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
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
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
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
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
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
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
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.
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.
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
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
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
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
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.
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
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.
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.
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
| 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
| 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.
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
In the following scheme are noted not only the great
factors in splanchnoptosia, but other detailed factors:
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.
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
Derangement of respiration is clinically evident
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
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.
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
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.
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.
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
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 Heisterís 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 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.
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
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
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
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.
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
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,
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.
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
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.
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
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.
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 Roseís
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.
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.
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.
The left colon is so infrequently dislocated from
the fact that it is rarely possessing a mesocolon that I omit its discussion
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.
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.
The treatment of coloptosia is medical, mechanical,
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.
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
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
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
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
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
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
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,
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
Treatment of Nephroptosia.
(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.
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
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
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
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
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.
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
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
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
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
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
| 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
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
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.
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.
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
| 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.
(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.
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
(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
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
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
(IV) Relaxation of the thoracic and abdominal
(V) Superimposed splanchnoptotic viscera.
(VI) Genital sub-involution (infection).
The Treatment of Genital Splanchnoptosia.
The treatment should be medical, mechanical, surgical.
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.
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.
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
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
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
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
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
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
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,
The similar conditions as regards haemogenous circulation
in splanchnoptosia may be practically applied to the lymphatic circulation
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
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.
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
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.
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.
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.
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.
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
(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
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
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
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
(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
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.
Presenting the fascia and muscles of the abdominal wall with the introduction
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
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,
(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
(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
(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.
Viscero-pexy on two organs-kidney and uterus-has
become unfortunately prevalent during the past decade.
Nephro-pexy should be performed for periodic hydro-ureter
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.
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,
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
(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
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,
(d) From the tractus vascularis, hyperaemia,
anaemial cardiac and aortic palpitation.
(e) From the tractus lymphaticus, congestion,
(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
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
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
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
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
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
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
(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
(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,
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
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?
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.
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