Focal Neurologic Signs Associated With Hyperkalemia K. STUART LEE, MD, BAYARD L. POWELL, MD, and PATRICIA L. ADAMS, MD, Winston-Salem, NG HYPERKALEMIA is a common electrolyte disturbance in patients with chronic renal disease. Muscle weak- ness or paralysis is a relatively common manifestation of hyperkalemia. The patient usually presents diffuse lower extremity weakness or an ascending paralysis; focal weakness, on the other hand, is uncommon. We report a case of focal neurologic deficit associated with severe hyperkalemia in a patient with chronic renal disease. CASE REPORT An 81-year-old man with end-stage renal disease due to hyper- tension was admitted to the hospital with malaise and persistently elevated BUN and creatinine values despite thrice weekly home peritoneal dialysis. He had a history of mild angina and mild congestive heart failure, but no transient ischemic attacks (TIAs) or strokes, At the time of admission, he had grade 2 hypertensive ret- inopathy and a grade 2/6 systolic murmur heard along the left ster- nal border. Neurologic and neurovascular examinations yielded normal findings. Scrum values were sodium 136 mEq/L, potassium 4.0 mEq/L, chloride 93 mEq/L, CO, 15 mEq/L, urea nitrogen (BUN) 97 mg/dl, glucose 106 mg/dl, and creatinine 40,8 mg/dl. Several days after admission, the patient became lethargic, but was arousable; he was oriented only to person. His pulse rate was 72 beats/ min and regular, and blood pressure 180/90 mm Hg. He had a flac- cid right hemiparesis, right facial weakness, deviation of the tongue to the right, and dysarthria. Deep tendon reflexes were absent on the right side, 2+ on the left side. Sensation of light touch and pin prick was intact. Arterial blood gas values were pH 7.29, Pco, 28 mm Hg, Po, 83 mm Hg, and HCO, 13.1 mEq/L. Serum electrolyte values were sodium 135 mEq/L, potassium 9.3 mEq/L, chloride 1 !4 mEq/L, CO, 11.9 mEq/L, and glucose 106 mg/dl. BUN and creatinine values were 59 mg/dl and 32.1 mg/dl respectively. The serum potassium deter- mination was repeated within an hour and showed a value of 9.9 mEq/L. Electrocardiography showed tall peaked T waves consistent with a diagnosis of hyperkalemia, Because the patient’s poor condition did not permit emergency hemodialysis, he was given several intravenous injections of 50% dextrose and insulin as well as sodium polystyrene sulfonate (Kay- exalate, a cation exchange resin) via nasogastric tube and rectally, and peritoneal dialysis was begun. Within four hours, the serum potassium value was 7.1 mEq/L, and he had only mild residual right- sided weakness; BUN and creatinine values were 57 and 28.4 mg/dl respectively. Within 12 hours of the start of therapy, the serum potassium value was 5.0 mEq/L; but despite 16 two-liter exchanges of peritoneal dialysate, the BUN value was 44 mg/dl and the creat- inine value 25.5 mg/dl. There was total reversal of the neurologic deficit, and he was alert and talkative. From the Section on Neurosurgery. Department of Surgery (Dr. Lee); Department of Medicine (Dr. Powell); and the Section on cphrology, Department of Medicine (Dr. Adams), Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC, Reprint requests to K. Stuart Lee, MD, Section on Neurosurgery, Bowman Gray School of Medicine, 300 S Hawthorne Rd, Winston-Salem, NC 27103. The patient's malaise continued to diminish, and he was dis- charged several days after the episode of focal neurologic deficit. The serum potassium value was within normal limits at the time of dis- charge. Although the patient received peritoneal dialysis every other day while in the hospital, the BUN value remained at 44 mg/dl and the creatinine value was 33.3 mg/dl on the day he was discharged. He was readmitted several months later because of severe nausea and vomiting, which were thought to be due to persistent uremia. The decision was made to begin chronic hemodialysis. During this admission, B-mode ultrasonic studies of the carotid arteries showed mild atherosclerotic plaque formation at the origin of the right internal carotid artery and severe atherosclerotic plaque formation at the origin of the left internal carotid artery. Despite those wor- risome findings, the patient has had no further episodes of neuro- logic deficit over 14 months of follow-up. DISCUSSION Neurologic disorders are common with chronic renal failure because of uremia itself, deranged metabolic parameters, or associated diseases such as hyperten- sion or atherosclerosis. In all but the latter, the expected presentation is a symmetrical deficit that usually resolves with correction of the underlying dis- ease. Our patient had all of the processes operative that would lead one to expect bilateral nervous system dis- ease, and yet a focal unilateral neurologic deficit developed. How might this presentation be explained? First, focal motor deficits have been reported in patients with renal disease and uremia. Sir William Osler! described spontaneous monoplegias and hem- iplegias in patients with chronic renal disease who had no gross lesions of the brain postmortem. Locke et al? noted transient hemiplegias in several patients with renal failure, two of whom had acute renal failure and were undergoing dialysis. Both of those patients had intermittently elevated serum potassium values, but no correlation could be made between the onset of the hemiplegia or reflex changes and any change in blood chemistry values. Knutson and Baker* stated that transient flaccid paralysis is relatively common in con- junction with uremia and described it in two patients. Plum and Posner' reported hemiparesis in ten of 45 patients with uremia and noted that the hemiparesis often cleared rapidly with dialysis. Thus, although our patient’s neurologic deficit could have been due to uremia, several factors argue against it. The patient had not had a similar episode of neu- rologic deficit over the several weeks before his admis- 792 dune 1984 e SOUTHERN MEDICAL JOURNAL © Vol77, No.6 sion to the hospital while he was being followed up for significant uremia. He was indeed uremic during his episode of neurologic dysfunction, but his BUN and serum creatinine values were lower at that time than when he had been admitted. Those values did improve slightly after peritoneal dialysis was begun during his episode of hyperkalemia and hemiparesis; however, although the peritoneal dialysis exchanges lasted longer than 12 hours, the neurologic signs had improved within four hours after glucose, insulin, and Kayexalate were given. Finally, the serum potassium level was the only metabolic variable to change acutely during the paralytic episode. When these factors are considered, it seems an oversimplification to attribute this episode of hemiparesis solely to the patient’s chronic uremia. Second, this patient did have a long history of hypertension, and he did have evidence of cerebro- vascular disease on noninvasive testing. Thus, itis pos- sible that his hemiparesis represented a transient ischemic attack (TIA) caused by an embolus from the left internal carotid artery. As noted, however, he had had no prior TIAs, nor has he had further episodes of neurologic deficit. His only known episode of neuro- logic dysfunction was accompanied by severe hyperkalemia. Third, there are many reports of muscle weakness or paralysis associated with hyperkalemia. The syn- drome of hyperkalemic periodic paralysis is a well rec- ognized example.5 An ascending paralysis resembling the Landry-Guillain-Barré syndrome has also been described in patients with hyperkalemia resulting from acute obstructive renal failure,® chronic renal failure,’ Addison’s disease,*'" and spironolactone therapy."! The paralysis in each of these patients resolved with treatment of the hyperkalemia, but in all cases the paralysis was a symmetrical weakness with loss of deep tendon reflexes. The neurologic deficit in our patient with hyperkalemia was unilateral and associated with preservation of deep tendon reflexes on the contralat- eral side. Therefore, we suggest an alternative expla- nation for his clinical course. It has been shown clinically and experimentally that localized areas of vascular insufficiency in the brain may be more sensitive to metabolic changes than areas with normal perfusion.'? After treating several hypo- glycemic patients with apparent localized cerebral lesons that resolved with treatment of the hypogly- cemia, Meyer and Portnoy’ studied the phenomenon in cats and monkeys by ligating the middle cerebral artery to produce hemiparesis. When the animals had recovered from the hemiparesis, the authors injected insulin and produced a hemiparesis on the side con- tralateral to the middle cerebral artery ligation. Treat- ment with intravenous glucose led to a rapid reversal of the neurologic deficit. Meyer and Portnoy there- Lee et al fore hypothesized that hypoglycemia in an area of greater cerebral ischemia than surrounding brain tis- sue might cause localized, reversible neuronal dys- function. Similar findings were observed in dogs undergoing ligation of the middle cerebral artery and then being subjected to systemic hyponatremia." The hyponatremia produced a hemiparesis contralateral to the middle cerebral artery ligation, and reversal of the hyponatremia led to rapid recovery. Portnoy!’ reported a case of an apparent TIA in a diabetic, hypoglycemic patient with stenosis of the internal carotid artery contralateral to the hemiparesis. The patient’s neurologic deficit improved rapidly when glucose was given. It is thus well documented that focal neurologic def- icit can follow partial or total occlusion of an intra- cranial or extracranial vessel and an accompanying metabolic abnormality. Although we can find no stud- ies using potassium similar to those cited using glucose or sodium, it is probable that our patient’s neurologic deficit can be explained by his left internal carotid artery stenosis and the superimposed hyperkalemia. SUMMARY A patient with end-stage renal disease had a flaccid hemiparesis in conjunction with severe hyperkalemia. The hemiparesis resolved with treatment of the hyperkalemia. The patient was later found to have extracranial vascular disease, and we propose that a severe metabolic abnormality associated with an area of relative cerebral ischemia caused the reversible neurologic deficit. References 1. Osler W: The Principles and Practice of Medicine. New York, Appleton-Cen- tury-Crofis Inc, 1892, p 738 . Locke S, Merrill. Tyler HR: Neurologic complications of acute uremia. Arch Intern Med 68: 19-529, 1961 . Knutson J, Baker AB: The central nervous system in uremia. Arch Neural Psychiatry 54: 130-140, 1945 . . Plum F, Posner JB: The Diagnosis of Stupor and Coma, Philadelphia, FA Davis Co, 1980, p 22 . Brooke MH: A Clinician's View of Neuromuscular Diseases, Baltimore, Wil- liams & Wilkins Co, 1977, pp 186-189 . 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Nenad 8:601-614, 1958 ype 14, Faris AA, Poser CM: Experimental production of focal neurologic deficit by systemic hyponatremia, Neurology 14:206-211, 1964 15, Portnoy HD: Transient “ischemic” attacks produced by carotid stenosis and hypoglycemia. Neurology 15:830-832, 1965 @ FOCAL NEUROLOGIC SIGNS AND HYPERKALEMIA 793