Kirstin Brandt eI al.Pfe' d eh e il ku n de 13 (199 7) 2 (J an uar -Feb ru an) [27][28][29][30][31][32][33][34] Atypical Myoglobinuria in grazing horsesIn autumn 1995 for the first time horses were taken to the clinic for horses in Hannover that showed symptoms of a muscular disease, not seen so far. None of the twelve patients survived this atypical myoglobinuria although extensive treatment was performed. At the same time other veterinarians reported on 103 cases. 99 of them died. Without exception all horses and ponies were not in training and kept on pasture just before the disease set on. In most of the cases more than one horse of a srngle pasture was affected. Different breeds, sexes and age groups were concerned. In the beginning all horses showed muscular tremor, stiffness and stagger. They were dull or apathetic. Heart rates and breathing frequencies were elevated. Appetite was maintained very long and only a few horses were painful. The rectal palpation revealed only a highly filled bladder. All patients showed a massive elevation of creatine kinase and myoglobinuria was characteristic, Treatment included infusion of isotonic solutions, analgesics, anti-inflammatory agents and doses of Vitamin E/selenium. Despite intensive medical care and treatment all horses came to recumbency within three days and finally died. In pathologic anatomical examinations various muscle groups showed a marked, acute rhabdomyolysis of type I fibres. Up to this day laboratory diagnostics, clinical, pathologic-anatomical, histological and toxicologrcal findings could not reveal the etiology of atypical myoglobinurla.

This study aimed to describe the inflammation, hydro-electrolyte and acid-base imbalances caused by generalised peritonitis (GP) and parietal fibrinous peritonitis (PFP) after caesarean section. After clinical examination, blood was sampled from 11 cows with PFP, 30 with GP and 14 healthy cows. Serum and plasma refractometry and glutaraldehyde tests were used to evaluate the inflammation level, while hydro-electrolytes and acid-base parameters were assessed using an EPOC® device. In addition to clinical signs of dehydration (>10%), blood analysis showed a high fibrinogen concentration (PFP: 8.64 ± 8.82 g/L; GP: 7.83 ± 2.45 g/L) and fast glutaraldehyde coagulation (<3 min) indicative of severe inflammation in both diseases compared to the control group (p < 0.05). Moreover, a severe decrease in electrolytes concentration (Na+: 126.93 ± 5.79 mmol/L; K+: 3.7 ± 1.3 mmol/L; Ca++: 0.89 ± 0.12 mmol/L; Cl−: 82.38 ± 6.45 mmol/L) and a significant increase in bicarbonate (30.87 ± 8.16 mmol/L), base excess (5.71 ± 7.42 mmol/l), L-lactate (8.1 ± 4.85 mmol/L) and creatinine (3.53 ± 2.30 mg/dL) were observed in cows with GP compared to the control group (p < 0.05). In contrast, few major perturbations were noticed in PFP, where only K+ (3.64 ± 0.25 mmol/L) and Ca++ (1.06 ± 0.09 mmol/L) were significantly modified (p < 0.05). In conclusion, a high dehydration and severe inflammation are induced by PFP and GP. Nevertheless, GP causes more electrolytes and acid-base disturbances than PFP.