A 57-year-old male with a history of chronic active alcoholism and secondary alcoholic liver disease, who required prior admission to the Psychiatric Acute Unit due to a manic condition related to alcohol intake.
He was admitted to Neurology from the emergency department for a week of progressive deterioration with impossibility of a standing position and decreased level of consciousness in the last 24 hours.
The patient was afflicted with TA of 120/75 mmHg, tachycardic, tachypneic and jaundice.
Cardiopulmonary auscultation was normal.
Neurologically, he had somnolence, mild bilateral mydriasis, bilateral facial weakness with normal cranial nerves, muscle weakness in the four limbs (lack of cooperation to balance) and generalized hyporeflexia.
No tremor or agitation were observed.
The emergency laboratory tests showed high blood glucose (233 mg/dL), normal renal function, hypokalemia, metabolic acidosis with normal lactate and respiratory alkalosis (pH: 7.3, bicarbonate: 11.9 mmol/L, 2.8 mmol/L).
Treatment was initiated with intravenous hydration (5% dextrose and saline), potassium replacement (K), administration of thiamine parenterally and hepatic antiencephalopathy measures.
The neurological status of the patient was similar in the inpatient ward.
Analytical control showed worsening of hypokalemia, severe hypophosphatemia, mild hypomagnesemia, hypernatremia, persistent acid-base balance disorders, and presence of methylketone in
We do not have chlorine levels at admission for the calculation of anion GAP, nor for the collection of fecal samples.
The electrocardiogram showed sinus rhythm and no abnormalities associated with electrolyte deficits.
At that time, the Nutrition Unit was consulted to collaborate in the management of the patient.
Hydration was continued only with 5% dextrose, without saline solution, the administration of parenteral thiamine was maintained, already initiated in the emergency room at a dose of 100 mg/day, and an aggressive intravenous replacement was performed.
Initially, 40 mmol of potassium phosphate was administered within 6 hours (corresponding in our case to about 0.55 mmol of P/kg of weight), after which a 24-hour infusion of potassium chloride (3 mEq/kg of potassium chloride) was initiated with 140 mEq/kg of
At the end of this period, acid-base balance abnormalities and hypernatremia had been corrected.
However, it was necessary to maintain this high rate of replacement of P (0.55 mmol of P/kg/day) and K (2 mEq of K/kg/day between potassium chloride and potassium phosphate) for 72 hours to achieve its normalization.
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 contributions.
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Simultaneously, the Neurology Department continued with diagnostic studies.
Computed tomography showed no evidence of acute endocraneal pathology, although there were evident signs of corticosubcortical deficiency.
The fluid had a slightly cephalometric appearance without severe cephalomotor activity, without cells, glucose 101 mg/dL, protein 95 mg/dL, and Adenosine deaminase 5.5 IU/L. The EEG showed focal evidence
At discharge, the patient was fully alert, with weakness 4/5 in the upper limbs and lower limbs.
Definitive diagnoses were: alcoholic sensitive ketoosis (AAC), severe hypokalemia and hypokalemia, mild hypomagnesemia, confusional state and severe polyneuro-motor atrioventricular septal defect.
