The pathophysiology of endotoxaemia, a leading cause of death in the horse, is beginning to be understood in greater detail. Endotoxin may be absorbed into the systemic circulation in a number of different ways: most commonly the body's normal defense mechanisms are disrupted or bypassed, or the normal clearance mechanisms overwhelmed. Following this wide-spread effects are observed, although the most significant are seen in the cardiovascular system. Fever, arterial hypoxaemia and signs of abdominal pain are also common. With increased understanding of the disease new therapeutic agents have become available, however, while the newer agents offer some advantages it is important to recognise that supportive care is the mainstay of treatment for endotoxaemia. Supportive care consists of aggressive fluid therapy (crystalloid, colloid and hypertonic), the administration of non-steroidal antiinflammatory drugs and, where appropriate, antimicrobials. The principles of supportive care are discussed in detail. Other therapies such as hyperimmune plasma, polymyxin B, pentoxifylline, dimethyl sulfoxide and heparin are commonly used in the treatment of equine endotoxaemia and their use is reviewed here. Furthermore, newer agents such as anti-tumour necrosis factor antibodies, detergent, activated protein C and insulin, which have yet to gain widespread acceptance but may have an important role in the treatment of endotoxaemia in the future, are examined.

A double-blind study was performed, in horses, to determine the potential toxic effects of the nonsteroidal anti-inflammatory drug, eltenac(4-[(2,6-dichlorophenyl) amino]-3-thiopheneacetic acid). Four treatment groups of six horses were formed. The drug was injected intravenously, once daily, at a dose level of 0.5 mg/kg, 1.5 mg/kg or 2.5 mg/kg for 15 days. A control group was injected with sterile saline solution. Horses were monitored for changes in appetite, physical examinations, biochemical evaluations and gastroscopic examinations. Complete post-mortem examinations were also performed. A few glandular gastric ulcers, mild in severity, developed in seven animals during the treatment period. This occurred more often in horses treated with high doses of eltenac (P = 0.02). A dose-dependent change of white blood cell (WBC) count and neutrophil count was noted. Total protein, albumin and globulin levels had dose-dependent decreases. One horse in the high dose group (2.5 mg/kg) developed ventral ooedema as well as hypoproteinaemia. Gross post-mortem and histological examination did not reveal any signs of drug related gastrointestinal, renal or hepatic abnormalities. Toxic effects of eltenac given intravenously were greatest in horses treated with 2.5 mg/kg of the compound for 15 days compared to other groups.

The findings of this first report of the clinical treatment of foals with refractory hypotension support the use of AVP and NE.