A 56-year-old man, who underwent right hemicolectomy-igmodectomy and terminal urticaria due to complicated colitis in 2003.
In 2004, bowel closure was performed and intestinal transit reconstruction was performed with good outcome.
6 years later he required ileal resection (100 cm) and construction of a definitive ileostomy due to intestinal obstruction due to adhesion syndrome that complicated after resection and initial anastomosis.
Five months after the ileostomy, the patient came to the emergency room due to an episode of sudden onset of tonic-clonic seizures and deviation of the oral commissure to the right.
Cranial CT, cranial MRI, ECG and chest X-ray showed no significant findings.
Laboratory data revealed hypoptasaemia, hypocalcaemia and hypomagnesaemia.
IV treatment was initiated with serum therapy/electrolytes for rehydration and correction of deficits and consultation with the Nutrition and Digestive Unit was requested.
During the nutritional assessment a very significant weight loss was observed in the last 3 months (12%).
Physical examination revealed loss of subcutaneous fat and muscle mass, absence of edema, and signs or symptoms of specific mental retardation.
The diet history shows good appetite with sufficient intake of a normal diet, with an ileostomy output of approximately 2,500 ml/day.
Nutritional status was compatible with moderate protein-energy malnutrition.
The patient was prescribed an absolute diet and started treatment with loperamide, feces suppression, parenteral nutrition via central route, with the therapeutic objective of reducing intestinal losses of water and electrolytes and total volume of stools.
After 7 days of treatment the output by the Ileostomy was reduced to 1,000 ml/day, so that oral tolerance is initiated and transition to soft oral diet poor residue supplemented with polymeric formula 2500 k isocal.
During the stay in IM she did not present new episodes of crisis or neurological focality highlighting an improvement in the nutrometabolic state.
The treatment at discharge consisted of: soft diet poor in residues supplemented with polymeric formula, 12 mg/d loperamide loperamide, 8 g/d and 10 ml of pidolate magnificent.
In a subsequent review during an outpatient visit, a further decrease in plasma magnesium (1.2 mg/dl) was observed, thus increasing the dose to 64 mEq/d.
At 15 days, the patient came to the clinic with recurrence of neurological symptoms.
Analytical analysis revealed Mg of 0.5 mg/dl, with hypokalemia and hypocalcemia, requiring rehospitalization for altered perfusion IV.
After analytical recovery, the patient is discharged with an increase in oral dose of Mg to 80 mEq/d, modification of loperamide by codeine (90 mg/d) and vitamin D supplementation (0.25 mcg/d).
During the following 3 months, the patient has required strict controls (every 15 days) of magnesemia and intravenous infusion on several occasions.
It has only been until normalization of output by ilestomy and intestinal adaptation, when magnesemia has been maintained in safe ranges.
Currently the patient has a good general condition and complete elimination of diarrhea (3 stools formed/d), so the diet has been extended including the incorporation of new foods.
It has gained 13 kg throughout the period and has been 4 months without the need for intravenous magnesium infusion, maintaining an oral dose of 80 mEq/d with good tolerance.
