Upper GI Flashcards
Mx of duodenal ulcer perforation
Suture closure and omental patch
Treat associated H.Pylori infection with triple therapy
Mx of gastric ulcer perforation
Suture closure and mental patch if pre-pyloric
Local excision and suture closure if in body
Causes of Upper GI Perforation
Duodenal ulceration
Gastric ulceration
Gastric carcinoma
Traumatic
Ischaemia secondary to gastric volvulus
Treatment of gastric volvulus
If perforation, need sub-totel gastrectomy
Surgical intervention in upper GI bleed
Massive haemorrhage requiring on-going resus is indication for surgical management
Failed endoscopic management
Re-bleeding, not amenable to repeat endoscopic therapy
Risk factors for oesophageal adenocarcinoma
GORD
Barret’s metaplasia
Nitrosamines
Risk factors for oesophageal squamous cell carcinoma
Smoking
Alcohol
Chronic achalasia
Strictures
Reduced intake of vegetables and fruit
Peak age for acute appendicitis
Uncommon <4, >80
Peak: teens to twenties
Types of acute appendicitis
Mucosal: mildest form only identified on histopathology
Phlegmonous: slow onset, slow progression
Necrotic: often due to bacterial infection with ischaemic necrosis, leads to perforation
Differential diagnosis of acute appendicitis
Children
- mesenteric adenitis
- Meckel’s diverticulitis
- Ovarian cyst
- Menstrual
Adult
Terminal ileum: Crohn’s, Meckel’s diverticulitis
Retroperitoneal: Pancreatitis, Renal colic
Ovarian: Ectopic pregnancy, Cyst infection
Complications of acute appendicitis
Perforation
Appendix mass
Abscess
- RIF
- Pelvic
Management of acute appendicitis
ACUTE APPENDICITIS, i.e. not appendix mass
=open or laparoscopic appendicectomy with IV antibiotics on induction
Management of appendix mass or abscess
IV antibtiotics
-Cefuroxime 750mg TDS and Metronidazole 500mg TDS
If settles –> delayed appendicectomy
Organised abscess –> percutaneous drainage
If symptoms persist or becomes peritonitic –> appendicectomy
Anatonical positions of the appendix
Pre-ileal – anterior to the terminal ileum – 1 or 2 o’clock.
Post-ileal – posterior to the terminal ileum – 1 or 2 o’clock.
Sub-ileal – parallel with the terminal ileum – 3 o’clock.
Pelvic – descending over the pelvic brim – 5 o’clock.
Subcecal – below the cecum – 6 o’clock.
Paracecal – alongside the lateral border of the cecum – 10 o’clock.
Retrocecal – behind the cecum – 11 o’clock.
Blood supply to appendix
Lies in own mesentery with sole blood supply from the appendicular artery
-terminal branch of the iliocolic artery
Thrombosis of the appendicular artery –> gangrene
Open approach to appendicectomy
Muscle splitting gridiron at McBurney’s point
Causes of Acute Peritonitis
=inflammation of peritoneal cavity
-primary and secondary causes
Primary = very rare
e.g. streptococcal infection from blood-borne spread
Managed with extensive lavage
Secondary = common If under 45 yrs, commonest is acute appendicitis Acute perforated diverticular disease Upper GI perforation Perforated large bowel due to malignancy Perforation secondary to gastric tumours Perforated ischaemic bowel Acute pancreatitis Peritoneal-dialsysis related Anastomotic leak Enteric injury
Locations of intra-abdominal abscess
Locations
- adjacent to offending organ
- pelvic e.g. appendicitis
- subphrenic e.g. upper GI perforation
Gynaecological causes of the acute abdomen
Mittelschmitz
Endometriosis
Ovarian cyst torsion
Tubo-ovarian infection / PID
Ectopic pregnancy
Causes of intra-abdominal abscess
Sigmoid diverticulitis
Acute appendicitis
Severe acute cholecystitis
Upper GI perforation
Post anastomotic leak
Infected acute pancreatitis
Post-trauma
Management of intra-abdominal abscess
IV antibiotics guided by sensitivities
IV fluids
Blood cultures
Antibiotics: e.g. Cefuroxime 750mg TDS, Metronidazole 500mg TDS
Percutaneous drainage (unless surgery needed to treat primary pathology)
Indications for surgery:
- surgery required for primary pathology
- failed IR drain
- IR drain not possible e.g. retroperitoneal or intramesenteric
Bilirubin level for clinically apparent jaundice
> 40mmol
Causes of pre-hepatic jaundice
=HAEMOLYTIC
Congenital structural abnormalities
- Hereditary spherocytosis
- Sickle cell disease
Autoimmune haemolytic anaemia
Transfusion reactions
Drug toxicity
Causes of hepatic jaundice
Increased UNCONJUGATED
- Gilbert’s: problem with uptake
- Crigler-Najjar: problem with conjugation
Increased CONJUGATED Infection -Viral (Hep A, B, C, EBV, CMV) -Bacterial leptospirosis or abscess -Parasitic amoebic
Drugs
- Paracetamol
- Anti-psychotics
- Antibiotics
Non-infective hepatitis
- Alcohol
- NAFLD
Causes of post-hepatic jaundice
Intraluminal
- Gallstones
- Thrombus
- Parasites (flukes)
Mural abnormalities bile ducts
- Cholangiocarcinoma
- Congenital atresia
- Sclerosing cholangitis
- Biliary cirrhosis
- Traumatic
Extrinsic compression
- Pancreatitis
- Tumours
- Lymphadenopathy
- Porta hepatic node (e.g. in gastric cancer)
MRCP
Magnetic resonance cholangiopancreatography
Indication: for extra-hepatic obstruction with no cause seen on USS
Complications of jaundice
Biliary infection
-E. coli, Psueodomonas
Coagulopathy
Relative immunosuppression and decreased protein synthesis
Hepatorenal syndrome
Management of acute obstructive gallstones
Fluid resuscitate e.g. 1000ml crystalloid
Hourly UO, catheter
10mg Vitamin K for 3 days if prolonged PT
IV Co-Amoxiclav
ERCP
ERCP
Endoscopic retrograde cholangiopancreatography
Interventions during ERCP
Sphincterotomy
- used for common bile duct stone extraction
- treatment of ampullarf strictures
Stent insertion
- plastic (easier to remove if further intervention planned)
- metal
Percutaneous transhepatic cholangiogram
PTC
Percutaneous drainage of the biliary system
Choledochoduodenostomy
Communication between common bile duct and duodenum
Constituents of bile
Bile salts
- primary: cholic, chenodeoxycholic
- secondary: deoxycholic, lithocholic
Phospholipids
Cholesterol
Increase in composition of cholesterol precipitates bile salt transformation to stones
Types of gallstones
Pure cholesterol
- 10%
- large 2.5cm stones
Pure pigment
- 10%
- black in colour = haemolysis
- brown in colour = chronic cholangitis e.g. parasites
Mixed stones
- 80%, by far most common
- multiple in number
Risk factors for gallstones
Increasing age
Female
Pregnancy
OCP
Obesity
Chronic haemolytic disorders
Long-term parental nutrition
Distal small bowel pathology e.g. Crohn’s
Presentation of gallstones
Biliary colic
Acute cholecystitis
Chronic cholecystitis
Mucocele
Empyema
Symptoms and signs of biliary colic
Intermittent severe epigastric / RUQ pain
Nausea & vomiting
Resolves after a few hours
Tenderness over gallbladder
Symptoms and signs of acute cholecystitis
Severe continuous RUQ pain
Radiates to back / right flank
Anorexia
Pyrexia
Tenderness over gallbladder
Murphy’s sign, palpation on inspiration
Complications of acute cholecystitis
Formation of abscess / empyema
Perforation –> biliary peritonitis
Cholecystoenteric fistula
-> if gallstones enters and obstructs ileum = Mirizzi’s syndrome
Mirizzi’s syndrome
Type I: cholecystoenteric fistula present
Type II - IV: no fistula
Pathology:
- Multiple gallstones become impacted in Hartmann’s such of gallbladder
- Leading to chronic inflammation
- Which leads to compression of the common bile duct (CBD), necrosis, fibrosis, and ultimately fistula formation into the adjacent common hepatic duct (CHD) or common bile duct (CBD).
Mucocele
Stone in the neck of gallbladder
Bile is absorbed BUT mucus secretions continue
Forms tense globular mass in RUQ
Hepatobiliary iminodiacetic acid scan
Hepatobiliary iminodiacetic acid (HIDA) scan
-used when USS unable to diagnose
Evaluate the gallbladder. It’s also used to look at the bile-excreting function of your liver and to track the flow of bile from your liver into your small intestine. A HIDA scan is often used with X-ray and ultrasound.
A HIDA scan might help in the diagnosis of several diseases and conditions, such as:
Gallbladder inflammation (cholecystitis)
Bile duct obstruction
Congenital abnormalities in the bile ducts, such as biliary atresia
Postoperative complications, such as bile leaks and fistulas
Assessment of liver transplant
Surgical management of acute cholecystitis
Cholecystectomy
Indications
- Symptomatic gallstones
- Patients who are high-risk, with asymptomatic gallstones
e. g. diabetics, pancreatitis, immunosuppression, porcelain gallbladder
Risks of cholecystectomy
5% are converted to open
Bile duct injury <1%
Bile leak 1%
Bleeding 2%
Complications of common bile ducts stones
Obstructive jaundice
Ascending cholangitis
Pancreatitis
Presentation of common bile duct stones
Nearly always due to secondary gallstones from there gallbladder
Rarely due to primary de novo stones in CBD
Causes:
- Obstructive jaundice
- Pancreatitis
- Ascending cholangitis
Can be asymptomatic found on USS
Courvoiser’s law
In a jaundice patient, a palpable gallbladder means that the diagnosis is NOT gallstones
= obstructing tumour
In gallstones –> small shrunken fibrotic gallbladder
Presentation of obstructive jaundice
Usually caused by stone in CBD
Can be caused by stricture or stenosis
Dark urine
Pale stool
Jaundice
Charcot’s triad
Swinging fever
RUQ pain
Jaundice
=ascending cholangitis
Investigations of common bile duct stones
Transabomdinal ultrasound = 1st line
-low accuracy for: distal CBD stones, obese, bowel gas
MRCP
-if USS inconclusive
ERCP
-if unable to tolerate MRCP for Investigation
OR
-intervention required e.g. sphincterotomy and extraction or stent insertion
Risks of ERCP
Endoscopic retrograde cholangiopancreatography
Hamorrhage
Acute pancreatitis
Ascending infection
Perforation (retroduodenal)
Risks increased with sphincterotomy
Indication for percutaneous transhepatic cholangiogram
in CBD stones, used when ERCP fails
Risks
- Sepsis
- Bile leak
- Tube migration
- Dehydration
Management of CBD stones in emergency setting
Unresolving gallstone pancreatitis
Ascending cholangitis
Mx: ERCP sphincterotomy and stone extraction or stent
Elective
-previous settled complications such as pancreatitis or cholangitis,
ERCP
All patients scheduled for cholecystectomy for gallbladder stones should have ERCP or MRCP
Causes of portal hypertension
Pre-hepatic
- Congenital portal vein atresia
- Portal vein thrombosis
- -> in neonates, secondary to umbilical sepsis
- ->Intra-abdominal sepsis
- Trauma
- Thrombosed portocaval shunt
Hepatic
- Cirrhosis
- Chronic hepatitis
- Parasitic disease (schistosomiasis)
Post-hepatic
- Budd-Chiari syndrome (hepatic vein thrombosis)
- Constrictive pericarditis
- Tricuspid incompetence
Management of massive variceal bleed
A to E approach
Transfuse O- negative
2 units FFP and 10mg vitamin K if iNR >1.5
Sengstaken tube, needs ITU and sedation
- Gastric balloon inflated first
- Traction applied, if arrests bleeding then left
- If no arrest, oesophageal balloon inflated
IV PPI
IV Terlipressin, 4mg IV bolus
Octreotide / somatostatin
Endoscopic banding
Transjugular intrahepatic portosystemic shunt
Or
Extrahepatic portocaval shunt
Causes of acute pancreatitis
Gallstones (60%)
Alcohol (30%)
Hyperlipidaemia
Hypercalcaemia (multiple myeloma)
Trauma: ERCP, post-surgery, cardiopulmonary bypass
Toxins
- Azathioprine
- Oestrogens
- Thiazides
- Isoniazid
- Steroids
- NSAIDs
Infection
- Mumps
- CMV
- Hepatitis B
- Mycoplasma
Venom
Idiopathic
Defining Acute Pancreatitis
Inflammatory cascade instigated by release of pancreatic enzymes trypsin, lipase, co-lipase, classically associated with a rise TNF-alpha, IL-2 and IL-6 leading to a systemic inflammatory response and multi-organ dysfunction
Classification of Acute Pancreatitis
Oedematous = 70%
Necrotising = 25%
Haemorrhagic = 5%
-associated with Grey Turner’s sign
Management of acute pancreatitis
A to E approach
1000ml plasma-lyte
Catheter, strict fluid balance
Low volume feeds
Glascow score
Consider HDU, Central line for central venous pressure, ionotropes and supportive therapy
Glascow Score
PaO2 <8kPa Age >55 years Neutrophilia >15,000 Calcium <2 Renal urea >16mmol Enzymes: ALT >200, LDH >600 Albumin <32g/L Sugar >10mmol
3 or more = HDU review
Signs of acute pancreatitis on AXR
Sentinel loop sign
Dilated proximal jejunal loop with colonic cut-off
Presentation of peptic ulcer disease
Peri-umbilical pain
Hx of heart burn / indigestion
Sudden-onset
Unremitting
Smoker or drinker
Investigations for peptic ulcer disease
ECG Urine dip Bloods CXR ?perforation ABG Fast scan / CT
Mx IV plasmalyte NBM NG tube Catheter Senior r/v Boradspectrum antibiotics Theatre booking CEPOD Anaesthetist
Management of perforated peptic ulcer
NO pneumoperitoneum and NO peritonitis –> likely conservative management with IV antibiotics
If acutely unwell and peritonitic –> UGRENT laparotomy
Surgical:
-omental graham patch repair via upper midline laparotomy
If recurrent ulcers despite maximal medical therapy
Consider surgical management
- Highly-selective parietal cell vagotomy
- Truncal vagotomy and pyelorolasty
- Vagotomy and antrectomy
Risk factors for hypertrophic pyloric stenosis
1 month old
Male > female
20% genetic
Presentation and signs of pyloric stenosis
Non-billous vomiting
Hungry, eager to feed
Dehydrated, floppy, sunken fontanelles, if delayed presentation
Abnormal palpable pylorus, olive-shaped mass
Distended
Metabolic abnormality seen in pyloric stenosis
Hypochloraemic hypokalaemic metabolic alkalosis
Diagnostic imaging for pyloric stenosis
Pylorus >3mm on USS
Hypoechoic ring
Management of pylorus stenosis
Paediatric ALS
IV /IO access
20ml/kg fluid bolus
Ramstedt pyloromyotomy
-circumumbilical incision
Resume feeding 12 - 24 hours post op
