Hyperkalemia-induced acute flaccid paralysis: a case report

Abstract

Acute flaccid paralysis is a medical emergency that may be caused by primary neuro-muscular disorders, metabolic alterations, and iatrogenic effects. Severe hyperkalemia is also a potential cause, especially in elderly patients with impaired renal function. Early diagnosis is essential for appropriate management.

Here, we report the case of a 78-year-old woman with hypertension and diabetes presenting to the emergency department because of pronounced asthenia, rapidly evolving in quadriparesis. Laboratory examinations showed severe hyperkalemia of 9.9 mmol/L, metabolic acidosis, kidney failure (creatinine 1.6 mg/dl), and hyperglycemia (501 mg/dl). The electrocardiography showed absent P-wave, widening QRS, and tall T-waves. The patient was immediately treated with medical therapy and a hemodialysis session, presenting a rapid resolution of electrocardiographic and neurological abnormalities. This case offers the opportunity to discuss the pathogenesis, the clinical presentation, and the management of hyperkalemia-induced acute flaccid paralysis.

Keywords: hyperkalemia, acute flaccid paralysis, hemodialysis, diabetes

Introduction

Hyperkalemia is associated with poor outcomes and a high mortality rate among the general population, and among patients with cardiac and renal disease [1,2]. Hyperkalemia-related clinical complications and deaths are determined mainly by the cardiac electrophysiological effects of elevated potassium levels [3]. Indeed, hyperkalemia may result in ventricular arrhythmias and sudden death. Moreover, hyperkalemia may also cause other physiologic perturbations, such as muscle weakness and paralysis, paraesthesia, and metabolic acidosis.

Here, we report a case of severe hyperkalemia presenting with dramatic neurological manifestations in the form of acute flaccid paralysis (AFP).

 

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Metformin and Diabetes: still has a sense of its use in paz. CKD stage II or is an additional risk factor?

Abstract

Pz woman of 62 years comes to P.S.G. for fatigue, low-grade fever, diuresis present. A history of hypertension refers to therapy for about five years, diabetes mellitus for about two years in therapy with Metformin 1gr x 3 gg / day.  Blood tests: BUN 195 mg / dL, creatinine 8.0 mg / dl, Ph 6877, HCO3 5.1 mmol / L BE -29.1 mmol / l. Rapid clinical deterioration with occurrence of arterial hypotension – 85/60 mmHg, stupor. Start therapy Bicarbonates ev, is positioned in Urgency CVC and it undergoes AFB with infusion of bicarbonates 2000 ml / h for 4 hours, blood flow rate 250 ml / min., the hemodynamics has been supported with dopamine infusion 200 mg: 2 vials in 250 cc of physiological vel 30 – 40 ml / h, The pc after undergoing three AFB, interrupted the dialysis for resumption of diuresis spontaneous and progressive improvement of renal function and blood pressure. Monitored, after discharge, the parameters of renal function decreased to within normal limits, clearance compatible with IRC II – III stage.

Conclusions: dehydration, fever, IRC II stadium, undiagnosed caused, in a very short time, an accumulation of metformin, which has been the cause of metabolic acidosis. The pc. saved thanks to the positioning of the CVC and to the AFB in the treatment with the infusion of large quantities of Bicarbonates e.v.

The use of metformin in pcs. > 50 years and / or creatinine clearance <60 ml / min., Must be subordinated to the preliminary study and periodic renal function.

 

Keywords: Metformin, Diabetes, IRA, metabolic acidosis

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Paziente di sesso femminile di 62 anni giunge al P.S.G. per astenia, malessere generale e riferita febbricola, in anamnesi riferisce ipertensione arteriosa in terapia antipertensiva da circa 5 anni, diabete mellito non insulino dipendente da circa 2 anni in terapia con Metformina 1 gr x 3/die. 

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