Critically Ill Horse with GI Disease Flashcards

1
Q

What are some conditions of the GI tract that lead to patients being ‘sick’, in horses and SA?

A
  • 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)
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2
Q

What is SIRS?

A

Systemic inflammatory response system (SIRS)

A self-amplifying dysregulated systemic inflammatory response

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3
Q

What can SIRS be triggered by and what can it result in?

A

–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

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4
Q

What was SIRS previously reffered to as?

Why is this different?

A

–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
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5
Q

What is sepsis?

A

–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

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6
Q

What is severe sepsis?

A

Sepsis with organ hypoperfusion or dysfunction

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7
Q

What is septic shock?

A

–Severe sepsis + systemic hypotension

  • Common in foals, rare in adult horses
  • Occurs in small animals
  • Hypotension usually doesn’t respond to drugs
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8
Q

What is multi-organ dysfunction syndrome?

How does the prognosis differ in SA compared to horses?

A
  • 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
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9
Q

What can multi-organ dysfunction sydrome be classed as?

A

–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)

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10
Q

What is disseminated intravascualr coagulation?

What is it associated with?

A
  • 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
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11
Q

What are the clinical signs of DIC in horses?

A

•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

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12
Q

What is the diagnosis for DIC?

A

•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)

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13
Q

What is a problem list and potential sequelae of GI disease (common things)?

A

–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

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14
Q

What is a problem list and potential sequelae of GI disease (less common things/specific challenges)?

A

–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

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15
Q

What is the likely success with the critically ill patient?

What does the prognosis correlate with?

A
  • 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
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16
Q

What are the clinical signs of hypovolaemia?

A
  • Congested or white MM – depending what phase we are in
  • Increased CRT
  • Increased HR
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17
Q

What is the clinical pathology of hypovolaemia?

A
  • 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
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18
Q

How can you monitor improvement in a patient with hypovolaemia?

A
  • 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
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19
Q

What is the approach to a hypovolaemic animal?

A

•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.

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20
Q

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?

A

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!

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21
Q

What is the skin tent, MM, CR, HR, lactate and other signs like for@

5% fluid deficit

8% fluid deficit

10-12% fluid deficit

A
22
Q

What fluid route should you avoid in animals that have ileus?

A

•Don’t use oral fluids in animals that have ileus

–If hypovolaemic, blood supply wont go to splenic circulation, fluid wont be absorbed – if we have ileus, also wont move through intestines and will distend stomach and SI – will cause discomfort and pain

–The fluid won’t be absorbed

–It will cause discomfort and pain

23
Q

What are the benefits for using oral versus paraenteral fluids?

A

•Don’t use oral fluids in animals that have ileus

–If hypovolaemic, blood supply wont go to splenic circulation, fluid wont be absorbed – if we have ileus, also wont move through intestines and will distend stomach and SI – will cause discomfort and pain

–The fluid won’t be absorbed

–It will cause discomfort and pain

  • Cheaper, but not always beneficial!
  • Again bigger problem in horses
  • Judge each case individually
  • Often OK if <5% fluid deficit – but not if its anymore!
24
Q

How can you correct hypovolaemia and electrolytes?

A

•For majority of animals – Hartmann’s or Lactated Ringers fine

–NO problem in neonates – they really like Lactated ringers as they like using lactate as an energy source.

–Hartmann’s probably best for all patients – even if increased lactate, can still use this fluid! Not acidic.

–Exception is an animal in intrinsic renal failure

•“The kidney as long as it is adequately perfused is smarter than the smartest internist”

–SO if the kidney is perfused it will sort out the acid-base and electrolyte abnormalities (within reason)

25
Q

What electrolytes are usually low in horses with hypovolaemia?

Small animals?

A

•Horses

–In animals that have food with-held in combination with resuscitation fluids develop – most fluid is low in these and most horses get these electrolytes from food:

  • Hypokalaemia
  • Hypomagnesaemia

–In animals with D++ often low Na and Cl – lost through the GIT

•Hypovolaemic animals

–Sl high Na and Cl

•Small animals

–Occ see hyperkalaemia and cardiac (ventricular) dysrhythmias secondary to m necrosis. Rarely also in horses with LCV

26
Q

What is the correction and prevention of electrolyte derangements?

A
  • Ideally need to initially measure and serially measure to ensure doing good and not doing harm esp imp re K+ and Ca2+
  • Horses NPO with concurrent administration of Lactated Ringers/ Hartmann’s

–WILL develop low K+ and Mg2+

–Low in fluid type

–Reliant upon diet

–Can supplement fluids safely – are tables available

27
Q

What is the monitoring with hypoproteinaemia?

A
  • Any problems with monitoring? If you’ve got an infection and too many Ig, this will mask it – this is a problem with doing it in house. Can have a normal TP and low albumin and high globulin – might pick this up with a larger buffy coat, which is often things such as fibrinogen and some Ig’s
  • Measure albumin on biochemistry, if you don’t have a biochem machine – TP and TS
  • Can end up with oedema – might be able to physically see it – oedema with other organs often occurs first and no way to measure it
28
Q

What is the treatment with hypoproteinaemia?

A
  • Plasma
  • Artificial colloids
    • Cellulose based ones – gel effusions
    • Starches – hydroxy ethyl starches but these have been removed from the market as they cause AKI in people and might do this is SA and no data in horses. Starches increase colloidal support but don’t increase TP as they aren’t really proteins! It wont increase even though its likely to be beneficial
29
Q
A
30
Q

What are some problems with using plasma?

A
  • Short half life and protein molecules are really small
  • With sick animals, the neutrophils produce chemicals that smash big wholes into the side of the BV so all of the small molecules you have can move out into interstitial space
  • Need a donor
  • Cheaper than artificial colloids but still a price with it
  • Reactions – immunogenic, it’s a foreign product from one animal to another and might make an immune reaction. Having a reaction to usually immunoglobulins and proteins – but we don’t always know! Some can be mild, some can be severe
  • Disease is another risk
31
Q

What are some problems with using colloids?

A
  • Might result in AKI
  • Can sometimes (gel effusions) can do what plasma does – leak out and promote development of oedema rather than increase colloid osmotic pressure
32
Q

What is activated with SIRS and sepsis?

What happens to blood vessels?

A

•Activation of the inflammatory cascade

–Some beneficial effects

–Some that lead to increasing severity of disease if out of control

  • Vasodilatation – a bit if a good thing! Should help to promote effusion, but if too much – will reduce BP and therefore reduce blood flow
  • Dysregulation of tissue perfusion
  • Leaky capillaries
33
Q

What is the management of the inflammatory response?

A
  • Anti-inflammatories
  • NSAIDs – as long as we have sorted hypovolaemia in SA, doesn’t matter in horses
  • GI bleeding with NSAID is much more of a problem with SA rather than horses
  • Steroids
  • Might be a bit counterintuitive
  • Play a role, maybe not right at the start, but if you are going to lose an animal as its inflammatory response is totally out of control, might need a bit of steroid to bring it down a bit – short acting steroids
  • Washing out abdomen – removing neutrophils
34
Q

What is the management of the organism triggering the response - with regards to the treatment of SIRS and sepsis?

A
  • Antibiotics if we think its bacterial disease
  • Bacteriocidal in a sick patient! Downside is that we release more bacterial products that trigger more inflammatory response – so may get worse before it gets better
  • Removal of FB if there is one
  • Can use anti-endotoxic drugs
  • E.g. Polymyxin B – the only anti endotoxic drug we have available
  • IV lidocaine
  • Anti-ileus and anti-inflammatory
35
Q

Name the Classifications of analgesic agents?

A
  • NSAIDS
  • Opioids
  • NMDA receptor antagonist
  • Ketamine
  • Alpha 2’s
  • Local anaesthetics
  • Randoms
  • Paracetamol
  • Tramadol
  • Gabapentin
36
Q

What are the potential side effects of:

NSAIDs

Opioids

Local anaesthetics

Alpha 2’s

Ketamine

A
  • NSAIDS
  • Renal dysfunction
  • Gastric ulceration in the dog, in the horse causes RDC ulceration
  • GI bleeding in SA – not in horses
  • Opioids
  • Can cause ileus, but can be caused by pain also – so balance to be had
  • Excitation
  • Dysphoria – in SA can make it hard to know whether they have had too much or whether there is something else wrong – horses like to box walk with opioids
  • LA’s
  • IV lidocaine most likely
  • Massive bolus needed for dysrhythmia
  • Can become ataxic, collapse, can behave weird – makes monitoring tough
  • Alpha2’s
  • Bradycardia
  • CVS effects and sedation – unless you want them to be sedated!
  • Ketamine
  • Eye ulcers but much worse in lab animals than in vet patients
  • No CVS effects
  • No excitation likely
37
Q

What is the monitoring for dysregulation of perfusion?

A
  • Use CRT – not always that helpful
  • Lactate – but this is sometimes trapped in the capillary beds
  • Capnograph possible – use animals intubated to get good measurements though
  • Kidney – end organ, look at urine output – not too challenging to measure in dogs and foals but more difficult in adult horses – more reliant on USG
  • Common and big problem, not brilliant at measuring it
38
Q

What is the treatment for the dysregulation of perfusion?

A
  • Fluids
  • Doesn’t mean they will get where we want them to go but an option
  • Norepinephrine, dopamine etc. – improve cardiac contractility and vasoconstriction – needs to be done as CRI sometimes
39
Q

What are some causes of ileus?

A

–Reduced perfusion to GI

–Opioids maybe

–Pain

–‘Stress’

–Inflammation that can be caused by a variety of diseases

40
Q

What are some potential treatments for ileus?

A

–Fluids and analgesia – may or may not include opioid depending on what camp you are in

–Motility agents – metaclopramide (2 – can cause severe neuro signs in horses that can make them dangerous), erythromycin (3) at sub anti-microbial doses and lidocaine (1) – numbers correspond to choice in horses

41
Q

What are some nutritional challenges that horses face when critcially ill?

Do you feed after surgery?

A

•To feed or not to feed following surgery

–Every other species is well ahead of us -we don’t know too much

–Differences between small animals and horses

–Adult horses can be starved for up to 48-72 hrs with minimal metabolic effects – but doesn’t mean we have the best effects!

  • Care with fat ponies and donkeys – max 12-24 hrs starvation as become hyperlipaemic and die
  • Ideally feed enterally

–Impossible if refluxing/ V++ and if they have ileus

–In SA – use anti-emetics to feed enterally

•If can’t feed enterally:

–Carefully monitor triglyceride concentrations (equine)

–Consider parenteral nutrition – either proteins and glucose IV or fats, protein and glucose IV

42
Q

How much use is 5% dextrose for paranterla nutrition?

What is partial and total parenteral nutrition?

A

•5% DEXTROSE DOES NOT PROVIDE NUTRITION FOR ANY ANIMAL IN THE VOLUME THAT WE CAN ADMINISTER IT!!! Low in calories and is free water.

–What’s going to happen if you administer free water?

–Although isotonic fluid when we give it, once its all goes into cells – basically tap water gone into then – goes hypotonic and causes cells to swell

•Partial parenteral nutrition

–40-50% dextrose +/- amino acids

•Dilute the dextrose and run side by side with Hartmann’s

–Only use IV glucose on own for max 24 hrs – otherwise not providing proteins and animal goes into catabolic state and starts breaking down its muscles and if its just had surgery, has negative impact on healing

–Glucose on own cheap; q exp when need to add AA

•Total parenteral nutrition

–40-50% dextrose + AA + lipid

–Q expensive

•Often don’t try to provide all caloric requirements– 10-40KCal/kg/day

43
Q

What are clinical signs of poor nutritional status?

What are some diagnostic tests?

A

•Clinical signs?

–Weakness

–Depression

–Weight loss and muscle loss

–Anorexia – they don’t eat, metabolic parameters go up and these suppress appetite

•Diagnostic tests?

–Blood glucose in SA and in foals – not helpful in adult horses as they don’t become hypoglycaemic as they don’t use glucose as a fuel in the way that carnivores do – they mobilise fats instead and increase in triglyceride concentration

–Cholesterol – in adult SA

44
Q

What does a period without food do to GI changes?

A

•Any period without food leads to GI changes

–Villi stunting

–Decreased absorptive capacity beyond that primary disease

•Human medicine

–Provide glutamine prior to re-feeding to ‘feed’ enterocytes – glutamine is a nutritional protein supplement often used by people who work out at the gym! Have used in periods of gut rest at horses, unsure if it works

–Q cheap – nutritional human supplement

  • Predisposes to mild gastric ulceration – usually reversible once you start to reverse the process
  • Controversial re prophylaxis and treatment

–Gastric acid has a purpose

–Prophylactic protein pump inhibitors as acid has a purpose! Don’t want a whole raft of bacteria getting in there that it cannot control!

45
Q

What are some managing changes in GI flora?

A

•Do nothing

–Commonly adopted

•Care re use of pre and pro-biotics

–Often no EBM to support their use

–May contain inappropriate or even pathogenic organisms

–Many unlikely to survive gastric acid

•Equids – Transfaunation

–‘Poo’ soup

–If animal lives in similar environment and in close contact with that horse, have similarly normal gut flora – with treatment (proton pump inhibitor to improve the likelihood of those good bugs in the poo soup that will make it to the small and large intestine) and poo soup, might be able to hasten to recolonisation of good bugs!

46
Q

What is thrombophelbitis?

WHat are some things that cna predispose to it?

What can you do to help prevent it?

A
  • Common complication following SIRS
  • The sicker they are, the more likely they are to get thrombophlebitis
  • What will likely predispose animals to developing this condition?

–Having a catheter

–Leaving catheter in too long

–Putting them in, in a non sterile way – they are at risk of bacteremia if they haven’t already got it!

•What can you do to help prevent it?

–Hand hygiene

–Aseptic prep in horses and often in very sick dogs

–Don’t contaminate the catheter

47
Q

What is the prevention and treatment for coagulation disorders?

A
  • Prevention:
  • Heparin – similar to warfarin, unfractionated or low MW – if used early in disease states, might help prevent getting into viscous cycle
  • Don’t use if spontaneously bleeding
  • Warfarin – similar to heparin but often don’t use
  • Treatment
  • Transfusion – could use whole blood? They missing clotting factors, which are in plasma – so want fresh plasma, the minutes plasma is frozen you reduce the amount of clotting factors
  • Little and often – will use it. One off doses of plasma often aren’t that helpful
48
Q

When are horses more at risk of laminitis?

What can we do to try and prevent this?

A
  • Horses following SIRS or sepsis at high risk of developing laminitis following resolution of GI signs
  • What can we do to try and prevent this?

–All the things we have said already

–Sorting SIRS

–Appropriate antibiotics

–Lots of fluids

–Heparin, polymyxin B

–Icing feet

–Foot pads – frog support

•Significant contributing factor to mortality in colitis and LCV

49
Q

When can you get ventricular dysrhythmias?

What should you do?

A
  • More common in dogs following GDV (and occasionally peritonitis and pancreatitis) and other causes of SIRS
  • Does occasionally occur in horses
  • Electrolyte abnormalities or ‘myocarditis’ secondary to SIRS
  • Try and regularly establish cardiac rhythms in dogs with GDV
  • Always check rhythms in animals with higher heart rates than expect for other clinical signs
50
Q

What is the approach to ventricular dysrhythmias?

A

–Check electrolytes – particularly potassium

–Check volume status

–IV magnesium sulphate – membrane stabiliser and should help to ensure ionised magnesium is normal, might the let the IV lidocaine work

–IV lidocaine (one off doses and if short term success try infusion)

–IV procainamide

51
Q

What is vomiting in SA and what drugs are available?

A
  • Remember that V++ is a protective mechanism
  • They are trying to remove something that is going to cause them harm! If you are SURE they don’t have an obstruction, then:
  • Parenteral anti-emetics improve welfare and increase likelihood of being able to feed with prolonged vomiting
  • Many drugs available

–Most effective are those acting at vomiting centre and chemoreceptor trigger zone – sometimes worth using more than 1 drug working at different sights on that pathway in order to get a positive outcome

–See SA lecture

52
Q

How can a critically ill patient get anaemia?

What do you treat with?

A
  • Can lose a dramatic amount of blood through GI tract
  • Remember that concurrent hypovolaemia will mask degree of anaemia due to haemoconcentration
  • Even more true in the horse re blood loss and PCV as splenic contraction can mask blood loss for up to 24 hrs
  • Treat with blood
  • Hypovolaemic patient – anaemia isn’t always as evident as how serious it is until you fix its haemoconcentration