Dogs and Cats 17 Flashcards
1
Q
what are the 3 components of haemostatic system
A
1) Primary haemostasis
○ Formation of the temporary platelet plug
2) Secondary haemostasis
○ Fibrin formation through the coagulation cascade
3) Fibrinolysis
○ Fibrin breakdown
2
Q
Primary haemostatic defects what is involved and causes
A
- Thrombocytopaenia ○ Decrease production, increase destruction, increase loss - Thrombocytopathia ○ NSAIDS, vWD, colloids (probably the bigger older ones) ○ Uraemia - Congenital ○ Von willebrands disease - Acquired ○ Immune-mediated thrombocytopaenia
3
Q
Secondary haemostatic defects what are 6 main diseases and the 2 most common
A
- Vitamin K antagnostis (rodenticides) - common
- DIC - common
- Bile duct obstruction - vit K needs bile to be reabsorbed
- Liver failure
- Haemophilia A (factor VIII)
- Haemophilia B (Factor IX)
4
Q
What are the 5 tests for haemostasis
A
1) blood smear
2) buccal mucosal bleeding time
3) activated clotting time
4) prothrombin time (PT)
5) activated partial thromboplastin time (aPTT)
5
Q
How does a blood smear help test for haemostasis, what is normal
A
○ Look for platelet clumping (esp cats) ○ Platelet number § One platelet per HPF - 15,000 on the total count § Normal is 10-20/100X HPF ○ Platelet size ○ Erythrocyte morphology § Regeneration § Other diseases - spherocytes § Schistocytes (RBC fragments)
6
Q
How does a Buccal mucosal bleeding times (BMBT) help test for haemostasis. what is normal and what does prolonged indicate
A
○ Assesses primary haemostasis - generally if platelet number is normal this is the next step
○ Normal <4mins up to 7mins - VARIABLE
○ Extremely methodology dependent
○ Prolonged and contraindicated with decrease platelets
○ Platelet dysfunction
§ Von willebrand disease
§ NSAIDS, antiplatelet drugs (clopidogrel)
§ Uraemia
7
Q
How does a activated clotting time (ACT) how assess haemostasis, what need to be careful of and how to do
A
○ Assesses intrinsic and common pathways (like PTT)
○ Activating agent: diatomaceous earth
○ Phospholipid source: sample platelets
§ Affected by platelet count (<10-20,000)
○ Temperature
○ Poor sensitivity (5-10% factor activity)
○ How to do
§ Use pre-warmed tubes and heating block
§ Begin timing when blood first enters tube
§ End point is first visual evidence of clot
§ Reference ranges vary
8
Q
Prothrombin time (PT) and Activated partial thrombplastin time (aPTT) how assess haemostasis and what if prolonged
A
Prothrombin time (PT) ○ Extrinsic and common pathway ○ Prolonged in factor VII deficiency § Vit K dependent and shortest half-life - so will see this first with rodenticide poisoning ○ Reference ranges vary ○ 25% greater than control Activated partial thromboplastin time (aPTT) ○ Intrinsic and common pathways ○ More sensitive than ACT ○ Most useful test for ICU patients ○ Reference ranges vary ○ 25% greater than control
9
Q
What are the 4 main steps in the diagnostic approach to bleeding patient
A
1) stablise
2) history
3) physical exam
4) Diagnostic tests
○ PCV/TS/CBC
○ Blood smear (platelet count/RBC morphology)
○ ACT or PT/aPTT
○ BMBT
○ Chem screen for organ assessment
○ Imaging to look for haemorrhage, masses and other disease
10
Q
In terms of history for a bleeding patient what are important aspects
A
○ Previous bleeding § Eruption of permanent teeth § Oestrus § Routine surgeries (neutering) § Venepuncture and vascular access § Trauma ○ Recent overt haemorrhage ○ Lameness ○ Dyspnoea ○ Appetite, drinking, activity ○ Stool colour ○ Other previous or concurrent illness ○ Medication/vaccination ○ Parents and siblings ○ Any rodenticides on the property
11
Q
What are some clinical signs of physical exam that suggest severe haemorrhage
A
○ Hypovolaemia
○ External haemorrhage
§ Epistaxis, gingival bleeding, haematemesis, haemoptyosis, haematuria, haematochezia, melaena or bleeding from a cutaneous wound
□ Melaena - upper GI bleeding
○ Signs referable to chronic anaemia
○ Organ dysfunction due to bleeding or concurrent disease
○ Concurrent disease per se
○ Mass lesions (the underlying cancer or haematoma)
12
Q
If a patient comes in after chest trauma in circulatory shock and respiratory distress what are the 5 stabilisation emergency treatments
A
1) resuscitative fluid therapy
2) Oxygen supplementation (flow-by oxygen (>4L/min)
3) Analgesia: 0.1mg/kg methadone IV
4) Stop external bleeding: wound pressure
5) Emergency diagnostics
13
Q
what are some emergency diagnostics to run on a traumatic bleeding dog
A
- PCV/TS
- Acid-base: BE, lactate
- Blood smear: plts
- PT, aPTT
- Blood type (DEA 1 pos/neg)
- Arterial blood gas
- TFAST/AFAST - to ensure not significant bleeding in chest or abdomen
- Monitoring:
○ Continuous ECG, SpO2, repeat MBSAs
14
Q
Resucitative fluid therapy what need to give, advantages and disadvantages
A
○ Isotonic crystalloids § Advantages □ Availability □ Quick, effective expansion of vascular volume § Disadvantages □ Not a long lasting effect - redistribution □ Not replacing what is lost □ Dilutional coagulopathy □ Anaemia □ Pulmonary oedema § TO PREVENT DISADVANTAGES □ Give fluid aliquot and then reassess ○ Blood products § Red blood cells § Clotting factors § Platelets § WHOLE BLOOD IDEAL
15
Q
What are some changes on blood smear that suggest regenerative anaemia
A
- Reticulocytes ○ Immature RBC ○ Only count aggregate reticulocytes in cats - the most immature ones ○ Magnitude should match anaemia ○ Use absolute reticulocyte counts Other changes that support regeneration - Polychromasia - ↑ MCV +/-↓ MCHC ○ Macrocytic and hypochromic / macrocytic nomorchormic - ↑ RDW - Nucleated RBC
16
Q
What are the main differences between haemorrhage and haemolysis
A
Haemorrhage - Total solids decreases - Normal RBC morphology - No agglutination - Moderate regenerative response - No haemoglobin free in circulation - Evidence of bleeding - body cavity, melena - Coombs negative - no complement and antibody sticking to red blood cells Splenomegaly no
17
Q
Clinical approach to anaemia what asking for with history
A
-Signalment
- Environment
- Travel history
- Fleas / flea control
- Ticks / tick control
- Endoparasite control
Vaccination status
- Current & prior medications / toxins - certain drugs can lead to RBC destruction or suppression of bone marrow
- Other diseases - known Haemangiosarcoma that are destroying RBCs
- Faecal colour - hematochezia, melena
- Trauma
- Prior / current diagnosis
18
Q
What finding on physical examination can suggest anaemia
A
- Jaundice, haemoglobinuria, splenomegaly: haemolysis
- Tachypnoea, muffled lung/heart sounds, abdominal distension: bleeding
- Bleeding ≥ 2 unrelated sites: coagulopathy
- Check for external bleeding: skin, urine, GI (rectal)
- Small kidneys: renal disease
- Testicular / abdominal mass: Sertoli / Ovarian tumour
- LN enlargement: Neoplasia
- Brown MM and swollen head: Paracetamol toxicity - IN CATS
- Cardiac murmur: Often secondary to anaemia
19
Q
What are the 2 types of haemolytic anaemia and the 6 main causes
A
- Extravascular ○ Spleen (liver, BM). Insidious onset. Mild or severe - Intravascular ○ Lysed within circulation. Acute onset. Haemoglobinaemia, haemoglobinuria - more severely unwell IF HAVE Both: Jaundice, bilirubinuria, ↑ [bilirubin] Causes 1. Immune mediated 2. Infectious 3. Toxin / Drug Inducted 4. Microangiopathic 5. Electrolyte 6. Congenital red blood cell defects
20
Q
Immune mediated haemolytic anaemia what is it and what are the 3 main things it results in
A
- Autoimmune disease
- Antibodies formed against self-red blood cells
- Coated red blood cells are targeted for destruction -> therefore destroyed or damaged so decrease lifespan
- Results in:
1) Extravascular haemolysis in liver / spleen - most common - generally slower onset
1. Macrophage removes the whole RBC due to complement binding OR
2. Macrophage removes only the part of the RBC with complement -> creating spherocytes
2) Intravascular haemolysis within circulation - less common - generally worse - Complement and/or antibodies attach to RBC resulting in lysing of that cell - haemoglobin free within blood -> haemoglobinuria
3) Destruction of red cell precursors in bone marrow – rare, non-regenerative (PRCA)
21
Q
Immune mediated haemolytic anaemia what are the main causes
A
○ Majority are idiopathic = primary: dogs > cats
○ Rest are secondary triggered by: cats > dogs
§ Infection
§ Cancer
§ Inflammation
§ Medications
§ Neonatal isoerythrolysis (type A kitten from type B queen
§ Vaccination?
22
Q
Immune mediated haemolytic anaemia typical signalment and what do the owners generally notice
A
Typical signalment
○ Young to young adult (2-7 yr)
○ Small to medium, often toy breeds - Maltese, schnauzers
○ +/- More females
○ Cats: Young < 6 yr, male, DSH/mix
What owners notice:
§ Lethargy, depression, weakness, anorexia
§ Collapse, increased respiratory rates
§ Vomiting, diarrhoea, increased thirst, eating strange objects (less frequently)
§ Cats: Pica, pu/pd
23
Q
Immune mediated haemolytic anaemia generally physical examination findings
A
§ Pale mucous membranes
§ Increased heart and respiratory rates, heart murmur, prolonged capillary refill time
§ Enlarged liver +/- spleen
§ Jaundice, orange coloured urine (intra-vascular haemolysis)
§ Abdominal pain, lymph node enlargement, fever
§ Red coloured urine
§ If concurrent immune mediate destruction of platelets (Evans syndrome)
□ Petechiae
□ Ecchymoses -> bruise easily especially with jugular vein - AVOID
□ Melena
24
Q
Immune mediated haemolytic anaemia blood smear and biochemistry results
A
§ Spherocytes
§ Auto-agglutination
□ Normal slide agglutination test
® ADD saline -> clearance of rouleaux with saline BUT NOT CLEARANCE OF AGGLUTINATION
□ Coombs test (direct antiglobulin test)
® Only perform if slide agglutination negative
® Detects for antibodies / complement against red blood cells
® False negatives common
® Not accurate after transfusion
○ Biochemistry
○ Increased bilirubin
○ Increased liver enzymes (ALP, ALT, AST) - tissue hypoxia
25
Diagnosis of immune mediate haemolytic anaemia
- Haemogram
○ Moderate to marked regenerative anaemia
§ Non regenerative (if early or bone marrow version)
○ Spherocytosis
○ Intravascular haemolysis (breakdown on red blood cells)
○ Auto agglutination
- Biochemistry
○ Increased bilirubin
○ Increased liver enzymes (ALP, ALT, AST) - tissue hypoxia
- Need good blood sample collection technique
26
what is involved with initial management of IMHA case
- Rest
- Oxygen – flow by, oxygen pen
- Get IV access
- Ensure have resuscitation code
- Collect blood samples: (EDTA (purple), blood smear, plain/Lit Hep (yellow/green), +/- citrate (blue)
○ PCV / TP and blood smear
○ Minimum data base (haemogram, biochemistry)
- Collect urine
27
When diagnose IMHA what need to do and how
Look for underlying cause – WHY? WHEN?
- Prior drug history (including vaccines, over the counter and preventative health-care)
- Travel history – ticks, heartworm, other infectious causes
- Prior diseases
- Prior transfusions, pregnancies
- Search for underlying cause - IMPORTANT as if malignant tumour wont help, if infectious cause and immunosuppress then can kill the animal
○ Chest x-rays
○ Abdominal ultrasound
○ +/- Cross match / blood typing
○ +/- Tests of clotting function
○ +/- Infectious disease panels (geographically dependant)
○ +/- Blood gas analysis
○ +/- Check bone marrow sample -> don't always do
- No underlying cause found -> primary IMHA
28
What are the 5 main treatments for IMHA
1) packed red blood cell transfusion
2) IV fluids as required
3) control vomiting/gastrointestinal ulcers as required
4) immunosuppressive dosese of prednisolone
5) antiplatelets - to reduce risk of embolic events - doesn't 100% prevent
29
Packed red blood cell transfusion in IMHA what could also give, how commonly need, and what should do before
○ Or whole red blood cells if not available
○ Required in 44-90% of cases
○ Ideally fresh products
○ Ideally cross match / blood typed for compatibility & reduced risk
§ Can be hampered by auto agglutination, previous transfusions
§ Essential if previous transfusions
§ If more than 5 days since transfusion, DEA 1.1-negative (“universal donor”) blood is ideal
30
Prednisolone in IMHA, what could also use, use until when and common side effects
○ Mainstay of initial treatment, rapid
○ Or IV dexamethasone day 1 then prednisolone day 2 onward
○ Until normal PCV and no spherocytes or auto agglutination, then slowly taper every 2-4 weeks while monitoring red cell count
○ Side effects common:
§ Increased thirst, increased urination, increased appetite, increased panting, muscle wasting, weakness, poor wound healing, gastrointestinal ulceration, increased liver enzymes and liver size, thin skin, hair loss, clots, increased risk of infection, diabetes, Cushing’s disease
○ First immunosuppressive medications tapered
31
What are the 2 other immunosuppressive medications used for IMHA, are they used with or without prednisolone
1) Azathipoprine - prednisolone sparing
| 2) cyclosporine - given with prednisolone
32
Azathioprine in IMHA how common, when start, when tapered, why used and main issues
○ Most common adjunctive immunosuppressant
○ Start early, several days / weeks to effect
○ Once a day for first week, then every other day, by mouth
○ Last drug to be tapered
○ Increases survival
ISSUES
○ Cytotoxic: Wear gloves, shouldn’t split tablets (compounding)
○ Side effects: Rare
§ Pancreatitis, bone marrow suppression (after 3-16 weeks), liver toxicity, anorexia, vomiting, diarrhoea
§ Monitor haemogram and liver enzymes
○ DO NOT USE IN CATS!!!!
33
Cyclosporine in IMHA when give, advantages and side effects
○ Give one hour before, or two hours after food
○ Given once to twice a day by mouth
○ For refractory cases
○ Can monitor blood levels prior to the next dose after 2-4 weeks
○ Rapid in action
○ Does not supress bone marrow
○ High cost, compounding
○ Side effects: vomiting, diarrhoea, anorexia, overgrowth of gums, papilloma-like skin lesions, hair loss, increased risk of infection, ?cancer
○ Manage gastrointestinal side effects with twice daily dosing / give with a small amount of food
34
Anti-platelets in the treatment of IMHA to reduce risk of embolic event what are the 2 main products to use and what increase
```
- Low dose aspirin once a day by mouth
○ Reduces but does NOT eliminate risk of embolic events
○ Increases short and long term survival
○ Practical
- Clopidogrel (Plavix)
○ Either alone or with aspirin
○ Safe
○ Similar short term survival to aspirin alone
```
35
monitoring and musing for IMHA patients what is involved
- Hospitalise initially
○ 24 hour care is ideal
○ Cage rest
- Monitor
○ PCV / TP every 12-24 hrs initially
§ Aim for improvement in anaemia, stable red cell count
§ Resolved autoagglutination and spherocytes
§ Care excessive venipuncture especially small patients or low platelets or DIC – use small (24G) needles, use peripheral veins and pressure bandage, provide extra bedding, enforced rest
○ For complications of IMHA and medications
○ Monitor vitals, appetite, thirst, urination, defecation
- Ensuring good nutrition, no raw meat!
○ Immunosuppressed, barrier nursing
36
IMHA prognosis, main risk period, main issues with treatment and negative prognostic factors
- Variable, poor to guarded
- High initial mortality rate, especially first 2 months
- 50-88% survive to discharge
- Risk of complications, treatment side effects, relapse
- Often expensive to treat, intensive at start, then maintenance for 6-12 months, possibly lifelong
NEGATIVE
- Increased bilirubin / jaundice
- Autoagglutination
- Increased band neutrophils
- severe anaemia
37
what are the 3 main complications of IMHA and prevalence
1) embolic events (clots) - most common
2) disseminated intravascular coagulation (DIC) - 20-45% of cases
3) relapse - 16% - restart treatment and taper more slowly - may need lifelong treatment
38
Embolic events (clots) as complication of IMHA where mainly occur, result from adn ris factors
○ Potentially devastating
○ Found in 10-80% of dogs at post-mortem
○ Especially to lungs, but any organ possible
§ Peracute severe respiratory distress
§ Often thoracic radiographs are normal
§ Minimal / no response to oxygen therapy
○ Result of systemic inflammatory response
§ Net increase in procoagulant activity
§ Decreased anticoagulant activity
§ Decreased clot breakdown
○ Risk factors – many unavoidable in treating the disease
§ Severely low platelets, low serum albumin, IV catheters, increased serum ALKP, prednisone, cytotoxic agents, blood transfusions
39
Immune mediated thrombocytopenia cause, treatment and prognosis
- Dx: Severe thromobcytopenia, +/- platelet bound antibodies, exclude other causes, response to Rx
- Rx: Underlying cause (secondary)
- Rest, GI protectants, IVFT, RBC transfusions, no NSAIDs
- Primary: Immunosuppressive prednisolone
- Prognosis: Generally good
○ ~ 70% respond, mortality ~ 20%, 25% recurrence and half of these refractory
40
What are the 2 main infectious causes of heamolysis
1) mycoplasma haemofelis
2) babaesiosis
- babesia canis
- babesia gibsoni
41
Mycoplasma haemofelis what are the 3 main types of infections and clinical signs
Types of infections
○ Acute: Severe haemolytic anaemia, to mild -> haemolysis and autoagglutination / Coombs positive
○ Chronic: Usually no anaemia
○ Subclinical: Carrier status, may clear, occasional reactivation - MOST CATS
Clinical signs:
○ Vary with species / strain / stage of infection / concurrent disease (FIV / FeLV)
○ Acute: Pale, lethargy, anorexia, weight loss, dehydration, pyrexia, splenomegaly, (jaundice)
42
Mycoplasma haemofelis transmission and diagnosis
- Transmission
○ Fighting, contaminated transfusions, ? transplacental,
- Diagnosis:
○ PCR on blood: Gold standard. Can use to monitor response to treatment
○ Cytology: Blood smear: useful in acute infection for rapid, bed-side diagnosis, but low sensitivity and false +ve and –ve possible
§ Can’t distinguish species
43
Mycoplasma haemofelis treatment and prognosis
- Treatment:
○ Doxycycline for 2 week minimum, can’t clear carrier state
○ Avoid corticosteroids
○ Supportive care: IVFT, transfusion, oxygen
- Prognosis: Generally good
44
Babesia what are the 2 species and how many subtypes, how transmitted and incubation period
- Transmitted: Ticks, transplacental, bite wounds, transfusions
- Babesia canis (3 subtypes)
○ B.canis var vogeli: Transmitted by brown dog tick, mildly pathogenic, most important form in Australia
○ 10-21 day incubation period
- Babesia gibsoni (2 subspecies)
○ Transmitted by dog fights, brown dog tick, transplacental, mildly pathogenic
○ 14-28 day incubation period
45
Babesia how many days for transmission to occur, results in and secondary complications
- 2 days for transmission to occur
- Results in
○ RBC fragility + anti-RBC Ab -> intravascular / extravascular haemolysis
○ Sludging of RBC -> organ failure + hypoxia
- Secondary complications: Renal / liver failure, ARDS, myocarditis, hypotension, pancreatitis, neurological signs, DIC, thrombocytopenia
46
Babesia diagnosis and treatment
```
- Diagnosis:
○ PCR (ideal)
○ Blood smear: Romanowsky stains
○ Serology (IFA)
- Treatment (most improve in 3-7 days):
○ Transfusions, Rx complications
○ B.Canis: Diminazene aceturate / imidocarb
○ B. Gibsoni: Atovaquone and azithromycin
```
47
Toxin/drugs that result in haemolysis what is the general history and changes on blood smear
- Dx: History of exposure:
○ Snake bite, carbimazole, certain antibiotics, onions, garlic, paracetamol, Zn, Cu
- Blood smear
○ Large numbers of Heinz bodies
○ Eccentrocytes - severe oxidative damage
48
what are 3 common causes of toxin/drug induced haemolysis
1. Oxidation of sulphydryl groups of globin chains in Hb
- E.g. Onions, Garlic
2. Direct damage to RBC membrane -> Intra / extra vascular haemolysis
- E.g. Zinc, Naphthalene, Cu, Snake bite
3. Oxidation of ferrous iron (Fe2+) to ferric ion (Fe3+) in haem -> methaemoglobin
- E.g. Paracetamol
49
Microangiopathic haemolytic anaemia what occurs, causes and diagnosis
- RBC haemolysis due to mechanical damage
○ E.g. Haemangiosarcoma, haemangioma, haematoma, DIC, splenic torsion, HW
- Dx / Rx: Typical RBC changes + find and Rx underlying cause
- Schistocytes: Fragments of RBC
- Acanthocytes: Projections on RBC surface
○ Cleared by spleen (extravascular haemolysis)
○ Usually mild anaemia (unless bleeding)
50
What electrolyte abnormality lead to a haemolysis, why and causes of this
- Hypophosphataemia -> RBC ATP depletion, ↑RBC rigidity, haemolysis
○ E.g. Insulin therapy during DKA treatment
○ E.g. Refeeding syndrome
○ Dx: Serum phosphate measurement
○ Rx: IV phosphate
51
How to hep differentiate when animal is pale from hypoperfusion or anaemia
hypoperfusion or anaemic -> TO DIFFERENTIATE DO PCV (could also determine whether icterus present (RBC destruction as well)
52
Acute vs chronic anaemia what are the main differences
- Reticulocytes <60 x 10^9/L
- Wait 3 days then ensure still below this -> ENSURE THAT IT IS NON-REGENERATIVE NOT JUST PRE-REGNERATIVE
- Have time to compensate for the reduced RBC mass -> very little clinical signs present
○ Possible clinical signs -> non-specific - lethargy, exercise intolerance, pica (mainly cats), pale MM
○ Depending on underlying cause -> splenomegaly, hepatomegaly, bleeding disorders - melena, petechiae
§ Pyrexia in animals with secondary or primary infections
53
What are the 7 main causes of non-regenerative anaemia and which generally have mild or severe anaemia
1. Chronic inflammation - mild
2. Endocrine disease - mild
3. Chronic kidney disease (IRIS!)
4. Bone marrow disorder - suspected if several cell lines are declined - severe anaemia
5. (Iron deficiency anaemia)
6. (Blood loss / haemolysis for the first 3 days: pre‐regenerative)
7. (Physiologic: puppy, pregnancy)
54
What indicates severe anaemia with PCV and is non or regenerative anaemia more common in dogs vs cats
```
PCV% severe
- Dogs <19
- Cats <15
Regenerative vs non-regenerative
- Dog -> regenerative more common
- Cat -> non-regenerative more common
```
55
If a patient with non-regenerative anaemia is symptomatic what are the 2 possible situations that ais occurring
1. Acute blood loss of haemolytic anaemia not yet mounted a response
- Pre-regenerative
2. Chronic anaemia
- Decompensated now because got to such a low threshold can no longer compensate
- Primary cause of anaemia is now taking over
56
If a patient with non-regenerative anaemia is symptmatic what need to treat with
- Needed PRIOR work up, if patient is SYMPTOMATIC
- Increase red cell mass: transfusion
○ Packed red blood cells
○ Synthetic haemoglobin (Oxyglobin®)
- Address the underlying disease (possible?)
○ Kidney disease is possible -> problem is the decrease in EPO -> replace this
○ Erythropeitin in CKD (darbepoetin)
§ 0.45mcg/kg/week SQ WITH iron supplementation!!
§ Monitoring: every 1‐2 weeks Aim: low end of PCV range
§ CAVEAT: antibodies production!
57
What is the workup involved in a chronic non-regenerative anaemia
- Review history (medication, infectious disease) / PE
- Laboratory
○ Haematology (reticulocytes), biochemistry, UA
○ Infectious diseases
○ FNA/biopsies
- Imaging
○ Chest and abdomen - looking for sites of infection or tumours
○ Abnormalities: FNA/biopsies (thrombocytes!)
- Bone marrow aspirates / biopsies - with non-regenerative - last step
○ Cytology and punch biopsy
58
What are some causes of bone marrow suppresion leading to chronic anaemia
- hyperoestrogenism - endogenous (sertolic cell tumour)
- Drug effects / hormones
○ Hyperoestrogenism (exogenous)
○ Chemotherapy (dose‐dependent)
○ Antibiotics (TMS, chloramphenicol)
○ Others: methimazole, griseofulvin, fenbendazole, phenobarbital
- Infectious agents - THIS NEEDS TO BE TREATED FIRST
○ Parvovirus, Ehrlichia, Anaplasma, FeLV, and FIV
- Myelophthisis
○ Neoplasia, fibrosis
- Idiopathic (immune‐mediated) - pure red cell aplasia
59
hypoestrogenism due to Sertoli cell tumour what are some signs associated, what results and how to treat, what occurs in cats
Clinical sign
- Feminising signs in a male non-castrated dog with pancytopenia
Treatment
- Remove source of oestrogen (Sammy -> castration) -> will result in bleeding and anaemic BUT NEED TO DO
- Severe neutropenia -> antibiotics
- Severe anaemia -> packed red blood cell
- Bone marrow usually recover, but it takes time!
- Cat
○ more sensitive, but rarely exposed
○ fatality due to liver disease
60
```
If have
History
- Chronic non‐regenerative anaemia (8 months)
- Polydipsia/polyuria
- Tiredness (agility dog)
Examination
- RR 24 / min T 38.6°C HR 80 / min
- Overweight (BCS 6/9)
- Increased undercoat
- Pain on hip extension
What thinking of cause, what also adds evidence
```
ENDOCRINE DISEASE
○ Clinical signs are secondary to the primary disease
○ Hypoadrenocorticism and hyperadrenocorticism
- mild anaemia - endocrine or inflammatory but if normal inflammatory mediators
- also pretty stable haematocrit over a few months
61
Pure red cell aplasia what is it, primary and secondary causes
BONE MARROW SUPPRESSION - non-regenerative
(type of IMHA) -> within the bone marrow not the blood
□ Primary
® Dog > cat
® Middle age female dogs (Labrador retriever?)
□ Secondary
® Immune mediated (mature lymphocytosis in BM)
® Infectious (Parvovirus, FeLV)
® Toxic (chloramphenicol, phenylbutazone (D), oestrogen (D))
62
Pure red cell aplasia treatment and outcome
□ Treatment
® Prednisolone 2mg/kg PO q12h
® Refractory: consider chlorambucil (2mg PO q48‐72h) or cyclosporine (5mg/kg PO q24h)
□ Outcome
® Good (23 out of 26 cats alive at two months)
® Aggressive treatment
® Time (3 to 5 weeks for resolution of the anaemia)...
® Might need long term treatment
63
Iron deficiency leading to non-regenerative anaemia what history can suggest this and haemoology results
```
END STAGE - leads to non-regenerative - chronic history
- History
○ Decreased exercise tolerance
○ Weight loss and decreased appetite
○ Diarrhoea (small bowel) for a month
Haematology
- MICROCYTIC ANAEMIA
```
64
Iron deficiency causes and treatment
```
- Causes
○ Inadequate iron intake (nursing animals)
○ Parasitism
○ Haematuria
○ Haemorrhage (external, pulmonary, GI)
○ Iatrogenic (multiple blood sampling)
- treatment
○ Remove primary cause (if feasible!)
§ Parasitic treatment (exo‐/endoparasites)
§ Coagulation disorders -> treat
§ GI ulcerations -> treat
§ Bleeding neoplastic process -> remove
○ Iron supplementation
§ Ferrous sulfate PO
□ Side effects: GI irritation, binds tetracycline
§ Iron dextran IM
□ Side effects: painful at injection site, hypersensitivity
```
65
Chrnic inflammation leading to chronic anaemia how common, how leads to anaemia and therefore diagnosis
- Chronic disease is the most common form of non-regenerative anaemia in cats and dogs
- Iron sequestration within the bone marrow secondary to sustained inflammatory or neoplastic processes
○ Therefore serum iron concentration and total iron-binding capacity are usually decreased and Hb saturation low but iron stores in the bone marrow are increased
- Diagnosis
○ Evaluate the bone marrow with staining aspirates with prussian blue
§ Often not needed - just identify the primary cause and treat that to resolve the anaemia
66
Chronic anaemia caused by renal disease why results, at what stage and treatment
- Chronic kidney disease occurs secondary to decreased erythropoietin production in kidney
○ Dependent on the kidney mass and only in ADVANCED renal disease
§ If severe anaemia but only in stage 1 or 2 of renal disease then other causes of erythropoietin decrease should be investigated
Treatment
- Replacement of the erythropoietin by subcutaneous injection
○ Patient can develop antibodies targeting EPO - anaemia will be more severe than prior to treatment - WORSE THAN DISEASE
○ THEREFORE - treatment only in advanced cases (PCV<20%) and only after warning the owners about potential risk
- Iron supplementation is usually needed to achieve the best result
67
Urinalysis results of: yellow, clear USG 1.038 +1 bilirubinuria, pH 8.5 Normal urine sediment
in a dog, anything abnormal
Some bilirubinuria is normla in dogs - if more than +1 start getting worried
68
What are the 2 main classifications of haemoabdomen and main organs that can cause this
1. Traumatic
2. Non-traumatic (Spontaneous)
○ Coagulopathic
○ Non-coagulopathic(neoplastic / torsion)
- Organs that can cause haemoabdomen
○ Liver, spleen, kidney, adrenal glands, major vessels
69
Traumatic haemoabdomen how common and main causes with clinical signs
○ Blunt(e.g.) Vehicular trauma
○ Penetrating trauma
§ Sticks, knives, gunshot, iatrogenic during surgery
○ Splenic, liver or renal rupture
○ Acute blood loss due to capsule rupture or avulsion of vessels
§ Tachycardia, pale mucous membranes, hypotension, weakness, collapse and death.
70
Non-traumatic haemoabdomen main causes
```
○ Coagulopathies –Refer to ECC lectures
○ Benign or malignant intra-abdominal neoplasia - splenic mass most common
§ Liver / Spleen / Kidney / Adrenal
○ Gastric dilatation and volvulus (GDV)
○ Liver lobe torsion
○ Splenic torsion
○ Post-surgical (e.g. OVH, GDV)
```
71
In terms of benign or malignant intra-abdominal masses what is the percetnage of the main ones in dogs ratios in cats
```
Dogs - cannot tell if benign or malignant splenic mass during surgery
- Haemangiosarcoma (HSA)(63.3%)
○ (Spleen or Liver)
- Splenic hematoma (26.6%)
- Splenic torsion (5%)
- Hepatocellular carcinoma (3.3%)
- Carcinomatosis (1.6%)
- Cats: 50% neoplastic : 50% non-neoplastic
```
72
What are the 3 things within the clinical approach for haemabdomen
```
1. Initial stabilization
○ IV Fluid therapy (bolus, assess response)
○ Abdominal compression (blunt trauma)
○ Oxygen therapy
2. Minimum database
○ TP/pcv, BG, BUN
3. Abdominal Ultrasound / Radiographs
○ Loss of serosaldetail / mass effect
○ Free fluid, mass
```
73
How to confirm haemoabdomen
Abdominocentesis or diagnostic peritoneal lavage
- Compare pcv of abdominal fluid to peripheral pcv
○ If similar → haemoabdomen
- Blood does not clot (no platelets)
- If clots → inadvertent splenic or vascular penetration
74
Haemabdomen what are 3 main indications for surgery and when shouldn't you
- Indications for surgery
○ Most spontaneous causes of haemoabdomen
○ No response to medical stabilization therapy
○ Deterioration of clinical signs
- Just as important as knowing if and when to cut is knowing when not to cut
○ Many traumatic causes of haemoabdomen can be managed successfully without surgery
○ Coagulopathic causes of haemoabdomen non-surgical -> generally rodenticide -> give vit K
75
Laparotomy for causes of haemabdomen what differentials would you do for
§ GI disorders –Foreign bodies / torsion / rupture
§ Urogenital abnormalities unresponsive to medical Rx
§ Abdominal disorders of unknown origin
§ Penetrating trauma
§ Acute abdomen
§ Generalized peritonitis
§ Diagnosis and treatment of portosystemic shunts
§ Splenic abnormalities
Uncontrolled abdominal haemorrhage
76
What are the branches of the aorta
1) celiac artery
- hepatic artery
- left gastric artery
- splenic artery
2) cranial mesenteric
3) right/left renal
4) testicular/ovarian
5) caudal mesenteric
77
With exploratory laparotomy for haemabdomen what need to be careful of with midline incision and what is the priority and how to achieve
1. Midline incision
○ Adequate exposure to exteriorize spleen
○ Be aware of acute decompensation when pressure of abdominal wall is released
2. Priority on controlling bleeding
○ Digital pressure on celiac artery and aorta will control most abdominal bleeding
○ Identify source of bleeding
§ If spleen is small (25-50% of N size) then it is probably NOT the cause of the bleeding
○ Look for clot –clamp proximally before removing
78
What are the 2 main ways bleeding is control with exploratory laparotomy for haemabdomen and what useful for
1) Pringle manoeuvre
○ Useful for control of hepatic bleeding
○ Temporary occlusion of hepatic artery and portal vein
§ digital pressure -caudal to stomach and cranial to celiac artery
2) Surgical haemostasis
○ Pressure / tamponade (temp. 5-10 minutes)
○ Ligation with suture ligatures or vessel sealing device - arterial side generally this is needed
○ Abdominal packing
○ Topical haemostatic agents
§ Gelfoam, Surgicel
79
Haemangiosarcoma (HSA) what breeds common in, metastatic rate and prevalence for malignant neoplasia vs benign mass, how many where then haemangiosarcoma therefore how many HSA as splenic mass
○ GSD, Labrador or Golden Retrievers increased incidence for HSA and haematoma
○ High metastatic rate >50% (liver, omentum, R atrium)
○ Prevalence
§ When a definitive diagnosis was obtained, malignant neoplasia was diagnosed most frequently and occurred in 24/30 (80%) dogs.
§ Hemangiosarcoma accounted for 21/30 (70%) diagnoses.
§ HSA = 2/3 of all cases
80
In dogs when haemoabdomen present how common are malignant massess and of these percentage that is HSA, what is the most common splenic mass in cat
§ HAS when haemoabdomen present
□ 76% of dogs have malignant mass (so 24% benign where surgical is curative)
□ 92% of malignant neoplasia is HSA
- Cats–Splenic masses most likely neoplastic lymphosarcoma, MCT
81
How to diagnose splenic masses and what anatomy need to be careful of
Diagnosis - Splenectomy -> biopsy to confirm malignant or benign
Vascular anatomy
- The splenic artery gives off 3 to 5 long primary branches (including one as pancreatic artery) as it courses in the greater omentum toward the ventral third of the spleen
- Branch of splenic artery → short gastric arteries
- Venous drainage is via the splenic vein into the gastrosplenic vein, which empties into the portal vein.
THEREFORE - ligate splenic vessels NEAR the spleen -> otherwise increase risk of pancreatis ishcaemia
82
Haemagiosarcoma prognosis with surgery alone, surgery + chem
```
- Surgery alone
○ MST was 86 days, 50 days,
○ 1 year survival rate of 6.25%
- surgery + CHEMOTHERAPY
○ Mean ST 267 days - 50% survived to this point, median 172 days
- Surgery + metronomic
○ Median and mean ST = 178 days
```
83
Splenectomy what are the main indications, when is partial done and what need to be caeful of with assumtions
```
- Indications:
○ Neoplasia
○ Trauma
○ Torsion
○ Splenic abscess
○ Immune mediated disease
- Complete versus partial splenectomy
○ Complete done most commonly
○ Partial if blunt trauma or known benign disease
- Just because large mass DOESN'T MEAN MALIGNANT
```
84
Splenectomy what are the 3 main parts to it
1) Ligate vessels near hilus of spleen
§ Silk or monofilament of multifilament suture
§ Encircling and transfixing ligatures for main splenic artery
2) Biopsy other organs as indicated (especially liver, lymph nodes, omentum, peritoneum)
§ Lavage abdomen thoroughly
§ Ensure all bleeding controlled
§ Histopathology
□ Submit entire spleen
3) Once remove spleen do exploratory laparotomy -> ensure nothing else an issue
85
What are the 5 main complications of splenectomy
1) cardiac arrhythimias
2) continued bleeding
3) vascular compromise to pancreas - damage to pancreatic artery arising from splenic artery
4) acute portal vein thrombosis - can be life-threatening
5) DIC
86
Cardiac arrhythmias caused by splenectomy what results, what need and criteria for treating
§ Ventricular premature contractions (VPCs)
§ Ventricular tachycardia higher in dogs with ruptured splenic masses than without rupture
§ Need continuous ECG monitoring
□ Often resolve with fluids after surgery
§ Myocardial ischaemia, ↓ cardiac return, hypovolemic shock
§ Criteria for treating:
□ HR > 150 bpm
□ Multiform ventricular beats
□ Hypotension during ventricular arrhythmias
87
Cardiac arrhythmias caused by splenectomy treatment
□ Lidocaine bolus (2mg/kg IV bolus) then CRI (30-80 ug/kg/min)
□ Supplemental O2
□ Treat hypovolaemia
88
Splenic torsion how common, presentation and diagnosis
- Uncommon
- Presentation
○ Large to giant breed dogs affected
○ Abdominal pain –vague clinical signs
○ Massively enlarged spleen –congestion
§ Torsion on pedicle occludes venous drainage → engorgement → block arterial supply
- Diagnosis on U/S or radiographs
○ Characteristic C shape of the spleen
89
Splenic torsion treatment
○ Do NOT derotate spleen -> release toxins if detorse
§ Inflammatory mediators, thrombi
○ Manually ligate vessels instead of staples
○ Careful inspection of pancreas for compromise
○ Prophylactic gastropexy
90
What are some non-splenic causes of haemabdomen in liver, adrenal, kidney and surgical
- Liver
○ Traumatic laceration
○ Neoplastic (HCC)
- Adrenal masses
○ Adrenalectomy
○ Retroperitoneal haemorrhage - within the retroperitoneal space -> move viscera ventrally
- Kidney
○ Trauma to parenchyma or renal vessels
- Surgical
○ Dropped ovarian pedicle or testicular artery
○ Iatrogenic laceration of major blood vessel
91
Liver massess what is most common, forms, prognosis and treatment
- Hepatocellular carcinoma (HCC) most common
- Massive, nodular or diffuse forms - just because it is big doesn't mean it is bad
- Good prognosis with surgery (no chemo)
○ MST > 1460 d, mean: 409 d
- Non-surgery group
○ MST –270 d, mean: 162 d
- Liver lobectomy with stapling devices
92
What are the main functions of the liver
- Carbohydrate metabolism
- Lipid metabolism
- Protein metabolism - urea, albumin, globulin, coagulation proteins
- Vitamin (fat and water soluble) metabolism
- Endocrine hormone metabolism
- Storage functions
- Digestive functions - bile
- Detoxification and excretory functions
93
what are some potential manifestations of liver disease
- Abdominal effusion
- Abnormal liver/shape
- Jaundice/bilirubinuria -
- Acholic faeces - no bile produced into the GIT due to obstruction
- Hepatic encephalopathy
- Coagulopathy
- Diarrhoea
- Anorexia
- Vomiting
- Dermatosis
- Weight loss
- Sedative/anaesthetic tolerance
94
What clinical signs suggest jaudice possible hepatic issues and how to help determine whether pre-hepatic, hepatic or post-hepatic
- Clinical signs
○ Icteric membranes, sclera and mouth
○ Acholic faeces -> obstruction of bile duct
○ Salivation - hepatic encephalopathy especially in cats
- WHERE ON THE PATHWAY IS THE ISSUE? -> pre-hepatic, hepatic or post-hepatic
○ Is the animal happy
○ What other systems appear to be affected
○ Is there abdominal pain - more likely to be hepatic disease in this case
○ Are there sigs of neurological abnormalities
- Assess the size and contour of the liver
95
What are the main causes of a smal and smooth, small and bumpy and large and bumpy liver
1) Small and smooth
§ Congenital vascular diseases - portosystemic shunts - NOT JAUNDICED
□ Lacking the circulation of the growth factors - ALL GOES TO THE KIDNEY - that gets big
2) Small and bumpy
§ End stage liver disease - cirrhosis, fibrosis
3) Large and bumpy
§ Neoplasia - adenoma (primary), metastatic
§ Nodular hyperplasia - excessive steroids
§ Abscesses/cysts
96
What are the main causes of a large and smooth liver and most common in cats
○ Large and smooth
§ Infiltrative disease - lymphoma, amyloidosis
§ Lipidosis - cats most common
§ Acute hepatitis
§ Vacuolar hepatopathy - generally not jaundice
§ Hard working
97
If thinking liver disease what must rule out first and what must be done
- You must rule out extra-hepatic disease before treating primary liver disease - especially when abdominal effusion or elevations of liver enzymes on routine biochemical screening are the only abnormalities
- Always do a full physical examination and take a thorough history prior to embarking on investigations that may end up expansive and invasive
98
Biochemistry in the diagnosis of liver disease what are the 3 main things used
1) liver enzymes
2) additional asssessment of liver function - liver products
3) serum bile acids
99
In terms of liver enzymes for assessment of liver what are the important ones, when significant and what important to remember
§ ALT,AST indicate hepatocellular repair or injury
□ Increase ALT > Increase AST in liver disease
§ ALP/GGT cholestasis
□ Any increase in cat is clinical important
□ Induced by stress and drugs in dogs
□ Increased in young animals
§ Not always increased in liver failure (liver no longer producing) and OFTEN increased in other diseases
100
What additional assessment of liver function in biochemistry will result in indication of liver disease
§ Decrease albumin
□ Not until <20% functional capacity left
§ Decrease glucose
□ Congenital or end-stage disease (<20%)
§ Decrease urea
□ Formed by the lvier, may be falsely increased if GI bleeding
§ Increase OR decrease cholesterol
§ Decrease coagulation factors
Increase in pro-thrombin time -> Vitamin K factors
101
Serum bile acids what responsible for, what reflect, when wouldn't you run, how done and what also affected by
§ Responsible for fat absorption
§ Reflects enterohepatic circulation and hepatocellular function
§ Only do if indicated clinically and not if high bilirubin
§ Test post-prandial bile acid levels
§ Bile acid stimulation test also affected by:
□ Steroid hepatopathy and extra-hepatic disease
□ Failure of GB to contract
□ Intestinal integrity transit time
□ Breed
