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ABSITE 2022 > Chapter 35 - Small Bowel++ > Flashcards

Chapter 35 - Small Bowel++ Flashcards

1
Q

What is absorbed in the small intestine?

A

nutrients and water

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2
Q

What is absorbed in the large intestine?

A

Water

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3
Q

In what portion of the duodenum are most ulcers?

A

bulb- 90% (1st part of duodenum)

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4
Q

What is contained in the second/descending portion of the duodenum?

A

ampulla of vater and duct of santorini

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5
Q

What portions of the duodenum are retroperitoneal?

A

descending (2nd) and transverse (3rd)

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6
Q

vascular supply of duodenum superiorly? inferiorly?

A

GDA superiorly, Inferior pancreaticoduodenal inferiorly

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7
Q

How long is the jejunem? how large are the vasa recta (long or short)?

A

100cm, long vasa recta

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8
Q

The jejunum is the maximum site of absorption for everything except:

A
  • iron - duodenum
  • Ca - duodenum
  • B12 - terminal ileum
  • Bile acids - ileum/terminal ileum
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9
Q

What percentage of NaCl is absorbed in the jejunum? water?

A

95%; 90%

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10
Q

What is the vascular supply of jejunum?

A

SMA

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11
Q

Hos long is the ileum?

A

150cm, short vasa recta, flat. Vascular supply from SMA

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12
Q

What is absorbed at the intestinal brush border?

A

maltase, sucrase, limit dextrinase, lactase

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13
Q

What is the normal diameter of small bowel? transverse colon? cecum?

A

3 6 9cm.

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14
Q

What is the terminal branch of the SMA?

A

Ileocolic

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15
Q

What do goblet cells do?

A

mucin secretion

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16
Q

What do paneth cells do?

A

secretory granules, enzymes

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17
Q

What do enterochromaffin cells do?

A

APUD, 5-Hydroxytryptamine release, carcinoid precursor

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18
Q

What do brunner’s glands produce?

A

alkaline solution

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19
Q

What are peyer’s patches? Where are they increased?

A

lymphoid tissue; increased in the ileum

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20
Q

What are M-cells?

A

antigen presenting cells in intestinal wall

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21
Q

What are the phases of gut motility?

A

I - Rest

II - acceleration and gallbladder contraction

III - peristalsis

IV - deceleration

Motilin is most important hormone in migrating motor complex

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22
Q

What is fat and cholesterol broken down by?

A

cholesterol esteras, phospholipase A, lipase, colipase in combination with bile salts -form micelles -TAG’s are reformed in intestinal cells and released as chylomicrons

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23
Q

What are chylomicrons made up of?

A

90%TAG’s, 10% phospholipids, cholesterol, protein

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24
Q

What percentage of bile salts are reabsorbed?

A

95% -50% passive- 45% ileum and 5% colon -50% active resorption in terminal ileum -conjugated bile is only absorbed in terminal ileum

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25
Q

What is bile acid conjugated to?

A

taurine and glycine can be deconjugated in the colon by bacteria and absorbed there

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26
Q

What are the primary bile acids?

A

cholic and chenodeoxycholic

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27
Q

What are the secondary bile acids?

A

deoxycholic and lithiocholic (from bacterial action on primary bile acids in the gut)

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28
Q

What can happen with the gall bladder after a terminal ileum resection?

A

develop stones secondary to inability to reabsorb bile salts

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29
Q

How is short gut syndrome diagnosed?

A
  • symptoms, not length of bowel
  • diarrhea, steatorrhea, weight loss, nutritional deficiency
  • lose fat, B12, electrolytes, water
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30
Q

What is a sudan red test?

A

checks for fecal fat

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31
Q

What is a schilling test?

A

checks for B12 absorption -radiolabeled B12 in urine

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32
Q

how much bowel do you need to survive with TPN?

A

75cm, 50cm with a competent ileocecal valve

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33
Q

What is the pathology of hypersecretion causing steatorrhea?

A

gastric hypersecretion of acid- increases motility- interferes with fat absorption -Interruption of bile salt resorption- interferes with micelle formation

Tx:control diarrhea- lomotil, codeine, decreased oral intake

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34
Q

Causes of Non-healing fistula?

A

FRIENDS F foreign body R radiation I irritable bowel E epithelialization N neoplasm D distal obstruction S sepsis/infection

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35
Q

High output fistulas normally occur where?

A

proximal bowel and are less likely to close with conservative management

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36
Q

What are most fistulas caused by?

A

iatrogenic -treat conservatively first -40% close spontaneously -can resect bowel secoment and perform primary anastamosis

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37
Q

Obstruction without previous surgery usually caused by what?

A

small bowel- hernia large bowel- cancer

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38
Q

Obstruction with previous surgery usually caused by what?

A

small bowel- adhesions large bowel- cancer

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39
Q

symptoms of bowel obstruction?

A

nausea, vomitting, crampy pain, failure to pass gas or stool -x-ray shows air fluid level, distended loops of small bowel, distal compression

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40
Q

What is the air with bowel obstruction from?

A

swallowed nitrogen

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41
Q

Conservative treatment for SBO?

A

NG IVF -cures 80% of partial SBO, 20-40% of complete SBO

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42
Q

What are the surgical indications for bowel obstruction?

A

Progressing pain, peritoneal signs, fever, increasing of WBC’s, signs of strangulation or perforation, failure to resolve

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43
Q

What is gallstone ileus?

A

-SBO from gallstone in terminal ileum -Air in biliary tree with SBO -caused by fistula bw gall bladder and second portion of duodenum -tx with stone removal -if sick leave fistula -if ok remove gall bladder, fix bowel

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44
Q

What is meckel’s diverticulum?

A

-A true diverticulum -2% of population -2 feet from ileocecal valve -fist 2 years of life

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45
Q

What is meckel’s diverticulum caused by?

A

failure of closure of omphalomesenteric duct 50% of all painless lower GI bleeds in children under 2

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46
Q

What is the most common tissue type found in meckel’s diverticulum? most common to cause bleeds?

A

Pancreas is most common type. Gastric mucosa most common to bleed

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47
Q

What is the most common presentation of meckels in adults?

A

obstruction

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48
Q

How do you localize a meckels?

A

Meckel’s scan (99Tc)- can do diverticulectomy

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49
Q

What do you do with duodenal diverticula?

A
  • observe unless symptomatic; need to rule out gallbladder disease as a cause
    • duodenal>jejunal>ileal
    • segmental resection vs excision if intraluminal
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50
Q

What are the first signs of Crohn’s disease?

A

Intermittent abdominal pain, diarrhea, weight loss, low grade fever -usually 15-35 at first presentation -increased in ashkenazia J’s

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51
Q

What are the extraintestinal manifestations of crohn’s?

A

arthritis, arthralgias, pyoderma gangrenosum, erythema nodosum, ocular diseases, stunted growth, B12/Folate deficiency

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52
Q

What is most comon first involved bowel portion in Crohn’s?

A

terminal ileum (40%) -10% anal perianal first -colon only 35% -small bowel only 20%

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53
Q

What is the pathology of Crohn’s disease?

A

transmural involvement segmental- skip lesions, cobblestoning, narrow deep ulcers, creeping fat fistulas

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54
Q

What is medical tx of Crohn’s?

A

5-ASA, sulfasalazine, steroids, azathioprine, methotrexate, remicade, Loperamide

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55
Q

What are the surgical indications for Crohn’s?

A
  • obstruction
  • abscess
  • hemorrhage
  • blind loop obstruction
  • EC fistula
  • Perineal fistula
  • ano/rectovaginal fistulas
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56
Q

What do u do with incidental finding of IBD with normal appendix in presumed appendicitis?

A

take appendix if cecum not involved

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57
Q

When is stricturoplasty indicated in patients with Crohn’s?

A

diffuse or recurrent strictures (failed endoscopic dilation), save small bowel length, 10% leakage/abscess/fistula rate with stricturoplasty

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58
Q

What are the complications from removal of terminal ileum?

A
  • decreased B12 uptake (megaloblastic anemia)
  • decreased bile salt uptake (leads to increased hepatic production and gallstones)
  • decreased oxalate binding secondary to increased intraluminal fat that binds calcium (leads to Ca oxalate kidney stones)
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59
Q

What are kulchitsky cells?

A

produce serotonin (enterochromoffin cell or argentaffin cells)

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60
Q

what is the breakdown product of serotonin?

A

5-HIAA can be found in urine

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61
Q

serotonin is part of what GI system?

A

amine precursor uptake decarboxylase system - APUD

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62
Q

what is the precursor to serotonin?

A

tryptophan

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63
Q

what can increased levels of tryptophan lead to?

A

niacin deficiency and pellagra

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64
Q

other than serotonin, what do carcinoid tumors also secrete?

A

bradykinin

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65
Q

When do you get carcinoid syndrome?

A
  • bulky liver mets
  • flushing and diarrhea, asthma symptoms, and right heart valve lesions
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66
Q

how do you treat carcinoid syndrome?

A
  • all pts get abdominal exploration unless unresectable
  • if resecting liver mets, also do cholecystecomy
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67
Q

What are the GI sx in carcinoid caused by?

A

vasoconstriction and fibrotic desmoplastic rxn

68
Q

what is a good test for localizing carcinoid when cant find it on CT?

A

octreotide scan

69
Q

where is the most common site for carcinoid?

A

appendix

70
Q

small bowel carcinoid is at increased risk for what?

A

multiple primaries and second unrelated malignancies

71
Q

what do you do with carcinoid in appendix?

A

2 cm or involving base - right hemi

72
Q

what do you do with carcinoid anywhere else in GI tract?

A

treat like ca- segmental resection w lymphadenectomy

73
Q

What is chemo for carcinoid?

A

streptozocin and 5FU

74
Q

what is a palliative tx for carcinoid?

A

octreotide

75
Q

what do you do for bronchospasm in carcinoid? flushing? false 5-HIAA is from what? what can exacerbate sx?

A

Aprotinin

alpha blockers

fruits

pentagastrin

76
Q

What causes intussusception in adults?

A
  • small bowel or cecal tumors
  • presents with bleeding or obstruction
  • tx: oncologic resection (ie w/ lymphadenectomy)
77
Q

what is most common small bowel tumor?

A

leiomyoma- usually extraluminal

78
Q

where are most adenomas of small bowel found?

A

ileum

79
Q

what inheritence is peutz-jehgers? What are sx?

A
  • autosomal dominant
  • jejunal and ileal hamartomas
  • mucocutaneous melanotic skin pigmentation
  • extraintestinal malignancies
  • slight increase in colon ca
  • lipomas, neurogenic tumors
  • hemangiomas
80
Q

what is most common small bowel malignancy?

A
  • adenocarcinoma
  • most in duodenum
  • may need whipple
  • carcinoid is becoming more prevalent
81
Q

what are risks for duodenal ca?

A
  • FAP
  • Gardners
  • polyps
  • adenomas
  • von Recklinghausen
82
Q

where are leiomyosarcomas of small bowel usually found?

A
  • jejunum and ileum
  • most extraluminal
  • hard to differentiate from leiomyoma
83
Q

where are small bowel lymphomas usually found?

A
  • ileum - greatest concentration of gut-associated lymphoid tissue
    • tend to be large (>5cm)
    • up to 25% present as perforation
  • mediterranean variant occurs in young males
    • they get clubbing
84
Q

what is obstruction rate with loop ileostomies?

A

1-2%

85
Q

what types of ostomies have increased risk of parastomal hernia?

A

loop colostomies

86
Q

what is most common stomal infection?

A

candida

87
Q

when do you get diversion colitis and from what?

A

Harmann’s pouch secondary to decreased short chain fatty acids- give short chain FA enemas

88
Q

what is most common cause of stenosis of stoma?

A

ischemia tx with dilation

89
Q

what are abscesses under stoma site caused by?

A

irrigation device

90
Q

what ostomy pts have increased risk of gallstones and uric acid stones?

A

ileostomy

91
Q

sx of appendicitis?

A
  • anorexia
  • periumbilical pain
  • vomiting
  • migrates to RLQ
  • can have Normal WBC
92
Q

most common age for appendicitis?

A

20-35

93
Q

what does appendicitis look like on CT?

A

diameter >7mm, wall >2mm, looks like bulls eye, fat stranding, no contrast in lumen

94
Q

What part of appendix is most likely to perf?

A

midpoint of antimesenteric border

95
Q

when is appendicitis non-operative?

A
  • walled off perforated appendix
  • perc drainage and interval appendectomy
  • f/u colonoscopy to ro perf’d colon ca
96
Q

why are children and elderly more likely to perf?

A
  • delayed dx
  • kids have higher fever, vomitting, diarrhea
  • elderly may be asymptomatic
  • infants rarely get it
97
Q

what do you do abt appendicitis in pregos?

A
  • most common cause of acute abdominal pain in 1st tri
  • more likely in second tri
  • more likely to perf in third tri (confused for contractions)
  • need to make incision where pain is - displaced superior
98
Q

what is fetal mortality with perf’d appendix?

A

35%

99
Q

what is a mucocele?

A
  • can be benign or malignant
  • mucous papillary adenocarcinoma - right hemi
  • if malignant - can get pseudomyxoma peritonei w/ rupture
100
Q

What percentage of pts with regional ileitis go on to have Crohn’s?

A

10%

101
Q

what do you do if you have presumed appendicitis but find ruptured ovarian cyst or thrombosed ovarian vein?

A

do appy anyway

102
Q

most common cause of ileus?

A
  • surgery
  • trauma
  • hypokalemia
  • ischemia
  • drugs
  • dilatation is uniform
103
Q

What do you get with typhoid enteritis?

A
  • bleeding/perforation
  • fever
  • headaches
  • maculopapular rash
  • leukopenia
  • tx with bactrim
104
Q

What gestational layers are the small bowel derived from?

A

endoderm (epithelial lining) and mesoderm (muscle and connective tissue)

105
Q

Where does the omphalomesenteric duct (vitelline duct) originate from? (fore, mid, or hindgut)

A

midgut

106
Q

During intestinal development, failure to complete the 270-degree rotation around the SMA causes what pathology?

A

intestinal malrotation

107
Q

At the confluence of the pre-arterial and post-arterial (SMA) intestinal segments, the vitelline duct joins the yolk sac and is obliterated before delivery. What is the pathology caused by the failure of this process?

A

Meckel diverticulum

108
Q

What are the portions of the duodenum?

A
  1. bulb
  2. retroperitoneal, plicae circulares (dissect for Kocher) - contains ampulla, the “C”
  3. inferior horizontal portion
  4. after the SMA/SMV crosses the duodenum (SMA syndrome occurs here)
109
Q

Chance fractures at the 2nd and 3rd lumbar vertebra can cause injury to what portion of the GI tract?

A

duodenum

110
Q

What portion of the duodenum is intimately associated with the uncinate process and important during surgical resection of the pancreas?

A

third

111
Q

Where does the ligament of Treitz originate from?

A

the right diaphragm crus

112
Q

The blood supply to the first portion of the duodenum?

A

GDA and supraduodenal branch of the proper hepatic artery

113
Q

What is the blood supply to the second and third portions of the duodenum?

A

the superior anterior and posterior pancreaticoduodenal arteries as well as the inferior anterior and posterior; these are branches from the GDA and SMA

114
Q

The fourth portion of the duodenum receives its blood supply from what?

A

the jejunal branch of the SMA

115
Q

What are some differences between the jejunum and ileum?

A
116
Q

What is the terminal artery of the SMA?

A

the ileocecal artery

117
Q

What are the blood vessels supplying the jejunum from the SMA?

A

the vasa recta

118
Q

What is the strongest layer of the bowel?

A

submucosa

119
Q

What layer is the myenteric plexus of Meissner in?

A

submucosa

120
Q

In the duodenum where are the Brunner glands? What do they do?

A

submucosa, secrete mucus and bicarb to neutralize acids

121
Q

What layer are the Peyer patches in the ileum, what do they do?

A

submucosa

122
Q

Enteroendocrine cells (aka APUD) secrete what?

A

GLP-1 and 2, gastrin, serotonin, substance P, VIP

123
Q

Enteroendocrine cells can give rise to what type of pathology

A

carcinoid

124
Q

What do goblet cells do in the small intestine?

A

secrete mucus - lubricate and protect

125
Q

What are the Paneth cells of the small intestine?

A

full of mitochondria, ribosomes, lysosomes - microorganism defense

126
Q

Where does most protein digestion and absorption occur?

A

duodenum and proximal jejunum, require around 1g/kg/d; body cannot use nitrogen efficiently, so it is excreted in urine as urea

127
Q

Describe protein digestion

A
  • starts in stomach: pepsin from chief cells in fundus
    • pepsin secreted 2/2 acidic env, gastrin, vagal
  • duodenum and jejunum: pancreatic peptidases
  • proteins degrade to AAs, dipeptides, tripeptides
  • cotransported with Na into cytoplasm
128
Q

What protein transports glucose and galactose into the small intestine cell?

A

SGLT-1

129
Q

How does glucose get into the portal system?

A

Na-K-ATPase dependent pump through GLUT-2; constant supply needed for CNS and RBC fct

130
Q

What does the majority of fat come in the form of?

A

cholesterol and phospholipids - essential for plasma membrane structure and function

131
Q

Describe fat digestion

A
  • mostly occurs in proximal small bowel
  • duodenum senses acid from stomach, release CCK from I cells
    • pancreas releases lipase, liver releases bile, gallbladder contracts, sphincter of Oddi relaxes
  • lipase - cleaves triglycerides to fatty acids (short, med, long)
  • products mix with bile - micelles (water soluble) - enter cell
  • in cell, triglycerides reform - form larger chylomicron
  • thoracic duct, then SVC
132
Q

What are some of the different properties of short, medium, and long-chain fatty acids?

A
  • short - water-soluble, used as fuel source enterocytes
  • medium - water-soluble, portal circulation, not in typical diet
  • long - primary energy storage, precurors to inflammatory mediators
133
Q

Where is calcium absorbed? How?

A
  • duodenum
  • stimulated through basolateral Ca-ATPase pump
  • hypocalcemia leads to PTH release
  • vit D increased - stim Ca-ATPase - Ca released into systemic circulation
134
Q

Where is iron absorbed?

A
  • duodenum
  • Fe2 state more easily absorbed
  • DMT1 is brush border transporter
  • ascorbic acid and ferric reductase make iron easier to absorb
135
Q

Describe B12 absorption

A
  • required for cellular nucleic acid production and mitosis
  • absorbed in terminal ileum (also bile)
  • binds with intrinsic factor from gastric parietal cells
  • taken up by transcobalamin 2 receptor
  • loss of transcobalamin 2 receptor or IF leads to hypersegmented neutrophils and megaloblastic anemia
136
Q

Where is ADEK absorbed?

A

jejunum

137
Q

Describe the small bowel’s role in immunology?

A
  • tight jcts b/w epithelial cells can disrupt and allow translocation
  • mucus inhibits bacterial growth, movement, attachment
  • Paneth cells produce toxic metabolites
  • M cells endocytose material to distribute to dendritic cells/macs
  • Peyer patches (most in ileum) - lymphocyte proliferation (can be lead point in intussuscx)
  • IgA prevents migration, neutralizes toxins
138
Q

How does erythromycin improve small intestine forward flow?

A
  • binds motilin receptor
  • causes MMC (basal pacemaker rhythm of SB)
139
Q

Where does the intestinal microbiome develop from?

A
  • breast milk
  • vaginal canal
140
Q

How do you manage GIST?

A
  • all greater than 2 cm should be resected w/o LADx
  • locally adv/metastatic - neoadj imatinib
  • if KIT+, and high risk of recurrence - adj imatinib
    • CT/MRI f/u q6 mo while taking adj, then cont close f/u after completion
  • small, low-risk tumors may not need f/u
141
Q

Short segment strictures (5-7 cm) should get what stricturoplasty?

A

Heinecke-Mikulicz - longitudinal incision with transverse closure

142
Q

Focal (<5 cm) strictures should be treated how?

A

can attempt endoscopic dilation if proximal, otherwise resection or Heineke-Mikulicz)

143
Q

When is bowel resection indicated for small bowel stricture in Crohns?

A

segment of small bowel is inflamed or perforated or when there is an abscess or fistula to an adjacent organ

ileocecal resection is performed when the terminal ileum is involved with Crohn disease

margins do not have to be pathologically negative and can include limited ulcers, take margins to palpably normal tissue

144
Q

How could you manage medium strictures (10-15 cm)?

A

Finney stricturoplasty - fold stricture into “U,” longitudinal incision, sew opposed edges together

145
Q

How could you manage a long (>15 cm) stricture?

A

Michelassi - divide stricture, stack in continuity, divide longitudinally, sew opposing edges in a side-to-side isoperistaltic fashion

146
Q

In patients with malignant bowel obstruction, what is a good pharmacological option that can help resolve nausea/vomiting?

A

octreotide

147
Q

In patients with NOMI, what vasodilator can be infused if supportive therapy has been maxed out?

A

papaverine

148
Q

In a patient previously treated for advanced cancer undergoes ex-lap for SBO. Serosa of the distal small intestine appears gray and opaque on surgery. What is this consistent with?

A

radiation injury

can lead to chronic, recurrent partial small bowel obstructions

149
Q

What intestinal abnormality is congenital diaphragmatic hernia associated with?

A

malrotation

strong predilection, found in up to 20% of patients with CDH

150
Q

How do you manage local duodenal adenocarcinoma?

A
  • 1st/2nd portion: pancreaticoduodenectomy
  • 3rd/4th portion: segmental resection
  • do regional lymphadenectomy

adenocarcinoma more likely to present proximally (as opposed to lymphoma and carcinoid - ileum); can bleed and obstruct

151
Q

If a feeding jejunostomy falls out, how do you manage this?

A
  • Make sure there is no peritonitis.
  • Tube replacement at the bedside.
  • If the tube is easily replaced, position in the intestinal lumen should be confirmed with a fluoroscopy study.
  • If the tube cannot be easily replaced and the time from surgery is less than 10 days, the patient will require emergent exploration for tube replacement and to avoid possible peritoneal contamination.
  • If the tube has been in place for at least 10 days, the tube may be replaced electively either in the operating room or with fluoroscopy guidance by IR.
152
Q

High ileostomy output is defined as…

A

greater than 1200 mL/d.

Loperamide can be used. Control lytes and monitor fluid status.

153
Q

Advantages of g-tube vs j-tube

A

bolus feeding, ability to decompress, decreased risk of obstructing tube

154
Q

How is decision-making for ileostomy vs colostomy made?

A
  • For temporary loop ostomy for diversion only: loop ileostomy
    • Reversal is easier compared with loop colostomy.
  • For permanent or immediate fecal diversion: colostomy
    • Particularly in older patients.
    • Has dec for dehydration, lyte abnormalities.
155
Q

A patient s/p colectomy w/ end ileostomy for cancer is set to undergo chemo but develops an ileostomy prolapse. How do you manage this?

A

The best treatment for ileostomy prolapse is to take down the ileostomy (rather than simply revise it), which can wait until the patient finishes chemotherapy unless he has severe symptoms or ischemia.

156
Q

Pt w/ FAP is discovered to have an ulcerated 3-cm periampullary mass. Biopsy shows to be a villous adenoma with high-grade atypia. What is your approach to the management of this patient?

A

Pancreaticoduodenectomy

Large, periampullary, sessile polyps with histologic evidence of high-grade atypia harbor a high risk of occult invasive cancer and so should be definitively resected with radical surgery.

157
Q

How do primary neuroendocrine tumors of the small bowel tend to present?

A
  • if metastatic past liver, can cause sx associated w/ endocrine disease
  • don’t perforate often (as opposed to lymphoma)
  • more likely to obstruct (as opposed to adenocarcinoma)
  • can bleed
158
Q

What extra-intestinal manifestations do not improve after resection of diseased bowel in Crohn’s.

A

hepatobiliary manifestations (primary sclerosing cholangitis and cirrhosis) and axial arthropathies (ankylosing spondylitis and sacroiliitis) do not resolve following resection

159
Q

How do you manage duodenal Crohn’s stricture?

A
  • Duodenal Crohn’s involving 1st and 2nd portions: gastrojejunostomy and vagotomy. Some form of vagotomy is necessary to avoid marginal ulcers.
  • Refractory strictures of 3rd and 4th portions: duodenojejunostomy.
  • Stricturoplasty can be used to avoid resection and conserve bowel for short strictures in the jejunum and ileum.
  • Pancreaticoduodenectomy is NOT performed for duodenal Crohn’s stricture (as opposed to adenocarcinoma or high-grade adenoma in FAP).
160
Q

Discuss mesenteric cysts.

A
  • rare, benign; but more common than omental
  • most commonly in small bowel, ileum
  • psx: nonspecific abdominal symptoms or as an incidental finding on routine imaging
  • dx: unilocular with solid component on imaging
  • tx: all get enucleation/cystectomy - may require resection of associated bowel if resection of the cyst results in compromise of blood supply to adjacent bowel; rarely will need resection
161
Q

PD catheters:

Where is the catheter placed?

What do you do if you find an incidental hernia?

How extensive does adhesion lysis need to be?

How long do pts have to wait before catheter use?

A
  • rectovesical/rectouterine
  • mesh repair intraop to prevent cath compx
  • selective LoA
  • normally 1-2 wks; 4-6 wks w/ hernia repair
162
Q

What are the top 2 presentations of pseudomyxoma peritonei?

A
  • increasing abdominal girth
  • inguinal hernia
  • CT scan shows liver scalloping
  • 2/2 rupture of tumor
  • Tx: HIPEC
163
Q

What is the most common cause of chylous ascites (abdominal chyle) in the Western world?

A
  • malignancy, specifically lymphoma
  • In the developing world, it is 2/2 TB and filiariasis
  • malignancy causing obstruction of lymphatic vessels at the base of the mesentery or the cisterna chyli
164
Q

How do you manage duodenal polyps in patients with FAP?

A
  • complete polypectomy at time of discovery (endoscopic)
  • ongoing surveillance
  • severity of Spigelman score guides tx (number, size, histology)
    • <4 is better, >20 is bad
    • size <4mm better, >10 mm is bad
    • tubulous is better, villous is bad
    • low grade is better, high grade is bad
  • Stage 0-III get increasingly more frequent surveillance
  • Stage IV can get duodenectomy
165
Q

How do you manage unruptured appendiceal mucinous neoplasms?

A
  • standard appendectomy for most cases
  • decision for more extensive resection can be made intraoperatively
  • can also be planned in patients with a complicated radiographic mucocele with involvement of the terminal ileum or cecum, and in patients with known adenocarcinoma with mesenteric or adjacent organ involvement
  • to ensure a complete resection of the lesion at appendectomy, can include a cuff of the cecum with the appendiceal specimen without encroaching on the ileocecal valve
  • if the base of the appendix is involved in the disease process so that a clear margin cannot be achieved by stapling, a partial cecectomy (with preservation of the ileocecal valve), ileocecectomy (resecting the ileocecal valve), or right colectomy can be performed; goal is clear margin
  • can resect the mesoappendix with the specimen so that the regional lymph nodes can be analyzed
  • if a right hemicolectomy is performed to achieve a negative resection margin, it should follow oncologic principles with high ligation of the ileocolic pedicle at its base
    • more extensive lymphadenectomy or routine right hemicolectomy performed solely to increase lymph node yield is not necessary for mucinous neoplasm of the appendix
    • unlike intestinal-type appendiceal tumors, rarely involves nodes
  • do not perform intraoperative frozen section during resection of appendiceal mucinous lesions, as the pathologies of these lesions are most often complex and unlikely to be diagnosed based upon a single frozen section.
166
Q

How do you manage ruptured appendiceal mucinous neoplasm?

A
  • rupture may result in peritoneal dissemination, so careful handling and resection of the lesion is paramount
  • resect the appendix, place in a retrieval bag before extraction
  • if lesion has ruptured but rupture is walled off, right hemicolectomy can be done to remove the contained rupture
  • more extensive surgery aimed at clearing peritoneal mucinous disease (ie, formal cytoreductive surgery) should only be conducted by surgeons with extensive experience with peritoneal malignancies after the return of final pathology
  • at nonspecialized centers, the initial surgery for a ruptured appendiceal mucinous lesion should be limited to an appendectomy or right hemicolectomy, peritoneal washing with fluid cytology, careful inspection of the abdominal cavity with documentation, and biopsy of any suspicious peritoneal lesions
  • the abdomen and surgical wounds should be thoroughly cleaned by irrigation to minimize tumor cell implantation
  • those with gross peritoneal spread of mucin (M1a/b according to American Joint Committee on Cancer [AJCC] staging) should then be referred to a specialized center for further evaluation and management depending on the final pathology
  • those with ruptured appendiceal mucinous lesion and mucin in the right lower quadrant but no gross peritoneal mucin (eg, T4a according to AJCC staging) should be closely followed with imaging and tumor markers, the frequency of which also depends upon the final pathology

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