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Small animal surgery I > Surgery of the stomach > Flashcards

Surgery of the stomach Flashcards

1
Q

What are the (general) treatment options for foreign bodies?

A
  • Stabilize the patient FIRST (don’t stop the vomiting)
    • Fluids/lytes/analgesics
    • Gastroprotectants
  • Specific therapies (toxins)
  • FB removal options:
    • Conservative
    • Endoscopy
    • Gastrotomy
    • Induce emesis
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2
Q

What are the indications for conservative management of foriegn body ingestion?

A

Patient consumes something small and benign (not sharp) that is likely to just pass through

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3
Q

How is endoscopy used and when is it indicated for foreign body removal? What about gastrotomy?

A
  • 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)
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4
Q

When should you induce emesis following a foreign body ingestion?

A

Toxins–want to get rid of them ASAP

(Also small objects that could cause obstruction if passed through)

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5
Q

What are some examples of specific therapies for FB ingestion?

A

Lead: chelation with EDTA

Zinc: transfusion

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6
Q

What are the predisposing factors for gastric foreign body?

A
  • Younger animals (“not as smart”)
  • Previous history of FB ingestion
  • Conditions that predispose to PICA (eating everything)
    • Pancreatic exocrine insufficiency
    • Hepatic encephalopathy
    • Iron deficiency
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7
Q

What are clinical signs associated with gastric outflow obstruction?

A
  • Intermittent vomiting
  • Dietary modification alters signs
  • Normal to decreased body condition
  • Abdominal distension but no pain
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8
Q

What are the causes of gastric outflow?

A
  • Congenital pyloric stenosis
  • Acquired outflow obstruction
    • FBs
    • Chronic hypertrophic pyloric gastropathy
    • Neoplasia
    • Inflammatory/infiltrative disease
    • Motility disorders
    • Ulceration with scarring
    • Extraluminal masses
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9
Q

Describe the blood supply to the stomach

A

R and L gastric arteries

Greater curvature: epiploic arteries

Fundic area: nerve bundle/fibers–gastric pacemaker (initiates normal contractions); avoid gastrotomy incision through pacemaker

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10
Q

Differentiate between congenital and acquired pyloric stenosis

A
  • 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
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11
Q

What pathology is associated with congenital and acquired pyloric stenosis?

A

Hypertrophy of the muscular layer of the pylorus (and/or mucosal layer for acquired); etiology is unknown (excess gastrin?)

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12
Q

Is pyloric stenosis the same in cats and dogs?

A

Not completely

  • Both species have vomiting as the major sign
  • Cats can also have regurgitation due to secondary esophagitis and esophageal dysfunction
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13
Q

Which digestive hormone has been implicated in the etiology of both congenital and acquired pyloric stenosis?

A

Gastrin

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14
Q

What diagnosis modality can be used to differentiate congenital and acquired pyloric stenosis? How?

A

Ultrasound

  • Congenital
    • Layer thickness
    • Differentiate neoplasia
    • U/S confirms diagnosis
  • Acquired
    • Pyloric wall and muscle thickness
      • Muscularis < 4mm
      • Pyloris < 9mm
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15
Q

What are the pathological classifications of acquired pyloric stenosis?

A
  • 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
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16
Q

What are the specific goals of surgical correction of acquired pyloric stenosis? What treatments are available?

A
  • Goal: reduce stenosis/increase gastric outflow
  • Treatments
    • Transverse pyloroplasty
    • Y-U pyloroplasty
    • Billroth 1
    • Biopsy
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17
Q

What is a Fredet-Ramstedt pyloromyotomy? What are the advantages/disadvantages?

A
  • 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
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18
Q

What is a Heineke-Mikulicz pyloroplasty? What are the advantages/disadvantages?

A
  • (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)
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19
Q

What is a Y-U pyloroplasty? What are the advantages/disadvantages?

A
  • 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
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20
Q

What is the Billroth 1 procedure? What are the advantages/disadvantages?

A
  • 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
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21
Q

Where should gastrotomy incisions for exploration and removal of FBs be made? Why?

A
  • 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
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22
Q

What are the principles/goals of suturing a gastrotomy incision? What factors influence closure choices?

A
  • 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
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23
Q

What are the indications for a gastrectomy?

A
  • Neoplasia
  • Ischemic injury (GDV)
  • Ulcer
  • Trauma
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24
Q

What are the advantages/disadvantages of suturing the stomach with inverting suture patterns?

A
  • 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
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25
Q

Differentiate between the Cushing, Lembert, and Connell suture patterns

A
  • 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
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26
Q

T/F: 60-70% of all gastric neoplasias are gastric adenocarcinomas

A

TRUE

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27
Q

What is the signalment of gastric adenocarcinomas?

A
  • 2.5:1 male:female
  • 7-10yrs
  • Rare in cats
  • Rough collie, Staff terrier, Belgian shepherd
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28
Q

What are the physical findings/pathology for gastric adenocarcinomas?

A
  • 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
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29
Q

What are the treatment options for gastric adenocarcinomas?

A
  • 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
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30
Q

What is the prognosis for gastric adenocarcinomas?

A

Poor, even with sx treatment

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31
Q

What is the signalment for leiomyosarcomas?

A

Usually middle aged–approx. 7yrs

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32
Q

What are the physical findings of leiomyosarcomas?

A
  • Smooth muscle origin
  • More common in cardia vs. pylorus
  • Single or multiple
  • Often ulcerate into gastric lumen
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33
Q

What is the prognosis for leiomyosarcomas?

A

MST = 21mo

Have high metastatic potential

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34
Q

What is the signalment for leiomyomas?

A
  • Often in older patients (> 15yrs)
  • Very slow growing
  • Often incidental finding
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35
Q

T/F: Leiomyomas are benign

A

TRUE

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36
Q

What is the treatment and prognosis for gastric leiomyomas?

A
  • Gastrotomy approach
  • Submucosal resection –> resect tumor and take minimal margins –> good to go
  • Prognosis = good–resection eliminates all signs
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37
Q

What is the signalment of pythiosis?

A
  • Young, large breed working dogs
  • Southeast U.S. (gulf states)
38
Q

What are the clinical signs of pythiosis?

A
  • Wt. loss
  • Vomiting
  • Diarrhea
  • Hematochezia
  • Sometimes palpable abdominal mass and increased mesenteric lymph nodes
39
Q

T/F: Pythiosis has a slow growth rate but an extensive nature

A

FALSE–has a fast growth rate

40
Q

What does pythiosis infiltrate?

A

Submucosa and muscularis layers of stomach and small intestines

41
Q

How can you diagnose pythiosis (oomycosis/pythium insidiosum)?

A
  • Endoscopy–difficult to find organism
  • Histo
    • Eosinophilic pyogranulomatous inflammation
    • Deep tissue samples of fibrotic material can reveal organism
  • ELISA tests for P. insidiosum antibodies
42
Q

How is pythiosis treated? What is the prognosis?

A
  • 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
43
Q

What is a Billroth II gastroenterostomy? When is it indicated?

A
  • 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
44
Q

What are some complications of the Billroth II procedure?

A
  • 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)
45
Q

What is the difference between acute gastric dilation, chronic gastric volvulus, and acute gastric dilation + volvulus?

A
  • 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
46
Q

What are the predisposing factors for GDV?

A
  • 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
47
Q

What foods decrease the risk of GDV?

A

Eggs or fish–very easily digested proteins

48
Q

What is the pathophysiology leading up to gastric dilation and volvulus (GDV)?

A
  • 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
49
Q

What are the 2 types of rotation in GDV?

A
  • Clockwise
    • Much more common
    • 70-360 degree rotation
    • Greater omentum covers stomach
  • Counterclockwise
    • Limited to 90 degree rotation
    • Greater omentum will not be visible
50
Q

What are the cardiovascular effects of GDV?

A
  • 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
51
Q

What are the respiratory effects of GDV?

A
  • Gastric distension–>impingement on diaphragm
  • Decreased excursions
  • Dec. tidal volume
  • Inc. CO2
  • Resp. acidosis
52
Q

What are the GI effects of GDV?

A
  • Vascular compromise of stomach mucosa
  • Mucosal hemorrhage and necrosis
53
Q

What are the metabolic effects of GDV?

A
  • 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
54
Q

What are the immune effects of GDV?

A
  • 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
55
Q

What are the renal effects of GDV?

A
  • Profound vasoconstriction attempting to increase blood pressure decreases GFR
  • Oliguria/anuria
  • Acute renal failure
56
Q

What is reperfusion injury? What is its role in GDV?

A
  • 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
57
Q

What are the clinical signs of GDV?

A
  • Distended painful tympanic abdomen
  • Active retching
  • Hypersalivation
  • Tachypnea
  • Tachycardia
  • Collapse
58
Q

How do you diagnose GDV?

A
  • Signalment (large breed dogs 10mo-14yr)
  • History
    • Looking/biting abdomen
    • Preying posture
    • Non-productive retching
    • Distended abdomen
59
Q

When you perform radiographs for a GDV patient, what is the patient’s position and what are the findings?

A
  • 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
60
Q

In which direction does the stomach most commonly move with GDV?

A

Clockwise

61
Q

What is the most common presentation for a GDV (rotation of stomach) and how is it confirmed?

A
  • 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)
62
Q

What are the key components of pre-operative stabilization of GDV patients (in the correct order)?

A
  • 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
  • Antimicrobials and free radical scavengers
  • Sx and post-sx treatment
63
Q

What are free radical scavengers (examples) and what is their potential benefit in treating GDV?

A
  • 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
64
Q

What methods can be used to decompress the stomach?

A
  • Orogastric intubation
    • Usually try first, may require sedation
  • Trocharization
    • Done when unable to pass orgastric tube
  • Emergency gastrostomy
65
Q

Why is the stomach decompressed prior to GDV sugery?

A
  • 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
66
Q

How do you perform orogastric decompression?

A
  • 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)
67
Q

How do you perform trocharization decompression?

A
  • 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
68
Q

When/how do you perform an emergency gastrotomy for treatment of GDV?

A
  • 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
69
Q

What treatment is used for GDV (other than surgical)?

A
  • 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
70
Q

T/F: Arrhythmias occur in 40-50% of GDV patients and can contribute to mortality

A

TRUE

Usually VPC’s

71
Q

What causes VPCs in GDV patients?

A
  • 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
72
Q

What are the advantages of early surgical correction in the management of GDV?

A
  • May complete surgery before arrhythmias emerge
  • Gastric repositioning improves bloodflow
73
Q

Which area of the stomach is most commonly affected by vascular compromise?

A

Greater curvature

(Gastric necrosis occurs in 10% of GDV patients)

74
Q

How is gastric necrosis due to GDV managed? How does this affect prognosis?

A
  • Partial gastrectomy
    • Techniques
      • Cut and sew
      • Stapling
      • Partial invagination
    • Ligate vessels
    • Remove necrotic tissue
  • Significantly worsens prognosis
75
Q

How is viability of the stomach typically assessed?

A
  • 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
76
Q

How is intestinal viability typically assessed?

A
  • 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
77
Q

What are the goals of a gastropexy?

A
  • Prevent volvulus from recurring
    • > 50% recurrence rate normally
  • Does not prevent dilation
  • Provide relatively anatomic position for pylorus
78
Q

What abnormalities in the spleen can occur with GDV and how are they treated?

A
  • 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
79
Q

What is the technique for an incisional gastropexy?

A
  • 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
80
Q

Describe the technique for a belt loop gastropexy

A
  • 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
81
Q

What is the technique for a circumcostal gastropexy?

A
  • 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
82
Q

Describe the technique for a tube gastropexy/gastrostomy

A
  • 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)
83
Q

What is the technique for an incorporating gastropexy?

A
  • 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)
84
Q

How is a laparoscopic-assisted gastropexy performed?

A
  • 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
85
Q

How is an endoscopically-assisted gastropexy performed?

A
  • 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
86
Q

When is the most critical time period for postoperative GDV patients? Why?

A

The 1st 4 days post-op are the most critical–when 95% of deaths following GDV occur

87
Q

When do GDV-associated arrhythmias usually occur?

A

12-36hrs after presentation

Usually VPCs and will subside 24-72hrs after surgery

88
Q

When should GDV-associated arrhythmias be treated?

A
  • 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)
89
Q

How are GDV-associated arrhythmias treated?

A
  • Lidocaine is drug of choice for initial management
  • Bolus 1-2mg/kg IV q5min
  • CRI (maintenance)
90
Q

What is the prognosis for GDV patients?

A
  • 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)
91
Q

Explain the prognosis-based lactate levels of GDV patients

A
  • 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

Small animal surgery I (25 decks)

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