Scot Med J 1992; 37: 83-84
0036/9330/92/105911083 $2.00 in USA 1992 Scottish Medical Journal
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ALCOHOLISM, HVPONATRAEMIA AND CENTRAL NEUROLOGICAL DAMAGE: MORE THAN PONTINE MYELINOLYSIS?
DJ.A. Adamson. RB.S. Laing.D. Nathwani Wards 25/26, Aberdeen Royal Infirmary, Foresterhill, Aberdeen
Abstract: Three patients with alcoholism and severe hyponatraemia are described. Permanent neurological damage occurredin eachcasewithcerebral. cerebellar orpontine damagefrom infarction or haemorrhagefollowing correction of the biochemical disturbance. No patient developed Central Pontine Myelinolysis (CPMJ. the condition usually associated withprofoundhyponatraemia and its correction. Key words: Alcoholism, hyponatraemia, iatrogenic correction, permanent neurological damage.
Introduction evere hyponatraemia is an unusual and potentially fatal condition, the management of which is controversial.l,2 We describe three patients with severe hyponatraemia resulting from alcohol abuse who underwent rapid correction of their biochemical derangement. Neurological sequelae included damage to the cerebrum, cerebellum, or pons. Central Pontine Myelinolysis (CPM) did not arise in any patient. We suggest that hyponatraemia and/or its treatment may result in unpredictable and diverse neurological damage other than the pontine demyelinatin!l lesions previously regarded as characteristic of this condition ."3-7
S
Case reports Case 1. A 33 year old man with a three year history of alcohol abuse was admitted to psychiatric care with the alcohol withdrawal syndrome characterised by increasing confusion and stupor. On admission his serum sodium was 104nunolll and potassium 1.4mmolll with a metabolic alkalosis (pH 7.64). He was immediately transferred to a medical unit where his Glasgow Coma Scale (GCS) score was nine - there was no focal neurological deficit. Blood pressure was 130n5 and clinical assessment of the cardiovascular system revealed no abnormality. The resting ECG was consistent with hypokalaemia. Urinary osmolality and sodium were 567mOsmlkg and 24nunoVl respectively and the serum osmolality was 221mOsmlkg. Liver function tests showed bilirubin 26umolll [
0036/9330/92/105911083 $2.00 in USA 1992 Scottish Medical Journal
~
ALCOHOLISM, HVPONATRAEMIA AND CENTRAL NEUROLOGICAL DAMAGE: MORE THAN PONTINE MYELINOLYSIS?
DJ.A. Adamson. RB.S. Laing.D. Nathwani Wards 25/26, Aberdeen Royal Infirmary, Foresterhill, Aberdeen
Abstract: Three patients with alcoholism and severe hyponatraemia are described. Permanent neurological damage occurredin eachcasewithcerebral. cerebellar orpontine damagefrom infarction or haemorrhagefollowing correction of the biochemical disturbance. No patient developed Central Pontine Myelinolysis (CPMJ. the condition usually associated withprofoundhyponatraemia and its correction. Key words: Alcoholism, hyponatraemia, iatrogenic correction, permanent neurological damage.
Introduction evere hyponatraemia is an unusual and potentially fatal condition, the management of which is controversial.l,2 We describe three patients with severe hyponatraemia resulting from alcohol abuse who underwent rapid correction of their biochemical derangement. Neurological sequelae included damage to the cerebrum, cerebellum, or pons. Central Pontine Myelinolysis (CPM) did not arise in any patient. We suggest that hyponatraemia and/or its treatment may result in unpredictable and diverse neurological damage other than the pontine demyelinatin!l lesions previously regarded as characteristic of this condition ."3-7
S
Case reports Case 1. A 33 year old man with a three year history of alcohol abuse was admitted to psychiatric care with the alcohol withdrawal syndrome characterised by increasing confusion and stupor. On admission his serum sodium was 104nunolll and potassium 1.4mmolll with a metabolic alkalosis (pH 7.64). He was immediately transferred to a medical unit where his Glasgow Coma Scale (GCS) score was nine - there was no focal neurological deficit. Blood pressure was 130n5 and clinical assessment of the cardiovascular system revealed no abnormality. The resting ECG was consistent with hypokalaemia. Urinary osmolality and sodium were 567mOsmlkg and 24nunoVl respectively and the serum osmolality was 221mOsmlkg. Liver function tests showed bilirubin 26umolll [
