Three case reports of the use of haemodiafiltration in the treatment of salicylate overdose.

Aspirin (acetylsalicylic acid) is widely available without prescription. Although self-poisoning is rare, if severe it may be life threatening. Haemodialysis has been recommended in severe cases when salicylate levels exceed 7.3 mmol l(-1). We describe three cases of severe salicylate poisoning, which were treated with continuous veno-venous haemodiafiltration (CVVHDF). All patients survived. The first case had already undergone haemodialysis before transfer to the ICU, where CVVHDF was commenced because salicylism persisted at 3 mmol l(-1). A small reduction in serum salicylate was noted. In the second case, serum salicylate decreased from 8.5 to 3.5 mmol l(-1) after 3 h of CVVHDF even though only minimal urine was produced. Our third case is a chronic overdose in whom serum salicylate decreased from 6.2 to 4 mmol l(-1) after 4 h and to 1.4 mmol l(-1) after a further 7 h. No bicarbonate was administered to this patient and elimination can only be attributed to CVVHDF and urinary clearance, which is known to be slow. We discuss the pathogenesis of severe salicylate toxicity and postulate that CVVHDF, which is widely used in the intensive care setting, may be a useful therapy in severely poisoned patients who are unstable and cannot undergo haemodialysis or in situations where haemodialysis is unavailable.

Prolonged vecuronium neuromuscular blockade associated with Charcot Marie Tooth neuropathy.

Charcot Marie Tooth (CMT) disease comprises a group of disorders characterized by progressive distal muscle weakness and wasting. Review of the anaesthetic literature produced conflicting reports concerning the responses to neuromuscular blocking drugs in these patients. We describe a case in which vecuronium 0.11 mg kg(-1) produced prolonged neuromuscular blockade lasting 115 min in a patient with the condition. Conduction velocity in the facial nerve is usually less affected than the ulnar or peroneal nerve in CMT patients. This nerve may be more useful in monitoring neuromuscular blockade, both in titrating the dose of neuromuscular blocking drug and ensuring adequate reversal at the end of a procedure. Recent advances in molecular biology have enabled identification of the underlying genetic abnormalities and pathophysiology of CMT. These advances are reviewed and implications of CMT for the anaesthetist discussed.

Issues for consideration in dihydropteridine reductase (DHPR) deficiency: a variant form of hyperphenylalaninaemia.

An adult male with intellectual disabilities demonstrated deterioration in many skills over a number of years and an increase in his temper outbursts was also reported. At 18 years of age, he had been diagnosed as having dihydropteridine reductase (DHPR) deficiency, but treatment had proved unsuccessful in the short term and was discontinued. Dihydropteridine reductase deficiency is a recessively inherited disorder of the amino acid metabolism resulting in a deficiency of tetrahydrobiopterin, an essential cofactor for phenylalanine, tyrosine and tryptophan metabolism. This causes a severe deficiency of neurotransmitters in the brain. Following further neurological examinations, treatment for the subject was recommenced at the age of 30 years. Few reports of late-diagnosis DHPR have been documented. This paper outlines one case report of DHPR, highlighting the importance of diagnosis, medical treatment and nursing care.

Client attachment in learning disabilities nurse education.

This paper describes the method by which the learning disabilities branch programme in Southampton has been adapted to reflect educational and practical changes. Emphasis is placed on integrating theory and practice through giving students extended contact with a caseload of patients with the support of a tutor and mentors. The authors report on the initial difficulties and benefits resulting from the new programme.

Autonomic neurone degeneration in equine dysautonomia (grass sickness).

Histological investigations were undertaken on four sympathetic autonomic ganglia and on the myenteric and sub-mucosal plexuses of the jejunum in healthy animals, in naturally occurring cases of acute, sub-acute and chronic equine dysautonomia and in ponies in which neuronal damage had been induced by the injection of acute grass sickness sera. The degree of neuronal damage is related to the type of dysautonomia. The coeliac-mesenteric ganglion reacts differently from other ganglia and is less severely damaged in cases of short duration. Extensive experimentally induced damage to the coeliac-mesenteric ganglion, even when jejunal damage is also present, is not associated with clinical illness. It is proposed that the rate of autonomic neurone loss and the extent of the damage may both influence the clinical manifestations of grass sickness.

Clinical equine dysautonomia and autonomic neuron damage.

Damage to the neurons of selected autonomic ganglia was quantified in relation to the severity of the clinical signs shown in acute, subacute and chronic cases of dysautonomia (grass sickness). No connection between the clinical severity of acute or subacute dysautonomia and the amount of neuronal damage in the superior cervical, stellate and coeliaco-mesenteric ganglia could be demonstrated. However, a higher proportion of normal neurons were found in chronic cases. Jejunal submucosal neuronal damage was correlated with clinical severity but further work is required to confirm this finding and to establish how widespread the alimentary neuronal lesions are in dysautonomia of different severities.

Clinical and biochemical features of grass sickness (equine dysautonomia).

An attempt has been made to assess the diagnostic value of clinical features seen at initial examination of horses with grass sickness, colic cases and cases submitted as possible grass sickness but diagnosed subsequently as some other condition. There appears to be no single pathognomonic sign for grass sickness. A range of signs has been associated with grass sickness but these are of value only when related to the length of illness and the history. Biochemical tests related to intestinal tissue damage, stress and dehydration were evaluated and most were found to be of value in diagnosing acute grass sickness. No evidence was found relating selected mineral or vitamin deficiencies to grass sickness, nor were protein changes specific. A marked fall in glutathione peroxidase values was associated with grazing rather than disease.

Secondary gastric impaction associated with ragwort poisoning in three ponies.

Poisoning with Senecio jacobaea (ragwort) is a common cause of chronic liver disease in horses in Britain. The major clinical signs are the result of hepatic failure but gastric impaction has recently been associated with the disease. The present paper describes three cases of secondary gastric impaction associated with ragwort poisoning. In each case the impaction was the cause of death or necessitated euthanasia.

Caecal intussusception in two ponies.

One case of caecocaecal intussusception (case 1) and one case of caecocolic intussusception (case 2) in ponies are described. Case 1 showed mild abdominal discomfort for seven days followed by sudden death whereas case 2 showed continuous moderate pain for three weeks. At post mortem examination, case 1 showed intussusception of the base of the caecum into the body whereas in case 2, the entire caecum had invaginated into the right ventral colon. Histopathological examination showed that the lesions in both animals had been present for a long time.