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  Table of Contents  
Year : 2020  |  Volume : 61  |  Issue : 2  |  Page : 102-105  

Minor blunt injury-induced rhabdomyolysis from a road traffic accident in Nigeria

1 Department of Medicine, Chukwuemeka Odumegwu Ojukwu University, Awka, Nigeria
2 Department of Medicine, Federal Medical Center, Umuahia, Nigeria
3 Department of Medicine, Nnamdi Azikiwe University, Nnewi, Nigeria
4 Department of Ophthalmology, Federal Medical Center, Owerri, Nigeria

Date of Submission22-Jul-2019
Date of Decision04-Dec-2019
Date of Acceptance27-Feb-2020
Date of Web Publication7-May-2020

Correspondence Address:
Dr. Ernest Ndukaife Anyabolu
Department of Medicine, Chukwuemeka Odumegwu Ojukwu University, Awka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/nmj.NMJ_114_19

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Rhabdomyolysis, though not a common complication of minor blunt trauma, may result in life-threatening acute kidney injury (AKI). Here is illustrated a case of a young male who sustained minor blunt injuries in a road traffic accident, which he overlooked and presented with features of severe AKI. The patient is a 24-year-old male, who presented with progressive weakness, difficulty in walking, and features of uremia, 14 days after he sustained minor blunt injuries and lacerations in a road traffic accident. Evaluation showed elevated serum creatine kinase, serum myoglobin, and severe azotemia. He was commenced on hemodialysis. He was also commenced on antibiotics, analgesic, and 5% dextrose/saline. He had three sessions of hemodialysis on alternate days. His condition improved remarkably after the first session of dialysis. He was discharged after 18 days on admission. Follow-up in the clinic showed a normal renal function. This case report shows rhabdomyolysis from minor blunt injuries sustained in a road traffic accident and complicated by severe AKI. The patient almost recovered full renal function with management.

Keywords: Acute renal failure, minor blunt injuries, Nigeria, rhabdomyolysis, road traffic accident

How to cite this article:
Anyabolu EN, Okoye IC, Chukwuonye II, Anyabolu AE, Dike KC, Ufoaroh CU. Minor blunt injury-induced rhabdomyolysis from a road traffic accident in Nigeria. Niger Med J 2020;61:102-5

How to cite this URL:
Anyabolu EN, Okoye IC, Chukwuonye II, Anyabolu AE, Dike KC, Ufoaroh CU. Minor blunt injury-induced rhabdomyolysis from a road traffic accident in Nigeria. Niger Med J [serial online] 2020 [cited 2023 Feb 7];61:102-5. Available from: https://www.nigeriamedj.com/text.asp?2020/61/2/102/283914

   Introduction Top

Rhabdomyolysis is a syndrome that derives from injuries to skeletal muscle.[1] Albeit the myriads nature of these injuries, rhabdomyolysis does not commonly result from common blunt injuries sustained in road traffic accidents.[1]

Injuries to the muscle cell, the sarcolemma, may disrupt many pumps like Na/K-ATPase, which regulates cellular electrochemical gradients.[2] Electrolyte composition is altered following energy depletion that disorganizes the cellular transport mechanisms.[3] Massive proteases and proteolytic enzymes that result from a rise in intracellular calcium, subsequently induce free oxygen radicals' regeneration. In turn, myofilaments are broken down by these substances and enzymes. Membrane phospholipids are also injured causing leakage of intracellular materials into the plasma. Creatine kinase (CK), phosphate, potassium, myoglobin, and urate are some of the materials unleashed into the plasma. Activated neutrophils and fluid infiltrate the muscles.[4] These will incite reperfusion injury and inflammatory cascade, which will cause perpetuation of the muscle breakdown.[5],[6]

In adults, rhabdomyolysis usually manifests with the triad of myalgia, muscle weakness, and dark urine.[7]

The incidence of rhabdomyolysis in Nigeria is not well defined. Myoglobin-induced rhabdomyolysis has not been well documented in Nigeria from the literature search, but worldwide, its incidence is conservatively put at 16%–33%.[8] Severe acute kidney injury (AKI) is a recognized complication of rhabdomyolysis.[9]

Levels of serum CK above 5 times the upper limit of normal establish the diagnosis of rhabdomyolysis.[10] Serum myoglobin may also be considered although this is not specific. Ancillary tests include high potassium levels and elevated lactate dehydrogenase.[1] Target treatment in rhabdomyolysis is the treatment of shock and reclamation of renal function.[11]

From the literature search, there was a paucity of reports on rhabdomyolysis from minor road traffic accidents in Nigeria. This has prompted the writing of this case which illustrated a patient with rhabdomyolysis attributable to minor blunt injuries sustained in a road traffic accident, overlooked by the patient.

   Case Report Top

The patient is a 24-year-old male, Igbo by tribe, and an undergraduate, resident in Enugu, Southeast Nigeria. He was referred from the Enugu State University Teaching Hospital staff clinic on account of persistent hiccups of 4 days and confusion of 2 days' duration. The patient was in apparent good health until about 14 days before presentation when he was involved in a road traffic accident, in which he sustained minor blunt injuries, bruises, and lacerations but no fractures. On presentation, he was seen, admitted, and managed by the General Surgical Unit of University of Nigeria Teaching Hospital, Enugu, Nigeria. Four days into the hospital admission in the surgical unit, he developed progressive weakness and worsening of the body pain, and hiccups which became so severe that the patient could not eat without fear of discomfort. As a result of the weakness, he was unable to walk around or bath himself. Two days later, the patient developed nausea and recurrent vomiting, which smothered on until he developed progressive confusion and altered sleep pattern. The patient later developed facial puffiness which was closely followed by bilateral swelling of the legs. The leg swelling progressed to the thigh; he had no associated fever or seizures. His urine volume was noticed to have reduced and a collected urine sample turned dark brown after 6 h. There was no history of hematuria or frothy urine. He had no bleeding from any orifice. There was no history of hypertension or diabetes mellitus. He had no known risk factor for muscular disease from history obtained, and there is no family history of muscular disease.

Physical examination revealed an acutely ill-looking young male. He was in respiratory distress, was afebrile (temperature 37.1°C), not pale, and not anicteric. There was no significant peripheral lymphadenopathy. He had bilateral pitting lower limb edema. Asterixis was present.

The significant observations on examination of the systems were that the patient was drowsy with flapping tremor and bilateral pitting lower limbs and facial edema. He had a pulse rate of 102 beats/min which was of small volume, with a blood pressure of 88/56 mmHg and respiratory rate of 34 cycles/min. Four lacerations and bruises, all dressed; they were neat and not offensive. He had a bilateral basal crepitation.

The assessment of AKI was made.

The following investigations were carried out: urinalysis, urine microscopy culture and sensitivity (MCS), full blood count (FBC), prothrombin time, activated partial thromboplastin time, serum electrolytes, urea, and creatinine (SEUC), serum calcium, serum phosphate, serum uric acid, fasting blood sugar, serum protein, serum CK, serum myoglobin, electrocardiogram (ECG), chest X-ray, and renal ultrasound scan. The results are shown in [Table 1], [Table 2], [Table 3], [Table 4].
Table 1: Biochemical investigation results of the patient

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Table 2: Urinalyses investigation results of the patients

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Table 3: Investigation results

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Table 4: Investigation results

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A diagnosis of rhabdomyolysis complicated by AKI was made.

Hemodialysis was commenced for the patient, intravenous fluid 5% dextrose/saline 1 L 8 hourly for 72 h, ciprofloxacin 200 mg 12 hourly for 72 h, and later converted to oral ciprofloxacin 500 mg 12 hourly for 7 days. The patient was also on tramadol 50 mg 12 hourly for 5 days. He regained full consciousness after the first session of hemodialysis. However, he received two further sessions of hemodialysis. His edema resolved within 15 days. The results are shown in [Table 1], [Table 2], [Table 3], [Table 4]. He was discharged after 18 days on admission. His first clinic check-up after 2 weeks showed that he had no edema and had normal BP. Laboratory evaluation at day 32 showed FBC, SEUC, urinalysis, serum CK, and serum myoglobin, and ECG results displayed in [Table 1], [Table 2], [Table 3], [Table 4]. He was stable and doing well. Further follow-up of this patient continued but was not captured, as this report was written 2 weeks after his discharge from the hospital.

   Discussion Top

The incidence of rhabdomyolysis is not well defined in Nigeria but seems to be low.[12] This index patient was the third case in our unit in 6 years suggesting that rhabdomyolysis is rare in this environment.

The causes of rhabdomyolysis include crush injuries, muscle compression, infections, and others.[13] There was no crush injury or muscle compression injuries in this index patient. Rhabdomyolysis could be accounted for by the blunt trauma; he sustained in the road traffic accident.

In rhabdomyolysis, muscle damage disrupts sarcolemma microstructures and electrolyte cellular transport mechanisms and alters electrolyte composition.[3] Our index patient had elevated serum CK, elevated serum myoglobulin, hyperkalemia, and hypocalcemia.[10]

Myalgia, weakness, and dark urine usually characterize rhabdomyolysis.[11] This patient under discussion had progressive severe weakness impairing ambulation. He also had dark urine, which is one of the signs of rhabdomyolysis.

Severe renal failure and disseminated intravascular coagulation are challenging outcomes of rhabdomyolysis.[14] Of note, this patient had severe acute renal failure; however, there were no features of intravascular coagulation.

Rhabdomyolysis accounts for 5%–25% of all adult cases of acute renal failure.[8] Nonetheless, myoglobin-induced acute renal failure, though not common, may warrant hemodialysis, albeit in short term. Our index patient had three sessions of hemodialysis with very good outcomes.

Some hereditary enzyme myopathies may potentiate rhabdomyolysis in the events of trauma.[15] Our index patient was a male but did not have a family history of muscle disease. However, he had trauma-associated rhabdomyolysis. Although drugs such as steroids, quinine, and antihistamines are known causes of rhabdomyolysis, the history of incriminating drugs was not obtained in our patients.

The diagnosis of rhabdomyolysis was based on compatible history of severe weakness and muscle pain with antecedent blunt trauma from a road traffic accident, dark urine, microscopic hematuria noted in the urinalysis, elevated serum creatine levels above 5 times the upper limit of normal,[10] elevated serum myoglobin levels, ancillary positive tests to hyperkalemia, neutrophil leukocytosis, hypocalcemia, and hypophosphatemia.[10] In addition, acute renal failure requiring dialysis was a complication of the rhabdomyolysis.[9]

The thrust of management is to correct cardiovascular insufficiency and address renal function impairment. Our patient received 3 L of 5% dextrose/saline/24 h. Hemofiltration is effective in removing large molecules like myoglobin from the bloodstream.[7] However, hemodialysis is the mainstay of renal replacement therapy in this condition. Our patient had three sessions of hemodialysis with correction of hyperkalemia. Most patients who have sustained renal impairment due to rhabdomyolysis fully recover their renal function.[2],[16],[17] A near similar picture was observed in this patient who had a progressive appreciation of the renal function.

   Conclusion Top

This case report shows rhabdomyolysis from minor blunt injuries sustained in a road traffic accident and complicated by severe AKI. The patient almost recovered full renal function with management.

Informed consent

Written informed consent was obtained from this patient.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for his clinical information to be reported in this journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity will not be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Beetham R. Biochemical investigation of suspected rhabdomyolysis. Ann Clin Biochem 2000;37:581-7.  Back to cited text no. 1
Chavez LO, Leon M, Einav S, Varon J. Beyond muscle destruction: A systematic review of rhabdomyolysis for clinical practice. Crit Care 2016;20:135.  Back to cited text no. 2
Brumback RA, Feeback DL, Leech RW. Rhabdomyolysis in childhood. A primer on normal muscle function and selected metabolic myopathies characterized by disordered energy production. Pediatr Clin North Am 1992;39:821-58.  Back to cited text no. 3
Sitprija V. Animal toxins and the kidney. Nat Clin Pract Nephrol 2008;4:616-27.  Back to cited text no. 4
Luck RP, Verbin S. Rhabdomyolysis: A review of clinical presentation, etiology, diagnosis, and management. Pediatr Emerg Care 2008;24:262-8.  Back to cited text no. 5
Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis–An overview for clinicians. Crit Care 2005;9:158-69.  Back to cited text no. 6
Cervellin G, Comelli I, Lippi G. Rhabdomyolysis: Historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med 2010;48:749-56.  Back to cited text no. 7
Chamberlain MC. Rhabdomyolysis in children: A 3-year retrospective study. Pediatr Neurol 1991;7:226-8.  Back to cited text no. 8
Petejova N, Martinek A. Acute kidney injury due to rhabdomyolysis and renal replacement therapy: A critical review. Crit Care 2014;18:224.  Back to cited text no. 9
Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2009;8:1553-61.  Back to cited text no. 10
Mannix R, Tan ML, Wright R, Baskin M. Acute pediatric rhabdomyolysis: Causes and rates of renal failure. Pediatrics 2006;118:2119-25.  Back to cited text no. 11
Oluyomi OO, Olugbenga EA, Adebode DA. Acute midney injuryrequiring hemodialysisin the tropics. Saudi J Kidney Dis Transpl 2012;23:1315-9.  Back to cited text no. 12
Karl AN, Marayana SM. Myoglobinuric and hemoglobinuric acute kidney injury. In: Greenberg A, Cheung AR, Thomas M, Falk RF, Jennette C, editors. Primer on Kidney Diseases. 5th ed. Philadelphia: Saunders Elsevier; 2009. p. 298-304.  Back to cited text no. 13
Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2000;11:1553-61.  Back to cited text no. 14
Scalco RS, Gardina A, Pitceathly RD, Zanoteli E, Becker H, Holton JL, et al. Rhabdomyolysis: A genetic perspective. Orphanet J Rare Dis 2015;10:51.  Back to cited text no. 15
Better OS. The crush syndrome revisited (1940-1990). Nephron 1990;55:97-103.  Back to cited text no. 16
Okpa HO, Bisong EM, Enang OE, Effa EE, Monjok E, Essien EJ. Predictors of chronic kidney disease among HIV-infected patients on highly active antiretroviral therapy at the university of Calabar teaching hospital, Calabar, South-South Nigeria. HIV AIDS (Auckl) 2019;11:61-7.  Back to cited text no. 17


  [Table 1], [Table 2], [Table 3], [Table 4]


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