Small bowel Flashcards
What is intestinal failure?
Failure to maintain adequate hydration, nutrition or electrolyte homeostasis in the absence of artificial support.
How much small bowel do we need to survive on?
It depends on which portion of small bowel and whether there is intact colon and whether this is in continuity.
If fully intact colon and in continuity then can survive on 35-40cm of small bowel.
If half colon e.g. small bowel to transverse colon anastomosis then need ~70cm of small bowel.
If end jejunostomy ~115cm.
In patients with high output stomas or entercutaneous fistulas what can be done to try reduce the output volume?
Medications:
- - Proton pump inhibitor. (Can be in a state of hypergastrinaemia in first 6 months post resection)
- Loperamide is concentrated in the enterohepatic circulation so is very dose dependent. Can give up to 64mg/day.
- Caution in use of codeine given its additive nature.
- Octreotide reserved for the worst because it has complications. causes gallstones, reduces motility, inhibits gut adaption.
Dietary:
- Limit hypotonic fluids to ~500ml/day
- Offer oral rehydration solution. Na 80mmol/L.
- fibre supplementation
Surgical:
- reverse stoma if appropriate
- repair fistula where possible
- re-entrant technologies/bag set up to input the output into a distal limb where anatomically possible.
How does the bowel adapt after significant resection resulting in short or near short gut?
It is slow - maximal adaption is at 2 years.
Nutritive and nonnutritive factors
Colon becomes a digestive organ.
Describe the different possible sites of internal herniation causing small bowel obstruction.
Anatomic normal defects
- Foramen of Winslow into lesser sac
Congenital abnormalities
- Paradudodenal
- Landzert fossa (left, IMV and left colic artery in free edge)
- Waldeyers fossa (right, SMA & SMV in free edge)
- Pericaecal
- ileocolic
- ilealcaecal
- paracaecal
- retrocaecal
- Intersigmoid fossa at root of messentery
- Supravesical into space of retzius. More commonly becomes external supravesical hernia rather than internal hernia.
- Transomental defect
- Transmesenteric
Acquired
- Transomental defect (trauma, iatrogenic
- Transmesenteric
- Retroanastomotic, risk post RenY 2-5%, colorectal surgery 0.65%.
- Post RenY
-Peterson’s space (between the roux/ailmentary limb and the transverse mesocolon (can occur whether retrocolic or antecolic roux limb).
- Brolins space (Mesojejunal window created by jejunojejunostomy)
- Transmesocolon through the mescolon defect created in retrocolic placement of roux/ailmentary limb.
How would you manage a perforated duodenal diverticulum?
How do you classify duodenal diverticulum?
Anatomic location (e..g D1, D2, D3, D4)
Aeitiology (congenital vs acquired)
True = all 3 layers (mucosa, submucosa and muscularis) vs false (mucosa and submucose prolapse out between muscularis)
Primary (usually D2, periampullary and false) vs secondary (invariably D1, true and usually due to inflammation e.g. PUD)
Usually mesenteric border.
Describe what a Meckels is, what pathology is associated with it and how/when to treat it.
Meckels diverticulum is a true diverticulum i.e. all layers of the wall that is due to incomplete obliteration of the intestinovitelline duct. it is the most common congenital small bowel abnormality and most common cause of GI bleed in paeds. it commonly contains heterotopic tissue (gastric and pancreatic)
It is associated with GI bleeding usually from the gastric heterotopic tissue screting acid and resultant ulcer on mesenteric wall or diverticulitis with inflammation usually due to the pancreatic herterotopic tissue or foreign body or food debris obstruction or tumour or small bowel obstruction due to intussception, volvulus, torsion or due to band between Meckels and abdominal wall or due to Meckels in external hernia i.e. Littres hernia.
Treatment depends on the presentation.
If incidental then usually can observe. Indications for resection either via diverticulectomy or segmental resection when found incidentally would be if its >2cm, palpable abnormality, associated with fibrous bands, if is possibly the cause of the pain in a diagnostic lap.
If treating due to bleeding then segmental resection as the ulcer is usually on the mesenteric border so a diverticulectomy won’t remove the ulcer however emerging practice to treat with diverticulectomy as risk of rebleeding once the gastric heterotopic tissue is gone is very low.
If treating due to inflammation then diverticulectomy often adequate however if perforated, base is inflamed or wide base >1/3rd diameter of small bowel or neck >2cm then would recommend segmental resection.
What is the ligament of Treitz?
The suspensory muscle of the duodenum - an extension of the right crus of the diaphragm and connects to the 3rd and 4th parts of the duodenum.
What are some ways post op ileus can be reduced?
- Minimally invasive surgery, reduced bowel handling, reduced operative time.
- Epidural
- Multimodal analgesia to reduce opiod use.
- Peripheral Opioid receptor antagonists
- Goal directed fluid administration
- Correction or electrolytes
- ERAS
What is the pathophysiology of ileus?
3 phases
1st phase = neurological
- noxious spinal signals stimulate enteric neural reflexes
- sympathetic system inhibits peristalsis.
2nd phase = inflammatory
- bowel manipulation and trauma activate macrophages and stimulate inflammatory response.
- inflammatory response inhibits peristalis.
- various neurohormonal peptides are aalso released e.g. nitrous oxide, VIP, substance P
3rd phase = resolution
- vagally parasympathetic mediated reduction of inflammatory response and return of peristalsis.
What is the pathogenesis of SBO?
Initial insult (aeitiology varied) followed by increased motility/contractility (clears the distal bowel often get diarrhoea preceding the obstipation) then as gut fatigues leads to dilation.
Inflammatory response
Bowel wall oedematous and increased pressure
Pressure overcomes venous pressure so becomes more congested and oedematous
Overcomes arterial pressure and becomes ischaemic
Ischaemic bowel and endoluminal damage results in bacterial translocation and SIRS.
systemic effects of hypovolaemia, metabolic alkalosis, respiratory compromise due to increased intrabdominal pressure, decreased venous return and raised diaphragm.
What are some common causes of SBO?
Extraluminal
- adhesions (congenital or iatrogenic or other acquired)
- neoplasms (peritoneal carcinomatosis or extrinsic compression)
- hernia (internal or external)
- volvulus
Intramural
- neoplasms
- strictures e.g, IBD, NSAIDs, diverticulitis, radiation enteropathy
- inflammation IBD, infective e.g. TB
- intussusception
Intraluminal
- food bolus
- foreign body
- bezoar
- gallstone ileus
- cystic fibrosis (Chronic Partial Distal Intestinal Obstruction Syndrome (DIOS))
Spot diagnosis. What are the causes and how is it treated?
Intussusception (target sign).
Most common in children usually at ileocaecal valve with no lead point. Peak incidence 6-9months. Most common cause of SBO in children. Due to lymphoid swelling and associated with viral illness. Can treat with pneumatic reduction using air or CO2 enema.
Rare in adults. In adults usually a lead point due a neoplasm. As such do not ‘untelescope’ and resect the intussuscepted portion and 5cm margin +/- oncological lymph node excision.
You are performing a diagnostic laparoscopy for right lower quadrant pain and presumed appendicitis in a young male. You see this appearance of the small bowel. What is your management?
This is fat creeping in the small bowel indicative of crohns disease.
If patient has appendicitis in combination with this then would still perform appendicectomy and post operatively refer to Gastroenterology.
If patient’s appendix appears normal I would not resect it but would take intraoperative photos of this appearance and post operatively would refer to gastroenterology. This may be the cause of the abdominal pain and as such treatment of acute Crohns flare with IV hydrocortisone to start with.
Going to need work up with colonoscopy
Describe the different kinds of stricturoplasty.
Heineke Mikulizc (longitudinal changed to transverse) for short segment (<7cm)
Finney (U shaped) for intermediate segment (>7-10cm)
Michelassi (side to side isoperistaltic anastomosis) for long segment of involved disease good for rosary bead sequential strictures not for long lead pipe segment that needs resection.
Jaboulay side to side anastomosis with bypassed strictured segment used when stricture too tight or thick to suture in.
Moskel- Walske-Neumayer (Y incision closed transversly as V in dilated portion) used when greatly different calibre between proximal and distal segments.
What are the differences in outcome for single vs double layer hand sewn anastomoses and hand sewn vs stapler?
No Significant Difference in Outcomes Between the Various Techniques
Single-Layer vs Double-Layer Hand-Sewn Anastomoses:
- No Difference in Anastomotic Leak Rates
- Single-Layer are Quicker to Perform
Hand-Sewn vs Stapled Anastomoses:
- No Difference in Anastomotic Leak Rates
- There are Some Conflicting Data with Strong Views Either Way
?Stapler high bleeding rate.
What is your management of high output stoma (>1.5L/day)
Simultaneous assess & resus particular attention to IVf and electrolyte replacement and correction of any reversible underlying cause e.g. sepsis, uncontrolled diabetes.
First line - psyllium husk or other water soluble fibre supplement
Second line - medication with loperamide, codeine
Others to consider
- octreotide
- PPI
- cholestryramine
ostomy reversal where appropriate
What are predictors of GIST recurrence?
Size >5cm
Mitotic rate >5/50hpf
Location more distal (colon higher chance than stomach etc).
What is the Spiegelman classification of duodenal polyps?
A classication of duodenal adenomas for patients with FAP to guide management and surveillance frequency. It utilises mitotic rate, polyp size and number and histology (tubule/villous nature) and severity of dysplasia.
Stage 0 = 0 points
Stage 1 = 1-4 points
Stage 2 = 5-6
Stage 3 = 7-8
Stage 4 = 9+
What is carcinoid syndrome?
Definition: Carcinoid syndrome is a clinical syndrome caused by the secretion of vasoactive substances, primarily serotonin (others include histamine, tachykinins, prostaglandins and kallikrein), by neuroendocrine tumours. It typically occurs in the setting of metastatic disease, particularly when the tumour metastasises to the liver or extra-abdominal bypassing the first pass metabolism.
The clinical features include episodic flushing, secretory diarrhoea, wheezing and bronchospasm, carcinoid heart disease and pellagra-like symptoms due to niacin deficiency (tryptophan shunted to serotonin synthesis).
What is the diagnosis? What is the pathophysiology? What is the treatment?
Median Arcute Ligament Syndrome - compression of the coeliac trunk by the median arcute ligament.
Usually due to a high take off of coeliac trunk or can be due to low position of median arcuate ligament.
Treat with transection of median arcuate ligament and coeliac plexus neurolysis in patients symptomatic (classic triad of symptoms = post prandial abdominal pain, weight loss and epigastric bruit).
What is the diagnosis? How is it diagnosed? How is it treated?
This appears to be SMA syndrome with a narrow (<25degree AMA angle and <8mm AMD distance).
It is often diagnosis of exclusion but supported by the above with proximal duodenal dilation.
Medical management:
- nutritional support and high calorie diet
- may require NJT
- correction of electrolyte abnormalities
- care for refeeding syndrome
- psychological support (many are associated with eating disorders, drug use etc)
Surgical management:
- Gastrojejunostomy bypasses the obstruction but given the obstruction is not relieved at risk of bile reflux gastritis and blind loop syndrome.
- duodenojejunostomy +/- division of the 4th portion of duodenum.
- Strongs procedure = division of the ligament of Treitz.
This is a slide of normal small bowel mucosa on the left and abnormal on the right. What condition does the bowel on the right display? What is the pathogenesis of this condition?
Coeliac disease.
Involves an abnormal T cell mediated response to Gliadin (component of gluten) which acts as an epitope which the body reacts to.
This leads to mucosal damage loss of brush border enzymes, loss of stimulus for pancreatic and bile secretion and exudation of protein across denuded mucosa.
Can see in this slide the villous atrophy, flattening of mucosal folds.
Other features include hypertrophy of crypts, increased intraepithelial lymphocytes, prominent submucosal vascularity
What treatment options are available for short gut or intestinal failure?
Dietary
- enteral feeding best at promoting intestinal adaptation and enterocyte health
- glutamine enterocyte main nutrient
- high calories, high CHO, high protein diets
- low oxalate to reduce change of nephrolithiasis
Pharmacological
- PPI/H2 blocker to reduce gastric hypersecretion
- slow transit agents e.g. loperamide, codeine
- cholestyramine may help reduce diarrhoea but can worsen steatorrhoea as binds bile salts (only works in patients with a colon)
- octreotide slows diarrhoea but concerns may inhibit gut adaptation & increases gallstones risk so reserved for IVF requirement >3L/day.
- fluid and electrolyte replacements esp Ca, Mg, zinc, iron
- Vit B12, Vit D
- PN or TPN
Surgical
- procedures to lengthen the bowel to increased surface area for absorption e.g. STEP & Bianchi procedures.
- procedures to reduce transit time e.g. formation of vavles or sphincters or antiperistaltic segments.
- intestinal transplant with or without other organs e.g. liver. best tolerated with liver transplant due to immunologic tolerance.
