A 20-year-old male with severe gastroesophageal reflux resistant to high doses (60 mg/day) with a history of habitual cocaine consumption and large amounts of alcohol on weekends.
Upper digestive tract endoscopy showed severe colitis and suggestive images of a esophagogastritis.
Esophageal pH monitoring revealed an intense GER with a DeMeester score of 193 (normal range < 14.72) and normal man showed a lower esophageal sphincter pressure of 325 mmHg.
With these tests the patient was proposed to perform a laparoscopic Nissen fundoplication.
Prophylaxis of thromboembolism was performed with 2,500 I.U. of low molecular weight heparin (Clexane®, Aventis Pharma, Spain) one dose 2 hours before surgery and one daily dose in the first three postoperative days.
The pneumoperitoneum was performed with CO2 at a maximum controlled pressure of 14 mmHg.
A Nissen fundoplication with irreabsorbable material was performed, sutured the diaphragmatic pillars.
There were no incidents during the intervention that lasted 105 minutes.
The postoperative period was uneventful during the first 72 hours and the patient was discharged asymptomatic.
On the seventh postoperative day, after a heavy ingestion of alcohol, soft drinks and food, the patient developed sudden instability of the back and intense, hemodynamic hyperthermia, abdominal distension and abdominal distension.
Laboratory tests showed leukocytosis with left shift with 12% of falls, metabolic acidosis (pH: 7.27) and prothrombin activity of 52%.
Abdominal CT showed intestinal loops, intraabdominal fluid, stasis liver and suspected portal venous thrombosis.
With the diagnosis of acute abdomen surgically intervened finding massive intestinal ischemia of the entire small intestine and part of the small intestine, portal thrombosis, stasis liver and a non-obstructive thrombus in the colon was not explored.
Doppler ultrasound confirmed complete thrombosis and pneumatosis of the main trunk of the portal vein, and gas in the intestinal wall.
The hepatic arteries and mesentery were permeable.
No additional surgical procedures were considered indicated.
The hypercoagulability study was normal and it was not possible to obtain a reliable urine sample to detect cocaine.
The patient rapidly recovered unfavorably, despite the initiation of anticoagulant therapy with heparin, with hemodynamic instability and irreversible acidosis, dying 24 hours after surgery.
Necropsy confirmed the diagnosis of massive mesenteric vein and portal vein thrombosis with hemorrhagic infarction of the entire small intestine and right colon, with acute mucosal ulcers and acute intestinal lumen thrombosis.
Submassive hepatic hemorrhagic infarction, left ventricular hypertrophy and dilatation and focal microcalcifications in lung parenchyma (typical finding in chronic users of inhaled cocaine).
The cause of death was hypovolemic and hemorrhagic shock secondary to portal vein thrombosis.
