoptosia.
    The tractus intestinalis is affected chiefly in splanchnoptosia by: (a) compromising of circulation, blood and lymph supply, i. e., congestion and decongestion, (b) trauma of nerve centers (ganglia), strands and nerve periphery, (c) complication from loss of peristalsis and atony of bowel muscle, (d) gastrointestinal catarrah and indigestion from excessive, deficient and disproportionate secretions.  Also dragging on the abdominal brain, an independent nerve center producing nausea, neurosis, headache, reflexes, and deranged sensation, secretion and motion on other viscera. (e) Dilatation of the stomach and duodenum, caused by the superior mesenteric vessels at the point where they cross the transverse segment.  The stomach is especially liable to dilatation from the above causes, where the prolapse of the enteron, enteroptosia, is sufficiently advanced to allow the enteronic loops to pass distalward into the lesser pelvis and particularly when the subject lies on the back, for then the superior mesenteric artery, vein and nerve are put on a stretch and they constrict vigorously the transverse portion of the duodenun. (f) the enteronic loops being dislocated (enteroptosia) into the plevis, peristalsis, secretion, circulation, sensation and nerve periphery are compromised, followed by catarrh, constipation and indigestion. (g) the colon, especially the colon transversum may lie in the lesser plevis producing similar compromising circumstances as in the enteron. (h) The appendages (liver, pancreas, and spleen) of the tractus intestinalis, in ptosis are compromised in circulation, secretion, absorption, sensation and nerve periphery.

CONSIDERATIONS OF GASTROPTOSIA AS PART OF SPLANCHNOPTOSIA.

    The stomach is fixed to the diaphragm by the oesophagus and part of the gastro-hepatic omentum (peritoneum).  It is fixed to the liver by the gastrohepatic omentum (peritoneum), hepatic artery, biliary duct and ligamentum hepato-duodenale and peritoneum (all important bands).  The stomach is fixed to the radix mesenterica by the gastric artery.  The root of the mesentery is not only an important gastric support, but a solid anchor, around which occur all visceral movements.  Besides the stomach rests on visceral shelves composed of the transverse colon and its mesentery, pancreas, duodenum and left kidney.  It is maintained on the visceral shelves by the abdominal muscles. The distal end of the stomach is bound to the diaphragm through the liver (gastro-hepatic and meshepaticon) and in a similar manner the proximal end of the stomach is bound to the diaphragm, through the spleen (gastro-splenic, lienorenal and suspensory ligament) which is, however, a band of limited strength.
 

Fig. 184.  Gastro-duodenal dilatation - gastroptosia.  This illustration is drawn from the subject.  This subject was 67 years old, dying of carcinoma of the ductus bilis et ductus pancreaticus.  It is a so-called transverse stomach, and as the stomach dilates it extends more distalward until in this case it extended to the pelvis.  Du and D presents the enormously dilated duodenum, obstructed by the superior mesenteric artery A and vein V. Observe the difference in dimension between the duodenum immediately to the right of the mesenteric vessels and that immediately to the left of them.  The jejunum, J., is normal in dimension, while the duodenum is as large as a man's arm.  A segment of the stomach and duodenum is resected at D to show the dimension of the distal duodenum. 1, a resected segment of the ventral surface of the duodenum in order to expose Vater's papilla. 0, elongated oesophagus.  In this subject the pylorus was dilated in proportion to the duodenum and gastrium.  This figure is from the same subject as Fig. 185.  I secured this specimen at an autopsy by the professional courtesy of Dr. Charles O'Byrne.

The Respiratory Movements of the Stomach.

    The diaphragm rests on the liver, stomach and spleen like a muscular dome, hence with  each  respiration  the  above  three  organs (if  the  stomach  be  distended) will act similarly - pass distalward according to the resistance offered by the muscles of the abdominal wall.  The distended stomach will move ventralward at each inspiration.  The stomach exists in the shape of a wedge with its base to the left.  The liver also exists in the shape of a wedge with its base to the right.  The apex of the liver wedge proximally overlaps the apex of the stomach wedge distally.  At every inspiration the apex of these wedges glide on each other, shortening the gastro-hepatic orrientum, while at each expiration the gastro-hepatic omentum is placed on tension.  The radix mesenterica or root of the mesentery having sent one of its branches to the liver - the hepatic artery - and the other branch to the stomach - the gastric artery - it remains the central axis around which the stomach and liver rotate.  A third branch of the radix mesenterica - the splenic artery - passes to the spleen, hence, the root of the mesentery is the central axis of the visceral rotation (in respiration) of the liver. stomach and spleen.  Strong fibrous sheaths of connective tissue and nerves radiate on the hepatic, gastric and splenic arteries to their respective viscera constituting an important band between the viscera and the immobile mesentery root.  The ventral elevation of the epigastrium at each inspiration is mainly due to: (a) The contraction of the diaphragmatic viscera (liver, stomach and spleen) distalward; (b) the apices of the liver and stomach wedges glide on each other toward their bases increasing their dorso-ventral diameters.  The degree of elevation of the epigastrium at each inspiration depends on the resistance of the abdominal wall and the splanchnoptotic state of the diaphragm and of the subdiaphragmatic viscera.
    Clinicians may observe that hepatic calculus is more frequent in splanchnoptosia but this is rationally explained by the facility in splanchnoptosia of infectious processes invading the biliary passages from lack of visceral drainage and stasis of tissue fluids - blood and lymph.  In splanchonptotics the ducts are flexed, especially the biliary ducts, obstructing the normal flow of visceral products.  Gastroptosia is practically constantly accompanied by gastric dilatation.  Gastric dilatation must be viewed as a result of displacements and not a cause.  In gastroptosia the vessels and nerve plexuses are traumatized, elongated, which impairs gastric innervation, circulation (lymph and blood), nourishment and a muscularis ending in dilatation.
    In general it may be noted that the coeliac axis (the immobile root of the mesentery vessels with strong fibrous and neural sheaths) is a secure support to the liver, stomach and spleen.  However, the visceral shelves of the subdiaphragmatic organs must not be overlooked.  The pancreas (with its corpus securely bound to the immobile coelac axis with strong fibrous tissue) is the strongest visceral shelf support.  The next strongest visceral shelf is the duodenum which in the adult is devoid of dorsal epithelial peritoneum but the strong fibrous subperitoneal tissue binds the whole proximal duodenum to the dorsal wall while the distal duodenum is solidly bound to the cruva of the diaphragm by the muscle of Treitz, (musculus suspensorius duodeni) and to the coliac axis by strong fibrous tissue.  Hence the duodenum and pancreas (both fixed to the root of the mesentery) are excellent visceral shelves for liver, stomach and spleen. (Duodenum and pancreas are the rara avis in hernia.) When the splanchnoptosia has advanced sufficiently to involve the proximal duodenum and head of the pancreas the duodenum is liable to present a diverticulum at the location of entrance of the ducts choledochus communis, while the pancreas being fixed in its middle (corpus) will locate its head near sacral promotory.
    Hepatoptosia and gastroptosia rest chiefly on two causes, viz: (a) relaxation of the abdominal walls; (b) constriction of the trunk by clothing.  In both (a) and (b) the normal respiration has become deranged.
 

Fig. 185.  Carcinoma completely obstructing the biliary and pancreatic ducts.  From same subject as Fig. 184.  Illustrates an X-ray of enormously dilated billary passages.  The biliary ducts (excepting the gallbladder, which was three to four times its normal dimension) had a capacity of 32 ounces, about six or seven times the natural capacity.  The ductus communis choledochus was over 11/4 inches in diameter.  The pancreatic duct admitted the index-finger.  The man, 69 years old, a giant in stature, weighing some 250 pounds with ordinary limited fat, lost 115 pounds in weight during three months illness.  The ductus cysticus, extending from II to IV, had seven Heister’s valves, and its lumen would admit a lead-pencil only.  At B the biliary ducts were deficient within the liver substance, but were really dilated on the surface.  T, the carcinonoma (divided with the scalpel), completely severing the lumen of the biliary and pancreatic ducts. There was enormous gastroduodenal dilation from the compression of the transverse duodenum by the superior mesenteric artery (A) and vein (V).  D, foldless, granular, proximal 2 1/2 inches of the duodenal mucosa; 1, entrance of duct's communis choledochus in the duodenum; Sa, ductus Santorini; P, ductus pancreaticus.  The ductus cornmunis choledochus and ductus pancreaticus, located between the carcinoma and Vater's diverticulum, were normal.  Da is the normal sized duodenum located distal to the compressing superior mesenteric vein (V) and artery (A).  Observe the vast dilatation of the duodenum proximal to the superior mesenteric artery (A) and vein (V).  I secured this rare specimen at an autopsy through the courtesy of Dr. Charles O'Byrne.

Gastroptosia.

    Gastroptosia or atonia gastrica signifies abdominal relaxation.  It includes distalward movement of the stomach and relaxation of the abdominal wall.  It is a part and parcel of splanchnoptosia.  Gastroptosia (or its equivalent atonia gastrica) practically includes the terms dilation of stomach, ectasis ventriculi, insufficiency of the stomach, gastric insufficiency, motor insufficiency, ischochymia (retention of cbyme), myasthenia, extasis gastrica, because it signifies abdominal relaxation and relaxation includes dilatation and motor insufficiency.  Therefore gastroptosia is a proper, comprehensive, scientific term which signifies ptossi, dilatation and motor insufficiency of the stomach.  Gastroptosia is of paramount importance to physicians as its existence is frequent in every day practice.
    In early embryonic life the stomach is absolutely vertical and the child is practically born with a vertical stomach and besides I have observed scores of permanently vertical stomachs in adult autopsies (perhaps from arrest of development).  With the growth of the child the stomach rotates following the atrophying liver.  In the adult the rotated stomach is supplied on its ventral surface (left) by the left vagus and on the dorsal surface (right) by the right vagus.  Food aids by its weight and distention to force the stomach distalward.  In gastroptosia the lesser curvature and pylorus moves distalward.
 

Fig. 186. This illustration presents the horizontal stomach, which in gastroptosia dilates from pylorus to cardiac extremity and passes distalward as in Fig. 184 - a gastro-duodenal dilatation.  Sig. represents the sigmoid flexure in a 180 deg. condition of physiologic volvulus.

Etiology.

    Gastroptosia arises from a variety of causes.  Disordered respiration with consequent descensus of the diaphragm and distorted distal thorax (ribs) is among the first disturbances.  In short gastroptosia coexists with splanchnoptosia.  Gastroptosia may be due to an abnormally distalward location of the diaphragm.  In hepatoptosia the liver forces the pylorus distalward and to the left. Relaxed abdominal walls, rapidly repeated pregnancies, infected puerperium (i. e., practically subinvolution of the abdominal wall), compression from waist bands, liver or spleen tumors, pleuritic effusions or adhesions, pericarditis are fruitful causes of gastroptosia.  I have observed in autopsies that peritoneal and especially omental adhesions play an extensive role in gastroptosia.
    Gastroptosia is congenital or acquired.  The acquired gastroptosia is discernible in the change in normal relations of the space in the proximal abdomen and distal thorax especially in the manifestation of respiration.  In general we observe at post mortems two forms of gastroptosia, viz.: (a) the whole stomach appears (with the lesser curvature and pylorus with a transverse position) moving caudal, (b) the distalward moving stomach assumes more or less a distinctly vertical position.
    I wish to state, that, from personal autopsic observation in the abdominal viscera in over 700 subjects, the stomach varies extensively: (a) in position, (b) in dimension, (c) in form.
    Gastroptosia may be due to constitutional defects or anomalies in both sexes.  The peculiar formed chest, as funnel shaped, chicken breast, may be observed in subjects with gastroptosia which is part and parcel of splanchnoptosia.  Gastroptosia occurs in subjects with tubercular habitus - constitutional defects.
 

Fig. 187.  This represents a vertical stomach.  During gastro-duodenal gastroptosia the chief gastric dilatation occurs at the distal end of the stomach.  The superior mesenteric, S, compressing the transverse duodenum, causes the gastro-duodenal dilatation.  This figure presents a non-descended cecum, and an ileum, 1, adherent to the ileopsoas muscle. 1, 2, 4 representing the dorsal insertion line of the meso-sigmoid.

    Gastroptosia (or splanchnoptosia) does not as a rule occur in strong robust subjects.  Obvious stigmata of degeneracy accompanying splanchnoptosia subjects with elongated narrow thorax are liable to gastroptosia because the diaphragm occupies an abnormally distalward location.  Pulmonary emphysemia or pleural effusions force the diaphragm distalward favoring gastroptosia (and concomitant splanchnoptosia).  Mechanical conditions may enhance stomachoptosia as supraumbilical hernia, inguinal or femoral hernia, peritoneal adhesions.  Rapidly repeated gestations present a large field of gastroptosia so fully discussed by Landau as well as rapid loss of large quantities of fat.  In multipara and subjects with loss of quantities of flesh the abdominal muscles become relaxed and lose their delicate active poise in maintaining the viscera in their normal physiologic position.

Gastric Dilatation in Splanchnoptosia.

    Many times I have observed in autopsy extensively dilated stomach, the existence of which in life had not been suspected, first, because the physical condition of the patient was favorable and second compensatory action between stomach and pylorus was still favorable.  A relation exists between the dimensions of the pylorus and that of the stomachs compensatory action.  I performed an operation on a woman who had vomited for years with a dilated stomach.  In this case the pylorus had dilated slightly and its flexion increasing by ptosis obstructed the free evacuations of the stomach contents.
 

Fig. 188.  illustrates gastroptosia.  The colon transversum forced distalward into the pelvis by the stomach. 1, liver with hepatoptosia; 2, stomach in the lesser pelvis; 3, 4, duodenum dilated; 5, the jejunum, normal caliber; 6, transverse colon.  This cut represents gastro-duodenal dilation-the second stage of splanchnoptosis. The artist neglected to present the duodenum dilated.

    Again we note autopsies in which a subject possesses a markedly dilated stomach with slight difficulty in evacuation of stomach contents through the pylorus because the pyloric ring had dilated proportionately with the stomach dilatation allowing free evacuation, free passage of food from stomach to duodenum, free drainage - here is compensatory dilatation - of stomach and pylorus, resembling that of the cardiac valves, however, suddenly the stomach and pyloric compensatory action may fail and the patient passes swiftly onward and swiftly downward - exactly as in valvular heart lesions.
    The etiology of gastroptosia may be sought chiefly in constitutional defects.  However, mechanical derangement is sufficiently obvious in gastroptosia.  Gastro-duodenal dilatation which plays such an extensive role in splanchnoptosia will be discussed and illustrated in a future chapter.  Combined gastro-duodenal dilatation due to the compression of the transverse duodenal segment by the superior mesenteric artery vein and nerve is a frequent condition and though I have published articles on it for a decade it is still but limitedly recognized.   The symtomatology may be practically negative or of the most aggravated kind.  It may be stated, in general, that gastroptosia is without symptoms so long as the stomach functionates normally which mainly prevails while the subject is in favorable physical condition.  Gastroptosia presents symptoms when detention and composition food occurs and general infection results.  Indirect symptoms may arise as in splanchnoptosia, e. g., fatigue, debility, constipation, insomnia.  Meinert insist that gastroptosia is a common cause of chlorosis.
The symptoms of gastroptosia are generally proportionate to the degree of stomachic dilatation.  Kussmaul originally observed that gastroptosia is frequently accompanied by a disturbance of the motor nerves of the stomach.  This may be due to the trauma traction on the vagi from change of gastric position.  Gastroptosia frequently coexists with multiple nervous symptoms, but the nervous symptoms may be due to splanchnoptosia. However, gastroptosia is a disease and is liable to be accompanied by disturbed motion, absorption, secretion and sensibility of the stomach.  Change of form and position of the stomach may not lead to any more nervous symptoms than change of form and position of the uterus, however dislocation of the uterus, i. e., permanent fixation, is the result of some disease.
    Malposition of the stomach does not produce neurasthenia any more than malposition of the uterus.  The position of a mobile viscus is not responsible for neurosis, for mulitple positions or multiple deviations must not be considered abnormalities.  It is disease that produces neurosis, not position of viscera.  Original disease which produced the malposition of the viscus should be held responsible for the nervous disturbance.  Again there can be no doubt that the symptoms of gastroptosia and nephroptosia are constantly mistaken for each other especially by the careless examining surgeon with a tendency to nephropexy.  There is no characteristic stomach contents peculiar to gastroptosia.  In gastroptosia pain is generally prevalent in the proximal abdomen and 'Lumbar regions.  It is true that subjects with gastroptosia (a part and parcel of splanchnoptosia) present multiple neurotic symptoms simulating disturbed mobility, secretion, absorption and sensibility of the stomach.  However, this may belong in the congenital debility or predisposition of the patient - due to the disturbance created by anatomically dislocated viscera and consequently pathologic physiology.  Gastroptosia increases the weight of the stomach.

Diagnosis.

    Gastroptosia is less recognized than nephroptosia which is diagnosed with more facility and besides the pexyites are more vigorously in search of nephroptotic victims.
    Percussion and auscultation with various quantities of fluid in the stomach may suggest the position and dimension of the stomach.
    Palpable epigastric pulsation, absence of projecting abdominal wall in the epigastrium and projecting abdominal walls in the hypogastrium aid in the diagnosing gastroptosia.
    The most exact method to determine the position and dimension of the stomach is by inflation, viz.: (a) by generation of gas within the stomach.  The most frequent method of gastric inflation practiced is by directing the patient to drink a glass of water containing some sodium bicarbonate and immediately to drink another glass of water containing tartaric acid whence carbonic acid gas is formed distending the stomach by air. (b) Another method to inflate the stomach is by introducing into the stomach a tube whence air is forced through it for distention, whence its form, position and dimension may be observed through the abdominal wall. (c) A third method of diagnosing the form, position and dimension of the stomach is by distending the stomach by fluid.
    When the major curvature is at or below the umbilicus and the pylorus and lesser curvature have moved distalward the diagnosis of gastroptosia is confirmed.  A healthy stomach maintains the position of its borders regardless of the subject's attitude.  In gastroptosia the borders of the stomach change according to the patient's position.  In gastroptosia with the patient in the erect posture the major stomach curvature and pylorus will be more caudal, while if the patient's posture is recumbent the pylorus and major curvature cephalad.  Succussion (splashing sound) is a method to diagnose gastroptosia by agitating air and water in the stomach through shaking the body.  The splashing sound may also be obtained by palpating the stomach while the patient is in the recumbent position.  A splashing sound elicited from the stomach means practically gastroptosia-relaxation, atony.  Some persons by practicing pressure of the abdominal muscles of the stomach can produce various sounds in the stomach.  Such persons perhaps possess abnormally a large stomach and powerful abdominal muscles, however, like a fakir have exaggerated an anomaly.  Gastroptosia may be diagnosed by transillumination, i. e., introducing an electric light in the stomach whence its contour may be observed.  This method was advocated in 1845 by Casenave, later in 1867 Milliot improved it by experimentation, however, Dr. Max Einhorn of New York practically first made successful use of (the gastrodiaphane) transillumination of the stomach in man and demonstrated the utility of gastro-diaphanes copy.
    Inspection may present a depression in the epigastrium and a projection in the umbilical region.  This method of diagnosis may be sufficient in spare persons to announce gastroptosia.  The X-ray may be used to note the position of the stomach by administering substances which will cast a shadow, as subnitrate of bismuth or metallic salts administered in capsules.  Treatment is medical, mechanical, surgical.

Treatment.

    1.  The medical treatment consists in regulation of diet and function.  The dietetic management consists in administering limited quantities of prescribed food at regular three-hour intervals.  The diet should be cereals, vegetables, milk and eggs.  All high seasoned food, pastry, pie, cake, spices, meat should be excluded to avoid fermentation.
    The most essential medical treatment consists in "visceral drainage" as ample sewerage the evacuating channels should be flushed.  Gastroptotics may live healthy with ample visceral drainage.  The tissues and tissue spaces in gastroptosia (splanchnoptosia) require flooding, washing, so that the subject may be free from waste laden blood and residual debris.  Every evacuating visceral tract (tractus intestinalis, perspiratorius, urinarius respiratorious) should perform maximum duty.  The sheet anchor treatment for gastroptosia is regulation of food and fluid, and maximum sewerage of visceral tracts.  Dietetics, hygiene, anatomic and physiologic rest, properly supervised tend extensively to the welfare in the life of a splanchnoptotic.
 

Fig. 189  illustrates the third stage of splanchnoptosia, viz.: gastro-duodenal dilatation. It shows the transverse-colon (5) in the lesser pelvis. The widely dilated stomach (1) is drawn leftward by hooks (10) from its bed to show the duodenum (2) dilated by the superior mesenteric artery, vein and nerve, (3) 4, the normal calibered loops of enteron; 6, right colon; 7, cecum; 8, the appendix.  Note the enteron loops crowded into the lesser pelvis.

    Mechanical treatment in gastroptosia judiciously applied affords wonderful relief.  Stomachic irrigation occasionally renders much comfort.  The treatment consists in the application of abdominal wall to support the viscera.  This is accomplished by various kinds of abdominal binders - elastic and non-elastic.  I use sometimes an abdominal binder within which is placed a pneumatic rubber pad which is distended with air to suit the patient's comfort.  Dr. E. A. Gallant employs a suitable fitting corset.  The adhesive strapping method of Achilles Rose is practical, rational and economical and affords excellent relief.  The recumbent position aids the patient. The mechanical method attempts the forcible reposition of the stomach to its physiologic position and there to maintain it by aids applied to the abdominal wall - a rational method.  Pregnancy practically relieves the gastroptosia for a season.  Splanchnoptotics experience more comfort from rational adhesive strapping (mechanical supports) than from surgical procedures.
    Surgical treatment in gastroptosia is a very limited field.  It espouses two methods, viz.: (a) The surgery is applied to the stomach itself as gastro-enterostomy, the Heinicke-Mickulicz operation (both tend to cure by visceral drainage) the replication of the stomach parietes or the attempt to shelve the stomach by omentum or mesentery (both unphysiologic, irrational).  (b)  The abdominal wall is employed to support the stomach as by incision and over-lapping like a double breasted coat, or by enclosing, uniting the two musculi recti abdominales in one sheath.  Both methods attempt to relieve by lessening the abdominal cavity and forcing the stomach into its normal physiologic position (both rational).  A third method is to perform gastropexy, i. e., suture the stomach to the abdominal wall (limited, irrational in general).

HEPATO-PTOSIA, COLOPTOSIA AND ENTEROPTOSIA IN SPLANCHNOPTOSIA.

Fixation of the Liver.

    The liver is firmly fixed to the diaphragm only.  It has the most extensive fixation to the diaphragm of any abdominal viscus, hence the action of the diaphragm in respiration will be the most comprehensive.  The structures which maintain the liver in contact with the concavity of the diaphragm are: (a) peritoneal folds; (b) connective tissue; (c) vessels; (d) abdominal muscles (most important).  The liver rests on a visceral shelf, composed of the stomach, duodenum, right kidney, pancreas and transverse colon.  The vena cava and hepatic veins by their intimate fusion with both liver substance and the diaphragm constitute a strong bond of union.  The dorsal mesentery of the liver-the mesepaticon meso-hepor is constituted by the extensive connective tissue which binds the right lobe of the liver to the distal concave surface of the diaphragm together with the reflexion of peritoneum which surrounds the connective tissue area.
    The mesepaticon forms the most important passive band of the liver and diaphragm.  The right and left lateral ligaments are mere extensions of the mesepaticon.  The suspensory ligament, the remnant of the ventral hepatic mesentery, is long and loose to allow respiratory movements.  An excellent example of what the respiratory movements of viscera may accomplish is observed in the bursa of Spiegel.  Spiegel's lobe moves proxinialward and distalward with each respiration and by this continual action has formed a diverticulum in the lesser sac of the peritoneum - Bursa spigelii.  The proximalward and distalward movements of Spiegel's lobe produced by the diaphragm in respiration is responsible for Spiegel's diverticulum in the peritoneurii.

Respiratory Movements of the Liver.

    If one studies the diaphragm it will be observed that its muscular contractions tend toward the radix mesenterica.  When the diaphragm contracts (inspiration) on the broad dorso-proximal dome-like hepatic surface it will force the liver distalward, - ventralward and medianward.  At every inspiration the liver pounds on the abdominal viscera distal to it like a hammer, especially in thoracic splanchnoptosia.  The degree of distalward movements of the liver in inspiration depends on the resistance offered by the muscles of the abdominal wall.  These movements of the liver in inspiration imposed on it by the diaphragm do not disturb its function, on the contrary doubtless aid in massaging the liver into vigorous function.
    The normal respiratory movements of the liver may become disturbed by relaxation of the diaphragm or abdominal walls which rob it of normal support.  Tight lacing may force the liver from its visceral niche and shelf whence the normal respiratory muscular action becomes ungeared.  Perihepatic peritoneal or pleuritic adhesions particularly distort respiratory muscular actions on the liver and consequent normal function.  Hepato-Ptosia is not a rare condition, especially when the liver has lost its visceral shelf and the abdominal walls become relaxed.

Etiology of Hepato-Ptosia.

    Hepato-Ptosia is a part and parcel of splanchnoptosia and depends on the same causes - as deranged respirations, relaxed abdominal walls, yielding of the diaphragm, hepatic ligaments and visceral shelves (kidney, duodenum transverse colon, pancreas, stomach) peritoneal and omental adhesions, plueritic effusions and exudates asthma, rapidly repeated pregnancies, hereditary or congenital debilities, persistent vomiting and coughing, hernia, tight waist band, corsets, trauma, congenital predisposition.
    The elongation of the hepatic ligaments are secondary to the relaxation of the abdominal wall.  Further etiologic factors in hepato-ptosia are the weight of the liver, cholelithiasis, weight of the gall-bladder, laxity or elongation of the hepatic ligaments (which are probably secondary to the relaxation of the abdominal wall), trauma as during parturition, disappearance of the visceral shelves.  The chief immediate course of hepato-ptosia is relaxation of the ventral abdominal wall.  The liver like the uterus rests on a floor or visceral shelf.

Frequency.

    Hepato-Ptosia occurs the most frequently in women.  During the past 15 years I have observed about one typical advanced clinical case a year; however, numerous subjects may be observed with a moderate degree of hepato-ptosia, especially those having a tendency to develop Riedel's lobe.  The frequency of hepato-ptosia is concomitant with splanchnoptosia, which is a common ailment.  Perhaps seven women suffer from hepato-ptosia to one man.  I have examined subjects of extreme hepato-ptosia in whom I could palpate the liver per vaginum.  The history of hepato-ptosia is recent, as Portal was among the first to call attention to it in autopsy (1804) and the first case described in the living was by Cantani in 1866.  Autopsies revealed its condition previous to that, but its interpretation remained unsolved.
    The liver lies in an excavation in the concavity of the diaphragm resting on a visceral shelf.  Its primary maintainers are the power of the abdominal wall.  Its secondary maintainers are the suspensory, coronary, triangular, ligaments and mes-hepaticon, mesohepar.  The elongation of these five supports allows distalward movements of the liver.  Floating liver is intimately associated with splanchnoptosia-is part and parcel of it-for in autopsy it is common to note the kidney, hepatic flexure, enteron passing distalward before the liver.  I have personally examined in the living and dead about a dozen typical, advanced, so called Riedel's lobes.  In every subject of marked Riedel's lobe splanchnoptosia was marked.  The vast majority of the subjects were women.
    First, when the right liver lobe becomes forced excessively distalward the costal margin tends to separate the proximal form the distal part of the lobe by compressing a crease in the liver.  The distal part of the right lobe which is extended distal to the costal margin becomes an increasing Reidel's lobe.  Second, the space between the distal costal margin land the proximal crest of the ilium allows Riedel's lobe to develop, as here the abdominal walls offer the direction of least resistance.

Symptomatology.

    The symptoms of hepato-ptosia are acute or chronic, partial or complete.  In general the clinical symptoms are dragging pain in the abdomen, nausea, vomiting, dizziness, constipation alternating with diarrhoea, ascites, a peculiar rhythmic distressing "hepatic" cough with numerous neurotic disturbances and malassimilation.  Curiously enough one not infrequently meets a subject with hepato-ptosia presenting no objective symptoms.

Diagnosis.

    The diagnosis rests on bimanual palpation, percussion, a mobile mass in right side, change in location of tumor by change of attitude.  Liver dullness changes with different positions and the liver may be felt in each different position.  The liver in hepato-ptosia may assume any position in the abdominal cavity.  If the kidney is not enlarged nephroptosia can be differentiated from hepato-ptosia; however, with enlarged kidney it may be impossible.  I have examined subjects with the best of experts in urology, where it was impossible to decide until peritonotomy was executed.
An excellent factor in diagnosis is to attempt to replace the liver with the patient recumbent, which if successful is confirmatory of hepato-ptosia; examine the liver in the erect and prone position.  As the liver passes distalward it is liable to rotate to the right on the ligamentum umbilicals as an axis.  A warning is offered that Riedel's lobe should be differentiated from hepato-ptosia.  Riedel's lobe is a direct extension distalward of the distal portion of the right hepatic lobe.  Its etiology, though obscure, appears to be associated with diseases of the gall-bladder, cholelithiasis or tight waist bands.
    The development of Riedel's lobe appears to be intimately connected with cholelithiasis; however, I have seen Riedel's lobe sufficiently frequent in both the living and the dead with no cholelithiasis present, to know it is not the only cause.
    Occasionally we can diagnose floating liver of' considerable degree accompanied apparently by no symptoms.  I have observed subjects of hepato-ptosia when a distinct bulging presented in the distal right quadrant of the abdomen with no symptoms.
    In hepato-ptosia the liver rotates on its pedicle (transverseaxis), the torsion of which compromises its anatomy and physiology (binary ducts, Portal vein, hepatic artery, lymphatics and nerves).  With change of position (hepato-ptosia) the liver experiences change of form.  Hepato-ptosia does not occur without dislocation and change of adjacent organs.  In hepatoptosia the change in form and position of the liver is not due merely to pressure of the abdominal wall (muscle or bony) but to the necessity of physiologic movement as liver rhythm and application of adjacent viscera against the liver by respiratory movements.  The liver is dislocated through disease, i. e., by pathologic physiology or pathologic anatomy of adjacent viscera or body walls.
 

Fig 190.  Coloptosia.  The transverse colon extends into the lesser pelvis.  Coloptosia increases the flexion of the flexura hepatica coli and the flexura linealis coli, increasing the difficulty and friction of fecal circulation.  Z The cupola of the sigmoid, presenting a physiological sigmoid volvulus.  CO Coecum located in the lesser pelvis, with the appendix Ap. 11.  Ileum, coursing proximalward and parallel with the right colon, assuming conditions favorable to an ileocecal volvulus.  X illustrates that during volvulus of the sigmoid it appropriates peritoneum, and formulates it into an additional elongated mesosigmoid.

Treatment.

    The treatment is: 1, Medical, such as diet, "visceral drainage," stimulation of the functions of the visceral tracts to a maximum degree of elimination by injesting liberal quantities of fluids at regular intervals, ample horizontal rests.  Forced nutrition aids in restoring the fat cushions.  The patient must avoid excessive or traumatic exertions. 2, Mechanical treatment consists in forcible reposition and maintaining the liver in its normal physiologic position.  Apply abdominal binders, adhesive strapping or an applicable, suitable corset (Gallanet).  The mechanical methods afford wonderful relief, especially Achilles Rose’s method of adhesive strapping.  3.  Surgical.  Hepatoplexy should be performed only as a last resort.  It has an extremely limited field of usefulness.  It has been performed over 50 times since its introduction in 1877 with doubtful results.  Overlapping the abdominal walls like a double breasted coat is more rational and secures more successful results, as such a procedure would diminish the abdominal cavity and force the liver in its normal dome-like excavation in the diaphragmatic concavity and on its normal visceral shelf.

Coloptosia.

    The colon has received some attention in splanchnoptosia from its relation to nephroptosia and hepato-ptosia gastroptosia: (a) Coloptosia transversal The dislocation of the middle of the transverse colon producing more or less of a curve with its concavity proximalward, is one of the most frequent factors in splanchnoptosia.  Dislocation of the colon is placed in relation with the relaxed abdominal wall with elongation of the mesocolon with constipation, with tight waist bands, with gastroptosia, nephroptosia, hepatoptosia; however, no one theory is satisfactory.
    It is true that by circular constriction of the abdomen one can force some viscera proximalward and many distalward.  However, at autopsy I found even in youth, in nuliipara in absence of corset, that the colon transversum may be located well distalward from the umbilicus.  We can observe that not only the mesocolon transversum was elongated but also the ligamenturn gastro-colicum, i. e., the visceral mesenteries were elongated.  With the elongated mesocolon transversum the transverse colon can assume various positions.
    In autopsy it is common to observe the middle of the transverse colon projection into the pelvis and not frequently the colon may lie in the lesser pelvis and on its floor.  The middle loop of the transverse colon can be moved with facility to any portion of the peritoneal cavity.  The enteronic loops may glide proximalward ventral to the transverse colon.  The right portion of the transverse colon is frequently prevented from distalward movements by reason of pathologic peritoneal adhesions binding it to the liver.  The mesocolon transversum measures generally 4 1/2 inches; however, in subjects of coloptosia, I have observed it nine inches in length and frequently six inches.  The membrana mesenterii propria. i. e., the submesocolic tissue, vessels and nerves, are elongated, attenuated.  Coloptosia transversum plays a prominent role in autopsic observations.
    Hepato-ptosia and nephroptosia may be advanced sufficiently to force the colonic hepatic flexure so far distalward that it becomes reversed.  In such cases the colon extends from the coecum obliquely across the abdomen to the spleen.  The clinical history of such patients was mostly unknown.  However, I am not convinced that these marked dislocations of the right and transverse colon manifested grave symptoms.  For the transverse colon in general will measure about 22 inches, and since the abdominal cavity between the points of the splenic and hepatic flexures is some 14 inches the transverse colon must assume a sinuous or looped course of more or less deviation from an extended line.

Coloptosia Dextra.

    The right colon becomes of significant interest in coloptosia on account of its relation to nephroptosia and hepato-ptosia, the appendix and tractus genitalis as well as to the fact that the colon dextrum not infrequently possesses a mesocolon.  The resistance to coloptosia dextra is chiefly offered by the ligamentum costo-colicum dextrum, which vigorously fixes the cecum, in many subjects, checks its distalward movements, preventing it from becoming a resident in the lesser pelvis (woman 20 %, man 10 %).
    The base or root of the right mesocolon is fixed to the ventral surface of the distal renal pole, hence maintains intimate relations to nephroptosia dextrum.  The right colon is about eight inches plus two inches for the cecum, assumes a sinuous or looped course in most bodies and the additional loops of moderate coloptosia dextra perhaps produce few symptoms.

Coloptosia Sinistra.

    The left colon is so infrequently dislocated from the fact that it is rarely possessing a mesocolon that I omit its discussion in coloptosia.

Coloptosia Sigmoidea.

    It is difficult to define splanchnoptosia of the sigmoid, as it has an extensive normal range of mobility.  In general it is 17 inches in length in woman' and 19 in man.  Its mesosigmold will average 2 1/2 inches.  The base of the mesosigmoid insertion-its foot-is but a few inches in length and hence the sigmoid will move about freely in the peritoneal cavity.  In autopsies the sigmoid may be found the most frequently in the lesser pelvis (65% to75%), in the right iliac fossa (15%), in the proximal abdomen (15%).  It may be in contact with the spleen, stomach, liver or cecum.  The most distinct reason for the nonsplanchnoptotic state of the sigmoid is that the trauma of the psoas produces more or less plastic peritonitis in the mesosigmoid (mesosigmoiditis) in 80% of subjects and the mesosigmoiditis contracts the mesosigmoid, fixing it to the Psoas muscle, preventing coloptosia sigmoidea.  It is claimed that in coloptosia of the sigmoid that it forms dangerous obstructing angulation which is yet to prove.

Symptomatology.

    The symptoms of coloptosia include many due to general splanchnoptosia.  Some of the symptoms are (a) constipation; (b) diarrhea - (a) and (b) alternating - (c) colonic catarrh, mucous colitis or which I prefer to term secretion neurosis of the colon.  The colonic secretion, absorption, sensations, and peristalsis may be excessive, deficient or disproportionate.  Fermentation, and borbyrigmusarise.  Dragging sensations, fatigue, debility, multiple nervous symptoms.  In general the symptoms of coloptosia are stenosis compromised and irregular caliber, dilatation, retention, obstruction, constipation, disturbed circulation and ennervation, relaxed abdominal wall, pendulous abdomen, practical relief of symptoms on assuming the prone position.
    The dislocation of the colon favors constipation because the defective abdominal wall has lost its effective power to force the faeces distalward.  Since in dyspepsia, nervopathies of the tractus intestinalis, no local subjective pain is experienced by the patient, we do not palpate the abdomen sufficiently frequently.  First and foremost we should palpate the abdomen to determine whether the pathologic physiology of the tractus intestinalis be secondary or primary.  Many diseases have an intestinal origin.  Dyspepsia refers to the stomach only.
    Splanchnoptosia is a disease of malnutrition.  Palpation of the tractus intestinalis attempts to explore systematically the various segments and susceptibility to pain caliber, contents, tension, and mode of fixation.  Simon's method of rectal exploration with the hand we discard as unsuitable.  In palpation of the abdomen we must devote sufficient time to understand the occasional variation in the aortic rhythm.  As to Glenard's colic cord we must consider the small contracted stomach, the pancreas and colon transversum, as any one may be mistaken for the "colic cord," Whatever this cord can be, found in perhaps 10% of splanchnoptotics, we should attempt to note its accessibility, position, length, form, volume, consistence, mobility, sensation.  In palpation the idea of gliding the intestinal segments under the hand or gliding the hand over them must be practiced.  The colic cord is located in the relation with the umbilicus.  In the diagnosis of coloptosia search should be made for colonicptosia, dilation, constriction, stenosis, atony, decalibration, obstruction, retention.
    Diagnosis of coloptosia may be confirmed by colonic inflation per rectum whence one can by inspection and percussion trace the course of the colon fairly accurately.  By palpation one may manipulate the colon.  Glenard mentions a diagnostic clue to coloptosia transverse which he calls "corde colique transverse" - the cord of the transverse colon.  I have practiced on this subject in the dead splanchnoptotic and it is my opinion that Glenard's cord of the transverse colon is simply the pancreas in general.  It may be possible from the direction, dimension, location, consistence, mobility, sensibility, inflation, of the "colic cord" to detect the transverse colon in splanchnoptosia.  The cecum and right colon will be best located by inflation whence inspection and percussion are further aids.  We must attempt to note the location, dimension, consistence, mobility of the cecum and right colon.
    In the diagnosis of coloptosia the means at hand are (a) inspection; (b) palpation; (c) distension, inflation;,(d) consistence; (e) mobility; (f) sensibility; (g) colonic peristalsis.

Treatment.

    The treatment of coloptosia is medical, mechanical, surgical.
    1.  Medical treatment is comprised in diet, regulation of function, ample anatomic and physiologic rest and appropriate hygiene.  First and foremost is what we term "visceral drainage." By appropriate food which results in ample faecal residue, copious fluids at regular intervals with established hours for evacuation.  It may be practically claimed that every case can be controlled.  If colonic secretion, absorption and peristalsis be appropriately stimulated by proper food and ample fluid the colonic circulation and innervation will practically remain normal and the coloptotic though necessarily afflicted with a certain amount of pathologic physiologic physiology will remain practically with a few symptoms.
    2.  Mechanical treatment comprises abdominal bands, corsets, adhesive strapping, prone attitude.  Adhesive strapping (of Achilles Rose), which is economical, practical and rational, has in my practice rendered much comfort to patients.
    3.  Surgical treatment in coloptosia is absolutely limited.  It comprises two methods, viz.: (a) operations on the colon itself, fixing it to the abdominal wall or other viscus - colopexy.  As coloptosia is but a part and parcel of splanchnoptosia, colopexy is limited in its range and rational application. (b) The surgical treatment of diminishing the space of the peritoneal cavity by incising the abdominal and reuniting by superposition, overlapping its fascial and muscular walls like a double breasted coat, though limited in application, is the more rational.  This treatment attempts forcible retroposition of the colon to its normal location and maintenance in its normal visceral shelf by the abdominal wall.

Enteroptosia.

    In enteroptosia the enteron passes distalward and ventralward.  In advanced cases the enteron passes almost entirely into the lesser pelvis.  In this condition the transverse duodenum is compressed against the vertebral column by the superior artery, vein and nerve - the axial cord of the mesenteron producing gastro-duodenal dilation.  If the abdominal wall becomes relaxed the mesenteron becomes elongated from the viscera following the walls, the enteronic loops pass distalward into the pelvis and ventralward in contact with the relaxed abdominal wall.  Besides the basal mesenteronic insertion on the dorsal wall passes distalward.
    In advanced enteroptosia, the enteron experiences mulitple flexions, stenoses, dilation, dislocation, compromising circulation (faecal, blood and lymph), peristalsis, decalibration and traumatizing nerve periphery.  In enteroptosia the enteron not only changes its location but also its form, hence pathologic physiology must be expected as altered secretion, absorption, peristalsis, and sensation.  The blood and lymph circulation is compromised by flexion, elongation, contraction or dilation of the vascular channels ending in malassimilation.
    The splanchnoptotic is continually in the condition of pathologic physiology.  In splanchnoptosia absorption, secretion and sensation are disturbed, the blood and lymph occupy the greater and lesser pelvis, hence the nerves and vessels are placed on tension, in which the soft walled veins and lymphatus suffer.  In the examination of the abdomen for enteroptosia, inspection, palpation, percussion, attitude, location the gliding movement, auscultation the belt test, gurgling, should be employed.  The consistence, limited dimension and multiple enteronic coils increase the difficulty in diagnosis.  The enteronic coils are confined in the colonic square, greater and lesser pelvis.  Attenuated abdominal walls aid in diagnosis.

NEPHROPTOSIA IN SPLANCHNOPTOSIA.

Fixation of the Kidney (tractus urinarius).

    The two most important factors maintaining the kidney in position are the muscular action of the diaphragm and abdominal wall.  The action of the diaphragm is direct, that of the abdominal muscles indirect through the adjacent viscera.  Ventral to the right kidney are the liver, duodenum, colon and enteron.  Ventral to the left kidney are the stomach, spleen, colon and enteron.  Next to the muscles in importance is the perirenal tissue - the fatty capsule in which the kidney lies imbedded.
    The perirenal areolar tissue binds the kidney to the diaphragm and at the proximal renal pole it fuses with the meshepaticon on the right si e while on the left side the perirenal tissue fuses with suspensory ligament of the spleen and coronary ligament.  A strong renal support is the renal pedicle composed of the renal artery, vein, nerve plexus, lymphatics and fibrous sheath which emanates from the radix mesenterica.  The renal pedicle limits the extent of renal motion because the renal artery arises so near the radix mesenterica - the coeliac artery - that its origin is practically immobile.  The kidney possesses no visceral shelf, simply a shallow renal fossa or niche.  It lies proximalward and distalward on the dorsal abdominal wall in a shallow renal groove.  Hence the structures or bands which maintain the kidney in position are: (a) the diaphragm and abdominal wall; (b) perineal capsule; (c) renal pedicle; (d) viscera (indirect).

Respiratory Movements of the Kidney.

    The respiratory motion of the kidney is due to the contraction of the diaphragm on its proximal dorsal surface.  The kidney experiences respiration movements which include all splanchnoptotic viscera.  The proximal dorsal surface of the kidney lies on the diaphragm (hence diaphragmatic area) while the distal dorsal surface lies on the lumbar structures (Psoas, (juadratus and transversal muscles, hence lumbar area).  Inspiration forces the kidney distalward and ventralward (rotation) by means of the diaphragm while expiration allows the return of the kidney to its physiologic location (to its renal niche in the abdominal wall).  No doubt the ratatory motion of the kidney if extensive produces pain from renal pedicle torsion. (Dietl's Crisis).
    The kidney becomes nephroptotic by decreasing its subdiaphragmatic space.  On the right side the liver and kidney completely occupy the right subdiaphragmatic dome and one or both must yield in splanchnoptosia when the subdiaphragmatic space is diminished, hence Riedel's lobe or nephroptosia or both results.  From clinical observation it may be observed that the right kidney is manifestly nephroptotic 10 fold more than the left and that woman have 10 fold more nephroptosia than man.  However, this is more apparent than real and refers rather to palpable degrees than to actualities.
    If one examines a series of embryos, no difference can be observed between the right and left kidneys in males and females, hence the difference in position and degree of nephroptosia is a post natal acquirement.  One special variable element arises and progresses after birth and that is the relation of the coecum to the kidney.  The difference in position of the kidnev begins in male and female at pubertas.  At pubertas in females the diameter of the interiliac space begins to increase more rapid than the diameter of the intercostal space producing a distalward expanding funnel in the body trunk and this truncated funnel is irregularly compressed by the construction of clothing aiding to force the viscera distal to the corset line of constriction.  In long trunked, waisted women the constriction of the corset may force the kidney proximalward dorsal to the liver surface.  In short waisted women the corset is the more liable to force the kidney distalward extending it from the costo-diaphragmatic space where it is palpated with facility.

The Relation of Nephroptosia to the Liver or Bile Ducts.

    The nephroptotic kidney maintains two relations with the liver, viz.: (a) The kidney may be extended distal to the liver when its peritoneal and subperitoneal tissue connections may produce traction on the biliary passages, flexing and obstructing them a distalward nephroptosia.  I published such a case with illustration in the Medical Critic, May, 1903.  In this subject a peritoneal band extended from the kidney to the ductus choledochus communis. (b) The nephroptotic kidney may pass proximalward on the dorsal surface of the liver.  This is proximalward nephroptosia - a symptomless dislocation.  The influence of the nephroptotic kidney on the colon (hepatic flexure) or coecum is marked, however, limited in clinical influence.
    Nephrotosia ends in compromising of the subdiaphragmatic space, as: (1) contraction of the diaphragm on a relaxed abdominal wall (as in respiration). (2) by collapse of chest walls (consequent to disease); (3) constriction of the trunk (by clothing).  The left kidney is limited in motion in nephroptosia because it is maintained in position by the splenic flexure of the colon.
    The production of appendicitis by nephroptosia, as reported by Edebohls. I have been unable to confirm clinically or by autopsy.
    Nephroptosia has no special influence on disease of the tractus genitalis.  In nephroptosia the essential element to observe is the ventralward displacement produced by axial rotation on the renal pedicle induced by the diaphragm and which constitutes the mobile kidney that rotates on its pedicle occasioning a "crisis." It is not the distalward nor proximalward dislocation of the kidney that produces the so-called crisis.

Nephroptosia, Ren Mobilis.

    Floating or movable kidney, Nephroptosia, has received the major attention in splanchnoptosia and has unfortunately been the scapegoat for the numerous symptoms belonging to general splanchnoptosia.  It is admitted that nephroptosia may be the most striking feature in the examination of the splanchnoptotic patient, however, in the vast majority of subjects it is but a part and parcel of splanchnoptosia.  What is nephropotsia?  It is understood to be excessive renal mobility. The kidney is a mobile organ, not absolutely fixed.  It moves with respiration, perhaps 1/2 an inch of range.  It is difficult to draw the line between a normally mobile kidney and a pathologic one except through complex clinical symptoms.
    Perhaps 10% of subjects only possessing palpably mobile kidney suffer from nephroptosia.  In my practice among women I have palpated and perceived mobile right kidney in 60% of subjects.      However, 60% of patients were not afflicted with nephroptosia - floating kidney - as no symptoms existed.  In some 700 personal autopsic abdominal inspections I found that the general movement of the right kidney in its fossal bed was one inch proximalward and one inch distalward.  The left kidney moved about one-quarter of an inch less in its proximalward and distalward translations.
 

Fig. 191.  This figure presents established hepatic dislocation. 1, diaphragm; 2, meshepaticon; 3, lobus dexter hepatis; 4, ligamentum suspensorium hepatis; 5, colon transversum ; 6, enteron.

    In the bodies of large men the right kidney would not infrequently move over 1/2 inches proximalward - a range of renal movements of over 3 inches (proximo-distalward).  (However, it is my opinion that the dorso-ventral renal motion - the axial rotation of the kidney on its neuro-vascular visceral pedicle that inflicts damage and pain.) These subjects during life had not complained of mobile kidney nor had it been diagnosed.  From the induration of the perirenal areola, fatty capsule, the kidney has a greater range of motion in the living than the dead.

Etiology of Nephroptosia.

    The main causes are: (a) a predisposing body form; (b) rapid loss of perineal fat; (c) rapidly repeated gestations; (d) heredity-degeneration, inferior anatomy and physiology; (e) yielding of diaphragmatic supports;. (f) debilitating disease, form and dimension of the renal fossa.  The renal fossa varies in form and dimensions within certain limits in different individuals.  The narrower the distal end of the renal fossa the more immobile the kidney.  The renal fossa is broader and shallower in woman than man, hence more ren mobilis in woman than man.  The broad, shallow fossa renalis connected with a funnel-shaped trunk accounts for increased renal mobility.

Frequency of Nephroptosia.

    I think that 10% of female adults are afflicted with symptomatic nephroptosia.  In 60% of adult women visiting my office I can palpate mobile kidney.

Age Relations of Nephroptosia.

    Nephroptosia is at its maximum frequency and extent at 40 years of age.

Diagnosis of Nephroptosia.

    Nephroptosia is diagnosed by bimanual palpation in the lumbar region while the patient assumes the dorsal, prone, semi-prone and erect attitude.  Mobile kidney should not be mistaken for neurosis.
    If, in nephroptosia, one can find distinct renal pain, renal tenderness, renal hypertrophy, and that the ureteral pelvis of the same side will contain a greater quantity of fluid than the other, periodic hydro-ureter has probably begun.  If in a kidney of extensive mobility irregular pain presents it is probably due to rotation of the kidney on its uretero-neuro-vascular pedicle (Dietl's crisis) and ureteral dilatation (periodic hydro-ureter) has probably begun.

Position of the Kidney.

    In about 15% of subjects the kidneys are of the same level.  Doubtless the combination of longer right renal artery, the erect attitude (force of gravity) and the liver explains the variation in position between the right and left calyces and pelvis (kidney).
    In mammals the right kidney lies more proximal than the left because the right renal artery is longer, the attitude or force of gravity tends proximalward and the liver does not wedge itself between the kidney and diaphragm so vigorously as in that of man.  Also the left liver half is much more developed in quadrupeds than man and hence the gastrium and spleen is more distalward than in man.  Hence taking into account the larger size of the right hepatic lobe and the larger volume of the embryonic liver which checks the growth of the Wolffian body proximalward (Strube) it would appear that the liver has considerable influence in the more distal position of the right than the left kidney.  There is an age and functional relation of the position of the kidney, especially in children and women.  A child's kidney is more distal than that of an adult on account of its relative small volume and large volume of the liver.  Also during reproduction when the elements of the abdominal wall (elastic, muscular and connective tissue) elongate and separate, allowing the kidney to move distalward.  Besides the splanchnoptosia that increase after 30 years of age lends data to an age and. functional relation of the renal position.
    The statement is common among general surgeons who are prone to perform nephropexy, that the right kidney, which is most frequently operated, extends distalward to crista iliaca.  However, if one will carefully examine l00 male and female cadavers in regard to the position of the kidney and iliac crestit it will be found that the distal pole of the male kidney will be chiefly ¾ of an inch proximal to the iliac crest and that the distal pole of the female kidney will average over 1/2 inch proximal to the iliac crest.  Perhaps in man 10% of right distal kidney poles touch the iliac crest and perhaps 20% in woman touch the iliac crest.
    The left kidney is more proximally located.  When the distal renal pole projects distal to the crest of the ilium pathologic conditions (splanchnoptosia) will probably exist.  The kidneys are located in an excavation (what I shall term renal fossa) on the dorsal wall of the abdominal cavity on each side of the vertebral column fixed to the diaphragm and lumbar muscle by the capsula adiposa renalis or perirenal tissue, anchored medially by the neuro-vascular renal pedicle and maintained ventrally by the intraabdominal pressure (adjacent viscera and abdominal wall).  A most excellent and practical standard, notwithstanding individual variations for kidney measurements and for the purpose of noting the position of the kidney is the crista iliaca.  I used it as the chief standard in all measurements in some 700 autopsies.  In general the distal pole of the kidney extends to the IV lumbar vertebra.  In the examination of over 620 cadavers (man 465, woman 155), the general average was that the right kidney was one finger 3/4inch) proximal to the iliac crest while the left kidney was 2 fingers (1 1/4 inches).
    The kidneys of woman were about 1/2 inch more distal than those of man.  In about 15 aloof the females the right distal kidney pole was on a level with the crista iliac.  These data have no relation with the artificial range of motion that one can impose on the kidney during life and in the cadaver.  The kidneys of males had not such a high per cent of distalward position nor such free motion as those of females.  However, individual variation is prominent for in some male cadavers I found the highest form of free mobility, e. g., in one large male cadaver the right kidney presented a proximalward range of 2 inches and a distalward range of 2 inches - a total vertical range of 4 inches.  Conclusions in regard to the factors affecting the position of the kidney: 1. The chief factors in retaining the kidney in position is the length of the neuro-vascular renal pedicle, in short the arteria-renalis. 2. Pressure and counter-pressure of adjacent viscera. 3. Intra-abdominal pressure (pelvic and thoracic diaphragm and ventral abdominal walls). 4. Bodily attitude and force of gravity.  In man the right kidney is located distalward to the left.  In quadrupeds, the right kidney is located proximal to the left.  In man and quadrupeds the right arteria renalis is the longer. 5. The shape of the trunk, especially of woman, is that of a funnel with the larger end distalward. 6. In woman age and functional relations aid in inducing nephroptosia. 7. The diminished amount of panniculus adiposus renalls, through absorption tends to nephroptosia. 8. Elongation and separation of the elements (fascia, muscle and elastic fiber) of the abdominal wall, relaxation are among the most potent factor as regards the position of the kidney. 9. The peritoneum aids in maintaining the kidney in position.  10.  The liver, in foetal and adult life, the long right renal artery, the absence of the colon on the ventral right renal surface, the shallow right renal bed or niche and the less strong perineal fascia in the right kidney makes the right kidney more mobile than the left.
 

Fig. 192.  This figure represents advanced hepatic dislocation. 1, diaphragms 1, hepaticon; 3, dexter et sinister lobus liepatis; 5, liganmentum rottindum hepatis.  The liver is advanced sufficiently distalward to conceal colon, enteron, and kidneys.

Symptoms of Nephroptosia.

    Among the chief disturbing symptoms of nephroptosia I think is renal anteversion, torsion of the renal pedicle with ureteral flexion.  Torsion of the renal pedicle can be observed in life only in the erect attitude as the recumbent position, immediately corrrects renal dislocation.  When the subject of nephroptosia sits or stands the proximal pole of the kidney moves ventralward producing torion or rotating of the renal pedicle (artery, vein, nerves, lymphatics) and flexion of the ureter.  Torsion of the renal pedicle, renal anteversion, compromises the renal lymph, venous and arterial vessels as well as traumatizes the nerves in the renal pedicle.  Doubtless the essential benefit of mechanical abdominal supports in nephroptosia is the correction of the renal anteversion and consequent correction of torsioned renal pedicle.  Doubtless Dietl's crisis is torsion of the renal pedicle.  Kidneys with extensive range of motion (3 to 4 inches) in the living may be accompanied with no symptoms.  We frequently observe this phenomena.  If the proximal pole of the kidney becomes detached from the diaphragm, as it does in nephroptosia renal anten,ersion begins its slow march which is continually accelerated by the distalward movements of the liver and spleen through the contracting diaphragm.  Renal anteversion and consequently torsion of renal pedicle may be observed in the large, spare splanchnoptotic multipara by palpating especially the right kidney.  During the last 15 years in some 700 autopsies I have tested the renal range of motion in large numbers.  The verticle or proximo-distal translation of renal motion is but a factor in nephroptosia.  I have found both in the living and dead that the dorso-ventral renal translation motion and the torsion or twisting of the renal pedicle are potent factors in the symptom-complex of nephroptosia.
    The dorsal-ventral movements of the kidney consists of ventralward motion only in a zone of perhaps 2 inches.
    Nephroptosia comprehends the view of clinical symptoms complex in which the role of dragging sensations, pain in the anterior crural and genitocrural nerves, gastric crisis, constipation, dyspepsia and various degrees of neuroses, violent palpitation in the epigastrium.  Pains in the sacral and lumbar region.  Dietl's crisis-paroxysmal attacks of severe and intense pain, nausea and vomiting.  Dietl's crisis may be due to torsion of the renal pedicle or to periodic hydro-ureter.  We may note improvement during pregnancy and discomfort during menstruation.  Increased symptoms during walking occur and relief of symptoms on assuming the prone position.  The above symptoms simulate those of splanchnoptosia.  Nephroptotic symptoms are generally an incident only in splanchnoptosia.  A warning is here offered pot to attribute symptoms to nephroptosia that belong to splanchnoptosia.  For practically nephroptosia and splanchnoptosia are coexistent.

Treatment of Nephroptosia.

I. Medical.

    (a)  Visceral drainage.  The most important treatment in nephroptosia (which practically coexists with splanchnoptosia) is what I shall term visceral drainage, i. e., maximum sewerage or flushing by ample fluids of the tractus intestinalis, urinarius and perspirations with liberal supply of coarse foods which leave an indigestible foecal residue to stimulate peristalsis in the colon. (b) Position.  Nephroptotics should assume the recumbent position as much as convenient for they possess inferior anatomy and physiology.  It relieves symptoms - acts as a prophylaxis and aids in curing by inducing the kidneys to persist in their normal prevertebral fossae. (c) Nutrition.  Improve nutrition in order to redeposit the perirenal areolar capsule. (d) Pregnancy.  Gestation improves nutrition (and acts as a temporary mechanical support).  (e) Massage. (f) Gymnastics. (g) Electricity.

II.  Mechanical.

    Mechanical treatment signifies forcible reposition and retention of the kidney in its normal physiologic location.  This is excuted by: (1) Attitude.  The horizontal position relieves symptoms and aids in curing the disease. (2) Abdominal binders. (a) These may be elastic or nonelastic and are applied during the day (or erect attitude). (b) An elastic binder which contains between the binder and abdomen a pneumatic rubber pad (Byron Robinson).  This binder is applied while recumbent and the pneumatic pad distended to suit the comfort of the patient. (3) The corset.  This method has been successfully conducted by Dr. E. A. Gallant of New York.  The corset is made under individual measurements, applied while in the prone position and removed for the recumbent attitude. (4) Adhesive strapping.  This is executed by means of adhesive straps applied to the abdomen and is known as Achilles Rose's method (also independently introduced by Dr. N. Rosewater of Cleveland, Ohio, and Dr. B. Schmitz of Germany).  Straps of adhesive plaster of various width are passed entirely around the body, elevating and maintaining the abdominal viscera in the normal physiologic position.  Rose's method of adhesive strapping is simple, economical, rational and of vast practical utility. (5) Pregnancy.  Gestation temporarily relieves the symptoms of nephroptosia.

The Effect of Relaxed Abdominal Wall and consequent splanchnoptosia in Nephroptosia.

    Women with relaxed abdominal walls frequently suffer with nephroptosia.  In regard to the nephroptosia, the renal secretion is deficient, excessive, or disproportionate.  The exact relations of factors of the nephroptosia and relaxed abdominal walls to the disturbed renal secretion are not easy to be determined.
    The disturbed renal secretion would appear to be mainly due to disturbed renal mechanism.  The renal artery, vein and ureter become compromised in relation to the nephroptosia.  The passing distalward of the kidney from relaxed abdominal walls stenoses the ureter and renal vein.  The blood pressure, in the renal vein is low, and hence light disturbed renal mechanism will easily compromise its blood flow.
    In nephroptosia the distal pole of the kidney approaches the vertebral column disproportionately, and hence compromises the lumen of the ureter, damming the urine.  Outside of disturbed urine flow from changed renal mechanism, equally disturbing factors in nephroptosia arise from trauma to the renal plexus.  The renal plexus is a large collection of nerve plexuses and ganglia, and besides it is directly connected with the ganglia coeliacum, the abdominal brain, the largest ganglia in the body, which, being a reflex center outside of the spinal cord, reorganizes the reflexes and sends them to all other abdominal viscera.  Thus the patient with nephroptosia complains of nausea and vomiting and dragging pains.  She gradually becomes neurotic from reflexes due to trauma on the renal plexus.  The damage in nephroptosia is, perhaps, in order:
    1.  Trauma of the renal plexus (and abdominal brain), producing a vicious circle by continuous reflexes on the abdominal viscera.
    2.  Traumatic stenosis of the vena cava, ovarian and renal veins.
    3.  Stenosis of the ureter with dislocation of the kidney, preventing drainage.
    4.  Trauma of renal artery.
    5.  A combined dislocation of the renal mechanism is changing the relation of the renal vein, artery and ureter, a disturbed mechanism of the uretro-ureteral triangle.
    6. The producing of deficient, excessive or disproportionate renal nephroptosis suffers nausea, headache, foul secretion.
    7.  The subject with right breath, gastric disturbances and constipation, accompanied by the stigmata of hysteria and other neuroses.  As nephroptosia is only a part and parcel of general splanchnoptosis, nephropexy, which should be (lone b), placing the kidney in the abdominal wall witbout sutures, must be limited in its local and general utility, practically to periodic hydroureter.
 

Fig. 193 presents a common condition found especially in the multipara.  The left kidney is presented as normal to compare the contrast. 1, right kidney with its distal pole projecting distal to the iliac crest; 2, the elongated right arteria renalis. 3, the ureter in a sinuous course.  B, point where vasa ovarica crosses ventral to the ureter (apex of uterovenous triangles of author).  A presents the apex of the utero-venous triangle of the left side. 4, left kidney 5, left ureter. 6, left arteria renalis. 0, oesophagus.  C, arteria coeliaca.  S, arteria mesenterica superior.  V, vena cava.

The Uretero-Venuous  Triangles.  (Byron Robinson.)

    In dissecting, one finds on the left side of the body a triangle formed by the ureter on the left side, the ovarian vein on the right side, and the renal vein on the proximal end or base.  The sides of the triangle are about 2 to 3 inches and the base (the renal vein) is about 1 inch.  The apex of the triangle is at the proximal arterio-ureteral crossing of the utero-ovarian artery, located proximal or distal to the iliac crest.
    This is what I term the left uretero-venous triangle. Its outlines are distorted in left nephroptosis.
On the right side of the body what I term the right uretero-venous triangle is formed by the ureter on the right side, the vena cava and ovarian vein on the left side, and the renal vein on the proximal end or base.  The right uretero-venous triangle is about an inch at its base (the renal vein) and 2 inches on its sides.  Its apex is at the proximal arterio-ureteral crossing of the utero-ovarian artery, and is located 1 1/2 to 2 inches distal to the iliac crest.  The significant factor in the right uretero-venous triangle is that in nephroptosia it becomes markedly distorted, compromising the lumen of the ureter, ovarian and the renal veins.  The uretero-venous triangles, bilateral distinct, constant structures, are significant landmarks in topographical anatomy.  I have not observed them named or described.  They vary considerably in size from the varying location of the apex at the crossing of the ureter by the ovarian vein and artery.  The apex of the uretero-venous triangle I have designated as the proximal arterio-ureteral crossing (of the utero-ovarian artery).  In nephroptosia the uretero-venous triangle is distorted and the lumen of the vein and ureter is compromised.

III Surgical.

    Nephropexy in general is irrational and unjustifiable (except in periodic hydroureter), because: (a), it is unphysiologic to fix mobile viscera; (b), the kidney, does not remain fixed; (c), the nephroptosia is but an incident, a fragment of splanchnoptosia; (d), the remaining - or adjacent viscera are deranged, splanchnoptotic; (e), the surgeon attempts to relieve one lesion or disease (excessive mobility) by producing another lesion or disease (fixtion) - which is the more irrational; (f). the multiple methods of nephropexy condemn it; (g), nephropexy does not remove the splanchnoptotic symptoms which coexist; (h), surgeons do not agree as to the indications for nephropexy, as the symptoms of nephroptosia are not proportionate to the degree of mobility; (1), the mortality of nephropexy is at least I per cent; (i), nephropexy should be systematically refused, discarded, condemned, for more rational methods (unless periodic hydroureter exist).  The therapeusis should be executed through the abdominal wall (medical, mechanical, surgical).  The incised abdominal walls should be superimposed, overlapped like a doublebreasted coat.  It is doubtfully justifiable to perform nephropexy on a replaceable kidney unless periodic h),droureter can be demonstrated.
Nephropexy should be performed only after all palliative measures have been tried.
    By observing the final results of nephropexy extending over a decade and including numerous subjects, it is not flattering.  Professor John A. Robison, of Chicago, relates to me personally that during the past ten years that a considerable number of his patients had visited different surgeons and had undergone the operation of nephropexy.  Dr. J. A. Robison asserts that he not only observed that the patients received no benefits from the nephropexy but that the results were damaging in almost every subject.

GASTRO-DUODENAL DILATATION IN SPLANCHNOPTOSIA.

A Phase or Complication in Splanchnoptosia.

    The dilatation of the Stomach and duodenum (gastro-duodenal dilation) is due to pressure of the superior Mesenteric artery, vein and nerve on the tranvserse segment of the duodenum.
In 1893, the time of the Chicago World's Fair while giving courses to physicians on abdominal visceral anatomy and its applied surgery, I became interested in the manner in which the transverse segment of the duodenum was compressed by the superior mesenteric artery, vein and nerve.  I well remember the discussions of the physicians in the classes at that time, who concluded that the superior mesenteric vessels and nerves would not obstruct the duodenum, because the duodenal contents were almost entirely fluid and gas.  However, we all observed that in a spare, though normal subject, the superior mesenteric vessels and nerves very suspiciously compressed the transverse duodenal segment.  We selected spare, fatless, subjects for visceral demonstration, and the distinct mechanical apparatus of mesenteric vessels and nerve clamping the transverse duodenum against the vertebral column as a base made an indelible impression.
 

Fig. 194. is a cut to illustrate the position of the duodenum and the superior mesenteric artery, vein and nerve. 1, the superior mesenteric vein; 2, superior mesenteric artery, the nerve not represented in the cut; 3, distal end of duodenum; 4 and 5, stomach; 6, hepatic artery; 7, splenic artery; 8, gastric artery, the hepatic and gastric arteries making what I shall term the gastrohepatic circle; 9, the oesophagus; 10, the gall-bladder; 11, the pylorus; 12, the duodenum; 13 and 16, gastro-epiploca sinistra et dextra; 17, spleen; 15, part of liver.  This ctit shows that the duodenum in the acute mesenterico-aortic angle is the acute mesenterico-vertebral - however, the real angle of strangulation.

    I have pursued the matter during the past thirteen years in subjects possessing visceral ptosis, and found that when the coils of enteron lie in the pelvis the superior mesenteric artery vein and nerve compress the transverse segment of the duodenum in such a manner that gastro-duodenal dialatation begins in the transverse segment of the duodeum immediately on the right side of the superior mesenteric vessels and nerve.  I have observed this so frequently in hundreds of autopsies that I know it to be an important factor in gastro-duodenal dilatation in persons suffering from visceral ptosis, splanchnoptosia.
 

Fig. 195. shows the relation of the duodenum transversum, pancreas, celiac axis, superior mesenteric artery, vein and nerve with the stomach drawn proximally. 1 and 2, superior mesenteric artery and vein; 3, aorta; 4 and 5, transverse segment of duodenum passing posterior to vessels; 6 and 7, pancreas; 8, spleen; 9, splenic artery; 10, hepatic, and 11, gastric arteries forming the gastro-hepatic circle; 13, portal vein; 14, duodenum ; 15 and 16, stomach; 17 and 18, epiploic arteries.  This cut shows how naturally the vessels could compromise the distalward-moving fecal current in the duodenum.  The fixation of the transverse segment of the duodenum by the musctilaris suspensorius and the fibromas band from the left crus of the diaphragm is not drawn in the cut.

    Previous to 1893 I had performed a considerable number of autopsies, but without detailed records of abdominal inspection.  Since 1893 I have detailed records of personal autopsic inspection of the abdomen in 165 adult females, and 480 adult males and some 50 children.  Besides, I have also pursued the study of visceral ptosis, and relaxed abdominal walls - splanchnoptosia in the living patients and abdominal sections.  In clinics and autopsy it is realized with facility that splanchnoptosia is a frequent, common disease.  I systematically examined in the 700 detailed autopsies the tractus intestinalis, tractus genitalis, the tractus urinarius and also the peritoneum.
    Since Glenard's celebrated labors on splanchnoptosia (1884) considerable study has been devoted to the position of the abdominal viscera.  The study of the position of the abdominal viscera has progressed, however, in an irregular method.  When Dr. Eugene Hahn, the brilliant Berlin surgeon, first introduced and performed nephropexy, superficial surgeons made a rush for a so-called new operation, with little idea that nephroptosia is only a part and parcel of general splanchnoptosia.  Visceral ptosis may begin in early years of age, and increases every subsequent decade of life.  My knowledge of splanchnoptosia or visceral ptosis was gained during the past twenty years by the personal autopsic inspection of 700 adult abdomens, 50 children, quite a number of fetuses with hundreds of peritonotomies.
    I have been for years attempting to prove, by postmortem examination and peritonotomies and celiotomies, that in a considerable number of cases dilatation of the stomach is caused through pressure of the superior mesenteric artery, nerve and vein on the transverse segment of the duodenum.  In these subjects the stomach does not begin to dilate at the pylorus, but in the duodenum at the right side of the superior mesenteric artery, vein and nerve.  The stomach alone is not dilated.  The compression of the duodenum by the superior mesenteric artery and vein and nerve is typically manifest in a subject with splanchnoptosia or visceral ptosis, and especially while lying on the back.  Practically it is not gastric dilatation - it is gastro-duodenal dilatation.
    In 700 autopsies I have noted perhaps 50 advanced typical subjects presenting some distinct and some extensive gastro-duodenal dilatation, which began in the duodenum on the right side of the superior mesenteric artery, vein and nerve.
    The careful dissector wonders why the superior mesenteric artery, vein and nerve, all bound in a strong fibrous bundle and tightly compressing the transverse segment of the duodenum, do not produce obstruction in the duodenal segment of the tractus intestinalis.  At first thought it is because the bowel contents in the duodenum is liquid or gas.  This may be always, or nearly always true in absolutely normal subjects, but in the numerous subjects with splanchnoptosia or visceral ptosis it is not true.  It must be remembered that gastro-duodenal dilatation is a phase or stage or a complication in progressive splanchnoptosia.  The more splanchnoptosia exists the more the loops of the enteron pass distalward into the lesser pelvis, dragging and tugging on the superior mesenteric artery, vein and nerve, which more and more tightly constricts the duodenum transversum, because the latter scarcely at all moves distalward.  If the subject possesses considerable splanchnoptosia, and for any reason lies considerable time on back, the gastro-duodenal dilatation may progress quite readily.
 

Fig. 196. is a cut to illustrate the final growing gastroduodenal dilatation dile to obstructing the duodenum by the superior mesetiteric arterv, vein and nerve.  The white portion of the stomach and duodenum represent the normal size, the adjacent dark portion is the dilated part. 1 and 2, the superior mesenteric vein and artery; 3, aorta; 4, the non-dilated portions of the duodenum, distal to the constricting vessels; 5 and 6, original normal stomach; 9 and 10, the non-dilated duodenum; 11, 12, 13 and 14, the dilated portions of the duodenum; 15, the hepatic, and 16 and 17, the gastric arteries forming the gastro-hepatic circle; 18, aorta; 19, celiac artery; 20, esophagus; 21, hepatic artery; 22, spleen; 23, pylortis.  In this cut the actite mesenterico-vertebral angle shows plainly how it strangles or obstructs the transverse duodenal segment in visceral ptosis.

    The most typical case in the living I have witnessed was one to whom Dr. Coons, of Chicago, called me in 1898.  The patient, a man, about 45 years of age, had been in bed perhaps 5 months with hip-joint disease.  He had some lordosis.  The abdomen was enormously distended, and he vomited continually.  I thought of some form of obstruction in the tractus intestinalis, and proposed that abdominal section gave the only faint hope of relief.  The patient quickly and cheerfully gave his consent.  I made an incision in the median abdominal line and found the abdomen absolutely filled from pelvic to thoracic diaphragm with a white, shiny distended cyst, which proved to be the enormously dilated stomach and duodenum.  If the subject bad been a woman the tumor would be immediately taken for an ovarian cyst.  In the patient's debilitated condition I could do nothing with such an enormous dilated stomach, and finding no apparent intestinal obstruction closed the abdominal incision.  The patient subsequently died   and an autopsy was allowed.  We found the enormously dilated stomach and duodenum gastroduodenal dilatation - caused by constriction of the superior mesenteric artery vein and nerve on the transverse segment of the duodenum.  The subject possessing considerable degree of splanchnoptosia and lordosis, with several months lying on his back in bed made the progress of the gastro-duodenal dilatation rapid in its course.          Gastro-duodenal dilatation - a slow, gradual, chronic process - doubtless accounts for numerous so-called idiopathic gastric dilations subsequent to laparotomies.  The explanation of acute gastric dilation (it is gastric-duodenal dilation) is an exacerbation of chronic gastro-duodenal dilation.  In every fifty autopsies I have noted typical cases where it was gastro-duodenal dilatation, not merely gastric dilatation.  In many cases one observes a slight dilatation which does not present itself as typical, but by careful examination and test by forcing the gascotis contents of the stomach through the duodenum distinct gastro-duodenal dilatation can be seen to begin at the right side of the band formed by the combination of the superior mesenteric artery, vein and nerve.
    One can easily experiment on the cadaver to prove that the obstruction lies at the point of the duodenum where it is crossed by the superior mesenteric artery, veins and nerve.  By placing the superior mesenteric artery, vein and nerve on a tension, i. e., by dragging the enteronic loops distalward and compressing the gas in the stomach, the obstruction is plainly visible by a distension of the duodenum at the right side of the structure (vessels and nerve) which constrict the duodenum transversum.  The dilatation is caused first by gas and second by fluids.  I have studied the subject of gastroduodenal dilatation from 1893 and since I have found no records of it in literature, except that of Albrecht, in 1899, six years after I began, it seems to be original.  The subject of gastro-duodenal dilatation as caused by the constriction of the superior mesenteric artery, vein and nerve is original with me. I published my first formal article in 1900.
 

Fig. 197. a profile view of the acute mesenterico-aortic (mesenterico-vertebral) angle presenting the method of duodenal obstruction by the mesenteric vessels.  This obstruction is especially increased when in visceral ptosis.  The loops of enteron drag on the superior mesenteric artery (3) and pass in the direction of the arrow toward the pelvis.  The mesentericoaortic angle (eventually the mesentericovert5bral angle) has already advanced to a partial obstruction of the duodenum. 1, duodenum; 2, aorta; 3, superior mesenteric artery; 4, superior mesenteric artery passing to coils of enteron; 5, superior mesenteric angle passing to colon; 6, transverse colon; 7, blades of omentum majus passing proximalward to gastrium; 3, blades of omentum majus passing distalward; 10, inferior mesenteric artery; 11, abdominal aorta lying between the origin of the superior and inferior mesenteric arteries.  The arrow points to the pelvis and indicates how the superior mesenteric artery clamps tighter and tighter the duodenum with advancing visceral ptosis.

    Dr. John M. T. Finney, associate professor of surgery in Johns Hopkins medical school, wrote the following in the Annals of Surgery: "It is a fact worthy of note in passing that Dr. Byron Robinson of Chicago in 1900 appears to have been the first one in this country to bring this condition to the attention of the profession in a publication.
    In 1896 I made an abdominal autopsy on a case for Dr. Holman.  We found extensive gastro-duodenal dilatation with marked distalward dislocation of the stomach (gastroptosia).
The woman vomited, I was informed, for a couple of years before her death, which appeared during life as a kind of marasmus.  Death was undoubtedly due to malassimilation, due to disturbances in the system caused by extensive gastro-duodenal dilatation.
    In 1895 Drs.  Fruth and Henry, of Ohio, referred to me a patient who had scarcely kept fluid or food long in the stomach for twenty months or more.  She was emaciated, and I could detect only a distended or dilated stomach.  The gastroptosia is easily detected, for, after the stomach is irrigated, it is pumped full of air and this method easily demonstrates its outline.  I thought this patient had a stricture of the pylorus, and perhaps a carcinoma, but she did not lose flesh nor had she paled sufficiently for malignancy.  On opening the abdomen all we found was an enormous gastro-duodenal dilatation which extended distal to the pelvic brim, yes, into the lesser pelvis.  I performed gastro-jejunostomy with my segmented rubber plates.  She made a favorable recovery, and wrote to me seven years after the operation that she was perfectly well.  Dr. Henry, of Fostoria, Ohio, her physician, reported in 1905, ten years subsequent to the operation, that she is well.  In hundreds of personal autopsic abdominal inspections I have noted the state of the duodenum and stomach since 1893, and gastro-duodenal dilatation is a common disease in subjects over 30 years of age, especially in multiparae, in whom I have palpated the liver partly resting in the lesser pelvis.  After fifteen years of observation of visceral ptosis I am convinced that gastroduodenal dilatation is the indirect cause of ill health and of many deaths in persons above thirty years of age.
    Gastro-duodenal dilatation is not found in normal subjects.  It would appear that the main disturbance in gastro-duodenal dilatation begins when the enteronic loop passes distalward over the pelvic brim or promontory.  It might appear strange that the mechanical arrangements of animal structure would tend to destroy its own existence.  A little study of this region will explain why the duodenal obstruction arises.  The gist of the explanation lies in the anatomic fact that (a) the transverse duodenal segment in the splanchnoptosia does not travel distalward as rapidly as does the enteron.  (b)  In adults the duodenum possesses a mesenterii membrana propria only (no Deritoneal mesentery).  It does not possess a peritoneal mesentery.  This fact alone explains why the duodenum does not move distalward as rapidly as the remaining enteron, which possesses a 6-inch mesenteron. (c) Again, the musculus suspensorius duodeni of Treitz arises adjacent to the coeliac axis and inserts itself into the duodenum, circumscribing limited motion to it - duodenum - practically imposing localized fixation on the doudenum.  This second important anatomic factor serves as a second explanation why the transverse segment of the duodenum does not pass as rapidly distalward as the enteron, which is maintained by an elongated mesentery. (d) A third explanation why the transverse duodenal segment does not pass distalward as rapidly as the enteron is that, the transverse duodenal segment maintained by the mesenterii membrana propria, does not yield and follow the relaxed abdominal walls as does the mobile enteron.  Hence, since the transverse segment of the duodenum does not travel distalward as rapidly as the enteron in visceral ptosis, it becomes clamped tighter and tighter in the diminishing acute angle between the vertebral column and the mesenteric cord (formed by the mesenteric vein, artery and nerve).  The chief clamping of the duodenum begins when the enteronic coils pass distalward into the lesser pelvis.  The expanding and proximalward moving uterus during pregnancy forces the enteronic coils proximalward, increasing the angle between the vertebral column and the mesenteric cord (superior mesenteric artery, vein and nerve), and this relieves the gastro-duodenal obstruction similar to an abdominal binder.
    One scarcely sees the duodenum in a hernia.  The text-books on hernia note that every organ of the abdomen has been found in hernia except the duodenum, pancreas and liver.  Dr. Lucy Waite and myself have made autopsies in which the stomach rested on the pelvic floor.  This extends tubular viscera and dislocates the parts so that partial obstruction arises from mesenterial vessels.
    Fig. 198 shows diagrammatically how the superior mesenteric artery, vein and nerve obstructs the transverse segment of the duodenum as it crosses the vertebral column.  Increasing enteroptosis (i. e., the passing of the enteron more and more into the lesser pelvis) makes more and more acute the mesenterico-vertebral angle, and. as the duodenum does not pass distalward as rapidly as the enteron, obstructs rapid progress. 1, vertebral column; 2 and 3, normal stomach ; 4, the dark outline represents the dilated portion; 5, superior mesenteric artery; 6, superior mesenteric vein; 5, 6, and 7 are bound by a strong sheath of connective tissue into a bundle as large as the little and ring finger.  Occasionally in visceral ptosis one must lift several pounds in order to elevate this superior mesenteric band from the duodenum. 8, the white, is normal duodenum; 9 and 11, dark, is the dilated portion of the duodenum due to the obstructing mesenteric vessels and nerve, hence the end result is gastro-duodenal dilatation; 11, the enteronic loops in the pelvis dragging the mesenteric vessels over the sacral promontory like a rope over a log.  The colon transversum is resected and removed P. S. In the abdomen of such a case of visceral ptosis as Fig. 184 the stomach would extend to the sacral promontory and the transverse duodenum would be relatively slightly moved distalward on account of its fixation apparatus (i. e., the musculus suspensorius duodeni and the fibrous band connecting the duodenum to the right crus of the diaphragrp).  In enteroptosia the superior mesenteric artery, vein and nerve must elongate and attenuate, unlike the uterine artery in pregnancy, which not only elongates, but thickens.
    In 1794, when Sir Astley Cooper and Mr. Cline performed an autopsy on Mr. Gibbon, one of the greatest of English writers and philosophers, they found the whole tractus intestinalis except the duodenum (and cecum) in the hernial sac.  The distinguished patient had suffered and died from a left inguinal hernia, and the fact of the long continued hernia and visceral ptosis shows that the transverse duodenum is the last segment of the tractus intestinalis to yield to the dragging hernial sac, the lax abdominal wall and intra-abdominal pressure.  For thirty years, in the case of Mr. Gibbon, the duodenum transversum had resisted traction of the hernial sac and intra-abdominal pressure and still practically retained its relative position.  The scrotal hernial swelling extended to his knees, placing all neuro-vascular visceral pedicles on high tension, as well as extending pathologically tubular viscera and visceral ligaments.
    I have observed no record of the duodenum or pancreas in a hernia.  My dissections appear to demonstrate the musculus suspensorius duodeni chiefly originates in the tissues about the coeliac axis, and is then inserted into the duodenum transversum as a broad, ribbon-like muscular band.  Besides a powerful fixation apparatus is given to the duodenum by a strong fibrous (and perhaps muscular) band, which, by traction, shows that it arises from the left crus of the diaphragm.  Hence, the coeliac axis and the crus of the diaphragm being the fixation apparatus of the transverse duodenum by means of the musculus suspensorius duodeni and the fibro-muscular band from the crus of the diaphragm, the duodenum transversum becomes the most fixed organ of the abdomen.

Diagnosis of Gastro-Duodenal Dilatation.

    To be useful to subjects afflicted with gastro-duodenal dilatation (a phase of splanchnoptosia) we must first and foremost establish the diagnosis.  The first postulate to entertain is that in established splanchnoptosia gastroduodenal dilatations phase, a step in the progress of splanchnoptosia-in all probability exists.  The gastric dilatation can be established with facility by aid of the sodium bicarbonate and tartaric acid test of the forcing of air in the stomach demonstrating the contour of the stomach.  If gastric dilatation exists in splanchnoptosia the probability is that duodenal dilatation also exists, i. e., gastro-duodenal dilatation is the probable diagnosis.  To my mind this explains the so-called acute idiopathic dilatation of the stomach subsequent to laparotomies.  A factor that increases gastro-duodenal dilatation is the dorsal position of the patient which is assumed almost immediately after the operation.  The trauma and infection resulting from manipulation of the viscera becomes suddenly manifest after the operation by paresis of the stomach and consequent rapid dilatation.  Splanchnoptotics do not resist infection vigorously.  The gastric fluids and gases accumulate and not being expelled distalward or proximalward distend the stomach.  There is nothing idiopathic in this condition.  The factors are evident, viz: (a) a preexisting gastro-duodenal dilatation (splanchnoptosia); (b) gastric (visceral) paresis from traumatic manipulation; (c) gastric (viscera) paresis from infection.  The stomach contents of patients suffering from so-called acute (idiopathic) gastric dilatation subsequent to peritonotomy seems to flow out of the mouth like a river - it resembles the facile flow from the verticle stomach of an infant.  The treatment for such patients is immediate and repeated gastric lavage furnishing immediate and wonderful relief.  All fluids and foods for such a patient should be by gradual slow rectal irrigation - say a pint of normal salt solution should be introduced in the rectum every two hours and require thirty minutes to flow from the fountain syringe into the rectum.
 

Fig. 199. (author) illustrates the superior mesenteric artery, vein and nerve bound in a large strong bundle and clamping the transverse segment of the duodenum, producing gastro-duodenal dilatation. 1, superior mesenteric vein; 2, nerve and third artery; 9, the duodenum on the right side of the vessels and nerve.  The artery, vein and nerve forms the mesenterico-aortic angle, but the actual compression angle is the mesenterico-vertebral angle.  The loops of enteron are drawn to the left in order to expose the vessels and nerve.

The Treatment of Gastro-Duodenal Dilation Due to Compression of the Superior Mesenteric Artery, Vein and Nerve.

Medical; (2) mechanical; (3) surgical

I.  Medical

    The medical treatment has regard to maintaining normal functions of the stomach (and other viscera), viz.: (a) sensation; (b) peristalsis; (c) secretion; (d) absorption.  The functions of the stomach are maintained by appropriate foods and fluids.

(A)  Fluids.

    The splanchnoptotic requires ample drainage of the tractus intestinalis (and urinanus).  The patient should drink eight ounces of fluid (the most useful is ½ to ¼ normal salt solution) every two hours for six times daily.  The fluids stimulate sensation, peristalsis, absorption, secretion in the stomach enabling the gastrium to wash itself, to irrigate its surface and by stimulation of its muscularis to evacuate itself.  The sodium chloride stimulates the gastric epithelium.  The fluid increases the blood volume (which especially stimulates gastric peristalsis), eliminates Waste laden material especially through the kidney and bowel.  In order to stimulate the tractus intestinalis to maximum function or activity I add to the eight ounces of one-half normal salt solution every two hours a part or multiple of an alkaline tablet composed of cascara sagrada (1-40 gr.), NaHCO3 (gr. 1), KHCO3 (1-3 gr.), MgSO4, (2 gr.), Aloes (gr. 1-3).  The tablet is used as follows: One-sixth to one tablet (or more as required to move the bowels, once daily) is placed on the tongue before meals and followed by 8 ounces of water (better hot).  At 10 a. m., 3 p. m., and bedtime one-sixth to one tablet is placed on the tongue and followed by a glassful of fluid.  In the combined treatment the fragment or multiples of sodium chloride tablet and alkaline tablet are both placed on the tongue together.  I employ for the sodium chloride solution or NaCl tablets of 12 grains each and use fragments of it.

(B) Foods.

    Appropriate foods are a necessity in gastroduodenal dilatation.  Food must be wholesome as cereals, vegetables, albuminoids.  All fermentative foods should be avoided, as pies, cakes, pastries, puddings, concentrated spices and condiments.  The appropriate food excites the functions of the stomach which promptly evacuates itself.  If food remains in the stomach for over 3 1/2 hours indigestion, fermentation will result.  In gastro-duodenal dilatation the essential necessity is rapid and complete gastric evacuation, i. e., maximum stomach drainage.  In gastro-duodenal dilatation two conditions exist, viz.: (a) one is where the pyloric ring dilates in proportion to the gastro-duodenal dilatation.  This condition permits favorable gastric evacuation; (b) the second condition is where the pyloric ring does not dilate in proportion to the gastro-duodenal dilatation.  This condition is unfavorable for proper gastric evacuation and is a serious menace to the splanchnoptotic.  It is a condition requiring surgical interference - gastro-jejunostomy.
    Maximum nourishment produces and maintains a normal panniculus adiposus which aids to maintain, support, viscera in their normal physiologic position.
 

Fig. 200.  An illustration of the clamping of the duodenum, in splanchnoptosia, by the mesenteric vessels.  D, duodenum, the enteronic coils are well distalward in the lesser pelvis.

Fig. 201 represents gastro-duodenal dilatation ending when the mesenteric vessels cross the transverse duodenum.

    Numerous subjects exist with advanced gastro-duodenal dilatation, but do not suffer marked symptoms because physical conditions are favorable and the pyloric ring is ample in dimensions to allow complete gastric evacuation.  In 1894 Dr. Lucy Waite and I performed an autopsy on a man 70 years of age.  We found gastro-duodenal dilatation advanced to the degree that the stomach rested on the pelvic floor.  No record of any symptoms existed during life because the pyloric ring was proportionately dilated with the gastrium and duodenum offering limited obstruction to the evacuation of the stomach contents.  Whereas in another autopsy in 1895 on a woman who vomited for two years with gastro-duodenal dilatation the data was reversed.  In this female subject I found enormous gastro-duodenal dilatation and the stomach projected practically to the lesser pelvic floor-however, the pyloric ring was remarkably limited in dimension and gastric contents were forced through with difficulty.  Residual food and fermentation occurred.  The continued combined treatment of the 3 pints of 1/4 sodium chloride solution and alkaline tablets 1-6 to 3, as required to move the bowels once daily, are the necessary visceral drainage treatment in gastro-duodenal dilatation (splanchnoptosia).  The alkaline and sodium chloride tablets take place of the so-called mineral waters.  I continue this dietetic treatment of fluids and foods for weeks, months (the splanchnoptotic requires lifelong treatment) and the results are remarkably successful especially in pathologic physiology of visceral tracts.  The urine becomes clarified like spring water and increased in quantity.  The tractus intestinalis becomes freely evacuated, regularly, daily.  The tractus vascularis increases in volume and power.  The blood is relieved of waste laden and irritating material.  The tractus cutus eliminates freely, and the skin becomes normal.  The appetite increases.  The sleep improves.  The patient becomes hopeful, natural energy returns.  The sewers of the body are drained and flushed to a maximum.  Subjects with gastroduodenal dilatation should take a limited quantity of food every three hours for four times daily so that the stomach may not be extensively distended or taxed.

II.  Mechanical.

    (1) Abdominal binders generally afford comfort and relief in gastroduodenal dilatation (if the pyloris is proportionately dilated).  The kinds employed are: (a) the author's pneumatic rubber pad placed within an abdominal binder and distended to suit the comfort of the patient (it should be removed at night). (b) E. Gallant's corset. (c) Achilles Rose's adhesive strapping.  The above mechanical contrivances afford vast comfort and relief in gastro-duodenal dilatation by: (1) forcing the viscera proximalward in their normal physiologic position.  It aids the stomach in evacuation. (2) They force the viscera (especially the enteron) proximalward and increase the dimension of the mesenterico-vertebral angle relieving the transverse duodenum of pressure and permitting free evacuation of stomach and duodenum.  Achilles Rose's rubber adhesive strapping is particularly useful-rational, practical, economical.
    (2) Position.  I found that by experimenting with the dead body that position had much to do with the pressure of the mesenteric vessels on the duodenum.  The pressure of the mesenteric artery, vein and nerve on the transverse segment of the duodenum is the greatest when (a) the patient lies on the back and the enteronic coils lie in the pelvis; (b) when lying on the abdomen the pressure is mainly relieved; (c) when the patient is turned on the side the pressure is relatively light.  Hence the best position of the patient in gastro-duodenal dilatations is lying on the abdomen; and second, lying on either side.  Lying on the back or standing increases compressions of the duodenum by the mesenteric vessels.

III.  Surgical.

    Surgical intervention should be applied to gastro-duodenal dilatation when all other therapeutic measures have been tested and failed.
    (1)  Visceral anastomosis or Gastro-jejunostomy.  I consider one of the most useful surgical methods to overcome extreme gastro-duodenal dilatation is gastro-jejunostomy.  It limits the food journey and time for fermentation, and facilitates gastro-duodenal drainage.  I proved in gastro-jejunostomy in dogs, ten years ago. that it will enable the stomach to completely evacuate itself, to contract because the food does not tarry in the stomach but passes immediately into the jejunum and ileum, the business portion of the tractus intestinalis.  Any segment of the tractus intestinalis containing no contents or over which no food travels will remain contracted.  Anyone can prove this by excluding a segment of the bowel from faecal circulation; it soon contracts and remains in that condition.
    Gastro-enterostomy is the most certain and useful of all operations for gastro-duodenal dilatation.  It affords the one necessity, gastric evacuation - complete visceral drainage.  I have reports of gastro-enterostomy for gastro-duodenal dilatation of 12 years' duration and perfectly well.
    (2)  Superposition of the abdominal wall.  Longitudinal overlapping of the abdominal wall resembling a double breasted coat is an excellent operation for some subjects afflicted with gastro-duodenal dilatation.  I perform it with permanently burned silver wire sutures, three to the inch.  In the Mary Thompson Hospital during the past five years its application has been remarkably successful.  The Mayos have advocated the proximo-distal superposition of the abdominal walls (especially in umbilical hernia).
    (3)  Resection of the duodenum.  The duodenum could be resected at a point to the right of the constricting mesenteric vessels and its divided ends reunited ventral to that of the constricting mesenteric vessels.  Perhaps it would be practically better to perform gastro-jejunostomy.
    (4)  Enclosing the musculi recti-abdominales in a single sheath.  My attention was called to the subject of lax abdominal walls by Prof.  Karl Schroeder, whose pupil I was for a year.
    In that year (1884-1885) Prof.  Schroeder, the greatest gynecologic teacher of his age, was at the zenith of his fame, and his clinic was vast; in fact, he tapped the whole of Europe for his material.  He discussed in his clear style the misfortune of lax abdominal walls, and he resected large oval segments of the abdominal wall lying between the diastatic recti-abdominales.  He then united the sheaths of the recti in the median line.  But Prof.  Schroeder said then to his pupils that he was not fully satisfied; however, it was the best surgery that he knew at that time.  Later German surgeons improved on Schroeder's idea by splitting the sheath of the recti and enclosing both the recti-abdominales in one sheath by uniting the recti sheaths ventral and dorsal to the recti muscles.
    In 1894, Prof. N. Senn, in his clinic, began splitting the sheaths of the recti-abdominales and uniting the sheaths anterior and posterior, enclosing both musculi recti-abdominales in a single sheath.
    In 1895, Dr. Orville W. MacKellar and I operated on a woman pregnant for five months for an ovarian tumor where the diastases, of the recti-abdominales was very marked, and the uterus, on coughing or extra intra-abdominal pressure, would project between the recti-abdominales.  We united the split sheaths of the recti ventrally and dorsally, enclosing the two musculi rectiabdominales in one sheath.  Dr. MacKellar reports to me that his case is perfectly well and the operation was a success.  Dr. MacKellar was at the delivery and the recti sheaths remain perfectly intact.  For a large postoperative hernia for the past four years at the Mary Thompson Hospital I have split the recti and enclosed them in a single sheath for every one with sufficient experience knows that the post-operative hernia of any considerable size in women over 35 is in nearly every case accompanied by visceral rtosis.  Dr. MacKellar and I have records to show that ten years after the Enclosing of the two recti-abdominales in a single sheath for visceral ptosis (utero-ptosis) the operation is a success.  The mesenteron is not to suspend the enteron but to act as a neurovascular visceral pedicle and to prevent the enteron from entanglement with either viscera.  It is the abdominal wall that holds the viscera in position.  Besides, I showed in 600 detailed records of personal autopsic abdominal inspections that in 96 per cent of subjects the enteron had a mesenteron sufficiently long to herniate through the inguinal femoral or umbilical ring.  Hence, the mesenteries must be viewed as neurovascular visceral pedicles, and not as suspensory organs, while the abdominal walls are the great supporters and retainers of the viscera.  And as every anatomist knows the recti-abdominales are among the chief regulators or governors of visceral poise, at least they retain the viscera in their first delicate normal balance.  Besides, enclosing the recti abdominales in a single sheath my plan of operating in very -extreme cases is to sever the recti-abdominales and invaginate one rectus sheath into the other and fix them with sutures.  This is similar to the "stove pipe" operation on the intestines that I presented to the profession in 1891 (Annals of Surgery, 1891 and "Practical Intestinal Surgery, " 1891).

TRACTUS GENITALIS IN SPLANCHNOPTOSIA.

Fixation of the Tractus Genitalis.

A. Pelvic diaphragm (primary support).

    Diaphragm pelvis consist of muculus levator ani plus its superior and inferior fascia.  What maintains the genital organs in their normal positions?
    (a) The form and function of the pelvic floor (levator ani with its proximal and distal fascia). (b) The position of the genitals and the adjacent viscera.  The mesenteries of the tractus genitalis (ligamenta lata) are not for mechanical support.  They are to conduct vessels, nerves, and to maintain structures in order for function.  It is true that the ligaments saco-uterina acts as vigorous supports if placed on tension but in their present normal state of existence they simply direct the cervix dorsalward.  The vagina extends from the pubus to the cervix and the sacro-uterine and the ligaments extend from the sacrum (rectum) to the cervix.  Hence the vagina and sacro-uterine ligaments act as a supporting beam on which the cervix and uterus is supported.  The same story, that the thoracic and abdominal viscera are chiefly maintained in position by their respective Walls, is true as regards the position of the pelvic viscera, and its walls.  The so-called uterine ligament (mesenteries of the genitals act only in pathologic relations as in sacropubic hernia).  As an anatomic demonstration that the pelvic floor supports the uterus one can observe (with evacuated bladder and rectum and uterus in physiologic position) that the transverse vaginal slit in the pelvic floor lies 2 inches ventral to the cervix (i. e., the corpus uteri lies doro-ventral across the transverse vaginal slit).  If pressure be exercised on the corpus uteri, exactly as intra-abdominal pressure is applied the previous position of the uterus will not be endangered, i.e., it will not enter the vaginal slit but simply force the pelvic floor distalward.  In other words the pelvic floor, the distal wall of the pelvic or levator ani maintains the tractus genitalis (uterus) in the normal physiologic position.  If one wishes (in the cadaver) to force the uterus through the vagina, vaginal slit in the pelvic floor the hand seize the fundus and corpus while the cervix is pushed vigorously distalward in the vaginal slit where the cervix may be observed in the entroitus vaginae.
    If the pressure is removed from the uterus it returns to its normal position.  One cannot force the corpus and fundus through the vaginal slit with any ordinary hand power.  During energetic forcing of the cervix through the vaginal slit the ligaments rotunda, ligaments lata and ligaments sacrouterina are scarcely put on tension (they are entirely secondary supports).  If all the uterine ligaments are severed and the experiment repeated the cervix can be forced through the vagina to the entroitus only.  The impossibility of forcing the corpus and fundus through the vaginal slit and entroitus vaginae is due to the increasing volume of the corpus and fundus on account of the addition of the oviducts, vessels, nerves, and ligaments lata.  The sacro-pubic hernia of senescence is due to atrophic conditions of the genitals which glide through the vaginal slit from diminutive volume.  Ziegenspeck claims that sacro-pubic hernia (uterine prolapse) is due to the difference between intra-abdominal pressure and atmospheric pressure.  Hence the primary support of the pelvic viscera (genitals) is the pelvic floor-levator ani with its proximal and distal fascia.  By relaxation it includes the tractus genitalis in splanchnoptosia.
    Diaphragma thoracis resembles diaphragms pelvis in physiology and anatomy.  Both have (a) a similar fixum punctum (circulatory bony origin), (b) similar punctum mobile (central tendon), (c) both support superimposed viscera, (d) both have three apertures for visceral transmission, (e) both diaphragms are respiratory, (f) both muscles by contsriction limit the apertures of visceral transmission, (g) both contract as a single muscle (h) both share in splanchnoptosia.  They differ in that contraction of the pelvic diaphragm draws the 3 visceral apertures proximalward and ventralward, while contraction of the thoracic diaphragm draws the visceral apertures distalward and dorsalward.

(B) Ligmenta Uterina (secondary supports).

    All uterine ligaments arise from the pelvic wall and become inserted in the lateral borders of the uterus.  They act as guy ropes, to maintain the uterus in a physiologic position in order to functionate.  The ligaments lata, the real neuro-vascular visceral pedicle is a physiologic support only not a mechanical serving as a conducting bed for vessels, nerves and tubular viscera.  These secondary uterine supports in splanchnoptosia become primary which is a pathologic condition.

Movements of late Tractus Genitalis During Respiration.

    To demonstrate that the diaphragm pelvis is a muscle sharing in respiration one need only to witness a single perineorrhaphy.  Whence the proximal. ward and distalward movements of the levator ani are evident.  To prove that the genitals share in respiration one need only to observe the regular motion of 6 month gestating uterus or the motion of the vagina and uterus in a coughing anaesthetized patient, whence not only the blue vagina everts through the vaginal slit, but the uterus may also be present at the pudendum.  The genitals and pelvic floor move with respiration.  The respiratory movements of the genitals are the chief factors in genital ptosis.  To illustrate if in a case of uterine prolapse or better sacro-pubic hernia the uterus may be returned to the pelvis and the patient told to force it distalward.  She immediately inspires deeply whence she retains the inspired air, fixes the thoracic diaphragm, and forces the uterus rapidly distalward through the vagina external to the pudendum.  She accomplishes this act by respiratory motion.  With relaxation of the pelvic the uterine fundus passes dorsalward and the cervix by this mechanism gains entrance to the vaginal slit in the pelvic floor whence intra-abdominal pressure forces the uterus distalward.  If the uterus loses its volume becomes atrophic, respiratory movements may force it distalward through the vaginal slit without loss of integrity of the pelvic floor.
    The continual respiratory trauma, when visceral supports are deranged, produce progressive sacro-pubic hernia.  From a study of the anatomic supports of the genitals it is evident how irrational are the surgical attempts to fix the uterus in some preconceived position by means of hysteropexy or the shortening of some secondary uterine support.  It appears that the function of respiration is not confined to a single location in the spinal cord, but extends to wide areas on its egress nerves so that man's trunk is a respiratory apparatus closed at the proximal and distal end by a diaphragm - both actively involved in respiratory movement.  The relaxation of the pelvic floor and consequent genital ptosis is simply a demonstration of the pathologic anatomy, and physiology of respiration.  The genitals present various grades of splanchnoptosia.  In the first place the portio vaginalis is found moved distalward in the pelvic axis, the corpus may be in normal anteflexion, but more frequent in a beginning of retroflexion - the whole uterus is excessively mobile.  In the second place the entire uterus lies parallel and against the sacrum (rectum).  The cervix is not infrequently fixed through parametritis posterior.  According to the degree of genital splanchnoptosia arise pain in the back and sacrum, radiating pain in the extremities, menstrual disturbances, venous congestion and constipation.  Later the cervix projects through the pudendum.  Advanced splanchnoptosia of the genitals presents prominent features of relaxation of the pelvic floor and venous congestion.

Etiology of Genital Ptosia.

The chief etiology of genital ptosia is:

    (I)  Results of parturition, i. e., elongation, separation or laceration of the pelvic floor tissue (the levator ani muscle and its proximal and distal fascia).
    (II)  Atrophy of the genitals.
    (III)  Respiratory movements forcing the genitals distalward (constantly forcing the deranged genitals in the direction of least resistance).
    (IV)  Relaxation of the thoracic and abdominal walls.
    (V)  Superimposed splanchnoptotic viscera.
    (VI)  Genital sub-involution (infection).

The Treatment of Genital Splanchnoptosia.

    The treatment should be medical, mechanical, surgical.

I. Medical.

    One of the essential remedies is visceral drainage.  Hot vaginal douche (with salt and alum as ingredients) increased to 12 quarts which contracts tissue (elastic, muscle, connective), massage, electricity, ample and horizontal rest are valuable means.  The boroglyceride tampon serves as an excellent remedy.  It is hygroscopic and may be prepared so that it can be worn one to several days.

II.  Mechanical.

    The horizontal position should be used as much and frequent as possible.  Abdominal binders (in which may be placed a pneumatic rubber pad) Achilles Rose's adhesive strapping, Galant's corset furnish much comfort.  Various kinds of pessaries may be worn.

III.  Surgical.

    Since the uterus is supported by the pelvic floor rational surgical proceedures should be applied to it in splanchnoptosia.  Relaxed pelvic floor means relaxed, elongated, fibrous separation of the levator ani with its superior and inferior fascia.  Hence perineorrhaphy should include the careful repair of the levator ani with its superior and inferior fascia.  It is fascia that supports, not muscle.  Ventral colporraphy aids in forcing the bladder proximalward and narrowing the vaginal exit.  The most effective and enduring operation for splanchnoptotic genitals is: (a) amputation of the cervix (if required), (b) ventral colporrhaphy (c) and extensive colpo-perineorraphy, i. e., an extended Tait flap splitting operation with reunion of the torn muscle and fascia of the levator ani.  In cases of uterine atrophy extensive vaginal narrowing is required.  For splanchnoptosia of the genitals hysterectomy should not be performed (as it renders supports less efficient).  The uterus is the key to the support of the genital viscera.  I have seen subjects of splanchnoptotic genitals where the uterus had been removed and subsequently the everted, distended vagina extended to the middle of the thigh with almost hopeless views of repair.  As to suspending or fixing the genitals to the abdominal wall proximal to the pelvis it is an irrational operation, unphysiologic and harmful.  The anatomy and physiology of the genitals belong to the pelvis.
    Ventral abdominal hysteropexy should not be performed in a reproductive subject.  Also patients do not present symptoms indicative of malposition of the uterus.  The position of the uterus has no special relation to disease.  As the symptoms do not emanate from the position of the uterus fixing it will have no relation to the symptoms (except to exacerbate them).  The symptoms of patients with retroversions for example emanate from other causes than the uterus.
 

Fig. 202. Represents the surgical procedure which encloses the musculi recti abdominales in a single sheath.  1 and 2 represent the anterior sheaths of the recti partially united in the middle lines. 10 and 12 represent the posterior sheaths of the recti partially united in the middle line. 5, the linea alba. 8 and 9 the recti sheaths lifted up-to show the recti muscles.  This operation I have employed for 5 years.

RESULTS OF RELAXED ABDOMINAL WALLS ON THE TRACTUS INTESTINALIS.

    In splanchnoptosia one of the most damaging influences rests on the tractus intestinalis - sensation, peristalsis, absorption and secretion are deranged.  The normal position of the tractus intestinalis with its appendages (liver, pancreas, and spleen), is changed disordered.  The circular band apparatus of the abdominal wall is relaxed.  The elongated neuro-vascular visceral pedicle allows the segments of the tractus intestinalis and its appendages to follow the relaxed abdominal wall, and hence move out of their normal physiologic range, compromising blood and lymph circulation and traumatizing nerve periphery.  There is at once a disproportionate action between traumatized nerve periphery and separated, elongated fascial and muscular fibres of the abdominal wall.  Muscular tone and nerve energy become deranged.  Since the abdominal wall becomes relaxed, the segments of the tractus intestinalis become dislocated permanently from a normal position.  Since the neuro-vascular visceral pedicles are not elastic, and not for the purpose of mechanical support, the viscera will pass distalward, i. e., in the direction of least resistance.  There is pathologic physiology and pathologic anatomy.  The spacious abdominal cavity allows the viscera to shift and glide from weight according to the position of the patient.  The mesenteries of course elongate when their essential support, the abdominal wall, yields.  The visceral supports or visceral fixation apparatus are (a) the abdominal wall, (b) the pelvic diaphragm, (c) the thoracic diaphragm (d) what I shall term "visceral shelves.  " Any yielding of any one of these segments a, b, c, or d increases the abdominal space and creates a disordered relation between viscera and supports with consequent pathologic physiology.  It may be a neurosis malassimilation from disordered circulation (lymph and blood), or it may be disordered visceral motion (peristalsis) from the trauma and infection of the ganglia mysenterica (Auerbach's ganglia) or disordered secretion from disordered action of the Billroth-Meissner plexuses from trauma and infection.  Constipation may occur.  The form of the abdomen 'Pendulous shows that the tractus intestinalis is dislocated distalward.  In aged and spare persons the actual form of the bowel segments and the peristaltic movements may be observed through the thin abdominal wall.  The tractus intestinalis in splanchnoptosia is manifoldly dislocated.  On account of the fact that while the subject of relaxed abdominal walls does not manifest the disease while lying on the back because the abdomen is flat, the autopsist does not observe the splanchnoptosia.  It is the clinician who is impressed with the splanchnoptosia, when the subject is in the erect attitude manifesting the "hanging belly," but the clinician loses his usefulness because he scarcely witnesses the autopsy.  It is the clinical and autopsic observation that demonstrates vividly the required data.  The great segments of the tractus intestinalis, gastrium, enteron, and colon, become disordered, deranged in relation, changed in situation.  The flexures of the tractus intestinalis become more flexed, rigid supports become elongated, secondary supports are put on tension and the lumen of the tractus intestinalis is stenosed, compromised in numerous places.  Canalization is compromised.  The rigid ligaments as the ligamentum hepato-duodenale, ligamentum costocolicum, will not yield as much as the adjacent slacker and weaker ligaments, hence the hepatic and splenic flexures become more and more flexed, stenosed.  Food passes them with difficulty.  For example, there are 5 points to consider in regard to the fixation apparatus of the duodenum, viz.:
    1.  The duodenum is as a whole fixed.  It has lost its peritoneal mesentery on both surfaces of the mesoduodenum and its middle mesenteric layer (membrana mesenterii propria) is fixed or coalesced to the dorsal wall.  It is also fixed by the musculus suspensorius duodeni, and the strong ligamentous band from the left crus of the diaphragm.  Also the head and body of the pancreas aid in fixing the duodenum.
    2.  The pylorus or proximal end of the duodenum is fixed to the vertebral column, to the liver, kidney and stomach.
    3.  The flexura duodenalis jejunalis or distal end of the duodenum is especially fixed by musculus suspensorius duodeni and the strong fibrous and ligamentous band from the left crus of the diaphragm.
    4.  The duodenum being fixed, it can not move distalward, while all the other abdominal organs glide distalward during splanchnoptosis.  Hence since the transverse segment of the duodenum becomes fixed it becomes compressed by the superior mesenteric artery, vein and nerve, inducing gastro-duodenal dilatation.  The compression of the duodenum is due to the mesenterico-aortic (vertebral) angle becoming more and more acute as the splanchnoptosia progresses, and finally, when the enteron lies mainly in the pelvis, the mesenterico-vertebral angle is very acute, allowing only a small space for the duodenum.  The passing distalward of the stomach stenoses the fixed pylorus, and the passing distalward of the enteron makes more and more acute the flexura duodeno-jejunalis, because the distal end of the duodenum especially is quite rigidly fixed.  The simple anatomic fact in splanchnoptosia is that the proximal end of the duodenum is dilated (with the stomach).  The ileo-cecal sphincter and angle are not so much stenosed, as both colon and distal ileum move distalward together, retaining the normal angle correlations.  The duodenum may be deranged by the mobile right kidney through the ligamentum duodeno-renale.  The dragging of the dislocated kidney aids to flex or stenose the duodenum, the retention of foods in the stomach, and thus enhances gastric fermentation, catarrh and dilatation.
 

Fig. 203.  Byron Robinson's rubber air pad for splanchnoptosia half distended.  It is to be placed inside an abdominal supporter. 1, side of rubber pad; 2, the rubber tube through which the rubber pad can be distended with air. (This rubber air pad is manufactured by John Drake & Co., of Chicago.)

The Flexura Coli Hepatica.

    The flexura coli hepatica suffers in splanchnoptosia, because as the stomach passes distalward it forces the colon transversum before it and hence makes more and more acute the hepatic flexure.  I have seen the transverse colon in the pelvis and 9 inches of it as an inguinal hernia.  It would at first appear impossible for the food to pass such acute colonic angles, but it should be remembered the peristalsis is continued by means of the activity of local segments.  However, since the hepatic flexure is generally an obtuse or right angle, its flexure is seldom drawn so acutely by the ligamentum hepatocolicum as to produce very vigorous stenosis.  Besides in splanchnoptosis the liver yields through its mesohepar and follows to some extent the distalward movements of the hepatic flexure, relieving its angle from acute flexing.

The Flexura Coli Lienalis.
 

    The flexura coli lienalis forms normally an acute angle.  It is the remnant of the ligamentum recto-lienalis of the lower mammals and quadrumana.  It is a distinct, direct apparatus fixing the colon to the costal wall and kidney.  In splanchnoptosia the splenic flexure is forced distalward and its angle made more acute.  The spleen also participates in the general splanchnoptosis passing distalward, gliding ventral to the colon, as shown in the autopsies, as far as the pelvic floor.  This increases the acuteness of the colonic flexure, obstructing the fecal current.  The stomach also forces the middle of the transverse colon distalward, which stenoses the hepatic and splenic colonic flexures in direct degree to the extent of the gastroptosia (splanchnoptosia).
 

Fig. 204. (Byron Robinson) profile view to illustrate the pressure of the rubber air pad on the abdomen. 1, distended pneumatic rubber pad; 2, wall of abdominal supporter over pneumatic rubber pad.

    Also the colon transversum in extensive distalward movements is often forced into a V-shaped condition, with acute adjacent panetel flexions becoming adherent by plastic peritoneal adhesions, due to bacteria or their products passing through the colonic mucosa, myocolon to the serosa, resulting in peritoneal exudates and organized peritoneal adhesions.  All dislocation of the viscera compromises function, peristalsis. sensation, absorption, secretion - fecal blood and lymph circulation and traumatizes nerve periphery.  Besides, splanchnoptosia is a general term.  The tractus intestinalis and its appendages, the tractus urinarius, the tractus genitatis, lymphaticus, vascularis and nervosus, all share in the distalward movement due to relaxed walls, - so that splanchnoptosia of the tractus intestinalis is made worse by the nephroptosia (especially on the right side.), hepatoptosia, splenoptosia and genital ptosis.  The enteroptosia is especially responsible for the gastroduodenal dilatation, because the duodenum cannot pass distalward from a definite fixation apparatus, and the superior mesenteric artery, vein and nerve - the constricting arm - compresses the transverse duodenum the more acutely the more the enteronic loops pass distalward into the pelvis.  Again, the distalward dislocation of the colon favors fecal accumulation, which favors migration of germs or their products through mucosa, muscularis into the peritoneum, inducing plastic peritoneal exudates and organized peritoneal adhesions.  The peritoneal adhesions compromise anatomy and physiology of the segments of the tractus intestinalis.  Again, a tractus intestinalis made defective by dislocation and fecal accumulation becomes an easy prey to muscular trauma.  Muscular trauma of the psoas, for example, makes over 70 per cent. of the peritoneal adhesions on the right side (adjacent to the appendix, cecum, and distal ilium), and over 80 per cent. on the left side (in the mesosigmoid).  Other abdominal muscles produce equal damage in proportion to their power of traumatism by trauma of their segments of the tractus intestinalis.  In minimum and maximum defect the more damage arises in the tractus intestinalis from muscular trauma than other visceral tracts.
    The fecal accumulations produce maximum damage when collected in the most dependent colonic segments, as the cecum, middle or transverse colon and sigmoid; besides it favors hernia, invagination and volvulus.  Doubtless it is the stenosed and superior flexed splenic flexures of the colon which produce the dull pain and fecal accumulation with dullness on percussion.  The multiple stenosing of various segments of the tractus intestinalis (and perhaps the ductus hepaticus) in splanchnoptosia is of a temporary character, because on change of the erect to the horizontal position the stenosis of the tractus intestinalis is damaging from the point of circulation, nourishment and assimilation.
    Splanchnoptosia induces trauma on secretary, sensory and motor nerves, it produces irregular congestion and decongestion, muscularis is impaired by irregular local contraction and dislocation.  Dislocation of the tractus intestinalis favors absorption of deleterious products.  The relaxed abdominal walls having lost their power of contraction, the fecal current is defectively driven distalward.  From loss of tone in the diaphragm, abdominal wall and pelvic floor, through excessive distention, defecation is difficult and hence fecal and gas accumulations are distressing.  Discomfort almost always attends the patient with any considerable degree of splanchnoptosia from traumatized nerves, or from distension with gas or food, from incapacity of the abdominal walls to maintain the viscera in the normal physiologic position.  If a subject with distinct relaxed abdominal walls be examined per vaginum or per rectum, stagnated fecal accumulation may be found in the sigmoid and if the cecum assume the pelvic position (female 20 per cent., males 10 per cent.), it may also be found occupied with feces.  The abdominal wall (thoracic and pelvic diaphragm) having lost its tone, defecation is not only difficult but defective.  Besides, long retained feces in the colon induce catarrh of the colon resulting in the absorption of toxic substances.  Meteorism arises in splanchnoptosia from excessive, deficient or disproportionate secretion and consequent fermentation, from stenosing of the tractus intestinalis, from loss of power in the abdominal walls, from catarrh due to constipation, from expansion of gas due to rise of the temperature after toxic absorption.  Such subjects have a foul-smelling breath from the gases being absorbed by the veins in the tractus intestinalis and becoming exhaled through the lungs.  Meteorism induces pain and discomfort from nerve pressure, and dislocated viscera and obstruction to circulation.  The results of splanchnoptosia are constipation, catarrh of the different segments of the tractus intestinalis, icterus through pressure, and stenosing of the ductus hepaticus.  Also the nephroptosia induces stenosing of the duodenum and ureter by flexing and rotation.
    Patients subject to splanchnoptosia suffer frequently from discolored skin and irregular kidney secretion, also from nausea, vomiting, irregular and obscure pains, with continual weakness, debility.  From these anatomic and physiologic considerations it is amply evident that in order to support the viscera in splanchnoptosia the thoracic and abdominal walls (with pelvic and thoracic diaphragm) must be forced into rational application.
    In splanchnoptosia it must be remembered that the anatomy thoracic and abdominal viscera (tractus respiratorius, intestinalis, vasculoris, genitalis, lymphaticus, urinarius nervosus) is dislocated and that the physiology of these seven visceral tracts is deranged.
    The chief aim of therapeutics in splanchnoptosia is to restore function, physiology.  We may live comfortable with pathologic anatomy, however, in general we live in discomfort with pathologic physiology.

CIRCULATION IN SPLANCHNOPTOSIA.

    In operating on the deep glands of the neck, where the large veins are isolated, it is very plain that respiration governs to a certain extent the venous circulation.  Now, the diaphragm, pelvic and thoracic, as well as the ventral abdominal walls are relaxed, it becomes evident in difficult defecation and in the same manner the venous circulation of the abdomen suffers from lack of pressure.  With relaxed abdominal walls, the abdominal veins (and the entire system) are congested and stenosis results.  As a sample of the evil effects of relaxed abdominal walls and consequent splanchnoptosis, in rapidly repeated pregnancy there is heart weakness, because the veins of the abdomen are too constantly, excessively occupied with excessive blood, robbing the heart of its required amount.  Since receiving instruction of Prof.  Schroeder, some twenty years ago, I continued the study and investigation of splanchnoptosia.  In relaxed abdominal walls one sees the distended veins of the extremities, and extensive and prominent veins of the pudenum, as well as the large hemorrhoidal nodes.  Besides frequent and free uterine hemorrhages occur.  Splanchnoptosia has deleterious effect on the pelvic organs by pressure and especially by obstructing the venous return flow.  In post mortems I have carefully noted that subjects with splanchnoptosia possess a plexus pampiniformis extended with straight, irregularly dilated veins.  Spiral and uniform calibered veins are normal.  In advanced splanchnoptosia the pelvic veins, especially the genitals and those of the rectum, are widely and irregularly dilated, containing enormous quantities of blood.  This causes hyperaemia, congestion and stasis of the pelvic organs, resulting in hemorrhage, malnutrition, and pathologic changes in the genitals as hypertrophy.  The liver suffers likewise from congestion, hyperaemia and blood stasis, for it drains the tractus intestinalis (spleen and pancreas) and the liver, by its dislocated position, compromises the blood current, especially in the portal and hepatic veins, besides, the dislocated liver drags or compresses the inferior vena cava, stenosing it.  Stagnation, stasis, congestion, hyperaemia are the characteristics of the circulation in the splanchnoptotic.
 

Fig. 205.  Byron Robinson's pneumatic rubber air pad is fitted to the abdomen inside the abdominal supporter. 2, 3 are rubber tubes passing between the limbs to fix the abdominal supporter.  It requires several days, a week for patients to become adjusted to the pad.  Patience on the part of the patient and encouragement on part of the physician will soon adjust the use of the pad.

    If the liver be dislocated to any considerable extent, which is frequent in gynecologic patients, the definite relations of the portal vein are disturbed, the liver veins and the inferior cava are dislocated or compromised, as the vena cava lies on the rigid dorsal wall.  Venous circulation is more physiologic and of complex delicate nature than arterial, which is more mechanical, and is easily compromised as is noted by the enlargement, conspicuously observed in the inferior and superior epigastric veins.  Continuous hyperaemia, congestion and stenosis in the dislocated. viscera produces pathologic changes in the organs themselves, impairing sensation, motion, secretion, absorption, and nutrition.  We have thus a vicious circle which might be called the visceral disease.  Relaxed abdominal walls and consequent splanchnoptosia disturb a wide area of complicated functions.  They distort an extensive and delicate mechanism, resulting in impaired respiration, circulation, sensation, motion, absorption, and secretion and in the end result in malnutrition and neurosis.
    Tension of the visceral vessels in splanchnoptosia limits their lumen and consequently more vigorous heart action is required to force the blood to the viscera - taxing the heart's power, ending in anaemia, congestion, throbbings, headaches, dizziness.  With loss of the controlling influence of the abdominal wall on the visceral circulation a fullness of feeling or weight in the abdomen may occur from visceral congestion and continuous congestion may lead to relaxation of visceral supports occurring in splanchnoptosia.
    In splanchnoptosia the visceral circulation is impeded by flexion, dilatation, constriction, decalibration, elongation, of vessels (and the accompanying plexiform nerve sheath is consequently traumatized).  In splanchnoptosia the veins from thin, flaccid walls, deficient muscularis and slow pressure current suffer more than the arteries which possess rigid walls, powerful muscularis and vigorous high pressure current.  Atonia gastrica is responsible for two important phenomena of visceral vessels, viz.: (a) flexion or angulation; (b) elongation and consequent decrease in lumen, decalibration.  Conspicuous examples of flexion or angulation of vessels may be observed in extensively distalward movements of the kidney which is frequently located in the middle of the abdomen on the pelvic brim and the spleen which Is not infrequently found located at any point from the kidney to the pelvic floor.  The distalward dragging of the viscera at different points on the visceral ligaments fixed to the abdominal wall flexes or angulates the vessels in extra-extended ligaments producing hyperaemia or anaemia, engorgement or ischaemia.  If one explores by dissection the abdominal visceral vessels in a normal subject and again in a splanchnoptotic subject by comparison it will be observed that the visceral vessels of the splanchnoptotic may be several inches longer than those of the normal subject, e. g., when the kidney lies in the iliac fossa or lesser pelvis, when the spleen lies on the pelvic floor, when the enteron lies almost completely on the pelvic floor.
    The visceral vessels become elongated in splanchnoptosia and elongation compromises the canals and lumen of the vessels, limiting vascular supply, inviting defective viscera, resulting in innervation, constipation, deficient secretion, limited and disordered peristalsis.  In enteroptosia the superior mesenteric artery and vein is the one set of vessels which suffers from dragging, trauma, from marked elongation of parietes and constriction of lumen.  The elongated superior mesenteric artery, vein and nerve constricts, stenoses the transverse segment of the duodenum by compression.  Thus in splanchnoptosia one distorted viscus compromises another.  It may be observed that the visceral vessels are compelled to elongate in splanchnoptosia as their base or origin, the aorta, is immobile.  In gestation the utero-ovarian artery elongates, experiences parietal hypertrophy, increases its spiralit y and diameter of its lumen.  However, gestation practically cures, symptomatically relieves splanchnoptosia for some six months.  In splanchnoptosia practically the opposite condition to that of the arteria uterina ovarica in gestation occurs in the visceral arteries, viz. : the visceral arteries elongate, decrease in diameter, diminish in spirality, experience parietal atrophy.  Finally during the elongation of visceral vessels vast sympathetic nerve trauma is inflicted on the plexiform, nodular network of nerves which ensheath the visceral vessels, damaging vascular function (especially rhythm) for the tractus vascularis and tractus nervosus is an automaton.  Hence, from the dragging of the viscera on their elongated tensioned vessels, from vessel extension, flexion and trauma on associated ganglia, excessive, deficient, or disproportionate circulation arises.  In splanchnoptosia palpatation, vigorous beating in the abdominal aorta which may be palpated from partial uncovering or exposure of the aorta by dislocated viscera and atrophy of the abdominal wall.  The arterial pulse beat is disordered - irregular, deficient, excessive.  Splanchnoptotics are afflicted frequently with debility, impending weakness, faint with facility and present rapid, variegated changes in circulation in different parts of the body.  The patient is flushed (congestion), pale (anaemic), mottled (disproportionate circulation).  They have headaches from irregular cerebral circulation and extensive abdominal venous stasis.  In autopsies on some advanced splanchnoptotics the numerous vastly distended blue veins presenting among the abdominal viscera suggest the idea that the patient had bled to death in his own abdominal veins.  The veins of the viscera and ganglia are engorged, flooded with stagnant venous blood surcharged with carbonic acid gas-while the arterial blood invigorated with life's messenger, oxygen, is excluded.
    The similar conditions as regards haemogenous circulation in splanchnoptosia may be practically applied to the lymphatic circulation in splanchnoptosia.
    The abdominal walls aid to regulate the circulation in the viscera (especially in the veins).  The abdominal vessels (veins) are a kind of reservoir for surplus blood by which blood pressure and other visceral supply is regulated.  If the abdominal muscles become deficient the blood will accumulate in the abdominal veins to the detriment of other viscera, e. g., the cerebro-spinal axis - manifesting many nervous phenomena.  The extensive venous stasis in the abdomen from atonia gastrica deranges visceral function (peristalsis, absorption, secretion, sensation) ending in malassimilation (indigestion, fermentation, meteorism, constipation).  The meteorism so frequent an accompaniment of the splanchnoptotic is a marked factor in disturbing circulation and digestion.  In the splanchnoptotic the dilatation of the blood vessels in the splanchnic area may lead to a decrease in general blood pressure and consequent increase of cardiac action.  The symptoms due to the pathologic physiology of circulation in the abdominal vessels are varied and numerous as rate, nature, force of peristalsis in the heart, and consequent effect on the abdominal viscera.  The extent of distention of the abdominal vessels would no doubt produce pathologic manifestations as dragging, feeling of fulness, weight.  Long continued congestion due to vaso-motor paralysis (from lack of abdominal pressure) may account for relaxation of visceral supports.  The manipulation of the plexiform nodular network ensheathing the arteries may be followed by palpation and be found tender, sensitive-indicating an irritable condition of the blood vessels, arteritis, arteriosclerosis, or a neuritis of the ensheathing nerve plexus (which is the more probable).
    Dilatation of the splanchnic vessels appear to be physiologically opposed to a similar condition of the peripheral vessels and the exquisite balance is due to a nerve mechanism.  Our remedies should be applied with 2 views, viz.: (a), to deplete the visceral congestion.  This can be especially accomplished by visceral drainage and aided by mechanical supports, the abdominal wall which regulates venous circulation (as by binders, Rose's strapping); (b), stimulate the peripheral or cutaneous vessels (by friction heat, chemicals) in order to entice the blood to the surface (as massage, salt rubs, hydrotherapy, wet cold pack).

TRACTUS NERVOSUS IN SPLANCHNOPTOSIA.

    The ideal nervous system consists of: (a) a ganglion cell (a central receiver and reorganizer), (b) a conducting cord (a transmitter), (c) a periphery (a sensory apparatus, a collector).  In splanchnoptosia the ideal nervous apparatus is deranged.  I am convinced from years of observation in the living and dead - that the tractus nervosus in splanchnoptosia indicates inferior anatomy and physiology with more facility than other visceral tracts.  Splanchnoptotics are prone to be afflicted with stigmata, degeneracy, a habitus.  They possess a weak, irritable nervous system.  They are not perfect physically or mentally.  Their anatomy and physiology are inferior structure and function of minimum perfection.  The nervous system is unstable.  Splanchnoptotics manifest defective resistance, and are incapacitated for sustained effort, presenting premature exhaustion on persistence mentally or physically.  Their tractus nervosus functionates under friction most of the time like some watches which maintain in correct time.  Splanchnoptoticsare chiefly congenital, physical unfortunates.  They are born with defects, stigmata, a habitus, a neuropathic predispositions condition or state which tends to degeneracy with facility.  One of the best terms to apply to subjects with excessive distalward movement of viscera, relaxed muscles, defective circulation, and defective nourishment is the word habitus, e. g., we meet the subjects with habitus splanchnopticus, habitus nervosus, habitus phthisicus, habitus dyspepticus.  The ensemble of symptoms associated with splanchnoptosia may well be termed habitus splanchnopticus.  It is heredity in so far that the subject possesses a predisposition and the main defect is inferior anatomy and physiology.  In the habitus splanchnopticus there is the gracile skeleton, the elongated, flat thorax, extensive intercostal space, acute epigastric angle, the sacculated pendulous abdomen, limited muscularis and panniculus adiposus, the labored respiration.  The costa fluctuans decirna of B. Stiller, the peculiar habitus in form - presenting evident pathologic physiology.  A marked factor in pathologic physiology of splanchnoptosia is the changed defective circulation, venous congestion.  Generally any subject with a "habitus" possesses an unstable nervous system.  The habitus splanchnopticus is perhaps more due to neuropathic disposition than to the splanchnoptosia, hence the term dyspepsia nervosa, or stigma dyspepticus.  The habitus neurasthenicus presents pathologic physiology of the tractus nervosus - a condition of exhaustion or weakness of the nervous system accompanied by physical and mental inefficiency.  Habitus neurasthenicus is a fatigue disease of the nervous system.  It is characterized by the presence of motor, sensory, psychic and visceral symptoms - all fatigued, tired, exhausted.  This habitus is especially characterized by weakness, or inefficiency and irritability of the tractus nervosus.  The physician can detect spots, of hyperaesthesia, spinal irritation, fatigue of, the special sense, auditory and retinal hyperaesthesia.  When the subject predisposed to the habitus splanchnopticus is afflicted with strain, as gestation, the care of growing children, extra mental or physical effort, the tractus nervosus habitus neurasthenicus - manifests itself deranged with rapidity and facility.  Also the instability of the tractus nervosus in splanchnoptosia is aggravated, irritated with facility in the habitus neurasthenicus by disease, as salpingitis, myometritus, pelvic peritonitis.  The weak, irritable tractus nervosus with its inherent defective vital power - its deteriorated anatomy and physiology - readily passes into a state of manifest pathologic physiology.
    In splanchnoptosia the nervous system is involved in manifold conditions.  In fact, in splanchnoptosia the nervous system is the central reference of investigators.  Hence, writers note that splanchnoptotics are afflicted with melancholia neurasthenia, nervous dyspepsia, neurosis, irritability, weakness and debility.  The splanchnoptotic experiences pain of various kinds in any portion of the abdomen.  They are afflicted with heavy feelings in the abdomen.  Pain radiates to the scapulae, especially in the region of the V to the VII dorsal vertebrae.  The pain is increased in the erect and decreased in the prone attitude (indicating nerve trauma).  Continuous standing, long labor or severe efforts increase the pain.  The multiple pain of the splanchnoptotic is described as dull, sticking, dragging, boring, cramps, faintness, lumbar and sacral pains.  Some have pain in many parts of the body.  The sensible visceral nerves and ganglia become traumatized, dragged by the dislocated viscera.  The visceral arteries are ensheathed by a ganglionated, plexiform network of nerves.  In splanchnoptotics the visceral arteries become elongated (sometimes several inches, in extra length) and their ensheathing nerves stretched, damaged, traumatized, altering their functions.  The pain is protean.  Hegar called it Lendenmarks symptome, i. e., lumbar cord symptoms.  The dislocated viscera drag on the great plexuses, resulting in irritability.  Hyperaesthesia and anaesthesia of the abdomen exist over the site of viscera - which suggests caution in pronouncing the stigmata of hysteria.  The plexus aorticus is frequently so stimulated that the vigorous, violent aortic pulsations may be mistaken for an aneurysm.  When no anatomic or histologic changes in the nerves can be demonstrated we are compelled to resort to such terms as neurosis, molecular disturbances in the nerve substance or peripheral.  Is splanchnoptosia due to a relaxation of the entire nervous system?  Splanchnoptosia attacks the motor nerves as it is shown by muscular fatigue. energy.  Evident incapacity for bodily labors present. The sensory nerves may suffer in splanchnoptosia as in anaesthesia and paraaesthesia.  The patient is sensitive to heat and cold.  Exaltation and depression occur.  The sympathetic nerve or nervus vasomotorius receives the brunt of the disease as is manifest in disturbed secretion, absorption. sensation and rhythm (peristalsis) of viscera.  Violent aortic palpation of the aorta exists.  Secretion, absorption and peristalsis may be excessive, deficient or disproportionate.

Frequency of Splanchnoptosia.

    In the vast majority of splanchnoptotics in general the viscera are displaced, prolapsed, and the visceral walls relaxed.  Splanchnoptosia is perhaps six times more prevalent in females than in males (some say ten).  I have no method to estimate the frequency of splanchnoptosia in my own practice except from the frequency of mobile ' kidney and in the personal autopsic abdominal inspection of over 650 adults and 75 children, infants, fetuses. 60% of the female patients in my practice present palpably mobile kidney, not splanchnoptosia, as no pathologic symptoms accompany many.  The difficulty of estimating the frequency of splanchnoptosia is due - and also the conditions of splanchnoptosia which present symptoms - to the different views of different authors.  I should estimate that 20% of the women with mobile kidney, in my private practice, have demonstrable splanchnoptosia - with attributable symptoms (i. e., 20% of 60% = 12%).  Part of this 20%, say 12%, do not suffer markedly, for in many the physical condition remains favorable.  Practically twenty years includes the clinical and autopsic study of splanchnoptosia, hence, older statistics are almost worthless.  Twenty years ago Mr. Lawson Tait, one of the greatest surgical geniuses of his age, and my own well-remembered teacher, denied movable kidneys.  The difficulty with statistics in splanchnoptosia is that it presents a wide range from the minimum scarcely perceptible to the maximum grade - an unsightly, sad appearance.  Hence we still lack a recognized standard to estimate the frequency of splanchnoptosia.

Symptomatology of Splanchnoptosia.

    Splanchnoptosia presents complex symptoms.  It may exist without recognizable symptoms or be accompanied by the most aggravated kind.  The general subjective symptoms of splanchnoptosia are (debility) a general sense of weakness; an impending irritable nervousness (neurosis), frequent relief in the prone position (attitude).  Practically, splanchnoptosia should be viewed as pathologic physiology, as a disease of symptoms and the object of the physician is to restore f unction.  Fatigue and pain are marked.  The general objective symptoms are: (abdomen) flattened pendulous abdomen especially in the epigastric region (Stellar's costalstigma), sensitiveness to pressure in the region of the tenth rib, palpation reveals excessive, multiple, visceral mobility.  A cord-like transverse colon (which is probably the pancreas) may be established by gliding it on the aorta.  A marked pulsation of the aorta, constipation.  A peculiar phenomenon may exist in splanchnoptosia which is in short that the intensity of the symptoms may not correspond to the degree of splanchnoptosia.  This doubtless depends on favorable or unfavorable physical conditions.  Marked splanchnoptosia may exist with practically no symptoms while a slight degree of splanchnoptosia may exist accompanied with striking symptoms.  Frequently the visceral ptosis is so slight that it is overlooked and consequently the treatment is misapplied.  An important matter in atonia gastrica, splanchnoptosia, is that symptoms are pronounced while the patient is in the erect attitude.  With the patient lying prone the symptoms diminish and may disappear.  This phenomenon deludes many physicians who consider merely that the patient requires physical rest.  Frequently I have noted immediate relief by supporting the abdomen with the hands from behind the patient (Glenard's belt test).  Besides the ordinary symptoms of fatigue, dragging, there is backache and side ache The backache in splanchnoptosia may be due to fatigue of the sacro-spinalis muscle simulating that observed in corpulent persons with fatty abdomen where the muscle becomes overworked in maintaining the center of gravity which is projected excessively ventralward.  In respiration in splanchnoptotics the expiratory power is not only lessened by loss of tone in the abdominal muscles but the floor of the thorax, the diaphragm, is dragged distalward by the distalward moving viscera.  The epigastrium may show a marked depression.  The relation of the diaphragm and ribs is disturbed, inducing shortness of breath on exertion.  To observe the splanchnoptotic one must examine in the prone and erect attitude with trunk clothing removed.  The patients frequently complain of weakness, dizziness, fatigue which may be enhanced by the distalward moving viscera dragging, traumatizing the splanchnic (sympathetic) nerves.  Most cases of splanchnoptosia are accompanied by pendulous abdomen, changed in form, however, with normal abdominal walls a single viscus may glide excessively distalward while mechanical pendulous abdomen may be caused by fat deposit.  Splanchnoptosia may exist without symptoms so long as the physical condition is favorable.  Atonia gastrica springs into prominence in association with neurosis and so-called nervous dyspepsia.  The symptoms of the splanchnoptotic are chiefly those of neurasthenia, neurosis.  Pain may be felt and is mainly referred to the lateral and dorsal region.  Splanchnoptosia is practically a unit though a general disease, seldom do single viscera suffer ptosis.  Exception may arise from sudden trauma, for example, instrumental parturition, sudden physical strain.  However, the ordinary case of recognizable splanchnoptosia, atonia gastrica, is general visceral ptosis with relaxed enclosing walls.  Splanchnoptosia must not be judged by the extent of dislocated viscera but by the degree of distress - the intensity of symptoms, the pathologic physiology.  The distalward dislocation of the diaphragm is an essential feature of splanchnoptosia.  Hence in marked subjects of splanchnoptosia the chest is deformed, the thoracic viscera occupy abnormal positions and the abdominal viscera are splanchnoptotic - the subject generally presents stigmata, physical defects, tubercular habitus, deformed distal thoracic borders.  A study of the subject of splanchnoptosia has exposed many previous puzzles.  A faint feeling after the morning rising, fatigue after exercise sense of weight in distal and dorsal abdomen, dragging in epigastrium, flatulence, constipation, frequent micturition, lends clues to widespread splanchnoptosia.  Neurasthenia, flaccid and pendulous abdomen, loss of flesh, diastasis, of the recti muscles shed light.  The aorta frequently strongly pulsates, and with spare subjects one feels what Glenard calls the "transverse colon cord, " however, I am fully satisfied at present after investigating these symptoms frequently in autopsies that this transverse band or "colon cord" is the pancreas mainly.

General Symptoms.

    Writers continually associate splanchnoptosia and nervous dyspepsia.  It seems to me such terms as nervous dyspepsia should be abandoned because later investigations have demonstrated that the various symptoms of splanchnoptosia are practically due to the malposition and consequent pathologic physiology of viscera.  In marked subjects of splanchnoptosia the symptoms of degeneracy present as B. Stillar's floating tenth rib (decima costa fluctuans) neurasthenia, so-called nervous dyspepsia.
    Splanchnoptotics may improve with advancing senescence.  This must mean that the neurosis and so-called nervous dyspepsia improves-not the splanchnoptosia for splanchnoptosia practically increases with senescence, that is after 35.  The explanation must lie in the adjustment and compensatory action of the splanchnoptotic organs.  The anatomy and physiology of the dislocated organs has become used to the order of things.  Meinert has written extensively on the relation of chlorosis and splanchnoptosia. it is more probable that the relations of chlorosis and splanchnoptosia are distant and rather that the defective constitutional power exposes the subject to both splanchnoptosia and clorosis - congenital and acquired defects which favor both diseases.
    The symptoms of splanchnoptosia are distension, expansion of thoracic and abdominal walls.  The thoracic and abdominal viscera are dislocated, succulated, flexed.  The visceral function (peristalsis, absorption, secretion, sensation) are disturbed.
    The symptoms of splanchnoptosia are functional, physiologic disturbances rather than definite marked anatomic or pathologic anatomy lesions.  The major visceral functions sensation, peristalsis, absorption, secretion are deranged. The visceral tracts, viz.: - Respiratory, circulatory, digestive, urinary, genital, nervous are compromised in physiology and anatomy.  Pathology is evident chiefly in pathologic physiology only.

GENERAL TREATMENT OF SPLANCHNOPTOSIA.

    The treatment should be medical, mechanical, surgical.

1. Medical Treatment.

    The essentials of medical treatment in splanchnoptosia are: (1), hygiene; (2), visceral drainage; (3), diet; (4), habitat; (5), avocation, electricity, spray, douche.  Advice is frequently of more value to a splanchnoptotic than medicine.
    Splanchnoptosia is practically a medical disease belonging to the internist.  The physician should treat not merely single organs but the patient.  Symptoms of general splanchnoptosia and neurosis should not be attributed to single dislocated organs as nephroptosia, hepatoptosia gastroptosia.  The subjective difficulties should be treated and not merely the clinical findings, because the patient may be suffering more severely than the physical findings indicate.  In splanchnoptosia the chief treatment consists in correcting the pathologic physiology of the thoracic and abdominal viscera as well as the restoration of the strength, firmness and elasticity of the enclosing walls.  Unfortunately the restoration of elasticity, of excessively extended muscle and connective tissue is difficult.  The aim of the physician should be restoration of function.  In splanchnoptosia there are four grand factors to consider; viz.: (a) relaxation of the thoracic and abdominal walls, (b) distalward movements of contained viscera (splanchnoptosia) (c) gastro-duodenal dilatation, (d) change of form of thorax, (flared), and abdomen (pendulous).  On these basic factors will rest the rock and base of our plans in treatment.

(1) Hygiene.

    Hygiene has reference to the method of living, the quantity and quality of ingested fluid and food, the exercise of functions, the quantity and quality of fresh air employed and the relations of environments.  In hygiene the advice of a physician is frequently more useful than drugs.

(2) Visceral Drainage.

    The splanchnoptotic suffers almost continually from pathologic physiology and the chief medical treatment consists in correcting diseased visceral physiology or function.  For the splanchnoptotic the most important treatment from beginning to end is ample visceral drainage.  The best diuretic is H20.  The sovereign visceral drainage fluid is different grades of physiologic salt solution.  I administer 8 ounces of 1/2 to 1/4 physiologic salt solution before each meal (better hot) and between meals, i. e., the subject drinks 8 ounces of 1/2 to 1/4 physiologic salt solution every 2 hours or 3 pints daily regardless of other fluids. (Note - sodium chloride should not be administered to subjects afflicted with parenchymatous nephritis.)
    The sodium chloride stimulates the epithelium of the tractus urinarius and tractus intestinalis.  In addition to the physiologic salt solution I administer on the tongue at the same time a part or multiple of an alkaline tablet (composed of: Cascara sagrada, one-fortieth of a grain; aloes, one-third of grain; NaHCO3, one grain; KHCO3, one-half grain; MgSO4, 2grain.) The sodium chloride tablet contains 11 grains.  The combined treatment consists in placing (1/6 to 2) alkaline tablets as required to produce one bowel movement daily and (1/2 to 1/4) sodium chloride tablet on the tongue (every two hours) followed immediately by a half a pint of H2O 6 times daily.  The plan of treatment I term the "visceral drainage" treatment, continuing it for weeks, months and the results are remarkably successful.  The urine becomes clarified resembling spring water and increased in quantity.  The tractus intestinalis becomes amply evacuated regularly daily.  The blood is drained of waste material.  The tractus cutis eliminates freely, and the skin becomes normal.  The appetite increases.  The sleep becomes improved.  The feelings become more hopeful.  The sewers of the body are vigorously drained and flushed.  The greatest principle in medicine and surgery - drainage - is accomplished.

(3) Diet.

    The diet influences visceral function equally with fluids, the main ideal of diet for the splanchnoptotic is that it shall be coarse, voluminous, and result in ample, indigestible faecal residue in order to stimulate the functions of the tractus intestinalis (peristalsis, absorption. secretion, sensation).  The kinds of foods for the splanchnoptotic should be (a) cereals (oatmeal, prepared wheat, rice, graham bread - i. e., the entire wheat as bran, shorts, and flour), (b) vegetables (cooked), (c) albuminoids (milk, eggs), (d) meats (limited in quantity).  Diet should be strictly regulated.  Food should be administered every three hours in limited quantities.  All fermentative substances should be avoided.  Fruits unless strictly regulated do more harm than good (from fermentative processes).  Pies, puddings, cakes, sugars, sauces, and condiments should be prohibited.  Diet should be wholesome and nutritive to produce fat for visceral padding whence the visceral shelves and fossae are increased and the abdominal wall thickened enabling it to diminish the abdominal cavity to aid in visceral reposition and maintenance in the normal physiologic position.  One of the essential pathologic conditions in splanchnoptosia is malnutrition, inanition.  Splanchnoptosia is best cured by rebuilding the organism which signifies normal blood and panniculus adiposus.  The practical therapeutics in splanchnoptosia is to improve the pathologic physiology, for splanchnoptotics live continually under pathologic physiology.  The visceral drainage treatment improves health.  It places visceral function and elimination at a maximum.  Hence, the subject is better prepared to institute local repair which means resisting and checking infection, absorbing exudates.  The visceral drainage treatment can be conducted at the patient's home, be it a cottage or a palace, without cessation of his occupation.  There is no necessity of making long sojourns to distant watering places to drink hissing sprudel or odorous mineral waters.

(4).  Habitat.

    Habitat or the environments of life are significant in the general treatment of the splanchnoptotic.  First and foremost, the splanchnoptotic should have ample fresh air night and day.  The window should be open all night summer and winter.  Clothing should be suspended from the shoulder avoiding all tight waist bands.  Physical exercise should be regular and practiced daily.

(5).  A vocation.

    The business or association of a splanchnoptotic is a matter of importance as he is unable mentally or physically to withstand persistent continued effort.  Mental and physical rest is necessary for the subject afflicted with inferior anatomy and inferior physiology.  Heavy labor he cannot endure.  Constant standing on the feet for hours exhausts the splanchnoptotic.  He should assume a horizontal position frequently in order to change the circulation and rest the fatigued muscles.  Assuming frequent physical rests the splanchnoptotic's inferior physiologic functions and inferior anatomic structures may maintain fair health and accomplish a reasonable degree of labor.

(6).  Electricity.

    Electricity is of considerable value in relaxed abdominal walls, especially faradization of the muscles.

(7).  The Cold Douche or Spray.

    The cold douche or spray is of limited value.  It can be applied to the abdomen, per vaginam or per rectum.

II.  MECHANICAL TREATMENT.

    The essentials of mechanical treatment is forcible reposition and maintenance of the viscera, on the visceral shelves and in the visceral fossae i.e., viscera are restored and maintained within the normal physiologic position.
    The object of mechanical treatment is forcible visceral reposition and retention of the organ (on their shelves in their fossae), i. e., in their normal physiologic position by means of the abdominal wall.  In the treatment the unfavorable standing posture, the excessive physical labor, the imperfect respiration in the distal zone of the chest and the absence of tone in the abdominal wall should be considered.  The dislocated viscera, in splanchnoptosia, are easily replaced, reduced to their physiologic range of action and maintained with facility through rational therapy applied to the abdominal wall.  The reposition of dislocated groups of viscera in splanchnoptosia to their normal physiologic range improves related visceral functions and structure.  Splanchnoptotics are mainly neurotics, mechanical reposition of the visceral on their visceral shelves and in their visceral fossa, ameliorates the neurosis, affords ample relief and comfort.  Splanchnoptotics are neurotics, consequently unable to judge; therefore, should not be informed as to the excessive mobility of individual organs.

(1).  Abdominal Supporters.

    Much utility, relief and comfort arises from the use of properly fitting abdominal supporters.  The kinds we have used are: (1), non-elastic, (2), elastic, and (3) the author's pneumatic ax shafted rubber pad which can be placed within an elastic or non-elastic abdominal binder and distended with air to suit the comfort of the patient.  The objection urged against the use of an abdominal binder in splanchnoptosia that it does not teach the muscles self-strength, is worthless as the objection against the use of a splint in fractures.  The fact to remember is that the abdominal muscles are extended, stretched beyond self or independent help.  Abdominal supporters do not cure, but properly fitting ones help the patient to relief, comfort and usefulness.  It is not sufficient to recommend an abdominal binder.  The physician should examine it to be sure that it fits properly, both for the grade of splanchnoptosia and for the avocation of the patient.  The difficulty of fitting a proper support is due to the varying position of the patient - walking, sitting or lying.  I have invented a rubber air pad which is the shape of an axe.  This is placed within a binder and subsequently distended with air through an attached rubber tube to the desired dimension.  The rubber pneumatic pad insures a uniform fitting of the abdomen like a water bed, whether spare or fleshy, and also the dimensions may be adjusted to the comfort, relief of the patient.  The binders are useful in moderate nephroptosia, which is the easiest of all portions of splanchnoptosia to aid, but when it has become advanced, binders are not only of little value but frequently harmful.  In severe or distinctly diagnosable hepatoptosia (with ' liver projected into the lesser pelvis, I have seen none or little utility in binders.  All tight waist bands should be removed, and the clothing should be suspended from the shoulders or from hooks on a corset waist.  If one experiments on a dead body with a tight-fitting corset, the organ which will suffer the most extensive displacement will be the right kidney.  All commercial tight corsets should be abandoned but a so-called waist corset is useful to adjust and from which to suspend clothing.
    Since a binder is to reposit the viscera by restoring elongated and separated fascial and muscular fibres of the abdominal walls it must fit snugly, especially in distal abdomen.  Unfortunately binders glide and slide and do not continually maintain a force on the distal surface (of the visceral shelf) of the viscera.  The viscera may glide distal to the binder.  Two rubber tubes must be employed passing between the limbs to fix the binder so that it will not slip proximalward. The binder generally only forces dorsalward and proximalward the abdominal wall, but the addition of the author's rubber pad adds to this the forcing of the viscera proximalward by acting like a pregnant uterus which elevates the viscera toward the thoracic diaphragm.  If the splanchnoptosia is not excessively advanced, the rubber visceral air pad being adjusted and distended with air while the patient lies on the back (Trendelenburg's posture) will prevent the viscera gaining the lesser pelvis-the dangerous ground for stenosis of ducts, vessels and viscera. and traumatizing nerve periphery.  The binder should be removed or loosened for the night's rest.

(2). Horizontal Position.

    A dominant factor in splanchnoptosia is venous congestion during erect attitude, hence the splanchnoptotic should assume especially the horizontal position.  When a patient with established splanchnoptosia assumes the erect attitude, the viscera in general pass distalward with the extra-expanded abdominal walls, the veins immediately enlarge, the abdominal wall is put on a tension, and it projects or bulges distal to the symphysis pubis sufficiently to conceal the genitals from the patient's view.  The patient in the erect attitude assumes a position of lordosis as in advanced pregnancy, in order to secure a compensatory weight balance.
    In the horizontal position the patient with splanchnoptosia should lie on the side and not on the back.  All patients with established splanchnoptosia suffer from gastro-duodenal dilatation (a phase in the progress of splanchnoptosia) due to pressure of the superior mesenteric artery, vein and nerve on the transverse segment of the duodenum. I experimented with dead subjects who had been afflicted with splanchnoptosia, and when such subjects were placed on the back, the viscera, especially the enteronic loops, passed distinctly more and more into the lesser pelvis, dragging and tugging on the superior mesenteric artery, vein and nerve, which compressed more and more the transverse segment of the duodenum.  When the subject of splanchnoptosia lies on the back, the enteronic loops glide into the lesser pelvis, which makes the superior mesenteric artery, vein and nerve approach closer and closer to The vertebral column and thus diminishing the superior mesenterico-vertebral angle, vigorously compressing the transverse duodenum.
I have observed personally splanchnoptosia and gastro-duodenal dilatation progress until the stomach completely occupied the abdomen like an ovarian cyst. (The more acute the mesenterico-vertebral angle becomes, the more the transverse duodenum segment is compressed.)   Pregnancy increases the (superior) mesenterico-vertebral angle, forcing proximalward the enteronic loops and thus releasing the transverse duodenum from pressure.  A great benefit in the wearing of an abdominal binder or Rose's strapping is to increase the (superior) mesenterico-vertebral angle, releasing the duodenum from compression and preventing increased gastro-duodenal dilatation.  Lying on the abdominal surface of the body, with a pillow under the thorax and the symphysis pubis would be the ideal position to insure the maximum (superior) mesenterico-vertebral angle (as it exists in quadrupeds) Hence the splanchnoptotic should lie in the horizontal lateral position as much as is convenient to increase the (superior) mesenterico-vertebral angle, to avoid venous congestion and to prevent the viscera from passing distalward, producing stenosis and flexion of the lumen of the vessels, ducts and viscera.  Lying on the back, or standing, diminishes the mesenterico-vertebral angle and increases the compression of the duodenum by the mesenteric vessels and nerves.

(3).  Massage.

    The massage of the abdominal wall as well as that of the tractus intestinalis aids materially in the treatment.  However, it is of limited value.

(4).  Achilles Rose's Adhesive Strapping.

    I wish to recommend strongly the strapping of the splanchnoptotic abdomen by rubber adhesive plaster introduced first by Dr. Achilles Rose of New York and independently later by Dr. N. Rosewater of Cleveland, Ohio, Dr. Walther Nicholas Clemm of Darmstadt, Germany, and Dr. B. Schmitz of Wildungen, Germany.
    Dr. Achilles Rose's strapping method is rational, economical and practical and affords prompt comfort and effective relief.  Abdominal binders slip and glide but adhesive straps will remain permanently in place and not slip.

Method of Applying the Adhesive Strap.

    Previous to applying the abdominal adhesive straps the abdominal skin should be thoroughly cleaned with soap and water and later alcohol to dissolve oily substances applied in the line of adhesive straps.  The patient should be strapped either in the standing position by elevating the abdominal wall (Glenard's belt  test) by the hands before the straps are applied or strapped in the Trendelenburg's position.
    Place an adhesive strap 2 inches in width around the trunk immediately proximal and parallel to the crest of the pubis, Poupart's ligament and crests of the ilia, superimposing or overlapping the adhesive straps on the medial dorsal line.  The dorsal position of the adhesive straps is located considerable proximal to the ventral position which endows the straps with its useful, visceral supporting properties.
    Secondly, apply a pyramid formed adhesive strap 3 inches wide ventrally and 2 inches wide dorsally immediately proximal and parallel to the first adhesive strap.  These two lateral adhesive straps overlap ventrally and dorsally.  This method of adhesive strapping forces the abdominal wall and viscera proximalward so that the relaxed portion of the abdominal wall is in the region of the umbilicus and stomach.  In other words the adhesive strapping reverses the position of the abdominal splanchnoptosia (atonia gastrica), i. e., the excessive mobile viscera and relaxed abdominal wall are transferred to the proximal end of the abdomen (instead of the distal end).  I allow the adhesive straps to remain in position for 10 days to a month.  Local bathing can be practiced with the adhesive straps in position (avoiding the moistening of the immediate region of the straps).  Beginners are apt to apply the strap too tightly.  Dr. E. Gallant of New York reports excellent results from his corset method of treatment.  Patients experience prompt and ample relief from mechanic supports, avoiding the danger of a fragmentary operation, its recurrence and the inevitable unfavorable cellular and peritonea] adhesions accompanying viscero-pexy.

(III).  SURGICAL.

    Surgery is not advised excepting for obvious pathologic lesions.  Splanchnoptosia cannot be cured by surgery though every abdominal viscus has imposed on it a " Pexy.  " Some surgeons encourage splanchnoptosia by allowing and advising the patient to leave the bed in an incredible limited time subsequent to an abdominal section or peritonotomy.  The treatment of splanchnoptosia is, in general, not by the scalpel, needle and suture.  The surgical therapeutics employed to relieve in splanchnoptosia are: (a) application to the abdominal wall, (b) viscero-pexy, (c) visceral anastomosis.

(A) Abdominal Walls.

    (1) Resection of portions of abdominal wall. (2) Union of musculi recti abdominalis in a simple sheath. (3) Superposition of abdominal wall.
    Resection of Portions of the Abdominal Wall.  The early attempts to diminish the abdominal cavity in splanchnoptosia originated from the gynecologists, particularly from Prof.  Karl Schroeder and Dr. Landau of Berlin, Germany.  I was a pupil of Dr. Theodore Landau in 1885 and his books, "Wander Niere" and "Wander Leber," have been for teachers and authors an unbounded source of credited and uncredited data.
    Union of the Musculi Recti Abdominales in a Single Sheath.  My attention was first called to the subject of relaxed abdominal walls by Prof. Karl Schroeder whose pupil I was for a year.  In that year (1884-lSS5) Prof.  Schroeder of Berlin, Germany, the greatest gynecologic teacher of his age, was at his zenith of fame, and his clinic was vast.  In fact, he tapped the whole of Europe for his material.  He discussed in his clear style the misfortune of lax abdominal wall lying between the diastatic recti abdominales.  He then united the sheaths of the recti in the median line.  But Prof.  Schroeder said then to his pupils that he was not fully satisfied, however, it was the best surgery that he knew at that time.  Later German surgeons improved Schroeder's ideas by splitting the sheaths of the two recti muscles and enclosing both muscles in one sheath by uniting the recti muscle sheaths dorsally and ventrally and dorsally to the recti muscles.
 

ABDOMINAL WALLS       Fig. 206.  Presenting the fascia and muscles of the abdominal wall with the introduction of sutures.

    In 1895, Dr. Orville W. MacKellar and I operated on a woman pregnant four or five months, where the diastases, the musculi recti abdominales was very marked, and the uterus, on coughing or extra intra-abdominal pressure, would project between the recti abdominales.  We united the split sheaths of the recti muscles ventral and dorsal, enclosing the two musculi recti abdominales in one sheath.  Dr. MacKellar reports to me at present (1906) that his patient is perfectly well, and the operation was a success.  Dr. MacKellar was at the delivery and the recti sheaths remained perfectly intact.  For the post-operative hernia, for years past at the Mary Thompson Hospital, I have split the recti and enclosed them in a single sheath.  Every one with sufficient experience knows that post-operative hernia of any considerable size, in women over 40, is in every case accompanied by splanchnoptosia.  Dr. MacKellar and I have records to show that 11 years after enclosing the two recti abdominales in a single sheath, for splanchnoptosia, the operation is a success.  The mesenteries are not for mechanical support to suspend the viscera, but to act as a neuro-vascular visceral pedicle, and to prevent the entanglement with other viscera.  It is the abdominal wall that maintains the viscera in position.
    Besides, I showed in over 600 detailed records of personal autopsic abdominal inspection, that in 96% of subjects the enteron had a mesenteron sufficient in length to herniate through the inguinal, femoral and umbilical rings.  Hence the mesenteries must be viewed as neuro-vascular visceral pedicles, and not as suspensory organs, while the abdominal walls are the essential supporters and retainers of the viscera.  And as every anatomist knows, the recti abdominales are among the chief regulators or governors of visceral poise, at least they retain the viscera in their first delicate normal balance.
    In uniting the two recti abdominales into a single sheath the operation may be performed without entering the peritoneal cavity or after laparotoiny.  During the past 4 years I have practically abandoned the union of the muscli recti abdominales in a single sheath for the operation of superposition, overlapping of the abdominal walls, taught me by Mr. Jordan Lloyd, of Birmingham, England, in 1891.
    Superposition of the Abdominal Walls.  In 1891 in a visit to Mr. Jordan Lloyd of Birmingham, England, he demonstrated to me the operation of superposition (overlapping) of the abdominal walls in abdominal section to strengthen the line of union.  He used a matras form of suture.  Since that time I have employed the superposition (overlapping, like a doublebreasted coat) of the abdominal wall.  Contrary to Mr. Jordan Lloyd, I employ the buried silver wire suture - some 3 to an inch.  The superposition or overlapping of the abdominal walls in splanchnoptosia is the most rational, effective, durable and successful of all parietal surgical procedures.  It diminishes, to the desired extent, the abdominal cavity, forcibly repositing organs on their visceral shelves and in their visceral fossae and retaining them in their normal physiologic position.  I have superposed, or overlapped, some abdominal walls as much as 3 inches on each side, diminishing the abdominal cavity by six inches of the ventral wall.  I observed that some patients with extensive superposition of the abdominal wall, and consequent diminution of the abdominal cavity, complained for a few months of compression feelings, as if the abdomen were too tight or constricted.

(B)  Viscero-pexy (fixation of organs).

    All abdominal viscera are physiologically mobile, hence, to perform viscero-pexy, or visceral immobilization, fixation of any organ, is unphysiological or in other words viscero-pexy produces a physiologic and anatomic lesion.  Excessive visceral mobility is exchanged for visceral fixation.  That is, to cure one disease (excessive visceral mobility), another lesion (visceral fixation) is substituted.  Therefore viscero-pexy is in general an irrational, harmful, surgical procedure.  However, in surgery as in other matters the lesser evil should be chosen, i. e., one should choose which is the greater evil, excessive visceral mobility or visceral fixation - visceropexy.  The lesion of viscero-pexy or visceral fixation is compromisation of physiology and anatomy, viz.: the lymph and blood circulation as well as peristalsis, absorption, secretion, sensation, are compromised.  Nerve periphery is traumatized.  The viscero-pexy in order of frequency have been the following: hystero-pexy, nephro-pexy, gastro-pexy, hepato-pexy, splenopexy and colo-pexy.  In general viscero-pexy is irrational surgery and will be limited in application, as:
    (a)  It attempts to cure one lesion (excessive visceral mobility) by producing another lesion (visceral fixation).  Which is the worse?  It is unjustifiable surgery that substitutes one pathologic visceral position for another (for a mobile, pathologic visceral position is no doubt less damaging than a fixed pathologic position).
    (b)  It attempts to cure a general defect or disease (splanchnoptosia - excessive visceral mobility) by fixation (a physiologic and anatomic lesion) of a single part (e. g., nephroptosia) fragment of the dislocated viscera.  Also, when, accidentally, by trauma ptosis of single viscera occur the distinct, marked symptoms and suffering are not indicated.  Instead of irrational, individual viscero-pexy, the diminution of the abdominal cavity is more rationally secured by Rose's abdominal strapping (or a binder) or by the superposition, overlapping of the abdominal walls (mechanical), as this does not produce the unfortunate peritoneal fixation lesions of viscero-pexy yet forcibly reposits the viscera on their normal anatomic shelves and within physiologic range.  If splanchnoptosia is to be cured by viscero-pexy it will require multiple visceral and parietal operations on one and the same patient as nephro-pexy, gastro-pexy, splenopexy, hepato-pexy, entero-pexy and in females (the usual subjects) utero-pexy.  Observe what extreme compromisation of visceral anatomy and physiology this would entail.  Besides, the thoracic and abdominal walls will require effective repair (diminution).  Hence a dangerous number of surgical. repetitions would confront the patient.
    (c) The viscero-pexy (a lesion of visceral fixation) is generally temporary as the viscus becomes practically eleased sooner or later from absorption of the adjacent artificial parieto-visceral exudate, from absorption or the yielding of suture, from the trauma of the visceral peristalsis, from adjacent muscular trauma, from the trauma of respiration (especially the diaphragm), from lack of support of the abdominal wall.
    (d)  The viscero-pexy compromises visceral function and structure. of which the most striking example is that of dystocia due to hystero-pexy have performed autopsy, the death being directly due to dystocia resulting from hystero-pexy.  Fixation damages other viscera similarly, perhaps according to the degree of solidarity of fixation.
    (e)  The peritonotomy or the invasion of the peritoneum alone, regardless of the viscero-pexy, may produce considerable damaging peritoneal adhesions, compromising not only the structure and function of the fixed viscus, but also of adjacent viscera.  Peritoneal adhesions are ample reasons in many subjects for primary or secondary peritonotomy.  I have shown in hundreds of autopsies that peritoneal adhesions damage viscera by compromising anatomy and physiology, e. g., especially in the caeco-appendicular, gall-bladder, sigmold and pelvic regions - that a peritonotomy is required.
    (f)  The patient is not suffering nor are the symptoms due to dislocation of single organs (in splanchnoptosia) - the suffering and symptoms are the result of general dislocation of viscera (splanchnoptosia-neurosis) and extra-expansion of the abdominal and thoracic walls, i. e., splanchnoptosia.
    (g)  Viscero-pexy is irrational because it compromises visceral function (peristalsis, absorption, secretion sensation) and structure (the connective tissue and the parenchyma of the organs is damaged).
    (h)  Viscero-pexy compromises circulation (blood and lymph).  It traumatizes nerve periphery.  It deranges nourishment, resulting in malassimilation, neurosis.
    (i)  Viscero-pexy is a pathologic surgical substitute for hygienic measures with a high cost and risk.  The anatomic rest (maximum quietude of voluntary muscles) and physiologic rest (minimum function of viscera) in bed, with mental hope of cure, tells the favorable story rather than the viscero-pexy.
    (j)  The patient recovers after the viscero-pexy from symptoms which did not practically belong to the organ attacked.  It was a mistake in diagnosis and an unnecessary operation.  e. g., to fix a retroverted state of the uterus is to substitute one pathologic condition for another, and also the subject is not suffering from the retroversion but either from complications or disease, as neurosis.
    (k)  Three views may be held on the favorable reports in viscero-pexy or visceral fixation, viz.: (1) the patient secures a period of favorite anatomic and physiologic rest in bed after the viscero-pexy - with mental hope of cure.  In other words the viscero-pexy is a hygienic measure with high price and risk. (2) The patient recovers after the viscero-pexy from symptoms which did not belong to the attacked organ.  The symptoms presented by the patient were due to other causes - especially neurosis (neurasthenia, hysteria).  It was a mistaken diagnosis.  Hence for individual viscero-pexy should be substituted rational hygienic measures and correct diagnosis.  Neurosis should not be mistaken for splanchnoptosia or enteroptosia. (3) A third view in the favorable reports of viscero-pexy is that they are prematurely published.  The operation from the anatomic and physiologic rest in bed, as well as diminution of the accompanying neurosis, has afforded temporary relief.  Individual viscero-pexy in the majority of subjects does not secure permanent relief.

INDIVIDUAL VISCERO-PEXY.

    Viscero-pexy on two organs-kidney and uterus-has become unfortunately prevalent during the past decade.

NEPHRO-PEXY.

    Nephro-pexy should be performed for periodic hydro-ureter only.
    If in nephroptosia one detects distinct renal pain, renal tenderness, renal hypertrophy and that the ureteral pelvis of the same side contains a greater quantity of urine than the pelvis of other side, periodic hydro-ureter has probably begun.  If in a kidney of extensive mobility, and irregular pain presents it is probably due to rotation of the kidney on its uretero-neurovascular-vascular-visceral pedicle (Dietl's crisis) and ureteral dilatation (periodic hydro-ureter) has probably begun.
As regards nephro-pexy there is practically one condition which indicates nephro-pexy and that is periodic hydro-ureter.  In this case the damage of periodic hydro-ureter is greater than - unphysiologic renal fixation - that of nephro-pexy.  Besides, nephro-pexy is generally not permanent; the kidney again appears in the field of nephroptosia.  The patient has assumed the risk of operation, with its consequent anatomic and physiologic damage, peritoneal and connective tissue adhesions, for temporary relief.  The multiple methods of executing nephro-pexy condemn it.  Practically every advocate of the irrational nephro-pexy pretends to possess his own method.  Also nephroptosia is but a fragment of splanchnoptosia, and to produce a single, pathologic, unphysiologic, harmful viscero-pexy to cure a general splanchnoptosia adds further damage to the patient. Nephro-pexy has perhaps a mortality of 2% (the dead are not reported - the living are reported).  In nephroptosia, the most rational treatment is mechanical reposition and retention of the kidney by means of mechanical supports (for 60% of adult women possess mo-bile kidney), it avoids operation with consequent connective tissue and peritoneal adhesions.  It is a doubtful justifiable surgical procedure to perform nephro-pexy on a replacable kidney, when the organ can be retained by mechanical means, i. e., by utilizing the abdominal wall through a binder-strapping - if no periodic hydro-ureter exists (because mechanical aids will reposit and maintain the kidney in its normal position a 1000 times more physiologic than fixation - nephro-pexy).  If nephro-pexy be performed (for periodic hydro-ureter) it should be executed according to the Senn method - i. e., the distal pole of the kidney should be placed in the wound in the abdominal wall and maintained there by a loop of gauze without sutures.  Later the kidney is fixed in this position by granulations and the skin is drawn over its longitudinal border by means of adhesive straps.

Hystero-pexy.

    As regards fixation of the genital organs we offer the following consideration: Hystero-pexy should not be performed on a reproductive subject. (Alexander operation is a pathologic surgical substitute for hygienic measures at a high cost and risk.  It demands repetition as frequent as man requires his hair cut.) Since the primary support of the genitals is the pelvic floor, rational surgery suggests pelvic floor repair for general support in visceral ptosis.  Anatomically and physiologically the genitals belong permanently in the pelvis.  The genital organs are permanent pelvic organs, hence it is irrational to remove them from the pelvis into the abdomen in order to fix them permanently to the abdominal wall - the genital nerve, lymph and blood apparatus are located in the pelvis in the resting state.
    To create new external supports external to the pelvis for the genitals (ventral hystero-pexy) is unphysiologic, pathologic, as it dislocates the organs and compromises structure and function - especially mobility and peristalsis beside disturbing adjacent organs.  The utility of ventral (abdominal) hysteropexy has not been established; however, its damaging effects have been recognized many hundreds of times: (a) in pain following the operation, (b) from dystocia, (c) in abortions, due to it, (d) in the necessity of surgical procedures in parturitions (as instrumental delivery symphysiotomy, Caesarian section, Porro operation), (e) in the necessity of producing abortions, (f) from postoperative hernia (Theilhaber reports 30% of hernia subsequent to ventral hystero-pexy - and these were practically originally aseptic subjects), (g) in the mortality of some, 2%.
    To forcibly substitute or transform secondary genital supports into primary ones or to create artificial ones is rarely applicable and of doubtful utility.  However, secondary supports are more rational than to create artificial new supports external to the pelvis.  The Alexander operation, of shortening the round ligaments, is imposing on a secondary uterine support (the round ligaments) the duty of a primary uterine support.

(B) Visceral Anastomosis.

    The anastomosis of viscera employed to relieve in splanchnoptosia are the stomach and enteron.  The reason for this is that gastro-duodenal dilatation is simply a phase in splanchnoptosia due to the compression of the duodenum by the superior mesenteric vessels.  Gastro-enterostomy allows the food to escape from the stomach into the enteron without first passing through the obstructed portion of the duodenum from the compression of the superior mesenteric artery vein and nerve.  With rapid stomach evacuation and no food in the duodenum the gastro-duodenal dilatation is quickly changed to gastro-duodonal contraction. (See discussion of gastro-duodenal dilatation.)

RESUME AS REGARDS SPLANCHNOPTOSIA.

    1. Splanchnoptosia presents two grand divisions, viz.: I. Thoracic splanchnoptosia which includes the factors of: (a) relaxation of the thoracic wall (with diaphragm), (b) thoracic splanchnoptosia (heart and lungs), (c) consequent deranged function of the thoracic viscera and wall (respiration and circulation). II.  Abdominal splanchnoptosia which includes the factors of: (d) relaxed abdominal walls (atonia gastrica), (e) splanchnoptosia of abdominal viscera (the six visceral tracks), (f) elongation of mesenteries (neuro-vascular visceral pedicle), (g) gastro-duodenal dilatation (due to compression of transverse portion of the duodenum by the superior mesenteric artery vein and nerve), (h) altered form of the abdomen (erect-pendulous, prone-projecting laterally).
    In general, in splanchnoptosia, canalization is compromised, nerve periphery traumatized, common visceral function (peristalsis, secretion, absorption, sensation) deranged; circulation (blood, and lymph) disordered; respiration disturbed - ending in malnutrition and neurosis.
Splanchnoptosia compromises the lumen of ducts, vessels and visceratubular canals - through flexion, stenosis, decalibration, elongation, constriction.
    2.  The numerous and complex groups of symptoms produced by splanchnoptosia must be considered independent of inflammatory processes.
    The symptoms of the splanchnoptotic are complex and numerous.  Each cause in splanchnoptosia produces a vicious circle of - pathologic physiology - pathologic effects on the visceral tracts - digestive, genital, urinary, lymphatic, vascular, nervous, respiratory -  impairing nourishment.  Splanchnoptosia is often mistaken and wrongly diagnosed as neurasthenia, nervous exhaustion, hysteria, spinal anaemia, menopause, nervous dyspepsia, and neurosis.
Splanchnoptosia appears to be chiefly of congenital disposition as its subjects are generally feeble, slender, atonic, neurotic, marked with a habitus, ill-nourished, deficient in vital force with marked inferior physiologic function and inferior anatomic structure, with apparently a hard struggle to battle for life and against its forces.  It seems sufficiently difficult for the splanchnoptotic to live merely - without attempting productive labors or to rear children.  Splanchnoptotics are inferior physically and incapable of sustained effort mentally.  They are easily fatigued and present a neurotic life.      Splanchnoptosia rests on evident inferior anatomy and inferior physiology - on stigma, on habitus, on heredity.  The heredity of the splanchnoptotic is habitus splanchnopticus.
    In splanchnoptosia the visceral tracts are deranged in function (manifesting pathologic physiology) and their anatomy is distorted (the elastic, muscular and connective tissue fibres are elongated and separated).  Splanchnoptotic organs are liable to become hypertrophic - e. g., spleen, liver, uterus - from hyperaemia (especially venous congestion).
    3.  In splanchnoptosia in common, the tractus intestinalis, urinarius, vascularis, respiratorius, lymphaticus, genitalis, experience excessive, deficient disproportionate function peristalsis, absorption, secretion, sensation); excessive mobility (distalward dislocation), obstruction (from flexion), pain.
    In splanchnoptosia the chief manifestation of distinctive characteristic features are:

    (a) From the tractus intestinalis, viz.: indigestion, fermentation, meteorism, constipation, malassimilation.
    (b)  From the tractus urinarius, hydro-ureter (periodic), axial rotation of renal pedicle (Dietl's crisis).
    (c)  From the tractus genitalis, hyperaemia, hypertrophy, abortion.
    (d)  From the tractus vascularis, hyperaemia, anaemial cardiac and aortic palpitation.
    (e)   From the tractus lymphaticus, congestion, decongestion, hyper-trophy.
    (f)  From the tractus nervosus, irritability (from trauma), instability, debility, neurosis.
    (g)  From the tractus respiratorius, excessive, deficient, disproportionate respiration.
    The splanchnoptotic is the typical subject of manifest pathology physiology (i. e., he lives in the zone between normal physiology and pathologic anatomy).
    Splanchnoptosia consists of a distalward dislocation of thoracic and abdominal viscera resulting from extra extended walls.  A viscus is dislocated when it is permanently fixed.  More adults have dislocated viscera (e. g., splanchnoptosia and from peritoneal adhesions) than normal ones.

    B.  Stillar's costal stigma or floating tenth rib - costa decima fluctuens - I have studied insufficiently to make authoritative statements.
    The objective appearance of the splanchnoptotic is neurotic, slender with gracile skeleton, flattened thorax, increased intercostal spaces, delicate and poorly nourished, pale, non-energetic; a sad, helpless picture.  Splanchnoptotics form a distinct class with peculiar characteristics resembling the class of tubercular subjects to which they are related.
    Splanchnoptosia is a general disease of the abdominal and thoracic viscera; the tractus respiratorius, intestinalis, vascularis, nervosus, urinarius, lymphaticus, genitalis are equally affected, but from anatomic mechanism and manifestations the tractus nervosus (neurosis) and tractus intestinalis (indigestion), appear to suffer the most.
    Since my clinic and private practice has consisted of 85% of women I cannot estimate the percentage of splanchnoptosia as regards sex; however, in over 650 personal autopsic abdominal inspections (475 men, 160 women) splanchnoptosia was amply evident in men.
    Rapidly repeated gestations play an influential role in progressive splanchnoptosia, as when the fascial, elastic and muscular fibre of some abdominal walls are once well elongated and separated (expanded) they do not return to normal.
    The second, third, fourth, fifth decades of life are the chief ages of suffering in splanchnoptosia.
The symptoms which chiefly predominate in splanchnoptosia are from the side of the nervous, digestive, and circulatory systems.  From the nervous sphere one observes mental depression, melancholy, excitability, irritability, and the nervous stigmata, as e. g., neurosis, hysteria, neurasthenia.  From the side of the circulatory system one observes hyperaemia, anaemia, cardiac, and aortic palpitations - excessive peristalsis.  The aorta may appear as a beating tumor which may be mistaken for aortic aneurysm, because the aorta (while in the prone attitude) is so extensively uncovered, exposed by separated viscera, presenting a protection of thin abdominal wall only.
From the side of the digestive system one observes indigestion, fermentation, meteorism, constipation.  These three groups of symptoms are marked in every advanced case of splanchnoptosia.
    I cannot agree with Meinert in attempting to establish an evident etiologic relation between chlorosis and splanchnoptosia.  I could observe no distinct relation in series of observation.
The large number of women who have not borne children, who have not laced tight, who have not suffered from ascites, nor wasting disease, however being afflicted with splanchnoptosia, indicates a predisposing or congenital factor.
    In splanchnoptosia there are two factors to study, viz.: (a) congenital and predisposing cause, (b) exciting cause.  The secondary or exciting causes are any forces which tend to debilitate (elongate and separate the fibres of the abdominal parietes), the abdominal wall, as rapidly repeated gestation, abdominal tumors, ascites, septic disease, constipation, and wasting disease, especially the disappearance of panniculus adiposus and adjacent to the viscera.  A congenitally defective system may persist in maintaining fair health; however, exciting or aggravating causes may precipitate invalidism with facility.
    Splanchnoptosia may exist with no recognizable symptoms, however, while the subject is in fair physical condition.  The rule is that splanchnoptosia may be accompanied by pathologic physiology (and pathologic anatomy) in part or all of the visceral tracts (thoracic or abdominal).
Splanchnoptosia is a general disease - not a local one.  It belongs to the area of respiration, which is the trunk.  This is well to remember when the pexyite is attempting to impose fixation on some single viscus (which should remain physiologically mobile).
    The physician should learn to discriminate the effects in splanchnoptosia from the different visceral tracts, e. g., nephroptosia and genital ptosis manifest almost identical symptoms.  The immediate relief by mechanical treatment of forcible reposition by adhesive strapping would decide in favor of nephroptosia as support from the abdominal walls is inefficient in genital ptosis.
    Observe how nephroptosia from trauma of the plexus renalis produces reflex svmptoms on the proximal end of the tractus intestinalis, ending in nausea, pain, malassimilation, constipation, neurosis.  Ureteral calculus induces vomiting, and sooner or later renal and gastric disease coexists.  Genital disease occasions more gastric disturbances than the reverse because the gastric functions (secretion, absorption, peristalsis, sensation) are deranged more effectually than those of the genitals.  Trauma or infection of the nerve periphery of any abdominal visceral system deranges the peristalsis, absorption, secretion, sensation of the other abdominal systems.  The connection between diseases of the tractus genitalsis (uterus) and tractus intestinalis (stomach) is profound and intimate.  Disease of the uterus and stomach frequently coexist.  A differential diagnosis of the symptoms arising from nephroptosia, from genital ptosis or from gastroptosia is often difficult, as similar symptoms may be referable to any one of these visceral tracts.  This may be due first to the nerve tract, the center of which is not in the brain or spinal cord but in the sympathetic nervous system - (e. g., cerebrum abdominale or cerebrum pelvicum).  From reflex action symptoms arise which relate to kidney, stomach or uterus.  The reflex tracts being anastomosis ovarica, anastomosis pudendo-baemorrhoidalis, anastomosis genito-gastrica, anastomosis cutaneo-cavernosa, anastomosis collateralis and the nervi splanchnici.  Also the anastomosis utero-coeliaca, anastomosis utero-cerebrospinalis, anastomosis reno-coeliaca.  The immediate routes of the reflex are direct connections of the vagus (excluding the ganglion abdominales) with the sympathetic nervous system.  The second manner in which the mistakes may occur are due to dislocation of the respective organs.  As splanchnoptosia is a general disease, local operation - viscero-pexy - as nephro-pexy, hysteropexv, hepato-pexy, gastro-pexy, colo-pexy, will evidently be of limited value.
    In diagnosis the patient's trunk should be divested of clothing.  Respiration should be observed in both the erect and prone attitude.  Every abdominal organ should be palpated in the erect and prone attitude.  Glenard's belt test may be employed.  Inspection, palpation, percussion, gastric distension and colonic inflation are decisive aids to diagnosis.
    Splanchnoptosia is congenital disease attacking the abdominal and thoracic viscera.  Observers associate with splanchnoptosia other stigmata as exopthalmic goiter, myxoedema, neurosis, defective physical form, Stiller's floating rib. It begins in disordered function - pathologic physiology - and structure of the tractus respiratorius.  Man must be considered to possess respiratory muscles in whatever location the spinal nerves supply the thoracic and abdominal wall.  The intercostal (thoracic) and lumbar (abdominal) nerves are not sharply separated in function.  Man's muscular trunk is a respiratory apparatus.  The diaphragm is the most important organ in splanchnoptosia.  The splanchnoptotic is mainly a neurotic (and hysteria if not present thrives well).  Mechanical reposition of organs through therapy applied to the abdominal wall rapidly ameliorates the symptoms and that is the general rational treatment.  The symptoms of the splanchnoptotic are chiefly those of neurasthenia with or without local distress or pain.  Pain may be experienced anywhere; however, it is chiefly referred to the small of the back.  The first impression one receives in studying splanchnoptosia is a picture of multiplicity, kaleidoscope, dissimilars.  However, with continued investigation the dislocated organs present themselves in groups and types.  In splanchnoptosia the viscera of the thorax, abdomen and pelvis share proportionally in the disease.

GENERAL CONCLUSION AS REGARDS SPLANCHNOPTOSIA.

    Splanchnoptotic (dislocated) organs are accompanied by more or less change of form and consequently function.  No dislocation in the form of an organ occurs without dislocation and change of form and relaxation of neighboring organs.  In splanchnoptosia the change of form of organs is not due merely to the pressure of opposing adjacent organs or the abdominal wall (muscle or skeleton) but the change of organ form is due to function or to physiology it is due to the physiologic necessity of visceral motion rhythm.  Practically no organ becomes dislocated without co-existing relaxation of the abdominal wall.  The dislocation of single organs does not occur without changing the relations of adjacent organs.

Pathologic Physiology.

    In the rise and progress of splanchnoptosia two matters should be held in view, viz.: (a) pathologic physiology, and (b) mechanical pathology.  Pathologic physiology is disordered function which is abnormal innumerable times before the pathologic anatomy is perceptible. it is true organs have a wide range of normal physiology but in splanchnoptosia the organs have progressed beyond the normal physiologic range and have entered the range of pathologic physiology.  In splanchnoptosia the pathologic anatomy is difficult to detect, judge and estimate.  However, it is plainly evident that the physiology of the organs and enclosing walls is pathologic because the functions are going wrong and it is the office of rational treatment to correct the erroneous physiology.  A large field of the pathologic physiology in splanchnoptosia is mainly mechanic - it is visceral and parietal dislocation hence mechanical pathology will demand the chief consideration in the subject.  First, in splanchnoptosia by appropriate stimulation (visceral drainage) of the organs affected with the sluggish, pathologic physiology to normal maximum action, tolerant, normal physiology is restored.    Second by the mechanic measure applied to the abdominal and thoracic walls the mechanical pathology is rationally removed.
    In splanchnoptosia the linea alba may be elongated and expanded, stretched to a thin blade.
In splanchnoptosia the organs should be first palpated in the horizontal or prone position and the outline marked with colored chalk, later in the erect position whence the difference in location of the viscera is plainly evident during the horizontal and erect attitude.  The percussion should be executed both in the standing and lying position and in each case the organs outlined with colored chalk.

Umbilicus.  A test of splanchnoptosia is the change of position of the umbilicus on coughing while standing and while lying.  With pendulus abdomen the umbilicus moves proximalward while standing and coughing but not while reclining. The amount of proximalward movement of the umbilicus is an index to the degree of splanchnoptosia.  If the proximal half of the rectus abdominalis be relaxed the umbilicus moves distalward.  In coughing while in the most erect attitude, the proximal half of the rectus is contracted and hence the umbilicus moves proximalward.  To make a diagnosis of splanchnoptosia the patient's clothing should be removed from the trunk.
    The symptoms of splanchnoptosia may be grouped into three phases, viz.: (a) the prodromal phase in which arises neurasthenia, hysteria hypochondria.  They are subjective symptoms.  Visceral dislocation and relaxed parietes may be insufficiently advanced to diagnose.  However, in this first stage the viscera becomes dislocated and the parietes become relaxed, the intra-abdominal pressure becomes reduced.  In this phase the circulation (lymph and blood) begins to be compromised, as well as visceral channels; secretions are diminished and toxic absorption becomes evident.
    (b)  The second stage of splanchnoptosia is characterized by dyspepsia, constipation, colic, headache, dizziness, insomnia, weakness, loss of flesh, marked visceral dislocation and relaxation of muscular parietes.  Anaemia, tympany and foecal stagnation exist.  Lack of intra-abdominal pressure is marked.  The visceral ligaments are elongated.
    (c)  The third stage of splanchnoptotic symptoms are characterized by multiple, many sided subjective symptoms.  The clinical picture is pronounced, body weight diminishes, capacity for nourishment is at a minimum, muscular weakness is at a maximum with scarcely sufficient capacity of forcing stool through the rectum.  Functional anuna and Psychical changes may exist.  Sensation is blunted.  Glandular secretions, absorptions and visceral peristalsis are extremely deranged.      Symptoms become manifold, and the patient is a pathologic picture.
    The treatment of splanchnoptosia is:
    I.  Medical (hygienic regulation of visceral function, diet, habitat, avocation).
    The medical treatment for splanchnoptosia is by means of ample visceral drainage of the tractus intestinalis and tractus urinarius which increases the volume of fluid in the lumen of the tractus vascularis and tractus lymphaticus, effectually sewering, draining the body of waste laden material.  It is visceral drainage, appropriate food, ample rest.
    II. Mechanical (forcible reposition and maintenance of viscera in their normal physiologic position - i. e., on their visceral shelves and in their. visceral fossae).
    The mechanical treatment consists in the employment of abdominal binders, especially Achilles Rose adhesive strapping (being rational, economical and practical).  The straps do not slip.  Also the author's abdominal binder within which is placed a pneumatic rubber pad which can be distended with air to suit the patient's comfort.  The splanchnoptotic must make the best of his hereditary burden and assume as much (horizontal) rest as possible.
    III. Surgical (superposition of the abdominal wall, viscero-pexy anastomosis.)
The surgical treatment consists of: (a) viscero-pexy, i.e., fixation of mobile viscus to the abdominal wall (extremely limited, as it attempts to cure one alleged visceral lesion - excessive mobility - by producing another visceral fixation). (b) Diminishing the abdominal cavity and forcing the mobile organs on their visceral shelves and visceral fossae by superposition (overlapping) the elastic, fascio-muscular apparatus of the abdominal wall like a double breasted coat (rational, practical). (c), Anastomosis as gastro-enterostomy.
    Some of the photographs in this chapter were executed by Dr. William E. Holland, from my wall charts.

A PARTIAL BIBLIOGRAPHY OF SPLANCHNOPTOSIA

    Rudolph Virchow - Virchow's Archiv., vol.  V, 1853.  An historical, critical and exact consideration of the affections of the abdominal cavity.
    Aberle, Rallet, Rayer, J. B. Morgazni, Kusmaul, Bayer, Hertzka, Lindner.
    Fischer-Benyon, Becker and Lenhoff, Frickhinger, Kiittner, Strauss, Chvostek, Memert, Kelling,  Huber, Flemer, Hufschmidt, Ewald, Brtiggeinzinn, B. Stiller, Bial, Obvortzow, Boaz, Ostertag.
Frantz Glenard - Articles from 1885 to 1906.  Book on splanchnoptosia (875 pages) published in 1899.
    Theodore Landau - Wander Nieve, 1881.
    Theodore Landau - Wander Leber, 1887.
    C.  Schwerdt - Beitrag (splanchnoptosia), 1897.
    J.  G. Sheldon - Is Nephroptosis Hereditary? 1903.
    Byron Robinson - Gastro-duodenal Dilatation, Cincin-Lancet-Clinic, Dec. 8, 1900.
    A. W. Lea - Enteroptosis, Medical Chronicle, 1902.
    Saunby - British Med.  Jr., Nov. 29, 1902.
    Beyea - Pennsyl.  Med.  Jr., Nov., 1902.
    Charles Adron - Splanchnoptosia in Pregnancy, Am.  Jr. Surg. and Gynecol., July, 1902.
    A. P. Francine - Gastroptosis, Philadel.  Med.  Jr., Jan. 3, l903.
    J. D. Steele - Analyses of 70 cases of gastroptosis, Am.  Jr. Med.  Assn., Nov. 8, 1902, also Jan. 25,1902.
    R. C. Coffev - A method of suspending the stomach, Philadel.  Med.  Jr., Oct. 11, 1902.
    Earnest Gallant - The Rational Treatment of movable kidney and associated ptosis, Am.  Jr.
Surg. and Gynecol., Dec., 1902, N. Y. Med.  Jr., April 29,1905.
    Robert J. Reed - Movable Kidney, Philadet.  Med.  Jr., Nov. 8,1902.
    L.  Schoeler - Movable Kidney, Virg.  Semi-Med.  Monthly, April 14,1899.
    J. E. Moore - Splanchnoptosis from a surgical standpoint, Jr. Am.  Med.  Assn., July 29, 1905.
    0.  Kraus - Emfluss des Korsetts, 1904.
    H.  Quincke - Enteroptose, Therapic de Gegenwart, XLIV, page 538.
    H. A. NcCullum - British Med.  Jr., Feb. 18,1905.
    Thomas R. Brown - Enteroptosis, American Medicine, July and August, 1903. Three articles.
    C. A. Meltzurg - Enteroptose und Intra-abdominales, Druck, 1898.
    Byron Robinson - Splanchnoptosia, Philadet.  Med.  Jr.. Nov. 30, Dec. 7,1901.
    J. M. Taylor - The Rational Treatment of visceral piosis, N. Y. Med.  Jr., Aug. 4, 1906.
    J. N. Le Conte - Gastroptosis, N. Y. Med.  Jr., July 25, 1903.
    Arthur Keith - Hunterian Lectures, Lancet, March 7, 1903.
    L. Krez - Frage der Enteroptose, 1892.
    H. Goelet - Annals of Gynecology and Pediatry, vol.  XV, 1903.
    M. L. Harris - Movable Kidney, Jr. Am.  Med.  Assn., June 1, 1901, Feb. 13,1904.
    C. A. Meltzurg - Gastroptose, Wiener Med.  Presse, July 28, Aug. 4, Aug. 11, Aug. 18, Aug. 25, 1895.
    J. Chalmers Da Costa - Nephroptosia, N. Y. Med.  Jr., Aug. 4,1906.
    Agness C. Vietor - Splanchnoptosia, Boston Med. and Surg.  Jr., Aug. 9, Sept. 9, 1906.
    Achilles Rose and R. C. Kemp - Atonia Gastrica (Book), 1906.
    R. Weissmann - Ueber Enteroptose, Monograph.