Pallor and Jaundice Flashcards
Definition of anaemia
Factors to consider when interpreting haematocrit (PCV)
Diagnostic approach to anaemia
Classification of bone marrow response
Peripheral signs of a regenerative response can be absent in:
Because the presence of a regenerative response is unreliable, a “mechanistic” approach to diagnosing anaemia is often used…
Locations of internal haemorrhage v. external haemorrhage
History foal:
* neurologically abnormal from birth: unable to stand, unable to nurse effectively, extremely hyper-responsive
* Physical examination largely unremarkable: mild scleral haemorrhage, several broken ribs
* Foal: laboratory eval
- stress leukogram (no toxic change)
- fibrinogen concentration normal
- complete failure of passive transfer
Eval Mare:
- moderate tachycardia (80-100/min)
- mild tachypnea
- pale pink MM
- distal extremities cool
- peripheral pulses weak
Colic eval:
- Decreased GI sounds all quadrants
- no reflux on passage of NGT
- Rectal exam: GIT unremarkable, repro tract large but no obvious abnormalities appreciated
Urogenital haemorrhage- rupture of the middle uterine artery
Colic in post-foaling mares diagnostic plan?
Further eval of post foaling mare
* PCV/TS normal, stress leukogram, serum biochem normal, vaginal exam (no tear appreciated in uterus, unable to exclude a tear), abdominal U/S (moderate volume of mildly hyperechoic (hypercellular) fluid with a swirling pattern), abdominocentesis (grossly hemmorhagic)
Urogenital haemorrhage
* Mares often markedly tachycardic (60-140 / min)
- tachycardia is inappropriate for level discomfort
* Rectal palpation
- may be able to palpate haematoma within broad ligament
- often unremarkable
- may exacerbate bleeding by increasing blood pressure
* Transcutaneous ultrasonography
- haemorrhage within broad ligament
- haemoperitoneum (confirm with abdominocentesis)
All of the above– combo.. C is probably the most– haemorrhage into the broad ligament = uncomfortable
** not ischaemic but shutting down
C is the right answer (D is also correct because splenic contraction does make it hard to tease out)
Give her transfusion now??
Hard to get a good cross match.. big deal in horses… so try a few things first! Restore vascular volume with fluid resuscitation… fluids would decrease PCV but you would improve tissue perfusion and that usually improves tissue perfusion…
Treatment plan for rupture of middle uterine artery with intra-abdominal haemorrhage
* Broad spectrum AMs
- Bacterial culture medium in abdomen
- cannot completely exclude uterine rupture
* Analgesics/ anti-inflammatory drugs
* Keep mare quiet
- Acepromazine: may cause milde hypotension
- rectal exam?
* Anti-fibrinolytics (formalin, amino-caproic acid)
Reasons not to perform a blood transfusion
Blood transfusion cross matching
Criteria for transfusion
Clinical signs suggesting decreased dissolved oxygen
Blood transfusion volume
* normal blood volume is 8% of body weight:
0.08 x 500 kg = 40 liters
* Should not take more than 20-25% blood volume: –> can take 8-10 liters from a 500 kg animal every 30 days
Adverse transfusion reactions
Yes
Anaemia
Equine Fluids
Only thing you need to know is when a horse is dehydrated and has poor vital signs we give it a bolus and monitor and check vitals after it has been administered and if it is still not stable we give it another but if it has stabilized we then move onto just a maintenance rate and a guesstimate of what its ongoing losses are
The bolus is at 20ml/kg/he
The maintenance is at 2ml/kg/hr
Liver disease in horses
Pyrrolizidine Toxicity
Know this– on exam!!
Pyrrolizidine Toxicity clinical signs? Diagnosis? Lesions?
Pyrrolizidine Toxicity prognosis? Management?
History foal:
birth 40 h prior to presentation
Birth unattended: placenta appeared grossly normal
Normal first 24 hours of life– passed normal meconium, normal urination, nursing normally
* Examined by rDVM at approx 24 hrs– physical exam normal, routine lab work normal, IgG >>> 800 mg/dL
But the following day… passing dark, red-colored urine– appeared to be straining to urinate
* Lying down more often than previous day
* Seemed mildly depressed
* did not appear to be nursing frequently
What is the most likely cause of icterus in this foal?
Discoloured urine: Haematuria, myoglobinuria, haemoglobinuria
Straining to urinate
Lethargic
Marked icterus
C. Intravascular haemolysis because discoloured urine– you wouldn’t see it appear in the urine
Icterus in foals
Diagnostic plan icterus in foal
PCV/TS concentration
CBC- fibrinogen concentration
Urinalysis
Blood culture- rule out sepsis because worried immunocompromised
Plasma biochem analysis
Coomb’s test OR
Mix the foals RBCs with the foals serum– positive or incompatible minor cross match we have our diagnosis
How are foals tricky with TP? AST and CK?
How are foals trick with GGT? And IgG concentration?
100 HR high but unsure as nervous because we just wrangled the foal
RR pretty low but normal??
Temperature mild pyrexia… anything above 39C
Really red serum– haemoglobinaemia– red pigment free in plasma.. bound to heptaglobin
Why normal haematocrit? Could be dehydrated or spleen is tricking us
Relationship between Hct: Hb should be about 3:1…. this one is 2 to 1… more Hb than RBCs… free haemoglobin floating around in the blood stream (most species)
** Why are we worried about high fibrinogen? Definitely inflammatory process… but we are worried about sepsis because it can take 2-3 days for fibrinogen to increase… could just be marked inflammatory process… but definitely a red flag
More band neutrophils than we would expect– related to marked inflamm response because marked haemolysis going on
TP within normal limits– most foals have total TP around 55.. so this is really increased.. dehydration, not inflamm because gamma globulins take a while to occur, intravascular haemolysis– proteins floating in the blood stream
* AST- hepatocellular enzyme– GGT is up too- cholestatic enzyme– when we look at the AST, we have to look at the CK too. CK is increased too (normal in foals– squeezed through birth canal, lying around, etc.)… AST is probably from muscles… But why GGT?? GGT is an enzyme that is in a lot of cells… so increase indicatees damage to and blockage of the biliary tract….enzyme that bind to a lot of epithelial membranes, including mammary glands.. colostrum has a high GGT content… can be used to assess passive transfer… so this is probably why it is increased
** Really high IgG– relatively consistent with foals with problems– high passive transfer
Likely haemoglobinuria
* rule out haematuria and myoglobinuria
* confidently say haemoglobin in the urine
Neonatal Isoerythrolysis
Somehow the mare has been exposed to these Aa+ antigens (unknown how).. mare develops Antibodies… And they are concentrated in colostrum and udder.. absorbed in the foal
A or B
C– she is bright and happy.. HR is okay… we are going to wait. Transfusion is a real issue.
Treatment of NI
Does the foal need a blood transfusion now?
Yes
Unable to find a compatible donor. Whose blood should we use?
A. Mare
B. Stallion
C.Either of those will be okay it is the first tranfusion
D. None of the above
D
A
Prevention of NI
