Dogs and Cats 17 Flashcards
what are the 3 components of haemostatic system
1) Primary haemostasis
○ Formation of the temporary platelet plug
2) Secondary haemostasis
○ Fibrin formation through the coagulation cascade
3) Fibrinolysis
○ Fibrin breakdown
Primary haemostatic defects what is involved and causes
- 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
Secondary haemostatic defects what are 6 main diseases and the 2 most common
- 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)
What are the 5 tests for haemostasis
1) blood smear
2) buccal mucosal bleeding time
3) activated clotting time
4) prothrombin time (PT)
5) activated partial thromboplastin time (aPTT)
How does a blood smear help test for haemostasis, what is normal
○ 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)
How does a Buccal mucosal bleeding times (BMBT) help test for haemostasis. what is normal and what does prolonged indicate
○ 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
How does a activated clotting time (ACT) how assess haemostasis, what need to be careful of and how to do
○ 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
Prothrombin time (PT) and Activated partial thrombplastin time (aPTT) how assess haemostasis and what if prolonged
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
What are the 4 main steps in the diagnostic approach to bleeding patient
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
In terms of history for a bleeding patient what are important aspects
○ 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
What are some clinical signs of physical exam that suggest severe haemorrhage
○ 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)
If a patient comes in after chest trauma in circulatory shock and respiratory distress what are the 5 stabilisation emergency treatments
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
what are some emergency diagnostics to run on a traumatic bleeding dog
- 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
Resucitative fluid therapy what need to give, advantages and disadvantages
○ 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
What are some changes on blood smear that suggest regenerative anaemia
- 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
What are the main differences between haemorrhage and haemolysis
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
Clinical approach to anaemia what asking for with history
-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
What finding on physical examination can suggest anaemia
- 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
What are the 2 types of haemolytic anaemia and the 6 main causes
- 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
Immune mediated haemolytic anaemia what is it and what are the 3 main things it results in
- 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)
Immune mediated haemolytic anaemia what are the main causes
○ 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?
Immune mediated haemolytic anaemia typical signalment and what do the owners generally notice
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
Immune mediated haemolytic anaemia generally physical examination findings
§ 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
Immune mediated haemolytic anaemia blood smear and biochemistry results
§ 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
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
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
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
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
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
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
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
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!!!!
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
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
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
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
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
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
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
What are the 2 main infectious causes of heamolysis
1) mycoplasma haemofelis
2) babaesiosis
- babesia canis
- babesia gibsoni
