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

1.2. Acute hepatopathies

1.2.1. Dogs Infection Leptospira (vaccinated for), adenovirus CAV-1 (vacc), bacterial endotoxaemia/septicaemia, liver fluke Toxicity/drug induced - most common Phenobarbitone, carprofen, potentiated sulphonamides, fungi, aflatoxins, mycotoxins Neoplasia (e.g lymphoma) Genetic - acute hepatic necrosis in young Bedlingtons with Cu storage disease

1.2.2. Cats Infectious - bacterial endotoxaemia/septicaemia, FIP, toxoplasmosis If acute, often bacterial Toxicity/drug related - diazepam, phenobarbitone, potentiated sulphonamides

1.3. Chronic hepatopathies

1.3.1. Dogs Inflammatory (idiopathic, chronic progression, eosinophilic and granulomatous,, hepatitis, genetic hepatopathy/immune mediated, Cu toxicosis? (Doberman) Cirrhosis - from hepatitis Neoplastic, primary or secondary Drug related Glucocorticoids Developmental/congenital - portosystemic shunts, portal vein hypoplasia, Cu storage disease

1.3.2. Cats Inflammatory Lymphocytic cholangitis - may also involve pancreas and gut, immune mediated Chronic neutrophilic cholangitis Amyloidosis Problems in kidney? Neoplasia - lymphoma, biliary carcinoma Infectious - FIP, toxo 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 Haemopoietic/hepatobiliary Red cell haemolysis, always have significant regenerative anaemia Pre-hepatic vs hepatic vs post-hepatic AND sepsis 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 Hepatic Post hepatic jaundice - biliary function Bilirubin >50 umol/L, almost certainly hepatobiliary If <50, with other clinical signs then non-hepatic (inflammatory leukogram, pyrexia) 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) 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 Gut bacterial protein metabolite affecting brain function Also ammonia? Reduce bacterial protein metabolism and ammonia absorption via antibiotics Reduce protein consumption, avoid red meat Surgery Liver bypassed fully or partially Not cleansing blood Less hepatotrophic substances Intrahepatic (large breeds), extrahepatic (small breeds and cats), or multuple shunt types - sometimes congenital, mostly secondary to hepatic cirrhosis 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 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 Is the patient systemically well? secondary systemic effects? Are these causes, or consequences Vomiting? Loss of appetite? Location - small bowel, large bowel, mixed 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) 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 Stress, dehydration, anorexia, pain, primary GI disease, toxin ingestion, insufficient fibre - stress common, but often not all the problem Complete vs partial? Anorexia present? Primary or non-GI? Proximal or distal GI? Lesion? History - husbandry history, diet (regular? treats? very common), medical history, eating? faeces production? 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 Stabilisation - Oxygen, warmth, fluids, nutrition, analgesia, prokinetics Warmth - lose heat quickly (high surface area:volume ratio) Beware of overheating 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 Nutrition - fibre to stimulate gut, get to voluntarily eat, otherwise syringe fed, or nasogastric tube (less stress) Analgesia - NSAIDs (meloxicam) Ensure well hydrated, consider gastroprotectants - gut stasis always a risk Opioids - buprenorphine See signs of pain Prokinetics 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 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. Diet, antibiotics, post-weaning, bacterial enteritis, Coccidiosis, Viral enteritis History important - toxic ingestion? bacterial toxins possible? medical history e.g. antibiotics disrupting gut flora? Stabilisation Specific treatment Coccidia treatment - Toltrazuril or Trimethoprim-sulphonamide Colestyramine - bind enterotoxins Antibiotics - with bacterial enteritis - Metronidazole Probiotics?

4. Vomiting

4.1. Vomiting?

4.1.1. Coordinated activity Emetic reflex following nauseous stimulus Visual receptors, vagal and sympathetic afferent neurones, chemoreceptor trigger zone, vomiting centre (medulla oblongata) Cerebral, vestibular (i.e. motion sickness, pain, smell, stress), GIT afferent/efferent, , CRTZ (or direct to vomiting centre) Nausea - depression, hypersalivation, swallowing, unwell Retching

4.2. Regurgitation?

4.2.1. Passive, no coordinated movements Induced/exacerbated by altered food consistency, exercise etc. From oesophagus - no bile, not digested 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 NEed blood transfusion and iron supplementation

5.3. Anaesthesia

5.3.1. History, PE, haematocrit, total protein (RBC), electrolytes, acid-base status, haematology, biochemistry 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 Compromised immune defences (debilitated, GI injury, extensive GI resections, long surgery) - may need prophylactic antibiotics Septic peritonitis fatal in 50% Small intestine and colon surgery - use broad spectrum antibiotic with anaerobic coverage (cephalosporin OR amoxycillin-clavulante) And Metronidazole (colon) targeting anaerobes 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 Compromised blood supply, traumatic technique - -ve impact on healing Hypoproteinaemia, chemo, radio, steroids - -ve impact on wound healing Septic peritonitis after intestinal wound breakdown 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 Suture material - monofilament Monocryl lasts longer than PDS-II Staples - eversion, inversion, apposition

5.6. Exploratory laparotomy

5.6.1. Diagnose and correct intra-abdominal disease Biopsies Along Xiphisternum Care around structures - blood vessels

5.7. Stomach surgery, Gastrotomy

5.7.1. Repair in two layers: Mucosa and Submucosa Serosa and Muscularis Inverted lembert - prevent leakage Simple continuous Indicated for gastric foreign bodies, neoplasia etc. Endoscopic retrieval of foreign body or gastrotomy Neoplasia - metastases?

5.7.2. Partial gastrectomy 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 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 Radiating blood vessels Biopsy - incision along anti-mesenteric border avoiding blood vessels - Ellipse for biopsy Clamp with atraumatic clamps/fingers Sutures through submucosa

5.10.2. Large intestine/Colorectal surgery Do not biopsy unless lesion identified/suspected - higher risk of wound breakdown Colotomy - full thickness biopsy, like enterotomy, but with delayed healing 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 Megocolon - Flaccid enlargement, distension with faeces, loss function of colonic muscle Primary (cats, idiopathic) Secondary (pelvic fracture, intrapelvic space-occupying lesion, colorectal neoplasia, abscess, perineal hernia, innappropriate diet) Chronic constipation, tenesmus, vomiting, anorexia, weight loss Large colon with faecal material, dehydration, poor BCS No other underlying cause for constipation Perianal surgery Anal sac impaction, inflammation, infection 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 Anal furunculosis - infection of deep hair follicle - ulcerations of skin and anus GSD Immune-mediated Uncomfortable!

5.10.3. Resection and anastomosis Ischaemic necrosis, neoplasia Adenoma/adenocarcinoma (local LNs, liver, Siamese cats) Lymphoma Leiomyoma/leiomyosarcoma (LNs, liver) Mast cell Duodenal polyps Assess GI tract viability Normal morpholoy, blood vessels, peristaltic muscle contractions, colour

5.10.4. Foreign body (like stomach) Enterotomy Multiple enterotomies (string) Encourage post-op oral nutrition Complications: ileus, strictures, short-bowel syndrome (malabsorption, malnutrition), intestinal incision dehiscence

5.10.5. Intussusception Dehydration, depression, abdominal pain, palpable tubular mass, protrusion from anus Ultrasound, radiography Reduction OR resection 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. Blood tests PVC/TS (total solids/proteins) Low/normal PCV = anaemia/haemorrhage TS can dec. before PCV Blood smear/haematology Inflammation - neutrophilia.neutropenia with left shift Blood glucose - Hypoglycaemia Sepsis, anorexia (puppies/kittens) Other cause (addisons, insulin secreting neiplasia, xylitol toxicity) Biochem Inc. BUN/creatinine + USG Bilirubin/ALT/ALKP for hepatic Pancraetic lipase - pancreatitis, small intestinal disease, peritonitis, liver dx Radiography GDV - R-lateral double bubble L-lateral - rotated pylorus on DV Dec. serosal detail (FF, juvenile, inflammation) SI dilation - repeat, contrast study, US Free has (around liver? - surgical emergency US - free fluid, guided abdominocentesis, full abdomen imaging Abdominocentesis - be careful of spleen Diagnose septic peritonitis, RHF Monitor triage - with large loss, could go into shock 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 IV fluids - shock, dehydration Antiemetics (Macropitant, Metaclopramide, Ondansetron) Gastroprotectants (Omeprazole) Antibiotics - with infection, or high risk Nutrition - enteral, parenteral Specific toxicity treatments Analgesia 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