Fulminating Uremic Pneumonitis Associated

with Acute Ischemic Nephropathy

(Lower Nephron Nephrosis)*

KENNETH M. HEARD, M.D., E. LEONARD POSEY, JR., M.D. and JOHN W. I,ONG, M.D.

Jackson, Mississippi

I iu a recent article on the subject of uremic

pneumonitis, Hopps and Wissler [I] espe-

cially emphasized the frequency of this lesion,

noting it in 62 per cent of 107 autopsy cases of

uremia. They also pointed out its relative fre-

quency in cases of uremia of short duration, the

lesion being present in sixteen (84 per cent) of

nineteen patients who had uremia for less than

one week. The case to be described here appears

to be an especially fulminating one, apparently

developing within two days of the onset of acute

renal shutdown, and resulting in the patient’s

death approximately three days later.

CASE REPOR’I

A seventy-five year old white housewife was ad- mitted to the Mississippi Baptist Hospital on the evening of September 16: 1956, complaining of epi- gastric cramping pain. The distress, which had been present since it awakened her from sleep on the night of September 13, was described as constant, moderate and occasionally “acute,” radiating into the left anterior chest as well as to the left subscapular region. There were no associated gastrointestinal complaints, the patient having continued to eat heartily, although feeling rather full postprandially. There had been no chills, fever or jaundice. The symptoms becoming progressively more intense, the patient sought medical aid after three days.

Previous similar attacks were denied. This admis- sion was the first hospitalization in her life. She had been told by a physician in another state that she had a “diseased heart” (no cardiorespiratory symptoms could be elicited by our questioning) and an “acid stomach” because of occasional heartburn, which she relieved symptomatically with baking soda. The only other finding of note in the systemic review was that for fifty-five years an indefinite mass had been present about the umbilicus which occasionally “stuck out like an egg.” The past history and family history were non-contributory.

Examination revealed the patient to be an alert, cheerful, cooperative elderly woman, well-developed and well-nourished, who did not appear to be acutely ill. Her blood pressure was recorded as 14Oj80 mm. Hg. The respiratory rate was 20 per minute; the pulse rate, 76 per minute; and the temperature, 98.6”~. No abnormalities were found on examination of the head, fundi, neck, heart, lungs and breasts. The abdomen was tender to palpation in the epigastrium, right upper quadrant and periumbilical region. Marked percussion tenderness was noted in the right upper quadrant. No rebound phenomenon was elicited. The liver, kidneys and spleen could not be palpated, nor were any masses evident. Peristalsis was moderately hyperactive. An umbilical hernia? egg-sized, was present. No costovertebral angle tenderness was found. Examination of the rectum, pelvis and extremities re- vealed no abnormalities.

On admission the hemoglobin was 13.3 gm. per cent and the hematocrit, 42 volumes per cent. The white blood cells numbered 9,100 per cu. mm. with 70 per cent segmented neutrophils, 23 per cent lymphocytes and 5 per cent monocytes. i\ urine specimen obtained by catheterization had a specific gravity of 1.016, a trace of albumin, no reducing substance and 2 to 6 red blood cells per high power field.

The admission diagnosis was cholelit hiasis with cholecystitis.

On September 17, blood chemistry studies found the serum amylase to be 48 units; the total bilirubin, 1.1 mg. per cent; blood glucose, 106 mg. per cent; alkaline phosphatase, 2.5 Bodansky units; thymol turbidity, 0.7 units; and blood urea nitrogen, 12.8 mg. per cent. Roentgen studies the same day failed to visualize the gallbladder twelve hours following tele- paque@ administration. Films of the upper gastroin-

testinal tract revealed a small hiatus hernia, but were

otherwise normal. An x-ray of the chest showed the aorta to be tortuous, the cardiac size and contour to be normal, and the lungs free of evidence of disease. The patient was advised to have her gallbladder re-

* From the Departments of Pathology, Medicine and Surgery, Mississippi Baptist Hospital, Jackson, Mississippi.

JANUARY, 1958 157

158 Fulminating Uremic Pneumonitis-Heard et al.

moved at once. She refused surgery because of her husband’s absence on business.

By the morning of September 18 there was tempera- ture of ~OO’F., distention, nausea, vomiting and marked tenderness in the right upper quadrant of the abdomen with rebound phenomenon. The total white cell count at this time was 20,500 per cu. mm. with 84 per cent segmented neutrophils, 3 per cent neutro- philic bands, 5 per cent lymphocytes and 8 per cent monocytes. It was felt that surgery could not await the husband’s return. On consultation, the surgeon agreed that immediate intervention was mandatory.

Surgery was undertaken at 1O:OO A.M. on September 18. The gallbladder was removed with relative ease; the pathologist reported diagnoses of “acute chole- cystitis and cholecystolithiasis.” Anesthesia was com- pletely uneventful. The patient’s blood pressure was 120/70 mm. Hg on leaving the operating room. No blood was given during surgery. In the recovery room the blood pressure dropped to 80/O mm. Hg and the patient became slightly cyanotic. Her pulse rate did not exceed 100 beats per minute; it was stated that the pulse always felt much stronger,than the blood pres- sure might indicate. Supportive measures included 500 cc. of whole blood and 50 cc. of a solution of hydrocortisone administered intravenously, oxygen and vasopressors. The response was slow; the patient was not returned to her room for five hours.

By the morning of September 19 she appeared much better clinically. The blood pressure was 94/60 mm. Hg, and the pulse rate was 90 per minute. The lungs were clear. The patient had become oliguric, how- ever, with a total urinary output of only 255 cc. from 7:00 A.M. September 19 to 7:00 A.M. September 20. The daily urine volumes for the remaining hospital days were 192 cc., 770 cc. and 540 cc. Every effort was made to avoid over-hydration and to keep the electrolytic balance as nearly normal as possible. A blood urea nitrogen was 31.3 mg. per cent. A urine specimen obtained from an indwelling bladder cathe- ter had a specific gravity of 1.017, and showed a trace of albumin. Innumerable red cells per high power field were noted. By the morning of September 20 the carbon dioxide combining power was 45.7 volumes per cent; the chlorides, 469 mg. per cent; the potas- sium, 4.6 mEq./L.; the sodium 122.9, mEq./L.; and the blood urea nitrogen, 45 mg. per cent.

Respiratory difficulty appeared on the afternoon of September 20, with orthopnea, cough of a hacking nature and mild cyanosis, unaffected by the admin- istration of oxygen by nasal catheter at 8 L. per minute. There was no clinical evidence of congestive failure; an electrocardiogram was interpreted as being within normal limits. Nevertheless, the patient was given digitalis, but it did not affect the patient’s condition.

A portable chest x-ray film on the morning of September 21 showed mottled shadows of increased density in both lung fields, extending out from the

hilar regions. The blood urea nitrogen had risen to 54.5 mg. per cent. The carbon dioxide combining power had declined to 37.2 volumes per cent. The chlorides were 478 mg. per cent, the potassium was 5.3 mEq./L. and the sodium was 126.7 mEq./L.

Despite the oliguria, the respiratory difficulty entirely dominated the picture by September 22. Subcrepitant and musical rales were apparent in both lung fields without signs of consolidation. The expira- tory phase was considerably prolonged. Cyanosis was marked. Breathing was of the “grunting” type. The sensorium became clouded. During the evening small amounts of bloody mucus were obtained on suctioning the trachea. During this entire period the blood pres- sure remained stable around 98/60 mm. Hg, with no cardiac dysfunction becoming apparent.

Breathing was labored in the extreme on the morn- ing of September 23, with much difficulty and effort in expiration. Only a small amount of mucus could be obtained by tracheal aspiration. The patient’s condition progressively declined as breathing became more impaired. Death occurred at approximately 9:30 A.M.

The chief autopsy findings of interest were in rela- tion to the heart, lungs and kidneys. The left pleural cavity contained approximately 1 L. of straw-colored fluid with some strands of fibrin contained therein. The lungs appeared quite voluminous, filling the pleural cavities. The combined weight of the lungs was 1,300 gm. The lower portion of the trachea, the mainstem bronchi and the segmental bronchi were filled with inspissated, rather firm grayish tan ma- terial. The pleural surfaces, bilaterally, were grayish- blue to pinkish blue but did not appear atelectatic. They varied from subcrepitant to firm on palpation. On transverse section all lobes presented rather uni- form grayish red, moderately firm dry surfaces from which only a moderate amount of foamy fluid could be expressed with rather marked pressure.

Fibrinous pericarditis was present, with a definite membrane of fibrin present over most of the heart. When peeled away this left slightly congested surfaces. The heart weighed 400 gm. There was a moderate degree of calcified atherosclerosis with no significant narrowing of any of the lumens, however, except in the left anterior descending branch. At a point ap- proximately 1.5 cm. from its origin it was narrowed, but not occluded. The endocardium and valves were all essentially negative in appearance.

The kidneys weighed 190 gm. each. The capsules stripped with ease leaving rather smooth, somewhat mottled tan renal surfaces. On transverse section there was some bulging of the cut surface with the cortical margins obscured and the cortex appeared quite pale. In several of the pyramids there were noted small punctate brown dots and linear brownish streaks at the corticomedullar’y junction.

Microscopically, examination of the heart con- firmed the fibrinous pericarditis noted grossly. (Fig. 1.)

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Fulminating Uremic Pneumonitis-Heard et al. 159

FIG. 1. Epicardial surface showing zone of fibrin deposi- tion with mild inflammatory reaction (urc-mic peri- carditis).

FIG. 2. Section of the lung showing- alvroli cnqorqcd with massive fibrinous exudate.

FIG. 3. Section of the lung with hyaline-membrane likr appearance of fibrinous pneumonitis.

There was quite a variation in the microscopic picture in various sections of the lungs, but fairly uniformly present were large plugs of fibrinous material within the alveoli. Frequently these were tremendous and distended the alveoli and connected through the pores of Cohn to adjacent alveoli. (Fig. 2.) In most areas there was a relatively scant cellular infiltrate accom- panying this process, this being predominantly mononuclear. In other areas there were larger num- bers of neutrophils, and in some there was evidence of interstitial pneumonitis in adjacent alveolar septae. Some fields showed fairly widely distended alveoli in which this fibrinous material was applied to the alveolar walls in the form of hyaline-appearing mem- branes. (Fig. 3.) Sections of small bronchi showed frequent erosion of the bronchial mucosa, a large plug of fibrinous exudate usually being adjacent to the eroded area. (Fig. 4.) ‘Also present in some of the bronchi were fairly large masses of mutinous material with entrapped neutrophils and macrophages. The

JANlTARY, 1958

FIG. 4. Small bronchial radicle showing erosion of wall with fibrinous exudate and collection of mutinous ma- terial. Evidence of more acute inflammation is noted here.

process in the lung was thought to consist basically of a so-called uremic pneumonitis, the massive fibrin com- ponent of the exudate being characteristic of this. A superimposed bacterial infection might also have been present because of the acuteness of the exudate in some areas. This could not be confirmed by bacteri- ologic studies because of prior arterial embalming.

Sections of the kidneys confirmed the presence of an acute ischemic nephropathy. Many glomeruli were congested. There was considerable interstitial con- gestion in the pyramidal portions. Pigment casts were present in moderately large numbers, these being reddish brown in color. (Fig. 5.) Frequently associated with these casts were degenerative changes in the tubular epithelium and occasional evidence of erosion of the casts into the interstitial tissue. (Fig. 6.) There were patchy zones of interstitial inflammatory reac- tion, the cells present being predominantly lympho-

160 Fulminating Uremic Pneumonitis-Heard et al.

FIG. 5. Numerous pigment casts in collecting $bules of FIG. 6. Large pigment cast with associated tubular kidney. necrosis.

cytes and macrophages. No vascular changes sugges- tive of a pre-existing arteriolar nephrosclerosis were present.

The final pathologic diagnoses in this case were: recent postoperative state following cholecystectomy for acute cholecystitis and cholecystolithiasis; acute ischemic nephropathy (lower nephron nephrosis) ; uremia (clinical); uremic pericarditis; massive uremic pneumonitis, bilateral; inspissated secretions in bron- chial tree; fatty metamorphosis, liver, with occasional zones of focal necrosis; umbilical hernia with in- carcerated portion of omentum; diverticulosis, colon; fibrous pleural adhesions, Ieft.

third postoperative day. During the final two days of this patient’s course respiratory difficulty dominated the clinical picture. This was char- acterized by an asthmatic type of respiration with subcrepitant and musical rales and expira- tory difficulty. Autopsy revealed a fibrinous pneumonitis characteristic of those cases previ- ously described as “uremic pneumonitis.” Concomitantly, a fibrinous pericarditis compati- ble with uremic origin had developed.

REFERENCES

SUMMARY

A case of a seventy-eight year old woman in whom shock and acute ischemic nephropathy developed following cholecystectomy for acute cholecystitis and cholecystolithiasis is presented. The blood urea nitrogen, which was normal prior to surgery, rose to 54.5 mg. per cent by the

1. HOPPS, H. C. and WISSLER, R. W. Uremic pneu- monitis. Am. J. Path., 31: 261, 1955.

2. BASS, H. E. and SINGER, E. Pulmonary changes in uremia. J. A. M. A., 144: 819, 1953.

3. CASTLEMAN, B. and TOWNE, V. W. Case records of the Massachusetts General Hospital. New England J. Med., 253: 72, 1955.

4. Clinicopathologic Conference, Mercy Hospital, Des Moines. J. Iowa State Med. Sm., 45: 477, 1955.

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