Incarcerated paraesophageal hernia complicated by pancreatic damage and unusual comorbidity: Two retrospective case series.

Autor: Haug, H.M., Johnson, E., Mala, T., Førland, D.T., Søvik, T.T., Johannessen, H.O.
Zdroj: International Journal of Surgery Case Reports; 2019, Vol. 54, p75-78, 4p
Abstrakt: Highlights • We present two cases of paraesophageal hernia that both needed total gastrectomy due to gangrene. • Both patients had clinical relevant comorbidities, respectively trisomy 21 and hereditary spastic paresis. • Due to compression from the dilated stomach one of the patients developed ischemia of the pancreas with leakage of peptidases which in turn caused anastomotic dehisence and intraabdominal abscess. • The pancreatic damage and anastomotic leakage was treated conservatively with repeated stenting and percutaeous drainage. • Immediate diagnosis and treatment for incarcerated paraesophageal hernias are vital to reduce morbidity and mortality. Abstract Introduction: About 1% of paraesophageal hernias (PEH) require emergency surgery due to obstruction or gangrene. We present two complicated cases of incarcerated PEH. Presentation of cases: A patient aged 18 with trisomy 21 was admitted after four days of vomiting and epigastric pain. CT scan revealed a large PEH. The stomach was massively dilated with compression of adjacent viscera and the celiac trunk. The stomach was repositioned laparoscopically and deflated by endoscopy in an attempt to avoid resection. During second look laparoscopy a gastrectomy was necessary. The patient was reoperated for intestinal obstruction, and treated for dehiscence of the esophagojejunostomy and a pancreatic fistula. A patient aged 65 with hereditary spastic paresis had two days history of emesis and epigastric pain. Upon arrival he was hemodynamically unstable and a CT scan revealed perforation of the herniated stomach. A subtotal gastrectomy without reconstruction was performed with vacuum closure of the abdomen. Later a gastrectomy was completed with a Roux-en-Y reconstruction. Except from reoperation for wound dehiscence after 14 days, the recovery was uneventful. Discussion: Trisomy 21 and hereditary spastic paresis may increase the risk of developing PEH. Challenges in regard to symptom evaluation may delay diagnosis. The pressure of the dilated stomach can give rise to ischemic and mechanical damage from compression of major blood vessels and organs. Urgent diagnosis and gastric deflation is required. Conclusions: In patients with known PEH or with comorbidity that may increase the risk of PEH, this diagnosis should be considered early on. [ABSTRACT FROM AUTHOR]
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