Small bowel Flashcards

1
Q

What is your framework for considering small bowel tumours

A

Non-neoplastic

  • haemangiomas
  • hamartomas
  • hyperplastic polyps
  • heterotopic tissue (in Meckel’s)
  • endometriosis & dermoid cysts

Neoplastic

  • Benign (adnomas, leiomyomas, lipomas most common)
    • adenomas (15% of benign SB tumours
    • leiomyomas
    • lipomas
    • fibromas
    • neurogenic tumours (neurofibroma & gangliocytic paraganglioma)
  • Intermediate: NET, GIST
  • Primary malignant (CALGary)
    • NET 44% (variable behaviour) - most common tumour in ileum
    • Adenocarcinoma 33% - most common malignancy in duo, decreases throughout rest of SB except in Crohn’s usu in ileum (70%)
    • Stromal tumours 17% - can develop in entire SB
      • GIST (variable behaviuor), leiomyosarcoma, liposarcoma
    • Lymphoma 8%
  • Secondary malignant
    • direct extension (from colonic, gastric, pancreatic or renal)
    • metastatic (melanoma, lung, breast, cervix, sarcoma, colon
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2
Q

Risk factors for small bowel tumours

A
  • congenital conditions
    • FAP (duodenal adenomas & adenocarcinoma)
    • HNPCC (adenocarcinomas throughout small bowel)
    • Peutz-Jeghers (increased risk adenocarcinoma)
    • Neurofibromatosis (leiomyosarcoma, adenocarcinoma, NET)
    • Cystic fibrosis
    • MEN1 assoc w NETs in rare cases
  • acquired conditions
    • chronic inflammation
      • Crohn’s (100x increased risk of adenoca in areas affected w active disease)
      • Coeliac disease (lymphoma & adenoca)
      • Other imunodeficiency states (incl pts on biologic agents) (increased risk non-Hodgkin lymphoma after long-term immunosuppression)
        • HIV: (lymphoma, Kaposi sarcoma)
      • Radiation
      • Smoking
  • pts w colon adenocarcinoma have higher risk of SB adenocarcinoma
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3
Q

Management of small bowel adenocarcinoma

A

determined by location & stage

  • R0 resection w locoregional LN resection = only curative tx
  • consider neoadj chemo if invasion into adjacent structures then re-evaluate 2-3mo later
  • non-infiltrating D1, D3, D4 tumour: can do duodenal resection if R0 resection possible
  • D2 tumours: pancreaticoduodenectomy + regional lymphadenectomy of periduodenal, peripanc & hepatic LNs as well as resection of involved vascular structures
  • Jej & ileal - resection & regional lymphadenectomy
  • TI - ileocaecectomy & R hemi w ligation of ileocolic artery & subsequent regional lymphadenectomy
  • currently no standard adjuvant protocol - most guidelines suggest consider if poorly differenitated or <10LNs; ?FOLFOX may increase OS in advanced disease
  • metastatic disease - FOLFOX or FOLFIRI firstline

Prognosis poor, prob bc of delayed presentation & presence of advanced disease at dx

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4
Q

What is the origin of small bowel neuroendocrine tumours?

A

Arise from enterochromaffin cells (considered neural crest cells) at the base of the crypts between intestinal villae

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5
Q

How are neuroendocrine neoplasms classified?

A
  • 2019 WHO histological grading scheme uses proliferative rate to startify the grades and requires both a mitotic count and the Ki-67 labeling index to be assessed; the higher of these two indices is used to define the final grade in cases where the mitotic rate and Ki-67 index are discordant
  • Poorly differentiated histology and high tumour grade are no longer considered equivalent & while it is true that nearly all poorly differentiated NECs have a high proliferation rate, not all G3 tumours are poorly differentiated
  • the most recent 2019 WHO classification of NENs recognises a category of high-grade (G3) well-differerentiated GEP NETs, & since poorly differentiated NECs are high grade by definition they are no longer assigned a grade
  • NENs also categorised based on embryologic site of origin & secretory product
    • foregut (resp tract, thymus)
      • characteristically produce low levels of serotonin (5-hydroxytryptamine) but may secrete 5-hydroxytryptophan or ACTH
    • midgut
      • high serotonin production
    • hindgut (distal colon, rectum)
      • rarely produce serotonin but may produce other hormones eg somatostatin & peptide YY

55% NETs from GI tract; 30% from bronchopulmonary system; rarer sites include kidneys or ovaries. Previously SB NETs most common (ileum), followed by rectum, appendix, colon and stomach; but since screening colonoscopy started, rectal NETs higher than SB NETs.

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6
Q

Describe the pathological features of NETs

A
  • on gross appearance, well-differentiated NETs of the tubular GIT are often well-circumscribed lesions in the submucosa or extending to the muscular layer/tend to infiltrate bowel wall & may extend through serosa, causing shortening & thickening of mesentery due to intense associated desmoplastic reaction
  • (while those arising in pancreas may be well circumscribed, multinodular or infiltrative)
  • cut surface appears red to tan, reflecting the abundant microvasulature, or sometimes yellow bc of high lipid content
  • well-differentiated NETs show a solid, trabecular, gyriform or glandular pattern, solid nests of uniform small cells w fairly round or oval nuclei, coarsely stippled (‘salt and pepper’) chromatin, and finely granular cytoplasm; little or no cellular pleomorphism, hyperchromasia or increased mitotic activity
  • poorly differentiated NECs are by definition high-grade carcinomas that resemble small cell carcinoma or large cell NEC of the lung - sheet-like or diffuse architecture, irregular nuclei & less cytoplasmic granularity
  • NETs are characterised by production of biologically active amines, which are stored in neurosecretory granules; secretion of these products by tumour cells can result in variety of clinical syndromes
  • most prominent agents secreted = serotonin & substance P; others include corticotropin, histamine, dopamine, neurotensin, prostaglandins, kinins, gastrin, somatostatin, pancreatic polypeptide, calcitonin

NB 30% of SB NETs have multiple synchronous nodules - check whole small bowel

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7
Q

What is carcinoid syndrome?

A
  • a term applied to constellation of sx mediated by various hormonal factors elaborated by some well-diff NETs of digestive tract & lungs which synthesise, store & release a variety of polypeptides, biogenic amines and prostaglandins
  • >90% of pts w carcinoid have metastatic disease, typically to liver
  • carcinoid syndrome affects <10% of pts w NETs
  • primarily assoc w metastatic tumours originating in the midgut; hindgut and foregut NETs uncommonly produce carcinoid syndrome
  • bc of firstpass metabolism of the vasoactive peptides responsible for carcinoid syndrome, hepatic mets or extra-abdo disease are necessary to elicit the syndrome
  • classic description: vasomotor, cardiac, GI manifestations
    • episodic attacks of cutaneous flushing, bronchospasm, diarrhoea & vasomotor collapse, also hepatomegaly & cardiac lesions most commonly right-sided heart valvular disease
  • humoral factors considered to contribute include serotonin, 5-HT (precursor of serotonin), histamine, dopamine, tachykinin, kallikrein, substance P, prostaglandin & neuropeptide K
  • carcinoid crisis = life-threatening form of carcinoid syndrome usu precipitated by a specific event eg aneasthesia, surgery or chemo
    • manifestations include intense flush, diarrhoea, tachycardia, hyper/hypotension, bronchospasm, altered metnal status
    • sx usu refractory to fluid resus & vasopressors
  • other functioning NETs of SB that produce specific clinical syndromes = comparatively rare
    • gastrinoma of duo - ZES (15% of gastrinomas in duo)
    • rarer: duodenal somatostatinomas, paragangliomas, high-grade NECs (rarely functioning)
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8
Q

What is the clinical presentation of small bowel NETs?

A
  • most asymptomatic & incidental
  • symptoms from mass effect
    • intermittent obstruction secondary to intralumninal tumour, or from mesenteric kinking & distortion brought on by tumour invasion & a secondary desmoplastic response
  • pain from vascular compromise secondary to large bulky mesenteric nodal mets or mesenteric vascular invasion +/- contribution from vasospastic effect of serotonin
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9
Q

What is the typical CT appearance of a SB NET?

A

solid mass with spiculated borders & radiating surrounding strands associated with linear strands within the mesenteric fat and kinking of the bowel +/- regional lymph nodes

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10
Q

How do you diagnose carcinoid syndrome?

A
  • initial test = 24hr urinary 5-HIAA (the end product of serotonin metabolism)
    • sens of >90%, spec of 90% for carcinoid syndrome; sensitivity low in pts w NETs w/o carcinoid syndrome
    • generally most useful in pts w primary midgut NETs which produce highest levels of serotonin; foregut and hindgut tumours may produce 5-HT and histamine but no test for urinary 5-HT
  • consider checking gastrin and VIP - some functional pancreatic neuroendocrine tumours can be assoc w severe diarrhoea
  • chromogranin A has low specificity - not recommended as screening test for diagnosis of a NET or carcinoid syndrome; may be appropriate tumour biomarker for pts w established dx of advanced NET in order to assess disease progression
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11
Q

Staging of small bowel NETs

A
  • Duodenum & ampulla:
    • T1 = mucosa or submucosa only, ≤1cm (duodenal) OR ≤1cm & confined within SOO (ampullary)
    • T2 = invades muscularis propria or is >1cm (duodenal) OR invades through sphincter into duodenal submucosa or muscularis propria, or is >1cm (ampullary)
    • T3 = invades pancreas or peripancreatic adipose tissue
    • T4 = invades visceral peritoneum (serosa) or other organs
    • N0 = no regional nodes; N1 = regional nodal involvement
    • M1 = distant mets; M1a = mets confined to liver; M1b = mets in at least one extra hepatic site (eg lung, ovary, nonregional LN, peritoneum, bone); M1c = both hepatic & extrahepatic mets
    • Stage 3 = T4 or N1
  • Jejunum & ileum:
    • T1 = invades lamina propria or submuocosa & is ≤1cm
    • T2 = invades muscularis propria or >1cm in size
    • T3 = invades through muscularis propria into subserosal tissue w/o penetration of overlying serosa
    • T4 = invades visceral peritoneum (serosal) or other organs or adjacent structures
    • N0 = no regional nodes; N1 = regional nodes <12; N2 = large mesenteric masses (>2cm) and/or extensive nodal deposits ≥12, espec those that encase superior mesenteric vessels
    • M1 = distant mets; M1a = mets confined to liver; M1b = mets in at least one extra hepatic site (eg lung, ovary, nonregional LN, peritoneum, bone); M1c = both hepatic & extrahepatic mets (same)
    • Stage 3 = involved nodes
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12
Q

Management of SB NETs

A
  • depends on tumour size, location & presence of metastatic disease
  • <1cm diameter w/o evidence of regional LN mets: segmental intestinal resection
  • >1cm with multiple tumours or w regional LN mets, regardless of size of primary tumour: wide excision of bowel & mesentery required
    • lesions of TI = R hemi
    • Small duo tumours can be excised locally but more extensive lesions may require pancreaticoduodenectomy
  • lap is safe
  • caution with anaesthesia: may precipitate carcinoid crisis characterised by hypotension, bronchospasm, flushing and tachyarrhythmias
    • carcinoid crisis is treated w IV octreotide - bolus of 50-100ug, whihc may be continued as an infusion at 50ug/hr
  • important to explore abdomen for multicentric lesions
  • often a large desmoplastic rxn causing shortening, folding & pleating of SB mesentery resulting in intestinal angina & obstruction; in cases where mesenteric disease appears to involve a large portion of mesentery, appropriate to dissect tumour off mesenteric vessels, w preservation of blood supply to unaffected bowel
    • extensive mobilisation of SB mesentery may be required
    • removal of mesenteric disease provides significant survival advantage & ensures most durable palliation for the pt
  • in pts w widespread metastatic disease, surgery may still be indicated bc definite role for surgical debulking which often provides beneficial symptomatic relief
    • also improves survival & slows progression of liver mets
    • liver mets may also be resected
  • medical therapy
    • somatostatin analogues (octreotide & lantreotide) - relieve sx of carcinoid syndrome & delay progression (though not all asymptmoatic pts treated initially)
    • everolimus (mTOR inhibitor) - can slow progression
    • others eg VEGF pathway inhibitors (sunitinib)
    • poor response to chemo but streptozocin, 5-FU and cyclophosphamide or temozolomide +/- capecitabine or cisplatin & etoposide in poorly diff NECs
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13
Q

What is required for a diagnosis of primary GI lymphoma?

A
  • no peripheral or mediastinal lymphadenopathy
  • normal WCC & differential on peripheral blood smear
  • tumour involvement must be predominantly in GI tract
  • no evidence of liver or spleen involvement
  • primary GI lymphoma = most common extranodal form of lymphoma; stomach (25%) & SB most common sites
  • risk factors: autoimmune diseases, immunodeficiency syndrome/drugs, Crohn disease, radiation therapy, nodular lymphoid hyperplasia
  • in SB, most common in ileum bc arises from lymphoid aggregates in submucosa & ileum is lymphoid follicle-rich

Can be low or high grade and of B or T cel origin

  • non-Hodgkin lymphomas
    • B cell lymphomas that most often involve GI tract: MALT type, DLBC, mantle cell, Burkitt and Burkitt-like
      • MALT occur most often in stomach; mantle cell in colon & SB
    • T cell less common - most often jejunal
  • primary/secondary involvement of GI tract by Hodgkin lymphoma = v rare
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14
Q

Causes of SBO

A

By frequency

  • developed world: adheisons (60%), malignancy (20%, mostly peritoneal disease), hernias (10%), Crohn’s (5%), other (5%)
  • developing world: hernia most common

By category

  • Extraluminal
    • adhesions
      • congenital
      • acquired - post-op, inflammatory, chemical (eg starch, talc)
    • neoplastic
      • peritoneal disease eg ovarian, pancreatic, gastric, colon
      • extraintestinal neoplasms
    • infection - eg diverticular abscess, TOA
    • hernia
      • primary
        • inguinal, femoral
        • paraduodenal, foramen of Winslow, diaphragmatic
      • secondary
        • incisional
        • post-op internal hernia after bariatric surgery
    • endometriosis
  • Intraluminal - bezoar, food bolus, enterolith, gallstone, foreign body
  • Mural
    • inflammatory
      • Crohn’s (acute flare or stenosis), TB, actinomycosis, eosinophilic gastroenteritis
      • vasculitides eg scleroderma
    • intussusception
    • congenital
      • duplication cyst
      • malrotation/volvulus
      • jejunal/ileal atresia
    • neoplastic
      • primary: NET, adenocarcinoma, GIST, lymphoma
      • secondary
    • trauma - haematoma
    • iatrogenic
      • post radiation stricture
      • anastomotic stricture
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15
Q

Pathophysiology of SBO

A
  • obstruction –> onset of vigorous SB peristalsis (both prox & distal to obstruction) to try & propel luminal contents past obstructing point –> colicky pain, usu in central abdo
    • can account for sometimes initial diarrhoea
    • later intestine becomes fatigued & dilates; contractions become less frequent & less intense
  • proximal dilatation of intestine and with time, bowel wall becomes oedematous, with loss of normal absorptive function & fluid is sequestered into bowel lumen; this & fluid loss thorugh vomiting –> hypovolaemia
    • loss of hydrogen & chloride ions –> alkalosis, hypochloraemia & hypokalaemia (from renal compensation)
  • ischaemic necrosis of bowel most commonly caused by twisting of bowel and/or its mesentery around an adhesive band or intestinal attachments; alternatively if bowel dilation is excessive, as intraluminal pressure increases in bowel, venous pressure is eventually surpassed –> oedema & congestion –> intramural vessels of SB become compromised so perfusion to intestine reduced –> ischaemia –> necrosis and perforation if process not interrupted
    • –> worsened, continuous (cf colicky) pain followed by perforation if left
  • if blood supply remains intact & bowel decompressed by vomitign & NG drainage, peristalsis will stop & colicky pain ceases, leaving dilated, non-functioning bowel
  • flora of SB changes dramatically in both type of organism (most commonly E coli, Strep faecalis & Klebsiella) & quantity increases markedly
    • increased bacteria translocating to mesenteric LNs & even systemic organs
    • bacterial translocation amplifies local inflammatory response in gut –> intestinal leakage & increased systemic inflammation +/- systemic sepsis & multiorgan failure
  • other consequences of bowel obstruction include increased abdo pressure, decreased venous return & elevation of diaphragm, compromising ventilation
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16
Q

Non-operative SBO management

A
  • non-operative management is successful in 65-80% of pts w adhesive SBO
  • gastrografin is a hypertonic water-soluble contrast that has both diagnostic & therapeutic properties
    • draws fluid into lumen of bowel due to its hypertonicity, decreasing intestinal wall oedema & stimulating intestinal peristalsis
    • identifies early pts who require surgery & those who dont’ thus reducing hospital stay & accelerating resolution of SBO in pts who would have resolved w/o surgery, but doesn’t reduce need for surgical intervention
    • contraindicated in pregnancy, presence of bowel compromise & has only been studied in pts w adhesive SBO therefore shouldn’t be given to pts w nonadhesive causes
    • aspirate to dryness, 100mL undiluted GG, clamp for 2-4hrs, AXR in 6-24hrs at convenient time
    • radiological appearance of contrast in colon within 24hrs predicts resolution in 99% of pts
    • failure of contrast to reach colon 24hrs later should influence but not dictate decision to operate; signif % of pts may require longer duration of nonop mx for successful resolution; most would wait up to 3-5days before operating (though stable pts w known frozen abdomens/other complicating factors may be observed for longer +/- w PN
  • pathologies other than adhesions that warrant trial of non-op mx:
    • inflammatory bowel disease - medical mx
    • infections SB disease eg TB - medical mx
    • colonic diverticulitis
    • radiation enteritis - higher risk of anastomotic leak so best avoid surgery
    • malignant obstruction
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17
Q

Options for malignant SBO

A
  • remember some are from adhesions not malignancy
  • no consensus/evidence re optimal strategy
  • weight risks & benefits, life expectancy, goals of care
  • medical mx - fluid diet, steroids, NG, PEG
  • surgical mx - resection, bypass, stoma, bail
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18
Q

Management of small bowel radiation enteritis

A
  • can present w acute abdomen during radiotherapy due to radiation enteritis or w acute-on-chronic attack many yrs later
  • if obstruction from fibrosis from prev radiotherapy: prolonged non-op mx even w IVN may be preferable to surgery - adhesions often dense & if SB injured, signif risk it might not heal whether repaired or anastomosed
    • if anastomosis necessary, should only anastomose irradiated bowel to non-irradiated bowel
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19
Q

Incidence of small bowel diverticular disease (excluding Meckel’s)

A
  • most common in 6th & 7th decades
  • symptomatic diverticula most common in duo (79%); jejunum or ileum in 18%; all 3 in 3%
  • 60% also have colonic diverticula
  • duodenal relatively common - 20% in autopsies
    • rare <40yrs
    • most common duo location is near ampulla
  • jejunoileal diverticula much more rare; 0.1-1.5% in autopsies
    • usually mulitple & localised to prox jejunum; distal jej & ileum less frequently affected
    • mainly in 60s+, often have connective tissue disorders
      *
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20
Q

Classificaiton of small bowel diverticular disease

A
  • congenital vs acquired
    • congenital - Meckel and intraluminal
  • intrluminal vs extraluminal
  • true vs false
    • true = all 3 coats of bowel present in wall of diverticulum (Meckel)
    • false = wall lacks proper muscle coat - mucosa & submucosa protrude througha. defect in muscle coat
      • extraluminal duodenal diverticula
      • most jejunoileal diverticula
  • by location - duodenal, jejunal, acquired

Vast majority are extraluminal and acquired

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21
Q

Aetiology of small bowel diverticula

A

Duodenal

  • extraluminal (most common) = false (acquired as a result of herniation through a defect caused by entrance of large vessels supplying bowel wall
    • combo of increased intraluminal pressures & intrinsic weakness of muscular layer thought to play a role
    • diverticula that are juxtapapillary/periampullary (located 2-3cm adjacent to ampulla) = assoc w inc risk of choledocholithiasis w bilirugin-containing pigment stones (also pancreatitis); poss mechanisms:
      • primary intraductal stones from biliary stasis due to extrinsic CBD compression
      • duo content reflux through incompetent SOO
      • stasis-assoc bacterial contamination of CBD allowing deconjugation of bilirubin glucuronide & precipitation of bile salts
  • intraluminal = ‘windsock diverticula’ - result from incomplete canalisation of foregut, producing duodenal diaphragm or web during embryonic development
    • lined on both sides w duo mucosa, and an eccentric opening is usu proximal in the sac

Jejunoileal

  • usu false (mucosa & submucosa only)
  • aetiology unclear but intestinal dysmotility & high intraluminal pressures thought to play a role; freqeuntly assoc w intestinal dysmotility conditions eg progressive systemic sclerosis, visceral neuropathies & myopathies
  • protrusion of mucosa through defects in lamina muscularis mucosae, where vasa recta penetrate bowel wall –> diverticula on mesenteric side of bowel
  • (Meckel - covered elsewhere - true diverticula on antimesenteric side)
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22
Q

Clinical presentation of SB diverticula

A
  • most asymptomatic, incidental
  • jejunoileal diverticula may present w early satiety, bloating, chronic abdo discomfort and diarrhoea/steatorrhoea due to bacterial overgrowth
  • duodenal diverticulosis most commonly presents w postprandial epigastric cramping pain & vomiting from partial or intermittent duo obstruction
  • complications:
    • SBO from volvulus or enterolith impaction
    • acute diverticulitis +/- complications of abscess, fistula or perforation)
    • GI bleeding secondary to diverticulitis w ulceration, diverticulosis w associated trauma, AV malformations
    • obstructive jaundice/recurrent pancreatitis -periampullary duo diverticulum can cause bile duct obstruction
    • iatrogenic perforation of periampullary diverticulum at ERCP

Pathophysiology of bacterial overgrowth/blind loop syndrome: 0.stasis of intestinal contents within distended diverticulum can –> bacterial overgrowth, deconjugation of bile salts & uptake of vit B12 by the bacterial flora –> malabsorption w hypoproteinaemia, steatorrhoea & megaloblastic anaemia, w or w/o neuropathy (essentially a blind loop syndrome)

23
Q

Management of complications of small bowel diverticula

A
  • asymptomatic - no treatment
  • SB bacterial overgrowth - antibiotics
    • for jejunoileal diverticula assoc w dyskinesia/pseudo-obstruction can give metaclopramide
  • symptomatic intraluminal duodenal diverticula - duodenotomy & excision usu necessary (endoscopic resection has been successful however)
  • obstruction from enterolith impaction - enterotomy & stone extraction or manual crushing & milking the stone distally into colon
  • choledocholithiaiss - ERC Pw sphincterotomy & stone removal then lap chole
  • acute diverticulitis - antibiotics +/- laparotomy & resection if perforation

Management of perforated duodenal diverticulum:

  • most common & effective = diverticulectomy - wide Kocher maneuver that exposes duo, diverticulum then excised & duo closed transversely or longitudinally, whichever produces least amount of luminal obstruction
    • care to identify ampulla to prevent injury to CBD & panc duct
  • for diverticula embedded deep within HOP: duodenotomy w invagination of diverticulum into lumen, which is then excised & wall is closed
  • for diverticula assoc w ampulla of Vater:
    • extended sphincteroplasty through common wall of ampulla in diverticulum
    • if CBD enters directly into diverticulum & diverticulum becomes obstructed: either choledochoduodenostomy or Roux-en-Y choledochojejunosotmy may be safer than attempting to excise diverticulum & reimplant bile duct
  • lap duodenal diverticulectomy safe & effective - endoscopic stapler most commonly used to traverse & resect diverticulum at its base & omental patch reinforcement over staple line
  • perforated diverticulum: may require excision of diverticulum & closure of duo w serosal patch from a jejunal loop
    • if surrounding inflam severe, divert enteric flow away from site of perforation w a gastrojej or duodenojejunostomy + interrupt duo continuity proximal to perforated diverticulum using pyloric closure w suture or row of staples
  • if diverticulum posterior & perforates into substance of pancreas, operative repair difficult & dangerous - consider wide drainage w duo diversion
  • consider surgical jejunostomy for pts w acute perforation to ensure nutrition repletion
24
Q

Aetiology, Investigation & Management of SB bleeding

A

Aetiology

  • commonest causes = vasc malformation, jejunal diverticula, peptic ulceration in a Meckel’s, SB tumour
  • other causes of ulceration:
    • vascular - vasculitis, GCA, amyloidosis, Behcet’s ischaemia
    • infections - TB, syphylis, typhoid, CMV, parasites, Campylobacter, Yersinia
    • autoimmue/inflammatory - crohn’s, SLE
    • metabolic - uraemia
    • iatrogenic/idiopathic - radiation, drug induced (NSAIDs, steroids)
    • neoplastic - lymphoma, adenocarcinoma, melanoma

Investigations

  • exclude gastroduodenal source
  • capsule endosocpy
  • double balloon endosocpy - can also allow for endoscopic therapies eg APC of vasc malformations & if endoscopic mx unsuccessful can tattoo lesion for surgical resection
  • limitations of CTA: mobility & variable anatomical layout of SB, which can make it difficult at laparotomy to pinpoint a radiologically identified bleeding point
  • red cell scan for Meckel’s
  • make every effort to localise preop

Management

  • embolisation risks ischaemia
  • interventions that can help localisation at laparotomy:
    • tattoo v double balloon endoscpy
    • vasc malformations eg haemangiomata may be visible at transillumination
    • intraop endoscopy
    • if bleeding appears brisk, segmental SB clamps can be placed throughout SB, resecting the segment that fills up w blood after period of waiting
    • laparosocpy not practical as bowel needs to be palpated & illuminated
  • if no bleeding point identified:
    • close abdomen and wait, hoping further bleeding doesn’t occur
    • or divide SB around its midpoint, bringing out 2 stomas; if bleeding recurs can be identified to one side & endscopy used to localise further
25
Q

Radiation enteritis - classification and pathogenesis

A

Classification

  • acute - affects 20-70%, transient
  • chronic - affects 5-15%, progressive
  • (initial toxicity generally resolves within a matter of wks; chronic changes can develop months-yrs later)

Pathogenesis

  • GI epithelium has high proliferation rate so susceptible to injury from rad & chemo
  • primary effect of rad = on mucosal stem cells within crypts of Lieberkuhn; stem cell damage, either directly or as a result of microvasc damage –> decreased cellular reserves for intestinal villi –> mucosal denudation w assoc intestinal inflammation, oedema, shortened villi, decreased absorption area
  • subsequent histo changes in chronic form include progressive obliterative vasculitis of blood vessels wtihin bowel wall & submucosal fibrosis –> eventually thrombosis, vasc insufficiency, chronic intestinal ischaemia
  • mucosal ulcerations can occur –> perforation, fistulas or abscess formation
  • as ulcers heal –> fibrosis & stricture
  • stasis –> SB bacterial overgrowth
  • these chronic changes can impair absorption of fast, carbs, proteins, bile saltes & vitB12 –> loss of water, electrolyte s& proteins in SB
    • lactase degradation can be impaired –> increased bacterial fermentation & flatulence, distension, diarrhoea
    • bile salt resorption may be impired –> inc amount sof conjugated bile salts in colon –> bile salts then deconjugated by bacteria –> intraluminal water retention w resultant diarrhoea
  • NB colon generally less radiosensitive than SB but when radiation injury does involve colon, can develop a pancolitis that mimics inflammatory bowel disease
26
Q

Risk factors for radiation enteritis

A
  • dose & schedule
  • limited bowel motility - increases amount of rad delivered to a specific segment of the intestines, eg if previous PID/endo/pelvic surgery
  • chemo - combined w RT increases risk
  • vascular disease - preexisting from smoking, diabetes, hypertension, atherosclerosis
  • collagen vascular disease - eg RA, SLE may have lower GI tolerance to rad
27
Q

Clinical presentation of radiation enteritis

A
  • Acute: diarrhoea, abdo pain, N&V, anorexia, malaise
    • rad-induced diarrhoea often appears during 3rd wk of tx - in 20-70% pts
    • sx typically disappear 2-6wks after completion fo RT; pts who develop acute SB toxicity may be at higher risk for later effects
  • Chronic:
    • typically presents 8-12mo after RT but may be yrs later
    • dysmotility, stricture formation, malabsorption, diarrhoea
    • bloating, excessive gas, borborygmi from SB bacterial overgrowth
    • bleeding/abdo pain from ulceration
    • fever from abscess formation
    • intermittent partial/complete SBO from strictures
    • labs: vit B12 def from SB bacterial overgrowth, hypoalbuminaemia, anaemia form malnutrition or bleeding
28
Q

Meckel’s diverticulum - rule of two’s

A
  • 2% of population
  • M:F 2:1
  • within 2feet of IC valve
  • can be 2 inches in length (though in practice size can vary)
  • a Meckel’s that bleeds is usually lined by 2 different types of mucosa: the native intestinal mucosa & a heterotopic mucosa (most common types of heterotopic mucosa = gastric; or pancreatic or colonic)
29
Q

Aetiology of Meckel’s diverticulum

A
  • results from incomplete closure of the omphalomesenteric, or vitelline duct, which connects the midgut to the yolk sac in the fetus, and normally undergoes obliteration at approx 8th wk of gestation
  • persistence of the omphalomesenteric duct beyond fetal development may result in variety of anaotmic patterns, incl omphalomesenteric cysts, omphalomesenteric fistulae that drain through umbilicus, and fibrous bands from diverticulum to umbilicus
  • remnant of L vitelline artery can also persist to form a mesodiverticular band, which connects the Meckel’s to the ileal mesnetery (& can cause obstruction)
  • most common form = a diverticulum w/o additional attachment = Meckel’s diverticulum
  • embryological origin of ectopic tissue within the walls of the diverticulum not known
30
Q

Discuss the pathological features of a Meckel’s diverticulum

A
  • antimesenteric border 45-60cm prox to IC valve
  • may exist in different forms, ranging from small bump to long projection communicating w umbo w persistent fibrous cord or to ileal mesentery via remnant of L vitelline artery forming a mesodiverticular band
  • usu = wide-mouthed diverticulum ~5cm length & 2cm wide
  • true diverticulum
  • 60% (and in 20% the proximal mucosa) have heterotopic epithelium - gastric most common (50%), pancreatic 5%, colonic less common
  • neoplasms in 0.5-3.2% - majority benign, NETs
  • lifetime risk of complications from Meckel’s = 4-6%
31
Q

Clinical presentation of a Meckel’s diverticulum

A
  • most asymptomatic/incidental
  • symptomatic
    • GI bleeding most common - 25-50%
      • most common symptomatic presentation in kids ≤2yrs and usu occurs <30yrs
      • usual source = ulceration of SB due to acid secretion by ectopic gastric mucosa within the diverticulum; site of mucosal ulceration & bleeding just adjacent to diverticulum
    • obstruction - 35% of symptomatic
      • from band adhesion (mesodiverticular band or fibrous band to abdo wall) or volvulus of SB around a fibrotic band attached to abdo wall
      • intussusception
      • abdo wall hernia w Meckel’s incarcerated = Littre’s hernia
    • diverticulitis - 10-20% of symptomatic
      • more common in adults
      • thought to be from obstruction of diverticular opening from enterolith, inflammatory tissue, food/other FB or tumour; can also occur from peptic ulceration from heterotopic gastric mucosa
    • neoplasms - usu incidental

Clinical features assoc w increased risk of developing sx = age <50, male, diverticulum lenght >2cm, presnece of histologically abnormal tissue

32
Q

Diagnosis of a bleeding Meckel’s

A
  • usualy have already had top & tail scopes
  • if diagnostic testing unhelpful or unstable may need exploratory laparotomy/laparoscopy
  • if brisk bleeding: conventional contrast angiography - dx established based on finding of an anomalous SMA branch feeding the diverticulum +/- active contrast extravasation (but not usu poss to embolise)
  • CT angiography (can detect bleeding as little as 0.3mL/min)
  • Meckel’s scan - in stable pts w less severe or intermittent GI bleeding & for whom suspicion of Meckel’s high
    • nuclear medicine study using 99m technetium pertechnetate which has affinity for gastric mucosa - given IV then scintigraphy performed to identify areas of ectopic gastric mucosa (but won’t see Meckel’s that doesn’t have gastric mucosa)
  • may also be dx on double-balloon enteroscopy or capsule endoscopy
33
Q

Management of Meckel’s diverticulum

A
  • incidental on imaging studies (adults & children) - do nothing (4-6% lifetime risk of complications & 5% risk of operative complications
  • asymptomatic Meckel’s found at operation
    • consider pt’s clinical status, lifetime risk of Meckel’s related complications & anatomic features assoc w developing sx
    • children (some say ≤8, some say to young adulthood) - resect
    • adults <50yrs, otherwise healthy, Meckel’s >2cm length or palpable abnormality - resect
    • adults >50yrs - only resect if palpable abnormality
  • symptomatic - resect (segmental resection)
34
Q

Management of SBO in ‘virgin abdomen’

A

There is data to indicate that even in pts w a ‘virgin abdomen’, adhesions are still the most common cause of SBO; underlying malignancy in only 10%, same prevalence in pts who have had previous surgery.

Non-operative management is successful in 615% with a recurrence rate of <10% over 4.5yr f/u

35
Q

What is the likelihood of a recurrent SBO after laparotomy for adhesiolysis?

A

20-30% get recurrent obstruction

After first adhesiolysis, on average 2.7 further ‘episodes’ per patient over 15yrs

36
Q

What is the pathophysiology of adhesions?

A

Adhesions can be primary or secondary (post-op or related to inflammation eg Crohn’s, previous diverticulitis)

  • The body deposits fibrin onto injured tissues as part of the body’s healing process after surgery
  • Usually local plasminogen activators initiate lysis of fibrin strands within 3days of their formation & mesodermal cells regenerate as early as 5 days after injury. Inadeqaute fibrinolysis due to decreased mesothelial plasminogen activity allows fibroblastic proliferation to produce fiborus adhesions.
  • surgery diminishes fibrolytic activity dramatically by increasing levels of plasminogen activator inhitiors and by decreasing tissue oxygenation; fibrinolysis can also be impaired by
    • thermal injury
    • desiccation
    • ischaemia
    • foreign bodies
    • blood
    • bacteria
    • some drugs
37
Q

What are some methods for preventing adhesion formation?

A

Methods are directed at mechanisms of adhesion formation; preventive measures may

  • minimise injury
  • introduce barrier between injured surfaces
  • prevent coagulation of the serous exudate
  • remove of dissolve the deposited fibrin
  • inhibit the fibroblastic response to the tissue injury
  • involve recombinant tissue plasminogen activator & novel fibrinolytics
  • technical measures (limit or prevent initial peritoneal injury)
    • gentle handling, avoid dmaage to serosa, meticulous haemostasis, keep surgical field moist
    • adequate irrigation & removal of infectious & ischaemic debris
    • remove talc/starch from gloves before entering peritoneal cavity
    • fine non-reactive suture mateiral where possible - avoid silk sutures in abdomen
    • lap surgery - smaller incisions, less handling of tissue, less exposure to FBs
  • barrier agents (don’t actively interfere w inflammation & wound healing but act as a spacer that separates injured surfaces of peritoneum, allowing these surfaces to heal w/o forming fibrinous attachments which eventually lead to adhesions)
    • include
      • solid materials (absorbable sheets, non-absorbable prosthetic materials)
        • Seprafilm (sodium hyaluronate-based carboxymethylcellulose sheet)
        • Interceed (oxidised regenerated cellulose sheet
      • viscous fluids introduced into abdomen
        • polyethylene glycol, hyaluronic acid - no great evidence
    • aimed at keeping damaged peritoneal surfaces separated during first 5-7 days after surgery til reepithelialisation
    • doo limit extent of adhesions but unclear if change clinical outcomes
  • pharmacologic therapies to interfere w or modify peritoneal response to injury - none approved for use
38
Q

What is the aetiology of intestinal non/malrotation?

A

Normal

  • midgut herniates out of abdominal cavity through umbilical ring at ~4th-5th wk of embryonic development
  • by 10th wk begins to migrate into abdominal cavity in a counterclockwise rotation around axis of SMA; eventually end up with a 270 degree rotation
  • DJ segment returns first and rotates beneath & to right of SMA to fix in LUQ at ligament of Treitz
  • caecocolic segment also rotates counterclockwise around SMA to rest in final position in RLQ
  • by week 12, this process of intestinal rotation is complete & colon becomes fixed to retroperitoneum
  • normal rotation & fixation result in a wide-based mesentery that extends form ligament of Treitz in LUQ to ICV in RLQ

Most anomalies of rotation result in an abnormally narrow mesenteric base which gives a risk of volvulus of the midgut.

  • Complete nonrotation of midgut = most common
    • neither DJ nor caecocolic limb undergoes correct rotation so SB located on right of abdomen & colon on left
  • Nonrotation of DJ limb, followed by normal rotation and fixation of caecocolic limb (usually partial caecocolic rotation of 90degrees rather than 100degrees) results in caecum ending up in mid-upper abdomen with the caecum fixated to the right lateral abdo wall by Ladd’s bands (bands of peritoneum that extend from colon across anteiror duodenum; can cause extrinsic compression & obstruction of duo
  • Others
    • reverse rotation of DJ limb –> duo rests anterior to SMA
    • reverse rotation of caecocolic limb –> transverse colon posterior to SMA
    • reverse rotation of DJ limb w normal rotation of caecocolic limb –> paraduodenal hernia; duo anterior to SMA & anteiror to duo, caecoclic limb rotates nromally & mesentery of right colon creates a pouch into which SB can herniate
  • 60% of children w intestinal malrotation have an associated anomaly; congenital diaphragmatic hernia, congenital heart disease & omphalocele common; also gastrocschisis, certain types of intestinal atresias, oesophageal atresia, biliary atresia, Meckel, complex anorectal malformations
39
Q

What are the clinical implications of intestinal malrotation/nonrotation?

A
  • volvulus bc narrow mesenteric base permits abnormal mobility of SB ie mesentery twists around SMA
  • duodenal obstruction from Ladd bands, or associated duo atresia or stenosis
  • most symptomatic pts present early in life (neonates or during first yr) but some. as older children/adults
  • asymptomatic
  • usu acute but sometimes chronic intermittent volvulus, or more subtle with early satiety or weight loss
  • im meomates can have duodenal obstruction from Ladd bands or associated duo atresia or stenosis - bilious vomiting w/o abdo distension
40
Q

What are th radiological findings for intestinal non/malrotation?

A
  • plain xray
    • gasless abdomen, mild intestinal dilatation or normal
    • NG extending into abnormally positioned duo
    • double-bubble sign w distal gas present (double-bubble w/o distal gas = more likely duodenal atresia); partial obstruction of duo causes distension of stomach & first part of duo
  • upper GI series
    • misplaced duo w ligament of Treitz on right side abdo
    • duodenum w ‘corkscrew’ appearance
    • duo obstruction which may appear simila to that seen w duodenal atresia (dilated stomach & prox duo), or may present w ‘beak’ appearance if volvulus present
    • normally duo should descend, cross midline then ascend to level of pylorus; any deviation from this normal course = malrotation or nonrotation
  • CT
    • 3rd part of duo doesn’t pass between mesenteric artery & duo
    • prox SB mostly located to right of midline
    • vertically oriented or reversed relative position of SMV and SMA (vein normally located to right of artery)
    • ‘whirlpool’ sign present indicating twisting of blood vessels around mesenteric pedicle
    • caecum in LUQ rather than RLQ
    • extraintestinal anomalies eg absence of panc uncinate process or polysplenia syndrome
41
Q

What is the surgical management of symptomatic malrotation

A

Ladd procedure; purpose is not to return the bowel to a normal configuration, which is anatomically impossible, but rather to minimise future risk of volvulus by

  • widening the base of the mesentery
  • placing bowel in position of nonrotation
  • to create adhesions which ‘hold’ intestine in place, making subsequent volvulus less likely

5 steps:

  1. Assessment of volvulus
    • eviscerate bowel to assess for volvulus/ischaemia; untwist counterclockwise if volvulus, resect any clearly non-viable bowel
  2. Division of Ladd bands, if present
    • fibrous bands that run between caecum & duo; can cause duo obstruction so should be completely divided
    • straighten duo w Kocher manoeuvre to prevent incomplete division of Ladd bands
    • unlike in neonate, Ladd bands in adults = quite thick & vascular therefore should be divdied w cautery
  3. Intermesenteric band division
    • fibrous bands between bowel loops other than caecum & duo; because they constrict the mesenteric base, these are also divided as part of Ladd procedure - ie widens base of mesentery
    • when doing this should ‘run’ entire bowel several times to ensure all bands divided
  4. Appendicectomy
    • frequently incorporated bc appendicitis dx often delayed w appendix being in aberrant position; audit showed no increased complication rate w appendicectomy - though in some may be useful to leave behind eg if may be required for urological reconstruction or appendicostomy for example
  5. Place viable bowel in position of nonrotation (ie SB on right, colon on left)
    • if viability of bowel in question, can close abdomen & relook in 24-36hrs
42
Q

Management of asymptomatic intestinal malrotation

A

Children

  • most pts w volvulus present in newbowrn period but not celar that risk of volvulus decreasees w age & difficult to determine on imaigng whether pt w rotational anomaly has a narrow-based mesentery which increases risk of volvulus
    • many recommend elective surgery espec for pts who are younger & at low risk for postop m&m
    • others advocate for laparoscopy to assess ombility of colon & width of mesentery
      • if narrow mesenteric attachment & potential colonic mobility do Ladd’s procedure
      • if atypical malrotation & wide mesenteric base (ligament of Trietz at or to left of midline but below pylorus) can be observed

Adults

  • if having appendicectomy & malrotation found on CT & confirmed intra-op, can add Ladd procedure to appendicectomy, espec if hx of chronic GI complaints
  • if asymptomatic & dx by imaging alone, choice between operative correction or continued watchful waiting controversial; many favour Ladd procedure due to potential risk of bowel ischaemia
43
Q

What is blind loop syndrome/bacterial overgrowth? What are its consequences?

A
  • rare condition resulting from bacterial overgrowth in stagnant areas of the small bowel
  • Predisposing factors:
    • immunodeficiency syndromes
    • structural - blind loop, jejunal diverticulae, SB stricture, enterocolic fistula
    • decreased SB motility eg scleroderma
    • decreased gastric acid secretion
  • Pathology
    • usual mechanisms to limit bacterial populations include:
      • continued flow of luminal contents from peristalsis & myoelectric complex
      • gastric acidity
      • local effects of immunoglobulins
      • prevention of reflux of colonic contents by ileocaecal valve
    • with stasis, number of bacteria increases
    • effects of bacterial overgrowth
      • bile salt deconjugation & dihydroxylation of bile salts in proximal SB –> steatorrhoea
        • deconjugated bile salts –> inadequate micelle formation to solubilise fat
        • unabsorbed FAs enter colon –> cause increased net secretion of water & electrolytes –> diarrhoea
        • hypocalcaemia occurs bc Ca is bound to unabsorbed FAs
      • anaerobic bacteria compete for & bind B12 –> malabsorption of B12 –> macrocytic anaemia
      • bacteria catabolise CHO & protein
      • may cause mucosal damage –> impairs absorption, incl CHO & protein
44
Q

What are the investigations for blind loop syndrome?

A
  • check fat-soluble vitamins & B12
  • can diagnose bacterial overgrowth with
    • culture of upper GI (jejunal) aspirate: bacterial counts of >10 to the power of 5 usu abnormal (gold standard)
    • indirect tests eg 14C-xylose or -cholylglycine breath tests; excessive bacterial use of 14C substrate –> increase in 14C-labelled CO2
      • accuracy of these limited, nevertheless most use this to dx SIBO as simple, non-invasive & widely available
  • after bacterial overgrowth & steatorrhoea confirmed, can perform Schilling test: labelled B12 given orally –> urine measured (if <7% excreted in urine, implies malabsorption; normal is 7-25%)
    • can be given again w IF to check correction; if corrects = pernicious anaemia; in bacterial overgrowth vitB12 excretion isn’t altered by addition of intrinsic factor)
    • can be given again after 5days tetracycline; if corrects implies bacterial overgrowth is a problem
45
Q

What is the management of blind loop syndrome?

A
  • IV B12 therapy
  • broad spectrum antibiotics - tetracyclines previously; rifaximin & metro = less resistance & also effective - 7-10days
  • ??octreotide may reduce bacterial overgrowth & improve abdo sx in pts w scleroderma??
  • surgical tx of underlying structural cause if possible
46
Q

Indications for surgery for small bowel & ileocolic Crohn’s

A
  • stenosis causing obstruction (obstruction most frequent)
  • enterocutaneous or intra-abdominal fistulae to other organs
  • intra-abdominal/retroperitoneal abscesses
  • acute or chronic bleeding
  • free perforation
47
Q

Discuss the classification and aetiology of SBO

A
  • Partial or complete
  • Luminal verus Mural versus Extrinsic
  • Most commonly - adhesions (6-17% after open surgery)
  • Congenital:
    • Congenital bands, malrotation, cystic fibrosis
  • Neoplastic:
    • Benign tumours (hamartomas, polyps)
    • Malignant (lymphoma, adenoCa rare)
    • Extrinsic tumours
  • Inflammatory:
    • Crohn’s, appendicitis
  • Structural:
    • Hernia, intussusception, gallstone ileus, volvulus, internal hernia
    • Foreign bodies
48
Q

Describe the staging of small-intestinal NET mesenteric masses.

How are they treated?

A
  • Stage I
    • Tumours located close to the intestine
    • Removed by limited ileal resection
  • Stage II
    • Tumours involving arterial branches close to the origin of the SMA
    • Require right hemicolectomy
  • Stage III
    • Tumours extend along, but do not invade, mesenteric trunk
    • May be free-dissected
  • Stage IV
    • Tumours encase the meseteric vessels and major branches
    • Non-resectable.
49
Q

How is the diagnosis of small bowel NETs confirmed?

A
  • History
    • Non-specific abdominal symptoms
    • Carcinoid syndrome
  • Exam not usualy helpful
  • Radiology
    • CT and MRI inefficient at diagnosing primary
    • May see spiculated mesenteric mass on CT
    • Bowel obstruction due to adhesions
    • Encasement of mesenteric vessels in advanced disease
  • Special Scans
    • “Octreoscan” - Somatostatin receptors 2 & 5 expressed by 90% of small bowel NETs
    • 68Ga-PET - high sensitivities for NETs.
50
Q

Classify the types and aetiology of ischaemic gut

A
  • Arterial or venous
  • Occlusive or non-occulsive
    • Occlusive
      • Thromboembolism (50%)
      • Thrombosis of arteries (25%) on pre-existing atheroma
      • Thrombosis of veins (5%)
      • Vasculitis
      • Dissection
      • Mechanical compression
    • Non-occlusive
      • NOMI - intense vasospasm
  • Reversible or irreversible
51
Q

What is the relative frequency of small bowel malignancy?

A

(CALGary)

  • Carcinoid (20-40%)
  • AdenoCa (35-50%)
  • Lymphoma (10-15%)
  • GIST (10-15%)
52
Q

Describe the incidence, classification, and aetiology of malrotation

A
  • Symptomatic malrotation occurs in 1:6000 births.
  • Some form occurs in 1/500 live births
  • Classified as:
    • Non-rotation (90%)
      • Neither proximal or distal limb of bowel rotate; duodenum on right and colon on left
      • High risk of torsion on narrow pedicle!
    • Malrotation
      • Duodenojejunal limb stays in position of non-rotation but cecocolic limb has partial rotation so loops over duodenum causing compression with Ladd’s bands

NB: Up to _62%_ of children who have intestinal malrotation have an _associated anomaly_; diaphragmatic hernia, omphalocoele, etc.

53
Q

What are the indications for surgery in the setting of small bowel obstruction?

A

Absolute

  • Peritonitis
  • Visceral perforation
  • Irreducible hernia
  • Peritonism

Relative

  • Palpable mass lesion
  • Virgin abdomen
  • Failure to improve (pain, high NG output)

Trial of initial conservative treatment

  • Incomplete obstruction
  • Previous surgery
  • Advanced malignancy
  • Diagnostic doubt (ileus?)