SA clinical pathology Flashcards
What liver features can be tested for by clinical pathology?
Hepatocellular injury -> leakage of enzymes
Cholestasis (reduced/blocked bile excretion) -> release of enzymes induced by retained bile
Hepatocellular function - decreased production or catabolism of substances
Hepatic portal circulation - decreased extraction of substances absorbed from GIT
Where are liver enzymes found normally?
ALP and GGT - on hepatocyte cell membranes
ALT, AST and SDH - in hepatocyte cytosol (and AST in mitochondria)
Which liver enzymes are there and what are they specific for?
ALT - largely liver specific (but also muscle), small animals
AST and LDH - liver and muscle
SDH and GLDH - liver specific in all species, used in large animals, SDH unstable
ALP and GGT - used in large animals as indicators of liver damage
What does it mean if there are increased liver ‘leakage’ enzymes in the blood?
Indicates hepatocellular damage
Myocyte damage can cause mild increase of AST, LDH +/- ALT (check CK)
Artefact (haemolysis) can increase AST and LDH (check serum/plasma quality)
Magnitude of increase correlates with degree of hepatocellular damage but not with reversibility of injury, prognosis or hepatic function
Short half lives: days in dogs, hours in cats (so even small increases may be significant in cats)
Which ‘cholestatic’ enzymes are there, used in small animals? What else can be used so assess if cholestasis?
ALP - good se for dogs but poor se for cats, scottish terriers have higher activities GGT - more specific Bilirubin Bile acids - more sensitive Cholesterol
What forms of ALP are there?
2 isoenzymes: intestinal and non tissue specific (I-ALP not generally detected in plasma as short half life so lost in GI tract)
Measurable isoforms:
- Liver-ALP (L-ALP) - serum half life of approx 70h in dog and 6h in cat (so insensitive in cats)
- Bone-ALP (B-ALP) - usually causes only mild increases, negative prognostic marker in osteosarcoma
- C-ALP - unique to dogs, induced by corticosteroids, product of I-ALP gene but produced in hepatocytes
What happens to senescent red cells to produce bilirubin (extravascular haemolysis)?
Breakdown of haem to bilirubin in macrophages of reticula-endothelial system (tissue macrophages, spleen, liver)
Unconjugated bilirubin is transported in blood via albumin to the liver
Taken up by facilitated diffusion by liver and conjugated with glucoronic acid
Conjugated bilirubin actively secreted into bile then into intestine
In intestine glucorionic acid is removed by bacteria and bilirubin is converted to urobilinogen
Some of urobilinogen is reabsorbed from gut and enters portal blood
Some of this participates in the enterohepatic urobilinogen cycel
Remainder of urobilinogen is transported in blood to kidney, converted to yellow urobilin and excreted
Types of hyperbilirubinaemia?
Prehepatic - secondary to haemolytic, check for anaemia
Hepatic - can be due to decreased bilirubin uptake, conjugation and excretion (so hepatocyte dysfunction and intrahepatic cholestasis)
Post-hepatic - secondary to obstruction of extra hepatic bile duct, serum cholesterol often high, ultrasound useful
How is bilirubin measured?
Total bilirubin Conjugated bilirubin (=direct bilirubin) Unconjugated = Til-DirBil (=indirect bilirubin)
Clinical signs of hyperbilirubinaemia?
Jaundice persists long after liver function turned to normal due to delta-bilirubin bound to albumin
If jaundice is due to delta-bilirubin there will be no bilirubinuria
Liver functions?
Detoxification
Synthesis of cholesterol, bile acids, plasma proteins, clotting factors
Breakdown of RBCs
Metabolism of carbohydrates, lipids and amino acids
Removal of bacteria
Storage of glycogen, iron, copper, vitamins
What markers are there of decreased hepatocellular function?
Decreased uptake and excretion of bilirubin and bile acids - increased (unconjugated) bilirubin and bile acids
Decreased conversion of ammonia to urea - increased ammonia, decreased urea
Decreased synthesis of metabolites - decreased albumin, cholesterol coagulation factors and inhibitors, glucose (but hypoalbuminaemia, hypoglycaemia, hypocholesterolaemia are insensitive markers for decreased liver function)
Decreased synthesis of coagulation proteins - decreased fibrinogen, increased PT and PTT
Decreased immunologic function - decreased clearance of toxins and antigens -> systemic stimulation -> increased Igs
What markers are there of alteration of hepatic blood flow (PSS)?
Decreased uptake and excretion of bile acids - increased bile acids (bilirubin not usually increased as major problem is the bile acids re-uptake from blood)
Decreased conversion of ammonia to urea - increased ammonia
Decreased immunologic function - decreased clearance of toxins and antigens -> systemic stimulation -> increased Igs
Where is ammonia produced and what happens to it?
Produced in GIT by protein digestion or bacteria metabolism
Enters liver via portal vein
Uptaken by hepatocytes to synthesise urea, amino acids, proteins
Urea diffuses to sinusoidal blood or bile canaliculi and is excreted through kidneys or intestine
Things to note when measuring blood ammonia?
Relatively insensitive
Only significant if raised (hepatic encephalopathy)
Not stable in vitro so should be measured immediately after blood sampled
Elevated in:
- congenital and acquired porto-systemic shunts and liver failure
Where are bile salts produced and what happens to them?
Produced by hepatocytes
Released into biliary system and then intestine - allow fat absorption and digestion
>90% then reabsorbed from ileum, enter portal vein, return to liver, re-circulate
Small amounts lost in faeces, replaced by liver
What can increased bile acids in the blood mean?
Reduced uptake/excretion by hepatocytes - reduced hepatocellular mass, impaired hepatocyte function
Disruption of enterohepatic circulation - portosystemic shunts, cholestasis/bile obstruction
No point measuring BA if bilirubin already increased (BA more sensitive)
Interpretation of fasting SBA?
> 25-30mmol/L are abnormal and indicate hepatobiliary pathology - can’t differentiate between cholestasis and liver failure
<25-30mmol/L cannot completely exclude portosystemic shunt, perform bile acid stimulation test (BAST) if still suspecting hepatic pathology
Interpretation of post prandial SBA? How to do it?
BA stimulation test/dynamic BA Take resting sample Fatty meal Post-prandial sample 2h after feeding >25-30mmol/L is abnormal and indicates hepatobiliary pathology - can't differentiate between cholestasis and liver failure
What extra hepatic diseases can cause elevation in liver enzymes?
Hypoxia GI and pancreatic disease Endocrine diseases (fat or glycogen accumulation) Sepsis = 'reactive hepatopathies'
How to determine if raised liver enzymes is due to ‘reactive hepatopathy’ due to extra hepatic disease?
Most have normal bile acids
Other markers of liver function will be normal - unless affected by primary disease
Bile acids may be markedly elevated in sepsis/SIRS/endotoxaemic shock
What haematology may be seen in liver disease?
Microcytosis - portosystemic shunts or severe liver insufficiency, likely due to altered iron transport or metabolism
Ovalocytes (elliptocytes) are frequently seen in cats with hepatic lipidosis
Acanthocytes - lipid disorders, disruption of normal vasculature (e.g. hepatic haemangiosarcoma)
Urinalysis in liver disease?
Often unremarkable but may see:
- isosthenuria or inappropriately low USG
- bilirubinuria (more than 2+ in dogs, any in cats)
- ammonium bitrate crystals or uroliths (40-70% of patients with portosystemic shunts)
Functions of the pancreas?
Exocrine acinar cells (98%) - secrete enzymes involves in initial digestion of food
- proteases (trypsin, chymotrypsin, elastase)
- lipases
- amylases
- high conc of bicarbonate in secretions
- aids B12 and zinc absorption
- antibacterial activity
- intestinal mucosal modulation
- proteases stored as inactive zymogens
Endocrine islet cells (2%) - secrete insulin and glucagon
Tests for exocrine pancreas integrity?
Amylase and lipase tests - identify injury to pancreatic cells (increases most often due to pancreatitis), pancreatitis should be based on a combo of these tests with compatible clinical and imaging signs (abdominal ultrasound)
DGGR - proven to correlate well with more specific tests and clinical pancreatitis, cut offs for pancreatitis diagnosis:
- >34 U/L in cats
- >216 U/L in dogs
Canine pancreatic lipase (cPL) - considered more specific and more sensitive than lipase and amylase, snap test available
TLI (trypsin like immunoreactivity) - used in dogs, cats, horses (species specific assays), detects trypsinogen, trypsin and trypsin bound to protease inhibitors, use in animals with clinical signs of maldigestion/malabsorption, high se and sp for exocrine pancreatic insufficiency, less useful fro pancreatitis, serum TLI < 2.5mg/L in dogs, < 8mg/L in cats
Amylase - function, half life, species used in?
Catalyses hydrolysis of complex starches Short half-life (hours) Salivary and intestinal not found in serum More useful in dogs than other species Can increase due to decreased GFR
Lipase - function, half life etc?
Catalyses hydrolysis of triglycerides
Very short half-life (2 hours)
Mostly from pancreas
Can increase (mildly) due to decreased GFR
Different tests have different positive and negative predictive value
Diagnosis of pancreatitis?
Elevation in lipase (and amylase) - suggestive but other causes possible, higher increase=higher likelihood, degree of increase doesn’t = severity of disease
Need compatible clinical signs
Additional tests - PLI (specific pancreatic lipase), ultrasound, fluid analysis, biopsy
Suggested criteria for diagnosis of acute pancreatitis in dogs?
Absence of surgical disease on abdominal radiographs or analysis of abdominal fluid
And abdominal ultrasound with evidence of primary pancretitis
And one or more of the following:
- Spec-cPL >400ug/L
- Positive SNAP-cPL
- Gross lipaemia
- Serum PE-1 >17.24 ng/ml
- Total lipase >3x the upper reference interval
Indications for cytology?
Lesion (nodule, mass, plaque) palpable externally or seen on imaging Organomegaly Cavitary effusion Cancer staging PUO
Problems reducing cytology sample quality?
Ruptured cells - incorrect sampling or smearing technique
Inadequate staining
Identifying cell types on cytology?
Inflammatory cells - neutrophilic, eosinophilic, lymphocytic, histiocytic, mixed
Tissue cells - expected from organ aspirated, abnormal cells
Normal cytology of skin and subutaneous tissue?
Few keratinocytes
Scant fat
Rare sebocytes
How to assess neoplastic cells and malignancy from cytology?
Cell arrangement
- discrete or cohesive
- any cytoarchitecture
Cell shape
- round, polygonal, spindle
Criteria of malignancy
- hypercellularity (in mesenchymal tumours)
- pleomorphism (anisocytosis, anisokaryosis)
- high/variable N:C ratio
- multinucleation
- karyomegaly
- mitoses (especially if atypical)
- nuclear moulding (rapid cell growth)
- large, angular, or variably sized nucleoli
Minimum of 3 criteria to be classified as malignant (nuclear are stronger) - adapt depending on specific organ/cell type, allow some with inflammation and in histiocytes
If absent criteria of malignancy -> benign or well differentiated malignant
How do round cell tumours, epithelial tumours and mesenchymal tumours typically present on cytology?
Round cell tumour - ‘sea’ of round, discrete cells
Epithelial tumour - ‘islands’ of cohesive polygonal cells
Mesenchymal tumour - spindle cells with indistinct edges embedded in extracellular ‘matrix’
What round cell tumours are there?
Histiocytoma Plasma cell tumour Mast cell tumour Lymphoma Transmissible venereal tumour (not in UK)
Histiocytoma - Typical presentation? Cytology?
Dome shaped, alopecia, may be ulcerated
Tend to regress in a few weeks
Often (but not only) in young dogs
Cytology - light blue cytoplasm fading into the background, small lymphocytes often present and may predominate at later stages, sometimes difficult to differentiate from plasma cell tumour and lymphoma
Histiocytic sarcoma - cytology?
Arises from interstitial dendritic cells
Usually marked cell pleomorphism with karyomegaluy and multinucleation
Localised or disseminated
Lymphoma - cytology?
Round cells with high nucleus to cytoplasm ratio
Large blasts (larger than a neutrophil)
Monomorphic population
Mast cell tumour - cytology?
Magenta granules in the cytoplasm - sometimes don’t stain well with Diff Quik (send some unstained slides to lab)
Poor granulation can be due to poor differentiation (usually means a more aggressive tumour)
Plasmacytoma - cytology?
Cutaneous plasmacytomas are usually benign
Can be well differentiated to pleomorphic (most commonly)
Deep blue cytoplasm, perinuclear halo, eusinophilic borders
Round, eccentric nucleus
Types of keratinising lesions?
Epidermal/follicular cysts - cysts lined by normal keratinised epithelium, keratin accumulates in centre
Hair follicle tumours - many types, mostly benign, often cytologically identical to cysts, sometimes basaxoid cells
Trichoblastoma - what is it? cytology?
Benign skin tumour
Scant amount of cytoplasm
Uniform nuclei
Sebaceous adenoma - cytology?
Raised cauliflower alopecic lesions
Clusters of cohesive heavily vacuolated cells
Cannot differentiate from hyperplasia on cytology
Hepatoid gland tumour - where? cytology?
Usually benign
Perianal or along thighs
Cutaneous
Clusters of ‘hepatic’ cells - similar to hepatocytes (large polygonal shaped cells, abundant pink-blue granular cytoplasm, prominent single nucleolus)
Surrounded by few ‘reserve’ cells - smaller and higher N:C ratio and oval nuclei
Squamous cell carcinoma - cytology?
Polygonal cells with variable tendency to cohesion
Typically marked pleomorphism
Often secondary neutrophilic inflammation
Anal sac adenocarcinoma - cytology?
Classically ‘naked nuclei’ appearance
Often cells form rosettes and ‘rows’
Sheets of bland looking cells but high metastatic potential!
Most common soft tissue sarcomas in dogs and cats?
Dogs: - perivascular and nerve sheath tumour - fibrosarcoma Cats: - fibrosarcoma/injection site sarcoma
What tumours are ‘confusing’ as not easily classified as round, epithelial or spindle?
Endocrine and neuroendocrine tumours
Histiocytic sarcoma, chondrosarcoma, osteosarcoma - may be round or spindle
Melanoma:
- well differentiated melanocytes are stellate
- undifferentiated melanocytes may be fixate, round, cuboidal with some tendency to cohesion
Are melanomas usually benign or malignant?
Usually benign and well differentiated in haired skin
Often malignant in nail beds, oral cavity
Lipoma - cytology?
Can’t differentiate from ‘normal’ subcutaneous adipose tissue
Where are erythropoietin and renin synthesised and where is vitamin A activated?
Erythropoietin: peritubular interstitial cells
Renin: juxtaglomerular cells
Vitamin D activation: proximal tubular cells
What electrolytes/substances and conserved and excreted by a healthy kidney?
Conserve:
- water
- amino acids/proteins
- glucose
- bicarbonate
- Na+ and Cl
- Mg2+ and Ca2+
Excrete:
- urea
- creatinine
- K+
- H+
- PO4
- ketones and lactate
- bilirubin
- haemoglobin and myoglobin
What is not filtered by glomerlar filtration and what is it restricted by?
Cells, proteins larger than albumin and most lipoproteins
Restricted by:
- size
- charge - albumin is size of pores but negatively charged
Which tests of renal function are there? What are they all useful to assess?
Biochemistry: nitrogenous waste excretion (urea and creatinine), degradation of lipase and amylase, electrolyte balance
Urinalysis
Haematology: erythropoietin secretion
Blood gas analysis: acid base balance (pH, BE, HCO3)
How can GFR be measured?
Directly with plasma clearance of creatinine or iohexol - impractical
Indirectly - urea and creatinine
SDMA
How much urea and creatinine is normally reabsorbed in the kidney?
Urea: up to 40%
Creatinine: not reabsorbed, a bit secreted
Causes for increased blood urea?
Decreased GFR
Mild increases:
- upper GI haemorrhage: protein catabolism, hypovolaemia/dehydration
- high protein diet
- recent meal
- catabolism (fever, starvation, corticosteroids)
Causes for decreased blood urea?
Severe liver disease or portosystemic shunt Low protein diet Aggressive fluid therapy PUPD - cause and effect Young animals Deficiency of enzymes in urea cycle
Causes of increased and decreased blood creatinine?
Increase: - decreased GFR - high muscle mass (mild increase) - high dietary protein - non creatinine chromagens Decrease: - reduced muscle mass - usually not clinically significant
Define azotaemia and uraemia?
Azotaemia = increased creatinine and/or urea Uraemia = complex of clinical signs seen in patients with renal disease: V+, D+, anorexia, weight loss, anaemia, ulcerative stomatitis, muscle tremors, convulsions, coma
All uraemic patients are azotaemic but not vice versa
Causes of pre-renal azotaemia? Clinical signs/pathology/how can you tell it is prerenal?
Dehydration or decreased CO (due to decreased blood flow to kidneys):
- clinical evidence of dehydration and/or hypovolaemia
- maximally concentrated USG (>1.030 in dogs, >1.035 in cats)
- urea often increased more than creatinine
- should respond to fluid therapy
Increased ammonia load (high protein diet, or GI haemorrhage)
- increased urea but not creatinine
- maximally concentrated USG
- signs of iron deficiency possible
Causes of renal azotaemia? Clinical signs/pathology/how can you tell it is prerenal?
Cause: decreased functional nephrons
Variable USG:
- isosthenuria (1.008-1.012) when >66% of nephrons lost
- suboptimal USG (>1.012 but <1.030 in dogs and <1.035 in cats)
- falls progressively
- cats can lose concentrating ability later than dogs
Causes of post renal azotaemia? Clinical signs/pathology/how can you tell it is prerenal?
Urinary tract rupture or blockage -> failure of urine output
Hyperkalaemia
If ruptured bladder:
- creatinine in abdominal fluid > blood
How good are urea and creatinine as markers of renal function?
Insensitive - only azotaemia when >75% of functional nephrons lost
What is SDMA produced from? Is it filtered by the kidneys? Benefits for kidney disease? When to measure? RI?
Produced from intranuclear demethylation of L-arginine
Freely filtered by glomerulus
More se and sp than creatinine:
- not influenced by muscle mass
- increases with 40% reduction of GFR
Measure when creatinine is normal or borderline to identify animals in IRIS stage 1/2 with absent or milf clinical signs
RI <14ug/L (+1 in puppies, kittens, greyhounds)
What electrolyte changes are seen with kidney disease?
Hyperphosphataemia:
- small animals have a high phosphate intake
- exception is horses as low diet P so tend to be hypo
Hyper or hypokalaemia:
- increased with acidosis, decreased urine output, marked decreased nephrons, anuria/oligura (AKI), bladder rupture, obstruction
- decreased with increased urinary losses (esp CKD), decreased intracellular stores, GI losses
Hypochloraemia:
- increased renal loss (follows Na)
- GI loss with vomiting
Hyper or hypocalcaemia
- hyper in horses
- hyper in low % of smallies (usually only tCa)
- most commonly hypo in smallies as decreased vit D and alimentation and tissue deposition
What does it mean if the USG is hyposthenuric?
Requires functioning nephrons
Diluted by kidneys
Typically ADH problem
When is a suboptimal USG significant? Cause?
If low USG + dehydration/azotaemia First look for non kidney causes: - lack of aldosterone or ADH - diuretics, glucocorticoids, glycosuria, medullary washout, pyelonephritis - low urea, Na or K, or high Ca If not, renal disease likely
Proteinuria: When is it significant? Causes?
Small amounts up to +1 may be normal More significant if low USG Causes: - glomerular damage (renal) - protein overload to glomerulus (pre-renal) or urinary tract inflammation (post-renal)
Urine protein:creatinine ratio: Why is this useful? Reference range for dogs and cats? What does it suggest?
Measure of proteinuria independent of urine concentration
>0.5 (dogs) >0.4 (cats) = proteinuric
0-2-0.5 - borderline
Elevated ratio in absence of an active sediment or hyperproteinaemia is a strong indicator of renal (often glomerular) disease
Glycosuria: When seen? Significance?
Seen with serum glucose >10mmol/L in dogs and >16.6mmol/L in cats
If serum glucose normal = renal glycosuria (failure of tubular reabsorption)
What is the normal urine pH for dogs and cats? What does it mean if different?
Usually 5.5-7
Low with metabolic acidosis
Can be inappropriately high with metabolic acidosis due to tubular dysfunction
Alkaline due to UTI with urease producing bacteria
What are casts un urine? Significance?
Cylindrical moulds of tubules composed of mucoproteins +/- cells
Occasionally hyaline and granular casts may be normal
Granular, cellular and waxy indicate tubular damage
Crystals in urine: How significant?
Fresh urine: likely developed in vivo
Stored urine: can precipitate post collection
Lots of normal animals have crystalluria
What types of crystals are there in urine? Significance? When formed?
Struvite:
- magnesium ammonium phosphate
- UTI, urolithiasis or normal
- form in alkaline urine and in vitro
Amorphous:
- urate in acidic pH: no clinical significance
- phosphate in alkaline pH, no clinical significance
Calcium oxalate di-hydrate:
- can be normal
- can form in vitro
- can be seen with ethylene glycol toxicity but not pathognomic
Calcium oxalate monohydrate:
- hyperoxaluric disorders or hypercalciuria (e.g. ethylene glycol toxicity or ingestion of oxalate rich foods like peanut butter)
Ammonium bitrate or uric acid:
- portosystemic shunts, liver disease, dalmatians
Cystine:
- associated with metabolic defect in tubular resorption of cystine (bulldogs)
Normal distribution of electrolytes?
ECF: Na, Cl, HCO3
ICF: K, P, proteins
Role of sodium? Causes of change? Controlled by?
Major cation in ECF responsible for preservation of electroneutrality - each Na ion balanced by an anion (2/3 Cl, bicarbonate) Maintains water in the body Usually narrow range Altered due to: - loss of Na and water (volume depletion) - loss of water alone (dehydration) Regulation of volaemia via RAAS Regulation of osmolarity via ADH
RAAS system?
Low BP, low perfusion pressure, renal ischaemia, low Na in DCT, sympathetic stimulation -> renin synthesis
Renin enzyme for angiotensinogen -> ANGI
ANG 1 -> ANG 2
-> Vasoconstriction -> increased BP
-> Aldosterone -> Na and water retention, K loss -> increased BP
ADH activation and action?
Increased blood osmotic pressure -> detected by osmoreceptors in hypothalamus -> ADH and thirst -> increases permeability of collecting duct -> water reabsorbed to prevent further dehydration
Thirst -> drinking reduces blood osmotic pressure
Causes of hyponatraemia?
Loss: - V+, sometimes D+ - kidneys (tubulopathy) - hypoadrenocorticism (no aldosterone) - loss into an effusion - iatrogenic (thiazides, furosemide) Volume overload: - CHF - (end stage renal failure) - iatrogenic Increased plasma osmolarity: - severe hyperglycaemia - mannitol
Reference for hypernatraemia in dogs and cats? Treatment?
> 160mmol/L in dogs
165mmol/L in cats
> 170mmol/L is life threatening
If chronic must correct slowly (too quick can cause CNS oedema)
low sodium fluid - 5% glucose, 0.45% NaCl
Furosemide as last resort?
Causes of hypernatraemia?
Most commonly due to loss of fluid with concurrent decreased intake or deficient ADH responses
Hypotonic fluid loss (most common): - GI losses - renal failure - post-obstructive diuresis - any cause of polyuria (DM, Cushing's) Free water loss: - heat stroke - pyrexia - diabetes insipidus deprived water - inadequate/inability to access water - adipsia (mini Schnauzers and cats) Excessive intake (uncommon): - incorrectly mixed milk/electrolyte solutions without water access Excessive reabsorption: - hyperaldosteronism Iatrogenic: - fludrocortisone - sodium phosphate enemas
What controls the K concentration in plasma? What happens to it?
K plasma concentration controlled by insulin, aldosterone and SNS
Freely filtered at renal glomerulus and then reabsorbed
K higher in serum than plasma
Reference for hyperkalaemia? Clinical signs?
K > 5.5mmol/L Muscle weakness Cardiac abnormalities (normally if >7.5) Bradycardia Bradyarrhythmias - atrial standstill, life threatening conduction abnormalities
Causes of artefactual hyperkalaemia?
Relatively common
Postal/aged samples:
- cell lysis
- esp if leucocytosis and/or thrombocytosis
K+ EDTA contamination: hyperkalaemia, hypocalcaemia, low ALP
Causes of true hyperkalaemia?
Decreased urinary excretion: - urethral obstruction - bladder/UT rupture - anuric/oliguric renal failure - hypoadrenocorticism (lack of aldosterone) Drugs: - beta blockers, ACE-I, and K sparing diuretics in combo with K supplementation Translocation ICF -> ECF: - insulin deficiency in ketoacidotic DM - tumour lysis syndrome - extensive crush/reperfusion injuries - necrosis-large thrombi Increased intake: - iatrogenic - excessive supplementation
Treatment for hyperkalaemia?
IVFT with K free or K depleted fluids Saline +/- 5% glucose Insulin and glucose? Calcium gluconate: - if cardiac effects - monitor on ECG Treat primary disease - correct acidosis
Reference for hypokalaemia? Clinical signs?
K < 3mmol/l Clinical signs: - muscle weakness - PU/PD, impaired urine concentration - anorexia - ileus - constipation Anorexia will always lead to hypokalaemia as there is always some loss of K
Causes of hypokalaemia?
Decreased intake: - anorexia - fluid therapy with K depleted fluids Translocation ECF -> ICF: - insulin - glucose containing fluids - catecholamines Increased loss: - gastrointestinal (vomiting, diarrhoea) Urinary - CRF in cats - diet-induced hypokalaemic nephropathy (low K, urinary acidifying diets) Post obstructive diuresis (esp cats) Mineralocorticoid excess: - HAC (more common if adrenal dependent) - primary hyperaldosteronism Drug therapy: - loop and thiazide diuretics - penicillins (unadsorbable anions increase lumen electronegativity)
Feline hypokalaemia myopathy: What is it?
Sudden onset myopathy
Often associated with elevated creatinine
Inherited form in Burmese cats
What is phosphate regulated by?
PTH promotes phosphate release from bone and excretion by kidneys
Causes of hyperphosphataemia?
Failure to excrete: - decreased GFR (pre-renal) - renal failure (esp chronic) - UT obstruction/rupture Increased release from bone: - young animals - (osteolysis) - feline hyperthyroidism Increased intake/absorption - high phosphate diet - hypervitaminosis D - mild post-prandial Increased renal reabsorption - primary HYPOparathyroidism (PTH has a phosphaturic effect) Spurious: - haemolysis: Tends to be mild - monoclonal gammopathy Tumor lysis syndrome, soft tissue trauma
Causes of hypophosphataemia?
Anorexia (cat) Shift from ECF to ICF: - insulin administration Decreased renal reabsorption GI loss (vomiting/diarrhea) Primary HYPERparathyroidism (PTH is phosphaturic) Reciprocally in hypercalcaemia of malignancy Hepatic lipidosis in cats Cushing’s in dogs
Forms of calcium in the body?
Total calcium:
- free calcium is biologically active (50% of total): regulated by PTH, vitamin D (calcitriol) and calcitonin
- protein bound (most bound to albumin, 40%)
- bound in other complexes (phosphate, bicarb)
Free calcium is unstable so must be measured ASAP
How to calculate corrected Ca for dogs? Problem?
Measured Ca - alb + 3.5
Need to convert units and not reliable in patients with kidney disease
Clinical signs of hypercalcaemia?
PUPD
Causes of hypercalcaemia?
Malignancy: - LYMPHOPROLIFERATIVE DISEASES - anal sac adenocarcinoma Renal failure Primary hyperparathyroidism Hypoadrenocorticism Bone lesions Young, growing animals Vitamin D toxicity Cholecalciferol rodenticide toxicity Artefact: lipaemia, hypovolaemia, haemolysis
Ddx acronym for hypercalcaemia?
H = Hyperparathyroidism, houseplants, hyperthyroidism (cats), HHM A = Addison’s, Vit A R = Renal disease, raisins (dogs) D = Vitamin D toxicosis, granulomatous dz I = Idiopathic (cats), infections, inflammatory O = Osteolytic N = Neoplasia, nutritional S = Spurius, Schistomosiasis
Clinical signs of hypocalcaemia?
Muscle tremors, twitches, cramps Seizures Facial pruritus in cats Lethargy, anorexia Restlessness, behavioural changes
Should you always supplement for hypocalacemia?
Not if due to hypoalbuminaemia (low total but normal ionised Ca)
Causes of hypocalcaemia?
Hypoalbuminaemia (but free Ca is WRI) Ethylene glycol toxicity (precipitates in tubules) Intestinal malabsorption (dog) Acute pancreatitis (dog) Eclampsia/puerperal tetany Idiopathic hypoparathyroidism Renal disease EDTA or citrate tube Iatrogenic hypoparathyroidism: - drugs (anticonvulsants, glucocorticoids, phosphate enemas) - nutritional - post thyroidectomy in cats
Anaemia severity?
Mild (30-36% in dogs, 20-24% in cats)
Moderate (18-29% in dogs, 15-19% in cats)
Severe (<18% in dogs, <14% in cats)
Stages of feline reticulocytes? How long do they last?
Aggregate reticulocytes: last 24h
-»
Punctate: last up to 10 days
Iron deficient anaemia - when seen? Regenerative or non regenerative? Most common cause? Treatment?
Chronic blood loss
Takes >1 month of continued bleeding for iron deficiency anaemia to develop
May be regenerative or non regenerative (will become non regenerative as iron depletes)
Microcytosis and hypochromic
Most common cause is GI haemorrhage
Treatment:
- blood/packed red cell transfusion if unstable, hypoxic, pre-op
- oral ferrous sulphate (best): 5mg/kg, or 50mg/cat sid divided up
- or IM iron dextran, only if vomiting etc (may cause anaphylactic shock)
Causes of chronic gastrointestinal haemorrhage?
NSAIDs Corticosteroids CKD Idiopathic GI ulceraton Neoplasia IBD Parasitism
Treatment of gastrointestinal haemorrhage?
Sucralfate
Cimetidine/ranitidine (H2 receptor antagonist)
Omeprazol
Misoprostol
What happens to blood cells with intravascular haemolysis?
Free Hb in blood
- > Binds to haptoglobin and is metabolised to bilirubin by liver
- > if haptoglobin saturated, Hb dissociates in dimers which passes freely through glomeruli -> haemoglobinuria
What causes cell ghosts on a blood smear?
Direct membrane damage by complement
Which Ig causes autoagglutination of blood?
IgM
What is cold agglutinin disease?
IgM antibodies
Agglutination -> capillary blockage, ischaemia, necrosis of extremities
Rare
What is the saline agglutination test?
1 drop blood and 9 drops saline
Rouleux will disappear
Agglutination will persist
When is the coombs test not useful for IMHA?
If agglutination already evident
Treatment for IMHA?
Immunosuppression -
Pred - 1-2mg/kg (reduce by 25% q3 weeks once remission)
Dex - emergency/anorexic, 0.3-0.6mg/kg IV/IM/SC/PO, may respond to this if didn’t to pred
Azathioprine - cytotoxic of choice for dogs only (use in combo with pred), monitor for myelosuppression side effect
Ciclosporin - to stabilise difficult cases
mycophenolate mofetil if others failed
Aspirin and clopidogrel
(Low MW heparin)
Transfusion if needed - increases risk of PTE, can’t cross match, shortened lifespan of RBCs, use packed RBCs
Fluids
Some dogs may be able to stop after months, some on for life
Side effects of azathioprine and ciclosporin?
Azathioprine: - GI - myelosuppression - pancreatitis Ciclosporin: - GI - gingival hyperplasia, hypertrichosis
Which puppies are affected by neonatal isoerythrolysis?
Very rate
DEA1.1 positive puppies with sensitised DEA1.1 negative bitch’s milk
Which kittens are affected by neonatal isoerythrolysis?
Rare Type A or AB kitten born to type B queen - British shorthair No previous transfusion required Avoid mating B queens with A or AB toms Foster kittens for first 24h
Transmission of Mycoplasma haemofelis? How to confirm diagnosis? Treatment?
Presumed fleas
PCR (smear is insensitive)
Once infected, always infected
Doxyxycline (5m/kg BID) for 21 days (remain carriers)
Prednisolone (1-2mg/kg BID) if immune mediated component
When does Mycoplasma haemocanis usually cause anaemia?
Splenectomised dogs
Causes of acanthocytes? What do they look like?
Multiple rounded projections of variable length, unevenly spaced
Liver disease, esp hepatic lipidosis Splenic HSA Lymphoma Glomerulonephritis Cholesterol metabolism abnormalities/ high cholesterol diets Occasionally in PSS
What are signs of oxidative damage to RBCs?
Methaemoglobinaemia
Heinz bodies
Eccentrocytes
What are heinz bodies?
Round, pale inclusions on inner surface or RBC membrane Aggregates of denatured Hb Highlighted by new methylene blue Oxidative damage <10% is normal in cats
Treatment for methaemoglobinaemia?
Methylene blue 1mg/kg once IV
Causes on non regenerative anaemia?
Primary or secondary marrow disease - need marrow sample to confirm
Lack of EPO due to kidney disease
Which drugs can cause bone marrow idiosyncratic drug reactions?
Oestrogen (dogs) antibiotics NSAIDs Anticonvulsants (phenobarbital) antivirals (cats) antifungals (griseofulvin in cats) methimazole (antithyroid drug used in cats)
Oestrogen toxicity: Cause? Effect on blood? Treatment?
Exogenous oestrogen Endogenous oestrogen - sertoli cell tumours Causes pancytopenia: - thrombocytopenia - neutrophilia then neutropenia - anaemia Treatment: - bactericidal Abs - blood/platelet rich tranfusions - remove any neoplasm - steroids? - most die!
Pure red cell aplasia: What is it? Cause? Treatment?
Only red cell line affected No erythroid precursors in the BM Myriad of causes (likely immune-mediated) Treatment: - remove any suspected initiating cause - cross matched transfusions - immunosuppressive therapy
What is aplastic anaemia? Treatment?
Misnomer: all cell lines affected - pancytopenia, not just anaemia! Treatment: - bactericidal Abs - blood/platelet rich tranfusions - remove any neoplasm - steroids? - most die!
What is myelofibrosis? Cause? Treatment?
Proliferation of collagen and reticulin fibres in bone marrow May be secondary to: - chronic damage of marrow stroma - retroviral infection - idiopathic Treatment: - crossmatched transfusions - immunosuppression - ?anabolic steroids
Anaemia of chronic disease: type of anaemia? Treatment?
Very common
Normocytic, normochromic non-regenerative anaemia
Mild to rarely moderate
>30% in the dog
>25% in the cat
Does not require specific therapy (it should resolve once underlying disease cured)
E.g. anaemia of CKD - reduced EPO, reduced abcs, also haemorrhage due to thrombocytopathies or GI ulceration
Treatment for anaemia of CKD?
Recombinant human EPO (darbepoitein) - risk of Ab response
Minimose blood loss - gut protectants, H2 blockers
Anabolic steroids? - little evidence
FeLV anaemia: type of anaemia? Why?
Usually non regenerative Occasionally macrocytic Multiple mechanisms: - red cell aplasia - aplastic anaemia - anaemia of chronic disease - myelodysplasia or myeloproliferative disease - acute leukaemia - IMHA (non region with FeLV)
FIV anaemia: type of anaemia?
Non regenerative
Due to erythroid dysplasia and maturation arrest
Usually granulocyte series more affected
Causes of relative polycytaemia/erythrocytosis?
Dehydration
Acute GI disease - e.g. haemorrhagic gastroenteritis
Severe hyperthermia -e.g. heat stroke
Splenic contraction - exercise, adrenaline release
Causes of absolute polycytaemia/erythrocytosis?
Primary - not due to increased EPO (e.g. myeloproliferative disorder, polyctyaemia vera)
Secondary - due to increased EPO:
- Appropriate due to generalised hypoxia (e.g. heart disease, lung disease, high altitude, chronic carbon monoxide exposure)
- Inappropriate without generalised hypoxia (e.g. tumours causing localised renal hypoxia, or more rarely a tumour producing EPO)
Treatment for absolute polycytaemia/erythrocytosis?
Remove the underlying cause if possible and stabilise with phlebotomy
10-20 mL/kg until resolution of clinical signs and PCV < 55% in dogs, <50% in cats (60-70% can be acceptable if due to chronic hypoxia)
Care maintaining volaemia
Can be repeated every 4-8 weeks
Chemotherapy (hydroxyurea) in case phlebotomy not effective
What blood tubes to use for full blood count, coagulation profile and biochemistry?
Full blood count: EDTA
Coagulation profile: citrate
Biochemistry: heparinised plasma or serum
Clinical signs of primary haemostasis?
Ooze from small wounds Petechial and ecchymotic haemorrhages Bleeding from mucous membranes - Epistaxis - Melaena
Differentials for thrombocytopenia?
Immune-mediated (primary or secondary)
Neoplasia
DIC (consumption)
Infectious diseases (destruction, consumption)
Breed related
- CKCS, Greyhounds, Shiba Inus may have ‘physiologically’ lower PLT concentration
Immune mediated thrombocytopenia (IMTP): Causes?
Most common causes of significant thrombocytopenia in dogs Usually marked (<20 x 109/L) Primary - more often females, Cocker Spaniels, Springers Secondary - Idiosyncratic drug reaction - Trimethoprim/sulpha, cephalosporins - Neoplasia - Viral disease (esp FeLV) - Ehrlichia - Vaccination (live virus)
When is there a risk of spontaneous haemorrhage in dogs and cats due to thrombocytopenia?
Dogs: Platelets < 50x109/l
Cats: Platelets < 30x109/l
Treatment of immune mediated thrombocytopenia IMTP?
Treat any underlying disease
Corticosteroids
Azathioprine
May need lifelong therapy (3-6 months initially)
When to suspect platelet dysfunction (thrombopathy)? Causes?
Normal platelet count and coagulation profile, but bleeding excessively causes: - azotaemia - von willebrand disease - hyperproteinaemia - BM disease - hepatic disease - NSAIDs, aspirin etc
How to test platelet function?
Buccal mucosal bleeding time
Clot retraction
What is Von Willebrand disease?
Deficiency of von willebrand factor
Inherited (dobermans pinscher) or acquired (severe aortic stenosis)
vWF is synthesised and stored by endothelial cells - vital for platelet adherence, binds to factor VIII and prolongs its half life
Type 1:
- most common
- autosomal
- partial quantitative
- bleeding from mucous membranes and bruising
- excessive haemorrhage during surgery
- all vWF multimers <50%
Type 2 and 3:
- type 2 is qualitative
- type 3 is severe quantitative, more severe
- both autosomal recessive
How to test for von willebrand disease?
BMBT increased - controversial, only if vWF <20%
Antigenic test
- separate titrate plasma asap and freeze
- level of vWf doesn’t correlate well with clinical disease
vWF function assays - for type 2
Genetic testing of breeds - Dobermann, poodle, manchester terrier, pembroke welsh corgi
Treatment for von willebrand disease?
Cryoprecipitate - Rich in factor VIII, fibrinogen and high MW multimers of vW factor Whole blood or plasma therapy DDAVP - 1-desamino-8-D-arginine vasopressin - Increases vWF release from endothelial cells - Type 1 Only - Can be given to donor
What are the results of clotting testing for the intrinsic and extrinsic pathways if disorder? Common?
Intrinsic - XII, XI, IX, VIII - normal platelet count - prolonged PTT - normal PT - normal FDPs Extrinsic - VII - normal platelet count - normal PTT - prolonged PT - normal FDPs Common pathway (or extrinsic and extrinsic) - X, V, II - normal platelets - prolonged PTT - prolonged PT - normal FDPs
Types of intrinsic pathway defects of clotting? Breeds?
Acquired - Hepatic disease - Heparin (remember ATIII): Sample contamination/therapy Hereditary - Hemophilia A (VIII), hemophilia B (IX) -- A more common than B -- Males: X-linked, GSDs, females are carriers -- Cavitary bleeding: hemarthroses/post-sx - Factor XI deficiency -- UNCOMMON -- Delayed hemorrhage post trauma/sx -- Kerry Blue Terriers - Factor XII deficiency -- No clinical signs -- Cats
Which clotting factors need vitamin K?
II, VII, IX, X
Usually both pathways affected
Types of intrinsic pathway defects of clotting? Breeds?
Acquired: - Vitamin K antagonism/deficiency - hepatic/hepatobiliary disease - usually both pathways affected Hereditary: - VII deficiency: less common, mild haemorrhage often associated with surgery, beagles
What causes intrinsic and extrinsic defects?
Acquired (common): - hepatic disease - vitamin K - DIC Hereditary: - X, II deficiencies: rare, severe hamorrhagic tendencies
Why does liver disease cause vitamin K malabsorption?
Vit K is absorbed with fat
Reduced excretion of bile can impair lipid digestion and vit K absorption
Anticoagulant rodenticides: What happens?
Coumarin and indandione derivatives
Vitamin K antagonists
Competitively inhibit vit K epoxide reductase
Vitamin K dependent factors remain inactivated as they cannot bind calcium
Diagnosis of vitamin K antagonism?
History of access to coumarins
Prolonged WBCT / ACT
Prolonged PT then PT and APTT
- PT first because factor VII has the shortest half-life (6 hours)
- Normal until coagulation factors run out
- 24-72 hours
Urine, liver and kidney samples can be frozen if dies
Presentation of acute DIC?
Presentation with thrombotic disease and/or bleeding diatheses Haemorrhage Thrombosis Multiorgan failure Metabolic acidosis
Lab abnormalities with DIC? Treatment?
Prolonged clotting times - Reduced ATIII (dog) - Thrombocytopenia - Schistocytes - Increased FDPs/D-dimer - Decreased fibrinogen Treatment - Treat underlying cause - Heparin, whole blood, plasma - ?ATIII
What are FDPs? When elevated?
Fibrinogen depredation products
Formed during depredation of fibrin (fibrinolysis) and fibrinogen (fibrinogenolysis)
Elevated in:
- DIC
- thrombotic disease
- reduced hepatic clearance
Can’t distinguish between plasmin action on fibrinogen and fibrin
What are D dimers?
Specific for breakdown of cross linked fibrin
= sensitive indicator of fibrinolysis in canine DIC
Presentation of chronic DIC?
Seen in association with many conditions Few clinical signs Generally normal coagulation screen ? Reduced or increased ATIII ? thrombocytopenia Increased FDPs Fibrinogen and coagulation times may be normal Generally better/good prognosis
Which conditions can lead to hyper coagulable states?
Immune mediated haemolytic anaemia Pancreatitis Nephrotic syndrome Hyperadrenocorticism Diabetes mellitus Cardiac disease
How long does it take neutrophils to mature in the BM? Average blood transit time?
Maturation time from blast to segmented neutrophil is 7 days (can be 2-3 days with inflammation)
Average blood transit time is 6-10h
Total neutrophil pool replaced 2.5 times daily
Leucocyte patterns with inflammation
Inflammatory leucogram:
- neutrophilia most common
- left shift (band neutrophils >1x10^9/L): acute inflammation
- neutropenia if high rate of consumption
- lymphopenia with acute viral infections
- lymphocytosis is rare (chronic inflammation causes lymphoid hyperplasia in tissues but doesn’t usual cause a peripheral lymphocytosis) - may see with chronic ehrlichiosis
What are regenerative and degenerative left shift?
Regenerative left shift = also neutrophilia
Degenerative left shift = normal or low mature neutrophils, poor prognostic indicator
What is toxic change?
Increased basophilia of cytoplasm, blue granules (Dohle bodies), vacuoles (foamy), less condensed chromatin
Of neutrophils
Due to reduced maturation time because of intense stimulation of myelopoiesis
Adrenaline response leucogram?
Due to excitement/fear Lymphocytosis: - due to splenic contraction - more frequent in cats - mature small lymphocytes Neutrophilia - less common - due to shift of neutrophils from marginated pool to circulating pool due to increased blood flow - no bands - no more than twice upper limit
Stress leucogram?
Due to chronic stress or excess endogenous/exogenous steroids
Lymphopenia:
- due to lymphocyte apoptosis induced by steroids
Neutrophilia:
- less common
- no bands
- may have hyersegmentation (longer time in circulation)
- no more than twice upper limit
- monocytosis
What haematological response is seen after bone marrow injury? Causes?
Neutropenia Bone marrow hypoplasia cause pancytopenia but neutropenia first to appear Causes: - chemo drugs - parvovirus - idiosyncratic drug reactions (e.g. phenobarbital, griseofulvin) - oestrogens - chronic ehrlichiosis - neoplasia
What causes:
- monocytosis
- lymphocytosis
- lymphopenia
- neutrophilia
- neutropenia
- left shift
- eusinophilia
- basophilia?
Monocytosis: Chronic inflammation, stress leucogram
Lymphocytosis: Adrenalin release in cats, if severe or atypical morphology: likely neoplastic (leukaemia)
Lymphopenia: Acute inflammation (e.g. acute viral infection), ‘Stress leucogram’ (due to endogenous or exogenous steroids)
Neutrophilia: usually due to inflammation, can also be due to chronic stress response (or steroid administration)
Neutropenia: overwhelming tissue demand, reduced bone marrow production or increased destruction (immune-mediated)
Left shift: acute inflammation
Eosinophilia: worm parasitism, allergy—type 1 hypersensitivity
Basophilia: usually follows eosinophilia and is due to similar causes
What is classed as leucopenia and leucocytosis on a low power field?
Leucopenia: <15 WBC in LPF 10x field
Leucocytosis: >45 WBC in a LPF 20x field
How much to blood transfuse equation?
k x weight(kg) x (required PCV - recipient PCV)/donor PCV
k = 90 in dogs
k = 66 in cats
= ml
What are the blood groups in dogs?
8 major erythrocyte antigens
DEA 1.1, 1.2, (1.3), 3, 4, 5, 7, 8
DEA 1 group:
- DEA 1.1 most important
DEA 1.2 also associated with transfusions reactions on second transfusion
Dog can be positive for 1.1 or 1.2, but not both
DEA 3, 5 and 7 may cause sensitisation
Dog donor selection for blood transfusion? How often can donate?
Ideally >28kg - can give a unit Friendly, healthy 8yo or less Preferably nulliparous Vaccinated more than 14d ago Never been abroad
Ideally DEA 1.1, 1.2, 3, 5 and 7 negative
Most greyhounds are 1.1 negative
For known 1.1 positive dog, can use 1.1 positive blood
PCV, TP/TS check prior to each donation
Minimum 28d between donations
When must blood be cross matched for dogs? Types of cross matching?
Not needed for first transfusion
Must be carried out if a second or subsequent transfusion is required
Major cross match:
- detects Abs in recipient plasma against donor red cells
Minor cross match:
- detects Abs in the donor against recipient red cells
- of little value unless donor has been previously transfused
When is it impossible/inaccurate to cross match blood for dog transfusions?
If auto agglutination already present
Inaccurate if on immunosuppressive therapy
What bag is blood collected in for blood transfusion to a dog? What to give donor following blood collection?
Human blood bag - CPDA-1 anticoagulant, citrate phosphate dextrose adenine
Give donor 2-3x volume of blood collected in crystalloids after donation
What blood groups do cats have?
A, B and AB (A is dominant to B - simple autosomal)
Type A:
- A/A or A/B
- express genes for A and B and the enzyme which converts B to A
- most common in DSH in UK
- may possess low tiered anti-B Abs (weak IgM agglutinins, and weak IgM and IgG haemolysins)
Type B:
- B/B
- express only gene for antigen B
- more common in British shorthair
- always possess high tiered anti-A Abs (mainly strong IgM haemolysins and haemagluttinins)
Type AB
- rare
- express genes for both NeuGC and NeuA and intermediate forms
- have no Abs to A or B
How to select a cat blood donor?
Friendly, healthy, preferably indoor (to avoid Mycoplasma haemofelis)
8-10yo or less
preferably nulliparous
vaccinated more than 14d ago
never been abroad
Ideally >4kg lean - can give 50ml cat unit
FeLV, FIV, M haemofelis negative
PCV >35%
Donor and recipient must be typed in advance
PCV, TP/TS checked prior to each donation
Min 28-42d between donations
Should cats be blood typed?
Yes donor and recipient every time
- transfusion of A blood to B cat produces very severe transfusion reaction
- transfusion of B blood to A cat results in mild-severe haemolytic reaction (dramatic reduction in rec cell lifespan = little benefit to patient)
- should transfuse AB cat with AB donor
- can give washed red cells
How to collect blood from a cat for transfusion?
Sedation - midazolam and ketamine
7ml CPDA-1 anticoagulant into 60ml syringe
Prime butterfly cannula with anticoagulant - use large gauge e.g. 19G
Make nick in skin with scalpel
Give donor 2-3x volume of blood collected in crystalloids
When to transfuse packed red cells, plasma and platelet rich plasma?
Packed red cells: when only red cells are required
Plasma: coagulopathies, hypoalbuminaemia
Platelet rich plasma: thrombocytopenia
Blood storage?
Whole blood and packed red cells: up to 4 weeks at 4-5 degrees C
- Have reduced oxygen carrying capacity
- Stored whole blood does not provide platelets or clotting factors
Plasma: freeze asap to preserve clotting factors (max delay 4-6h)
Warm to 30-37C gently to use
Where to do intra osseous blood transfusion? Where else if no other option?
Bone marrow cavity of proximal femur?
Intraperitoneal: poor, slow uptake, only 40% RBCs absorbed
Speed of blood transfusion?
Hypovolaemic: 22ml/kg/hr
Normovolaemic: 5-10ml/kg/hr
CV or renal dysfunction: 2-4ml/kg/hr (2 in cats)
Half rate for packed RBCs
Blood transfusion reactions in dogs?
Haemolysis Circulatory overload Pyrexia due to: - acute haemolysis - sepsis - hypersensitivity (type 1) Hypocalcaemia Vomiting Contamination Infectious disease transmission Tachycardia due to: - anaphylaxis - shock - sepsis Jaundice due to: - severe haemolysis
Blood transfusion reactions in cats?
Face pawing Restlessness Tachypnoea Pyrexia Urticaria Vomiting
When is the most acute, severe haemolysis seen with blood transfusions?
Sensitised CEA 1.1 negative dog receiving 1.1 positive blood (previously had 1.1 positive transfusion)
Type B cat receiving type A blood
Less acute:
- CEA 1.2 sensitised dogs
- other CEA incompatibities (CEA 3, 5, 7 - 4-5 days later)
- type A cats given type B blood
Treatment for haemolysis during blood transfusion?
Stop tranfusion Crystalloid fluids IV corticosteroids if shock Oxygen Antihistamines - chlorpheniramine Adrenaline
Causes of blood haemolysis in vitro of collected blood?
Bacterial contamination - likely if stored produce are used
Overheating
Freezing - can’t freeze whole red cells
What to do if pyrexia during blood transfusion? Cause?
Increased by 1 degree or more Fairly common, usually transient Abs to platelets, WBCs or plasma proteins Bacterial contamination - rare Slow or stop transfusion and monitor Rule out haemolysis Assess for bacterial contamination
Hypocalcaemia during blood transfusion: Why happens? Signs? What to do?
Citrate anticoagulant chelates calcium Inappropriate volumes infused rapidly Impaired citrate metabolism - severe hepatopathy Signs: - ear twitching - vocalisation - cardiac dysrhythmias Supplement Ca
Vomiting during blood transfusion: Cause? What to do?
Usually due to: - rapid administrationn - feeding Stop tranfusion Determine if other cause Do not feed before, during or immediately after transfusion
Circulatory overload during blood transfusion:
Common if too rapid administration Pulmonary oedema - tachypnoea, dyspnoea, cough tachycardia STOP TRANSFUSION Oxygen Frusemide
