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
Dysregulation of perfusion in SIRS/sepsis
Vasodilation as result of SIRS/sepsis
Positive inotropes – dobutamine – increase force of contraction – improve cardiac output
Vasopressors – norepinephrine – increased tone in vessels so increased perfusion pressure
Ileus
Causes
Treatments
Consequence of GIT disease
SI strangulating obstructions
Causes
- Pain
- Abdominal surgery – gut handling and stretch
- Drugs – anaesthetic drugs
- GI abdominal disease/inflammation (peritonitis)
Treatments
- Prokinetics – lidocaine, metacloprimide, neostigmine
- Analgesia – treat the pain causing ileus
- Treatment of primary disease
- Restoration of perfusion
Particular concern in horses as can lead to gastric distention and rupture as cannot vomit – manual removal with NG tube
Should you feed critical patient - SIRS sepsis
- Adult horses can be starved for 48-72hours with minimal effect
Care with fat horses and donkeys – 12-24 hours – hyperlipaemia
Ideally feed enterally – better for GIT – impossible if refluxing and have ileus
If cant feed enterally – monitor triglyceride concentrations – if increase breaking down fat reserves – parenteral nutritions – glucose infusions to total parenteral nutrition
5% dextrose does not provide nutrition – low in calories and is free water – can lead to cell rupture – no place
Partial
40-50% dextrose +/- amino acids - Only use IV glucose on own for max 24h
- Glucose on own is cheap – quite expensive with adding AAs
Total parenteral - 40-50% dextrose + AAs + lipid
- Quite expensive
Often don’t try to provide all calorie requirements – 10-40 Kcal/kg/day – often start lower at 5Kcal
Thrombophlebitis
Broad spectrum antibiotics
Antiinflammatory
Systemic – aspirin and other NSAIDs to suppress platelet formation
Topical – DMSO, hot packs
Heparin – or analogues
Vasodilators – glyceryltrinitrate
Raise head – risk of swelling head – improve drainage
Alternative venous access – lateral thoracic vein, cephalic
With bilateral thrombosis – tracheostomy – oedema of head – URT obstruction
Surgical procedures to strip vein and or graft – rarely undertaken
Thrombosis treatment
Heparin
Clopridogrel
Aspirin
Ventricular dysrhythmias
Occasionally occur in horses
Electrolyte abnormalities or myocarditis secondary to SIRS
Always check rhythms in animals with higher heart rates than expected for other clinical signs
Can often compromise cardiac output and perfusion will improv if can be resolved
Approach
- Check electrolytes
- Check volume status
- IV magnesium sulphate – membrane stabiliser
- IV lidocaine – one off doses and if short term success – try infusion
- IV procainamide – not readily available
Anaemia
Can lose dramatic amount of blood through GIT
Concurrent hypovolaemia will mask degree of anaemia due to haemoconcentration
Blood loss and PCV – splenic contraction can mask blood loss for up to 24 hours
