Ulcerative colitis complicating pregnancy and the puerperium

Ulcerative colitis complicating pregnancy and the puerperium

ULCERATIVE COLITIS COMPLICATING THE BY (CHARLES S. KARNES, A.B., M.D., PIIILADET,I~IEIA, (From the Obstetri.cal Department PREGNANCY AND ...

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ULCERATIVE

COLITIS

COMPLICATING

THE BY

(CHARLES

S.

KARNES,

A.B., M.D., PIIILADET,I~IEIA,

(From

the Obstetri.cal

Department

PREGNANCY

AND

PUERPERIUM*

of the

School

AND

HELEN

14.

M.D.,

HAYES,

PA. of Medicine

of Temple

University)

ulcerative colitis was first described C HRONIC Hale White in 1888. But the disease received

as an entity by W. little attention, until, within the past one or two decades, it has been the subject of much intensive study. Bargen, to whom the profession is indebted for much information, began his investigations in 1923. It is variously named ulcerative, suppurative, rectocolitis gravis.

. The disease may be acute, fulminating, or gradual in onset. There is a strong tendency to recurrence in apparently cured cases. It occurs far most frequently between twenty and forty years of age, not infrequently before twenty. Ulceration of the colon is the essential pathologic condition. The process usually begins in the rectum and sigmoid, but in some 80 per cent, the higher levels are finally reached, even the lower ileum. Logan1 in a review of 117 cases says : “Chronic ulcerative colitis is a most serious disease from the standpoint of both morbidity and mortality. It is a chronic disease of long duration ending quickly from toxemia or perforation.” As to the active infective agent or agents, investigators differ. Bargrn and Log+ of The Mayo Clinic, as a result of admirable experimental research, report isolation in 45 of 60 cases of a gram-positive lancet-shaped diplostrcptococcus as the exciting cause. Bargenz isolated the same diplococcus from tonsils and abscesses of teeth. Cultures introduced intravenously into animals, produced, in onethird of the number, colonie ulcers like those in man. Frequently tonsillectomy or removal of infected teeth has resulted in acute temporary exacerbations of the disease. This suggests the presence of the causative bacteria in these foci. Other earnest workers have not been able to confirm the findings of Bargen, and most authorities are disposed to designate, as the commonly exciting cause, the intestinal organisms always present in the ~01011, namely, the colon bacillus, staphylocnrrus and streptococcus. Ordinarily they are nonpathogenic to the intestine. But Kendall states, “Normal intestinal organisms may multiply with abnormal luxuriance, leading, through unusual conditions, to abnormal reactions in the alimentary canal. ” Among such unusual conditions Yeomnnss mentions food toxins, severe constipation, injuries, pregnancy and labor, and acute general infections. Yeomans states, also, that, generally, no definite predisposing cause can be assigned. However, in his series of 100 cases, the onset dated, in six cases, from dietary indiscretion; five, severe constipation; three, exposure; two cases each, pyorrhea and root abscesses, influenza, injury, and pregnancy. The onset followed parturition in *Real1

before

the

Ohstetricnl

Society

of Philadelphia, 907

Febrnary

5, 1931.

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one case. He adds, “These ering resistance, during which usual virulence. ”

OF

OBSTETRICS

factors are the normal

mainly intestinal

AND

GYNECOLOGY

significant bacteria

in temporarily may assume

lowan un-

We present three cases of ulcerative colitis complicating pregnancy and the puerperium, a fourth one to be added in discussion. CASE University of labor.

L-M. H., Hospital,

white, July

forty-two 30, 1930,

years at full

old, para x. Admitted to the Temple term, well advanced in the first stage

Patient’s parents both died of Bright’s disease. Five living children, four dead at about two years of age. Patient was under prenatal care only the last two and a half months of pregnancy. Within this time, no serious ill symptoms were present. During the period of her prenatal care, however, she lost some four pounds in weight, her blood pressure arose from 108 systolic at first to I43/100, on

Fig.

Fig.

1.

Fig. l.-Case 1. Section occupied by necrotic tissue, and edema can be seen in Fig. Z.-Case 1. Section, there are many bacteria. bacilli.

admission. abnormality. half hours

Meanwhile, A healthy of labor.

of colon. Mucosa is completely fibrin and leucocytes. Leucocytic the submucoba and muscle coat. of colon. XbOOO. In the edematous There are elongated diplococci

the urine showed a slight trace of child was delivered spontaneously

2.

destroyed. inflltration, and

Its site hyperemia

inflammatory pseudo-diphtheria

albumin, but after eight

is

tissue

no other and one-

Abdominal pains, at first believed to be after-pains, marked the puerperium throughout. Abdominal tenderness was soon manifest. There were very frequent, The stools were never grossly bloody. fetid stools, tympany, and great prostration. Fever, 100” on admission, soon arose to 103.6” and subsequently remained excessive of a remittent type. Note that, on admission, the maternal heart rate was 100. There was progressive heart acceleration throughout the course. A probable diagnosis of Enteritis was made. It was believed to be a ease of septic infection Such the postmortem showed, the pathologist giving but not of puerperal origin. as cause of death, acute ulcerative ileocolitis. Death occurred on the ninth day of the puerperium.

BARNES

AND

HAYES

:

Late in the case, hemoglobin was 45 per blood cells 9,600, differential count normal. ative, both antemortem and postmortem.

ULCERATIVE

909

COLITIS

cent. Red blood Widal negative.

cells 2,870,000, Blood eulturc

white neg-

CASE 2.-H. W., colored, thirty-three years of age, admitted to the Philadelphia General Hospital July 12, 1928, approximately seven months pregnant. Four healthy children living. No history of serious illness or of complicated pregnancy or childbirth. Chief complaint on admission, (‘Cannot see, sleepy. ” Illuess began one week before admission with headache and spots before the eyes. Edema of the lower extremities present. Two convulsions occurred before admission. Blood pressure on admission 280/150 minimum blood pressure 184/124. Free venesection was done, morphino sulphate given, glucose intravenously, later magnesium sulphate by the same route. Within a few hours after admission, four severe convulsions occurred, each lasting several minutes. Colonic irrigation was repeatedly given, fluids forced. Delivery of a small stillborn fetus occurred the day subsequent to admission. Improvement failed to follow delivery, unconsciousness and coma prevailing. Uranalyses showed extreme kidney damage, albumin, blood, casts. Phenolphthalein test, none first hour, 5 per cent second hour. Blood urea 18, blood sugar 150. Clinical diagnosis : eclampsia; acute tubular nephritis. Yet, throughout the puerperium, ending by death in five days, there was abdominal distention, abdominal pain and tenderness developing, with frequent liquid stools, foul, black, later blood stained. The temperature varied Pathologic diagnosis :

little acute

from the ulcerative

normal, colitis.

pulse 95 to 195. Chronic diffuse nephritis.

CASE 3.-G. F., colored, aged thirty-five years. Admitted to the Philadelphia General Hospital, December 3, 1930. Father died of “a stroke,” mother living, an epileptic. Six children living and well. Tonsillectomy in 1924. Two previous pregnancies, were complicated by serious toxemia. August, 1925, near term, with preeclamptic toxemia, patient gave birth, in the Samaritan Hospital, to a stillborn child. Labor was induced. On admission, her blood pressure was 260/150. X-ray showed many apical abscesses of the teeth. The urine showed no abnormality except a cloud of albumin and a few leucocytes. Again, February, 1927, she was admitted to the same hospital, with toxemia, five months pregnant. Blood pressure 160/90, urine as before; blood, hemoglobin 50 per cent, otherwise approximately normal. Patient refused to remain more than four days for treatment. For one week before admission to the Philadelphia General Hospital, patient is said to have complained of headache, pain in the back, nausea and vomiting, blurred vision; reported also, to have had oliguria and hematuria. She had, within a few hours before admission, two severe convulsions. When admitted, temperature was 98”, pulse 120, there was noisy restless delirium, and mouth soiled with bloody Physical examination revealed no gross abnormalities. An apparently mucus. pregnant uterus reached midway from symphysis t,o umbilicus. Blood pressure was 230/120. Urine showed a cloud of albumin, many leucocytes, many hyaline and granular casts. Blood Wassermann was negative. Red blood cells 2,610,OOO; white blood cells 18,250; hemoglobin 55 per cent. Differential count was normal ; urea nitrogen 55, later 70 to 150; sugar 166; creatinine 3.1, later 6.4 to 12.6. Spinal tap, fluid clear, under no excess pressure. The patient received sedation, temporarily, with sodium amytal. Treatment included veneseetion, glucose and magnesium sulphate intravenously, dry hot packs, colonic irrigation. Fluids given freely by hypodermoclysis and intravenously. Patient became comatose, from which she aroused but little throughout the course. The last day of illness tremor was present, and one convulsion occurred. Abortion

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of a four months’ pregnancy occurred the day following admission. Blood pressure had meanwhile become subnormal; following delivery, 110/65. No improvement in general condition occurred. Patient died five days subsequent to admission. Clinical diagnosis: An acute exacerbation of a chrouic nephritis, complicated by an early pregnancy; uremia, pyelonephritis; heart failure. Pathologic report, cause of death : chronic nephritis; ulcerative enterocolitis.

It seems that colitis, as a complication of pregnancy and the puerVery few books mention colitis. perium, has been seldom recognized. Berkeley and Bonney4 casually remark that inflammation of the sigDeLee5 moid has been described as a complication of pregnancy. mentions, as possibly a part of the pathology of puerperal septicemia, Medical literature, we believe, contains gastritis, enteritis and colitis.

comparatively

little.

Review

of the complete files of the AMERICAN JOURNAL OF OBSTETRICSAND GYNECOLOGY fails to find mention of colitis. Search, also, of the last ten volumes of Surgery, Gynecology and Obstetrics, and of the Supplement, Intervmtional Abstracts of Surgery, is rewa.rded by little upon the general subject, none upon its relation to pregnancy. Positive diagnosis of ulcerative colitis, in pregnancy or the puerperium, which may require the barium enema and the x-ray or the sigmoidoscope, is frequently difficult. Symptoms of the condition are not unlikely to be obscured by the symptoms of other grave conditions or to be mistaken for the symptoms of the latter: Successful treatment, which may require ileotomy, to divert the fecal current, may be, in such cases, of doubtful expediency.

BdRfSES

AND

HAYES:

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COIJTIS

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In only one of our cases was a probable diagnosis made. The symptoms in all, however, if properly comprehended and analyzed, point pain, tenclcrquite definitely to the condition : Abdominal distention, ness, very frequent foul, dark liquid stools (blood stained at t,imes), prostra.,tion, anemia, tachycardia in all, fever in the septic case. Bargen. and Weber” observe: that a septic type of fever occurs in the severe fulminating cases. Review of the records at the Philadelphia General Hospital of 100 patients dying apparently of toxemia of pregnancy or of puerperal sepsis, yielded 18 cases submitted to postmortem examination. Two of our cases are of this latter number. A third case was reported, by the pathologist : “Intestines, mucosa coat,ed with thin membranous exudate.” A fourth case, “Mucous membrane of the large bowel is the seat of small hemorrhagic points.” The remaining 14 cases, showed “no gross pathology of the mucosa of the intestines.” The few cases we present justify certainly no positive conclusions, but suggest, we believe, some pertinent comments. Reca,ll conditions inherent in pregnancy, most of them accepted by the profession: Increased metabolism due to the growing fetus with its see-undines, and to tissue normally added to the maternal organism (many pounds). Both anabolism and katabolism are at high tension. The organs of elaboration, assimilation and excretion are subjected to an overload. Logan has expressed the belief that the basic etiologic factor in ulcerative colitis is metabolic disturbance. Kidneys, liver, one or perhaps bot,h, partially fail in their function. A toxemia of pregnancy ensues. We believe every pregnant woman to be more or less toxic. BargenT report,s that in his series of 268 cases, 3 showed renal insufficiency. He says, “Renal insufficiency as a complication of severe dysfunction of the colon is serious. Demonstrable renal injury has occurred only rarely in this series. Evidence of such impairment has included alhuminuria, hematuria, edema, increased blood urea, and elevation of blood pressure, as well as changes in the ocular fundi.” Renal insufficiency, with the above symptoms, is a frequent complication of pregnancy. The colon is called upon in pregnancy for extra work in its large function of excretion, both mechanical and absorptive. How essential it is, we realize, that the bowel, in pregna.ncy, regularly perform its excretory function ! Excess of toxic material weakens the resistance of the mucosa. Constipation, inertia of the bowel, due partly to mechanical interference by the enlarged uterus, is another factor contributing to colon dysfunction. The blood and lymph streams of the bowel, perhaps polluted, suffer in like manner, mechanical interference also. In many cases, the whole organism of the pregnant woman has a lowered resistance to the inroads of various complicating diseases. What a melancholy example of this the pregnant woman presented in the

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severe epidemic of influenza of 1918! The morbidity and the mortality were terrific. It is quite plausible that labor may traumatize the bowel, especially one already diseased. Could there be a group of conditions better suited than these outlined as predisposing to the primary development of a colitis in the pregnant and parturient, or one more favorable especially for an acute exacerbation of a preexisting bowel lesion? This seems particularly so in cases of grave toxemias or infections of pregnancy or of the puerperium. Bacteria, normally present in the colon or others accidentally introduced, even though not violently virulent, or blood-borne organisms, find but little resistance to their invasion of the bowel wall and to their destructive inroads of the tissues. Our studies have led us to the conviction that colitis is a more frequent complication of pregnancy than the profession has realized; that the severe form, illustrated by cases herewith presented, is probably not uncommon in pregnancy and in grave puerperal conditions, and not rarely the chief decisive factor in fatality. Doubtless the latter was true in our cases. Indeed one, of our patients, Case 1, showed no pathology that could be ascribed directly to pregnancy or to the puerperium, strongly suggesting that the symptoms of the disease under discussion may so simulate those of a puerperal condition as to lead to a false diagnosis. We hope the presentation of this limited study will stimulate closer observation and more intensive investigation of the pregnant, parturient and puerpera, especially of those apparently septic or toxemit; and secure, in fatal cases, when possible, a postmortem. By such a course we venture to hazard the prediction that the future will reveal a considerable number of cases of ulcerative colitis complicating pregnancy and the puerperium. REFERENCES (1) Logan, A. H.: Northwest Med. 18: 1, 1919. (1) Bmgen, J. Arnold: Arch. Int. Med. 45: 561, 1930. (3) Peomans, Frank C.: Simple Ulcerative Colitis, (4) Berkeley, Comyns, Proctology, New York, 1929, D. Appleton & Company. and Bomey, Victor: The Difficulties and Emergencies of Obstetric Practice, 1904, The Principles and Practice of P. Blakiston’s Son & Co. (5) DeLee, Joseph B.: Obstetrics, 1928, W. B. Saunders Company. (6) Barge%, J. Arnold, and Web-r, Obst. 50: 694, 1930. (7) Bargen, J. Awwkz: Ann. Int. Harry M. : Surg. Gynec. Med. 3: 336, 1929. Santee, H. E.: Ann. Surg. 87: 704, 1928. 2211 6204

LOCUST LIMEKILN

STREET. PIKE (For

discussion,

see page

946.)