UPPER GASTROINTESTINAL BLEEDING (UGIB)
Bleeding from the oesophagus to the ligament of Treitz
CLINICAL PRESENTATION
EPIDEMIOLOGY
Haematemesis
Incidence 60/100,000 per year
Melena
Mortality rate 8%-10%
Clinical signs of blood loss
Resuscitation
APPROACH TO PATIENT Cannulation of 2 peripheral veins (or CVC)
Assessment of haemodynamic stability Volemic expansion (saline solution, Ringer’s
Vital signs (HR, BP, RR), general appearance lactate)
Diuresis Blood transfusion (if required)
Shock index (HR/BP, >1) Urinary catheter
Blood test (CBC, blood group, renal function, Diagnostic studies
coagulation) Upper GI endoscopy
X-ray, CT
PEPTIC ULCERS
Most common cause of UGIB (47%)
Causes
CAUSES
NSAIDs overuse; H. pylori infection
Peptic ulcer
Classification
Gastritis
Forrest’s classification
Oesophagitis
Diagnosis
Angiodysplasia
Upper GI endoscopy
Mallory-Weiss lesion
Therapy
Neoplasia
Medical therapy (PPI, stop NSAIDs, H. pylori
Oesophageal varices
eradication)
Dieulafoy lesion
Endoscopic therapy (diathermoregulation,
injection of vasoconstrictive or sclerosing
agents, clip placement)
PORTAL HYPERTENSION
Fibrosis due to liver cirrhosis results in increase pressure in portal system
Complications
Oesophageal varices: creation of oesophageal varices in all cirrhotic patients (30% will bleed)
Gastric varices
Ectopic varices (e. g. duodenal, colonic, etc.)
Portal hypertensive gastropathy: diffuse gastritis
Management
Prevention of 1st variceal bleeding: medical therapy (non-selective -blocker), endoscopic therapy
Therapy for variceal bleeding: resuscitation, vasoactive drugs (terlipressin, somatostatin,
octreotide), antibiotics (SBP prevention), endoscopy (band ligation, sclerotherapy, Sengstaken-
Blakemore tube, self-expandable oesophageal stent), radiological placement of transjugular
intrahepatic shunt (TIPS)
Prevention of bleeding recurrences
LOWER GASTROINTESTINAL BLEEDING (LGIB)
Bleeding from the ligament of Treitz to the anus
CLINICAL PRESENTATION EPIDEMIOLOGY
Haematochezia Incidence 40/100,000 per year
Proctorrhagia Mortality rate 5%
APPROACH TO PATIENT
,Assessment of haemodynamic stability Volemic expansion
Vital signs (HR, BP, RR), general appearance Blood transfusion (if required)
Diuresis Urinary catheter
Shock index Diagnostic studies
Blood test (CBC, blood group, renal function, Colonoscopy
coagulation) Angio-CT
Resuscitation Angiography
Cannulation of 2 peripheral veins (or CVC) Surgery
OBSCURE GASTROINTESTINAL BLEEDING
CAUSES
(OGIB)
Diverticula: most common in Western countries
Bleeding whose location and source cannot be
Benign anorectal masses: internal
identified
haemorrhoids, anal fissures
Obscure-overt GIB: obscure location but visible
Colitis: ischemic colitis (elderly), IBD (younger,
bleeding
ulcerative colitis, Chron’s disease)
Obscure-occult GIB: obscure location and
Neoplasia
detection with FOBT or chronic iron-deficiency
Polyps
anaemia
Angiodysplasia
Causes
Post-endoscopic
Angiodysplasia, tumours, others (NSAID-related
Post-surgery
bleeding, TB, CD, coeliac disease, vasculitis)
Miscellaneous
Diagnosis
Unknown
FOBT, upper GI endoscopy/colonoscopy
Others: radiation-induced colitis, infectious
Videocapsule endoscopy (VCE)
haemorrhagic colitis, vasculitis, solitary rectal
Double ballon enteroscopy (DBE)
ulcer, colonic varices and hypertensive portal
Scintigraphy, angio-CT, CT enterography, MRI
colopathy, Meckel’s diverticulum
enterography, angiography
GALLSTONES DISEASES
Diseases of the gallbladder and biliary tree caused by gallstones
GALLSTONE TYPES
Pure cholesterol gallstones
Cholesterol crystals; more common in Western
EPIDEMIOLOGY
countries
20mln of Americans
Pure pigment gallstones
Mortality rate: 0.12%
Black gallstones (calcium bilirubinate, increased
Increased incidence due to DM, metabolic
haemolysis)
syndrome, and obesity
Brown gallstones (calcium palmitate, infections,
de novo formation in bile duct)
Mixed gallstones
Cholesterol, pigment, calcium, bilirubin salts
RISK FACTORS Oral contraceptive
Independent Dietary
Ageing High calories
Female gender Low fibres
Race Low cis-unsaturated fats
Family history High refined carbohydrates
Lifestyle Associated conditions
Low grade physical activity Metabolic syndrome
Prolonged fasting Obesity
Rapid weight loss Hyperinsulinism
Pregnancy and parity (multiple, one close to the Oestrogen replacement therapy
,other) Gallbladder or intestinal stasis (or both)
BILIARY OBSTRUCTION
BILIARY COLIC Obstruction of the common bile duct
Symptomatic uncomplicated gallstone disease Signs and symptoms
Signs and symptoms Colic pain, persistent, sometimes intermittent
Transient and intense pain in RUQ, radiation to or absent (elderly)
right shoulder and right back region Nausea and vomiting
Nausea and vomiting Itching and jaundice (if complete obstruction)
Onset: after meal, night, early morning Diagnosis
Duration: 1-4h (peak at 30min) Clinical presentation
Recurrence: 50% of patients Blood tests: elevated AST, ALT, GGT, ALP,
Diagnosis bilirubin
Clinical presentation US: first-level, poor SE (50%)
Blood tests: normal or transiently elevation of MRCP: gold standard, no for stones <5mm
AST, ALT, GGT, ALP (if gallstone migration) Endoscopic US (EUS): for stones <5mm, high
US NPV
Treatment Treatment
Acute phase: fasting + hydration, NSAIDs Fasting + hydration
Post-acute phase: low-fat diet, UDCA Pain management: NSAID, paracetamol, opioid
(10mg/Kg/day in 2-3 doses, only if <10mm non- ERCP: diagnosis and stone removal
calcified gallstone), laparoscopic Subsequent laparoscopic cholecystectomy
cholecystectomy (pigment or calcified gallstone) Others: cholangioscopy during ERCP,
cholangioscopy-guided laser lithotripsy
ACUTE CHOLECYSTITIS ACUTE CHOLANGITIS
Inflammation and/or infection of the Infection of the biliary tract due to biliary
gallbladder wall obstruction
Signs and symptoms Signs and symptoms
Persistent and intense pain in RUQ Charcot’s triad: septic fever with chills,
Nausea, vomiting, low-grade fever jaundice, RUQ pain
(sonographic) Murphy’s sign Reynold pentad: septic fever with chills,
Complications jaundice, RUQ pain, shock, altered mental
Hydropic gallbladder status
Gallbladder empyema Complications
Emphysematous cholecystitis Systemic sepsis
Gallbladder perforation (biliary ileus) Multiple liver abscesses (long antibiotic
Haemorrhagic cholecystitis therapy)
Diagnosis Intravascular coagulation syndrome
Clinical presentation Diagnosis
Blood tests: leucocytosis, high CRP, elevated Clinical presentation
AST, ALT, GGT, ALP, bilirubin Blood tests: leucocytosis, high CRP, elevated
US: gallbladder wall thickening (>3mm), AST, ALT, GGT, ALP, bilirubin
pericholecystic fluid, gallbladder distension, US: first-level, poor SE (50%)
acoustic shadowing MRCP: gold standard, no for stones <5mm
CT: extension of inflammation, gallstone type, Endoscopic US (EUS): for stones <5mm, high
complications NPV
Treatment Treatment
Fasting + hydration Fasting + hydration
Pain management: NSAID, paracetamol, opioid Pain management: NSAID, paracetamol, opioid
Antibiotics: 3rd gen cephalosporin + Antibiotics: piperacillin/tazobactam, ampicillin
metronidazole (mild), piperacillin/tazobactam Urgent ERCP: stone removal
(moderate-severe) Laparoscopic cholecystectomy: within first 48h
, Laparoscopic cholecystectomy: within first 48h or after resolution of symptoms
or after resolution of symptoms Others: nasal-biliary tube, biliary stenting
OTHER CHOLECYSTIC DISORDERS
Porcelain gallbladder
Rare manifestation of chronic cholecystitis; calcium deposition in gallbladder wall; high risk of
gallbladder cancer (2%-3%); prophylactic cholecystectomy
Cholesterolosis of the gallbladder
Accumulation of lipids in submucosa of gallbladder wall; diffuse form (strawberry gallbladder) or
localised form (cholesterol polyp, no acoustic shadowing)
Gallbladder adenomyomatosis
Benign hypertrophy of mucosal epithelium of gallbladder; Rokitansky-Aschoff sinuses; possible
polyp formation; cholecystectomy if polyp >10mm, sessile, and age >50y/o
Acalculous cholecystitis
Recurrent episodes of biliary colic in absence of stones; motility dysfunction and reduced EF;
cholecystectomy
Acute acalculous cholecystitis
5%-10% of acute cholecystitis; necroinflammatory disease; risk factors are vasculitis, DM, torsion
of gallbladder, obstructive adenocarcinomas, infections, prolonged delivery, severe trauma/burns
Low phospholipid associated cholelithiasis (LPAC) syndrome
ABCB4 gene deficiency, no MDR3 production; phospholipids are not transported in biliary tract,
cholesterol crystal formation and bile duct luminal membrane injuries; biliary symptoms after
cholecystectomy; hyperechoic intrahepatic foci or comet tail images within intrahepatic bile duct
ACUTE PANCREATITIS (AP)
Acute inflammation of the pancreas which may involve the peripancreatic fat and distant organs
CLNICAL DEFINITION
EPIDEMIOLOGY
Two out of three criteria:
Mean age: 40-60y/o
1- Acute onset of typical pancreatic pain
Incidence: 5-6/100,000 in Italy, 13-45/100,000
2- Increase of amylases or lipases >3-times
in US
ULN
2nd cause of hospitalisation and 15th cause of
3- Radiological imaging (CT or MRI)
death for GI diseases
compatible with pancreatitis
CAUSES
SIGNS AND SYMPTOMS
Obstructive
Symptoms
Alcohol
Abdominal pain
Toxins (tobacco, scorpion venom)
Vomit
Drugs (6-MP, valproate, sulphonamides,
Paralytic ileus
diuretics)
Shock (high mortality)
Metabolic alterations: hypertriglyceridemia (3rd
Dyspnoea (high mortality)
most common cause, 2%-5%)
Oliguria or anuria
Infections: virus (CMV, HBV, EBV), bacteria (TB,
Neurologic signs
Salmonella), fungi (Aspergillus, Candida),
Signs of infections
parasites (Toxoplasma, Ascaris lumbricoides)
Haemorrhage
Vascular disorder
Signs
Trauma
Ecchymosis of abdominal wall (Cullen sign,
Post-surgery
Grey-Turner sign)
Post-ERCP pancreatitis (PEP): 7% of ERCP,
Panniculitis
prevention with indomethacin or diclofenac
Thrombophlebitis
Hereditary-genetic-familial (CF)
Subcutaneous fat tissue necrosis
Others (diabetes, hypercalcaemia)
Signs of chronic hepatitis
Controversial
Bleeding from the oesophagus to the ligament of Treitz
CLINICAL PRESENTATION
EPIDEMIOLOGY
Haematemesis
Incidence 60/100,000 per year
Melena
Mortality rate 8%-10%
Clinical signs of blood loss
Resuscitation
APPROACH TO PATIENT Cannulation of 2 peripheral veins (or CVC)
Assessment of haemodynamic stability Volemic expansion (saline solution, Ringer’s
Vital signs (HR, BP, RR), general appearance lactate)
Diuresis Blood transfusion (if required)
Shock index (HR/BP, >1) Urinary catheter
Blood test (CBC, blood group, renal function, Diagnostic studies
coagulation) Upper GI endoscopy
X-ray, CT
PEPTIC ULCERS
Most common cause of UGIB (47%)
Causes
CAUSES
NSAIDs overuse; H. pylori infection
Peptic ulcer
Classification
Gastritis
Forrest’s classification
Oesophagitis
Diagnosis
Angiodysplasia
Upper GI endoscopy
Mallory-Weiss lesion
Therapy
Neoplasia
Medical therapy (PPI, stop NSAIDs, H. pylori
Oesophageal varices
eradication)
Dieulafoy lesion
Endoscopic therapy (diathermoregulation,
injection of vasoconstrictive or sclerosing
agents, clip placement)
PORTAL HYPERTENSION
Fibrosis due to liver cirrhosis results in increase pressure in portal system
Complications
Oesophageal varices: creation of oesophageal varices in all cirrhotic patients (30% will bleed)
Gastric varices
Ectopic varices (e. g. duodenal, colonic, etc.)
Portal hypertensive gastropathy: diffuse gastritis
Management
Prevention of 1st variceal bleeding: medical therapy (non-selective -blocker), endoscopic therapy
Therapy for variceal bleeding: resuscitation, vasoactive drugs (terlipressin, somatostatin,
octreotide), antibiotics (SBP prevention), endoscopy (band ligation, sclerotherapy, Sengstaken-
Blakemore tube, self-expandable oesophageal stent), radiological placement of transjugular
intrahepatic shunt (TIPS)
Prevention of bleeding recurrences
LOWER GASTROINTESTINAL BLEEDING (LGIB)
Bleeding from the ligament of Treitz to the anus
CLINICAL PRESENTATION EPIDEMIOLOGY
Haematochezia Incidence 40/100,000 per year
Proctorrhagia Mortality rate 5%
APPROACH TO PATIENT
,Assessment of haemodynamic stability Volemic expansion
Vital signs (HR, BP, RR), general appearance Blood transfusion (if required)
Diuresis Urinary catheter
Shock index Diagnostic studies
Blood test (CBC, blood group, renal function, Colonoscopy
coagulation) Angio-CT
Resuscitation Angiography
Cannulation of 2 peripheral veins (or CVC) Surgery
OBSCURE GASTROINTESTINAL BLEEDING
CAUSES
(OGIB)
Diverticula: most common in Western countries
Bleeding whose location and source cannot be
Benign anorectal masses: internal
identified
haemorrhoids, anal fissures
Obscure-overt GIB: obscure location but visible
Colitis: ischemic colitis (elderly), IBD (younger,
bleeding
ulcerative colitis, Chron’s disease)
Obscure-occult GIB: obscure location and
Neoplasia
detection with FOBT or chronic iron-deficiency
Polyps
anaemia
Angiodysplasia
Causes
Post-endoscopic
Angiodysplasia, tumours, others (NSAID-related
Post-surgery
bleeding, TB, CD, coeliac disease, vasculitis)
Miscellaneous
Diagnosis
Unknown
FOBT, upper GI endoscopy/colonoscopy
Others: radiation-induced colitis, infectious
Videocapsule endoscopy (VCE)
haemorrhagic colitis, vasculitis, solitary rectal
Double ballon enteroscopy (DBE)
ulcer, colonic varices and hypertensive portal
Scintigraphy, angio-CT, CT enterography, MRI
colopathy, Meckel’s diverticulum
enterography, angiography
GALLSTONES DISEASES
Diseases of the gallbladder and biliary tree caused by gallstones
GALLSTONE TYPES
Pure cholesterol gallstones
Cholesterol crystals; more common in Western
EPIDEMIOLOGY
countries
20mln of Americans
Pure pigment gallstones
Mortality rate: 0.12%
Black gallstones (calcium bilirubinate, increased
Increased incidence due to DM, metabolic
haemolysis)
syndrome, and obesity
Brown gallstones (calcium palmitate, infections,
de novo formation in bile duct)
Mixed gallstones
Cholesterol, pigment, calcium, bilirubin salts
RISK FACTORS Oral contraceptive
Independent Dietary
Ageing High calories
Female gender Low fibres
Race Low cis-unsaturated fats
Family history High refined carbohydrates
Lifestyle Associated conditions
Low grade physical activity Metabolic syndrome
Prolonged fasting Obesity
Rapid weight loss Hyperinsulinism
Pregnancy and parity (multiple, one close to the Oestrogen replacement therapy
,other) Gallbladder or intestinal stasis (or both)
BILIARY OBSTRUCTION
BILIARY COLIC Obstruction of the common bile duct
Symptomatic uncomplicated gallstone disease Signs and symptoms
Signs and symptoms Colic pain, persistent, sometimes intermittent
Transient and intense pain in RUQ, radiation to or absent (elderly)
right shoulder and right back region Nausea and vomiting
Nausea and vomiting Itching and jaundice (if complete obstruction)
Onset: after meal, night, early morning Diagnosis
Duration: 1-4h (peak at 30min) Clinical presentation
Recurrence: 50% of patients Blood tests: elevated AST, ALT, GGT, ALP,
Diagnosis bilirubin
Clinical presentation US: first-level, poor SE (50%)
Blood tests: normal or transiently elevation of MRCP: gold standard, no for stones <5mm
AST, ALT, GGT, ALP (if gallstone migration) Endoscopic US (EUS): for stones <5mm, high
US NPV
Treatment Treatment
Acute phase: fasting + hydration, NSAIDs Fasting + hydration
Post-acute phase: low-fat diet, UDCA Pain management: NSAID, paracetamol, opioid
(10mg/Kg/day in 2-3 doses, only if <10mm non- ERCP: diagnosis and stone removal
calcified gallstone), laparoscopic Subsequent laparoscopic cholecystectomy
cholecystectomy (pigment or calcified gallstone) Others: cholangioscopy during ERCP,
cholangioscopy-guided laser lithotripsy
ACUTE CHOLECYSTITIS ACUTE CHOLANGITIS
Inflammation and/or infection of the Infection of the biliary tract due to biliary
gallbladder wall obstruction
Signs and symptoms Signs and symptoms
Persistent and intense pain in RUQ Charcot’s triad: septic fever with chills,
Nausea, vomiting, low-grade fever jaundice, RUQ pain
(sonographic) Murphy’s sign Reynold pentad: septic fever with chills,
Complications jaundice, RUQ pain, shock, altered mental
Hydropic gallbladder status
Gallbladder empyema Complications
Emphysematous cholecystitis Systemic sepsis
Gallbladder perforation (biliary ileus) Multiple liver abscesses (long antibiotic
Haemorrhagic cholecystitis therapy)
Diagnosis Intravascular coagulation syndrome
Clinical presentation Diagnosis
Blood tests: leucocytosis, high CRP, elevated Clinical presentation
AST, ALT, GGT, ALP, bilirubin Blood tests: leucocytosis, high CRP, elevated
US: gallbladder wall thickening (>3mm), AST, ALT, GGT, ALP, bilirubin
pericholecystic fluid, gallbladder distension, US: first-level, poor SE (50%)
acoustic shadowing MRCP: gold standard, no for stones <5mm
CT: extension of inflammation, gallstone type, Endoscopic US (EUS): for stones <5mm, high
complications NPV
Treatment Treatment
Fasting + hydration Fasting + hydration
Pain management: NSAID, paracetamol, opioid Pain management: NSAID, paracetamol, opioid
Antibiotics: 3rd gen cephalosporin + Antibiotics: piperacillin/tazobactam, ampicillin
metronidazole (mild), piperacillin/tazobactam Urgent ERCP: stone removal
(moderate-severe) Laparoscopic cholecystectomy: within first 48h
, Laparoscopic cholecystectomy: within first 48h or after resolution of symptoms
or after resolution of symptoms Others: nasal-biliary tube, biliary stenting
OTHER CHOLECYSTIC DISORDERS
Porcelain gallbladder
Rare manifestation of chronic cholecystitis; calcium deposition in gallbladder wall; high risk of
gallbladder cancer (2%-3%); prophylactic cholecystectomy
Cholesterolosis of the gallbladder
Accumulation of lipids in submucosa of gallbladder wall; diffuse form (strawberry gallbladder) or
localised form (cholesterol polyp, no acoustic shadowing)
Gallbladder adenomyomatosis
Benign hypertrophy of mucosal epithelium of gallbladder; Rokitansky-Aschoff sinuses; possible
polyp formation; cholecystectomy if polyp >10mm, sessile, and age >50y/o
Acalculous cholecystitis
Recurrent episodes of biliary colic in absence of stones; motility dysfunction and reduced EF;
cholecystectomy
Acute acalculous cholecystitis
5%-10% of acute cholecystitis; necroinflammatory disease; risk factors are vasculitis, DM, torsion
of gallbladder, obstructive adenocarcinomas, infections, prolonged delivery, severe trauma/burns
Low phospholipid associated cholelithiasis (LPAC) syndrome
ABCB4 gene deficiency, no MDR3 production; phospholipids are not transported in biliary tract,
cholesterol crystal formation and bile duct luminal membrane injuries; biliary symptoms after
cholecystectomy; hyperechoic intrahepatic foci or comet tail images within intrahepatic bile duct
ACUTE PANCREATITIS (AP)
Acute inflammation of the pancreas which may involve the peripancreatic fat and distant organs
CLNICAL DEFINITION
EPIDEMIOLOGY
Two out of three criteria:
Mean age: 40-60y/o
1- Acute onset of typical pancreatic pain
Incidence: 5-6/100,000 in Italy, 13-45/100,000
2- Increase of amylases or lipases >3-times
in US
ULN
2nd cause of hospitalisation and 15th cause of
3- Radiological imaging (CT or MRI)
death for GI diseases
compatible with pancreatitis
CAUSES
SIGNS AND SYMPTOMS
Obstructive
Symptoms
Alcohol
Abdominal pain
Toxins (tobacco, scorpion venom)
Vomit
Drugs (6-MP, valproate, sulphonamides,
Paralytic ileus
diuretics)
Shock (high mortality)
Metabolic alterations: hypertriglyceridemia (3rd
Dyspnoea (high mortality)
most common cause, 2%-5%)
Oliguria or anuria
Infections: virus (CMV, HBV, EBV), bacteria (TB,
Neurologic signs
Salmonella), fungi (Aspergillus, Candida),
Signs of infections
parasites (Toxoplasma, Ascaris lumbricoides)
Haemorrhage
Vascular disorder
Signs
Trauma
Ecchymosis of abdominal wall (Cullen sign,
Post-surgery
Grey-Turner sign)
Post-ERCP pancreatitis (PEP): 7% of ERCP,
Panniculitis
prevention with indomethacin or diclofenac
Thrombophlebitis
Hereditary-genetic-familial (CF)
Subcutaneous fat tissue necrosis
Others (diabetes, hypercalcaemia)
Signs of chronic hepatitis
Controversial
