He was treated with intravenous infusion of insulin-dextrose and calcium gluconate for hyperkalemia. Table 1 Serum laboratory test results during patient’s hospital course Open in a separate window Open in a separate window Figure 1 Electrocardiogram showing tall T-waves, absent P-waves and widening of QRS complexes His CSF exam revealed a protein of 68 mg/dL, Rabbit polyclonal to Myocardin glucose of 90 mg/dL and a CSF cell count of 2 leukocytes/mm3. can be complicated by pneumonia, sepsis, pulmonary embolism, respiratory paralysis or cardiac arrest.[1] Analysis of GBS is usually based on clinical exam and is supported by nerve conduction studies and cerebrospinal fluid (CSF) exam.[2] Mild elevation in serum creatine kinase (CK) level have been seen in early stage of GBS, but marked elevation of CK in GBS is an extremely rare getting.[3] We present the case of GBS with marked elevation in serum CK, serum myoglobin levels and prolonged hyperkalemia BML-284 (Wnt agonist 1) as a result of connected acute rhabdomyolysis, which is a potentially life-threatening condition. Case Report The present case report is about a 24-year-old Indian man who presented with 20 days history of weakness of both lower and upper extremities. The weakness began all of a sudden in both lower extremities, which progressed to both top extremities over 2 days. He was limited to bed for 15 days prior to admission in hospital. Five days of fever preceded the onset of weakness by 10 days. He had no sensory or bladder symptoms. He had no history of stress, toxin exposure, illicit drug or alcohol misuse. On general exam, he was afebrile, having a pulse rate of 106/min, blood pressure of 110/70 mmHg and respiratory rate of 18/min. There were no pressure sores or any muscle mass tenderness present on physical exam. On neurological exam, he had flaccid, areflexic, genuine engine quadriparesis with strength graded as 2/5 in both lower extremities and 3/5 in both top extremities. Bilateral plantar reflexes were not elicitable. His laboratory checks on hospital day 1 exposed hyperkalemia, elevated liver enzymes (aspartate aminotransferase, 274 IU/L; alanine aminotransferase, 476 IU/L), leukocytosis (14,100/mm3) and deranged renal profile [Table 1]. His electrocardiogram showed tall T-waves, absent P-waves and widening of QRS complexes consistent with severe hyperkalemia [Number 1]. He was treated with intravenous infusion of insulin-dextrose and calcium gluconate for hyperkalemia. Table 1 Serum laboratory test results during patient’s hospital course Open in a separate window Open in a separate window Number 1 Electrocardiogram showing tall T-waves, absent P-waves and widening of QRS complexes His CSF exam exposed a protein of 68 mg/dL, glucose of 90 mg/dL and a CSF cell count of 2 leukocytes/mm3. Electrophysiological studies confirmed the presence of acute engine and sensory axonal neuropathy. It showed low amplitude of compound muscle mass action potential and nerve action potential, with near normal conduction velocity and the presence of fibrillation and positive razor-sharp wave potentials consistent with axonal neuropathy. His serological checks were bad for leptospira, dengue, human being immunodeficiency disease, antinuclear antibodies, hepatitis B disease and hepatitis C disease. His blood and urine ethnicities were sterile. Thyroid stimulating hormone and free thyroxine levels were within the research range. Immunoglobulins could not be given to him for the treatment of GBS due to monetary constraints. On hospital day time 2, he developed hypotension. Inotropic support (noradrenalin and dopamine) was started after adequate fluid repletion. On hospital day BML-284 (Wnt agonist 1) 3, he was not able to lift his head off the pillow and cough out his secretions. He was put on a mechanical ventilator for respiratory failure. In view of rising renal guidelines, oliguria, proteinuria (2+ on urine dipstick test) and prolonged hypotension, peritoneal dialysis was started [Table 1]. A possibility of coexisting chronic renal insufficiency or acute rhabdomyolysis was kept in view of the presence of persistent hyperkalemia, hyperphosphatemia (10.8 mg/dL), hyperuricemia (14.2 mg/dL), hypocalcemia (7.4 mg/dL) and high anion space metabolic acidosis. His renal profile prior to admission was normal and there was no evidence of chronic kidney disease on abdominal ultrasonography. His biochemical analysis on day time 3 of admission exposed serum CK of 7002 U/L (n. 38-174), lactate dehydrogenase (LDH) of 1250 U/L (n. 91-180), serum myoglobin levels were above 10,000 g/L (n. 10-46) and urine myoglobin levels were 25.7 g/L (n. 0-1000). His serum CK was 279 U/L and 44 U/L on day time 2 of admission (in our hospital) and 3 days prior to admission (in additional private hospital from where he was referred) respectively [Table 1]. No evidence of muscle BML-284 (Wnt agonist 1) mass necrosis was seen in muscle mass biopsy. A final analysis of GBS complicated by acute kidney injury (AKI) and rhabdomyolysis was made. His hyperkalemia persisted despite all.
