Equine medicine Flashcards
Describe the possible manifestations and causes of chest pain?
Usually pleural in origin. Largely parietal as visceral pleura has very few nociceptors. manifestations: pain on palpation (NB feel between ribs - pleurodynia). reluctance to move or lie down, elbows abducted, chest wall splinted, shallow rapid respiratory excursions, grunting. Common causes: pleuritis, pleuropneumonia, lung abscess, peumonia. Less common: mediastinal mass, fractured rib, osteomyelitis, myopathy, ruptured oesophagus
Describe the manifestations and possible causes of abdominal pain
Spectrum of signs from mild depression, stretching, lip curling, grunting, flank watching, burxism, pawing, rolling, violent thrashing.
Causes: colic, the syndrome of abdominal pain. Most commonly gastrointestinal related. Colic is a syndrome not a diagnosis of its own right. Be aware of false colics. eg urinary pleural, laminitis - that may look like a GI type colic case.
What are the manifestations of pain in the extremities?
Altered stance or gait. Reflex contraction of flexor muscles with acute stimulus. Numerous orthopaedic diseases, some inflammatory conditions e.g purpura haemorrhagica, cellulitis, staphylococcal skin infections.
What are the manifestations of neck and back pain?
Guarding, reluctance to be tacked up, ridden, pain on palpation. in the Neck: reluctance to lower head or move neck, splinting, pain on palpation. Causes: numerous orthopaedic conditions e.g fractures, thrombophlebitis, myopathy e.g exertional rhabdomyolysis.
What are the manifestations of urinary pain?
If urinary pain is severe it can resemble a serious gastrointestinal obstruction. Prolonged posturing, absent poor or intermittent urine flow, straining, grunting with micturition. foals: need to see if straining to urinate for instance with ruptured bladder, which may look slightly different to defaecatory tenesmus, for instance with meconium retention. NB the difference in signs is not always apparent.
What is neuralgia?
Defined as pain in a nerve or along the course of one or more nerves. Poorly understood in animals but some evidence that animals can suffer from syndromes that have been better described in people.
Describe the pathogenesis of headshaking seen in horses
Multiple possible causes. 2 have increased attention: photic and trigeminal neuralgia. Most cases are idiopathic. Trigeminal nerve V provides sensation to the face. Evidence of this nerves involvement: if nerve block performed of infraorbital nerve some horses clinical signs improve. Block of posterior ethmoidal nerve gives some improvement. Photic: perhaps a form of optic trigeminal summation. Horses improve at night, indoors, with masks/lens. Some forms of idiopathic headshaking are like a trigeminal neuralgia in man. (Microvascular compression and pathological changes in nerve root and ganglion or suggestion of degenerative change in brainstem nucleus). The trigeminal nerve could be hypersensitive and fire impulses in response to trigger factors (e.g sunlight, wiind, increased blood flow, dust, warm, cold etc). If suspiscion of photic or trigeminal component treat with cyproheptaine or carbamazepine. Avoidance of stimuli e.g masks, nets, lens, hoods. Surgical compression of the infraorbital nerve using platinum coils has been described. Some improvement but self trauma still a problem. Permanent tracheostomy effective in some horses (thought to be because airflow bypasses nasal cavity where trigger factors are thought to act).
What is the normal body temperature for an adult horse? How is this maintained?
Adult approximate range is 38.1+-0.5, with average around 38.0C. Nenatal foals slightly higher ranging from 37.8-38.9. Maintenance of body temperature neuronally controlled in negative feedback system. Hypothalamus and autonomic and behavioural effector systems. In horses, sweating is important for evaporative heat loss.
What is hyperthermia?
A significant elevation in body temperature in which the core body temperature set point is unaltered. Causes can include: increased heat production, heat absorption, impairment of heat loss, CNS disorders disturbing hypothalamus, certain toxins or drugs e.g erythromycin may cause hyperthermia in hot weather especially in the foal, hyperkalaemic periodic paralysis, exercise (heat production may exceed ability of heat loss mechanisms). e.g fans, water sprays etc. Antipyretic drugs e.g nsaids have no effect. Heat stroke, anhiidrosis, malignant hyperthermia has been reported.
What is fever and what may cause a fever? how does fever differ from hyperthermia?
Differs from hyperthermia in fever the core body temperature set point is elevated. Initiated by various infections, inflammatory, immunological, neoplastic or traumatic conditions. complex interaction of many cytokines especially IL-1, TNF-a, IFN. These cytokines have a pyrogenic actions amongst many other actions. They act locally, systemically and in the brain. the production of arachidonic acid and prostaglandins important as COX inhibitors have antipyretic actions. They have no effect on normal body temperature. Febrile state also accompanied by metabolic, haematological and immunological staes. The cytokine cascade can lead to an acute phase response. Therefore monitoring fever is important. Infectious causes: numerous. Viral e.g respiratory viruses. Bacterial e.g streptococcus equi, salmonela spp. Neoplasic conditions such as lymphosarcoma, squamous cell carcinoma, immunological/inflammatory - various conditions including prpura haemorrhagica, urtcaria, pemphigus foliaceus. Miscellaneous eg hepatic disorders, hyperkalaemic period paralysis, foreign bodies, thrombphlebitis, drug reactions etc.
Describe a through investigation of pyrexia of unknown origin
Most febrile conditions are caused by infeectious diseases and may be diagnosed with history and clinical examination or they may run their course and recover within 2 weeks with n o aetiological diagnosis being made. But some fevers may be ore chronic or even intermittent and can be difficult and frustrating to diagnose. A thorough history including document the fever record, vaccination history, are others affected, movement of animals on and off premises to events etc, drug administrations. A thorough clinical exam, reeectal temperature preferably more than twice a day, discharges: nasal, vaginal etc. Auscultation, percussion chest. Lymph nodes, rectal exam. Ancillary examinations: endoscopy respiratory tract, ultrasound chest, abdomen, radiography of chest, abdominocentesis, thoracocentesis if indicated. Laparoscopy/laparotomy only if really suspect abdominal disease and if surgery really indicated. Biopsies, fluid aspirates.
Describe the aetiology of neonatal pneumonia. What is the treatment?
A common sequel to bacteraemia and septicaemia. Initial signs often non specific eg dullness and fever. Tachypnoea - 35/min - normal rate immediately post partum is 60-89/min, declining to 30/min by 1h, more common than coughing and nasal discharge. Bronchoscopy, trans tracheal aspirate culture, ultrasonography and radiopgrahy are useful. Haematology and clinical chemistry are less sensitive and specific. Treat with antibiotics, ideally based on culture and sensitivity. Suitable include penicillin/gentamicin, ceftiofur or cefquiome. Supplement IgG if there is concurrent FPT. Intensive nursing, oxygen by mask or trans nasal tube. IV fluids and frequent turning of recumbent foals are essential. Prognosis dependent on speed of treatment, type of bacteria, severity of lung damage and presence of sepsis in other structures.
What is the affect of a prepartum EHV-1 infection in a mare?
While EHV-1 usually causes outbreaks of abortion in last trimester, occasionally it leads to birth of extremely weak foals which die despite attempted treatment. Confirm by PCR or detection of pathognomonic histological inclusion bodies in foals liver lungs and thyms. Most stud mares are vaccinated against EHV1 & 4, but protection is incomplete.
What is neonatal fractured rib syndrome? How can it be treated?
Many foals develop rib fractures as a result of thoracic compression during forceful expulsion. Most are asymptomatic or cause only local injury (pain, swelling, haemorrhage). Potentially fatal sequelae include haemothorax, pneumothorax, laceration of the lung, percardium, myocardium and diaphragm. Careful thoracic palpation and ultrasnography are useful. The affected segment can be stabilised with adhesive bandage an the foal confined to a stable for a few weeks. Surgical stabilisation is required for flail chest?
What is meconium aspiration in foals?
In utero stress may cause foals to defecate and gasp, leading to Prepartum aspiration of meconium. This causes obstruction and chemical injury of airways. Affected foals have meconium staining on the coat and a brown coloured, bilateral nasal discharge at birth. Treatment involves nursing and broad spectrum antibiotics. Aspiration of meconium from airways can be attempted.
What is dysmaturity in foals? why do these foals have a poor prognosis?
Inadequate lung maturation may lead to increasingly severe expiratory effort and lung dysfunction. Provide surfactant, respiratory support, antibiotics. Poor prognosis <300 days gestation.
How does infection with rhodococcus equine pneumonia occur? What is the treatment and prophylaxis?
Occurs primarily on intensive rearing farms in warm, dry climates. Foals probably infected as neonates, by inhalation or ingestion of environmental bacteria, but do not develop clinical signs until 2-6 months old. Bacteria reside intracellularly, particularly in phagocytes, leading to multifocal Pulmonary abscessation. Signs include ill thrift, debility, progressive dyspnoea ad less commonly coughing and nasal discharge. Systemic spread may cause abscessation in other structures including mediastinal and mesenteric lymph nodes, joints, physes and GIT. all in contact foals should be screened, because early detection and treatment improves the outcome. Prolonged treatment with rifampin and erythromycin, clarithromycin or azithromycin is required. Hyperimmune serum is available in some countries. Prophylaxis can include - improved managemet, reduce stocking desity, collect faeces from paddocks, rotate paddocks, move water and feed areas around paddocks to prevent development of dusty areas, administration of appropriate prophylactic antibiotics to neonates or administration of specific hyperimmune serum. Vaccines are under development.
What is Streptococcus equi var zooepidemicus infection?
A common recurrent problem in groups of growing foals. Nuisance rather than concern. cough, nasal discharge, slight submandibular lymph node enlargement, intermittent mild and pyrexia, but animals are not sick. Administer penicillin and turn out to pasture or ignore. May wax and wane over several weeks.
How do you identify the aetiology of infectious respiratory disease in adults?
Identification of aetiology of outbreaks is often not possible on clinical grounds alone beecause of common presenting signs, including pyrexia, dullness, anorexia, coughing, mucoid to mucopurulent to purulent asal discharge and bilateral enlargement of submandibular lymph nodes. Influenza is likely cause if outbreak spreads rapidly and strangles is likely when horses have marked submandibular lymph node abscessation. Vaccinated horses may still develop clinical infections. Where detailed laboratory investigation is performed, cause is not determined in 40% of cases, while in others, multiple agent are identified. For virus screen submit some of the following; nasopharyngeal swabs, tracheal aspirates, BALF ,s erum or heparinised blood. For virology, respiratory secretions should be submitted in virus transport medium. Influenza is detected rapidly in secretions by ELISA. culture of influenza and EHV from secretions takes several weeks, so is more useful for disease epidemiology than clinical diagnosis. Paired serology takes 2-3 weeks. culture of bacteria in nasopharyngeal swabs or tracheal aspirataes.
How should respiratory Infection outbreaks be managed in horses?
Antiviral drugs are rarely used. Rest is important. maintain horses in clean air environment (well ventilated stable, shaving bedding and fed haylage from ground to encourage gravitational drainage of secretions). Antibiotics often administered if horse remains febrile for 4-5 days, respiratory secretions become purulent or if marked respiratory signs occur, particularly in young or very old horses. Clenbuterol may aid mucociliary clearance.
Describe EHV1 and EHV4 infections
Probably the commonest equine respiratory infection. EHV1 occasionally causes respiratory disease, but more commonly causes outbreaks of abortion and encephalomyopathy. All horses acquire EHV early in life, and probably all become asymptomatic carriers of latent vius which may redrudesce following sterss or intercurrent disease. Immunity to natural infection is short lived and horses may be repeatedly infected, especially following mixing of horses at sales or races. EHV4 is particularly problematic in young horses in trainig. EHV causes prolonged immunosuppression. EHV vaccines are not very effective but may afford some protection in younger racehorses.
What is equine viral arteritis? What are the clinical signs?
Clinical sigs are variable including general signs of respiratory disease, severe conjunctivitis, profound depression and Periorbital oedema due to vasculitis. It is venereal spread. Effective vaccines are available.
What is the causative organism of strangles? how does it spread?
Streptococcus equi var equi - spreads rapidly via direct contact and via fomites. bacteria remain viable in environment for weeks- months. Signs of classical strangles include pyrexia, bilateral purulent nasal discharge, dysphagia and marked sweling of submadibular and occasionally other head lymph nodes. Atypical strangles cases have no lymph node abscessation and may be misclassified as viral respiratory disease unless culture/PCR is doe. Diagnosis is confirmed by culture or PCR of bacteria in nasal, nasopharyngeal or guttoral pouch swabs/washes or detection in serum antibodies using ELISA. biochemical identification required to differentiate bacteria from streptococcus zooepidemicus var zooepidemicus, a common commensal of nasopharyx.
How is strangles treated and what are the possible sequelae?
Treatment; penicillin treatment early in disease course may stop clinical progression, but unclear if horses develop immunity so must be done in conjunction with effective isolation. Do not administer antibiotics to horses with lymph node abscesses. Nursing care important as described for viral cases. Sequelae include bastard strangles which is a rare complication whereby abscessation occurs in other tissues including mediastinal ad mesenteric lymph nodes and physes. Affected horses present with fever, malaise, weight loss and signs related to local abscessation. Poor prognosis. Purpura haemorrhagica is an immune mediated vasculitis occuring 1-3 months after strangles infection. Signs include generalised oedema, petechiation, pyrexia, commonly resulting in multi organ failure. High mortality. Treat with immunosuppressive doses of dexamethasone, penicillin and supportive care. Guttoral pouch empyema may also occur
What is recurrent airway osbtruction?
Airway inflammatory response to pro inflammatory agents in inhaled organic dust, originating from poorly conserved hay and straw. Controlled exposure to hay/straw may be done to exacerbate clinical signs and thereby aid diagnosis of mild clinical signs. Risk factors include >5yo, poor stable hygiene, genetic predisposition, respiratory infections and exposure to hay /straw early in life. Coughing is most sensitive indicator of equine pulmonary disease and most frequent presenting sign. Clinical signs reflect airway inflammation and obstruction, especially of the bronchioles. coughing is most sensitive indicator of equine pulmonary disease and most frequent presenting sign for RAO. coughing is usually exacerbated by exercise and poor exercise tolerance is common. Bilateral mucopurulent nasal discharge is present in 55% of cases. the remainder have o nasal discharge because they swallow the increased volumes of mucopus. Overt expiratory dyspnoea leads to tachypnoea, expiratory heaving and development of heave lie. Severely affected horses have audible wheezes or crackles.
Describe how environmental management can be used to treat Recurrent airway obstruction (heaves)?
This is essential and highly effective. All sources of airborne organic dust may be eliminated, ideally by keeping horses permanetly at pasture. when this is not possible, shavings or paper bedding must be used and all wet bedding removed daily. do not use deep litter shavigs or paper as they rapidly develop mould and bacterial cotamination. haylage, chopped dried alfalfa, silage or complete cubed diets are suitable low dust feedstuffs. Feeding soaked hay is ineffective as the dust challenge is not fully eliminated and additionally the nutritive content of the hay is reduced. To provide adequate ventilation the top door is kept open permanently and a louvered vent inserted in the back wall of the stable. Affected horses should be housed as far as possible from potential sources of organic dusts, such as stables containing hay and straw, waste bedding and barns. Treatment of acute RAO - tur out or house in dust free evironment, best rescue drug is atropine, but adverse effects preclude its repeated use, follow up with clenbuterol or inhaled sallbutamol, inhaled beclomethasone or oral prednislone. maintain hydration to avoid respiratory secretion becoming tenacious.
What is summer pasture associated obstructive pulmonary disease? (SPAOPD)
Similar clinicopathological features to RAO, but affects pastured horses with no access to hay/straw. clinical disease occurs between spring and autumn, with remission during winter. Some horses have both SPAOPD and RAO. Severe and potentially fatal dyspnoea rather than coughing and nasal discharge is the usual presenting sig. Crackles and whezes commonly detected on auscultation. Diagnosis usualy made on basis of history and clinical findings although marked neutrophilia of tracheal mucus and BALF may be helpful. Aetiology is unknown, but likely represents a pulmonary hypersesitivity to inhaled pollens or outdoor moulds. Intradermal antigen testing with a wide variety of antigens has failed to identify the cause. management is more problematic than for RAO. Some horses may improve when moved to a different environment. If this is not feasible. horses should be housed in a dust free environment as for RAO. Bronchodilators in combination with oral or inhaled glucocorticoids are usually administered as bronchodilators alone commonly give only a partial and temporary improvement.
What is inflammatory airway disease?
A syndrome characterised by coughing, exercise intolerance, increased volumes of neutrophiilic mucopus within lower airways and occasionally nasal discharge. Horses are not depressed, sick or pyrexic and do not have the overt airway obstruction that characterises RAO. In contrast to RAO, which invariably affects older horses, all ages of horse may develop IAD. IAD is commonly identified at the start of traiing. Syndrome may self resolve within a couple of weeks or may persist for months ot years with chronic cases being frustrating to manage. Many affected horses have a history consistent with a preceding, acute onset infectious respiratory disease. Aetiology is unclear but appears multifactorial,including bacteria and inhaled dust/edotoxin. Treatment is largely symptomatic, including rest and provision of a dust free environment. While those horses with significant bacterial infections may benefit from antibiosis, antibiotic therapy alone is ineffective in many cases. Antibiotics should ideally be selected based on culture and sensitivity of tracheal aspirates. Oxytetracycline, ceftiofur, cefquinome, enrofloxacine or TMPS are commonly used. Some horses with chronic IAD respond favourably to oral or inhaled glucocorticoids. Oral alpha interferon has been shown to be effective in some studies but is expensive. IAD does not cause overt airway obstruction so bronchodilators probably not indicated.
Describe lungworm infestation in horses
Normally with dictyocaulus arfieldi - uncommon today because of widespread use of effective athelmintics. Occurs in summer or autumn, in horses pastured with donkeys, which are atural and usually asymptomatic, reservoir hosts. Infectios in horses are usually no patent and consequetly the baermann faecal flotation technique is unreliable for diagosis. Diagnosis confirmed by demonstrating eosiophilia in tracheal mucus or BALf, rarely by endoscopic visualisation of larvae within the trachea or in respiratory secretions or by positive response to anthelminics. Affected horses and in contact horses and donkeys should be given an avermectin or bezimidazole and moved to a clean pasture.
What is idiopathic pulmonary eosinophilia?
Most eosinophilic lung diseases which affect horses in the UK are unrelated to lungworm. These include eosiophil dominated acute alveolitis, chronic small airway diseases and chronic interstitial diseases. these are of unknown aetiology but often respond favourably to corticosteroids.
What are interstitial restrictive lung diseases
Poorly understood and uncommoly recognised. Characterised by acute or chronic inflammatory alveolitis with i njury to type I epithelial cells and endothelial cells. Serum proteins leak into alveoli leadig to pulmonary oedema in acute cases. inflammatory cells infiltrate alveoli and interstitium. If horses survive this early injurious phase inflammatory response resolves or interstitial fibrosis and granuloma develop over a period of weeks to years. Cause is not identified in majority of cases. Interstitial disease reduces lung compliance, causing predominantly inspiratory dyspnoea. Crackles, especially end inspiratory and wheezes are common. Nasal discharge and coughing are uncommon. Radiography reveals interstitial or mixed interstitial /alveolar pattern. Early inflammatory phase must be treated aggressively to prevent development of fibrosis. Putative causal agents should be eliminated. Immunosuppressive dosages of glucocorticoids are usually indicated. Frusemide may reduce pulmonary oedema. Bronchodilators are rarely effective.
What is pulmonary oedema and how does it present in horses?
Causes include acute URT obstruction, cardiac failure, alveolitis/interstitial lung disease, smoke inhalation, neoplasia, plant and drug toxicity, immune mediated and volume overload. Sings include frothy nasal discharge, increased inspiratory effort and widespread fine crackles on auscultation. Endoscopy - frothy fluid within airways. Radiography - diffuse interstitial or mixed interstitial. Treatment - correct underlying cause where possible eg for URT obstruction insert tracheostomy tube, frusemide, intranasal oxygen, and where appropriate, antibiotics and corticosteroids.
How does thoracic neoplasia present in the horse?
Rare. Most cases have lymphosarcoma or metastatic disease, with primary lung neoplasia being rare. Clinical signs are variable and include weight loss, anorexia, pyrexia, dyspnoea, chronic coughing, pleural effusion, ventral oedema and jugular distension. thoracic radiography, ultrasonography, thoracocentesis, pleuroscopy and cytology of pleural fluid or a tracheobronchial aspirate may aid diagnosis.
How do pulmonary abscesses and pleuropeumonia occur?
Often follows prolonged transport, when pulmonary defences are compromised or as a sequel to aspiration of saliva and food. A wide range of aerobic and anaerobic bacteria may be involved, commonly mixed infections. Initially bacteria colonise lung causing localised pneumonia. Extension of inflammatory response to adjacet pleura causes sterile inflammatory effusion termed a parapeumonic pleural effusion. systemic antibiosis alone may be effective at this stage. Extension of bacterial infection into pleura induces production of larve volumes of infected purulent effusion which requires drainage. Large amounts of fibrin are formed lining the pleural surfaces and resulting in locule formation. The organisation phase is characterised by significant fibrin deposition resulting in a thick pleural peel which limits thoracic expansion. Affected horses are sick with lethargy, anorexia, pyrexia, ventral oedema and varying degrees of respiratory distress. Pleural pain causes reluctance to move, base narrow stance, elbow abduction, soft muffled coughing and fast shallow ventilation. These signs may be misinterpreted as signs of colic, laminitis or hypocalcaemia. Malodorous breath suggests anaerobic infection or lung necrosis and is a poor prognostic sig.
What is pleural effusion caused by in the horse?
Causes include thoracic neoplasia, b acteerial leuropneumonia, penetrating chest wall wounds, concurrent peritonitis, congestive heart failure, hypoproteinaemia, chylothorax ad diaphragmatic hernia. Identify effusion by auscultation, percussion and ultrasoography. Pleural fluid analysis can facilitate differentiation of transudate, modified transudate and exudate. Perform cytological examination for neoplastic cells and aerobic and anaerobic culture and gram smear for bacteria. Treat underlying cause and perform thoracocentesis.
What is exercise induced pulmonary haemorrhage?
During very fast exercise most horses bleed from dorsocaudal lung, because of very high pulmonary capillary pressures, sub atmospheric inspiratory pressures and presence of other predisposiing URT, LRT and cardiac disorders. Most bleeds are asymptomatic however marked EIPH can cause epistaxis, poor exercise perforamce, pulling up and very rarely, death. Excessive coughing is not a feature of EIPH. Diagnosis is confirmed by bronchoscopy, fresh blood is visible in trachea and large bronchi for a few days following a bleed, while Haemosiderin tinted secretions are visible in trachea and large bronchi for a few days following a bleed, while haemosiderin tinted secretions are visible for up to 1 week. Haemosiderophages can be identified in tracheal aspirates and BALF for many months following a bleed. Treatment is largely unsatisfactory but includes rest treatment of underlying cardiac URT and LRT disorders, nsaids to reduce interstitial lung fibrosis, dust free environment and training at slower speeds. Pre race administration of frusemide is permitted in some countries but is of questionable efficacy. Non responsive horses should be retired to less demanding disciplines.
What is diarrhoea? what is the result of diarrhoea?
Passage of faecal material with increased water content. In adult horses - almost exclusively due to disorders of the large intestines, although may be a secondary response to another disease process e.g edotoxaemia, liver disease. Acute diarrhoea may result in sigificat water and electrolyte losses and acid base disturbances.
What are the different mechanisms of diarrhoea?
Malabsorption; decrease i functioal absorptive surface area (decreased fluid absorption and retention), increased secretion: increased solute and water secretion by inflamed colon. Abnormal motility: decreased transit time eg stress/excitement. Osmotic overload e.g carbohydrate overload/magnesium sulphate administration. Increased hydraulic pressure from blood to intestinal lumen e.g congestive cardiac failure, inflammatory bowel disease.
Name the potential causes of acute diarrhoea?
Infectious; salmonella typhiumurium, clostridium difficile, clostridium perfringens, parasitic cyathostomiasis, toxic - NSAIDS, others - atbiotic usage, carbohydrate overload.
What are the potential causes of chronic diarrhoea?
Chronic salmonellosis, chronic cyathostomiasis, lawsonia intracellularis, sand, NSAID toxicity, granulomatous eteritis, lymphocytic plasmacytic enteritis, multisystemic eosinophilic epitheliotrophic disease. Disruption in normal physiological processes 9abnormal VFA synthesis or absorption). Non GI-
Liver disease, congestive heat failure, renal disease.
Describe a general treatment approach to acute diarrhoea?
Fluid/ electrolyte / protein replacement - orally via indwelling nasogastric tube if no small intestinal ileus, 4-8L every 20-30 min. IV fluids preferred in most cases - isotonic sodium chloride or lactated ringers: volume ad rate depends on degree of fluid and electrolyte losses. Hypertonic NaCl - if severe hyponatraemia, contraindicated if severely dehydrated ad should always be followed by administration of isotonic solutions. Colloids - protein losses may result in interstitial oedema formation, drop in oncotic pressure may worsen with crystalloid fluid administration. Colloids - more effective and longer duration of plasma volume expansion. When using synthetic colloids - plasma protein may be poor indicator of plasma oncotic pressure. Control of colonic inflammation and reduction in fluid secretion - prostaglandins likely play a large role in infectious diarrhoea, COX inhibitors - anti secretory effects however PGE2 and PGI2 are critical for mucosal repair therefore NSAID use is controversial. Other anti inflammatory drugs - metronidazole, bismuth subsalicylate. Control of endotoxaemia with low dose NSAIDS. Promotion of mucosal repair - sucralfate, misoprostol, psyllium mucilloid increases productio of SCFAs. Control of pain - alpha2 agonists, butorphanol, lidocaine. Antibiotics indicated in neutropaenic horses. Increased risk of septicaemia either from primary bacterial cause or GI bacteria breaching a compromised mucosal barrier.
Describe a general treatment approach to an undifferentiated CHRONIC diarrhoea
Change diet: hay and alfalfa good source of easily digestible protein. Stop NSAID and antibiotic therapy if this could be possible cause. Caecal traunsfaunation or probiotics. Larvicidal dose anthelmintics & corticosteroids if suspect cyathostomiasis. May need to wait several weeks to determine whether this is effective. Corticosteroids - last resort, may improve inflammatory enteritis. Since may have malabsorption best to give injectable dexamethasone therapy for first week then 1.1g/kg prednisolone every other day orally. Taper dose off over at least a 2 week period. May need intermittent or long term low dose therapy. Not a high success rate.
What is colic?
Clinical signs consistent with abdominal usually gastrointestinal pain. Be aware of false colics - origin of pain from non GI structures. colic is not a diagnosis. Commonly encountered problem in equine practice.
Describe the common behavioural findings seen with colic in horses
Mild colic - stretching of the abdomen, looking at flanks, teeth grinding, yawning. Moderate colic - pacing up the box, pawing the ground, kicking at belly, crouched stance, grunting, frequent getting up and down, prolonged periods in lateral recumbency. Severe colic: includes many of the above signs in addition to generalised sweating, rolling and self inflicted trauma.
What history should be take for evaluation of the colic patient?
History - when were the clinical symptoms first noticed, how rapidly have the symptoms proressed, what when ad how much feed an water intake, how much faeces urine, repeated episodes of colic? weight loss?, worming programme? at grass:grass sickness, intestinal parasitism, tympanic colic, recent changes in diet? stages of work? (horses in work that are given time off commonly get mild immpactions), bedding: horses that eat their bedding may get impactios, season: incidence of grass sickness peaks in spring/summer, in the winter season there is often an increased frequency of primary impactions.
Describe how the degree and nature of pain is important in a clinical examination of a colic patient
Intermittent, cotinuous, increasing or decreasing.
Visceral pain - most commo: increased peristalsis, distension, ischaemia, stretching of mesentery.
Parietal pain: less common, inflammation of the pareital peritoneum, tend to be immobile, boarding of the abdomen, resent external abdominal compression.
Abdominal distension - indicates large colon and or Caecal distension in the adult horse.
Rectal temperature - increase with anterior enteritis, colitis, peritoitis, and intestinal abscessation.
decrease coupled with a rapid weak pulse indicates shock - grave prognosis.
What do the possible different colours of mucous membrane ad capillary refill time of a colic patient tell you?
Pink - seen with mild impactions, simple colics.
Pale - anaemic, seen with intrabadominal haemorrhage
Red /injected: haemoconcentration and vasodilation, results from endotoxaemia.
Brick red - further deterioration
toxic/dirty brown - later stages of endotoxic shock, may show toxic lie in periodontal region, cyanotic suggests grave prognosis, euthanasia probably best.
CRT best assessed from oral mucous membranes, reflects circulatory status. Normal <2 seconds. Increasing CRT indicates a progressively inadequate peripheral perfusion.
Why is abdominal auscultation important in a colic patient?
Auscultate for several minutes i each of 4 sites (right/left/orsal/ventral). Note site ad nature of the sounds heart - haustral short duration,2-4 per minute, peristaltic longer duratio once every 2-4 minutes, caecal filling, caecal emptying. Increased gut sounds may be heard with spasmodic or tympanitic colics. Decreased gut sounds usually heard with most other types of colic, grass sickness and various metabolic systemic disorders. Generally the quieter the abdomen the more serious the problem. Percussing the abdomen will often elicit a ping over the tympanitic areas especially over a distended caecum.
Describe what May be detected on a rectal examination of a colic patient?
Only the caudal 1//3 of the abdominal cavity is palpable. Foals and small ponies too small to permit examination. Adequate restraint - necessary to ensure the safety of the personnel and horse. It is not possible to palpate small intestinal loops in a normal horse. The jejunum has a long mesenteric attachment and moves away from the hand. Palpation of distended loops of small intestine is one indication in which referral should be considered. It may be necessary to perform rectal examinations at hourly or two hourly intervals. Specific abnormal rectal findings include; Impaction of the pelvic flexure - very common, often easily diagnosed on rectal examiatio, feels like a doughy mass. Secondary impaction of the pelvic flexure occurs in some conditions with colonic stasis. Absorption of fluid from the colon. Small intestinal distension: may be palpable in grass sickness, enteritis, strangulating obstructions, small intestinal impactions, intussusceptions and non strangulating infarctions. Caecal intussusception - may be palpated as a mass within the caecum. Ileocaecal intussusception may be detected as a paiful, oedematous ass within the caecal base, likely to also result in small intestinal distension. Large intestinal gaseous distension - occurs in a number of conditions including primary flatulent colic, transverse or small colon obstructioon, large colon displacements, large colon torsions. nephrosplenic entrapment of large colon - occurs when the left large colon migrates dorsally between the spleen and the body wall and ultimately hooks over the nephro splenic ligament. colon may be palpated in left/dorsal abdominal quadrant running in a dorsoventral direction. May palpate colon overlying the nephrosplenic ligament. Intra abdominal abscess formation or neoplasia - may be palpable per rectum if situated in a suitable position. Can range in size from golf ball sized to football sized.
When is the passage of a nastogastric tube indicated?
For diagnosis of gastric distension with as or liquid, since gastric reflux is nor normally spontaneous it is always necessary to pass a stomach tube to determine if excessive fluid/gas is present. Relief of gastric distension, administration of therapeutic agents directly into the stomach. Conditions that result in gastric dilation/reflux include: acute grass sickness, ileus, small intestinal strangulating obstruction, proximal jejunitis, some cases of large intestinal obstruction.
When should abdominal paracentesis be done?
should be considered in most cases of colic unless confident they are simple medical colics. Interpretation - initial response of the peritoneum to inflammation or ischaemia is an increase in protein and fibrinogen levels. Fibrinogen >0.1g/l is suggestive of an acute inflammatory response or haemoabdomen. With progressive insult - leukocyte counts WBC increase. Acute Ischaemia is characterised by a Neutrophilia and increased erythrocytes due to diapedesis. Acute inflammatory responses such as Abscessation or bacterial peritonitis may increase neutrophils counts without increasing red blood cell numbers. chronic inflammatory conditions show increases in both neutrophils and mononuclear cells. Peritoneal fluid may remai ormal in horses with devitalised bowel if inflammatory debris is trapped, as occurs in epiploic entrapment and intussusceptions. Purulent fluid see in peritonitis. Serosanguinous fluid indicative of infarction in which there is leakage of HB and RBCs from the intestine. Fresh blood from intra abdominal haemorrhage or iatrogeic haemorrhage. Digesta - ruptured viscus.
What are the suggested indications for surgery/euthanasia of colics?
Severe continuous pain showing no or only short duration improvement with analgesia. Pulse >60, progressively rising and weakening. Progressive cardiovascular collapse: PCV >55, injected or cyanotic mms despite fluids, rectal findings positive for acute abdominal diseas.e progressive reduction in the intestinal motility or continual gas reflux. incraesing abdominal distension. Serosanguinous peritoneal fluid with increased protein and WBCs. If none of the seven criteria are preset, treat medically but reassess at short intervals so that any subsequet development of indications for surgical therapy can be detected early and treated appropriately.
What medical treatment can be used for colic patients?
Avoid large volumes of fluids/liquid paraffin orally if intestinal motility is reduced.
NSAIDS - act peripherally by inhibiting prostagladin production, do not depress gut motility some have potent endotoxin properties. Excess usage side effects include gastrointestinal ulceration, renal papillary necrosis and blood dyscrasias. options include phenylbutazone, flunixin, ketoprogen.
Opioids - very potent analgesics, temporarily prolong gut transit time, cause respiratory and cardiovascular depressio, do nto mask the clinical signs of endotoxaemia. options include butorphanol, morphine.
Sedatives - provide good sedation along with varying degrees of visceral analgesia. side effects include reduced gut motility, ataxia and bradycardia. often used in combination with a opioid. options include romifidine, xylazine, detomidine. Spasmolytic drugs; buscopan compositum contains metamizole and butylscopolamine- commonly used first line of treatment.
Laxatives best used in conjunction with fluid therapy when treating impactions. important to ensure good intestinal motility before administration. Optios include liquid paraffin, dioctyl sodium sulfosuccinate, oral magesium sulphate.
IV fluids - often essential in cases of severe dehydration nor endotoxic shock, administration in the field often quite difficult. very effective in softening intestinal impactions. Options include polyionic fluid, isotonic glucose salie, sodium bicarbonate, hypertonic saline.
What is icterus?
Yellow coloration of the sclera and mucous membranes resulting from increased tissue and serum bilirubin. Usually indicative of; decreased excretion of bilirubin with liver or biliary tract disease, increased production of bilirubin with haemolytic anaemia, impaired hepatic uptake or conjugation of bilirubin with liver disease. Accumulation of conjugated bilirubin results in more pronounced jaundice than unconjugated bilirubin therefore most pronounced jaundice seen with hepatic or biliary obstructive disease. Icterus more likely with acute liver disease compared with chronic liver disease. Fasting/anorexia in the horse can result in an increase in unconjugated bilirubin.
What are the the clinical signs of equine liver disease? when do they appear?
Develop only when 60-70% of hepatocytes are destroyed, signs of hepatic failure may appear suddenly, often history of gradual weight loss, decreased appetite and recurrent bouts of photosensitisation before hepatic failure develops. Most die within a few weeks. Most signs are non specific; depressin, anorexia, weight loss, mild to severe abdominal pain. Some signs are more suggestive; icterus, photosensitisatio, pruritus, hepatic encephalopathy, coagulopathy, petechiae, bilateral laryngeal paralysis.
How is equine liver disease treated?
Largely supportive util adequate liver function returns or regeneration occurs. acute failure best progosis. chronic liver disease with extensive fibrosis - hopeless prognosis. treatment of horses with hepatic ecephalopathy rarely warranted. General principles - remove from source of hepatotoxins. Dietary mangement with high carbohydrate diet, low protein, antibiotics only indicated when suppurative cholangitis or abscesation suspected, tracheostomy may be required if bilateral laryngeal paralysis corticosteroids - no evidence to indicate inhibit development of liver fibrosis. may be contraindicated as increase metabolic load on liver. May be indicated in cases of chronic non suppurative cholangiohepatitis. Treatment of hepatic encephalopathy - sedation; only if horse is uncontrollable and poses a danger to handlers. Correction of metabolic, fluid and electrolyte abnormalities, reduction in GIT production/absorption of potential neurotoxins - reduce number of anaerobes and gram negative urea splitting organisms. Lactulose - reduces intestinal neurotransmitter production and absorption.
What are the different methods of assessing weight in horses?
By eye, Body condition scoring e.g method of carroll and huntigdo, point score, weight tape and calculations - based on algorithms calculated from girth and or other anatomical points, weigh bridge - most accurate and least available, regular calibration required. Owners should be encouraged to regularly condition score their horses.
What are the differentials for weight loss?
Management, physiology etc;
Poor nutrition; amouts and or types/quality
Increased metabolic demads: exercise, pregnancy, vices
Hierarchy/pecking order
Inability to access
Old age
Disease:
Dysphagia
Maldigestion and malabsortion - parasites, IBDz, neoplasia, liver disease
Increased consumption or loss (parasites, IBDz, Neoplasia, PPID, EGS, renal disease, liver disease, cardiac disease, infections and sepsis, chronic pain)
Why is history and signalment important in the approach to diagnosis in the weight loss case?
Age - parasitism occurs more often in the young and problems like equine proliferative enteropathy are only features of weanlings living in relatively crowded coditions. Neoplasia more common i older animals. History of dental disease/routine floating - many abnormalities such as diastema, caudal hooks may be missed without a proper examination. Feeding history - amounts and types - are they matched nutritionally to the metabolic needs. Medicatio history; any history of repeated or cotinual NSAID use? antibiotics? worm history - very important, best case scenario is to obtain information relating to faecal egg worm counts, but remember that these do not reflect encysted cyathostome numbers, only adults. Even though the owner thinks they have a good worming regime, that may not be the case. Any diarrhoea noted by the owner? Diarrhoea generally means large intestinal problem i the hose. Any lethargy? water intake?
What further diagnostic techniques should be considered on first visit?
Rectal examination - obtain a fresh faecal sample. Abdominal paracentesis - peritonitis, neoplastic masses. Faecal analysis - blood, mucous, presence of small redowmr larvae, assessment of fibre length, indicatio of poor mastication. Haematology - significant neutrophilia with neoplasia and other inflammatory disease. Biochemistry - initial panel for evaluation of weight loss should include proteins, fibrinoge, alkaline phosphatase, liver screen - GLDH and GGT, assessment of urea and creatinine.
What is the symptomatic treatment of weight loss?
Assess weight and set date for re evaluation. Dietary change - ad lib good quality grass, hay, haylage. High energy feed e.g sugar beet young stock, mix, veteran diets, add oil to ration. Stop/start any long term medication for example phenylbutazone may be a potential cause of colitis or protein loss. Anthelmintic therapy: probably always worth giving a larvicidal dose of anthelmintics despite apparent adequacy of an anthelmintic regime. If high suspisio of cyathostome infestation then using either a single dose of moxidectin or the older regimen of repeating regime of 5 day fenbedazole followed by ivermectin may be used.
What is equine metabolic syndrome?
Term currently used to describe and explain obese horses or ponies prone to laminitis. Also known as peripheral cushings disease and obesity dependent laminitis. Insulin resistance may be a key factor. If an animal is obese and suffers recurrent bouts of laminitis then it probably has underlying metabolic predisposition to the obesity and the laminitis.
How can insulin sensitivity and glycaemic status be measured?
Insulin resistance is thought to play a major role in EMS. Fasting glucose and insulin test may be carried out in conjunction with tests to rule out ECF. starve of concentrations for 12 hours prior to testing. water ad grass hay may still be fed up until the sampling without invalidating the test. Increased levels of insulin provide evidence of insulin resistance, while increased glucose levels in a non stressed individual suggest severe IR/type 2 DM. Oral glucose tolerace test - horse or pony is starved of concentrates for 12 hours before test. Water is removed for 1 hour prior to test. Glucose is administered and blood glucose and insulin levels are tested prior to administration and at various points after. Blood gluocose should double within two hours and reduce to normal levels within 6 hours. Increased peak in glucose or delay to return to normal levels is indicative of relative insulin resistance.
How can Equine metabolic syndrome be managed/treated?
Control of calorific intake with judicious exercise in those individuals where this is possible. If there is an identifiable underlying cause then this should be treated appropriately. for example those animals with ECF should be treated with pergolide.
What strategies can be used with feeding horses with equine metabolic syndrome?
Feeds with a low glycaemic index should be chosen. Complete starvation should be avoided. Rich grass should be avoided as the sugar content can be very high. Restricted grazing practice must be balanced with the need for exercise therefore use of grass muzzles or night grazing may be advantageous. Grass hay is generally good but may be variable in soluble carbohydrate /sugar content therefore best practice is to encourage owners to have it analysed for non structural carbohydrate. Soaking hay may also reduce the soluble CHO as it gets trapped in the water. If further feeding is required then use other low GI foods. Alfalfa chaff is good extra ration.
Should horses with Equine metabolic syndrome be exercised?
May improve insulin sensitivity. Can be difficult if active laminitis. Placing an animal out to grass in theory is beneficial but can be difficult at the high risk times of year. Night grazing may be beneficial.
What are the possible causes of paresis and weakness? What are the key historical and clinical findings?
rhabdomyolysis, botulism, equine motor neurone disease, hyperkalaemic period paralysis, hypocalcaemia, myasthenia gravis. Fasiculuation/muscle twitchig, narrow based stance, icreased periods of recumbency, low head carriage at rest and during exercise, reluctance to bear weight when a limb is raised sudden rapid recumbency, dysphagia.
What are the possible causes of spasticity and hypertonia? What are the key historical findings with spasticity?
Rhabdomyolysis, tetanus, hypocalcaemia, shivering and stiff horse syndrome. Key historical findigs: fasciculation, trismus, stiff and stilted gait, other bizarre gait abnormalities.
Describe the pathophysiology of botulism
Caused by the toxin of clostridium botulinum, a gram positive anaerobic spore forming bacteria found ubiquitously in soil. toxin is thought to block acetylcholine release at the neuromuscular junction, peripheral cholinergic nerve terminals in autonomic ganglia, and post ganglionic parasympathetic nerve endings. C botulinum grows best in eutral or alkaline pH and grows ad produces toxin anaerobic environments such as decaying vegetable matter and animal carcasses. Silage provides a suitable medium for growth and toxin production. animal carcasses may be accidently baled into bales or chopped into cubes or pellets. Three modes of intoxication possible; Ingestion, of preformed toxin, growth of the agent in the GI system, or contamination of wounds. In adult horses in the UK, botulism is usually secondary to eating big bale silage.
What are the clinical signs of botulism in horses?
May be acute in onset with dyspnoea, severe diffuse paresiis and rapid progression to recumbency. In some horses the onset and progression are slower, occuring over several days. Weakness and trembling which improves during periods of recumbency. Inability to fully retract the tongue, dysphagia and drooling of the saliva, flaccidity of the tail, gradual onset of clinical signs is associated with a better prognosis cf acute onset. In fatal cases, death occurs quietly, in non fatal cases, recovery takes weeks to months.
What are the clinical signs of botulism in foals?
Initially appear alert, progression is associated with paresis, stilted gait and most prominent and generalised muscle trembling - shaker foals. ptosis and decreased tail tone is frequently evident. dysphagia is present despite a normal appetite. May show slow PLR, ileus, constipation and urine retention. Death is caused by respiratory paralysis or complications such as pneumoia. Mortality in this form >90%.
What is the treatment of botulism?
Definitive diagnosis by identification of toxin in serum, GI contents or food. Treatment mainly symptomatic. in cases of wound contamination or toxicoinfectious botulism, antibiotic therapy is indicated. Antibiotics associated with neuromuscular weakness should be avoided if possible e.g aminoglycosides, tetracyclines and procaine penicillin. Antitoxin not widely available for clinical use in the UK. Preention with good husbandry, vermin control, adequate disposal of carcasses, avoiding the use of spoiled foodstuff and poor quality silage.
Describe the pathophysiology of tetanus?
Caused by clostridium tetani - a large gram positive spore forming bacillus. found in soil and is a commensal in the GI tract of man and domestic animals. the spores of C tetani can persist in the environment for many years. In the body, requires anaerobic conditions to survie. The common sites of contamination includes; puncture wounds, surgical wouds, mucosal wounds and ulers, umbilical cord, retained placenta and Haematogenous spread to devitalise tissue. It produces a potent exotoxin - tetanospasm causes spastic contractions of striated muscles. Tetanospasm acts primarily on the CNS transported partly by the vascular system and partly by retrograde axonal migration along the motor nerves to the ventral horns of the spinal cord grey matter. Thought to act mainly by preveting the release of inhibitory neurotransmitters from the intereurons at the motor synapses in the spinal cord. Locally further tissue necrosis and exudation is aided by another toxin, tetanolysin.
What are the clinical signs of tetanus in the horse?
Horse very susceptible to toxin but may take a few days to several weeks to appear. first signs are usually a change in the horses gait (stilted action) and demeanour. May also notice a difficulty in eating at this stage (spasm of muscle of prehension, mastication and swallowing). Generalised spastic muscular contractions are provoked by external stimuli, especially evident in the third eyelid when the cheek is tapped or when fingers are snapped infront of the eye. The disease may worsen dramatically over the ext 24 hours or take several days, the horse will stand square on four stiff limbs with its head and neck extended and the tail raised. it will have an anxious expression with the nostrils flared, eyelids retracted and ears erect. Sweating and tachycardia may result. Drooling may be seen due to involvement of the pharyngeal and laryngeal muscles - food and water may be regurgitated down the nose or pass into the lungs. progression to recumbency and death often from convulsions leading to respiratory and cardiac arrest.
What is the treatment for tetanus?
in each case - consider the prognosis and the welfare aspects, recumbent adult animals should be destroyed. Cases with the best prognoses show mild clinical signs over several days and are still able to eat and drink. Quiet dark stable, peat or shavings bedding, elevate food and water soft moist food quiet gentle handing, acetyopromazine, sodium benzylpenicillin, procaine penicillin, antitoxin, hydrogen peroxide in wound. Prevention with vaccinatio.
What is the pathogenesis of acute rhabdomyolysis?
Common in working horses and ponies. Vast majority sporadic and associated with exercise. excessive glycogen > lactic acid and 02 radicals > coagulative necrosis > further muscle hypoxia > prevents muscular relaxation. Signs occur during or sometimes immediately following exercise. A minority of cases signs may eve occur on leaving the stall/box or following minimal exercise. With acute tying up both hind limbs are usually affected - especially gluteal, femoral and lumbar muscles. Affected horses develop a stiff gait and may refuse to move. Palpation reveals affected muscle groups to be painful, hard and swollen. The animal is frequently distressed, sweating, wiht increased temperature, HR and Rr. In severe cases the urine may be red/brown in colour due to the presence of myoblobin. The excess myoglobin may lead to renal failure due to the accumulation within the renal tubules. If the horse is oliguric, poor prognostic sign.
What laboratory findings can help you diagnose Acute rhabdoymolysis?
Elevations in the serum levels of enzyme creatinine kinase, aspartate aminotrasnferase and lactate dehydrogenase. the degree of increase reflects the degree of muscle damage. CK is the most specific for skeletal muscle damage. CK rises first and disappears first followed by LDH and then AST. LDH peaks at approximately 15 hours and may reach several thousant. AST peaks at 24 hours and may reach many thousand. The presence of myoglobin in the urine. When using a dipstick this cannot be distinguished from blood. Pathological findings - extensive pale discolouration of affected muscles.. Degeneration and swelling of muscle fibres histologically.
What are the General treatment measure sin one off/acute cases of tying up?
Rest - further muscular activity exacerbates the disease therefore doo not move the hors. Some very mild cases have been reported to respond to walking out but if in doubt, do not move. Analgesics - NSAIDs highly recommended. Fluids - consider oral fluids for mild cases, i/v for more severe. may of these cases are alkalotic, therefore HCO3 would be contraindicated. If unable to check the elctrolyte and acid base status best to give a balanced electrolyte solution. Diuretics are usually contra indicated unless despite vigorous fluid therapy the horse is still oliguric. Sedatives - ACP, may help alleviate anxiety and muscle spasm. Corticosteroids - short acting steroids may play a useful role in stabilising cellular membranes, however be aware of the risks of laminitis with high doses of potent corticosteroids. Calcium carbonate and calcium gluconate have been cited as being useful in severe cases as calcium may be depleted.
What is the treatment for chronic rhabdomyolsis?
Reduced carbohydrate, increased intake of food AFTER increased workload, Continual exercise with adequate warm ups and without breaks in routine, turnout is beneficial, stress avoidance especially important in recurrent ER cases. Acepromazine to reduce stress of training, dantrolene - reducing post exercise levels of CK. Salt - may sweat profusely resulting in loss of sodium and chloride. Vitamin E and selenium - believed to be useful due to their suspected involvement in oxidative reduction reactions within the cells.
List the potential differentials for collapse/falling in the horse or pony?
Seizures, Cervical vertebral stenosis, narcolepsy, inappropriate sleep, botulism, arrhthmias, haemorrhage, heart failure, aorto iliac thrombosis, neurocardiogenic collapse, hypocalcaemia, hypoglycaemia, monensin toxicosis, systemic anaphylaxis, air emboli, musculoskeletal abnormality, severe myopathy.
Describe The initial management of very sick foals
control seizures with diazepam, if hypothermic provide heat lamp or blankets ( blood culture vial. Treat navel with 0.05% chlorhexidine if moist - repeat for several days. Give tetanus antitoxin if mare not vaccinated within the last 4-6 weeks of gestation. LAsts approx 3 months.
Where is a heart murmur commonly heard in a foal?
Pansystolic murmur at cranial left heart base for up to 7 days in a oal, due to PDA or functional murmur. Palpate thorax for fractured ribs.
How is failure of passive transfer of antibody detected in foals?
Measure neonatal serum IgG from 8-24h onwards. Cannot do when >2 weeks since foals own IgG production will affect results. Single radial immunodiffusion kits - most accurate, highly specific. CITE test - accurate and suitable for field use. Normal IgG at 21 hours old >8g/l. FPT is partial or complete. Partial FPT (4-8g/l) may not need treatment if foal is clinically normal and in clean environment. Treat complete FPT <4g/l otherwise foal susceptible to sepsis.
What is the treatment of FPT in foals?
If 24 hours old - intestinal absorption of IgG ceased, so give 1-2L equine plasma IV. First litre over 60 minutes and slower rate subsequently. Rare complications include tachypnoea, shivering, aaphylaxis, volume overload.
What is neonatal Isoerythrolysis? (NI)
An immune mediated haemolytic anaemia. destruction of the foals RBCS by Colostral antibodies which are directed against foals RBC membrane alloantigens. Most incompatibilities are due to alloantigens Aa and Qa. Problem occurs when foal inherits Aa or Qa alloantigens from Aa or Qa +ve stallion and when RBC of mare are negative for these antigens - during birth of the foal, foetal blood often leaks into maternal circulation and mare makes anti Aa or Qa antibodies. As antibodies peak at 9 days after foaling they are not transferred in colostrum at first pregnancy thus do not get NI in first partum mares, however in subsequent pregnancies mare produces increasing amounts of these antibodies which are excreted in colostrum. If subsequent foals are Aa or Qa positive these antibodies cause NI. Normal at birth, signs begin from 6-8 hours, anaemia with weakness, icterus and rarely haemoglobinuria, depressio, anorexia, progressing to collapse and death.
What is the treatment of neonatal isoerythrolysis?
Prevent further absorption of mares colostral Ig - give alternative milk until foal is >24hours old. Milk mare thoroughly and regularly and discard colostrum. Blood transfusion equired if PCV <10-12% or if PCV reducing rapidly. Can transfuse thoroughly washed RBC from mare - wash 3x in saline, then administer 1-21 of 50% suspension of RBCs in saline. Alternatively transfuse whole blood from Aa, Qa alloantigen negative horse or stallion or gelding that has never had a transfusion. Collect blood into transfusion bags as plasma and administer whole blood via iline filter. Prevention - dont mate Aa or Qa ive mares with Aa or Qa +ve stallions. Test at risk mares serum for alloatibodies. in last 2 weeks of gestation when levels are increasing.
What is neonatal septicaemia in the foal?
The major cause of neonatal mortality, prognosis guarded. prompt therapy critical for success. portal entry GIT, lung, umbilicus, iatrogenic. Rarely acquired in utero, if so are sick at birth. Most acquired post partum - sigs develop 48-96 hours. Bacteria are usually ubiquitous environmental bacteria - maiinly gram negative, E. coli, salmonella, Klebsiella, actinobacillus, pseudomonas. And less often gram +ve streps, staphs, rhodococcus equi, clostridia. Initially have non specific signs reduced apeptiet, decreased sucking, dullness, increased recumbency, pyrexia, rapid progression to signs of multisystem involvement - meningitis, diarrhoea, colic, tachypnoea, resp distress, lameness, swollen joints, omphalophlebitis, uveitis, petechiae, scleral injection.
What laboratory results would you find in neonatal septicaemia?
Blood or body fluid cultures vry useful. collect samples before administration of antibiotics, ideally when foal is pyrexic. do not collect blood from indwelling iv catheter since may have surface contaminants. Do aerobic and anaerobic cultures. WBC counts may be normal, increased or decreased depending on stage of infection may need to follow progress of counts. Presence of bad and toxic neutrophils is suggestive of sepsis. Septic foal are often thrombocytopenic. Fibrinogen increased after 24hours. IgG may be low. Hypglycaemia, low pao2, metabolic acidosis.
What is the treatment of neonatal septicaemia in foals?
While awaiting culture results - use broad spectrum antibiotics e.g penicillin plus getamici, cetiofur or cefquinome. change therapy if necessary after culture and sensitivity results obtained . Treat for 1-2 weeks after clinical signs of sepsis have resolved. often need antibiotics for 1-2 months especially if persistent infection. Local therapy eg joint lavage, pleural drainage, umbilical surgery etc. IgGs - may need supplementing since may will have FPT.
What is foal heat diarrhoea?
Occurs at 6-14 days. Due to alteration in colonic microflora and epithelium as they adapt from milk to grass diet and perform corpophagy. Transient self curing diarrhoea. No Treatment required but watch in case it isn’t foal heat diarrhoea - reconsider diagnosis if becomes sick with pyrexia, depression, dehydration.
Describe rotavirus in the foal
Main cause of foal diarrhoea. Widespread in equine population. Adults probably source for foals. survives for over 9 months in enviroment. Many foals 1 month have mild enteritis only. Profuse watery, non foetid diarrhoea, depression. Mainly affects small intestine - stunting of villi & loss of absorptive capacity together with increased intestinal secretion. Diagnosed using ELISA or latex agglutination -submit faecal sample. Treat with specific antisera orally or treat symptomatically. Avoid overstocking. Vaccinate mare in ,9,10th month of gestation with inactivated equine rotavirus to provide Colostral protection.
What other Causes of infectious diarrhoea are there in foals?
Salmonellosis: mare is most likely source.commonly mild enteritis but may cause severe septcaemia. Clostridium perfringens type A B & C causes foetid necrotising haemorrhagic enteritis in 1-2 day old foals. commonly causing death within 48 hours. Septicaemia; dairrhoea is commoon presenting sign in septicaemia. Aeromonas spp probable primary cause of diarrhoea in foals. E. coli. Coronavirus and adenovirus. Cryptosporidium. Strongyloides westeri.
How should Diarrhoeic foals be managed?
Fluid therapy - critical since likely have dehydration, metabolic acidosis, and reduced Na, Cl, K. For mild dehydration administer isotonic electrolyte solutions orally little and often. Severe dehydration usually requires IV fluids. Antibiotics controversial and probably overused. Not idicated in nutritional, viral and parasitic diarrhoea. Only give in foals 1 day only as get undernutrition
Describe the aetiology and clinical signs of gastroduodenal ulceration in foals?
Probably multifactorial. Stress important - consequently most sick foals are given GDU prophylaxis. Can be iatrogenic - foals susceptible to NSAID toxicity. NSAIDs inhibit PG synthesis causing gastric mucosal vasoconstriction and ischaemia. Most foals have a few ulcers on the non glandular side of the margo plicatus without symptoms. Symptomatic ulcers occur from day 1 onwards causing anorexia, salivation, colic after sucking, dorsal recumbency, odotopresis, regurgitation of mucoid/watery gastric fluid. Proton pump inhibitor most effective and most commonly used.
What are the clinical signs of meconium retention? how can this be treated?
Meconium usually voided within a few hours. Retentio mainly in males due to narrow pelvis. Signs start at 6-24 hours, restless, straining, lifting tail, rolling, lying on back, attempts to urinate. Straining may reopen urachus - drip urine in conjunction with straining. Treatment using warm soapy water as enema using soft tube inserted 10-12’’. Forceps or rectal spoons not recommended.
What is tyzzers disease?
Uncommon in the UK - infectious necrotic hepatitis caused by clostridium piliformis. Affects foals 1-6 weeks old, sudden death or acute abdominal pain, depression. Penicillin recommended, b ut most foals die. Usually PM diagnosis.
What is uroperitoneum? how does this occur in foals?
Urine leakage from ruptured bladder or rarely from patent urachus or ureters. common in colt foals. ladder defect always on dorsal midline. probably ruptures when foals abdominal pressure increases during delivery. signs onset 3-7 days old. Usually only some of urine passes into peritoneal cavity so most foals still urinate exteernally. PRogressive onset of abdominal distension lethargy, tachypnoea, tachycardia, circulatory failure, mild abdominal pain. Diagnosis made on signs, ultrasonography of abdomen and bladder and peritoneal fluid analysis. Uro peritoneum confirmed by demonstrating ratio of creatinine in peritoneal fluid: serum >2:1. Most foals develop azotaemia, hyperkalaemia, hyponaetramemia, hypochloraemia and metabolic acidosis. due to metabolic derangements this is a medical emergency - attempt to drain abdomen via catheter, administer IV saline to correct Na loss and hyperkalaemia. correct hypoglycaemia, administer abx. Once stabilised performs surgical bladder closure.
What is perinatal asphyxia syndrome?
Exact pathogenesis unclear and likely multifactorial but involves peripartum cerebral hypoxia/ischaemia. Signs of cerebral dysfunction appear after several hours to 1 day - localised seizures of face and limbs, disorientation, ataxia, loss of righting and suck reflexes, loss of affinity for dam, central blindess, barking vocalisation, loss of thermoregulation, erratic breathing pattern, increasing recumbecy, coma or general seizures, o specific treatment. Steroids often administered but no evidence of efficacy. cotrol seizures using diazepam slow IV. Many stabilise by 2-3 days but flul recovery takes several weeks.
What does the umbilical stump comprise of?
2 umbilical arteries which connect internal iliac arteries to placenta and which after birth become round ligaments of the bladder. 1 umbilical vein which connects placenta to hepatic portal vein which becomes the round ligament lying within the falciform ligament after birth. Urachus - connects foetal bladder to allantoic cavity.
Describe an umbilical infection/Abscessation in the foal?
Infection occurs usually <1 week old. Most commonly have infection confined to external umbilicus with local heat, pain, swelling and commonly no systemic effects. These can be effectively drained or treated with systemic antibiotics. More concerning is infection of internal umbilicus - ultrasound useful to detect infection - often have secondary septicaemia. usually require surgical removal as rarely respond to antibiotics alone.
What is a parent urachus?
Associated with navel ill, septicaemia, increased abdominal pressure due to straining or prolonged recumbency. usually occurs soon after when dried umbilical stump drops off. easily recognised because urine drips from umbilicus and urethra when urinate. perform ultrasound examination to determine if urachus is infected. Infected urachus requires surgical removal, while uncomplicated patent urachus usually resolves simply with correction of underlying cause eg retained meconium.
When does a diagnosis in equine medicine usually NOT warrant antimicrobial therapy?
Strep equi subspp equi, subsolar abscess,diarrhoea, purely viral infections. Sulphonamides are ineffective in purulent and necrotic tissue. Aminoglycosides are ineffective in an abscess.
Describe the activity of trimethoprim sulphonamides?
equitrim an norodine. Both inhibit folic acid synthesis, individually are bacteriostatic but synergistically are bactericidal. Act against gram positive and gram negative but not anaerobes. Purulent and necrotic tissue inactivate sulphonamides. Time dependent. give BID not SId. Fatal cardiac dysrhythmias may occur with concurrent use of A2 agonists and IV TMPS.
Describe the activity of penicillin
Inhibits cell wall synthesis, bactericidal, gram positive,g ram negative and anaerobic effective. Time depedent. Benthazine penicillin G - give single long acting injection. Do not use as fails to reach MIC. Adverse effects to penicillin - inadvertent IV injection - ataxia/seizure like activity, hypersensitivity - urticaria, angiooedema, rapid IV administration - colic, loose faeces.
Describe the activity of the cephalosporins
Active against gram +ve, Gram-ve, aaerobes. Inhibits cell wall synthesis. Bactericial. Time dependent.
Describe the activity of the aminoglycosides
Amikacin - pumped across cell membrane & inhibit protein synthesis. Are bactericidal. active against gram ive. Concentration dependent. Side effects include Nephrotoxicity especially if dehydrated and NSAIds, ototoxicity, muscle irritation if IM.
Describe the activity of the tetracyclines
Inhibit bacterial protein synthesis, are bacteriostatic, concentration and time dependent, Active against gram positive, gram negative and anaerobes. Effective against intracellular pathogens - ehrlichia, rickettsial organisms, lawsonia. Oxytetracycline - Ca binding = treatment for flexural limb deformity in foals.
Describe the activity of the fluoroquinolones
Inhibit DNA gyrase responsble for supercoiling bacterial DNA, bactericidal, concentration dependent, active against gram =ve, gram -ve, not anaerobes. active against rickettsia ehrlichia.
Why should the macrolides not be used in adult horses?
Cause severe and fatal colitis. Hyperthermia with concurrent respiratory distress. Rhodococcus equi highly susceptible. Bacteriostatic. Very active against gram positive. Inhibit bacterial protein synthesis.
How does rifampin work?
Inhibits RNA polymerase. Bactericidal. Gram positive. Anaerobes. synergistic with macrolides - for rhodococcus equi. Always use in combination with another class of Antibiotics. rapidly develop resistance.
What is the difference between active and passive vaccination?
Active vaccination induces an antigen specific immune response in the vaccinated animal by administration of dead or live antigen or DNA capable of expressing protein antigens n vivo. Success of vaccination often depends on the effective use of an adjuvant, a compound capable of amplifying and directing immune responses. Passive vaccination is accomplished by administering preformed antibodies either as a plasma transfusion or in a concentrated form.
What are horses currently vaccinated for and when?
Equine influenza - 5-6 months of age, 4-6 weeks later, 5 months later.
Equine herpes virus - EHV1, EHV4
Tetanus - toxoic 2 vaccines 1 month apart then boosters every 2-3 years.
Equine viral arteritis - establishment of EVA negative status of stallions prior to vaccination is important.
Streptococcus equi - 2 vaccines 4 weeks apart. Booster every 3-5 months. live modified strain of S equi, submucosal. reduces clinical sigs only. Serological ELISA test positive.
What are the common equine parasites?
Cyathosomes small strongyles/redworms
Large strongyles large redworms e.g strongylus vulgaris
Ascarids (large roundworm) - immunity by 2 years
Aoplocephala (tapeworm) - 6 month cycle
Gasterophilus bots - 12 months to mature, tx once yearly
Strongyloides weteri - natural immunity by 6 moths, acquired via mares milk.
Oxyuris (pinworm) - irritation only. the most pathogenic equine nematode worldwide = cyathostome. Encysted larvae in large colon with subsequent en masse emergence later winter/early spriing.
What diagnostic tests can be used to detect worms?
FWEC - strongyles and ascarids, doesn’t detect immature or encysted strongyles.
Tapeworm ELISA - measures atibody, levels take at least 16 weeks to decline.
What anthelmintics can be used for routine treatment?
Febendazole
Pyratel
Ivermectin
Moxidectin
What anthelmintics can be used for strategic treatment?
Fenbendazole - 5 day course for encysted redworms.
Pyrantel - double dose for tapeworm.
Ivermectin - bots and lungworms.
Moxidectin - bots and encysted cyathostome larvae.
What anthelmintics are not safe for use in pregnant and lactating mares?
Moxidectin & praziquantel - safe for foals > 6.5 months old but not pregnant/lactating mares.
How should pasture be managed to avoid high worm burdens?
Avoid high stocking density/overgrazing, avoid horses with high faecal egg counts, avoid presence of young horses, twice weekly removal of faeces from pasture, alternative species grazing.
What is anthelmintic resistance?
failure of anthelmintic to perform as expected. Ca be due to suboptimal dsiing - encourage owners to use weigh tapes. increasingly due to resistance - particularly Benzimidazoles in relation to cyathstomes. over worming using interval programme promotes resistance. importance of refugia in retaining susceptible population of worms. at moment no new wormers in manufacture - can not fully rely on chemotherapeutic.
What is the average gestation length in the mare
342 days - range 321 -385 days. Do not induce parturition in the mare. Even if the mare has gone over her expected due date the foal is almost certainly not viable until normal parturition is ready to take place.
What are the signs of impending parturition?
Enlarged abdomen
Mammary development - 3-6 weeks prepartum, major changes within 2 weeks of term, initially straw coloured discharge, udder distends with colostrum 2-3 days prepartum, teat waxig lasts up to 48 hours, increase in calcium and magnesium content of milk, at term calcium >10mmol/l. Relaxation of sacrosciatic ligaments over last few weeks and vulva in last few hours. Relaxation of cervix. Foaling aids - measurement of milk calcium can be useful. Mares may wear a monitoring alert that sets of an alarm when the mare is recumbent for prolonged periods. this can result i false alarms and miss foalings. Some people have cameras in the stable that can be programmed into the tV in the house or an iphone.
Foalert is a small magnetic device that is sutured to the vulva - when parturition begins the magnet is opened and sets off an alarm that rings a mobile phone.
Describe stage 1 of parturition
Lasts approximately 2-4 hours, uterine contractions start, cervix relaxes and dilates, restlessness, colicky signs, patchy sweating. In some mares delivery of the foal may be delayed for several hours or days. the end of 1st stage labour is marked by rupture of the allantochorion at an avascular area, the cervical star, and release of straw coloured watery allantoic fluid. The foal rotated to a dorso sacral position just before birth. The amnion should protrude through the vulvar lips within 5 minutes of the rupture of the allantoochorion.
Describe stage II labour
Lasts less than 30 minutes;
Assume lateral recumbec, abdominal contractios, foal is delivered covered by amnion, the equine placenta separates from the endometrium rapidly and foetuses not delivered within a relatively short time of onset of 2nd stage labour are deprived of oxygen. Prolonged 2nd stage labour is an emergency. Normal presentation is anterior, dorso sacral, extended. Do not cut the umbilical cord - you may allow excessive bleeding.
Describe stage III labour
Expulsion of the placental membranes usually occurs within 1 hour with the allantoochorion turned inside out. NB always examine the placenta for completeness.
What is dystocia in the mare
Dystocia exists when 1st or second stage labour is prologed or not progressive and should always be considered an emergency. if o progress occurs within 10 minutes of onset of straining, a veterinary examination is needed. The foal will need to be delivered within an hour. Dystocia is most often caused by abormal presentation with long foetal extremities predisposing the mare to problems with delivery. Examination of the birth canal and feotus is necessary to determine the cause of the dystocia. The foetus is particularly at risk from placental detachment, hypoxia and damage to the respiratory centre.
What are the differennt causes of dystocia in the mare?
Primary uterine inertia - usualy due to voluntary suppression of foalig caused by disturbance. Cervix is partially ope. chorioallantois intact. Leave the mare alone for 20 minutes. Mare can have dilated cervix for 12 hours and foal normally. Important to remember that progress needs to be quick when mare on stage II. Can induce parturitio. Secondary uterine inertia - usually caused by foetal malpresetation. Failure of abdominal expulsive effort or obstruction of the birth canal. fetopelvic disproportion is rarely a problem in mares.
What are the indications for caesarian section in the mare?
Transverse presetatio, uterine torsio, malposture of living foetus which cannot be corrected rapidly, oversized foetus, and maternal pelvic deformities. The time from induction of anaesthesia to foal removal s hould be less than 20 minutes. usual approach is by midline laparotomy. Until the foetus is removed general anaesthesia should be maintained in a light plane to avoid respiratory depression. The uterus is incised along its greater curvature. Uterine contents should be treated as contaminated and carefully drained to the outside. the live foal should be placed alongside the mare with the umbilical cord left intact. The use of a continuous interlocking suture through all the layers of the uterine wall and around the entire margin of the incision controls intraluminal haemorrhage - a significant cause of maternal mortality. The uterus is closed with invertig sutures taking care to exclude any placenta. Administer oxytocin if the placenta was not removed.
How are bacterial venereal diseases treated?
Klebsiella and pseudomonas are difficult to treat - often treated with combination of topoical washings with pevidine followed by drying and packing the penis with gentamicin cream or 1% silver nitrate daily for 1-2 weeks. collect serial swabs over several weeks for cultural examination to monitor success of treatment. taylorella is sensitive to most antibiotics and antiseptics. Wash penis daily for 3-5 with 2% chlorhexidine followed by topical application of nitrofurazone or penicillin ointment. can treat penis with broth culture of normal microflora at end of treatment.
What are the signs of equine viral arteritis?
Signs may vary from none at all to severe systemic illness including fever, depression, filling of the lower limbs, conjunctivitis with periorbital oedema, nasal discharge, urticarial rashes, and oedematous plaques and ventral oedema. Infected mares may abort 7-10 days later. Infection is via the respiratory or venereal route. virus localises in the accessory sex glands of stallion and 30% of infected stallions continue to shed the virus indefinetly. shedder stallions are always seropositive but not all seropositive stallions are shedders. Mares do not become carriers. seropositive mares with a stable or declining antibody titre are thought not to infect stallions or in contact animals.
What are the major causes of PUPD in a horse?
Primary psychogenic polydipsia, PPID, Primary renal disease.
Less common; pscyogenic salt consumption, diabtes insipidus, drug induced
What are the baseline diagnostic tests for investigating alterations in urinary function?
Urinalysis very important. USG normal 1.020-1.050. Isothenuric 1.008-1.014. Hyposthenuric 75% loss of total tubular function. Protein levels: albumin may decrease with glomerular disease or tubular diseases. Electrolytes - sodium decrease, chloride decrease, calcium increase, phosphate decrease, potassium increase may. Glycaemic status: glucose, insulin and ACTH. Ideally done on resting sample after starving of concentrates for 12 hours for accurate interpretation.
What tests can be carried out if there are no signs of renal disease?
Water deprivation tests - tests the ability of the kidneys to concentrate urine in the face of water deprivation. Complete water deprivation test involves taking all fluid sources away and measuring USG gravity over succeeding hours. Important to evaluate hydration status . Must check renal function before carrying this out : to omit this would be negligent and dangerous.ADH stimulation test - animals which fail to concentrate after both Water deprivation tests have diabetes insipidus - either central or nephrogenic. Aimals with central DI should rapidly concentrate urine when given ADH analogue.
What is equine cushings disease/ pituitary pars intermedia dysfunction (PPID)
Due to the overproduction of proopiomelanocortin (POMC) peptides from pars intermedia. (PI) . the resultant increase in adrenocorticotrophin levels, coupled with the possible potentiating effects of other POMC Peptides e.g endorphins, insulin like molecules on ACTH causes dysregulated cortisol secretion.
What are the clinical signs of equine cushing’s disease?
Hirsutism - increased cortisol may lead to increased androgen production from the adrenal glands. Hyperhidrosis due to hirsutism and effects of compression on thermoregulatio. Laminitis due to effects of glucocorticoids on metabolism, vascular function, skin function, bone function. Lethargy & poor demeanour, fat redistribution due to cortisol dysfunction, predisposition to infections, weight loss due to muscle wastage, PUPD due to hyperglycaemia (secondary diabetes mellitus), polyphagia blindness, seizures.
How is ECD diagnosed?
Demonstration of clinical signs described may be justification alone in making a diagnosis of ECD, particularly the pathognomonic sign of hirsutism. Other tests can be used including - basal glucose, basal insulin, basal cortisol (too poor sensitivity) and basal ACTH.
What is the treatment for Equine Cushings disease?
May be no need to provide specific medication to some cases of ECD. sensible conservation measures to manage ECD cases include those recommended for aged animals in genreal. Good attention should be paid to feeding, dentistry, anthelmintic regimes and the early detectio of clinical abnormalities. Clipping the excessively long haircoat may be advantageous. Regular farriery is paramount and horses or ponies should be monitored for signs of laminitis, chronic or acute. In the absence of chronic orthopaedic disease, continued exercise may be beneficial in enhancing insulin sensitivity and offsetting any effects of abnormal cortisol status. Cases of particular concern are those that have a history of laminitis or evidence of chronic laminitic changes in the feet. In these cases early therapy may be sensible. All cases with evidence of resting hyperglycaemia and signifcant increases in insulin should be treated as these have a poorer prognosiis long term without therapy.
What are the main causes of incontinence in horses?
reflex/upper motor neurone bladder, eg EHV-1 infection, EPM
Paralytic/lower motor neurone bladder e.g polyeuritis equi, EHV1, trauma
Non neurogenic (most common)- inflammatory/irritant e.g cystitis, urolithiasis, myogenic (detrusor atony leading to sabulous urolithiasis), neoplasia, ectopic ureter, breeding trauma, hypo oestrogenism.
What is the treatment for urinary incontinence in horses?
Generally futile with the exception of EHV1, EPM infection and cystitis. Palliative care - drainage and flushing, washing and vaseline, antibiotics vs secondary cystitis. Some mares have responded to oestrogen, A adrenergic blockers: decrease urethral sphincter thus facilitating urination with UMN problems.. Parasympathomimetics; promote detrusor function.
What is uraemia?
The clinical signs associated with increased nitrogenous compounds in the blood stream: signs include anorexia, weight loss, bedraggled hair coat.
What is azotaemia?
Azotaemia refers to the abnormal increase in biochemical parameters (urea creatinine and other non protein nitrogenous compounds) that occur in renal disease. This can be further defied in the following; pre renal azotaemia (decreased real perfusion), renal Azotaemia (acute/chronic renal failure), post renal azotaemia (obstructive disorders, uroperitoneum)
Describe the differeent causes of acute real failure in horses
Acute tubuler necrosis; toxicity due to drugs: aminoglycosides, NSAIDS, polymixinB, pigments Hb, Mb, vitamins D and K3, heavy metals, acorns. Aminoglycosides accumulate in interstitial cells, NSAIDs cause papillary ecrosis, may affect vascular function, Vitamin D causes tissue mieralisation.
Vascular: vasomotor nephrotpathy - dehydration, shock, hypotension, adverse drug reactions.
Acute glomerulonephropathy: immune mediated e.g purpura haemorrhagica, bacterial mediated e.g strep E coli
acute interstitial nephritis - unknown cause - adverse drug reactions.
Primary bacterial - leptospirosis. - L interrogans pomona
Describe the different types of chronic renal failure in horses?
Glomerular disease - proliferative glomerulonephritis, membranous glomerulonephritis, membrano proliferative glomerulonephritis. Disease affecting the glomeruli predominantly. types differ in histological changes. Probably immune mediated.
Chronic interstitial nephritis - sequel to acute tubuler necrosis, vascular abnormalities and pyelonephritis. Histological changes to tubule cells and interstitial inflammatory cells predominate.
End stage kidney disease - gross and histological severe changes comprising both tubular and glomerular disease - primary cause unidentifiable.
Describe general treatment for Acute renal failure in horses
Fluid therapy - balanced fluids with regular monitoring of electrolyte status. care regarding over hydration and oedema formation. Monitor urination - if the hors remains oliguric within the first 24 hours of therapy then this must be addressed. Poor prognosis for these cases. Ideally creatinine should decrease by at least 30% in the first 24 hours of therapy, otherwise prognosis poor. animals which respond should be slowly weaned off fluid therapy but may need continued electrolyte supplementation at least in the short term.
Describe the general treatment of chronic renal failure
Fluid therapy foor 24-48 hours to evaluate for response to therapy with decreases in creatinine. Identify any primary abnoralities and treat if possible e.g urinary stones, pyelonephritis. Dietary - correct any electrolyte or acid base abnormalities, small frequent varied meals encourage appetite. Avoid high calcium foodstuffs e.g alfalfa. Poor renal function leads to hypercalcaemia. Increase CHO intake e.g using oils, but maintain adequate protein. Anabolic steroids - may stimulate appetite. Blood ad plasma transfusions for anaemia and hypoalbuminaemia respectively. Horses with a plasma creatinine 400mol/l and a BUN <15:1 may have an acceptable existence for some months or even years.
What are the most common differential diagnosis for haematuria in horses?
Urethral tears - in geldings and stallions, quarter horses, at the end of urination.
Cystitis/UTI/Urolithiasis - other clinical signs concurrent e.g stranguria, pollakiuria.
Idiopathic renal haematuria - mostly arabs, sudden onset, observe blood from one/both ureters.
Neoplasia - e bladder, urethra, penis, sheath.
Drugs - NSAIDS
Vaginal varicosities - mares, especially multiparous
Exercise induced haematuria - usually microscopic, may see bladder lesions.
Non urinary systemic disease - haemolysis, acute mypathiies, coagulopathy.
What investigative techniques are suggested for haematuria?
Differentiate haematuria from Hburia/ Mburia. Smal amounts of Rbcs will lead to scattered spots on the dipstick. microscopic evaluation may reveal numerous red cells. spin down urne and look for pellet of cells rather than discoloured urine. Separate glomerular from non glomerular bleeding - evaluate morphology of cells: numerous numbers of more variable appearance are noted in glomerular disease. Evaluate timing of haematuria; throughout urination; kidneys, ureters, bladder. Begiinning of urination; distal urethra. end of urination: proximal urethra and bladder neck.
Describe lice infection in horses (pediculosis)
Lice infestation with biting louse Damalinia equi and sucking louse haematopinus asini. Very common an cause pruritus scaling and alopecia. Often occurs in winter on poorly managed/congregated horses. Common in cushingoid horses. Diagnosis: demonstration of lice or ites. Treatment: insecticidal shampoos, sprays or powders usually containing pyrethrins or yrethroids. Two applications at 14 day intervals are usually sufficient.
Describe Chorioptic mange in horses
Caused by chorioptes equi, primarily affects distal limbs of heavily feathered horses. Carrier horses with no clinical signs can perpetuate the infection. Infection spread by beddig, brushes, contact. Affected horses stamp and bite limbs. Scaling and exudation are present with secondary bacterial infections. Diagnosis: presence of mites in superficial scrapings. Treatment includes removal of hair and scabs combined with application of insecticides including permethrins and fipronil to affected horses ad in contacts. systemic ivermectin may be useful. Seleen shampoo can reduce pruritis.
Describe trombiculosis in horses
T autumnalis (small orange/yellow coloured mites). Sucking mite -disease associated with nymphal form. Pruritus of head/legs of grazing horses in late summer/autumn. Diagnose with groomings. Treatment : topical insecticides.
