Congenital portosystemic shunts (PPS) are abnormal vascular communications that allow blood from the intestine to bypass the liver, and are classified as intrahepatic or extrahepatic. Clinical signs are generally related to the nervous, gastrointestinal or urinary systems, and are often vague. In addition, changes present on routine blood analysis are often mild and non-specific. For this reason, alternative tests are required for a diagnosis. Diagnostic tests include serum bile-acid concentrations, ammonia tolerance test, portography, ultrasonography and/or scintigraphy. Medical therapy involves reducing absorption of encephalopathic toxins from the gastrointestinal tract and may prolong survival. Surgical therapy is aimed at attenuation of the shunting vessel and provides improved survival rates. The traditional approach has been complete or partial ligation of the shunt. More recent approaches have involved slow, progressive attenuation with ameroid constrictors or cellophane banding. Overall, prognosis following surgical therapy is good in dogs and fair in cats.

The dosage of medetomidine and ketamine recommended in the literature for immobilising tigers produced severe cardiopulmonary depression in this animal. A reduced dosage of medetomidine and higher dosage of ketamine provided adequate restraint with decreased cardiopulmonary depression.

Gastric dilatation-volvulus (GDV) is a disease in which there is gross distension of the stomach with fluid or gas and gastric malpositioning. It causes pathology of multiple organ systems and is rapidly fatal. It is common in large- and giant-breed dogs. The disease appears to have a familial predisposition. Thoracic depth/width ratio also appears to predispose dogs to GDV. Implicated dietary factors include dietary particle size, frequency of feeding, speed of eating, aerophagia and an elevated feed bowl. A fearful temperament and stressful events may also predispose dogs to GDV. Abdominal distension, non-productive retching, restlessness, signs of shock, tachypnoea and dyspnoea are possible clinical signs. Initial treatment includes treatment of shock and gastric decompression. Surgical treatment should be performed promptly. There are no studies comparing the use of different anaesthetic agents in the anaesthetic management of GDV. Pre-medication with an opioid/benzodiazepine combination has been recommended. Induction agents that cause minimal cardiovascular changes such as opioids, neuroactive steroidal agents and etomidate are recommended. Anaesthesia should be maintained with an inhalational agent. Surgical therapy involves decompression, correction of gastric malpositioning, debridement of necrotic tissue, and gastropexy. Options for gastropexy include incisional, tube, circumcostal, belt-loop, incorporating, and laparoscopic gastropexy. Expected mortality with surgical therapy is 15-24%. Prognostic factors include mental status on presentation, presence of gastric necrosis, presence of cardiac arrhythmia and plasma lactate levels. Prophylactic gastropexy should be considered in dogs identified as being at high risk.

In this case of VAE-associated anaesthetic death, it is further speculated that underlying pulmonary disease, in the form of pulmonary calcification, may have contributed to an increased sensitivity to the adverse effects of VAE.

Responses by the veterinarians taking part in this survey indicated that they had a reasonably good standard of anaesthetic practice. A physical examination was carried out preanaesthesia, and premedication including analgesia was routinely administered to most patients. A dedicated anaesthetist usually monitored patients and most respondents reported they had access to basic anaesthetic monitoring equipment. Areas where changes could lead to improved anaesthetic practice were increased use of I/V catheterisation, endotracheal intubation, and supplementary oxygen, and reduced I/V fluid rates.