GI critically ill Flashcards
What is SIRS
Systemic inflammatory response syndrome
A self amplifying, dysregulating systemic inflammatory response
Triggered by
- Bacterial toxins
Lipopolysaccharides derived from G-ve bacteria cell wall
S aureus
Burns, neoplasia, pancreatitis
Can result in coagulopathies
Previously referred to as endotoxaemia
- Inflammation leading to cell death and apoptosis
LPS has some direct roles - Lipopolysaccharides
Includes non-LPS bacterio
What is sepsis
Sepsis - SIRS plus culture proven infection
Severe sepsis – sepsis with organ hypoperfusion or dysfunction
Septic shock
- Severe sepsis + systemic hypotension
Common in foals, rare in adult horses
Occurs in small animals
What is Multi-organ dysfunction syndrome
Altered organ function in an acutely ill animal such that haemostasis cannot be maintained without intervention
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
Disseminated intravascular coagulation - DIC
Consumptive coagulopathy
Pathological activation of coagulation
- Microvascular clotting
- Haemorrhagic diathesis
- Consumption of procoagulants
Associated with
- SIRS, sepsis, septic shock
- MODS
Systemic neoplasia
Enteritis and colitis
DIC - disseminated intravascular coagulation
Clinical signs
- In large animals – usually thrombosis rather than spontaneous haemorrhages
- Petichial haemorrhages
- Bleeding following trauma – venepuncture, surgical sites, nasogastric intubation
DIC - disseminated intravascular coagulation
Diagnosis
- 3/5 abnormalitites
- Thrombocytopenia
- Prolonged prothrombin time
- Prolonged activated partial thromboplastin time
- Increased fibrin degradation products
- Decreased antithrombin 3
- Low fibrinogen – not often used as reference range <4g/l
Assessment of volume status
Clinical exam
- Heart rate
- CRT
- Jugular filling time
- Peripheral temperatures
- Demeanour
- Lactate
- PCV/TP
- Creatinine
How to estimate fluid deficit
5% - 1-3 S skin tent, Moist/tacky mm, <2s CRT, normal HR, <3 lactate, dec urine output
8% - 3-5 skin tent, tacky mm, 2-3s CRT, normal to 50% above normal HR, 3-6 lactate, dec arterial pulse quality
10-12% - 5+ skin tent, dry mm, >4s CRT, 50% above normal HR, >6 lactate, dec jugular fill, poor pulse, sunken eyes
Equine maintenence fluids
2-3ml/kg/day
50ml/kg
Hypovolaemic horse
Electrolytes
Estimate fluid deficit %
Maintenence - 50% as bolus and 50% over next 6-8h + maintenence for this time
For majority – hartmanns or lactated ringers is fine
- No problem in neonates
- Exception in animal in intrinsic renal failure
The kidney – as long as adequately perfused – is smart – will sort out acid-base and electrolyte imbalanced within reason
Oral or parenteral fluids
Do not use oral fluids in animals with ileus - fluid wont be absorbed and will cause pain
Cheaper
Okay if <5% deficit
Electrolyte imbalance in horse
In horses with food withheld in combination with resuscitation fluids develop
- Hypokalaemia
- Hypomagnesemia
In animals with diarrhoea – often low Na and Cl lose through GIT
Hypovolaemia animals – slightly high Na and Cl -haemoconcentration – restore with circulating volume
Ideally need to initially measure and serially measure to ensure doing good and not harm – especially K+ and Ca2+
Horses with NPO (no oral feed?) – with concurrent lactate ringers/hartmanns
- will develop low K+ and Mg2+
- Low in fluid type
- Reliant upon diet
- Can supplement fluids safely – tablets are available
Hypoprotenaemia
Problems with monitoring – can be affected by volume status – hypovolaemia – artificially increases so when restore circulating volume – massive hypoproteinaemia
Treating
- Plasma – relatively safe horse to horse – will also provide some clotting factors
- Commercially available products
SIRS and sepsis
How to treat
Activation of inflammatory cascade
- Some beneficial effects
- Some that lead to increasing severity of disease if out of control
Vasodilation – hypotension and reduced perfusion – leaky capillaries – oedema
Treatment
- Antimicrobial drug administration
- Fluid resuscitation and pressure support
- Treatment for inflammation, endotoxaemia and coagulopathy
Early recognition – critical for successful outcome
Analgesia in critial patient
NSAIDs
Opiods – not butorphanol – limited effects
- Opioids do not cause ileus – pain is a cause of ileus
Paracetamol
Alpha-2 agonists
Ketamine
Lidocaine – controversial but good effects for visceral analgesia – could be a prokinetic and could offset harm of NSAIDs
