Equine 8 Flashcards
what is SIRS triggered by
bacterial toxins
- lipopolysaccharide derived from gram negative bacteria
- gram positive organisms partocularly S aureus
- burns, neoplasia, pancreatitis (small animals)
lead to inflammation causing cell death and apoptosis
what is SIRS
self-amplifying dysregulated systemic inflammatory response
what is sepsis
SIRS plus culture proving infection (humans, generally just assume in animals)
what is severe sepsis
sepsis with organ hypoperfusion or dysfunction (measure with renal output)
what is septick shock
severe sepsis plus systemic hypotension
common in foals, rare in adult horses
what is multi-organ dysfunction syndrome
altered organ function in an acutely ill animal such that haemostasis cannot be maintained without intervention - horses inevitably die
what is primary MODs
resulting from well-defined insult where the organ dysfunction occurs early and is a direct consequence of the insult itself e.g. burns, neoplasia
what is secondary MODs
organ failure not in direct response to the insult but as a consequence of SIRS
what is DIC
disseminated intravascular coagulation - pathological activation of coagulation
- microvasculature clotting
- haemorrhagic diathesis
- consumption of procoagulants
what is DIC associated with
SIRS
sepsis
septic shock
MODs
what are the clinical signs of DIC in horses
thrombosis
petechial haemorrhage more common in foals
rarely - bleeding following trauma
how is DIC diagnosed in horses
3 of the 5 below = Thrombocytopenia = Prolonged prothrombin time ○ Prolonged activated partial thromboplastin time ○ Increased fibrin degradation products = Decreased antithrombin 3 also low fibrinogen but not often used
what are the common sequelae of GI disease in horses
SIRS or sepsis Hypovolaemia ○ acute pre-renal disease Dysregulation of perfusion ○ Some patients have ok circulation but capillary beds shut down (exchange site) so tissues become hypoxic Hypoproteinaemia Ileus Nutritional challenges ○ Poorly functioning gut doesn't absorb food effectively ○ Hypovolaemia means blood supply to GIT is reduced Change in gut flora Thrombophlebitis Coagulation abnormalities Pain
what are the less common sequelae to GI disease in horses
Ventricular dysrhythmias ○ Especially with GDV/LCV (dog/horse) Laminitis (horse) Vomiting (dogs, cats) Electrolyte abnormalities ○ Common ○ K increase in GDV ○ Low Na and Cl with diarrhoea ○ Increased Na and Cl with hypovolaemia and low Mg and K - colic - Mg and K increased by eating ○ Treat if life-threatening, otherwise leave kidneys to sort Anaemia
which factors must be corrected early in the critically ill patient to improve prognosis
hypovolaemia
electrolyte disturbances
hypotension
SIRS - some cases need surgery
need appropriate use of antimicrobials
what are the clinial signs of hypovolaemia in horses
- mm colour congested or white
- increased CRT
- increased HR
what are the clinical pathological signs of hypovolaemia in horses
• Increased creatinine - horse • Increased urea and creatinine - dog - USG >1.030 in conjunction with other signs • Increased lactate • PCV and TP
what factors are used to monitor improvement of hypovolaemia in horses
• HR normalising
• Improved demeanour
• Repeat USG or starting to produce urine when previously anuric
• Repeat bloodwork max q4hours
○ Repeat lactate
§ Produced by cells. If you have had capillary bed shut down then fluids given, the beds open up and then lactate will double so need to take care with interpretation
describe the approach to hypovolaemia in horses
• Assess percentage fluid deficit (not dehydration)
• Calculate maintenance rates
○ Adults = 2ml/kg/hr
○ Neonates 2x adult rate ~5ml/kg/hr
• Replace 50% fluid deficit as bolus as fast as you can
○ Large bore, short catheter, hang fluids from a height
○ Re-examine animal at this point
• Replace remaining 50% and maintenance over the next 6-8 hours
○ Include fluid estimate of loss due to reflux/diarrhoea etc
○ Need to correct underlying problem
why should oral fluids be avoided in cases of ileus
- won’t be absorbed
- will distend small intestines as not moving through
- will cause discomfort/pain
what electrolyte imbalance may be seen in horses that have had food withheld with resuscitation fluids
hypokalaemia
hypomagnesemia
which electrolyte imbalance may be seen in horses that have diarrhoea
low Na
low Cl
which electrolyte imbalances may be seen in hypovolaemia
slightly high Na and Cl
which electrolyte imbalance may be seen in horses with LCV
hyperkalaemia and cardiac dysrhythmias secondary to muscle necrosis (rare)
how is hypoproteinaemia monitored in horses
- Total protein/total solids using refractometer
- Albumin on biochemistry
- Oedema - can see peripheral but not around organs
- Total protein will be affected by albumins and globulins so could have very low albumin and very high globulins - Buffy coat will be bigger
how is hypoproteinaemia treated in horses
colloidal support
- plasma
- cheap, immunogenic, disease transmission risk, short half-life
- artificial
- cellulose based e.g. gelofusine
- may promote oedema
- hydroxyethyl starches (don’t use)
- don’t use especially in foals
- will support but won’t increase protein
how is SIRS and sepsis treated in horses
NSAIDs or steroids IV lidocaine wash out abdomen surgery bactericidal antibiotics if needed antiendotoxic drugs - po;ymixin B
how is dysregulation of perfusion monitored
urine output - difficult in adult horses. use USG
capnograph
lactate
CRT
how is dysregulation of perfusion treated
fluids
sympathomimetics
- dobutamine CRI
- dopamine
why is ileus a concern in horses
leads to gastric distension and rupture as they cannot vomit
what may cause ileus in the horse
reduced perfusion to GIT pain stress inflammation opioids
how is ileus treated in horses
fluids analgesia pro-motility agents - lidocaine - metaclopramide (can cause neuro signs) - erythromycin at sub-antimicrobial doses (abx resistance issues)
how long may adult horses be starved for with minimal metabolic effects
- 48-72 hours
- fat ponies and donkeys max 12-24 hours due to hyperlipaemia risk
what effects does starvation have on the GI system
villi stunting
decreased absorptive capacity
predisposes to mild GI ulceration (usually reversible)
how soon should horses be fed after surgery and what methods may be used
asap
- enteral ideal but impossible if refluxing and have ileus
- 5% dextrose (doesn’t provide enough nutrition)
- PPN - 40-50% dextrose and amino acids
- TPN - 40-50% dextrose, amino acids and lipid
how is nutritional status monitored in horses
clinical signs - weakness, depression, weight loss, anorexia
blood glucose (not adults as don’t become hypoglycaemic)
triglyceride concentration
creatine kinase (will be high due to boxing etc)
how are changes in GI flora managed in horses
do nothing common
no EBM to support use of pre- or pro- biotics
transfaunation via NG tube (pre-treat with proton-pump inhibitor)
what predisposes horses to thrombophebitis
catheter placement - particularly if left in too long or placed in non-sterile way. cheap, hard, platic catheters worse
how is thrombophlebitis prevented in horses
good hygiene
aseptic prep before catheter placement
what are the signs of coagulation disorders in horses
- bleeding
- petechial haemorrhage
- thrombi
how are coagulation disorders prevented in horses
low molecular weight heparin in early disease states not if already bleeding
how are coagulation disorders treated in horses
transfusion - missing clotting factors so use fresh plasma little and often
how is laminitis following SIRS prevented
treat SIRS early fluids appropriate antibiotics heparin polymixin B icing feet foot pads - frog support
when may ventricular dysrhythmias occur in horses and dogs
dogs - following GDV and other causes of sepsis
horses - occasionally secondary to muscle necrosis. myocarditis secondary to SIRS
always check ECG in animals with higher HR than expected for other clinical signs
how should ventricular dysrhythmias be approached
check electrolytes check volume status +/- fluid bolus IV magnesium sulphate - membrane stabiliser IV lidocaine IV procainamide
describe anaemia in horses
can lose a lot of blood via GIT
concurrent hypovolaemia can mask degree due to haemoconcentration especially due to splenic contraction
treat with blood transfusion
