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