Case Report

Acute onset quadriparesis with sine wave: a rare presentation

Abstract

Secondary hyperkalemic paralysis is a rare disease entity, and initial presentation with sine wave pattern is even rarer. We report a case of acute onset flaccid quadriparesis due to hyperkalemia and sine wave pattern in electrocardiogram.

A 56-year-old diabetic woman presented to our emergency department with a history of acute onset flaccid quadripar- esis and slight breathlessness for 1 hour. For the last 15 days, the patient was having repeated episodes of vomiting; and her urine output had progressively decreased, she had no history of fever, diarrhea, trauma, vaccination, or similar neurologic episode before. The patient had poorly controlled diabetes, renal failure, and hypertension for many years. On examination her vitals were: temperature, 98 ?F; respiratory rate, 20/min; heart rate, 130/min; and blood pressure, 150/90 mm Hg.

Examination of neurologic system revealed conscious and oriented patient with areflexic paralysis of both lower limbs. Power in lower limb was 2 of 5, and both planters were mute. Power in both upper limbs was 3 of 5, and reflexes were diminished. There was no sensory deficit, and all Cranial nerves were normal. Cardiovascular and gastrointestinal systems were normal; examination of respiratory system revealed bilateral basal crypts. Bedside electrocardiogram (ECG) showed broad-complex tachycardia suggestive of sine wave pattern (Fig. 1). Blood was sent for biochemistry immediately. Keeping in view the clinical picture of the patient and the sine wave pattern in ECG, the patient was provisionally diagnosed as a case of acute onset hyperkalemic flaccid

quadriparesis. She was treated with 10 mL of 10% Calcium gluconate intravenously and 20 units of regular insulin in 50 mL of 50% dextrose. Patient improved after treatment, which was reflected in her subsequent ECG (Fig. 2). Investigations done in the emergency department showed profound dyselec- trolytemia with serum potassium, 8.9 mEq/L; sodium, 131 mEq/L; Blood sugar, 486 mg%; absent urinary ketones; blood urea, 150 mg%; and serum creatinine, 2.2, suggesting hyperkalemia consequent to acute renal failure. Repeat potassium after treatment showed potassium to be 7.8 mEq/

L. Patient was subsequently referred to the department of nephrology for consideration for renal replacement therapy.

Secondary hyperkalemic paralysis is a rare but potentially life-threatening event. If ECG is not done in a timely fashion, the ascending flaccid quadriparesis with no sensory deficit may mimic Guillain-Barre syndrome [1]. Autonomic distur- bance a remarkable feature of Gullian Barre Syndrome is not a recognized feature of hyperkalemic ascending paralysis, although it has been described in other situations associated with hyperkalemia [2]. The exact mechanism of secondary hyperkalemic paralysis is not clear though. It is thought by some to be due to the direct action of potassium on the muscle fiber and cell membrane [3,4], whereas others believe that a functional peripheral neuropathy induced by high serum potassium level is responsible [1,5]. electrocar- diogram generally does not correlate well with serum potassium levels and can show changes ranging from normal to tall T waves with wide QRS, to sine wave pattern and asystole [6,7] as seen in our patient. Management of hyperkalemia includes monitoring vital signs, repeated ECGs, assessment of serum potassium levels, calcium gluconate injection, insulin and dextrose infusion, sodium polystyrene sulfonate regimens, and renal replacement therapy if needed.

Fig. 1 Pretreatment ECG showing broad-complex tachycardia suggestive of sine wave pattern.

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Fig. 2 Posttreatment ECG showing improvement.

Arif Wahab MD

R.B. Panwar MD Govt. Centre of Cardiovascular Sciences and Research

Bikaner, India E-mail address: [email protected]

Vipin Ola MBBS

Department of Internal Medicine

S.P Medical College

Bikaner, India

Shaista Alvi MD Department of Medicine J.N.M.C.H, A.M.U, Aligarh, India

doi:10.1016/j.ajem.2010.05.021

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