Acute Abdomen Module 1 Flashcards
What is vomiting?
The forceful expulsion of contents of the stomach and the proximal small intestine
What is vomiting triggered by?
The vomiting centre contains alpha-adrenergic and serotonin receptors that can be stimulated directly by irritants of indirectly following input from 4 principle area
- Chemoreceptor trigger zone: lies within the brain near vomiting zone - not protected by the BBB and this means easily permeated by irritants regardless of lipid solubility and molecular size
- Irritants: serotonin, neurokinin, histamine, acetylcholine, dopamine, opioids - Vestibular Nuclei - motion sickness
- Inner ear stimuli travel via CN8 stimulating histaminic, muscarine and NMDA receptors - Cerebral cortex and thalamus - emotionally charged sites and smells that cause nausea and emesis
- Enkephalageneric opioid anad bzp receptors
- Upper GI tract: irritation and distension of the upper GI tract
- Vagal and sympathetic afferent impulses to the v+ centre
How do you differentiate between vomiting and regurgitation?
Vomiting :
- prodromal signs of nausea - lipsmacking/nausea
- Active abdominal contractions
- May occur at any time
- Digested food
- Bile may be present
Regurgitation:
- No prodromal signs
- Passive ejection of food
- Usually shortly after eating
- Usually undigested food
- No bile
What are ddx for regurgitation
Oesophageal disease
- Hypomotility/megaoesophagus : congenital, primary idiopathic, secondary to MG, NM disease, – - Addisons, dysautonimia, lead toxicity
- Oesphagitis - drugs, reflux, lupus myositis
- Obstruction - Stricture, FB, vascular ring anomaly, hiatal hernia, GI intussusception
Ddx for vomiting
GI v. Ex-GI
GI
- Obstructions: FB, intuss, GDV, neoplasia, mesenteric torsion
- Dietary - allergy/intolerance/indescretion
- IBD
- GI ulceration
Ex. GI
- Uraemia
- Pancreatitis
- Endocrine: DKA, Addisons, hyperthy
- Liver disease
- Infections - pyo/peritonitis/prostatis
- Drug/toxin induced
- Vestibular disease
When v+ what questions should be asked and examined at PE?
- Toxins/diet/fb potential
- PUPD
- Weight loss
- Vaccination and travel history
- Drugs around house/or he is on
always do a rectal exam with d+ - anal glands/prostate/iliac ln - Check under tongue
- Abdo palp and ballottement
What tests would you run for vomiting ddx?
- Minimum database: PCV/TP, glucose, lactate, urea, blood smear, BG, electrolytes
- Biochemistry/haematology (neutropenia, imha, absence of stress leukogram, anaemia, PCV.TP for haem)
- PLI/Lipase (40% lipase not elevated with pancreatitis)
- Cortisol/ACTH stim
- Urinalysis - dipstick/usg/culture - renal v. Pre-renal
- Faecal analysis - snap Parvo and culture
- Imaging: survey rads abdo and thorax, pocus
Second line diagnostics-
Upper GI contrast- contraindicated in GI perf
Upper GI endoscopy
What are anti-emetic options?
- Maropitant - neurokinin receptor antagonist - centrallly and peripherally GI tract
- Low risk of SE, can combine
- Hypoplasa BM in puppies <8weeks - Metaclopromide
- Antiemetic via dopamine atangonaism acting both central and peripherally, also has gastric and pro-kinetic action and increase tone in the lower oesophgeal sphincter via agonism of serotonin
- Monitor for Aki with renal compromised animals
- Can have seizures/excitement and tremors
- Not really in cats as minimal dopamine receptors for cats to v+ - Ondansetron
- Serotonin receptor antagonist with both peripheral and central action
- Highly effective anti-emetic
- Oral and IV - Phenothiazines
- Chlorpromazine - dopamine and histamine receptor antagonist that acts centrally and v+ centre
- Used at lower doses than sedation
- Care with hepatic disease
What are GI protectant options and what are they used for?
- Ranitidine - reversible H2 antagonists - also promotes acetylcholinesterase inhibition which can prolong effects of acetylcholine on smooth muscle - prokinetic
- Slows metabolism of some drugs: metronidazole lidocaine - therapeutic overdose - Famotidine - H2 antagnists -
- Omeprazole/Pantoprazole - proton pump inhibitor - irreversible inhibitor - body needs to make new pumps and takes 2-3 days to reach maximal acid suppression
- IV better - as oral meds have first pass metabolism so take longer
- SE: dysbiosis, diarrhea, increased risk of aspiration pneumonia - Misprostol - prostaglandin analogue - acid inhibitory and mucosal protective, stimulates secretion of music and bicarb and increases gastric mucosal blood flow
- Reduces aspirin induced ulcers
- No effect on current ulcer and can cause abortion (people/animals) - Sucralfate - local barrier - complex of aluminium hydroxide and sucrose to form a past and binds to positively charged proteins of eroded mucosa
- Absorbs other drugs so administer at least 2 hours later any other drugs
Initial diagnostic plan for acute abdomens
Minimum database: PCV/TP, glucose, urea, lactate, blood smear and manual platelet count, Blood gas, electrolytes, BP, ECG, +/- coags/lungworm
What are the landmarks for AFAST
- Diaphragmatic-hepatic view: midline immediately caudal to xiphoid : can look for fluids between liver lobes, GB, angle cranially and can quick check pericardial/pleural space
- Spleno-renal view: left flank immediately caudal to last rib and ventral to lumbar muscles, can assess retroperitoneal fluid
- Cysto-colic view: midline over and immediately cranial to bladder
- Hepato-renal view: right flank immediately caudal to last rib and ventral to lumbar muscles : retroperitoneal fluid
GB wall edema - halo on GB wall
- Anaphyalxis
- Pericardial effusion
- RH failure
- Fluid overload
- GB disease
Stomach contracts 3x per min - no contraption - ileus
Pneumoperitoneum - B-lines over solid organs - kidneys
Risks: haemorrhage, infection, damage to orange
Left lateral best for sampling as best to miss the spleen
What are the tests that can be preformed on abdominal fluids
- Glucose
- Lactate
- Creatinine
- Potassium
- Total bil
- PCV/TS
- Smear
- Culture
What are the types of fluid that can be aspirated from an abdomen and how can they be identified?
- Haemoabdomen: PCV serum to fluid, not clotting, no/low platelets, erythrocytes within macrophages
- Uroabdomen: K+ serum to fluid >1.4x is 100%, creatinine >2x to that of peripheral blood is 100%
- Septic peritonitis: intracellular bacteria and degenerate neutrophils, glucose 1.1mol/L lower than peripheral bloods os 100% , lactate 2mmol/l high than peripheral blood 100%
- Bile peritonitis: total bil twice that of peripheral blood, bile pigment on cytology (golden-brown/blue-green/dark brown/black)
Steps to stabilisation of the acute abdomen
- Aggressive fluid resus
- Crystalloids
- Colloids
- Hypertonic saline - if no dehydrated
- Plasma - Anti-arrhythmic therapy
- sustained tachycardia over 160-180 with fluid correction, CE of poor CO (hypotension/decreased mentation), R on T
- Lidocaine - 2mg/kg bolus up to 3x followed by CRI - Analgesia
- Opioid
- Epidural
- Paracetamol
- - Anti-emetics
- Maropitatnt
- Metoclop - not if blockage
- Ondansetron
What are GDV risk factors
- 1st degree relatives with GDV
- higher thoracic depth to width ratio
- Lean body condition
- Advancing age
- Eating quickly/FB
- Laxity/agenesis of perigastric ligaments
- Stressy dog
- Diet related: dry food only, raise food bowls
- Failure of normal eructation and pyloric outflow mechanisms
