Surgery of the stomach Flashcards
What are the (general) treatment options for foreign bodies?
- Stabilize the patient FIRST (don’t stop the vomiting)
- Fluids/lytes/analgesics
- Gastroprotectants
- Specific therapies (toxins)
- FB removal options:
- Conservative
- Endoscopy
- Gastrotomy
- Induce emesis
What are the indications for conservative management of foriegn body ingestion?
Patient consumes something small and benign (not sharp) that is likely to just pass through
How is endoscopy used and when is it indicated for foreign body removal? What about gastrotomy?
- Endoscopy: use graspers on scope for small, regular FBs
- Can’t use for sharp objects (i.e., bone)
- Gastrotomy: open up stomach and remove object
- Large or sharp objects (unable to be removed via endoscopy)
When should you induce emesis following a foreign body ingestion?
Toxins–want to get rid of them ASAP
(Also small objects that could cause obstruction if passed through)
What are some examples of specific therapies for FB ingestion?
Lead: chelation with EDTA
Zinc: transfusion
What are the predisposing factors for gastric foreign body?
- Younger animals (“not as smart”)
- Previous history of FB ingestion
- Conditions that predispose to PICA (eating everything)
- Pancreatic exocrine insufficiency
- Hepatic encephalopathy
- Iron deficiency
What are clinical signs associated with gastric outflow obstruction?
- Intermittent vomiting
- Dietary modification alters signs
- Normal to decreased body condition
- Abdominal distension but no pain
What are the causes of gastric outflow?
- Congenital pyloric stenosis
- Acquired outflow obstruction
- FBs
- Chronic hypertrophic pyloric gastropathy
- Neoplasia
- Inflammatory/infiltrative disease
- Motility disorders
- Ulceration with scarring
- Extraluminal masses
Describe the blood supply to the stomach
R and L gastric arteries
Greater curvature: epiploic arteries
Fundic area: nerve bundle/fibers–gastric pacemaker (initiates normal contractions); avoid gastrotomy incision through pacemaker

Differentiate between congenital and acquired pyloric stenosis
- Congenital
- Hypertrophy of circular muscles
- Brachycephalic breeds (Boston terrier)
- Siamese cats (rare)
- Etiology unknown (excess gastrin?)
- Signs start at weaning
- Acquired
- Chronic hypertrophic pyloric gastropathy
- Stress major factor (along w/ any drug that mimics CNS)
- Mucosal and/or muscular hypertrophy
- Usually both tissue layers affected (unlike congenital)
- Small breeds–Lhaso apso, Shih Tzu
- Excitable or vicious
- Middle aged males
- Chronic hypertrophic pyloric gastropathy
What pathology is associated with congenital and acquired pyloric stenosis?
Hypertrophy of the muscular layer of the pylorus (and/or mucosal layer for acquired); etiology is unknown (excess gastrin?)
Is pyloric stenosis the same in cats and dogs?
Not completely
- Both species have vomiting as the major sign
- Cats can also have regurgitation due to secondary esophagitis and esophageal dysfunction
Which digestive hormone has been implicated in the etiology of both congenital and acquired pyloric stenosis?
Gastrin
What diagnosis modality can be used to differentiate congenital and acquired pyloric stenosis? How?
Ultrasound
- Congenital
- Layer thickness
- Differentiate neoplasia
- U/S confirms diagnosis
- Acquired
-
Pyloric wall and muscle thickness
- Muscularis < 4mm
- Pyloris < 9mm
-
Pyloric wall and muscle thickness

What are the pathological classifications of acquired pyloric stenosis?
- Grade 1 = muscular hypertrophy
- Rare
- Can look like congenital (use age + signalment to differeniate)
- Grade 2 = muscular and mucosal hypertrophy
- Most common
- Grade 3 = mucosal hyperplasia and muscular and submucosal inflammation
What are the specific goals of surgical correction of acquired pyloric stenosis? What treatments are available?
- Goal: reduce stenosis/increase gastric outflow
- Treatments
- Transverse pyloroplasty
- Y-U pyloroplasty
- Billroth 1
- Biopsy
What is a Fredet-Ramstedt pyloromyotomy? What are the advantages/disadvantages?
- 2cm incision through seromuscular layers of pylorus
- Advantages
- Quick and easy
- Lumen unopened–no risk of spilling abdominal contents
- Disadvantages
- Congenital pyloric stenosis only
- Stenosis may reoccur
What is a Heineke-Mikulicz pyloroplasty? What are the advantages/disadvantages?
- (Transverse pyloroplasty)
- 3-5cm full thickness, going into lumen
- Suture transversely–will significantly widen pyloric area
- Simple interrupted or continuous
- Advantages
- Mucosa exposed–can take biopsy
- Reoccurrence unlikely
- Disadvantages
- Lumen opened–risk of abdominal spillage
- Not usually effective with acquired pyloric stenosis (usually only works with grade 1)
What is a Y-U pyloroplasty? What are the advantages/disadvantages?
- Transport antral wall to pyloric region–>wider pylorus
- Advantages
- Will resolve grade 2 (most common)
- Allows mucosal resection
- Disadvantages
- Shortens gastric emptying time
- Must avoid hepatoduodenal ligament as can damage common bile duct

What is the Billroth 1 procedure? What are the advantages/disadvantages?
- Complete removal of the pylorus (pylorectomy with gastroduodenostomy)
- Very severe grade 3’s
- Advantages
- Abnormal tissue completely removed
- Larger increase in gastric outflow
- Disadvantages
- Technically difficult–much more advanced/complicated
- Longer procedure
- Increased risk of leakage

Where should gastrotomy incisions for exploration and removal of FBs be made? Why?
- Ventral midline approach from xyphoid to pubis
- Want to avoid vessels in the lesser curvature of the stomach that might be hit if you don’t stay along midline
- Want to avoid gastric pacemaker
- Stab incision in center of vessels
What are the principles/goals of suturing a gastrotomy incision? What factors influence closure choices?
- Submucosa is the holding layer–apposition of submucosa results in strong closure
- If you can invert the tissue (serosa-serosa contact) you can form a fibrin seal that will aid in a water-tight closure (required)
- Reduced gastric volume or tissue pliability complicate closure
- Closure technique is influenced by the pathology (if any) in the stomach wall and surgeon preference
What are the indications for a gastrectomy?
- Neoplasia
- Ischemic injury (GDV)
- Ulcer
- Trauma
What are the advantages/disadvantages of suturing the stomach with inverting suture patterns?
- Advantages
- Will allow fibrin seal formation which facilitates water-tight closure
- Disadvantages
- Impossible to do with very thickened walls
- Don’t get submucosa-to-submucosa contact (though should still be strong enough)
- Will not use in resection situations–length of stomach wall has already been shortened enough
Differentiate between the Cushing, Lembert, and Connell suture patterns
- Cushing = goes through submucosa but doesn’t go through mucosa or into the lumen
- Connell = same as Cushing but goes full thickness
- Lembert = double inverting
T/F: 60-70% of all gastric neoplasias are gastric adenocarcinomas
TRUE
What is the signalment of gastric adenocarcinomas?
- 2.5:1 male:female
- 7-10yrs
- Rare in cats
- Rough collie, Staff terrier, Belgian shepherd
What are the physical findings/pathology for gastric adenocarcinomas?
- Usually found at pyloric antrum and lesser curvature
- Metastasis–regional LN, liver
- Diffuse, thickened, and non-distensible
- Linitis plastica (leather bottle stomach)
- Ulcerated mucosal plaques
- Discrete polyploid
What are the treatment options for gastric adenocarcinomas?
- Aggressive surgical excision (> 5cm margins, remove regional LN for staging/biopsy)
- Palliative bypass procedure (non-resectable obstructive lesions)
- Chemotherapy (?)
- Gastrectomy
- Billroth 1
- Billroth 2
- Cholecystoenterostomy
What is the prognosis for gastric adenocarcinomas?
Poor, even with sx treatment
What is the signalment for leiomyosarcomas?
Usually middle aged–approx. 7yrs
What are the physical findings of leiomyosarcomas?
- Smooth muscle origin
- More common in cardia vs. pylorus
- Single or multiple
- Often ulcerate into gastric lumen
What is the prognosis for leiomyosarcomas?
MST = 21mo
Have high metastatic potential
What is the signalment for leiomyomas?
- Often in older patients (> 15yrs)
- Very slow growing
- Often incidental finding
T/F: Leiomyomas are benign
TRUE
What is the treatment and prognosis for gastric leiomyomas?
- Gastrotomy approach
- Submucosal resection –> resect tumor and take minimal margins –> good to go
- Prognosis = good–resection eliminates all signs
What is the signalment of pythiosis?
- Young, large breed working dogs
- Southeast U.S. (gulf states)
What are the clinical signs of pythiosis?
- Wt. loss
- Vomiting
- Diarrhea
- Hematochezia
- Sometimes palpable abdominal mass and increased mesenteric lymph nodes
T/F: Pythiosis has a slow growth rate but an extensive nature
FALSE–has a fast growth rate
What does pythiosis infiltrate?
Submucosa and muscularis layers of stomach and small intestines
How can you diagnose pythiosis (oomycosis/pythium insidiosum)?
- Endoscopy–difficult to find organism
- Histo
- Eosinophilic pyogranulomatous inflammation
- Deep tissue samples of fibrotic material can reveal organism
- ELISA tests for P. insidiosum antibodies

How is pythiosis treated? What is the prognosis?
- Surgical excision with 3-4cm borders
- Combined with medical treatment
- Itraconazole and terbinafine
- Immunotherapy–P. insidiosum vaccine
- Monitor for recurrence w/ ELISA 2-3mo post-op
- Prognosis: guarded to poor
What is a Billroth II gastroenterostomy? When is it indicated?
- Remove part of the proximal duodenum and stomach (gastrojejunostomy)
- Indicated when resection of the stomach is so proximal to limit end to end anastomosis
- Allows extensive gastrectomy without tension on suture
What are some complications of the Billroth II procedure?
- Alkaline gastritis (bile and pancreatic secretions flow into stomach)
- “Blind loop” syndrome–gastric contents move orally and putrefy
- Marginal ulceration–ulceration of jejunal mucosa (not used to seeing acidic contents)
What is the difference between acute gastric dilation, chronic gastric volvulus, and acute gastric dilation + volvulus?
- Acute gastric dilation
- No volvulus seen
- Distended stomach but in a normal position
- Chronic gastric volvulus
- Slight malposition
- Vomiting and eructation
- Gastropexy
- Acute GDV
- Distension of the stomach and rotation of the stomach on its mesenteric axis
- Surgical disease
- Also called gastric torsion
What are the predisposing factors for GDV?
- Large/giant breeds (G. dane, St. Bernard, S. poodle)
- Deep chested dogs
- Inc. depth to width ratio
- Harder to eructate
- 1st degree relative
- Faster eating
- Larger volumes daily
- Raised food bowls
- Post prandial activity
- Fats and oils
- Restricting water before/after feeding
- Age–ligaments
- Post splenectomy (?)
- Underweight dogs
- Intact females
- Males >> females
- Temperament
What foods decrease the risk of GDV?
Eggs or fish–very easily digested proteins
What is the pathophysiology leading up to gastric dilation and volvulus (GDV)?
- Distension from gas/fluid
- Distension alters pyloric/esophageal sphincter position
- Limited eructation and bacterial fermentation causes further distension
- Further distension –> body of stomach rotates clockwise along the long axis of the esophagus
- Rotation of the body causes pylorus to rotate cranioventrally from right to left
- Pylorus will rest along the left body wall on top of the esophagus and the gastric body to the right

What are the 2 types of rotation in GDV?
- Clockwise
- Much more common
- 70-360 degree rotation
- Greater omentum covers stomach
- Counterclockwise
- Limited to 90 degree rotation
- Greater omentum will not be visible
What are the cardiovascular effects of GDV?
- Increased intra-abdominal pressure
- Compression of low pressure veins
- Cd vena cava, portal and splenic veins
- Poor venous return
- Decreased preload, perfusion, CO and BP
- Patients go into shock–need fluids ASAP
- Catecholamines
- Vasoconstriction–>dec. perfusion
- Tachycardia, tries to inc. BP
- Arrhythmias (40-50%)
- Myocardial hypoxia
- Metabolic acidosis–> dec. contractility
- Myocardial depressant
- Reperfusion
What are the respiratory effects of GDV?
- Gastric distension–>impingement on diaphragm
- Decreased excursions
- Dec. tidal volume
- Inc. CO2
- Resp. acidosis
What are the GI effects of GDV?
- Vascular compromise of stomach mucosa
- Mucosal hemorrhage and necrosis
What are the metabolic effects of GDV?
- Poor tissue perfusion
- Cellular hypoxia
- Anaerobic metabolism
- Inc. lactate
- Metabolic acidosis
- Liver/kidney buffer
- Convert lactate to pyruvate
- Organs compromised from poor perfusion
- Compounds acidosis
What are the immune effects of GDV?
- Source of pathogenic bac. is GIT
- Hypoxemia–>mucosal ischemia
- Loss of protective barrier
- Bacterial translocation
- Damage to mucosal-assoc. lymphatics (ischemia from obstruction)
- Portal hypertension–compromised reticular endothelium
What are the renal effects of GDV?
- Profound vasoconstriction attempting to increase blood pressure decreases GFR
- Oliguria/anuria
- Acute renal failure
What is reperfusion injury? What is its role in GDV?
- Tissue flow absent, then returned when GDV is corrected
- Anaerobic metabolism
- Accumulation of waste products + toxic oxygen radicals
- Toxins released into general circulation
- Capillary permeability
- Altered vascular tone
- Platelet activation
- Vascular occlusions
- Fever
- Negative inotrope
- Neutraphils
- No reflow phenomenon
What are the clinical signs of GDV?
- Distended painful tympanic abdomen
- Active retching
- Hypersalivation
- Tachypnea
- Tachycardia
- Collapse
How do you diagnose GDV?
- Signalment (large breed dogs 10mo-14yr)
- History
- Looking/biting abdomen
- Preying posture
- Non-productive retching
- Distended abdomen
When you perform radiographs for a GDV patient, what is the patient’s position and what are the findings?
- Do not perform until medical stabilization
- Do NOT take a VD view–may predispose to reflux and aspiration
-
Right lateral is most diagnostic
- Gastric dilation with compartmentalization
- Malposition of pylorus
- Double bubble

In which direction does the stomach most commonly move with GDV?
Clockwise
What is the most common presentation for a GDV (rotation of stomach) and how is it confirmed?
- 180 degrees clockwise rotation most common
- Can confirm rotation is clockwise because the omentum will be covering the stomach (isn’t visible in the counterclockwise direction)
What are the key components of pre-operative stabilization of GDV patients (in the correct order)?
- Goal is to stabilize CV, resp, and renal systems initially
- Fluids
- Crystalloids 45-90ml/kg IV
- Crystalloids 10-40ml/kg + colloids 10-20ml/kg/day increases survival
- 7% hypertonic saline
- Blood sample
- Decompression
- Pain management
- Fluids
- Antimicrobials and free radical scavengers
- Sx and post-sx treatment
What are free radical scavengers (examples) and what is their potential benefit in treating GDV?
- Free radical scavengers
- Acetylcysteine
- Vitamins C and E, selenium
- Deferoxmaine–ferric iron chelator
- Lidocaine–also drug of choice if VPCs develop and provide analgesia
- Scavenger of ROS
- Help to prevent reperfusion injury
What methods can be used to decompress the stomach?
- Orogastric intubation
- Usually try first, may require sedation
- Trocharization
- Done when unable to pass orgastric tube
- Emergency gastrostomy
Why is the stomach decompressed prior to GDV sugery?
- Improves CV and resp function
- Done prior to surgery because the more stabilized patients are when they go into sx, the better off they’ll be
- *Perform AFTER fluid/volume support
- Can cause CV instability from endotoxins
How do you perform orogastric decompression?
- Stiff but flexible large bore tube with bite block
- Nose to last rib
- Gavage pump
- 2 buckets
- Lubricate tube
- Blow in tube to help through esophageal sphincter (but do NOT force it)

How do you perform trocharization decompression?
- 10-14g catheter or needle
- Clip and sx prep 6cm patch in cranial abdomen
- Find tympanic area
- Insert catheter firmly
- Gently decompress
- Remove when stops

When/how do you perform an emergency gastrotomy for treatment of GDV?
- If unable to decompress by OG tube or trocharization and other surgical treatment must be delayed
- Requires sedation and local block over right paracostal region
- 10cm skin incision through abdominal muscle
- Isolate stomach and suture stomach to incision on abdominal wall
- Incision into stomach
What treatment is used for GDV (other than surgical)?
- Oxygen therapy
- Helps offset poor ventilation
- Pain control
- Drugs with minimal CV effect
- Correct electrolyte/acid-base imbalances
- Glucocorticosteroids contraindicated–NEVER give to GDV patients
T/F: Arrhythmias occur in 40-50% of GDV patients and can contribute to mortality
TRUE
Usually VPC’s
What causes VPCs in GDV patients?
- Etiology is unknown
- Myocardial hypoxia decreases CO and tachycardia decreases coronary blood flow
- Metabolic acidosis decreases myocardial contractility and CO
- Myocardial depressant factor–cellular ischemia from decreased organ perfusion and (-) inotropic effects
- Reperfusion injury compromises cardiac function
What are the advantages of early surgical correction in the management of GDV?
- May complete surgery before arrhythmias emerge
- Gastric repositioning improves bloodflow
Which area of the stomach is most commonly affected by vascular compromise?
Greater curvature
(Gastric necrosis occurs in 10% of GDV patients)
How is gastric necrosis due to GDV managed? How does this affect prognosis?
- Partial gastrectomy
- Techniques
- Cut and sew
- Stapling
- Partial invagination
- Ligate vessels
- Remove necrotic tissue
- Techniques
- Significantly worsens prognosis

How is viability of the stomach typically assessed?
- Peristalsis–dead stomach wall loses its ability to contract
- Serosal color
- Pink/red = good
- Black, green, gray = bad
- Palpate for thinning or friability
- Pulsation of vessels
- Bleeding cut surfaces suggests that blood supply to the area is still viable
How is intestinal viability typically assessed?
- Peristalsis
- Important
- If moving = (probably) still alive
- Pinch test: see if it stimulates contraction
- Color: pink, glistening = good
- Pulsation of mesenteric vessels
- Bleeding of cut surface
- Wall thickness and texture
- Fluorescin infusion
- Woods lamp shows fluorescence if blood supply patent
- Oximetry probe–check for oxygenation and perfusion
What are the goals of a gastropexy?
- Prevent volvulus from recurring
- > 50% recurrence rate normally
- Does not prevent dilation
- Provide relatively anatomic position for pylorus
What abnormalities in the spleen can occur with GDV and how are they treated?
- Venous congestion–usually self-limiting
- Vessel thrombosis–splenectomy
- Splenic torsion–splenectomy if severe
- Can usually detorse and it will return to normal
- If clots, reperfusion, and platelet circulation spleen will appear black = dying –> splenectomy
What is the technique for an incisional gastropexy?
- Most common
- 3-6cm incision right ventro-lateral wall
- Perpendicular to and 6-8cm lat to celiotomy
- Through peritoneum and T. abdominal m.
- Incision pyloric antrum/stomach
- Serosal and muscular layer
- Suture far incision first
- Suture 2/0 or 3/0 abs
Describe the technique for a belt loop gastropexy
- Parallel incisions 2cm apart to create tunnel
- Right abdominal wall
- Peritoneum/muscle
- Parallel 4cm incisions 3cm apart through serosa/muscular near pyloric antrum
- Base at G. curvature
- Pull suture through ‘belt loop’ incision on abdominal wall
- Creates very good adhesion–strong and effective
What is the technique for a circumcostal gastropexy?
- Create tunnel around right 11th-12th rib
- Must palpate–don’t want to go into thoracic cavity (BAD)
- Create stomach flap with base near lesser curvature
- Suture with 2/0 or 3/0
- Very strong
Describe the technique for a tube gastropexy/gastrostomy
- Incision through R abdominal wall caudal to last rib
- Purse string suture in stomach
- 14-20 fr foley or mushroom tip catheter
- Suture tube to pyloric antrum area with mattress sutures
- Suture stomach to abdominal wall
- Secure with a finger trap
- Inflate with saline
- Tube is clamped and bandaged; usually removed in 5-10days
- Heals by second intention
- Advantages: prevents recurrent dilation, allows feeding
- Disadvantage: not as strong as other methods (but usually strong enough)
What is the technique for an incorporating gastropexy?
- Stomach wall incorporated into linea alba incision (celiotomy incision)
- Not recommended–surgical nightmare if you have to go back into the abdomen later–stomach and adhesions in the way
- Only indicated if patient requires abrupt discontinuation of anesthesia (crashing/complications)
How is a laparoscopic-assisted gastropexy performed?
- Dorsal recumbency
- 2 ports
- Camera port–midline
- Instrument port–R abdominal wall
- ID pyloric antrum
- Grasp with laparoscopic Babcock forceps
- Extend working port incision to exteriorize stomach
- Place stay sutures in stomach
- Confirm orientation of stomach
- Perform incisional gastropexy
- Advantage: less invasive, can be done prophylactically
- Disadvantage: need equipment, not done to treat GDV
How is an endoscopically-assisted gastropexy performed?
- Use endoscope to find pyloric antrum
- Manipulate to R ventral lateral abdomen
- Will see light through skin
- Place stay suture
- Make incision and perform incisional gastropexy
When is the most critical time period for postoperative GDV patients? Why?
The 1st 4 days post-op are the most critical–when 95% of deaths following GDV occur
When do GDV-associated arrhythmias usually occur?
12-36hrs after presentation
Usually VPCs and will subside 24-72hrs after surgery
When should GDV-associated arrhythmias be treated?
- Associated w/ weakness or syncope
- Persistent tachycardia >150bpm
- Pulse deficits or poor pulse quality
- Multifocal VPCs
- Will not always treat–drug of choice is lidocaine (can be arrhythmogenic and problematic)
How are GDV-associated arrhythmias treated?
- Lidocaine is drug of choice for initial management
- Bolus 1-2mg/kg IV q5min
- CRI (maintenance)
What is the prognosis for GDV patients?
- 10-33% mortality rate
- One of the leading causes of death in large/giant breed dogs
- Can correlate duration and severity of signs with survival
- Recumbant patients = higher mortality
- 44x more likely to die
- < 10% recurrence rate w/ gastropexy (very high w/o it)
Explain the prognosis-based lactate levels of GDV patients
- Lactate > 6mmol/L = higher incidence of gastric necrosis
- 50% mortality w/ gastric necrosis
- Lactate < 6mmol/L = 99% survival
- Lactate > 6mmol/L = 58% survival
- Percentage changes in lactate in response to treatment may be a better indicator of survival rates