Management of the critically ill horse with GI disease Flashcards

GI disease but many of these apply to the otherwise critically ill horse in the hospital setting

1
Q

Common potential sequelae of GI dz

A

▪ SIRS or sepsis
▪ Hypovolaemia
– Acute pre-renal disease
▪ Dysregulation of perfusion
▪ Hypoproteinaemia
– From PLE
▪ Ileus
▪ Nutritional challenges
▪ Change in gut flora
▪ Thrombophelbitis
▪ Coagulation abnormalities
▪ Pain

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2
Q

Less common/species- specific potential sequelae of GI dz

A

▪ Ventricular dysrhythmias
– LCV (large colon volvulus)
▪ Laminitis
– Sometimes seen as a consequence of SIRS/sepsis
▪ Electrolyte abnormalities
– Common
-> Low Na and Cl with D++
-> Inc Na and Cl with hypovolaemia and low Mg and K in colic
▪ Anaemia

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3
Q

What does the prognosis of the critically ill pt correlate to?

A
  • measures of SIRS
    – Higher the SIRS scores or the progression of SIRS into sepsis -> poorer prognosis

From human medicine:
▪The sooner abnormalities are corrected appropriately within 24 hours, the more likely they are to survive
– Hypoproteinaemia and electrolyte disturbances
– Appropriate use of antimicrobials
– Correction of decreased CO/hypotension
– Correction of sepsis/SIRS

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4
Q

How to assess volume status

A

Clinical Exam
▪Heart rate
▪Capillary Refill time
▪Jugular filling time
▪Temperature of extremities
▪ Demeanour

Clinical Pathology
▪ Lactate
▪ PCV/TP
▪ Creatinine

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5
Q

Approach to the hypovolaemic animal

A

▪Assess percentage fluid deficit
▪Calculate maintenance rates (2-3ml/kg/hr) (aka 50ml/kg/day)
▪Replace 50% of fluid deficit as a bolus
▪Then replace the remaining 50% and maintenance requirements of the next 6-8 hours
▪Don’t forget to include fluid estimate of loss in vomit/reflux, diarrhea etc.

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6
Q

Measures of 5% fluid deficit

A

Skin tent: 1-3s

MM: moist/tacky

CRT: <2s

HR: normal

Lactate: <3mmol/L

Other: decreased urine output

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7
Q

Measures of 8% fluid deficit

A

Skin tent: 3-5s

MM: tacky

CRT: 2-3s

HR: normal to 50% above normal

Lactate: 3-6mmol/L

Other: decreased arterial pulse quality

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8
Q

Measures of 10-12% fluid deficit

A

Skin tent: 5+s

MM: dry

CRT: >4s

HR: 50% above normal +

Lactate: >6mmol/L

Other: decreased jugular fill, poor pulse quality, sunken eyes, cold extremities

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9
Q

Contraindications for oral fluids

A
  • don’t use oral fluids in animals that have ileus
    – the fluid won’t be absorbed
    – it will cause discomfort and pain
    – not for more than 5% fluid deficit
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10
Q

The use of Hartmanns/lactated ringers

A
  • for the majority of animals it is fine
  • not a problem in neonates
  • NOT for an animal in intrinsic renal failure
    – if the kidney isn’t properly perfused it won’t sort out the acid-base and electrolyte imbalances
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11
Q

Causes of electrolyte imbalances

A

In horse that have food withheld in combination with resuscitation fluids develop
▪ Hypokalaemia
▪ Hypomagnesaemia
(Bc K and Mg are primarily obtained from the horses diet)

In animals with diarrhea, often low Na and Cl lost through GIT

Hypovolaemic animals
▪Slightly high Na and Cl (due to haemoconcentration, therefore should be sorted with restoration of volume)

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12
Q

Correction and prevention of electrolyte derangements

A

▪Ideally need to initially measure and serially measure to ensure doing good and not harm, especially important RE K+ and Ca2+
▪Horses NPO with concurrent administration of lactate ringers/hartmann’s
– WILL develop low K+ and Mg2+
– Low in fluid type
– Reliant upon diet
– Can supplement fluids safely – tablets are available

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13
Q

Hypoproteinaemia - what can it be affected by? How to treat

A

▪Problems with monitoring?
– Can be affected by volume status

▪ Treating
– Plasma
-> Safest and also provides clotting factors
– Commercially available products
-> But potential complications with these products

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14
Q

What do SIRS and sepsis lead to?

A

▪Activation of the inflammatory cascade
– Some beneficial effects
– Some that lead to increasing severity of disease if out of control
▪ Vasodilation
-> widespread vasodilation can cause hypotension and reduced perfusion
▪Dysregulation of tissue perfusion
▪Leaky capillaries
-> fluid extravasation and oedema

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15
Q

Treatment of SIRS and Sepsis

A

▪Treatment of sepsis requires an intensive care approach that includes:
– Antimicrobial drug administration
– Fluid resuscitation and pressure support
– Treatment for inflammation, endotoxaemia and coagulopathy.
▪Early recognition of sepsis and prompt antimicrobial drug treatment
are critical for a successful outcome

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16
Q

Analgesia

A

▪ NSAIDs
▪Opioids (not butorphanol as limited analgesic effects)
–Opioids do not cause ileus, pain is a cause of ileus
▪ Paracetamol (can be used in combination with NSAIDs)
▪Alpha-2 agonists
▪ Ketamine
▪ Lidocaine

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17
Q

How to fix dysregulation of perfusion due to vasodilation from SIRS/sepsis

A

▪Positive inotropes
– Dobutamine
-> increases force of contraction and CO
▪ Vasopressors
– Norepinephrine
-> result in increased tone in the vessels and therefore increased perfusion pressure and so hopefully better perfusion to tissues

Priority for these cases is to restore vascular volume in these pts - correct hypovolaemia. Many of these pts will still have hypotension despite normovolaemic - so we will need to give drugs to help improve cardiac output and blood pressure.

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18
Q

Causes of ileus

A

▪ Pain
▪Abdominal surgery
– Occurs post op due to gut handling
▪Drugs
▪GI/abdominal disease and inflammation
– Commonly seen in horses with SI strangulating obstructions

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19
Q

Potential tx for ileus

A

▪ Prokinetics
▪ Analgesia
▪ Treatment of primary disease
▪ Restoration of perfusion

20
Q

Why are we particularly concerned about ileus in horses?

A
  • can lead to gastric distension and rupture as they can’t vomit
  • removal of NG reflux is important part of tx
21
Q

To feed or not to feed following surgery?

A

▪Differences between small animals and horses
▪Adult horses can be starved for up to 48-72 hours with minimal effect
▪Care with fat ponies and donkeys – max 12-24hrs

22
Q

Would you ideally feed enterally or parenterally?

A
  • enterally
  • but impossible if reflex and have ileus
23
Q

If you can’t feed enterally what do you need to carefully monitor? What do you need to consider instead?

A
  • carefully monitor triglyceride []
  • consider parenteral nutrition
24
Q

Use of 5% dextrose

A
  • none
  • doesn’t provide nutrition for any anima
  • low in calories
  • is free water
    -> can result in rupture of the cells
25
Q

PPN

A

= partial parenteral nutrition
▪ 40-50% dextrose +/- amino acids
▪ Only use IV glucose on own for max 24hrs
– 24+ can cause insulin dysregulation
▪ Glucose on own is cheap; quite expensive when need to add AA

26
Q

TPN

A

= total parenteral nutrition
▪ 40-50% dextrose + AA + lipid
▪Q expensive

27
Q

With parenteral nutrition do you aim to provide all caloric requirements?

A
  • no
  • usually 10-40kCal/kg/day
28
Q

Things to monitor to monitor nutrition status

A

▪Weight
▪PE
▪Hydration status ▪Metabolic lab work ▪Blood glucose
▪TS
▪ Triglycerides
▪ BUN
▪ Electrolytes

29
Q

What does any period without food lead to?

A
  • GI changes
    – Villi stunting
    – Decreased absorptive capacity
  • Predisposes to mild gastric ulceration
30
Q

Managing changes in GI flora

A

▪Do nothing
– Commonly adopted
▪Care RE use of pre and probiotics
–Often no EBM to support their use
–May contain inappropriate or even pathogenic organisms
–Many unlikely to survive gastric acid
▪Equids – transfaunation
– Shown improvement in d+, appetite and speed of recovery

31
Q

Thrombophlebitis tx

A

▪ Broad spectrum antibiotics
– Used to prevent bacterial infection establishing within the thrombus
▪ Anti-inflammatories
– Systemic
-> Aspirin (to prevent further clot formation)
-> Other NSAIDs (will cause platelet activation)
– Topical (questionable benefit)
-> DMSO
-> Hot packs
▪ Heparin
– or analogues
– to prevent further clot build up
▪ Vasodilators
– Glyceryltrinitrate
– to try improve blood flow around the thrombus
▪Raise head
– For those where it is severe they have a risk of swelling of the head
– so raising it can help reduce swelling and promote drainage from the head

32
Q

Thrombophlebitis management

A

▪Alternative venous access
– Lateral thoracic
– Cephalic
▪With bilateral thrombosis, tracheostomy may be required (bc oedema of the head can result in upper airway obstruction
▪Surgical procedures to strip and/or graft the vein have been described but are rarely undertaken

33
Q

Coagulation disorders

A
  • excessive bleeding
  • excessive thrombosis
34
Q

Causes of excessive bleeding

A
  • hypocoagulation is the most common cause
    – can be caused by decreased amount or function of components of primary or secondary haemostasis
  • hyperfibrinolysis
    – been proposed to contribute to increased bleeding in several dz states, including trauma and postpartum haemorrhage
  • increase anticoagulant activity
    – can occur iatrogenically
35
Q

Causes of excessive thrombosis

A
  • hypercoagulation
  • hypofibrinolysis
  • decreased anticoagulant activity

It’s rare to encounter excessive thrombosis as a primary condition in horses.

Inflammation causes a variety of changes that promote both primary and secondary haemostasis and inhibit fibrinolysis and anticoagulant activity

36
Q

Tx for excessive thrombosis

A
  • Low-molecular-weight heparin
  • Unfractionated heparin
  • Clopidogrel
  • Aspirin

Prevents further clot formation around the thrombus

37
Q

Benefits of low-molecular-weight heparin vs unfractionated heparin

A

Low-molecular-weight heparin:
- less side effects and more predictable dose response
- difficult to monitor with aPP, requires measurement of anti-Xa activity or possibly viscoelastic coagulation testing
- Decreased jugular vein thrombosis cf unfractionated heparin

Unfractionated heparin:
- RBC agglutination and decreased platelet count possible
- degree and duration of effect unpredictable

38
Q

What are horses following SIRS or sepsis at a high risk of developing, following resolution of GI signs?

A
  • laminitis
39
Q

How to prevent laminitis post SIRS/sepsis

A
  • early identification and tx of SIRS/primary dz
  • icing
40
Q

Ventricular dysrhythmias

A

▪Occasionally occurs in horses
▪Electrolyte abnormalities or ‘myocarditis’ secondary to SIRS
▪Always check rhythms in animals with higher heart rates than expected for other clinical signs
▪These often compromise cardiac output and perfusion will improve if they can be resolved

41
Q

Approach to tx of ventricular dysrhythmias

A

▪Check electrolytes
▪Check volume status
▪IV magnesium sulphate – membrane stabilizer
▪IV lidocaine (one off doses (4/5 doses)and if short term success try infusion)
▪IV procainamide
– not readily available in most practices

42
Q

What can hypovolaemia mask and why?

A
  • anaemia (to a degree)
  • due to haemoconcentration

splenic contraction can mask blood loss for up to 24 hrs

43
Q

Parenteral nutrition for those struggling to control blood glucose

A
  • add in insulin to PPN/TPN and start at 5kCal/day
44
Q

What can BUN indicate?

A
  • a horse is burning its own protein reserves
45
Q

Where is the lateral thoracic vein accessed?

A
  • just behind the forelimb
46
Q

Is excessive thrombosis or excessive bleeding more common in equids?

A
  • excessive thrombosis