Clinical Geriatrics

Introduction

Acute ascending paralysis secondary to hyperkalemia is a serious but reversible medical emergency. While the adverse effects of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with renal failure are very well known, it is important to remember that they can cause serious damage even in patients with preserved renal function in the setting of dehydration.

Case Presentation

A 75-year-old woman was admitted to the Emergency Service with generalized weakness and paresthesias. She had a history of chronic edema of the lower limbs, which was being treated with furosemide 40 mg per day. The patient’s symptoms started 2 weeks prior to admission with progressive weakness of her legs and increasing edema. Highly exudative lesions were observed in the pretibial area. Amoxicillin-clavulanic and ibuprofen were prescribed with no effect. At admission, the patient was anuric with paresthesias in the upper limbs and severe weakness in all of her extremities. She reported reducing her intake of fluids over the previous 2 days.

Physical examination confirmed the presence of edema and flaccid quadriparesis. No fever and no meningism were present. The electrocardiogram (EKG) showed a nodal rhythm, 60 beats per minute, with wide QRS complexes and peaked T-waves (Figure 1a). The urine sediment, chest radiography, and magnetic resonance imaging scan of the brain were normal. The blood analyses showed a potassium level of 9.4 mEq/L, BUN 227 mg/dL, creatinine 4 mg/dL, pH 7.29, PCO2 83 mm Hg, and HCO3 12 mEq/L.

A clinical diagnosis of NSAID nephropathy with severe hyperkalemia and secondary acute renal failure was made; this was felt to include a prerenal component due to dehydration. The patient was transferred to the Monitored Care Unit. Treatment with organic resins, insulin, glucose, and salbutamol was initiated to lower the serum potassium level. Parenteral hydration was effective, and dialysis was not needed. In 24 hours, the patient was normokalemic, and her renal function became normal in 48 hours. EKG abnormalities disappeared within 6 hours after insulin and glucose treatment (Figure 1b). The neurological symptoms disappeared within 3 hours. A determination of creatinine clearance performed at that time was normal. The suppurative process in the lower limbs responded to topical measures and systemic antibiotics. The patient was moved to a general medical floor, where she had a complete recovery.

Discussion

Neurological symptoms associated with hyperkalemia were first described in 1953.1 However, there are fewer than 30 cases in the literature reporting the neurological disorder as the first symptom. The paralysis usually starts distally with an ascending course, mimicking Guillain-Barré syndrome or a spinal cord injury.2,3 The level of potassium leading to the paralysis reportedly ranges from 7.0 to 11.2, with a mean of 9.0 mEq/L.2 Complete symmetric paraplegia in the proximal muscles, areflexia/hyporeflexia, distal dysesthesia, and no abnormalities of the cranial nerves are the typical findings.2

The prognosis of secondary hyperkalemic paralysis is good, with symptoms promptly resolving after hemodialysis or after glucose and insulin infusion.4 Recovery from motor paresis typically starts within 1 hour of starting the latter procedure, even when potassium levels are still high.