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mm with a normal differential; whole blood urea nitrogen (BUN), 14 mg/100 ml; and
fasting blood sugar, 106 mg/100 ml.
During the rst two hospital days the patient was treated with bed rest, sodium
restriction, and diuretics; her condition improved and she lost 4 kg in weight. On
the third hospital day, however, intermittent bigeminal rhythm was noted, and her
rash became urticarial and pruritic. Digitoxin, chlorothiazide, and penicillin were
discontinued, and on the sixth hospital day prednisolone was given because of
progressive worsening of the rash. On the morning of the eighth day, while walking,
the patient developed severe midepigastric pain, a sensation of fullness in the right
upper quadrant, and nausea. On examination the abdomen was soft, bowel sounds
were present, and there was moderate tenderness in the midepigastrium and right
upper quadrant. The heart rate was 120 beats per minute and the blood pressure was
150/90mm Hg. The WBC was 15,000/cu mm, and roentgenograms of the abdomen
were unremarkable. Electrocardiograms (ECG) and roentgenograms of the chest
were unchanged in comparison to those obtained at the time of admission. The
abdominal pain abated, but 12hours later the systolic blood pressure was 80mm
Hg. At this time the serum sodium was 138 mEq/liter; potassium, 6.7 mEq/liter;
chloride, 82 mEq/liter; carbon dioxide content, 12 mEq/liter; blood sugar, 35 mg/100
ml; serum amylase, 136 Somogyi units; and BUN, 30 mg/100 ml. Repeat blood sugar
was 27 mg/100 ml; repeat serum potassium was 7.5 mEq/liter; and the arterial blood
had a pH of 7.27, Po
, 71mm Hg, and PCO2, 27mm Hg. Intravenous uids containing
2
glucose (25 gm), sodium bicarbonate (7.5 gm) and metaraminol (in amounts sufcient
to maintain the systolic blood pressure at 90mm Hg), digitoxin, and nasal oxygen
were administered, and within one hour the abdominal pain had subsided and the
patient improved. Two hours later the blood sugar was 135 mg/100 cc, and the BUN
was 41 mg/100 ml. The serum potassium was 6.1 mEq/liter; sodium, 132 mEq/liter;
chloride, 79 mEq/liter; and carbon dioxide, 12 mEq/liter.
During the next six hours the abdominal pain gradually returned, associated
with generalized abdominal tenderness with rebound and rigidity and absent
bowel sounds. Astool contained occult blood. Dilated loops of small bowel, with
air-uid levels, were seen on roentgenograms. The blood pressure, which had been
about 100mm Hg systolic during the previous six hours, without the administration
of vasopressors, suddenly dropped to 50mm Hg systolic, and the patient became
disoriented and irrational. Intravenous metaraminol, antibiotics, prednisolone, and
plasma were given, and an exploratory laparotomy was performed. The peritoneal
cavity contained approximately 500 ml of turbid, brown uid with a fecal odor. The
serosal surfaces of the stomach, duodenum, and proximal 10cm of the jejunum
appeared normal. The small bowel distal to this point, however, was dilated and
cyanotic, and in some areas appeared to be necrotic. The ascending and transverse
colon were gray but appeared viable; the descending colon, from the splenic
exure to the pelvic brim, was black. The superior and inferior mesenteric arteries
were nonpulsatile and severely constricted, but no localized obstruction could be
detected at any point. Cardiac arrest occurred at the conclusion of the operation, and
resuscitation was unsuccessful.
Pathologic Findings.—At autopsy, the stomach and duodenum were normal,
but the mucosa of the jejunum, ileum, and colon varied from black to red in
color (Figure 1). The serosa of the entire small and large intestine was smooth
and glistening, but of dark color. No thrombi or emboli were found in any of the
mesenteric vessels, and the mesenteric arteries contained no atheromata. Numerous
histologic sections of small and large intestine were examined; some areas were
normal while others showed distinct pathologic changes. The most frequent lesion
observed was hemorrhagic necrosis of the mucosa (Figure2). In some areas of the
bowel this was the only abnormal nding. At other sites, however, the muscularis
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CASE 38 INTESTINAL INFARCTION FROM MESENTERIC ARTERIAL INSUFFICIENCY
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Figure 1 Gross appearance of intestine. Distribution of lesions was irregular and
segments of involved mucosa were hemorrhagic.
Figure 2 Section of intestine disclosing hemorrhagic necrosis of mucosa and
severe dilatation of submucosal blood vessels. Although not apparent in this photomicrograph, there was focal degeneration and necrosis of the smooth muscle of the
muscular layer (hematoxylin and eosin, × 25).
mucosae and muscularis externa were also necrotic. In addition, the submucosa
was edematous, contained acute inammatory cells, and its vessels, particularly
the veins, were markedly distended by erythrocytes. Variations between these
two lesions commonly were seen. The serosa in all sections was intact and free of
inammatory cells, and no mucosal ulcerations were present. Sections of the liver,
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Figure 3 Section of liver disclosing massive necrosis of hepatic lobules. Hepatic
architecture was barely discernible (hematoxylin and eosin, × 84).
which weighed 1,700 gm, disclosed massive centrolobular congestion and necrosis,
and occasionally infarction of entire lobules (Figure3). Sections of the kidneys were
unremarkable, except for a few old small cortical infarcts.
The heart revealed typical rheumatic mitral valve disease, and the valve orice
was both stenotic and regurgitant (Figure4). An organized thrombus lled the left
atrial appendage. The right ventricle, tricuspid valve ring, and right atrium were
dilated, but the tricuspid leaets and chordae were normal. There was hemorrhagic
infarction of the lower lobe of the left lung, and the pulmonary artery to this lobe
was completely occluded by a brin clot.
COMMENT
Several reviews have emphasized the difcult diagnostic problem posed in the
clinical differentiation of nonobstructive and obstructive mesenteric arterial
insufciency.
1–6
The majority of patients with either of these lesions have underlying
cardiac disease, and then manifest signs and symptoms related to the abdomen.
Abdominal pain, tenderness and distention, nausea and vomiting, bloody diarrhea,
and leukocytosis may occur with both conditions. Although abdominal and cardiac
manifestations are similar in both obstructive and nonobstructive mesenteric
arterial insufciency, evidences of ischemia in other organ systems is an important
diagnostic nding favoring the presence of the nonobstructive lesion. The basic
physiologic abnormality in nonobstructive mesenteric arterial insufciency is
an inadequate cardiac output, and the intestine is but one of several areas which
receive an insufcient supply of blood. When the cardiac output is abnormally
low, the distribution of arterial ow is also abnormal and, by means of selective
vasoconstriction, oxygenated blood is shunted to the more vital body areas, such as
the heart and brain, and away from the peripheral and splanchnic vascular beds.
Intestinal ischemia of the nonobstructive type is, therefore, often associated with
evidences of decreased perfusion of other body regions, and manifestations of
central nervous system, renal, and hepatic ischemia favor this diagnosis. The present
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7–9
CASE 38 INTESTINAL INFARCTION FROM MESENTERIC ARTERIAL INSUFFICIENCY
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Figure 4 Heart. Top, Opened left atrium, mitral valve, and left ventricle. Organized
thrombus was present in left atrial appendage. Mitral valve leaets and chordae tendineae were brotic, shortened, and focally calcied. Bottom, Mitral valve orice as
seen from left ventricle (left) and from left atrium (right). Valve was both stenotic and
incompetent.
patient, for example, had evidence of inadequate blood ow to the kidneys (oliguria,
azotemia) and liver (hypoglycemia), as well as to the bowel (abdominal pain), before
clinical signs of intestinal necrosis appeared. Hypoglycemia has been reported
in one other patient with severe cardiac decompensation and nonobstructive
mesenteric arterial insufciency, and may be an important indicator of ischemia
of the liver.
10
Hypoglycemia in the present patient appears to have resulted from
hepatic ischemia, since necrosis of entire hepatic lobules was found at autopsy.
In addition, the patient described had severe metabolic acidosis, an abnormality
which is also more likely to occur in nonobstructive mesenteric arterial insufciency
11,12
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than in association with an isolated obstruction of the superior mesenteric artery.
Metabolic acidosis, due to tissue hypoxia and anaerobic oxidation, is a consequence
of inadequate cardiac output of any cause, and in patients with cardiac failure
often indicates a generalized perfusion insufciency.
13–15
It is possible that in the
present patient cardiac decompensation, with a sudden fall in cardiac output, was
precipitated by the pulmonary embolus, but the embolus was not evident from the
physical, radiographic, and electrocardiographic examinations performed soon
after the onset of abdominal pain. Digitalis intoxication also may have been a
precipitating factor in this patient.
The diagnostic differentiation of obstructive and nonobstructive mesenteric
arterial insufciency is of vital importance when specic treatment becomes
necessary. Organic obstruction of the superior mesenteric artery, or one of its major
branches, by an embolus or thrombus necessitates early operative intervention and
restoration of a patent aterial lumen before intestinal necrosis occurs.
5, 16, 17
In contrast,
laparotomy prior to bowel infarction is contraindicated in patients with arterial
insufciency secondary to an inadequate cardiac output, since further reduction in
cardiac output and intestinal perfusion may result from anesthesia and operative
manipulation of the intestine. Optimal therapy in patients with nonobstructive
mesenteric arterial insufciency must be directed to measures which will increase
systemic blood ow: vigorous treatment of cardiac failure, maintenance of adequate
blood and extracellular uid volumes, correction of metabolic abnormalities,
intestinal decompression, and reduction of an abnormally high hematocrit reading.
Obviously, vasopressors should be avoided whenever possible and vasodilatation
by serial epidural blockade may be of benet.
18
Operation may prove necessary in a
patient with nonobstructive mesenteric arterial insufciency, but when the clinical
ndings indicate this diagnosis, laporatomy should be performed only if denite
signs of intestinal infarction appear.
SUMMARY
A patient is described in whom nonobstructive mesenteric arterial insufciency
caused focal infarction of the bowel and liver. The precipitating cause was a
strikingly diminished cardiac output, the result of rheumatic mitral stenosis and
congestive heart failure. Nonobstructive mesenteric arterial insufciency, rather
than mesenteric embolus or thrombosis, was indicated by evidences of inadequate
perfusion of other organ systems resulting in oliguria, hypoglycemia, and metabolic
acidosis.
GENERIC AND TRADE NAME OF DRUG
Chlorothiazide—Diuril
REFERENCES
1. Berger, R. L., and Byrne, J. J.: Intestinal gangrene associated with heart disease,
Surg Gynec Obstct 112:529, 1961.
2. Ende, N.: Infarction of the bowel in cardiac failure, New Eng J Med 258:879, 1958.
3. Glotzer, D. J., and Shaw, R. S.: Massive bowel infarction: An autopsy study
assessing the potentialities of reconstructive vascular surgery, New Eng J Med
260:59, 1960.
4. Ming, S. C., and Levitan, R.: Acute hemorrhagic necrosis of the gastrointestinal
tract, New Eng J Med 263:59, 196 0.
5. Shaw, R. S.: Vascular lesions of the gastrointestinal tract, Surg Clin N Amer
39:1253, 1959.
6. Wilson, R., and Qualheim, R. E.: A form of acute hemorrhagic enterocolitis
aficting chronically 111 individuals, Gastroenterology 27:431, 1954.
44
CASE 38 INTESTINAL INFARCTION FROM MESENTERIC ARTERIAL INSUFFICIENCY
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7. Corday, E., et al: Mesenteric vascular insufciency: Intestinal ischemia induced
by remote circulatory disturbances, Amer J Med 33:365, 1962.
8. Corday, E., and Williams, J. H.: Effect of shock and vasopressor drugs on the
regional circulation of the brain, heart, kidney, and liver, Amer J Med 29:228,
1960.
9. Lillehei, R.C.: The intestinal factor of irreversible hemorrhagic shock, Surgery
42:1043, 1957.
10. Aklerfer, H. H., and Richardson, J. H.: Hepatic hypoglycemia and infarction of
the bowel, Arch Intern Med 112:96, 1963.
11. Clarke, W. T. W.: Centrilobular hepatic necrosis following cardiac infarction,
Amer J Path 26:249, 1950.
12. Ellenberg, M., and Osserman, K. E.: The role of shock in the production of cen-
tral liver cell necrosis, Amer J Med 11:170, 1951.
13. Clowes, G. H. A., Jr., et al: Effects of acidosis on cardiovascular function in surgi-
cal patients, Ann Surg 154:524, 1961.
14. Huckabee, W. E.: Lactic acidosis, Amer J Cardiol 12:663, 1963.
15. Litwin, M. S., et al: Acidosis and lacticacidermia in extracorporeal circulation:
The signicance of perfusion ow rate and the relation to preperfusion respiratory alkalosis, Ann Surg 149:188, 1959.
16. Rutledge, R. H.: Superior mesenteric artery embolectomy, Ann Surg 159:529, 1964.
17. Zuidema, G. D., et al: Superior mesenteric artery embolectomy, Ann Surg 159:548,
1964.
18. Jackson, B. B., and Lykins, R.: Serial epidural analgesia in mesenteric arterial
failure, Arch Surg 90:17 7, 196 5.
19. Bachrach, W. H., and Thorner, M. C.: Hemorrhagic enteropathy complicating
myocardial infarction, Amer J Cardiol 11:89, 1963.
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Case 56 Roentgenogram of the Month
William C. Roberts, MD,* Gonstan VV. Berard, MD and Nina S. Braunwald, MD
Bethesda, Maryland
Benjamin Felson, M.D., Editor
Harold Spitz, M.D., Co-Editor
A 45-YEAR-OLD WHITE MAN WITH RHEUMATIC mitral stenosis and aortic
regurgitation underwent replacement of both mitral and aortic valves with StarrEdwards prostheses on April21, 1964. In October, 1964, he developed fulminating
hepatic decompensation secondary to probable serum hepatitis superimposed on
cardiac cirrhosis, and was treated thereafter with high doses of a corticosteroid. In
January, 1965, he developed fever, night sweats, anorexia and dyspnea. Figures1 and 2
were obtained at that time. He died on February27, 1965.
Figure 1
For reprints, please write: Dr. William C. Roberts, Laboratory of Pathology, Clinic of
Surgery, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014.
From the Clinic of Surgery, National Heart Institute and the Pathologic Anatomy Branch,
*
National Cancer Institute, National Institutes of Health.
46 DOI: 10.1201/9781003409281-7
Figure 2
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CASE 56 ROENTGENOGRAM OF THE MONTH
DIAGNOSIS: Pulmonary Nocardiosis
The teleoroentgenogram and tomogram demonstrate an area of consolidation with
an irregular central cavity. Figure3A is a cut surface of the left upper lobe showing
the cavity. Nocardia asteroides organisms, which were cultured from the sputa during
life and from the pulmonary cavity at necropsy, are shown in Figure3B (Brown and
Brenn stain; x1200).
Systemic nocardiosis, which is virtually always caused by N. asteroides, usually
begins in the bronchial mucosa and spreads through the bronchial wall to the
pulmonary parenchyma, resulting in extensive necrosis of tissue with the formation
of conuent abscesses.
1
The infection may be chronic or acute or even fulminating.2
N. asteroides are aerobic, Gram-positive and variably acid-fast, delicate, branching
lamentous fungi which break up into bacillary forms of varying lengths.
Pulmonary-cutaneous stulas and granules are less common than in actinomycosis.
Hematogenous spread results in metastatic lesions throughout the body, most
commonly to the brain.
The diagnosis of pulmonary nocardiosis is made by staining a smear of the
sputa specically for bacterial organisms (Brown and Brenn stain). The organism
grows on a variety of simple media, including blood agar, but a three to four week
period is required before the typical colonies are identiable.
Sulfonamides (4–8 gm daily in adults) constitute the treatment of systemic
nocardiosis, and the therapy should be continued for two to three months after all
signs and symptoms of the disease have disappeared.
2
The nocardiosis in this patient represents an infection in one whose resistance
had been lowered by a combination of chronic diseases (cardiac and hepatic) and
steroid therapy, although nocardiosis may occur as a primary disease.
2, 3
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Figure 3
REFERENCES
1. WEED, L. A., ANDERSEN, H. A., GOOD, G. A. AND BAGGENSTOSS, A. H.:
“Nocardiosis. Clinical, bacteriologic and pathologic aspects,” New Engl. J. Med.,
25 3:113 7, 1 9 55.
2. FREESE, J. W., YOUNG, W. G., JR., SEALY, W. C. AND CONANT, N. F.: “Pulmonary
infection by Nocardia asteroides. Findings in eleven clinical cases,” J. Thor. and
Cardiovas. Surg., 46:537, 1963.
3. SALTZMAN, H. A., CHICK, E. W. AND CONANT, N. F.: “Nocardiosis as a com-
plication of other diseases,” Lab. Invest., 11:1110, 1962.
48
CASE 65 QUADRIVALVULAR RHEUMATOID HEART DISEASE
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Case 65 Quadrivalvular Rheumatoid Heart Disease
Associated with Left Bundle Branch Block*
Deborah F. Carpenter, MD,† Abner Golden, MD and William C. Roberts, MD‡
Washington, D. C.
The clinical and necropsy ndings are described in a sixty-ve year old woman
with rheumatoid arthritis and rheumatoid nodules in the heart, lungs, joints and
subcutaneous tissue. Signs of aortic and mitral regurgitation, congestive cardiac
failure and left bundle branch block were observed clinically and necropsy
revealed numerous rheumatoid nodules in all four cardiac valves as well as in
the adjacent myocardium and in the pericardium. The extensive nature of the
cardiac involvement by rheumatoid granulomas is the most unusual aspect of
this patient’s illness.
NONSPECIFIC obliterative pericarditis is frequently observed at autopsy in
patients with rheumatoid arthritis but the nding of rheumatoid nodules in the
heart is unusual. Granulomas histologically indistinguishable from those of the
subcutaneous tissues have been described in the pericardium, myocardium and
endocardium, including the cardiac valves. They are usually few in number and
involve only one valve or a limited area of myocardium or pericardium. Similar
lesions have at times been described in lung, pleura, larynx, vertebrae, skeletal
muscle, peripheral nerve, esophagus, kidney, spleen, eyes and dura.
Described herein are the clinical and postmortem ndings in a patient with
rheumatoid arthritis who had mitral and aortic valvular regurgitation, severe
congestive cardiac failure and left bundle branch block. Numerous rheumatoid
nodules were present in all four cardiac valves, in large areas of myocardium
including the conduction system and in the pericardium.
CASE REPORT
A sixty-ve year old white woman (D.Y., No. 98266) died on March 15, 1966, in
congestive cardiac failure. Although she apparently had had systemic hypertension
at one time, she had been well until age fty when signs and symptoms of
rheumatoid arthritis appeared, with progressive involvement of the knees, ankles,
hips, wrists, shoulders and cervical vertebrae. She received adrenocorticotropic
hormone, nitrogen mustard, gold, prednisone, whirlpool therapy and intra-articular
hydrocortisone at various times. Approximately six months before death signs and
symptoms of right- and left-sided congestive cardiac failure appeared. She lost 35
pounds, became bedridden mainly because of dyspnea, and two days before death
became obtunded and was hospitalized.
On examination, the blood pressure ranged from 140/60 to 105/30mm. Hg, the
pulse was 80 per minute, respiration 12 per minute and the temperature was normal.
* From the Department of Pathology, Georgetown University School of Medicine and Medical
Center, Washington, D. C. Manuscript received November10 1966.
†
Present address: Pathologic Anatomy Branch, National Cancer Institute, National Institutes
of Health, Bethesda, Maryland.
‡
Present address: Laboratory of Pathology, Clinic of Surgery, National Heart Institute,
National Institutes of Health, Bethesda, Maryland.
DOI: 10.1201/9781003409281-8 49
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