Laminitis in the horse: a review

Laminitis has been a recognized disease since early Greek and Roman times, but it is still bothering both practitioners and scientists. In the last decade a lot of new fundamental research has been done to elucidate the pathogenesis of laminitis. New insights into the pathogenesis, the predisposing factors (including nutritional overload, endotoxaemia, shock, management, etcetera), clinical and radiological signs, differential diagnosis, therapy, and prognosis of the disease are described. The data, however, are not always in agreement with each other, giving further proof of the complexity of the syndrome.     

Phenylbutazone in the horse: a review

Phenylbutazone is an acidic, lipophilic, non-steroidal anti-inflammatory drug (NSAID). It is extensively metabolized in the horse. The metabolites so far identified, oxyphenbutazone, gamma-hydroxyoxyphenbutazone, account for some 25-30% of administered dose over 24 h. The plasma half-life of phenylbutazone and termination of its pharmacological action are determined primarily by its rate of hepatic metabolism. Phenylbutazone acts by inhibiting the cyclooxygenase enzyme system, which is responsible for synthesis of prostanoids such as PGE2. It appears to act on prostaglandin-H synthase and prostacyclin synthase, after conversion by prostaglandin-H synthase to reactive intermediates. It markedly reduces prostanoid-dependent swelling, edema, erythema, and hypersensitivity to pain in inflamed tissues. Its principal use in the horse is for treatment of soft tissue inflammation. Phenylbutazone is highly bound (greater than 98%) to plasma protein. After i.v. injection, blood levels decline with an elimination half-life of 3-10 h. The plasma kinetics of phenylbutazone may be dose dependent, with the plasma half-life increasing as the drug dosage level increases. Plasma residues of the drug at 24 h after a single i.v. dose of 2 g/450 kg average about 0.9 microgram/ml, but considerable variation occurs. If dosing is repeated, the plasma residue accumulates to give mean residual blood levels of approximately 4.5 microgram/ml on Day 5 after 4 days of dosing. Approximately similar blood levels are found after a combination of oral and i.v. dosing. Experiments on large numbers of horses in training have been undertaken to ascertain the population distributions of residual blood levels after such dosing schedules. Absorption of phenylbutazone from the gastrointestinal tract is influenced by the dose administered and the relationship of dosing to feeding. Access to hay can delay the time of peak plasma concentration to 18 h or longer. Under optimal conditions, the bioavailability of oral phenylbutazone is probably in the region of 70%. Paste preparations may be more slowly absorbed than other preparations and yield higher residual plasma levels at 24 h after dosing, but further controlled studies are required. Phenylbutazone is easily detected in the plasma and urine of horses but concentrations in saliva are low. It is quantitated for forensic purposes by HPLC. The variability of this method between laboratories is about +/- 25%. Increasing urinary pH increases the urinary concentration of phenylbutazone and its metabolites up to 200-fold.(ABSTRACT TRUNCATED AT 400 WORDS)     

Rectal tears in the horse: a literature review

Rectal tears are a relatively rare complication of rectal palpation, mating, or dystocia, and idiopathic rectal perforation is an incidental finding. Rectal tears can be classified according to a 3 or a 4-grade system. This article describes medical and surgical treatment for rectal tears.     

Trimethoprim/sulfonamide combinations in the horse: a review

Van Duijkeren, E., Vulto, A.G., van Miert, A.S.J.P.A.M. Trimethoprim/sulfonamide combinations in the horse: a review. J. vet. Pharmacol. Therap. 17 , 64–73. The indications for use, side-effects, and pharmacokinetic parameters of trimethoprim, sulfonamides and their combinations in the horse are reviewed. Trimethoprim/sulfonamide (TMPS) combinations are used for the treatment of various diseases caused by gram-positive and gram-negative bacteria, including infections of the respiratory tract, urogenital tract, alimentary tract, skin Joints and wounds- TMPS combinations can be administered orally, since absorption from the gastrointestinal tract is relatively good. However, peak serum concentrations can vary significantly between individual horses. Feed intake affects serum concentrations after oral administration. Concentrations of non-bound trimethoprim (TMP) and sulfadiazine (SDZ) in synovial fluid and peritoneal fluid are equal to serum concentrations after intravenous (i.v.) administration, and high concentrations are found in urine. Concentrations of TMP and sulfamethoxazole (SMX) in cerebrospinal fluid after i.v. administration exceed the minimum inhibitory concentration for common equine pathogens. The volume of distribution is 1.5-2.71/kg for TMP and 0.3-0.7 1/kg for various sulfonamides. The plasma half-life of TMP is 1.9-4.3 h, whereas the plasma half-lives of the different sulfonamides vary between 2.7 and 14.0 h. About 50% of total TMP is bound to plasma proteins. The binding of sulfadox-ine to plasma proteins depends on total plasma concentration and varies between 14% and 72%. The binding of other sulfonamides to plasma proteins may range from 33% for sulfaphenazole (SPZ) to 93% for sulfadimethoxine (SDM). Sulfonamides are metabolized by acetylation of the para-amino (N₄) group and by hydroxylation of the methyl group and the pyrimidine ring. The metabolic pathways of TMP in the horse are not fully known. Bacterial resistance to TMPS combinations is still relatively low. The sensitivity of different micro-organisms may vary with the relative activity of the sulfonamide used in the combination. The advised oral and i.v. dose rate is 15–30 mg/kg (in a 1:5 TMP/S ratio) with a dose interval of 12 h. The acute toxicity of TMPS is low, but there have been several reports of death after i.v. administration, probably due to vagal stimulation and subsequent bradycardia and vasodilatation caused by the pharmaceutical formulation (excipients, solvents) used. Future research should concentrate on establishing the optimum pyrimidine/sulfonamide combination and its dosing regimen for antimicrobial therapy in horses.     

Muscle fatigue in the horse: A review

The onset of fatigue within a muscle depends on several factors, including the duration or intensity of work and amount of training. In aerobic work over prolonged time it appears to be the level of glycogen stored within the muscle fibers that becomes limiting. In anaerobic work the limiting factor may be a combination of the amount of substrate available to the cell and the ability of the cell to continue working at low pH. Further work is needed to establish which is the most limiting of these two factors, levels of stored glycogen or accumulating levels of lactate and concomitant lowering of muscle pH.     

Lead toxicosis in the horse: A review

Lead intoxication is rarely diagnosed in horses and can present a major challenge to the equine practitioner because of the variety of clinical signs. Horses with lead poisoning can develop gastrointestinal disturbances, neurological abnormalities, haematological changes, or nonspecific signs of weight loss, weakness and rough hair coat, which makes early diagnosis difficult. Fortunately, lead analysis of whole blood is routinely available and can confirm intoxication. Because of the well‐described lead‐induced peripheral neuropathies in horses, a thorough neurological examination is essential in the investigation of a suspect case. Once diagnosed, the source of lead has to be identified and further exposure prevented. Intoxication can be treated by administering chelating drugs and providing symptomatic and supportive care.     

Calmatives for the excitable horse: a review of L-tryptophan

Preparations that contain tryptophan are marketed world wide as calmative agents to treat excitable horses. Tryptophan is the amino acid precursor for serotonin, a neurotransmitter implicated in sedation, inhibition of aggression, fear and stress, in various animal species and humans. Experiments have shown that tryptophan supplementation decreases aggression in humans, dogs, pigs, poultry, and fish, and that it may reduce fearfulness and stress in calves, vixens and poultry. However, behavioural characteristics more closely linked to excitement, such as hyperactivity in dogs, are not modified by tryptophan supplementation. Research using a variety of animals other than horses, has shown that the behavioural response to tryptophan supplementation varies with age, breed and gender, and can be modified by diet, exercise, social status, and level of arousal. Significantly, the response is species-dependent, and there are no scientific publications that confirm the efficacy of tryptophan as a calmative in excitable horses. The few studies where tryptophan has been administered to horses suggest that low doses (relative to those contained in commercial preparations) cause mild excitement, whereas high doses reduce endurance capacity, and cause acute haemolytic anaemia if given orally, due to a toxic hindgut metabolite. As tryptophan continues to be used as an equine calmative, there is an urgent need for research to confirm its efficacy in horses, and to establish a safe therapeutic dose range. In the meantime, available data suggest that it would be imprudent to rely on tryptophan to calm the excitable horse, and instead, that a greater effort should be made to identify the underlying causes of excitability, and to explore more appropriate non-pharmacological remedies.     

Warfarin: a review with emphasis on its use in the horse

Warfarin or dicoumarol prevents the production of functional clotting factors II, VII, IX and X. Navicular disease and thrombophlebitis are examples of equine thrombotic diseases in which warfarin has been used therapeutically. The initiation of anticoagulant therapy is relatively simple but attending veterinarians must be aware of the potential risks in order to minimize them. These risks include epistaxis, bleeding into the gastrointestinal tract and at the venipuncture site, and increased susceptibility to hematoma formation following local trauma. Vitamin K, especially vitamin K₁ is a swift and specific antidote for warfarin toxicity.     

Incarcerated umbilical hernia in the horse: a case with a review of the literature

Umbilical hernias are common in foals. This article provides a review of the literature and presents a case of an 1.5-year-old Friesian mare with an incarcerated umbilical hernia. After reposition of the incarcerated intestine (with a lot of effort), the practising veterinarian referred the mare to the Department of Equine Sciences. Preperforative peritonitis was diagnosed, presumed to be caused by necrotic bowel. After laparotomy, this tentative diagnosis was confirmed. The necrotic part of the small intestine was resected and intensive medical treatment was started. Initially, the mare recovered well, but seven days after surgery her general condition deteriorated and she had to be euthanized. At necropsy, impaction of the stomach and rupture of the stomach wall were found. The impaction was probably a result of the generalized peritonitis.     

Visceral prolapse after castration in the horse: a review of 18 cases

During a 10 year period, 18 horses were treated surgically because of visceral prolapse after castration. Surgery was successful in six cases of omental prolapse and in eight out of 12 cases of intestinal prolapse. To minimise the risk of visceral prolapse, the authors prefer half-closed castration, with proper ligation of the parietal vaginal tunic, to open castration. If adequate treatment is started promptly, prognosis in cases of visceral prolapse is favourable.     

Fever of unknown origin in the horse: a review of 63 cases

Fever of unknown origin (FUO) is a syndrome characterised by prolonged, unexplained fever associated with non-specific signs of illness such as lethargy, inappetence and weight loss. This paper reviews the details of 63 horses affected by FUO. The cause was found to be infection in 43 per cent of the cases, neoplasia in 22 per cent, immune-mediated diseases in 6.5 per cent and miscellaneous diseases in 19 per cent; the cause remained undiagnosed in 9.5 per cent.     

Medical treatment of osteoarthritis in the horse - a review

The medical treatment of osteoarthritis (OA) in the horse is one of the most utilized therapeutic regimens in the equine practice. It is important to understand the anatomy of synovial joints and the pathophysiology of the disease process to treat OA adequately. Once a thorough understanding of the disease process is comprehended the proper combination of systemic nonsteroidal anti-inflammatory drugs (NSAIDs), intraarticular steroids, viscosupplementation and chondroprotectants can be used to treat the disease and inhibit further progression of degenerative changes to the cartilage surface. The equine practitioner is faced with many choices for controlling inflammation in OA. This review presents the background and appropriate uses of various NSAIDs such as phenylbutazone, flunixin meglumine, ketoprofen, naproxen, and carprofen as well as their associated toxicities. Various steroid formulations exist for intraarticular (IA) administration and much has been learned in the past decade regarding correct dosage, frequency of administrations, indications and toxicity. This review presents IA steroids and their indications in addition to various chondroprotective drugs that also exist to control inflammation and provide viscosupplementation. Data are also given on disease modifying OA drugs such as glucosamine and chondroitin sulphate that have more recently become available to the equine practitioner.     

Ectopic ureter in the horse: Three cases and a review of the literature

Ureterovesicular anastomosis resulted in resolution of the clinical signs of urinary incontinence in three horses with unilateral ectopic ureter. Follow-up of two of the horses ten months and three years later indicated no further urinary tract problems; the third horse died four days after surgery from intestinal infarction.

Diagnosis can be readily confirmed by antegrade or retrograde ureterography, or endoscopic visualization of the ectopic ureteral openings. Nephrectomy appears indicated in cases of unilateral ectopic ureter with associated ipsilateral urinary tract infection or hydronephrosis, providing the contralateral kidney has normal function. Ureterovesicular anastomosis appears to be indicated in the management of unilateral ectopic ureters in the absence of ascending urinary tract infection or hydronephrosis, and in cases of bilateral ectopic ureters.