A 57-year-old man with a history of chronic active alcoholism and secondary alcoholic liver disease, who had previously been admitted to the Acute Psychiatric Unit for manic symptoms related to alcohol intake. He was admitted to Neurology from the emergency department due to clinical symptoms of progressive deterioration over a week's time, with the impossibility of bipe-destation and a decrease in the level of consciousness in the last 24 hours. The patient was afebrile, with a BP of 120/75 mmHg, tachycardic, tachypneic and icteric. Cardiopulmonary auscultation was normal. Neurologically, he presented somnolence, mild bilateral mydriasis, bilateral facial weakness with the rest of the cranial nerves normal, muscle weakness in all four limbs (lack of cooperation for balance) and generalised hyporeflexia. No tremor or agitation was observed. Emergency laboratory tests showed elevated blood glucose (233 mg/dL), normal renal function, hypokalaemia, metabolic acidosis with normal lactate and respiratory alkalosis (pH: 7.3, bicarbonate: 11.9 mmol/L, base excess: -14.4 mmol/L, pO2: 104 mmHg, pCO2: 24 mmHg, lactate: 2.8 mmol/L). Treatment was started with intravenous hydration (5% dextrose and saline), potassium (K) replacement, parenteral thiamine administration and hepatic anti-encephalopathy measures. On the hospital ward, the patient's neurological condition was similar. Laboratory tests showed worsening hypokalaemia, severe hypo-phosphataemia, mild hypomagnesaemia, hypernatraemia, persistent acid-base balance disturbances and the presence of methylketone in urine. We do not have chlorine levels on admission to calculate the GAP anion, nor ketone bodies in the blood. The electrocardiogram corresponded to sinus rhythm and showed no alterations associated with electrolyte deficits.
At that time, the Nutrition Unit was consulted to assist in the management of the patient. Hydration was continued with 5% dextrose only, without saline, the administration of parenteral thiamine already started in the ED was maintained at a dose of 100 mg/day and aggressive replacement of the different deficits was carried out intravenously. Initially, 40 mmol of monopotassium phosphate was administered in 6 hours (corresponding in our case to about 0.55 mmol of P/kg body weight), after which a 5% glucose perfusion with 140 mEq of potassium chloride (2 mEq of K/kg body weight) and 24 mEq of Mg (3 g of magnesium sulphate) was prescribed over the following 24 hours. By the end of this period the acid-base balance abnormalities and hypernatraemia had been corrected. However, it was necessary to maintain this high replacement rate of P (0.55 mmol P/kg/day) and K (2 mEq K/kg/day between potassium chloride and monopotassium phosphate) for 72 hours to achieve normalisation. Figure 1 shows the daily evolution of serum K, P and Mg levels until complete correction. The analytical improvement was accompanied by clinical improvement, which allowed oral supplementation with progressive withdrawal of parenteral intake.

Simultaneously, the Neurology Department continued to carry out diagnostic studies. Computerised axial tomography showed no evidence of acute endocranial pathology, although there were clear signs of corticosubcortical atrophy. The cerebrospinal fluid had a slightly xanthochromic appearance, without cells, with glucose 101 mg/dL, protein 95 mg/dL, and Adenosine deaminase 5.5 IU/L. The electroencephalogram showed rapid low-voltage baseline activity, without asymmetries, focality or triphasic components; and the electromyogram suggested severe axonal predominant polyradicular sensory-motor involvement of the lower extremities (LES) and mild involvement of the upper extremities (EESS).
At the time of discharge the patient was fully alert, with weakness 4/5 in EESS and EEII. Definitive diagnoses were: alcoholic ketoacidosis (AKA), severe hypophosphataemia and hypokalaemia, mild hypomagnesaemia, and confusional syndrome and acute axonal sensory-motor polyradiculoneuritis secondary to severe hypophosphataemia.