Week 5 - GI Flashcards
Where is the gallbladder located?
between quadrate and right medial lobes
How many hepatic ducts do dogs and cats have?
Dogs → 2-7
Cats → 1-5
Where does the commons bile duct lie?
from first hepatic duct to major duodenal papilla
What blood vessels supply the liver?
-Hepatic artery (20% of blood supply and 50% of O2) – more oxygenated blood
-Portal vein (80% of blood supply and 50% of O2)
What is the blood supply for the gallbladder?
Cystic artery (branch of hepatic artery)
Cholecystectomy is what?
Removal of gallbladder, stops at cystic duct
What is the ductal anatomy for a dog and cat? What’s the main difference?
Dogs
-Major duodenal papilla: Exit for CBD + Pancreatic duct SEPARATELY
-Minor duodenal papilla:: Exit for accessory pancreatic duct (V. IMP)
Cats
-Major duodenal papilla: Exit for CONJOINED CBD + PD
-Minor duodenal papilla: Only present in 20% of cats
Major difference: only 20% of cats have minor duodenal papilla. so if you damage the major duodenal papilla, you’ll have ramifications
What are some pre-operative considerations for hepatic surgery?
- hemorrhage
-Bleeding can be profuse and life-threatening
-Check coagulation profiles
-Blood type and cross-match patients
-Consider pre-treatment in some patients
-Be familiar with surgical techniques to prevent massive bleeding (e.g. use of stapling devices, pringle maneuver etc.) - hypoglycemia
-Rarely a major problem in hepatic resections
-Can occur in very small or debilitated patients - Anesthesia/drug metabolism
-Avoid drugs that undergo hepatic metabolism or are hepatotoxic
4.Bacteria
-Significant proportion of cats and dogs have resident hepatic microflora of mostly enteric origin
-Bile cultures more likely to yield positive culture than hepatic parenchyma
–make sure to empty entire gallbladder to prevent leakage and so hole can heal without leakage
-Good empirical choices of antibiotics
–fluoroquinolone with amoxicillin-clavulanate or clindamycin
What are the 3 indications for liver surgery?
- Liver biopsy
‣ For investigation of diffuse hepatopathies or mass lesions - Liver lobectomy
‣ Neoplasia
‣ Liver abscesses
‣ Liver lobe torsion
‣ Trauma - intrahepatic portosystemic shunt
‣ Mostly treated using an interventional stent and coil approach
What are the 4 techniques for a liver biopsy?
- SUTURE FRACTURE TECHNIQUE
-for diffuse hepatopathy - look for a liver lobe with pointed margin
-Blood vessels and bile ducts will be ligated - PLACEMENT OF OVERLAPPING SUTURES
-Helpful when areas that cannot be easily looped around need to be sampled
-Overlapping suture bites are taken to prevent bleeding - SKIN PUNCH TECHNIQUE
-Skin punch used to harvest biopsy “cylinder”
-Can fill biopsy holes with cores of gelatin sponge - LAPAROSCOPIC LIVER BIOPSY
-Subumbilical camera port, one instrument port in cranial left or right quadrant
What should you consider when biopsying a mass lesion off the liver?
▸ Many are very vascular and might bleed profusely
▸ If possible biopsy using a suture ligation technique for
added security or consider fine needle aspirate to see how
much it bleeds
▸ Other option is to go straight to liver lobectomy
What are tumor types of the liver?
‣ Metastatic lesions (most common)
‣ Primary liver tumors
-Hepatocellular carcinoma/adenoma - better prognosis than others
-Bile duct tumors (cholangiocellular carcinoma)
-Mesenchymal tumors
-Neuroendocrine tumors (carcinoids)
-Liver tumors can be massive, nodular or diffuse
CS of tumors: anorexia, lethargy, inappetence
What does a liver resection entail?
▪ Can be partial or complete
▪ Performed with blunt dissection and suture ligation or surgical staplers
‣ Thoracoabdominal stapler (TA-Covidien Inc.)
▪ Need knowledge of hepatic anatomy and blood supply
▪ Can resect up to approximately 70% of the liver acutely
How would you diagnose and treat a liver abscess?
▪ Uncommon, in older dogs with non-specific clinical signs: vomiting, lethargy, anorexia
▪ Can be single or multifocal
▪ Dx: Abdominal ultrasonography ± aspiration
▪ Micro-organisms: E. Coli, Staph spp. Enterococcus spp., Clostridium spp.
▪ Treatment:
‣ Medical: antibiotics and aspiration
‣ Surgical: lobectomy
‣ Drainage and alcoholization
Biliary tract surgeries encompass what dz/pathologies?
-mucoceles
-bile peritonitis
-extra hepatic biliary obx
What are the 3 classifications for extra hepatic biliary obx?
- extraluminal
-pancreatitis
-neoplasia - intraluminal
-cholelithiasis
-FB
-neoplasia - intramural
-neoplasia
▪ Inflammatory (~70%)
- Cholangiohepatitis (93%)
- Cholecystitis (89%)
- Cholelithiasis (40%)
- Pancreatitis (47%)
- Hepatic lipidosis (28%)
▪ Neoplastic (~30%)
- pancreatic adenocarcinoma
- biliary adenocarcinoma
▪ Occasional
- diaphragmatic hernia, fluke, FB
How do you diagnose EHBO?
▪ Hyperbilirubinemia
▪ Increased serum alkaline phosphatase, alanine
aminotransferase, gamma-glutamyl transferase
▪ Leucocytosis
▪ Hypoalbuminemia
▪ Urinalysis: Bilirubinuria or bilirubin crystals in the urine are
common.
▪ Coagulation profile: PT, PTT
▪ Fecal examination: Acholic feces, Trematode eggs - cats
▪ Plain radiography
-Cranial organomegaly
-Cholelithiasis – most radio-opaque
-peritonitis
▪ Abdominal ultrasound
-CBD & GB distension
-Note that distension doesn’t confirm obstruction
-Choleliths, neoplastic lesions, mucoceles
How does bile peritonitis happen? What causes it?
-Trauma
-Ruptured gall bladder mucocele
-Necrotizing cholecystitis
-Secondary to all causes of EHBO
Is bile peritonitis an emergency?
YES, it is an emergency
▪ Bile is an important adjuvant in peritonitis
▪ Causes chemical peritonitis
▪ Treatment of underlying leakage is imperative
▪ Thorough abdominal lavage
▪ Abdominal drainage – Open v. closed??
How do you DIAGNOSE bile peritonitis?
▪ Laboratory parameters:
-Hyperbilirubinemia
▪ Imaging
-Plain radiography
-Abdominal ultrasound
▪ Cytology of effusion
-bile pigments
▪ Abdominocentesis
-if bilirubin in effusion is ≥2X serum considered diagnostic
Examples of hepatic pathologies and coinciding surgeries:
▪ Cannot demonstrate patency of CBD
→ Biliary re-routing
▪ Functional EHBO but can catheterize
→ Biliary stenting/cholecystostomy
▪ Biliary mucocele/cholelithiasis/GB neoplasia or trauma
→ Cholecystectomy
▪ Traumatic injury to common bile duct
→ Primary closure or biliary rerouting
Why do mucoceles happen?
▪ Underlying lesion is cystic mucinous hyperplasia of gallbladder
▪ GB full of thick gel-like congealed bile
▪ C/S – from silent to EHBO ± rupture
What is the treatment of choice for mucoceles?
▪ Cholecystectomy is treatment of choice
How do you DIAGNOSE a mucocele?
▪ Primarily an ultrasonographic diagnosis
▪ Early lesion – bile sludge accumulation
- CAREFUL - Not all bile sludge
cases progress into mucocele
▪ Later – Classical stellate appearance (“kiwi” gall bladder)
-look like a kiwi
What is post-op care after liver surgery?
▪ Continued fluid therapy
▪ Electrolytes and acid-base status
▪ Nutrition
▪ Antibiotic therapy
▪ Open abdominal drainage if deemed necessary
What are post-op complications after liver surgery?
▪ Further leakage of bile
▪ Peritonitis
▪ Hemorrage
▪ Pancreatitis
▪ Re-obstruction of biliary tree
▪ Ascending cholangiohepatitis with re-routing procedures
▪ Sepsis
What are the 3 functions of the colon?
- Fermentation of and nutrient production from indigestible ingesta by colonic flora (mainly bacterial)
* Vitamins
* Short chain fatty acids
* Etc. - Electrolyte and water absorption (mainly ascending & transverse)
- Storage of feces (mainly descending colon)
What’s the difference between constipation and obstipation?
- Constipation - infrequent, difficult evacuation of dry/hard feces (still productive)
- Obstipation - severe constipation, unable to defecate (requires medical intervention)
What are some predisposing factors for feline constipation?
- Sedentary lifestyle
- Obesity?
- Hx of trauma
- Dehydration - like from CKD, etc
- Diet: some low fiber diets or diet high in indigestible material (e.g., bone fragments in cats that hunt)
- Underlying cause (see next)
What are functional obstipation? (vs. Mechanical)
-issue with colon propelling feces
- Neurologic disease
-Pelvic trauma (neurologic)
-Sacrocaudal luxations (AKA tail pull injuries)
-Dysautonomia
-Ganglionopathies (e.g., Hirschsprung’s disease) - Dehydration
-systemic disease (e.g., CKD, DM/DKA, chronic vomiting, neoplasia)
-lack of water access or anorexia - Electrolyte changes (severe)
-hypokalemia
-hypercalcemia
What are mechanical obstipation? (vs. Functional)
-physical obx
INTRALUMINAL
* colorectal masses
* Strictures
* atresia ani in kittens
* foreign bodies
EXTRAMURAL
* Orthopedic stenosis or fractures (trauma)
* masses
* pelvic trauma orthopedic, soft tissue
* Manx sacral deformity
Underlying causes for CONSTIPATION
- Idiopathic megacolon
-a diagnosis of exclusion
-cause unknown but suspected to be a disturbance in colonic smooth muscle contraction - Chronic enteropathy (anecdotally)
Top causes of feline OBSTIPATION
- Idiopathic megacolon (62%)
- Orthopedic (23%)
- Neurologic (11%) - hanging tail
What should a DIAGNOSTIC WORKUP for constipation/obstipation be?
- CBC
- Chemistry panel (with lytes)
- Urinalysis
- History
- Neurologic examination
- Sedated rectal exam
-Palpate for masses/ stricture/ stenosis
-Palpate pelvis for fractures/ stenosis - Radiographs
-Evaluation of amount and character of feces
-Evaluation of fractures, stenosis, mass, FB - Abdominal ultrasound
-extraluminal masses (similar to rads but
better soft tissue detail) - (Colonoscopy/proctoscopy)
-Intraluminal lesions (mass, stricture) - (Contrast radiographs)
-Barium enema if colonoscopy not possible
Colonic diameter (at the biggest/most dilated point) / L5
<1.3 normal
>1.5 megacolon
How do you treat an obstipated cat BEFORE manual deobstipation?
- Hospitalization
-rehydration with iv fluid therapy
-Serial warm water enemas 10ml/kg
-Monitoring of electrolytes (especially with frequent enemas, plus cats almost always have hypokalemia)
-if none of this works, THEN manually deobstipate
What is deobstipation?
-done under GA with e-tube bc the dilation of the colon can cause vomiting
-manual evacuation of colon
How do you MEDICALLY MANAGE a constipated/obstipated animal?
Overall strategy:
1. First time offenders may require less aggressive intervention
2. Recurrent offenders warrant more aggressive treatment
3. Obstipated cats need to be hospitalized
4. Address any underlying disease
5. Lifestyle changes
-increase physical activity to activate GI motility
-Intentional weight loss
-Diet
-can give prokinetics (cisapride, serotonin 5-HT4 agonist)
-fiber/laxatives
-ensure hydration
What considerations should be made for a diet of a constipated/obstipated animal?
- Canned diet to increase water intake
2 strategies:
Fiber:
-High fiber diets
-Fiber additions
–psyllium 1teasp-1tblsp/meal
–canned pumpkin 1-4 tblsp/ meal (careful with carb content!)
Highly digestible (minimal residue) diet to reduce stool volume
What stool softeners can be given to cats?
- Miralax® powder (OTC) ~1/4 tsp/cat po bid
- Lactulose syrup (Rx) ~0.5mL/kg po bid-tid
- both are hyperosmotic polysaccharide laxatives
- titrate “to effect” for a soft, but formed stool
Which part of the pancreas is responsible for glucose metabolism?
Endocrine - islet cells
* α cells – glucagon (15-20%)
* β cells – insulin, amylin (65-80%
* δ cells – somatostatin (3-10%)
* PP cells – pancreatic polypeptide
* ɛ cells - ghrelin <1% (mainly
produced by stomach)
What is the exocrine pancreas in charge of?
acinar cells and ducts
- Digestive enzymes
- Bicarbonate ions
- Intrinsic Factor (IF) (in cats sole source, in dogs + stomach) - important for B12
- Bactericidal peptide
What’s the difference between dogs and cats and their common bile ducts, pancreatitic ducts, and accessory pancreatic ducts?
DOGS
-Common bile duct enter and pancreatic duct enter close but NOT MERGED at the major duodenal papilla
CATS
-Common bile duct and and pancreatic
duct MERGE before opening at the major
duodenal papilla
Only 20% of cats have an accessory pancreatic duct. Most dogs have an accessory pancreatic duct.
There are two forms for pancreatitis:
Can be clinically indistinguishable
ACUTE
* fully reversible inflammation
* neutrophilic inflammation
* interstitial edema
* necrosis (mesenteric fat necrosis)
CHRONIC
* Irreversible histopathologic changes
* Lymphoplasmacytic inflammation
* fibrosis
* cystic acinar degeneration
* can complication of acute pancreatitis
* immune-mediated?
* Cats > dogs
*clinial course: subclinical or mild to shock, multi-organ failure, recurrent acute-on-chronic episodes, and death
Why doesn’t the pancreas auto digest itself
There are protective mechanisms such that enzymes are as zymogens/proforms - they are activated via enterokinase.
Acute pancreatitis is the result of____________
trypsinogen activation
-once trypsinogen converts to trypsin, it starts a cascade for the other enzymes to be activated
- Autoactivation of cationic trypsinogen
- Activation of zymogens by thrombin
* Bacterial toxemia
* Ischemia
* Hypoxia - Apical block of zymogen granule secretion >
colocalization of lysosomal proteases and zymogen granules - Biliary-pancreatic reflux > enterokinase entering
What perpetuates acute pancreatitis?
- Increased vascular permeability
- Influx of neutrophiles
- Loss of apical paracellular barriers
What is the pathway of acute pancreatitis?
- zymogen activation
- cell injury (bc activated zymogens are supposed to digest cells)
- pain
- systemic enzyme leakage
and SIRS > MODS -multiple organ dysfunction (ARDS, AKI, DIC, arrythmias) - Shock, Poor perfusion, hypoxia
What are complications of acute pancreatitis?
- Acute kidney injury (AKI)
- Systemic Inflammatory Response Syndrome (SIRS)
- Multiple organ dysfunction syndrome (MODS)
- Acute respiratory distress syndrome (ARDS)
- Pseudocysts, necrosis, abscesses
- Chronic pancreatitis
- Exocrine pancreatic insufficiency (EPI)
- Diabetes mellitus
Is pancreatitis sterile?
YES, inflammation occurs without microorganisms involvement
What is the etiology of pancreatitis?
*idiopathic
*risk factors
-breed - yorkie, mini schnauzer
-Hypertriglyceridemia
*Triglycerides > 862 mg/dL (> 9.7 mmol/L)
4.5x higher likelihood of having increased
cPLI
-Obesity
*Obesity is associated with HT and marked
increased cPLI, but not with clinical signs
-Dietary Indiscretion
*Access to trash and table scraps
*high-fat diet ?
-Endocrine Disoders
*Cushing’s
*Hypothyroidism
*Diabetes mellitus (DKA)
-concurrent disease
*chronic enteropathies
-Drugs
*documented in dogs: potassium bromide, phenobarbital, calcium, and L-asparaginase, many other single case reports
What are some CS of pancreatitis?
Lethargy
Hyporexia
Vomtining
Diarrhea
Weight loss
Dyspnea
What are some physical exam findings of pancreatitis?
*Dehydration
*Hypothermia or hyperthermia/pyrexia
*Abdominal pain (30% in cats)
*Icterus
*Abdominal mass/ cranial abdominal organomegaly
What will US usually look like with ACUTE PANCREATITIS?
*Pancreatic enlargement
*Hypoechoic pancreas
*Hyperechoic surrounding mesentery
*Abdominal effusion
*Cysts or abscesses
*Sensitivity 11-67% (severity-, machine-, and operator-dependent)
-enlarged hypoechoic pancreas with
hyperechoic surrounding mesentery is classic for
acute pancreatitis
What will US usually look like with CHRONIC PANCREATITIS?
*Hyperechoic or mixed echogenicity
*Dilated common bile duct
*Enlarged pancreas
*Irregular margins
*Pancreatic nodular hyperplasia can be normal in older cats and dogs!!
*Very unspecific
remember – never make a diagnosis of pancreatitis based on imaging findings alone!
What does a CBC usually look like with pancreatitis?
- Nonregenerative anemia
-GI hemorrhage
-Anemia of inflammatory disease - Increased PCV?
-dehydration - Leukocytosis/leukopenia
- +/- toxic change/left shift
- Thrombocytopenia
-consumption
What does a Chemistry usually look like with pancreatitis ?
- elevated ALT, ALP
-direct insult by digestive enzymes, hypoxia - hyperbilirubinemia
-biliary obstruction - Hypercholesterolemia and/or
hypertriglyceridemia
-biliary obstruction, pre-existing
What happens to calcium with pancreatitis?
HYPOCALCEMIA
*Pancreatic lipase: Pancreatic lipase reacts
with mesenteric fat to generate free fatty acids
> free fatty acid > chelate calcium salts >
precipitation of calcium soaps (saponification)
*Hypoalbuminemia
*Hypovitaminosis D (concurrent enteropathy!)
What is the cPLI?
*Quantitative and qualitative test (SNAP) available for testing for PANCREATITIS
*Sensitivity ranges from 64-93%
*Specificity 74%
*No correlation with disease severity
*Increases reported with other diseases including Cushing’s disease, IVDD, IMHA
In addition to cPLI, Precision PSL also tests for pancreatitis measuring what?
*1,2-o-dilauryl-rac-glycero glutaric acid (6’ methyl
resorufin)-ester (DGGR)
*Reference range 24-140 IU/L
*Sensitivity 93%
*Specificity 53%
*Moderate correlation with
spec cPL
Severe outliers noted with
Boxers
What is the greyzone PLI references?
CAT
3.6-5.3
DOG
201-399
A diagnosis of pancreatitis is based on what?
combo of:
signalment
clinical signs
laboratory findings
imaging findings
How do you TREAT ACUTE pancreatitis?
Fluid therapy
*balanced isotonic crystalloids
-LRS, Plasmalyte
*colloidal support
-Hetastarch
Nutrition
*Enteral feeding should be prioritized
*Oral, NG/NE tube, E tube
*Appetite stimulants
–Capromorelin (EntyceⓇ) – ghrelin
receptor agonist
–Mirtazapine
*Combine with anti-emetic
Antiemetics
*5HT3 antagonists
*ondansetron 0.2-0.5 mg/kg IV q 12-24h
*NK1 antagonists
*maropitant 1 mg/kg SQ q 24h
Analgesics
*partial & full μ-agonists
*buprenorphine 0.005-0.01 mg/kg SQ q 4-6h
*methadone 0.1-0.5 mg/kg SQ q 2-4h
How do you treat CHRONIC pancreatitis?
treatment of concurrent/underlying
conditions:
-hypertriglyceridemia
*low-fat diet
*omega-3 fatty acids (fish-oil)
*gemfibrozil, benzafibrate, etc.
-chronic enteropathy
*history, chemistry panel
*cobalamin, folate
Controversial or NOT recommended pancreatic treatment
- antimicrobials
-pancreatitis is usually sterile - steroid
-no benefits seen in humans - NSAIDs
-may potentially cause pancreatitis - acid suppressants
-not indicated unless evidence of ulceration is present - plasma transfusion
-controversial but usually not indicated unless patient is actively bleeding from DIC - surgical intervention
-not indicated unless pancreatic abscess is present
What are the 3 different clinical syndromes of gastric dilation/volvulus?
-Gastric dilation
-Gastric dilation/volvulus - torsion
-Chronic volvulus
The fundus is normal on which side of the stomach/body? How about pylorus?
Fundus - Left
Pylorus - Right
this is flipped with GDV
What are some intrinsic and extrinsic factors that contribute to GDV development?
INTRINSIC FACTORS
-Increased thoracic depth to width
ratio (deep chested dogs)
-First-degree relatives affected
-increasing age
-underweight dogs
EXTRINSIC FACTORS
-Dogs fed once daily
-Dogs fed from a raised food bowl
-Behavior that promotes aerophagia
-stress
-Happy” or “easygoing” dogs are protected
Which breeds are more disposed to developing GDV?
-great danes
-irish setters
-standard poodles
-weimaraners
-rottweilers
Common signalment for GDVs
▸ Large and Giant breeds predominate
▸ 10 months to 14 years
▸ No sex predilection
CS of GDV
▸ Retching, non-productive vomiting
▸ Hypersalivation
▸ Restlessness
▸ Abdominal distention
▸ Weakness
▸ Collapse
PE findings of GDV
▸ Distended, tympanic cranial abdomen
▸ Splenomegaly
▸ Hypovolemic shock
- pale, dry mucous membranes
- weak pulses
- prolonged capillary refill time
- tachypnea
- arrhythmias
Lactate is a biomarker associated with _____________
global hypoperfusion
If >6mmol/L at presentation associated with higher chance of gastric necrosis
Lactate has an effect on prognosis:
Final prognosis WORSE in dogs with:
▸ final lactate >6.4mmol/L (after fluid resuscitation)
▸ change in absolute lactate ≤4mmol/L
▸ % change in lactate ≤42.5%
▸ Initial Lactate <4mmol/L may be associated with fewer complications
▸ Initial Lactate of >6mmol/L may increase GN and complications
▸ DON’T USE LACTATE AS A REASON NOT TO DO SURGERY
How do you DIAGNOSE a GDV?
▸ Clinical signs
▸ Plain radiography
-Right lateral (lay animal on the right side)
-Ventrodorsal view
How do you TREAT/MANAGE GDV?
▸ SURGICAL EMERGENCY!!
▸ Hemodynamic stabilization
▸ Gastric decompression
▸ Surgical management
-Correction of rotation ± gastric necrosis
-Prophylactic gastropexy
▸ Post-operative management
How do you implement gastric decompression for GDV?
OROGASTRIC TUBE
–reach last rib
▸ Use no or mild sedation
-opioid ± diazepam/midazolam
-avoid acepromazine
▸ Administer oxygen
TROCARIZATION
- Aseptically prepare an area in the right or left paracostal space at site of greatest tympany
- 18g over the needle catheter
- Perform stabbing motion
- Remove stylet
- Can usually hear or smell gastric contents
When you open up the abdomen – what do you do to the stomach in a GDV?
-untwist the stomach
-asses viability once decompressed
-any possible gastric resection
What type of suture patterns should you use for GDV?
-simple continuous - simplest and quickest
open gastropexy and has been shown to be highly against recurrence of GDV
Gastropexy should be done on ______ side for a GDV
RIGHT
-take bites only in seromuscular layer
Post-Op care for GDVs
▸ Fluid therapy
▸ Analgesics
▸ Gastric wall protection
-H2 receptor antagonists
-Coating agents
-Proton pump inhibitors
▸ Antibiotics
▸ Promotility agents (bc post-op ileum)
- e.g metoclopramide
Post-Op complications for GDVs
▸ Cardiac arrythmias
▸ Aspiration pneumonia
▸ DIC
▸ Pancreatitis
▸ Hypoproteinemia
▸ Post-operative ileus and regurgitation
▸ Ongoing gastric necrosis
▸ Dehiscence of gastric resection site
What is Acute Abdomen?
-Any animal the presents to the hospital with acute abdominal pain, or unstable condition due to abdominal disease
What causes Acute Abdomens?
-Pancreatitis
-Peritonitis
-Pyometra
-Prostatitis
-Pyelonephritis
-Trauma
-Abdominal Hernia
-Sepsis
-Neoplasia
-GI obstruction
-GI perforation
-GI torsion
-Infarctions
-The list goes on an on and on!
What are the 6 signs of perfusion on PE?
-Mentation
-Mucous membrane color
-Capillary refill time
-Heart rate
-Pulse quality
-Extremity temperature
