Intestinal Obstruction
Intestinal obstruction is a partial or complete blockage of the small or large bowel that prevents the normal passage of intestinal contents, leading to proximal dilation, fluid accumulation, and potential ischemia.
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]:
- Mechanical obstruction — implies a physical barrier to the aboral progress of intestinal contents (i.e., peristalsis is present and working against an obstruction) [1]
- 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.
- 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
| Age Group | Common Causes |
|---|---|
| Neonates (0–28 days) | Intestinal atresia, malrotation with volvulus, meconium ileus, Hirschsprung's disease, anorectal malformations |
| Infants (1–36 months) | Intussusception (most common abdominal emergency in early childhood), incarcerated inguinal hernia |
| Children | Incarcerated hernia, adhesions, intussusception |
| Adults | Adhesions (~60–74%), hernias (~10%), neoplasm (~5%), Crohn's disease (~7%) for SBO [1]; colorectal cancer, volvulus, diverticular stricture for LBO |
| Elderly | Colorectal cancer (15–20% of patients with colorectal cancer present with IO [1]), sigmoid volvulus, incarcerated hernia, faecal impaction |
III. Risk Factors
Understanding risk factors is essentially understanding "what predisposes the bowel to being blocked or to stopping working."
- 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)
- 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])
- 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
- 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
IV. Anatomy and Function Relevant to Intestinal Obstruction
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]
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]
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)
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]
Anatomy Pearl
The caecum is the most likely site of perforation in LBO with a competent ileocaecal valve because it has the largest diameter. By Laplace's law (Wall Tension = Pressure × Radius), the caecum experiences the greatest wall tension for any given intraluminal pressure.
V. Etiology
The causes of intestinal obstruction are best organised by:
- Mechanism: Mechanical vs. Functional
- Level: Small bowel vs. Large bowel
- 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].
| Cause | Pathophysiology | Notes |
|---|---|---|
| Adhesions | Congenital; post-inflammation; formed after abdominal surgery [1]. Fibrous bands form during peritoneal healing after surgical trauma, infection, or radiation. These bands can kink, compress, or angulate bowel loops. | The most common cause of SBO in Western countries [1]. Accounts for ~74% of SBO admissions [1]. Lower abdominal and pelvic surgery (appendicectomy, colorectal surgery, gynaecological surgery) carry highest risk. |
| Hernias | Bowel herniates through a defect (inguinal canal, femoral canal, umbilical ring, incisional site) and becomes trapped (incarcerated). If the bowel lumen is obstructed, it is "obstructed"; if blood supply is also compromised, it is "strangulated." | ~3–10% of SBO [1][4]. Incarcerated hernias are the leading cause of complications (ischaemia, necrosis, perforation) related to bowel obstruction [3]. In children, incarcerated inguinal hernia is the MC surgical cause of SBO [4]. |
| Volvulus | Twisting of bowel around its mesentery → luminal obstruction + vascular compromise | Small bowel volvulus is less common than sigmoid; may occur in malrotation |
| Intraperitoneal malignancy | Extrinsic compression or carcinomatosis peritonei | Ovarian, gastric, colorectal secondaries |
| Cause | Pathophysiology | Notes |
|---|---|---|
| Tumour (primary or secondary) | Lymphoma, GIST, adenocarcinoma grow within the bowel wall narrowing the lumen | ~5% of SBO [1] |
| Strictures | Fibrotic narrowing from Crohn's disease, radiation, anastomotic scarring, drug-induced (e.g. NSAIDs, potassium chloride) | Crohn's disease accounts for ~7% of SBO [1] |
| Intussusception | A proximal segment of bowel (intussusceptum) telescopes into a distal segment (intussuscipiens). In adults, usually caused by a pathological lead point (polyp, tumour, Meckel's diverticulum). | Most common in infants 6–36 months (usually idiopathic) |
| Cause | Pathophysiology | Notes |
|---|---|---|
| Foreign bodies | Physical blockage of the lumen | Ingested objects, bezoars |
| Gallstones (gallstone ileus) | A large gallstone erodes through the gallbladder wall into the adjacent duodenum via a cholecystoenteric fistula, then impacts at the terminal ileum (narrowest part of SB). Bouveret's syndrome: stone stuck at duodenum/stomach causing gastric outlet obstruction [4]. | Rigler's triad on AXR: pneumobilia + SBO + ectopic gallstone [4] |
| Bezoars | Accumulation of indigestible material — trichobezoar (hair), phytobezoar (plant fibre) | More common in patients with prior gastric surgery or gastroparesis |
| Worms | Masses of roundworms (Ascaris lumbricoides) can physically occlude the lumen | Endemic areas; less common in HK |
| Meconium ileus | Inspissated, sticky meconium in neonates with cystic fibrosis (thick secretions due to CFTR dysfunction) | Almost pathognomonic for CF in a neonate |
High Yield – SBO Etiology Data
From the landmark Miller et al. study referenced in the lecture slides [1]:
- Adhesions: 74% of patients / 68% of admissions
- Crohn's disease: 7% / 11%
- Neoplasm: 5% / 5%
- Hernia: 3% / 3%
- Radiation injury: 1% / 1%
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].
| Cause | Pathophysiology | Notes |
|---|---|---|
| Colorectal cancer | Intraluminal/intramural mass progressively narrows the colonic lumen. 15–20% of patients with colorectal cancer present with intestinal obstruction [1]. | Characteristics: more advanced cancer, elderly patients with comorbidity, high operative mortality and morbidity, worse prognosis [1]. Most commonly at sigmoid (narrowest lumen). |
| Volvulus | Twisting of bowel around its mesentery → closed-loop obstruction + vascular compromise. Sigmoid volvulus (70%) is most common, followed by caecal volvulus (25%) [4]. | Sigmoid volvulus: older males, elongated mesosigmoid, chronic constipation. Caecal volvulus: younger females, congenital hypermobile caecum. |
| Diverticulitis | Acute inflammation → oedema → luminal narrowing. Chronic/recurrent → fibrotic stricture. | More common in sigmoid (Western) or right colon (Asia) |
| Stricture | Anastomotic, radiation, ischaemic, endometriotic [1] | Post-surgical stricture at anastomotic site; radiation enteritis/colitis causing fibrosis |
| Extrinsic compression | Metastasis, pelvic/extraperitoneal tumour [1] | Ovarian, uterine, prostatic malignancies |
Congenital anomalies are the primary causes [2]:
| Cause | Key Features |
|---|---|
| Intestinal atresia | Atresia can occur from oesophagus to anus [2]. Most common site is jejunum and ileum. Duodenal atresia associated with Down syndrome. |
| Malrotation | Arrest of normal 270° rotation → abnormal position of duodenojejunal junction and caecum → Ladd's bands may compress duodenum → predispose to midgut volvulus |
| Meconium disease | Meconium ileus (CF) — thick, inspissated meconium; Meconium plug syndrome — colonic dysmotility |
| Hirschsprung's disease | Absence of ganglion cells in distal bowel (from failed craniocaudal migration of neural crest cells) → functional obstruction of the aganglionic segment → proximal dilatation |
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)
Paralytic ileus = failure of transmission of peristaltic waves secondary to neuromuscular failure in the myenteric (Auerbach's) plexus and submucosal (Meissner's) plexus [3].
| Category | Causes | Mechanism |
|---|---|---|
| Post-operative ileus | The most common cause [4]. | Any abdominal procedure causes peritoneal inflammation → inhibitory sympathetic reflexes + local inflammatory mediators (IL-6, prostaglandins) → paralysis of smooth muscle. A degree of paralytic ileus is common after any abdominal procedure with variable duration of 24–72 hours [3]. |
| Intra-peritoneal | Peritonitis, intra-abdominal abscess [1] | Peritoneal inflammation activates inhibitory sympathetic pathways |
| Inflammatory/infective | Inflammatory/infective conditions [1] | Same mechanism as above |
| Intestinal ischaemia | Ischaemic bowel cannot contract effectively | |
| Retroperitoneal | Retroperitoneal haematoma/infection; aortic, spinal, urological operations; pancreatitis [1] | Retroperitoneal inflammation irritates the sympathetic chain/coeliac plexus → reflex ileus |
| Reflex ileus | Fracture of spine or ribs, retroperitoneal haemorrhage [3] | As above |
| Metabolic | Hypokalaemia, hypothyroidism, uraemia, diabetic ketoacidosis | K⁺ is essential for smooth muscle repolarisation; ↓K⁺ → membrane hyperpolarisation → ↓contractility. Thyroid hormone maintains basal metabolic rate of smooth muscle. |
| Drug-induced | Opiates, anti-cholinergics [3] | Opiates: μ-receptor activation → ↓ACh release from myenteric plexus → ↓peristalsis. Anti-cholinergics: block muscarinic M₃ receptors on smooth muscle → ↓contraction. |
(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].
- 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]
- 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
- Idiopathic
- Familial visceral myopathy [3]
| Feature | Pseudo-obstruction | Mechanical Obstruction |
|---|---|---|
| Bowel sounds | Normal | High-pitched / tinkling (early); absent (late) |
| PR examination | Dilated rectum | Collapsed, empty rectum |
| Pain | Distension but not much pain | Colicky, significant |
| AXR | Gas in rectum present | Absent rectal gas |
VI. Classification
Intestinal obstruction can be classified along several axes. This matters clinically because the classification determines urgency, likely cause, and management approach.
- Small bowel obstruction (SBO)
- Large bowel obstruction (LBO)
- Mechanical — peristalsis works against a physical barrier
- Functional — absence or inadequacy of peristalsis without mechanical barrier
- Paralytic ileus
- Pseudo-obstruction
- 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)
- Chronic vs. Acute [1]
- Acute: sudden onset, often surgical emergency
- Chronic: insidious, often from slowly growing tumours or strictures; may have intermittent subacute episodes
- 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]
- Intraluminal (within the lumen)
- Intramural (within the wall)
- Extramural (outside the wall)
Strangulation vs. Simple Obstruction
A common exam mistake is failing to distinguish simple from strangulating obstruction. Strangulation implies compromised blood supply and is a time-critical surgical emergency. Clinical clues to strangulation include: constant (non-colicky) pain, peritoneal signs (guarding, rebound), tachycardia, fever, leucocytosis, and metabolic acidosis with raised lactate. Do not wait for these signs to develop — if in doubt, operate early.
VII. Pathophysiology
Understanding the pathophysiology of IO is essential because every clinical feature and complication can be traced back to these mechanisms.
When a mechanical obstruction occurs, the bowel proximal to the obstruction dilates due to:
- 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]
- 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
- 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
This is a major source of morbidity and mortality in IO:
| Mechanism | Explanation |
|---|---|
| Decreased oral intake | Nausea, vomiting, and NPO status |
| Vomiting | Loss of fluid containing Na⁺, K⁺, Cl⁻, H⁺ [3] → hypochloraemic, hypokalaemic metabolic alkalosis (loss of H⁺ and Cl⁻ from gastric secretions) |
| Defective intestinal absorption | Oedematous bowel wall cannot absorb water and electrolytes normally [4] |
| Fluid sequestration in bowel lumen | Fluid is trapped ("third-spacing") within the dilated bowel, effectively lost from the circulating volume |
| Transudation into peritoneal cavity | Transudation of fluid into extracellular space and peritoneal cavity [3] — increased hydrostatic pressure in congested bowel wall drives fluid into the peritoneum |
The net effect is hypovolaemia → tachycardia, hypotension, oliguria, prerenal AKI.
Strangulation represents the most dangerous evolution of IO:
- 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
- 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
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
The progressive pathophysiology can be summarised in a cascade:
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
- 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
- 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
- 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)
- 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
| Feature | Proximal SBO | Distal SBO | LBO |
|---|---|---|---|
| Pain | Periumbilical, colicky, frequent | Periumbilical, colicky | Infraumbilical, colicky; may be less intense initially |
| Vomiting | Early, profuse, bilious | Later onset, may become feculent | Late or absent; if present, feculent |
| Distension | Minimal/absent | Moderate | Marked |
| Constipation | Late | Present | Early and prominent |
| Dehydration | Severe (early vomiting) | Moderate | Less prominent initially |
B. Signs
- 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]
- 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
- 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)
- Tympanic (hyper-resonant): due to gas-filled, distended bowel loops
- Shifting dullness: suggests free peritoneal fluid (ascites from transudation)
- 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
- 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
| Sign | Mechanism |
|---|---|
| Constant (non-colicky) pain | Continuous ischaemic irritation of peritoneum |
| Peritonism (guarding, rigidity, rebound) | Peritoneal inflammation from ischaemia/necrosis/perforation |
| Tachycardia, fever | Systemic inflammatory response/sepsis |
| Leucocytosis | Inflammatory response |
| Metabolic acidosis / Raised lactate | Anaerobic metabolism in ischaemic bowel |
| Bloody PR | Mucosal sloughing from ischaemic bowel |
Bilious vomiting in a neonate is malrotation with midgut volvulus until proven otherwise — it is a surgical emergency [2][5].
| Feature | Significance |
|---|---|
| Bilious (green) vomiting | Obstruction distal to ampulla of Vater; think malrotation with midgut volvulus as the most dangerous cause |
| Non-bilious projectile vomiting | Obstruction proximal to ampulla; think pyloric stenosis (if 2–8 weeks old) or oesophageal/proximal duodenal atresia |
| Failure to pass meconium within 24–48 hours | Think Hirschsprung's disease, meconium ileus, anorectal malformation |
| Abdominal distension | Lower obstruction (ileal/colonic); may be absent in proximal obstruction |
| "Double bubble" sign on AXR | Duodenal atresia (dilated stomach + proximal duodenum, no distal gas if complete) |
- Colicky abdominal pain — episodic screaming with drawing up of legs, child appears well between episodes
- "Redcurrant jelly" stools — bloody mucus per rectum from venous congestion and mucosal ischaemia of the intussuscepted segment
- "Sausage-shaped" mass — usually palpable in the RUQ (because the ileocolic intussusception pushes along the course of the colon)
- "Dance sign" — emptiness in the RIF (because the caecum has been dragged upwards)
- 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]
Don't Forget Hernia Orifices!
A common exam and clinical pitfall is forgetting to examine all hernia orifices (bilateral inguinal, femoral, umbilical, and incisional sites) in a patient presenting with intestinal obstruction. An incarcerated hernia can cause bowel obstruction and is easily missed if the groin is not exposed. Always check the groin — especially in elderly patients presenting with SBO.
IX. Neonatal Intestinal Obstruction — Detailed Pathophysiology by Cause
- 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
- 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]:
- Weeks 4–5: Rapid growth of midgut → physiological herniation through the umbilicus
- Weeks 6–10: The midgut undergoes a 270° counter-clockwise rotation around the SMA axis
- 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
- "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
- 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
X. Closed-Loop Obstruction — Special Entities
- 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]
- 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]
High Yield Summary
Definition: IO = any impediment to aboral passage of intestinal contents. Mechanical (physical barrier) vs. Functional (ileus/pseudo-obstruction).
Epidemiology: SBO accounts for ~80% of mechanical IO. LBO ~15%. Most common causes: SBO = adhesions > hernia > cancer; LBO = cancer > volvulus > diverticulitis.
Risk Factors: Prior surgery (adhesions), hernia, malignancy, medications (opiates, anticholinergics), metabolic (hypoK, hypothyroid).
Pathophysiology cascade: Obstruction → proximal dilatation (gas + fluid) → ↑ intraluminal pressure → venous congestion → oedema → arterial compromise → ischaemia → necrosis → perforation → peritonitis/sepsis. Dehydration from vomiting, third-spacing, impaired absorption.
Cardinal Features (4): Pain (colicky → constant if strangulation), Vomiting (early in proximal SBO; late/feculent in distal), Distension (greater with distal obstruction), Absolute constipation (complete obstruction).
Key Signs: Dehydration, high-pitched tinkling bowel sounds (early) → absent (late), abdominal tenderness (peritonism = strangulation), empty rectum on PR (mechanical LBO), visible peristalsis, hernial orifices must be checked.
Closed-loop obstruction: Obstruction at 2 points, rapid ischaemia risk. Examples: LBO + competent ileocaecal valve, volvulus, hernia.
Neonatal IO: Bilious vomiting = malrotation with midgut volvulus until proven otherwise. Key causes: intestinal atresia, malrotation, meconium disease, Hirschsprung's disease.
Classification: By anatomy (SBO/LBO), mechanism (mechanical/functional), completeness (partial/complete), complexity (simple/strangulating/closed-loop), relation to wall (intra/intramural/extramural).
Active Recall - Intestinal Obstruction (Definition to Clinical Features)
[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.
Before diving into specific causes, the clinician must answer three sequential questions:
- Is there truly an obstruction? (vs. a mimic like paralytic ileus, gastroenteritis, or a medical cause of acute abdomen)
- If yes, is it mechanical or functional?
- 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.
Key Lecture Point
The differential is best organised by:
- Level: SBO vs. LBO
- Mechanism: Mechanical vs. Functional
- Age group: Adult vs. Neonatal/Paediatric
- Mimics: Conditions that present like IO but are not
C. Differential Diagnosis of Small Bowel Obstruction (Adults)
| Category | Differential | Key Distinguishing Features | Why it causes SBO |
|---|---|---|---|
| Extramural | Adhesions (~60–74%) [1][3] | History of prior abdominal/pelvic surgery; recurrent episodes; may resolve with conservative Mx | Fibrous bands kink, compress, or angulate bowel loops → luminal obstruction |
| Incarcerated hernia (~10%) [4] | Tender, irreducible groin/umbilical/incisional lump; check hernial orifices [7] | Bowel loop trapped within hernial sac → lumen obstructed ± vascular compromise | |
| Volvulus | Acute onset, may have signs of ischaemia | Twisting of mesentery obstructs lumen AND blood supply simultaneously | |
| Intraperitoneal malignancy | Peritoneal carcinomatosis (ovarian, gastric, CRC); ascites, weight loss, cachexia | Extrinsic compression of bowel loops by tumour deposits or malignant adhesions | |
| Intramural | Tumour (lymphoma, GIST, adenoCA) ~5% [1] | Subacute onset, weight loss, anaemia, may have palpable mass | Intramural growth narrows the lumen from within the wall |
| Strictures (Crohn's, radiation, anastomotic, drug-induced) [1] | History of Crohn's disease (~7% of SBO [1]), prior RT, NSAID use, or previous anastomosis | Chronic inflammation → fibrosis → fixed narrowing of lumen | |
| Intussusception | Adults: suspect a pathological lead point (polyp, tumour, Meckel's) | Proximal segment telescopes into distal → luminal obstruction + venous congestion | |
| Intraluminal | Gallstone ileus | Elderly female, Rigler's triad (pneumobilia + SBO + ectopic gallstone) [4]; Bouveret's syndrome if GOO [4] | Large stone erodes via cholecystoenteric fistula → impacts at terminal ileum (narrowest SB segment, 2 feet proximal to IC valve) [4] |
| Bezoar (trichobezoar / phytobezoar) | Psychiatric history (trichotillomania), prior gastric surgery, gastroparesis | Accumulated indigestible material physically blocks lumen | |
| Foreign body | History of ingestion (children, psychiatric patients, prisoners) | Physical blockage | |
| Worms (Ascaris) | Endemic area, multiple worms form a bolus | Physical blockage by worm mass | |
| Faecal impaction | Elderly, immobile, opioid use, chronic constipation | Inspissated stool acts as intraluminal plug |
| Differential | Key Distinguishing Features | Why it mimics IO |
|---|---|---|
| Paralytic ileus / Post-operative ileus [4] | History of recent surgery (clinically significant if > 72h post-op [4]), peritonitis, or metabolic derangement; hypoactive bowel sounds [4]; no transition point on imaging | No peristalsis → gas and fluid accumulate → distension and vomiting, but no mechanical barrier |
| Ogilvie's syndrome [3][4] | Hospitalised patient with severe comorbidity; normal bowel sounds; dilated rectum on PR [4]; gas in rectum on AXR | Autonomic imbalance → colonic aperistalsis without mechanical cause |
| Drug-induced ileus | Opioids, anticholinergics, CCBs in drug history | Pharmacological suppression of myenteric plexus activity |
| Metabolic ileus | HypoK, hypothyroidism, uraemia, DKA | Electrolyte/hormonal derangement impairs smooth muscle contractility |
Common causes of LBO: Cancer of colon, Volvulus, Diverticular stricture, Pseudo-obstruction [7]
| Category | Differential | Key Distinguishing Features | Why it causes LBO |
|---|---|---|---|
| Neoplastic | Colorectal cancer | More advanced cancer, elderly patients with comorbidity, high operative mortality and morbidity, worse prognosis [1]; change in bowel habit, weight loss, anaemia, PR bleeding, palpable mass | Progressive intraluminal growth narrows the colonic lumen; 15–20% of CRC patients present with IO [1] |
| Volvulus | Sigmoid volvulus (70%) | Older males, chronic constipation, institutionalised; coffee bean sign on AXR [4]; bird's beak sign on contrast enema [4] | Twisting of sigmoid around narrow mesosigmoid → closed-loop obstruction |
| Caecal volvulus (25%) | Younger females, congenital hypermobile caecum; dilated SB on AXR | Failed fusion of ascending colon mesentery → mobile caecum twists | |
| Inflammatory | Diverticular stricture | History of recurrent diverticulitis; LLQ (Western) or RLQ (Asia) pain; fibrotic narrowing | Chronic inflammation → fibrosis → fixed stricture of colonic lumen |
| Stricture | Anastomotic / Radiation / Ischaemic / Endometriotic [1] | Prior surgery, RT, vascular disease, or endometriosis history | Fibrotic narrowing from healing/scarring process |
| Extrinsic | Metastasis / Pelvic tumour [1] | Known primary (ovarian, uterine, prostatic); pelvic mass on examination | External compression of colon by adjacent tumour mass |
| Pseudo-obstruction | Ogilvie's syndrome | As above; diagnosis of exclusion [4] | Functional, not mechanical |
| Toxic megacolon | IBD history, C. difficile infection, antibiotic use; bloody diarrhoea; systemic toxicity (fever, tachycardia, leucocytosis) [3] | Total or segmental colonic dilatation with systemic toxicity → mimics obstructive LBO but mechanism is inflammatory paralysis |
Sigmoid Volvulus vs. Toxic Megacolon vs. Ogilvie's
These three conditions all present with massive colonic dilatation and can look similar on AXR. Differentiation is crucial because management is completely different:
- Sigmoid volvulus: coffee bean sign, absent rectal gas, no systemic toxicity initially → endoscopic decompression
- Toxic megacolon: systemic toxicity, bloody diarrhoea, IBD/C. difficile history → medical management ± colectomy
- Ogilvie's: hospitalised patient, no systemic toxicity, normal bowel sounds, dilated rectum, gas in rectum on AXR → supportive ± neostigmine ± colonoscopic decompression
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.
| Differential | Age at Presentation | Vomiting | Distension | Meconium | Key Diagnostic Clue |
|---|---|---|---|---|---|
| Malrotation with midgut volvulus | Days 1–28 (often first week) | Bilious (always pathological) [2] | May be minimal | May have passed normally | Upper GI contrast study showing DJ junction malposition; surgical emergency |
| Duodenal atresia | Day 1 | Bilious (if distal to ampulla) or non-bilious (if proximal) | Epigastric only (proximal obstruction) | May pass normally | "Double bubble" sign on AXR; association with Down syndrome [3] |
| Jejunoileal atresia | Day 1–2 | Bilious | Progressive | Absent or scant | Multiple dilated loops with air-fluid levels; no gas in rectum |
| Meconium ileus | Day 1–2 | Bilious | Marked | Absent (inspissated) | Ground-glass appearance on AXR (Neuhauser sign); association with cystic fibrosis [3] |
| Hirschsprung's disease | Day 1–3 (or later in short-segment) | Bilious (late) | Progressive, massive | Delayed > 48h (failure to pass meconium in 90%) [3] | "Blast sign" on PR; contrast enema showing transition zone; rectal suction biopsy (gold standard) |
| Anorectal malformation | Day 1 | Late | Progressive | Absent; no visible anus | Absent/abnormal anus on perineal inspection |
| Necrotising enterocolitis (NEC) | Premature neonates, days 2–14 | Bilious | Marked, tender | Bloody stools | Pneumatosis intestinalis on AXR; portal venous gas |
| Incarcerated inguinal hernia | Any neonatal age | May or may not be present | Variable | Variable | Palpable, irreducible groin swelling; especially in premature males |
| Pyloric stenosis | 2–8 weeks | Non-bilious, projectile | Epigastric only | Normal | Palpable "olive" mass in epigastrium; hypochloraemic, hypokalaemic metabolic alkalosis; pyloric muscle thickening on USS |
Bilious Vomiting in a Neonate
Bilious vomiting in a neonate = malrotation with midgut volvulus until proven otherwise. This is a surgical emergency because the entire midgut can infarct within hours if the volvulus is not reduced. Do NOT wait for further investigations if the clinical picture is suspicious — obtain an urgent upper GI contrast study and call the paediatric surgeon immediately.
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:
| Mimic | Why it mimics IO | How to differentiate |
|---|---|---|
| Acute pancreatitis | Severe epigastric pain, vomiting, ileus (reflex ileus from retroperitoneal inflammation) | Elevated amylase/lipase; CT findings; pain radiating to back; no transition point on AXR |
| Acute mesenteric ischaemia | Severe abdominal pain "out of proportion to examination," vomiting, distension | AF or embolic source; raised lactate; CT angiography showing SMA occlusion; pain early, signs late |
| Acute peritonitis (e.g., perforated peptic ulcer) | Board-like rigidity, absent bowel sounds, vomiting | Free gas on erect CXR; history of PUD/NSAID use; peritonism from the outset (not progressive as in strangulated IO) |
| Gastroenteritis | Vomiting, diarrhoea, colicky abdominal pain, may have distension | Diarrhoea is prominent (not constipation); infective contacts; self-limiting; AXR non-specific |
| Diabetic ketoacidosis | Severe abdominal pain ("pseudoperitonitis"), vomiting, dehydration | Hyperglycaemia, ketonuria, metabolic acidosis; no mechanical obstruction on imaging |
| Acute urinary retention | Suprapubic distension, pain, inability to void | Palpable bladder, confirmed by USS/catheterisation; no features of bowel obstruction on AXR |
| Ruptured AAA | Acute abdominal/back pain, hypotension, distension | Pulsatile abdominal mass; CT angiography; haemodynamic instability disproportionate to IO features |
| Location | IO-related DDx | Non-IO Mimics |
|---|---|---|
| RLQ | Caecal volvulus, appendiceal mass causing SBO, Crohn's stricture | Acute appendicitis, right-sided diverticulitis (Asia), ovarian torsion, ectopic pregnancy, ureteric colic [3][4] |
| LLQ | Sigmoid volvulus, diverticular stricture, CRC | Acute diverticulitis, ovarian torsion, ectopic pregnancy, ureteric colic |
| Central/diffuse | Adhesive SBO, generalised peritonitis from perforated strangulated bowel | Perforated viscus, ruptured AAA, acute mesenteric ischaemia, DKA [4] |
| Epigastric | High SBO (duodenal), GOO from pyloric stenosis (neonates) or gastric cancer (adults) | Acute pancreatitis, acute MI, perforated PUD [4] |
G. Differential Diagnosis — Specific Scenarios
| DDx | Differentiating Features |
|---|---|
| Toxic megacolon | Total or segmental colonic dilatation with systemic toxicity; bloody diarrhoea; history of IBD or C. difficile (antibiotic use) [3] |
| Ogilvie's syndrome | Acute dilatation without anatomic obstruction; hospitalised, severely ill; abdominal distension is the most common presentation [3]; normal bowel sounds; gas in rectum |
| Obstructing CRC | Subacute history of change in bowel habit, weight loss; CT showing mass not volvulus |
| DDx | Differentiating Features |
|---|---|
| Meckel's diverticulum | Painless massive PR bleeding (vs. painful colicky episodes in intussusception); Technetium-99m pertechnetate scan positive [3] |
| Malrotation with midgut volvulus | Bilious vomiting ± PR bleeding; typically neonatal; upper GI contrast diagnostic |
| Bacterial colitis | Diarrhoea predominant, infective contacts, stool cultures positive |
| Septic shock | Lethargy and coma may mimic the inter-episode lethargy of intussusception, but haemodynamic instability, fever, and septic markers distinguish [3] |
| Henoch-Schönlein purpura | Purpuric rash over buttocks/legs, arthralgia, haematuria; abdominal pain from bowel wall haematoma ± intussusception (HSP itself can cause intussusception) |
| DDx | Differentiating Features |
|---|---|
| Malrotation of gut | Bilious vomiting, may have minimal distension; upper GI contrast diagnostic |
| Hirschsprung's disease | Delayed meconium passage, abdominal distension, blast sign on PR; rectal biopsy confirmatory |
| Meconium ileus | Ground-glass appearance (Neuhauser sign) on AXR; association with CF; sweat chloride test |
| Intestinal atresia | Level-dependent presentation; double bubble (duodenal), triple bubble (jejunal), microcolon (ileal/colonic) |
| Meconium plug syndrome | Occurs in up to 1:500 newborns; colonic dysmotility or abnormal meconium consistency; often resolves with contrast enema [3] |
| Small left colon syndrome | Infant of diabetic mother; transient left colon dysmotility; contrast enema shows small-calibre descending colon [3] |
| Internal anal sphincter achalasia | Similar to short-segment Hirschsprung; rectal biopsy shows normal ganglia (differentiates from HD) [3] |
This is a high-yield exam comparison. The key is to combine clinical features, examination findings, and imaging.
| Feature | Mechanical SBO | Paralytic Ileus | Pseudo-obstruction |
|---|---|---|---|
| Pain | Colicky [1] — intermittent, cramping | Mild, diffuse, non-colicky | Distension but not much pain [4] |
| Vomiting | Profuse in SBO [4] | Present but less dramatic | Variable |
| Distension | Variable (depends on level) | Diffuse | Often marked |
| Constipation | Complete (obstipation) if complete obstruction | Variable; may pass flatus | Variable |
| Bowel sounds | Increased [1] — high-pitched, tinkling (early); absent (late, if strangulation) | Hypoactive or absent [4] | Normal [4] |
| PR examination | Empty, collapsed rectum | Variable | Dilated rectum [4] |
| AXR | Dilated proximal loops + collapsed distal; transition point; absent rectal gas | Diffuse gas throughout SB and LB; no transition point | Dilated colon; gas present in rectum [4] |
| CT abdomen | Transition point identified; proximal dilatation, distal collapse | No transition point; diffuse dilatation | Dilated colon, no mechanical cause |
| History | Prior surgery, hernia, malignancy | Recent operation, peritonitis, metabolic disorder, drugs | Hospitalised, severely ill, metabolic disturbance |
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":
| Red Flag | Pathophysiological Basis |
|---|---|
| Constant (non-colicky) pain | Continuous ischaemic injury to bowel wall irritating peritoneum |
| Tachycardia and hypotension [7] | Hypovolaemia + sepsis from bacterial translocation |
| Fever, leucocytosis | Systemic inflammatory response to ischaemic/necrotic bowel |
| Metabolic acidosis / raised lactate | Anaerobic metabolism in ischaemic bowel tissue; lactate is a sensitive marker of bowel ischaemia |
| Peritoneal signs (guarding, rigidity, rebound) [7] | Parietal peritoneum irritated by transmural necrosis or perforation |
| Bloody PR discharge | Mucosal sloughing from ischaemic bowel |
| Absent bowel sounds | Bowel has become non-viable → no peristaltic activity |
High Yield Summary — Differential Diagnosis of IO
-
First question: Is it truly IO or a mimic? (Pancreatitis, mesenteric ischaemia, DKA, peritonitis, GE, urinary retention can all mimic IO)
-
Second question: Mechanical or functional? — Differentiate by bowel sounds (↑↑ = mechanical; ↓/absent = ileus; normal = pseudo-obstruction), PR exam (empty rectum = mechanical LBO; dilated = pseudo-obstruction), and imaging (transition point = mechanical)
-
Third question: If mechanical, SBO or LBO? — SBO: ABC (Adhesions, Bulge/hernia, Cancer); LBO: Cancer, Volvulus, Diverticular stricture, Pseudo-obstruction
-
Neonatal IO: Bilious vomiting = malrotation with midgut volvulus until proven otherwise. DDx includes intestinal atresia, meconium disease, Hirschsprung's disease, NEC.
-
Sigmoid volvulus DDx: Toxic megacolon (systemic toxicity, bloody diarrhoea, C. difficile) vs. Ogilvie's (hospitalised, normal bowel sounds, dilated rectum, gas in rectum)
-
Always check: hernial orifices, surgical scars, medications (opioids, anticholinergics), metabolic panel (K⁺, TFT, glucose), strangulation signs (constant pain, peritonism, fever, lactate)
Active Recall - Differential Diagnosis of Intestinal Obstruction
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
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.
IO is diagnosed when the combination of:
- Clinical features: ≥ 1 of the cardinal features (colicky pain, vomiting, distension, absolute constipation) in an appropriate clinical context
- Radiological confirmation: Imaging demonstrating dilated bowel proximal to a transition point with collapsed distal bowel (mechanical) OR diffuse dilatation without transition point (functional)
- 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.
IO is a Clinical-Radiological Diagnosis
Unlike many medical conditions, intestinal obstruction does not have a formal set of "diagnostic criteria" with sensitivity/specificity thresholds. The diagnosis is made by putting together the clinical picture (cardinal features + risk factors + examination findings) with imaging (AXR and/or CT). The role of investigations is to confirm the obstruction, localise the level, identify the cause, and detect complications (especially strangulation).
The following algorithm represents the systematic approach to a patient with suspected IO, integrating the questions from the lecture slides [1]:
D. Investigation Modalities — Detailed Guide
The investigations for IO can be grouped into:
- Bedside tests
- Blood investigations
- Imaging (the cornerstone)
- Endoscopy
Each test has a specific role in answering one or more of the key diagnostic questions.
| Test | Rationale / What You're Looking For |
|---|---|
| Urinalysis [7][8] | Exclude urological mimics (UTI, ureteric colic — haematuria); assess concentration (dehydration) |
| Pregnancy test [7][8] | Mandatory in all women of childbearing age to exclude ectopic pregnancy (a mimic of acute abdomen) and to guide imaging decisions (avoid CT radiation) |
| Point-of-care glucose | Exclude DKA as a cause of "pseudoperitonitis" and ileus |
| ECG [8] | Exclude acute MI — inferior MI can present with epigastric pain and vomiting mimicking high SBO |
Bloods: CBC, ABG/VBG, LRFT, amylase, lactate ± septic work-up [4]
| Test | What It Tells You | Why / Pathophysiological Basis |
|---|---|---|
| CBC with differential [4][7][8] | Leucocytosis (↑ WCC) | Suggests strangulation, ischaemia, perforation, or underlying infection. The stress response and bacterial translocation from ischaemic bowel both drive leucocytosis. |
| Anaemia (↓ Hb) | May indicate chronic blood loss from underlying malignancy (CRC) or acute haemorrhage from strangulated/necrotic bowel | |
| Haemoconcentration (↑ Hb/Hct) | Dehydration from vomiting and third-spacing | |
| ABG / VBG [4][8] | Metabolic alkalosis | From vomiting — loss of H⁺ and Cl⁻ from gastric secretions. This is the classic acid-base disturbance in proximal SBO with profuse vomiting. |
| Metabolic acidosis with raised lactate | Sensitive marker for bowel ischaemia [3]. Anaerobic metabolism in ischaemic bowel produces lactate; also reflects tissue hypoperfusion from hypovolaemia. This is a red flag for strangulation. | |
| LRFT (Liver and Renal Function Tests) [4][8] | ↓ K⁺ (hypokalaemia) | Due to hypovolaemia and impaired absorption secondary to oedematous bowel wall [4]. Also from vomiting (direct K⁺ loss + renal K⁺ wasting from metabolic alkalosis via ↑ HCO₃⁻ delivery to distal nephron + RAAS activation) [3]. |
| ↓ Na⁺, ↓ Cl⁻ | Losses in vomitus (gastric secretions rich in Na⁺, Cl⁻, H⁺) | |
| ↑ Urea and Creatinine | Pre-renal AKI from dehydration (third-spacing + vomiting + reduced intake) | |
| ↑ Urea:Creatinine ratio ( > 20:1) | Suggests pre-renal cause — urea is passively reabsorbed in the proximal tubule when flow rate is low | |
| LFT [3][8] | Rule out hepatic pathology; check albumin (nutritional status, malignancy) | |
| Amylase [4][8] | ↑ Amylase | Can be mildly elevated in IO (from bowel ischaemia, peritoneal irritation); markedly elevated → think pancreatitis as the cause of ileus. Elevated in approximately half of patients with intestinal ischaemia [3]. |
| Serum lactate [3][4] | ↑ Lactate | Sensitive marker for bowel ischaemia [3]. Lactate > 2 mmol/L should raise suspicion of strangulation. Rising serial lactate is particularly concerning. |
| CRP [8] | ↑ CRP | Non-specific inflammatory marker; very high CRP may suggest perforation/peritonitis |
| Group and Save / Cross-match [8] | Preparation for surgery | Any patient with suspected strangulation or who may need laparotomy should have blood available |
| Septic work-up [4] | Blood cultures if febrile | Bacterial translocation from ischaemic bowel → bacteraemia |
The Lactate-Alkalosis Paradox
In IO, you might see metabolic alkalosis (from vomiting) AND metabolic acidosis (from ischaemia) co-existing. This creates a mixed acid-base picture. Always interpret the ABG in context: if vomiting has been profuse but lactate is also rising, suspect concurrent strangulation. An ABG that "looks normal" might actually be a mixed disorder with opposing forces cancelling out — always check the anion gap.
3. Imaging — The Cornerstone of Diagnosis
Erect CXR: free gas, aspiration pneumonia, gastric distension, NG tube position [4]
| Finding | Significance | Why |
|---|---|---|
| Free gas under the diaphragm (pneumoperitoneum) | Bowel perforation | Gas escapes from a perforated viscus into the peritoneal cavity and rises to the highest point (subdiaphragmatic space in the erect position). This is a surgical emergency — do NOT delay for further imaging. |
| Aspiration pneumonia | Complication of IO | Vomiting in a patient with impaired consciousness or reduced GCS → aspiration of gastric/intestinal contents |
| Pleural effusion / consolidation | Thoracic pathology mimicking abdominal pain | Basal pneumonia can cause referred abdominal pain and ileus |
| NG tube position | Confirm correct placement | Before starting NG aspiration |
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]:
| Feature | Small Bowel | Large Bowel |
|---|---|---|
| Mucosal folds | Valvulae conniventes (plicae circulares) — cross the entire width of the lumen | Haustra — do NOT cross the entire width (only partial indentations) |
| Location | Central in the abdomen | Peripheral (frame the abdomen) |
| Diameter | Dilated if > 3 cm (SB) | Dilated if > 6 cm (colon) or > 9 cm (caecum) |
| Number of loops | Multiple (many loops if distal SBO) | Fewer, larger loops |
| Finding | Description | Significance |
|---|---|---|
| Dilated proximal bowels with distal collapsed bowel [3] | Gas-filled loops proximal to obstruction; no or little gas distally | Confirms mechanical obstruction and helps localise the level |
| Air-fluid levels [3] | Multiple, at different heights within the same loop ("stepladder" pattern in SBO) | Fluid trapped in distended loops; gas sits on top in erect film |
| Gasless abdomen [3] | Complete absence of visible gas | Complete filling of loops of bowel with sequestered fluid [3] — a completely fluid-filled obstructed bowel shows no gas shadows. This is an easily missed finding! |
| Absent colonic/rectal gas | No gas seen in the colon/rectum | Suggests complete SBO (all gas proximal to obstruction) or distal LBO |
| Coffee bean sign [4] | Large, ahaustral, bent loop arising from pelvis/LLQ with 3 converging white lines | Sigmoid volvulus — the 3 lines represent the 2 walls of the dilated sigmoid and the mesenteric root |
| Pneumobilia [4] | Gas in the biliary tree (linear gas over hepatic area) | Air in the biliary tree [1] → think gallstone ileus (Rigler's triad: pneumobilia + SBO + ectopic gallstone) [4]. Other DDx: post-ERCP, post-cholecystectomy, emphysematous cholecystitis |
| Double bubble sign | Two rounded gas shadows (stomach + proximal duodenum) with no distal gas | Duodenal atresia in neonates; associated with Down syndrome |
AXR Findings Suggesting Complications (Strangulation/Ischaemia) [1][3]:
| Finding | Description | Significance |
|---|---|---|
| Thumbprinting sign [3] | Normal haustration becomes thickened at regular intervals appearing like thumbprints projecting into the lumen [3]. Caused by bowel wall thickening usually caused by oedema [3]. | Suggests bowel wall ischaemia/oedema — mural haemorrhage or submucosal oedema causes the mucosa to bulge into the lumen |
| Pneumatosis intestinalis [1][3] | Gas tracking within the bowel wall — appears as linear or bubbly lucencies within the wall | Gas-producing bacteria have invaded the ischaemic bowel wall (transmural necrosis allows bacterial infiltration). This is a late and ominous sign indicating bowel necrosis. |
| Free peritoneal gas (pneumoperitoneum) [1] | Gas under the diaphragm (erect CXR) or between bowel loops (supine AXR — Rigler's sign / double-wall sign) | Perforation has occurred — surgical emergency |
| Double-wall sign (Rigler's sign) [3] | Both sides of the bowel wall are visible because gas is present both inside the lumen and outside in the peritoneal cavity | Confirms free intraperitoneal gas (perforation) |
| Portal venous gas | Linear branching gas shadows overlying the liver periphery | Gas has entered the portal venous system from necrotic bowel — extremely ominous sign |
AXR Pattern by Level [3]:
| Type | AXR Pattern |
|---|---|
| High SBO | Little evidence of dilated small bowel loops [3] — short segment proximal to obstruction, often gasless |
| Low SBO | Multiple dilated small bowel loops [3] — central, with valvulae conniventes |
| LBO | Dilated colon proximal to obstruction [3]; dilated small bowel if ileocaecal valve is incompetent [3] |
The Gasless Abdomen Trap
A completely gasless abdomen on AXR can be easily dismissed as "normal" — but in the context of IO, it means the obstructed loops are completely filled with fluid and no gas is visible. This is actually a sign of complete, early obstruction where swallowed air has not yet accumulated but massive fluid sequestration has occurred. Always correlate with clinical features; if suspicion is high, proceed to CT.
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 Finding | Description | What It Means |
|---|---|---|
| Transition point | Abrupt change from dilated proximal loops to collapsed distal loops | Localises the exact site of mechanical obstruction |
| Small bowel faeces sign | Particulate matter in the dilated SB lumen with a faecal appearance | Suggests complete or near-complete SBO with prolonged stasis (bacterial fermentation of SB content) |
| "Target sign" [3] | Alternating hypodense and hyperdense layers | Indicative of intussusception [3] — concentric rings represent the layers of invaginated bowel wall and mesentery |
| "Whirl sign" [3] | Rotation of small bowel mesentery — swirling of mesenteric vessels and fat around a central axis | Indicative of volvulus [3] — the mesentery and its vessels twist around the axis of rotation |
| "Apple-core" lesion [3] | Annular narrowing of the colonic lumen with shouldered margins | Indicative of colorectal cancer [3] — circumferential tumour growth creates the characteristic shelf-like narrowing |
| Pneumatosis intestinalis [3] | Gas within the bowel wall | Bowel wall necrosis with bacterial invasion — ominous sign |
| Bowel wall thickening [3] | Mural thickening > 3 mm in SB, > 5 mm in colon | Oedema from venous congestion, ischaemia, or inflammation |
| Reduced or lack of bowel wall enhancement [3] | Bowel wall does not take up IV contrast | Indicates ischaemia — compromised arterial supply means contrast cannot reach the bowel wall. This is a key finding to look for when assessing viability. |
| Oedematous and thickened mesentery [3] | Mesenteric fat stranding, haziness | Venous congestion → fluid transudation into mesentery |
| Engorgement of mesenteric vessels [3] | Dilated, congested mesenteric veins | Impaired venous return from obstructed bowel |
| Portal venous gas [3] | Gas in the portal venous branches within the liver | Extremely ominous — gas from necrotic bowel has entered the portal system. Strong indication for emergent surgery. |
| Rigler's triad [4] | Pneumobilia + SBO + ectopic gallstone | Pathognomonic of gallstone ileus |
| Free fluid / free gas | Ascites or pneumoperitoneum | Perforation (gas) or transudation/ischaemia (fluid) |
| "Beak sign" | Tapering of bowel lumen to a point at the site of obstruction | Seen in volvulus (the twisted mesentery compresses the bowel to a beak-shaped endpoint) |
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.
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]:
| Aspect | Details |
|---|---|
| Indication | Suspected adhesive SBO only — NOT for LBO, NOT if perforation suspected (although gastrografin is water-soluble and safe, unlike barium) |
| Technique | 100 mL of gastrografin administered orally or via NG tube. X-ray is taken every 30 minutes until 4 hours (delayed film) [3]. The 2-hour film is the most important [3]. |
| Diagnostic role | Detects the level of obstruction and whether it is partial or complete [3]. If contrast reaches the colon by the 2-hour film → partial obstruction → likely to resolve conservatively. If contrast fails to reach the colon by 4–24 hours → complete obstruction → likely needs surgery. |
| Therapeutic role | Water-soluble contrast is both diagnostic and therapeutic [3]: (1) Draws fluid into lumen of bowel due to hypertonicity (osmotic effect, ~2000 mOsm/L) → reduces bowel wall oedema; (2) Decreases intestinal wall oedema and stimulates intestinal peristalsis [3] → may resolve partial adhesive obstruction. |
| Evidence | Studies show gastrografin reduces the need for surgery in adhesive SBO and shortens hospital stay. If contrast reaches the caecum within 24 hours, the probability of resolution without surgery is ~99%. |
Gastrografin — Diagnostic and Therapeutic
Gastrografin is a hyperosmolar, water-soluble contrast agent (~2000 mOsm/L). When given orally in adhesive SBO, its hypertonicity draws water into the bowel lumen, which paradoxically reduces bowel wall oedema (by osmotically pulling interstitial fluid from the oedematous wall into the lumen) and stimulates peristalsis. The 2-hour film is the key timepoint — if contrast is in the colon by 2 hours, the patient almost certainly has a partial obstruction that will resolve conservatively.
Water-soluble enema for LBO: to differentiate mechanical vs functional [4]
| Aspect | Details |
|---|---|
| Indication | Suspected LBO — particularly to differentiate mechanical obstruction from pseudo-obstruction; also to identify the site of obstruction |
| Agent | Gastrografin or other water-soluble contrast (NOT barium in acute setting — barium peritonitis risk if perforation) |
| Findings | Bird's beak sign in sigmoid volvulus (contrast tapers at twist point) [4]; mass lesion in CRC; diverticular stricture; transition zone in Hirschsprung's (dilated proximal ganglionic → narrow aganglionic distal segment) |
| Caution | Do NOT order colonoscopy/barium enema in acute settings: risk of perforation and chemical peritonitis [4] |
- 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
Lower gastrointestinal endoscopy [1]: Diagnostic AND Therapeutic
| Aspect | Details |
|---|---|
| Diagnostic role | Not usually the initial investigation but can aid in diagnosis when LBO cannot be excluded on imaging; allows biopsy of obstructing mass (CRC) |
| Therapeutic roles [1] | Decompression in sigmoid volvulus and pseudo-obstruction [1]; Stenting (self-expanding metallic stents / SEMS for palliation or bridge-to-surgery in left-sided CRC) [1] |
| Caution | To avoid excessive insufflation of gas [1] — already distended bowel can perforate with further gas insufflation. Use CO₂ insufflation where possible (absorbed faster than air). |
| Contraindication | Do NOT order colonoscopy/barium enema in acute settings [4] if perforation is suspected. AVOID endoscopy for acute abdomen: sealed-off perforation may open by gas insufflation during endoscopy [8]. |
Specific endoscopic scenarios:
| Scenario | Endoscopic Approach |
|---|---|
| Sigmoid volvulus | Flexible sigmoidoscopy de-rotation with cautious insufflation [4] — first line! Successful reduction: sudden expulsion of gas and stool. Leave rectal tube in situ for 24 hours. |
| Obstructing CRC | SEMS stenting [4] — either as bridge-to-surgery (allows elective 1-stage resection) or palliation in unresectable disease |
| Pseudo-obstruction | Colonoscopic decompression [4] — bowel prep not required; limit air insufflation |
| Caecal volvulus | Colonoscopic de-rotation ± caecopexy — high recurrence rate [4] |
| Condition | Investigation | Key Findings |
|---|---|---|
| Gallstone ileus | AXR + CT | Rigler's triad: pneumobilia + SBO + ectopic gallstone [4] |
| Intussusception (paediatric) | Ultrasound (first-line in children) | "Target sign" / "doughnut sign" on transverse view; "pseudokidney sign" on longitudinal view |
| Air/saline enema | Diagnostic AND therapeutic — pneumatic or hydrostatic reduction | |
| Malrotation | Upper GI contrast study (gold standard) [3] | Abnormal position of DJ junction; corkscrew/beak sign |
| Hirschsprung's disease | Contrast enema | Transition zone (narrow distal aganglionic → dilated proximal ganglionic); delayed 24-hour film shows contrast retention |
| Rectal suction biopsy (gold standard) | Absence of ganglion cells in submucosal plexus; hypertrophied nerve trunks; elevated acetylcholinesterase staining | |
| Anorectal manometry | Absence of recto-anal inhibitory reflex (RAIR) — normally, rectal distension causes relaxation of the internal anal sphincter; in HD, the aganglionic sphincter cannot relax | |
| Meckel's diverticulum | Technetium-99m pertechnetate scan ("Meckel's scan") [4] | Ectopic gastric mucosa actively secretes chloride → pertechnetate (a chloride analogue) accumulates → focal uptake in RLQ. Pre-med with H₂ blockers to prevent secretion of isotope. |
| Pseudo-obstruction | AXR (daily), CT, water-soluble contrast enema [4] | Dilated colon, gas in rectum, no transition point; CT to rule out mechanical cause |
| CRC causing LBO | Colonoscopy with biopsy (gold standard for CRC diagnosis) [4] | Histological confirmation; CEA for prognostication (not diagnostic — low sensitivity/specificity) [4] |
| Diagnostic Question | How Answered | Key Investigation |
|---|---|---|
| Is there IO? | Clinical features + AXR showing dilated bowel ± air-fluid levels | History, examination, AXR |
| Mechanical or functional? | Transition point (mechanical) vs. diffuse dilatation (functional); bowel sounds; PR exam | AXR, CT, clinical examination |
| SBO or LBO? | Valvulae conniventes (central) = SBO; Haustra (peripheral) = LBO [7] | AXR, CT |
| What is the cause? | CT identifies mass, hernia, volvulus, intussusception, gallstone, etc. | CT abdomen with contrast |
| Simple or strangulated? | Clinical (peritonism, fever, tachycardia) + Lab (↑ lactate, acidosis, ↑ WCC) + CT (no bowel wall enhancement, pneumatosis, portal venous gas) | Clinical + Bloods + CT |
| Partial or complete? | Gastrografin follow-through (contrast reaching colon = partial) | Gastrografin follow-through |
| Is there perforation? | Free gas on erect CXR / CT; Rigler's sign on AXR | Erect CXR, CT |
High Yield Summary — Diagnosis of IO
-
IO is a clinical-radiological diagnosis — no formal scoring criteria exist. Combine cardinal features + imaging.
-
First-line imaging: Erect CXR (rule out perforation) + Supine and Erect AXR (confirm IO, distinguish SBO vs LBO, detect complications).
-
AXR systematic review [1]: Dilated loops? Air-fluid levels? Gas in colon/rectum? Strangulation signs (thumbprinting, pneumatosis, free gas)? Massive colonic dilatation? Air in biliary tree?
-
CT abdomen with IV contrast is more sensitive than plain AXR [1] — identifies transition point, cause, viability (bowel wall enhancement), and complications. Use rectal contrast for LBO.
-
Gastrografin follow-through for adhesive SBO: diagnostic AND therapeutic. 2-hour film is key. Contrast in colon = partial obstruction = likely to resolve conservatively.
-
Key bloods: Lactate (ischaemia), ABG (alkalosis from vomiting vs acidosis from ischaemia), K⁺ (hypokalaemia), WCC (infection/strangulation).
-
Endoscopy: Diagnostic and therapeutic — decompression in sigmoid volvulus/pseudo-obstruction; stenting in CRC. Caution: avoid excessive gas insufflation [1].
-
Neonates: Upper GI contrast study is gold standard for malrotation; contrast enema + rectal biopsy for Hirschsprung's.
Active Recall - Diagnosis of Intestinal Obstruction
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
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.
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]
- 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
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
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
- 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
Metoclopramide in Complete Mechanical Obstruction
Do NOT give metoclopramide in complete mechanical bowel obstruction. Metoclopramide is a D₂ antagonist and 5-HT₄ agonist that increases peristaltic activity. In a complete mechanical obstruction, increased peristalsis against a fixed barrier can worsen distension, pain, and theoretically precipitate perforation. Use ondansetron or cyclizine instead for anti-emesis.
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
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
D. Conservative (Non-Operative) Management
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
| Component | Details |
|---|---|
| Intravenous fluid and electrolytes [1] | As above — crystalloid resuscitation, K⁺ replacement |
| Nasogastric decompression [1] | Free drainage + Q4h aspiration |
| Nutrition [1] | TPN if prolonged fasting anticipated |
| Frequent monitoring [1] | Vitals, abdominal signs, bloods (WCC, lactate), serial AXR |
| Gastrografin follow-through [3][4] | For adhesive SBO — diagnostic AND therapeutic (see Investigations section) |
Resolution of obstruction [1]:
- Less abdominal distension
- Reduction of nasogastric output
- Passage of flatus and bowel movement
- Resolution in abdominal X-rays
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]
The 72-Hour Rule
Conservative management for adhesive SBO should be given a fair trial of 48–72 hours with close monitoring. However, if at any point signs of strangulation develop (constant pain, peritonism, rising lactate, fever), the trial must be abandoned immediately and the patient taken to theatre. The 72-hour clock is a maximum, not a target — clinical deterioration always trumps the clock.
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:
| Indication | Reasoning |
|---|---|
| Strangulated hernia | Blood supply to bowel is compromised → ischaemia → necrosis → perforation within hours if not relieved |
| Suspected/proven strangulation | Same as above — the ischaemic clock is ticking |
| Peritonitis | Indicates perforation has already occurred OR transmural necrosis with bacterial translocation — source control is mandatory |
| Pneumoperitoneum | Free gas = perforation = surgical emergency |
| Pneumatosis cystoides intestinalis | Gas in the bowel wall = transmural necrosis = imminent perforation |
| Closed-loop obstruction | No decompression possible in either direction → rapid pressure build-up → rapid ischaemia → rapid perforation |
| Volvulus with peritoneal signs | Volvulus is inherently a closed-loop obstruction; peritoneal signs indicate ischaemia has already supervened |
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.
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:
| Criterion | Viable | Non-viable |
|---|---|---|
| Colour | Dark colour becomes lighter (after release of obstruction, reperfusion improves colour) [3] | Dark colour persists [3] |
| Mesenteric vessels | Visible pulsation in mesenteric arteries [3] | No detectable pulsation [3] |
| General appearance | Shiny serosa [3] | Dull and lusterless [3] |
| Musculature | Firm, peristalsis may be observed [3] | No peristalsis [3] |
| Additional intra-op assessment | Pink serosa, bleeding from marginal arteries [4]; intra-op Doppler USG; fluorescein injection → Wood's lamp [4] | Absence of these findings |
If there is doubt, the "second-look laparotomy" approach (re-exploring at 24–48 hours) may be used [4].
G. Cause-Specific Management
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]
| Phase | Management | Details |
|---|---|---|
| Initial | Conservative ("Drip and Suck") | NPO, IV fluids, NG decompression, monitoring |
| 48–72h assessment | Gastrografin follow-through | If contrast in colon by 4h → partial → continue conservative. If not → complete → surgery. |
| Surgery | Enterolysis (lysis of adhesions and release of constricting bands) [1] | Resection only on causative adhesions and remaining adhesions (if present) should be left in situ unless angulation is present as division of these adhesions will only cause further adhesion formation [3] |
| If non-viable bowel | Resection + anastomosis or stoma | Primary anastomosis if conditions favourable; stoma if contamination/instability |
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?
- 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
4. Intussusception
| Phase | Management | Details |
|---|---|---|
| Pre-reduction | Stabilisation: IV fluids, prophylactic antibiotics [3] | Resuscitation before any intervention |
| Non-operative reduction (first-line) | Pneumatic (air/CO₂) or hydrostatic (saline) reduction under ultrasound guidance [3] | Pneumatic technique using air or CO₂ reduces intussusception more easily and is more advantageous if perforation occurs [3]. Ultrasound is now the intervention of choice for guidance (over fluoroscopy) [3]. |
| Success criteria | Appearance of water and bubbles in terminal ileum; free flow of contrast or air into terminal ileum; relief of symptoms; disappearance of abdominal mass [3] | |
| Post-reduction | Observation with hospitalisation for 12–24 hours [3] | Patient usually presents with fever after successful reduction due to bacterial translocation or release of endotoxin or cytokines [3]. Watch for recurrence. |
| Surgical indications | Critically ill patient; suspected bowel perforation; refractory to non-operative reduction [3] | |
| Surgical technique | Manual reduction at operation [3] | Gently compressing most distal part of intussusception towards its origin [3]. If reduction fails or lead point identified → resection with primary anastomosis. |
Contraindications to non-operative reduction [3]:
- Peritonitis
- Perforation
- Haemodynamic instability / septic shock
- Clinical features of prolonged ischaemia
- 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]:
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 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]:
| Option | Description | Indication |
|---|---|---|
| Hartmann's operation [1] | Resection without anastomosis [1] — the tumour-bearing segment is resected, the distal rectum is closed as a rectal stump (Hartmann's pouch), and the proximal end is brought out as an end colostomy. Reversal is a second operation. | Most common emergency procedure [4]; unstable patient, contaminated field, unprepared bowel |
| Primary resection and anastomosis [1] | Segmental resection with primary anastomosis (on-table lavage) [1] — the colon proximal to the anastomosis is lavaged intra-operatively to remove faecal loading, reducing leak risk. | Only for very good risk patients [4]; stable patient with viable bowel |
| Subtotal colectomy with anastomosis of ileum and distal colon/rectum [1] | Remove the entire loaded colon → anastomose ileum to rectum/sigmoid. Avoids the issue of faecal loading entirely. | Synchronous tumours, cecal perforation from closed-loop obstruction, non-viable proximal colon |
| Endoscopic stenting (SEMS) [4] | Self-expanding metallic stent placed across the obstructing tumour endoscopically | For left-sided tumour except very large or distal rectal tumour (risk of tenesmus and pain) [4] |
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]
- Palliation [4]: for patients unfit for or declining surgery
2-stage: most common [4]:
Hartmann's vs. Primary Anastomosis
The fundamental question in emergency left-sided colonic surgery is: can I safely join the bowel ends together, or is it safer to bring out a stoma? Anastomotic leak in an emergency setting carries up to 50% mortality. Therefore, Hartmann's is the safer default unless the patient is stable, the bowel is viable and relatively clean, and the surgeon is experienced. On-table lavage allows primary anastomosis by washing out the faecal-loaded proximal colon intra-operatively.
6. Volvulus
Sigmoidoscopic decompression (recurrence: 50%) [1] Surgery (perforation, strangulation or failed decompression): Resection [1]
| Phase | Management | Details |
|---|---|---|
| Initial | NPO, drip and suck, IV antibiotics [4] | Standard IO resuscitation |
| First-line | Flexible sigmoidoscopy de-rotation with cautious insufflation [4] | Successful reduction: sudden expulsion of gas and stool [4]. Leave rectal tube in situ for 24h for decompression → serial AXR [4]. |
| Failed decompression / Ischaemia | Urgent laparotomy [4] | Emergency Hartmann's operation: rectal stump + colostomy [4]. Or sigmoidectomy → primary anastomosis + on-table lavage if conditions favourable [4]. Paul-Mikulicz procedure: removal of volvulus + double-barrel colostomy for future anastomosis [4]. |
| Elective (recurrence prevention) | Elective sigmoidectomy [4] | For young patients or elderly with recurrent volvulus [4]. Recurrence rate of endoscopic decompression alone is ~50% [1] → definitive surgery reduces this. |
H. Management of Functional Obstruction
| Management | Details | Rationale |
|---|---|---|
| Drip and suck | NPO, NG decompression, IV fluids | Remove accumulating secretions; maintain hydration |
| Treat underlying cause | Correct electrolytes (K⁺, Ca²⁺, Mg²⁺); treat sepsis; discontinue offending drugs (opioids, anticholinergics) | Addressing the root cause allows the myenteric plexus to recover |
| Oral gastrografin (hyperosmotic) [4] | Stimulates peristalsis via osmotic effect | |
| Prokinetics [4] | Erythromycin (motilin agonist — stimulates gastric and small bowel motility), metoclopramide (D₂ antagonist/5-HT₄ agonist) | Pharmacologically stimulate peristalsis |
| Pethidine [4] | No effect on gut motility c.f. morphine [4] | Preferred analgesic in ileus if opioid needed; however, limited use due to toxicity concerns |
| Ambulation | Encourage early mobilisation post-operatively | Physical activity promotes return of bowel function |
Pseudo-obstruction Management [1]:
- To exclude mechanical obstruction
- Nasogastric tube feeding and enemas
- Colonoscopic decompression
- Rectal tube decompression
- Neostigmine
- Caecostomy
| Step | Management | Details |
|---|---|---|
| 1. Supportive (first-line, up to 72h) [4] | Decompression: drip and suck, rectal tube [4]; ambulation [4]; remove underlying cause: electrolyte disturbance, discontinue causative drugs [4] | First-line if no peritonism and caecal diameter < 12 cm |
| 2. IV Neostigmine [1][4] | Acetylcholinesterase inhibitor → ↑ acetylcholine at muscarinic receptors on colonic smooth muscle → stimulates contraction | S/E: bradycardia → requires cardiac monitoring [4]. Contraindicated in mechanical obstruction (would worsen). Atropine should be at bedside. |
| 3. Colonoscopic decompression [1][4] | Endoscopic aspiration of gas from the colon | Bowel prep not required (little propulsion); limit air insufflation to reduce risk of perforation [4] |
| 4. Caecostomy [1] | Surgical or percutaneous placement of a tube into the caecum for decompression | Last resort if all other measures fail; avoids laparotomy in frail patients |
| Urgent surgery | If caecal diameter > 12 cm [4] or peritonism develops | Risk of perforation is critical |
Management [9]:
- Medical: NPO, TPN, IV antibiotics
- Surgical indications: pneumoperitoneum, clinical deterioration, failure of medical Rx
- Operative options: Resection + stoma; Resection + primary anastomosis [9]
| Condition | Management | Key Points |
|---|---|---|
| Malrotation with midgut volvulus | Emergency Ladd's procedure: detorse volvulus counter-clockwise, divide Ladd's bands, broaden mesenteric base, appendicectomy (incidental — caecum is now in LIF), place SB on right and LB on left | Time-critical; delay → midgut infarction → short-gut syndrome or death |
| Duodenal atresia | Duodenoduodenostomy (diamond anastomosis) | Bypass the atretic segment; check for associated anomalies (Down syndrome, cardiac) |
| Jejunoileal atresia | Resection of atretic segment + primary anastomosis; tapering enteroplasty for size discrepancy | Proximal dilated bowel may need tapering to match calibre of distal collapsed bowel |
| Meconium ileus | Non-operative: Gastrografin enema (hyperosmotic → draws water into lumen → loosens inspissated meconium). Operative: if failed enema or perforation → enterotomy and irrigation or resection + stoma. | Confirm CF with sweat chloride test / genetic testing |
| Hirschsprung's disease | Initial: rectal irrigations with saline for decompression. Definitive: abdominoperineal pull-through operation (Soave, Duhamel, or Swenson) — resect aganglionic segment, bring ganglionic bowel to anus [3]. | Laparoscopic-assisted and transanal approaches now preferred [3] |
| NEC [9] | Medical: NPO, TPN, IV antibiotics. Surgical: pneumoperitoneum, clinical deterioration, failure of medical Rx. Resection + stoma or resection + primary anastomosis [9]. | Premature neonates; serial AXR looking for pneumatosis, portal venous gas, pneumoperitoneum |
| Intussusception (paediatric) | Non-operative pneumatic/hydrostatic reduction (first-line) → surgical manual reduction or resection if failed | As detailed above |
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]
| Cause | Operative Procedure |
|---|---|
| Adhesive SBO | Enterolysis [1] — lysis of causative bands only |
| Incarcerated hernia | Hernia repair ± bowel resection if non-viable |
| Gallstone ileus | Enterolithotomy [4] ± cholecystectomy + fistula repair |
| Intussusception (paediatric) | Manual reduction → resection if irreducible or lead point |
| CRC (right-sided) | Right / extended right hemicolectomy + primary anastomosis [1] |
| CRC (left-sided) | Hartmann's [1] or segmental resection with on-table lavage + primary anastomosis [1] or subtotal colectomy [1] |
| Sigmoid volvulus | Sigmoidectomy (Hartmann's or primary anastomosis) |
| Caecal volvulus | Right hemicolectomy [4] |
| Non-viable bowel (any cause) | Resection of non-viable intestine [3] + stoma or anastomosis depending on conditions |
- 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
High Yield Summary — Management of IO
-
All patients: Resuscitation first — "Drip and Suck" (IV fluids + NG decompression). NPO, antibiotics if complicated, monitoring.
-
Conservative Mx indicated for: partial obstruction, adhesive SBO, Crohn's stricture, radiation stricture, disseminated malignancy. Monitor for 48–72h. Gastrografin is both diagnostic and therapeutic.
-
Urgent surgery indicated for: strangulated hernia, proven/suspected strangulation, peritonitis, pneumoperitoneum, pneumatosis intestinalis, closed-loop obstruction, volvulus with peritoneal signs.
-
Adhesive SBO: Conservative Mx ~50–80% effective. Gastrografin follow-through guides decision. Surgery = adhesiolysis; resect only causative bands.
-
Obstructing CRC: Right-sided → resection + primary anastomosis. Left-sided → Hartmann's (most common emergency procedure) or primary anastomosis with on-table lavage (good-risk patients) or SEMS bridge-to-surgery.
-
Sigmoid volvulus: Endoscopic decompression first-line (50% recurrence → consider elective sigmoidectomy). Caecal volvulus → right hemicolectomy.
-
Pseudo-obstruction: Supportive → neostigmine → colonoscopic decompression → caecostomy.
-
Bowel viability: Assess colour change, pulsation, shiny serosa, peristalsis. Non-viable → resect.
-
Neonatal IO: NPO + TPN + IV antibiotics. Surgery if pneumoperitoneum, deterioration, or failed medical Rx.
Active Recall - Management of Intestinal Obstruction
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:
- Local complications (arising from the bowel itself)
- Systemic complications (arising from the body's response to the obstruction)
- Post-operative / treatment-related complications
- Disease-specific complications (unique to certain causes of IO)
A. Local Complications
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]:
| Category | Features |
|---|---|
| Clinical (Signs) | Fever, tachycardia, peritoneal signs (guarding, rigidity, rebound tenderness) [3] |
| Clinical (Symptoms) | Continuous or worsening abdominal pain [3] — the transition from colicky to constant pain is a critical red flag. Colicky pain means the bowel is still alive and contracting; constant pain means the bowel is dying and continuously irritating the peritoneum. |
| Biochemical | Leucocytosis, metabolic acidosis [3] — WCC rises from systemic inflammatory response; lactate rises from anaerobic metabolism in ischaemic tissue; metabolic acidosis results from both. |
| Radiological | Pneumoperitoneum, pneumatosis intestinalis, portal venous gas [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]
The Strangulation Mortality Gap
The mortality jump from 2% (simple) to 10–30% (strangulated) [1] tells you everything about why early recognition and intervention matter. The clinical clue is the transition from colicky to constant pain — this should trigger immediate escalation. Do not wait for peritonism, fever, and raised lactate to all appear; any ONE of these in the right context mandates urgent surgical exploration.
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
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
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
B. Systemic Complications
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):
| Mechanism | Effect |
|---|---|
| Vomiting | Loss of H₂O, Na⁺, K⁺, Cl⁻, H⁺ → hypochloraemic, hypokalaemic metabolic alkalosis |
| Third-spacing | Fluid sequestered in bowel lumen and peritoneal cavity → effectively lost from circulation |
| Reduced oral intake | NPO + nausea → no fluid input |
| Defective intestinal absorption | Oedematous bowel wall cannot absorb water/electrolytes [4] |
| Transudation | Hypersecretion and loss of fluid to extracellular space and peritoneal cavity [1] |
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
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
Pathophysiology cascade:
- Bacterial translocation from ischaemic bowel → bacteraemia
- Systemic inflammatory response (SIRS): fever/hypothermia, tachycardia, tachypnoea, leucocytosis/leucopenia
- Sepsis → septic shock → MODS (renal failure, respiratory failure, hepatic dysfunction, DIC, cardiovascular collapse)
This is the mechanism underlying the high mortality of strangulated obstruction.
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
C. Post-Operative / Treatment-Related Complications
These complications arise from the surgical treatment of IO rather than from the obstruction itself.
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
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
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)
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
- 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
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
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
D. Disease-Specific Complications
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]
- 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]:
- 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]
- 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]
| Category | Complication | Pathophysiological Basis |
|---|---|---|
| Local | Strangulation / Ischaemia | ↑ Intraluminal pressure / direct compression / mesenteric vessel occlusion → venous congestion → arterial compromise → ischaemia |
| Perforation | Transmural necrosis → loss of wall integrity → spillage of luminal contents | |
| Closed-loop obstruction | Obstruction at 2 points → rapid pressure rise → accelerated ischaemia and perforation | |
| Bacterial translocation | Mucosal barrier breakdown from ischaemia → bacteria cross bowel wall → bacteraemia, peritonitis | |
| Systemic | Dehydration and electrolyte disturbance | Vomiting, third-spacing, reduced intake, defective absorption |
| Aspiration pneumonia | Regurgitation of stagnant bowel contents → aspiration into lungs | |
| Sepsis / MODS | Bacterial translocation → SIRS → septic shock → organ failure | |
| VTE (DVT/PE) | Virchow's triad: stasis, dehydration/hypercoagulability, endothelial injury | |
| Post-operative | Anastomotic leak | Poor healing at bowel join → faecal peritonitis |
| Recurrent adhesive SBO | Surgery causes new adhesions → recurrent obstruction (~30%) | |
| Wound infection | Contaminated/dirty surgical field | |
| Post-operative ileus | Peritoneal inflammation, electrolyte disturbance, opioids | |
| Short bowel syndrome | Extensive resection → insufficient absorptive surface | |
| Stoma complications | High output, parastomal hernia, prolapse, retraction, skin excoriation |
The prognosis of IO depends entirely on whether complications develop:
| Scenario | Mortality |
|---|---|
| Non-strangulating obstruction | 2% [1] |
| Strangulating obstruction | 10–30% [1] |
| Emergency surgery for colonic obstruction | More than 10% [1] |
| Faecal peritonitis from perforation | 30–50% |
| Neonatal midgut volvulus with extensive necrosis | Very high; survivors may have lifelong SBS |
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
High Yield Summary — Complications of IO
-
Strangulation is the most feared complication: mortality jumps from 2% (simple) to 10–30% (strangulated). Accelerated in closed-loop obstruction and volvulus.
-
Signs of strangulation: constant pain (not colicky), fever, tachycardia, peritonism, leucocytosis, metabolic acidosis/raised lactate, pneumatosis intestinalis, portal venous gas.
-
Perforation: end-stage of ischaemia → faecal peritonitis → sepsis → death. Caecum is most vulnerable site in LBO (Laplace's law: largest radius = greatest wall tension).
-
Systemic: Dehydration (hypoK, metabolic alkalosis from vomiting; metabolic acidosis from ischaemia), aspiration pneumonia (prevented by NG decompression), sepsis/MODS (from bacterial translocation), VTE.
-
Post-operative: Anastomotic leak (especially left-sided colonic surgery — why Hartmann's is preferred), recurrent adhesive SBO (~30%), wound infection, post-op ileus, short bowel syndrome, stoma complications.
-
Disease-specific: HAEC in Hirschsprung's (up to 45%); perforation in intussusception reduction ( < 1%); adhesive SBO after Ladd's procedure.
-
Emergency surgery for colonic obstruction mortality > 10% — driven by comorbidity and advanced malignancy.
Active Recall - Complications of Intestinal Obstruction
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)
High Yield Summary
Definition: IO = any impediment to aboral passage of intestinal contents. Mechanical (physical barrier) vs. Functional (ileus/pseudo-obstruction).
Epidemiology: SBO accounts for ~80% of mechanical IO. LBO ~15%. Most common causes: SBO = adhesions > hernia > cancer; LBO = cancer > volvulus > diverticulitis.
Risk Factors: Prior surgery (adhesions), hernia, malignancy, medications (opiates, anticholinergics), metabolic (hypoK, hypothyroid).
Pathophysiology cascade: Obstruction → proximal dilatation (gas + fluid) → ↑ intraluminal pressure → venous congestion → oedema → arterial compromise → ischaemia → necrosis → perforation → peritonitis/sepsis. Dehydration from vomiting, third-spacing, impaired absorption.
Cardinal Features (4): Pain (colicky → constant if strangulation), Vomiting (early in proximal SBO; late/feculent in distal), Distension (greater with distal obstruction), Absolute constipation (complete obstruction).
Key Signs: Dehydration, high-pitched tinkling bowel sounds (early) → absent (late), abdominal tenderness (peritonism = strangulation), empty rectum on PR (mechanical LBO), visible peristalsis, hernial orifices must be checked.
Closed-loop obstruction: Obstruction at 2 points, rapid ischaemia risk. Examples: LBO + competent ileocaecal valve, volvulus, hernia.
Neonatal IO: Bilious vomiting = malrotation with midgut volvulus until proven otherwise. Key causes: intestinal atresia, malrotation, meconium disease, Hirschsprung's disease.
Classification: By anatomy (SBO/LBO), mechanism (mechanical/functional), completeness (partial/complete), complexity (simple/strangulating/closed-loop), relation to wall (intra/intramural/extramural).
High Yield Summary — Differential Diagnosis of IO
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First question: Is it truly IO or a mimic? (Pancreatitis, mesenteric ischaemia, DKA, peritonitis, GE, urinary retention can all mimic IO)
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Second question: Mechanical or functional? — Differentiate by bowel sounds (↑↑ = mechanical; ↓/absent = ileus; normal = pseudo-obstruction), PR exam (empty rectum = mechanical LBO; dilated = pseudo-obstruction), and imaging (transition point = mechanical)
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Third question: If mechanical, SBO or LBO? — SBO: ABC (Adhesions, Bulge/hernia, Cancer); LBO: Cancer, Volvulus, Diverticular stricture, Pseudo-obstruction
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Neonatal IO: Bilious vomiting = malrotation with midgut volvulus until proven otherwise. DDx includes intestinal atresia, meconium disease, Hirschsprung's disease, NEC.
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Sigmoid volvulus DDx: Toxic megacolon (systemic toxicity, bloody diarrhoea, C. difficile) vs. Ogilvie's (hospitalised, normal bowel sounds, dilated rectum, gas in rectum)
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Always check: hernial orifices, surgical scars, medications (opioids, anticholinergics), metabolic panel (K⁺, TFT, glucose), strangulation signs (constant pain, peritonism, fever, lactate)
High Yield Summary — Diagnosis of IO
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IO is a clinical-radiological diagnosis — no formal scoring criteria exist. Combine cardinal features + imaging.
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First-line imaging: Erect CXR (rule out perforation) + Supine and Erect AXR (confirm IO, distinguish SBO vs LBO, detect complications).
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AXR systematic review [1]: Dilated loops? Air-fluid levels? Gas in colon/rectum? Strangulation signs (thumbprinting, pneumatosis, free gas)? Massive colonic dilatation? Air in biliary tree?
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CT abdomen with IV contrast is more sensitive than plain AXR [1] — identifies transition point, cause, viability (bowel wall enhancement), and complications. Use rectal contrast for LBO.
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Gastrografin follow-through for adhesive SBO: diagnostic AND therapeutic. 2-hour film is key. Contrast in colon = partial obstruction = likely to resolve conservatively.
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Key bloods: Lactate (ischaemia), ABG (alkalosis from vomiting vs acidosis from ischaemia), K⁺ (hypokalaemia), WCC (infection/strangulation).
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Endoscopy: Diagnostic and therapeutic — decompression in sigmoid volvulus/pseudo-obstruction; stenting in CRC. Caution: avoid excessive gas insufflation [1].
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Neonates: Upper GI contrast study is gold standard for malrotation; contrast enema + rectal biopsy for Hirschsprung's.
High Yield Summary — Management of IO
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All patients: Resuscitation first — "Drip and Suck" (IV fluids + NG decompression). NPO, antibiotics if complicated, monitoring.
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Conservative Mx indicated for: partial obstruction, adhesive SBO, Crohn's stricture, radiation stricture, disseminated malignancy. Monitor for 48–72h. Gastrografin is both diagnostic and therapeutic.
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Urgent surgery indicated for: strangulated hernia, proven/suspected strangulation, peritonitis, pneumoperitoneum, pneumatosis intestinalis, closed-loop obstruction, volvulus with peritoneal signs.
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Adhesive SBO: Conservative Mx ~50–80% effective. Gastrografin follow-through guides decision. Surgery = adhesiolysis; resect only causative bands.
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Obstructing CRC: Right-sided → resection + primary anastomosis. Left-sided → Hartmann's (most common emergency procedure) or primary anastomosis with on-table lavage (good-risk patients) or SEMS bridge-to-surgery.
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Sigmoid volvulus: Endoscopic decompression first-line (50% recurrence → consider elective sigmoidectomy). Caecal volvulus → right hemicolectomy.
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Pseudo-obstruction: Supportive → neostigmine → colonoscopic decompression → caecostomy.
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Bowel viability: Assess colour change, pulsation, shiny serosa, peristalsis. Non-viable → resect.
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Neonatal IO: NPO + TPN + IV antibiotics. Surgery if pneumoperitoneum, deterioration, or failed medical Rx.
High Yield Summary — Complications of IO
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Strangulation is the most feared complication: mortality jumps from 2% (simple) to 10–30% (strangulated). Accelerated in closed-loop obstruction and volvulus.
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Signs of strangulation: constant pain (not colicky), fever, tachycardia, peritonism, leucocytosis, metabolic acidosis/raised lactate, pneumatosis intestinalis, portal venous gas.
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Perforation: end-stage of ischaemia → faecal peritonitis → sepsis → death. Caecum is most vulnerable site in LBO (Laplace's law: largest radius = greatest wall tension).
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Systemic: Dehydration (hypoK, metabolic alkalosis from vomiting; metabolic acidosis from ischaemia), aspiration pneumonia (prevented by NG decompression), sepsis/MODS (from bacterial translocation), VTE.
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Post-operative: Anastomotic leak (especially left-sided colonic surgery — why Hartmann's is preferred), recurrent adhesive SBO (~30%), wound infection, post-op ileus, short bowel syndrome, stoma complications.
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Disease-specific: HAEC in Hirschsprung's (up to 45%); perforation in intussusception reduction ( < 1%); adhesive SBO after Ladd's procedure.
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Emergency surgery for colonic obstruction mortality > 10% — driven by comorbidity and advanced malignancy.
Intestinal Ischemia
Intestinal ischemia is insufficient blood flow to the intestines, either acute or chronic, caused by arterial occlusion, venous thrombosis, or nonocclusive hypoperfusion, potentially leading to bowel infarction and necrosis.
Intussusception
Intussusception is the telescoping of a proximal segment of bowel into an adjacent distal segment, causing intestinal obstruction and potentially compromising mesenteric blood supply.