ABSTRACT
The HELLP syndrome (haemolysis, elevated liver blood tests and low platelets) is a serious complication in pregnancy characterized by haemolysis, elevated liver enzymes and low platelet count occurring in 0.5 to 0.9% of all pregnancies and in 10-20% of cases with severe preeclampsia. Hepatic capsular rupture is a rare yet dramatic complication of HELLP syndrome. The majority of cases occur in multiparous women over the age of 30. Classically it presents with acute onset right upper quadrant pain in the presence of constitutional symptoms such as vomiting and pyrexia. However, symptoms and signs are usually non specific. Spontaneous hepatic rupture can be preceded by signs of hypovolaemic shock; yet the diagnosis is infrequently made prior to emergent laparotomy. We present the case of a 35 year old nulliparous woman with a second trimester gestational hepatic rupture associated with HELLP syndrome. We briefly discuss the aetiology, diagnostic difficulties and treatment options associated with this rare presentation.
ABSTRACT
Diaphragmatic rupture due to trauma is both well recognised and uncommon. The difficulties in diagnosing traumatic diaphragmatic rupture at the first admission are the most common causes of latent morbidity and mortality. Herniation of the abdominal viscera is the most common sequel with strangulation and perforation the most serious complication. This case outlines the delayed presentation of diaphragmatic rupture and herniation presenting as an acute tension faecopneumothorax. We review the relevant literature, with particular emphasis on the difficulties in diagnosis at presentation.
ABSTRACT
BACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.
