Wajahat Aziz, Jamal Zafar, Sohail Aziz.
Periodic paralysis - an unusual complication of poorly controlled diabetes mellitus.
J Pak Inst Med Sci Jan ;7(2)8(1,2):547-9.

A 47 year old diabetic lady was admitted for recurrent attacks of flaccid paralysis and hyperkalemia. She had diabetes mellitus for the past 20 years and developed diabetic nephropathy and chronic renal failure. She also had Addisons disease for the past 4 years. She had since been advised insulin therapy because of inadequate control of diabetes on oral hypoglycaemic agents. Her present admission was on account of generalised weakness of five days duration. She had history of similar episodes over the last six months. Each episode of flaccid quadriplegia was accompanied with depressed reflexes. There was no associated sensory loss. Blood biochemistry revealed hyperkalemia in the range of 5.7-6.5m Eq/1. In her previous admissions, she was diagnosed as hyperkalemic periodic paralysis and was treated with calcium and glucose/insulin infusion. During this admission, whilst she was having an episode of weakness, the nervous system examination revealed a flaccid paralysis with grade I/V weakness, along with reduced tone and absent reflexes. There was no evidence of sensory loss or myotonia. Rest of the general physical examination was normal apart from diabetic retinopathy. In between the episodes of weakness her nervous system examination was completely normal. Her blood glucose was 440mg/dl and the serum potassium was 6.8 mEq/1. The renal functions were mildly de-ranged and there was no evidence of acidosis or ketosis. The patient was treated with calcium and insulin infusion. Attempt to find a precipitating or stressful factor was unrewarding, the dose of steroids was appropriately increased. The patient responded satisfactorily and the blood glucose and serum potassium came within normal limits. During the remainder of the stay in the hospital, she developed four episodes of paralysis. During each of these episodes the same biochemical abnormality was repeatedly noticed. It was interesting to note that the hyperkalemia always followed an upsurge in the blood glucose levels. The patient was started on conti nuous intravenous insulin to which she responded by having no further episodes of weakness, or blood biochemical changes. Later she was switched to split dose of subcutaneous insulin and she remained symptom free and was sent home. She continued to improve in the follow-up period after repeated motivation to continue with the insulin regimen.

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