JC60 (Surgery) - Intestinal Obstruction Flashcards
Difference in presentation between small bowel and large bowel obstruction*
□ Small bowel obstruction (SBO):
→ High: early, profuse vomiting with rapid dehydration and minimal distension
→ Low: predominant pain with central distension, colics
□ Large bowel obstruction (LBO): early, pronounced distension with mild pain and minimal vomiting
Differentiate simple, closed loop and strangulated obstructions *
□ Simple: one obstructive point w/o vascular compromise
□ Strangulated: viability of bowel is threatened due to compromised blood supply
□ Closed loop: ≥2 obstructive points
Define causes of dynamic/ mechanical intestinal obstruction *
Intraluminal
Stool impaction in bed-ridden patients
Gallstone ileus
Trycho- (hairs) and phytobezoars (vegetable)
Foreign bodies
Intramural
Inflammatory strictures, eg. Crohn’s, radiation, ischaemic, anastomotic, drug-induced, endometriotic
Tumours and malignant strictures
Intussusception
Extramural
Adhesions
Incarcerated hernia
Volvulus
Diverticular disease
Other external compression, eg. LNs, peritoneal carcinomatosis, SMA syndrome
Define causes of adynamic/ functional intestinal obstruction (/)
Paralytic ileus (absent peristalsis)
- Post-operative
- Infectious, i.e. intra-abdominal sepsis
- Reflex ileus due to intra-abdominal inflammatory process
- Metabolic, eg. hypoK, uraemia commonest
Pseudo-obstruction (dysfunctional peristalsis)
- Small intestinal: idiopathic, familial visceral myopathy
- Acute colonic: toxic megacolon, Ogilvie syndrome
- (Chronic colonic:)
□ Degenerative, eg. MSA, DM
□ Paraneoplastic, eg. SCLC, carcinoids, thymoma
□ Autoimmune, eg. scleroderma, dermatomyositis, SLE
□ Infectious, eg. Chagas’ disease
□ Genetic, eg. mitochondrial ds
Explain the pathophysiology of proximal dilatation and distal collapse in intestinal obstruction
Distal collapse:
- Bowel exhibits normal peristalsis and absorption distal to obstruction, collapses after emptying contents
Proximal dilatation:
- Increased peristalsis and progressive dilatation, result in flaccidity and paralysis later
- Accumulation of bacteria overgrowth in gut, causing transmural spread and gas accumulation
- Fluid accumulation due to bowel wall edema and low absorption
Causes of bowel strangulation **
Complications of bowel strangulation
Features of strangulation
Causes:
→ External pressure, eg. hernia orifices, adhesions or bands
→ Interrupted mesenteric blood flow, eg. volvulus, intussusception
→ High intraluminal pressure esp in closed loop obstruction
Consequences:
→ Haemorrhagic infarction occurs in ischaemic segment
→ Peritonitis and septicaemia due to ↑permeability to luminal bacteria and toxins
→ Hypovolemic shock due to sequestration of blood if long-segment strangulation
Causes of closed loop bowel obstruction
Consequence of prolonged obstruction
Closed loop obstruction: ≥1 obstruction points
Causes:
→ Volvulus
→ Incarcerated hernia
→ Lower bowel obstruction + competent ileocaecal valve (occurs in 1/3)
Consequences: cannot decompress into prox. bowels
- High risk of strangulation + perforation
Causes of small bowel obstruction **
Intra-luminal
Intra-mural
Extra-mural
Intra-luminal:
- Foreign body
- Gallstones
- Bezoars
- Worms
Intra-mural
- Tumor
- Strictures: Crohn’s, radiation, anastomotic, drug
- Intussusception
Extra-mural
- Adhesions**
- Hernia
- Volvulus
- Intraperitoneal malignancy
Causes of large bowel obstruction **
CA colon (commonest, 50-60%)
Colonic diverticulitis
Caecal and sigmoid volvulus
External tumour compression: metastasis, pelvic/ extraperitoneal tumors
Strictures (ischaemic, anastomotic, radiation, endometriotic)
Faecal impaction
Causes of intestinal adhesions **
Pathogenesis
Complications
Causes:
→ Congenital adhesions
→ Post-inflammatory: following severe peritonitis (eg. appendicitis, cholecystitis, PID)
→ Post-operative: ↑risk if open surgery
Pathology:
peritoneal irritation → local fibrin production → early fibrinous adhesions
→ late vascularization and replacement by fibrous adhesions
Complications:
→ IO affecting lower SB
→ Chronic abdominal/pelvic pain with dyspareunia
→ Infertility due to tubal blockage
Prevention of intestinal adhesions **
Prevention in surgery: commonest in appendicectomy and gynaecological procedures
→ Good surgical technique with gentle handling of bowel and laparoscopic surgery
→ Less contact with irritants, eg. removal of powder from gloves, ↓contact with gauze
→ Barriers to keep damaged peritoneal surfaces separated, eg. solid (sodium hyaluronate, oxidized cellulose), liquid (PEG, icodextrin, hyaluronate)
→ Saline lavage
Intestinal adhesion
Classical imaging sign
Management
CT: ‘fat-bridging’ sign showing cord-like mesenteric fat bridging across peritoneum
Mx of adhesive IO:
Supportive management: ‘drip and suck’
□ ABCs: resuscitation if unstable
□ Nil per oral until resolution
□ NG tube suction
□ IV fluid/electrolytes:
→ Secure large bore IV access
→ Give Ringer’s lactate/NS ± K+ supplements and correct acidosis
□ ± others: monitor UO, prophylactic broad-spectrum Abx, CVP monitoring for resuscitation
Adhesiolysis if refractory to conservative Tx or features of strangulation
Gallstone ileus
Pathogenesis
Imaging sign
Management options
Pathogenesis:
erosion of gallstone into bowel through cholecystoenteric fistula
→ gallstone (usu >2cm) impacts at small bowel → ‘ball-valve’ effect causing recurrent SBO attacks
Imaging sign: Rigler’s triad (pneumobilia, SB IO, obstructing gallstone)
Management: crush stone intraluminally → milk fragment into caecum to for removal
- Enterolithotomy
- ± cholecystectomy and closure of cholecystoenteric fistula
Intussusception **
Causes in children and adults
Pathogenesis
Major sites in GIT
S/S
Imaging signs
Management
Causes:
Children: 90% idiopathic but may be a/w previous URTI/GE (?due to hypertrophic Peyer patches)
Adults: ALWAYS a/w pathological lead-points (usu intraluminal lesions in SB), eg. polyp, submucosal lipoma, Meckel’s diverticulum, GIST, carcinoma
Pathology: occurs when proximal gut (intussusceptum) invaginates into distal segment (intussusceptiens)
Site: majority ileocolic (90%) in children vs colocolic in adults
S/S: classically IO with currant jelly stools
Intussusception **
Imaging sign
Management
CT: characteristic target (donut) lesions
Mx:
→ Children: hydrostatic or pneumatic pressure by enema
→ Adults: bowel resection to r/o CA
Volvulus **
Pathogenesis
3 main types
Pathology: twisting of a portion of bowel about its mesentery
→ >180o torsion → obstruction to lumen
→ >360o torsion → mesenteric vascular occlusion
Sigmoid volvulus (60%)
Caecal volvulus (30%)
Small bowel volvulus (rare)
Sigmoid volvulus /
Risk factors
Pathogenesis
S/S
→ RFs: Asians, elderly institutionalized pt with Hx of constipation or chronic psychotropic drug use
→ Pathology: narrow mesentery + long sigmoid colon with fecal loading → predispose to twisting of sigmoid colon
→ S/S: usu insidious onset of LBO Sx but may be fulminant (17%) in younger pt
Sigmoid volvulus **
Imaging signs
Management options
Ix:
Plain AXR shows coffee bean sign
Barium enema shows bird’s beak or ace-of-spade sign
(NOT done usually due to risk of perforation)
Mx:
- Sigmoidoscopic decompression by applying pressure at apex of volvulus (75-95% successful rate but 50% recurrence rate)
- Sigmoid resection/ sigmoidectomy with primary anastomosis or Hartmann’s procedure
Caecal volvulus /
Risk factors
S/S
Imaging signs
RFs: more common in middle-aged female with congenitally mobile caecum
S/S: classical IO Sx w/ midline/Lt-sided palpable tympanic swelling (25%) ± Sx of ischaemia
Dx: AXR (coffee bean caecum) and CT scan (‘whirl sign’)
Management of caecal volvulus **
Mx: surgical detorsion + caecopexy ± caecostomy (if unstable)
ileocecal resection/R hemicolectomy with 1o anastomosis (if stable
Small bowel volvulus /
Pathogenesis
Risk factors
Section of bowel invovled
Most caused by adhesions to abdominal wall and female pelvic organs
RFs:
- malrotation of gut (both DJ junction and ileocaecal valve at RUQ → short mesenteric attachment),
- Meckel’s diverticulum (fibrous band as axis)
Pathology: usu involve midgut (D2 to transverse) and rotate about SMA as axis
Cardinal features of IO
(1) Colicky abdominal pain
(2) Abdominal distension
(3) Nausea/vomiting
(4) Constipation/obstipation
(5) Increased bowel sounds
Describe onset, character and site of abdominal pain in IO
□ Onset: usually sudden and severe
□ Nature: initially colicky (initial hyperperistalsis) and gradually becomes a mild and more constant diffuse pain (distension with hypoperistalsis)
□ Site: periumbilical (SBO) or lower abdomen (LBO), usu poorly localized
Difference in abdominal distention between small vs large bowel obstruction
□ SBO: usu at centre of abdomen, ↑ for distal obstruction ± visible peristalsis (‘ladder-like’)
□ LBO: usually a late feature, RLQ hyperresonant bulge if closed loop
Differentiate content of vomitus in different types of intestinal obstruction
Vomitus: digested food (GOO) vs bilious (high SB) vs feculent (low SB) vs none (LB)
Associated Signs of IO (apart from 4 cardinal features) **
Bowel sounds: initially hyperactive (high-pitched tingling if SBO), later absent
Dehydration: usu in SBO due to ↑↑vomiting and fluid sequestration
Pyrexia: rare and may indicate ischaemia, perforation or underlying inflammation/abscess
Tenderness: indicates impending/established ischaemia
Peritoneal signs: indicates impending/overt infarction or perforation
Clinical features of bowel strangulation
how is it different from normal, uncomplicated IO?
- Constant, severe pain (cf colicky abdominal pain)
- Tenderness: severe (cf no/mild)
- Peritoneal signs: guarding, rigidity
- Blood in vomitus
- Fever and shock
Outline history taking for IO
□ Cardinal features: pain, vomiting, abd distension, constipation/obstipation
□ Features of strangulation: constant, severe pain with peritoneal signs and shock
□ Other associating symptoms suggestive of underlying aetiology
□ Previous Hx of IO
□ Past abdominal Hx:
→ abd/pelvic surgery for adhesive IO
→ severe abd inflammation for adhesive IO
→ CA or abd/pelvic irradiation
□ RFs for underlying aetiology:
→ RFs for ischaemic bowel: atherosclerotic RFs, CVD, stroke
→ RFs for malignancy: LOW, LOA, prev CA, FHx
Outline P/E for suspected IO
□ General:
→ Vitals and features of dehydration for haemodynamic instability
→ LNs for malignant obstruction
□ Abdomen:
→ Inspection: distension, scars (prev surgery), visible peristalsis
→ Palpation: peritoneal signs, masses, hernia (must be checked esp femoral, easily strangulated)
→ Auscultation: BS, succession splash (GOO)
→ DRE: rectal masses, impacted stools
Imaging investigations for IO **
Erect/supine AXR***
Contrast CT abdomen (if AXR non-diagnostic or complications)
Water soluble contrast study by gastrografin (GGF) - for adhesive IO
Lower endoscopy - for large bowel obstruction or decompression
Features of IO on erect/supine AXR
Air-fluid levels on erect AXR:
→ >5 air-fluid levels diagnostic of IO
Proximal dilation with distal collapse on supine AXR
→ ‘3-6-9 rule’: dilation defined as SB diameter >3cm, LB >6cm, caecum >9cm
Gasless abdomen on supine AXR
→ String of pearls sign: collection of small itnraluminal gas along superior bowel wall separated by valvulae conniventes
AXR features of the following causes of IO:
Volvulus
Intussusception
Ulcerative colitis
Gallstone ileus
Fecal impaction
→ Volvulus: coffee bean sign (LLQ to RUQ in sigmoid, RLQ to LUQ in caecal)
→ Intussusception: sausage-shaped opacity
→ UC: thumb-printing (thickened bowel wall) or lead-pipe colon
→ Gallstone ileus: Rigler’s triad
→ Faecal impaction: multiple faecal densities throughout colon/rectum
Features of IO on contrast CT abdomen
□ Proximal dilation + distal collapse with air-fluid levels
□ Thickening of bowel walls: wall thickening >3mm, submucosal and mesenteric oedema
□ Transition point marking level of obstruction
Signs of Strangulations and perforation from IO
P/E signs and imaging signs
Strangulation: Increase abd pain and tenderness, blood in vomitus
- Thumb-printing due to oedematous haustral folds
- Loss of normal mucosal pattern
- Pneumatosis cystoides intestinalis: transmural gas due to necrotic bowel
- Pneumatosis portalis: gas in portal vein or IMV
Perforation:
- Pneumoperitoneum: double wall (Rigler’s) sign, free gas under diaphragm
Contrast CT features of the following causes of IO
Intussusception
Volvulus
CA colon
→ Target sign for intussusception
→ Whirl sign and ‘X-marks-the-spot’ sign for volvulus
→ Apple-core sign for CA colon
Serological investigations for suspected IO
□ CBC, L/RFT: infection, anaemia, dehydration
□ ABG + lactate: acidosis (ischaemia), alkalosis (vomiting)
□ Amylase to r/o acute pancreatitis
□ Erect CXR + E/S AXR for perforation and strangulation
Ddx intestinal obstruction
□ Acute GE: may have abdominal pain and vomiting but usu a/w diarrhea as predominant symptom
□ Adynamic ileus: usually a/w milder, constant pain with no demonstrable clear transition point/aetiology on CT
□ Pseudo-obstruction: usually chronic with stool-filled rectum on PR and no demonstrable clear transition point/aetiology on CT
General supportive treatment for IO
Supportive management: ‘drip and suck’
□ ABCs: resuscitation if unstable
□ NPO until resolution: 70% SBO recover with bowel rest and decompression
□ Nasogastric tube: passive connection with aspiration or continuous/intermittent suction
□ IV fluid/electrolytes:
→ Secure large bore IV access
→ Give Ringer’s lactate/NS ± K+ supplements and correct acidosis
□ ± others: monitor UO, prophylactic broad-spectrum Abx, CVP monitoring for resuscitation
Clinical indications for urgent surgical treatment of IO
Clinical indications for surgery
(1) Continuous (>4d) or worsening abdominal pain ± peritonitis
(2) Blood in vomitus
(3) Fever, ↑WBC, tachycardia: Shock
(4) Metabolic acidosis
(5) Radiological features of strangulation or perforation (pneumoperitoneum/ pneumatosis intestinalis..etc)
(6) ↑risk for complications, eg. closed loop, incarcerated hernia, volvulus, adult intussusception
Surgical treatment options for uncomplicated IO**
Adhesion
Strictures
Hernia
Bolus/ Foriegn body
Intussusception
Uncomplicated IO:
- Operative decompression
- Bowel resection if non-viable bowels
Specific causes:
- Adhesiolysis (enterolysis) for adhesive IO
- Stricturoplasty for Astrictures
- Hernia repair for incarcerated hernia
- Bolus removal by breaking down, pushing to colon then removal with enterotomy
- Surgical reduction of intussusception
Conservative treatment for small bowel obstruction
Supportive Tx: NPO, NGT decompression, IVF/E ± nutrition
Serial monitoring of vitals, abdominal signs, AXRs for any Cx/resolution
Water soluble contrast study - adhesive IO
- 100mL undiluted GGF given orally or via NGT
- hyperosmolar → ‘laxative-like’ effect
Monitoring methods for resolution of IO **
↓abdominal distension
↓ Nasogastric output
Passage of flatus and bowel movement
Resolution on AXR
Intestinal obstruction **
Non-surgical/ operative management options
Indications for non-operative treatment
Supportive care: IV fluid and electrolytes, Nasogastric tube decompression, Nutrition, Frequent monitoring
Non-operative decompression of sigmoid volvulus
→ Instrument: sigmoidoscopy or Ryle’s tube
Endoscopic stenting for malignant obstruction
Indications: Partial obstruction:
- Adhesions
- Crohn’s disease
- Radiation stricture
- Disseminated malignant disease
Endoscopic stenting for large bowel obstruction **
Technique
Indications
Technique: Endoscopic or Fluoroscopic guidance
Uses: (2)
- Palliation for severe disease - Avoid surgeries and stomas
2, Bridge to surgery
- Avoid emergency surgery
- More bowel preparation
- More time to stage disease before op
- Lower operative mortality and morbidity
- Lower stoma rate
Large bowel obstruction **
Surgical management options
Surgical management: required for ~75% of LBO
□ Resection with 1o anastomosis or no anastomosis (i.e. staged resection)
□ Non-resection: proximal stomal decompression or bypass
Surgical treatment of large bowel obstruction **
Factors for surgery
Patient condition
IC valve competence
Heavy bacterial and fecal load
Edematous proximal colon
Poor patient condition - Cancer, Malnutrition
Surgical treatment option specific to right colonic obstruction **
- One-staged (main)
→ Right hemicolectomy: removal up to hepatic flexure + ileocolostomy
→ Extended Rt hemicolectomy: removal up to proximal transverse colon + ileocolostomy
- Two-staged operation: patient or bowel condition is not favourable
-
Non-resection: patients with short-life expectancy and high-risk surgical candidates
→ Loop ileostomy or loop caecostomy for palliative decompression
→ Surgical bypass
Surgical treatment options specific to left colonic obstruction **
One-staged operation: patient is stable w/ long life-expectancy
→ Segmental resection with 1o ileocolonic anastomosis (a/w risk of synchronous tumour)
→ Subtotal colectomy with 1o ileocolonic/ileorectal anastomosis
Two-staged (Hartmann’s) operation: *** main ***
→ Sigmoidectomy with loop or temporary end colostomy
→ ± subsequent anastomosis + closure of stoma
Three-staged operation: condition very poor or CA rectum
→ Defunctioning transverse loop colostomy (loop ileostomy does not work if ileocaecal valve is competent)
→ Resection with 1o anastomosis
→ Closure of colostomy
Paralytic ileus **
intra-abdominal and retroperitoneal causes
Extra-abdominal causes
intra-abdominal:
- Post-operative
- Peritonitis/ abscess
- Inflammatory/ infective conditions
- Intestinal Ischemia
Retroperitoneal:
- Hematoma
- Infection
- Aortic/ spinal/ urological operations
- Pancreatitis
Extra-abdominal causes
- Metabolic: electrolyte, uraemia, hypothyroidism, lead poisoning
- Medication: anticholingergics, antihistamines, opiates
- Spinal injury/ operation
Post-operative ileus /
Pathophysiology
Definition for Dx
Post-operative ileus: period of inhibition of activity after abdominal/retroperitoneal operations
Aetiology:
→ Reflex inhibition by inhibitory local neural reflexesafter organ manipulation
→ Cytokine and other serum factors, eg. NO, VIP, secreted as inhibitory neurotransmitters from gut
→ Use of opioid analgesics for post-op pain control
Definition of prolonged ileus: on or after post-op day 4, there is ≥2 of
→ Nausea or vomiting
→ Inability to tolerate oral diet over preceding 24h
→ Absence of flatus over preceding 24h
→ Abdominal distension
→ Radiological confirmation
Post-operative ileus **
Management options
Mx of prolonged ileus:
Supportive: NPO + IV fluid ± NGT suction (if severe vomiting)
□ NGT decompression
□ Treatment of underlying cause
□ Daily P/E + AXR for monitoring and assessment
□ Prokinetics (eg. domperidone, erythromycin) if prolonged
□ Laparotomy if sustained ileus >7d
Post-operative ileus /
Prevention methods
Early feeding w/o routine NGT
Epidural anaesthesia and analgesia instead of GA with systemic opioids
Laparoscopy instead of open to achieve less manipulation, maintenance of peritoneal milieu and ↓pain and stress
Gentle intestinal manipulation during surgery
Use of NSAIDs over opioids
Paralytic ileus **
S/S
□ S/S of underlying cause, eg. peritoneal signs, pain
□ Abdominal pain: tends to be diffuse, constant and less severe (cf mechanical IO)
□ Abdominal distension with bloating: gradually becomes more marked and tympanitic
□ Constipation
□ Effortless vomiting
□ Inability to tolerate oral diet
□ Sluggish/absent bowel sounds
First-line investigations for paralytic ileus **
Rule out mechanical IO and look for underlying causes:
□ Review drugs
□ CBC: anaemia (bleeding), leukocytosis (infection, ischaemia, abscess)
□ RFT: hypoK, hypoMg, uraemia
□ LFT, amylase: biliary sepsis, pancreatitis
□ E/S AXR
□ Contrast CT ± GGF study
Compare mechanical SBO and paralytic ileus /
- Abdominal distention
- Bowel sounds
- Constipations
- Pain character
- Vomiting
- Peritoneal signs
- Fever
- AXR signs
Post-operative ileus /
Risk factors
Surgery:
- Prolonged surgery
- Lower GI surgery
- Open surgery
Post-operation complications:
- Intra-abdominal inflammation
- Delayed enteral feeding
- Blood loss and transfusion
- Perioperative opioid use
Intestinal pseudo-obstruction *
Acute and chronic causes
Acute: Ogilvie’s syndrome (acute colonic pseudo-obstruction) or toxic megacolon
Chronic: may be neuropathic, myopathic or due to abnormalities in interstitial cell of Cajal
Ogilvie’s syndrome *
Definition
Pathogenesis
Clinical features
Ddx
Ogilvie’s syndrome: Massive, PAINLESS dilatation of colon without anatomic obstruction
Pathogenesis: unknown, probably due to impairment of ANS
Clinical features: Typical IO features, Bedridden patients with severe extra-colonic diseases, Severe gaseous distention of colon on Xray
Diagnosis of exclusion after excluding toxic megacolon or mechanical IO
□ Toxic megacolon: bowel dilatation a/w systemic toxicity with Hx of severe bloody diarrhoea
□ Mechanical obstruction: usu cramping pain with SB air-fluid levels and ‘cut-off’ sign on AXR
Ogilvie’s syndrome *
Management
□ Conservative Tx as initial Mx for up to 24-48h
→ Mx of underlying condition, eg. stop opioids, correct electrolytes
→ NPO + NGT on intermittent suction
→ Frequent reassessment with P/E, CBC, electrolytes, AXR Q12-24h
□ Neostigmine if caecal diameter >12cm or fails conservative Mx
□ Colonoscopic/ Rectal tube decompression if fail neostigmine
□ Surgical or percutaneous caecostomy if fail colonoscopic decompression
Intestinal ischemia
Differentiate mesenteric ischemia and ischemia colitis
Mesenteric ischaemia referring to ischaemia of SB
→ Acute mesenteric ischaemia due to embolism, hypoperfusion, thrombosis
→ Chronic mesenteric ischaemia usually due to mesenteric atherosclerosis
Ischaemic colitis referring to ischaemia of colon
→ Acute ischaemic colitis usually due to non-occlusive causes (95%)
→ Chronic ischaemic colitis
Mesenteric ischemia
Causes
Occlusive
1. Arterial embolism (50%): AF, mural MI, AAA, VHD
- ‘Jejunal-sparing’ strongly suggests embolic cause
- IMA rarely affected due to thin calibre
2. Arterial thrombosis (15-25%):
- Usu occurs at origin of SMA or coeliac a.
- Other causes: abd trauma, infections, mesenteric dissection
Venous thrombosis (5%):
- Idiopathic, eg. due to thrombophilia
- Secondary, eg. due to malignancy, prior abd surgery
Non-occlusive:
→ Systemic hypotension, eg. shock, HF, peri-op hypotension, CPB, dialysis
→ Aortic insufficiency, eg. AAA repairs
→ Vasoconstrictors, eg. digoxin, α-agonist, adrenaline
Mesenteric ischemia /
Clinical features
Clinical features:
□ Severe abdominal pain that is out of proportion to examination
→ Embolic: sudden severe peri-umbilical pain ± N/V and diarrhoea (usu not bloody)
→ Thrombotic: worsening of chronic postprandial abdominal pain, food aversion and weight loss
→ Non-occlusive: variable, may be non-specific in early stages progressing to severe abd pain
□ Metabolic acidosis with ↑lactate, followed by hypovolemic shock
Risk factors of mesenteric ischemia /
→ Embolic: elderly with AF, other evidence of embolism (eg. limb ischaemia)
→ Thrombotic: known PAD with multiple atherosclerotic RFs, background of post-prandial discomfort with weight loss
→ Non-occlusive: may be overshadowed by precipitating disorders, eg. ↓BP, CHF, hypovolemia, arrhythmias
Investigations for mesenteric ischemia /
□ Bloods: metabolic acidosis with ↑serum lactate, marked leukocytosis with neutrophilia
□ AXR: non-specific, normal in 25%
→ May show ileus, bowel wall thickening and pneumatosis intestinalis (if advanced)
□ Contrast CT abdomen ***
□ MRI Venogram: more sensitive for venous occlusion
□ Mesenteric arteriogram if in doubt or for intervention
Mesenteric ischemia /
Management: conservative and surgical options
□ Supportive: NPO, NGT decompression, IV fluid, O2 supplement
□ Stop all vasopressors
□ Systemic anticoagulation by unfractionated heparin
□ Other drugs: empirical Antibiotics, PPI
Endovascular intervention:
→ Pharmacomechanical thrombolysis, Angioplasty with stenting
Immediate surgery if features of advanced ischaemia
→ Abdominal exploration by laparotomy
→ Revascularization by open SMA embolectomy or SMA bypass
→ Bowel resection
→ Delayed closure with second-look laparotomy to reassess viability ~24-48h post-op
Ischemic colitis /
Areas of GIT affected and vascular supply
Watershed areas between major arterial supplies are particularly prone to ischaemia
→ Griffiths’ point (splenic flexure) at site of communication of ascending Left colic a. with marginal a. of Drummond
→ Sudeck’s point (rectosigmoid junction) between left colic a. and sup. rectal a.
Ischemic colitis **
Causes
Aetiology: due to hypoperfusion of colon
Non-occlusive (95%): Characteristically affects the watershed areas of colon
e.g. Congestive heart failure, shock, colonic obstruction, medication, iatrogenic (AAA repair, CABG…), Increase coagulability
Occlusive: uncommon
→ Embolic and thrombotic: rarely occurs w/o SB ischaemia (i.e. SMA occlusion)
→ Venous thrombosis (very uncommon)
Acute colonic ischemia **
S/S
Sudden onset cramping abdominal pain:
Mild-to-moderate rectal bleeding develops ≤24h of onset of abdpain
Tenderness over intestines
□ Blood: ↑↑WBC, metabolic acidosis, ↑serum lactate, ↑LDH, ↑CPK, ↑amylase
□ Stool culture + C. difficile toxin to r/o infectious diarrhoea
□ AXR: distension, thumbprinting, pneumatosis
Ischemic colitis /
Define 3 Clinical phases and S/S
Hyperactive phase: severe abd pain with frequent passage of bloody loose stools
Paralytic phase:
→ Pain diminishes and becomes more continuous and diffuses
→ Abdomen becomes more tender and distended
→ ↓bowel sounds with no passage of blood stools
Shock phase: massive fluid, protein and electrolytes leaking through damaged mucosa
Ischemic colitis *
Investigations and characteristic findings
Contrast CT with IV ± oral contrast
→ Segmental oedema and thickening of bowel wall
→ Target sign due to hypodense submucosal oedema
→ Pneumatosis coli or portalis suggest advanced ischaemia
Colonoscopy with minimal air insufflation
→ May show oedematous, friable mucosa
→ Bluish haemorrhagic nodules of submucosal bleeding
Differentiate between the presentation of acute small bowel ischemia vs acute ischemic colitis /
acute small bowel ischaemia which usu shows
→ Wider range of onset age (vs 90% >60y in LB)
→ Typical acute precipitating cause (uncommon in LB)
→ Patient appears severely ill
→ Pain usually severe but tenderness not prominent early
→ Bleeding uncommon until very late
Ischemic colitis**
Treatment
Conservative for low or moderate risk individuals (≤3 RFs)
→ NPO, NGT on suction (if ileus)
→ IV fluid, Abx ± TPN
→ Rectal tube decompression of distended colon
→ ± antithrombotic
Abdominal exploration for high-risk individuals and those with infarction/necrosis
→ Emergency laparotomy
→ Resection of ischaemic segments ± 1o anastomosis
→ Second-look procedure
Features suggestive of severe ischemic colitis with infarction or necrosis /
(1) Ongoing pain out of proportion of P/E or with peritoneal signs
(2) Haemodynamic instability or sepsis, persistent fever
(3) Involvement of Rt colon
(4) Pneumatosis coli or portalis, or perforation (free gas) on AXR
(5) Gangrene on colonoscopy
Indications for urgent bowel surgery
