Variations of serum potassium level and risk of hyperkalemia in inpatients receiving low-molecular-weight heparin.

OBJECTIVES: To observe the variations of serum potassium level in patients receiving low-molecular weight heparin, assess the consequent risk of hyperkalemia and evaluate the clinical contributory factors. METHODS: A prospective study was performed on consecutive inpatients treated with low-molecular-weight heparin as indicated by the attending physicians. The changes of serum potassium level observed within 5-8 days were tested by univariate and multivariate analysis according to demographic and clinical variables and concomitant pharmacological therapy. RESULTS: Four hundred and sixteen patients (mean age 73 years; 64% female) were enrolled in the study over 15 months. After receiving nadroparin or enoxaparin (mean daily dosage: 76.3 anti-factor Xa unit/kg) for a median 6-day period, their mean (+/-SD) serum potassium level increased from 4.2+/-0.5 mmol/l to 4.5+/-0.5 mmol/l ( P<0.0001). This change was significantly correlated with baseline potassium, interval between potassium samplings, history of hypertension or renal insufficiency, and marginally with aldosterone antagonist treatment. Hyperkalemia, defined as potassium exceeding 5.5 mmol/l, developed in ten patients (2.4%) and the highest value observed was 7.6 mmol/l; by multivariate logistic-regression analysis, history of diabetes was the only significant independent predictor (odds ratio 6.5; 95% C.I.=1.7-24.8). CONCLUSION: Short-term treatment with low-molecular-weight heparin induces a significant increase in serum potassium level but the related incidence of relevant hyperkalemia is low. However, given the high absolute number of patients currently exposed to the risk in many clinical settings and the limitation of risk prediction, clinicians should prevent this life-threatening complication by a high index of suspicion and, accordingly, a quite routine monitoring of serum potassium.

Heparin-induced life-threatening hyperkalemia.

Hyperkalemia may occur in many clinical settings and lead to serious events. Heparin-induced hyperkalemia is presumably less well recognized than other untoward effects of heparin treatment and more frequent than commonly perceived. To draw attention to this clinically relevant occurrence, we report 2 cases of life-threatening bradyarrhythmia associated with heparin prescription. Heparin-induced hyperkalemia is mediated by an enzymatic block in the synthesis of aldosterone; however, in most cases severe hyperkalemia occurs in the presence of additional factors influencing potassium homeostasis. Patients treated with heparin should be stratified and adequately monitored according to the outlined risk profile.