Caroline Spelta equine health Flashcards

GIT, Neuro, haemat, card, resp

1
Q

(five observations in each categorie; mild, modertae and severe).

Describe signs of mild, moderate and severe signs of colic in the equine ?

A

Colic is not a disease but a syndrome (signs of colic)

Mild colic
- inappetence
- restlessness
- weight shifting
- flank watching
- stretching out
- posturing to urinate
- intermittent pawing

Moderate colic
- continuous pawing (front foot)
- head tossing
- penile protrusion
- yawning
- flehmening
- up and down
- dog sitting
- kicking at abdomen

Severe signs of colic
- violent pawing
- violent rolling
- collapsing / throwing themselves on the ground
- refusal to stand frim lateral recumbency

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2
Q

Identify a minimum of ten differentials for colic ?

A

Differentials for colic
(any condition which causes abdominal pain)

GIT
- stomach; ulcers, choke
- small intestine; endotoxaemia, hernia, volvulus, intussusception, IBD, ileus
- colon; sand impaction, right/left dorsal displacement, infarction, colitis
- distension, ischaemia and inflammation
Distension
- abnormal gas production / obstruction
- impaired motility / ileus
- extraluminal compression causing obstruction, neoplasia
- ischaemia, strangulation
extra-abdominal
- hepatic pain
- renal pain
- urinary system pain
- peritoneal pain
- reproductive system pain eg dystocia, testicular torsion
- laminitis
- cardiovascular; heart failure
- neurological; hendra, botulism
- metabolic hypocalcaemia

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3
Q

Describe why horses are predisposed to colic ?

A

Colic is the most common

Horses hind gut fermenter

Predisposition
Very large fermentative vat
- unable to reructate from fermentative vat

Domestication
- changed diet
- changed use / housing / management

Poor gastrointestinal design
- U turns, pelvic flexure
- Bottlenecks caecocolic valve

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4
Q

You identify colic; what follow up diagnostic tests could be utilised ?

A

Colic; Follow up diagnostic tests

  1. Baseline
    - Baseline values can be used to measure the horses response to treatment
    - Temperature 37-38.5
    - HR 36 +/- 10
    - Respiratory rate 12 +/- 4
    - Gut sounds +<2sec, digital pulses +
    - pressence of manure its volume and consistency
    - abdominal contour
    - auscultation, percussion and succussion (ping for gas on the right caecum)
    - secondary complications
  2. Nasogastric tubing
  3. Abdominal palpation per rectum
  4. Abdominocentesis - fluid analysis and cytology
  5. Abdominal ultrasound
  6. Gastroscopy
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5
Q

Describe the indication and safe technique for nasogastric intubation ?

A

Nasogastric intubation

Indication - pain
- primary indication is gastric decompression / comfort / effective pain relief
- horses stomach is only 10-15L
- evidence of apin
- tachycardia >60bpm pass stomach tube immediately
- provides an effective pain relief in cases of stomach distension
- if significant reflux returned, leave the tube in place with a one way valve (glove finger slit tip)
**
Procedure**
- Two bucket technique “in” and “out”
- use clean water in one bucket and put reflux into second bucket
- Total reflux = initial clean water - net reflux
- Significant reflux >4.5 L

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6
Q

Equine; Describe how you would carry out abdominocentesis ?

A

Abdominocentesis
Abdominocentesis of peritoneal fluid - changes in health of organs, especially intestine reflected as physical and cytological changes in fluid.

Can be used to differentiate
1. Intestinal injury (predominately small intestine); inflammation, ischaemia
2. Peritoneal cavity disease; - Peritonitis, bowel

Procedure
- lignocaine / local anaesthetic
- most ventral aspect of the linea alba, midline to slightly to the right (spleen located on the left)
- teat cannula or 18 guage needle

Sample collection
- Lithium heparin (green) = lactate, biochemistry
- EDTA; cytology
- Plain tube (red); bacterial culture

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7
Q

Describe your baseline for a physical examination of a horse ?

A

Physical exam - The key items

Temperature 37-38.5
Heart rate 36 +/- 10
Respirator 12 +/- 4
CRT <2 sec
Gut motility and digital pulses

  • Demeanor
  • Mucous membranes - colour, CRT
  • GIT sounds = (borborygmi), absent vrs present, hypomotile, herpermotile, ileocaecal flush
  • peripheral pulse qaulity
  • Abdominal contour
  • Abdominal auscultation, percussion and succussion (ping for gas distended viscus (caecum on the right).
  • Always assess for secondary complications.
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8
Q

How can naso gastric intubation be useful diagnostically ?

A

Objective measurements and findings
- Pain relief
- reflux present or absent (gastric accumulation or retrograde flow from the small intestine).
- normal volume 1-2 L
- if significant reflux leave the tube in

Assess PH
- Acidic = gastric outflow obstruction
- Alkaline = small intestine - retrograde flow
- Clinical response alleviation of pain and resultant decrease in heart rate.

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9
Q

What can a clinician detect upon rectal palpation in the horse ?

A

Abdominal palpation per rectum
Safety first - palpation of painful structures can elicit significant injury to the Veternarian.

What can we identify
- bowel distension; large vrs small
- pressence of tight bands (displacement or volvulus)
- large or small colon impactions
- masses or hernias
- ruptured viscus (bowel perforation) - loss of negative pressure and gritty serosa

Left dorsal quadrant
- caudal edge of the spleen
- nephrosplenic space
- nephrosplenic ligament
- left kidney

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10
Q

Identify potential issues with abdominal centesis ?

A

Complications of abdominocentesis

Enterocentesis
- seeding of bacteria into the peritoneal cavity (peritonitis)
- most commonly occurs in cases of large intestinal impaction
- broad spectrum antibiotic therapy - 5 days

Splenic tap
- sample PCV > systemic PCV
- unlikely to result in life threatening complication
- possible to induce splenic rupture

Omental evisceration
Haemorrhage

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11
Q

Describe what we should observe in a healthy patients peritoneal fluids ?

A

Normal peritoneal fluid

Colour
- normal; pale yellow / straw coloured
- blood may indicate; latrogenic contamination, splenic tap, diapedesis of RBCs
**
Transparency**
- normal is clear, should be able to read the news paper through sample
- Turbid; increased nucleated cells or inflammation

Protein
normal <20g/L
- high abdominal fluid protein - intestinal injury

Cytology
TNCC < 5 x 10^9 cells/L
normal; mononuclear (macrophages, some lymphocytes and non degenerate neutrophils
- peritoneal inflammation > 5 x 10^9 cells/L
- Bacterial peritonitis/ toxic change >25 x 10 ^ 9
- haemorrhage

Microbiology (red cap plan tube)
- bacterial culture and susceptability

Lactate (Ischaemia)
- Lactate is an indicator of tissue ichaemia normal <2m(mol/L
- Must compare plasma lactate to pertoneal lactate
- Plasma; reflects every body organ
- Peritoneal fluid; ultrafiltrate of plasma
- Peritoneal lactate >1.5x plasma lactate
- suggestive of local production of lactate within the abdominal cavity (ie tissue ischaemia)

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12
Q

Describe the indications and procedure procedure for gastroscopy / Duodenoscopy ?

A

Gastroscopy / Duodenoscopy

Indications
- recurrent colic
- poor performance
- notusually indicated in an acute colic episode

Procedure
- horses require 16 hours of fasting
- evaluation of stomach and proximal duodenum
- 3m scope required (adult horses)
- Detection of; gastric tumours, gastric emptying defects, impactions, equine gastric ulcer syndrome (EGUS)

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13
Q

Describe PCV / TP in the equine patient ?

A

PCV / TO
Simple and useful diagnostic test

PCV (Packed cell volume)
High indications
- haemoconcentration, splenic contraction (adrenaline) primary increase in red cell mass
- >54% at admission = increased mortality
- Low indications
- haemorrhage, haemolysis, failure of production

PCV must always be assessed in conjunction with total protein
- there may be multiple problems occuring in the same patient
- dehydration ^ PCV and TP

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14
Q

NSAIDS; Provide three examples, mechanism of actions, and dosgae in the equine patient ?

A

NSAIDS

MOA
- inhibition of the enzyme cycloxogenase COX, preventing the production of prostoglandins.
**
Flunixin meglumine**
- most effective NSAID for visceral and (occular pain)
- analgesic, anti-pyretic and anti-inflammatory
- reliable and predicatable analgesic effect
- onset: 15 mins
- duration 12 hours
- 1.1 mg/kg dose IV/PO q 12h
- never administer IM = clostridial myonecrosis

Meloxicam
- only licensed NSAID for use in foals
- no adverse effects at 2x dose for 7 days
- less inhibition of small intestinal mucosal repair after ischaemic injury than flunixin
- 0.6 mg/kg IV or PO (never IM)

Phenylbutazone
- most effective for musculoskeletal pain, fair soft tissue analgesia
- increasing dose does not increase analgesic effect (but will prolong duration until elimination)
- ideally no doses less then 12 hours apart
- 2.2-4.4 mg/Kg IV or PO (never IM)

More is not better - there is ceiling effect of analgesia (If your NSAID is not working, reconsider diagnosis +/- implement other analgesic protocol)

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15
Q

Provide examples of alpha-2 agonists and their indications, duration of action and potential contraindications ?

A

Alpha-2 Agonist (Treatment analgesia)

Sedatives, but effective short duration
- useful to give immediate control of signs of abdominal pain and allow diagnostic procedures to be performed safely.

Duration of action
- Xylazine; 20 mins
- Romifidine; 30 mins
- Detomidine; 30-45 mins

Disadvantages / Contraindications
- profound decrease in GIT motility as well as cardiovascular and respiratory depression
- ataxia
- increased sweating and urine production
- violent behaviour (RARE) = Alpha 2 angries

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16
Q

Provide an example, MOA and contraindication for the use of opiods in horses ?

A

Horses Opiods (treatment, analgesia)

Effective analgesics
Butorphanol 0.02-0.1 mg/kg IV q 4-12 hrs

Significant side effects
- agitation and hyperexcitability
- always administer in conjunction with an Alph-2 agonist (the only exemption is a really sick horse)
- inhibition of gastrointestinal motility - decreases faecal output.

17
Q

Describe the MOA, action and contraindication of Lignocaine ?

A

Lignocaine

MOA; Na channel blocker

Administration / effect
Local anaesthetic; intrarectal (topical)
- 20ml of 2% solution, increases rectal wall
- compliance
- may aid abdominal palpation and reduce rectal tear

1.3 mg/kg IV bolus
- analgesic, antiinflammatory - prokinetic (small intestine)
- reduces factors that may inhibit intestinal motility

Contraindication (Toxicity)
- skeletal muscle tremors, ataxia, seizures, collapse, and cardiac arrest
- care to not overdose (especially hypoproteinaemic patients)

18
Q

Describe the action and contraindication in the use of parafin oil ?

A

Parafin oil (mineral oil)

Actions
- measure of GIT gastrointestinal time
- 18hr, oil staining around the perineum
- 1-2 L
- takes up space where water could be administered

Contraindications
- hind leg dermatitis, cellultis if large volumes administered
- aspiration could cause a fatal pneumonia

19
Q

Reccomned laxatives for use in the equine patient ?

A

Laxatives for use in the equine patient

Magnesium sulphate
- irritant cathartic

Dioctyl sodium succinate (DSS)
- surface active agent with wetting and emulsifying properties
- reduces surface tension and allows water and fat to penetrate ingesta

Never co administer with Parafin oil - will faciliatte absorption of parafin into the circulation !

20
Q

Describe the component of a gram negative bacteria that results in endotoxaemia; and its structural components ?

A

Endotoxin - Lipopolysaccharide (LPS)

Endotoxin - is the structural components of the outer layer of gram negative bacteria (Lipopolysaccharide)
- which comprises 75% of the outer cell wall
- heat stable, in contrast to secreted toxins
- functions in the bacteria as a permeability barrier

Structural components
O specific chain
- highly variable between between different bacteria serotypes
- determines immunospecificity

Core polysaccaride region
- linking section conserved between strains

Lipid A
- highly conserved amongst all gram negative bacteria
- anchors LPS to the outer membrane
- is the toxic principle of LPS.

21
Q

Describe the pathophysiology of endotoxaemia in horses ?

A

Pathophysiology of endotoxaemia in horses.
(Pressence of endotoxin in the blood stream)

  1. Endotoxin released
    - rapid bacterial replication or death
    - bacteraemia (gram-ve in circulation), localised infection, endogenous / exogenous from GIT, translocation
  2. Endotoxin is absorbed across the gut barrier
    - facilitated by damaged gut barrier function
  3. Endotoxin becomes free in the blood stream

Innate immune response - pattern recognition

Sepsis
- systemic inflammatory response to bacterial infection
SIRS - Systemic inflammatory response **syndrome **
- A general systemic inflammatory process independant of cause
**MODS Multiple organ dysfunction syndrome **
- Insufficiency of two or more organ systems eg. azotaemia
**MOFS Multiple organ failure syndrome **
- Failure of 2 or more organ systems eg laminitis, DIC

22
Q

Describe how an acute injury to the equine GIT may predispose to endotoxaemia ?

A

Endotoxin / LPS and the GIT

Acute gastrointestinal injury (colic) increases GIT permeability to LPS.

Permeability increased;
- GIT rupture
- local ischaemia; stangulating lipoma
- inflammation; anterior enteritis
- systemic acidosis
- LPS detected in up to 40% of colic cases at admission.

23
Q

Describe the deleterious effects of endotoxin pressence in the blood stream ?

A

The deleterious effects of endotoxin in horses

  1. Interact with mononuclear phagocytes (monocytes and macrophages).
    - cytokines
    - Eicosanoids
    - Tissue factor
    - Kinins
    - free radicals
  2. Endotoxin contacts blood plasma
    - endotoxin interacts with normal plasma and tissue proteins to initiate enzymatic reactions.
    - important mediators of inflammatoionand haemostasis
    - margination, activation and extravasation of neutrophils
    - neutropenia

Inflammation = protective + destructive

24
Q

Define and describe (CARS) the bodys response to endotoxaemia ?

A

Cars ( Compensatory anti-inflammatory response syndrome)

Most horses don’t die - CARS
- stimuli evoke with delayed kinetics anti-inflammatory molecules that rein in the inflammatory response and restore homeostasis.
- horses at this stage are susceptable to opportunistic infections

25
# 4 cellular changes Describe the resultant host pathology resulting from endotoxaemia ?
Host pathology; Endotoxaemia This causes - increased procoagulant activity - reduced deformability of blood cells - altered vasomotor tone (dysfunction in blood vessel constriction) - vascular leak These changes on the cellular level result in; - hypoxia and lactic acidosis - multiple organ failure (MOFS) - multiple organ dysfunction (MODS)
26
Describe the clinical signs of equine endotoxaemia ?
Equine endotoxaemia; Clinical signs - hyperaemic (excess blood within vessels) - toxic + brick red / purple musculoskeletal membrane - anorexia - lethargy - sweating - discomfort - recumbancy - decreased borborygami - Tachypnoea (rapid breathing) - Tachycardia (rapid heart rate) Thrombosis (local coagulation), mucosal petechiae, and potential haemorrhage
27
# 5 observations Describe your strategy for diagnoses of endotoxaemia ?
Endotoxaemia Reflect number one disease +/- organ failure (renal, liver, blood gas) 1. Leukopenia due to neutropenia +/- band neutrophils - most specific indicator - toxic change less condensed chromatin and cytoplasmic basophilia (ribosomal RNA retention) - rebound neutrophilia on recover 2. Hypocalcaemia - cytokine induces parathyroid gland insufficiency, vitamin D deficieciency and impaired Ca metabolism 3. Hypoglycaemia - increased activity of neutrophils requires glucose - especially evident in foals 4. Coagulopathy - thrombocytopenia - hypofibrinogenaemia 4 Haemoconcentration
28
Identify the five strategies we apply to treat endotoxaemia in the horse ?
The five strategies to treat endotoxaemia in the horse 1. Inhibition of LPS release into the circulation 2. Scavenging 3. Inhibition of cellular activation by LPS 4. Inhibition of inflammatory mediator synthesis 5. Supportive care Supportive care - fluid therapy - acid base balance - management of coagulopathy - monitor - nutritional support
29
Describ the treatment strategy of endotoxaemia in the equine patient ?
5 Principles of treatment 1. Inhibition of LPS release into circulation. - nantimicrobial, ceftiofur sodium - beware killing bacteria may initially increase endotoxin 2. Scavenging LPS - Polymixin B, binds to lipid A of the LPS 3. Inhibition of cellular activation by LPS - Ethyl pyruvate - blocks the production of proinflammatory mediators - blocks LPS binding to macrophages 4. Inhibition of inflammatory mediator synthesis - flunixin meglumine (potentially nephrotoxic) - lignocaine (anti-inflammatory) - antioxidants 5. Supportive care - fluid therapy - acid base balance - management of coagulopathy