An Acute Kidney Injury Associated Rhabdomyolisis as a

Complication After High Level Spinal Cord Injury in a Rural Hospital: a Case Report
Jeffrey Chandra1, Runi Asmarani2
1General physician, dr. H. Marsidi Judono General Hospital, Belitung
2Neurology resident, Department of Neurology RSUP dr. Kariadi, Semarang

Abstract
Complications of acute kidney injury after spinal cord injury are not commonly seen. Rhabdomyolisis or massive muscle cell damage is an acute and emergency condition that must be treated

quickly. Male, 83 years old, came to the Emergency Department at dr. H. Marsidi Judono General Hospital, had spastic tetraparesis (upper extremity 222/222 and lower extremity 111/111) and frontal

region hematoma of cranial after a motorcycle accident. On examination, the patient was compos mentis but experienced neurogenic shock and spinal cord lesions were found as high as Thoracal III-

IV. Patient receives neurogenic shock treatment and treated in the ICU, and further laboratory and imaging evaluations were performed before the patient finally went home with a neurological

sequele, tetraparesis with the same muscle strength as well as when he was arrived. Thirteen days later, the patient came back to the hospital with a loss of consciousness accompanied by hematemesis

melena. Laboratory tests found an increase in serum creatinine and urea levels, and hypokalemia. A history of kidney disease has never been experienced before. As a result of immobilization and

lack of movement during homecare, a large decubitus ulcer was found in the gluteus region with necrotic tissue. Rhabdomyolisis is strongly suspected to be the cause of acute kidney injury in this

case which should have been identified and treated earlier to prevent secondary disease. Tetraparesis after spinal cord injury that causes immobilization is an important sign but often missed of care,

so that pressure ulcer can occur on the skin that can continue to damage deeper tissue, such as muscle cells and underlying bone. Complications of acute kidney injury associated rhabdomyolysis after

spinal cord injury are expected to be a concern for clinicians, to reduce morbidity and mortality. 

Keywords : Spinal Cord Injury, Rhabdomyolisis, Acute kidney Injury

Background: Discussion:
Spinal cord injury has a several severe complications, one of which is a kidney dysfunction. Renal function impairment complication can be found in spinal injury patient with medulla

Decreased kidney function in spinal cord injuries usually due to neurogenic bladder, urinary tract spinalis lesions, generally due to neurogenic bladder, recurrent urinary tract infections, and

infections, or nephrolithiasis. On the other hand, acute kidney injury is rarely encountered in acute nephrolithiasis.1,2 Tetraparesis is known to reduce kidney function due to autonomic nervous

complications of spinal cord injury. Acute muscle cell disintegration or rhabdomyolysis is an system disorders and urinary dysfunction.1 In this case, in less than a month, there was an

emergency condition that can occur due to trauma, alcohol use, certain drugs (e.g. statins), and increase in serum creatinine and urea levels, without having a history of previous kidney

infection. The incidence of acute kidney injury associated rhabdomyolysis after spinal cord injury is problem. Renal hypoperfusion with renal artery vasoconstriction caused by neurogenic shock

rare, but it is important for clinicians to reduce the morbidity and mortality rates of spinal cord may occur in these patients so that renal function decreases.3 However, adequate fluid

injury. resucitation minimizes kidney injury and the objective data indicate a good renal function after

resuscitation. Rhabdomyolisis is suspected of causing this acute kidney function impairment,

with grade IV decubitus ulcers in the gluteus due to immobilization, signifying the process of

Case: tension and / friction occurs between the layers of the skin with internal tissue support such as

Male, 83 y.o, had spastic tetraparesis (upper extremity 222/222 and lower extremity 111/111) and muscle and then causes muscle cell death.4 Muscle cell necrosis can be seen by hypocalcemia

frontal region hematoma after a motorcycle accident. Patient was compos mentis (E4 V5 M6), because the dead myocytes will shorten causing continuous muscle contractions so that massive

airway breathing clear, BP 60/33 mmHg, pulse 50 x / min, without external bleeding and FAST calcium influx into the intracellular.4 Myoglobin, enter the blood circulation and kidney,

examination was clear. Hypesthesia was found from both toe tips to the level of Thoracal III-IV, caused clogging and damaged tubules with results in a decrease glomerular filtration.5

suspected to have spinal cord lesions (ASIA, AIS C). The patient has a history of controlled Manifestations of hematemesis melena can be caused by uremic gastropathy after kidney

hypertension without renal impairment or diabetes. Neurogenic shock treatment is performed by damage and stress ulcers due to immobilization which subsequently causing hypovolemic

loading fluids and installing vasopressors. Blood tests showed a decrease in hemoglobin without shock. This situation itself is like a circle of death, because hypovolemic shock reduces renal

electrolyte disturbances or kidney disfunction. Cervicothoracolumbosacral imaging are suspected of perfusion and finally the kidney function decreases. Rhabdomyolysis as a cause of acute kidney

spinal cord injury without vertebral column fractures. Non-contrast head CT scan showed frontal injury in patients with spinal cord injuries should be known earlier but often not recognised by

hematosinus and hemorrhage in the cerebellum, which is thought to be a result of the coup-counter clinicians. Rita et al, according to their study, revealed that 51.5% acute spinal cord injuries had

coup mechanism. After being treated for four days in the ICU and four days in a ward, the patient rhabdomyolysis and more than half of them 53.5% had acute kidney injury.6

was about to be referred to neurosurgeon but he rejected and went home with a neurological sequele

of spastic tetraparesis with the same motoric strength as the patient arrived. Thirteen days later, the

patient came back to the hospital with decreased consciousness and hematemesis melena. Patient Conclusion:
was somnolence (E3 V5 M6), with BP 62/33 mmHg, pulse is weak and cold acral. Fluid and
Complications of acute kidney injury associated rhabdomyolysis after spinal cord injury are
vasopressor were given to overcome hypovolemic shock. Grade IV decubitus ulcer was found in the
expected to be a concern for clinicians. The prognosis will be better if it is detected and treated
gluteus region. Laboratory results showed Hemoglobin 5.1 g/dL, Ureum 366 mg/dL and Creatinine
earlier. Serum creatinine, urea, urinalysis to assess renal function as well as serum electrolytes
2.8 mg/dL, and Hypocalcemia of 6.1 mg/dL
and creatine kinase can help in directing suspicion of rhabdomyolysis. No less important, careful

physical examination can detect decubitus ulcer and muscle atrophy as a sign of occuring muscle

cell death. Finally, education about home care is very important for spinal cord injury patients.

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