Intestinal Obstruction

I. Definition

Intestinal obstruction (IO) refers to any condition that impedes the normal passage (aboral progress) of intestinal contents through the gastrointestinal tract.

This can occur by two fundamentally different mechanisms ^[1]:

1. Mechanical obstruction — implies a physical barrier to the aboral progress of intestinal contents (i.e., peristalsis is present and working against an obstruction) ^[1]
2. Ileus (functional obstruction) — implies failure of peristalsis to propel intestinal contents with no mechanical barrier ^[1]

The distinction matters enormously because management is completely different: mechanical obstruction often requires surgical intervention, whereas functional obstruction is usually managed conservatively by treating the underlying cause.

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II. Epidemiology

• Intestinal obstruction is a common surgical emergency ^[3]
• Small bowel obstruction (SBO) is more common and is involved in ~80% of cases of mechanical IO ^[3]
• Large bowel obstruction (LBO) accounts for about 15% of intestinal obstruction ^[1]
• LBO usually occurs at the sigmoid colon ^[1]
• SBO accounts for approximately 12–16% of all surgical admissions and ~20% of all emergency surgical admissions worldwide
• In Hong Kong, adhesive SBO is extremely common given the high volume of prior abdominal surgery; however, incarcerated hernias (particularly inguinal hernias) remain a leading cause in the elderly population
• In neonates, congenital anomalies — including intestinal atresia, malrotation, meconium disease, and Hirschsprung's disease — are the predominant causes ^[2]

Age-specific patterns

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III. Risk Factors

Understanding risk factors is essentially understanding "what predisposes the bowel to being blocked or to stopping working."

Medical History [3][4]

• Hernia — an incarcerated hernia traps bowel within it, creating obstruction
• Abdominal infection or inflammation — leads to adhesion formation or stricturing (e.g., Crohn's disease, tuberculosis, diverticulitis)
• Abdominal malignancy — intraluminal growth narrows the lumen; peritoneal carcinomatosis causes extrinsic compression
• Previous intestinal obstruction — recurrence risk is high, especially with adhesive disease (~30% recurrence)

Surgical History [3][4]

• Previous abdominal or pelvic surgery — the single biggest risk factor for adhesive SBO; any peritoneal breach triggers an inflammatory-fibrotic healing cascade
• Previous abdominal irradiation — causes radiation enteritis → stricture formation from fibrosis (radiation injury accounts for ~1% of SBO ^[1])

Drug History [3][4]

• Opiates — activate μ-receptors on myenteric plexus → ↓ acetylcholine release → ↓ propulsive peristalsis
• Anti-cholinergics (anti-histamines, anti-spasmodics, anti-depressants, anti-psychotics) — block muscarinic receptors on smooth muscle → ↓ peristalsis

Other Risk Factors

• Chronic constipation — predisposes to faecal impaction (LBO), sigmoid volvulus (by distending and elongating the sigmoid)
• High-fibre diet in certain populations — bulky stools can predispose to sigmoid volvulus
• Bedbound / immobility — predisposes to pseudo-obstruction and volvulus
• Metabolic derangements — hypokalaemia, hypothyroidism, uraemia → all impair smooth muscle contractility
• Pregnancy — hormonal laxity of ligaments, physical compression by gravid uterus

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IV. Anatomy and Function Relevant to Intestinal Obstruction

A. Small Bowel

The small bowel (duodenum → jejunum → ileum) is approximately 6–7 metres long and is the primary site of nutrient absorption and fluid handling.

• Blood supply: Superior mesenteric artery (SMA) via jejunal, ileal and ileocolic branches
• Mesentery: The small bowel hangs from a mesentery attached to the posterior abdominal wall; this mobility makes it susceptible to adhesive kinking, volvulus, and herniation
• Wall layers: Mucosa → submucosa → muscularis propria (inner circular, outer longitudinal) → serosa
• Nerve supply: Myenteric (Auerbach's) plexus between the muscle layers controls peristalsis; submucosal (Meissner's) plexus controls secretion and absorption
  • This is why functional obstruction (paralytic ileus) involves neuromuscular failure of these plexuses

Key anatomical points:

• The duodenojejunal flexure (ligament of Treitz) is the landmark dividing proximal from distal SBO; obstruction proximal to this causes early bilious vomiting
• The terminal ileum is the narrowest portion of the small bowel (approximately 2 feet proximal to the ileocaecal valve), which is why gallstones (gallstone ileus) and other intraluminal objects typically impact here ^[4]
• A lesion at the ileocaecal valve presents as small bowel obstruction ^[1]

B. Large Bowel

The large bowel (caecum → ascending → transverse → descending → sigmoid → rectum) is approximately 1.5 metres long; its primary functions are water absorption and faecal storage.

• Blood supply: SMA (caecum to proximal 2/3 of transverse colon) and IMA (distal 1/3 of transverse to rectum)
• Unique anatomy:
  • Taeniae coli — three longitudinal muscle bands (rather than a complete layer) leaving the wall structurally weaker between them
  • Haustra — sacculations between the taeniae
  • These structural features are why diverticula form at the weakest point where vasa recta penetrate the circular muscle ^[4]
• Sigmoid colon — has its own mesentery (mesosigmoid), making it mobile and prone to volvulus; also has the narrowest lumen → highest intraluminal pressure (Laplace's law) ^[4]
• The rectum is never affected by diverticula because its outer longitudinal muscle is a complete circumferential layer ^[4]

C. The Ileocaecal Valve

This is a critical structure in IO:

• Competence of the ileocaecal valve determines the clinical features of distal colon obstruction ^[1]
• Competent valve (~1/3 of population): prevents retrograde flow of colonic contents into the ileum → creates a closed-loop obstruction between the valve and the distal obstruction → rapid caecal distension → high risk of perforation (especially when caecal diameter > 9–12 cm, per Laplace's law: T = P × r, so the caecum, having the largest radius, is most prone to perforation)
• Incompetent valve (~2/3 of population): allows decompression of colonic contents retrograde into the small bowel → presents with features more like SBO (distension, vomiting)

D. Neonatal Anatomy

Embryonic development of the gut ^[3] is critical to understanding neonatal causes:

• The GI tract is derived from foregut (oesophagus to mid-duodenum), midgut (mid-duodenum to proximal 2/3 transverse colon), and hindgut (distal 1/3 transverse colon to upper anal canal)
• The midgut undergoes a complex 270° counter-clockwise rotation around the SMA during weeks 4–12 of gestation
• Arrest of this rotation → malrotation → predisposes to midgut volvulus (a surgical emergency)
• Neural crest cells migrate craniocaudally during weeks 4–7 of gestation to form the enteric ganglia; failure of this migration → Hirschsprung's disease ^[3]

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V. Etiology

The causes of intestinal obstruction are best organised by:

1. Mechanism: Mechanical vs. Functional
2. Level: Small bowel vs. Large bowel
3. Relation to bowel wall: Intraluminal vs. Intramural vs. Extramural (for mechanical causes)

A. Mechanical Obstruction

(i) Small Bowel Obstruction (SBO)

Most common causes of SBO: Adhesions, Malignancy, and Hernias ^[3]. The mnemonic "ABC" — Adhesion, Bulge (hernia), Cancer — is a useful aide-mémoire ^[4].

Extramural (Extrinsic) Causes

Intramural Causes

Intraluminal Causes

(ii) Large Bowel Obstruction (LBO)

Most common causes of LBO: Malignancy and Volvulus ^[3]. Specifically: Cancer, Volvulus, Diverticulitis, Stricture (anastomotic, radiation, ischaemic, endometriotic), Extrinsic compression (metastasis, pelvic/extraperitoneal tumour) ^[1].

(iii) Neonatal Causes of Intestinal Obstruction

Congenital anomalies are the primary causes ^[2]:

Additional neonatal causes include:

• Anorectal malformations (imperforate anus)
• Incarcerated inguinal hernia (especially in premature males)
• Necrotising enterocolitis (NEC) — primarily affects premature neonates
• Small left colon syndrome — occurs in infants of diabetic mothers

B. Functional Obstruction (Non-mechanical)

(i) Paralytic Ileus

Paralytic ileus = failure of transmission of peristaltic waves secondary to neuromuscular failure in the myenteric (Auerbach's) plexus and submucosal (Meissner's) plexus ^[3].

(ii) Pseudo-obstruction

Pseudo-obstruction = clinical picture of obstruction in the absence of a mechanical cause or intra-abdominal disease ^[3]. Obstruction in the absence of a mechanical cause — associated with underlying neuropathy or myopathy ^[3].

Acute Colonic Pseudo-obstruction (Ogilvie's Syndrome)

• Characterised by acute dilatation of the colon in the absence of an anatomic lesion that obstructs the flow of intestinal content ^[3]
• Occurs in hospitalised patients in association with a severe illness or after surgery and in conjunction with a metabolic imbalance or administration of medications ^[3]
• Abdominal distension is the most common clinical presentation ^[3]
• Pathophysiology: Autonomic imbalance (↓ parasympathetic / ↑ sympathetic) → aperistalsis ^[4]
• Aetiology: metabolic disturbance (DM, hypoK, hypothyroidism, uraemia), drugs (opioids, CCBs), trauma/post-op, neurological diseases (Parkinson's, MS) ^[4]

Chronic Colonic Pseudo-obstruction

• Toxic megacolon: Characterised by total or segmental colonic dilatation with systemic toxicity ^[3]. Occurs as a complication of IBD, infectious colitis (commonly associated with Clostridium difficile), ischaemic colitis, volvulus, diverticulitis and obstructive colorectal cancer. Bloody diarrhoea is the most common clinical presentation ^[3].
• Hirschsprung's disease: Chronic functional obstruction from aganglionic segment

Small Intestinal Pseudo-obstruction

• Idiopathic
• Familial visceral myopathy ^[3]

Differentiating Features: Pseudo-obstruction vs. Mechanical Obstruction [4]

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VI. Classification

Intestinal obstruction can be classified along several axes. This matters clinically because the classification determines urgency, likely cause, and management approach.

A. Anatomical Classification [3]

• Small bowel obstruction (SBO)
• Large bowel obstruction (LBO)

B. Mechanical vs. Functional Classification [3]

• Mechanical — peristalsis works against a physical barrier
• Functional — absence or inadequacy of peristalsis without mechanical barrier
  • Paralytic ileus
  • Pseudo-obstruction

C. Completeness [1]

• Partial vs. Complete obstruction ^[1]
  • Partial: some gas/fluid still passes → patient may still pass flatus, diarrhoea may occur (overflow)
  • Complete: no passage of gas or stool → absolute constipation (obstipation)

D. Chronicity [1]

• Chronic vs. Acute ^[1]
  • Acute: sudden onset, often surgical emergency
  • Chronic: insidious, often from slowly growing tumours or strictures; may have intermittent subacute episodes

E. Complexity [1]

• Simple obstruction — obstruction of the lumen, usually at one point only ^[1]; blood supply intact
• Strangulating obstruction — blood supply to bowel impaired ^[1]; constitutes a surgical emergency due to risk of ischaemia, necrosis, perforation
• Closed-loop obstruction — lumen occlusion in at least 2 points ^[1]; a segment of intestine is obstructed in two locations creating a segment with no proximal or distal outlet ^[3]
  • Presents with minimal abdominal distension since only a short segment of intestine is distended ^[3]
  • Can rapidly lead to complications such as ischaemia, necrosis and perforation ^[3]
  • Examples: LBO with competent ileocaecal valve, volvulus, hernia containing a loop of bowel, afferent loop syndrome (post-Billroth II gastrectomy) ^[4]

F. Relation to Bowel Wall (for mechanical causes) [3]

• Intraluminal (within the lumen)
• Intramural (within the wall)
• Extramural (outside the wall)

Classification Summary Diagram

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VII. Pathophysiology

Understanding the pathophysiology of IO is essential because every clinical feature and complication can be traced back to these mechanisms.

A. Proximal Dilatation [3][4]

When a mechanical obstruction occurs, the bowel proximal to the obstruction dilates due to:

1. Accumulation of gas:
   • Swallowed air (the major source; ~70% nitrogen which cannot be absorbed)
   • Bacterial fermentation — significant overgrowth of both aerobic and anaerobic organisms producing CO₂, H₂, and methane ^[3]
2. Accumulation of fluid:
   • Saliva, bile, pancreatic secretions, and gastric secretions ^[3] — the GI tract normally secretes 6–8 litres of fluid per day, most of which is reabsorbed. Obstruction prevents distal reabsorption → massive fluid accumulation in the proximal bowel
3. Peristaltic response:
   • Initially, increased peristalsis attempts to overcome the obstruction ^[4] — this is why early bowel sounds are high-pitched and hyperactive ("tinkling")
   • Eventually, the bowel fatigues and becomes atonic

B. Distal Collapse [3][4]

• Bowel below the obstruction exhibits normal peristalsis and absorption ^[3]
• Eventually becomes empty and collapses ^[3]
• This is why PR examination in mechanical LBO typically reveals an empty, collapsed rectum (in contrast to the dilated rectum of pseudo-obstruction)

C. Dehydration and Electrolyte Imbalance [3][4]

This is a major source of morbidity and mortality in IO:

The net effect is hypovolaemia → tachycardia, hypotension, oliguria, prerenal AKI.

D. Pathogenesis of Strangulation [3]

Strangulation represents the most dangerous evolution of IO:

1. Impaired venous and lymphatic return → venous and lymphatic congestion resulting in oedematous tissues ^[3]
   • Venous pressure rises → increased capillary hydrostatic pressure → oedema and haemorrhagic infarction of the bowel wall
2. Compromised arterial blood supply → bowel ischaemia, necrosis and subsequently perforation ^[3]
   • As intramural oedema worsens, even arterial inflow is eventually compressed
   • Ischaemic bowel loses its mucosal barrier → bacterial translocation across the bowel wall into the peritoneal cavity and bloodstream → peritonitis, sepsis, multi-organ failure

E. Closed-loop Obstruction — Special Pathophysiology

In closed-loop obstruction (e.g., LBO with competent ileocaecal valve, volvulus):

• The trapped segment cannot decompress in either direction
• Intraluminal pressure rises rapidly
• The caecum (largest diameter) is at highest risk of perforation by Laplace's law (Wall Tension = Pressure × Radius)
• Caecal diameter > 9 cm on imaging is a warning sign; > 12 cm is considered critical with imminent perforation risk

F. Systemic Consequences

The progressive pathophysiology can be summarised in a cascade:

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VIII. Clinical Features

Cardinal features of IO = Abdominal pain + Distension + Vomiting + Absolute constipation ^[3]

The clinical presentation depends on the level (proximal vs. distal), completeness (partial vs. complete), type (simple vs. strangulating), and duration of obstruction.

A. Symptoms

1. Abdominal Pain

• Sudden onset ^[3]
• Colicky in nature — paroxysms of pain coinciding with increased peristaltic activity ^[3]
  • Why colicky? The bowel contracts vigorously trying to push contents past the obstruction → intermittent smooth muscle contraction → intermittent pain → relief between spasms
• Located in periumbilical region (small bowel) or infraumbilical (large bowel) ^[3]
  • Why periumbilical for SBO? The small bowel is a midgut-derived structure; visceral pain from the midgut is referred to the periumbilical region (T9–T10 dermatome)
  • Why infraumbilical for LBO? The hindgut-derived colon refers pain to the infraumbilical/suprapubic region (T11–L1 dermatome)
• Progression from cramping to more focal and constant pain may indicate peritoneal irritation related to complications such as bowel ischaemia and necrosis ^[3]
  • Why does it become constant? Ischaemic bowel causes continuous irritation of the visceral and then parietal peritoneum → constant, localised, somatic pain that is worsened by movement

2. Vomiting

• The more distal the obstruction, the longer it takes for the onset of nausea and vomiting ^[3]
  • Why? In proximal SBO, the stomach fills quickly with regurgitated secretions → early vomiting. In distal SBO or LBO, there is a large capacitance reservoir that must fill before retrograde flow reaches the stomach.
• Character of vomitus changes from digested food to feculent material as obstruction progresses due to enteric bacterial overgrowth ^[3]
  • "Feculent" does not mean actual faeces — it is the foul-smelling product of bacterial fermentation in stagnant small bowel contents
• Bilious vomiting in a neonate is malrotation with midgut volvulus until proven otherwise — this is a surgical emergency ^[2][5]
• In proximal SBO: vomiting is early, profuse, and bilious → leads to rapid dehydration and metabolic alkalosis
• In LBO: vomiting is late and may be feculent; some patients never vomit

3. Abdominal Distension

• The more distal the obstruction, the greater the distension ^[3]
  • Why? More bowel length is available proximal to the obstruction for gas and fluid accumulation
• Proximal SBO: minimal or absent distension (short segment of bowel proximal to obstruction)
• Distal SBO: moderate distension
• LBO: marked, generalised distension (entire colon and potentially ileum if valve is incompetent)

4. Absolute Constipation (Obstipation)

• Inability to pass faeces and flatus ^[3]
• Feature of complete intestinal obstruction ^[3]
• Why? In complete obstruction, nothing passes the obstruction point → distal bowel empties its residual contents → then nothing more can pass
• In partial obstruction, some flatus or even diarrhoea may still be present (overflow diarrhoea)
• Note: patients may pass stool/flatus from bowel distal to the obstruction in the early hours — this does NOT exclude obstruction

Summary: Clinical Presentation by Level

B. Signs

1. General Examination

• Dehydration: dry mucous membranes, decreased skin turgor, sunken eyes, tachycardia, hypotension
  • Why? Loss of fluid from vomiting, third-spacing, and reduced oral intake
• Tachycardia: may be from dehydration or pain; persistent tachycardia with fever raises concern for strangulation/sepsis
• Fever: suggests strangulation, perforation, or intra-abdominal sepsis
• Hernia sites must be examined — always check groin (inguinal and femoral), umbilical, and any surgical scars for incisional hernias
  • Incarcerated hernias are the leading cause of complications related to bowel obstruction ^[3]

2. Abdominal Inspection

• Distension: as described above; assess degree
• Surgical scars: suggest adhesive obstruction
• Visible peristalsis: may be visible through the abdominal wall in thin patients with SBO — represents hyperperistalsis of bowel proximal to obstruction trying to overcome it ("ladder pattern")
• Hernia orifices: groin, umbilicus, incisional sites

3. Abdominal Palpation

• Tenderness:
  • Mild diffuse tenderness is common in uncomplicated IO
  • Localised tenderness, guarding, rebound tenderness → suggests peritonism from strangulation, ischaemia, or perforation
  • A tender, irreducible lump at a hernia site = obstructed/strangulated hernia until proven otherwise
• Palpable mass: may represent the obstructing lesion (tumour), distended closed-loop, or intussusception ("sausage-shaped mass" in the RUQ in paediatric intussusception)

4. Abdominal Percussion

• Tympanic (hyper-resonant): due to gas-filled, distended bowel loops
• Shifting dullness: suggests free peritoneal fluid (ascites from transudation)

5. Auscultation

• Early / Simple obstruction: High-pitched, tinkling bowel sounds — "borborygmi" — representing hyperactive peristalsis trying to overcome the obstruction
• Late / Strangulation: Absent bowel sounds — the bowel has fatigued or become necrotic → no more peristalsis
• Paralytic ileus: hypoactive or absent bowel sounds ^[4]
• Pseudo-obstruction: normal bowel sounds ^[4] — this is a key differentiating feature

6. Digital Rectal Examination (PR)

• Essential in every patient with suspected IO
• Empty rectum in mechanical LBO (distal bowel has been evacuated)
• Dilated rectum in pseudo-obstruction ^[4]
• May reveal:
  • A rectal mass (colorectal cancer)
  • Blood on glove ("redcurrant jelly" mucus in intussusception; blood from ischaemic mucosa)
  • Faecal impaction
  • An empty ballooned rectum in Hirschsprung's disease (after which a gush of stool/gas may be released — "blast sign")

C. Special Clinical Features by Cause

Strangulated Obstruction — Warning Signs

Neonatal Intestinal Obstruction — Key Features [2][5]

Bilious vomiting in a neonate is malrotation with midgut volvulus until proven otherwise — it is a surgical emergency ^[2][5].

Intussusception (Paediatric) — Classic Triad [3]

1. Colicky abdominal pain — episodic screaming with drawing up of legs, child appears well between episodes
2. "Redcurrant jelly" stools — bloody mucus per rectum from venous congestion and mucosal ischaemia of the intussuscepted segment
3. "Sausage-shaped" mass — usually palpable in the RUQ (because the ileocolic intussusception pushes along the course of the colon)
4. "Dance sign" — emptiness in the RIF (because the caecum has been dragged upwards)

Sigmoid Volvulus — Classic Features [4]

• Elderly, male, institutionalised/bedbound patient with chronic constipation
• Massive abdominal distension (often asymmetric)
• Coffee bean sign on AXR — dilated sigmoid arising from pelvis/LLQ, ahaustral, with 3 lines of sigmoid wall converging at the twist point ^[4]
• Bird's beak sign on contrast enema — tapering of contrast at the twist point ^[4]
• Whirl sign on CT ^[4]

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IX. Neonatal Intestinal Obstruction — Detailed Pathophysiology by Cause

Given the emphasis in the lecture slides ^[2][5][6], let us elaborate on the major neonatal causes:

A. Intestinal Atresia [3]

• Atresia is a congenital defect of a hollow viscus that results in complete obstruction of the lumen ^[3]
• One of the most frequent causes of bowel obstruction in newborns ^[3]
• Most commonly affected site: jejunum and ileum (jejunoileal atresia); least common: colon ^[3]
• Duodenal atresia causes complete obstruction; duodenal stenosis causes partial obstruction only ^[3]

Pathogenesis: Two theories depending on location:

• Duodenal atresia: Failure of recanalization — during weeks 4–8 of gestation, the duodenal lumen becomes obliterated by epithelial proliferation and then normally recanalizes. If this fails → atresia or stenosis.
• Jejunoileal atresia: Vascular accident — an in-utero mesenteric vascular insult (thrombosis, volvulus, intussusception) causes segmental ischaemic necrosis → resorption → atresia. This is why jejunoileal atresia is NOT associated with other congenital anomalies (unlike duodenal atresia).

Classification (Grosfeld) ^[3]:

• Type I (mucosal web): Intact bowel wall with intraluminal mucosal membrane
• Type II (fibrous cord): Atretic ends connected by fibrous cord, mesentery intact
• Type IIIa (mesenteric gap defect): Atretic ends separated by a V-shaped mesenteric gap
• Type IIIb (apple-peel / Christmas tree): Proximal jejunal atresia with the distal bowel spiralling around a single SMA branch — carries high mortality
• Type IV (multiple atresia): Multiple atretic segments ("string of sausages")
• Type III is the most common; Type I is the least common ^[3]

Associations ^[3]:

• Duodenal atresia: Down syndrome (trisomy 21) — ~30%; cardiac, renal, vertebral, biliary anomalies
• Jejunoileal atresia: Cystic fibrosis (meconium ileus)
• Colonic atresia: Hirschsprung's disease

B. Malrotation [3][5][6]

• Intestinal malrotation occurs when normal rotation of the embryonic gut is arrested or disturbed during in utero development ^[3]
• Majority of patients present during neonatal period or within the first year of life ^[3]

Normal embryology ^[3]:

1. Weeks 4–5: Rapid growth of midgut → physiological herniation through the umbilicus
2. Weeks 6–10: The midgut undergoes a 270° counter-clockwise rotation around the SMA axis
3. Week 10–12: Return to abdomen with the duodenojejunal junction fixing to the left of midline (at the ligament of Treitz) and the caecum fixing in the RIF; the mesentery then fuses broadly to the posterior abdominal wall

What goes wrong in malrotation:

• The rotation is incomplete → the duodenojejunal junction fails to reach its normal position → the caecum fails to descend to the RIF
• Ladd's bands: Peritoneal bands extend from the malpositioned caecum across the duodenum to fix in the RUQ → extrinsic compression of the duodenum
• Narrow mesenteric base: The unfixed mesentery has a dangerously narrow pedicle → the entire midgut can twist around the SMA → midgut volvulus → catastrophic midgut ischaemia if not corrected within hours

Associated conditions ^[3]: CDH (~100%), CHD (40–90%), heterotaxy syndrome, omphalocele (31–45%), gastroschisis, intestinal atresia, oesophageal atresia, biliary atresia, Meckel's diverticulum

C. Hirschsprung's Disease [3]

• "Hirschsprung" → named after Harald Hirschsprung who described it in 1886
• Occurs in 1 in 5000 live births; male predominance (M:F = 3:1 to 4:1) ^[3]
• Predominant gene: RET proto-oncogene — loss-of-function mutation → impaired neural crest cell migration and differentiation ^[3]

Pathogenesis ^[3]:

• Defect in craniocaudal migration of neuroblasts from the neural crest
• Migration begins at week 4 and should reach the distal colon by week 7 of gestation ^[3]
• Failure of cells to reach the distal colon leaves that segment aganglionic and therefore non-functional ^[3]
• The aganglionic segment remains tonically contracted (because ganglia normally provide inhibitory relaxation via NO and VIP) → functional obstruction → proximal bowel dilates

Clinical features ^[3]:

• Failure to pass meconium within 24–48 hours of birth (90% of neonates with HD)
• Abdominal distension
• Bilious vomiting
• "Blast sign" on PR: explosive release of gas and stool when the examining finger is withdrawn
• Later presentation: chronic constipation in children (short-segment disease)
• Complication: Hirschsprung-associated enterocolitis (HAEC) — explosive, foul-smelling diarrhoea, abdominal distension, fever, sepsis → can be life-threatening

D. Intussusception [3]

• Intussusception = invagination (telescoping) of a part of intestine into itself ^[3]
• Most common abdominal emergency in early childhood ^[3]
• Most common cause of intestinal obstruction in infants between 6–36 months ^[3]
• Male predominance (M:F = 3:2) ^[3]
• Location: most often at ileocaecal junction (ileocolic intussusception) ^[3]

Pathogenesis ^[3]:

• Idiopathic (75%): Hypertrophy of Peyer's patches in lymphoid-rich terminal ileum secondary to viral infection (URTI, gastroenteritis) acts as a lead point
• Pathological lead point (more common in adults or children > 6 years): Meckel's diverticulum, polyps, lymphoma, duplication cysts, HSP
• The intussusceptum (proximal segment) drags into the intussuscipiens (distal segment) → venous congestion → mucosal oedema and haemorrhage → "redcurrant jelly" stool → if untreated, arterial compromise → necrosis → perforation

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X. Closed-Loop Obstruction — Special Entities

A. Hernia-related Closed-Loop Obstruction [3][4]

• Definitions ^[4]:
  • Reducible: hernia contents can be returned to the abdomen
  • Incarcerated: contents are trapped but the bowel lumen is not obstructed
  • Obstructed: bowel lumen is obstructed (closed-loop IO) but blood supply intact
  • Strangulated: blood supply also compromised → ischaemia → gangrene
  • Richter's hernia: only one sidewall of bowel is incarcerated → ischaemia without obstruction ^[4]
  • Reduction-en-masse: apparently reducing the sac but did not push contents out → still strangulated ^[4]
• Incidence of strangulation: femoral > indirect inguinal > direct inguinal ^[4]

B. Gallstone Ileus [4]

• Gallstone erodes through the GB into adjacent bowel through a cholecystoenteric fistula ^[4]
• Bouveret's syndrome: stone stuck at duodenum/stomach → GOO ^[4]
• Cholecystoduodenal fistula (MC): stone travels through SB → impacts at terminal ileum, 2 feet proximal to the ileocaecal valve (narrowest part of SB) ^[4]
• AXR: Rigler's triad — pneumobilia + SBO + ectopic gallstone (usually in RIF) ^[4]
• Management: Enterolithotomy — exploratory laparotomy → proximal enterotomy (NOT over the stone because of ulceration) → milk the stone proximally for extraction ^[4]

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Active Recall - Intestinal Obstruction (Definition to Clinical Features)

1. Name the 4 cardinal features of intestinal obstruction and explain how the level of obstruction affects each feature.

Your answer

Grade

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Pain (periumbilical for SBO, infraumbilical for LBO), Vomiting (early and bilious in proximal SBO, late and feculent in distal), Distension (greater with more distal obstruction), Absolute constipation (complete obstruction). More distal = more distension, later vomiting; more proximal = earlier vomiting, less distension.

2. What is the most common cause of SBO in adults, and what is the most common cause of LBO? Give the approximate percentage for SBO.

Your answer

Grade

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SBO: Adhesions (approximately 60-74%). LBO: Colorectal cancer. 15-20% of CRC patients present with IO.

3. Explain the pathophysiological cascade from simple mechanical obstruction to perforation.

Your answer

Grade

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Obstruction leads to proximal dilatation from gas and fluid accumulation, then increased intraluminal pressure causes venous and lymphatic congestion, then bowel wall oedema, then arterial compromise causing ischaemia, then necrosis, then perforation leading to peritonitis and sepsis. Bacterial translocation occurs at the ischaemia stage.

4. A neonate presents with bilious vomiting on day 1 of life. What is the most important diagnosis to exclude and why?

Your answer

Grade

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Malrotation with midgut volvulus. It is a surgical emergency because the entire midgut can twist around the SMA, leading to catastrophic midgut ischaemia and necrosis within hours if not surgically corrected via Ladd procedure.

5. Explain why a competent ileocaecal valve in the presence of a distal colonic obstruction is dangerous.

Your answer

Grade

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A competent ileocaecal valve prevents retrograde decompression into the ileum, creating a closed-loop obstruction. This causes rapid rise in intraluminal pressure, particularly in the caecum which has the largest diameter. By Laplace law (Tension = Pressure x Radius), the caecum is at highest risk of perforation when diameter exceeds 9-12 cm.

6. List 4 clinical features that suggest strangulation has occurred in a patient with bowel obstruction.

Your answer

Grade

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Any 4 of: constant non-colicky pain, peritoneal signs (guarding, rigidity, rebound tenderness), tachycardia, fever, leucocytosis, raised lactate or metabolic acidosis, bloody PR discharge, absent bowel sounds.

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References

^[1] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (pp. 3, 4, 9, 21–23, 30, 39, 41, 42) ^[2] Lecture slides: GC 205. The newborn baby is vomiting repeatedly Neonatal intestinal obstruction and other GI emergencies.pdf (p. 5) ^[3] Senior notes: felixlai.md (Intestinal Obstruction, Intestinal Atresia, Intestinal Malrotation, Hirschsprung Disease, Intussusception, Volvulus sections) ^[4] Senior notes: maxim.md (sections 4.3 Intestinal Obstruction, Volvulus, Gallstone Ileus, Hernia, Diverticular Disease, Meckel Diverticulum, Pseudo-obstruction) ^[5] Lecture slides: Neonatal Surgery.pdf ^[6] Lecture slides: Case Study – Paediatric Surgery Bilious vomiting of new-born_ACH Fung.pdf

Differential Diagnosis of Intestinal Obstruction

The differential diagnosis of intestinal obstruction is essentially the process of determining why the bowel is obstructed — and, crucially, whether it is truly obstructed at all. Many conditions mimic the cardinal features of IO (pain, distension, vomiting, constipation) without an actual mechanical barrier, and some mechanical causes masquerade as others. The approach must be systematic.

A. The Core Clinical Question: Is This Really Intestinal Obstruction?

Before diving into specific causes, the clinician must answer three sequential questions:

1. Is there truly an obstruction? (vs. a mimic like paralytic ileus, gastroenteritis, or a medical cause of acute abdomen)
2. If yes, is it mechanical or functional?
3. If mechanical, what is the specific cause and is there strangulation?

Severity of each symptom depends on the level of obstruction ^[1] — this principle is central to the differential because a high SBO presents very differently from an LBO.

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B. Systematic Framework for the Differential Diagnosis

The differential is best organised by:

1. Level: SBO vs. LBO
2. Mechanism: Mechanical vs. Functional
3. Age group: Adult vs. Neonatal/Paediatric
4. Mimics: Conditions that present like IO but are not

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C. Differential Diagnosis of Small Bowel Obstruction (Adults)

Most common causes of SBO: Adhesions, Bulge (hernia), Cancer — mnemonic "ABC" ^[3][4]

(i) Mechanical Causes

(ii) Functional Causes (Mimicking or Co-existing with SBO)

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D. Differential Diagnosis of Large Bowel Obstruction (Adults)

Common causes of LBO: Cancer of colon, Volvulus, Diverticular stricture, Pseudo-obstruction ^[7]

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E. Differential Diagnosis of Neonatal Intestinal Obstruction

Causes of neonatal intestinal obstruction ^[2]:

• Intestinal atresia (oesophagus to anus)
• Malrotation
• Meconium disease
• Hirschsprung's disease

The key differentiating feature in neonates is the character of vomiting (bilious vs. non-bilious) and the timing/passage of meconium.

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F. Differential Diagnosis by Presenting Feature

Sometimes patients present with a dominant symptom rather than the full tetrad. Here is a feature-based differential approach:

(i) Abdominal Pain + Distension + Vomiting — "Is it really IO?"

(ii) Acute Abdomen by Location — Cross-referencing IO Mimics [4]

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G. Differential Diagnosis — Specific Scenarios

(i) DDx of Sigmoid Volvulus [3]

(ii) DDx of Intussusception (Paediatric) [3]

(iii) DDx of Neonatal IO [3]

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H. Differential Diagnosis Algorithm

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I. How to Differentiate Mechanical SBO from Paralytic Ileus from Pseudo-obstruction

This is a high-yield exam comparison. The key is to combine clinical features, examination findings, and imaging.

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J. Red Flags in the Differential — When to Suspect Strangulation

Any patient with suspected IO who develops the following should be considered to have strangulated obstruction until proven otherwise — this changes the differential from "which cause?" to "emergent surgery NOW":

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Active Recall - Differential Diagnosis of Intestinal Obstruction

1. Name three clinical and investigational features that differentiate mechanical SBO from paralytic ileus from pseudo-obstruction.

Your answer

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Bowel sounds: increased/high-pitched in mechanical SBO, hypoactive/absent in paralytic ileus, normal in pseudo-obstruction. PR exam: empty collapsed rectum in mechanical LBO, variable in ileus, dilated rectum in pseudo-obstruction. AXR: transition point with absent rectal gas in mechanical, diffuse gas with no transition point in ileus, dilated colon with gas in rectum in pseudo-obstruction.

2. A 75-year-old woman presents with features of distal SBO. She has no surgical history and no hernias. AXR shows SBO with pneumobilia. What is the likely diagnosis and what is the classic triad on AXR?

Your answer

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Gallstone ileus. Rigler triad: pneumobilia, SBO, and ectopic gallstone (usually in RIF at ileocaecal valve area). Stone erodes from gallbladder into duodenum via cholecystoenteric fistula and impacts at terminal ileum, the narrowest SB segment.

3. List four differential diagnoses for massive colonic dilatation and explain how you differentiate them.

Your answer

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Sigmoid volvulus (coffee bean sign, absent rectal gas, no initial systemic toxicity), Caecal volvulus (dilated SB, arises from RLQ, haustral markings), Toxic megacolon (systemic toxicity, bloody diarrhoea, IBD or C. difficile history), Ogilvie syndrome (hospitalised patient, normal bowel sounds, dilated rectum on PR, gas in rectum on AXR, diagnosis of exclusion).

4. In a neonate with bilious vomiting, what are the top four differential diagnoses and which one must be excluded first and why?

Your answer

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Top four: malrotation with midgut volvulus, intestinal atresia (jejunoileal or duodenal if distal to ampulla), meconium ileus, Hirschsprung disease. Must exclude malrotation with midgut volvulus first because the entire midgut can infarct within hours from SMA compromise if the volvulus is not surgically reduced.

5. Name three medical conditions that can mimic intestinal obstruction and explain the mechanism by which each mimics IO.

Your answer

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Any three of: (1) Acute pancreatitis - retroperitoneal inflammation causes reflex ileus via sympathetic chain irritation; (2) DKA - autonomic neuropathy and metabolic derangement cause ileus and severe abdominal pain (pseudoperitonitis); (3) Acute mesenteric ischaemia - ischaemic bowel loses motility and causes distension, pain, vomiting; (4) Hypokalaemia - K+ essential for smooth muscle repolarisation, low K+ causes bowel paralysis.

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References

^[1] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (pp. 3, 9, 10, 39) ^[2] Lecture slides: GC 205. The newborn baby is vomiting repeatedly Neonatal intestinal obstruction and other GI emergencies.pdf (pp. 3, 5) ^[3] Senior notes: felixlai.md (Intestinal Obstruction, Volvulus, Intussusception, Intestinal Atresia, Malrotation, Hirschsprung Disease, Meckel's Diverticulum, Diverticulitis, Appendicitis sections) ^[4] Senior notes: maxim.md (sections 4.3 Intestinal Obstruction, Paralytic Ileus, Pseudo-obstruction, Volvulus, Gallstone Ileus, Acute Abdomen DDx) ^[7] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p. 28)

Diagnosis of Intestinal Obstruction

A. Diagnostic Approach — The Key Questions

The lecture slides lay out a systematic framework of questions that must be answered sequentially ^[1]:

Does the patient have intestinal obstruction? Ileus vs. mechanical obstruction? What is the site and cause of obstruction? Small bowel vs. large bowel? Is the obstruction simple or strangulated? What investigations should be performed? Should the patient be treated conservatively and for how long? What are the indications for surgery? What are the surgical options? ^[1]

There is no single "diagnostic criterion" for IO the way there is for, say, rheumatoid arthritis. Instead, IO is a clinical-radiological diagnosis — you combine history, examination, blood tests, and imaging to answer the questions above. Let us walk through each layer.

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B. Diagnostic Criteria — Clinical-Radiological Diagnosis

IO is diagnosed when the combination of:

1. Clinical features: ≥ 1 of the cardinal features (colicky pain, vomiting, distension, absolute constipation) in an appropriate clinical context
2. Radiological confirmation: Imaging demonstrating dilated bowel proximal to a transition point with collapsed distal bowel (mechanical) OR diffuse dilatation without transition point (functional)
3. Laboratory support: Blood results consistent with dehydration, electrolyte derangement, or ischaemia

There is no universally agreed scoring system, but the diagnosis is essentially clinical + imaging. The clinical picture raises the suspicion; imaging confirms and characterises it.

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C. Diagnostic Algorithm

The following algorithm represents the systematic approach to a patient with suspected IO, integrating the questions from the lecture slides ^[1]:

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D. Investigation Modalities — Detailed Guide

The investigations for IO can be grouped into:

1. Bedside tests
2. Blood investigations
3. Imaging (the cornerstone)
4. Endoscopy

Each test has a specific role in answering one or more of the key diagnostic questions.

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1. Bedside Tests [7][8]

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2. Blood Investigations

Bloods: CBC, ABG/VBG, LRFT, amylase, lactate ± septic work-up ^[4]

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3. Imaging — The Cornerstone of Diagnosis

(i) Erect Chest X-ray (CXR)

Erect CXR: free gas, aspiration pneumonia, gastric distension, NG tube position ^[4]

(ii) Abdominal X-ray (AXR) — Supine and Erect

Erect and supine AXR ^[4]. The lecture slides outline a systematic approach to AXR interpretation ^[1]:

Key questions to answer on AXR ^[1]:

• Are there dilated bowel loops?
• Are air-fluid levels present in erect film?
• Any gas in the colon and the level of cut-off?
• Any evidence of strangulation: thumbprinting, pneumatosis cystoides intestinalis, free peritoneal gas?
• Any massive dilatation of colon?
• Any air in the biliary tree?

Why two views?

• Supine AXR is better for identifying the transition point (where dilated bowel meets collapsed bowel) and overall gas pattern ^[4]
• Erect AXR shows air-fluid levels (gas rises above fluid in distended loops), though the number of air-fluid levels does not affect management ^[4] — what matters is whether there is obstruction and at what level

How to distinguish SBO from LBO on AXR ^[7]:

AXR Findings in IO ^[3][1]:

AXR Findings Suggesting Complications (Strangulation/Ischaemia) ^[1][3]:

AXR Pattern by Level ^[3]:

(iii) CT Abdomen — The Definitive Investigation

CT scan: more sensitive than plain abdominal X-rays ^[1]

CT is now the investigation of choice for confirming IO, identifying the cause, and detecting complications. The lecture slides emphasise the following ^[1]:

CT for SBO ^[1]:

• Level of obstruction (transition between dilated and collapsed loop)
• Lesions (tumour, foreign bodies)
• Viability of bowel (intravenous contrast)

CT for LBO ^[1]:

• Intravenous contrast, rectal contrast
• Site of obstruction (transition of dilated loop and collapsed loop)
• Mass lesion
• Perfusion of bowel wall
• Distant disease in case of malignancy

CT Protocols:

• SBO: CT with IV contrast (to assess bowel wall enhancement/viability). Oral contrast is generally NOT given in acute SBO because the patient is vomiting and the contrast will take too long to reach the obstruction point.
• LBO: CT with IV contrast + rectal contrast ^[1] — rectal contrast helps delineate the distal obstruction point and differentiate mechanical from pseudo-obstruction.

(iv) Gastrografin (Water-Soluble Contrast) Follow-Through

Gastrografin meal and follow-through is indicated in adhesive IO only ^[3]

This is a particularly important investigation because it is both diagnostic AND therapeutic ^[3]:

(v) Water-Soluble Contrast Enema

Water-soluble enema for LBO: to differentiate mechanical vs functional ^[4]

(vi) Upper GI Contrast Study (Neonates)

• Gold standard for diagnosing intestinal malrotation ^[3]
• Uses barium or water-soluble contrast to visualise the duodenum
• Classical findings:
  • "Corkscrew" appearance of the duodenum (abnormal position and rotation)
  • "Beak" appearance at the volvulus point
  • Clearly misplaced duodenum with ligament of Treitz on the right side of the abdomen ^[3]
  • Dilatation of stomach and proximal duodenum in duodenal obstruction

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4. Endoscopy

Lower gastrointestinal endoscopy ^[1]: Diagnostic AND Therapeutic

Specific endoscopic scenarios:

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5. Special Investigations by Cause

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E. Interpretation Framework — Putting It All Together

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F. Summary: Investigation Hierarchy

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Active Recall - Diagnosis of Intestinal Obstruction

1. List the 6 key questions to ask when reviewing an AXR of a patient with suspected intestinal obstruction, as per lecture slides.

Your answer

Grade

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1. Are there dilated bowel loops? 2. Are air-fluid levels present on erect film? 3. Any gas in the colon and the level of cut-off? 4. Any evidence of strangulation (thumbprinting, pneumatosis intestinalis, free peritoneal gas)? 5. Any massive dilatation of colon? 6. Any air in the biliary tree?

2. Explain the diagnostic AND therapeutic role of gastrografin follow-through in adhesive SBO. When is the most important film taken?

Your answer

Grade

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Diagnostic: Detects level of obstruction and whether partial or complete. If contrast reaches colon by 2 hours, obstruction is partial and likely to resolve. Therapeutic: Hyperosmotic contrast draws fluid into the lumen, reduces bowel wall oedema, and stimulates peristalsis. The 2-hour film is the most important.

3. On CT abdomen, name 4 findings that suggest bowel ischaemia or strangulation in a patient with IO.

Your answer

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Any 4 of: Reduced or absent bowel wall enhancement (lack of contrast uptake), pneumatosis intestinalis (gas in bowel wall), portal venous gas, bowel wall thickening, oedematous/thickened mesentery, engorgement of mesenteric vessels, free fluid.

4. How do you differentiate SBO from LBO on plain AXR? Name 3 distinguishing features.

Your answer

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1. Mucosal folds: valvulae conniventes (cross full width) in SBO vs haustra (partial) in LBO. 2. Location: central loops in SBO vs peripheral in LBO. 3. Diameter: dilated if greater than 3 cm for SB vs greater than 6 cm for colon (greater than 9 cm for caecum).

5. Name the classic radiological triad of gallstone ileus and explain the pathophysiology.

Your answer

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Rigler triad: pneumobilia, SBO, and ectopic gallstone (usually in RIF). Pathophysiology: large gallstone erodes through gallbladder wall into duodenum via a cholecystoenteric fistula (usually cholecystoduodenal). The fistula allows air to enter the biliary tree (pneumobilia). The stone travels through the small bowel and impacts at the terminal ileum (narrowest part, 2 feet from IC valve).

6. A neonate presents with bilious vomiting. What is the gold standard investigation to confirm malrotation and what are two classical findings?

Your answer

Grade

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Gold standard: Upper GI contrast study (barium or water-soluble). Classical findings: Corkscrew appearance of the duodenum and misplaced duodenojejunal junction (ligament of Treitz on the right side of the abdomen). Also: beak appearance at volvulus point, dilatation of stomach and proximal duodenum.

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References

^[1] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (pp. 2, 15, 18, 44, 46) ^[3] Senior notes: felixlai.md (Intestinal Obstruction – Diagnosis, Intestinal Malrotation – Diagnosis, Mesenteric Ischaemia – Diagnosis, Intussusception – Diagnosis, Intestinal Atresia sections) ^[4] Senior notes: maxim.md (sections 4.3 Intestinal Obstruction – Investigations, Volvulus – Investigations, Gallstone Ileus – Investigations, Pseudo-obstruction – Investigations, CRC – Investigations) ^[7] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (pp. 12, 29) ^[8] Senior notes: maxim.md (section 2.4 Acute Abdomen – Investigations)

Management of Intestinal Obstruction

A. Overarching Principles

The management of IO follows a logical sequence that mirrors the diagnostic questions from the lecture slides ^[1]:

Management: initial resuscitation followed by determination of the site and cause of obstruction ^[1] Decision on surgery and timing of surgery important ^[1] High mortality if complications occur ^[1]

Every patient with suspected IO requires simultaneous resuscitation and assessment. The key management decision is whether the patient needs conservative (non-operative) management or urgent surgical intervention — and if conservative, for how long before you pull the trigger on surgery.

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B. Management Algorithm — Master Overview

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C. Initial Management — All Patients ("Drip and Suck")

Every patient with IO, regardless of cause, requires the same initial resuscitation package. The mnemonic is "Drip and Suck" ^[3][4]:

Resuscitation: ABC. NPO, O₂, IV access, analgesics, anti-emetics ^[4]

1. Nil Per Os (NPO)

• All patients should be made NPO to limit bowel distension ^[3]
• Why? Any oral intake adds to the accumulating gas and fluid proximal to the obstruction, worsening distension, vomiting risk, and aspiration risk

2. IV Fluid Resuscitation ("Drip")

Intravenous fluid and electrolytes ^[1]

• External loss due to vomiting + internal loss due to sequestration of fluid in the bowel as part of the non-functional ECF (third-space loss) leading to intravascular volume depletion ^[3]
• Crystalloids: normal saline (0.9% NaCl), Ringer's lactate, or Hartmann's solution ^[3]
• K⁺ replacement may be indicated but should be given cautiously in patients with AKI from severe dehydration ^[3]
  • Why cautious? In AKI, the kidneys cannot excrete potassium effectively → risk of hyperkalaemia even though the patient is total-body K⁺ depleted. Always check K⁺ and renal function before replacing.
• Monitoring: Strict fluid balance (input/output charting), urine output (target > 0.5 mL/kg/h), serial U&Es
• In severe hypovolaemia: may need rapid fluid boluses (e.g. 500 mL over 15 min) guided by clinical response

3. Nasogastric Tube Decompression ("Suck")

NG tube / Salem sump tube (suck): free drainage + Q4h aspiration to decompress proximal bowel and reduce N/V ^[4]

• Achieved by non-vented (Ryle) or vented (Salem Sump) tube ^[3]
• Placed on free drainage with 4-hourly aspiration ^[3]
• Functions ^[3]:
  • Decompression proximal to obstruction — removes accumulated gas and fluid from the stomach/proximal SB, reducing intraluminal pressure
  • Reduce risk of aspiration during induction of anaesthesia and post-extubation — a stomach full of bilious/faeculent fluid is a massive aspiration risk during intubation
• NG output monitoring: Volume, colour (bilious = distal to ampulla obstruction), reducing output suggests resolution
• Salem Sump (double-lumen) is preferred over Ryle (single-lumen) because the vent lumen prevents the tube from adhering to the gastric mucosa during suction, reducing mucosal injury

4. Pain Relief

• Pain management with opioids is reasonable although pain from mechanical bowel obstruction in general is often not amenable to treatment with analgesics ^[3]
• In practice: IV paracetamol as first-line, then careful titration of IV morphine/fentanyl
• Pethidine has no effect on gut motility c.f. morphine ^[4] — this makes it theoretically preferable in ileus, but its use is declining due to norpethidine toxicity risk
• Anti-emetics: metoclopramide (prokinetic — aids peristalsis, but contraindicated in complete mechanical obstruction as it increases peristalsis against the obstruction → risk of perforation), ondansetron, or cyclizine

5. Antibiotic Prophylaxis

Antibiotics: if suspect bowel perforation; IV ceftriaxone + metronidazole ^[4]

• Broad-spectrum antibiotics due to bacterial overgrowth ^[3]
• Mandatory for all patients undergoing surgery for intestinal obstruction ^[3]
• Warranted especially in patients with complicated obstruction ^[3]
• Why? Bacterial translocation from ischaemic/distended bowel → bacteraemia. Enteric organisms include Gram-negatives (E. coli, Klebsiella) and anaerobes (Bacteroides) → need cover for both
• Regimen: IV ceftriaxone (Gram-negative cover) + IV metronidazole (anaerobic cover) ^[4]; or amoxicillin-clavulanate; or piperacillin-tazobactam in severe sepsis

6. Monitoring

Frequent monitor of vital signs, abdominal signs and X-rays ^[1]

• Monitor: vitals (temp, BP/P), abdominal tenderness, WBC, ABG ^[4]
• Urine output via catheter
• Serial abdominal examination (looking for developing peritonism)
• Serial AXR if on conservative management

7. Nutrition

Nutrition when prolonged fasting is anticipated ^[1]

• If NPO likely to exceed 5–7 days (or if the patient is already malnourished), start total parenteral nutrition (TPN) or peripheral PN
• Why? Prolonged starvation leads to catabolism, impaired wound healing, and immunosuppression — all of which worsen surgical outcomes

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D. Conservative (Non-Operative) Management

Indications for Conservative Management [1]

Non-operative treatment is appropriate for ^[1]:

• Partial obstruction
• Adhesions
• Crohn's disease
• Radiation stricture
• Disseminated malignant disease

Why conservative management works in these situations:

• Partial adhesive obstruction: The bowel is kinked or compressed but not completely occluded → oedema resolves with bowel rest and decompression → the partial obstruction opens up. Conservative management is approximately 80% effective for adhesive SBO ^[4].
• Crohn's stricture: Active inflammation may respond to medical therapy (steroids, biologics) → oedema subsides → lumen opens
• Radiation stricture: Acute-on-chronic inflammatory oedema may settle with bowel rest
• Disseminated malignancy: Surgical cure unlikely; focus on palliation with decompression ± endoscopic stenting

Conservative Management Protocol [1][3]

Signs of Resolution [1][3]

Resolution of obstruction ^[1]:

• Less abdominal distension
• Reduction of nasogastric output
• Passage of flatus and bowel movement
• Resolution in abdominal X-rays

When to Abandon Conservative Management

Unresolved obstruction → surgical treatment (duration of conservative treatment controversial, usually 48 hours) ^[1]

• Duration of observation = 48–72 hours in which if no improvement is seen then the patient should be surgically explored ^[3]
• Some centres use gastrografin follow-through to guide this decision: if contrast has not reached the colon by 4 hours → adhesive IO is unlikely to resolve → book for surgery ^[4]

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E. Indications for Urgent Surgery

Indications for urgent surgery ^[1]:

• Incarcerated, strangulated hernia
• Suspected or proven strangulation
• Peritonitis
• Pneumoperitoneum
• Pneumatosis cystoides intestinalis
• Close-loop obstruction
• Volvulus with peritoneal signs

Why each of these is urgent:

Surgical management should be delayed until resuscitation is complete provided there is no sign of strangulation or evidence of closed-loop obstruction ^[3]

This is an important principle: even urgent surgery benefits from a brief period (30–60 min) of aggressive fluid resuscitation to optimise the patient haemodynamically — but this should NOT delay definitive surgery for hours.

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F. Surgical Principles

Surgical principle: Treat underlying cause + resection of non-viable bowels ^[4] Anastomosis: Primary anastomosis (usually SB) or double-barrel ileostomy for observation ^[4]

Assessment of Bowel Viability at Surgery [3][4]

When the abdomen is opened, the surgeon must assess whether bowel is viable or not before deciding on resection:

If there is doubt, the "second-look laparotomy" approach (re-exploring at 24–48 hours) may be used ^[4].

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G. Cause-Specific Management

1. Adhesive SBO

Clinical features of small bowel obstruction with previous abdominal surgery ^[1] Success rate of non-operative treatment: about 50% ^[1] Indications for surgery: Non-responsive to conservative treatment; Clinical features of strangulation ^[1]

The lecture slides also highlight the controversies ^[1]:

• Duration of conservative treatment
• Administration of water-soluble contrast: Differentiates partial from complete obstruction; Therapeutic effect?; Reduced operating rate?; Shorten hospital stay ^[1]

2. Strangulated/Obstructed Hernia

Inguinal exploration: look for viability (~6P: cold, pulsation, pallor, peristalsis) → hernia repair (if viable) or resection + stoma (if non-viable) ^[4]

• Manual reduction should not be performed ^[4] — Why?
  • Recurrence likely ^[4]
  • Risk of peritonitis due to ischaemic bowel ^[4] — pushing necrotic bowel back into the abdomen causes faecal peritonitis
  • Reduction "en masse" ^[4] — the sac may appear reduced but the contents remain incarcerated within the sac just deep to the fascia → still strangulated
• Proceed to urgent inguinal exploration → assess viability → hernia repair (with mesh if viable, without mesh in contaminated field) or bowel resection + stoma if non-viable

3. Intraluminal Obstruction (Bezoar, Gallstone Ileus)

MC site: distal ileum / ileocaecal valve ^[4]

Operative treatment: small bowel obstruction ^[1]:

• Foreign bodies (Bezoars, gallstones) ^[1]:
  • Break down and push to colon ^[1]
  • Enterotomy and removal ^[1]

For gallstone ileus specifically ^[4]:

• Enterolithotomy to relieve SBO ^[4]
• Exploratory laparotomy → proximal enterotomy (NOT over the stone because of ulceration) → milk the stone proximally for extraction ^[4]
• Same-session or elective cholecystectomy + fistula repair

4. Intussusception

Paediatric (Ileocolic)

Contraindications to non-operative reduction ^[3]:

• Peritonitis
• Perforation
• Haemodynamic instability / septic shock
• Clinical features of prolonged ischaemia

Adult

• Almost always has a pathological lead point → requires surgical resection (not enema reduction)

5. Obstructing Colorectal Cancer

This is a complex management decision that depends on tumour location, patient fitness, and presence of complications.

Emergency surgery: if signs of ischaemia / perforation. Choice depends on risk of anastomotic leak vs morbidity of externalising a stoma ^[4]

Right-sided Obstruction (Caecum to Splenic Flexure) [1]

Right-sided obstruction: caecum to splenic flexure ^[1]:

• Resection and anastomosis if the patient is stable (right or extended right colectomy) ^[1]
• Resection without anastomosis if the patient or the bowel condition is not favourable ^[1]
• Non-resection: Stoma or bypass (advanced tumour) ^[1]

Why is right-sided easier? The terminal ileum (which is anastomosed to the remaining colon) is usually healthy and not loaded with faeces → lower risk of anastomotic leak → primary anastomosis is usually safe.

Left-sided Obstruction [1]

Left-sided obstruction is more challenging because the proximal colon is distended and loaded with faeces → higher risk of anastomotic leak if primary anastomosis is performed.

Options ^[1]:

SEMS as bridge-to-surgery ^[4]:

• Must first do CT to r/o closed-loop obstruction (perforation → T4 tumour) ^[4]
• Bridge to elective surgery: wait 2–4 weeks before surgical resection ^[4]
  • Avoid EOT (better fluid/nutrition, bowel prep) — higher chance of successful anastomosis ^[4]
  • Allow 1-staged procedure (no stoma) ^[4]
  • Allow complete oncological staging ^[4]
• Palliation ^[4]: for patients unfit for or declining surgery

2-stage: most common ^[4]:

• Resectable tumours: Hartmann's procedure (resection + end colostomy + close distal end as rectal stump → reversal of stoma) ^[4]
• Unresectable tumours: proximal diversion loop colostomy/ileostomy or double-barrel stoma (Paul-Mikulicz) ^[4]

6. Volvulus

Sigmoid Volvulus [1][4]

Sigmoidoscopic decompression (recurrence: 50%) ^[1] Surgery (perforation, strangulation or failed decompression): Resection ^[1]

Caecal Volvulus [3][4]

• Volvulus is usually ischaemic and requires resection ^[3]
• Right hemicolectomy ^[4] is preferred
• Colonoscopic de-rotation ± caecopexy (fixation of caecum to RIF) — high recurrence ^[4]
• Decompression and reduction of volvulus if viable followed by caecopexy ^[3]

7. Diverticular Disease Causing LBO [4]

• Elective: 1-stage (resection + primary anastomosis) ^[4]
• Emergency: 2-stage (Hartmann) ^[4]

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H. Management of Functional Obstruction

1. Paralytic Ileus [4]

2. Pseudo-obstruction (Ogilvie's Syndrome) [1][4]

Pseudo-obstruction Management ^[1]:

• To exclude mechanical obstruction
• Nasogastric tube feeding and enemas
• Colonoscopic decompression
• Rectal tube decompression
• Neostigmine
• Caecostomy

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I. Neonatal Intestinal Obstruction — Management Principles

Management ^[9]:

• Medical: NPO, TPN, IV antibiotics
• Surgical indications: pneumoperitoneum, clinical deterioration, failure of medical Rx
• Operative options: Resection + stoma; Resection + primary anastomosis ^[9]

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J. Operative Treatment Summary Table

Operative treatment: small bowel obstruction ^[1]:

• Enterolysis (lysis of adhesions and release of constricting bands)
• Repair of hernia
• Foreign bodies (bezoars, gallstones): Break down and push to colon; Enterotomy and removal
• Bowel resection: Strangulation with gangrenous bowel; Unhealthy bowel ^[1]

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K. Post-operative Considerations

• NG tube: Continue until bowel function returns (passage of flatus, reduced NG output)
• Fluid management: Continue IV fluids until oral intake re-established
• VTE prophylaxis: LMWH + TED stockings (IO patients are high-risk: immobility, dehydration, malignancy)
• Nutrition: Early enteral feeding when safe; TPN if prolonged ileus
• Adhesion prevention: Careful surgical technique, minimise peritoneal trauma; consider adhesion barriers (e.g. Seprafilm — hyaluronate-carboxymethylcellulose membrane) though evidence is variable
• Stoma care: If stoma created → early stoma nurse input, patient education, psychological support
• Monitor for complications: Anastomotic leak (fever, tachycardia, peritonism days 3–7 post-op), wound infection, recurrent obstruction

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Active Recall - Management of Intestinal Obstruction

1. List the 7 indications for urgent surgery in intestinal obstruction as per the lecture slides.

Your answer

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1. Incarcerated/strangulated hernia. 2. Suspected or proven strangulation. 3. Peritonitis. 4. Pneumoperitoneum. 5. Pneumatosis cystoides intestinalis. 6. Closed-loop obstruction. 7. Volvulus with peritoneal signs.

2. Explain the components of 'Drip and Suck' and the rationale for each.

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Drip = IV fluid resuscitation (crystalloids) to replace losses from vomiting, third-spacing, and reduced intake. Suck = NG tube decompression (free drainage + Q4h aspiration) to decompress proximal bowel, reduce vomiting, and lower aspiration risk. Also includes NPO to limit further bowel distension.

3. For a left-sided obstructing colorectal cancer, describe 3 surgical options and the indication for each.

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1. Hartmann procedure (resection + end colostomy + rectal stump) - most common emergency procedure; for unstable patients or unfavourable bowel conditions. 2. Segmental resection + primary anastomosis with on-table lavage - for stable, good-risk patients with viable bowel. 3. Subtotal colectomy + ileorectal anastomosis - for synchronous tumours or non-viable proximal colon. Also SEMS stenting as bridge-to-surgery for stable patients without closed-loop obstruction.

4. What are the 4 criteria used at surgery to assess bowel viability?

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1. Colour: dark colour becomes lighter after release (viable) vs persists (non-viable). 2. Mesenteric pulsation: visible pulsation in mesenteric arteries (viable) vs absent (non-viable). 3. Appearance: shiny serosa (viable) vs dull and lusterless (non-viable). 4. Musculature: firm with peristalsis (viable) vs no peristalsis (non-viable). Additional: bleeding from marginal arteries, intra-op Doppler, fluorescein with Wood lamp.

5. Describe the stepwise management of Ogilvie syndrome (acute colonic pseudo-obstruction).

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Step 1: Supportive management up to 72h if no peritonism and caecum less than 12 cm (drip and suck, rectal tube, ambulation, correct electrolytes, stop causative drugs). Step 2: IV neostigmine (acetylcholinesterase inhibitor; requires cardiac monitoring due to bradycardia risk). Step 3: Colonoscopic decompression (no bowel prep needed; limit air insufflation). Step 4: Caecostomy (last resort). Urgent surgery if caecum greater than 12 cm or peritonism develops.

6. Why should manual reduction NOT be performed for a strangulated hernia? Give 3 reasons.

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1. Recurrence is likely (hernia defect not repaired). 2. Risk of peritonitis due to pushing ischaemic/necrotic bowel back into the abdomen. 3. Risk of reduction en-masse where the sac is apparently reduced but contents remain incarcerated within the sac just deep to the fascia, so the bowel is still strangulated.

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References

^[1] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (pp. 25, 27, 28, 29, 32, 33, 37, 49, 52, 53, 62, 66, 67) ^[3] Senior notes: felixlai.md (Intestinal Obstruction – Treatment, Intussusception – Treatment, Volvulus – Treatment, Hirschsprung Disease – Treatment) ^[4] Senior notes: maxim.md (sections 4.3 Intestinal Obstruction – Management, Volvulus – Management, CRC – Emergency surgery, Pseudo-obstruction – Management, Paralytic Ileus – Mx, Mesenteric Ischaemia – Management, Gallstone Ileus – Management) ^[9] Lecture slides: Neonatal Surgery.pdf (p. 40)

Complications of Intestinal Obstruction

Complications of IO are the reason this condition carries significant mortality. Understanding them requires tracing the pathophysiology we've already established to its logical endpoints. Every complication is a consequence of either (a) the obstruction itself and its downstream effects, or (b) the treatment of the obstruction.

High mortality if complications occur ^[1]

We can categorise complications into:

1. Local complications (arising from the bowel itself)
2. Systemic complications (arising from the body's response to the obstruction)
3. Post-operative / treatment-related complications
4. Disease-specific complications (unique to certain causes of IO)

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A. Local Complications

1. Strangulation (Bowel Ischaemia → Necrosis)

This is the most feared and time-critical complication of IO. The lecture slides emphasise ^[1]:

Compromise of blood supply, leading to necrosis and perforation of bowel (accelerated in close-loop or strangulating obstruction) ^[1]

Pathogenesis ^[3]:

• Blood supply is compromised when bowel dilatation is excessive ^[3]
• Bowel becomes ischaemic and leads to necrosis or perforation ^[3]

Causes of strangulation ^[3]:

• ↑ Intraluminal pressure — progressive accumulation of gas and fluid raises the pressure inside the bowel lumen → compresses first the thin-walled veins (lower pressure) → venous congestion → further oedema → eventually compresses arteries → ischaemia
• Direct pressure on bowel wall — constricting band (adhesion), hernia ring, or twist (volvulus) compresses the bowel externally
• Interrupted mesenteric blood flow — volvulus twists the mesenteric pedicle directly occluding the SMA/SMV branches; hernia ring compresses mesenteric vessels within the hernial neck

Why is this accelerated in closed-loop obstruction? Because in a closed-loop, gas and fluid cannot escape in either direction → intraluminal pressure rises much faster than in a simple, single-point obstruction → ischaemia develops within hours, not days.

Features suggestive of strangulation ^[3]:

Prognosis ^[1][3]:

• Non-strangulating obstruction: mortality 2% ^[1]
• Strangulating obstruction: mortality 10–30% ^[1]
• Morbidity and mortality are dependent on duration of ischaemia and its extent ^[3]
• Any length of ischaemic bowel can cause significant systemic effects secondary to sepsis and dehydration ^[3]

2. Perforation

Perforation is the endpoint of untreated ischaemia — the necrotic bowel wall loses its structural integrity and breaks down.

Pathophysiology:

• Transmural necrosis → loss of all wall layers → luminal contents (bacteria, faecal matter) spill into the peritoneal cavity
• In LBO with a competent ileocaecal valve: the caecum is the most likely site of perforation because it has the largest diameter (Laplace's law: Wall Tension = Pressure × Radius) → caecal diameter > 9–12 cm on imaging is critical ^[4]
• In closed-loop obstruction: perforation can occur at the site of maximal distension within the closed loop itself

Consequences of perforation:

• Faecal peritonitis: massive bacterial contamination of the peritoneal cavity → overwhelming sepsis → multi-organ failure
• Free gas (pneumoperitoneum): visible on erect CXR or CT
• Mortality of faecal peritonitis is very high (up to 30–50%)

Clinical features: Sudden worsening of pain (may paradoxically improve briefly as distension is released), followed by board-like rigidity, absent bowel sounds, haemodynamic collapse

3. Closed-Loop Obstruction

While this is primarily a type of obstruction, it is also considered a complication because any obstruction can evolve into a closed-loop situation:

• Obstruction inside closed loop → impaired blood flow → risk of necrosis and perforation ^[4]
• Examples: malignant stricture of colon + competent ileocaecal valve, volvulus, hernia, afferent loop syndrome ^[4]
• Why is this a complication? A patient with a left-sided colonic tumour may initially have a partially competent ileocaecal valve that becomes fully competent as colonic distension increases → converting a simple LBO into a dangerous closed-loop obstruction

4. Bacterial Translocation

Pathophysiology:

• Normal intact bowel mucosa acts as a barrier preventing intraluminal bacteria from entering the bloodstream
• In IO: mucosal ischaemia → loss of mucosal barrier integrity → bacteria and endotoxins cross the bowel wall into the mesenteric lymph nodes, portal venous system, and peritoneal cavity
• Bacterial overgrowth ^[1] in the stagnant, dilated bowel amplifies this process — the longer the obstruction persists, the greater the bacterial load
• This is the mechanism by which uncomplicated IO can progress to sepsis and multi-organ dysfunction syndrome (MODS) even before frank perforation occurs

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B. Systemic Complications

1. Dehydration and Electrolyte Disturbance

Complications: Systemic — dehydration, electrolyte disturbance ^[4]

This is arguably the most common complication and is present to some degree in almost every patient with IO.

Pathophysiology (already covered in detail, summarised here):

Consequences:

• Hypovolaemic shock: tachycardia → hypotension → oliguria → pre-renal AKI → multi-organ failure if uncorrected
• Hypokalaemia: can cause cardiac arrhythmias (U waves, flat T waves, prolonged QT), muscle weakness, and paradoxically worsens ileus (K⁺ is essential for smooth muscle repolarisation — a vicious cycle)
• Metabolic alkalosis (from vomiting) or metabolic acidosis (from ischaemia/dehydration) → mixed acid-base disorders are common
• Pre-renal AKI: reduced renal perfusion from hypovolaemia → elevated urea and creatinine

2. Aspiration Pneumonia

Complications: Systemic — aspiration pneumonia ^[4]

Pathophysiology:

• In IO, the stomach and proximal bowel are filled with regurgitated, stagnant, bacteria-laden fluid
• If the patient vomits (especially while supine or during anaesthetic induction), this fluid can be aspirated into the tracheobronchial tree
• Aspiration of acidic gastric contents → chemical pneumonitis (Mendelson's syndrome)
• Aspiration of bacteria-laden intestinal contents → aspiration pneumonia
• Why NG decompression is protective: draining the stomach reduces the volume of gastric/intestinal fluid available for aspiration

Clinical features: Cough, dyspnoea, fever, tachypnoea, crackles on auscultation, new infiltrate on CXR (typically right lower lobe — more vertical right main bronchus)

Prevention: NG decompression, semi-recumbent positioning (30° head-up), rapid sequence induction (RSI) with cricoid pressure during anaesthetic induction

3. Sepsis and Multi-Organ Dysfunction Syndrome (MODS)

Pathophysiology cascade:

1. Bacterial translocation from ischaemic bowel → bacteraemia
2. Systemic inflammatory response (SIRS): fever/hypothermia, tachycardia, tachypnoea, leucocytosis/leucopenia
3. Sepsis → septic shock → MODS (renal failure, respiratory failure, hepatic dysfunction, DIC, cardiovascular collapse)

This is the mechanism underlying the high mortality of strangulated obstruction.

4. Venous Thromboembolism (DVT/PE)

Pathophysiology:

• IO patients have Virchow's triad in full force:
  • Stasis: immobilisation (bed rest), reduced venous return from hypovolaemia
  • Endothelial injury: surgical trauma (if operated)
  • Hypercoagulability: dehydration → haemoconcentration; systemic inflammation; underlying malignancy
• Prevention: LMWH prophylaxis (e.g. enoxaparin 40 mg SC daily), TED stockings, early mobilisation

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C. Post-Operative / Treatment-Related Complications

These complications arise from the surgical treatment of IO rather than from the obstruction itself.

1. Anastomotic Leak

Pathophysiology:

• After bowel resection and anastomosis, the two joined bowel ends must heal together
• Risk factors for leak: poor blood supply to bowel ends, tension on the anastomosis, malnutrition, steroid use, contaminated field, unprepared bowel (faecal loading), emergency surgery (vs. elective)
• Why is leak dangerous? Intestinal contents spill into the peritoneal cavity → peritonitis → sepsis → MODS
• Left-sided colonic obstruction carries higher leak risk because the heavy bacterial and faecal load in proximal colon and oedematous unhealthy proximal colon ^[1] make primary anastomosis risky
  • This is precisely why Hartmann's procedure (resection without anastomosis) is the safer default in emergency left-sided colonic surgery ^[4]
  • And why primary anastomosis is risky ^[1] in this context

Clinical features: Typically presents days 3–7 post-op with fever, tachycardia, abdominal pain, peritonism, rising inflammatory markers, foul/faeculent drain output

Management: Return to theatre for washout ± re-anastomosis or stoma formation; IV antibiotics; ICU support

2. Recurrent Adhesive Obstruction

Pathophysiology:

• Surgery for adhesive SBO (adhesiolysis) itself causes peritoneal trauma → new adhesion formation → recurrent SBO
• This creates a frustrating cycle: each operation to treat adhesions can cause more adhesions
• Risk: ~30% of patients who undergo adhesiolysis will develop recurrent SBO
• Prevention: Minimise peritoneal trauma during surgery (meticulous haemostasis, gentle tissue handling, minimal serosal drying); consider adhesion barriers (e.g. Seprafilm); laparoscopic approach where possible (less peritoneal trauma than open surgery)

3. Wound Infection (Surgical Site Infection)

Pathophysiology:

• IO surgery is often performed in contaminated or dirty fields (bacterial overgrowth in stagnant bowel, possible perforation)
• Faecal contamination during surgery → wound contamination → SSI
• Prevention: Prophylactic IV antibiotics, meticulous surgical technique, wound lavage

4. Paralytic Ileus (Post-operative)

• A degree of paralytic ileus is common after any abdominal procedure with a variable duration of 24–72 hours ^[3]
• Prolonged ileus ( > 72 hours) is a complication in itself and can occur after any IO surgery
• Causes of prolonged post-op ileus: intra-abdominal sepsis, electrolyte disturbance (particularly hypokalaemia), opiate analgesics, excessive bowel handling during surgery
• Management: Correct underlying cause, drip and suck, prokinetics, early mobilisation, minimise opioids

5. Short Bowel Syndrome (SBS)

Pathophysiology:

• If extensive bowel resection is required (e.g. massive midgut necrosis from volvulus, mesenteric ischaemia, or multiple resections for recurrent adhesive SBO), the remaining bowel length may be insufficient for adequate nutrient and fluid absorption
• Defined as < 200 cm of remaining small bowel (or < 100 cm without colon in continuity)
• High risk of short gut syndrome: diarrhoea, steatorrhoea → dehydration, malabsorption, weight loss ^[4]

Clinical consequences:

• Malabsorption → malnutrition, weight loss, fat-soluble vitamin deficiency (A, D, E, K)
• Chronic diarrhoea and steatorrhoea
• Dependence on TPN (parenteral nutrition)
• Complications of TPN: central line infections, hepatic steatosis, cholestasis, metabolic bone disease

6. Stoma-Related Complications

If a stoma is created (e.g. Hartmann's procedure, defunctioning ileostomy):

• High output stoma: particularly ileostomy → significant fluid and electrolyte losses (Na⁺, K⁺, Mg²⁺, HCO₃⁻) → dehydration, renal impairment
• Parastomal hernia: weakening of abdominal wall around the stoma site
• Stoma prolapse: intussusception of bowel through the stoma
• Stoma retraction: stoma sinks below skin level → poor appliance fit → skin excoriation
• Skin excoriation: contact dermatitis from intestinal effluent (especially alkaline ileal output)
• Psychological impact: body image concerns, social isolation

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D. Disease-Specific Complications

1. Obstructing Colorectal Cancer [1]

Obstructing colorectal cancer: more advanced cancer, elderly patients with comorbidity, high operative mortality and morbidity, worse prognosis ^[1]

• Prognosis of emergency surgery for colonic obstruction: mortality more than 10% ^[1]
  • Comorbidity ^[1] and advanced malignancy ^[1] are the key drivers of this high mortality
• Patients presenting with CRC as an emergency obstruction tend to have more advanced-stage disease (larger tumours, higher T stage, more nodal involvement) compared to those diagnosed electively
• Emergency surgery carries higher leak rates, higher infection rates, and higher stoma rates compared to elective surgery
• Left-sided obstruction is particularly challenging ^[1]:
  • Competence of ileocaecal valve (closed-loop obstruction → perforation) ^[1]
  • Heavy bacterial and faecal load in proximal colon ^[1]
  • Oedematous, unhealthy proximal colon ^[1]
  • Poor general condition of patient: malignancy and malnutrition, dehydration ^[1]
  • Primary anastomosis is risky ^[1]

2. Hirschsprung-Associated Enterocolitis (HAEC) [3]

• The most severe and lethal complication of Hirschsprung's disease ^[3]
• Can occur before surgery, in the immediate post-operative period, or years after definitive repair
• Pathogenesis: Stasis in aganglionic segment → reduced protective mucin production → bacterial overgrowth → bacterial translocation through the compromised mucosa → bowel wall invasion by colonic organisms → can lead to perforation, peritonitis, septic shock, and death ^[3]
• Incidence as high as 45% ^[3]
• Clinical features: Explosive, foul-smelling diarrhoea, abdominal distension, fever, sepsis
• Management: IV fluid resuscitation, IV antibiotics, repeated rectal irrigations (saline) through rectal tube, diverting ileostomy/colostomy if refractory ^[3]

3. Intussusception — Complications of Reduction [3]

• Perforation ( < 1%) ^[3] — risk factors include age < 6 months, long duration of symptoms, and higher pressure during reduction ^[3]
• Recurrence: approximately 5–10% after successful non-operative reduction; higher in children with pathological lead points
• Post-reduction fever: Patient usually presents with fever after successful reduction due to bacterial translocation or release of endotoxin or cytokines ^[3]

4. Malrotation with Midgut Volvulus — Complications of Ladd's Procedure [3]

• Small bowel obstruction from adhesions ^[3]
• Short bowel syndrome (if resection is necessary when necrotic bowel is present) ^[3]
• Recurrent volvulus (rare but possible if mesenteric base not adequately broadened)

5. Intestinal Atresia — Post-Operative Complications [3]

• Poor feeding and vomiting ^[3]
• Volume depletion ^[3]
• Electrolyte imbalance ^[3]
• Aspiration pneumonia ^[3]
• Anastomotic stricture
• Short bowel syndrome (especially in Type IIIb apple-peel atresia with limited bowel length)

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E. Complications Summary Table

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F. Prognosis

The prognosis of IO depends entirely on whether complications develop:

Key prognostic factors ^[1]:

• Duration of obstruction before treatment (longer = more ischaemia = worse outcome)
• Presence of strangulation
• Patient comorbidity (especially in elderly with obstructing CRC)
• Stage of malignancy (if cancer is the cause)
• Timeliness of surgical intervention

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Active Recall - Complications of Intestinal Obstruction

1. What is the mortality of non-strangulating vs strangulating bowel obstruction?

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Non-strangulating: 2%. Strangulating: 10-30%. This dramatic increase is because strangulation causes bowel ischaemia leading to necrosis, perforation, bacterial translocation, peritonitis, sepsis and multi-organ failure.

2. Explain the pathophysiology of bacterial translocation in IO and its systemic consequences.

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Mucosal ischaemia from distension and venous congestion causes loss of mucosal barrier integrity. Bacteria (amplified by bacterial overgrowth in stagnant bowel) and endotoxins cross the bowel wall into mesenteric lymph nodes, portal venous system, and peritoneal cavity. This leads to bacteraemia, SIRS, sepsis, septic shock, and multi-organ dysfunction syndrome.

3. Why is the caecum the most likely site of perforation in LBO with a competent ileocaecal valve?

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By Laplace law (Wall Tension = Pressure x Radius), the caecum has the largest diameter (radius) of any part of the colon. For any given intraluminal pressure, it experiences the greatest wall tension. Combined with a competent IC valve creating closed-loop obstruction, pressure rises rapidly in the caecum. Perforation risk is critical when caecal diameter exceeds 9-12 cm.

4. List 4 reasons why primary anastomosis is risky in left-sided emergency colonic surgery.

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1. Heavy bacterial and faecal load in the proximal colon. 2. Oedematous, unhealthy proximal colon with poor healing capacity. 3. Competence of ileocaecal valve may create closed-loop obstruction risking perforation. 4. Poor general condition of the patient (malnutrition, dehydration, comorbidity from malignancy). These factors all increase the risk of anastomotic leak.

5. Name 3 post-operative complications specific to IO surgery and explain one in detail.

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Anastomotic leak, recurrent adhesive SBO, post-operative ileus, short bowel syndrome, wound infection, stoma complications. Detail for any one, e.g.: Recurrent adhesive SBO - surgery for adhesions causes peritoneal trauma which triggers a fibrotic healing cascade forming new adhesions. Approximately 30% of patients who undergo adhesiolysis will develop recurrent SBO, creating a frustrating cycle.

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References

^[1] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (pp. 8, 38, 42, 50, 54, 67) ^[3] Senior notes: felixlai.md (Intestinal Obstruction – Complications, Hirschsprung Disease – Complications, Intussusception – Treatment/Complications, Intestinal Atresia – Complications, Malrotation – Complications, Intestinal Ischaemia, Diverticulitis – Complications) ^[4] Senior notes: maxim.md (sections 4.3 Intestinal Obstruction – Complications, Closed-loop IO, Mesenteric Ischaemia – Management, CRC – Emergency surgery)