Sixty-three year old woman with a personal history of kyphoscoliosis, restrictive respiratory insufficiency and diverticulosis.
The patient presented with peritonitis secondary to perforated diverticulitis, treated with the Hart-mann technique. Postoperatively, she developed an entero-cutaneous fistula, treated with oral enteral nutrition. Given her refusal to undergo surgery, she was discharged with this treatment, when she presented a debit of 200 ml/day, and periodic outpatient check-ups were scheduled, which she did not attend.
Three months later, she went to the emergency department for presenting in the previous days with asthenia, anorexia, nausea, dizziness, abdominal pain, decreased stool output through the colostomy and a significant increase in fistula output, sometimes with a haematic appearance. He was afebrile, with a BP of 85/50 mmHg and presented with diffuse pain on abdominal palpation. During his stay in the ED, he presented a decreased level of consciousness that improved after administration of intravenous fluids.
Laboratory tests showed: haemoglobin 12.3 g/dl; leucocytes 10,400/mm3; glycaemia 102 mg/dl; urea 426 mg/dl; creatinine 2.9 mg/dl; total protein 9.3 g/dl; Ca 10.5 mg/dl; Na 104 mEq/l; K 6.9 mEq/l; Cl 73 mEq/l; HCO3 17 mmol/l; urinary Na 6 mEq/l. She was diagnosed with dehydration, acute renal failure, metabolic acidosis, severe hyponatraemia and hyperkalaemia. Given the suspicion of acute adrenal insufficiency, treatment was started with hydrocortisone and continued with IV fluid replacement, with good clinical and analytical response. Subsequent blood tests showed a drop in haemoglobin concentration to 7.6 g/dl and she received a transfusion of two red blood cell concentrates.
She was admitted to internal medicine and subsequently transferred to surgery with a diagnosis of intestinal obstruction. On the sixth day of admission she was started on parenteral nutrition. The patient was fully conscious, haemodynamically stable, without oedema and renal function, hyponatraemia and hyperkalaemia had normalised. She weighed 68 kg and was 145 cm tall (BMI 32 kg/m2). The composition of the TPN was: total volume 2500 ml, 1500 kcal, N 11 g, glucose 200 g, lipids 40 g, Na 120 mEq, K 60 mEq, Mg 15 mEq, P 15 mEq, Zn 12 mg, Ca 12 mEq. The following day the patient reported paresthesia in the hands and perioral region. Thiamine i.m. was administered empirically. A few hours later, she began to present a picture of decreased level of consciousness and bradypsychia, with preserved motility in the extremities. The clinical picture progressed during the following day, presenting with a fluctuating level of consciousness deterioration, with aphasia and paraparesis in MSI and becoming stuporous. She was afebrile and her blood pressure was 130/70 mmHg. NTP was discontinued, she was maintained on serum therapy and empirical vitamin supplementation. Head CT scan was normal. She was transferred to the ICU and, given the suspicion of metabolic encephalopathy, an EEG was performed, which showed non-convulsive status epilepticus, and treatment with IV phenytoin was started. Laboratory tests showed: Hb 10.7 g/l; 12,800 leukocytes with 71.5% granulocytes; glycaemia 91 mg/dl; creatinine 0.5 mg/dl; Na 143 mEq/l; K 2.6 mEq/l; P 0.5 mg/dl; Mg 1.5 mg/dl; CPK 31 UI/l. The ECG showed no arrhythmias. Arterial blood gas analysis was similar to the previous one.
She was diagnosed with severe hypophosphataemia with hypomagnesaemia and hypokalaemia. Phosphate salts were administered i.v., as well as magnesium and potassium, with good clinical response, progressively improving the neurological situation until normalisation. She was again transferred to surgery and parenteral nutrition was restarted, progressively increasing the caloric intake and with a higher intake of phosphorus, magnesium and potassium. During her admission she also presented several complications: phenytoin intoxication with neurological symptoms, and sepsis due to Candida spp. related to the central catheter, from which she recovered without sequelae. Oral enteral nutrition and modified oral diet were progressively introduced and TPN and IV fluids were discontinued. Since the diagnosis of adrenal insufficiency was not confirmed and there was significant dehydration on admission that could explain the analytical alterations, corticosteroids were progressively decreased until they were discontinued, without the appearance of symptoms or signs of adrenal insufficiency. Cortisol after ACTH stimulation (250 mg) was 43.9 µg/dl at 30 minutes, reflecting a normal adrenal reserve.
The patient refused intestinal transit reconstruction surgery. Enterocutaneous fistula persisted with a debit of approximately 300 cc/day. The patient was discharged with good clinical and analytical status.
Table I shows the evolution of phosphorus, magnesium and potassium levels during admission.