Acute Abdomen Module 2

Question 1

What are the steps of placing a stomach tube in GDV

Answer 1

1. Pre-measure the tube from the level of the nares to the last rib and place a tape marker
2. In an awake patient use a roll of medical tape or conforming bandage as a mouth gag through which the tube can be passed
3. Lubricate the tip and advance into oesophagus
4. Gentle pressure and a twisting motion can be applied if the meets resistance at the entrance of the stomach - blowing into the tube can also help
5. Correct tube placement is check in a conscious patient by pasting neck to ensure the tube ad trachea can be felt as two separate tubes
6. Decompression - lavage
7. When the tube is withdrawn it is essential to occlude or kink the end to prevent aspiration of stomach contents

Question 2

What are the steps for stabilising a GDV?

Answer 2

1. Aggressive fluid resus
   - Two wide bore catheters placed bilaterally and fluid pressure bagged in as shock disease in large dogs are usually litres
   - Isotonic crystalloids + hypertonic saline
2. Gastric decompression
   - Trocharisation - fast, easy and doesn’t require sedation
   - Orogastric intubation
3. Anti-arrhythmic therapy
   - Lidocaine
   - Analgesia
   - Lidocaine
   - Opioids
4. Anaesthesia
   - BZP/Opioid induction - avoid propofol
5. B/S abs if perforation/aspiration/pneumonia/prolonged GDV/neutropenia
   - Co-amox and cefuroxime

Question 3

Explain the different shocks a septic patient can present with

Answer 3

1. Hypovolemic shock - due to third space loss of fluids/dehydration/vomiting
2. Distributive shock: - loss of vasomotor tone between endogenous vasoconstrictors and vasodilators
   - Vasopressin deficiency - not a continuously made
   molecule, takes time to regenerate
   - NO plays a major role in vasodilatory state -
   increased production secondary to inflammatory
   factors - this leads to CS of: hyperaemic mm, short
   CRT, tachycardia, hyper dynamic pulses
   - Dysregulation of inflammatory factors and
   coagulation - pro inflame factors up regulate coag
   cascade - procoagulant state - will progress to
   hypocoagulanle state
3. Endothelial, mitochondrial and microcirculatory abnormalities - altered oxygen extraction ratio
   - Damage to glyococalyx
   - Activation of neutrophils and vascular permeability
   - Loss of vascular smooth muscle auto regulation

Cardiogenic shock - myocardial dysfunction

Question 4

What is the glyococalyx

Answer 4

• Layer between blood flow and endothelium
• Alters coagulation
• Localised production of NO if shear injury

Question 5

Outline the treatment plan for sepsis

Answer 5

Start with 1 and then if no response –> 2 then if no improvement try –> 1 again and if still no improvement step 3

1. Fluid resuscitation - make sure euvolaemic
   - Isotonic fluids –> hypertonic saline –> plasma (FP/FFP is clotting factors)

Vasopressors
Norepi/Noradrenaline - first choice
Should be using lowest dose to maintain BP >60mmHg
Start low and increase every 14 mins until normotensive or max dose

Myocardial dysfunction - echo to check for fractional shortening
Pimobendan - q12hrs for 24-48hrs, oral is okay - doesn’t increase o2 consumption
Dobutamine - increases O2 consumption

Broad spectrum IV - started as soon as sepsis confirmed - aspirate fluids
Some sepsis do not present with fluid at the beginning due to level of dehydration - serial POCUS
Coamox (20mg/kg q4-6hrs) +/- clinda or Cefuroxime + metro of marbo

Hypoglycaemia treatment
CRI best - 0.5g/kg of dextrose diluted 1:2 and administered for 5-10mins
2.5%-5% dextrose as often as necessary
If supplementing over 5% - give through a central line
CIRCI treatment
Sundrome in a subset of people with sepsis - where BP doesn’t response to fluid or vasopressor thought to be due to impaired hypothalamic-pituitary-adrenal axis function caused reduced cortisol modulation of vascular tone
Only for the patients where all the above has been exhausted
Hydrocortisone (1:1 mineralocorticoid and glucocorticoid function) 2.5-3mg/kg/day CRI
Calcium - check that ionised is above 1.1 ideally

Steps of stabilising a haemoabdomen

Fluid resuscitation
Crystalloid required - keep MAP 60mmHG and SBP 90mmHg
Autotransfusions - if massive losses - bleeds that occur between 1-24hrs do not need anticoagulant
Give through filter or giving set
Abdominal counter pressure
Oxygen
Pain relief

Question 6

Outline the treatment plan for sepsis

Answer 6

Start with 1 and then if no response –> 2 then if no improvement try –> 1 again and if still no improvement step 3

1. Fluid resuscitation - make sure euvolaemic
   
   • Isotonic fluids –> hypertonic saline –> plasma
     (FP/FFP is clotting factors)
2. Vasopressors
   
   • Norepi/Noradrenaline - first choice
     Should be using lowest dose to maintain BP
     >60mmHg
     - Start low and increase every 14 mins until
     normotensive or max dose
3. Myocardial dysfunction - echo to check for
   fractional shortening
   - Pimobendan - q12hrs for 24-48hrs, oral is okay -
   doesn’t increase o2 consumption
   - Dobutamine - increases O2 consumption
4. Broad spectrum IV - started as soon as sepsis
   confirmed - aspirate fluids
   - Some sepsis do not present with fluid at the
   beginning due to level of dehydration - serial
   - POCUS
   - Coamox (20mg/kg q4-6hrs) +/- clinda or
   Cefuroxime + metro of marbo
5. Hypoglycaemia treatment
   - CRI best - 0.5g/kg of dextrose diluted 1:2 and
   administered for 5-10mins
   - 2.5%-5% dextrose as often as necessary
   - If supplementing over 5% - give through a central
   line
6. CIRCI treatment
   - Syndrome in a subset of people with sepsis -
   where BP doesn’t response to fluid or
   vasopressor thought to be due to impaired
   hypothalamic-pituitary-adrenal axis function
   caused reduced cortisol modulation of vascular
   tone
   - Only for the patients where all the above has
   been exhausted
   - Hydrocortisone (1:1 mineralocorticoid and
   glucocorticoid function) 2.5-3mg/kg/day CRI
7. Calcium - check that ionised is above 1.1 ideally

Question 7

Steps of stabilising a haemoabdomen

Answer 7

1. Fluid resuscitation
   - Crystalloid required - keep MAP 60mmHG and
   SBP 90mmHg
2. Autotransfusions - if massive losses - bleeds that
   occur between 1-24hrs do not need anticoagulant
   - Give through filter or giving set
   - Abdominal counter pressure
3. Oxygen
4. Pain relief

Question 8

How is abdominal counter pressure achieved for a haemoabdomen?

Answer 8

• Used to try and slow bleeding in
  haemodynamically compromised patients
• Abdominal wraps are shown to reduce blood
  vessel diameter
  
  • Likely not useful for arterial bleeds
• Can compromise flow to hind limbs
• Contraindicated in patients with concurrent
  thoracic injuries or disease

1. Hindlimbs must be included in the wrap - to avoid
   excessively compromised venous return
2. Cast padding or towels are applied round the
   hindlimb, warming fireman in a barber pole
   technique and incorporating 50% overlap during
   wrapping
3. Next a layer of adhesive or cohesive bandage is
   applied for the padding again using a barber pole
   technique and incorporating 50% overlap of layers
   during wrapping
4. As the warp is continued cranially over the
   abdomen the patients heart rate, blood pressure,
   resp rate and oxygenation should be monitored
5. The wrap is continued to just caudal to the 13th
   rib - (if 13th rib included can cause resp
   compromise)
6. Should be able to get one finger under
7. Removal: wraps should be removed very slowly
   starting at the cranial end and using scissors to
   cute a couple of CM of warp every 15mins -
   monitor patient closely
8. Maximum length that wrap can stay in place is 12
   hours

Question 9

Steps to treat uroabdomen

Answer 9

1. Fluid therapy
   - Hypovolaemic shock
   - Hartmanns
2. Hyperkalaemia Treatment
   - Decreased cell excitability = cardiac bradycardia’s
   which are more pronounced in atria
   - K >7.5 insulin/dextrose
   - Calcium gluconate
3. Pain relief
   - Chemical peritonitis painful - opioid
4. Urinary diversion
   - Indwelling urinary catheter or abdominal
   catheter.- MILA attached to a urine collection
   system under local block
5. ABs
   - Likely with rupture
   - Confirm and sample first
   - >5 neutrophils per high power field on urine
   sediment exam

Question 10

Stabilisation of penetrating injuries

Answer 10

1. Survey radiographs for ruptures/hernias/gas
2. POCUS for free fluid
3. Fluid stabilisation
4. Pain relief
5. Abs post taking samples

Question 11

Explain the endocrine and exocrine portions of the pancreas?

Answer 11

Endocrine portions: consists of islets of langerhans - which secret insulin and glucagon and pancreatic hormones

Exocrine portions: acini cells and make up 98% of pancreatic volume
- They produce and secrete digestive enzymes
including proteases, amylases and lipases
- These enzymes are mostly produced and stored
within the acing cells as pro-enzymes and
zymogens
- Trypsinogen and chymotrupsinogen - which are
activated within the duodenum to trypsin and
chymotrypsin = they function to break down
ingested proteins within the duodenal lumen and
trypsin is the acitvotr of other proenzymes

Question 12

What are the three key protective mechanisms safeguarding the pancreas against auto digestion?

Answer 12

1. Enzymes are produced, stored and secreted in
   their inactive pro-enzyme form and are not
   activated till they reach the duodenum
2. Acinar cells produce inhibitor enzyme - serine
   protease inhibitor kazal type 1 - which works to
   inhibit any trypsin that has been prematurely
   activated within the acinar cells
3. Zymogens are stored within the membrane
   bound granules until hey are secreted from the
   acinar cells - these are kept away from
   intracellular environment

Question 13

What is pancreatitis triggered by?

Answer 13

Triggered by inappropriate early activation of zymogens within the pancreas and in particular early activation of trypsinogen to trypsin
- pancreas susceptible to ischaemia and episodes
of hypotension and oxidative stress which triggers
the above
- If sufficient pro-enzumes are activated within the
acinar cells the normal safeguards are
overwhelmed = local inflame = cytokines = SIRs =
third spacing of fluid = hypovolaemia/hypotension
= mods/aki/ards/dic

Question 14

Management step for pancreatitis?

Answer 14

1. Fluid therapy
   - Treat hypovolaemia - v+/third spacing and
   dehydration
   - Crystalloid boluses to resus and then correct
   dehydration
   - Reassess fluid plan at least twice daily
   - Consider jugular catheter placement
   - Plasma
2. Analgesia
   - NSAIDs - contraindicated
   - Regional anaesthesia - epidural catheter
   placement
3. Other Drugs
   - Multimodal anti-emetic therapy -
   maropitant/metaclop
   - Omeprazole - considered in patients with signs of
   gastric ulceration (haematemesis, meleana) or
   oesophagitis (regurg/eructation)
   - Abs - not routinely recommended, cats can have
   concurrent cholangiohepatitis
4. Plasma Transfusions
   - FFP contains macroglobulins - protease inhibitors
   that may activate circulating proteases - can also
   replace lost coagulation factors
   - No improvement in outcomes shown in studies
   - FP can be used as a natural collid - good for
   preservation of glycocalyx
5. DM mx - neutral insulin to manage temporarily

Question 15

Why is early enteral nutrition recommended?

Answer 15

1. Enterocytes receive nutrition from the gut lumen
   and without a supply of nutrients leads to
   mucosal atrophy, enterocyte apoptosis, increased
   mucosal permeability and bacterial translocation
2. Enteral nutrition should typically be started within
   24hrs of hospitalisation
3. If patient hasn’t eaten in 3-5 days need to
   introduce in increments
   • Day 1: 33%
   • Day 2: 66%
   • Day 3: 100%