A Rare Case of Lumbosacral Plexopathy Secondary to Severe Rhabdomyolysis Following Kratom, Cocaine, and Heroin Use

Abstract

INTRODUCTION: Lumbosacral (LS) plexopathy can be difficult to diagnose as it is not commonly encountered in clinical practice. Disease severity is related to the underlying etiology however, progressive neurological deterioration is often seen if proper intervention is not executed promptly. LS plexopathy secondary to severe rhabdomyolysis has been reported in a small number of case reports. We present a rare case of LS plexopathy caused by severe rhabdomyolysis following concurrent use of kratom, cocaine, and heroin. CASE PRESENTATION:A 25 year old male with a history of schizophrenia presented to the emergency department (ED) after experiencing numbness and tingling in his lower extremities following cocaine, heroin and kratom use the day prior. On presentation, the patient became increasingly lethargic and sustained a cardiac arrest while in the ED. CPR was performed for 9 minutes before ROSC was achieved. Labs were remarkable for potassium of 8, BUN 35, creatinine 4.03, and creatine kinase of >100,000 consistent with rhabdomyolysis. The patient was also found to have compartment syndrome of his left lower extremity requiring emergent fasciotomy. He was admitted to the medical intensive care unit where he remained intubated and underwent hemodialysis for acute renal failure. On day 4 of admission, the patient was successfully liberated from the ventilator. At this point, flaccid paralysis and loss of sensation of his bilateral lower extremities were noted on exam. Work up including CT and MRI of the spine were significant for severe paraspinal edema and myonecrosis consistent with rhabdomyolysis. EMG of the lower extremities revealed mild chronic partial denervation with abnormal spontaneous activity in the proximal and distal right leg muscles. Oral Prednisone was initiated with improvement in the patient's lower extremity paralysis after five days of therapy. The patient completed a three week steroid taper with continued improvement in his exam. He was discharged to rehab. At one month follow-up, he showed near complete resolution of his neurologic deficits. DISCUSSION:The LS plexus includes a network of nerves that are formed by the anterior rami of the lumbar and sacral spinal cord which supply the lower back, pelvis and legs. LS plexopathy often presents with lower back and lower extremity weakness, pain, paresthesias, numbness and tingling. LS plexopathy is typically caused by trauma, diabetes, neoplasms and pregnancy. Complications of LS plexopathy may include progressive neurological deterioration, intractable pain, recurrent infections, joint contracture and bedsores.CONCLUSIONS: LS plexopathy secondary to severe rhabdomyolysis is rare, described in only a few case reports. Treatment often relies on addressing the underlying etiology and should be geared towards preventing further nerve damage as LS plexopathy can cause significant detriment to the quality of life of a patient.

Cocaine-Induced Rhabdomyolysis Causing Lumbosacral Plexopathy in an Adult Male

“…Acute kidney injury (AKI) may develop secondary to volume depletion and intratubular heme pigment cast formation [ 1 ]. Lumbosacral plexopathy and compartment syndrome may develop in rare cases secondary to tissue edema [ 2 ]. The acuity, rapidity, and severity of the presenting symptoms should raise suspicion regarding the possibility of the aforementioned complications aggravating the effects of rhabdomyolysis.…”

“…The lumbosacral plexus is a network of nerves formed by the anterior rami of the lumbar and sacral spinal cord [ 2 ]. It innervates the lower back, pelvis, and legs.…”

“…It innervates the lower back, pelvis, and legs. Lumbosacral plexopathy can result from compression from surrounding structures, masses, or edema [ 2 ]. It presents with lower back and lower extremity weakness, pain, paresthesia, numbness, or tingling [ 2 ].…”

“…Lumbosacral plexopathy can result from compression from surrounding structures, masses, or edema [ 2 ]. It presents with lower back and lower extremity weakness, pain, paresthesia, numbness, or tingling [ 2 ]. When severe, it can lead to intractable pain, progressive neurological deterioration, and joint contracture [ 2 ].…”

“…It presents with lower back and lower extremity weakness, pain, paresthesia, numbness, or tingling [ 2 ]. When severe, it can lead to intractable pain, progressive neurological deterioration, and joint contracture [ 2 ]. Treatment often centers around promptly addressing the underlying etiology with a view to preventing further nerve damage [ 2 ].…”