Case Report: Drug induced hyperkalemia presenting as acute flaccid quadriparesis

Introduction

Hyperkalemia is a frequently encountered clinical problem. Hyperkalemic paralysis occurs primarily in genetic defects due to sodium channelopathy. Though numerous other etiologies can cause hyperkalemia, neuromuscular paralysis is unusual. Prompt diagnosis and management ensues complete and rapid reversal of symptoms¹. This atypical presentation is a challenge to the clinican. In the case presented herein, early initiation of treatment saved the patient without the need of invasive ventilation or hemodialysis.

Case report

A 66 year old man presented with a history of weakness of both lower extremities followed by weakness in the upper extremities for a duration of 12 hours. There was no history of numbness, paresthesia or sensory loss. The patient did not have any symptom suggestive of cranial nerve involvement, raised intracranial tension and autonomic dysfunction. He had a past history of coronary artery disease (anterior wall myocardial infarction with moderate left ventricular dysfunction) and had undergone percutaneous transluminal coronary angioplasty. The patient was taking Aspirin (75 mg once daily), Ramipril (2.5 mg once daily) and Spironolactone (25 mg once daily) for the past year.

On examination the patient was attentive, oriented and hemodynamically stable. Nervous system examination revealed hypotonia of all four limbs with a power of grade 2. Deep tendon reflexes were absent. Remaining neurological examination and other system examination were within normal limits. Clinically a possibility of acute inflammatory demyelinating polyradiculoneuropathy was considered. Laboratory investigations are depicted in Table 1.

An electrocardiogram (ECG) showed tall peaked T waves (Figure 1), prolonged PR interval and loss of P waves conspicuous of hyperkalemia (Figure 2). The patient was immediately initiated on antihyperkalemia measures, where the dose was guided by clinical response. Calcium gluconate, insulin-dextrose solution infusion, nebulization with beta 2 agonist and oral potassium binding agent (calcium polystyrene sulfonate) were administered. ACE inhibitors (Ramipril 2.5 mg once daily) and Spironolactone (25 mg once daily) were stopped. Arterial blood gas analysis revealed mild metabolic acidosis.

Figure 1. Electrocardiogram showing tall peaked T waves.

Figure 2. Prolongation of PR interval with widening of QRS complex.

Serum potassium levels subsequently normalized after 12 hours of treatment. The patient showed rapid clinical improvement, without the requirement of haemodialysis. He was able to walk on the second day and on examination had grade 5 power in all limbs. An ECG taken after correction of hyperkalemia (after 12 hours of treatment) showed normal sinus rhythm. The patient was detected to have deranged renal function with evidence of chronic kidney disease using ultrasonography, which might have contributed to his hyperkalemia. A portable chest radiograph did not show evidence of fluid overload. Nerve conduction was normal.

On follow up after two months the patient was doing well without any neurological symptoms. His serum creatinine was 2.4 mg/dl and serum potassium was 4 meq/l. He is being monitored regularly by the nephrologist.

Discussion

Clinical manifestations of hyperkalemia are often nonspecific. Patients may present with vague aches and pains, muscle cramps, fatigue or sometimes palpitations. Cardiac arrhythmias are life threatening. Neuromuscular paralysis is not a common presentation of hyperkalemia and is frequently seen with hypokalemia. There are only isolated reports of hyperkalemia presenting as flaccid paralysis^2,3. Weakness in hyperkalemia occurs in an ascending manner, starting in the lower limbs and sometimes leads to respiratory distress requiring invasive ventilation. In the present case, weakness progressed rapidly, but did not involve the respiratory muscles and the patient improved without the need of respiratory support.

The exact molecular mechanism by which hyperkalemia produces neurological dysfunction is not yet elucidated. It is hypothesized to be due to abnormal membrane depolarization. Resting membrane potential of cell membranes is maintained by the difference in concentration of extracellular and intracellular potassium ions. When the extracellular potassium increases in hyperkalemia, it blunts the transmission of nerve impulse to muscle fiber⁴.

In a report by Evers et al., renal dysfunction was the most common cause of secondary hyperkaemic paralysis, as in our case⁵ Other etiologies include excessive dietary intake of potassium, metabolic acidosis, medications that inhibit the renin angiotensin aldosterone system, medications that cause transcellular shift of potassium (Digoxin) and increased tissue catabolism as in tumor lysis and trauma. Succinylcholine used for rapid sequence intubation can cause fatal hyperkalemia, and sometimes result in a similar presentation⁶. Serial electrocardiographic changes in hyperkalemia are described by Aslam et al.,⁷ Electrocardiographic changes may not always correlate with degree of hyperkalemia.

Conclusion

The present case highlights the importance of considering hyperkalemia as a differential diagnosis in patients presenting with acute flaccid paralysis. Regular monitoring of serum potassium should be done in patients on potassium sparing diuretics and other potassium altering drugs. Patients with chronic kidney disease should be carefully watched for development of any complication of hyperkalemia.

Consent

Written informed consent for publication of their clinical details and clinical images was obtained from the patient.

Data availability

All data underlying the results are available as part of the article and no additional source data are required.