GI and hepatic Flashcards
3 stages to known ingestion/exposure
Decontamination
Assessment of effects
Treatment of symptoms
Decontamination if eaten - mucous membranes or stomach
Mucous membrane absorption; rapid, you’ve already missed the boat by presentation.
Gastric transit – Induce emesis or gastric decontamination
Window of opportunity; 2-8 hours in dogs, 2-12 hours in cats.
Apomorphine – licensed in dogs (very effective)
Alpha-2 agonist e.g. xylazine, medetomidine – not licensed but can be used in cats (moderately effective)
Avoid neurologically compromised patients e.g. obtunded due to aspiration risk
Avoid caustic substances “home remedies” e.g. hydrogen peroxide and causing oesophagitis and potential major complications
Stomach lavage; orogastric tube placed and warmed saline or hartmann’s used to flush the stomach
Always kink the tube on removal to avoid aspiration
Intestinal absorption
Arguably you could try to reduce intestinal transit time e.g. with laxatives but this will likely cause fluid and electrolyte losses unnecessarily.
Adsorbants – Activated charcoal
Does not work for all toxins (in the unknown toxin always worth trying)
‘Activation’ makes the charcoal massively porous which increases the surface area hugely
Carbon is reactive, and as a result some molecules will react with this surface and resultantly ‘bind’ to the surface of the carbon (adsorption)
Bound carbon-toxin -> defaecated
Causes black poo!!
Licensed formulation in UK is a liquid
Could be an aspiration risk
Powder available – off licence
Decontamination by skin exposure
Spot on products - quick
Some toxins not absorbed rather groomed and ingested
Decontamination is now surface based
Washing the skin is primarily performed with water
Can apply activated charcoal topically before washing off – messy!
Lipid soluble toxins can be removed easily with soap E.g. fairy liquid
Prolonged washing e.g. several minutes, can increase absorption of some chemicals (“wash in effect”)
Don’t use dilute bleach!
Take care when drying – absorption through abrasions
Decontamination by inhalation exposure
Very rare, but realistically decontamination for your patient is not possible.
Be careful yourself!
e.g. attending a scene to retrieve an animal
Washing the patient and aerosolising any toxin
Appropriate PPE e.g. a mask is always a good idea!
Decontamination by exposure that becomes toxin once metabolised
Once toxins are in the blood stream, we still have the opportunity to prevent them being metabolised:
The solution to pollution is dilution
The simplest approach is fluid therapy
Increase GFR and promote renal excretion
Increased organ perfusion and transit of compounds
E.g. 2 x Maintenance in the normally hydrated patient
Lipid infusion
Works well for lipid soluble compounds
Some evidence in humans for improved outcomes in non-lipid soluble
Fatty acids are a cardiac energy source
Minimal side effects – pulmonary lipid embolus, ?ARDS
Assessment of unknown toxin absorption
Neuro – seizures, ataxia, sedation
Cardiovascular – arrythmias, tachycardia, bradycardia, hypotension, hypertension
Gastrointestinal – vomiting and diarrhoea
But some will require investigations;
Renal – azotaemia, inappropriate USG
Hepatic – jaundice, elevations in ALT, ALP, bile acids
Haematological;
Clotting – prothrombin time, activated partial thromboplastin time, thromboelastography, point-of-care ultrasound
Anaemia – PCV, HCT.
Cardiovascular – ECG
Treatment of unknown toxin ingestion
Primarily symptomatic based on the system:
Neuro – Seizure control;
Diazepam IV x 3
Levetiracetam, phenobarbital IV
Propofol CRI
Hepatic damage – Supportive in nature
SAMe, Ursodeoxycholic acid, Silybin (milk thistle)
Acute Kidney Injury
IVFT +/- diuretics depending on urine output
Dialysis
Cardiovascular and Respiratory
Anti-arrythmics (e.g. lidocaine, amiodarone), beta-blockers (e.g. propranolol), parasympatholytics (e.g. atropine)
Blood pressure management – Fluid therapy, vasopressor (e.g. nor-adrenaline) or anti-hypertensives (e.g. amlodipine)
Oxygen therapy
Gastrointestinal
Vomiting – may not want to stop in the acute phase
Irretractable vomiting – anti-emetic (e.g. maropitant, metoclopramide, ondansetron) and fluid therapy
Diarrhoea – fluid therapy, gastro-intestinal diet
Haematological
Clotting – Vitamin K1, Plasma
Anaemia – Packed Red Blood Cells/Whole Blood.
Ingestion of ibuprofen - NSAID
COX inhibitors – reducing prostaglandin production.
PGE2 and PGI2 play important roles in:
Maintaining afferent renal blood flow
Maintaining GI mucous production, mucosal blood flow and cell turnover
Clinical signs – Haemorrhagic vomiting/diarrhoea, AKI.
Ibuprofen – 10mg/kg GI signs, 100mg/kg renal signs
Specific treatments:
H2 blockers – ranitidine/cimetidine
Proton pump inhibitor – omeprazole
Prostaglandin analogue – misoprostol (not in the pregnant patient)
Intralipid infusion
Ingestion of aspirin
Very similar to other NSAIDs but may have greater inhibition of Thromboxane in addition to prostaglandin inhibition.
Thromboxane (TXA2) is important for platelet function
Clinical signs
Thrombocytopathy – bleeding e.g. prolonged BMBT
Other NSAID associated
Treatment as for NSAIDs. Bleeding is unlikely to be significantly associated with death before other damage.
Paracetamol ingestion
Mechanism of action is believed to be via COX but there are other theories….
Metabolised by the liver, primarily by glucuronidation then sulphate conjugation.
Those pathways can become saturated, cytochrome P450 oxidises the excess into N-acetyl-p-benzoquinone (NAPQI) – which is really horrible!
NAPQI is de-toxified by glutathione – but glutathione stores can be exhausted.
Another potential metabolite produced is para-aminophenol (PAP) also not nice!
NAPQI causes
- Hepatic cell necrosis
- Nephrotoxicity
Glutathione or PAP causes
- Methemoglobinemia
- Prevents haemoglobin releasing oxygen
Clinical signs:
Brown mucous membranes (methemoglobin)
Jaundice, abdominal pain, lethargy, vomiting (direct hepatic damage)
AKI
Signs of hypoxia to tissues – brady or tachy arrythmias, peripheral oedema (especially the neck in dogs), respiratory distress.
Diagnostic clue – brown blood! In cats, Heinz body anaemia is suggestive.
Treatment:
N-acetyl cysteine – glutathione precursor which binds the toxic metabolites
H2 receptor antagonists (e.g. ranitidine) may reduce CP450 oxidation
Ascorbic acid (Vit C) may reduce methaemoglobin to haemoglobin
Liver support – SAMe, UDA, Silybin
AKI support – IVFT
GI support
Chocolate - theobromine and caffeine
Both examples of Methyl-Xanthines:
Increase catecholamine release
Increases cAMP -> increased intracellular calcium in cardiac and skeletal muscle (see first year cardiac action potential lecture)
Inhibits adenosine receptors
Primarily affects the cardiac rhythm and CNS.
Clinical signs:
Hyperactivity – important to ask owners about this!
Vomiting/diarrhoea
Arrythmias (usually tachy) with VPCs, tachypnoea
Seizures
Coma
Death
Treatment – as per system with some specifics:
Entero-hepatic recycling – so charcoal every 4-6 hours.
Severe cases may need intubation, and urinary catheterisation.
Xylitol ingestion
A sugar-alcohol, that mimics glucose but without a calorific contribution
Commonly a result of dogs eating chewing gum, can be found in other things, including some peanut butters (check the label).
Stimulates insulin release and hepatotoxic
Prolonged hypoglycaemia - 12-48 hours
Liver failure – within 72 hours
Weakness, collapse, seizures, coma, death
Jaundice
Diagnostic clues
- Hypoglycaemia
- Elevated ALT
Specific treatment:
Hepato-protectants – sAME, UDA, Silybin
Glucose supplementation
Oral vs IV
Bolus vs CRI
Try to avoid causing further insulin spikes
Pyrethroid exposure
Permethrin
Found in insecticides such as “Raid” and ant powders, as well as some “old school” flea products.
Cats are particularly susceptible as they lack the enzyme glucuronyl transferase required for the glucuronidation pathway.
Primarily act on neural axons (sodium channels):
Ataxia, tremors, disorientation and seizures
Dyspnoea and respiratory arrest
Hypersalivation and vomiting
Uncontrolled seizuring can cause rhabdomyolysis and subsequent AKI
Diagnosis is usually based on known exposure and clinical signs.
Treatment – general principles, but decontamination may involve the skin e.g. flea products.
Intralipid is excellent – permethrin is highly lipophilic!
Household cleaning produce exposure
Many household cleaning products contain either strong acids or alkalis, as a result they are all toxic.
Damage is primarily due to surface contact, in the case of ingestion this will the mucosa, particularly oral, oesophageal and gastric.
Clinical signs – oral pain, dysphagia, regurgitation, vomiting, etc.
Gastric decontamination is dangerous – risk of worsening oesophagitis
Dilution is the solution to pollution – oral water, or washing exposed surfaces with water
Severe oesophagitis can develop post exposure including strictures
Ethylene glycol - anti freeze exposure
Anti freeze is sweet tasting and similar in structure to alcohol. This means it’s tasty and rapidly absorbed!
Ethylene glycol is metabolised into glycoaldehyde, glycolic acid and oxalic acid.
Glycoaldehyde is neurotoxic, glycolic acid produces a severe acidosis and oxalic acid binds calcium leading to calcium oxalate crystal formation in several organs.
Mortality is high! Cats are particularly susceptible (1.5ml/kg compared to 6.6ml/kg for dogs)
Clinical signs:
Vomiting, lethargy, ataxia (looking drunk) – <12 hours
Tachyarrythmias, tachypnoea, hypocalcemia – 12-24 hours
AKI and Death – 24-72 hours
Diagnosis:
Increased osmolality due to EG <1h; not often available in first opinion
Acid/base analysis – profound normochloraemic metabolic acidosis
Hypocalcemia (ionised preferably)
Renal damage – Azotaemia, hyperkalaemia
Urinalysis – 3 - 6h may find calcium oxalate monohydrate crystals
Woods lamp on paws/mouth – some anti-freeze contains fluorescein dye
Ethylene glycol point of care tests are available
Specific Treatment (Don’t get your hopes up – be realistic with the owners)
Slowing the production of toxic metabolites is key – alcohol dehydrogenase
Medical ethanol (20%)
Vodka diluted with saline (20%)
2 – 3 days – formulary has guidelines.
Dialysis has improved outcomes – referral.
Rat poison - warfarin - exposure
Inhibit vitamin K epoxide reductase – i.e. they inhibit vitamin K synthesis.
Vitamin K is important in production of clotting factors II, VII, IX and X
Coagulopathy 36-72 hours post ingestion
Diagnosis:
PT prolongation initially (factor VII has the shortest half life)
aPTT prolongation follows
Cavitatory (large) bleeds – e.g. haemothorax
Petechiae are unlikely to be present!
Treatment specifics:
Vit K1 injectable initially, followed by oral – up to 8 weeks!
Fresh Frozen Plasma transfusion in severe cases – clotting factors
Raisin/grapes exposure
Toxic substance is not known – Tartaric acid has been implicated but the jury is still out.
Resultantly there is no known toxic dose – so any exposure should be considered serious.
However, retrospective reviews have highlighted a low degree of AKI developing after exposure – it’s difficult to gauge how worried we should actually be as a result.
Clinical sign – AKI
Treatment – general principles; including recommendation of IVFT for 48-72h in non-azotaemic animals.
Dialysis has improved outcomes where AKI is confirmed.
Recreational drugs exposure
- Cocaine, marijuana, opiates, ketamine
Cocaine – hyperactive, hyperthermia, tachyarrythmias, vomiting, ataxia, seizures.
Treatment – General principles, don’t forget the hyperthermia.
Marijuana – Vomiting, ‘paranoia’, ataxia, depression, coma, urinary incontinence
Treatment – general principles, Urinary Catheter, Intralipid, anxiolytics
Opiates (e.g. heroin) – Depression, lethargy, vomiting, constipation, hypoventilation
Treatment – general principles, reversal – naloxone, consider ventilating short term.
Ketamine – Ataxia, hallucinations, aggression, cataplexy (K-hole) and loss of patent airway
Treatment – general principles and consider intubation
Lily exposure
Toxic substance not known (probably a steroidal glycoalkaloid).
Cats are very sensitive – minimal ingestion can lead to AKI
Dogs are less sensitive – usually just GI signs
Any part of the plant is toxic – including the stamen and pollen – which cats will play with because they are ‘floppy’
Treatment is as per AKI, and dialysis has improved outcomes.
Consider the exposure though, particularly pollen…
Decontamination should also involve clipping/washing paws and around the mouth to prevent further exposure through grooming.
Onions, garlic, leeks, chives exposure
Large quantities need to be eaten for toxicity to develop, cats may be more sensitive.
Sulphur containing compounds which can cause:
Haemolysis
Heinz-body anaemia
Clinical signs:
Vomiting and diarrhoea
Tachycardia, tachypnoea, pale mucous membranes (anaemia)
Treatment:
General principles, in severe cases consider a transfusion.
Tremogenic mycotoxins exposure
Fungal metabolites (Penitrem A) that are neurotoxic – usually found on mouldy food!
Clinical signs:
Muscle tremors
Hyperaesthesia
Seizure, coma, death (thankfully very rare)
Treatment
General principles
But – diazepam is ineffective for the tremors, instead methocarbamol (trade name: Robaxin) should be used, but is off licence.
Intralipid may be useful as Penitrem A is considered lipid soluble.
Word of advice:
The prognosis for these cases is usually good but they can look severe – owner management is half the challenge!
Physiology of vomiting
Vomiting is an active reflex mediated via the emetic centre that can be stimulated via the chemoreceptor trigger zone (CRTZ) or GI tract, cerebral cortex, or vestibular system.
The CRTZ is full of various receptors and samples the blood for endogenous (e.g. azotaemia - renal, ammonia – hepatic, inflammatory mediators) or exogenous (e.g. drugs/toxins) substances.
This means in vomiting there are several systems to consider as possible causes.
Acute vs chronic vomiting
Important to begin differentiating possible causes.
Acute is more likely to be toxic, obstructive, inflammatory, infectious
Chronic is more likely to be chronic inflammatory, chronic infectious, metabolic/endocrine, neoplastic
But there is always cross-over! Consider the neoplastic mass growing for a while…
Acute vomiting
GI Tract – obstructive (FB, Neoplasia, parasitic, constipation, intussusception, volvulus), inflammatory (gastritis, gastroenteritis, colitis), mucosal insult (Dietary indiscretion, intolerance, sudden change in diet, toxins), infectious (bacterial/viral/parasitic), gastric stretch (you ate too much!)
Cerebral cortex – head trauma, sudden changes in ICP
Vestibular system – motion sickness, idiopathic vestibular disease, otitis interna
CRTZ
Endogenous: any systemic metabolic or endocrine disease resulting in acute changes e.g. DKA, Addisons, AKI, pancreatitis, acute hepatitis, peritonitis, prostatitis, pyometra, electrolyte disturbances, acid-base disturbances.
Exogenous: Toxins/Drugs
Chronic vomiting
Chronic vomiting
GI Tract – Chronic inflammatory (gastritis, gastroenteritis, colitis, chronic enteropathy), mucosal insult (Dietary intolerance), infectious (bacterial/viral/parasitic) obstructive (pyloric FB, Neoplasia, parasitic, constipation)
Cerebral cortex – Neoplasia/SOL, CNS disease
Vestibular system – chronic vestibular damage, otitis interna, neoplasia, cerebellar disease
CRTZ
Endogenous: any systemic metabolic or endocrine disease resulting in chronic changes e.g. diabetes mellitus, Addisons, chronic renal failure, liver failure, chronic pancreatitis, electrolyte disturbances, acid-base disturbances, hyperT4 (cats)
Exogenous: Toxins/Drugs less likely
Physiology of regurgitation and dysphagia
Physiology:
Passive expulsion of food from the pharynx or oesophagus.
This is a failure of swallowing (Dysphagia) and/or subsequent movement of food down the oesophagus to the stomach.
Realistically we should therefore be considering anatomy, particularly muscular and neurological systems involved in eating and swallowing.
Oesophagus – proximal and distal sphincters, food moves between them via peristalsis, controlled by the muscular wall (dogs – striated, cats – striated proximally and smooth distally)
What is dysphagia
Failure to prehend/bite (mouth) and initially swallow (pharynx):
Pain – on closing (e.g. dental disease, stomatitis) or on opening (e.g. retrobulbar abscess) or both (fractured jaw, TMJ disease).
Failure of neuro-muscular control – cranial nerves disease (V, VII, IX, X, XII), CNS disease, masticatory myositis, Botulism, myasthenia gravis.
Obstruction – pharyngeal FB, polyp, neoplasia, abscessation, lymphadenopathy
What is regurgitation
Failure to pass the oesophagus:
Dilatation (megaoesophagus) – may be congenital or occurring via either being active stretch (e.g. a chronic obstruction) or passive stretch (weak muscular wall, dysmotility) or idiopathic.
Obstruction – intraluminal (internal), mural (wall) or extramural (external)
Intraluminal – foreign body, stricture (e.g. secondary to oesophagitis)
Mural – neoplasia, inflammation
Extramural – Vascular ring anomaly, Hiatal Hernia, SOL (neoplasia)
Neuro-muscular disorder – Myasthenia gravis, botulism, tetanus, distemper, dysautonomia, peripheral neuropathy (e.g. autoimmune), Addisons, Hypothyroidism
Vomiting (active) vs regurgitation/dysphagia - passive
speak to the owner.
Vomiting is usually associated with retching, abdominal effort and lots of noise!
Regurgitation is passive, the food just ‘plops’ out, no retching, less noise.
The timing after food can be variable, so not that reliable, but does it look partially digested?
Treating regurgitation
Regurgitation - depends on the cause:
Megaoesophagus - Difficult to manage!
Omeprazole (PPI) – risk of worsened aspiration.
Feed from a height – 5-10 minutes! Small balls rather than big amounts. Could consider a feeding tube. Prognosis is often poor for chronic regurgitation.
Treat any concurrent/underlying disease e.g. hypothyroidism, PRAA, etc.
Oesophagitis – Pain relief!! Feeding Tube (bypass the oesophagus)
Oesophageal Foreign body – remove it, endoscopy, consider referral – rupture -> thoracotomy
Treating vomiting
Vomiting:
Consider the cause and treat the underlying.
Be aware – reaching for drugs may just mask the problem e.g. FB.
Maropitant – NK1 antagonist -> helps with centrally mediated Nausea e.g. metabolic, CRTZ, Vestibular
Metoclopramide – D2 receptor antagonist and 5-HT3 receptor antagonist -> Dual effect, CRTZ and lower oesophageal sphincter, BUT prokinetic so if FB present could rupture the GI Tract
Ondansetron – 5HT3 – centrally acting (CRTZ)
Nutrition:
Especially in chronic cases where BCS is reducing.
Consider feeding tubes – bypass the problem if you can; NO/NG tube, O tube, PEG tube.
TPN/PPN – parenteral nutrition; ideally a central line is required so not often a routine first opinion approach but it is feasible with good nursing.
Gastroprotectants
Omeprazole – Proton Pump Inhibitor, reduced H+ secretion -> useful for gastric ulceration (and reducing CSF production e.g. Syringomyelia). Long term use -> Dysbiosis. <3-4 weeks.
Misoprostol – Prostaglandin analogue – Increases mucosal blood flow and therefore healing e.g. ulcers – DON’T USE IN PREGNANCY – primarily used for NSAID tox
H2 Receptor antagonists e.g. cimetidine – reduce acid secretion, effectiveness is questionable, minimal research in small animal and not supportive.
Sucralfate – polyionic surfactant (anion) binds to damaged mucosa (positively charged proteins exposed) – weak evidence for use in oesophagitis, probably not helpful in gastric ulceration – use liquid not tablets.
How to localise vomit
Drinking ability normal if form stomach
Poor if from oropharynx,oesophagus
No pain on swallowing with stomach
pH will be +-<5 if from stomach
WIll be immediately after eating if from oropharynx or oesophagus
Will be bile if from stomach unless pyloric obstruction
Clinical signs of nausea
Hypersalivation
Lethargy
Anorexia
Lip smacking
Burping
Why is my patient vomiting
History – Diet, toxin exposure, medications, trauma
Clinical exam (peripheral receptors)
Non specific/Normal
Signs of nausea
Abdominal pain
Diarrhoea
Neurological exam (vomiting centre/vestibular)
Normal
Bloodwork (CRTZ); haematology, biochemistry, electrolytes, cPli, cortisol, pH
Non specific/Normal
Dehydration
Mild liver parameter elevations
Mildly elevated leukogram
Specific tests based on localisation
Ultrasound, Radiography, Endoscopy
Acute intestinal disease - vomiting - ddx
Trauma - foreign body, intussusception
Toxin - dietary indiscretion or drugs
Inflammatory - acute enteritis
- Immune mediated - dietary indiscretion, idiopathic
- Infectious - bacterial, viral, parasitic, protozoal
Main D/dx:
Obstruction (Foreign body or intussusception)
Acute enteritis
Dietary indiscretion/Toxin
Idiopathic lymphocytic/plasmacytic or eosinophilic
Infectious
Does it have a foreign body?
Do I have a foreign body?
Scavenger
Acute, severe vomiting
Abdominal pain or palpable obstruction
Pathophysiology
Obstruction - Increased pressure - Dilation and compromised perfusion - Inflammation/Necrosis - Vomiting
Diagnosis
Plain/Contrast Radiography
Ultrasonography
(CT)
(Endoscopy)
Treatment
Removal
Does it have intussusception?
Pathophysiology
Vigorous contraction of a segment of intestine into the lumen of the adjacent relaxed segment.
Obstruction Increased pressure Dilation and compromised perfusion Inflammation/Necrosis Vomiting
Causes
Idiopathic
Parasitism
Masses
Foreign bodies (linear)
Diagnosis
Ultrasound
Treatment
Surgery
Treatment of acute vomiting if not FB or intussusception?
Treatment
Symptomatic
Diet
IVFT
Anti-emetics - maropitant, metoclopramide
Chronic intestinal disease - vomiting ddx
Inflammatory
Immune mediated chronic enteritis
Dietary indiscretion
Idiopathic (Lymphocytic Plasmacytic/Eosinophilic)
Infectious chronic enteritis - SIBO
Neoplastic
Adenocarcinoma, Leiomyosarcoma, Mast Cell Tumour, Alimentary Lymphoma
Polyp
Metabolic
Endocrine; Addisons, DM, hyperT4
Hepatic, renal etc
Anomalous
Lymphangiectasia
If suspecting neoplasia for chronic vomiting - protocol
Clinical signs:
Chronic vomiting
Chronic diarrhoea
Melaena
Haematemesis
Weight loss
Clinical exam:
Lymphadenopathy?
Abdominal mass?
Abdominal pain?
Bloodwork:
Often normal
Dehydration?
Leukocytosis?
Hypercalcemia?
Anaemia?
High urea? (GI bleeding)
Gammopathy?
Elevated hepatic enzymes?
Radiography:
Abdominal mass
Constricting lesions or filling defects on contrast
Ultrasound:
Intestinal mass
Loss of wall layering
Reduced motility
Lymphadenopathy
Diagnosis
Biopsy (surgical or endoscopy) for diagnosis and grading
Staging with bloodwork and FNA/biopsy of local lymph nodes +/- spleen/liver
Treatment:
Surgery
Chemotherapy for mast cell tumours
Prognosis:
Grade dependent but usually 200-300 days
75% have mets at diagnosis
Mast cell tumours carry a very poor prognosis
If suspecting lymphoma for chronic vomiting - protocol
Clinical signs:
Chronic vomiting
Chronic diarrhoea
Melaena
Haematemesis
Weight loss
Clinical exam:
Lymphadenopathy?
Abdominal mass?
Abdominal pain?
Bloodwork:
Often normal
Dehydration?
Leukocytosis?
Hypercalcemia?
Anaemia?
High urea? (GI bleeding)
Gammopathy?
Elevated hepatic enzymes?
Radiography:
Abdominal mass
Constricting lesions or filling defects on contrast
Ultrasound:
May look similar to enteritis
Thickened abdominal wall on ultrasound
Loss of intestinal wall layering
Reduced motility
Lymphadenopathy
Diagnosis:
Biopsy/FNA for diagnosis or grading
Staging with bloodwork and FNA/biopsy of local lymph nodes +/- spleen/liver
Treatment:
Surgery
Chemotherapy (COP, CHOP, LOPP)
Prognosis:
Grade and lineage dependent (4-18m)
Poor in dogs except for colorectal
Better in cats
Anatomy of pancreas
Right and left lobes
Closely associated with duodenum and stomach
Dogs - 2 ducts – one opens next to common bile duct on major duodenal papilla, other on minor duodenal papilla
Cats – Single duct – fuses with bile duct before opening on major duodenal papilla Design flaw
Role of the pancreas
Pancreatic acinar cells - secrete digestive enzymes – zymogens – inactive form.
Enzyme inhibitors preventenzymes digesting pancreatic tissue
Zymogens secreted into intestinal lumen -cleaved by enterokinase which activates them
Ifenzyme activation happens in pancreas can lead to pancreatitis
Endocrine tissue – 1-2% of the pancreas, found in islets oflangerhans.
Common pancreatic diseases assocaited with vomiting
Acute pancreatitis
Inflammation of the pancreas
Sudden onset
Little or no permanent changes after recovery
Chronic pancreatitis
Continuing inflammatory disease
Irreversible morphological changes – fibrosis and atrophy
Can lead to permanent impairment of function
Risk factors for pancreatic disease
Hereditary– Min Schnauzers,Yorkshire Terriers, Boxers, CockerSpaniels, Poodles and Dachshund. Siamese and Bengal cats.
Hyperlipidaemia– Miniature Schnauzers (idiopathichypertriglyeridaemia)
High fat meal? (not in cats)
Obesity? (not in cats)
Cats – GI disease/vomiting - leading to bile reflux
Pancreatic ischaemia and hypoxia
shock, severe acute anaemia, dehydration, hypotension during GA,occlusion of venous outflow during abdominal surgery
Pancreatic trauma - RARE
eg. due to surgical biopsy, surgical manipulation, blunt abdominal trauma
Common pathway – decreased secretion of pancreatic juices - premature activation of digestive enzymes – damages the pancreas – inflammation leads to pancreatitis
Clinical signs of pancreatic disease
Acute pancreatitis:
Lethargy/weakness
Anorexia – suspect pancreatitis in any cat not eating/behaving normally
Vomiting
Diarrhoea
Severe acute pancreatitis:
Shock
Collapse
Abdominal pain
Cranial abdominal mass
Mild ascites
Dehydration
Fever
Jaundice - uncommon
Test findings with acute and chronic pancreatitis
Changes on CBC, biochem and urinalysis - nos specific and variable
Haem - anaemia, haemoconcentration, leukocytosis
Biochem - azotemia (prerenal),
increase liver enzymes (ALP),
hyperbilirubinaemia,
hyper or hypoglycaemia,
hypoalbuminaemia
hypertriglyceridaemia
Hypercholesterolaemia
Electrolytes
Hypokalaemia
Hypochloraemia
Hyponatraemia
Hypocalcaemia
cPL and fPL - specific and sensitive test for pancreatitis
If need urgent result then run Snap cPL. If negative the dog doesn’t have pancreatitis. If positive, send sample away for spec cPL to confirm diagnosis.
cTLIandfTLI(trypsin like immunoreactivity)
less sensitive and less specific
Increase rapidly in early stages of pancreatitis but decline quickly
Limited diagnostic utility
Amylaseandlipase
Non-specific assay
Influenced by hepatic, renal, intestinal disease and neoplasia
Don’t use to confirm pancreatitis
Radiography:
Evidence of pancreatitis rarely seen
Useful to rule out other differentials
Decreased detail/ground glass appearance cranial abdomen
Displacement of abdominal organs
Abdominal ultrasound:
Enlargement of pancreas
Localised peritoneal effusion
Decreased echogenicity – pancreatic necrosis
Hyperechogenicity – pancreatic fibrosis – chronic pancreatitis
Pancreatic duct dilation
User-dependent
Treatment plan for pancreatitis
Correct underlying fluid and electrolyte abnormalities
Treat underlying cause
Analgesia - buprenorphine, methanone, morphine, fentanyl patch, ketamine, or lidocaine CRI
Antiemetics - maropitant, ondanstron, metaclopramide
Antibiotics - if infectious cause identified - TMPS, enrofloxacin, metronidazole, clindamycin
Steroids
Start feeding once vomiting controlled
- High carb, low fat
Enteral feeding for anorexic cats
- NO tube
- Oesophagostomy tube
Outpatient support of cats:
Sub cutaneous fluids – 80-100ml Hartmann’s.
Administer via butterfly cannular (from bag or via syringe)
Maropitant 1mg/kg s/c or oral (off-license)
Mirtazapine – 2mg/cat transdermal
Buprenorphine 0.01-0.03mg/kg q 6-8h (sub-lingual or in-clinic im inj)
Complications of pancreatitis - pancreatis pseudocyst
Signs similar to pancreatitis
Significance unclear
Fluid of low cellularity
Treat medically or surgically
Complications of pancreatitis - pancreatic abscess
Bacterial infection only rarely present
Clin signs and lab abnormalitiessimilar topancreatitis
May palpate mass in cranial abdomen
Surgical excision best avoided unless evidence of enlarging mass +/-sepsis and not responding to medical therapy
Antimicrobials of questionable value
Long term treatment of pancreatitis
Prognosis
Avoid high-fat meals
Fat restricted diet – if recurrent bouts of pancreatitis
Oral pancreatic enzyme supplements
Cats with recurrent episodes – trial prednisolone 1mg/kg q 12-24h for 1 week tapering to 0.5mg/kg EOD as needed.
Prognosis
Unpredictable and varies in severity
Difficult to give accurate prognosis
Most cases given supportive care respond spontaneously and do well long term
Acute pancreatitis can be life-threatening
Poor prognosis if continue to refuse food or can’t tolerate food
Hypocalcaemia with acute necrotizing pancreatitis in cats has poor prognosis
Pancreatic neoplasia
Adenomas, adenocarcinoma, sarcoma
adenocarcinoma more common
Clinical signs:
Similar to chronic pancreatitis;
- vomiting, anorexia, diarrhoea, weight loss
May have signs associated with metastatic lesions eg lameness, dyspnoea, bone pain
Cats - paraneoplasic alopecia – shiny skin disease – alopeica of ventrum, limbs and face.
Laboratory abnormalities
Lab results may be unremarkable
May have neutrophilia,anaemia, hypokalaemia, bilirubinaemia, azotaemia, hyperglycaemia, increased liver enzyme activities
Some dogs have very high serum lipase
Hypercalcaemia can occur
Imaging findings
Radiography:
- decreased contrast cranial abdomen
- may see mass
- spleen may be caudally displaced
Ultrasonography
- soft tissue mass in region of pancreas
- if peritoneal effusion present – sample it for cytology
- FNA of mass can be attempted – only successful in 25% of cases
Diagnosis
Often made at ex-lap or at post-mortem
Biopsy and histology required to establish definitive diagnosis
Treatment
Adenomas
Benign – only treat if cause clin signs
If find mass during ex-lap – partial pancreatectomy to establish diagnosis
Adenocarcinomas
Often metastatic disease present by time of diagnosis.
Sites of metastatic disease – liver, abdominal and thoracic lymph nodes,mesentery, intestines,lungs.
If no gross metastatic lesions, surgical resection can be attempted
Clean surgical margins rarely achieved
Overall prognosis is grave
Nodular hyperplasia
Nodular hyperplasia
Occurs frequently in older cats and dogs
Small nodules found throughout exocrine portion of the pancreas
No capsule – adenomas have a capsule
Doesn’t lead to functional change
Doesn’t cause clinical signs
Usually incidental finding
Pancreatitis - histology
Pancreatitis
Oedematous tissue
Soft
Swollen
Fibrinous adhesions
Serosanguinous free abdominal fluid
Severely affected areas may be liquified
Pseudocysts
Haemorrhages (pancreas and omentum)
Abdominal fat necrosis
Histology – multifocal infiltration of neutrophils plus haemorrhage, necrosis, oedema and vessel thrombosis
Pathogenesis of acute gastritis
Treatment of acute gastritis
Disruption to mucosal barrier
Gastroparesis
Treatment of “Acute gastritis”
Time
Reduce toxin exposure
Fluid therapy if necessary
Anti-emetics - Maropitant (Ondansetron)
Reduce acid damage
Highly digestible diet- Low fat, low fibre, wet OR Hypoallergenic (e.g. Purina HA) fed little and often
- Proton pump inhibitors
- H2 antagonists
- Antacids
- Synthetic prostaglandins
- Sucralfate
Prokinetics
- Cisapride/Metoclopramide
Pathogenesis of chronic gastric disease
Gastroparesis - biochem, US, contrast radiography
Disruption to mucosal barrier - Bloods, US, gastroscopy, biopsy
Obstruction - Bloods, plain and contrast radiography, US
