Week 5 - GI Flashcards

1
Q

Where is the gallbladder located?

A

between quadrate and right medial lobes

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2
Q

How many hepatic ducts do dogs and cats have?

A

Dogs → 2-7
Cats → 1-5

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3
Q

Where does the commons bile duct lie?

A

from first hepatic duct to major duodenal papilla

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4
Q

What blood vessels supply the liver?

A

-Hepatic artery (20% of blood supply and 50% of O2) – more oxygenated blood

-Portal vein (80% of blood supply and 50% of O2)

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5
Q

What is the blood supply for the gallbladder?

A

Cystic artery (branch of hepatic artery)

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6
Q

Cholecystectomy is what?

A

Removal of gallbladder, stops at cystic duct

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7
Q

What is the ductal anatomy for a dog and cat? What’s the main difference?

A

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

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8
Q

What are some pre-operative considerations for hepatic surgery?

A
  1. 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.)
  2. hypoglycemia
    -Rarely a major problem in hepatic resections
    -Can occur in very small or debilitated patients
  3. 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

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9
Q

What are the 3 indications for liver surgery?

A
  1. Liver biopsy
    ‣ For investigation of diffuse hepatopathies or mass lesions
  2. Liver lobectomy
    ‣ Neoplasia
    ‣ Liver abscesses
    ‣ Liver lobe torsion
    ‣ Trauma
  3. intrahepatic portosystemic shunt
    ‣ Mostly treated using an interventional stent and coil approach
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10
Q

What are the 4 techniques for a liver biopsy?

A
  1. SUTURE FRACTURE TECHNIQUE
    -for diffuse hepatopathy - look for a liver lobe with pointed margin
    -Blood vessels and bile ducts will be ligated
  2. 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
  3. SKIN PUNCH TECHNIQUE
    -Skin punch used to harvest biopsy “cylinder”
    -Can fill biopsy holes with cores of gelatin sponge
  4. LAPAROSCOPIC LIVER BIOPSY
    -Subumbilical camera port, one instrument port in cranial left or right quadrant
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11
Q

What should you consider when biopsying a mass lesion off the liver?

A

▸ 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

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12
Q

What are tumor types of the liver?

A

‣ 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

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13
Q

What does a liver resection entail?

A

▪ 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

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14
Q

How would you diagnose and treat a liver abscess?

A

▪ 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

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15
Q

Biliary tract surgeries encompass what dz/pathologies?

A

-mucoceles
-bile peritonitis
-extra hepatic biliary obx

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16
Q

What are the 3 classifications for extra hepatic biliary obx?

A
  1. extraluminal
    -pancreatitis
    -neoplasia
  2. intraluminal
    -cholelithiasis
    -FB
    -neoplasia
  3. 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

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17
Q

How do you diagnose EHBO?

A

▪ 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

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18
Q

How does bile peritonitis happen? What causes it?

A

-Trauma

-Ruptured gall bladder mucocele

-Necrotizing cholecystitis

-Secondary to all causes of EHBO

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19
Q

Is bile peritonitis an emergency?

A

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??

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20
Q

How do you DIAGNOSE bile peritonitis?

A

▪ Laboratory parameters:
-Hyperbilirubinemia

▪ Imaging
-Plain radiography
-Abdominal ultrasound

▪ Cytology of effusion
-bile pigments

▪ Abdominocentesis
-if bilirubin in effusion is ≥2X serum considered diagnostic

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21
Q

Examples of hepatic pathologies and coinciding surgeries:

A

▪ 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

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22
Q

Why do mucoceles happen?

A

▪ Underlying lesion is cystic mucinous hyperplasia of gallbladder

▪ GB full of thick gel-like congealed bile

▪ C/S – from silent to EHBO ± rupture

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23
Q

What is the treatment of choice for mucoceles?

A

▪ Cholecystectomy is treatment of choice

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24
Q

How do you DIAGNOSE a mucocele?

A

▪ 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

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25
Q

What is post-op care after liver surgery?

A

▪ Continued fluid therapy

▪ Electrolytes and acid-base status

▪ Nutrition

▪ Antibiotic therapy

▪ Open abdominal drainage if deemed necessary

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26
Q

What are post-op complications after liver surgery?

A

▪ Further leakage of bile
▪ Peritonitis
▪ Hemorrage
▪ Pancreatitis
▪ Re-obstruction of biliary tree
▪ Ascending cholangiohepatitis with re-routing procedures
▪ Sepsis

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27
Q

What are the 3 functions of the colon?

A
  1. Fermentation of and nutrient production from indigestible ingesta by colonic flora (mainly bacterial)
    * Vitamins
    * Short chain fatty acids
    * Etc.
  2. Electrolyte and water absorption (mainly ascending & transverse)
  3. Storage of feces (mainly descending colon)
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28
Q

What’s the difference between constipation and obstipation?

A
  • Constipation - infrequent, difficult evacuation of dry/hard feces (still productive)
  • Obstipation - severe constipation, unable to defecate (requires medical intervention)
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29
Q

What are some predisposing factors for feline constipation?

A
  • 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)
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30
Q

What are functional obstipation? (vs. Mechanical)

A

-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
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31
Q

What are mechanical obstipation? (vs. Functional)

A

-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

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32
Q

Underlying causes for CONSTIPATION

A
  1. Idiopathic megacolon
    -a diagnosis of exclusion
    -cause unknown but suspected to be a disturbance in colonic smooth muscle contraction
  2. Chronic enteropathy (anecdotally)
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33
Q

Top causes of feline OBSTIPATION

A
  • Idiopathic megacolon (62%)
  • Orthopedic (23%)
  • Neurologic (11%) - hanging tail
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34
Q

What should a DIAGNOSTIC WORKUP for constipation/obstipation be?

A
  • 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
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35
Q

Colonic diameter (at the biggest/most dilated point) / L5

A

<1.3 normal
>1.5 megacolon

36
Q

How do you treat an obstipated cat BEFORE manual deobstipation?

A
  • 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

37
Q

What is deobstipation?

A

-done under GA with e-tube bc the dilation of the colon can cause vomiting

-manual evacuation of colon

38
Q

How do you MEDICALLY MANAGE a constipated/obstipated animal?

A

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

39
Q

What considerations should be made for a diet of a constipated/obstipated animal?

A
  • 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

40
Q

What stool softeners can be given to cats?

A
  • 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
41
Q

Which part of the pancreas is responsible for glucose metabolism?

A

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)

42
Q

What is the exocrine pancreas in charge of?

A

acinar cells and ducts

  • Digestive enzymes
  • Bicarbonate ions
  • Intrinsic Factor (IF) (in cats sole source, in dogs + stomach) - important for B12
  • Bactericidal peptide
43
Q

What’s the difference between dogs and cats and their common bile ducts, pancreatitic ducts, and accessory pancreatic ducts?

A

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.

44
Q

There are two forms for pancreatitis:

A

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

45
Q

Why doesn’t the pancreas auto digest itself

A

There are protective mechanisms such that enzymes are as zymogens/proforms - they are activated via enterokinase.

46
Q

Acute pancreatitis is the result of____________

A

trypsinogen activation

-once trypsinogen converts to trypsin, it starts a cascade for the other enzymes to be activated

  1. Autoactivation of cationic trypsinogen
  2. Activation of zymogens by thrombin
    * Bacterial toxemia
    * Ischemia
    * Hypoxia
  3. Apical block of zymogen granule secretion >
    colocalization of lysosomal proteases and zymogen granules
  4. Biliary-pancreatic reflux > enterokinase entering
47
Q

What perpetuates acute pancreatitis?

A
  • Increased vascular permeability
  • Influx of neutrophiles
  • Loss of apical paracellular barriers
48
Q

What is the pathway of acute pancreatitis?

A
  1. zymogen activation
  2. cell injury (bc activated zymogens are supposed to digest cells)
  3. pain
  4. systemic enzyme leakage
    and SIRS > MODS -multiple organ dysfunction (ARDS, AKI, DIC, arrythmias)
  5. Shock, Poor perfusion, hypoxia
49
Q

What are complications of acute pancreatitis?

A
  • 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
50
Q

Is pancreatitis sterile?

A

YES, inflammation occurs without microorganisms involvement

51
Q

What is the etiology of pancreatitis?

A

*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

52
Q

What are some CS of pancreatitis?

A

Lethargy
Hyporexia
Vomtining
Diarrhea
Weight loss
Dyspnea

53
Q

What are some physical exam findings of pancreatitis?

A

*Dehydration
*Hypothermia or hyperthermia/pyrexia
*Abdominal pain (30% in cats)
*Icterus
*Abdominal mass/ cranial abdominal organomegaly

54
Q

What will US usually look like with ACUTE PANCREATITIS?

A

*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

55
Q

What will US usually look like with CHRONIC PANCREATITIS?

A

*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!

56
Q

What does a CBC usually look like with pancreatitis?

A
  • Nonregenerative anemia
    -GI hemorrhage
    -Anemia of inflammatory disease
  • Increased PCV?
    -dehydration
  • Leukocytosis/leukopenia
  • +/- toxic change/left shift
  • Thrombocytopenia
    -consumption
57
Q

What does a Chemistry usually look like with pancreatitis ?

A
  • elevated ALT, ALP
    -direct insult by digestive enzymes, hypoxia
  • hyperbilirubinemia
    -biliary obstruction
  • Hypercholesterolemia and/or
    hypertriglyceridemia
    -biliary obstruction, pre-existing
58
Q

What happens to calcium with pancreatitis?

A

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!)

59
Q

What is the cPLI?

A

*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

60
Q

In addition to cPLI, Precision PSL also tests for pancreatitis measuring what?

A

*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

61
Q

What is the greyzone PLI references?

A

CAT
3.6-5.3

DOG
201-399

62
Q

A diagnosis of pancreatitis is based on what?

A

combo of:

signalment
clinical signs
laboratory findings
imaging findings

63
Q

How do you TREAT ACUTE pancreatitis?

A

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

64
Q

How do you treat CHRONIC pancreatitis?

A

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

65
Q

Controversial or NOT recommended pancreatic treatment

A
  1. antimicrobials
    -pancreatitis is usually sterile
  2. steroid
    -no benefits seen in humans
  3. NSAIDs
    -may potentially cause pancreatitis
  4. acid suppressants
    -not indicated unless evidence of ulceration is present
  5. plasma transfusion
    -controversial but usually not indicated unless patient is actively bleeding from DIC
  6. surgical intervention
    -not indicated unless pancreatic abscess is present
66
Q

What are the 3 different clinical syndromes of gastric dilation/volvulus?

A

-Gastric dilation

-Gastric dilation/volvulus - torsion

-Chronic volvulus

67
Q

The fundus is normal on which side of the stomach/body? How about pylorus?

A

Fundus - Left
Pylorus - Right

this is flipped with GDV

68
Q

What are some intrinsic and extrinsic factors that contribute to GDV development?

A

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

69
Q

Which breeds are more disposed to developing GDV?

A

-great danes
-irish setters
-standard poodles
-weimaraners
-rottweilers

70
Q

Common signalment for GDVs

A

▸ Large and Giant breeds predominate

▸ 10 months to 14 years

▸ No sex predilection

71
Q

CS of GDV

A

▸ Retching, non-productive vomiting

▸ Hypersalivation

▸ Restlessness

▸ Abdominal distention

▸ Weakness

▸ Collapse

72
Q

PE findings of GDV

A

▸ Distended, tympanic cranial abdomen
▸ Splenomegaly
▸ Hypovolemic shock
- pale, dry mucous membranes
- weak pulses
- prolonged capillary refill time
- tachypnea
- arrhythmias

73
Q

Lactate is a biomarker associated with _____________

A

global hypoperfusion

If >6mmol/L at presentation associated with higher chance of gastric necrosis

74
Q

Lactate has an effect on prognosis:

A

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

75
Q

How do you DIAGNOSE a GDV?

A

▸ Clinical signs

▸ Plain radiography
-Right lateral (lay animal on the right side)
-Ventrodorsal view

76
Q

How do you TREAT/MANAGE GDV?

A

▸ SURGICAL EMERGENCY!!

▸ Hemodynamic stabilization

▸ Gastric decompression

▸ Surgical management
-Correction of rotation ± gastric necrosis
-Prophylactic gastropexy

▸ Post-operative management

77
Q

How do you implement gastric decompression for GDV?

A

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

78
Q

When you open up the abdomen – what do you do to the stomach in a GDV?

A

-untwist the stomach
-asses viability once decompressed
-any possible gastric resection

79
Q

What type of suture patterns should you use for GDV?

A

-simple continuous - simplest and quickest
open gastropexy and has been shown to be highly against recurrence of GDV

80
Q

Gastropexy should be done on ______ side for a GDV

A

RIGHT

-take bites only in seromuscular layer

81
Q

Post-Op care for GDVs

A

▸ Fluid therapy

▸ Analgesics

▸ Gastric wall protection
-H2 receptor antagonists
-Coating agents
-Proton pump inhibitors

▸ Antibiotics

▸ Promotility agents (bc post-op ileum)
- e.g metoclopramide

82
Q

Post-Op complications for GDVs

A

▸ Cardiac arrythmias
▸ Aspiration pneumonia
▸ DIC
▸ Pancreatitis
▸ Hypoproteinemia
▸ Post-operative ileus and regurgitation
▸ Ongoing gastric necrosis
▸ Dehiscence of gastric resection site

83
Q

What is Acute Abdomen?

A

-Any animal the presents to the hospital with acute abdominal pain, or unstable condition due to abdominal disease

84
Q

What causes Acute Abdomens?

A

-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!

85
Q

What are the 6 signs of perfusion on PE?

A

-Mentation
-Mucous membrane color
-Capillary refill time
-Heart rate
-Pulse quality
-Extremity temperature