Management of Rhabdomyolysis and Acute Renal Failure Following Strenuous Exercise in Young Adult: A Case Report

Introduction: Rhabdomyolysis is severe and life threating condition in which skeletal muscles are damaged by dissolution of striped muscles. Acute kidney injury (AKI) has been widely reported (13% - 50%) as a complication of Rhabdomyolysis in which the main pathophysiological mechanisms are intra-renal vasoconstriction, intraluminal cast formation (Tamm-Horsefall) and direct myoglobin toxicity. In this report we are going to describe the management of Acute Kidney Injury due to Rhabdomyolysis that is not responding to vigorous rehydration. Objective: Reporting about acute renal failure induced by Rhabdomyolysis due to Excessive Exercise and dehydration in young patient. Case Report: A 20 years male came to the outpatient clinic complaining of sever lower limb pain, back pain and vomiting. He was anuric and hypertensive (BP = 150/90 mmHg) with serum creatinine and urea levels of 15.72 mg/dl and 235 mg/dl, respectively. The diagnosis was based on the laboratory finding of creatine kinase = 3127 IU/l. The patient, then, has been referred to the emergency department. The Management plan was based on two arms: Emergency Management with Urgent Hemodialysis for AKI and high fluid replacement therapy. Patient started to recover after three hemodialysis sessions but the peak of recovery was noted after starting manual fluid replacement therapy with a target urine output of greater than 2 ml/kg, a urine pH of greater than 6. Manual fluid replacement therapy consisted of loop diuretics, intravenous fluids and intravenous sodium bicarbonate 1.26%. Full recovery was noted after one month of hospital admission with inpatient care and regular follow-up. A follow-up after one month has been set to assess the patient progression and monitor his kidney functions. Relevance and Impact: Home messages and lessons are;Firstly, young adults are vulnerable to Rhabdomyolysis, second, the diagnosis of Rhabdomyolysis can be made on the clinical bases but a confirmatory laboratory test of Creatine Kinase is mandatory, and lastly’ acute kidney injury needs to be treated urgently. Also, reducing the risk of infection is one of the management objectives to achieve recovery.

Miller Fisher Syndrome Induced by Chemotherapy in Known Case of Acute Lymphocytic Leukaemia: A Case Report

Introduction: Guillain-Barre Syndrome (GBS) is an acute-onset autoimmune-mediated neuropathy. Guillain-Barre Syndrome can be divided into three subtypes: acute inflammatory demyelinating poly-radiculo-neuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN). About 20% of patients with GBS develop respiratory failure and require mechanical ventilation. We are presenting a variant of GBS (Miller Fisher Syndrome, or MFS), which has been confirmed by nerve conduction studies along with the triad of ophthalmoplegia, ataxia, and areflexia. The objective of this study is to present a rare case of chemotherapy-induced GBS. Important clinic findings: A 25-year-old gentleman with acute lymphocytic leukemia on active chemotherapy treatment presented with lower limb weakness. This weakness started after his fifth chemotherapy session. After the sixth chemotherapy, he developed complete paralysis of the left lower limb. Later, he developed right lower limb paralysis. He was also complaining of eye dryness and incomplete closure of both eyes. While inpatient, he developed upper-limb weakness. His chemotherapy consisted of MESNA, cyclophosphamide, doxorubicin, vincristine, cyorabine, and methotrexate. He had ptosis and ophthalmoplegia in the left abducent and right oculomotor regions. He had bilateral facial nerve palsy. He was hypotonic with power grade 3 in the upper limbs and grade 0 in the lower limbs with areflexia. His sensation was intact in the upper limbs but lost in the lower limbs. His planter reflexes were mute. Diagnoses and Management: Intravenous immunoglobulins were given for 5 days. A nerve conduction study showed severe demyelinating sensorimotor polyradoculoneuropathy with secondary axonal loss. The triad of ataxia, ophthalmoplegia, and areflexia was consistent with MFS. The patient improved over the course of the hospital stay but did not reach full recovery. Conclusion: Although GBS is uncommon, it must be taken into account when making a differential diagnosis for any patient presenting with progressive weakness. Drug history is important in all GBS cases.