Alimentary Disease in Small Animals

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Alimentary Disease in Small Animals by Mind Map: Alimentary Disease in Small Animals

1. Hepatic Disease

1.1. Diagnosis

1.1.1. Clinical pathology

1.1.1.1. Liver enzymes (ALT, ALP, GGT, AST), Bilirubin, bile acids, albumin/globulin (changes mean severe disease), cholesterol (important in liver function), glucose, urea (may be low), ammonia

1.1.2. Imaging - ultrasound more helpful for lesion location

1.1.3. Biopsy

1.1.3.1. Ultrasound guide, exploratory laparotomy, define the lesion, invasive and expensive

1.2. Acute hepatopathies

1.2.1. Dogs

1.2.1.1. Infection

1.2.1.1.1. Leptospira (vaccinated for), adenovirus CAV-1 (vacc), bacterial endotoxaemia/septicaemia, liver fluke

1.2.1.2. Toxicity/drug induced - most common

1.2.1.2.1. Phenobarbitone, carprofen, potentiated sulphonamides, fungi, aflatoxins, mycotoxins

1.2.1.3. Neoplasia (e.g lymphoma)

1.2.1.4. Genetic - acute hepatic necrosis in young Bedlingtons with Cu storage disease

1.2.2. Cats

1.2.2.1. Infectious - bacterial endotoxaemia/septicaemia, FIP, toxoplasmosis If acute, often bacterial

1.2.2.2. Toxicity/drug related - diazepam, phenobarbitone, potentiated sulphonamides

1.3. Chronic hepatopathies

1.3.1. Dogs

1.3.1.1. Inflammatory (idiopathic, chronic progression, eosinophilic and granulomatous,, hepatitis, genetic hepatopathy/immune mediated, Cu toxicosis? (Doberman)

1.3.1.2. Cirrhosis - from hepatitis

1.3.1.3. Neoplastic, primary or secondary

1.3.1.4. Drug related

1.3.1.4.1. Glucocorticoids

1.3.1.5. Developmental/congenital - portosystemic shunts, portal vein hypoplasia, Cu storage disease

1.3.2. Cats

1.3.2.1. Inflammatory

1.3.2.1.1. Lymphocytic cholangitis - may also involve pancreas and gut, immune mediated Chronic neutrophilic cholangitis

1.3.2.2. Amyloidosis

1.3.2.2.1. Problems in kidney?

1.3.2.3. Neoplasia - lymphoma, biliary carcinoma

1.3.2.4. Infectious - FIP, toxo

1.3.2.5. Congenital - vascular shunts

1.4. Treatment

1.4.1. Supportive fluids, electrolytes balance, antibiotics, diet, anti-oxidants

1.4.2. Ursodeoxyholic acid (secondary bile acid)

1.4.3. anti-inflammatories, corticosteroids, specific treatments

1.5. Jaundice/Icterus

1.5.1. Bilirubin from b/d of Hb

1.5.1.1. Haemopoietic/hepatobiliary

1.5.1.1.1. Red cell haemolysis, always have significant regenerative anaemia

1.5.1.2. Pre-hepatic vs hepatic vs post-hepatic AND sepsis

1.5.1.2.1. Pre-hepatic haemolysis - immune mediated haemolyticanaemia, microangiopathic, RBC damage, congenital, Babesia infection, toxins (Heinz body anaemia, onions, garlic, zinc)) - RBCs b/d in bloodstream/vessels

1.5.1.2.2. Hepatic

1.5.1.2.3. Post hepatic jaundice - biliary function

1.5.1.2.4. Bilirubin >50 umol/L, almost certainly hepatobiliary If <50, with other clinical signs then non-hepatic (inflammatory leukogram, pyrexia)

1.5.1.3. Low renal threshold of bilirubin in dogs - normal bilirubinuria Cats = pathological

1.5.2. Non-hepatic - fever, starvation, sepsis, significant inflammation - especially cats, increased bilirubin, less to intestines (rate-limiting step)

1.5.2.1. Interference of bilirubin transport by inflammatory mediators

1.6. Hepatic encephalopathy

1.6.1. Neuro dysfunction due to liver failure - from congenital portosystemic shunts (most common), acquired shunt, sudden hepatic failure

1.6.1.1. Gut bacterial protein metabolite affecting brain function Also ammonia?

1.6.1.1.1. Reduce bacterial protein metabolism and ammonia absorption via antibiotics Reduce protein consumption, avoid red meat Surgery

1.6.1.2. Liver bypassed fully or partially Not cleansing blood Less hepatotrophic substances

1.6.1.2.1. Intrahepatic (large breeds), extrahepatic (small breeds and cats), or multuple shunt types - sometimes congenital, mostly secondary to hepatic cirrhosis

1.6.1.3. Clinical signs related to eating, neuro signs, intermittent GIT signs, stunted growth, PU/PD, prolonged anaesthetic/sedative recovery, hypersalivation in cats, behaviour, seizures, copper colour irides in cats

1.6.1.3.1. Dec. serum albumin and/or globulin, slight inc in ALT and ALP, increased fasting blood ammonia, inc. fasting and post prandial serum bile acids, ammonium biurate crystals, erythrocyte microcytosis (dec. MCV), blood urea low, hypoglycaemia (i.e seizure) in small breeds

2. Diarrhoea

2.1. Classification: chronicity and location

2.1.1. History important Acute vs chronic Acute - treat symptomatically, self resolving (e.g. parvo, dietry indiscretion, something transient) Chronic - investigate, not often

2.1.1.1. Is the patient systemically well? secondary systemic effects? Are these causes, or consequences

2.1.1.1.1. Vomiting? Loss of appetite?

2.1.1.2. Location - small bowel, large bowel, mixed

2.1.1.2.1. Diagnostics: faecal anlysis, TLI (pancreatic insufficiency in small bowel D), endoscopy, therapeutic trial, biopsy, ultrasound Full blood count (FBC) Target product profile (TPP) (bacterial vs not) Faecal panels, cultures, ID toxins Metranidazole Small bowel only - Serum TLI (Trypsin like immunoreactivity, if suspect EPI) Cobalamin and folate - supplementation? Ultrasound - duodenal wall, jejunum/ileum, mucosa/muscularis thickened? Biopsy - endoscopy, laparotomy (if hypoproteinaemic, thickened intestinal walls, significant weight loss, hypercalcaemic, suspected neoplasia, unwilling to follow diagnostic plan) - don't biopsy chronic until: wormed, metranidazole, ruled out secondary GI disease (SB) Antibacterial trial? - Tetracycline, Tylosin Dietary trial (novel proteins, inc. fibre diet)

2.2. Alteration in normal defacation pattern - soft, unformed, increased water content and/or increased frequency Straining of large bowel to empty even though not much, or have a lot of faeces

2.2.1. Confuse with vaginal discharge? Anal sac discharge? Straining looks like constipation in lower bowel disease? Owner may not know if diarrhoea or not?

3. Small mammal GI disease

3.1. Faster GI transit time, hindgut fermenters, caecotrophy, fibre essential for gut motitlity, can't vomit

3.1.1. Certain oral antibiotics can cause reduction in intestinal bacteria - overgrowth of others (e.g. Clostridium) - toxin production, rapid death (rapid metabolism)

3.1.1.1. PLACE rule - cannot give orally Penicillins Lincosamides Aminoglycosides Cephalosporins Erythromycin

3.1.2. Gut stasis not a diagnosis Associated with anorexia usually Can be fatal or resolve successfully

3.1.2.1. Stress, dehydration, anorexia, pain, primary GI disease, toxin ingestion, insufficient fibre - stress common, but often not all the problem

3.1.2.1.1. Complete vs partial? Anorexia present? Primary or non-GI? Proximal or distal GI? Lesion?

3.1.2.1.2. History - husbandry history, diet (regular? treats? very common), medical history, eating? faeces production?

3.1.2.1.3. Clinical exam - dental exam, first principles Gut sounds reflect stasis (although could be temporary stress) - absence important if consistent, with normal droppings before AND after consult

3.1.2.2. Stabilisation - Oxygen, warmth, fluids, nutrition, analgesia, prokinetics

3.1.2.2.1. Warmth - lose heat quickly (high surface area:volume ratio) Beware of overheating

3.1.2.2.2. Fluids - dehydrated animal, or food in gut for long time dehydrate in the gut Maintenance higher than cats and dogs IV possible, often divided between IV and SC

3.1.2.2.3. Nutrition - fibre to stimulate gut, get to voluntarily eat, otherwise syringe fed, or nasogastric tube (less stress)

3.1.2.2.4. Analgesia - NSAIDs (meloxicam) Ensure well hydrated, consider gastroprotectants - gut stasis always a risk Opioids - buprenorphine See signs of pain

3.1.2.2.5. Prokinetics

3.1.2.3. Blood tests - systemic disease (lead/zinc levels good indicator), elevated glucose (elevated glucose is serious, diabetes not common) GA not always desirable, gastrocopy limited by full stomach, biopsy = risk of dehiscence and infection Hard to define lesion

3.1.2.3.1. Many can resolve with symptomatic treatment, but may have recurrence

3.1.3. Diarrhoea Acute vs chronic? Systemic signs if acute? Small vs large intestine? mixed? diarrhoea, or caecotroph? - may not eat caecotrophs as obese, bad teeth, spinal arthritis etc.

3.1.3.1. Diet, antibiotics, post-weaning, bacterial enteritis, Coccidiosis, Viral enteritis

3.1.3.1.1. History important - toxic ingestion? bacterial toxins possible? medical history e.g. antibiotics disrupting gut flora?

3.1.3.2. Stabilisation

3.1.3.3. Specific treatment

3.1.3.3.1. Coccidia treatment - Toltrazuril or Trimethoprim-sulphonamide

3.1.3.3.2. Colestyramine - bind enterotoxins

3.1.3.3.3. Antibiotics - with bacterial enteritis - Metronidazole

3.1.3.3.4. Probiotics?

4. Vomiting

4.1. Vomiting?

4.1.1. Coordinated activity

4.1.1.1. Emetic reflex following nauseous stimulus Visual receptors, vagal and sympathetic afferent neurones, chemoreceptor trigger zone, vomiting centre (medulla oblongata)

4.1.1.1.1. Cerebral, vestibular (i.e. motion sickness, pain, smell, stress), GIT afferent/efferent, , CRTZ (or direct to vomiting centre)

4.1.1.2. Nausea - depression, hypersalivation, swallowing, unwell

4.1.1.2.1. Retching

4.2. Regurgitation?

4.2.1. Passive, no coordinated movements

4.2.1.1. Induced/exacerbated by altered food consistency, exercise etc. From oesophagus - no bile, not digested

4.2.1.1.1. Persistent, suggests disease, can't treat symptomatically - investigate oesophagus

4.3. Gagging? - unproductive retrograde pharyngeal movements

4.4. Coughing?

5. GI surgery

5.1. Disease of wall of gastrointestinal tract Partial/complete obstruction of GI tract

5.2. Need to correct alkalosis, acidosis, electrolyte imbalance, dehydration etc. prior to surgery

5.2.1. IV isotonic crystalloids IV K+ supplementation

5.2.2. GI bleeding - haematemesis, melaena (vomit blood, digested blood faeces) - anaemia and hypoalbuminaemia

5.2.2.1. NEed blood transfusion and iron supplementation

5.3. Anaesthesia

5.3.1. History, PE, haematocrit, total protein (RBC), electrolytes, acid-base status, haematology, biochemistry

5.3.1.1. If not fit enough, stabilise and IV supplementation

5.4. Infection risks

5.4.1. Bacteria within GI tract (e.coli) in small intestine and colon

5.4.1.1. Compromised immune defences (debilitated, GI injury, extensive GI resections, long surgery) - may need prophylactic antibiotics

5.4.1.1.1. Septic peritonitis fatal in 50%

5.4.1.1.2. Small intestine and colon surgery - use broad spectrum antibiotic with anaerobic coverage (cephalosporin OR amoxycillin-clavulante) And Metronidazole (colon) targeting anaerobes

5.4.1.2. Dec. chance (colon - mechanical preparation (enema) Low residue diet, at least 12-24 hour starvation recommended

5.5. Healing - submucosa strongest layer (high collagen)

5.5.1. Rate decreases along GI tract - wound breakdown

5.5.1.1. Compromised blood supply, traumatic technique - -ve impact on healing

5.5.1.2. Hypoproteinaemia, chemo, radio, steroids - -ve impact on wound healing

5.5.1.3. Septic peritonitis after intestinal wound breakdown

5.5.1.3.1. Bacteria - endotoxin, cytokines, vasodilation, increased permeability of capillaries, fluid and protein in peritoneal cavity, hypovolaemia with dec. vascular oncotic pressure, hypovolaemic shock, systemic inflammatory response, Disseminated intravascular coagulation (DIC), and death

5.5.2. Repair - suture pattern choice - full thickness appositional, simple interrupted, simple continuous

5.5.2.1. Suture material - monofilament Monocryl lasts longer than PDS-II

5.5.2.2. Staples - eversion, inversion, apposition

5.6. Exploratory laparotomy

5.6.1. Diagnose and correct intra-abdominal disease Biopsies

5.6.1.1. Along Xiphisternum

5.6.1.2. Care around structures - blood vessels

5.7. Stomach surgery, Gastrotomy

5.7.1. Repair in two layers: Mucosa and Submucosa Serosa and Muscularis

5.7.1.1. Inverted lembert - prevent leakage

5.7.1.2. Simple continuous

5.7.1.3. Indicated for gastric foreign bodies, neoplasia etc.

5.7.1.3.1. Endoscopic retrieval of foreign body or gastrotomy

5.7.1.3.2. Neoplasia - metastases?

5.7.2. Partial gastrectomy

5.7.2.1. Same principle as gastrotomy, consider staples (eversion)

5.8. Liver

5.8.1. Biopsy - based on clinical signs, blood tests, US imaging, visualisation at surgery Nodules, masses

5.8.1.1. Consider FNA and trucut biopsy first under US guidance

5.9. Pancreas

5.9.1. Biopsy - take edge away from blood vessel, or from limb (not so many crucial blood supplies)

5.10. Intestinal surgery

5.10.1. Small intestines

5.10.1.1. Radiating blood vessels Biopsy - incision along anti-mesenteric border avoiding blood vessels - Ellipse for biopsy Clamp with atraumatic clamps/fingers

5.10.1.1.1. Sutures through submucosa

5.10.2. Large intestine/Colorectal surgery

5.10.2.1. Do not biopsy unless lesion identified/suspected - higher risk of wound breakdown

5.10.2.1.1. Colotomy - full thickness biopsy, like enterotomy, but with delayed healing

5.10.2.1.2. Resection Majority - loss of reservoir and absorptive capacities, inc faecal frequency, watery - >6cm associated with faecan incontinence Preserve ileocaecolic junction - ileal function, prevents retrograde bacteria into SI and bacterial overgrowth

5.10.2.2. Megocolon - Flaccid enlargement, distension with faeces, loss function of colonic muscle

5.10.2.2.1. Primary (cats, idiopathic) Secondary (pelvic fracture, intrapelvic space-occupying lesion, colorectal neoplasia, abscess, perineal hernia, innappropriate diet)

5.10.2.2.2. Chronic constipation, tenesmus, vomiting, anorexia, weight loss Large colon with faecal material, dehydration, poor BCS No other underlying cause for constipation

5.10.2.3. Perianal surgery

5.10.2.3.1. Anal sac impaction, inflammation, infection

5.10.2.3.2. Anal sac apocrine gland adenocarcinoma - highly malignant, 50% mets at diagnosis Paraneoplastic syndrome (hypercalcaemia, PU/PD) Diagnosis and staging - PE, haematology, biochem, urinalysis, FNA, incisional biopsy, radiography/US

5.10.2.3.3. Anal furunculosis - infection of deep hair follicle - ulcerations of skin and anus GSD Immune-mediated Uncomfortable!

5.10.3. Resection and anastomosis

5.10.3.1. Ischaemic necrosis, neoplasia

5.10.3.1.1. Adenoma/adenocarcinoma (local LNs, liver, Siamese cats) Lymphoma Leiomyoma/leiomyosarcoma (LNs, liver) Mast cell Duodenal polyps

5.10.3.2. Assess GI tract viability

5.10.3.2.1. Normal morpholoy, blood vessels, peristaltic muscle contractions, colour

5.10.4. Foreign body (like stomach)

5.10.4.1. Enterotomy Multiple enterotomies (string)

5.10.4.1.1. Encourage post-op oral nutrition

5.10.4.1.2. Complications: ileus, strictures, short-bowel syndrome (malabsorption, malnutrition), intestinal incision dehiscence

5.10.5. Intussusception

5.10.5.1. Dehydration, depression, abdominal pain, palpable tubular mass, protrusion from anus

5.10.5.1.1. Ultrasound, radiography

5.10.5.1.2. Reduction OR resection

5.10.5.1.3. Enteroplication - good prognosis in young

6. Abdominal pain

6.1. Acute pain, associated with acute organ disease

6.1.1. History, PE (triage) - emergency? Stabilisation? Localise pain, masses, fluid thrill etc.

6.1.1.1. Blood tests

6.1.1.1.1. PVC/TS (total solids/proteins) Low/normal PCV = anaemia/haemorrhage TS can dec. before PCV

6.1.1.1.2. Blood smear/haematology Inflammation - neutrophilia.neutropenia with left shift

6.1.1.1.3. Blood glucose - Hypoglycaemia Sepsis, anorexia (puppies/kittens) Other cause (addisons, insulin secreting neiplasia, xylitol toxicity)

6.1.1.1.4. Biochem Inc. BUN/creatinine + USG Bilirubin/ALT/ALKP for hepatic Pancraetic lipase - pancreatitis, small intestinal disease, peritonitis, liver dx

6.1.1.2. Radiography

6.1.1.2.1. GDV - R-lateral double bubble L-lateral - rotated pylorus on DV

6.1.1.2.2. Dec. serosal detail (FF, juvenile, inflammation) SI dilation - repeat, contrast study, US Free has (around liver? - surgical emergency

6.1.1.3. US - free fluid, guided abdominocentesis, full abdomen imaging

6.1.1.3.1. Abdominocentesis - be careful of spleen Diagnose septic peritonitis, RHF Monitor triage - with large loss, could go into shock

6.1.1.4. Diagnostic peritoneal lavage (if suspect peritonitis with no/minimal effusion) Exploratory laparotomy - surgical emergencies, no further plan

6.1.2. Distension of capsule/organ (neoplasia, dilation)

6.1.3. Traction (mesenteric torsion)

6.1.4. Ischaemia (infarction, necrosis)

6.1.5. Inflammation (e.g. gatrosnteritis)

6.1.6. VITAMIN D - Vascular (thrombosis, haemorrhage), Infection/Inflammation/Immune-mediated, Toxin/Trauma, Anomalous, Metabolic, Iatrogenic/Idiopathic, Neoplasia/Nutrition, Degenerative

6.1.7. Medical management

6.1.7.1. IV fluids - shock, dehydration

6.1.7.2. Antiemetics (Macropitant, Metaclopramide, Ondansetron)

6.1.7.3. Gastroprotectants (Omeprazole)

6.1.7.4. Antibiotics - with infection, or high risk

6.1.7.5. Nutrition - enteral, parenteral

6.1.7.6. Specific toxicity treatments

6.1.7.7. Analgesia

6.1.7.7.1. Pure opioids (methadone, morphine, fentanyl) Partial agonist opioid (buprenorphine) Ketamine infusion Lidocaine infusion - arrythmias Avoid NSAIDs (meloxicam, carprofen) - risk ulceration, kidney injury, contraindicated in anaesthesia