Gastrointestinal Surgery Flashcards
ACUTE ABDOMEN
Acutely ill where signs and symptoms are chiefly abdominal; Abdominal pain and tenderness,
Colicky pain, Distention and swelling etc
ACUTE ABDOMEN Investigations and Management
• Investigations – U&E, FBC, Amylase, LFT, CRP, ABG (? Ischaemia), Blood cultures
o AXR, CT and USS Abdo, CXR if >50yrs or Peritonitis; ECG if >50yrs
o Rigler’s Double Wall Sign and Football Sign – Pneumoperitoneum
o Sentinel Loop – Focal area of Adynamic ileus provides clues as to source of
inflammation e.g. Appendicitis, Pancreatitis
• Initial Management – Management of Shock (Oxygen, Fluid resuscitation), Crossmatch and
G+S, Antibiotic Prophylaxis, Pain Management, Nil by mouth in case of emergency surgery
o Broad spectrum regime e.g. Cefuroxime and Metronidazole
Differential Diagnosis • Organ Rupture
(Spleen, Aorta, Ectopic Pregnancy); Hypovolaemic shock would be key
presentation; History of blunt (Spleen, may occur weeks after) or penetrating (Liver) trauma
o Always exclude pregnancy in females of reproductive age
Differential Diagnosis • Peritonitis
(Peptic Ulcer Disease, Diverticulum, Ruptured Appendicitis, Bowel Perforation, Gallbladder perforation); Prostration, Shock, Lying still and pain on coughing
o Abdominal rigidity + Guarding, Absent bowel sounds, Tenderness ± Rebound
Differential Diagnosis • Local Peritonitis
Diverticulitis, Cholecystitis, Salpingitis, ± Abscess formation
Differential Diagnosis • Colic
– Regular, waxing/waning pain rhythm caused by spasm of hollow viscera e.g. Intestine Ureter, Bile ducts (NB: Gallbladder pain typically dull and constant)
Differential Diagnosis • Intestinal Obstruction
Vomiting, Nausea, Anorexia, Colic and Constipation (Discussed in
subsequent section)
Differential Diagnosis
• Surgical Emergencies
Mesenteric Ischaemia, Acute Pancreatitis, Ruptured AAA
Differential Diagnosis
Medical Causes
Irritable Bowel Syndrome, MI, Infective (Pneumonia, Gastroenteritis, Herpes Zoster, Typhoid, Cholera), Metabolic (Diabetic Ketoacidosis, Porphyria, Thyroid)
Peritonitis
• Acute inflammation of the Peritoneal cavity; Primary Peritonitis typically due to streptococcal
infection via bloodstream; Secondary causes more common
• Secondary Peritonitis – Appendicitis, Ruptured Diverticular disease, Upper GI perforation,
Perforated ischaemic bowel, Perforated tumours, Acute Pancreatitis
• Could also be Post-operative complication, Complication of Peritoneal dialysis
Presentation of Peritonitis
• Anorexia, Fever, Severe Generalised abdominal pain which may radiate to shoulders and
back; Worsen on movement, coughing and sneezing
• Tachycardia, Guarding, Abdominal rigidity, Palpable masses
Diagnosis and Management of Peritonitis
• Investigations – FBC (Neutrophilia), CRP, Amylase, CT Abdomen, Exploratory laparoscopy
• Emergency Management – Large IV access, Catheterisation, Blood for FBC, U&E, CRP,
Amylase, G+S, NBM and ABG
Anatomy of Appendix
• Vermiform appendix located at the end of the Caecum
near the Ileocaecal junction; Has its own mesentery
(Mesoappendix) and sole blood supply (Appendiceal
Artery, Br Ileocaecal artery)
• Most commonly Retrocaecal, also Pelvic or Subcaecal
• Taenia Coli converge at base of the Appendix
Presentation of Appendicitis
• Classically central pain migration to RIF associated with N+V, Anorexia; Occurs in less than half
• Most common presentation Abdominal pain exacerbated by movement; Generally unwell,
weak, cold, clammy; Migratory pain is strongest symptom associated with Appendicitis
• Guarding, Rebound or Percussion tenderness suggests Local Peritonism; Rosving’s and Psoas
sign are of limited diagnostic value
• If no signs of Peritonism, Normal blood results and Normal US, Very low risk of Appendicitis
• Alvarado score (≥7 predictive; <5 against) – RIF tenderness (2), Rebound Tenderness (1), RIF
migratory pain (1), Anorexia (1), N+V (1), Fever (1), Leukocytosis (2), Left shift neutrophils (1)
Pathology of Appendicitis
• Neutrophilic infiltrate of the Muscularis Propria (Circular and Longitudinal layers)
• May progress to Perforation, forming a Mass (Densely adherent Caecum and Omentum
forming a mass), RIF abscess (Retrocaecal) and Pelvic abscess (Pelvic)
• Caused due to blockage of the appendix opening leading to increased pressure, decreased
perfusion and increased bacterial growth leading to inflammation and distention
o Blockage commonly caused by calcified faeces or inflamed lymphoid tissue
Differential Diagnosis for RIF Pain Children
Non-specific Adenitis, Merkel’s Diverticulum, Ovarian cyst/Menstrual symptoms
Differential Diagnosis for RIF Pain Adults
Crohn’s, Merkel’s Diverticulitis, Gastroenteritis, Pancreatitis, Renal colic, Ectopic
pregnancy, Ovarian cyst, Infection, Menstrual pain
Differential Diagnosis for RIF Elderly
Caecal Diverticulitis, Caecal tumours, Sigmoid Diverticulitis, Ovarian cysts, tumours
Management of Acute Appendicitis
• A-E Assessment
• FBC, U&E, CRP, Blood cultures, Crossmatch if required
o Beta HCG for Women of Childbearing Age
o Urinalysis – Renal Colic, UTI; NB: Pyuria can occur due to Appendicitis in 40%
o Elevated WBC, CRP, Neutrophilia suggestive of Appendicitis
• CT with IV contrast offers best chance of diagnosis; CI in Pregnancy and Young; Alternatively,
US or MRI; Identifies inflammatory response to Appendicitis
• IV Antibiotics given at induction; continued if perforated
• Evidence of Sepsis require urgent surgery; IV Abx alternatively for high-risk, or unfit
• Open or Laparoscopic Appendicectomy – Open approach involves Gridiron incision over
McBurney’s point (1/3 between Umbilicus and ASIS)
INTESTINAL OBSTRUCTION
- Mechanical/Functional obstruction of the Intestine which can occur distal to Duodenum
- Presents with Abdominal pain, Distention, Vomiting ± Faecal, Constipation
Small Bowel Obstruction
tends to be Colicky, central pain; Vomiting may occur before constipation while Large Bowel Obstruction tends to be lower in the abdomen and felt for
longer; Constipation occurs earlier and vomiting may be less prominent
Complicated by Dehydration, Electrolyte disturbances, Aspiration, Respiratory compromise
due to distention, Bowel Ischaemia or perforation
Simple obstruction
One point and no vascular compromise
Closed loop obstruction
2 points forming loop of grossly distended bowel; >12cm requires
urgent decompression
Strangulation
Compromise of blood supply; Sharper pain, more constant and localised;
Peritonism, Fever and ↑WBC (Mesenteric Ischaemia)
Small Bowel Causes
• Adhesions from previous surgery (Most common cause) • Hernia, Volvulus and Intussusception • SMA syndrome • Ischaemic strictures • Foreign body (and Gallstone Ileus) • Neoplasms – e.g. MALT Lymphoma • Inflammatory Strictures – Crohn’s • Pseudo-obstruction (Functional) • Intestinal Atresia
Large Bowel Causes
- Neoplasms
- Constipation, Faecal Impaction
- Diverticular disease
- Hernia, Volvulus and Adhesions
- Inflammatory Strictures – UC, Crohn’s
- Colon Atresia
- Pseudo-obstruction e.g. Hirschsprung’s
- Narcotic Drug use
Post-operative Ileus
Recovery time of 0 – 24 hours for Small bowel, 24 – 48 hours for
Stomach, 48 – 72 hours for Colon
o Reduced bowel motility = Absence of pain and bowel sounds
Paralytic Ileus
If obstruction is more than >72 hours post-operative
Primary Chronic Intestinal Pseudo-obstruction
Kawasaki’s, Chagas’, Parkinson’s,
Hirschsprung’s; Treated with Neostigmine or Colonoscopic decompression
Investigations of Obstruction
• AXR, CT Abdo, US Abdo, Biopsy of any masses; Presence of more than six gas-fluid levels on
supine and erect radiographs; Non-straight fluid levels
• Presence of water-soluble contrast in Caecum on abdominal radiograph within 24 hours (e.g.
Gastrografin) predicts conservative resolution
Resuscitation and Emergency Management of Obstruction
• 5.5% of small bowel obstruction ultimately fatal if treatment delayed; Strangulation and Large
Bowel Obstruction require surgery, Ileus and Small Bowel Obstruction can initially be
managed conservatively
• Nasogastric Tube, IV Fluids to rehydrate; Analgesia and Catheterize to monitor fluid status
• Treatment of the causative lesion e.g. Endoscopic stenting as palliation or bridging to surgery
Oesophageal Cancer Adenocarcinoma
Associated with GORD and Barrett’s Metaplasia, Dietary nitrosamines (e.g.
Smoked or fresh fish, Pickled fruit)
o Commonest in Western Europe, occurs in lower third of Oesophagus
o 5× more common in males
Oesophageal Cancer Squamous Carcinoma
Associated with Smoking, Alcohol, Poor diet, Chronic Achalasia and
Chronic caustic strictures
o Commonest in Japan, North China and South Africa, anywhere in Oesophagus
o 3× more common in males
Differential Diagnosis for Dysphagia (Difficulty) and Odynophagia (Pain on swallowing)
• Neurological causes – Stroke, Tumours, Neurodegenerative disease, Peripheral Neuropathy
• Mechanical Obstruction – Tumours, Inflammatory masses, Hiatus Hernia, Zenker’s
Diverticulum, Schatzhi Rings, Oesophageal webs, MSK issues
• Muscular issues – Muscular dystrophy, Achalasia, Hypertonic sphincter, Nutcracker
Oesophagus, Oesophageal Atresia
Presentation of Oesophageal Cancer
• Dysphagia – >45yrs new onset Dysphagia is tumour until proven otherwise
• Screened on follow up for Barrett’s Oesophagus/GORD; High grade dysplasia associated with
occult adenocarcinoma in 30% of patients
• Hematemesis, Cervical and Para-Aortic Lymphadenopathy, Hepatomegaly (Metastases)
• Other symptoms of local invasion e.g. Dysphonia (Recurrent Laryngeal Nerve), Cough and
Haemoptysis, SVC obstruction, Horner’s Syndrome
Oesophageal Cancer Risk Factors
Alcohol consumption, Tobacco use (any form), Radiation exposure, Obesity,
Red and processed meats, High temperature drinks, Diet lacking in fruits and vegetables
Oesophageal Cancer Investigations
• Flexible Oesophagoscopy/OGD and Biopsy
• Barium swallow indicated for failed intubation or suspected post-cricoid carcinoma which
might not be seen on endoscopy
• Endoluminal Ultrasound for invasiveness of tumour; CT regional staging and PET scan for
occult disseminated disease for patients considered for potentially curative treatment
Staging of Oesophageal Cancer
Tumour T1 = To Lamina/Submucosa T2 = To Muscularis Propria T3 = To Adventitia T4 = To adjacent structures Node N0 = No nodes (except Coeliac) N1 = Regional node involved (except Coeliac) Metastasis M0 = No distant metastasis M1 = Spread to other parts of the body e.g. Hepatic, Peritoneal, Coeliac Lymph
Oesophageal Cancer Curative Treatment
• Squamous Carcinoma – Radical Radio and Chemotherapy; Neoadjuvant Chemotherapy with Radical surgical resection • Adenocarcinoma – Neoadjuvant Chemotherapy with Radical surgical resection for large tumours; Surgical resection, Endoscopic Mucosal Resection (EMR) or Ablation for small or dysplastic disease
• Most present with incurable disease and require palliation; Dysphagia managed by Self-
Expanding Metal Stenting (SEMS) and External Beam Radiotherapy
• Systemic chemotherapy for treatment of metastases
GASTRIC CARCINOMA
Adenocarcinoma is common; can also be Gastrointestinal Stromal Tumours (Connective
tissue origins), Neuroendocrine (Carcinoid) or Lymphoid (Lymphoma)
o Adenocarcinoma – Most common >50yrs, 3× more common in males
GASTRIC CARCINOMA Risk factors
Nitrosamines, Chronic atrophic gastritis, Blood group A and H. pylori
GASTRIC CARCINOMA Presentation
Dyspepsia (New onset >45yrs Adenocarcinoma unless proven otherwise), Weight loss, Anorexia, Lethargy, Dysphagia (rare)
o Palpable Epigastric masses, Supraclavicular lymph nodes (in disseminated disease)
o Iron Deficiency Anaemia (due to chronic blood loss), Acute upper GI bleeding
Differential Diagnosis for Weight Loss (5% body weight over 6 months)
• Voluntary – Psychological causes (Anorexia Nervosa, Bulimia), Bariatric surgery, Lifestyle
• Involuntary – Malignant disease (Cachexia), Gastrointestinal (e.g. Coeliac) Endocrine
(Hypermetabolism), Cardiopulmonary (Cardiac cachexia), Alcohol, Muscular wasting diseases
Differential Diagnosis for Nausea
• Metabolic – Diabetic Ketoacidosis, Tubular Acidosis and Uraemia, Hypercalcaemia, Adrenal
Insufficiency, Liver failure, Toxins e.g. Chemotherapy, Antibiotics, etc.
• Neurological – Disequilibrium, Space-occupying Lesions, Hydrocephalus
• Gastrointestinal – Obstruction, Infection, Inflammatory disorders, Biliary colic
• Other causes – MI, Psychiatric illness (Anorexia, Bulimia, Depression), Malignant disease
H pylori
• H pylori associated with Non-Cardia Gastric cancer; 6× higher risk likely due to persistent
inflammation and Peptic Ulcer Disease (due to Mucosal erosion) leading to increased
malignant predisposition
• Linked to lower risks of Cardia Gastric cancer and Oesophageal Adenocarcinoma – Likely due
to decrease in stomach acidity in long term H pylori colonisation
GASTRIC CARCINOMA Investigations and Management
• Gastroscopy; Barium Meal X-Ray if
contraindicated
• Staging by CT CAP, Endoluminal Ultrasound,
Laparoscopy if considering resection
• Majority of tumours metastatic or
unresectable due to local metastasis
• Early Gastric Cancer (T1/2, N0/1, P0 H0)
o Attempted curative resection;
Radical gastrectomy with
Neoadjuvant Chemotherapy; Pre- and post-operative Chemotherapy
• Advanced Gastric Cancer – Local ablation, Palliative Chemotherapy for disseminated disease
Presentation of Acute GI Bleeding
• Haematemesis – Vomiting of bleed, indicating bleeding proximal to duodenojejunal junction
o Peptic Ulceration (Gastric or Duodenal) – Fresh with clots, may be with food
o Oesophageal Varices – Large amounts of dark red blood, features of portal HTN
o Oesophageal Trauma (e.g. Mallory-Weiss) – Small volumes of bright blood
o Aortoenteric Fistula – Large amounts of fresh blood
• Melaena – Passage of altered blood due to bleeding below gastro-oesophageal junction
Acute GI Bleeding Emergency Resuscitation and Investigations
• Large IV access; Fluid resuscitation up to 1000ml if tachycardic or hypotensive; Emergency
Type O Blood transfusion if extremis, otherwise wait for cross-matched blood; Catheterise
• Insertion of a Sengstaken-Blakemore Gastro-oesophageal Tube to stop bleeding
• FBC, U&E, LFT, Cross-match (at least 3 units if severe), Clotting (FFP and Vit K if INR > 1.4)
• Urgent Oesophageal-Gastro-Duodenoscopy (OGD) within 24 hours
• Angiography – May be suitable if bleeding was due to interventional radiology
Treatment of Gastrointestinal Bleeding
• Start IV Proton Pump Inhibitors and discontinue NSAIDs • Blood Transfusion if heavy blood loss or drop in Hb/Symptomatic Anaemia • Surgical Intervention if Massive Haemorrhage, Failure of Endoscopic intervention or Rebleeding which is unsuitable for Endoscopic intervention
Stages of Hypovolaemic Shock
Class I <750ml, <15% of blood volume, <100 bpm, UO >30, slightly anxious Class II 750-1500ml blood loss 15-30% blood loss Lower pulse pressure UO: 20-30 Mildly anxious Replace with IV crystalloids Class III and IV treat with blood transfusion
Occult Gastrointestinal Bleeding
• Presents initially as positive Faecal Occult Blood Test and/or Iron Deficiency Anaemia
• Thorough review of history and examination, especially drug history (NSAID use), family
history (Vascular abnormalities, Colorectal Cancer)
• Common causes include Reflux Oesophagitis, Ulceration, Varices, Duodenitis, Infections,
Meckel’s Diverticulum, Inflammatory Bowel Disease (Coeliac, Crohn’s, Ulcerative Colitis),
Diverticular disease, Vascular abnormalities
• Investigations – CT Imaging, OGD, Colonoscopy, Capsule and Balloon Enteroscopy
Prevention of Peptic Ulcer
- Lifestyle Advice – ETOH, Smoking cessation, reduce NSAID use
- PPI or H2 blockers, Antacids (e.g. Gaviscon)
- H pylori Eradication Therapy (Metronidazole, Clarithromycin, PPI)
Enterohepatic Circulation
• Blood enters the liver through the Hepatic Portal Vein (Formed of Superior Mesenteric,
Splenic and other smaller veins) as well as Left and Right Hepatic Arteries; Leaves the Liver
through the Inferior Vena Cava
• Bile leaves through the Left and Right Hepatic Ducts; Merge together to form the Common
Hepatic Duct, joints the Cystic Duct to form the Common Bile Duct which enters the second
part of the Duodenum at the Major Duodenal Papilla after merging with the Pancreatic Duct,
where it is guarded by the Sphincter of Oddi
• Bile salts are only reabsorbed at the Ileum; Re-enters Enterohepatic circulation for recycling
Metabolism of Haemoglobin and Bilirubin
• Haemoglobin broken down into Haem and Globin chains; Globin chains are recycled into
amino acids in the Liver
• Haem is broken down to form Iron (Which is recycled) and Biliverdin; Biliverdin is reduced to
form Unconjugated Bilirubin; Conjugation to Glucuronic acid by Liver enzymes (e.g. UDP
Glucuronosyltransferase) and excretion into Bile
• Dehydroxylation of Bile salts by Bacteria forms lipid soluble,
deconjugated bile acids (Urobilinogen) which are passively
reabsorbed; C/f Ionized conjugated primary bile salts need
active transport
• Some reabsorbed Urobilinogen excreted in urine as Urobilin;
Some Urobilinogen converted to Urobilin and Stercobilin in the
Colon is excreted in the faeces
Presentation and History of Jaundice
• Serum Bilirubin normally 3 – 17 μmol/L; Jaundice is clinically
apparent at levels around 50 μmol/L
• History taking – Family history of blood disorders, Recent travel, Change in
drugs/medications, Recent surgery/anaesthesia, History of Gallstones, Alcohol intake, Fever
• Investigations – FBC, Blood film, Clotting time, Hepatitis screen, Immunological tests (e.g.
Anti-Mitochondrial Antibodies in PBC)
Pre-Hepatic Causes
- RBC Abnormalities
- Autoimmune Haemolytic Anaemia
- Transfusion Reactions
- Drug Toxicity
Post-Hepatic Causes
- Gallstones
- Thromboembolism
- Parasitic Obstruction
- Tumour
- Congenital Atresia
- Sclerosing Cholangitis
Hepatic Unconjugated Hyperbilirubinaemia
o Gilbert’s Syndrome – Deficiency/Abnormality of Unconjugated Bilirubin Uptake
o Crigler-Najjar Syndrome – Abnormality in Conjugation enzymes
Hepatic Conjugated Hyperbilirubinaemia
o Infection – Viral (e.g. Hepatitis A, B, C, EBC CMV), Bacterial (e.g. Leptospirosis, Parasitic (e.g. Amoebic) o Drugs – e.g. Paracetamol overdose, Antipsychotics, Antibiotics o Non-infective Hepatitis E.g. Alcohol
Urobilinogen and Bilirubin content of stool and urine
• Urine Bilirubin is present in Obstructive causes (but Urobilinogen absent)
• Urine Urobilinogen in Pre-Hepatic causes (Bilirubin not normally found; Unconjugated
Bilirubin not water soluble)
• Gilbert’s Syndrome – High Urobilinogen but absence of Urinary Bilirubin
Mechanisms of Drug-induced Jaundice
- Haemolytic Anaemia – NSAIDs, Cephalosporins (Immune-related), G6PD related
- Drug-induced Hepatocellular Hepatitis – Paracetamol overdose, Alcohol abuse
- Hepatocanalicular hepatotoxicity – Chlorpromazine, Erythromycin
Management of Jaundice
• Hx – Hepatitis Exposure, Duration of Illness, Prodromal Illness, Dietary factors, IVDU or
Tattoos, MSM or Commercial Sex, Blood Transfusions, ETOH Intake, Travel, FMHx, Surgery,
Environmental Factors, Systemic symptoms
• O/E – Hepatomegaly, Splenomegaly, Ascites; Palpable (? Painless) Gallbladder
• Ix – FBC, U/Es, LFTs (AST, ALT, ALP, GGT), Albumin, Clotting, Ultrasound Abdomen
o Size of Biliary Ducts and Level of Obstruction if present; 75% of stones can be
identified on US, and nearly all tumours
o FNAC or Needle Biopsy for tissue diagnosis
Liver Cancer and Metastatic Disease
• Commonest tumours of Liver are through Metastasis due to Portal drainage system; Primary
tumours often in Pancreas, Colon, Stomach, Oesophagus and Breast
• 35% of patients who died of malignant disease have liver metastases; Soil and Seed
hypothesis, Mechanical hypothesis
Hepatocellular Carcinoma (HCC)
• 90% of Primary liver tumours but less than 1% of new cancers in the UK; Common in Africa
and Asia, more common in males
• Arises from Liver Parenchymal cells; spreads via local invasion through Portal vein or Hepatic
vein to other sites e.g. Lung metastasis
• Commonly presents as rapid deterioration of pre-existing cirrhosis
• Risk factors – Cirrhosis (HBV, HCV, ETOH XS), Aflatoxin exposure, Contraceptives, Androgens
Cholangiocarcinoma
More commonly Extrahepatic Biliary tree; Common sites include CBD, Common Hepatic duct
or Confluence of Hepatic ducts (Klatskin tumour)
Adenocarcinoma of the Gallbladder
- Associated with Gallstones, Ulcerative Colitis, Primary Sclerosing Cholangitis
- Often incidental finding cholecystectomy for RUQ pain; Gallbladder mass/obstructive jaundice
- Spread directly to Hepatic tissue, Hilar lymph nodes, or through blood vessels (Incurable)
Ampullary Carcinoma –
Small, early onset painless obstructive jaundice = Best prognosis
before invasion/metastasis
Fibrolamellar Hepatocellular Carcinoma (FHCC/FLC);
Rare; affects younger patients (30 –
40yrs); Does not occur in background of liver disease
o Presents as large, Vascular mass; Histology – Laminated fibrous layers
Angiosarcoma
o Less than 1% of Liver tumours, most common Sarcoma of the Liver
o Associated with Arsenic, Vinyl Chloride, Anabolic steroids and Contraceptives
Diagnosis of Liver Cancer
• AFP >500ng/ml; US Abdomen, Needle Biopsy, ERCP and Cytology; MRCP alternatively;
Percutaneous Transhepatic Cholangiography (PTC) and Biliary stenting
• CT staging for local spread and metastasis
Treatment of Liver Cancers • Surgical Resection
Needs to be fit for major surgery; No evidence of Metastasis or Lymph
node involvement, Tumours suitable for complete resection
o Partial Hepatectomy for HCC
o Liver Transplantation for HCC of Chronic Hepatitis
o Radical Cholecystectomy or Bile duct with reconstruction
o Pancreaticoduodenectomy (Whipple’s Procedure)
Treatment of Liver Cancers • Palliative Care
Endoscopic or Percutaneous Biliary Stenting, Percutaneous Thermal or
Radiofrequency Ablation of HCC
o Chemotherapy is of minimal benefit in Primary Liver/Biliary cancers
Gallstones Presentation
• Obstructive Jaundice, Biliary Colic (Intermittent severe Epigastric and RUQ pain), Nausea and
Vomiting, Tenderness over Gallbladder
• Murphy’s sign – Pain over gallbladder on inspiration
• Empyema, Abscess formation, Perforation and Biliary Peritonitis
• Cholecytoenteric Fistula leading to Gallstone ileus
• If CBD stone – Anorexia, Nausea, Itching, Dark urine and pale stools, low grade bile infection
o Ascending Cholangitis – Charcot’s Triad; Constant severe RUQ pain, Obstructive
Jaundice and high swinging fever
o CBD stones cause 60% of Acute Pancreatitis
Pathogenesis of Gallstone Formation
• Excessive Cholesterol relative to Bile salts and Lecithin leading to precipitation
• 10% Pure Cholesterol stones; Often solitary, large and round
• 10% Pure Pigment stones; Black (Haemolytic disease) and Brown (Chronic Cholangitis and
Biliary Parasites)
• 80% Mixed stones; Most common, often multiple stones
Risk Factors of Gallstone Formation
• Age, Female (Pregnancy, use of Oral Contraception), Multiparity
• Obesity, Chronic Haemolytic disorders (Pigment stones), Long Term
Parenteral disorders (Alteration of Bile content)
• Previous surgery (Vagotomy or Ileal/distal small bowel resection)
Management of Gallstones
• FBC, U&Es + Cr, LFTs (Conjugated Bilirubin and Alkaline Phosphatase),
Blood cultures, Serum amylase, AXR, Transabdominal Ultrasound
• MRCP if ultrasound inconclusive; ERCP if unable to tolerate or for
therapeutic interventions
o Endoscopic Sphincterotomy, Lithotripsy and Biliary Stent insertion
o Percutaneous Transhepatic Cholangiography if failure of ERCP
• Cholecystectomy – Laparoscopic, day case surgery; Indicated for symptomatic gallstones,
Asymptomatic but at risk of complications (Diabetic, Porcelain gallbladder, Pancreatitis,
Immunosuppressed patients)
• Medical Management – Percutaneous Drainage of Gallbladder, Dissolution therapy and
Extracorporeal Shockwave Lithotripsy (latter two rarely used)
Differential Diagnosis for Epigastric Pain
• Cholangitis and Biliary Colic, Intestinal Obstruction, Perforated Peptic ulcer, Hepatitis,
Mesenteric Ischaemia, Appendicitis, Pancreatitis
• Pulmonary and Pleural disease, Aortic dissection/AAA, Inferior MI
Anatomy of the Pancreas and Pancreatic Duct
• Uncus, Head, Neck, Tail; Head around Duodenum while Tail in contact with Spleen
• Receives blood supply from branches of Coeliac (Splenic, Pancreatoduodenal, etc) and drains
into Splenic vein (into Hepatic Portal vein)
• Pancreatic Duct drains exocrine secretions of the Pancreas; Joins Common Bile duct at the
Ampulla of Vater/Sphincter of Oddi
o Exocrine secretions – Bicarbonate (Centroacinar cells), Digestive Enzymes (Basophilic
cells) including Trypsinogen, Chymotrypsinogen, Pancreatic Lipases and Amylases
o Proteases secreted as Zymogens; Need to be converted e.g. By Enteropeptidase into
active forms (Trypsin, Chymotrypsin)
• Endocrine – Insulin (β cells) and Glucagon (α cells) from the Islets of Langerhans; Others include Somatostatin (δ cells) and Pancreatic Polypeptide (γ/PP cells)
Presentation of Acute Pancreatitis
• Severe Epigastric pain radiating to back; Severe Nausea and Vomiting
• Fever, Dehydration, Hypotension, Tachycardia, Epigastric tenderness, Guarding, Rigidity
• Grey-Turner’s sign (Left flank bruising) and Cullen’s sign (Periumbilical bruising) in 1-3% of
Haemorrhagic pancreatitis
• Classification of Acute Pancreatitis
o Oedematous (70%) ± Phlegmon production
o Severe/Necrotising (20%) with peripancreatic pseudocyst formation
o Haemorrhagic (5%)
• Hypocalcaemia due to precipitation and sequestration of Calcium as well as Albumin
depletion; Inflammatory reaction can lead to pulmonary complications e.g. ARDS
Causes of Acute Pancreatitis
- Common: Idiopathic, Gallstones, Ethanol, Traumatic, Steroids
- Mumps, Autoimmune, Snake/Scorpion bites, Hypercalcaemia, ERCP, Drugs
Management of Acute Pancreatitis
• Fluid resuscitation, catheterise; Consider central line and HDU management
• Investigations – FBC, U&E, LFT, Amylase/Lipase, G+S, Clotting panel
• AXR may reveal Gallstones and Pancreatic calcification; CT imaging; Ultrasound needs to be
done within 48 hours of admission
• Glasgow Imrie Criteria to assess severity of Acute Pancreatitis
• Urgent ERCP and stone extraction
• CT guided Pancreatic Aspiration for
Infected Necrosis; Early feeding to
reduce risk of Stress Ulceration and
Bacterial translocation
• Surgical debridement of proven
Infected Necrosis
• Mortality associated with Pancreatic
Necrosis and Sepsis (including MODS)
Chronic Pancreatitis Presentation and Pathogenesis
• Recurrent or persistent abdominal pain from the pancreas due to irreversible destruction and
fibrosis of Pancreatic parenchyma; Associated with Exocrine or Endocrine insufficiency
o Pain worsens with food and alcohol intake
o Anorexia, Weight loss, Steatorrhea, Insulin dependent Diabetes Mellitus
• May occur following Acute Pancreatitis, or progressive de novo
• May affect whole Pancreas or focal disease; Head tends to be affected more in alcohol abuse
• Glandular atrophy, Duct Ectasia, Microcalcification and Intraductal stone formation, Cystic
changes due to duct occlusion, Features of Acute Pancreatitis
Causes of Chronic Pancreatitis
• Acute Pancreatitis especially due to Alcohol abuse
• Pancreatic Duct obstruction; Cysts, Tumours, Congenital abnormalities, Strictures (Iatrogenic,
Parasitic), Cystic Fibrosis
• Autoimmune disease e.g. Primary Biliary Cirrhosis (PBC), Primary Sclerosing Cholangitis
Pancreatic Function Tests
• Secretin Stimulation Test – Secretin normally stimulates production of pancreatic fluid high in
bicarbonate; Duodenal secretions aspirated over 2 hours after administration of Secretin by
Nasoduodenal tube
• Faecal Elastase Test – Measurement of Elastase by ELISA from stool sample
Management of Chronic Pancreatitis
• Lifestyle – Reducing alcohol intake, Encourage diet rich in antioxidants (Vit A, C, E, Selenium),
Lower in fat with adequate carbohydrates and protein
• Treatment for Gallstones, Autoimmune disease and other underlying causes
• Pancreatic Exocrine supplementation (Creon)
and Diabetic control
• Analgesia – Oral Morphine Tablets or Coeliac
Plexus block
Surgical Management of Chronic Pancreatitis
- Pancreaticoduodenectomy (Whipple’s)
- Partial Pancreatectomy of Head (Frey) or Distal
- Pancreatojejunostomy (Peustow/Duval)
- Surgical resection of Cysts, Fistulas, Obstructions
Pancreatic Carcinoma
Fourth Commonest solid organ cancer; Increasing
incidence occurring mostly in 60 – 70yrs
Head (65%) of Pancreas Carcinoma
Obstructive
Jaundice and Palpable Gallbladder, Epigastric/LUQ
pain which may radiate to the back, Hepatomegaly
(due to Metastasis), Anorexia, Nausea and
Vomiting, Fatigue, Dyspepsia and Pruritus
Body (25%) and Tail (10%) of Pancreas Carcinoma
Usually asymptomatic; Weight loss and back pain,
Epigastric mass, Jaundice and Diabetes Mellitus
• Thrombophlebitis Migrans; Splenic vein thrombosis
leading to Splenomegaly
Pathogenesis
Ductal Adenocarcinoma (90%), Mucinous Cystadenoma/Cystadenocarcinoma (7%) and Islet cell tumours (3%) including Functional Tumours e.g. Insulinoma
Pancreas Carcinoma Diagnosis and Investigations
• FBC, LFT, Blood sugar, Elevated CA 19-9 (Level correlates to tumour volume), Transabdominal
Ultrasound, Doppler Ultrasound, Dual phase CT, CT angiography
• CT/Ultrasound guided FNAC, ERCP; PET Scanning for metastasis
• Exploratory Laparoscopy to rule out Peritoneal disease
Pancreas Carcinoma Risk Factors
- Cigarette smoking, Age, High fat diet, Diabetes Mellitus, Alcohol abuse, Chronic Pancreatitis
- Hereditary factors; 1 in 20 have family history of Pancreatic Cancer
Pancreas Carcinoma Treatment
• Palliative Treatment; 95% not suitable for resection due to presence of metastasis, local
invasion, lymphadenopathy, age or comorbidity
o Relief of Jaundice – ERCP and Stenting, Percutaneous Biliary drainage,
Cholecystojejunostomy and Choledocojejunostomy
o Gastrojejunostomy to relieve Duodenal obstruction
o Pain management – Oral morphine, Coeliac Plexus block (by Chemical Ablation)
• Curative treatment – Whipple’s procedure, Total and Distal Pancreatectomy; Adjuvant
Chemotherapy improves prognosis
• Poor prognosis; 5-year survival even in resectable disease is 12%
Polyp
Growth of the lining of the large bowel; Stalked (Pedunculated), Flat and spreading (Sessile) or combination of both
Colorectal Cancer
Second commonest tumour and commonest GI malignancy; 3× more
common in males; predominantly Adenocarcinoma
o Rectal – Presents with Rectal bleeding and bloody stools, Changing in bowel habits
(Difficulty, Sensation of incomplete evacuation, and Pain (Tenesmus)
o Descending to Sigmoid – PR bleeding (sometimes clotted), Increased bowel
frequency, variable consistency, mucous PR, bloating and flatulence
o Right sided – Iron deficiency Anaemia might be the only presentation
• Up to 40% present as emergencies – Large
Bowel Obstruction, Perforation and Peritonitis,
Acute PR blood loss
Differential Diagnosis for Rectal Bleeding
• Haemorrhoids, Anal fissure, Prolapse, Angiodysplasia • Proctitis, Proctocolitis and Colitis, Diverticular disease, NSAID induced ulceration • Rectal and Colonic tumours
Differential Diagnosis for Constipation
• Defined as <2 bowel movements per week; or less than normal habit; or difficulty, straining or
pain; or sense of incomplete evacuation
• Lifestyle (Diet, Exercise, Fluid intake), Age, Environment, Pain, Psychological, Idiopathic
• Irritable Bowel Syndrome, Diverticulosis, Fissures, Strictures
• Anal or Colorectal Carcinoma, Pelvic masses
• Pelvic muscle dysfunction, Pseudo-obstruction
• Nerve injury (Trauma, Surgery), Neuropathy, Aganglionosis
• Hypercalcaemia, Hypothyroidism, Hypokalaemia, Porphyria, Lead poisoning
• Narcotics, Anticholinergics, Iron, Aluminium Antacids, Diuretics, Calcium Channel Blockers
Risk Factors for Colorectal Cancer
• Lifestyle – Diet, Sedentary lifestyle, Obesity, Smoking, Heavy alcohol use
• Age, History of Polyps or Cancer, Inflammatory Bowel Disease, Type 2 Diabetes, Racial and
Ethnic background
• 5 – 10% due to Inherited familial syndromes – Familial Adenomatous Polyposis (FAP),
Hereditary Non-Polyposis Colorectal Cancer (HNPCC/Lynch Syndrome), Turcot syndrome (like
FAP producing Medulloblastomas or like FAP producing Glioblastomas), Peutz-Jeghers
syndrome, MUTYH associated polyposis
o FAP – Autosomal dominant/recessive, Mutations of Adenomatous Polyposis Coli
(APC) gene leading to defective APC (Type of Tumour Suppressor Protein)
o HNPCC – Autosomal dominant, Mutations of DNA mismatch repair genes leading to
defective mismatch repair causing microsatellite instability
Pathogenesis of Colorectal Adenomas/Adenocarcinoma
• Ordered process; Initiation, Promotion and Progression; Colorectal Adenoma – Benign
glandular tumour of the colon and rectum; Pre-cancerous lesion of Adenocarcinoma
• <10% of Adenomas become cancerous but 95% of Adenocarcinoma develop from Adenomas
• Hyperplastic polyps generally not associated with Colorectal cancer unless on the Right side
• Mutation of Adenomatous Polyposis Coli gene (loss of Heterozygosity) leads to development
of early Adenoma; Accumulation of other mutations (e.g. KRAS, DCC/DPC4) leads to Late
Adenoma, Loss of p53 Tumour Suppressor Gene leads to progression to Adenocarcinoma
Management of Colon Cancer
• Hemicolectomy where possible with Anastomosis; LND up to root of mesentery
o Obstruction carries greater morbidity and mortality; Preoperative Decompression by
Stenting can allow surgery to be done as elective rather than emergency
• Adjuvant Chemotherapy with 6/12 5FU and Folinic acid, or Oral Capecitabine reduces risk of
death and improves 5yr survival for node-positive disease; Less benefit for node negative
Screening and Management Strategies for Colon Cancer Syndromes
• Faecal Occult blood test (FOBT), PR examination, Flexible Sigmoidoscopy, Colonoscopy,
Virtual CT Colonoscopy, Barium enema XR or Capsule endoscopy
• Lynch Syndrome – Colonoscopy every 1 – 2 years; Beginning from age 20 – 25 or 5 years
before earlier age of diagnosis in the family, whichever is sooner
o Lynch Syndrome in Females – Yearly Pelvic examination, Pelvic ultrasound,
Endometrial Biopsy from age 30-35; Consider prophylactic Oophorohysterectomy
• Familial Adenomatous Polyposis – Colonoscopy ± OGD every (few) years, 100% chance of
colorectal cancer by 50yrs; Total colectomy prevents inevitable development
• H pylori testing and eradication therapy
Population Screening for Colorectal Polyps and Cancers
• Numbers Needed to be Screened estimated 688 for Colorectal Cancer (2001)
• Colonoscopy remains most accurate at a single application vs other screening tools
• Colonoscopy is relatively safe (3.1 serious harms per 1000 procedures) while Flexible
Sigmoidoscopy is safer (3.4 per 10,000); Moderate specificity and sensitivity
DIVERTICULAR DISEASE
Outpouching of the intestinal wall usually occurring at
sites of entry of perforating arteries; Occurs at point of
weakness where the outer longitudinal coat is
discontinuous
o Diverticulosis – Presence of Diverticula;
Diverticular disease – Symptomatic diverticula;
Diverticulitis – Inflammation of the Diverticulum
o NB: Diverticular disease does not occur in the rectum (has full longitudinal coat)
• Associated with hypertrophy of surrounding colonic muscle and thickening of the mucosa
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• Epidemiology – 30% of people in Westerners 60 yrs; Peak age of presentation at 50 – 70yrs
DIVERTICULAR DISEASE Presentation
• Majority asymptomatic (incidental finding of barium enema); Pain presents in LIF
• Diarrhoea, Nausea, Fever, Tachycardia, Tenderness; May present as spontaneous bleeding
but not associated with inflammation
Acute Diverticulitis
• Rapid onset LIF pain; Colonic wall shows acute neutrophil infiltrate into Subserosa
• May progress to Peri/Paracolic mass (Thickening due to infection) which may produce pus
leading to formation of abscess; Perforation of abscess leads to Purulent Peritonitis; Direct
bowel perforation leads to Faeculent Peritonitis – High fever, Severe pain, Rigidity, Guarding
• Diverticular Fistula – Colovesticular/Colovaginal; Leads to recurrent UTI/Vaginal discharge
• Stricture Formation – Colonic Fibrosis/Narrowing; Recurrent colic, Distention and Bloating
Management of Diverticular Disease
• Double contrast Barium Enema for elective diagnosis
• Colonoscopy – Poor measure of extent but indicated if any suggestion of co-existent
malignancy, CT Abdomen to identify complications
• High fibre, High fluid intake, Stool softeners (e.g. Dulcolax)
• IV Antibiotics if Perforated (Cefuroxime, Metronidazole) or during Acute Infective
Exacerbations (Amoxicillin, Gentamicin, Metronidazole); Recurrence prevented by 6-week
course of oral antibiotics
• Surgical Management – Resection of affected segment (Segmental Colectomy); Primary
anastomosis or Proximal End Colectomy with Oversewing of the Distal end (Hartmann’s Type)
• Strictures may be electively resected or Dilated by balloon; Segments with Fistulas resected
o Surgery indicated if Unresponsive to Medical therapy, Undrainable sepsis or Free
perforation of the bowel
Acute Mesenteric Ischaemia
Disruption of blood supply to the Small Intestine; May be due
to SMA Thrombosis/Embolism, Mesenteric Vein Thrombosis, or Non-Occlusive disease
o Venous Thrombosis more common in younger patients in hypercoagulable states
o Non-Occlusive – Occurs in low-flow states reflecting poor cardiac output
• Classic Triad – Severe pain without abdominal signs, Setting of rapid hypovolaemic shock
• Investigations – ↓Hb, ↑WCC, ↑Amylase, Metabolic Acidosis
o AXR: “Gasless Abdomen”, CTA/MRA will reveal obstruction
o New techniques involve measuring mucosal O2 tension, MR Oximetry of SMA
• Treatment – Antibiotics (Gentamicin, Metronidazole ± Amoxicillin), Fluid Resuscitation,
Heparinisation and Thrombolytics by Angiography catheter if indicated, Surgical resection of necrotic bowel and revascularisation if possible
• Complications – Septic Peritonitis, Progression to SIRS and MODS
Chronic Mesenteric Ischaemia (Intestinal Angina)
• Severe, Colicky post-prandial abdominal pain, ↓Weight, Upper abdominal bruit ± PR
bleeding, Malabsorption, Nausea/Vomiting
• Tends to have history of vascular disease
• Investigated with CTA/MRA, Doppler Ultrasound; Surgery if risk of Acute Mesenteric
Ischaemia; Other options include Percutaneous Transluminal Angioplasty with Stenting
(Lower risk of morbidity and mortality but higher restenosis rates)
Ischaemic Colitis – Disruption of blood supply to the Large intestine
• Hyperactive Phase – Abdominal pain and Haematochezia
• Paralytic Phase – Widespread pain, General Abdominal Tenderness, ↓Motility and absent
bowel sounds on examination
• Shock Phase – Shock and Metabolic acidosis 2o
to dehydration
HAEMORRHOIDS Anatomy
• Upper 2/3rd lined with Simple Columnar
Epithelium; Lower ends have folds of mucous
membrane (Anal valves); Receives blood supply
from Superior Rectal artery (Br IMA) and drains
into IMV (Portal circulation)
• Pectinate/Dentate Line between two parts of the
Rectum (Hindgut Proctoderm Junction)
• Lower 1/3rd lined with Stratified Squamous
Epithelium that blends with skin; Receives blood
supply from Inferior Rectal artery (Br Int Iliac via
Int Pudendal)
o Hilton’s White Line indicates junction between Unkeratinised and Keratinised
Stratified Squamous Epithelium
o Anal verge; point where perianal skin becomes continuous
Physiology of Continence/Defaecation
• Faeces stored within the Rectum Ampulla; Increased volume leads to distention, which
stimulate stretch receptors causing desire to defecate
• Reflex contraction of Rectal muscle, Relaxation of Internal Anal Sphincter (Autonomic control)
and Initial contraction of External Anal Sphincter (Somatic control); Urge can then be acted
upon by increasing intra-abdominal pressure consciously
• Faecal incontinence – Anorectal abnormalities, Spinal cord defects, Pelvic floor weakness
(Especially Puborectalis), Overflow, Drugs (e.g. Nitrates, Diarrhoea/Constipating drugs)
Presentation of Haemorrhoids
• Fresh Rectal bleeding often with stool or dripping right after defecation; May be accompanied
by mucous and pus discharge, Severe anaemia
• PR exam; Prolapsing piles are obvious, Internal Haemorrhoids not palpable (seen instead on
Proctoscopy and Sigmoidoscopy)
• Weight loss, Tenesmus and changes in Bowel habits are uncommon and may be due to other
diseases e.g. Malignancy
Classification of Haemorrhoids
• Grade I: Remains within the Rectum • Grade II: Prolapse through the Anus on defection but spontaneously reduced • Grade III: Prolapse through the Anus on defection but manually reduced • Grade IV: Permanently Prolapsed
Management of Haemorrhoids
- Grade I: Increased fluid/fibre intake; Topical analgesia, Stool softeners, Short term steroids
- Grade II and III or failed I: Rubber band ligation, Sclerosants (I and II), Infra-red Coagulation
- Surgical Management – Excisional Haemorrhoidectomy, Stapled Haemorrhoidopexy
Haemorrhoids Risk Factors
- Chronic Diarrhoea or Constipation, High fat low fibre diet, Obesity, Alcoholism
- Sedentary lifestyle, Loss of pelvic floor tone, Anal intercourse
Fistula
Abnormal connection between two epithelial surfaces; Very common especially in
otherwise fit young adults; Assoc with Crohn’s disease; Occasionally Obesity, Diabetes
Mellitus; Rarely Trauma or Anorectal Tumours
ANAL FISTULAS
which penetrates through; Often presents initial as
Acute Perianal Abscess; Classification depends on
extent of penetration
Acute Perianal Abscess
Rapid onset Severe
Perianal or Perineal Pain; Swelling, Erythema of
Perianal Skin with Fever and Tachycardia
Recurrent Perianal Abscess
Recurrent Intermittent
sepsis typified by gradual build-up of pressure
sensation and swelling and Perianal skin; Discharge
of purulent fluid with blood
Chronic Perianal Discharge
Persistent Low-grade sepsis of Fistula track with Chronic
Discharge of Seropurulent fluid via punctum
Management of Fistula-in-ano
• Perineal and Rectal Examination might reveal Palpable Fibrous track
• Examination under Anaesthesia might be indicated; Endoanal Ultrasound identifies course
• MRI Pelvis – Most sensitive method of determining track; Useful for identification of occult
Perianal or Pelvic Sepsis
• Flexible Sigmoidoscopy for any associated disease e.g. Crohn’s Disease; Appropriate
treatment of underlying Inflammatory Bowel Disease
• Antibiotics reduce symptoms of underlying sepsis but cannot treat underlying Fistula
Surgical Management of Fistula-in-ano
• Drainage of Acute sepsis; Prevention of Recurrent Sepsis by insertion of loose Senton suture
E.g. Silastic Sling
• Fistulotomy for Low Fistula-in-ano – Track should be laid out and Chronic Granulation should
be removed and allowed to heal
spontaneously
o Low risk of incontinence due to
minimal division of Sphincter tissues
• Fistulectomy with Endorectal Flap
Advancement – Removal of Fistula Track
and Closing Internal opening
• Cutting Seton – Division of the Sphincter
tissue between Fistula and Perianal skin;
Small risk of incontinence
• Fistula can be filled with Fibrin glue
ANAL CANCER
• Typically, Squamous Cell Carcinoma near Squamocolumnar Junction; Associated with Human
Papillomavirus; Other types include Adenocarcinoma, Lymphoma, Sarcoma and Melanoma
• May present as Pain/Pressure in Anus/Rectum, Change in Bowel Habit, Palpable mass, Rectal
Bleeding, Itching or Discharge; Bleeding might be severe
• Risk Factors – HPV Infection (Especially HPV16, 18), Anal Intercourse or Multiple Sexual
Partners, Smoking, Immunosuppression, History of other Pelvic Cancers
• Carcinoma-in-situ, Anal Intraepithelial Neoplasia for ablation (E.g. Infrared Photocoagulation)
• Surgery – Associated with incontinence due to excision of Internal and External Sphincter;
Current gold standard is Chemoradiotherapy – 5FU, Mitomycin and Radiation
• 10-20% develop Distant Metastases following treatment; Chemotherapy – Platinum
Chemotherapy, Anthracycline, Antimetabolites
RECTAL PROLAPSE
• Partial Thickness (Usually just Mucosa) or Full Thickness (Involves layers of Rectal Wall); Full
Thickness can also be confined within Rectum (Intussusception)
• Commonest in Post-Menopausal Women, Multiparous, Chronic Straining and Defection
Disorders (Associated with weakness of Pelvic Floor and Sphincter Complex) and Slow Transit
Constipation; Occasionally occurs in children suffering constipation, but usually self-limiting
• Mucosa involved in Prolapse undergoes Chronic changes – Glandular branching, Gland
misplacement, Thickening of Muscularis Mucosae and Excess Submucosal Collagen
Deposition; Inflammation and Focal Ulceration; May result in Solitary Rectal Ulcer
Presentations of Rectal Prolapse
• Mucosal Prolapse – Discharge of Mucus and Small Volume Faecal Straining, Pruritus and
occasionally Small Volume Rectal Bleeding
• Internal Full Thickness Prolapse – Sensation of fullness/mass, Tenesmus etc
• External Full Thickness Prolapse – External prolapsing mass after defecation which might
require manual reduction; Mucus and Faecal Soiling with occasional Bright Red Rectal
Bleeding (Large Volume if Ulcerated)
Management of Rectal Prolapse
• Rigid Sigmoidoscopy to illustrate Mucosal Inflammation; Prolapse might be demonstrable on
straining during Rectal Examination
• Defecating Proctogram – Demonstrate Internal Prolapse if suspected; Useful to confirm
diagnosis if unclear or demonstrate associated problems with Pelvic Floor and Rectocoele
• Colonic Transit if suspected Slow Transit Constipation
• Avoidance of Straining and Adaption of Defaecatory Habit (Biofeedback)
• Avoidance of Constipation (Stool Softeners, Bulking Agents)
Surgical Management of Rectal Prolapse
• For Mucosal Prolapse – Recurrent banding or Dilute Phenol Injection to eliminate excess
Mucosa or Excision; Stapled Anopexy (Procedure for Prolapse and Haemorrhoids)
• Delorme’s Perineal Rectopexy – Mucosal Excision with Sutured Plication of Rectal Muscle to
shorten to reduce change of recurrent Prolapse; Ideal for Frail/Elderly but least successful
with high Recurrent rates
• Altmeier’s Perineal Rectal Resection – Mucosal and Rectal Muscle Excision with Sutured
Perineal Anastomosis; Increased morbidity due to anastomosis
• Transabdominal Rectopexy – Mobilisation of the Rectum and Suturing to Presacral Fascia;
Highest success rate of prevention of recurrence of Prolapse; May be combined with Sigmoid
Resection if marked associated constipation
Hernia
Abnormal Protrusion of Viscus or Part of Viscus through weakness in containing wall;
May be Congenital (Associated with Developmental Disorder, or Failure of complete
obliteration of Umbilical opening) or Acquired
o Ageing, Previous Surgery, Increased Intra-Abdominal Pressure increases risk
• Hernia comprises Sac (Peritoneal Lining of Hernia), Neck (Level of defect) and Contents
(Bowel, Omentum)
• Hernias can be Reducible, Incarcerated (Cannot be reduced due to Narrow Neck/Adhesions;
Risk of Strangulation), Obstructed (Due to Kinking; Usually goes on to Strangulation)
o Strangulation – Blood supply to the contents cut off = Ischaemic/Infarction
o Venous/Lymphatic Occlusion, Oedema and Increased Venous Pressure, Impedance to
Arterial Flow, Bowel Necrosis and Perforation
• Third most common cause of Bowel Obstruction (after Adhesions and Cancer)
Inguinal Hernia
• Most common cause of Abdominal Hernia; 8× more common in Males • Classified Direct or Indirect based on relationship to Inferior Epigastric Artery (Surgically) • Can be both (Pantaloon Hernia) • Most are asymptomatic until lump is noticed in groin; Aching or Dragging sensation especially towards the end of the day • Some onset of pain and bulge due to specific activity
Indirect Hernia
Occurs at any age but usually Young Congenital (Patent Processus Vaginalis) • Occluding Internal Ring Controls Hernia • Strangulation is more likely Herniotomy for Infants; Adults treated similarly to Direct
Direct Hernia
Uncommon in Children/Young adult Acquired Weakness Medial – Rarely descends to Scrotum • Occlusion Internal Ring does not control Hernia • Strangulation is rare • Open Mesh Repair, Laparoscopic Repair
Management of Inguinal Hernia
• If diagnosis uncertain – Ultrasound, CT/MRI (Highly accurate)
• Patients with symptoms or have had episodes of irreducibility/Bowel Obstruction should be
offered repair; Elderly, Immobile patients/high morbidity should be observed if asymptomatic
55
• Repair may be by Open surgery or Laparoscopic approach (Transperitoneal or Pre-Peritoneal
Space); Open approach can be done under Local Anaesthesia in some cases
• Tension-free Reinforcement of the Transversalis Fascia (TVF) – The non-absorbable mesh is
placed in front of the TVF in Open surgery and behind it in the Laparoscopic approach
• Mesh may be fixed in place by Sutures (Open approach) or Tacking (Laparoscopic)
• Patients advised to avoid heavy lifting and staining 2 weeks post-op; Lifetime recurrences is
low (1-2%); Laparoscopic approach recommended for Recurrent or Bilateral Hernias
Femoral Hernia
• Femoral Hernias are more common in Women than Men; Occurs through the tissues of the
Femoral Canal; Higher risk of Strangulation due to Bony and Ligamentous surfaces
• 30% present as Emergencies of which half for Bowel Resection for Strangulation/Ischaemia
• Presents Inferolateral to Pubic Tubercle and Medial to Femoral Pulse; Might be asymptomatic
until Incarceration or Strangulation occurs and might be mistaken for Upper Medial Thigh
Swelling; Differentia includes Low Inguinal Hernia, Lipoma, Lymph Node, Varicosity of
Saphenous Vein (Which is compressible and disappears on lying flat), Femoral Artery
Aneurysm or Psoas Abscess (Lateral to Femoral Pulse rather than Medial)
Management of Femoral Hernia
• All Femoral Hernias should be repaired due to high risk of Strangulation; Once Hernia has
been reduced, Femoral Canal should be narrowed by Interrupted Sutures to prevent
Recurrence without narrowing neighbouring Femoral Vein
• Infrainguinal Approach – Incision below Inguinal Ligament; Does not interfere with Inguinal
structures but unable to provide exposure for Small Bowel resection; For Elective Surgery
• Inguinal Approach – Above Inguinal Ligament with Posterior Wall of Inguinal Canal being
dissected (Inguinal Ligament); Requires Inguinal Repair during closure but allows for Small
Bowel surgery if required, usual approach for emergency presentation
INCISIONAL HERNIA
• Hernia occurring through the tissues where Incision was made; Sac is made up of Peritoneum,
Internal Eventuated or Subcutaneous Scar Tissue
• Most commonly in the Abdomen; Up to 10% of Midline Laparotomy to some degree; Less
common with Muscle Splitting or Transverse Incisions
• Predisposing Factors – Wound Infection, Steroid Use, Anaemia, Malnutrition
Presentation of Incisional Hernia
• Peak time of presentation is up to 5 years after Surgery; Variable extent of Defect
• Risk of Strangulation is maximal if Defect is Small/Medium
• Large Chronic Herniation might be accompanied by retraction of remaining Lateral Abdominal
Wall Tissues resulting in Permanent Herniation due to insufficient room in revised cavity
Management of Incisional Hernia
• Considerations before Surgical Intervention – Risk of Complications/Strangulation without
surgery, Likelihood of complete reduction, Fitness for surgery and Risk of Respiratory
Function compromise if large hernia is reduced
• Small (<4cm) Defects can be repaired by Simple Sutures
• Medium to Large (>4cm) Defects might require placement of Mesh between Posterior Rectus
Sheath and Rectus Abdominis; If below Umbilicus, Mesh is placed in Pre-Peritoneal Space;
Mesh is fixated and Anterior Rectus Sheath is closed
• Laparoscopic approach – Underlay Intraperitoneal Mesh might create potential for Bowel
Adhesion or Fistula Formation; PTFE mesh have reduced Adhesive complications
• Custom-made Support Corset if not for surgery
ABDOMINAL TRAUMA
• Blunt Trauma – Most frequently affects Spleen (45%), Liver (40%), Retroperitoneum (15%);
Compression/Crushing resulting in Rupture; Deceleration Injury leading to Tearing/Avulsion
o Very common in RTCs especially in Fatal incidents, High speed (>50mph) etc
• Stab wounds and Low Velocity gunshot wounds can cause damage by Lacerating or Cutting;
Stab wounds involve Liver (40%), Small Bowel (30%), Diaphragm (20%), and Colon (15%)
• High Velocity gunshot wounds transfer more kinetic energy; Further injury due to Cavitation,
Tumble and Fragmentation; Small Bowel (50%), Colon (40%), Liver (30%) and Vessel (25%)
• Primary Survey – Assume Intra-Abdominal Bleeding is Hypotensive despite Resuscitation and
without obvious cause of Blood Loss
o Emergency Laparotomy if critical unstable; Abdominal CT Scan if Patient is stable
Secondary Survey
• History – Patient and Collateral, Mechanism of Injury, Prehospital condition and treatment
• Anterior Abdomen – Lower Thorax, Perineum, Log roll for Posterior; Look for Abrasions,
Contusions, Lacerations, Penetrating wounds, Distention, Evisceration
• Palpation for Tenderness, Guarding, Rebound Tenderness, Pregnancy; Auscultate for Bowel
Investigations in Abdominal Trauma
• Focused Abdominal Sonography for Trauma (FAST); Morrison’s (Hepatorenal) Pouch,
(Rectouterine) Pouch of Douglas, Perisplenic and Pericardium
o Also used as screening for patients without major risk factors for abdominal injury
• Diagnostic Peritoneal Lavage (DPL) – Superseded by FAST for Unstable and CT for Stable;
Useful for identification of free intraperitoneal fluid (e.g. Intra-abdominal bleeding)
o Aspiration of Blood, GI contents/Faeces or Bile indicates Laparotomy
• CT – Investigation of choice for Haemodynamically stable patients if there is not emergency
indication for Laparotomy
Indications for Resuscitative Laparotomy
• Life-threatening Blunt Abdo Trauma
• Unresponsive Hypotension despite
adequate Resuscitation with no other
cause of bleeding found
Indications for Urgent Laparotomy
• Blunt Trauma with positive Lavage or Free blood on Ultrasound with Unstable Circulatory Status • Blunt Trauma with evidence unstable for Conservative Management • Clinical Features of Peritonitis • Knife Injury associated with visible viscera, Peritonitis, Haemodynamic instability or setting of Sepsis • Gunshot Wound (GSW)
