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Drafts of absite from online deck > Chapter 30: Stomach COPY > Flashcards

Chapter 30: Stomach COPY Flashcards

1
Q

Stomach transit time

A

3-4 hours

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2
Q

Where does stomach peristalsis occur?

A

Distal stomach (antrum)

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3
Q

How is gastroduodenal pain sensed

A

Through afferent sympathetic fibers T5-T10

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4
Q

Components of the celiac trunk

A

Left gastric
Common hepatic artery
Splenic artery

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5
Q

Branches of the splenic artery that supply the stomach

A

Left gastroepiploic and short gastric

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6
Q

Blood supply to the greater curvature

A

Right and left gastroepiploics, short gastrics

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7
Q

What is the right gastroepiploic a branch of?

A

Gastroduodenal artery

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8
Q

Blood supply of lesser curvature

A

Right and left gastrics

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9
Q

What is the right gastric a branch off?

A

The common hepatic artery

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10
Q

Blood supply of the pylorus

A

Gastroduodenal artery

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11
Q

Mucosa lining the stomach

A

Simple columnar epithelium

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12
Q

What do cardia glands secrete?

A

Mucus

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13
Q

Fundus and body glands

A

Chief cells

Parietal cells

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14
Q

Produces pepsinogen (1st enzyme in proteolysis)

A

Chief cells

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15
Q

Release hydrogen and intrinsic factor

A

Parietal cells

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16
Q

What stimulates parietal cells?

A

Acetylcholine (vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells) cause H+ release

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17
Q

What is the pathway of acetylcholine (vagus nerve) and gastrin?

A

Activates phospholipase (PIP -> DAG + IP3 + Increase Ca); Ca-calmodulin activates phosphorylase kinase -> H+ release

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18
Q

What is the pathway of histamine?

A

Activates adenylate cyclase -> cAMP -> activates protein kinase A -> increased H+ release

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19
Q

How do phosphorylase and protein kinase A work?

A

Phosphorylate H+/K+ ATPase to increase H+ secretion and K+ absorption

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20
Q

Blocks H+/K+ ATPase in parietal cell membrane (final pathway for H+ release)

A

Omeprazole

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21
Q

Inhibitors of parietal cells

A

Somatostatin, prostaglandins (PGE1), secretin, CCK

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22
Q

Binds B12 and the complex is reabsorbed in the terminal ileum

A

Intrinsic factor

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23
Q

Antrum and pylorus glands

A 
Mucus and HCO3- secreting glands.
G cells (gastrin).
D cells (somatostatin)
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24
Q

Secreting glands - protect stomach

A

Mucus and HCO3- (Antrum and pylorus glands)

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25
Q

Release gastrin - reason why antrectomy is helpful for ulcer disease

A

G cells

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26
Q

What inhibits G cells?

A

H+ in duodenum

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27
Q

What stimulates G cells?

A

Amino acids, acetylcholine

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28
Q

Secrete somatostatin, inhibit gastrin and acid release

A

D cells

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29
Q

In duodenum; secrete alkaline mucus

A

Brunner’s glands

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30
Q

Released with antral and duodenal acidification

A

Somatostain, CCK, and secretin

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31
Q

What are the causes of rapid gastric emptying?

A

Previous surgery (#1), ulcers

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32
Q

What are the causes of delayed gastric emptying?

A

Diabetes, opiates, anticholingerics, hypothyroidism

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33
Q

(Hair) - hard to pull out

Tx?

A

Trichobezoars

- Tx: EGD generally inadequate; likely need gastrostomy and removal

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34
Q

(fiber) - often in diabetics with poor gastric emptying

Tx?

A

Phytobezoars (fiber)

Tx: enzymes, EGD, diet changes

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35
Q

Vascular malformation; can bleed

A

Dieulafoy’s ulcer

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36
Q

Mucous cell hyperplasia, increased rugal folds

A

Menetrier’s disease

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37
Q
  • Associated with type II (paraesophageal) hernia
  • Nausea without vomiting; severe pain; usually organoaxial volvulus
    Treatment?
A

Gastric volvulus

Tx: reduction and Nissen

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38
Q
  • Secondary to forceful vomiting
  • Presents as hematemesis following severe retching
  • Bleeding often stops spontaneously
A

Mallory-Weiss tear

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39
Q

What type of volvulus is a gastric volvulus?

A

Organoaxial volvulus

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40
Q

Dx/Tx: Mallory Weiss Tear

A

EGD with hemo-clips; tear is usually on the lesser curvature (near GE junction)

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41
Q

Where is the Mallory Weiss Tear located?

A

Usually on the lesser curvature (near GE junction)

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42
Q

What if you have continued bleeding after EGD with hemo-clips for Mallory Weiss tear?

A

If continued bleeding, may need gastrostomy and oversewing of the vessel.

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43
Q

What is the physiologic effect of vagotomy?

A

Both truncal and proximal forms increase liquid emptying -> vaguely mediated receptive relaxation if removed (results in increased gastric pressure that accelerates liquid emptying)

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44
Q

Vagotomy:

Divides vagal trunks at the level of the esophagus; decreases emptying of solids

A

Truncal vagotomy

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45
Q

Vagotomy:

  • highly selective
  • divides individual fibers, preserves “crow’s foot”, normal emptying of solids
A

Proximal vagotomy

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46
Q

Emptying of solids: truncal vs proximal vagotomy

A

Truncal: decreased emptying of solids

Proximal: normal emptying of solids

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47
Q

How can you increase solid emptying with truncal vagotomy?

A

Addition of pyloroplasty to truncal vagotomy results in increased solid emptying.

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48
Q

Physiologic effects of truncal vagotomy

  • Gastric effects
  • Nongastric effects
  • Diarrhea
A
  • Gastric: decreased acid output by 90%, increased gastrin cell hyperplasia
  • Nongastric: decreased exocrine pancreas function, decreased postprandial bile flow, increased gallbladder volumes, decreased release of vaguely mediated hormones
  • Diarrhea: MC problem following vagotomy
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49
Q

MC common problem following vagotomy

A

Diarrhea (40%)

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50
Q

What causes diarrhea following vagotomy?

A

Caused by sustained MMCs (migrating motor complex) forcing bile acids into the colon

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51
Q

Name that vagotomy: both nerve trunks are divided at the level of the diaphragmatic hiatus

A

Truncal vagotomy

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52
Q

Name that vagotomy: division of the vagal fibers that supply the gastric funds. Branches to the antropyloric region of the stomach are not transected, and the hepatic and celiac divisions of the vagus nerves remain intact.

A

Proximal gastric vagotomy

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53
Q

Risk factors: upper gastroinestinal bleeding

A

Previous UGIB, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting.

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54
Q

Dx/Tx: UGIB

A

EGD (confirm bleeding is from ulcer); can potentially treat with hemo-clips, Epi injection, cautery

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55
Q

Mgmt: UGIB with slow bleeding and having trouble localizing source

A

Tagged RBC scan

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56
Q

UGIB: biggest risk factor for rebleeding at the time of EGD

A 
#1 spurting blood vessel (60%) chance of rebleed
#2 visible blood vessel (40% chance of rebleed)
#3 diffuse oozing (30% chance of rebleed)
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57
Q

Highest risk factor for mortality with non-variceal UGIB

A

Continued or re-bleeding

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58
Q

Treatment: patient with liver failure is likely bleeding from esophageal varices, not an ulcer

A

EGD with variceal bands or sclerotherapy; TIPS if that fails

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59
Q
  • From increased acid production and decreased defense

- Most common peptic ulcer; more common in men

A

Duodenal ulcers

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60
Q

Location of duodenal ulcers

A

Usually in 1st part of the duodenum; usually anterior.

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61
Q

Complications of duodenal ulcers:

  • Anterior
  • Posterior
A
  • Anterior ulcers perforate

- Posterior ulcers bleed from gastroduodenal artery

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62
Q

Symptoms: epigastric pain radiating to the back; abates with eating but recurs 30 minutes after
- Dx/Tx?

A

Duodenal ulcer

  • Dx: endoscopy
  • Tx: PPI, triple therapy for H. pylori -> bismuth salts, amoxicillin, and metronidazole/tetracycline (BAM or BAT)
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63
Q

What has decreased incidence of surgery for ulcer?

A

Surgery for ulcer rarely indicated since PPIs

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64
Q

What do you need to rule out in patients with complicated ulcer disease?

A

Need to rule out gastrinoma

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65
Q

Gastric acid hyper secretion.
Peptic ulcers.
Gastrinoma.

A

Zollinger-Ellison Syndrome

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66
Q

Surgical indications for duodenal ulcer

A

Perforation. Protracted bleeding despite EGD therapy. Obstruction. Intractability despite medical therapy. Inability to rule out cancer. PPI with duodenal ulcer complication.

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67
Q

Duodenal ulcer: if patient has been on a PPI and has complications

A

If a patient has been on a PPI, an acid-reducing surgical procedure is required in addition to surgery for any complications

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68
Q

Surgical options (acid-reducing surgery) for duodenal ulcers

A
  • Proximal vagotomy
  • Truncal vagotomy and pyloroplasty
  • Truncal vagotomy and antrectomy
  • Reconstruction after antrectomy - Roux-en-Y gastro-jejunostomy (best)
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69
Q

Surgery duodenal ulcer: lowest rate of complications, no need for astral or pylorus procedure; 10-15% ulcer recurrence, 0.1% mortality

A

Proximal vagotomy

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70
Q

Ulcer recurrence / mortality after proximal vagotomy

A
  • 10-15% ulcer recurrence

- 0.1% mortality

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71
Q

Ulcer recurrence / mortality after truncal vagotomy and pyloroplasty

A
  • 5-10% ulcer recurrence

- 1% mortality

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72
Q

Ulcer recurrence / mortality after truncal vagotomy and antrectomy

A
  • 1-2% ulcer recurrence (lowest rate of recurrence)

- 2% mortality

73
Q

Why is roux-en-y gastro-jejunostomy the best procedure for reconstruction after antrectomy?

A

Less dumping syndrome and reflux gastritis compared to Bilroth I (gastro-duodenal anastomosis) and Billroth II (gastro-jejunal anastomosis)

74
Q

Most frequent complication of duodenal ulcers

A

Bleeding (usually minor but can be life threatening)

75
Q

Definition of major bleeding in duodenal ulcer

A

> 6 units of blood in 24 hours or patient remains hypotensive despite transfusion

76
Q

Tx: bleeding from duodenal ulcer

A

EGD 1st - hemoclips , cauterize, Epi injection

77
Q

Surgery: bleeding duodenal ulcers

A

Duodenotomy and gastroduodenal artery (GDA) ligation.

  • Avoid hitting common bile duct (posterior) with GDA ligation
  • If patient has been on a PPI, need acid-reducing surgery as well
78
Q

Initial treatment of choice for obstruction from duodenal ulcer

A

PPI and serial dilation

79
Q

Surgical options: duodenal ulcer obstruction

A

Antrectomy and truncal vagotomy (best); include ulcer in resection if it’s located proximal to ampulla of Vater

80
Q

What do you need to rule out in duodenal ulcer obstruction?

A

Need to biopsy area of resection to rule out CA

81
Q

Duodenal ulcer perforation: % will have free air

A

80% will have free air

82
Q
  • patient usually have sudden epigastric pain; can have generalized peritonitis
  • pain can radiate to the prevocalic gutters with dependent drainage of gastric content
A

Duodenal ulcer perforation

83
Q

Tx: duodenal ulcer perforation

A 
Graham patch (place momentum over the perforation)
- Also need acid-reducing surgery if the patient has been on a PPI
84
Q

Definition of intractable duodenal ulcers

A

> 3 months without relief while on escalating doses of PPI

85
Q

What is diagnosis of intractable duodenal ulcers based on?

A

Based in EGD mucosal findings, not symptoms

86
Q

Tx: intractability of duodenal ulcers

A

Acid-reducing surgery

87
Q
  • Older men, slow healing
  • 80% on lesser curvature of the stomach
  • Symptoms: epigastric pain radiating to the back; relieved with eating but recurs 30 minutes later; melena or guaiac-positive stools
A

Gastric ulcers

88
Q

Risk factors for gastric ulcer

A

Male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress (burns, sepsis, and trauma), steroids, chemotherapy

89
Q

Where are most gastric ulcers located?

A

80% on lesser curvature of the stomach

90
Q

What is difference in mortality between gastric and duodenal ulcer hemorrhage?

A

Hemorrhage is associated with higher mortality than duodenal ulcers.

91
Q

Gastric ulcers: best test for H. pylori

A

Histiologic examination of biopsies from antrum

92
Q

Test for H.pylori, detects urease released from H. pylori

A

CLO test (rapid urease test)

93
Q

Type 1 Gastric ulcer

A

Lesser curve low along body of stomach; due to decreased mucosal protection

94
Q

Type 2 gastric ulcer

A

2 ulcers (lesser curve and duodenal); similar to duodenal ulcer with high acid secretion

95
Q

Type 3 gastric ulcer

A

pre-pyloric ulcer; similar to duodenal ulcer with high acid secretion

96
Q

Type 4 gastric ulcer

A

Lesser curve high along cardia of stomach; decreased mucosal protection

97
Q

Type 5 gastric ulcer

A

Ulcer associated with NSAIDS

98
Q

What gastric ulcers are associated with decreased mucosal secretion?

A

Type 1 and 4

99
Q

What gastric ulcers are similar to duodenal ulcer with high acid secretion?

A

Type 2 and 3

100
Q

What type of gastric ulcer is associated with NSAIDS?

A

Type 5

101
Q

Surgical indications for gastric ulcers

A

Perforation, bleeding not controlled with EGD, obstruction, cannot exclude malignancy, intractability (> 3 months without relief - based on mucosal findings)

102
Q

Tx: gastric ulcer

A

Truncal vagotomy and antrectomy best for complications; try to include the ulcer with resection (extended antrectomy) - need separate ulcer excision if that is not possible (gastric ulcers are resected at time of surgery due to high risk of gastric CA)

103
Q

What are poor options for surgical repair of gastric ulcers?

A

Omental patch and ligation of bleeding vessels are poor options for gastric ulcers due to high recurrence of symptoms and risk of gastric CA in the ulcer.

104
Q
  • Occurs 3-10 days after event; lesions appear in fundus first
  • Tx: PPI
  • EGD with cautery of specific bleeding point may be effective
A

Stress gastritis

105
Q

Where do lesions in stress gastritis appear?

A

Lesions appear in fundus first

106
Q

Chronic gastritis type: associated with pernicious anemia, autoimmune disease

A

Type A (fundus)

107
Q

Chronic gastritis type: associated with H. pylori

A

Type B (antral)

108
Q

Treatment Chronic Gastritis

A

PPI

109
Q

Pain unrelieved by eating, weight loss

A

Gastric cancer

110
Q

Where are 40% of gastric cancers located?

A

Antrum

111
Q

Gastric cancer-related deaths in Japan

A

Accounts for 50% of cancer-related deaths in Japan

112
Q

Dx: gastric cancer

A

EGD

113
Q

Risk factors: gastric cancer

A

Adenomatous polyps, tobacco, previous gastric operations, intestinal metaplasia, atrophic gastritis, pernicious anemia, type A blood, nitrosamines

114
Q

15% risk of gastric cancer.

- Tx: endoscopic resection

A

Adenomatous polpys

115
Q

Gastric cancer metastases to ovaries

A

Krukenberg tumor

116
Q

Gastric metastasis to supraclavicular node

A

Virchow’s node

117
Q

Increased in high-risk populations. Older men. Japan. Rare in United States

Surgical treatment: try to perform subtotal gastrectomy (need 10-cm margins)

A

Intestinal-type gastric CA

118
Q

Low risk populations. Women. Most common type in the United States.
Diffuse lymphatic invasion, no glands.

Surgery: total gastrectomy bc of diffuse nature of linitis plastica

A

Diffuse gastric cancer

119
Q

Prognosis: intestinal-type gastric CA vs diffuse gastric cancer

A

Less favorable prognosis than intestinal-type gastric CA (overall 5-YS - 25%)

120
Q

Margins for intestinal-type gastric CA

A

need 10 cm margins

121
Q

Chemotherapy for gastric cancer

A

Poor prognosis:

- 5 FU, doxorubicin, mitomycin C

122
Q

Gastric cancer: management of metastatic disease outside area of resection

A

Contraindication to resection unless performing surgery for palliation.

123
Q

When to consider palliation of gastric cancer?

A
  • Obstruction - proximal lesions can be scented; distal lesions can be bypassed with gastrojejunostomy
  • Low to moderate bleeding or pain - Tx: XRT
124
Q

What if surgical management fails for palliation of gastric cancer (stents, gastrojejunostomy, XRT)?

A

If these fail, consider palliative gastrectomy for obstruction or bleeding.

125
Q

Most common benign gastric neoplasm, although can be malignant

Symptoms: usually asymptomatic, but obstruction and bleeding can occur

A

Gastrointestinal stromal tumors (GISTs)

126
Q

How do GISTs look on ultrasound?

A

Hypoechoic on ultrasound; smooth edges

127
Q

Dx / Tx: GIST

A

Dx: biopsy - are C-KIT positive

Tx: resection with 1 cm margins; Chemotherapy with imatinib (Gleevac, tyrosine kinase inhibitor) if malignant

128
Q

Chemotherapy for malignant GIST

A

Imatinib (Gleevax; tyrosine kinase inhibitor)

129
Q
  • Related to H. pylori infection

- Usually regresses after treatment for H. pylori

A

Mucosa-associated lymphoid tissue lymphoma (MALT lymphoma)

130
Q

When are GIST considered malignant?

A

> 5 cm or > 5 mitoses / 50 HPF (high-powered field)

131
Q

What will be positive in biopsy of GIST?

A

C-KIT

132
Q

MC location of MALT lymphoma

A

Stomach

133
Q

Treatment: MALT lymphoma

A

Triple-therapy antibiotics for H. pylori and surveillance.

If MALT does not regress, need XRT.

134
Q

What if MALT lymphoma does not resolve with triple therapy antibiotics for H.pylori?

A

If MALT does not regress, need XRT

135
Q
  • Have ulcer symptoms
  • Usually non-Hodgkin’s lymphoma (B cell)
  • Overall 5-year survival rate > 50%
A

Gastric lymphomas

136
Q

MC location for extra-nodal gastric lympoma

A

Stomach

137
Q

Dx: Gastric lymphoma

A

EGD with biopsy

138
Q

Primary treatment modalities of gastric lymphoma

A

Chemotherapy and XRT are primary treatment modalities; surgery for complications

139
Q

When is surgery indicated for gastric lymphoma?

A

Surgery possibly indicated only for stage 1 disease (tumor confined to stomach mucosa) and then only partial resection is indicated

140
Q

Overall 5-year survival rate for gastric lymphoma

A

> 50%

141
Q

Criteria for patient selection for bariatric surgery (need all 4)

A
  • BMI > 40 kg/m^2 or BMI > 35 kg/m^2 with coexisting comorbidities
  • Failure of nonsurgical methods of weight reduction
  • Psychological stability
  • Absence of drug or alcohol abuse
142
Q

What type of obesity is worse prognosis in general population?

A

Central obesity

143
Q

Operative mortality in morbid obesity

A

1%

144
Q

What gets better are surgery for morbid obesity?

A

DM, cholesterol, sleep apnea, HTN, urinary incontinence, GERD, venous stasis ulcers, pseudotumor cerebri, joint pain, migraines, depressions, PCOS, NASH

145
Q
  • Better weight loss than just banding.
  • Risk of marginal ulcers, leak, necrosis, B12 deficiency, IDA, gallstones
  • Perform cholecystectomy during operation if stones present
  • UGI on POD 2
A

Roux-en-Y gastric bypass

146
Q

Failure rate of roux-en-y gastric bypass

A

10% failure rate due to high-carbohydrate snacking

147
Q

What are the signs of a leak after roux-en-y gastric bypass?

A
  • Ischemia: MCC leak

- Signs of leak: increased RR, increased HR, abdominal pain, fever, elevated WBCs

148
Q

Dx / Tx: leak after roux-en-y gastric bypass

A

Dx: UGI

Tx: early leak (not contained) -> re-op; late leak (Weeks out from surgery, likely contained) -> percutaneous drain, antibiotics

149
Q

Incidence of marginal ulcers after roux-en-y gastric bypass

A

Develop in 10%

Tx: PPI

150
Q

Management of stenosis after roux-en-y gastric bypass

A

Usually responds to serial dilation

151
Q

Complications of roux-en-y gastric bypass

A
  • Leak
  • Marginal ulcers
  • Stenosis
152
Q

MCC leak after roux-en-y gastric bypass

A

Ischemia

153
Q

After roux-en-y gastric bypass:

  • Hiccoughs, large stomach bubble
  • Dx: AXR
  • Tx: G-tube (gastrostomy tube)
A

Dilation of excluded stomach postop

154
Q

s/p roux-en-y gastric bypass:

  • nausea and vomiting, intermittent abodminal pain
  • AXR shows dilated SB
A

Small bowel obstruction

- Surgical emergency

155
Q

Why is SBO s/p roux-en-y gastric bypass a surgical emergency?

A

Due to the high risk of small bowel herniation, strangulation, infarction and subsequent necrosis.

  • Tx: surgical exploration
156
Q
  • these operations are no longer done
  • a/w liver cirrhosis, kidney stones, and osteoporosis (decreased calcium)
  • need to correct these patients and perform roux-en-y gastric bypass if encountered
A

jejunoileal bypass

157
Q
  • can occur after gastrectomy or after vagotomy and pyloroplasty
  • occurs form rapid entering of carbohydrates into the small bowel.
  • can almost always be treated medically (and dietary changes)
A

Dumping syndrome

158
Q

2 phases of dumping syndrome

A
  • Hyperosmotic load causes fluid shift into bowel (hypotension, diarrhea, dizziness)
  • hypoglycemia from reactive increase in insulin and decrease in glucose (2nd phase rarely occurs)
159
Q

Tx: dumping syndrome

A

Small, low-fat, low-carb, high-protein meals; no liquids with meals, no lying down after meals; octreotide

160
Q

Surgical options for dumping syndrome (Rarely needed)

A
  • Conversion of Billroth 1 or Billroth 2 to Roux-en-y gastrojejunostomy
  • Operations to increase gastric reservoir (jejunal pouch) or increased emptying time (Reversed jejunal loop)
161
Q

postprandial epigastric pain associated with n/v; pain not relieved with vomiting

A

Alkaline reflux gastritis

162
Q

Dx / Tx: alkaline reflux gastritis

A

Dx: evidence of bile reflux into the stomach; histologic evidence of gastritis

Tx: PPI, cholestyramine, metoclopramide

163
Q

Surgical options for alkaline reflux gastritis

A

Conversion of Billroth 1 or Billroth 2 to Roux-en-Y gastrojejunostomy with afferent limb 60 cm distal to gastro jejunostomy

164
Q
  • Delayed gastric emptying

- Symptoms: n/v, pain, early satiety

A

Chronic gastric atony

165
Q

Chronic gastric atony:

Dx / Tx / Surgical options

A

Dx: gastric emptying study

Tx: metoclopramide, prokinetics

Surgical option: near total gastrectomy with roux-en y

166
Q
  • Early satiety

- Actually want this for gastric bypass patients

A

Small gastric remnant

167
Q

Small gastric remnant:

Dx / Tx / Surgical option

A
  • Dx: EGD
  • Tx: small meals
  • Surgical option: jejunal pouch reconstruction
168
Q
  • With billroth 2 or roux-en-y; caused by poor motility

- Symptoms: pain, steatorrhea (bacterial beconjugation of bile), B12 deficiency (bacteria use it up), malabsorption

A

Blind-loop syndrome

169
Q

What causes blind-loop syndrome with billroth 2 or roux-en-y?

A

Caused by bacterial overgrowth (E coli, GNRs) from stasis in afferent limb

170
Q

Dx: blind-loop syndrome

A

EGD of afferent limb with aspirate and culture for organisms

171
Q

Tx: blind loop syndrome

A

Tetracycline and flagyl, metoclopramide to improve motility

172
Q

Surgical option: blind-loop syndrome

A

Re-anastomosis with shorter (40-cm) afferent limb to relieve obstruction

173
Q
  • Symptoms of obstruction - n/v, abdominal pain
  • Dx: UGI, EGD
  • Tx: balloon dilation
  • Surgical option: find site of obstruction and relieve it
A

Efferent-loop obstruction

174
Q
  • Secondary to non-conjugated bile salts in the colon (osmotic diarrhea)
  • Causes by sustained postprandial organized MMCs
A

Post-vagotomy diarrhea

175
Q

Tx / Surgical option: post-vagotomy diarrhea

A

Tx: cholestyramine, octreotide

Surgical option: reversed interposition jejunal graft

176
Q

What causes post-vagotomy diarrhea?

A

Reversed interposition jejunal graft

177
Q

Management: duodenal stump blow-out

A

Place lateral duodenostomy tube and drains

178
Q

Potential PEG complications

A

Insertion into the liver or colon

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