A 34 year old male, engaged in some industrial work in Noida, with no significant past history, presented to the casualty (
The weakness was bilateral and involved both the proximal and distal group of muscles. He had no respiratory or swallowing difficulty, and there was no evidence of any cranial nerve involvement. The patient further denied any parenthesis or any recent H/O diarrhea or respiratory tract infection. He however complained of vague aching generalized pain. He denied any H/O trauma to neck.
He, however admitted to H/O generalized weakness of his body around a fortnight back, which had resolved after receiving some iv fluids (probably K+ containing, No documents were available with the patient) in a nearby hospital. His parents, siblings and children didn’t have any similar episode in past. He admitted to tobacco chewing, but no other addictions or extramarital sexual exposure otherwise.
On physical examination, the patient appeared normal in overall appearance with average built. He was conscious, well oriented to time, place and person with average intelligence and intact speech. His heart rate was 106/min, and blood pressure was 130/86mm of Hg. There was no pallor, icterus, cyanosis, clubbing or edema. No JVP distension, goiter or lymphadenopathy was appreciated.
Single breath count was 20. Cardiac examination revealed tachycardia with regular rhythm and no murmur. Examination of the chest and abdomen was unremarkable.
Neurologic examination revealed flaccid paralysis of all extremities, involving both proximal and distal group of muscles. Power was Grade 2 in all major muscle groups. Deep tendon reflexes were markedly diminished to absent, even with reinforcement. Plantar was B/L unresponsive. All modalities of sensation were intact and so were the bladder and bowel functions. Cranial nerve functions and higher mental functions were grossly intact.
Complete haemogram, liver function tests and kidney function tests were normal. Routine examination of urine was unremarkable. Blood Sugar Random was normal at 114 mg%. K+ level was low at 2.5mg/dl during the episode. Changes suggestive of hypokalemia, in the form of flattened T waves were also noted in ECG recorded simultaneously.
The patient was started on iv K+ replacement, 20 meq of KCl was mixed in a pintof normal saline and slow iv infusion was started. Around 30 mins later, the patient began to notice some improvement subjectively- which continued – and around one and half hours later, the patient’s neurologic symptoms had completely resolved. The patient was even able to stand on his own and move about in the ward. He was then sifted to oral K+ supplementation and later started on oral Acetazolamide prophylaxis. Further recheck of his K+ level was done, and was found to be 3.8 meq/dl.
Further studies were performed to determine the etiology of patient’s hypokalemia. Urine Na+ and K+ and serum Aldosterone and renin levels were measured to rule out adrenal involvement and were found to be normal. Thyroid function tests were also well within range.