We report the case of an 84-year-old woman who presented with progressive lower limb edema (one year of evolution), with the appearance of erythema and blistering lesions in the two months prior to admission.
The patient's history included only type 2 diabetes mellitus under oral antidiabetic treatment.
She had undergone a subcapital fracture of the right hip and left inguinal hernia repair one year before admission (without intestinal resection).
In the directed anamnesis, the patient reported an altered intestinal rhythm after previous herniorrhaphy, with episodes of constipation alternating with other episodes of diarrhea consulted due to the fact that we had not drunk and increased abdominal perimeter,
Location site: 8 kg.
She did not report abdominal pain.
Upon arrival at our hospital, the patient had a blood pressure of 100/57 mmHg, temperature of 2oC, and heart rate of 90 bpm.
Capillary glycemia 80 mg/dl showed poor nutritional status (weight 36 kg, body mass index 16).
The jugular venous pressure and the cardiopulmonary auscultation were normal and the abdomen was slightly distended, tympanic, with increased sounds, hydrocephalus and no masses or organomegaly.
The lower limbs presented edema with fovea up to the knee, accompanied by phlogistic signs and blistering, some of them eroded.
In the initial tests, normocytic normochromatic anemia of 10.7 g/dl was noteworthy, with preservation of the rest of the series.
The erythrocyte sedimentation rate was 52 mm and the biochemistry only showed hypoproteinemia and hypoalbuminemia (total proteins 4.31 g/dl, serum albumin 1.99 g/dl).
The chest X-ray, electrocardiogram and echocardiogram performed, reasonably ruled out the existence of heart disease.
There was also no nephropathy or proteinuria.
The suspicion of protein loss of digestive origin and the semiology of abdominal exploration, abdominal radiography and abdominal CT with intravenous contrast were performed.
After clinical manifestations, treatment was initiated with total parenteral nutrition and intestinal obstruction with nasogastric tube.
The subsequent surgical treatment was diagnostic and therapeutic.
Laparotomy revealed a 20 cm stenosed intestinal loop (jejunal), which was resected and thermo-terminal anastomosis was performed.
The anatomopathological study ruled out a neoformative process or acute focal ischemia, being informed as a segmental mucosal and mural infarction, with dense chronic inflammatory infiltrate of lymphoplasmacytic type, prior to the theoretical intervention zone.
The patient was discharged, asymptomatic, ten days after admission.
At that time, serum albumin was 2.52 g/dl, and 5 months later, upon outpatient review, 3.83 g/dl.
The final diagnosis was malalignment secondary to intestinal stenosis.
