What is the aetiology of small-bowel obstruction?
- Adhesions (60%): usually secondary to previous abdo surgery
- Hernia
- Malignancy
- Crohn’s disease
What is the pathophysiology of small-bowel obstruction?
- Mechanical obstruction is most common
- Obstruction leads to bowel distension above the block with increased fluid secretion into the distended bowel
- Also leads to proximal dilatation above the block (causes increased secretion and swallowed air in the SB)
- More dilatation causes decreased absorption and mucosal wall oedema
- Increased pressure with the intramural vessels becoming compressed, resulting in ischaemia and/or perforation
- Untreated obstruction leads to ischaemia, necrosis and perforation
What is the presentation of small-bowel obstruction?
- Pain – initially colicky then diffuse (higher in abdo than large bowel obstruction)
- Profuse vomiting following pain (occurs earlier than in large bowel obstruction)
- Less distension than large bowel obstruction
- Nausea and anorexia
- Tenderness suggests strangulation and urgent surgery is required
- Constipation with no passage of wind occurs late
- Increased bowel sounds
How is small-bowel obstruction investigated?
- Abdominal x-ray: central gas shadows that completely cross the lumen, no gas in large bowel, distended loops of bowel proximal to obstruction, increased bowel sounds
- Examination of hernia orifices and rectum
- FBC essential
- CT is gold standard to localise lesion accurately
How is small-bowel obstruction managed?
- Aggressive fluid resuscitation
- Bowel decompression
- Analgesia and antiemetic
- Antibiotics
- Surgery to remove obstruction
What is the aetiology of large bowel obstruction?
- 90% due to colorectal malignancy
- Volvulus is most common cause in African countries
What is the pathophysiology of large bowel obstruction?
- Similar to SBO, but colon proximal to obstruction dilates
- Increased colonic pressure and decreased mesenteric blood flow results in mucosal oedema
- Can compromise arterial blood supply and cause mucosal ulceration
In colonic volvulus: - 360o axis rotation results in a closed loop obstruction
- Fluid and electrolytes shifts into the closed loop
- Results in increased pressure and tension in the loop causing impaired colonic blood flow
What is the presentation of large bowel obstruction?
- Abdominal pain is more constant than in SBO
- Abdominal distension
- Bowel sounds normal then increased then quiet later
- Palpable mass e.g. hernia, distended bowel loop or caecum
- Late vomiting which is more faecal like (suggestive of LBO)
- Vomiting may be absent
- Constipation
- Fullness/ bloating/ nausea
How is large bowel obstruction investigated?
- DRE (empty rectum, hard stools, blood)
- FBC is essential (see low Hb if chronic occult blood loss)
- Abdominal XR (peripheral blood shadows proximal to the blockage, caecum and ascending colon distended)
How is large bowel obstruction managed?
- Aggressive fluid resuscitation
- Bowel decompression
- Analgesia and antiemetic
- Antibiotics
- Surgery to remove obstruction (if due to malignancy, then colorectal stents followed by elective surgery)
What is the aetiology of bowel pseudo-obstruction?
- 80% is a complication of other conditions:
- Intra-abdominal trauma, pelvic, spinal and femoral fractures
- Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic, neuro
- Intra-abdominal sepsis
- Pneumonia
- Drugs e.g. opiates and antidepressants
- Metabolic disorders e.g. electrolyte disturbances, malnutrition
What is the presentation of bow pseudo-obstruction?
- Rapid and progressive abdominal distension with pain
How is bow pseudo-obstruction investigated?
- XR shows gas-filled large bowel
How is bowel pseudo-obstruction managed?
- Treat underlying problem e.g. withdrawal of opiate analgesia
- IV neostigmine
What is the pathophysiology of diverticulitis?
- Low fibre diet increases intestinal transit time and decreases stool volume resulting in increased intraluminal pressure and colonic segmentation, which predisposes to diverticular formation
- Commonly form where vasa recti penetrate the colonic all, and food particle or faecal material may contribute to the development of infection
What are the risk factors of diverticulitis?
- Low dietary fibre
- Age >50
- Western diet
- Obesity (BMI>30)
- Use of NSAIDs
What is the presentation of diverticulitis?
- Lower left quadrant pain
- Leukocytosis
- Fever
- Rectal bleeding
- Guarding and tenderness in lower left quadrant
- Bloating
- Constipation
What are the differential diagnoses of diverticulitis?
- Endometriosis
- Colorectal cancer
- Appendicitis
- Ulcerative colitis
- Crohn’s disease
- UTI
- Pyelonephritis
- Ischaemic colitis
- Pelvic inflammatory disease
- IBS
How is diverticulitis investigated?
- FBC with differential (polymorphonuclear leukocytosis)
- Abdominal x-ray (free air in bowel perforation)
- Abdo CT (thickening of bowel wall, mass, abscess)
How is diverticulitis managed? (Asymptomatic and symptomatic)
- No treatment if asymptomatic
- Symptomatic then dietary modification and fibre supplementation + oral antibiotic therapy
What is the aetiology of gastritis?
- Most commonly due to H. Pylori infection
What is the pathophysiology of gastritis?
- H. Pylori infection induces a severe inflammatory response with gastric mucin degradation
- NSAIDs and alcohol decrease gastric mucosal blood flow with loss of the mucosal protective barrier
What are the risk factors of gastritis?
- Helicobacter pylori infection
- NSAID use
- Alcohol use/ toxic ingestion
- Previous gastric surgery
- Critically ill patients
- Autoimmune disease
- Immunocompromised
What is the presentation of gastritis?
- Dyspepsia/epigastric discomfort
- Nausea, vomiting and loss of appetite
- Fever
- Acute abdominal pain
- Cognitive impairment
