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Acute Kidney Injury Due to Rhabdomyolysis Following a Minor Accident

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Acute Kidney Injury Due to Rhabdomyolysis Following a Minor Accident International Journal of Current Medical And Applied Sciences, 2016, March,10(1),04-05. CASE REPORT Acute Kidney Injury Due to Rhabdomyolysis Following a Minor Accident . Naik M.R 1. , Umar Quadri Syed 2, Atul Jadhav 3, Anirudha Londhe 3 & Saurabh Bhutada 3 1 Professor, 2Assiatant professor, 3Post-Graduate Student, Department of Medicine, Mahatma Gandhi Missions Medical College, Aurangabad [MS] , INDIA. ------------------------------------------------------------------------------------------------------------------------------------------------------------------- Abstract: Rhabdomyolysis is commonly seen with injuries associated with damage to the muscles. The pathogenesis includes the release of muscle proteins like myoglobulin into the blood stream which can lead to electrolyte disturbances, hypovolemia, metabolic acidosis, coagulopathies, and myoglobinuric assault of the kidneys by tubular clogging and necrosis resulting in renal failure. Significant muscle trauma is generally required to develop full blown manifestations of rhabdomyolysis like renal failure and hyperkalemia. We report a rare case of rhabdomyolysis in a patient with blunt injury to back due to fall from height without significant muscle damage. A 45 year old male patient was admitted withblunt injury to back and fracture of 2 nd and 3 rd intercostal ribs following a fall from height. Investigations showed elevated serum creatinine, urea levels, with anaemia and hyperkalemia. X- Ray was done suggestive of left sided pleural effusion. USG chest suggestive of moderate fluid in pleural cavity. Inter Costal Drain (ICD) was inserted which was hemorrhagic in nature suggestive of hemothorax. USG abdomen showed no evidence of intra abdominal bleeding or major organ injury. The patient was in non-oliguric renal failure with a rapid rise in serum creatinine and grossly elevated Serum creatine phospho kinase (CPK) and without myoglobulin in urine. A provisional diagnosis of Rhabdomyolysis with Acute Kidney Injury (AKI) with hemothoraxwas made and he was given intermittent hemodialysis, and judicious IV fluids. He gradually improved and after 4 sessions of hemodialysis, creatinine normalized and patient had good urine output. He was discharged on the 20 th day after ICD drain was removedas patient was clinically stable and had no complaints. Key words: Acute Kidney Injury; Creatine Phospho Kinase, Hemodialysis, Non-Oliguric Renal Failure , Rhabdomyolysis , diabetes mellitus. Introduction: Rhabdomyolysis is a condition characterized by myocyte cell membrane results in the release of large dissolution of skeletal muscles with liberation of of quantities of myoglobin, a nephrotoxin, which results in toxic intracellular contents from the myocytes into the tubular clogging, necrosis of tubular cells and circulatory system (Myo-muscle, Rhahdo-striated and sloughing [2]. Lysis is breakdown) which triggers a common Case report: rhabdomyolysis cascade irrespective of the primary 45 years old male admitted with history of blunt insult [1]. It is generally caused by severe muscle trauma to back due to fall from height. Patient had damage secondary to traumatic crush injuries, non complaint of chest discomfort. Patient was conscious, traumatic muscle injuries like burns, oriented with vitals as Pulse-96/min, BP-120/70 mm of necrotizinginfections, seizures, intense exercise, Hg. Cardiovascular system was normal. extremes of heat and cold exposure etc. Damage to Address for correspondence: Dr.Umar Quadri Syed , Access this Article Online Assistant Professor, Department of Medicine, Website: Mahatma Gandhi Missions Medical College, Aurangabad [MS], India. www.ijcmaas.com Email: [email protected] How to cite this article: Subject: Umar Quadri Syed: Acute kidney injury due to Rhabdomyolysis Medical Sciences following a minor accident . International Journal of current Medical and Applied sciences; 2016, 10(1), 04-05. Quick Response Code IJCMAAS,E-ISSN:2321-9335,P-ISSN:2321-9327. Page | 04 Naik M.R., Umar Quadri Syed, Atul Jadhav, Anirudha Londhe & Saurabh Bhutada Patients ECG was within normal limit. X-ray chest skeletal musclesas well as reduced clearence as a result Suggestive of fracture of 2 nd and 3 rd left intercostal ribs of renal shutdown [3].This coincided with elevated and left sided moderate pleural effusion. USG Chest CPK and urea being disproportionately low for suggestive of moderate fluid in pleural cavity. ICD was creatinine. Hb does not immediately fall after external inserted and was suggestive of hemorrhagic fluid. blood loss as intravascular fluid shift takes at least 24 Other lab investigation were done and were as Hb- 6.0 hours to dilute the blood and hence should be gm/dl; TLC- 7920/mm 3; Platelets- 99,000/mm 3, Urea- periodically checked. This explains the delayed fall of 320 mg/dl, Creatinine- 10.3 mg/dl, Na +-123meq/L, K +- Hb in this case. Patients with trauma will have myocyte 5.3meq/L, ABG suggestive of severe metabolic acidosis. membrane damage leading to release of large amounts Patient was having normal urine output. Initially of potassium and phosphate into extracellular patient was treated with crystalloids with compartment as this electrolytes are mainly approximately 3 litres of normal saline over 24hrs. concentrated within the cells [4]. Similarly, sodium and Correction of hyperkalemia was given as calcium calcium which are mainly extracellular, may influx into gluconate & insulin in dextrose by i.v. route. Patient cells due to concentration gradient leading to was also incidentally was detected as diabetic and was hyponatremia and hypocalcemia, which is put on regular insulin subcutaneously. Patient was compounded by large volume of fluid therapy, as is provisionally diagnosed as C/O Rhabdomyolysis and so seen in this case. CPK levels are generally elevated CK total levels and urine for myoglobulin was send for immediately and can remain so for variable periods of examination. time. Myoglobin released from damaged muscles can On 2 nd day patient had increase in serum urea and clog renal tubules and can lead to AKI but initiation of creatinine levels to 375 mg/dl and 11.3 mg/dl timely hemodialysis is extremely important in as it not respectively. Patient had normal urine output but only helps in removing uremic toxins but also in patient was taken for hemodialysis due to persistent managing metabolic complications. Establishing good hyperkalemia and metabolic acidosis. urine output is critical in determining the prognosis as Report of CK total was 58,097 IU/L and urine for it flushes the toxic products and reduces the contact myoglobulin was negative. Patient was diagnosed as period with tubular epithelial cells. Electrolyte C/O Rhabdomyolysis with non-oliguric renal failure. imbalance and renal failure are the causes of mortality Patient underwent 4 hemodialysis within next 10 days and if they are addressed properly, the outcome should due to persistant hyperkalemia, metabolic acidosis and be good. rising trend of creatinine and urea. After 4 sessions of Conclusion: dialysis patient’s condition improved clinically and labs Rhabdomyolisis requires high index of suspicion in any were creatinine-1.4 mg/dl; Urea- 28 mg/dl; CK total- patient with major or minor muscle injury, who 212 IU/L. Patients ICD was removed on 14 th day as develops acute kidney injury and metabolic drain output was decreased. Patient was discharged on disturbances. Aggressive fluid therapy and timely 20 th day with insulin therapy for diabetes. hemodialysis can reduce the mortality. Absence of Discussion: urinary myoglobulin and adequate urine output does This case highlights the importance of keeping not rule out possibility of acute kidney injury in case of rhabdomyolysis in mind in any patient with rhabdomyolysis. unexplained renal failure (raised serum urea and References: creatinine levels). The severity of renal disease 1. Russell TA. Acute renal failure related to generally coincides with the severity of muscle damage Rhabdomyolysis: pathophysiology, diagnosis, and but this is not a rule in every case. Often, AKI following collaborative management. Nephrol Nurs J. trauma is attributed to shock and volume depletion. 2000;27:567-577 The rapidity of rise in creatinine, unresponsiveness to 2. Bosch X, Poch E, Grau JM; Rhabdomyolysis and acute fluid therapy and worsening metabolic derangements kidney injury. N Engl J Med,2009, 361:62–72 in spite of supportive therapy has pointed to the 3. Gronert GA. Cardiac arrest after succinylchoiine: possibility of rhabdomyolysis AKI in this case. The mortality greater with rhabdomyolysis than receptor diagnosis is delayed in many cases as muscle injury can upregulation. Anesthesiology. 2001:94:523-529 be mild and is way from being significant such as 4. Moore KP, Holt SG, Patel RP, et.al. A causative role for intramuscular injections, focal muscle ischemia, redox cycling of myoglobin and its inhibition by intraoperative torniquets, tight dressings, prolonged alkalinization in the pathogenesis and treatment of splintings and drugs causing muscle disease like rhabdomyolysis-induced renal failure. J statins. BiolChem,1998,273:31731–31737. In this case, a rise in the creatinine from 10.3 mg/dL to 11.3 mg/dL over one day is due to release from Conflict of interest: None declared No source of funding. Logic Publications @ 2016, IJCMAAS, E-ISSN: 2321-9335,P-ISSN:2321-9327. .
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