Causes of sudden death related to oesophageal carcinoma

Two cases of recently diagnosed oesophageal squamous-cell carcinomas in men, both aged 72 years, are reported that resulted in rapid clinical deterioration and death from upper-airway occlusion and haemorrhage, respectively. In the first case, direct growth of the tumour from metastatic deposits in the paratracheal lymph nodes through the wall of the trachea resulted in lethal acute airway occlusion. In the second case, local extension of the tumour through the wall of the oesophagus into the adjacent aorta resulted in an aorto-oesophageal fistula which led to catastrophic and fatal haemorrhage. Although rare, oesophageal squamous-cell carcinomas may cause unexpected death due to quite different mechanisms, and result in the need for a detailed medico-legal assessment.

Diaphragmatic lesions and fatal haemorrhage in Texel sheep

Twelve Texel sheep were found to have diaphragmatic lesions, with or without thoracic haemorrhage, at postmortem examination over a period of two-and-a-half years. Presenting clinical signs ranged from general malaise or mild respiratory stertor, to severe acute respiratory distress or sudden death. Gross postmortem findings included focal areas of diaphragmatic haemorrhage, diaphragmatic musculature necrosis or diaphragmatic rupture with herniation of abdominal viscera into the thoracic cavity. In some cases, acute severe fatal haemorrhage from either thoracic vessels or the diaphragmatic lesions was observed. Histopathology confirmed an acute event leading to the sudden death of affected animals, but also suggested a pre-existing chronic degenerative lesion of unknown aetiology affecting the diaphragmatic muscle. This case report suggests diaphragmatic lesions, with or without fatal thoracic haemorrhage, as a differential for respiratory distress or sudden death in young Texel sheep.

Surgical Management of Recurrent Cervico-Vaginal Prolapse by Ovario-Hysterectomy in Stray Cows: A Report of 12 Cases

Pre and postpartum genital prolapse in cows is often a chronic and recurrent condition. Cervicovaginal prolapse is a very painful and serious condition due to which most of the animals undergo severe straining and may become recumbent. It is assumed that the occurrence of prolapse has a genetic predisposition in both cattle and sheep. It is regarded as an emergency condition and should be managed before excessive oedema, mucosal trauma, contamination and fatal haemorrhage lead to a grave prognosis.

Clinical picture of heparin-induced thrombocytopenia (HIT) and its differentiation from non-HIT thrombocytopenia

SummaryHIT is an acquired antibody-mediated disorder strongly associated with thrombosis, including microthrombosis secondary to disseminated intravascular dissemination (DIC). The clinical features of HIT are reviewed from the perspective of the 4Ts scoring system for HIT, which emphasises its characteristic timing of onset of thrombocytopenia. HIT antibodies recognize multimolecular complexes of platelet factor 4 (PF4)/heparin. However, a subset of HIT sera recognise PF4 bound to platelet chondroitin sulfate; these antibodies activate platelets in vitro and in vivo even in the absence of heparin, thus explaining: delayed-onset HIT (where HIT begins or worsens after stopping heparin); persisting HIT (where HIT takes several weeks to recover); spontaneous HIT syndrome (a disorder clinically and serologically resembling HIT but without proximate heparin exposure); and fondaparinux-associated HIT (four distinct syndromes featuring thrombocytopenia that begins or worsens during treatment with fondaparinux), with a new patient case presented with ongoing thrombocytopenia (and fatal haemorrhage) during treatment of HIT with fondaparinux, with fondaparinux-dependent platelet activation induced by patient serum (“fondaparinux cross-reactivity”). Ironically, despite existence of fondaparinux-associated HIT, this pentasaccharide anticoagulant is a frequent treatment for HIT (including one used by the author). HIT can be confused with other disorders, including those with a) timing similar to HIT (e. g. abciximab-associated thrombocytopenia of delayed-onset); b) combined thrombocytopenia/thrombosis (e. g. symmetrical peripheral gangrene secondary to acute DIC and shock liver); and c) both timing of onset and thrombosis (e. g. warfarin-associated venous limb gangrene complicating cancer-associated DIC). By understanding clinical and pathophysiological similarities and differences between HIT and non-HIT mimicking disorders, the clinician is better able to make the correct diagnosis.