Horses 3 Flashcards
What are some reasons not to perform a whole blood transfusion
○ Transfusion reactions are potentially fatal
§ High degree of blood type polymorphism
§ Identifying a completely compatible blood donor nearly impossible
○ Risk of transmitting infectious diseases (EIA)
○ Recipients rapidly develop antibodies directed against transfused RBCs
§ Increased workload for the RE system
○ Impairs bone marrow response to anaemia by blunting production of erythropoietin
what is ideal but not necessary on first transduction UNLESS and how to perform (2 types)
Cross-matching is ideal but not absolutely necessary on first transfusion:
○ Unless anaemia is immune mediated
○ Testing performed to avoid serious blood group mismatching
1. Major cross match
§ Donor erythrocytes and recipient serum
§ Whether recipient has antibodies against donor RBCs
2. Minor cross match
§ Recipient erythrocytes and donor serum
§ Presence of antibodies in donor serum (against recipient RBCs)
Blood transfusions what are the criteria
○ Acute anaemia PCV <12%
○ Chronic anaemia PCV <8-10%
○ PCV has decreased to 18-24% in a 24 hour period or shorter
○ Clinical signs and clinicopatholic indicators of decreased DO2, are more important than the PCV
§ Tachycardia (especially if HR is increasing)
§ Clinical signs of hypoxic tissue injury
□ Decreased GI motility
□ Muscle weakness
□ Cold extremities and weak peripheral pulses
□ Depression (decreased CNS DO2)
□ Cold sweats
Volume of transfusion can you replace entire deificit, how done and how much can take from donor horse
○ In neonates it is possible to replace entire deficit - care with volume overload
○ In adults usually impractical to replace entire deficit
§ Given to effect
§ Replacing 20-40% of the calculated deficit is usually sufficient
- Donor horse
○ Normal blood volume is 8% of body weight
§ Should not take more than 20-25% of blood volume
□ Can take 8-10L from a 500g animal every 30 days
what are some adverse transfusion reactions
○ Tachypnoea and dyspnoea ○ Tachycardia ○ Fever ○ Restlessness ○ Defecation ○ Piloerection ○ Muscle fasciculations ○ Sudden collapse
Hyperbilirubinaemia what are the 4 main mechanisms, result from and what clin path findings expect
a. Haemolytic (prehepatic)
§ Rapid destruction of RBC causes release of bilirubin into blood
§ Expect an increase in unconjugated (bilirubin)
§ Animal expected to be anaemic
§ Release of hepatic enzymes into blood (ALT, AST, GLDH, SDH)
b. Hepatocellular (hepatic)
§ Hepatic injury or dysfunction impairs uptake and conjugation of bilirubin -> take liver biopsy to test for this in horses
§ Expect an increase in unconjugated (bilirubin)
c. Post-hepatic (obstructive)
§ Obstruction of bile flow causes regurgitation (reflux) of bilirubin into the circulation -> cholestatic liver disease
§ Expect an increase in conjugated (bilirubin)
§ Reflux of enzymes lining biliary tract into bloodstream (GGT, alkaline phosphatase (AP or ALP - not as specific)
d. Anorexia (in horses ONLY)
§ Horses that have been anorectic for more than 1-2 days are mildly icteric
§ Unconjugated bilirubin increase
What are some common clinical signs of liver disease and why occur
- Jaundice
- Weight loss - frequently the only sign of hepatic disease
- Depression and anorexia - might be an manifestation of hepatic encephalopathy
- Mild-moderate abdominal pain (colic) colic can be gastrointestinal or extra-gastrointestinal
- Hepatic encephalopathy -> signs can include severe depression, apparent blindness or impaired vision, compulsive walking, circling, head pressing
- Skin photosensitivity and pruritis - phylloerythrin synthesised by bacteria from chlorophyll within the GI tract is normally removed from the blood by liver and excreted in the bile -> 12% of horses with liver failure display photosensitivity
- Coagulopathies
- Haemoglobinaemia and haemoglobinuria
What are the 4 main laboratory indicators of hepatic disease
1) indicatiors of hepatocellular injury - GLDH, SDH, AST, LDH, AST
2) indications of biliary tract obstruction - GGT, ALP
3) indicatiors of hepatic function - bilirubin concetration, serum bile acids, ammonia, PT
4) non-specific indicatiors - hypoalbimaenia (chronic), increase PCV, low urea
in terms of laboratory indicators of hepatocellular injury what are the main ones, where found and value
○ GLDH -> hepatocellular mitochondrial enzyme, poor stability
○ SDH -> hepatocellular cytoplasmic enzymes, after acute injury returns to normal within 4-5 days making it useful in monitoring liver disease in horses, poor stability
○ AST -> also found in large amounts in skeletal and cardiac muscle so look at CK
○ LDH -> also found in many tissues so LIMITED VALUE
○ ALT -> NOT OCCUR in equine liver and is NOT USEFUL in assessing liver damage
In terms of laboratory indicators of biliary tract obstruction what are the 2 main ones, where located and value
○ GGT -> epithelial lining of biliary tract - obstruction results in reflux of GGT back into blood stream, very long half-life and activity can remain increased for weeks after clinical signs, very stable in collected samples
○ ALP -> also found in intestinal tissue and bone
what are the 4 other laboratory indicators of hepatic function, how measure and what indicate hepatic disease
1) Bilirubin concentration -> with fasting or anorexia can increase and associated with mild jaundice
§ If fasting then conjugated takes up about 10% of total bilirubin
§ If conjugated portion exceeds 20-25% of total then cholestasis more likely
2) Serum bile acids (SBA) -> can be measured regardless of feeding (horses don’t have gallbladder), increase indicator of acute or chronic liver damage and decreased hepatic function
3) Blood ammonia -> difficult to measure, only increase with severe hepatocellular damage, thought to contribute to the signs of hepatic encephalopathy but no good relationship between concentration
4) Prolonged of clotting time (pro-thrombin time (PT) and activated partial thromboplastin time (aPTT) -> need to be measured before performing a liver biopsy
apart from the laboratory tests what two other tests can be used to diagnose liver disease and what can asses
1) ultrasound
○ Assess
§ Size: sharp edges and should not extend ventral to the costochondral junctions on the right
□ Rounded margins suggest hepatomegaly
§ Echogenicity: more echodense than the kidney and less than the spleen, should also be uniform in appearance
§ Presence of dilated bile ducts and biliary calculi
○ Mainly used to guide a liver biopsy, can also detect other problems hepatic abscesses, tumours, parasitic cysts or traumatic laceration
2. Liver biopsy
○ Percutaneous are usually performed at site determined by ultrasound
○ Samples submitted for culture and histology although culture of liver samples appears to have low sensitivity
how to assess the liver via ultrasound
○ Imaged on the right side just ventral to the lung fields and dorsal to the costochondral junction - can extend caudally so contacts the right kidney
○ Small amount of liver seen on left just caudal to the left ventricle (between 8 and 10th intercostal spaces) - echogenicity of the liver can be compared to the spleen
treatment of liver failure what are the principles
- Largely supportive and should be directed toward alleviation of clinical signs, particularly those associated with hepatic encephalopathy
1. Antimicrobial therapy - broad spectrum
○ If infectious process is suspected -> suppurative cholangitis or cholelithiasis
2. Management of hepatic encephalopathy (HE)
3. Nutritional support
4. Corticosteroid therapy
○ Controversial, may be used in immune mediated liver conditions
How to manage hepatic encephalopathy is the treatment of liver failure
○ Sedation: horses with severe neurological dysfunction will require sedation - xylazine
○ Provision of glucose: oral or intravenous administration can result in dramatic reversal of neurological dysfunction
○ Reduction of ammonia production:
§ Oral administration of neomycin sulfate to reduce ammonia producing bacteria
§ Lactulose given orally every 6 hours acidifies colonic contents
what is involved in the nutritional support in the management of liver failure
○ If the animal is not eating or drinking, administration of electrolyte solutions and glucose via nasogastric tube might be indicated
○ Feeds containing low level of high quality proteins are recommended to reduce the “workload” of liver
○ Parenteral administration of B-complex vitamins might decrease the demands on the liver for production
how common is liver disease in horses and the 4 main causes (which is most common)
not so common
1. Pyrrolizidine alkaloid toxicity - most common cause
○ Other toxicities occur occasionally
2. Serum hepatitis (Theiler’s disease)
3. Tyzzer’s disease (Cl.piliformis)
4. Cholangiohepatitis/choledocholithiasis
○ Bacterial and/or immune-mediated
Pyrrolizidine toxicity what caused by, when does toxicity occur and clinical signs
- Senecio spp (ragwort) and Echium plantagineum (Paterson’s curse)
- Usually unpalatable; ingestion occurs only if other feed stuffs limited
- Acute intoxication possible but chronic progressive hepatopathy more common
- Onset of clinical signs is often abrupt
○ Chronic weight loss
○ Variable icterus
○ Photosensitisation (about 25% of cases)
○ Hepatic encephalopathy
Pyrrolizidine toxicity diagnosis, prognosis and management
- Diagnosis
○ Liver biopsy is essential for accurate diagnosis
§ Classical histopathological lesions include:
□ Fibrosis
□ Megalocytosis
□ Bile duct proliferation - Prognosis
○ Often poor
○ Progressive hepatocyte loss, fibrosis and destruction of the normal hepatic architecture
○ Presence of signs of hepatic encephalopathy suggest a poor prognosis - Management
○ Management of horses exposed to toxin but not yet showing clinical signs is important
§ Contaminated feed or hay MUST be removed
Icterus in a foal what are some likely differentials
- Neonatal isoerythrolysis - intravascular haemolysis
○ DISCOLOURED URINE - Liver disease - infectious causes - clostridia
- Sepsis - liver hypoxia
- Haemorrhage (rib or long bone fractures - generally lame though
- Anorexia (generally low level icterus)
- EHV-1 (abortion, weak, new born foals)
how to determine between myoglobin and haemoglobin with red urine
Myoglobin - would expect CK to be much higher AND PLASMA WOULD BE CLEAR
also look under microscope to see red blood cells in urine if haemorrhage
What immunoglobin G concentration is adequate and what commonly at at 24 hours and what does high fibrinogen levels indicate
- Adequate is 800mg/dL
- more often 1,500-1,800mg/dL at 24 hours
High fibrinogen in young foal ->Acute inflammatory response
AST and CK increase in foal what can indicate
§ AST released by several tissues including liver and muscle
§ CK activity also increased -> muscle injury
§ Common finding in new born foals
§ Clinically significant rhabdomyolysis -> INCREASE CK activity
Neonatal isoerthryolysis what results in with clin path and what else need to consider with inflammation
- Neonatal isoerythrolysis with intravascular haemolysis
○ Results in hyperbilirubinaemia, haemoglobinaemia, hyperbilirubinuria - Inflammatory response
○ Probably related to intravascular haemolysis BUT must always consider SEPSIS in neonates
Neonatal isoerthrylosis how occurs and what are the 2 main things that may result
- The situation needed
○ Mare Aa negative - no antigens and Stallion Aa positive - does have antigens
○ Foal -> Aa positive - has antigens that mare does not - AT some point mare is exposed to antigens and becomes SENSITISED
○ Breeding trauma, during foaling, transfusions - UNSURE - Udder concentrates the antibodies against foals RBC antigens
- When foal drinks, gets antibodies, lyses of RBC
Antibodies coat erythrocytes and may act as either
a. Haemolysins (intravascular haemolysis)
b. Agglutinins (extravascular haemolysis)
Neonatal isoerthrylosis treatment plan
- Prevent nursing from the mare
○ Feed safe milk or milk replacer via a NGT
○ Gut “closes” at approx 18-24 hours - ensure enough colostrum - Intravenous fluids
○ Correct dehydration
○ Prophylaxis against pigment nephropathy - Prophylactic broad-spectrum antimicrobials
- MONITOR - very important
○ PCV, HR, RR, Lactate and blood gas
○ Urine, creatinine and bilirubin - if PCV gets worse - NEED BLOOD TRANSFUSION (around 15%)
If unable to find a compatible donor for the foal with neonatal isoerthryolysis what blood should be used
- NOT THE STALLION
○ Foal has Aa antigens and ant-Aa antibodies from mare within blood
○ If give stallion blood -> those RBC haemolysed straight away - Mare
○ Doesn’t have antigen that antibodies react against BUT DOES HAVE MORE ANTIBODIES
§ Need to wash these RBC to remove as many antibodies as possible
□ Whole process takes a long time - about 8 hours
What are some prevention strategies for neonatal isoerthryolysis
- More common in mares with previous NI foal
○ Attend high risk foaling/pregnancy
○ Prevent ingestion of colostrum (24-36h)
§ Muzzle foal, find safe source of colostrum
§ Identify blood donors - Blood type mares and avoid incompatible pregnancies
- Monitor titres against Aa or Qa antigens in the mares serum in the last 3 months of pregnancy
- Jaundice foal agglutination test - test colostrum against foal’s blood prior to ingestion
What is the surviival rate for foals with dystocia and what is important
- Mares generally does well
- Survival rate for foals 42% only 1/3rd of successful birth survive
○ Difference between survival and non-survival 15 mins
§ NEED TO GET ONTO IT QUICKLY
What are 4 things within the history that suggest a high risk mare
1. Unhealthy uterine environment ○ Repeated breedings ○ Abortion or premature birth ○ Premature placental separation ○ Placentitis - ascending infection through the cervix -> faecal contamination -> POOR CONFORMATION 2. Previous dystocia ○ Contracted tendons 3. Prolonged pregnancies ○ Approx 340 days (320-350 days) ○ Some mares just give birth earlier or later -> above is a reference RANGE § Need to determine what is normal for that mare 4. Previous sick foals
What are 4 events during current pregnancy that indicate a high risk mare
- Premature lactation - indicates placentitis
○ Loss of colostrum - need to be ready to provide foal with colostrum - Disease during gestation
○ Reduced O2 -content/delivery
○ Elaboration of prostaglandins
○ Recurrent colic - Excess abdominal enlargement
○ Hydrops (amnii, allantois)
○ Body wall defects - pre-pubic tendon rupture - MORE COMMON
§ Cannot generate abdominal force to get foal out, stage II longer than needs to be - Prolonged gestation
What events during parturition indicate a high risk mare
- Poor udder development - problem with colostrum levels
- Dystocia
○ Stage I: 30min to 4 hours
○ Stage II: 20-30min - important
○ Stage III: 30-60min to 3 hours (start to get nervous) - Premature placental separation
- Meconium staining
- Abnormalities of the placenta
○ Weight/gross/microscopic
when evaluating the neonate what need to look at/ask about
1) foal behaviour
2) PE- cardiovascular. respiratory, abdomen, musculoskeletal,
3) laboratory evaluation - blood culture sensitivity, complete blood count, biochemistry, serum IgG concetration, arteril and/or venous blood gas (evaluate lungs)
in terms of foal behaviour what is normal times for important things as well as urination
○ Sternal within 5 mins ○ Suckle reflex within 20min § Often present at birth ○ Standing within 1 hour ○ Nursing within 2 hours § Some normal foals take longer ○ Meconium § Passes within 24 hours ○ Urination § May not urinate for 12 + hours § First urine will be quite concentrated § After that -> 1.005 or less generally - due to fluid diet
Evaluating the cardiovascular system in foal what are normal findings
§ HR 60-140/min - resting should be 60 but when you place your hand on them will increase
□ Can be very low immediately after birth
□ Arrhythmias common - but should resolve
□ Continuous (machinery) murmur - patent ductus arteriosus
□ Left-sided, soft, systolic murmur
What can cause a persistent bradycardia and tachycardia in a foal
§ Persistent bradycardia □ Hypothermia/hypoglycaemia/hypoxaemia § Persistent tachycardia □ Sepsis, hypovolaemia □ Pain, fever, excitement □ congenital defects
Evaluating the resiratory system in foal what is normal and how to assess
§ Respiratory rate approx 30-40/min within first hours
§ Recumbent foals often appear dyspnoeic
□ NE may cause an abnormal respiratory pattern
§ Auscultation is not very sensitive
□ Lack of adventitial sounds does not preclude disease
□ Dependent lung often sounds very wet - can hear harsh lung sounds/crackles
® Need to come back and auscultate after gotten back up
§ Other modalities for investigating the lungs
□ Ultrasound
□ Radiography
□ Blood gas measurements - recumbent foals can be hypoxic - arterial O2 down to 70
Evaluating the abdomen in foals what assessing for, how assess and what can locate
colic § Amenable to palpation □ Meconium □ Umbilical structures □ Bladder □ Intussusceptions § Ultrasonography - more sensitive in foals than adults § Radiography
Evaluating the Musculoskeletal system in a foal what evaluting for
§ Angular limb deformities § Flexor laxity/contraction § Incomplete ossification □ Radiograph capri (and tarsi) § Fractured ribs - generally doesn't cause an issue
Flexor laxity in foals what breed most common in, presentation, cause and treatment
□ Standardbreds □ Foals often struggles to rise □ Difficulty standing to nurse □ Distal limb edema □ trauma to palmar/plantar aspect □ Resolve as foal gains strength and becomes more active ® Heel extensions ® Avoid bandaging
