GIT management and diagnosis Flashcards
GI causes of finger clubbing
My Inflamed Liver:
Malabsorption
Inflammatory bowel disease
Liver cirrhosis
Abdominal exam clinical signs to look out for initially
Confusion: end stage liver disease/hepatic encephalopathy
Jaundice: high bilirubin from acute hepatitis, liver cirrhosis, cholangitis, pancreatic cancer
Pallor: underlying anaemia
Abdominal distension: ascites or bowel obstruction or organomegaly
Hyperpigmentation: haemochromatosis
Oedema: liver cirrhosis
Cachexia: malignancy and advanced liver failure
Hernias: coughing may make these more pronounced
Also look for:
stoma, surgical drains, feeding tubes, mobility aids, vital signs, fluid balances and prescriptions
Hand clinical signs for abdominal problems
Palmar erythema: red heel or palm: chronic liver disease (normal in pregnancy)
Dupuytren’s contracture
Koilonychia: spoon shaped nails associated with iron deficiency anaemia (eg in Crohn’s disease)
Leukonychia: Whitening nail bed - hypoalbuminaemia eg end stage liver disease, protein losing enteropathy
Finger clubbing: IBD, coeliac disease, liver cirrhosis, lymphoma of GIT
Asterixis (flapping tremor): hepatic encephalopathy or renal failure
Arms and axillae clinical signs for abdominal disease
Bruising: clotting problems secondary to liver disease
Needle marks: increased risk of viral hepatitis
Acanthosis nigricans: insulin resistance or GI malignancy (stomach cancer most common)
Hair loss: iron deficiency anaemia and malnutrition
Facial clinical signs for abdominal disease
Conjunctival pallor: anaemia
Jaundice: acute hepatitis, liver cirrhosis, cholangitis, pancreatic cancer
Corneal arcus and Xanthelasma: hypercholesterolaemia
Kayser-fleischer rings: Dark rings around iris - Wilsons disease (liver cirrhosis)
Perilimbal injection: inflammation adjacent to iris associated with IBD
Glossitis: smooth enlarged tongue - iron, B12 and folate deficiency
Oral candidiasis: immunosuppression
Aphthous ulceration: round ulcers inside mouth - stress, trauma, iron, B12 and folate deficiency
Hyperpigmented macules: Peutz-Jeghers syndrome
Enlargement of the left supraclavicular lymph node (Virchow’s node) - metastatic abdominal malignancy
Chest and abdomen clinical signs of abdominal disease
Spider naevi: liver cirrhosis, pregnancy, combined oral contraceptive (more than 5 = pathology)
Gynaecomastia: liver cirrhosis, digoxin and spironolactone medications
Caput medusae: engorged paraumbilical veins associated with portal HTN (liver cirrhosis)
Striae: ascites, malignancy, Cushings, obesity, pregnancy
Cullen’s sign: bruising around umbilicus - late sign of haemorrhagic pancreatitis
Grey-Turner’s sign: bruising in flanks - late sign of haemorrhagic pancreatitis
Stoma assessment
Location: type of stoma (e.g. colostomies are typically located in the left iliac fossa, ileostomies and urostomies are typically located in the right iliac fossa).
Contents: can be stool (e.g. colostomy or ileostomy) or urine (e.g. urostomy).
Consistency of stool: note if it is liquid (ileostomy) or solid (colostomy).
Spout: colostomies are flush to the skin with no spout whereas ileostomies and urostomies have a spout.
Murphy’s sign
- Position your fingers at the right costal margin in the mid-clavicular line at the liver’s edge.
- Ask the patient to take a deep breath.
If the patient suddenly stops mid-breath due to pain, this suggests the presence of cholecystitis (known as “Murphy’s sign positive”).
Causes of splenomegaly
Portal hypertension secondary to liver cirrhosis Haemolytic anaemia Congestive heart failure Splenic metastases Glandular fever
Anatomy of the colon and relevant clinical points
The widest area of the colon is the cecum, the narrowest is the sigmoid colon; meaning any blockages have highest likelihood of perforation in the sigmoid and chance of diverticulitis is highest in the sigmoid colon
Divisions of the abdomen and contents
right hypochondriac: liver, gallbladder, right kidney, small intestine
epigastric region: stomach, liver, pancreas, duodenum, spleen, adrenal glands
left hypochondriac: spleen, colon, left kidney and pancreas
right lumbar: gallbladder, liver and right colon
umbilical: umbilicus, parts of small intestine, duodenum
left lumbar: descending colon and left kidney
right iliac fossa: appendix and cecum
pelvic/hypogastric: bladder, sigmoid colon, uterus, reproductive organs
left iliac fossa: descending colon, sigmoid colon
water and electrolyte turnover in GIT
On average/24h (in rounded numbers)
+ 2000 CC Water intake (drinking and eating)
+ 8000 CC Secreted water in upper GI
(Saliva, gastric, duodenal, intestinal secretions, and bile)
_______________
+ 10,000 CC Water, exposed to the small intestinal mucosa
- 9000 CC Water, absorbed by the small intestinal mucosa - 90%
_______________
+ 1000 CC Water, exposed to the colon mucosa
- 900 CC Water, absorbed by the colon mucosa - 90%
_______________
+ 100 CC Water, lost in stool (≡ 1% of the 10,000 CC)
If this 1% becomes 2%, it means diarrhoea!
If this 1% becomes 0.5%, it means constipation!
In conditions like obstruction, diarrhoea and perforation, water and electrolyte imbalance is a major and early issue.
Considering 70-80% of body weight in neonates is composed of water, these disorders are more dangerous in children.
Define acute abdomen
An abdominal condition of abrupt onset associated with severe abdominal pain resulting from (ethiology):
Inflammation
Obstruction
Infarction
Perforation
Rupture of intra-abdominal organs.
Acute abdomen requires urgent evaluation and diagnosis, because it may indicate a condition that requires urgent surgical intervention.
Presenting complaint of acute abdomen
SOCRATES characteristics of pain
Site - Where is the pain, is it localized, in a region, or generalized?
Diffuse
Epigastrium, Peri-Umbilical, Hypogastrium
Four Quadrants
Onset - Gradual, rapid, or sudden? Intermittent or constant? Happened before?
Character - Sharp, stabbing, dull, aching, tight, sore, colicky, burning?
Radiation - Does it spread to other areas e.g. back or shoulder?
Associated symptoms - Nausea, Vomiting, Dysuria, Jaundice?
Timing - Does it occur at any particular time?
Exacerbating or Relieving factors.
Surgical history - Does the pain relate to surgical interventions? / Severity
Characteristics
Sharp in nature
Well-localised
Made worse by movement or cough
Relieved by lying still
Mild forms – dull in nature and vague description from patient
Severe forms – nausea and vomiting, poorly-localised
Foregut – epigastrium
Midgut – peri-umbilical
Hindgut – suprapubic
Interpreting abdominal imaging
Check the name, date and type of imaging
Ask about clinical findings
Describe the image (type, position, view, plain/contrast) and landmarks
Describe abnormalities
Translate these abnormalities to pathologies
Differential pathologies
Management plan and further investigations if needed
Acute abdominal series XR
Indicated for:
Determining the amount of bowel gas and possibly bowel distension
Assess air fluid levels
Query pneumoperitoneum
Projections used:
AP supine: most information is gathered via this view
PA erect AXR: This clarifies air-fluid levels
PA erect chest XR: This is for greater sensitivity for pneumoperitoneum and to exclude any chest pathologies which may be presenting with abdominal pain
Modified view (for those who cannot stand):
AP supine
Left lateral decubitus view: most sensitive for intraperitoneal free gas evaluation
AP supine chest view
In order to adequately evaluate for free intraperitoneal gas, the patient should be positioned in the erect and decubitus views for enough time to allow small amounts of free gas to drift up to the diaphragm or lateral liver edge, respectively. This often takes ~5-10 minutes
KUB XR
Indicated for visualising any calcifications within the urinary tract (kidneys, ureter, urinary bladder and urethra)
Is an AP projection
Taken with patient lying straight, supine, taken on full inspiration to squash all organs down to fit in one image
Intestinal obstruction types
Mechanical: physical blockage of the intestinal lumen (either through extra, intra or inter-mural means) such as adhesion bands, neoplasms and hernias
Paralytic Ileius (pseudo-obstruction): a functional condition causing loss of peristalsis, such as bacterial or viral infections, electrolyte imbalances etc.
Mechanical bowel obstruction complications
Loss of intra-luminal fluid and vomiting leads to hypovolaemia, water and electrolyte imbalances
Bowel distension and intraluminal and intramural pressures increase which can lead to intestinal ischaemia and necrosis due to perfusion impairment (STRANGULATED BOWEL OBSTRUCTION) is a vascular emergency
Luminal flora of the bowel changes and BACTERIAL OVERGROWTH occurs
Perforation
Respiratory distress (elevated diaphragm)
Aspiration pneumonitis
Acute renal failure
Bowel obstruction investigations/diagnosis
History of bowel changes (prior abdominal operations may suggest adhesions, abdominal disorders)
Abdominal examination; assess for hernias or previous scar tissues
Bloods: FBC, U+Es, Amylase, LFTs, CRP, clotting screen
ABG (strangulation)
Urinary output
In partial or early (first 1-2 days) small bowel obstruction they may appear identical to an ileus, therefore follow up imaging is usually used to see how it involves and then determine the cause
Acute abdominal series Ix:
AXR supine
AXR upright
CXR upright
CT scan more sensitive for SBO detection
Small bowel obstruction and causes
Caused by lesion obstructing lumen of the bowel
Results in dilatation of bowel proximal to obstruction and compression after obstructing lesion
caused by: Adhesions Tumors Hernia Irritable bowel disease Intussusception (tunneling within bowel) Intraluminal lesions other than tumors (foreign body, gallstones, bezoars)
bowel obstruction diagnostic criteria
Dilated small bowel loops >3 cm (SBO) >5/6cm LBO
Air-fluid levels
Paucity of air in colon (lack of air past the obstruction if complete obstruction)
SBO:
Can look very similar to ileus when early within first few days, need follow up monitoring to see how it develops
Will show dilated loops of small bowel >3cm
Transition point
Collapsed bowel distal to transition point
Maybe a small bowel faeces sign: stool seen within the small bowel
Closed loop bowel obstruction
Obstruction of a loop of bowel in 2 separate places
Will not see any significant dilatation proximal to the closed loop
Often caused by adhesions from prior surgery
Can result in strangulation (surgical emergency)
There will be blocked blood flow to bowel resulting in necrosis
Imaging will show wall thickening and decreased enhancement of bowel wall
Closed loop obstructions need immediate surgical management due to high risk of perforation from strangulation
Strangulated bowel and red flags
Refers to ischaemia/infarction of an obstructed loop of bowel
Most commonly seen in context of a closed loop obstruction
Will show reduced mural enhancement on CT scan
Red flags: indicate early surgical interventions:
Patient is usually more ill than expected
Severe abdominal pain disproportionate to clinical findings suggests ischaemia (sharp, constant, localised pain with peritonism)
Localised abdominal tenderness and rigidity
Tachycardia
Fever
Marked raised leukocytes
Acidosis
Comparison of SBO and paralytic Ileus
Both conditions cannot promote bowel contents (impaired motility)
Both show distended loops of small intestine detected by XR or CT
OBSTRUCTION physically blocks the contents: the lumen is closed
ILEUS: the paralysis of the intestinal wall muscles makes contents stagnant: the lumen in open, this is a FUNCTIONAL obstruction
Ileus has no hyper-secretion and therefore no colic usually
Bowel sounds are absent/diminished in ileus but are hyperactive in SBO
Ileus is temporary motility disorder, reversed by correction of the cause
Localised functional paralytic Ileus and causes
Dilatation of a loop(s) of small bowel called sentinel loops are seen on AXR
Results from abdominal pathology causing focal inflammation of the small bowel
Causes: Cholecystitis Pancreatitis Appendicitis Diverticulitis Ureteral stones
Generalised functional Ileus and causes
Most often post operative
Involves the entire bowel, large and small
Cause of generalised function ileus: operations, infection and inflammation, electrolyte imbalances, drugs
Abdominal surgery
Infection: sepsis, intra-abdominal abscess, peritonitis, pneumonia, electrolyte abnormalities (hypokalaemia, hypomagnesemia, hypermagnesemia, hyponatremia)
Medication: anticholinergics, opiates, phenothiazines, CCB, tricyclic antidepressants
Hypothyroidism
Retroperitoneal haemorrhage
Spinal cord injury
Myocardial infarction
Mesenteric ischaemia
Paralytic Ileus presentation
Inability to tolerate liquids or solids by mouth
Nausea
Lack of flatus or bowel movements
Vomiting and abdominal distension MAY occur
Large bowel obstruction and causes
Far less common than small bowel (20% bowel obstructions)
Causes:
Malignancies
Diverticular disease
Colonic volvulus
Bowel obstruction presentation
Nausea and vomiting Abdominal colics Abdominal distension Lack of wind/gas passage ie constipation or obstipation Loss of lots of fluid: hypovolemic
Upper obstruction (small intestine):
Vomiting occurs earlier on
Distance between colics are SHORTER
Abdominal distension and constipation are LATE presenting
Lower obstruction (large intestine): Abdominal distension and constipation occur earlier on Distance between colics is longer Vomiting occurs later on *in complete obstruction, symptoms are complete, but in partial obstruction symptoms are more mild usually and they may also develop diarrhoea (hyper-secretion)*
SBO and LBO AXR comparisons
SBO: Central gas shadows No gas in large bowel Mucosal folds (valvulae conniventes) completely cross lumen May show fecal impact sign
LBO:
Peripheral gas shadows
Dilation >6 cm
Gas proximal to blockage but not in rectum (unless PR exam done beforehand)
Mucosal folds (haustra) do NOT cross all lumen width
Bowel obstruction management
ALL bowel obstructions need fluid resuscitation and correction of electrolyte imbalances
Conservative: usually successful secondary to adhesions, Ileus and partial obstructions
- Monitor patient regularly, regular examinations and imaging to monitor progress, NBM, if signs of strangulation, ischaemia, peritonitis or toxaemia then ready for emergency surgery
Surgical intervention: strangulation, frank perforations, peritonitis, LBO all need immediate surgical intervention
Fluid resus steps
Two large IV lines administer saline or hartmann
Bloods: FBC (Hb, WCC), U+Es (Na, K), CRP, amylase, lipase, group and save
NBM, NG tube insertion
Catheterise
Fluid balance chart
ABG needed if in shock, suspected ischaemic bowel or pancreatitis
Acute appendicitis
Appendix is attached to cecum found in left inguinal fossa (RIF)
Most common acute abdomen complaint
Highest incidence between 10-20 years but can occur at any age
Very wide range of presentations
Acute appendicitis causes and pathophysiology
Causes:
Fecalith (poop rock)
Undigested seeds
Pinworm infection
Pathophysiology:
Obstruction blocks the blind ending lumen
The appendix continues secreting fluid and becomes oedematous
Causing inflammation of the appendix and leading to compression of afferent visceral nerves nearby causing pain
Can lead to gangrene if the obstruction of blood vessels supplying the organ persists
Acute appendicitis presentation
Epigastric or periumbilical pain that moves to the right inguinal fossa (RIF)
Gradual pain onset, constant and moderate-severe
Peritonism: Shows guarding and rebound tenderness or percussion tenderness in RIF
Tachycardia
Fever
Anorexia
Nausea may be present but vomiting is rare
Constipation in adults, diarrhoea in children
Rovsing’s sign (pain greater in RIF than LIF when LIF pressed)
Psoas sign (pain on flexion and internal rotation of right hip if appendix close relation to obturator internus)
Acute appendicitis complications
Perforation: if faecolith present and diagnosis delayed can cause generalised peritonitis Gangrenous appendix Appendix abscess (usually treat with drainage or antibiotics) Appendix mass (inflamed and covered with omentum) diagnosed with US/CT, early surgery or conservative NBM and antibiotics treatment used +/- delayed appendectomy
Acute appendicitis investigations
Bloods: neutrophil leucocytosis, elevated CRP
CT scan has high diagnostic accuracy!!
Mcburney’s point +ve
acute appendicitis management
Mild: rest GI and antibiotics for inflammation
Appendectomy +/- antibiotics
Laparoscopic appendicectomy (esp. Good for women and obese with suspected gangrenous perforation)
Meckels diverticulum
Outpouching of the lower part of the small intestine
It is a remnant of the vitello-intestinal duct (leftover umbilical cord should obliterate during fifth week foetal development)
Most common congenital defect of the GIT (2-3% population)
Usually asymptomatic
The majority of symptomatic pts begin presenting before age 2
Meckel’s diverticulitis occurs in 20% patients who become symptomatic, it is clinically indistinguishable from appendicitis
Meckels diverticulum disease of 2s
2% people have this
2:1 M:F ratio
2 inches in length usually
2 more common ectopic tissues: pancreas and stomach
2 complications other than diverticulitis: obstruction, bleeding
2 mechanisms of obstruction: secondary intussusception (inverted diverticulum acts as lead point), volvulus (loops around band between diverticulum and umbilicus)
Meckels disease presentation, diagnosis and management
Presentation:
GI bleeding
Obstructive symptoms
Diagnosis:
technetium -99m pertechnetate scan (Meckel’s scan)
Management:
Asymptomatic - no treatment needed
Symptomatic - monitoring
Meckel’s diverticulitis - laparoscopic surgery
Peritonitis
Inflammation of the peritoneum
Generally secondary generalised bacterial infection
Common complication of many abdominal pathologies
Classification:
Chemical, viral, bacterial (primary or secondary)
Local peritonitis - localised tenderness
Generalised peritonitis - generalised tenderness
Causes of peritonitis
Post-surgical eg anastomotic leak, enteric injury (30%)
Acute perforated appendicitis (most common esp <45 yrs (20%)
Acute diverticulitis (most common in elderly)
Peptic ulcer perforation - 10% (or other upper GI perforation)
Perforated acute cholecystitis
Perforated tumours (colonic or gastric)
Perforated ischaemic bowel (eg acute mesenteric ischaemia)
Acute pancreatitis
Peritoneal dialysis-related
Peritonitis pathophysiology
Widespread absorption of toxins from large, inflamed surface (peritoneum)
Paralytic ileus with loss of fluid, electrolytes and protein
Gross abdominal distension with elevation of diaphragm, increases susceptibility to lung collapse and pneumonia
Primary (rare): monomicrobial, typically streptococcal. Probable port of entry via the bloodstream
Secondary (common): polymicrobial, gram - and +ve and anaerobes. Portal of entry from intra-abdominal organs (secondary to perforation, ischaemia or infection of other organs etc)
Usually shows mixed faecal flora (E.coli, strep facalis, pseudomonas)
Peritonitis presentations
Anorexia
Fever
Severe generalised abdominal pain, radiating to shoulder and back
Abdo pain worse with movement, coughing, sneezing
Alleviated when lying still
Tachycardia
Generalised abdominal tenderness, rebound tenderness, guarding and rigidity
Max tenderness may indicate underlying cause if in one particular area
May be abdominal mass present
Advanced stages: Distended abdomen and tympanic on percussion Increasingly toxin and ill Feculent vomit Sunken eyes (severe dehydration) Rapid, febril pulse (shock) Moist, cold, cyanosed skin (shock) drowsy/confused (shock)
Peritonitis investigations
ABCDE assessment and act accordingly
Analgesia
Find cause: Bloods show infection markers, Abdo CT scan confirms or excludes acute pancreatitis or locates probably source of pathology
Laparoscopy
Prep patient for possible surgery: most causes of peritonitis need surgery, however, acute pancreatitis is contraindicated for surgery!
Management of peritonitis
Early: IV antibiotics (wide coverage) eg metronidazole 500mg IV tds + Cefuroxime 750mg IV tds
Oxygen therapy, serum therapy (IVI), correction of electrolyte abnormalities
Definite specific management should then be based on diagnosis of cause: surgery, medications ect.]
if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy
Bacteroides fragilis - antibiotics in peritonitis needs to cover this bacteria (common gut flora causing abdo infections)
Local peritonitis causes
Diverticulitis
Cholecystitis
Salpingitis
Appendicitis
local peritonitis presentation and investigation
Presentation:
Localised tenderness/rebound tenderness
Presentation of cause
Investigations: Bloods CT US CXR AXR *if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy*
Gastroenteritis
(adults)
An infection of the GIT, nonspecific term to describe a condition with a combination of nausea, vomiting, diarrhoea and abdominal pain
About 20% of the UK develops every year
Viral infections cause 30-40% of gastroenteritis in adults (higher in children)
Management is not usually dependent on cause as it is never isolated and the responsible agent never diagnosed
(children):
Infective gastroenteritis in young children by the sudden onset of diarrhoea with/without vomiting
Mostly due to viral infection but can be from bacterial or protozoal infections.
Usually resolves within days but can cause severe dehydration and become life threatening
Gastroenteritis causes
children:
Retrovirus most common (56%), campylobacter spp., salmonella spp., norovirus, E.coli
Cause never isolated and responsible agent never diagnosed
adults:
A variety of viral (norovirus, rotavirus, adenovirus), bacterial (E. coli, salmonella, staph.aureus toxins) and parasitic pathogens
Gastroenteritis risk factors
Poor hygiene, lack of sanitation
Compromised immunity
Achlorhydria: lack of HCL in digestive juices (especially for salmonella and campylobacter) can result from acid-suppressing drugs
Poorly cooked food, cooked food left too long, insufficient reheating etc
Gastroenteritis presentations
History of eating mispreppared food (incubation usually around 24-36 hours for virus’, few hours to 4 days for bacillary dysentery and 7-10 days for parasites) or may have recently been to exotic location
Vomiting and nausea
Abdominal pain
Diarrhoea (bloody diarrhoea may indicate bacterial infection especially E. coli)
Pyrexia (in adults can indicate invasive organism)
Complications of gastroenteritis
Dehydration and electrolyte disturbance
Haemolytic uraemic syndrome (HUS): AKI, haemolytic anaemia and thrombocytopenia
Reactive complications such as urticaria, reactive arthritis, erythema nodosum etc.
IBS
Gastroenteritis investigations
Vitals: temp, BP, pulse, HR, respiratory rate
Abdominal examination to exclude other diagnoses (appendicitis)
Assess for dehydration
Stool microscopy, culture and sensitivity if there is blood/mucus in stool or the patient is immunocompromised or the patient has been abroad to anywhere other than western europe, north america, australia or NZ recently, if diarrhoea has not improved by day 7 or uncertain diagnosis.
Unwell patients may need FBC, renal function and electrolytes
Gastroenteritis prevention and management
Prevention:
Good hand hygiene
Good food hygiene and preparations (cooking)
Management:
All dysentery and food poisoning are notifiable diseases
Hospital admission if unable to retain oral fluids, features of shock or severe dehydration
Assess the extent of dehydration and manage accordingly, patient education of infection prevention, advising small light meals, avoiding spice or heavy food while ill.
Oral rehydration salt (ORS) can be used in frail elderly patients
Advise exclusion from work or other settings until at least 48 hours after being free from diarrhoea and vomiting
Can advise antimotility drugs if these will enable quicker resolution to essential activities in those with mild to moderate diarrhoea (loperamide 1st line). AVOID if blood or mucus in stool or high fever present
CHILDREN
Encourage fluid intake and normal breastfeeding etc. but avoid solid foods if during rehydration therapy
Offer oral rehydration salts to those at increased risk of dehydration
Racecadotril can be used with oral rehydration in infants over 3 months
Monitor vitals very well.
Gastroenteritis red flags
Appears unwell or deteriorating Altered responsiveness Sunken eyes Tachycardia Tachypnoea Reduced skin turgor
Signs of shock
Decreased level of consciousness Pale or mottled skin Cold extremities Decreased level of consciousness Tachycardia Tachypnoea Weak peripheral pulses Prolonged capillary refill Hypotension
Dehydration assessment
Mild: lassitude (weak, lacks energy), anorexia, nausea, light-headed, postural hypotension
Moderate: apathy (lack of interest or concern), tiredness, dizzy, muscle cramps, dry tongue, sunken eyes, reduced skin elasticity, postural hypotension, tachycardia, oliguria
Severe: profound apathy, weakness, confusion, shock, tachycardia, marked peripheral vasoconstriction, hypovolemia, oliguria or anuria
Cholelithias
70% patients with gallstones are asymptomatic and have no issues
Can cause acute or chronic cholecystitis, biliary colic, pancreatitis or obstructive jaundice
Biliary colic is most common, caused by gallstone impacting in the cystic duct or the ampulla of Vater, blocking the tubes.
Second most common is acute cholecystitis, caused by gallbladder distension and subsequent necrosis and ischemia of mucosal wall
Cholelithias pathophysiology
Bile is formed of cholesterol, phospholipids and bile pigments, stored in the gallbladder before passing into the duodenum
the cystic duct travels from the GB, joins the common hepatic duct to form the common bile duct, joined by the pancreatic duct close to the duodenum to form the hepatopancreatic ampulla of Vater which deposits bile into the duodenum.
Gallstones form as a result of supersaturation of bile
Types of gallstone
Cholesterol stones: composed purely of cholesterol from excess cholesterol production. Highly linked to poor diet and obesity.
Pigment stones: composed purely of bile pigments from excess bile pigments production. Commonly seen in those with haemolytic anaemia
Mixed stones: mixture of both
Risk factors for cholelithias
5 Fs: Fat, forty, fertile, female, family history
Increasing age
Positive family history
Female
Loss of bile salts (after obesity surgery)
Diabetics (metabolic syndrome)
Oral contraception, particularly in young women
Management of cholelithias
Case by case basis: very small risk of complications so mostly a ‘watch and wait’ policy
Younger patients are more likely to develop complications more frequently due to having gallstones for longer - monitor more frequently
Modify risk factors if possible
Biliary colic
Occurs when the gallbladder neck becomes impacted by a gallstone.
No inflammatory response, but the contraction of the gallbladder against the occluded neck will cause pain
Over 50% symptomatic pts with gallstones will present with biliary colic
Biliary colic presentations
Sudden, dull pain
Colicky
Focussed often in the RUQ, although may radiate to epigastrium and/or the back
Pain may be precipitated by consumption of fatty foods (stimulates CCK release from duodenum, causing contraction of GB)
Nausea/vomiting
Often relieved quickly with pain relief
Cholecystitis
Inflamed gallbladder
Most often caused by gallstones
More common in women
25% pts with cholelithias will present with acute cholecystitis
Cholecystitis pathology
Most individuals with gallstones are asymptomatic, the gallstones mostly stay within the gallbladder and cause no harm
Cholecystitis is usually caused when a gallstone seemingly becomes stuck in the cystic duct
Bile then builds up in the gallbladder, which becomes distended and the walls of the gallbladder consequently become inflamed or may even become infected
Infection is more prone to complications
Repeated attacks of acute cholecystitis leads to chronic cholecystitis; the walls of the gallbladder become thickened and scarred and the gallbladder becomes shrivelled
Risk factors for cholecystitis
5 Fs: fat, fertile, female, forty, family history
Gallstones or biliary sludge Hospitalisation for trauma or acute biliary illness Female Increasing age Obesity Rapid weight loss Pregnancy Crohn's disease Hyperlipidaemia
Cholecystitis presentation
Upper abdomen pain, usually worse on the right side under the ribs (RUQ) continuous epigastric pain
May radiate to the back or to the right shoulder and tends to last several hours
Nausea and vomiting
Fever, lethargy
+ve Murphy’s sign
May have previous history of cholecystitis
Murphy’s sign positive: increased pain when placing hand under the ribs on the right hand sign and asking patient to take deep breath, putting pressure on the gallbladder
Cholecystitis investigations
Vitals: BP, temperature, pulses, urine output
Abdominal examination including Murphy’s sign
Ultrasound: thickened GB walls (>3mm), gallstones
Bloods: WWC raised, mildly abnormal liver enzymes
CT of abdomen if indicated
Magnetic resonance cholangiopancreatography (MRCP): shows potential defects in biliary tree with almost 100% sensitivity
trans-abdominal US is most sensitive!! = FIRST LINE
Management of acute cholecystitis
Acute cholecystitis:
Opioid (morphine or pethidine) given parenterally and/or diclofenac by suppository - overcomes absorption difficulties due to vomiting.
Pain lasting >24 hours with fever needs hospital admission
IV antibiotics (coamoxiclav + metronidazole)
Open cholecystectomy surgery to remove stones in emergency - very rarely perform cholecystectomy for acute cases
Sepsis 6 if septic
Management of chronic cholecystitis
Laparoscopic cholecystectomy preferred Percutaneous cholecystostomy (surgical drainage) is useful for those not fit for cholecystectomy *Post op complications are rare but include bile duct injury, fat intolerance and post-cholecystectomy syndrome (abdominal pain, jaundice or dyspeptic symptoms*
Prognosis is good however there is a high chance they may experience more bouts of cholecystitis which is why usual treatment is to remove the gallbladder entirely
Cholangitis and causes
Infection of the biliary tract
Associated with high morbidity and mortality if untreated
Cause:
Biliary outflow obstruction
Gallstones
ERCP (iatrogenic)
Cholangiocarcinoma
Most common organisms are E. coli, Klebsiella and enterococcus
Pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy and parasitic infections (rare)
Cholangitis pathophysiology ad risk factors
Pathophysiology:
During obstruction the stasis of fluid combined with elevated intraluminal pressure allows bacterial colonisation of the biliary tree to become pathological
Risk factors:
Oral contraceptive
Fibrates
Lipid-rich diet
Cholangitis presentation
Charcot’s triad: jaundice, fever, RUQ pain
RUQ pain Fever Jaundice (when bilirubin >50 umol/L) Pruritus (as result of bile accumulation) Pale stool Dark urine Pyrexic Rigors Confusion Hypotension, tachycardia May have history of cholelithias, recent biliary tract procedure (ERCP/cholecystectomy) or previous history of cholangitis
Cholangitis investigations
Bloods: FBC (Hb and WCC) shows leukocytosis, LFTs (raised ALP and GGT)
Blood cultures
Biliary tract USS shows bile duct dilation >6mm and may indicate underlying cause
GOLD STANDARD: ERCP is diagnostic and therapeutic
Cholangitis management
Vitals: check for sepsis, manage as needed
Gain IV access for fluid resus
Routine bloods and blood cultures taken early
Broad spectrum antibiotics therapy (co amoxiclav + metronidazole)
Definitive management given via endoscopic biliary decompression (ERCP +/- sphincterotomy and stenting)
PTC percutaneous transhepatic cholangiography 2nd line
In long term may need cholecystectomy if gallstones are underlying cause
Acute pancreatitis
Sudden inflammation of the pancreas
Typically caused by hypersecretion of backflow (obstruction) of exocrine digestive enzymes, resulting in autodigestion of the pancreas
Can be mild or life threatening
With effective treatment has good prognosis
Acute pancreatitis pathology
Occurs when digestive enzymes are activated before release into the duodenum and so attack the pancreas
If the enzymes enter the bloodstream other organs can become affected which can lead to life threatening shock symptoms
Pancreatic damage can be classified into two major categories: interstitial oedematous (most common, better prognosis) and necrotising (5-10% cases, more severe)
The damage is potentially reversible whereas chronic pancreatitis results in irreversible damage from ongoing inflammation
Causes of acute pancreatitis
I GET SMASHED
Iatrogenic Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune disease Scorpion sting Hypercholesterolaemia/hypertriglyceridaemia ERCP Drugs: thiazides, septrin, tetracyclines, azathioprine
Risk factors of acute pancreatitis
Male Increasing age Obesity Smoking Family history
Acute pancreatitis presentations
Severe, sudden epigastric pain
Sharp, stabbing pain, may radiate to sides or back if cholecystitis present too
Vomiting
Pain rapidly crescendos, duration likely 1 day
May have history of biliary colic, recent surgery or illness
Exacerbated by movement, alleviated partially by leaning forward or adopting foetal position
Tetany may occur from hypocalcemia (secondary to fat necrosis)
Acute pancreatitis investigations
Abdominal examination: epigastric tenderness, abdominal distension
Cullen’s sign: periumbilical bruising (LATE sign of retroperitoneal haemorrhage)
Grey-Turner’s sign: flank bruising (LATE sign of retroperitoneal haemorrhage)
Bloods: FBC, CRP, U+Es, LFTs, Lipase, serum amylase, VBG, ABG, Beta-hCG (rule out pregnancy and permit safe investigation of XR and CT)
ECG to ensure no MI
Urinalysis
CXR to look for free gas under diaphragm (pneumoperitoneum)
USS - abdominal ultrasound
CT of abdomen and pelvis
glasgow-Imrie scale
Diagnosis of acute pancreatitis
two of three criteria
Abdominal pain + history suggestive of acute pancreatitis
Serum amylase/lipase of over 3 times upper limit of normal
Imaging characteristic of acute pancreatitis
Classification of acute pancreatitis
Mild: most common, no organ dysfunction/complications, resolves within 1 week
Moderate: initially some evidence of organ failure which improves within 48 hours
Severe: persistent organ dysfunction >48 hours with local or systemic complications
Management of acute pancreatitis
PANCREAS:
Perfusion: fluid resus and oxygenation
Analgesia
Nutrition: enteral feeding <48 hours
Clinical: APACHE II or APACHE I scores to assess need to transfer to HDU
Radiology: USS for gallstones, choledocholithias and local complications. CECT after 48-72 hours pain onset to determine degree and extent of necrosis. Percutaneous catheter drainage USS guided helpful to manage necrosis
ERCP: within 72 hours if cholangitis or severe acute pancreatitis with persistent obstruction
Antibiotics: empirical ABs if infection suspected
Surgery: multiorgan failure with necrosis not responding to conservative management
Predict severity using the glasgow-Imrie scale, predict mortality using APACHE II scoring
Once diagnosis is confirmed, largely supportive management: fluid resuscitation, analgesia (IV paracetamol and opioids)
Nil-by-mouth until initial pain improves - gradual feeding re-introduced via oral feeding or nasojejunal feeding
Antiemetics: IV ondansetron
Calcium derangement corrected
Control glucose
Antibiotics for prophylaxis PRN
Infected necrotic tissue needs to be removed via: percutaneous drainage or surgical necrosectomy
Gallstone pancreatitis:
Obstructed bile duct needs ERCP to relieve obstruction with/without sphincterotomy to dilate the sphincter of Oddi to allow removal of ductal stones, biliary sludge etc.
Cholecystectomy for all patients with gallstone pancreatitis during same admission of acute episode
Alcoholic pancreatitis:
Benzodiazepines for withdrawal agitation and seizures
Thiamine, folate and B12 replacement
Glasgow-Imrie scale: PANCREAS
PaO2 <7.9 Age >55 Neutrophils/WCC >15 Calcium <2 Renal function/ urea >16mmol Enzymes (LDH >60) Albumin <32 g/l Sugar >10mmol
*if CRP >150mg/l likely to be severe
Chronic pancreatitis and cause
Chronic inflammation resulting in progressive and irreversible damage to the pancreas parenchyma
Male to female ratio 4:1
Cause: Chronic alcohol abuse (60%) Idiopathic (30%) Hyperlipidaemia Infection (viral and bacterial) Hereditary (CF) Autoimmune
Presentation of chronic pancreatitis
Chronic pain, complicated by recurring attacks of acute pancreatitis (acute-on-chronic pain)
Typically in epigastrium and back
Nausea and vomiting
Endocrine insufficiency (secondary to islet of langerhans damage)
Exocrine insufficiency (secondary to acinar cell damage causing malabsorption - weight loss, diarrhoea, steatorrhoea)
Abdo examination: soft abdomen but tender epigastrium, may have signs of cachexia and malabsorption
Chronic pancreatitis investigations
Urine dip
Bloods: FBC, CRP, serum amylase/lipase (often not raised in established disease), BLOOD GLUCOSE, LFTs (obstructive jaundice)
Faecal elastase level will be low
Chronic pancreatitis management
Treat underlying cause (alcohol cessation, statin therapy for hyperlipidaemia)
Analgesia (opioid or neuropathic analgesics)
Enzyme replacement for malabsorption
Vitamins A, D, E and K (fat soluble)
Regularly check for endocrine insufficiency, (HbA1c annually) treat as needed, also screen bone density regularly
Cholesterol and pigment gallstones
Cholesterol gallstones often appear yellow and are the most common type of gallstone. Scientists believe that cholesterol stones are caused by bile that contains:
too much cholesterol
too much bilirubin
not enough bile salts
The cause of pigment stones is not known. They seem to occur in people who have:
cirrhosis of the liver
biliary tract infections
hereditary blood disorders in which the liver makes too much bilirubin
Choledocelithias
(also called bile duct stones or gallstones in the bile duct) is the presence of a gallstone in the common bile duct.
Choledocelithias presentation
abdominal pain in the RUQ or epigastric region
fever
jaundice (yellowing of the skin and eyes)
loss of appetite
nausea and vomiting
clay-colored stools
Pain severity can vary throughout, can be sporadic or can linger
Complications of choledocelithias
Cholangitis
Biliary cirrhosis
pancreatitis
Choledocelithias investigations
transabdominal ultrasound (TUS)
abdominal CT scan
endoscopic ultrasound (EUS)
endoscopic retrograde cholangiography (ERCP)
magnetic resonance cholangiopancreatography (MRCP)
percutaneous transhepatic cholangiogram (PTCA)
complete blood count
bilirubin
pancreatic enzymes
liver function tests
Choledocelitheias management
stone extraction via biliary endoscopic sphincterotomy (BES) using balloon/basket device
fragmenting stones (lithotripsy)
surgery to remove the gallbladder and stones (cholecystectomy)
surgery that makes a cut into the common bile duct to remove stones or help them pass (sphincterotomy)
biliary stenting
Intussusception
Common in infants 3-12 months
Boys:girls 3:1 ratio
Usually occurs in the ileocecal region (usually ileum telescoping into cecum)
Primary: 95% in infants and children, most often due to lymphoid hyperplasia from peyer’s patches
Secondary: adults mostly, much less common, lead point/apex is a polyp, tumour or inverted Meckel’s diverticulum etc.
Low mortality within 24 hours, but very high in irreducible or gangrenous cases
Pathophysiology:
Telescoping of portion of the intestine
Mesentery is dragged alongside proximal bowel wall into the distal lumen, obstructing venous return
Causes Oedema, mucosal bleeding and increased pressure
If arterial flow is compromised then causes ischaemia, necrosis and perforation can result
Intussusception presentation
classic triad: sudden severe paroxysmal colicky pain, bilious vomiting, red currant jelly stools
Colicky abdominal pain and guarding Leg flexing Fever (if septic) Lethargy Vomiting Blood in stool: red currant jelly stool Poor feeding Dance’s sign: empty RIF + sausage shaped mass in mid/RUQ Abdominal distension Signs of shock in late presentation
Intussusception investigations
USS if stable may show bullseye sign, doughnut sign or crescent in doughnut Diagnostic enema (CI if peritonitis, shock, perforation or pt unstable) shows meniscus sign/coiled spring sign
Intussusception management
Acute: clinically stable, no CI to contrast enema reduction:
NBM, nasogastric tube, Fluid resus and contrast enema reduction
Broad spectrum antibiotics IF sign of infection/ischaemia
Clinically unstable or CI contrast enema
Fluid resus and surgical reduction
Broad spectrum antibiotics IF sign of infection/ischaemia
Achalasia
Rare disorder of the oesophagus making it difficult to swallow food or drink
Motility disorder of the lower oesophageal or cardiac sphincter
This layer of muscle has impaired peristalsis and failure of relaxation causing functional stenosis or stricture
Exact cause is unknown but can occur secondary to other conditions such as oesophageal cancer
Tends to present in adult life, children is very rare
achalasia pathophysiology
Muscle tone and activity are controlled by a balance of excitatory transmitters such as ACh and substance P and inhibitory transmitters such as NO and Vasoactive intestinal peptide (VIP)
The interstitial cells of Cajal (cells within the intestinal wall which provide the pacemaker function of the musculature) are thought to be involved in the condition
Autoimmune reactions to viral infections and genetic factors have also been implicated to trigger the condition
Achalasia presentation
Dysphagia
Food bolus impaction
Regurgitation (may also induce regurgitation to reduce pain)
Retrosternal chest pain in some pts, after eating
Heartburn also common and can be aggravated by treatment
Weight loss
Nocturnal cough (later sign of disease)
Inhalation of refluxed contents - inhalation pneumonia incidences! (later sign)
Achalasia investigations
Examinations are unlikely to reveal anything!! Sometimes high incidences of inhalation pneumonia may indicate
CXR may show signs of inhalation or may show dilated oesophagus behind the heart (rare to see in practice)
Barium swallow (contrast material) to rule out malignancy
Endoscopy
Manometry GOLD STANDARD: detects up to 9-% cases, high resting pressure in cardiac sphincter, incomplete relaxation on swallowing and absent peristalsis. If this shows normal results but there are symptoms of achalasia then pseudoachalasia might be present
Lower oesophageal pH monitoring to exclude GORD
Achalasia management
CCB and nitrates may reduce pressure in lower oesophageal sphincter but only effective in 10% pts.
Heller myotomy is considered best treatment if pts are fit, performed by laparoscope (success rate 85-95%, low complication rate)
For older pts can use pneumatic dilatation: insert balloon and inflate to rupture muscle while leaving mucosa intact (multiple dilations over months or years has better success rates)
Endoscopic injection of botulinum toxin
Peroral endoscopic myotomy and endoscopic stent
Achalasia complications
Nocturnal inhalation
Aspiration pneumonia
GORD (from treatments)
Oesophageal cancers
Dyspepsia
Indegestion Complex of upper GI symptoms present for typically more than four weeks Includes abdominal pain or discomfort Heartburn Acid reflux Nausea Vomiting
Dyspepsia presentation and red flags
Epigastric discomfort Fullness and bloating Excessive flatus Nausea Fatty food intolerance
Red flags:
Weight loss
Recurrent vomiting
Dysphagia
Evidence of GI bleeding (blood in stool etc)
Urgent 2WW referral for chronic GI bleeding or for >55 years with weight loss
Dyspepsia investigations
Abdominal exam: always check for masses
Bloods: FBC for iron deficiencies
Test for helicobacter pylori
Endoscopy (considered in >55 years who are treatment resistant, raised platelet count, nausea or vomiting, previous Barrett’s oesophagus)
Dyspepsia management
Uninvestigated without alarm features:
Review medications: NSAIDs, steroids, Ca antagonists, nitrates, theophyllines, bisphosphonates
Lifestyle advice: smoking cessation, regular meals, cease excessive alcohol consumption, avoid triggering foods, reduce stress, anxiety and depression if needed
Antacids for occasional symptom relief
Test for H.pylori and treat if positive
Empirical acid suppression (with proton pump inhibitors) for 1 month with full dose, continue long term either PPI, H2RA on lowest effective dose (eg ranitidine)
Investigate to find underlying cause and treat best as possible
Review at end of treatment course to confirm outcome
H pylori eradication 1st line
Lansoprazole 30 mg, omeprazole 20–40 mg, esomeprazole 20 mg, pantoprazole 40 mg, or rabeprazole 20 mg.
7-day triple therapy regimen of:
PPI twice-daily and amoxicillin 1 g twice-daily and
Either clarithromycin 500 mg twice-daily or metronidazole 400 mg twice-daily.
PENICILLIN ALLERGY: 7-day triple therapy regimen of:
A PPI twice-daily and clarithromycin 500 mg twice-daily and metronidazole 400 mg twice-daily.
If the person is allergic to penicillin and has had previous exposure to clarithromycin, offer a 7–10 day triple therapy regimen of:
A PPI twice-daily and metronidazole 400 mg twice-daily and levofloxacin 250 mg twice-daily.
If re-testing is indicated, wait at least 4 weeks (ideally 8) after initial eradication therapy
Oesophagitis and presentation
Inflammation of the oesophagus lining, mostly due to reflux of stomach contents leading to chronic irritation
Presentation: Heartburn Upper chest and abdomen pain Nausea Bloating Dyspepsia (indigestion) Tend to be related to meal intake Persistent cough particularly at night Mouth and gum problems, bad breath
Endoscopic grading of oesophagitis
Stage 1: Single of multiple erosions on single fold. May be exudative or erythematous
Stage 2: Multiple erosions on multiple folds. May be confluent
Stage 3: Multiple circumferential erosions
Stage 4: Ulcer, stenosis or oesophageal shortening
Stage 5: Barrett’s epithelium. Columnar metaplasia in form of circular or non-circular extensions (Islands or tongues)
OR
A - one or more mucosal breaks <5mm none extending to tops of mucosal folds
B - one or more mucosal breaks >5mm none extending between tops of two mucosal folds
C - mucosal breaks extending between tops of two or more mucosal folds, involving <75% mucosal circumference
D - mucosal breaks involving >75% mucosal circumference
GORD
Acid from stomach leaks up into oesophagus, usually as result of cardia sphincter weakening
2-3 x more common in men
25% adults experience heartburn
5% have daily symptoms
Spectrum of disorders ranging from the most common endoscopy negative GORD to oesophageal mucosal damage, which can progress to ulceration, stricture (although only 8% will have mod-severe oesophagitis)
GORD pathophysiology
Gastro-oesophageal reflux is a natural protective mechanism of the lower oesophagus
If reflux is prolonged or excessive it can cause breakdown of protection with inflammation of the oesophagus (oesophagitis)
Abnormalities of the lower oesophageal sphincter may facilitate excessive reflux of the gastric and sometimes bile contents into the oesophagus
Reflux of duodenal contents (bile) is more severe
GORD risk factors:
Increased intra-abdominal pressure Weak cardiac sphincter Smoking Alcohol Fat Coffee Pregnancy Obesity Tight clothes Large meals Surgery in achalasia of the cardia Systemic sclerosis Hiatus hernia Drugs: tricyclic antidepressants, NSAIDs, anticholinergics, nitrates, CCBs
*most of these factors increase intra-abdominal pressure
GORD presentations
Heartburn, related to eating, lying down, stooping, straining
Relieved by antacids
Retrosternal discomfort
Acid brash (regurgitation of acid or bile)
Water brash (excessive salivation)
Odynophagia (pain on swallowing) can indicate stricture or severe oesophagitis
Atypical symptoms: found in up to 50% cases
Chest pain
Epigastric pain
Bloating
GORD investigations
ENDOSCOPY - gold standard
Bloods: FBC to exclude anaemia
Barium swallow
Oesophageal pH monitoring (24 naso-oesophageal study or wireless pH capsule)
Dyspepsia red flags
Dysphagia
Dyspepsia with weight loss, proven anaemia or vomiting
Dyspepsia >55 years with <1 onset or continuous symptoms since onset
Dyspepsia with at least 3 risk factors
GORD management
Lifestyle: reduce weight, smoking cessation, decreased alcohol consumption, raise head of bed at night, small regular meals, avoid hot drinks and eating <3 hours before going to bed, avoid triggering drugs (nitrates, NSAIDs, anticholinergics, antidepressants)
PPI full dose for one month (two months if severe oesophagitis), can add H2RA (ranitidine) at bedtime, or switch entirely to H2RA if needed with confirmed oesophagitis
H. pylori eradication if indicated
Long term acid suppression for recurring symptoms after initial management (healing dose for one-two months then taper to lowest dose providing symptom relief)
Referral for endoscopy
Surgery: laparoscopic insertion of magnetic bead band
Review patients annually if on long term treatments or as needed
Peptic ulcer disease and causes
Break in inner lining of stomach, duodenum or lower oesophagus
Gastric ulcers in stomach, duodenal ulcers, oesophageal ulcers
Helicobacter pylori infection associated with 95% duodenal ulcers and 80% gastric ulcers
Pathophysiology:
Stomach mucosa is prone to ulceration from: breakdown of protective layer of the stomach and duodenum and an increase in stomach acid (stress, excessive caffeine, smoking, spicy foods etc)
Cause: H pylori NSAIDs Pepsin Smoking Alcohol Bile acids Steroids Stress Changes in gastric mucin consistency (genetically determined)
Peptic ulcer disease presentation
very nonspecific presentation sometimes
Epigastric pain usually 1-3 hours postprandial, may sometimes wake patient in night
Relieved by food (DUODENAL ulcer)
Worsened by food (GASTRIC ULCER)
Nausea and vomiting
Oral flatulence
Bloating, distension and intolerance of fatty foods
Heartburn (sometimes)
Posterior ulcer may cause pain radiating to back
Symptoms relieved by antacids
Epigastric tenderness
Succussion splash (if gastric emptying is slow)
Melaena
Haematemesis
Dyspepsia
Iron deficiency anaemias
SILENT Peptic ulcer disease risk factors
can present with unheralded perforation or bleeding
Increasing age Male sex Smoking H pylori infection Absence of atrophic gastritis
PUD investigations
Bloods: FBC for iron deficiencies
H pylori testing
Endoscopy
PUD management
Lifestyle: avoid triggering medications, smoking cessation
H pylori +ve = eradication treatment, follow up for proof of eradication
PPIs or H2RA for H pylori -ve
Exclude rare conditions (if not caused by common eg infection or NSAIDs) such as Zollinger-Ellison syndrome - take samples from ulcer and mucosa
Treat bleeding ulcers PRN (correct fluid loss, transfusions, surgical interventions)
Annual reviews for regular intermittent treatments
GI associated symptoms for history taking
Abdominal pain Nausea and vomiting Change in bowel motions, constipation, diarrhea, incontinence Blood in stool Anorectal pain, masses or sensation of incomplete emptying (tenesmus) Weight change Jaundice Dysphagia Dyspepsia
GI history taking past medical history conditions
Common GI disorders: GORD Peptic ulcer disease IBD; Crohn’s, ulcerative colitis Coeliac disease Diverticular disease Anorectal disease; fissures, fistulas, ulcers, haemorrhoids Hernia; inguinal, femoral, umbilical ventral IBS
Hepatobiliary disease: Liver cirrhosis Alcoholic liver disease Non-alcoholic fatty liver disease Hepatitis B or C Chronic pancreatitis
also ask about procedural history!
Antiemetics examples and function
Antidopaminergics:
- Metoclopramide
- Domperidone
- Droperidol
- Antagonise dopamine D2/3 receptors
Serotonin receptor blockers (5-HT):
- Ondanstetron
- Selectively inhibit serotonin receptors
Phenothiazines:
- Prochlorperazine
- Blocks D2 receptors and alpha adrenoreceptors
Gastric secretion modulators examples and functions
H2 receptor antagonists:
- Ranitidine
- Inhibits histamine H2 receptors, decreasing acid H+
Proton pump inhibitor (PPIs):
- Omeprazole
- Esomeprazole
- Pantoprazole
- inhibit H+/K+ ATPase (acid secretion)
Laxatives examples and functions
Bulking agents:
- Psyllium
- carbohydrates that retain water
Osmotic laxatives:
- MgSO4 (epsom salt)
- Lactulose
- Macrogol 3350
- Osmotically draws water into the GIT
Secretory laxatives:
- Senna
- Sodium picosulphate
- Stimulate GI elec. and water secretion
Stool softeners:
- Docusate sodium
- Softens faeces, doesn’t affect motility
IBD medications
Systemic corticosteroids:
- Prednisolone
- Hydrocortisone
- Systemic anti-inflammatory action
Aminosalicylates:
- Mesalazine
- Sulfasalazine
- Adenosine release, decreases inflammation
Thiopurines:
- Azathioprine
- Mercaptopurine
- Inhibits purine synthesis decreasing DNA synthesis
Methotrexate:
*Inhibition of IL-1 and other cytokines
TNF-Inhibitors:
- Infliximab
- Adalimumab
- Inhibit tumour necrosis factor alpha, decreasing inflammation
Abdominal regions and related pains and conditions
RUQ pain: Hepatobiliary Hepatic flexure Right renal Right lower lobe pathology Gallbladder pathology
RLQ pain: Colonic Appendicitis Gynaecologic Right renal pathology
Generalised pain: Bowel obstruction Perforation Bacterial peritonitis IBD
Epigastrium: Hepatobiliary Gastric Pancreatic Vascular or cardiac pathology
LUQ pain: Gastric Pancreatic Splenic flexure Spleen Left renal Left lower lobe Vascular pathology
Umbilical:
Gastric
Small bowel
Vascular pathology
LLQ pain:
Colonic
Gynaecologic
Renal pathology
Suprapubic:
Colonic
Gynaecologic
Right renal pathology
Moving from umbilical to RLQ:
Characteristic of appendicitis
Abdominal character and radiating pain and indications
Character:
Dull, diffuse pain - visceral pain eg from intra-abdominal organs
Sharp, localised pain - parietal pain eg from peritoneum
Burning pain in epigastrium - suggestive of oesophagitis, gastritis or peptic ulcer disease
Radiation:
To flank: renal or biliary cause
To back: pancreatitis, ruptured AAA, aortic dissection, duodenal ulcer
To shoulder: diaphragm irritation eg intra-abdominal gas or blood
GI associated symptoms and indications
Nausea and vomiting
Feculent vomiting: bowel obstruction
Bloating: gastroparesis
Diarrhoea: gastroenteritis
Constipation: faecal impaction or bowel obstruction
Lack of flatus: bowel obstruction
Blood in stool: diverticulitis or ischaemic colitis
Frank PR blood: lower GI bleed or massive upper GI bleed
Haematemesis or melaena: peptic ulcer
Fevers: infection (appendicitis, peritonitis, cholecystitis, diverticulitis, cholangitis etc)
RUQ/LUQ pain with cough and fever: pneumonia
Heartburn: gastritis, peptic ulcer
Dysuria: cystitis, pyelonephritis
Haematuria: nephrolithiasis
Vaginal discharge: pelvic inflammatory disease
Anorexia: appendicitis
Weight loss: malignancy
GI exacerbating and relieving factors and indications
Exacerbating factors:
Coughing or movement: peritonitis, perforation, pancreatitis
After eating: gastric ulcer, gastritis, cholelithiasis, mesenteric ischaemia
Eating fatty foods: cholelithias
Alleviating factors:
Eating: duodenal ulcer
Vomiting: small bowel obstruction
Regurgitation: achalasia
Vomiting and nausea timing indications
Worst in morning: pregnancy, alcohol intake, uraemia, raised intracranial pressure
Vomiting 1-2 hours after eating: gastric outlet obstruction
Vomiting during meals: anorexia/bulimia
Is it affecting daily lifestyle
Are they able to keep any solid or fluids down at all
Were they in contact with any sick coworkers or family or friends etc.
Causes of hematochezia
Lower GI bleed
Inflammation: IBD, diverticular disease, infectious colitis, ischaemic colitis
Mass: carcinoma, polyp
Anorectal disorder: haemorrhoids, fissure, fistula, ulcer, anal SCC
Arteriovenous malformation
Trauma
Massive upper GI bleed:
Variceal bleed
Peptic ulceration
GI Bleeding history taking and indications
Blood on toilet paper only: anorectal disorder
Blood in stool: colorectal disease
Blood in toilet bowl: high volume bleed
Heavy bleeding: diverticular bleed or AV malformation
Minor bleeding: haemorrhoids, polyp, cancer
RED FLAG
Weight loss: cancer
presyncope/syncope: hypovolaemia
Melaena and causes
Jet black, tarry, sticky, foul-smelling stool
Highly suggestive of upper GI bleeding
Medications containing iron and bismuth can also cause stools to look similar in appearance
CAUSES:
Oesophageal: varices, AVM, tumour, oesophagitis, Mallory-Wiess tear
Gastric: gastritis, gastric ulcer, gastric carcinoma, hiatus hernia
Duodenal: duodenal ulcer, duodenitis
GI causes of weight loss
peptic ulcer disease, obstruction, IBD, chronic pancreatitis, coeliac disease, gastric bypass surgery
toxic megacolon
When IBD cause the colon to expand, dilate and distend >6cm (toxic colitis with dilated colon = toxic megacolon)
The colon is becomes obstipated (no gas or faeces)
Is life threatening and may lead to perforations
Toxic megacolon risk factors
Ulcerative colitis Crohn’s colitis Pseudomembranous colitis Infectious colitis HIV/AIDS immunosuppression Discontinuation of IBD medications Antimotility agents
Toxic megacolon presentation
Fever/chills Tachycardia Mental status alterations Diarrhoea Abdominal pain and tenderness Hypotension Abdominal distension
Toxic megacolon investigations
History of risk factors (IBD, medications)
Clinical diagnosis from presentation and history
Bloods: FBC, electrolytes, albumin levels, lactic acid, CRP, blood cultures
Stool samples
CT of abdomen/pelvis
Acute AXR series
Toxic megacolon management
1st line resus and monitoring
Broad spectrum antibiotics
Supportive care
Nasogastric decompression
With suspected severe C difficile colitis: antibiotics
With inflammatory colitis: IV corticosteroids
No improvement within 72 hours: surgery
Diverticular disease and complications
Out-pouching of the wall of the gut
May be result of smooth muscle over activity
Mostly asymptomatic but can cause a wide array of symptoms and complications
Diverticulitis is inflammation of a diverticulum and can be caused by infection
Classification:
Congenital ‘true’ diverticula: all 3 coats of bowel are present in the wall (eg Meckel’s diverticulum)
Acquired ‘false’ pulsion diverticula: no muscularis layer, herniation of mucosa and muscularis mucosa through the colonic wall where main blood vessels penetrate the colonic wall (eg sigmoid diverticula, Zenker diverticulum)
complications Diverticulitis Segmental colitis Lower GI bleeding Infection Abscess Perforation Peritonitis Fistula formation Obstruction
Diverticular disease risk factors
Low fibre diet Western diet >50 years BMI >30 NSAID use
Diverticular disease presentation
majority asymptomatic found incidentally on colonoscopy History: presence of risk factors LLQ abdominal pain (colicky persisting pain) After eating, relieved by defecation Leukocytosis Fever Guarding in LLQ, tenderness Bloating Constipation, obstipation Diarrhea Anorexia Nausea Flatulence *pain and tenderness on right side as well as if pt is on steroids indicates sigmoid diverticular disease*
Diverticular disease management
Asymptomatic: no treatment needed
Symptomatic diverticular disease:
1st line: diet modification increase fibre with Oral antibiotics
Symptomatic diverticulitis (uncomplicated):
1st line analgesia and oral antibiotics with Low residue diet
2nd line IV antibiotics to cover gram -ve and anaerobes, analgesia and low residue diet
Symptomatic diverticulitis (complicated): 1st line with rectal bleeding: endoscopic haemostasis, supportive therapy, low residue diet and analgesia 2nd line surgery plus all above aside from endoscopic haemostasis
Unresponsive to IV antibiotics or with >3cm abscess, perforation, fistulae, obstruction: 1st line radiological drainage/surgery, IV antibiotics, analgesia and low residue diet
Recurrent diverticulitis:
Elective surgery
Ischaemic bowel disease
Group of disorders caused by acute or chronic processes, arising from occlusive or nonocclusive aetiologies resulting in decreased blood flow to the GIT
May range from transient to reversible to fulminant (sudden and severe)
Classification:
Acute mesenteric ischaemia (further split into embolic, thrombotic or venous)
Colonic ischaemia (most common with best prognosis)
Chronic mesenteric ischaemia
Ischaemic bowel disease risk factors
Old age Smoking Hypercoagulable states AF MI Structural heart defects Vasculitis history
Ischaemic bowel disease presentations
Abdominal pain and tenderness (general or specific depending on area of ischaemia) Hematochezia/melaena Diarrhoea Weight loss Abdominal bruit (stenosis of vessel)
Ischaemic bowel disease investigations
Bloods: FBC (leukocytosis, anaemia, haemoconcentration), serum lactate, coagulation, ABG
Acute abdominal series
ECG
CT scan
Sigmoidoscopy or colonoscopy
Mesenteric angiography, duplex US or MRI angiography if indicated
Ischaemic bowel disease management
Evidence of infarction, perforation or peritonitis:
1st line fluid resus and supportive measures
Empiric antibiotics
Exploratory laparotomy or laparoscopy
Correct underlying cause (eg embolectomy, heparinization if clot is cause etc)
No evidence of infarction, perforation or peritonitis:
1st line supportive measures
Empiric antibiotics
Correct underlying cause
Chronic mesenteric ischaemia:
1st line surgical systemic mesenteric bypass
If pt not suitable for surgery: Percutaneous angioplasty and stenting 1st line
Non Acute colonic ischaemia:
1st line segmental colectomy
OR following chronic stricture as result of healing after an ischaemic event 1st line is endoscopic dilation or segmental resection
diverticular disease investigations
uncomplicated diverticulitis:
CBC, U+A + culture
Abdo and pelvic CT scan
Colonoscopy or barium enema (rule out cancer)
CT virtual colonoscopy and Ba enema if severely stenotic
Complicated diverticulitis:
AXR: rule out air perforation or obstruction
Colonoscopy rule out cancer
CT cystogram rule out colovesicular fistula
Barium enema rule out colovaginal fistula
Small bowel series to rule out coloenteric fistula
Helicobacter pylori and testing
Gram -ve aerobic bacteria
Lives in the stomach
Causes damage to epithelial lining of stomach resulting in gastritis, ulcers and increased risk of cancer
It avoids acidic environment by forcing its way into the gastric mucosa, exposing the underlying epithelial cells to the acid
Also produces ammonia to neutralise stomach acid and other chemicals which directly damaged epithelial cells
Testing:
Must be done >2 weeks without PPI use for accurate result
Urea breath test (radio labelled c13)
Stool antigen test (now most used)
Rapid urease test (performed during endoscopy by taking small biopsy)
Barrett’s oesophagus
Metaplasia from squamous to columnar epithelial cells in the oesophageal lining
Typically causes improvements in patients reflux symptoms as the cells are now more protected against the acid
Considered a premalignant condition for adenocarcinoma of the oesophagus
Treatment is with PPI (omeprazole)
Ablation treatment during endoscopy using photodynamic, laser or cryotherapy also used to destroy dysplastic cells allowing healthy squamous ones to regrow
Constipation
Normal bowel habit is considered to pass stool between 3x per day and 3x per week
Constipation is characterised by difficulty emptying bowels with fewer bowel movements than normal for that individual
Can also mean: faeces are too hard, it may hurt or they have diarrhoea alternating with constipation
Acute <12 weeks, chronic >12 weeks
Primary = idiopathic/functional constipation
Secondary = organic/due to known cause or condition
Constipation common causes
Diet low in fibre Dehydration Low exercise levels Poor toilet routine Drugs: opioids, antimuscarinics Diabetes IBS Elderly Pregnancy
Investigations for constipation
History taking
Abdominal exam and PR exam
Bloods: FBC, U+E, Ca, TFTs if indicated to look for underlying cause if suspected
Constipation management
Lifestyle:
Increase dietary fibre (fruits, veg, whole wheat and bran).
Increase exercise regimen
Short duration constipation:
1st line: bulk-forming laxative (Ispaghula husk 1 sachet BD)
2nd line: osmotic laxative (Macrogol 1 sachet BD), try lactulose if not tolerated
3rd line: stimulant laxative (Senna, 7.5mg BD) to stimulate peristalsis
Opioid induced:
Osmotic laxative and stimulant laxative in combination
OR docusate (both in one)
Titrate dose up until 3x stools per week, then titrate down as needed
Chronic
As per short term constipation
Prucalopride or lubiprostone can be tried if at least two laxatives from different classes are tried at highest tolerance for at least 6 months, only in women. If it is not effective within 4 weeks the benefits v risks should be weighed up
Treat as though faecal impaction if this fails
Bulk producing constipation drugs
function:
Increase faecal mass, stimulating peristalsis
Must be taken with plenty of fluid
CI: swallowing difficulties, intestinal obstruction, colonic atony, faecal impaction, opioid cause constipation
Examples: Bran powder 3.5g 2-3x daily with food Ispaghula husk 1 sachet BD, sit upright for 1 hour after use Methylcellulose Sterculia
stool softeners
Side effects can include anal seepage, lipoid pneumonia, malabsorption of fat-soluble vitamins
examples:
Arachis oil enemas lubricate and soften impacted faeces
Liquid paraffin should NOT be used for prolonged period
Stimulant laxatives
Increase motility
CI for obstruction
Avoid prolonged use as may cause colonic atony and hypokalaemia
examples:
Bisacodyl tablets 5-10mg at night or suppositories 10mg in the morning
Senna 2-4 tablets at night (7.5mg BD)
Docusate sodium and dantron: associated with colonic and liver tumours. Reserve use for very elderly and terminally ill
Glycerol suppositories
Sodium picosulfate for rapid bowel evac. For procedures
Osmotic agent laxatives
Retain fluid in bowel
examples:
Lactulose: discourages growth of ammonia producing organisms. 15ml/12 hour or in hepatic encephalopathy 30-50ml/12 hourly
Mg salts rapid bowel evac
Macrogels for long term management
Enemas and suppositories
Useful additional treatment for constipation
examples:
Sodium phosphate enemas and glycerin suppositories may be useful
Sodium salts should be avoided as they cause sodium and water retention
Phosphate enemas rapid bowel evac
Excessive use of soapy tap water enemas may lead to water intoxication
Obstructed defecation syndrome
The urge to defecate but an impared ability to expel the faecal bolus
Symptoms include unsuccessful evacuation, excessive straining, pain, bleeding after defecation and sense of incomplete evacuation
Women, especially multiparous women are more likely to present with these symptoms
Often associated with structural defects in the retum
Managements include diet changes, biofeedback, laxatives, pelvic floor retraining
Surgery can also be considered for unresponsive cases
Faecal impaction
Large hard mass of stool stuck in the colon or rectum, causing obstruction that cannot be pushed out
More common in those who already have bowel problems
Can be caused by untreated constipation, overuse of laxatives, IBS, colon cancer, ageing, opiates, diverticulitis
Faecal impaction presentation
Liquid diarrhea leaking from rectum Pain or abdominal discomfort Nausea or vomiting Feeling need to push Headache Unintentional weight loss Feeling full/loss of appetite Fever Confusion/irritation Incontinence
Faecal impaction diagnosis
Clinical history: how often they evacuate bowels and when last time was, how often they’re constipated, how much they have drunk or eaten, if they use laxatives, which medications they take
Abdominal and PR exam
AXR in some cases
Faecal impaction management
As per constipation but with more rapid dose titration
Inadequate response: suppository (Bisacodyl soft stool or bisacodyl with glycerol for hard stools)
Mini enema (docusate or sodium citrate)
Sodium phosphate or arachis oil retention enema (may need to be repeated)
Diarrhoea
Defined as 3+ loose or liquid stools per day (or more frequently than normal for that individual)
Acute <4 weeks (NICE says <14 days)
Persistent diarrhea >14 days
Chronic >4 weeks
Cause of acute diarrhoea
Medications: laxatives, allopurinol, AT2 antagonists, antibiotics (C drugs), metformin, Mg containing antacids, NSAIDs, PPIs, SSRIs C difficile from certain antibiotics Infections such as salmonella, E coli Constipation with ‘overflow’ diarrhea Anxiety Food allergies Acute appendicitis, intestinal ischaemia IBS/IBD
Assessment and investigations of patient with diarrhoea
Determine frequency, severity, quantity and character of stools
Red flag symptoms: blood, recent antibiotic or hospital treatment, persistent vomiting, weight loss, painless, watery, high volume, nocturnal symptoms disturbing sleep
Other symptoms: fever, recent travel, contact with sick people, stress, anxiety, clinical presentation of appendicitis etc.
Assess for dehydration
Consider comorbidities and increased risk of complications
Consider rectal exam particularly in >50 years
investigations:
Stool specimen if pt is unwell, immunocompromised, recently received antibiotics, blood in stool, persistent >7 days, occurs after foreign travel to anywhere other than western EU, north america, NZ or australia
Investigations for underlying cause if chronic cause suspected
Bloods for ALL chronic cases: FBC, U+E, B12, folate, ferritin, TFTs, ESR, LFTs, CRP, coeliac disease
Management of diarrhoea
Oral rehydration therapy (salts to reabsorb water into the body) 1 sachet in 200ml water after every loose motion. Can also add to infant feeds
Loperamide, 2x 2mg capsules on onset and one after every loose motion, max 16mg daily (CI if blood or pt is febrile or severe abdominal pain, larger doses increase CV risk, QT prolongation, cardiac arrest). Naloxone used to reverse effects
Travellers diarrhoea: ciprofloxacin antibiotic 500mg BD for 3 days
Hospital admission needed if vomiting, unable to retain fluids, features of severe dehydration or shock, elderly, blood diarrhea, abdominal pain/tenderness suggestive of cause
IBS
AKA inflamed colon/spastic colitis Psychosomatic illness Relapsing functional disorder of the large intestine, characterised by abdominal pain, change of bowel habit, bloating and abdominal distension Almost twice as common in women Peak prevalence ages 20-30 Approx. 10-20% of adults are affected
IBS aetiology and subclasses
No structural lesion, no single explanation
Seems to involve abnormal smooth muscle activity +/- visceral hypersensitivity and abnormal central processing of painful stimulant
Associated with increased stress and poor coping strategies
Possible disturbed GI motility from abnormal bowel transit time
Subclasses: IBS with constipation (IBS-C): loose stools <25% and hard stools >25% of time IBD with diarrhea (IBS-D): loose stools >25% and hard stools <25% time IBS mixed (IBS-M): both hard and soft stools >25% time
IBS presentation
Alternating obstipation and diarrhea, can be continuous or intermittent Flatulence Vertigo Loss of appetite Pressure and bloating with relief on defecation Mild pressure or pain in left lower abdomen, no muscular defense Inconspicuous bowel sounds Excessive mucus in faeces Lethargy Nausea Backache Bladder symptoms
IBS diagnostic criteria
Must have at least 6 month history of either:
Abdominal pain or discomfort
Bloating
Change in bowel habit
If abdominal pain is either relieved by defecation or associated with bowel frequency or stool form AND at least 2 of the following are present:
Altered passage of stool (straining, urgency, incomplete evac)
Abdominal bloating, distension or hardness
Symptoms aggravated by eating
Passage of mucus rectally
IBS investigations
Diagnostic criteria
Bloods: FBC, ESR, CRP, coeliac screen, faecal calprotectin
CA 125 for ovarian cancer
If indicated: TFTs, USS, Colonoscopy, faecal occult blood, hydrogen breath tests
IBS management
Lifestyle:
Regular meals, plenty of fluids, reduce alcohol and fizzy drink intake, limiting high fibre foods
Avoid sorbitol for diarrhea
Flatulence: increase oats and linseeds (1 tablespoon/day)
Referral to dietician for those whose diet plays a large role in symptoms
CBT for psychosomatic treatment
Medications: high rate of placebo effect in IBS
Antispasmodics for spasm and abdominal pain (Mebeverine 135mg TDS, Alverine citrate 60-120mg TDS, Peppermint oil 1-2 capsules 3x daily) CI with obstruction or paralytic ileus
Antimuscarinics (dicycloverine hcl 10-20mg TDS, hyoscine butylbromide 10mg TDS-20mg QDS) CI obstruction and ileus, angle-closure glaucoma, severe ulcerative colitis, toxic megacolon side effects CAN’T SEE, CAN’T PEE, CAN’T SHIT, CAN’T SPIT
Antimotility (loperamide: 1st line diarrhea choice)
Bulk forming laxatives (Ispaghula)
Tricyclic Antidepressants (amitriptyline 5-10mg at night) or SSRIs
CBT
Linaclotide
IBD
Umbrella term for two main diseases causing inflammation of the GIT
Ulcerative colitis and crohn’s disease
Both involve inflammation of the GI walls and are associated with periods of remission and exacerbation
Crohn’s vs ulcerative colitis
Crohn’s: crows NESTS:
No blood or mucus (usually)
Entire GIT involved
Skip lesions on endoscopy
Terminal ileum most affected and Transmural (full thickness) inflammation
Smoking is a risk factor (don’t set a nest on fire)
*cobblestoning mucosa and aphthous/linear ulcers endoscopic appearance
*also associated with weight loss, strictures and fistulas**
Crypt abscesses and granulomas only present in Crohn’s
Ulcerative colitis: U-C- CLOSEUP: Continuous inflammation Limited to colon and rectum only Only superficial mucosa affected Smoking is protective Excrete blood and mucus Use aminosalicylates Primary sclerosing cholangitis *endoscopic appearance is diffuse continuous mucosal involvement*
IBD general presentation and investigations
Diarrhea
Abdominal pain
Passing blood
Weight loss
Ix:
Routine bloods for anaemia, infection, thyroid, kidney and liver function
CRP for inflammation and active disease
Faecal calprotectin raised (90% sensitive for IBD in adults)
Endoscopy with biopsy is diagnostic
USS, CT, MRI for complications like fistulas, abscesses, strictures
Crohn’s disease
An IBD characterised by inflammation of the entire GIT (transmural granulomatous inflammation)
Likely to have strong family history
Associated with excess mortality compared to general population
Onset has two age peaks: ages 15-30 is largest and ages 50-70 is second peak
Also rapidly increasing in children
Usually spares the rectum (less likely GI bleed)
Crohn’s disease risk factors
Genetic family history of IBD
Smoking increases 3-4 fold risk
Intercurrent infections (URTI, enteric infections)
NSAIDs
Crohn’s disease presentation
Variable symptoms
Diarrhea (may be bloody and become chronic >6weeks)
Abdominal pain
Weight loss
Acute exacerbation periods with remissions or less active disease
Malaise
Anorexia
Fever
Children may show poor growth, delayed puberty, malnutrition and bone demineralisation
Hypotension, tachycardia, pyrexia in acute exacerbations
Anal or perianal lesions
Mouth ulcers
Finger clubbing, erythema nodosum, pyoderma gangrenosum
Large joint arthritis
Fatty liver, sclerosing cholangitis (rare)
Renal stones
Malnutrition
Amyloidosis
Crohn’s disease investigations and staging tools
Bloods: FBC, CRP, U+E, LFTs, *CRP useful for assessing relapse**
Stool culture
Faecal calprotectin raised
Ileocolonoscopy and biopsy to confirm
Perianal disease: pelvic MRI gold standard
Laparoscopy
staging:
- CDAI and PCDAI criteria
Crohn’s management - inducing remission
1st line oral prednisolone, IV hydrocortisone or other glucocorticosteroid for 12 months
Immunosuppressant (specialist): azathioprine, mercaptopurine, methotrexate, infliximab, adalimumab
Referral for rectal bleeding and abdominal pain, change of bowel habit, weight loss, iron deficiency anaemia
Hospital admission if severe pain, tenderness, diarrhea >8x/day, bowel obstruction, fever and systemically unwell
Crohn’s management - maintaining remission
Smoking cessation is vital
Tailored to individual based on side effects, preference and nature of disease, may not require medications while well
1st line azathioprine or mercaptopurine
Alternatives: methotrexate, infliximab, adalimumab
Surgery when disease only affects the distal ileum is possible to resect the area and prevent further disease flares. Can also be used to treat strictures and fistulas secondary to CD
Poisoning investigations
ECG
U+E, glucose, anion gap +/- lactate, osmolal gap
LFTs, clotting
ABG
Paracetamol level, salicylates, theophylline, digoxin, lithium, antiepileptics if indicated
Urinalysis
CXR if pulmonary oedema or aspiration
CT scan of brain to exclude other causes of altered conscious
Poisoning general management
ABCDE assessment and act accordingly
History: how much, when, what route of administration, has there been vomiting, past medical history, current medications and allergies, suicide note/suicide risk, third party history for context
Cardio, respiratory, abdominal, neurological examinations
Vital signs: temperature, pupils, BP, HR
Muscle rigidity
Skin - cyanosis (methaemoglobinaemia), very pink (carboxyhaemoglobinaemia, cyanide, hydrogen sulphide), blisters (barbiturates, tricyclic antidepressants (TCAs), benzodiazepines), needle tracks, hot/flushed (anticholinergics).
Breath - ketones (diabetic/alcoholic ketoacidosis), ‘bitter almonds’ (cyanide), ‘garlic-like’ (organophosphates, arsenic), ‘rotten eggs’ (hydrogen sulphide), organic solvents.
Mouth - perioral acneiform lesions (solvent abuse), dry mouth (anticholinergics), hypersalivation (parasympathomimetics)
Poisoning - charcoal removal
Single-dose activated charcoal is the preferred method of decontamination in many cases.
Patients should have had a significant overdose, be co-operative, without impairment of consciousness and not thought to be likely to fit imminently.
Ideally it is used in a 10:1 ratio with the ingested drug - the usual dose is 50 g for an adult (children: 1 g/kg).
It may be repeated in one hour if necessary (oral, nasogastric tube). Its large surface area adsorbs many drugs but has its limitations.
It may not be be effective if given after the first hour or in cases of poisoning with iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon or strong acids or alkalis.
Paracetamol overdose overview symptoms and management
Presentation:
Hepatocellular necrosis (indicated by right subcostal pain and tenderness)
Nausea and vomiting
Treatment:
Acetylcysteine reduced severity of liver damage if given <24 hours ingestion
Monitor for signs of liver failure
Tricyclic antidepressants overdose presentation and management overview
Presentation:
Dry mouth, coma, hypotension, hypothermia, hyperreflexia, extensor plantar responses, convulsions, respiratory failure, cardiac conduction defects, dilated pupils, urinary retention, hallucinations, delirium and confusion
treatment: Supportive measures to clear airway IV lorazepam or diazepam for convulsions Activated charcoal <1 hour Correct hypoxia and acidosis Monitor cardiac activity
SSRIs overdose presentation and management overview
presentation:
Nausea, vomiting, agitation, tremor, nystagmus, drowsiness, sinus tachycardia, convulsions
treatment:
Supportive
Activated charcoal <1 hour
Convulsions treated with lorazepam, diazepam
Benzodiazepines overdose presentation and management overview
presentation:
Drowsiness, ataxia, nystagmus, respiratory depression, coma
treatment:
Flumazenil injection Reverses CNS and respiratory depression. However if person has also taken tricyclic antidepressant or has epilepsy must be cautions as can cause seizures or arrhythmias
Activated charcoal <1 hour
Coeliac disease
Multi Genetic disorder associated with HLA types DQ2 (90%) or DQ8, plus other genetic or environmental factors.
Family tendency 10-15%
Approx 1 in 100 people in the UK have coeliac disease, however only 10-20% will be diagnosed
Highest incidence in ages 50-69
Coeliac disease presentation
wide variation of signs and symptoms, many cases are asymptomatic
Persistent unexplained abdominal or GI symptoms
Faltered growth
Unexpected weight loss
Severe or persistent mouth ulcers
Unexplained iron, vit B12 or folate deficiency
Type 1 diabetes
Autoimmune thyroid disease
IBS in adults
1st degree relatives of people with coeliac disease
Dermatitis herpetiformis (classic manifestations of CD)
Gluten sensitivity
NICE recommendation for coeliac screening in..
Metabolic bone disorder
Unexplained neuro symptoms (ataxia, epilepsy, dementia, depression)
Unexplained subfertility or recurrent miscarriage
Persistently raised liver enzymes without known cause
Dental enamel defects
Down’s or Turner syndrome
All newly diagnosed type 1 diabetics are screened for coeliac disease*
Coeliac disease investigations
only accurate if gluten diet is eaten during diagnostic process
Autoantibodies: total IgA and tTG 1st line. IgA EMAs if weakly positive.
For children: total TgA and IgA tTG 1st line. IgG EMA, IgG DGP or tTG if IgA is deficient
FBC: anaemia, iron and folate deficiency, B12, ferritin, LFTs (elevated transaminases which should return to normal on gluten free diet), Ca and albumin
Small bowel barium studies to exclude other causes of malabsorption
Biopsy needed for confirmation by GI endoscopy or suction capsule
Coeliac disease complications and referrals
Referrals to GI specialist:
Young people with +ve serological tests for endoscopic biopsy
Children with +ve serology to paediatric specialist for further investigation
-Ve serology to gastro specialist if CD still suspected for further investigation
Complications: Deficiencies eg vit D and iron Osteoporosis Cancer Ulcerative jejunitis Functional hyposplenism Anxiety, depression Male infertility Poor foetal outcome in UNDIAGNOSED pregnancy women, but not diagnosed
Coeliac disease management
Gluten free diet (no wheat, barely, rye, bread, cakes etc) seems to be only effective treatment
Refractory CD: consider prednisolone initial management while waiting specialist advice
If after GFD excluded but symptoms persist/serology is high for >12 months refer for endoscopic biopsy
Annual review to measure weight, height, review symptoms, assess diet and adherence, need for specialist dietitian or nutritional advice
Consider DEXA scan, regular bloods for long term complications monitoring
Types of hernia
Groin Hernias: - Inguinal (direct/indirect) - Femoral hernia Ventral hernias: - Umbilical, para-umbilical hernia - Epigastric hernia Incisional hernia
Reducible = can be pushed back into right place
Irreducible = implies the hernia sac is not reducible
Incarcerated: contents are stuck inside by adhesions without any obstruction or strangulation
Obstructed: content is bowel content and is obstructed (typically small or large intestine obstruction). Some obstructed hernias can become strangulated also.
Strangulated: content of the hernia is NOT bowel, but there is ischaemia. Patient becomes toxic and needs urgent surgery
All these terms describe the condition of the contents of the hernia
Usually strangulation happens after obstruction
Inguinal hernias
An inguinal hernia is a protrusion, or movement of abdominal contents, from within the abdominal cavity. This tissue then protrudes, or emerges, at the exit point, the superficial inguinal ring.
Location: inguinal hernias are most commonly found superomedial to the pubic tubercle.
Femoral hernia
Femoral hernias occur just below the inguinal ligament when abdominal contents pass through a naturally occurring weakness in the abdominal wall called the femoral canal.
It is important to note that the femoral canal is narrow and is bordered medially by thesharp edge of the lacunar ligament. Therefore, femoral hernias are at higher risk of strangulation and obstruction.
more common in women
Location: femoral hernias are typically found inferolateral to the pubic tubercle and medial to the femoral pulse.
Umbilical hernia
Umbilical hernias, as the name suggests, occur at the site of the umbilicus and are common. They can be large but are typically low risk for strangulation.
Location: umbilical region
Incisional hernia
Incisional hernias occur at the sites of previous operations where tissue integrity has been compromised.
Location: incisional hernias present as a bulge or protrusion at or near the site of a previous surgical incision.
Sliding hernia
Generally the hernial sac is a protruded part of parietal peritoneum
In sliding hernia, the wall of the viscus (caecum, sigmoid etc) forms a portion of the hernial sac. The remainder of the sac being formed by parietal peritoneum
Mostly expected to see these hernias as large inguinal hernias
Important to classify sliding hernias before surgery to allow dissection of hernia sac from organ forming wall
Richters hernia
Aka parietal hernia
Abdominal hernia where only a portion of bowel wall is herniated
Expect to see this in femoral hernia
Likely to present with ischaemia, may end in perforation
Hernia history and investigations
History: Groin lump, swelling Obstructive symptoms Strangulated symptoms May be reducible or not Cough impulse if irreducible
Investigations:
Zeimann’s technique of palpation (index finger on deep inguinal ring, middle finger on superficial ring, ring finger over saphenous opening after reducing hernia content. patient asked to cough and impulse felt in finger corresponding to hernia)
USS
CT scan for incisional hernia
MRI - good in sports groin with pain
Contrast radiology - especially for inguinal hernia
Laparoscopy - useful to identity contralateral inguinal hernia
Hernia management
Pain, tenderness and skin colour changes may imply high risk of strangulation
Femoral hernia should always be repaired
Pts with symptoms or have episodes of irreducibility or bowel obstruction etc should be offered surgical repair
Elderly, immobile pts or those with high morbidity if asymptomatic or mild may be observed (watch and wait policy)
Groin of truss is of limited symptomatic benefit for these non-surgical pts
Compare indirect, direct and femoral groin hernias
indirect: 80% cases, can strangulate, usually young age, often congenital (patent processes vaginalis), lateral to inferior epigastric artery, often descends to scrotum, treatment is herniotomy in infant and open mesh repair/laproscopic repair in adults
direct: 20% cases, early reduced, rarely strangulate, more common in older patients, acquired weakness in abdominal wall, medial to inferior epigastric artery, rarely descends to scrotum, treated with open mesh repair or laparoscopic repair
femoral hernias: more common in females, frequently strangulate and frequently irreducible
Groin hernias and causes
Herniation through defects in the abdominal wall, above or below the inguinal ligament in the groin area
Include inguinal (direct and indirect) and femoral hernias
Indirect inguinal hernias are most common groin hernia
Inguinal hernias are common in male infants due to the patent processus vaginalis
Uncommon in female infants: should have androgen insensitivity syndrome tests
Women more commonly have femoral hernia
Men indirect inguinal
Elderly men more commonly direct inguinal hernias
causes: Coughing COPD Obesity Straining: constipation or prostatism Pregnancy Low birth weight Family history of hernia Valsalva maneuver Ascites Upright position Congenital connective tissue disorders Defective collagen synthesis Previous RLQ incision Arterial aneurysms Smoking Heavy lifting Physical exertion
Hernia examination
Always assess both sides of the groin to avoid missing pathology
Typical hernia pathology:
Single lump in inguinal region
+ve cough impulse (unless incarcerated)
Soft on palpation
Reducible (unless incarcerated)
Unable to get above lump during palpation
Painless (unless incarcerated)
Bowel sounds on auscultation (unless incarcerated)
Differentiation of subtypes:
Assess relationship to pubic tubercle (inguinal typically above and medial to, femoral typically below and lateral to)
Reducibility: can it be flattened out with changing positions (supine) or by applying pressure. Ask pt to lie supine and observe for reduction. If still present, try to reduce with pressure.
A hernia that is TENDER and IRREDUCIBLE may be strangulated and needs urgent surgica review
If inguinal hernia suspected: determine if direct or indirect
Locate deep inguinal ring (midway between ASIS and pubic tubercle), manually reduce hernia with compression towards the deep inguinal ring starting at the inferior aspect. Once reduced, apply pressure over deep inguinal ring and ask patient to cough
If it reappears, it’s more likely to be DIRECT, if not, then more likely is INDIRECT (unreliable test - needs further imaging)
Haemorrhoids
Aka piles
Abnormally swollen vascular mucosal cushions that are present in the anal canal
Pathology:
3 vascular mucosal cushions which help maintain anal continence
Typically described as being present at left lateral, right posterior and right anterior positions (varies)
When these become enlarged it leads to dilation of the local veins and protrusion into and through the anal canal - haemorrhoids
Internal vs external haemorrhoids
Depending on origin in relation to the dentate line (situated 2cm from anal verge and marks transition between the upper and lower anal canal)
External haemorrhoids originate below the dentate line and are covered by modified squamous epithelium (anoderm) which is richly innervated with pain fibres
External can also be more itchy (pruritic) and painful
Internal haemorrhoids arise above the dentate line and are covered by columnar epithelium, which have NO pain fibres
Therefore are not sensitive to touch, temperature or pain (unless they become strangulated)
Internal H are further graded by degree of prolapse (1-4)
Haemorrhoid risk factors
Constipation Straining Ageing Conditions increasing intra abdominal pressure (pregnancy, labour, ascites, pelvic mass) Chronic cough Heavy lifting Exercising Genetics (congenital weaknesses) Low fibre diet
Haemorrhoid presentations
Bright red, painless, rectal bleeding
Typically occurs with defecation and seen as streaks of blood on toilet paper (not in stool)
Anal itching or irritation
Feeling of rectal fullness, discomfort or incomplete evacuation (tenesmus)
Soiling due to mucus discharge or impaired continence
Pain
Strangulated haemorrhoids are extremely painful, acutely thrombosed external haemorrhoids
Difficult to palpate internal haemorrhoid as internal mucosal folds also get in the way
Haemorrhoids investigations and diagnosis
Investigations:
Digital rectal exam/PR, even though internal haemorrhoids often not palpable
Bloods: FBC, ESR/CRP
faecal calprotectin test
Diagnosis:
Clinical history and PR exam
May be asymptomatic or can have history of intermittent symptoms lasting from few days to few weeks
Can have both internal and external at once
Haemorrhoids management (lifestyle and creams)
Conservative (lifestyle)
Constipation avoidance: good dietary fibre intake, adequate fluids
Good toilet habits: clean and dry. Cleanse with moistened towelettes and pat (not rub) dry
Advise against stool withholding and undue straining
Medications
Analgesia: paracetamol (avoid NSAIDs if bleeding), avoid opioids (constipation causing)
Topical astringents, lubricants, anaesthetics and corticosteroids for symptom relief
Anusol (astringent and emollient)
Anacal (heparinoid)
Anodesyn (local anaesthetic)
Germoloids (lidocaine and astringent)
Anusol HC Plus (hydrocortisone and astringent)
Proctosedyl (anaesthetic and hydrocortisone)
Local anaesthetics can cause anal skin sensitisation
Steroids cause thinning of anal skin
HOW TO USE:
Generally used morning and night and after bowel movements
Anaesthetic containing prep should only be used for a few days due to skin sensitisation
Corticosteroid containing prep used no longer than 7 days as may lead to skin atrophy, contact dermatitis and skin sensitisation. Avoid excessive application
Haemorrhoids management (removal) and referrals
Non-surgical: rubber band ligation injection sclerotherapy infrared coagulation/photocoagulation bipolar diathermy and direct current electrotherapy
surgical:
haemorrhoidectomy
stapled haemorrhoidectomy
haemorrhoid artery ligation
hospital admission:
Strangulated external haemorrhoids <72 hours onset for reduction or excision
Internal haemorrhoids that prolapsed or swollen, incarcerated and thrombosed (haemorrhoidectomy may be needed)
Perianal sepsis
Non-urgent referral:
Fourth degree haemorrhoids or third degree haemorrhoids that are too large for non-operative measures (haemorrhoidectomy may be needed).
Perianal haematoma (a blue or dark coloured swelling at the anal verge) if symptoms are for less than 24 hours duration for clot evaluation.
Combined internal and external haemorrhoids with severe symptoms (surgery may be required).
Thrombosed haemorrhoids when bleeding is problematic, or there is chronic irritation or leakage.
Large skin tags (surgical excision may be required).
coloRectal neoplasm
Colorectal and anal cancers
Primarily SCC
Anal margin tumours are usually well differentiated. More common in men with good prognosis
Anal canal tumours are poorly differentiated, more common in women with worse prognosis
2:1 F:M ratio
60% 5 year survival rates
rectal neoplasm risk factors
HPV
Anal intercourse and high lifetime number of sexual partners (increased HPV risk)
Male with male sex
HIV/immunosuppression
Women with cervical cancer history or cervical intraepithelial neoplasia (CIN)
Immune suppression in transplant recipients
Smoking
Rectal neoplasm presentation
Anal pain Tenesmus (incomplete emptying feeling) Rectal bleeding Anal mass or ulceration Rectovaginal fistula (advanced)
Rectal neoplasm investigations and management
Diagnosis clinical
Proctoscopy and biopsy to confirm
Faecal immunology test FIT
FBC, LFT, U+E, CRP, ESR
Management:
2WW referral
Surgical excision + radio or chemotherapy with lymph node excisions depending on severity and spread
Red flags for 2WW referral: anal mass or anal ulceration
colon cancer
Mostly adenocarcinomas which evolve from polyps
May be present for 10+ years before malignancy develops
National screening program for bowel cancer - FIT and scope
Bowel cancer is 4th most common cancer in UK
Risk factors for colon cancer
Family history of colorectal neoplasms <60 years old
Past history of colorectal neoplasms
IBD
Polyposis syndromes: Gardner’s syndrome, Turcot’s syndrome etc.
Hereditary non-polyposis colorectal cancer (HNPCC)
Hormonal factors: nulliparity, late age first pregnancy, early menopause
Diet rich in meat and fat, poor fibre, folate and Ca intake
Sedentary lifestyle: smoking, high alcohol intake
Diabetes
Previous irradiation: asbestos exposure etc
History of small bowel cancer, endometrial cancer, breast cancer or ovarian cancer
Colon cancer
Change of bowel habit: diarrhoea or constipation
Rectal bleeding
Loss of weight
Abdominal pain
Tenesmus
Iron deficiency anaemia especially in men and postmenopausal women (unexplained = RED FLAG)
DVT, abdominal or rectal masses, occult blood in faeces (uncommon)
Colon cancer investigations
FIT: detects small amounts of blood in stool samples using antibodies specific to human Hemoglobin
FBC, LFTs
Colonoscopy and biopsy GOLD STANDARD
CT colonography in those unfit for colonoscopy but doesn’t include biopsy
Colon cancer management
2WW referral
Surgery, chemo or radiotherapy or sometimes biological agents such as cetuximab
Resection of bowel and stoma may be expected
Red flags: 40+, unexplained weight loss and abdominal pain, 50+ unexplained rectal bleeding, 60+ iron deficiency or changes in bowel habit, tests how occult blood in faeces
General red flags: abdominal pain, change in bowel habit, weight loss, iron deficiency anaemia
Hepatic neoplasms
Primary liver cancers
Often presents as complication of cirrhosis, usually following chronic viral hepatitis or alcoholic liver disease
Most common primary liver cancer is hepatocellular carcinoma
Hepatoblastoma more common in children
Other includes cholangiocarcinoma
Hepatic neoplasms risk factors
HBV/HCV infection
Chronic HBV infection most common cause of HCC in the world
HCV most common cause in EU
Co infection of both increases HCC risk further
Alcoholism
Genetic haemochromatosis
Primary biliary cirrhosis
Metabolic syndrome (HTN, diabetes and obesity)
Smoking
Saharan africa and asian foods (high concentrations of aflatoxins)
Hepatic neoplasms presentation
RUQ abdominal pain Abnormal LFTs and liver function Hepatomegaly Upper abdominal masses Jaundice Pruritus (from bile build up) Splenomegaly Bleeding oesophageal varices Weight loss Confusion and hepatic encephalopathy Abdominal distension due to ascites
Hepatic neoplasms investigations and management
Investigations:
USS/other imaging
Biopsy for confirmation in secondary care
Bloods: LFTs, clotting screen, bone profile (albumin)
Management: 2WW referral for biopsy in secondary care Surgical resection Thermal ablation Systemic chemotherapy Transarterial chemoembolization Selective internal radiation therapy Red flags: upper abdominal mass consistent with enlarged liver - 2WW USS
Pancreatic neoplasms
Pancreatic cancer
Categorised into exocrine and endocrine tumours
Mostly exocrine tumours
Infiltrating ductal adenocarcinomas 90% pancreatic cancers
Majority arise from head, neck or uncinate process
90% periampullary malignancies arise from pancreas and remaining 10% from the distal common bile duct, ampulla of Vater and duodenum
Metastases most commonly in the liver, peritoneum and lungs
Low survival rate 5% 5 years due to patients presenting notoriously late on in disease, only less than one fifth present with localised, potentially curable tumours
Risk factors for pancreatic neoplasms
Smoking High BMI Red meat intake high, low fruit and eg Diabetes High alcohol intake Chronic and hereditary pancreatitis both associated with increased risk Family history Family cancer syndromes: BRCA1 and 2, familial adenomatous polyposis, Peutz-Jegers syndrome, familial melanoma syndromes, Gardner's syndrome IBD Periodontal disease Peptic ulcer disease
Pancreatic cancer presentation
very late usually
Abdominal epigastric pain radiating to back
Dull pain worse when supine, eased by leaning forward
Loss of appetite
Jaundice
Weight loss
Palpable gallbladder (Courvoisier’s sign, painless jaundice)
Nausea and vomiting
Endocrine cancer may produce symptoms from secretions of hormonal (diabetes etc)
Pancreatic cancer investigations and management
Investigations:
CT scan most sensitive
USS
Bloods: FBC (anaemia, thrombocytosis), LFTs (raised bilirubin, ALP, GGT), serum glucose (hyperglycaemia)
Diagnosis needs biopsy (secondary care often)
Management:
2WW referral for biopsy
Surgery to remove tumour
Red flags: 60+ abdo pain and weight loss, back pain and weight loss, new onset diabetes, change of bowel habit and weight loss, nausea and vomiting with weight loss
40+, jaundice
Oesophageal neoplasm and risk factors
Mostly SCC or adenocarcinomas
M:F 2:1 ratio
Risk factors:
Male
Tobacco and alcohol
Barrett’s oesophagus (precursor of adenocarcinoma)
Chronic inflammation and stasis from any cause increases risk of SCC eg strictures due to caustic injury or achalasia
Tylosis and Paterson-Brown-Kelly syndrome
Obesity for AC but reduced risk of SCC
Family history of hiatal hernia for AC
Oesophageal cancer presentation
varies and can overlap with gastric neoplasms Dysphagia Odynophagia Acid reflux Loss of appetite Weight loss Hoarse voice Melaena Retrosternal pain Intractable hiccups Anaemia
Oesophageal neoplasm Ix and Mx
Investigations: Endoscopy GOLD STANDARD Biopsy to confirm Bloods: FBC, U+E, LFTs, glucose, CRP CXR
Management:
2WW referral
Surgery alone or with chemo or radiation therapy
Red flags: dysphagia, haematemesis >55 years with weight loss, upper abdo pain, reflux or dyspepsia
Non-urgent referral for >55 years with treatment resistant dyspepsia, upper abdo pain with low Hb levels OR raised platelet count with nausea, vomiting, weight loss, reflux, dyspepsia, upper abdo pain, or nausea and vomiting with, weight loss, reflux, dyspepsia or upper abdo pain
Gastric cancer
Stomach carcinoma Starts anywhere inside stomach or stomach wall 50% involve pylorus 25% less curve 10% cardia 2-8% gastric cancers are lymphomas 5 year survival rate approx 20% Majority of pts present with advanced disease
Stomach cancer risk factors
Increasing age (95% >55) Male Poor socio-economic status Helicobacter pylori can double risk Diet low in fruit and veg and high in salt and preserved foods Smoking Atrophic gastritis Pernicious anaemia Post-gastrectomy Menetrier’s disease Family history Blood group A Hypogammaglobulinaemia
Gastric cancer presentation
Dysphagia Abdominal pain Acid reflux Loss of appetite Weight loss Anaemia
Gastric cancer Ix and Mx
Investigations:
Endoscopy GOLD STANDARD
Biopsy to confirm
Bloods: FBC and LFTs
Management:
2WW referral
Surgery to remove tumours
All pts should be screened for nutritional deficiencies and considered for nutritional support
Red flags: upper abdo mass consistent with stomach cancer, dysphagia,haematemesis, >55 years with weight loss, upper abdo pain, reflux or dyspepsia
Non-urgent referral for >55 years with treatment resistant dyspepsia, upper abdo pain with low Hb levels OR raised platelet count with nausea, vomiting, weight loss, reflux, dyspepsia, upper abdo pain, or nausea and vomiting with, weight loss, reflux, dyspepsia or upper abdo pain
GI endoscopy medication advice
Aspirin, continue taking as normal
Warfarin, continue, stop 4 days pre-op and if high risk start LMWH PRN
Dipyridamole, continue, stop 24 hours pre-op if high risk
Clopidogrel/prasgurel/ticagrelor, continue, stop 7 days pre-op if high risk switch to aspirin for 7 days if not already taking or CI
Rivaroxaban, stop 24 hours pre-op
Dabigatran, stop 1-4 days before op according to eGFR/procedure bleed risk
Apixaban, stop 24-48 hours pre-op according to procedure bleed risk
ACEi/A2RB, stop on day if BP well controlled (140/80), monitor eGFR
Diuretics, stop on day of procedure, confirm electrolyte levels an eGFR
NSAID, consider stopping on day and restarting after 3 days, confirm electrolytes and eGFR
Lithium and any other medications, do not take within 1 hour bowel cleansing medication to avoid reduced absorption, confirm electrolytes and eGFR
Colonoscopy bowel preparation medications and contraindications
Moviprep sachets 2x2
Citramag SF sachets 2, senna 7.5mg tablets x10
Klean prep sachets 4
CI for bowel prep: GI obstruction, retention, ileus or perforation Severe IBD, ulceration or colitis Toxic megacolon Reduced consciousness level Dysphagia Ileostomy Hypersensitivity to ingredients
Patient information for colonoscopy bowel preps
No solid food should be eaten at least 2 hours before taking bowel cleanse
Diarrhea is expected, stay at home close to toilets
Drink plenty of clear fluid (water) throughout
Side effects: nausea, vomiting, bloating, abdo pain, anal irritation, sleep disturbance
Can lead to dehydration, dizziness, headaches, confusion
Allergic reaction may include rash, itching, redness and swelling
ASA classification
I Normal healthy patient II Mild systemic disease III Severe systemic disease IV Severe systemic disease constant threat to life V Moribund patient not expected to survive without operation VI Declared brain dead - organs being removed for donor purposes
Patient performance status
Standard criteria measuring how the disease impacts patients daily living
0-5 description
0: fully active, able to carry on all pre-disease performance without restriction
1: restricted in strenuous activity but ambulatory able to carry out work of light nature
2: ambulatory and capable of all selfcare but unable to carry out any work activities, up and about >50% waking hours
3: capable of only limited selfcare, confined to bed or chair >50% waking hours
4: completely disabled, cannot carry out selfcare, totally confined to bed or chair in waking hours
5: dead
Food intolerance and allergy
Adverse reactions to food, this will be recurring each time the person ingests that food
Symptoms depend on the mechanisms of reaction but range from vomiting and diarrhea and skin reactions (eczema, urticaria) to anigio-oedema, severe respiratory distress and anaphylaxis
Classification:
Immunological reactions (food ALLERGY): IgE and non-IgE mediated (delayed and acute reactions)
Non-immunological reactions (food INTOLERANCE)
Common foods: Milk Eggs Fish and seafood Peanuts Sesame Tree nuts Soy beans Wheat Kiwi fruit
Food intolerance or allergy history taking
Why food allergy suspected What foods are implicated (complete list needed including how it was prepared) Symptoms occurring after eating What age symptoms started How much food needed to cause it Do symptoms occur every time it’s eaten How long do symptoms last Do they follow pattern Frequency of occurrence Worst reaction they had Setting of reaction Personal or family history of allergy Feeding history, age of weaning, formula or breast fed Previous treatments, diet exclusions and results of that Is diet nutritionally adequate
Food allergy presentation
Pruritus
Erythema
Diarrhoea
Abdominal pain are all common in both types of reaction
IgE mediated:
Acute urticaria - localised or generalised
Acute angio-oedema, commonly mouth, lips, face, eyes
Oral itching, nausea and vomiting
Colicky abdominal pain
Nasal itching, sneezing, rhinorrhoea, allergic conjunctivitis
Cough, shortness of breath, wheezing and bronchospasm (or history of asthma)
Other signs of anaphylaxis, feeling of impending doom, CV collapse
Non-IgE mediated: Atopic eczema Reflux Infantile colic Stools: loose/frequent/blood/mucus Constipation Perianal redness Pallor and tiredness Faltered growth Food aversion or avoidance
Food allergy investigations
Food diary
Skin prick tests for specific IgE antibodies to suspected foods
Measurement of serum allergen IgE (ELISA) and fluorescent enzyme immunoassay tests
Atopy patch testing or oral food challenges
Trial elimination diet (2-6 weeks normally) then reintroduce to see if symptoms improve then return
Anaphylaxis management
ABCDE assessment
High flow oxygen with reservoir mask
Lay patient flat, raise legs, in pregnancy use left lateral tilt 15 degrees
Adrenaline 0.5micrograms IM adults >12 years old, 0.3 micrograms age 6-12, <6 years 150 micrograms
Establish airway
UV access and rapid fluid challenge
Chlorphenamine after initial resus (dose age dependent)
Hydrocortisone (dose age dependent)
Continual vitals monitoring
Food allergy/intolerance management
Food avoidance
Dietician referral
Antihistamines for less severe symptoms
Adrenaline for severe anaphylactic reactions
Medical emergency bracelet PRN
Informing relatives, schools, carer education etc
Prognosis:
Most children ‘grow out’ of allergy to eggs, milk, wheat and soya. May be due to maturation of gut or immune responses that are responsible for allergy
Sensitivity to peanuts, seafood, fish, tree nuts are rarely lost
Anal fissures
Tear in the mucosa of the anal canal just inside the anal margin
Commonly causes pain on defecation
Mostly responds well to topical or conservative management but refractory cases can need surgery
Second most common complication after pregnancy (first being haemorrhoids)
Acute <6weeks
Chronic >6 weeks (uncommon)
Primary: no apparent cause
Secondary: due to underlying conditions such as constipation, IBD, STI, trauma (surgery, sexual), pregnancy and childbirth or rectal malignancy
Aeitology is unclear but thought to be related to increased anal tone.
Anal fissures presentation and investigations
History of pain with defecation (passing shards of glass)
Can persist several hours after passing
Fresh blood on toilet paper
May have a history of constipation, IBD etc.
Investigations:
Clinical history
PR exam (only external examination if fissures are seen)
Abdominal exam
Anal fissures management
Increase dietary fibre gradually to avoid bloating, shallow warm baths after movements may ease pain
Correct anal hygiene, especially in children, keep dry and clean, advise against stool withholding and undue straining during movements which can worsen
GTN 0.4% ointment for those with >1 week symptoms without improvement, use twice daily for 6-8 weeks (read CI first) also warn pt if bleeding, that they may bleed slightly more than normal with GTN application before healing.
For extreme pain prescribe short course (few days) topical lidocaine 5% ointment used before passing stool, apply 1-2mL PRN
Diltiazem ointment (unlicensed)
Botulinum toxin injections
Oral analgesia PRN for pain, can also prescribe laxatives for constipation, treat underlying condition PRN
Referral for children with non-healing <2 weeks, adults with ongoing pain 6-8 weeks, whose symptoms are still present 12-16 weeks after healing, consider earlier referral in elderly
Recurrent or chronic cases may need surgery (sphincterotomy) to correct fissure and loosen anal tone
follow ups:
Primary anal fissure: in children, return if unhealed after 2 weeks or earlier if painful. In adult, review if unhealed after 6-8 weeks or earlier PRN
Secondary anal fissue follow ups will depend on underlying cause
Advise primary anal fissue when healed they should contiue to keep dietary and lifestyle measures in place to reduce risk of recurrence
gastritis
Gastric mucosal inflammation
Bacterial acute and chronic gastritis are caused by H pylori infection
Erosive gastritis may occur in response to NSAID/alcohol long term use, doesnt typically cause inflammation but can lead to bleeding and ulceration in stomach lining
Stress gastritis is most commonly related to mucosal ischaemia in critically ill patients, ranging from superficial to deep mucosal damage known as stress ulceration
Autoimmune gastritis is diffuse mucosal atrophy characterised by auto-antibodies to parietal cells and intrinsic factor, resulting in inflammatory infiltration and atrophy
Gastritis presentation and complications
Presentation: Can start suddenly or develop slowly Pain in epigastric or RUQ abdomen Loss of appetite, feeling full in upper abdomen Dyspepsia Bloating Retching Nausea and vomiting
Complications:
Stomach ulcers
Haematemesis
Gastritis acute and chronic management
Acute gastritis management:
GI bleeding: urgent hospital referral, IV access, fluid resus and stabilisation, urgent OGD if needed.
If related to NSAIDs, aspirin, alcohol then bleeding usually resolves quickly, stop aspirin or NSAID and initiate PPI
Antacids can reduce irritation and may resolve symptoms
Chronic gastritis:
H pylori associated: treat with eradication immediately
NSAID related gastritis: stop NSAID if possible, if not then after ulcer healing offer long term gastric protection or consider substitution to newer Coc-2 selective NSAID (celecoxib or etoricoxib)
Pyloric stenosis
Caused by diffuse hypertrophy and hyperplasia of smooth muscle of antrum and pylorus of stomach
Pyloric muscle hypertrophy results in narrowing of the pyloric canal which results in easy obstruction
Usually presents in infants aged 2-8 weeks
Occurs in 1 in 500 live births
More common in males than females (4:1 ratio)
Genetically linked, early exposure to erythromycin in first 2 weeks of life
Pyloric stenosis presentation
Onset of vomiting around 2-8 weeks of age
Non-bilious vomiting for several days often projectile, usually 30-60 minutes after a feed with baby remaining hungry
Vomiting increases in intensity over several days
Persistent hunger
Weight loss
Dehydration
Lethargy
Infrequent of absent bowel movements
Stomach wall peristalsis may be visible
Enlarged pylorus, described as an ‘olive’ may be palpated in the RUQ or epigastrium at start of feed
Pyloric stenosis investigations and management
Investigations:
USS, best test
Serum electrolytes to correct imbalances
Management:
Correct electrolyte imbalances and dehydration
Ramstedt’s Pyloromyotomy (can be done laparoscopically)
Prognosis is excellent unless diagnosis delayed and patient suffers severe dehydration
Mallory-weiss syndrome
Characterised by UGIB from mucosal lacerations in UGIT, usually the gastro-oesophageal junction or gastric cardia
Emergency medical condition (mortality 6-13%)
Majority are caused by peptic ulcers
Common between ages 30-50
Most patients present with single tear, usually just below the gastroesophageal junction on the lesser curve of the stomach, but may be associated with other lesions
Cause:
Haematemesis usually occurs after prolonged or forceful bout of retching, vomiting, coughing, straining or hiccupping
Mallory-weiss syndrome pathology and risk factors
Repeated/forceful vomiting causes acute increase in intra-abdominal pressure against closed glottis (very sudden and strong valsalva manoeuvre)
Sudden forceful contraction of stomach also increases intra-oesophageal pressure
Mucosal tear usually occurs at gastro-oesophageal junction/gastric cardia causing arterial bleeding
risk factors:
Excessive alcohol ingestion
Conditions predisposing to retching and vomiting eg gastroenteritis, bulimia, renal disease, raised intracranial pressure, hepatitis, COPD, bronchiectasis, whooping cough, hiatus hernia, NSAIDs
Mallory-weiss syndrome presentation and investigations
History of haematemesis following bout of retching or vomiting
Melaena
Dizzy or syncope
Abdominal pain and features from initial cause of vomiting
investigations:
Assess blood loss using rockall scoring system to assess the UGIB
Bloods: FBC, coagulation studies
Renal function, urea, creatine, electrolyte levels
Group and save
ECG and cardiac enzymes to rule out MI
Mallory-weiss syndrome management
ABCDE assessment
Resus, maintain airway, high flow oxygen and correcting dehydration and fluid loss
Once stable, take history and perform examinations
Endoscopy to stop the bleeding (should be performed within 24 hours)
Most will stop bleeding spontaneously, few need endoscopic intervention
Rockall score calculated post-endoscopy (<3 low risk, >3 needs close observation as high risk)
Careful monitoring (urine output, BP and vitals) and those with high risk of rebleeding should be monitored for at least 48 hours
PR exam for anal fissures
Ask pt to lie comfortably in lateral position and gently part buttocks
Acute anal fissures are superficial and well-demercated edges
Chronic are wider, deeper, muscle fibres visible in base. Edges often swollen, skin tag may be visible at end of fissure
Primary are usually singular, occur in posterior midline of anus, although few cases may be seen in anterior midline (especially in women)
Secondary may have irregular outline, be multiple, or occur laterally
Anal spasms and pain may prevent full visualisation of fissure. When fissure cannot be seen, pain occurs with gentle pressure on anal margin
Anal fissure important history taking
Symptoms:
Anal pain with defecation
Severe and sharp when passing stool, followed with deep burning pain persisting hours afterwards
Bleeding may occur with defecation. When present usually seen small quantity of bright red blood on stool or toilet paper
Anal spasm and tearing sensation on passing stool commonly reported
Duration of symptoms:
Acute anal fissures are present <6 weeks
Chronic anal fissures present for >6 weeks
Features of underlying cause, including:
Dietary and bowel habits; constipation, diarrhea, recent changes
Previous anorectal trauma; anal surgery and obstetric history
Associated symptoms; abdo pain or weight loss
Family history of colorectal cancer, IBD etc.
STI possibility
Recent pregnancy
Anorectal abscess/fistula
Thought to be caused by plugging of anal ducts that drain anal glands in anal wall, helping ease passage of faecal matter through mucus secretion
ducts: supralevator ischiorectal intersphincteric perianal
Anorectal abscess/fistula presentation
Pain in perianal region
Exacerbated when sitting
Localised swelling, itching, discharged
Severe abscesses can present with systemic features: fever, rigors, general malaise, septic features
Erythematous, fluctuant, tender perianal mass, which may be discharging pus or have surrounding cellulitis
Deeper abscesses may not have any obvious external signs, however produce severe tenderness on digital rectal exam, therefore need further examination under anaesthesia for full assessment
Anorectal abscess/fistula management
Arrange same day incision and drainage (can be performed in primary care if lesion is small and superficial) otherwise refer to colorectal or general surgical unti dependin gon local protocol
Paracetamol for pain/fever
If response insufficient offer NSAIDs (ibuprofen, naproxen) if not CI
Associated cellulitis: oral antibiotics (flucloxacillin mild or co-amoxiclav for severe)
Post-drainage advise lifestyle changes to reduce risk of recurrence such as: meticulous peri-anal hygiene, baths, showers, removal of hair
Fistula and management
Small tunnel that develops between end of bowel and skin near the anus
Usually the result of an infection near the anus causing a collection of pus (abscess) in nearby tissue, eating away a small tunnel in tissue, but can occur without bacterial infection also
When pus drains, can leave small channel behind
Usually do not get better on their own
management
same day admission for surgical review
Pilonidal disease
Chronic skin problem found most often in sacrococcygeal region
Cleft between buttocks just below base of spine
Characterised by one or more sinus tracts; these are cavities with narrow opening on skin surface (pilonidal sinus)
Most cases, the cavity is filled with nests of hair - hence pilonidal (means hair nest). Non-inflamed lump known as pilonidal cyst. If the sinus becomes infected a pilonidal abscess may form, pilonidal disease, cysts may be asymptomatic and need no intervention. When abscesses form, always need intervention
Pilonidal disease cause
Congenital - born with small holes/pits near base of spine (enlarged hair follicles)
Follicular occlusion: some people genetically prone to this. May also suffer from hidradenitis suppurativa, acne conglobata and dissecting cellulitis (follicular occlusion syndrome/tetrad)
When subjected to friction and motion the follicles are injured and disrupted so hair pokes through wall of follicle into surrounding skin setting up foreign body reaction
Neighbouring hairs or free hairs from other parts of body collect in pit and invade small opening created by distorted hair follicles
Skin and perineal bacterial (staph. Aureus, bacteroides species etc) invade and cause infection
Pilonidal disease risk factors
2-3x more common in men Coarse, curly or crinkly hair Obesity Family predisposition Poor hygiene Prolonged sitting or buttock friction causing increased sweating Repeated local injury Co-existing hidradenitis suppurativa
Pilonidal disease presentation
Small painless pit or dimple at base of spine
Large painful abscess
Progressive tenderness
Particularly after prolonged periods of sitting
Pain, redness, swelling
Small hole or holes draining fluid that may be clear, cloudy or bloody
If infected, draining pus may smell foul
Fever, malaise, nausea
Visible or lumpy tracts 2-5 cm long in chronic or recurrent disease
Pilonidal disease management
Asymptomatic: no treatment needed
Advice to keep clean, hair free and cyst may self resolve
Persistent and inflamed cysts (acute pilonidal abscess) are incised and drained to reduce inflammation
Occasionally abscesses need to be cut out completely to remove hair nests and skin debris, this reduces rate of recurrence to about 15%
Persistent or complex pilonidal disease can benefit from surgical intervention - consider referral if heavily impacting quality of life, requires packing for several follow ups until complete healing after intervention to ensure proper healing without sinus healing (carried out by nurses/tissue viability)
Rectal polyps and risk factors
Very common >50 years
Slightly more common in men
Can develop single or multiple
Exact cause unknown, thought to be by body producing too many cells in lining of the bowel
These extra cells then form into a bump (polyp) is a benign tumour
Risk factors: Family history of polyp or bowel cancer Condition affecting the gut eg colitis, crohn’s etc Obesity Smoking
Rectal polyps presentation and investigation
Asymptomatic
Incidental findings on scoping
Larger polyps may cause mucus in poo, diarrhea, abdominal pain
investigations:
Colonoscopy
Wire loop can be used during this to cauterise polyp and remove it
Rarely some bowel will be removed with the polyp, this is very severe cases where polyp has some cell changes; the polyp is very large or there are lots of polyps
Polyps and cancer
Usually benign
Some can be adenomas with increased chance of malignancy if not removed
It’s believed most bowel cancers develop from adenoma polyps
Very few polyps will turn into cancer but takes many years for this to happen
Because of risk of bowel polyps developing into cancer, your dr will always recommend treatment
Clostridium difficile
Bacterial infection commonly affecting those who have recently been on antibiotics
Easily spread to others
Notifiable condition: must notify authority of all cases once confirmed
Normally in the bowel but kept under control by other gut flora
Some antibiotics interfere with flora balance and increase risk of c. diff multiplying and producing toxins producing illness
Once out of the body the bacteria become spores and can spread to others, can survive for long periods of time so regular disinfecting of all surfaces needed
Considered infectious until at least 48 hours after symptoms clear up
C. difficile risk factors
Taking broad spectrum antibiotics, several types at once or long term antibiotics
Hospital or care home settings
>65 years
IBD
Cancer
Kidney disease
Immunosuppressed conditions
Taking PPI medications (reduced stomach acid)
Bowel surgery history
Antibiotics more risky are: fluoroquinolones, cephalosporins, penicillins and clindamycin
the 5 Cs: cephalosporins carbapenems clindamycin ciprofloxacin co-amoxiclav
C difficile presentation and management
Diarrhea several times daily (foul smelling) Fever Loss of appetite Nausea Abdominal pain
Management:
Hospitalisation for severe infection to correct dehydration and electrolyte imbalances
Mild can be treated at home
Isolation needed to reduce risk of spreading to others
Stopping causative antibiotics
10-14 day course of antibiotics known to kill C. diff, may need to be repeated if symptoms return or persist (vancomycin, fidaxomicin, metronidazole)
Rarely, surgery to removal damaged section of bowel
Hepatitis
Inflammation of the liver
Can be acute or chronic
Pathology:
Liver cell necrosis and inflammatory cell infiltration in liver
Divided into acute or chronic type based on clinical and pathological criteria
Acute and chronic causes of hepatitis
Acute: Viral Non-viral Alcohol Toxins Drugs Ischaemic Autoimmune Metabolic diseases
Chronic: Viral Alcohol Drugs Non-alcoholic steatohepatitis Autoimmune Hereditary
Presentation of hepatitis
Can be asymptomatic Fatigue Pruritus Muscle and joint aches Nausea and vomiting Jaundice Fever (viral)
typical biochemical findings of hepatitis
liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.
Viral hepatitis
Five types, A-E
Most people commonly affected by A, B and C
Management:
Have a low threshold for screening patients that are at risk of hepatitis C
Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
Refer to gastroenterology, hepatology or infectious diseases for specialist management
Notify Public Health (it is a notifiable disease)
Stop smoking and alcohol
Education about reducing transmission and informing potential at risk contacts
Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
Hepatitis A (HAV) and presentation
Most common type of acute viral hepatitis
RNA virus
Spread by faecal-oral route, ingestion of contaminated foods (shellfish, clams) or water
Most infections are in childhood/young patients
Incubation 2-6 weeks
Presentation:
Nonspecific prodromal symptoms (fever, malaise, anorexia, nausea and vomiting, arthralgia)
Jaundice (rare in children)
Can cause cholestasis, causing dark urine and pale stools
Hepatosplenomegaly
Adenopathy
HAV investigations and management
Investigations:
AST and ALT increased (3-6 weeks post-exposure)
Management:
Notifiable disease: notify public health
Supportive, alcohol cessation, basic analgesia
Usually self limiting infection resolves within 3-6 weeks
Prevention: good hygiene, avoid risky foods when travelling and vaccinations
Hepatitis B HBV
DNA virus
Spread via blood products, IV drug abusers, sexual partners, direct contact (horizontal transmission)
Vertical transmission is from mother to child during parturition is most common means of transmission worldwide
Horizontal transmission occurs particularly in children through minor abrasions or close contact with other children
Acute hepatitis B:
Incubation 1-5 months
Pathology:
HBV penetrates hepatocytes, in immunocompetent adults will elicit strong cellular immune response and clears the infection
5-10% remain chronic carriers and a risk to others
1% will have fulminant liver failure/fulminant hepatitis
acute HBV presentation and investigations
Asymptomatic Nonspecific prodromal symptoms (fever, malaise, anorexia, nausea, arthralgia) Jaundice (rare in children) Hepatosplenomegaly Adenopathy
Investigations:
AST and ALT increased (3-6 weeks post-exposure)
Management of acute HBV and complications
No specific therapy, supportive management if symptomatic
Some cases use interferon alfa-2a, Tenofovir, Entecavir
Have low threshold for patients at risk, screen for other blood borne diseases (HIV, all hepatitis virals and other STIS)
Refer to GI, hepatology or infectious diseases for specialist management
Notify public health for all cases
Smoking cessation and alcohol
Education of reducing transmission and informing potential at risk contacts
Test for complications: fibroscan for cirrhosis, USS for hepatocellular carcinoma
Antiviral meds can slow progression and reduce infectivity
Liver transplant for end-stage liver disease
Complications:
Short term: 5-10% become carriers, 1% have fulminant hepatitis
Long term (in carrier state): cirrhosis, HCC, cholangiocarcinoma
Hepatitis serology
Antigens:
HBsAg (active infection) appears in blood 6 weeks- 3 months after acute infection and then disappears
HBeAg (viral replication) rises early and usually declines rapidly
Persistence of both of these antigens indicates chronic hepatitis
Antibodies:
Anti-HBs (implies vaccination or past or current infection) appear late and indicates immunity. If all else negative but this is positive, likely immune from vaccination
anti-HBc (implies past or current infection) is first to appear and persists for many months. IgM implies active infection, high titre = acute while low titre = chronic infection. IgG indicates past infections when HBsAg is negative
anti-HBe appears after anti-HBc and indicates low risk
Window period:
Diagnosis of viral hepatitis made by finding the antigen or antiviral antibody in serum
For HBV, antigens may be detectable after 6 weeks-3 months
Early negative result does not exclude acute HBV infection
Hepatitis C HCV and presentation
RNA virus
Spread via blood products, IVDU, sexual contact
Most common in UK is IV drug users (IVDU)
In developing countries is blood products
Incubation 2-6 months
No vaccination but is now curable with direct acting antiviral meds (1 in 4 make full recovery, 3 in 4 become chronic)
Presentation: Early is mild or asymptomatic with only 10% jaundice 85% have silent chronic infection 25% have cirrhosis in 20 years 4% of corrhotic patients develop HCC
HCV investigations
Most patients are not diagnosed until they present years later, with elevated serum aminotransferase levels (LFTs) found on routine biochemistry or with symptoms and signs of chronic liver disease and cirrhosis
LFTs
anti-HCV antibodies confirms exposure
HCV-PCR confirms ongoing infection
Liver biopsy or elastography (if PCR +ve) to assess liver damage and need for treatment. Elastography is assessment of tissue elasticity and stiffness by USS or MRI
Window period:
Diagnosis made by finding viral antiviral antibody in serum
For HCV antibodies are detectable after 8 weeks (2 months)
Management of HCV
Alcohol cessation to reduce risk of cirrhosis and HCC
All patients with chronic infection need direct acting antiviral therapy (INF-alpha + Ribavirin) over 8-12 weeks
Prognosis based on other risk factors (alcohol, HIV, HBV)
Prevention is avoiding needle stick injuries, safety measures
Liver transplant for end stage liver disease
Hepatitis D HDV overview
Incomplete RNA virus, needs HBV present for assembly (attaches to HBsAg)
5% HBV carriers have HDV co-infection, especially in IVDUs
Complication:
Acute liver failure
Cirrhosis
Investigations:
anti-HDV antibody
HBsAg +ve (if +ve request HDV AB also)
Management:
INF-alpha (limited success)
May need liver transplant
Prevention: HBV vaccination prevents HDV infection
Hepatitis E (HEV) overview
RNA virus similar to HAV
Transmitted by faecal-oral route
Common in indo-china
More common than HAV in UK
Mortality is high in pregnancy
Produces only mild illness, virus cleared within 1 month and no treatment is needed
Rarely progresses to chronic hepatitis/liver failure, more so in immunocompromised pts
Investigation:
Anti-HEV antibody
Management:
Conservative
Vaccine available in china
Fulminant hepatitis/fulminant hepatic failure overview
Pathology:
Hepatic failure with encephalopathy
Acute liver damage from any cause may cause massive liver cell necrosis with encephalopathy
Cause:
In the UK, viral hepatitis and paracetamol overdose are the most common causes
Presentation:
Hepatic encephalopathy
Severe jaundice
Severe coagulation
management:
Most with need specialist liver unit
Emergency liver transplantation usually
80% mortality without transplant
chronic hepatitis and causes
Sustained inflammatory disease of the liver, lasting >6 months
Principal cause worldwide is viral hepatitis HBV and HCV
Viral hepatitis is also most common cause of cirrhosis and HCC
Causes: HBC/HDV HCV Autoimmune Drugs: methyldopa, nitrofurantoin, isoniazid, ketoconazole Hereditary: wilson’s disease IBD Alcohol
Chronic hepatitis (HBV)
Persistence of HBsAg in serum for >6 months after acute infection
Most patients clear virus after acute infection and only small % progress to chronic
Progression depends on several factors: virulence of virus, immunocompetence of patient, age of patent
When acquired at birth (vertical transmission) or early childhood, cellular immune response does not occur and chronic infection normally develops
Risk of chronic liver disease, cirrhosis, HCC
Chronic HBV hepatitis management
Antiviral (INF-alpha, lamivudine, adefovir, entecavir, tenofovir) treatment for those with HBV DNA >20,000 IU/ml and elevated ALT
Inactive HBV carrier (normal ALT and HBV DNA <2000 IU/ml) are low risk for progressive liver disease and not given antivirals
autoimmune hepatitis
Rare cause of chronic hepatitis
Unknown exact cause but could be genetic predisposition triggered by environment eg viral infection causing T cell mediated response against liver cells
Types:
Type 1; Occurs in adults. Typically women in late 40-50s. Presents around menopausal time with fatigue, features or liver disease. Takes less acute course than type 2.
Type 2; Occurs in children. Teenagers or early 20s present with acute hepatitis with high transaminases and jaundice
autoimmune hepatitis Ix and Mx
Type 1 show antinuclear antibodies (ANA), anti smooth muscle AB (anti-actin), anti soluble liver antigen (anti-SLA/LP)
Type 2 show anti-liver kidney microsomes-1 (anti-LKM1) and anti-liver cytosol antigen type 1 (anti-LC1)
Diagnosis confirmed with liver biopsy
Management:
High doses of prednisolone tapered over time while immunosuppressants (particularly azathioprine) are introduced
Liver cirrhosis
Chronic inflammation of the liver and damage to liver cells
When hepatocytes are damaged, they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver
Fibrosis affects the structure and blood flow through the liver, causing increased resistance in vessels, leading to portal HTN
Cirrhosis with encephalopathy, ascites or variceal haemorrhage = decompensated cirrhosis
Cirrhosis without complications = compensated cirrhosis
Pathology:
Results from necrosis of liver cells followed by fibrosis and nodule formation
Results in impaired hepatocyte function and gross distortion of liver
Leading to portal HTN
histopathology
Micronodular cirrhosis: uniform, small nodules <3mm diameter caused by alcohol damage or biliary tract disease
Macronodular cirrhosis: nodules of variable size caused by chronic viral hepatitis
Liver cirrhosis causes
most common Alcoholic liver disease Non alcoholic fatty liver disease Hepatitis B Hepatitis C Less common: Autoimmune hepatitis Primary biliary cirrhosis Haemochromatosis Wilson's disease alpha-1 antitrypsin deficiency Cystic fibrosis Drugs: amiodarone, methotrexate, sodium valproate
Liver cirrhosis presentation
Jaundice from raised bilirubin
Hepatomegaly but can shrink if more cirrhotic
Splenomegaly from portal HTN
Spider naevi
Palmar erythema from hyperdynamic circulation
Gynaecomastia and testicular atrophy in males from endocrine dysfunction
Bruising from abnormal clotting
Ascites
Caput medusae: distended paraumbilical veins from portal HTN
Asterixis
Cirrhosis with encephalopathy, ascites or variceal haemorrhage = decompensated cirrhosis
Cirrhosis without complications = compensated cirrhosis
Liver cirrhosis Ix
Enhances liver fibrosis ELF blood test is first line GOLD STANDARD for non alcoholic fatty liver disease (<7.7 indicates none to mild fibrosis, 7.7-9.8 moderate, >9.8 = severe fibrosis)
LFT: normal or slight elevation of ALT, AST
FBC: thrombocytopenia
Albumin
USS to screen for nodularity. Corkscrew arteries may show from compensated reduced portal blood flow
Hyponatremia indicates more severe liver disease
Test for viral antibodies and antigens to screen for viral hepatitis
Alpha-fetoprotein is tumor marker for HCC can check every 6 months screening in patients with cirrhosis along with USS
Child-puge score and MELD score for cirrhosis
CP score to determine severity of cirrhosis and prognosis base on bilirubin, albumin, INR, ascites and encephalopathy
MELD score: recommended by NICE to be used every 6 months in patients with compensated cirrhosis. Takes into account bilirubin, creatinine, INR and Na and if they need dialysis or not. Gives % estimated 3 month mortality and helps guide referral for liver transplant
Liver cirrhosis management
Irreversible and progressive, manage only complications such as varices
USS and alpha-fetoprotein every 6 months for HCC
Endoscopy every 3 years in patients with known varices
End stage cirrhosis needs liver transplant
High protein, low sodium diet
MELD score every 6 months
Liver cirrhosis complications
Malnutrition, muscle wasting
Portal HTN, varices and variceal bleeding
Ascites, spontaneous bacterial peritonitis
Hepato-renal syndrome
Hepatic encephalopathy (decline in brain function as result of severe liver disease, due to not being able to remove toxins from blood, leading to brian damage)
HCC
Hepatorenal syndrome overview
occurs in liver cirrhosis. Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads to hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.
Hepatic encephalopathy overview
also known as portosystemic encephalopathy. It is thought to be caused by the buildup of toxins that affect the brain. One toxin that is particularly worth remembering is ammonia, which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. There are two reasons that ammonia builds up in the blood in patients with cirrhosis: Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver altogether and enters the systemic system directly.
By giving laxatives we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce the number of bacteria in the gut producing ammonia.
Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes to personality, memory and mood.
hepatic encephalopathy precipitating factors and management
Constipation Electrolyte disturbance Infection GI bleed High protein diet Medications (particularly sedative medications)
Management
Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
Nutritional support. They may need nasogastric feeding.
Oesophageal varices and presentation
Usually present as result of portal HTN
Most common cause of portal HTN is cirrhosis
Presentation:
History of alcohol abuse, drug abuse, HBV or liver disease
Signs of liver disease: jaundice, telangiectasia, ascites
Postural hypotension
Dizziness
Pallor
Signs of shock: cold extremities, drowsiness etc
Oesophageal varices management
Approach is usually the same as approach to upper GI bleeding, then later diagnosed as bleeding oesophageal varices
ABCDE assessment
Management of shock: oxygen, IV infusion, transfusion, ITU
Blood transfusion
Emergency endoscopy/surgery to locate and fix bleed
If stable: IV, bloods, G+S, NBM, IV infusion, clotting corrected: vit K, FFP, platelets
For suspected varices: terlipressin (vasopressin) IV 1-2mg/6hr for <3 days g
Broad spectrum IV antibiotics eg ciprofloxacin, tazocin (piperacillin/tazobactam) IV 4.5g/8hr
Both given before endoscopy:
Treated with balloon tamponade (temporary for uncontrolled bleeding) called sengstaken-blakemore tube
Band ligation, sclerotherapy, fulguration, laser
Danis oesophageal stent
TIPS: transjugular intrahepatic portosystemic shunts causes reduction in portal pressure and collapse of varices
** Blakemore not used in MW tear due to more likely being from arterial bleeding - will put pressure on vessels witch is CI for arterial but good for venous bleeds**
Portal HTN
Abnormally high pressure in hepatic portal vein
Clinically significant portal HTN is defined as hepatic venous pressure >10mmHg
Pathology:
Portal vein comes from superior mesenteric vein and splenic vein
Delivers blood to liver
Liver increases resistance increases blood pressure in portal vein, increasing back-pressure in portal system (portal HTN)
Causes sites where the portal system anastomoses with the systemic system to dilate and become tortuous (varices)
One of these shunts is through the lower oesophageal veins, which if portal HTN is present, will dilate and come to the surface as varices
Vulnerable to bleeding
Sites varices occur at: Gatro-oesophageal junction Ileocaecal junction Rectum Anterior abdominal wall via umbilical vein (caput medusae)
Causes of oesophageal varies
Prehepatic: blockage of vein before liver. Eg Congenital atresia or stenosis, or vein thrombosis
Hepatic: cirrhosis (most common cause), chronic hepatitis, idiopathic, nodular, toxins etc
Posthepatic: blockage of hepatic veins or venules eg constrictive pericarditis, right heart failure etc
Oesophageal varices presentation
For causes of liver disease:
History of jaundice.
Alcohol consumption.
Blood transfusion, especially abroad; lifestyles that predispose to hepatitis B or hepatitis C.
Family history - eg, Wilson’s disease or hereditary haemochromatosis.
For complications of portal hypertension:
Haematemesis or melaena - suggest bleeding varices.
Lethargy, irritability and changes in sleep pattern - suggest encephalopathy.
Increased abdominal girth, weight gain - suggest ascites.
Abdominal pain and fever - suggest spontaneous bacterial peritonitis.
Pulmonary involvement is common in patients with portal hypertension
Ix for oesophageal varices
Clinical diagnosis
Dilated veins in anterior abdo wall and around umbilicus (caput medusae)
Splenomegaly
Ascites
Bloods: LFT, U+E, FBC, clotting screen
USS for organomegaly, portal blood flow, thrombosis
CT or MRI for vasculature if inconclusive
Endoscopy for varices
Indirectly measure portal pressure by hepatic venous pressure gradient (HVPG)
Oesophageal varices management
Conservative: salt restriction and diuretics
Propranolol reduced portal HTN (non-selective beta blocker) or nitrates and other vasoactive drugs (terlipressin and octreotide)
Shunt procedures to create anastomoses between portal and hepatic veins
Treat underlying cause
Liver transplant
Boerhaave syndrome overview
Rare but potentially fatal condition characterised by transmural (complete) tear of the distal oesophageal induced by sudden increase in pressure
Diagnosis made by classic triad of vomiting, abdominal pain or chest pain and subcutaneous emphysema but often this does not present
Hamman’s sign: crunching sound on auscultation of heart due to pneumomediastinum
Treatment can be conservation, surgical or endoscopic
oesophageal strictures
Types:
Benign: GORD, corrosives, medication, radiotherapy, endoscopic Tx of varices, post-op, prolonged NGT
Malignant
Webs: mucosa and submucosa only
Rings: mucosa, submucosa and muscle
External compression: in neck of mediastinum
Schatzki’s ring:
Thin circumferential ring in distal oesophagus
Only involves mucosa and submucosa (should be named web)
Usually appears at proximal part of hiatus hernia
Cause uncertain, congenital and acquired factors eg GORD
Usually presents in >50 years
Chronic intermittent dysphagia to solid food
Non-progressive
Benign oesophageal strictures causes
Peptic: secondary to GORD (most common)
Ingestion of corrosives
Medications: alendronate, iron, NSAIDs, KCl
Radiotherapy
Endoscopic treatment of oesophageal varices (sclerotherapy, thermal fulguration etc.)
Post-op
Prolonged nasogastric tube placement
Oesophageal strictures presentation
Dysphagia (progressive worsening from solids to liquids means worsening of stricture)
Heartburn
Impaction of food
Weight loss
Chest pain
Cough and wheeze from food aspiration or acid
Asymptomatic (incidentally found on endoscopy or barium swallow)
Oesophageal strictures investigation
Abdominal exam: tenderness, organomegaly, lymphadenopathy
Bloods: ferritin, LFTs (ALP increase)
CXR
Barium swallow + endoscopy GOLD STANDARD
CT
Endoscopic USS (EUS) for staging or metastasis
Difference between benign and malignant oesophageal strictures on imaging
Benign: long segment concentric and smooth tapering no shouldering no mucosal irregularity
Malignant: short segment eccentric, irregular narrowing shouldering is seen usually associated with mucosal irregularity
complications of oesophageal strictures
Aspiration pneumonitis
Complete obstruction of foods (solid food impaction)
Malnutrition
Bleeding or perforation from stricture dilatation
Oesophageal strictures management
Benign stricture or rings:
Endoscopic dilatation
Endoscopic incisional therapy long term PPI reducing need for number of dilatations
Malignant:
Surgical excision (oesophagectomy)
Radiotherapy
Oesophageal stent (palliative)
Oesophageal stricture due to GORD overview
most common cause of stricture
presents with gradually worsening dysphagia
treated with endoscopic dilatation and long term PI therapy
Chronic GORD may also underlie development of Schatzki ring
Management of upper GI bleeding
ABCDE assessment intervene as needed
protect airway, keep NBM
insert 2 large bore IV cannula for fluid resus
take bloods: FBC, LFT, glucose, clotting screen, G+S
rapid IV fluid infusion
Blood transfusion PRN
continue fluids until stable
correct clotting abnormalities (vit K, FFP, platelets)
If risk of varices give Terlipressin IV 1-2mg/6hours and broad spectrum antibiotics
consider referral to HDU/ICU
consider CVP line for fluids (aim for >5cmH2O)
catheterise and monitor UO (>30mL/hour aim)
notify surgeons of severe bleeds
urgent endoscopy for diagnosis and control of bleeding after adequate Jesus (urgent <24 hours, if blood clotting and patient more stable <72 hours)
Causes of UGIB
PUD (35-50%) Gastroduodenal erosions 8-15% Oesophagitis 5-15% Mallor-weiss tear 15% Varices 5-15% Upper GI malignancy Vascular malformations Bleeding diathesis Swallowed blood: facial trauma, nose bleed, dental bleed, haemoptysis etc.
Typical symptoms of UGIB
Haematemesis
Altered bowel habit: dark tarry stools (melaena), fresh rectal bleeding
Abdominal pain: typically epigastric but can be diffuse
Presyncope or syncope: due to hypovolemia and secondary to cerebral hypoperfusion
Hypotension/postural hypotension
Tachycardia
Decreased UO
Signs of shock (cyanosis, cool and clammy)
Dark, clotted blood being vomited indicates bleeding is no longer active can endoscopy within 72 hours (non-emergency)
Abdominal tenderness
Hematochezia: passage of fresh red blood per rectum, which can occur in context of profuse UGI haemorrhage due to rapid transit of blood through the GIT
UGIB red flags
60< years Continued bleeding Hemodynamically unstable Liver disease or known varices Significant comorbidity
UGIB Blatchford score
Calculated prior to endoscopy based on lab parameters
Used to identify low risk patients who do not need any intervention (blood transfusion, endoscopic therapy or surgery etc.) when presenting with upper GI haemorrhage
takes into account: blood urea, haemoglobin (different values men and women), systolic BP, pulse, meleana, syncope, hepatic disease, cardiac failure
UGIB rockall score
Important to identify those at risk of ongoing bleeding and death
Post endoscopy score provides most accurate risk assessment
With increasing age is increased risk of death
Mortality <40 years is negligible
Mortality increases to 30% >90 years
Patients with evidence of active bleeding and signs of shock have 80% risk of death
Those with non-bleeding visible vessel at endoscopy have 50% chance or re-bleeding
takes into account age, shock, comorbidities, diagnosis and major surgical history?
LFTs
Alanine transaminase ALT Aspartate aminotransferase AST Alkaline phosphatase ALP Gamma-glutamyltransferase GGT Bilirubin Albumin Prothrombin time PT
- ALT, AST, ALP and GGT used to distinguish between hepatocellular damage and cholestasis*
- Bilirubin, albumin and PT used to assess livers synthetic function*
If ALT has >10 fold increase and ALP has <3 fold increase then suggests hepatocellular injury
Vice versa suggests cholestasis
Marked raised ALP with raised GGT strongly suggests cholestasis - without suggests non-hepatobiliary cause (bone breakdown increasing ALP instead of liver)
Bilirubin >50/60 shows jaundice
Unconjugated bilirubin = normal urine colour
Conjugated = darker urine colour
White stools = post hepatic cause
ASTALT = cirrhosis and acute alcoholic hepatitis
Causes and LFT results of hepatic derangement
ALT
acute hepatocellular damage: Very high
chronic hepatocellular damage: Normal or high
cholestasis Normal or high
ALP
AHD: Normal or high
CHD: Normal or high
cholestasis: Very high
GGT
AHD: normal/high
CHD: normal/high
cholestasis: very high
Bilirubin
AHD: high/very high
CHD: normal/high
cholestasis: very high
causes of AHD:
Poisoning
Infection (HAV, HBV)
Liver ischaemia
causes of CHD: Alcoholic fatty liver Non-alcoholic fatty liver Chronic infection (HBV, HCV) Primary biliary cirrhosis Alpha-1 antitrypsin deficiency Wilson’s disease Haemochromatosis
Clotting screen normal values and effects of anticoagulants and anti platelets
Prothrombin time 12-13 seconds
INR 0.8-1.2 (2-3 if warfarin)
APTT 35-45 seconds
Thrombin time 10-15 seconds
Anticoagulant medications will: Increase PT/INR Increase APTT Antiplatelets (clopidogrel and aspirin): Increase overall bleeding time But won’t affect PT or APTT
Perforation and bleeding
Hole in wall of GIT
May occur anywhere from oesophagus to anorectal junction
Delay in resus and definitive surgery can rapidly progress into septic shock, multi-organ dysfunction and death
Needs to be first consideration during diagnosis to be excluded with acute abdominal pain
Causes:
Most commonly peptic ulcers and sigmoid diverticulum
Chemical: PUD, foreign body
Infection: diverticulitis, cholecystitis, meckel’s diverticulum
Ischaemia: mesenteric ischaemia, obstructive lesions (cancers, strangulated hernia etc) resulting in bowel distension, ischaemia and necrosis
Colitis: toxic megacolon (C. diff, UC)
Iatrogenic: recent surgery, endoscopy, NGT insertion
Trauma: high force over small surface area, shear forces from acceleration-deceleration
Presentation of perforation
Abdominal pain
Systemic symptoms: vomiting, lethargy, malaise
Peritonism
Oesophageal perforation: chest/neck pain may radiate to back, pain usually pleuritic, vomiting, respiratory symptoms
Investigations for perforation
CT GOLD STANDARD (XR cannot rule out a perforation) , confirms presence of free air, location of perforation and potentially underlying cause
Raised WCC + CRP
Lactate
Acute AXR series
Pneumomediastinum/widened mediastinum if oesophageal perforation
Management for perforation
ABCDE, act as needed, bloods, fluid resus etc.
Antibiotics prophylaxis
Surgical treatment: omental (graham) pouch used to close peptic ulcer perforation, Hartmann’s procedure to resect diverticula and thorough washout
Conservative management: elderly or frail or CI for surgery or with localised perforation + peritonism with no evidence of generalised contamination on CT, usually <5mm perforation
Oesophageal perforation
Full rupture to oesophagus has mortality 50-80%
Full thickness rupture of oesophageal wall
If spontaneous (vomiting etc) often called Bperhaave’s syndrome
Results in leaking stomach contents into mediastinum and pleural cavity, triggering severe inflammatory response, rapidly overwhelming the body
Results in collapse, multi organ failure and death
Causes:
Two most common causes are iatrogenic (endoscopy etc) or after severe forceful vomiting
Rare but mostly occur in patients with otherwise normal oesophagus
Presentation and Ix of oesophageal perforation
Presentation: Mackler's triad: retrosternal chest pain, respiratory distress and subcutaneous emphysema following severe vomiting or retching (actually only seen in 15% patients) Epigastric pain Back pain Dyspnea Shock
Investigation:
Bloods: routine and G+S also
CT chest abdomen pelvis with IV and oral contrast to show air/fluid in mediastinum or pleural cavity
CXR evidence of pneumomediastinum or intrathoracic air fluid levels
Management of oesophageal perforation
Often septic and hemodynamically unstable: need septic 6 and IV fluids and blood transfuion PRN
Spontaneous perforation needs immediate surgery to control leak and wash out chest (thoracotomy usually performed with on table endoscopy to determine perforation site and site of incision)
Decomperess oesophagus via trans- gastric drain or endoscopically placed NGT
Nutritional support - feeding jejunostomy
Patients need CT scan with contrast 10-14 days before starting oral intake to check for leakage
Iatrogenic perforations are often more stable than spontaneous and may be suitable for conservative management:
ICU/HDU, antibiotics and antifungal cover,
NBM for 1-2 weeks with NGT insertion for drainage
Total parenteral nutrition (TPN) or feeding jejunostomy insertion
Chest drain
Boerhaave syndrome overview
Transmural Oesophageal rupture secondary to forceful vomiting and/or retching
Thought to occur due to forceful ejection of gastric contents in unrelaxed oesophagus against closed upper cricopharyngeus
Risk factors:
Male
Alcoholism
Presentation: Mackler’s triad: vomiting, chest pain, subcutaneous emphysema (only actually seen in 15% cases) Epigastric pain Back pain Dyspnea Shock
Treatment:
Surgery gold standard
Conservative methods like oesophageal stenting can be used also
GI bleeding/haemorrhage
Can be upper (oesophagus, stomach or duodenum) Or lower (intestines, rectum or anus) All will need PR exam
Common causes of upper GI bleeding: Peptic ulcers Oesophageal varices Mallory weiss tears Oesophagitis (most often from GORD)
Common causes of LGIB: Diverticular disease IBD Tumours Colon polyps Haemorrhoids Anal fissues Proctitis
UGIB overview
Presentation of UGIB: Haematemesis Coffee ground vomiting Abdominal pain Meleana - black tarry stools Significant blood loss: pale, weak, dizzy, syncope, SoB Raised urea (blood digestion)
Investigations:
Glasgow-Blatchford score GBS for low and high risk
Takes into account, haemoglobin, BUN, systolic BP, sex, HR, meleana, syncope, hepatic disease history and cardiac failure
Management: ABCDE IV fluids ad bloods taken Blood transfusion PRN IV PPI pantoprazole 40mg Endoscopy to directly inject medicine, cauterise ulcer or clam/clip off bleeding vessel
LGIB presentation and management
Rectal bleeding
Abdominal pain
Significant blood loss: pale, weak, dizzy, SoB
management: Based on underlying cause If unknown: CT with contrast/colonoscopy IV fluids to maintain BP Blood transfusion PRN
Alcoholic liver disease
Effects of long term excessive consumption of alcohol on the liver
Onset and progression varies
May be genetic predisposition to harmful effects of alcohol on the liver
Recommended alcohol consumption: 14 units/week (no more than 5 in one day, spread evenly over >3 days)
Progression:
Alcohol related fatty liver: drinking leading to build up of fat in the liver. If stopped, process is fully reversible within around 2 weeks.
Alcoholic hepatitis: alcohol over a long period causes inflammation in the liver. Binge drinking is associated with the same effects. Mild cases are usually reversible with permanent abstinence.
Cirrhosis: many hepatocytes replaced with scar tissue. Function impaired, portal HTN likely. Irreversible changes. Drinking cessation can prevent further damage while continuing has very poor prognosis
Alcoholic liver disease presentation and investigations
Jaundice Hepatomegaly Spider naevi Palmar erythema Gynaecomastia Bruising Ascites Caput medusae Astrexis
Investigations: Bloods: FBC, LFTs, clotting screen, U+Es USS/fibroscan Endoscopy CT and MRI Liver biopsy to confirm
Alcoholic liver disease management
Alcohol cessation
Detox regimen (benzodiazepine given every 1-4 hours for 5-7 days, IV high dose B vitamins, pabrinex, and low dose oral thiamine after)
Nutritional support (thiamine and vitamins) and high protein diet
Steroids for short term
Treat complications
Liver transplant
Alcohol withdrawal: 6-12 hours: tremor, sweating, headache, craving, anxiety 12-24 hours: hallucinations 24-48 hours: seizures 24-72 hours: delirium tremens
Non-alcoholic fatty liver disease
Part of metabolic syndrome group of chronic health conditions relating to increased risk of heart disease, stroke and diabetes
Estimated up to 30% adults have this
Characterised by fatty deposits in hepatocytes interfering with function
Asymptomatic initially but can progress to hepatitis and cirrhosis
Stages: Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis Fibrosis Cirrhosis
Non-alcoholic fatty liver disease risk factors and investigations
Obesity Poor diet and low activity Type 2 diabetes High cholesterol Middle age< Smoking High blood pressure
Investigations: USS of liver Hepatitis B and C serology Autoantibodies (ANA, SMA, AMA, LKM-1) Immunoglobulins Caeruloplasmin (wilson’s disease) Alp1 antitrypsin Ferritin and transferrin saturation
Non-alcoholic fatty liver disease management
Weight loss
Exercise
Smoking cessation
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
Liver fibrosis can refer to specialist for vitamin E or pioglitazone treatment
Wilson’s disease and presentation
Excessive accumulation of copper in the body and tissues
Caused by mutation in wilson disease protein on chromosome 13
Autosomal recessive disease
Presentation: depending on where copper deposition is most predominant: Hepatic problems (40%) Neuro problems (50%) Psychiatric problems (10%) Kayser-fieischer rings in cornea (brown rings around iris) Haemolytic anaemia Renal tubular damage Osteopenia
Wilson’s disease investigations and management
Investigations:
Clinical exam: kayser-fleischer rings, physical signs of liver disease etc
Gold standard is serum ceruloplasmin - low suggestive of Wilson’s disease (not specific)
Liver biopsy
24 hour urine copper assay
MRI brain changes
Management:
With copper chelation using:
Penicillamine
Trientene
Gastritis diagnosis
Clinical via history taking Abdominal exam/PR exam H pylori testing (antigen, breath) Endoscopy Barium swallow and AXR
Gastritis acute and chronic causes
Acute causes: H pylori Alcohol NSAIDs Stress Bile acid reflux (usually post surgical)
Chronic: Chronic h pylori infection Crohn’s Sarcoidosis Autoimmune (atophic)
Ulcerative colitis
Idiopathic chronic inflammation of the colon, follows course of relapse and remission
Most common form of inflammatory bowel disease
Peak incidence in late adolescence and early adulthood
Can be associated with extraintestinal symptoms occasionally
More often see GI bleeding
Presents with diffuse continuous involvement of mucosa
Occurs in 8-15 people per 100,000
Characterised by remissions and exacerbations
Likely autoimmune condition triggered by colonic bacteria causing GI inflammation
UC disease classifications
Distal disease: left sided colitis, colitis confined to the rectum and sigmoid colon
More extensive disease includes left sided colitis (up to splenic flexure), extensive colitis (up to hepatic flexure) and pancolitis (affecting whole colon)
Patients with pancolitis may have involvment of terminal ileum due to incompetent ileocecal valve
UC presentation
Bloody diarrhea
Colicky abdominal pain
Urgency or tenesmus (feeling of incomplete emptying of bowels)
Disease limited to rectum may present with constipation and rectal bleeding
Malaise, fever
Weight loss
Tachycardia, hypotension, febrile, dehydrated
Erythema nodosum
Episcleritis
Ankylosing spondylitis
Primary sclerosing cholangitis
UC investigations
Clinical history
Bloods: FBC, renal function, U+Es, LFTs, ESR, CRP, iron studies, B12, folate
Faecal calprotectin to differentiate between IBS
C difficile testing
Colonoscopy and biopsy to confirm
CT, MRI
Barium fluoroscopy
UC disease severity, indications for hospitalisation and surgery
Disease severity:
Subacute: moderately to severe active ulcerqative colitis that would normally be managed in outpatient setting and does not need hospitalisation or urgent surgical intervention
Mild: fewer than four stools daily, no more than small amount of blood in stools, no anaemia, pulse rate <90, no fever and normal ESR and CRP
Moderate: 4-6 stools daily with more blood in stool. No anaemia, pulse rate <90, no fever, normal ESR and CRP
Severe: 6+ stools dailys, visible blood in stools, at least one feature of systemic upset (fever, pulse >90, anaemia, ESR and CRP raised)
Indications for hospital referral:
Severe colitis
Moderate disease fail to respond to steroids within 2 weeks
Respond partially to treatment should be seen urgently in outpatient setting treated for refractory colitis
Indications for surgery:
Severe abdominal pain and fever should raise concern of toxic megacolon or fulminant colitis
Haemorrhage
Elective surgery for intractability, complications of med therapy, cancinomas
Management of ulcerative colitis
Inducing remission:
Mild to mod 1st line aminosalicylate (mesalazine) oral or rectal
2nd line corticosteroids (prednisolone)
Severe: 1st line IV corticosteroids (hydrocortisone)
2nd line IV ciclosporin
Maintaining remission:
Aminosalicylate (mesalazine) oral or rectal
Azathioprine
Mercaptopurine
Panproctocolectomy (removing colon and rectum) and permenant ileostomy or ileo-anal anastomoses (J pouch) where ileum is folded back on itself into larger pouch that functions like a rectum, collecting stools prior to person passing the motion
Hiatus hernia
Herniation of part of abdominal viscera through oesophageal aperture of the diaphragm
Vast majority of them only involve herniation of the gastric cardia through hiatal aperture
Rarely hernias with a large defect can allow other organs to enter the thoracic cavity, such as the spleen and pancreas
Over half peoples with reflux esophagitis have been found to present with hiatus hernia
Cause:
Widening of oesophageal hiatus
Pulling up of stomach due to oesophageal shortening
Pushing up of stomach by increased intra-abdominal pressure
Acid reflux barrier is lost, the larger then hernia the more impaired the clearance of acid (thereby exacerbates GORD)
Hiatus hernia classifications
Sliding hiatus hernia: gastro-oesophageal junction slides up into thoracic cavity (85-95% cases)
Para-oesophageal (rolling) hiatus hernia: gastro-oesophageal junction remains in place, but part of the stomach herniates into chest next to the oesophagus (5-15% cases)
Many are mixed presentation
Alternative classifications:
Type I: sliding; GOJ migrates above diaphragm. Stomach remains in longitudinal alignment and fundus below the GOJ
Type II: pre paraesophageal hernias; GOJ remains in normal place, portion of fundus herniates through hiatus
Type III: combination of I and II; both GOJ and fundus herniate through hiatus. Fundus superior to GOJ
Type IV: structures other than stomach (omentum, colon, small bowel) lie within hernia sac
Hiatus hernia risk factors
Obesity Pregnancy Ascites Genetic predisposition Previous gastro-oesophageal surgery Trauma to chest or abdomen Skeletal deformities such as scoliosis, kyphosis and pectus excavatum
Hiatus hernia presentations
Exacerbation of GORD symptoms Volvulus or ischaemia symptoms Retrosternal burning (heartburn) especially on bending or lying down Reflux Dysphagia Can be asymptomatic Chest pain Epigastric pain Excessive fullness Nausea
Hiatus hernia investigations and management
CXR
Barium studies
Endoscopy
Oesophageal manometry
Management:
Lifestyle: avoid increase in intra-abdominal pressure (tight clothes), raise head of bed at night, avoid eating <3 hours before bed, weight loss, smoking cessation, alcohol avoidance
PPIs usually needed long term
Surgical: laparoscopic fundoplication or gastropexy
Poisoning management overview
ABCDE assessment and act accordingly
History: how much, when, what route of administration, has there been vomiting, past medical history, current medications and allergies, suicide note/suicide risk, third party history for context
Cardio, respiratory, abdominal, neurological examinations
Vital signs: temperature, pupils, BP, HR
Muscle rigidity
Skin - cyanosis (methaemoglobinaemia), very pink (carboxyhaemoglobinaemia, cyanide, hydrogen sulphide), blisters (barbiturates, tricyclic antidepressants (TCAs), benzodiazepines), needle tracks, hot/flushed (anticholinergics).
Breath - ketones (diabetic/alcoholic ketoacidosis), ‘bitter almonds’ (cyanide), ‘garlic-like’ (organophosphates, arsenic), ‘rotten eggs’ (hydrogen sulphide), organic solvents.
Mouth - perioral acneiform lesions (solvent abuse), dry mouth (anticholinergics), hypersalivation (parasympathomimetics)
ABCDE approach to poisoning
ABCDE: Eyes (dilated pupils indicate tricyclics, cocaine, amphetamine; pinpoint pupils indicate opiates; nystagmus indicates alcohol, benzodiazepines, phenytoin) Breath (bitter almond smell of cyanide indicates alcohol or organic solvents) burns around mouth (corrosive substances like paraquat, glue) hyperventilation (salicylates) needle marks (recreational drug abuse)
Identify substance: if pt is unconscious, third party evidence of what has been taken. Time of ingestion, associated alcohol consumption, past and current medical history (esp if renal or liver disease), symptoms noticed since poisoning (vomiting may have removed some substance already, hematemesis caused by iron overdose, salicylates, alcohol)
Elimination: activated charcoal (decontamination) decreases absorption within 1 hr of digestion (preferred), antidote administration, gastric lavage (no longer recommended due to aspiration risk; only indicated in life threatening amount ingested within previous hr and poison cannot be removed via other methods. May be useful for drugs such as lithium and iron which aren’t charcoal absorbed), dialysis (peritoneal, haemodialysis), diuresis (alkaline, acid change urinary pH to increase substance excretion in urine) whole bowel irrigation (when substance would not be absorbed by activated charcoal)
Specific and general treatment of pt condition
Period of observation
Psychiatric assessment
Common drug overdoses and antidotes
Given for certain poisons which can either prevent poison working or reverse it’s effects
Glucagon injection for insulin and beta-blockers
N- acetylcysteine for paracetamol
Flumazenil for Benzodiazepines
Fab fragments for Digoxin
Naloxone for opiates
Ethyl alcohol for methanol overdoses
Alcohol poisoning symptoms and management
Ataxia, dysarthria, nystagmus, and drowsiness, which may progress to coma, with hypotension and acidosis.
managed supportively, maintaining clear airway, reduce risk of aspiration of gastric contents, blood glucose monitoring and administration if needed
Salicylates poisoning symptoms and management
Hyperventilation, tinnitus, deafness, vasodilation, sweating, coma (very severe)
Monitor plasma salicylate, pH and electrolytes
Activated charcoal <1hour ingestion if >125mg/kg aspirin taken
Replace fluid losses and correct electrolyte imbalances
Opioid overdose symptoms and management
Coma, respiratory depression and pinpoint pupils, nausea and vomiting
Naloxone injection or infusion. Short half life (might only last for 15-20 minutes) so must be monitored for top up or continuous doses if needed
Administration of IV used for rapid diagnosis of opiate poisoning. Should show significant improvement in condition within 1-2 mins
Monitor for aspiration of vomit, monitor pupils, RR, BP, sepsis, signs of hep B/C or HIV screen if indicated (drug users etc)
Paracetamol overdose symptoms and management
Hepatocellular necrosis (indicated by right subcostal pain and tenderness) Nausea and vomiting
Acetylcysteine reduced severity of liver damage if given <24 hours ingestion Monitor for signs of liver failure Given by IV 150mg/kg initial dose 50mg/kg over next 4 hours 100mg/kg over next 6 hours
Side effects:
anaphylaxis
Hypotension
Rash
Nausea and vomiting
Only given if over paracetamol level threshold due to side effects so must take bloods first
100mg/l at four hours after ingestion is toxic
Tricyclic antidepressants and SSRI poisoning symptoms and management
Tricyclic antidepressants
Dry mouth, coma, hypotension, hypothermia, hyperreflexia, extensor plantar responses, convulsions, respiratory failure, cardiac conduction defects, dilated pupils, urinary retention, hallucinations, delirium and confusion
Supportive measures to clear airway IV lorazepam or diazepam for convulsions Activated charcoal <1 hour Correct hypoxia and acidosis Monitor cardiac activity
SSRIs
Nausea, vomiting, agitation, tremor, nystagmus, drowsiness, sinus tachycardia, convulsions, can cause QT prolongation
Supportive: guard airway if vomiting, ensure patient safety and take good history of if anything else has been taken
Activated charcoal <1 hour
Convulsions treated with lorazepam, diazepam
Benzodiazepines poisoning symptoms and management
Drowsiness, ataxia, nystagmus, respiratory depression, coma
Flumazenil injection Reverses CNS and respiratory depression. However if person has also taken tricyclic antidepressant or has epilepsy must be cautions as can cause seizures or arrhythmias
Activated charcoal <1 hour
Beta blockers overdose symptoms and management
Bradycardia, hypotension, syncope, heart failure, conduction abnormalities
Maintain airway, supportive care Unclear benefit but can give charcoal <1 hour Fluid resuscitation Vasopressors and inotropes Glucagon for severe hypotension Sodium bicarb for metabolic acidosis
CCB poisoning symptoms and management
Nausea, vomiting, dizziness, agitation, confusion, coma, hypotension
Charcoal <1 hour
Calcium chloride or calcium gluconate injections
Atropine sulfate to correct bradycardia
Lithium poisoning symptoms and management
Apathy, restlessness, vomiting, diarrhea, ataxia, weakness, dysarthria, muscle twitching, tremor
Gastric lavage <1 hour
Whole bowel irrigation considered for significant ingestion
Seek advice from national poisons info service
types of drug clearance
Preventing absorption
Renal clearance
Hepatic clearance
Preventing absorption:
Activated charcoal: Repeated doses of charcoal are given after overdose with:
Carbamazepine
Dapsone
Phenobarbital
Quinine
Theophylline
*vomiting may reduce effectiveness
*should NOT be used with petroleum distillates, corrosive substances, alcohols, malathion, cyanides and metal salts (Fe and lithium)
(not doing anymore) - emesis and gastric lavage
Promotion of renal clearance:
IV fluids
Alkalinisation of urine Administer sodium bicarbonate for salicylates
Hemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, sodium valproate
Hepatic elimination:
Not generally exploited in overdose management due to the liver being post-intestinal so most substance would be absorbed into the body by then
Main strategy is promotion of renal clearance
