Pathophysiology of acute laminitis

This article reviews research findings relating to the pathophysiology of acute laminitis in horses. The data presently available suggest that the onset of the condition may be due to constriction of the postcapillary vessels in the digit, leading to increased capillary hydrostatic pressure and movement of fluid into the interstitial space.     

The pathophysiology of developmental and acute laminitis.

This review implies that although we know more regarding the enigma of developmental and acute laminitis today than previously, there is still more to investigate. As these investigations are conducted and interpreted, new and more effective preventive and therapeutic regimens are likely to be developed, tested, and made available. As this occurs, the impact of laminitis should undoubtedly decrease. Unfortunately, due to the lack of clinical symptoms in the developmental phase and the shortness of the acute phase, it is also evident that the two sequelae of acute laminitis, subacute and chronic laminitis, are likely to continue to pose a major problem for some time.     

奶牛蹄叶炎的预防与治疗

奶牛蹄叶炎又名奶牛蹄壁真皮炎,是奶牛生产中常见的一种疾病。生产上兽医治疗常用到中药青黛散治疗疗效显著。为防止本病的发生,应在饲养中本着科学饲喂,营养全价,饲养管理与奶牛生产相适应,按需、按个体发育与生产特点供给营养需要的原则供给奶牛日粮。奶牛作为奶牛养殖场主要的经济效益来源,必须保证奶牛体况良好才能有稳定的产奶量,然而在生产中常常会遇到奶牛患蹄部疾病而影响产奶,严重者甚至造成奶牛的淘汰,所以在日常的饲养管理中应做好综合性的预防,减少本病的发生。     

Animal welfare in prevention and therapy of laminitis

Laminitis is a systemic disease which is manifested as a non infectious condition in the foot. The management of feeding and housing conditions is necessary to treat the endocrinological and metabolic disturbances of laminitic horses. The Equine Metabolic Syndrome (EMS) is predisposing for developing laminitis, and it is characterised by obesity, insulin resistance, hypertension and dyslipidaemia. A genetical predisposition is supposed and EMS is accompanied by a lack of exercise and inadequate energy intake. Laboratory examinations are of great importance for diagnosis. Analyses of insulin, glucose and ACTH are of interest. Several approaches to treat laminitis are available, including pharmacological and orthopaedic strategies as well as the management of the feeding and housing conditions. However, the prophylaxis to prevent laminitis has to be emphasised. Predisposed horses should be detected and adequately treated; especially weight reduction in obese horses is in the focus of interest. Horses in the acute stage of laminitis have to be stabled. Furthermore redistributing weight from the most stressed wall is necessary to prevent pain and to minimise laminar damage and displacement of the distal phalanx. In cases of displacement of the distal phalanx a close communication between the veterinarian and the authorised farrier is necessary, in these cases treatment should be supported by x-ray diagnosis. Horses have to be treated with NSAISs to ensure a proper therapy to consider animal welfare. Horses have to be fed with hay and supplemented with minerals and vitamins. Feeding exclusively straw and feed restriction has to be avoided.     

Glucocorticoid therapy and the risk of equine laminitis

Although glucocorticoids have been used successfully for the treatment of noninfectious inflammatory diseases of horses for more than 35 years, their use has been attended by a fear of the induction of laminitis. This paper reviews the evidence for this fear and the possible mechanisms whereby glucocorticoids could participate in laminitis induction. Although the association of laminitis with elevated serum cortisol in pituitary pars intermedia dysfunction suggests that chronic exposure to glucocorticoids may be part of laminitis pathogenesis, review of published reports and databases suggests that glucocorticoid‐induced laminitis is a relatively rare occurrence. However, several of the actions of glucocorticoids are similar to those known to be involved in laminitis pathogenesis. Glucocorticoid administration can induce insulin resistance, lead to vascular dysfunction that potentiates vasoconstriction, and interfere with keratinocyte proliferation and differentiation as well as matrix integrity, all mechanisms that could possibly induce laminitis. Drug formulation, dose and route of administration, and the systemic and hoof disease history of the horse must all be considered when assessing laminitis risk during glucocorticoid treatment. Generally, local glucocorticoid administration presents little risk as does systemic treatment of recurrent airway obstruction without concurrent disease. Caution should be used however in horses that are overweight and/or insulin resistant, or have had a recent bout of acute laminitis of alimentary or endotoxic origin. Overall, however, the risk of laminitis after glucocorticoid treatment, especially local use, is acceptable compared to the many benefits of these drugs.     

The pharmacologic basis for the treatment of developmental and acute laminitis.

Each horse with laminitis is presented to the veterinarian at a different stage in progression of the condition and with varying severity. The pathogenic timing is often unknown and is difficult to determine. Because timing and severity are related to both the lesion's severity and responsiveness to treatment, these factors are critical to treatment selection and success. It is erroneous to assume that each horse with laminitis should receive each treatment. It is therefore important to ascertain as logically and objectively as possible the pathophysiological stage of development of each horse when it is examined. Therapeutic failure may result from inappropriate interpretation of the clinical signs and pathophysiologic condition of the patient in order to coordinate a treatment regimen.     

Bovine laminitis: clinical aspects, pathology and pathogenesis with reference to acute equine laminitis

This review deals with the features of clinical and subclinical laminitis in cattle. Prominent clinical signs of acute laminitis are a tender gait and arched back. The sole horn reveals red and yellowish discolourations within five days. In subacute and chronic cases clinical signs are less severe. In chronic laminitis the shape of the claws is altered. Laminitis is frequently followed by sole ulceration and white zone lesions. Blood tests showed no significant changes for laminitic animals. Arteriographic studies of claws affected by laminitis indicated that blood vessels had narrowed lumens. Gross pathology revealed congestion of the corium and rotation of the distal phalanx. Histopathologic studies indicate that laminitis is associated with changes of the vasculature. Peripartum management and nutrition are important factors in its aetiology. It is hypothesised that laminitis is evoked by disturbed digital circulation. In the pathogenesis of acute laminitis three factors are considered important: the occurrence of thrombosis, haemodynamic aspects of the corium, and endotoxins which trigger these pathologic events.     

Supportive therapy in the anesthetized horse

In conclusion, vigilant supportive care is necessary to prevent morbidity and death in the anesthetized horse. Because some of the equipment and drugs are specialized and the consequences of some postanesthetic complications are severe, availability of those items must be confirmed prior to anesthesia. Proper positioning and padding will help to reduce the incidence of postanesthetic myopathy-neuropathy syndrome in these large patients. Adequate tissue perfusion is important and can be achieved by controlling anesthetic depth, increasing intravascular volume with fluid administration, and by administering sympathomimetic agents.     

The role of endotoxin in the pathogenesis of acute bovine laminitis

To study the possible role of endotoxin in the pathogenesis of bovine laminitis, local and systemic injections of endotoxin (E. coli 0111 B4) with different doses were given to three groups of four cows each. Clinical and haematologic parameters indicated an acute-phase response, including positive plasma ethanol gelation (soluble fibrin), the occurrence of fibrin degradation products and decreased thrombocyte counts. Local Shwartzman reactions were not evoked. Clinical examination of the claws and the gait of the animals revealed no signs of laminitis. However, on histopathological examination of the claw corium signs of laminitis such as vacuolisation of the Stratum basale, lymphocyte and leucocyte infiltration and thrombosis were found. These results indicate that endotoxin indeed may be involved in the pathogenesis of laminitis. For the development of a clinical acute laminitis model in cattle either another dosage, other toxins or factors in addition to the endotoxin used in this experiment are needed.     

Equine laminitis: cryotherapy reduces the severity of the acute lesion

REASONS FOR PERFORMING STUDY: The hypometabolic and vasoconstrictive effects of cryotherapy could prevent the development of laminitis. OBJECTIVES: To use distal limb cryotherapy to prevent laminitis induced by alimentary carbohydrate overload. METHODS: Laminitis was induced in 6 Standardbred horses that had one front limb continuously cooled in an ice/water mixture. Lameness evaluation, blinded lamellar histological grading and analysis for lamellar matrix metalloproteinase-2 (MMP-2) mRNA expression were used to evaluate the severity of laminitis. RESULTS: Cryotherapy was well tolerated and effective in cooling the feet. In each horse no lameness was observed in the treated limbs. Laminitis histology scores in the treated limbs were significantly less than those of the corresponding untreated forelimbs (P < 0.05). Laminitis histology scores in the treated limbs were also significantly less than those of the untreated limbs (fore- and hind) as a group (P < 0.05). Expression of MMP-2 mRNA in the iced feet was significantly (P < 0.05) less than that detected in the untreated feet. CONCLUSIONS: Cryotherapy, when applied to one foot, markedly reduced the severity of acute laminitis in this study. We propose that vasoconstriction (preventing delivery of haematogenous trigger factors) and hypometabolism (reduction in lamellar MMP activity) were the primary therapeutic mechanisms. POTENTIAL RELEVANCE: Although further research is needed, we suggest cryotherapy as a potentially effective prophylactic strategy in horses at risk of developing acute laminitis.     

Voluntary limb-load distribution in horses with acute and chronic laminitis

OBJECTIVES: To compare limb-load distribution between horses with and without acute or chronic laminitis. ANIMALS: 10 horses with carbohydrate-induced acute laminitis, 20 horses with naturally occurring chronic laminitis, and 20 horses without foot abnormalities (controls). PROCEDURES: Limb-load distribution was determined, using a custom-designed system that allowed simultaneous quantification of the mean percentage of body weight voluntarily placed on each limb (ie, mean limb load) and the SD of the mean load over a 5-minute period (ie, load distribution profile [LDP]). Load distribution profile was used as an index of frequency of load redistribution. RESULTS: Mean loads on fore- and hind limbs in control horses were 58 and 42%, respectively, and loads were equally and normally distributed between left and right limbs. In addition, forelimb LDP was greater, compared with hind limbs, and was affected by head and neck movement. In comparison, limb-load distribution in horses with chronic laminitis was characterized by an increase in the preferential loading of a forelimb, a decrease in total forelimb load, and an increase in LDP that was correlated with severity of lameness. In horses with carbohydrate-induced acute laminitis, mean limb loads after onset of lameness were not different from those prior to lameness; however, LDP was significantly decreased after onset of lameness. CONCLUSION AND CLINICAL RELEVANCE: Quantification of limb-load distribution may be an applicable screening method for detecting acute laminitis, grading severity of lameness, and monitoring rehabilitation of horses with chronic laminitis.     

Expression of endothelin in equine laminitis.

Biosynthesis of endothelin-1 (ET-1), the most potent endogenous vasoconstrictor yet identified, is increased following myocardial infarction (MI) in man. Pathological events which occur in the connective tissues of the equine hoof during laminitis are similar in some respects, to changes occurring in the myocardial connective tissues following MI in man. The objective of this study was to determine whether ET-1 expression in connective tissues obtained from the hoof of laminitic horses is increased compared with tissues obtained from healthy horses. Expression of ET-1 in connective tissues of the equine hoof was measured following tissue extraction from 3 groups of horses: horses in which acute laminitis had been induced by the administration of starch; chronically foundered horses; nonlaminitic horses. The concentration of ET-1 in laminar connective tissues obtained from all laminitic horses (1573.0 +/- 392.8 pg/g of tissue; n = 10) was increased when compared with tissues obtained from nonlaminitic horses (392.5 +/- 117.4 pg/g of tissue; n = 5) (P<0.05). The concentration of ET-1 in laminar connective tissues obtained from the experimentally induced, acute laminitic horses (1043.6 +/- 254.4 pg/g of tissue; n = 7) and from the spontaneously affected, chronic laminitic horses (2808.3 +/- 878.6 pg/g of tissue; n = 3) was increased compared with the control group (P<0.05, P<0.01, respectively). The concentration of ET-1 in laminar connective tissues obtained from the chronic laminitic horses was greater than that of the experimentally induced, acute laminitic group (P<0.05). It is suggested that the data provide a strong argument that increased ET-1 expression in the connective tissues of the equine hoof represent a potentially important and hitherto unrecognised component of the pathophysiology of equine laminitis. Further studies are needed to determine whether inhibitors of ET-1 converting enzyme or antagonists of ET-1 receptors might be useful in the treatment and prevention of laminitis in horses.     

The digital pathologies of chronic laminitis.

This review indicates that the patient-to-patient uniqueness commonly seen in chronic laminitis represents the variable presence of the digital pathologies. Although some degree of mechanical failure is always present, the secondary metabolic and growth dysplasias, vascular pathologies, and sepsis may or may not be evident. The presence and severity of these pathologies appear to have a more significant impact on the prognosis of individual cases than does the displacement of the distal phalanx. It should be reiterated that it is often the combined presence of these individual pathologies that gives rise to the patient that is totally refractory to treatment. In the absence of these pathologies, many horses with significant displacement of the distal phalanx are not in pain and are not in need of treatment. It thus follows that a key to the improved rehabilitation of difficult patients is focusing research on the physiopathology and diagnosis of these nonmechanical problems.