Gastrointestinal (3) Flashcards
Define haemorrhoids
Enlargement, engorgement and protrusion of the haemorrhoidal vascular cushions in the anal canal which have a tendency to bleed or prolapse
Describe haemorrhoid classification
Internal haemorrhoids lie ABOVE the dentate line
External haemorrhoids lie BELOW the dentate line
Dentate line = divides upper 2/3 and lower 1/3 of the anal canal and represents the hindgut-proctodeum junction
1st Degree - haemorrhoids that do NOT prolapse
2nd Degree - prolapse with defecation but
reduce spontaneously
3rd Degree - prolapse and require manual reduction
4th Degree - prolapse that CANNOT be reduced
What are the risk factors of haemorrhoids?
Age 45-65
History of constipation
Increased intra-abdominal pressure: pregnancy and ascites
Presence of space occupying pelvic lesion
Prolonged straining
Derangement of the internal anal sphincter
Portal hypertension
Summarise the epidemiology of haemorrhoids?
More common in white patients
Most common at 45-65 years
Very common
What are the presenting symptoms of haemorrhoids?
Usually ASYMPTOMATIC
Bleeding - bright red blood on the toilet paper and drips
into the pan after passage of stool. NOT mixed with stool.
ABSENCE of alarm symptoms (weight loss, anaemia, change in bowel habit, passage of
clotted or dark blood, mucus mixed with the stool)
Itching Anal lumps Prolapsing tissue Perianal pain Sensation of incomplete evacuation
What are the signs on physical examination of haemorrhoids?
1st or 2nd degree haemorrhoids are NOT usually visible on external inspection
Internal haemorrhoids are NOT normally palpable on DRE unless they are thrombosed
Haemorrhoids are usually visible on proctoscopy
Anal mass
Tender palpable perianal lesion
What are the appropriate investigations for haemorrhoids?
DRE
Anoscopic examination
Proctoscopy
Colonoscopy/flexible sigmoidoscopy - exclude IBD, cancer
FBC - check for anaemia
Stool for occult haem - if no haemorrhoidal tissue seen on examination
What is the management of haemorrhoids?
Conservative:
High-fibre diet and increased fluid intake
Bulk laxatives
Topical creams (e.g. local anaesthetics, corticosteroids)
Injection Sclerotherapy - Induces fibrosis of the dilated veins
Banding - Barron’s bands are applied proximal to the
haemorrhoids which then fall off after a few days.
Infrared photocoagulation
Surgery:
Reserved for symptomatic 3rd and 4th degree haemorrhoids
Milligan-Morgan haemorrhoidectomy - excision of three haemorrhoidal cushions
Stapled haemorrhoidectomy is an alternative method
Post-operatively the patient should be given laxatives
to avoid constipation
What are the possible complications of haemorrhoids?
Anaemia Thrombosis Incarceration Faecal incontinence Pelvic sepsis Anal stenosis Bleeding Prolapse Gangrene
Injection Sclerotherapy Complications Prostatitis Perineal sepsis Impotence Retroperitoneal sepsis Hepatic abscess
Haemorrhoidectomy Complications Pain Bleeding Incontinence Anal stricture
What is the prognosis of haemorrhoids?
Often chronic with high rate of recurrence
Treatment results in resolution or improvement of symptoms with low rates of recurrence.
Surgical haemorrhoidectomy confers the best long-term effect with less than 20% symptom recurrence.
Define hepatocellular carcinoma
Primary malignancy of the liver parenchyma usually in a cirrhotic liver
What is the aetiology/risk factors of hepatocellular carcinoma?
Associated with chronic liver damage:
Cirrhosis Chronic HBV infection Chronic HCV infection Chronic heavy alcohol use Diabetes Obesity Family history Aflatoxin – Aspergillus flavus toxin on stored grains Autoimmune conditions e.g. PBC, PSC, haemochromatosis Metabolic conditions e.g. alpha-1 antitrypsin deficiency OCP Smoking Male
Summarise the epidemiology of hepatocellular carcinoma
COMMON
1-2% of all malignancies
LESS common than liver metastases
High incidence in regions where hepatitis B and C are endemic
What are the presenting symptoms of hepatocellular carcinoma?
Malaise Weight loss Loss of appetite/anorexia Abdominal distention Jaundice RUQ pain Early satiety Leg oedema
History of Exposure to Carcinogens:
High alcohol intake
Hepatitis B or C (e.g. sexual activity, IV drug use)
Aflatoxins
What are the signs on physical examination of hepatocellular carcinoma?
Cachexia Lymphadenopathy Hepatomegaly (may be nodular) Jaundice Ascites Bruit over the liver Hepatic encephalopathy Splenomegaly Asterixis Spider naevi Palmar erythema Fetor hepaticus
What are the appropriate investigations for hepatocellular carcinoma?
Bloods FBC - low MCV and platelets Urea - high Sodium - low ESR LFTs - high ALP, AST, ALT, bilirubin, low albumin Clotting Alpha-fetoprotein - tumour marker for liver cancer Hepatitis serology
PT time - normal or elevated
Imaging:
Abdominal US
CT/MRI - GOLD STANDARD for staging
Histology/Cytology - Ascitic tap my be sent for cytological analysis
Define a hernia
- Direct Inguinal
- Indirect Inguinal
- Femoral
- Epigastric
- Umbilical
Abnormal protrusion of a viscus through a defect in its containing compartment and its coverings into an abnormal position
Inguinal hernias are above and medial to pubic tubercle
Direct Inguinal Hernia:
Protrusion of the hernial sac directly through a weakness in the transversalis fascia and posterior wall of the inguinal canal.
Arises medial to the inferior epigastric vessels
WEAKNESS IN ABDOMINAL WALL EVOLVES INTO LOCALISED HOLE
Indirect Inguinal Hernia:
Protrusion of the hernial sac through the deep inguinal ring, following the path of the inguinal canal. Occurs lateral to inferior epigastric artery. Due to lax deep ring or patent processus vaginalis.
Femoral hernia - inferior and lateral to the pubic tubercle.
Epigastric – at site of midline union of rectus muscles
Umbilical – present in 3% at birth (normally resolves <3 years), transversalis fascia defect
What is the aetiology/risk factors for an inguinal hernia?
Congenital - abdominal contents enter the inguinal canal through a patent processus vaginalis
Acquired - due to increased intra-abdominal pressure along with muscle and transversalis fascia weakness. Degeneration, fatty changes etc
Risk Factors: Male Prematurity Chronic lung disease Age Obesity Raised intra-abdominal pressure (e.g. chronic cough) Constipation Bladder outflow obstruction Intraperitoneal fluid (e.g. ascites) Connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome) Smoking Family history AAA Previous RLQ incision Heavy lifting BPH
Summarise the epidemiology of hernias
COMMON
Peak age in adults: 55-85 yrs
9 x more common in MALES
Groin hernias affect 27% of men and 3% of women at some point in their life
What are the presenting symptoms of hernias?
Asymptomatic
Patient notices a ‘lump in the groin’
May cause discomfort and pain
May be irreducible
May present because it has increased in size
May present because of complications (e.g. bowel obstruction) - nausea and vomiting, constipation
What are the signs on physical examination of a hernia?
Visible or palpable groin lump that extends to the scrotum (males) or labia (women)
Check for cough impulse
Indirect hernias can be reduced and controlled by applying pressure over the deep inguinal ring
Auscultation - there may be bowel sounds over the hernia
Tenderness if strangulated
Check for signs of complication
What are appropriate investigations for hernia?
Mainly a clinical diagnosis
Bloods: FBC U&Es CRP Clotting Group and save (if operation is likely)
ABGs - may show lactic acidosis from bowel ischaemia
Imaging:
Erect CXR - check for perforation
USS - exclude other causes of groin lump
AXR - check for obstruction
What is the management for hernias?
If small, asymptomatic hernia then watchful waiting
Surgical
Usually elective repair of uncomplicated hernias
Mesh Repair - The hernia is surgically reduced and a mesh is inserted to reinforce the defect in the transversalis fascia
Laparoscopic Mesh Repair
Prophylactic antibiotics given
EMERGENCY: If obstructed or strangulated, laparotomy with bowel resection may be indicated if the bowel is
gangrenous - NG feeding, fluid resuscitation
What are the possible complications of hernias?
Incarceration
Strangulation
Bowel obstruction
Surgery Complications: Pain Wound infection Haematoma Penile/scrotal oedema Mesh infection Testicular ischaemia Urinary retention Bowel obstruction
What is the prognosis of hernias?
Prognosis is excellent after surgical repair.
The incidence of recurrent hernia with mesh repair is reported to be less than 2%.
Moderate to severe chronic groin pain is reported to occur in 10% to 12% of patients after inguinal hernia repair.
Groin pain higher incidence after open repair compared to laparoscopic repair.
Define hiatus hernia
The protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm. It most commonly contains a variable portion of the stomach but can contain transverse colon, omentum, small bowel, or spleen.
What are the types of hiatus hernia?
Congenital
Traumatic
Non-traumatic
Sliding (90-95%) - the hernia moves in and out of the chest. Usually protrusion of gastro-oesophageal junction followed by body of stomach above diaphragm which causes a decreased LOS pressure.
Paraoesophageal (rolling) (5-10%) - the hernia goes through a whole in the diaphragm next to the oesophagus. The fundus or body of stomach usually herniate and the gastro-oesophageal junction remains below the diaphragm.
This can produce rotation and twisting of the stomach, leading to intermittent strangulation with obstruction and ischaemia.
What is the aetiology/risk factors of a hiatus hernia?
Aetiology is unknown however can be congenital, traumatic and non-traumatic (sliding or para-oesophageal)
Risk factors: Obesity Previous gastro-oesophageal procedure Elevated intra-abdominal pressure: Chronic cough, Ascites, Multiparity, pregnancy Low-fibre diet Male Advanced age Structural abnormality of oesophageal hiatus Chronic oesophagitis
Summarise the epidemiology of hiatus hernias
Estimates of the prevalence of hiatus hernia in western populations range up to 50%.
The prevalence may be lower in eastern populations.
The incidence of symptomatic cases of hiatus hernia is closely related to the diagnosis of GORD
Sliding hernias are the most common.
70% of patients are over 70 years old.
What are the presenting symptoms of hiatus hernias?
Mostly asymptomatic
Sliding hernias most likely to cause symptoms. Present with symptoms of GORD:
Heartburn
Regurgitation
Waterbrash
Chest pain (oesophageal spasm)
Dysphagia/odynophagia (oesophagitis)
Haematemesis
Cough/wheeze (aspiration)
What are the signs on physical examination of hiatus hernias?
No signs
What are the appropriate investigations for hiatus hernias?
CXR - gastric air bubble may be seen above the diaphragm
Upper gastrointestinal series (X ray of upper GI tract) - shows intrathoracic stomach
OGD - inflammation of oesophagus and proximal migration of gastro-oesophageal junction
CT or MRI
Oesophageal manometry or pH monitoring - double hump configuration
Bloods
FBC - check for iron deficiency anaemia
What is the management of a hiatus hernia?
Medical:
Modify lifestyle factors (e.g. lose weight)
Inhibit acid production (e.g. PPIs)
Enhance upper GI motility
Surgical with or without anti-reflux procedure:
Necessary in a MINORITY of patients - those with complications of reflux disease despite medical treatment or pulmonary complications (e.g. aspiration pneumonia)
Nissen Fundoplication:
The stomach is pulled down through the oesophageal hiatus and part of the stomach is wrapped (360 degrees) around the oesophagus to make a new
sphincter and reduce the likelihood of herniation
What are the possible complications of hiatus hernias?
Oesophageal: Intermittent bleeding Oesophagitis Erosions Barrett's oesophagus Oesophageal strictures
Non-Oesophageal:
Incarceration of para-oesophageal hiatus hernia - strangulation and perforation
Gastric volvulus
Obstruction
Surgical complications: Dysphagia Haemorrhage Fundal necrosis Diarrhoea
What are the possible complications of a hiatus hernia?
Generally GOOD
Sliding hernias have a better prognosis than rolling hernias
Define intestinal ischaemia
Obstruction of a mesenteric vessel causing reduced blood flow to the GI tract leading to bowel inflammation, odeoma, ulceration, ISCHEMIA AND NECROSIS.
Most commonly affects the splenic flexure (the watershed between the SMA and IMA).
Explain the aetiology of intestinal ischaemia
Embolus (60%)
Thrombosis (40%)
Can be a consequence of: Volvulus Intussusception Bowel strangulation Failed surgical resection
Arterial inflow obstruction: Atheroma Thrombosis Embolism (cardiac arrhythmia) Vasculitis
Venous outflow obstruction
Reduced perfusion - Hypotension, Shock
What are the risk factors of intestinal ischaemia?
AF Endocarditis (can throw emboli)
Arterial Thrombosis: hypercholesterolaemia, hypertension, diabetes mellitus, smoking
Venous Thrombosis: portal hypertension, splenectomy, septic thrombophlebitis, OCP, thrombophilia
Old age
Hypercoagulable states
Myocardial infarction
History of vasculitis
Summarise the epidemiology of intestinal ischaemia
Uncommon
More common in elderly (60-80 years)
More common in those with co-morbidities (AF, MI, atherosclerosis)
What are the presenting symptoms of intestinal ischaemia?
Severe acute colicky abdominal pain Vomiting/nausea Rectal bleeding History of chronic mesenteric artery insufficiency Gross weight loss Post-prandial abdominal pain History of heart or liver disease Melaena Diarrhoea
What are the signs on physical examination of intestinal ischaemia?
Diffuse abdominal tenderness Abdominal distension Tender palpable mass (ischaemic bowel) Bowel sounds may be absent Disproportionate degree of cardiovascular collapse Abdominal bruit Fever Tachycardia
What are the appropriate investigations for intestinal ischaemia?
Diagnosis based on clinical suspicion or after laparotomy
AXR - thickening of small bowel folds and signs of obstruction, bowel dilation and thickening of walls
Bloods: ABG - lactic acidosis FBC - leukocytosis, anaemia U&Es LFTs Clotting - underlying prothrombotic condition Lactate - elevated Cross-match
Mesenteric Angiography if stable
ECG - may show arrhythmia
Erect CXR - check for perforation
Contrast CT/CT angiogram
Sigmoidoscopy/colonoscopy
Define intestinal obstruction
A mechanical disruption in the patency of the GI tract, resulting in a combination of vomiting, absolute constipation, and abdominal pain.
Explain the aetiology/risk factors of intestinal obstruction
Small bowel: Previous surgery (adhesions) – 80% Hernia Crohn’s disease Malignancy Appendicitis Volvulus Intussusception (children) Ileus
Large bowel:
Malignancy (90%)
Volvulus (5%)
Benign stricture (3%)
Summarise the epidemiology of intestinal obstruction
COMMON
More common in the ELDERLY due to increasing incidence of adhesions, hernias and malignancy
Lifetime incidence between 0.1% and 5% in patients who have not undergone previous surgery
Rises to over 60% in patients who have undergone previous surgery
What are the presenting symptoms of intestinal obstruction?
Severe gripping colicky pain with periods of ease Abdominal distension Frequent vomiting (it may be bile-stained or faeculent) Absolute constipation Obstipation (failure to pass stool or flatus) Nausea Fever
What are the signs on physical examination of intestinal obstruction?
Abdominal distension Abdominal tenderness Peritonitis - absent bowel sounds, guarding, rebound tenderness Palpable abdominal mass Palpable rectal mass Tachycardia Hypotension Tinkling bowel sounds or no bowel sounds if advanced Visible peristalsis Abdominal scars from previous surgeries
DRE - hard faeces or empty rectum
Signs of malignancy - Weight loss, Rectal bleeding
What are the appropriate investigations for intestinal obstruction?
Abdo X-Ray: Dilated intestinal loops, valvulae conniventes (small bowel - diameter more than 3cm) or haustra (large bowel - diameter more than 6cm)
Partial SBO: gas throughout the abdomen and into the rectum
Complete SBO: no distal gas, and staggered air-fluid levels
Complicated SBO: free air under the diaphragm suggestive of perforation; thumb-printing of the bowel suggestive of ischaemia
Bloods:
FBC - high WCC
Urea - increased if dehydrated
Electrolyes - low K+, Na+
Abdo CT
Water soluble contrast enema
Barium follow through
What is the management of intestinal obstruction?
IV fluid resuscitation and nasogastric decompression
Electrolyte replacement
Monitor vital signs, urine output, fluid balance
Correction of underlying cause
Analgesia and anti-emetic
Pre-operative prophylactic antibiotic and surgery (emergency laparotomy)
What are the complications of intestinal obstruction?
Dehydration Bowel perforation Peritonitis Toxaemia Gangrene of ischaemic bowel wall Sepsis Multi-organ failure Intra-abdominal abscess Short bowel syndrome
What is the prognosis of intestinal obstruction?
Medical emergency.
Patients treated in a timely manner have a very good prognosis.
In untreated patients, obstruction progresses to intestinal necrosis, perforation, sepsis, and multi-organ failure.
Define liver abscess
Purulent collections in the liver parenchyma that result from bacterial, fungal, or parasitic infection of the liver which has spread from: Biliary tree Portal vein (from appendicitis) Hepatic vein Bacteraemia Trauma
Explain the aetiology of liver abscess
Pyogenic (producing pus): E.coli Klebsiella sp. Streptococcus milleri Enterococcus Bacteroides Staphylococci
Amoebic:
Entamoeba histolytica
What are the risk factors of liver abscess?
Biliary tract abnormalities Age >50 years Malignancy Diabetes mellitus Interventional biliary or hepatic procedures Travel in endemic areas Underlying malignancy
Summarise the epidemiology of liver abscess
Uncommon Higher incidence in Asia Slightly more common in men Incidence increases with age Pyogenic most common in industrial world Amoebic most common worldwide Fungal infections can occur in immunocompromised
What are the presenting symptoms of liver abscess?
Abdominal pain - RUQ/epigastric may be referred to shoulder Nausea and vomiting Cough, SOB, chest pain Weight loss Fatigue Fevers and chills Anorexia Night sweats Jaundice Diarrhoea History of foreign travel
What are the signs on physical examination of liver abscess?
RUQ tenderness Hepatomegaly Ascites Signs of pleural effusion in right lower zone - dullness to percussion, reduced breath sounds Signs of shock Jaundice
What are the appropriate investigations for liver abscess?
Bloods:
FBC - Mild anaemia, Leukocytosis, elevted neutrophil
LFTs - High ALP, mildly high bilirubin and AST and ALT, low albumin
High ESR and CRP
PT to see if aspiration can occur
Liver USS - guide aspiration of abscess
Contrast enhanced CT abdo
Blood cultures: Amoebic and hydatid serology
Stool MC&S - for E. histolytica
Culture of aspirated fluid and gram stain
CXR - check for right pleural effusion or atelectasis, raised hemidiaphragm
Aspiration and culture of the abscess material
Define liver failure
Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy.
Describe the classification of liver failure
Liver failure is classified based on the time interval between the onset of jaundice and the development of encephalopathy.
Hyper-acute = <7 days Acute = 1-4 weeks Sub-acute = 4-12 weeks
Explain the aetiology of liver failure
Viral:
Hepatitis A, B, C, D and E
Drugs: Paracetamol overdose, idiosyncratic drug reactions, long-term alcohol use
Autoimmune hepatitis Budd-Chiari syndrome Pregnancy-related Malignancy (e.g. lymphoma) Haemochromatosis Mushroom poisoning (Amanita phalloides) Wilson's disease
What are the risk factors of liver failure?
Alcohol abuse
Poor nutritional status (depletion of glutathione stores)
Pregnancy (hepatitis E)
Chronic hepatitis B
What are the three main features of liver failure? Describe their pathogenesis
Jaundice: decreased secretion of conjugated bilirubin
Encephalopathy: Nitrogenous products (e.g. ammonia) is absorbed in the gut and goes via the portal circulation to the liver. If the liver is failing, these toxic products can go through the liver and reach the brain and exert its effects
Coagulopathy: Reduced synthesis of clotting factors and reduced platelets. Platelet functional abnormalities associated with jaundice or renal failure
Summarise the epidemiology of liver failure
Paracetamol overdose accounts for over 50% of acute liver failure in the UK
Rare
What are the presenting symptoms of liver failure?
May be asymptomatic Fever Nausea and vomiting Abdominal pain Jaundice Malaise
What are the symptoms of hepatic encephalopathy?
Sleep reversal -> Lethargy -> Somnolence -> Stupor
Reduced awareness and attention span -> Poor memory and confusion
What are the signs on physical examination of liver failure?
Jaundice Asterixis Bruising or bleeding Encephalopathy Fetor hepaticus Hepatomegaly
Abdo or RUQ tenderness
Ascites and splenomegaly (less common if acute or hyper-acute)
Signs of secondary causes (e.g. bronze skin colour, Kayser-Fleisher rings in Wilson’s)
Pyrexia: may indicate infection or liver necrosis
Signs of hepatic encephalopathy • Asterixis • Hyperreflexia • Nystagmus • Clonus • Rigidity
Signs of cerebral oedema
• Hypertonia
• Decerbrate posturing
• Loss of pupillary reflexes
What are appropriate investigations for liver failure?
Identify the cause: Viral serology Paracetamol levels Autoantibodies (e.g. ASM, Anti-LKM) Ferritin (haemochromatosis) Caeruloplasmin and urinary copper (Wilson's disease)
Bloods:
FBC - low Hb (if GI bleed), high WCC (if infection)
U&Es - May show renal failure (hepatorenal syndrome)
Glucose
LFTs - high bilirubin, high AST, ALT, ALP, GGT, low albumin
ESR/CRP
Coagulation screen
ABG: to determine blood pH
Group and save
Liver US/CT
Ascitic Tap: If neutrophils > 250/mm3 = spontaneous bacterial peritonitis
Doppler scan of hepatic or portal veins: check for Budd-Chiari syndrome
EEG: monitor encephalopathy
What is the management of liver failure?
Resuscitation - ABC
Treat the cause:
N-acetylcysteine for paracetamol overdose
Treatment/prevention of complications:
Monitor - vital signs, PT, pH, creatinine, urine output, encephalopathy
Manage encephalopathy: lactulose and phosphate enemas
Antibiotic and antifungal prophylaxis
Hypoglycaemia treatment
Coagulopathy treatment - IV vitamin K, FFP, platelet infusions
Gastric mucosa protection - PPIs or sucralfate
AVOID sedatives or drugs metabolised by the liver
Cerebral oedema - decrease ICP with mannitol
Renal Failure:
Haemodialysis
Nutritional support
Surgical - liver transplant
What are the possible complications of liver failure?
Infection Coagulopathy Hypoglycaemia Disturbance of electrolyte balance and acid-base balance Disturbance of cardiovascular system Hepatorenal syndrome Cerebral oedema (causing raised ICP) Respiratory failure
What is the prognosis of liver failure?
Depends on severity and aetiology
Define Mallory-Weiss tear
A tear or laceration of the lining of the oesophagus along the right border of or near the gastro-oesophageal junction which causes upper GI bleeding as a result of recent violent vomiting or straining to vomit.
What is the aetiology of Mallory-Weiss tear?
Coughing Retching Vomiting Straining Hiccups Closed-chest pressure or cardiopulmonary resuscitation Acute abdominal blunt trauma Alcohol Medications (aspirin or NSAIDs).
Most common causes: chronic alcohol abuse, bulimia, trauma, intense coughing and gastritis.
Hiatal hernia is considered a precipitating factor, causing an oesophageal tear to occur.
Conditions that may induce vomiting:
GI disease: food poisoning, infectious gastroenteritis, peptic ulcer disease, malrotation, intussusception, volvulus, gastric outlet obstruction, and gastroparesis
Hepatobiliary disease: hepatitis, gallstones, and cholecystitis
Renal disease: nephrolithiasis, renal failure, and ureteropelvic obstruction
Neurological disease: tumours, hydrocephalus, congenital disease, trauma, meningitis, pseudotumour cerebri, migraine headaches, and seizures
Psychiatric disease: anorexia nervosa, bulimia, and cyclic vomiting syndrome.
Summarise the epidemiology of Mallory-Weiss tear
Common - 50-150 per 100,000 people per year
Mortality between 8-14%
Mallory-Weiss tear responsible for 3-15% of upper GI bleeds
More common in men
In women of childbearing age, most common cause is hyperemesis gravidarum
Most common between 30-50 years
What are the presenting symptoms of Mallory-Weiss tear?
Small and self-limiting haematemesis - flecks or streaks of blood mixed with gastric contents and/or mucus, coffee ground vomit, bright-red bloody emesis
Light headedness/dizziness (symptoms of hypovolaemia)
Dysphagia
Odynophagia
Meleana
Abdominal pain
Involuntary retching
What are the signs on physical examination of Mallory-Weiss tear?
Postural hypotension
Signs of anaemia - tachycardia, pallor, fatigue
What are appropriate investigations for Mallory-Weiss tear?
Bloods: FBC - may show anaemia Urea - high if ongoing bleeding LFTs - normal, rule out underlying liver-disease PT - normal
CXR - usually normal, used to check for oesophageal perforation
OGD - DIAGNOSTIC OF MWT. Tear or laceration shows as red longitudinal defect
What is the management of a Mallory-Weiss tear?
80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own
Urgent evaluation and monitoring
Endoscopy with or without intervention
If bleeding does not stop - Surgery
Injection sclerotherapy
Coagulation therapy
Arteriography
If severe blood loss - transfusions
Anti-reflux medications may also be prescribed
What are the possible complications of a Mallory-Weiss tear?
Boerhaave’s Perforation - spontaneous perforation of oesophagus resulting from a sudden increase in intraoesophageal pressure combined with negative intrathoracic pressure
Re-bleeding
Hypovolaemic shock
Hypokalaemia due to vomiting
What is the prognosis of a Mallory-Weiss tear?
For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy.
Prognosis is excellent in patients without associated disease or complications.
A routine second endoscopic evaluation is not recommended unless the patient remains symptomatic after initial treatment.
Re-bleeding occurs in 8-15% of patients, usually within 24 hours.
Define acute pancreatitis
A sudden inflammation of the pancreas due to autodigestion by its own enzymes with variable involvement of other regional tissues or remote organ systems.
Mild: minimal organ dysfunction and uneventful recovery
Severe: organ failure and/or local complications i.e. necrosis, abscesses and pseudocyst
Explain the aetiology of acute pancreatitis
Most common causes are gallstones and ethanol I - diopathic - 10-20% G - allstones E - thanol T - rauma S - teroids M - umps A - utoimmune S - scorpion sting H - yperlipidaemia/hypercalcaemia E - RCP D - rugs (diuretics, valproic acid, azathioprine)
Summarise the epidemiology of acute pancreatitis
In the UK - 50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors.
Gallstone pancreatitis is more common in white women >60 years of age
Alcoholic pancreatitis is seen more frequently in men
Peak age = 60 years old
What are the presenting symptoms of acute pancreatitis?
Severe sudden onset epigastric pain which radiates to the back and is better on bending over/leaning forwards Pain made worse by movement Nausea Vomiting Anorexia
What are the signs on physical examination of acute pancreatitis?
Cullen sign - bruising around umbilicus
Grey-Turner’s sign - bruising across flanks
Epigastric tenderness without guarding or rebound
Decreased bowel sounds if severe
Fever
Shock - tachypnoea, tachycardia, hypotension
Signs of hypocalcaemia - Chocstek’s sign (Facial muscle spasm when facial nerve is tapped), Trousseau’s sign (Carpopedal spasm when pressure cuff is applied).
Signs of cause:
Hepatomegaly - alcohol
Xantholasma - hyperlipidaemia
Parotid grand swelling - mumps
What are the appropriate investigations for acute pancreatitis?
Bloods:
FBC - leukocytosis, increased haematocrit
Amylase and lipase - more than 3 times upper limit of normal
CRP/ESR - raised
U&Es (to check for dehydration)
Serum calcium - LOW - saponification: calcium binds to digested lipids from pancreas to form soap
LFTs - may be deranged if gallstone pancreatitis or alcohol
ABG - hypoxia or metabolic acidosis
USS: check for evidence of gallstones in biliary tree
Erect CXR: may be pleural effusion. Rule out perforation
AXR: exclude other causes of acute abdomen
CT Scan: if diagnosis is uncertain or if persisting organ failure - show inflammation, necrosis, pseudocysts
What is the management of acute pancreatitis?
Fluid resuscitation Analgesia Bowel rest if necessary Cessation of alcohol ERCP and elective cholecystectomy post-pancreatitis if gallstones are cause
What are the possible complications of acute pancreatitis?
Local: Pancreatic necrosis Liquefactive haemorrhagic necrosis Pancreatic pseudocyst Pancreatic abscess
Systemic: DIC ARDS Pleural effusion Sepsis Multiorgan dysfunction Renal failure Hypocalceamia
Long term: CHRONIC PANCREATITIS
What is the presentation of a pancreatic pseudocyst?
Following a bout of acute pancreatitis:
Abdominal pain
Anorexia/loss of appetite
Palpable mass in abdomen
Pancreatic abscess presents the same but with fever and high WCC
What is the prognosis of acute pancreatitis?
80% of patients with acute pancreatitis have mild disease and will improve within 3 to 7 days of conservative management.
Overall mortality rate is low (approximately 5%)
Mortality rate rises to 25% to 30% in severe acute pancreatitis
Define chronic pancreatitis
Persistent inflammation of the pancreas causing progressive injury to the pancreas and surrounding structures, resulting in irreversible scarring, calcification and parenchymal atrophy leading to loss of endocrine and exocrine function.
Summarise the aetiology of chronic pancreatitis
Main causes are alcohol (70%) and idiopathic (20%) Repeated bouts of acute pancreatitis Gallstones Tumour causing duct obstruction Trauma Cystic fibrosis Hyperlipidaemia Hypercalcaemia
Summarise the epidemiology of chronic pancreatitis
Most common cause in children = cystic fibrosis
Prevalence 0.04-5%
Alcoholic chronic pancreatitis presentation 36-44y/o
What are the presenting symptoms of chronic pancreatitis?
Repeated bouts of epigastric pain which radiates to the back
Pain relieved by sitting forward
Pain can be aggravated by eating or drinking alcohol
Weight loss
Steatorrhoea - greasy, smelly stools
Bloating
What are the signs on physical examination of chronic pancreatitis?
Weight loss
Jaundice - if caused by pancreatic tumour causing obstruction of CBD
Epigastric tenderness
What are the appropriate investigations for chronic pancreatitis?
Bloods:
Serum amylase/lipase - may be normal due to pancreatic insufficiency
Bilirubin and ALP - may be elevated if due to tumour compressing CBD
Glucose - high due to Diabetes mellitus following loss of endocrine function
Ig4 high if autoimmune
Ultrasound - may show gallstones
ERCP or MRCP: may show stenosis and dilatation of ducts - chains of lakes pattern
AXR: pancreatic calcification
CT Scan: May show pancreatic calcification and pancreatic cysts
Tests of pancreatic exocrine function: Faecal elastase (pancreatic exocrine function) - LOW
72hr stool collection - high fat due to fat malabsorption
What is the management of chronic pancreatitis?
Adequate fluid intake Alcohol cessation Low fat meals Reduce meat intake Glycaemic control Oral pancreatic enzyme replacement Nutritional supplements
What are the possible complications of chronic pancreatitis?
Local: Pseudocysts Biliary duct stricture Duodenal obstruction Pancreatic ascites Pancreatic carcinoma
Systemic: Diabetes mellitus Vitamin A, D, E, K (fat soluble vitamins) deficiency Steatorrhoea Chronic pain syndromes Dependence on strong analgesics
What is the prognosis of chronic pancreatitis?
Ten-year survival after diagnosis is 20% to 30% lower than the general population
Chronic pain usually decreases
Depends on aetiology
Leading cause of death in alcoholic pancreatitis is CVS disease
