SUMMARY Mean normal values for PaO2 and max Δ Ppl for horses were determined. Using 2 standard deviations below (PaO2) and above (max Δ Ppl) the mean normal values as a guide, horses affected with COPD were satisfactorily distinguished from other horses in a series of 100 animals. The frequency of occurrence of 20 different clinical parameters in affected, not affected and possibly affected horses was examined statistically. Poor work performance and a history of previous febrile illness occurred more often in COPD horses than in others. The presence of a chronic cough, dyspnoea, double expiratory effort, increased breathing sounds, wheezing and crepitant breathing sounds occur more frequently in COPD horses than in others and the presence of prolonged coughing was highly indicative of COPD. Crepitant breathing sounds (observed only in horses in the affected group), wheezing and increased respiration sounds were observed in a high proportion of horses affected with COPD, but a diagnosis of COPD based solely on these parameters would lead to an unacceptably low number of cases being recognised. While radiological examination appeared to be helpful, x‐ray films were in general difficult to interpret. Haemato‐logical examination was of no help in the diagnosis of COPD. The beneficial effect of removing affected horses from contact with hay and straw was recorded. RÉSUMÉ Les valeurs moyennes normales de PaO2 et les valeurs maximales de Ppl ont été déterminées chez le cheval. En employant les déviations standards au dessous pour PaO2 et au dessus pour Ppl des valeurs moyennes, on peut distinguer les chevaux atteints dans une série de 100 chevaux. La fréquence d'apparition de 20 paramètres cliniques différents fut déterminée de manière statistique pour les chevaux atteints, suspects et indemnes. Une aptitude physique insuffisante et les commémoratifs d'une maladie fébrile antérieure ont été constatés plus souvent chez les chevaux atteints de MPCO. L'existence d'une toux chronique, de dyspnée, d'une expirationà deux temps et les bruits respiratoires crépitants ou sifflants est plus fréquente chez les chevaux atteints de MPCO que chez les autres. Les bruits respiratoires crépitants (seulement observés chez les chevaux atteints de MPCO), les bruits respiratoires sifflants et l'intensité accrue des sons respiratoires furent constatés chez un grand nombre de chevauxà MPCO; toutefois le diagnostic de MPCO étayé par ces seuls paramètres serait par trop restrictif. Les examens radiologiques furent utiles mais les clichés furent trop souvent difficilesà interpréter. L'hématologie n'apporta aucune aide. On nota l'intérét qu'il y avait de soustraire les animaux malades du contact des fourrages, paille ou foin. ZUSAMMENFASSUNG Normale Durchschnittswerte für PaO2 und Δ Ppl max wurden bestimmt. Die Verwendung von zwei Standard‐abweichungen unter (PaO2) oder über (Δ Ppl max) dem Mittelwert erlaubte die zufriedenstellende Unterscheidung von Pferden mit COPD und von anderen Pferden in einer Reihe von 100 Tieren. Die Frequenz des Auftre...

Summary Sesamoid lameness poses many problems to the clinician. Owing to the complexity of the fetlock joint and its components, it is often difficult to determine the exact nature and site of the pathological changes on clinical examination. Accurate diagnosis is dependent on radiological examination but changes seen on such examinations may not be demonstrable until the condition has become chronic. Many of the lesions of the sesamoids seen on radiological examination are difficult to interpret and they relate to the clinical picture, and thus need not necessarily provide an accurate guide to the prognosis. Most cases of sesamoid lameness are related to previous primary soft tissue damage, and treatment should, in the initial stages, be directed toward this. While the prognosis should always be guarded, many animals will recover to soundness, in spite of marked pathological changes in the area. Résumé Les boiteries sésamoidiennes posent de nombreux problèmes cliniques. A cause de la complexité de l'articulation du boulet et de ses éléments il est souvent difficile de prèciser la nature et le site exact des changements pathologiques lors d'un examen clinique. Un diagnostic satisfaisant dépend souvent d'un examen radiographique; mais les changements décelables par cette technique peuvent n'etre appréciables que lorsque la condition pathologique est devenue chronique. Bien des lésions au niveau des sésamoides, rencontrées lors d'un examen radiographique, sont d'interprètation délicate, difficiles à rattacher au contexte clinique; partant elles n'ont pas nécessairement une grande utilité dans le pronostic. La plupart des boiteries sésamoidiennes sont dues à une lesion initiale des tissus mous et le traitement devrait, à son début, tenir compte de ce fait. Le pronostic doit toujours etre réservé. Pourtant de nombreux animaux retrouvent une aptitude fonctionnelle normale en dépit de déformations pathologiques marquées de cette région. Zusammenfassung Gleichbeinlahmheiten stellen den Kliniker vor viele Probleme. Wegen der komplexen Verhältnisse im Fesselgelenk ist es oft schwierig die genaue Natur und den Sitz pathologischer Veränderungen durch die klinische Untersuchung zu eruieren. Die genaue Diagnose hängt ab von der Röntgenuntersuchung, aber sichtbare Veränderungen treten oft erst auf, wenn der Zustand chronisch geworden ist. Viele Gleichbeinläsionen, die im Röntgenbild zutage treten, sind schwer zu beurteilen und mit dem klinischen Bild zu korrelieren. Das Röntgenbild gibt deswegen nicht unbedingt zuverlässige Anhaltspunkte für die Prognose. Die meisten Gleichbeinlahmheiten stehen in Beziehung mit vorbestehenden Schäden des umgebenden Gewebes und die Behandlung sollte zu Beginn darauf Rücksicht nehmen. Die Prognose muss vorsichtig gestellt werden, obgleich viele Tiere trotz deutlichen Veränderungen an den Gleichbeinen sich klinisch wieder erholen. Sumario La claudicacion sesamoidea posee varios problemas para el clinico. Sabiendo lo complejo de la articulacion del menudillo es dificil determinar exactamente la na...

A 50-year-old man, with a known weekly alcohol intake of almost 100 units, presented to his GP feeling drowsy. Routine blood tests revealed a profound hyponatraemia of 100 mmol/litre, and he was referred to hospital for investigations. On admission he was drowsy, but had a Glasgow Coma Scale score of 15, an abbreviated mental test score of 10/10 and an entirely normal neurological examination. Liver function tests were consistent with excessive alcohol consumption. He had been prescribed bendroflumethazide and clomipramine (a tricyclic antidepressant) by his GP. In view of their potential tocause hyponatraemia these were subsequently withheld and he was fluid restricted to 1.5 litres per day. His sodium level rose gradually and on day 5 of admission it had increased to 122 mmol/litre. He was discharged on day 8 having been advised to stop drinking. Less than a week after discharge he represented to his GP with symptoms of excessive sweating, shaking, constipation, disorientation and dysarthria. He was febrile at 38.6°C , and had a blood pressure of 180/90 mmHg. Electrolytes were normal (Na+ 135 mmol/litre). Although he denied consuming any alcohol since his initial admission, his symptoms were consistent with acute alcohol withdrawal and he was treated accordingly. He failed to improve on two attempts at reducing doses of chlordiazepoxide. His dysarthria progressed until his speech was difficult to understand and his swallow became unsafe. He continued to spike temperatures throughout the admission and although a catheter specimen of urine was positive for enterococcus, treatment with a prolonged course of antibiotics had not resolved his fever. A computed tomography scan of his head and a lumbar puncture were performed. Other than cortical atrophy in keeping with alcohol abuse, neither investigation provided any answers. It was considered that his symptoms could be explained by autonomic dysfunction. In view of his corrected hyponatraemia, central pontine myelinolysis was suggested and a magnetic resonance imaging head scan was performed (Figure 1). This confirmed the presence of central hyperintensity on the water sensitive sequences within the central pons, in keeping with an osmotic demyelination syndrome. Additionally these changes were identified within the caudate nuclei, possibly accounting for the patient's inability to fully control voluntary movement. The ongoing temperatures without sepsis suggested hypothalamic involvement. Following diagnosis this patient failed to improve. Treatment became supportive, and he died 7 weeks later.

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