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CASE REPORT  
Year : 2014  |  Volume : 7  |  Issue : 2  |  Page : 136-138
Chromium induced AKI: case with protean implications


Department of Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India

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Date of Web Publication8-Dec-2014
 

   Abstract 

Poisoning with chromium is fatal and rarely reported. We report a case of a 25-year-old man who developed severe acidosis, gastrointestinal hemorrhage, acute kidney, and hepatic injury following homicidal ingestion of chromium. Patient improved after multiple cycles of alternate day hemodialysis.

Keywords: Chromium, AKI, hemodialysis

How to cite this article:
Khan R, Quaiser S, Sharma A, Haque SF. Chromium induced AKI: case with protean implications. Ann Trop Med Public Health 2014;7:136-8

How to cite this URL:
Khan R, Quaiser S, Sharma A, Haque SF. Chromium induced AKI: case with protean implications. Ann Trop Med Public Health [serial online] 2014 [cited 2019 Sep 22];7:136-8. Available from: http://www.atmph.org/text.asp?2014/7/2/136/146409

   Introduction Top


Chromic acid is a strong metal acid, and acute poisoning is very rare, but very serious with severe skin injury, renal, and liver failure. The majority of published cases were suicide attempts with lethal outcomes. [1],[2],[3] We describe the case of a 25-year-old man who presented to the Department of Medicine, Jawaharlal Nehru (JN) Medical College, Aligarh with ingestion of 100 ml of chromic acid poison used in the industrial setup for chrome plating with homicidal intent. Patient was treated with hemodialysis for 20 days and was discharged after 22 days of hospitalization. The patient is now on regular follow-up in Nephrology Outpatient Department of JN Medical College with normal renal function tests (RFTs).


   Case Report Top


A 25-year-old man referred to our hospital 3 days after ingestion of chromium acid mixed with a cold drink with homicidal intent. At presentation, his vitals were stable, and he complained of abdominal discomfort. Renal and liver failure were absent at presentation but appeared later in the course of the disease. There was the absence of any evidence of caustic injury to the oral or upper gastrointestinal (GI) mucosa, and his pupils were normally reacting. His complete blood counts RFTs and liver function tests were within normal limits on day 1. On day 2 post admission, patient started having decreased sensorium and shortness of breath. Urine output decreased to 50 ml in 24 h. His RFTs were acutely deranged from baseline normal values to serum creatinine 8.2 mg/dl, blood urea 95 mg/dl. Arterial blood gas analysis revealed metabolic acidosis with pH 7.2, bicarbonate 12.5, serum potassium 3.5, serum sodium 135, and oxygen saturation 95.5. Ultrasonography of the abdomen showed normal sized kidneys with maintained echo texture and color Doppler study revealed normal renal arteries.

Patient also developed upper GI bleeding for which he was immediately shifted to critical care ward (medicine intensive care unit) and taken for emergency hemodialysis. Upper GI fresh bleeding continued for 2 days for which was managed with 3 units of packed red blood cells, and 1 unit of platelet-rich-plasma was transfused. With this, platelet count rose to 88,000 from 5000.

Liver function tests revealed elevated liver enzymes and bilirubin values (aspartate aminotransferase 95, alanine transaminase 114, alkaline phosphatase 16, bilirubin total 3, direct 1.5, indirect 1.5, prothrombin time 14, international normalized ratio 1.8).

He was treated with intermittent hemodialysis, no chelating agents or other methods for enhancing elimination were used. Patient underwent 7 cycles of alternate day hemodialysis in which his RFT fluctuated. During the next 15 days, the renal function deteriorated despite daily increase in urine output. RFT fluctuated from a peak of serum creatinine 15.6 and blood urea 125 to a nadir of serum creatinine 1.6 and blood urea 52. Gradually upper GI bleed subsided, urine output returned to 1400 ml/day from a nadir of 50 ml/day [Table 1]. Renal biopsy was discussed but was not considered due to refusal by patient party and deranged blood parameters. Patient was kept under close observation, and his blood counts, renal functions and urine output gradually improved. Patient was discharged after 22 days of in hospital treatment in stable condition.
Table 1: Clinical and biochemical profi le of patient

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   Discussion Top


Solutions containing chromium ions have many industrial applications which include chrome plating, textile printing, and dyeing. Of the three valencies in use (Cr 2+ , Cr 3+ , Cr 6+ ), the hexavalent form (Cr 6+ ) is considered the most hazardous. [4] Hexavalent chromium readily crosses cell membranes, causing cellular damage. The resulting cellular damage leads to GI bleeding, hemolysis and hepatic and renal damage. In the present case report, aggressive hemodialysis between day 2 and 20 after injury caused a progressive decrease in chromium levels poisoning and renal failure with improvement in GI and liver functions.

To the best of our knowledge, there is only one case reported of fatal chromic acid poisoning with acute renal failure in India by Varma et al. [5] In another study, successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation was also reported in Austria. [6]

No proven antidote is available for chromium poisoning. Acute poisoning is often fatal regardless of therapy. Treatment in cases of acute high-level chromium exposure is usually supportive and symptomatic. Fluid and electrolyte balance is critical. Appropriate supportive measures may include ventilatory support, cardiovascular support, and renal and hepatic function monitoring. [7]

Dialysis toxicological analysis of blood taken 5 h after chromium ingestion and before dialysis was initiated showed a chromium concentration of 3.4 mg/l. An amount of 1 g chromium is believed to be a lethal dose for humans there are reports suggesting that chromium blood concentrations of 10 mg/l or more are inevitably lethal. [2]

Renal failure was the most serious complication. Progression to anuria is associated with poor prognosis. Initial oliguric/anuric phase could be explained by the combination of both direct chromic acid-induced intrinsic renal azotemia (both tubular and glomerular) and peripheral edema with volume depletion and hemoconcentration. [4],[7],[8]

Affected patients should be monitored carefully for evidence of GI bleeding, hemolysis, coagulopathy, seizures, and pulmonary dysfunction. [8]

Hemodialysis and charcoal hemoperfusion do not substantially enhance chromium removal from the body if renal function remains normal. [7] However, if renal failure ensues, hemodialysis may be necessary for management of the renal failure itself.

Peritoneal dialysis or hemodialysis is of great value to aid the removal of circulating chromium and is of use in treating established renal failure. [9]


   Conclusion Top


There are several interesting points to be noted in this case report: Absence of caustic injury to the mucosa of the upper GI tract, [10] course of organ failure with no specific elimination treatment attempted and recovery after prolonged hospitalization. The patient was discharged after 22 days of hospitalization in good condition, with normal liver and renal function but without the need of maintenance hemodialysis.

We emphasize the importance of timely intensive care for patients with accidental or unintentional poisoning with chromic acid or similar chemical substances and keeping a watchful eye for such emergencies needing specialized care .

 
   References Top

1.
Loubières Y, de Lassence A, Bernier M, Vieillard-Baron A, Schmitt JM, Page B, et al. Acute, fatal, oral chromic acid poisoning. J Toxicol Clin Toxicol 1999;37:333-6.  Back to cited text no. 1
    
2.
Pedersen RS, Mørch PT. Chromic acid poisoning treated with acute hemodialysis. Nephron 1978;22:592-5.  Back to cited text no. 2
    
3.
Baresic M, Gornik I, Radonic R, Zlopasa O, Gubarev N, Gasparovic V. Survival after severe acute chromic acid poisoning complicated with renal and liver failure. Intern Med 2009;48:711-5.  Back to cited text no. 3
    
4.
Dayan AD, Paine AJ. Mechanisms of chromium toxicity, carcinogenicity and allergenicity: Review of the literature from 1985 to 2000. Hum Exp Toxicol 2001;20:439-51.  Back to cited text no. 4
    
5.
Varma PP, Jha V, Ghosh AK, Joshi K, Sakhuja V. Acute renal failure in a case of fatal chromic acid poisoning. Ren Fail 1994;16:653-7.  Back to cited text no. 5
    
6.
Stift A, Friedl J, Längle F, Berlakovich G, Steininger R, Mühlbacher F. Successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation. Transplantation 2000;69:2454-5.  Back to cited text no. 6
    
7.
Chromium Toxicity Treatment and Management. Case Studies in Environmental Medicine, 2008. Available from: http://www.atsdr.cdc.gov/csem/chromium/treatment_management.html. [Last cited on 2008 Jan 24].  Back to cited text no. 7
    
8.
Geller R. Chromium. In: Sullivan JB Jr, Krieger GR, editors. Clinical Environmental Health and Toxic Exposures. 2 nd ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2001.  Back to cited text no. 8
    
9.
Schiffl H, Weidmann P, Weiss M, Massry SG. Dialysis treatment of acute chromium intoxication and comparative efficacy of peritoneal versus hemodialysis in chromium removal. Miner Electrolyte Metab 1982;7:28-35.  Back to cited text no. 9
    
10.
Xiang J, Sun Z, Huan JN. Intensive chromic acid burns and acute chromium poisoning with acute renal failure. Chin Med J (Engl) 2011;124:2071-3.  Back to cited text no. 10
    

Top
Correspondence Address:
Ruhi Khan
Department of Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh - 202 002, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.146409

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