Critically Ill Horse with GI Disease Flashcards
What are some conditions of the GI tract that lead to patients being ‘sick’, in horses and SA?
- Retained foetal membranes
- Septic peritonitis
- Large colonic torsion – GDV in dog, almost same in bad things that we see
- Bacteraemia – usually seen 2ndary in larger animal
- GI perforations – probably more common in SA than horses
- Post-surgical contamination
- If we have bacteria somewhere other than the GI tract, will end up with bad things – e.g. rupture in SA (chemical peritonitis)
What is SIRS?
Systemic inflammatory response system (SIRS)
A self-amplifying dysregulated systemic inflammatory response
What can SIRS be triggered by and what can it result in?
–Triggered by
•Bacterial toxins
–Lipopolysaccharide (LPS/endotoxin) derived from gram negative bacteria
–S aureus – gram positive organisms
–Burns, Neoplasia, Pancreatitis (SA, not equine) – not infectious organisms
–Can result in coagulopathies
What was SIRS previously reffered to as?
Why is this different?
–Stopped using this term as assumes it’s the endotoxins causing the clinical signs, which is isn’t always?
–Inflammation leading cell death and apoptosis
- LPS has some direct roles
- Includes non-LPS bacteria
What is sepsis?
–SIRS plus : Culture proven infection (in humans)
–Veterinary patients – a likely bacteraemia we have got, as blood culture is difficult and get lots of false negatives
What is severe sepsis?
Sepsis with organ hypoperfusion or dysfunction
What is septic shock?
–Severe sepsis + systemic hypotension
- Common in foals, rare in adult horses
- Occurs in small animals
- Hypotension usually doesn’t respond to drugs
What is multi-organ dysfunction syndrome?
How does the prognosis differ in SA compared to horses?
- Horses -> probably gonna die, can reverse in SA
- Altered organ function in an acutely ill animal such that haemostasis cannot be maintained without intervention. SA’s will bleed, horses will clot and form microthrombi
What can multi-organ dysfunction sydrome be classed as?
–Classified as either primary or secondary
•Primary
–resulting from well-defined insult where organ dysfunction occurs early and is a direct consequence of the insult itself
»Burns and neoplasia
•Secondary
–Organ failure not in direct response to the insult but as a consequence of a host response (SIRS)
What is disseminated intravascualr coagulation?
What is it associated with?
- Death is coming!
- “Consumptive coagulopathy”
- Pathological activation of coagulation
–microvasculature clotting
–haemorrhagic diathesis
–consumption of procoagulants
•Associated with
–SIRS, SEPSIS, SEPTIC SHOCK
–MODS
- systemic neoplasia
- enteritis and colitis
What are the clinical signs of DIC in horses?
•In large animals, DIC is usually manifested by thrombosis rather than spontaneous haemorrhage
–petechial haemorrhages – esp in foals
–bleeding at following trauma – rare compared to in SA
- Venipuncture
- surgical sites
- nasogastric intubation
•
What is the diagnosis for DIC?
•3 out of 5 abnormalities of
–Thrombocytopenia
–Prolonged prothrombin time
–Prolonged activated partial thromboplastin time
–Increased fibrin degradation products
–Decreased anti-thrombin 3
–(Low fibrinogen – not used very often as ref range <5 g/L)
What is a problem list and potential sequelae of GI disease (common things)?
–SIRS or sepsis
–Hypovolaemia
•Accompanies acute pre-renal disease
–Dysregulation of perfusion
•Oxygen and ATP delivery occurs in capillary beds and in some patients, they have okay circulation but capillary beds shut down and their tissues go hypoxic and don’t receive what they should
–Hypoproteinaemia
•PLE and consumption of protein too fast
–Ileus
–Nutritional challenges
•If you have ileus and GI disease, wont have blood flow to GI track
–Change in gut flora
–Thrombophlebitis
–Coagulation abnormalities
–Pain
What is a problem list and potential sequelae of GI disease (less common things/specific challenges)?
–Ventricular dysrhythmias
•Esp GDV/LCV
–Laminitis
–Vomiting (dogs and cats)
–Electrolyte abnormalities
- Common
- K+ inc in GDV
- Low Na and Cl with D++
- Inc Na and Cl with hypovolaemia and low Mg and K – colic
- Electrolytes need to be sorted imminently if they are life threatening e.g. potassium, but largely slightly low Na and Cl – kidney can probably sort that better than we can! Sort perfusion to kidneys and they don’t have renal disease, then a lot of these will resolve by themselves
–Anaemia
What is the likely success with the critically ill patient?
What does the prognosis correlate with?
- Prognosis correlates with measures of SIRS
- Extrapolated from human medicine
–The sooner abnormalities are corrected appropriately within 24 hours, the more likely survival
- Hypovolaemia and electrolyte disturbances
- Appropriate FIRST use of antimicrobials – if you get the right one the first time, better outcome
- Correction of decreases in CO/ hypotension
- Correction of sepsis/SIRS
What are the clinical signs of hypovolaemia?
- Congested or white MM – depending what phase we are in
- Increased CRT
- Increased HR
What is the clinical pathology of hypovolaemia?
- Increased creatinine in the horse and increases urea and creatinine in the dog
- Assessing renal function – USG more than 1030 is indicative of hypovolaemia
- Lactate (use alongside USG)
- PCV and TP – challenges with using these
How can you monitor improvement in a patient with hypovolaemia?
- Repeat USG
- Normalising heart rate
- Improving demeanour
- Don’t have to keep taking blood samples in order to assess patient! You can assess the horse and see if you are going in the right direction – might need to quantify it, but can get a good idea from how they are
What is the approach to a hypovolaemic animal?
•Assess percentage fluid deficit (its not dehydration!!)
–10% of bodyweight? Take their body weight and knock a 0 off
•Calculate maintenance rates
–How do they differ between adults and neonates?
–Neonate – require double the rate
–Shock rate - 50-90ml/kg in SA can be used.
•Replace 50% of fluid deficit as a bolus
–30kg labrador – 1.5 litres as bolus – it’s the reexamination of the animal that becomes really important
–Cannot be too fast as a bolus!!!
•Then replace the remaining 50% and maintenance requirements over the next 6-8 hours
–Don’t forget to include fluid estimate of loss in vomit/ reflux, diarrhoea etc.
If a patient has a high lactate, the horse is on fluid therapy and looks improved and then you measure the lactate again - why does this happen?
Lactate produced by cells where the blood is from the capillary bed, if you give fluids and the horse looks better and now its lactate is 8 and higher than it was – you have to give it time to wash the lactate out and don’t measure it too quickly!