Acute Reversible Tetraplegia Induced by Hyperkalemia in a Patient with Paravertebral Mass due to Lymphoma

Abstract

Acute onset of tetraplegia is a medical emergency. Hyperkalemia has been described as a very uncommon cause of tetraplegia. A 79 year old male presented with an acute onset of tetraplegia. His past medical history was significant for stage III follicular lymphoma diagnosed 4 years ago that 1 month prior to the admission progressed with biopsy-proven transformation to a diffuse large B-cell lymphoma. Recent CT and PET scans revealed multiple active lesions including a large paravertebral mass measuring 29 cm×12 cm×7 cm starting in the axial level of the diaphragm involving left psoas, the left renal vein and encasing the aorta. Multiple skeletal lesions, as well as numerous lymph nodes were found. The liver and spleen were also compromised. His surgical history was remarkable for radical prostatectomy for localized prostate cancer. The patient did not have previous history of renal failure and his blood urea nitrogen and creatinine were within normal range (15 mg/dL and 0.8 mg/dL, respectively). Case PresentationTwo days prior to presentation, the patient began experiencing malaise, weakness and myalgia in his lower extremities, which progressed to paraparesis several hours later, and he was unable to ambulate without assistance. Thereafter he developed weakness in both upper extremities. On the day of admission he suddenly became completely tetraplegic. He denied seizures, chorea, rigidity, spasms, recent trauma, or any recent febrile or viral illness. He did admit to have experienced recent poor oral intake related to his generalized malaise, with no vomiting or diarrhoea and he denied recent use of non-steroidal anti-inflammatory drugs or any other new medications, including steroids).On admission his vital signs were all within normal limits; the blood pressure was 136/76 mmHg, heart rate was 68 per minute, respiratory rate was 18 per minute, and temperature was 36.6 degrees Celsius. He was alert and oriented, in no distress with flaccid tetraplegia, areflexia, preserved cranial nerve function, normal rectal sphincter tone and absent plantar responses. The electrocardiogram showed wide QRS complexes, a shortened QT interval and tall peaked T waves. Laboratory testing revealed a serum potassium of 9.3 mEq/L, sodium 120 mEq/L, urea nitrogen 81 mg/dL, creatinine 9.9 mg/dL, calcium 8.5 mg/dL, phosphorus 4.1 mEq/L, creatine kinase 126 units/L, uric acid 9.6 mg/ dl, Lactate Dehydrogenase (LDH) 1118 mg/dl (LDH was 1114, two weeks earlier), aspartate transaminase 28 IU/L, alanine transaminiase 23 IU/L, and alkaline phosphatase 65 IU/L. Imaging studies were negative for hydronephrosis and there was no evidence of spinal cord involvement on chest, abdominal and pelvic CTs performed only two weeks before the admission.While spinal cord compression was considered in the differential diagnosis, however hyperkalemia induced flaccid paralysis with severe acute renal failure were more likely causes and the decision was to initiate treatment of hyperkalemia and renal failure before proceeding with dedicated studies to...