Intestinal Obstruction — Small vs Large Bowel, X-ray Signs, Volvulus, Intussusception and Management

Intestinal obstruction means that bowel contents cannot pass normally along the gut. It is one of the commonest surgical emergencies: small bowel obstruction (SBO) alone accounts for 15% to 20% of hospital admissions for acute abdominal pain and about 80% of all bowel obstructions; the rest are large bowel obstructions (LBO).

• Mechanical vs functional — mechanical obstruction has a physical barrier; functional obstruction (paralytic ileus, pseudo-obstruction) is failure of peristalsis without a block.
• By site of the mechanical block — intraluminal (gallstone ileus, foreign body, bolus), intramural (tumour, Crohn stricture) or extrinsic (adhesions, hernia, volvulus).
• Simple vs strangulated — simple obstruction blocks the lumen without ischaemia; strangulated obstruction compromises the blood supply and can progress to necrosis and perforation.
• Open-loop vs closed-loop — a closed loop is blocked at both ends (volvulus, a band, or a colonic block with a competent ileocaecal valve) and is at high risk of ischaemia and perforation.
• Complete vs partial, and small vs large bowel — these decide the clinical picture and whether a trial of non-operative treatment is safe.

The site of the block also shapes the small-bowel picture. Proximal SBO gives heavy vomiting, little distension and early dehydration and electrolyte loss. Distal SBO gives more distension, later vomiting and slower systemic upset.

Adhesions form after as many as 97% of common abdominal operations such as appendicectomy, colectomy and gynaecological surgery; the risk of SBO rises with the number of previous operations. Women are more prone to adhesive SBO (gynaecological surgery), men to hernia-related obstruction — so always examine the hernial orifices in a patient with SBO.

Gallstone ileus is a rare intraluminal cause: a gallstone enters the bowel through a biliary-enteric fistula and usually impacts near the ileocaecal valve. Imaging shows the Rigler triad — small bowel obstruction, pneumobilia and an ectopic gallstone. Colonic volvulus is uncommon in the United States (about 4% of LBO) but causes around half of colonic obstructions in the 'volvulus belt', which includes India, Africa, the Middle East, South America and Russia.

1. Proximal distension with swallowed air and secretions; peristalsis above the block first increases (colic), while the bowel below collapses.
2. Third-space loss — the wall becomes leaky, so fluid and electrolytes are lost into the lumen and peritoneal cavity; with vomiting and poor intake this causes dehydration and hypovolaemia, sometimes prerenal acute kidney injury.
3. Electrolytes — vomiting produces hypokalaemia, hyponatraemia and metabolic alkalosis; lactic acidosis suggests ischaemia.
4. Venous congestion and ischaemia — rising wall pressure impairs venous return, then arterial inflow, leading to mucosal ischaemia, bacterial translocation (notably E. coli) and, finally, necrosis, perforation and peritonitis.
5. Systemic response — fluid loss, translocation and ischaemia drive SIRS, septic shock and multiorgan failure; delayed treatment of strangulation carries a mortality above 25%.

In LBO the ileocaecal valve matters. If it is incompetent, the colon decompresses into the small bowel and the patient eventually vomits. If it is competent, the colon becomes a closed loop that keeps distending. The caecum has the largest diameter and thinnest wall, so it is the usual site of perforation — progressive right iliac fossa pain warns of impending caecal perforation.

The cardinal features are colicky abdominal pain, vomiting, abdominal distension and absolute constipation (obstipation). Vomitus starts as gastric content and becomes bilious as the block becomes more distal. Partial obstruction may still allow some stool or flatus early on.

• History — previous abdominal surgery (adhesions), known hernia, weight loss or change in bowel habit (colorectal cancer), Crohn disease, radiotherapy, opioids or anticholinergics (dysmotility).
• Examination — dehydration and tachycardia; distension; visible peristalsis in thin patients; check the hernial orifices; scars; rectal examination for an empty rectum, mass, blood or faecal impaction.
• Bowel sounds — may be hyperactive or high-pitched early; they may become absent with strangulation or ischaemia.
• Investigations — CBC, electrolytes and renal function, blood gas and lactate, amylase/lipase, and blood cultures if sepsis is suspected.

A supine abdominal radiograph (with an erect film or erect chest X-ray) is often the first image. In high-grade SBO the triad of multiple air-fluid levels, distended small bowel loops and absent colonic gas is characteristic, but plain films are insensitive — about 50% to 80% for SBO — and cannot reliably show the cause or strangulation.

Look also for complications: free gas under the diaphragm or Rigler sign (perforation), and gas in the bowel wall (pneumatosis) or portal venous gas, which suggest ischaemia. Portal venous gas reaches the periphery of the liver, whereas pneumobilia stays central.

• CT abdomen — the gold standard for SBO. It confirms the diagnosis, finds the transition point and cause (hernia, tumour, gallstone), and separates simple from strangulated obstruction. Closed-loop configuration, signs of ischaemia and free fluid mean surgery without delay.
• Ultrasound — no radiation and repeatable; a small bowel loop over 3 cm suggests obstruction or ileus, and a thick-walled non-compressible loop beside a collapsed loop marks the transition point. It does not replace CT.
• Water-soluble contrast (Gastrografin) — both diagnostic and therapeutic in adhesive SBO (see management).
• Contrast enema — reliably separates a mechanical LBO from pseudo-obstruction and may show or even reduce a volvulus.
• MRI — for pregnant patients or when CT is contraindicated. Colonoscopy (minimal insufflation) gives tissue in suspected cancer; the whole colon must be assessed because of synchronous lesions.

1. Resuscitate ('drip') — isotonic IV fluids (Ringer lactate or normal saline); correct hypokalaemia and metabolic alkalosis.
2. Decompress ('suck') — nasogastric tube to relieve vomiting and distension and reduce aspiration risk; keep the patient nil by mouth.
3. Antibiotics covering gram-negative and anaerobic gut flora when strangulation or perforation is suspected.
4. Early surgical review and serial examination, vital signs and lactate.

In adhesive SBO without peritonitis, strangulation or ischaemia, the WSES Bologna guidelines make non-operative management the strategy of choice; a trial can safely continue for up to 72 hours. A water-soluble contrast (Gastrografin) challenge helps decide: if contrast has not reached the colon on an X-ray 24 hours after it is given, non-operative treatment is very likely to fail.

Surgery is tailored to the cause: adhesiolysis (open or laparoscopic), hernia reduction and repair, resection of non-viable bowel with primary anastomosis or a stoma, and a second-look laparotomy when viability is doubtful. For left-sided malignant LBO, a self-expanding colonic stent can decompress the colon as a bridge to elective surgery or as palliation; emergency surgery often needs a stoma and carries higher morbidity. Recurrent SBO occurs in 12% to 32% after surgery.

A volvulus needs a redundant loop on a narrow-based mesentery. By site, colonic volvulus involves the sigmoid (about 80%), caecum (about 15%), transverse colon (3%) and splenic flexure (2%).

Intussusception is telescoping of one bowel segment (the intussusceptum) into the adjacent distal segment. In children it is usually idiopathic, most often the ileum entering the caecum (ileocolic), with a peak age of 6 to 18 months and a male-to-female ratio of about 3:1. It rises during viral gastroenteritis seasons; adenovirus is the strongest associated infection. Only about 10% have an anatomic lead point (Meckel diverticulum, polyp, duplication).

• Symptoms — episodic colicky pain with the child drawing the legs up, vomiting (may be bilious), then lethargy.
• Classic triad — pain, a palpable sausage-shaped mass and 'red currant jelly' stool (blood, mucus and sloughed mucosa) — but the jelly stool appears in only a minority, so any bloody stool in an infant should raise the possibility.
• Dance sign — emptiness of the right lower quadrant on palpation.
• Ultrasound is the test of choice: a target or doughnut sign, usually about 3 cm across, on transverse section.
• Treatment — air (pneumatic) or hydrostatic contrast enema, which both confirms and reduces it; surgery (laparoscopic or open) if enema reduction fails or complications occur.

Adult intussusception is different: it causes only about 1% of bowel obstructions, presents with vague or intermittent pain, and in more than 90% has a pathological lead point, most often a neoplasm. CT is preferred for diagnosis, and enema reduction is not used — adults usually need resection.

With malrotation, the small bowel mesentery has a narrow base and can twist around the superior mesenteric artery, cutting off blood supply to most of the midgut. Ladd bands run from the caecum across the second part of the duodenum and can also obstruct it. Midgut volvulus can occur at any age but is most common in the first few weeks of life.

• Bilious vomiting is usually the first feature; an infant with sudden bilious vomiting, upper abdominal distension and deterioration needs urgent evaluation.
• Imaging — upper GI contrast study (stable child, no peritonitis) may show a corkscrew jejunum or complete duodenal obstruction with small bowel lying on the right; ultrasound shows the SMV anterior to or left of the SMA and the whirlpool sign.
• Treatment — emergency laparotomy: untwist the bowel counterclockwise ('turning back the hands of time'), then the Ladd procedure — divide the Ladd bands so the duodenum falls to the right and the caecum to the left, and perform an appendicectomy.
• Complication — delayed treatment causes gangrene of most of the small bowel and short bowel syndrome.

Paralytic ileus is functional obstruction from failed peristalsis — after surgery, with electrolyte disturbance, sepsis or drugs such as opioids. It is treated supportively: bowel rest, correcting metabolic abnormalities, cutting down opioids, and sometimes a prokinetic such as metoclopramide.

Acute colonic pseudo-obstruction (Ogilvie syndrome) is massive colonic dilatation without a mechanical block, usually in critically ill men over 60. It is thought to reflect excess sympathetic over parasympathetic activity. Patients may still pass flatus; pain is less prominent; X-ray shows marked caecal and colonic dilatation with gas reaching the rectum, and air-fluid levels are typically absent. A contrast enema separates it from mechanical LBO.