Acute renal failure after chromic acid injection.

Case Reports Acute Renal Failure After Chromic Acid Injection TED F. BADER, MD Denver

ACUTE CHROMIUM INGESTION causes a clinical syndrome of acute gastroenteritis, toxic hepatitis, a bleeding diathesis and renal failure due to acute tubular necrosis.',2 It was fatal in 6 of 13 cases reported in the literature of patients treated with peritoneal dialysis or hemodialysis.1-5 Before the advent of dialysis, this syndrome appears to have been uniformly fatal.2 3 This report provides the first description of an intravenous injection of chromic acid causing acute renal failure. All other cases have occurred with oral ingestion or immersion.

Report of

a

Case

The patient, a 31-year-old male prisoner, injected an unknown amount of a chemical cleaning compound called "Alodina 1000," which is composed of 60% chromic acid and 40% potassium fluozirconate. He is a drug addict who thought he could get "high on the acid." For the next three days he suffered nausea, vomiting, dark red urine and loose reddish stools. Seven days after injection, he reported for medical care with the chief complaint of depression and nausea. He was admitted to the prison psychiatric service. A medical consult was obtained with the discovery of the following serum values: creatinine 19.1 mg per dl, blood urea nitrogen 190 mg per dl, aspartate aminotransferase 17 IU per liter; sodium 126, potassium 4.2, chloride 80 and bicarbonate 19 mEq per liter. The patient was oliguric. A urinalysis showed a protein level of 30 mg per dl, trace ketones, 3 + hemoglobin, a few renal tubular epithelial cells and casts and 0 to 5 erythrocytes. No pigmented casts were noted. He had a history of hepatitis in 1976 and the intravenous drug abuse of heroin, cocaine, phencyclidine hydrochloride and "anything else I can find." Eight months previously, a urine specimen had no protein or blood. His blood pressure was 132/98 mm of mercury. A physical examination showed no abnormalities except for mild difficulty with tandem gait. A repeat creatinine done 24 hours later showed a level of 21.0 mg per dl. Eight days after the above injection, a random urine specimen for chromium measured by atomic absorption (Smith, Kline & French Laboratories) gave a result of 3,640 yg per liter (normal 0 to 10). He was transferred to the dialysis center where he underwent dialysis through a left subclavian access catheter on days 9, 10, 11, 12 and 14 of his illness. (Bader TF: Acute renal failure after chromic acid injection. West J Med 1986 May; 144:608-609) From the Health Programs, United States Penitentiary, Lompoc, Califomia. Formerly Chief of Health Programs at the US Penitentiary, Dr Bader is now affiliated with the Department of Intemal Medicine, St Luke's Hospital, Denver. Reprint requests to Ted F. Bader, MD, Dept of Intemal Medicine, St Luke's Hospital, 601 East 19th Ave, Denver, CO 80203.

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On the 18th day, the patient complained of left pleuritic and left calf pain. A pulmonary angiogram showed an embolus in the right lower lobe pulmonary artery. Anticoagulation was started with intravenous administration of sodium heparin, switched to warfarin sodium (Coumadin) by mouth. Dialysis was repeated two more times after the 19th day and the patient was discharged on the 23rd day with a creatinine level of 3.5 mg per dl and a creatinine clearance of 38 ml per minute. No further dialysis was done. On day 48, his serum creatinine level was 1.5 mg per dl and creatinine clearance was 64 ml per minute. Despite careful control of the prothrombin time within the therapeutic range, a large gluteal hematoma forced discontinuation of the warfarin therapy after five weeks. The patient was normotensive and felt well three months after the initial

injury. Comments Three areas are worthy of comment in this case: the lack of liver toxicity, the occurrence of a pulmonary embolus and the unusually rapid rise in the serum creatinine level. Liver injury is a usual result of acute chromium intoxication.2 The liver function test results were normal in this patient despite a urinary chromium level much higher than those causing toxic hepatitis in industrial workers with long-term exposure.6 Because the usual mode of chromium intake has been an oral ingestion with resulting hepatic injury, one possible explanation could be that an intravenous injection avoids the first highly concentrated pass through the portacaval system. In addition, the patient sustained a much smaller, if any, amount of intestinal necrosis than he otherwise might have. It is of interest that he still had symptoms of gastroenteritis during the first three days after injection. It is unlikely that a short-lived liver toxicity was missed since two well-documented cases had shown a 12- to 48-day range of liver abnormalities.12 Bleeding tendencies occur frequently in patients with acute uremia from any cause. There is also a tendency towards a bleeding diathesis in cases of acute renal failure due to chromium toxicity.2'3'5 An angiographically proved pulmonary embolus was thought to be very unusual in this case. Initially the serum creatinine level was felt to be too high at a value of 19.1 mg per dl at presentation on day 7 to be explained entirely by acute renal failure. It could be argued that acute renal failure occurred in addition to chronic renal insufficiency. The best evidence against this hypothesis in the current case is the fact that his serum creatinine value returned to 1.5 mg per dl at day 48. In fact, others have reported without comment an unusually rapid rise in serum creatinine in the setting ofthis metallic intoxication. Kaufman and co-workers noted a serum creatinine level of 10.5 mg per dl on day 1 of an acute oral ingestion of potassium dichromate in a 14-year-old boy.3 Schiffl and associates reported a serum creatinine level of 8.9 mg per dl on day 2 in a 19-year-old worker who fell into a chromic acid bath.4 THE WESTERN JOURNAL OF MEDICINE

CASE REPORTS

Increases in serum creatinine leVels of greater than 1 mg per dl per day are thought to reflect hypercatabolism.l While creatinine production from muscle stores of creatinine is thought to be constant, increased formation has been noted in patients with muscular dystrophy.8 It could be speculated that the high levels of creatinine occurred in this patient as a result of muscle damage and a catabolic state. Muscle studies were not done. An intriguing idea explored in this case was the possibility that the chromic acid interfered with the picric acid-creatinine complex to give a falsely elevated photometric creatinine result. Serial dilutions, however, of chromic acid serum concentrations done with a Beckman automated analyzer did not yield any false-positive values. The unexpectedly high serum creatinine levels in this case of poisoning remain to be explained. REFERENCES 1. Pedersen RS, Mdrch PT: Chromic acid poisoning treated with acute hemodialysis. Nephron 1978; 22:592-595 2. Friestedt B, Lindqvist B, Schultz A, et al: Survival in case of acute oral chromic acid poisoning with acute renal failure treated by hemodialysis. Acta Med Scand 1965; 177:153-159 3. Kaufman DB, DiNicola W, McIntosh R: Acute potassium dichromate poisoning. AmJ Dis Child 1970; 1 19:374-376 4. Schiffl H, Weidmann P, Weiss M, et al: Dialysis treatment of acute chromium intoxication and comparative efficacy of peritoneal versus hemodialysis in chromium removal. Miner Electrolyte Metab 1982; 7:28-35 5. Sharma BK, Singhal PC, Chugh KS: Intravascular hemolysis and acute renal failure following potassium dichromate poisoning. Postgrad Med J 1978; 54:414-415 6. Pascale LR, Waldstein SS, Engbring G, et al: Chromium intoxication with special reference to hepatic injury. JAMA 1952; 194:1385-1389 7. Schrier RW: Acute renal failure. Kidney Int 1979; 15:205-216 8. Doolan PD, Alpen EL, Theil GB: A clinical appraisal of the plasma concentration and endogenous clearance of creatinine. Am J Med 1962; 32:65-79

Serous Adenocarcinoma of the Ovary Presenting as a Large Liver Cyst JONATHAN R. HIATT, MD Los Angeles HEATHER FURNAS, MD Stanford, California RONALD K. TOMPKINS, MD Los Angeles

LIVER CYSTS are congenital, infectious or posttraumatic, but rarely are they neoplastic. The presentation of ovarian adenocarcinoma as a liver cyst has not been reported previously.

gradual abdominal swelling and radiation of her pain to the back and sternum. She was admitted to another hospital, where ultrasonography and computed tomography (CT) of the upper abdomen (Figure 1) showed a large subcapsular cystic mass in the right lobe of the liver. Percutaneous aspiration returned 1,500 ml of serosanguineous fluid upon which cytology and bacterial culture were negative. The fluid reaccumulated over two weeks, and bilateral pleural effusions developed. Visceral angiography determined that the large mass in the right lobe ofthe liver was avascular. Specimens of lung and liver biopsies, thoracentesis and cyst aspirate showed no malignancy or bacteria (aerobic, anaerobic, mycobacterial or fungal). The patient was transferred to the University of California, Los Angeles, Medical Center. She said that she had not had jaundice, weight loss or anorexia. She had traveled to Tijuana for one day one year earlier. She had consumed alcohol heavily in the remote past but had never used birth control pills or estrogens. There was no history of significant abdominal trauma. The family history was positive for gastric cancer. On examination she appeared anicteric but chronically ill. Breath sounds were decreased at both lung bases. The cardiac examination was normal. The abdomen was distended, with a tense mass in the right upper quadrant obscuring the liver edge and extending 8 cm below the costal margin. There was no splenomegaly. Her hemoglobin was 10 grams per dl, with a normal leukocyte count and differential. Electrolyte, glucose and creatinine levels and coagulation studies were normal. Other laboratory values were as follows: bilirubin 0.4 mg per dl, aspartate aminotransferase 50 U per liter, alanine aminotransferase 71 U per liter, and alkaline phosphatase 1, 185 IU per liter (normal < 106). A urinaly$is showed 3 to 6 erythrocytes and 60 to 80 leukocytes. A chest radiograph showed bilateral pleural effusions, right more than the left, and an electrocardiogram was normal. At operation, the right lobe of the liver was displaced posteromedially by a huge unilocular liver cyst. The left lobe was normal, and the common duct was exposed and appeared patent. On abdominal exploration there was bilateral ovarian enlargement, with the left ovary measuring 5 cm and the right 3 cm. Salpingo-oophorectomies were done, and frozen sec-

Report of a Case The patient, a 67-year-old white woman, was admitted to the hospital for treatment of a large liver cyst. She had had a cholecystectomy seven years earlier, followed by intermittent pressure-type pain in the right upper and lower quadrants. Four months before admission, increased abdominal pain developed, associated with shortness of breath, vomiting and temperature to 39.4°C (103°F). A month later she had (Hiatt JR, Furnas H, Tompkins RK: Serous adenocarcinoma of the ovary presenting as a large liver cyst. WestJ Med 1986 May; 144:609-610) From the Department of Surgery, University of California, Los Angeles, School of Medicine. Dr Fumas is now a Resident in Plastic Surgery, Stanford University School of Medicine, Stanford, California. Reprint requests to Jonathan R. Hiatt, MD, UCLA Medical Center, Room 72-1 82E CHS, Los Angeles, CA 90024.

MAY1986 * 144 * 5

Figure 1.-A computed tomographic scan of the upper abdomen shows a large cystic mass contiguous with the right lobe of the liver. 609