Acute Onset Distal Motor Weakness following a Heavy Meal - medIND

46 downloads 91 Views 349KB Size Report
Electrocardiography revealed prominent u- ... Electrocardiographic evidence of U waves in a ... Practical Electrocardiography BI Waverly Pvt Ltd, New.
IMAGES IN CLINICAL MEDICINE

Acute Onset Distal Motor Weakness following a Heavy Meal Parvez Kumar*, S Dwivedi*

A 24 years old male presented with weakness of both upper and lower limbs for 24 hours duration. Weakness started on getting up from sleep following a heavy meal. The patient was normotensive, non-diabetic, and without any preceding headache, vomiting, altered sensorium, gastro-intestinal upset, or viral illness. On examination, pulse was 90/minute, regular, blood pressure – 130/80 mm of Hg CNS examination revealed normal higher mental functions with intact cranial nerves.

On investigation, total leucocyte count was 7,900/cubic mm, random blood sugar, urea and serum creatinine were 106 mg/dl, 36 mg/ dl, and 0.9 mg/dl respectively. Electrocardiography revealed prominent uwaves (Fig. 1). Serum sodium and potassium were 141 and 1.8 meq/litre respectively. In view of low serum potassium patient was given potassium orally. Patient completely recovered after 8 hours following oral potassium supplementation. His follow-up

There was grade I-II/V strength in all groups of muscles of elbow, wrist, knee, and ankle while grade V/V at shoulder and hip joints. All sensory modalities were intact. Chest, cardiovascular, and abdominal examination was unremarkable

electrocardiogram (Fig. 2) was normal with serum potassium level of 3.8 meq/litre.

* Department of Medicine, BP Koirala Institute of Health Sciences, Dharan, Nepal.

Comments Electrocardiographic evidence of U waves in a patient with acute onset areflexic motor weakness suggests hypokalaemic paralysis. It usually occurs following a heavy meal or

exercise. Gastrointestinal and renal losses of potassium, thyrotoxicosis, and barium carbonate ingestion are well known causes of secondary hypokalaemic paralysis 1,2 . Hypokalaemia can be controlled by oral or intravenous potassium supplementation3. Serum potassium level during the episode of motor weakness is usually less than 3 meq/litre 4. Hypokalaemia induced motor weakness may be induced by injection of insulin, epinephrine, fluorohydrocortisone, or glucose 5 . The characteristic ECG change is prominent Uwaves with reversal in amplitude of T and U waves6. Normal U wave is in same direction as the T-wave but 10% of it’s amplitude. In the present case clinical suspicion of hypokalaemia was made on the basis of U-wave, which reversed completely along with abolition of symptoms following correction of potassium level. Such paralysis are usually areflexic and flaccid.

204

References 1.

Agarwal AK, Gupta S, Wali M, Sangla KS. Hypokalemic Paralysis. In Manoria PC (ed). Medicine Update. Dristi Offset, Bhopal 1996; VI (IV): 260-5.

2.

Agarwal AK, Ahlawat SK, Wadhwa S et al. Periodic paralysis secondary to gastrointestinal potassium loss. J Assoc Phys Ind 1994; 42: 261-2.

3.

Aminoff MJ. Nervous System. In: Tierney LM, Mcphee SJ, Papadakis MA (ed). Current Medical Diagnosis and Treatment, Lange Medical book, Prentice Hall international Inc, Stamford 1996; 35: 858-914.

4.

Walton J. Disorders of Muscle. In: Brain’s Diseases of Nervous System. Oxford Medical Publications, Oxford 1993; 10: 656.

5.

Rowland LP. Familial Periodic Paralysis. In: Merritt’s Textbook of Neurology, The Williams & Wilkins Co., USA 1995; 9: 781.

6.

Wagner GS. Electrolyte Abnormalities. In: Marriott’s Practical Electrocardiography BI Waverly Pvt Ltd, New Delhi 1994; 9: 180.

Journal, Indian Academy of Clinical Medicine



Vol. 2, No. 3



July-September 2001