Horses 3 Flashcards
(101 cards)
1
Q
What are some reasons not to perform a whole blood transfusion
A
○ 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
2
Q
what is ideal but not necessary on first transduction UNLESS and how to perform (2 types)
A
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)
3
Q
Blood transfusions what are the criteria
A
○ 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
4
Q
Volume of transfusion can you replace entire deificit, how done and how much can take from donor horse
A
○ 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
5
Q
what are some adverse transfusion reactions
A
○ Tachypnoea and dyspnoea ○ Tachycardia ○ Fever ○ Restlessness ○ Defecation ○ Piloerection ○ Muscle fasciculations ○ Sudden collapse
6
Q
Hyperbilirubinaemia what are the 4 main mechanisms, result from and what clin path findings expect
A
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
7
Q
What are some common clinical signs of liver disease and why occur
A
- 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
8
Q
What are the 4 main laboratory indicators of hepatic disease
A
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
9
Q
in terms of laboratory indicators of hepatocellular injury what are the main ones, where found and value
A
○ 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
10
Q
In terms of laboratory indicators of biliary tract obstruction what are the 2 main ones, where located and value
A
○ 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
11
Q
what are the 4 other laboratory indicators of hepatic function, how measure and what indicate hepatic disease
A
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
12
Q
apart from the laboratory tests what two other tests can be used to diagnose liver disease and what can asses
A
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
13
Q
how to assess the liver via ultrasound
A
○ 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
14
Q
treatment of liver failure what are the principles
A
- 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
15
Q
How to manage hepatic encephalopathy is the treatment of liver failure
A
○ 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
16
Q
what is involved in the nutritional support in the management of liver failure
A
○ 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
17
Q
how common is liver disease in horses and the 4 main causes (which is most common)
A
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
18
Q
Pyrrolizidine toxicity what caused by, when does toxicity occur and clinical signs
A
- 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
19
Q
Pyrrolizidine toxicity diagnosis, prognosis and management
A
- 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
20
Q
Icterus in a foal what are some likely differentials
A
- 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)
21
Q
how to determine between myoglobin and haemoglobin with red urine
A
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
22
Q
What immunoglobin G concentration is adequate and what commonly at at 24 hours and what does high fibrinogen levels indicate
A
- Adequate is 800mg/dL
- more often 1,500-1,800mg/dL at 24 hours
High fibrinogen in young foal ->Acute inflammatory response
23
Q
AST and CK increase in foal what can indicate
A
§ 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
24
Q
Neonatal isoerthryolysis what results in with clin path and what else need to consider with inflammation
A
- Neonatal isoerythrolysis with intravascular haemolysis
○ Results in hyperbilirubinaemia, haemoglobinaemia, hyperbilirubinuria - Inflammatory response
○ Probably related to intravascular haemolysis BUT must always consider SEPSIS in neonates
25
Neonatal isoerthrylosis how occurs and what are the 2 main things that may result
1. The situation needed
○ Mare Aa negative - no antigens and Stallion Aa positive - does have antigens
○ Foal -> Aa positive - has antigens that mare does not
2. AT some point mare is exposed to antigens and becomes SENSITISED
○ Breeding trauma, during foaling, transfusions - UNSURE
3. Udder concentrates the antibodies against foals RBC antigens
4. When foal drinks, gets antibodies, lyses of RBC
Antibodies coat erythrocytes and may act as either
a. Haemolysins (intravascular haemolysis)
b. Agglutinins (extravascular haemolysis)
26
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%)
27
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
28
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
29
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
30
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
```
31
What are 4 events during current pregnancy that indicate a high risk mare
1. Premature lactation - indicates placentitis
○ Loss of colostrum - need to be ready to provide foal with colostrum
2. Disease during gestation
○ Reduced O2 -content/delivery
○ Elaboration of prostaglandins
○ Recurrent colic
3. 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
4. Prolonged gestation
32
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
33
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)
34
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
```
35
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
36
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
```
37
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
38
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
```
39
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
```
40
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
```
41
Flexor contraction in foals presentation, cause and treatment
```
□ Foals often struggles to rise
□ Difficulty standing to nurse
□ Trauma to dorsal aspect of limb
□ Extensor rupture
□ Resolves as becomes more active
® Physiotherapy
® Bandaging/splints
® Toe extensions/heel elevation
® Oxytetracycline (kidney worried about) - relaxation of the tendons
```
42
What is important to look at in the complete blood count of foal and why
§ Fibrinogen concentration
§ Changes to the leukogram
□ Leukopenia - overwhelming inflammation
□ Leucocytosis
□ Inversion of the N:L ratio
□ Toxic changes
□ SEPTIC foals can have NORMAL white cell counts
43
What look at with haemogram of foal and what disease can suggest
□ Many ill neonates are mildly-to-moderately anaemic
® PCV 22-28%
□ Severe anaemia more common in neonatal isoerythrolysis or blood loss
® Rib/long bone fractures
® Umbilical injury
® Trauma
44
What need to look at in biochemistry of foals as what can be detected
```
§ Acute phase proteins
□ Fibrinogen
□ Serum amyloid A
§ Blood glucose
§ Creatinine and BUN
□ Glomerular filtration rate
□ Creatinine often increased in sick foals - acute renal injury - COMMON
§ Liver enzymes
□ Reset values in foals
□ AST and CK often slightly increased due to birthing process
§ Bilirubin
□ Sepsis
□ Neonatal isoerythrolysis
§ Muscle enzymes (AST and CK)
```
45
Serum IgG concentration when is max, half life, what concentration suggest partial and complete failure and what leads to a decrease
§ Maximum plasma concentration at approx 18 hours
§ T1/2 in healthy foals approx 12 to 25 days
§ Partial failure of passive transfer: 400-800mg/dL
§ Complete failure of passive transfer: <400mg/dL
§ Serial evaluation -> IgG can be normal but overtime decrease due to the following two reasons:
□ Consumption (antigen-antibody complexes) - INFECTION
□ Catabolism (negative energy balance)
46
What are the 4 main causes of sick neonate and what is important to remember
```
1. Sepsis
○ Systemic inflammatory response
2. Neonatal encephalopathy
○ Hypoxic-ischemic encephalopathy
○ Neonatal maladjustment syndrome
○ Dummy foals
3. Prematurity/dysmaturity
4. Rupture bladder
Distinguishing these is hard so therapeutic treatment is quite broad (BELOW)
```
47
What are the 6 main things needed in treatment of neonatal disease
1) treatment/prevention of underlying infection - antibacterials (gentamicin, ampicillin, penicillin)
2) haemodynamic support
3) supportive care to maintain organ function - nutritional support
4) inhibition of pro-inflammatory mediators - anti-inflammatories/analgesia
5) intensive nursing care and monitoring - MOST IMPORTANT THING
6) Plasma transfusion
48
Haemodynamic support with treating neonatal disease what is involved and what need to be careful of
```
○ Intravenous fluid therapy
§ Vasopressors (to increase vascular tone) and inotropes (to increase cardiac output)
○ Neonatal fluid requirements probably higher
§ Maintenance = 80mL/kg/day
○ Care to avoid oedema
§ Monitor carefully for pulmonary oedema
○ Care with sodium load
§ Hartmann's [Na+] = 140mmol/L
```
49
Nutritional support in the treatment of neonatal disease what do healthy foals drink/gain and therefore what need to provide
○ Healthy foals
§ Drink 20-25% of their bodyweight in mare's milk/day
§ Gain approx. 1kg/day in bodyweight
○ Meet MER in critically ill foals
§ Approx. 10% of bodyweight in mare's milk/day
§ Indwelling feeding tube if unable to nurse or drink from a bottle/bucket
Consider early institution of TPN in foals that do not tolerate enteral feeding
50
What anti-inflammatories/analgesia use in neonatal disease
○ Many of the diseases affecting foals have an inflammatory basis or are painful
§ Typically rely on NSAIDS
§ Care with nephrotoxicity
§ PK are different in foals (-> SID)
- Consider opioids (butorphanol) in very painful conditions or with renal dysfunction
51
plasma transfusion for neonatal disease when use, how and reactions
§ Foals older than 12 to 18 hours
§ Foals that are unable to nurse or will not tolerate enteral nutrition
§ Reactions are uncommon (approx. 10%)and typically mild
§ Administer slowly initially and through an in-line filter
52
foal colic what are important history things to ask and how to differentiate between surgical and medical and diagnosis
History
- Age/duration/progression of signs
- Normal previously/foaling
- Nursing
- Type/dose of analgesics
Surgical vs medical: determined by proper history and thorough physical exam
- Cannot rectal
- Hard to interpret pain: foals are dramatic
- Better ability to ultrasound thoroughly: penetration
DIFFERENTIAL VIA AGE AND ULTRASOUND
53
What are some mild colic signs for foals
- Mild meconium impactions or rotavirus (dxa)
- Restlessness
- Attempts to pass manure
- Tail swishing
- Straining to urinate/frequent urination
- Walking round stall not nursing
Mare runs milk when not nursing - so ask if mare is running milk
54
What are some more severe signs of colic in foals
- Abdominal distension (small OR large intestine in foal)
- Lying down/on back or rolling
- Sweating
- NGT any foal with ongoing mild signs or severe signs
55
6-24 hours old foals what are the 3 common causes and the most common
1) meconium impactions - most common
2) Congenital atresias - colon, rectum, anus
3) Paint foals: primarily white and with (frame) overo dam AND sire: risk of ileocecal aganglionosis (lethal white foal)
56
Meconium impactions what age cause colic in, how formed, when should be passed and higher risk foals
6-24 hours
○ Glandular secretions from GI tract, amniotic fluid and cellular debris
○ Should be passed by 24-26 hours of age
Higher risk foals
- In utero sepsis
○ Hypoglycaemia and sympathamomimetic release: can induce hypomotility
○ Ensure no systemic illness if present as meconium impaction
○ Anticipate impaction in sick neonates
- More common in colts (narrow pelvic canal)
57
Meconium impaction diagnosis
- Lack of meconium
- Contrast radiographs/ultrasonography - meconium: mixed echogenicity in LI, surrounded by ring of gas (white reflections)
58
Meconium impaction what are the 4 main treatment options
1) Commercial enemas just inject into rectum - a lot of time this is already done by the farm hands -> you are doing the next one
2) Retention enema -> warm water or acetylcysteine retention (most aggressive) enemas generally effective
3) Analgesia
4) Minority -> may require surgery - generally at this point prognosis is not good
59
Retention enema what are the 6 steps in how to perform on a foal
1) Sedate: diazapam 0.1mg/kg IV or 1mg/foal butorphanol IV
2) buscopan 0.1-0.2mg/kg IV - Relaxation of these hypermotile segments will allow the enema to percolate around impaction more effectively (most neonate, mature TB foals 50Kg at birth)
3) 40ml of 20% acetylcysteine + 160ml of water
4) Lubricated 12-14Fr cuffed foley catheter introduced p/r and cuff gently inflated
5) Infuse 200ml slowly and plug end of catheter
6) Tape end to foal tail and leave 15mins
- Cap repeat several times a day
60
lethal white foals resulting in colic what occurs, prevention, which form of pain is most common and common myths
○ Inadequate development of enteric nervous system - WILL ALWAYS BE LETHAL
- Colon often narrow/absent
- Lack of peristalsis: ileus -> proximal intestine distended -> meconium and gas - NO CURE
○ Predominately white foal
○ DNA test for "frame" gene
○ Different overo (types of paint horse) that can pass on the gene
Frame overo -> the most common one
Common myths around lethal white foals
- All overos carry the lethal allele - no just mainly frame
- All totally white foals from two overo parents are lethal whites
- Lethal whites are totally white
61
2-5 day old foals what are the 4 main causes of colic and 2 others that look like colic but aren't
1. Enteritis
2. Intussusceptions
3. Gastroduodenal ulceration (bruxism/sick)
4. Small intestinal
BOTTOM TO -> generally may think is colic but won't be
1. Ruptured bladder - will also generally have abdominal distention, dull
2. Inguinal hernias - generally not colicking
62
2-5 day old foals colic diagnosis and 3 main indications for surgical lesions
- Ultrasonography helpful in ddx
○ Distended SI (>2.5cm in foal)
○ No motility: suggestive SI volvulus
- Large amount of peritoneal fluid + history infrequent urination: suggests ruptured bladder
- Severe signs colic: NOT pathognomonic for surgical lesions (foals are dramatic)
- BUT: inability to control it required an exploratory laparotomy
Indications for surgical lesions
○ Tachycardia >120bpm
○ Non responsive to pain medication
○ Absence of fever - suggest surgical lesions
63
SI obstruction leading to colic in 2-5 day old foals clinical signs, lab findings, ultrasound and treatment
- Severe colic signs - surgery (treatment)
○ Bruxism - excessive teeth grinding or jaw clenching
○ Reflux from nares (clients think nasal discharge) - spontaneously reflux
- NEED TO PASS A NGT
○ Gastric/small intestinal distension - abdominal distention
- Lab findings non-specific
○ Dehydration secondary to fluid losses into GI tract
- Ultrasound
○ Hypomotile SI distention >2-3cm
○ If SI distension, esp with thickened (oedematous) wall surgery is warranted
64
3-5month old foal what is the most common cause of colic, general history, why results and prognosis (why)
```
Ascarid impaction
○ Dewormed a week prior
○ Large worm 'kill' resulting in physical obstruction -> not dead when you cut them out though
○ Poor prognosis for survival
- Ascarids release toxins
- Inflammation from surgery
- Prolonged ileus common
- High risk adhesions
- Foals are often unthrifty
```
65
Ascarid impaction diagnosis and treatment (which is preferred and indications for surgery)
○ Diagnosis
- May see on ultrasound
- Linear hyperechoic structures
- In distended small intestines
- Can be present in reflux
○ Treatment
1. Medical - preference as surgical survival is crap
- Encourage them to pass: enteral fluids/oils
- Flunixin - analgesia/antiinflammatory
- Decompression via NGT
- IV fluid support
- Risk of rupture with medical BUT prognosis with surgery poor
2. Indications for surgery - possibly just euthanasia due to the poor prognosis
® Inability to control pain
® Ultrasound deterioration/lack of improvement
® Uncertain diagnosis
66
Ascird impaction prevention advice
- Pre-treat foals within the same paddock as other foal -> flunixin and drench prior to worming
- Resistance is becoming common
- Moxidectin is currently effective
- Good worming essential q4-6 weeks
- Eggs live in environment for up to 8 years
- All foals will pick up ascarid eggs
- Adults can do damage before eggs laid: FEC misleading
- Immunity develops at 1-2 years of age
67
Up to 2 year old foal what is the most common cause of colic, what occurs, presentation, diagnosis and 3 main types
Intussusception
- Telescoping of bowel into itself: large or small intestinal
- Partial obstruction progressing to complete
- Gradual necrosis of intussuscepted bowel
- Abdominal tap may be misleading (fluid sequestered)
- Intermittent low grade pain - progresses to violent
- Target lesions on ultrasound - pathognomonic
- Types
○ Jejunojejunal
○ Ileocaecal
○ Caecocolic
68
Herniation in foals which location most common, how different to adults and therefore how may present
- Inguinal (common), umbilical
- Most do not strangulate the bowel - resolve spontaneously - not normally colicky
○ This is in contrast to the situation in adult horses - much more open in a foal
69
Inguinal hernia in foals what present as, what advise, if cannot what do next and indications for surgery
present for scrotal swelling - more likely to have gut involved
○ Advise repeated manual reduction
○ Often resolved within a few days
○ If not
§ Manual reduction
§ Gentle pressure toward inguinal ring
§ Easiest if foal recumbent: can be done standing
§ May keep popping out but if keep reducing and will eventually stay in
○ Indications for surgery
§ Non reducible, heat, pain - infection/inflammation - not common
§ Subcutaneous (rather than within tunic)
§ Increasing size/client frustration
○ NB castration performed at the same time
70
Umbilical hernia in foals what generally present as, and treatment
generally doesn't have gut involved -> no colic
○ Reduce in size as foal grows
○ Indications for surgery
§ >2 fingers width
○ How to reduce
§ Elastrator: GA, dorsal recumbency, squeeze content away before application (risks catching gut)
§ Surgical closure - expensive
71
6 month old foal with colic what is the most likely differential, why, risk factors and typically history
Gastroduodenal ulceration
- Ulceration more often clinically significant in foals - Can be life threatening (peritonitis due to gastric rupture/obstruction due to stricture)
- Bowel stricture during healing - not acidic (foal doesn't have acidic environment while on milk)
- Risk factors
○ Stress, starvation (illness), can be secondary to sepsis/neonatal
○ NSAID (reduction PGEs and mucosal blood flow, bicard and mucus secretion
- Typically history
○ Previous sickness
○ May be unthrifty
72
Gastroduodenal ulceration at what age does it lead to colic, typical clinical signs and diagnosis
6 months
- Typically clinical signs
○ Depression and intermittent nursing - low grade colic
○ Bruxism, ptyalism
○ Lay in dorsal recumbancy
- Diagnosis
○ Reflux (partial obstruction), stomach enlarged on US
○ May not see SI distension (location of stricture)
○ Do this via endoscope -> only need 2 hours of fasting
○ OR barium study
§ Delay = barium in stomach after 2 hours
§ Could be inflammatory as a result of ulceration OR stricture (fibrosis further down the healing pathway from ulcer)
- If stricture it is permanent and will need surgical intervention
73
Gastroduodenal ulceration treatment options and prognosis
1) Medical management
○ IV fluid support (CRI or q4-6 hours)
○ Gastric decompression
○ Anti-ulcer medications
○ Anti-inflammatories - flunixin -> TO DETERMINE WHETHER INFLAMMATORY OR STRICTURE
○ If comfort is maintained: continue medical in hopes there is no stricture
○ Expect improvement in 2-3 days if inflammatory
§ Improving reflux
§ Improved bruxism/ptyalism
§ Nurse/eat without pain
2) Lack of response: surgical bypass indicated (guarded prognosis with surgery) - this case the stricture so fibrosis is the issue
74
what are the 6 main principles for fluid therapy
1) why are we giving fluid therapy
2) route
3) what type
4) rate administer
5) volume give out
6) monitoring
75
what are the main reasons you give fluid therapy
○ Fluids most often administered in emergency situations
○ Restore vascular volume and tissue perfusion
○ Correct electrolyte imbalances
○ Correct acid-base derangements (usually an acidosis)
○ Meet maintenance in patients unable to drink
○ Nutritional support
○ Dieresis of patients in acute renal failure
76
What is preferred type if IV fluid therapy, example and why
- Balanced, buffered, isotonic and polyionic fluid usually preferred for IV administration to foals
○ Hartmann's (lacted ringers), normosol-R or similar
○ Balanced = electrolyte composition mimics plasma
Buffered = helps to eliminate an acid load
77
what IV fluids do you use in calves that wouldn't use in horses and why the difference
- Isotonic bicarbonate solutions are widely used during resuscitation of very acidaemic calves
○ Followed by administration of a balanced crystalloid
○ WHY DON'T WE ADMINISTER BICARBONATE TO FOALS
§ Bicarb moves Ph closes to neutral BUT not treating the underlying problem
□ Need to restore their perfusion (hypovolaemia) -> that is what is causing acidaemia -> reduced tissue perfusion and anaerobic tissue metabolism -> lactic acidosis
® Once you restore this the acidosis will resolve
§ If give too much bicarb
□ Overshot and start to create acidosis in CNS - not totally benign
§ Difference with calves -> want to make them feel better, don't have the time and economics to address the whole problem
78
in terms of knowing the volume to be administered what are the principles
- Traditionally, fluid plans have been formulated using:
1. An estimate of initial fluid deficit
2. Standard estimates for maintenance requirements
3. Estimate of on-going losses
79
In step 1 of knowing the volume to be administered what is the traditional approach and how specific
Assessing fluid status (deficit) in foals via MM, CRT, HR, other clinical signs - can also use clin pathology
- Pretty non-specific -> can be caused by other things not just fluid deficit
- Nice starting point but NOT THE BE ALL END ALL -> will probably need to adjust based on response
○ For a 50kg foal that is moderately dehydrated (estimated 8%) - GETTING TO THE 8% IS THE SUBJECTIVE PART
§ Deficit = (50 x 0.08) x 100 = 400.0ml = 4L
80
what are some other clinical signs that can help identify fluid requirements
```
○ Increased heart rate
○ Skin tenting
○ Slow jugular refill
○ Weak peripheral pulses
○ Cool extremities
○ Decreased urine production (often assessed subjectively)
○ Eye position (not as useful in foals)
○ Decreased blood pressure
```
81
What clinical pathology can help quantify fluid deficits
○ PCV
§ Splenic contraction (less pronounced in foals)
○ Total protein (or albumin) concertation
§ Many diseases accompanied by protein loss
§ Protein low in neonates before passive transfer
○ Creatinine concentration
§ Assess renal function
§ Sick foals often have an increased [creatinine]
○ Blood lactate concentration
§ [LAC] higher in neonatal foals for first 1-3 days of life
82
In step 1 of knowing the volume to be administered what is a better approach
- BETTER - more physiological approach to fluid therapy that better identifies the key goals of a fluid plan
1. Resuscitation phase: rapidly restores vascular volume and organ perfusion
2. Rehydration phase: restores interstitial and intracellular fluid over a more prolonged period
3. Maintenance phase: provides for maintenance fluid requirements and on-going losses
○ Still need to calculate maintenance requirements and on-going losses once resuscitation is complete
83
How does resuscitation therapy occur in terms of volume to be administered and steps afterward
○ For horse requiring rapid fluid resuscitation, concentrate on rapidly correcting hypovolaemia
i. 20mL/kg administered as a relatively rapid bolus (approx. 30-60mins)
□ 1L for a 50kg foal, 10L for a 500kg adult -> over an hour
ii. Patients are assess between boluses
□ Use what we used to determine the deficit
iii. Boluses repeated until resuscitation is complete or the patient has received 60-80mL/kg
iv. After 3-4 boluses the patient is careful re-evaluated
□ If vascular volume is inadequate -> additional boluses administered
□ If vascular volume is adequate but tissue perfusion remains poor - inotrope or vasopressor therapy
84
Why is a physiological approach to fluid therapy better than just calculating fluid deficit in terms of knowing volume to be administered initally
○ Recognises the importance of restoring vascular volume (and tissue perfusion) as quickly as possible
○ Removes need to estimate a fluid deficit
§ Boluses are continued until patients vascular volume is restored
§ Emphasizes importance of patient monitoring
85
what are the standard estimates for maintenance requirements (step 2 in amount of administer)
- Maintenance fluid requirements more closely related to metabolic rate
- Adults: 40-60mL/kg/day
- Foals: 80-100mL/kg/day
86
how to calculate ongoing losses with step 3 to identify the volume to be administered
- Guess -> 1.5 or 2x maintenance????
| - Where monitoring is important as hard to do properly
87
Rate of fluid administration what does it depend on, traditional and better approach
- Fluid rate depends on the patient, severity of disease and practical limitations
- Using the traditional approach
○ Correction of half of moderate-to-severe deficit over 2-6 hours
○ Correction of the remainder occurs over the following 18-22 hours
○ For correction of a mild deficit, the deficit volume can be added to the daily fluid requirements
- Using the resuscitation approach - BEST
○ Administer 20mL/kg over 30-60mins
88
Monitoring fluid therapy what needs to be monitored
- Careful physical examination is needed
○ Measurements should be performed at frequent intervals as trends are generally more informative
- Clinicopathologic markers
○ PCV, [TS], urine output and specific gravity, and [LAC]
○ Na+, K+, Ca2+, Mg2+
- Additional monitoring techniques
○ Blood pressure monitors, central venous pressure
89
Define SIRS and sepsis
- Systemic inflammatory response syndrome
○ Immune/inflammatory response normally protective
○ Extends beyond the site of initial injury or is activated beyond its normal level of control
○ Mediated by a cascade of pro-inflammatory messenger molecules (cytokines)
- Sepsis
○ Life-threatening organ dysfunction caused by a dysregulated host response to infection
90
Define compensatory anti-inflammatory response and mixed anti-inflammatory response syndrome
- Compensatory anti-inflammatory response syndrome
○ Balancing cascade of anti-inflammatory mediators
○ Occasionally response is too vigorous
○ Reduces hosts ability to kill pathogens
○ Results in overwhelming infection
- Mixed anti-inflammatory response syndrome
○ Dysfunction of both pro-inflammatory and anti-inflammatory responses may occur simultaneously
91
What results from SIRS and sepsis in general terms
○ Inflammation is intimately related to coagulation
§ Activation of one tends to lead to activation of the other
§ Coagulopathy may result in microvascular thrombosis
§ Impaired end-organ perfusion
§ Multiple organ dysfunction
92
Equine neonatal sepsis clinical signs and main causes
- Clinical signs and metabolic derangements
○ Due to in part result of host immune response -> response to the presence of bacteria or the toxins
- Usually acquired from the environment
○ GIT tract
○ Respiratory tract
○ Umbilicus
○ In utero infection
- Primary/secondary (bacteriaemic and haematogenous spread) infections
Most commonly streps, staphs and E.coli from environment
93
Equine neonatal sepsis complications
○ Pneumonia
○ Enteritis
○ Omphalitis
○ Septic arthritis or osteomyelitis - swollen joints are infected until proven otherwise
§ Rarely caused by trauma -> synoviocentesis, radiographs - repeat every 2-3 days if needed
○ Meningitis
94
Equine neonatal sepsis diagnosis
1. suspecision - clinical signs - hypovolaemia
2. CBC - leukopaenia with left shift, fibrinogen increase (inflammation at least 24 hours)
3. biochemistry - Hypoglycaemic (inadequate nursing, sepsis), Hyperbilirubinaemia (sepsis), decrease in IgG (used to fight infection)
4. Blood gas - Metabolic acidosis , Hypoxaemia, Hyperlactatemia (inadequate perfusion)
5. blood culture - MAIN DIAGNOSTIC - is the goal bacteriamic (almost always in foals) - most commonly E.coli
95
what does a positive base excess mean in blood gas and what result in and why
Base excess -> metabolic acidotic -> hypoperfusion can add to this
- ADDING IN H+ ion concentration -> decrease pH
Low CO2 as respiratory compromising for low pH -> WANT TO MOVE EQUATION AWAY FROM PRODUCTION OF H+
- Need to reduce CO2 by increasing respiratory rate -> shift equation the opposite way
96
What are the 6 main important things in terms of treatment for neonatal sepsis
1) antibiotics - broad spectrum or depending on blood culture - ampicillin, penicillin, gentamcin
2) fluid - haemodynamic support
3) respiratory support
97
fluid haemodynamic support in the treatment of neonatal sepsis what is needed, maintenance and what need to be careful of
§ IV fluid therapy usually sufficient
□ Inotropes to increase CO
□ Vasopressors to increase vascular tone
§ Neonatal fluid requirements probably higher
□ Maintenance = 80mL/kg/day
§ Care to avoid oedema - monitor carefully for pulmonary oedema
§ Care with sodium load - hartmann's [Na+] = 140mmol/L
98
respiratory support in the treatment of neonatal sepsis what is needed in most cases and position needed
§ Many septic foals benefit from respiratory support
§ Intra-nasal O2 insufflation sufficient in most cases
□ Nasal cannula to the level of the pharynx
□ Begin at 5L/min - adjust rate based on arterial blood gas analyses
□ Add humidifier to not dry up nasal passages
§ Maintain in sternal recumbency
□ Alternate sides frequently in foals in lateral recumbency
99
Nutritional support in the treatment of neonatal sepsis what is normal amounts, what is needed to meet MER and what should consider
§ Healthy foal drink 20-25% of BW in milk/day
□ 120-150kcal/kg/d
§ Meet MER in critically ill foals
□ Approx. 50kcal/kg/d
□ Equates to approx. 10% of bodyweight in mares milk/day
□ Feeding tube if unable to nurse or drink from a bottle/bucket
§ Consider early institution of TPN in foals that do not tolerate enteral feeding
□ Monitor glucose, triglycerides and electrolytes
100
Plasma transfusion for neonatal sepsis when needed and what nursing and supportive care is needed
Plasma transfusion
§ Foals older than 12 to 18 hours
§ Foals that are unable to nurse or will not tolerate enteral nutrition
§ Hyperimmune plasma
Nursing and supportive care
§ Intensive, good quality nursing care is perhaps the most important aspect to ensure good outcomes
□ Keep the foal clean and dry
□ Flip and stand recumbent foals up frequently
□ Physiotherapy
□ Meticulous attention to catheter sites
□ Frequent and careful monitor to detect changes
101
What is the prognosis for neonatal sepsis and common complication
○ 70% survive to hospital discharge
§ 50% for foals that are blood culture positive
○ Septic arthritis secondary complication
§ 84% survived to discharge
§ 40% started at least once
§ 24% raced 5 times or more
§ Mean age to race 1757 days
○ Slower and less likely to get in the races
