Gastrointestinal (2) Flashcards
1
Q
What is Gastro-oesophageal reflux disease (GORD)?
A
Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
2
Q
What is the aetiology of Gastro-oesophageal reflux disease (GORD)?
A
- The lower oesophageal sphincter (LOS) regulates food passage from the oesophagus to the stomach
- Episodes of transient lower oesophageal sphincter relaxation are a normal phenomenon, but they occur more frequently in GORD
- This causes reflux of gastric contents into the oesophagus
3
Q
What is the epidemiology of Gastro-oesophageal reflux disease (GORD)?
A
- GORD is a common condition that affects between 10% and 30% of people in developed countries
- All age groups are affected but risk increases with age and obesity
- FH association
4
Q
What are the features of GORD?
A
- Substernal burning discomfort or heartburn:
a. Aggravated by lying supine or bending
b. Large meals and drinking alcohol - Regurgitation of gastric contents
- Dysphagia (caused by formation of peptic stricture after long-standing reflux)
- Bloating/ early satiety
- Pain relieved by antacids
5
Q
What are the features of aspiration from GORD?
A
RARE, may result in:
1. Voice hoarseness
2. Laryngitis
3. Nocturnal cough and wheeze with (out) pneumonia
6
Q
What are the indications for an upper GI endoscopy in GORD?
A
- Age > 55 years
2 Symptoms > 4 weeks or persistent symptoms despite treatment - Dysphagia
- Relapsing symptoms
- Weight loss
7
Q
What is the gold standard test for GORD?
A
24-hr oesophageal pH monitoring
Often performed if endoscopy is indicated and negative
8
Q
How is the management of GORD divided?
A
Endoscopy findings
9
Q
What is the management of GORD if endoscopy shows oesophagitis?
A
- Full dose proton pump inhibitor (PPI) for 1-2 months
- If response then low dose treatment as required
- If no response then double-dose PPI for 1 month
10
Q
What is the management of GORD if endoscopy does not show reflux disease?
A
- Full dose PPI for 1 month
- If response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
- If no response then Histamine type 2 receptor antagonist or prokinetic for one month
11
Q
What is the management of GORD that has not been investigated by endoscopy?
A
- Review medications for possible causes of dyspepsia
- Lifestyle advice
- Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
12
Q
What are some of the complications of GORD?
A
- Oesophagitis
- Ulcers
- Anaemia
- Benign strictures
- Barrett’s oesophagus
- Oesophageal carcinoma
13
Q
What is Gastroenteritis?
A
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
14
Q
What is Infectious Colitis?
A
Inflammation of the colon due to a virus or bacteria
15
Q
What is the aetiology of Gastroenteritis and Infectious Colitis?
A
Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water
16
Q
What is traveller’s diarrhoea?
A
- Defined as at least 3 loose to watery stools in 24 hours with or without one of more of:
a.abdominal cramps
b. fever
c. nausea/ vomiting or
d. blood in the stool - The most common cause is Escherichia coli
17
Q
What is acute food poisoning?
A
- Describes the sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin
- Typically caused by Staphylococcus aureus, Bacillus cereus or Clostridium perfringens
18
Q
What are some of the causative bacterial organisms for gastroenteritis?
A
- E.coli: traveller’s diarrhoea
- Giardiasis
- Cholera
- Shigella
- Staph Aureus
- Campylobacter
- Baccilus cereus
- Amoebiasis
19
Q
What is the typical presentation of gastroenteritis caused by E.coli?
A
Watery stools
Abdominal cramps and nausea
Common amongst travellers
20
Q
What is the typical presentation of gastroenteritis caused by Giardiasis?
A
Prolonged, non-bloody diarrhoea
21
Q
What is the typical presentation of gastroenteritis caused by cholera?
A
- Profuse, watery diarrhoea ‘rice water stools’
- Severe dehydration resulting in weight loss
- Not common amongst travellers
22
Q
What is the typical presentation of gastroenteritis caused by shigella?
A
- Bloody diarrhoea
- Vomiting and abdominal pain
23
Q
What is the typical presentation of gastroenteritis caused by staphylococcus aureus?
A
Severe vomiting
Short incubation period
24
Q
What is the typical presentation of gastroenteritis caused by Campylobacter?
A
- A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
- May mimic appendicitis
- Complications include Guillain-Barre syndrome
25
What is the typical presentation of gastroenteritis caused by Bacillus cereus?
Two types of illness are seen:
1. vomiting within 6 hours, stereotypically due to rice
2. diarrhoeal illness occurring after 6 hours
26
What is the most common cause of gastroenteritis?
Norovirus
27
What are the signs of Gastroenteritis and Infectious Colitis on physical examination?
1. Diffuse abdominal tenderness
2. Abdominal distension
3. Bowel sounds are often increased
If severe:
a. Pyrexia
b. Dehydration
c. Hypotension
d. Peripheral shutdown
28
What are the investigations for gastroenteritis and infective colitis?
1. Bloods: FBC, blood culture (helps identification if bacteriaemia present), U&Es: dehydration
2. Stool:
a. Faecal microscopy for polymorphs, parasites, oocysts, culture, electron microscopy (used to diagnose viral infections)
b. Analysis for toxins, particularly for pseudomembranous
colitis (Clostridium difficile toxin)
29
What is the management for Gastroenteritis and Infectious Colitis?
Most infections are self-limiting:
1. Bed rest
2. Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt)
3. IV rehydration may be necessary in those with severe vomiting
4. Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter)
Public health:
-Often a notifiable disease
-Educate on basic hygiene and cooking
30
What are the complications of Gastroenteritis and Infectious Colitis?
1. Dehydration
2. Electrolyte imbalance
3. Pre-renal failure
4. Secondary lactose intolerance (particularly in infants)
5. Sepsis and shock (particularly Salmonella and Shigella)
6. Haemolytic uraemic syndrome is associated with toxins from E. coli
7. Guillian–Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis
31
What is diarrhoea?
> 3 loose or watery stool per day:
1. Acute diarrhoea < 14 days
2. Chronic diarrhoea > 14 days
32
What are the causes for acute diarhhoea?
1. Gastroenteritis: may be accompanied by abdominal pain or nausea/vomiting
2. Diverticulitis: lassically causes left lower quadrant pain, diarrhoea and fever
3. Antibiotic therapy: ,ore common with broad spectrum antibiotics (C diff)
4. Constipation causing overflow: A history of alternating diarrhoea and constipation may be given -may lead to faecal incontinence in the elderly
33
What are the causes of chronic diarrhoea?
1. IBS: Very common, most consistent features are abdominal pain, bloating and change in bowel habit (constipation or diarrhoea)
2. UC: Bloody diarrhoea may be seen, crampy abdominal pain and weight loss are also common
3. Crohn's disease: less likely compared to UC
4. Colorectal cancer: depends on site of tumour
5. Coeliac disease: children may present with failure to thrive, diarrhoea and abdominal distension
34
What are some other conditions in which diarrhoea may be a feature?
1. Thyrotoxicosis
2. Laxative abuse
3. Appendicitis
35
What is gastrointestinal perforation?
Also known as ruptured bowel
36
What is the aetiology of gastrointestinal perforation?
The most common causes of GI perforation are peptic ulcers (gastric or duodenal) and sigmoid diverticulum
37
What are the different causes of gastrointestinal perforation?
1. Chemical: peptic ulcer, foreign body
2. Infection: diverticulitis, cholecystitis
3. Ischaemia: mesenteric ischaemia, malignancy (LBO)
4. Inflammation: toxic megacolon (C. diff or UC)
38
What are the traumatic causes of gastrointestinal perforation?
Iatrogenic:
1. Recent surgery (including anastomotic leak)
2. Endoscopy or overzealous NG tube insertion
3. Penetrating or blunt trauma: Shear forces
Direct rupture:
1. Excessive vomiting leading to oesophageal perforation (Boerhaave Syndrome)
39
What is the most common cause of gastrointestinal perforation?
Ulcerative disease: duodenal ulcers causing 2- to 3-times more than gastric ulcers do
40
What are the presenting symptoms of gastrointestinal perforation?
1. Main feature is pain: typically this is rapid onset and sharp in nature
2. Patients are systemically unwell therefore may also have associated malaise, vomiting, and lethargy
3. Thoracic perforation: such as a oesophageal rupture
a. Pain, ranging from chest or neck pain to pain radiating to the back, typically worsening on inspiration
b. There may be associated vomiting and respiratory symptoms
41
What are the signs of gastrointestinal perforation on physical examination?
1. Patients will look unwell and often have features of sepsis
2. On examining their abdomen, they will have features of peritonism: may be localised or generalised (a rigid abdomen)
3. Thoracic perforation:
auscultation and percussion may reveal signs of a pleural effusion
42
What is the gold standard investigation for gastrointestinal perforation?
CT scan: demonstrating air outside the gastrointestinal tract
43
What are the findings of gastrointestinal perforation on abdominal x-ray (and chest x-ray)?
1. Free air under the diaphragm
2. Rigler’s sign: both sides of the bowel wall can be seen, due to free intra-abdominal air acting as an additional contrast
3. Psoas sign: loss of the sharp delineation of the psoas muscle border, secondary to fluid in the retroperitoneum
44
What is the management of gastrointestinal perforation?
1. Conservative:
a. For patients who have localised perforation (diverticular disease) or sealed upper GI perforation without generalised peritonism
b. Can also be for patients not suitable for surgery e.g. elderly patients with extensive co-morbidities
2. Medical: Prophylactic broad spectrum antibiotics, should be given to almost all patients, particularly those requiring surgery
3. Surgical:
a. Identification and management of underlying cause e.g. repairing perforated peptic ulcer with an omental patc, resecting a perforated diverticulae (e.g. via a Hartmann’s procedure)
45
What are the complications of gastrointestinal perforation?
1. Infection: peritonitis and sepsis
2. Haemorrhage
46
What is the prognosis of gastrointestinal perforation?
1. Most patients require urgent surgery
2. Prognosis is dependent on early recognition and prompt resuscitation
47
What is haemochromatosis?
An autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation
48
What is the aetiology of haemochromatosis?
Caused by inheritance of mutations in the HFE gene on both copies of chromosome 6
49
What is the epidemiology of haemochromatosis?
1. 1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
2. Prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis
50
What are the early features of haemochromatosis?
Often asymptomatic and initial symptoms are often non-specific e.g. lethargy and arthralgia
51
What are the features of haemochromatosis?
1. Early symptoms: fatigue, erectile dysfunction and arthralgia (often of the hands)
2. 'bronze' skin pigmentation
3. Diabetes mellitus
4. Liver:
a. Stigmata of chronic liver disease
b. Hepatomegaly
c. Cirrhosis
d. Hepatocellular deposition
5. Arthritis (especially of the hands)
52
What are some of the cardiac and endocrine features of haemochromatosis?
1. Cardiac failure secondary to dilated cardiomyopathy
2. Hypogonadism: secondary to cirrhosis and pituitary dysfunction = hypogonadotrophic hypogonadism
53
What is important to exclude in suspected haemochromatosis?
Causes of secondary iron overload e.g. multiple transfusions
54
What are the signs of Haemochromatosis on physical examination?
May be normal, but with severe iron overload:
1. Skin: Pigmentation (slate-grey) resulting from increase in melanin deposits
2. Liver: Hepatosplenomegaly
3. Heart: Signs of heart failure, arrhythmias
4. Hypogonadism: Testicular atrophy, loss of hair, gynaecomastia
55
What are the best investigations to screen for iron overload?
1. In the general population: transferrin saturation is considered the most useful marker (plus ferritin)
2. In family members: genetic testing for HFE mutation
56
What is a typical iron study profile in a patient with haemochromatosis?
1. Transferrin saturation > 55% in men or > 50% in women
2. Raised ferritin (e.g. > 500 ug/l) and iron
3. Low TIBC
57
What other investigations are useful in haemochromatosis?
1. Iron studies: specifically transferrin
2. LFTs
3. MRI for liver and cardiac involvement
4. Liver biopsy: now only for patients with suspected cirrhosis
58
What is the management for haemochromatosis?
1. First line: Venesection
2. May use desferrioxamine as second line
59
What should be monitored during venesection as part of the management for haemochromatosis?
Transferrin saturation:
Should be kept below 50% and the serum ferritin concentration below 50 ug/l
60
What are the complications of haemochromatosis?
Reversible with treatment:
1. Cardiomyopathy
2. Skin pigmentation
Irreversible:
1. Liver cirrhosis
2. Diabetes mellitus
3. Hypogonadotrophic hypogonadism
4. Arthropathy
61
What are haemorrhoids?
Vascular-rich connective tissue cushions located within the anal canal: become haemorrhoids when they become enlarged, congested and symptomatic
62
How can haemorrhoids be classified?
External and internal:
1. External:
a. originate below the dentate line
b. prone to thrombosis
c. may be painful
2. Internal:
a. originate above the dentate line
b. do not generally cause pain
c. Can be graded
63
What is the grading system of internal haemorrhoids?
Grade I: Do not prolapse out of the anal canal
Grade II: Prolapse on defecation but reduce spontaneously
Grade III: Can be manually reduced
Grade IV: Cannot be reduced
64
What is the aetiology of haemorrhoids?
1. Excessive straining due to either chronic constipation or diarrhoea (most common)
2. Increase in intra-abdominal pressure by pregnancy or ascites
3. Presence of space-occupying lesions within the pelvis may cause a concomitant decrease in vascular return and increase in anal vascular engorgement
65
What is the epidemiology of haemorrhoids?
1. Prevalence is approximately 4% and is more common in white patients than in black patients
2. Presentation peaks between the ages of 45-65 years
66
What are the clinical features of haemorrhoids?
1. Painless rectal bleeding (most common symptom)
2. Can be itchy: pruritus
3. Pain, usually only if thrombosed
4. Faecal incontinence with third or fourth degree haemorrhoids
67
What are the signs of haemorrhoids on physical examination?
1. Tender palpable perianal lesion: can form adjacent to the anal canal on the anal margin when there is acute thrombosis
2. Internal haemorrhoids are not usually palpable on DRE
3. Anal mass: may be present with prolapsing haemorrhoids
68
What are the investigations for haemorrhoids?
1. Anoscopic examination: most specific and conclusive diagnostic test
2. Colonoscopy/flexible sigmoidoscopy: exclude serious pathology such as inflammatory bowel disease or cancer
3. Bloods only if there is concern that the patient has experienced significant prolonged rectal bleeding and signs of anaemia are present
69
What is the management of haemorrhoids?
1. Conservative: soften stools by increasing dietary fibre and fluid intake
2. Medical: topical local anaesthetics and steroids may be used to help symptoms
3. Surgical: ranges from outpatient treatment to newer treatments
70
What is the outpatient treatment for haemorrhoids?
Rubber band ligation
71
Who is eligible for surgical management of haemorrhoids?
Reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments
72
What are the new surgical techniques in the management of haemorrhoids?
Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy
73
What are the features of an acutely thrombosed external haemorrhoid?
1. Typically present with significant pain
2. Examination reveals a purplish, oedematous, tender subcutaneous perianal mass
74
What is the management of an acute thrombosed external haemorrhoid?
1. Patient presents within 72 hours: then referral should be considered for excision
2. Otherwise patients can usually be managed with stool softeners, ice packs and analgesia
3. Symptoms usually settle within 10 days
75
What are the complications of haemorrhoids?
1. Anaemia from continuous or excessive bleeding
2. Acute thrombosis of a haemorrhoid
3. Incarceration: prolapsing haemorrhoidal tissue can become incarcerated and be unable to be reduced into the anal canal, causing severe pain- urgent surgical haemorrhoidectomy
4. Faecal incontinence
76
What leads to the best long term prognosis of haemorrhoids?
Surgical haemorrhoidectomy: lowers the risk of recurrence
77
What is a haemorrhoidectomy?
An operation to remove haemorrhoids-swollen blood vessels in the anal canal
78
What are the indications for a haemorrhoidectomy?
1. Relieve persistent discomfort/pain
2. Prevent bleeding from the anus
3. Surgically correct strangulated haemorrhoids: when the anal sphincter squeezes the prolapsed haemorrhoid and interrupts blood flow
79
What are the possible complications of a haemorrhoidectomy?
From surgery:
1. Bleeding
2. Constipation
3. Infection
4. Excessive bleeding (seek advice)
Further complications of haemorrhoids:
1. Incontinence of stool: very rare (less than 1%)
2. Recurrent haemorrhoids
80
What is hepatocellular carcinoma?
Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver
81
What is the epidemiology of hepatocellular carcinoma?
The third most common cause of cancer worldwide
82
What are the most common causes of hepatocellular carcinoma?
1. Chronic hepatitis B is the most common cause worldwide
2. Chronic hepatitis C is the most common cause in Europe
83
What is the main risk factor for developing hepatocellular cancer?
Liver cirrhosis
84
What are the most common causes of liver cirrhosis?
Secondary to:
1. Hepatitis B and C
2. Alcohol
3. Haemochromatosis
4. Primary biliary cirrhosis
85
What are some of the risk factors of hepatocellular cancer?
1. Alpha-1 antitrypsin deficiency
2. Glycogen storage disease
3. Drugs: OCP, anabolic steroids
4. Porphyria cutanea tarda
5. Diabetes mellitus, metabolic syndrome
6. Male sex
7. Aflatoxins: Aspergillus flavus fungal toxin found on grains or biological weapons
86
What are the features of hepatocellular cancer?
1. Tends to present late, features of liver failure:
a. Jaundice
b. Ascites
c. RUQ pain,
d. Hepatosplenomegaly
e. Pruritus
2. Possibly present as decompensated chronic liver disease: encephalopathy, asterixis, spider naevi
87
What is the tumour marker for hepatocellular carcinoma?
AFP: alpha-fetoprotein, will be raised, has high sensitivity
88
What is the screening for hepatocellular carcinoma?
Ultrasound ± AFP in high risk groups:
1. Patients with liver cirrhosis secondary to Hep B and C, haemochromatosis
2. Men with liver cirrhosis secondary to alcohol
89
What is the management of hepatocellular carcinoma?
1. In early disease: surgical resection
2. Definitive management: liver transplantation
3. Radiofrequency ablation
4. Transarterial chemoembolisation
5. Sorafenib: a multikinase inhibitor
90
What is the prognosis of hepatocellular carcinoma?
A very aggressive type of cancer, depends upon stage and overall functional status of the liver
91
What is a hernia?
The protrusion of abdominal or pelvic contents through a weakness in the muscle or tissue wall that holds it in place e.g. the abdominal wall
92
What are the different types of hernia?
1. Inguinal hernia
2. Femoral hernia
3. Umbilical
4. Paraumbilical
5. Epigastric
6. Obturator
93
What are the risk factors for abdominal wall hernias?
1. Obesity
2. Ascites
3. Increasing age
4. Surgical wounds
94
What are the features of abdominal wall hernias?
1. Palpable lump
2. Cough impulse
3. Pain
4. Obstruction: more common in femoral hernias
5. Strangulation: may compromise the bowel blood supply leading to infarction
95
What is the cough impulse for inguinal hernias?
Helps to distinguish between direct and indirect inguinal hernias:
1. Reduce the hernia and occlude the deep internal ring with 2 fingers
2. Ask the patient to cough (or stand)
3. If the hernia is restrained it is indirect
4. If not it is direct
96
What is an inguinal hernia?
1. Accounts for 75% of abdominal wall hernias
2. Around 95% of patients are male
3. Above and medial to pubic tubercle
4. Presents as a groin lump: disappears on pressure or when lying down
5. Discomfort and ache often worse with activity
4. Strangulation is rare
97
What is a femoral hernia?
1. Below and lateral to the pubic tubercle
2. More common in women, particularly multiparous ones
3. High risk of obstruction and strangulation
4. Surgical repair is required
98
What is an epigastric hernia?
1. Lump in the midline between umbilicus and the xiphisternum
2. Risk factors include extensive physical training or coughing (from lung diseases), obesity
99
What is an incisional hernia?
May occur in up to 10% of abdominal operations
100
What is an obturator hernia?
1. A hernia which passes through the obturator foramen
2. More common in females and typical presents with bowel obstruction
101
What is the management of inguinal hernias?
1. Treat medically fit patients even if they are asymptomatic
2. A hernia truss may be an option for patients not fit for surgery but probably has little role in other patients
3. Mesh repair is associated with the lowest recurrence rate:
1. Unilateral inguinal hernias are generally repaired with an open approach
2. Bilateral and recurrent inguinal hernias are generally repaired laparoscopically
102
What advice should be given to patients who had open repair management of their inguinal hernia?
Return to non-manual work after 2-3 weeks (following laparoscopic repair after 1-2 weeks)
103
What are the complications of inguinal hernia mesh repair?
Early: bruising, wound infection
Late: chronic pain, recurrence
104
How are femoral hernias diagnosed?
Usually clinical, although ultrasound is an option
105
What are some of the differentials for a femoral hernia?
1. Lymphadenopathy
2. Abscess
3. Femoral artery aneurysm
4. Hydrocoele or varicocele in males
5. Lipoma
6. Inguinal hernia
106
What is the management of femoral hernias?
1. Surgical repair is a necessity, given the risk of strangulation, and can be carried out either laparoscopically or via a laparotomy
2. Hernia support belts/trusses should not be used for femoral hernias (risk of strangulation)
3. In an emergency situation, a laparotomy may be the only option
107
What are the complications of a femoral hernia?
1. Incarceration: where the herniated tissue cannot be reduced
2. Strangulation: surgical emergency!
3. Bowel obstruction: surgical emergency
4. Bowel ischaemia and resection due to the above, which may lead to significant morbidity and mortality for the patient
108
What is femoral hernia strangualtion?
1. A surgical emergency where the blood supply to the herniated tissue is compromised, leading to ischemia or necrosis
2. These hernias will be tender and likely non-reducible, and may also present with a systemically unwell patient
109
What are the investigations for a strangulated hernia?
1. Imaging can be used in cases of suspected strangulation, however, it is not considered necessary and is more useful in excluding other pathologies
2. FBC and ABG analysis can help point towards the diagnosis by showing:
a. Leukocytosis
b. Raised lactate
110
What is the management of a strangulated femoral hernia?
Surgical repair, a laparotomy may be the only option
111
What type of hernia carries a high risk of strangulation?
Femoral hernias
112
What is a hiatus hernia?
Describes the herniation of part of the stomach above the diaphragm
113
What are the two types of hiatus hernia?
1. Sliding: (95% of hiatus hernias), the gastroesophageal junction moves above the diaphragm
2. Rolling: the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
114
What are the risk factors for hiatus hernias?
1. Obesity
2. Increased intra-abdominal pressure e.g. ascites, multiparity
115
What are the features of a hiatus hernia?
1. Heartburn
2. Dysphagia
3. Regurgitation
4. Chest pain
116
What is the most sensitive test for a hiatus hernia?
Barium swallow
117
How are hiatus hernias commonly found?
Incidentally: due to presenting symptoms the patients have an endoscopy which shows the displacement of the gastroesophageal junction
118
What is the management of hiatus hernias?
1. Conservative: all patients benefit from weight loss
2. Medical: proton pump inhibitor therapy
3. Surgical: only really has a role in symptomatic paraesophageal hernias (other part of the stomach herniates)
119
What is intestinal ischaemia and how can it be divided?
Bowel ischaemia:
1. Acute mesenteric ischaemia
2. Chronic mesenteric ischaemia
3. Ischaemic colitis
120
What are the predisposing factors for intestinal ischaemia?
1. Increasing age
2. AF (mesenteric ischaemia)
3. Other causes of emboli: malignancy, endocarditis
4. CVD risk factors: HTN, smoking, DM
5. Cocaine (ischaemic colitis in young people)
121
What are the features of intestinal ischaemia?
1. Abdominal pain
2. Rectal bleeding
3. Diarrhoea
4. Fever
122
What is a common feature in acute mesenteric ischaemia?
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings
123
What are the findings of intestinal ischaemia on bloods?
Elevated white blood cell count and lactic acidosis
124
What is the investigation of choice for intestinal ischaemia?
CT
125
What is acute mesenteric ischaemia caused by?
1. Typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel e.g. superior mesenteric artery
2. Classically patients have a history of AF
126
What is the management of acute mesenteric ischaemia?
1. Urgent surgery is usually required
2. Poor prognosis, especially if surgery delayed
127
What is chronic mesenteric ischaemia?
1. A relatively rare clinical diagnosis due to it's non-specific features
2. May be thought of as 'intestinal angina'
3. Colickly, intermittent abdominal pain occurs
128
What is ischaemic colitis?
1. Describes an acute but transient compromise in the blood flow to the large bowel
2. This may lead to inflammation, ulceration and haemorrhage
129
Where is a common site for ischaemic colitis?
More likely to occur in 'watershed' areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries
130
What are the signs of ischaemic colitis on abdominal x-ray?
'Thumbprinting' may be seen due to mucosal oedema/haemorrhage
131
What is the management of ischaemic colitis?
1. Usually supportive
2. Surgery may be required in a minority of cases if conservative measures fail
3. Indications for surgery include:
a. Generalised peritonitis
b. Perforation
c. Ongoing haemorrhage
132
What is small bowel obstruction?
Where the passage of food, fluids and gas, through the small intestines becomes blocked
133
What are the common causes of small bowel obstruction?
1. Adhesions (e.g. following previous surgery): most common
2. Hernias
134
What are the features of small bowel obstruction?
1. Diffuse, central abdominal pain
2. Nausea and vomiting
2. Typically bilious vomiting
4. 'constipation' with complete obstruction and lack of flatulence
5. Abdominal distension may be apparent, particularly with lower levels of obstruction
6. 'tinkling' bowel sounds (more common in early bowel obstruction)
135
What is the first line imaging in small bowel obstruction?
Abdominal x-ray: distended small bowel loops with fluid levels
1. Considered dilated if small bowel is >3cm diameter
136
What is the definitive investigation for small bowel obstruction?
CT: most sensitive, particularly in early obstruction
137
What is the management of small bowel obstruction?
1. Intial steps:
a. NBM
b. IV fluids
c. nasogastric tube with free drainage
2. Some patients settle with conservative management but otherwise will require surgery
138
What is large bowel obstruction?
When the passage of food, fluids and gas, through the large intestines becomes blocked
139
What is the most common cause of large bowel obstruction?
Tumours:
1. 60% of cases
2. Can be the initial presenting complaint of colonic malignancy (30% of cases)
3. Particularly more distal colonic and rectal tumours, as these tend to obstruct earlier due to the smaller lumen diameter
140
What are the causes of large bowel obstruction?
1. Tumours (60%)
2. Volvulus
3. Diverticular disease
141
What are the clinical features of large bowel obstruction?
1. Feature suggestive of obstruction plus underlying causes (e.g. any recent symptoms suggestive of colorectal cancer)
2. Absence of passing flatus or stool
3. Abdominal pain
4. Abdominal distention
5. Late: nausea and vomiting, may suggest a more proximal lesion
6. Peritonism: if there is associated bowel perforation
142
What is the first line investigation for large bowel obstruction?
Abdominal x-ray:
1. Normal diameter limits are 10-12 cm for caecum, 8 cm for ascending colon, and 6.5 cm for recto-sigmoid
2. Diameter greater than this is diagnostic of obstruction
3. Presence of free intra-peritoneal gas indicates colonic perforation
143
What is the best investigation for large bowel obstruction?
CT:
1. High sensitivity and specificity for identifying obstruction (over 90% each)
2. Can identify the aetiology of obstruction itself
144
What is the management of large bowel obstruction?
1. Initial steps:
a. NBM
b. IV fluids
c. nasogastric tube with free drainage
2. Urgency of management depends on whether perforation is suspected
3. If the cause of obstruction itself does not require surgery: conservative management for up to 72 hours can be trialled
4. Around 75% will eventually require surgery
5. IV antibiotics will be given if perforation suspected or surgery planned
145
What is the surgical management of large bowel obstruction?
1. Emergency surgery necessary if: there is any overt peritonitis or evidence of bowel perforation,
2. Procedure:
a. Irrigation of the abdominal cavity
b. Resection of perforated segment and ischaemic bowel
c. Address the underlying cause of the obstruction itself
146
What is the difference in imaging in small and large bowel obstruction?
On abdominal x-ray:
Small bowel:
1. Maximum normal diameter = 35 mm
2. Valvulae conniventes extend all the way across
Large bowel:
1. Maximum normal diameter = 55 mm
2. Haustra extend about a third of the way across
147
What is Ileus?
1. The slowing of GI motility accompanied by distention, in the absence of a mechanical intestinal obstruction
2. Diagnosis of exclusion after bowel obstruction has been ruled out
3. It usually occurs in response to physiological stress, including surgery, sepsis, metabolic derangements, and Gl diseases
148
What are the complications of Intestinal obstruction?
1. Intestinal necrosis
2. Sepsis
3. Multi-organ failure
4. Intestinal perforation: lead to intra-abdominal abscess
5. From surgery: short bowel syndrome: extensive removal of small intestine resulting in inadequate absorption of enteral nutrition
149
What are Liver abscesses?
Localised infections in the liver parenchyma resulting in a walled off collection of pus
150
What is the aetiology of liver abscesses?
The most common organisms:
1. Staphylococcus aureus in children
2. Escherichia coli in adults
151
What are the presenting symptoms of a Liver abscess?
1. Non-specific symptoms: fever, malaise, nausea, anorexia, night sweats, weight loss
2. RUQ or epigastric pain, which may be referred to shoulder (diaphragmatic irritation)
3. Diarrhoea
4. 1/3 of patients have chest symptoms, including cough, shortness of breath, and chest pain
152
What are the appropriate investigations for Liver abscesses?
1. Bloods:
a. Inflammatory and infection markers
b. LFTS: raised ALP (most common finding), prothrombin time
c. Blood cultures: pyogenic abscesses
2. Ultrasound:
a. Can be used to guide aspiration of the abscess
b. Gram stain and culture of aspirated abscess fluid
3. Non-contrast CT: demonstrates hypodense liver lesions, gas within the lesion is highly suggestive of a pyogenic abscess
153
What is the management of liver abscesses?
Drainage (typically percutaneous) and antibiotics:
1. amoxicillin + ciprofloxacin + metronidazole
2. If penicillin allergic: ciprofloxacin + clindamycin
154
What are Liver cysts?
Fluid filled sacs in the liver, that can be congenital
155
What is the aetiology of Liver cysts?
1. Inherited disorders can cause cysts, including polycystic liver disease, congenital hepatic fibrosis
2. Majority of cystic disease is caused by simple cysts- caused from a malformation of your bile ducts
156
What is the epidemiology of Liver cysts?
1. Congenital causes are present at birth
2. Simple cysts are estimated to affect between 1% and 2.5% of the population
3. Affect all ages, but occur more frequently in the population as age increases
157
What are the presenting symptoms/signs of Liver cysts?
1. Usually have no symptoms
2. Larger cysts may occasionally cause some dull pain and/ or swelling RUQ- hepatomegaly
158
What are the investigations for Liver cysts?
1. Bloods:
a. FBC: lack of signs of infection: abscess
b. CRP: elevated if inflamed
c. LFTs: elevated AlkPhos and bilirubin if bile duct is obstructed
2. Ultrasound or CT scan: localise structure of mass, exclude abscess
3. Aspiration of fluid: exclude infection
159
What is the management of Liver cysts?
1. Simple liver cysts generally do not require treatment unless they become large enough to cause pain
2. Aspiration and then stick the walls together using sclerosant or remove part of the wall of the cyst, called laparoscopic de-roofing
160
What is acute liver failure?
Describes the rapid onset of hepatocellular dysfunction leading to a variety of systemic complications
161
What are the causes of acute liver failure?
1. Paracetamol overdose
2. Alcohol
3. Viral hepatitis (usually A or B)
4. Acute fatty liver of pregnancy
162
What are the features of acute liver failure?
1. May be asymptomatic
2. Jaundice
3. Fever, nausea, malaise
4. Abdominal pain
163
What are the signs of liver failure on examination?
1. Bruising: coagulopathy: raised prothrombin time
2. Hypoalbuminaemia
3. Hepatic encephalopathy
4. Renal failure is common ('hepatorenal syndrome')
164
What is Budd-Chiari syndrome?
1. A very rare condition involving the occlusion of the hepatic veins that drain the liver
2. It presents with the classical triad of abdominal pain, ascites, and liver enlargement
165
What is the pathogenesis of the manifestation in Liver failure?
1. Jaundice: decreased secretion of conjugated bilirubin
2. Encephalopathy: increased delivery of gut-derived products into the systemic circulation and brain
from the reduced extraction of nitrogenous products by liver and portal systemic shunting- ammonia may play a part
3. Coagulopathy: reduced synthesis of clotting factors and so reduced platelets (hypersplenism if chronic portal hypertension)
166
What are the investigations for Liver failure?
A to E approach:
1. Bloods:
a. LFTs: hyperbilirubinaemia, elevated liver enzymes
Prothrombin time >1.5
b. FBC: thrombocytopenia
c. U&Es for renal failure
2. ABG: metabolic acidosis. elevated lactate- presence of acidosis is an important prognostic indicator, particularly in paracetamol overdose
3. Identify cause e.g. paracetamol level, urine toxicology, pregnancy, viral hepatitis serology, autoimmune markers
167
What tests are the most accurate marker of liver function?
Prothrombin time and albumin
168
What is the management for Liver failure?
1. Resuscitation (ABC approach): ITU care and specialist unit support essential
2. Treat the cause if possible: N-acetylcysteine for paracetamol overdose
3. Invasive ventilatory support often required plus coagulopathy treatment: IV Vitamin K, FFP, platelet infusions if required, gastric mucosa protection (PPI)
4. Antiviral therapy should be considered
4. Avoid: Sedatives or drugs metabolized by the liver
5. Liver transplantation should be considered in all patients with acute liver failure who fulfil prognostic criteria for a high risk of mortality
169
What is the prognostic criteria for a high risk of mortality in Liver failure?
According to the United Network for Organ Sharing (UNOS):
1. Age >18 years
2. Life expectancy without a liver transplant of <7 days
3. Onset of encephalopathy within 8 weeks of the first symptoms of liver disease
4. Absence of pre-existing liver disease
4. Admission to an intensive care unit, and 1 of the following:
a. Ventilator dependence
b. Requirement of renal replacement therapy
c. INR >2.0
170
What are the contraindications of Liver transplantation?
1. Severe infection or septic shock
2. Brain death
3. Severe cardiopulmonary disease or ARDS
4. Multi-organ failure
5. Extrahepatic malignancy
6. Others: ongoing alcohol or illicit drug abuse, or a history of repeated suicide attempts
171
What are the complications of Liver failure?
1. Rapidly progressing hepatic encephalopathy
2. Coagulopathy
3. Infection
4.. Hepatorenal syndrome (concurrent hepatic and renal failure)
5. Metabolic disorders: hypoglycaemia, acid–base and electrolyte disturbances
6. Cerebral oedema
7. GI bleeding due to coagulopathy
172
What is the prognosis of Liver failure?
Depends on the severity and aetiology:
1. Secondary to paracetamol overdose, acute hepatitis A, or shock liver is associated with a favourable prognosis
2. In contrast, resulting from idiosyncratic drug-induced liver injury, acute hepatitis B, or indeterminate cause has a much lower rate of spontaneous recovery
173
What is hepatic encephalopathy?
1. Often associated with acute liver failure it may also be seen with chronic disease
2. Features:
a. Confusion
b. Asterix/ liver flap
174
What are the grades of hepatic encephalopathy?
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
175
What are the precipitating factors for hepatic encephalopathy?
1. Infection e.g. spontaneous bacterial peritonitis
2. GI bleed
3. Post transjugular intrahepatic portosystemic shunt
4. Constipation
5. Drugs: sedatives, diuretics
hypokalaemia
6. Renal failure
176
What is the management of hepatic encephalopathy?
1. Treat any underlying precipitating cause
2. NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
a. Lactulose promotes the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
177
What is Mallory-Weiss tear?
A syndrome characterised by a tear or laceration often along the right border of, or near, the gastro-oesophageal junction
178
What is the aetiology of a Mallory-Weiss tear?
Most cases seem to occur as a result of a sudden rise in abdominal pressure or transmural pressure gradient across the gastro-oesophageal junction with a corresponding low intrathoracic pressure e.g. retching, vomiting, chronic cough
179
What are the causes of a Mallort-Weiss tear?
1. Coughing (chronic e.g. COPD, bronchiectasis)
2. Retching, vomiting and straining
3. Closed-chest pressure or cardiopulmonary resuscitation
4. Acute abdominal blunt trauma
5. Alcohol and medications (aspirin or other NSAIDs)
6. Chemotherapeutic agents
7. Hiatal hernia, which is present in 40% to 100% of people with MWT, is considered by many to be a precipitating factor, causing an oesophageal tear to occur
180
What is the epidemiology of Mallory-Weiss tears?
1. Admission to hospital for non-variceal upper GI bleeding is common
2. Age of presentation may vary but is most common in people aged between 30- 50 years
3. More common in men than in women in a ratio of 3:1
4. In women of childbearing age, the most common cause is hyperemesis gravidarum (severe nausea and vomiting)
181
What are the presenting symptoms and signs of a Mallory-Weiss tear?
1. Haematemesis: varies from flecks or streaks of blood mixed with gastric contents and/or mucus, blackish or ‘coffee ground’, to a bright-red bloody emesis
2. Light headedness/dizziness
3. Postural/orthostatic hypotension
182
What is the typical history of a Mallory-Weiss tear?
Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting (rare to have malena)
183
What are some differentials for an acute upper GI bleed?
Oesophageal:
1. Varices
2. Oesophagitis
3. Cancer
4. Mallory-Weiss tear
Gastric:
1. Ulcer
2. Cancer
3. Gastritis
Duodenal:
1. Ulcer
184
What is the Glasgow-Blatchford score for assessing acute upper GI bleeds?
The first assessment which helps clinicians decide whether patient patients can be managed as outpatients or not
185
What is the Glasgow-Blatchford score for assessing acute upper GI bleeds?
The first assessment which helps clinicians decide whether patient patients can be managed as outpatients or not
186
What is the blatchford score?
Assessing the admission risk for patients who present with an acute upper GI bleed (if 0 may be considered for early discharge):
1. Urea level
2. Haemoglobin
3. Systolic BP
4. Others including:
a. Pulse
b. Melena
c. Syncope
d. Hepatic disease
e. Cardiac failure
187
What is the best investigation for acute upper GI bleed?
Endoscopy within 24 hours - but should only be performed after resuscitation
188
What is the resuscitation of patients with an acute upper GI bleed?
1. ABC, wide-bore intravenous access x 2
2. Platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
3. Fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time or activated partial thromboplastin time greater than 1.5 times normal
4. Prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
189
What is the specific management for a Mallory-Weiss tear?
Usually ceases spontaneously
190
What is the management of an acute upper GI bleed divided into?
Variceal vs non-variceal bleeding
191
What is variceal bleeding?
1. Complication of portal hypertension secondary to liver cirrhosis
2. Usually associated with large volumes of blood (can haemorrhage)
3. Often associated with haemodynamic compromise
4. May stop spontaneously but re-bleeds are common until appropriately managed
192
What is the management of variceal bleeding?
1. Terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
2. Band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
3. Transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
193
What is the management of non-variceal bleeding?
1. NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper GI bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
2. If further bleeding then options include repeat endoscopy, interventional radiology and surgery
194
What are the complications of Mallory-Weiss tears?
1. MI or infraction: usually related to the acuity, severity of bleeding, and associated CAD
2. Hypovolaemic shock/death: usually related to acuity and severity of bleeding; however, it is rare in patients with early stabilisation and prompt treatment
3. Oesophageal perforation:
Gastric ischaemia
4. Metabolic disturbance: intractable vomiting
195
What is the prognosis of Mallory-Weiss tears?
1. For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy
2. Prognosis is excellent in patients without associated disease or complications
3. A routine second endoscopic evaluation is not recommended unless the patient remains symptomatic after initial treatment
196
What is Nasogastric tube insertion?
The insertion of a tube from the patients nose into their stomach for either feeding or aspiration
197
What are the indications of Nasogastric tube insertion?
1. To empty the upper gastrointestinal tract or for feeding
2. Insertion may be for prophylactic or therapeutic reasons e.g. bowel obstruction
198
What are the possible contraindications of a NG tube insertion?
1. Ear, nose and throat abnormalities or infections
2. Facial/neck fractures including base of skull
3. Possible strictures of the oesophagus
4. Oesophageal varices
5. Anatomical abnormalities (oesophageal diverticulae)
6. High risk of aspiration
199
What are the possible complications of Nasogastric tube insertion?
Main: aspiration and tissue trauma- if placed incorrectly into the trachea and lung it can cause pneumonia and death
200
How is an NG tube insertion checked that it is in the correct position?
pH test (NG tube is aspirated and the contents are checked using pH paper) and CXR
201
What is Nissen fundoplication?
Surgical procedure to treat severe and ongoing acid reflux (GORD) and hiatal hernia
202
What is Non-alcoholic fatty liver disease?
1. Now the most common cause of liver disease in the developed world
2. Includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis (in non-alcoholics)
203
What is the aetiology of non-alcoholic fatty liver disease?
It is largely caused by obesity and describes a spectrum of disease ranging from:
1. Steatosis - fat in the liver
2. Steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH)
3. Progressive disease may cause fibrosis and liver cirrhosis
204
What is non-alcoholic steatohepatitis (NASH)?
1. A term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse
2. It is relatively common and thought to affect around 3-4% of the general population
3. The progression of disease in patients with NASH may be responsible for a proportion of patients previously labelled as cryptogenic cirrhosis
205
What are the associated factors in non-alcoholic fatty liver disease?
1. Obesity
2. T2 DM
3. Hyperlipidaemia
4. Jejunoileal bypass
5. Sudden weight loss/starvation
206
What are the features of non-alcoholic fatty liver disease?
1. Usually asymptomatic
2. Hepatomegaly
3. ALT is typically greater than AST
4. Increased echogenicity on ultrasound
5. Absence of chronic alcoholic disease signs
207
What are the signs of chronic alcoholic disease?
1. Spider naevi
2. Palmar erythema
3. Dupuytren's contracture
4. Gynaecomsastia
5. Parotid gland enlargement
208
What are the guidelines on investigation and management of non-alcoholic fatty liver disease?
1. No evidence to support screening for NAFLD in adults, even in at risk groups (e.g. T2DM)
2. The guidelines are therefore based on the management of the incidental finding of NAFLD - typically asymptomatic fatty changes on liver ultrasound
209
What are the initial investigations that would be performed in patients presenting with features of non-alcoholic fatty liver disease?
1. Bloods:
a. FBC
b. LFTs: deranged, AST>ALT, elevated GGT and Alk Phos
2. Test for aetiology e.g. HbA1c
3. Ultrasound
210
What are the features of non-alcoholic fatty liver disease on ultrasound?
1) Diffuse hyperechoic echotexture (bright liver)
2) Increased liver echogenicity compared with kidney
3) Vascular blurring
4) Deep attenuation
211
What investigation is recommended in patients with non-alcoholic fatty liver disease on ultrasound?
Enhanced liver fibrosis (ELF) blood test:
1. To check for advanced fibrosis
2. A combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1
3. An algorithm based on these values results in an ELF blood test score, similar to triple testing for Down's syndrome
212
What is the management of patients with advanced fibrosis secondary to non-alcoholic fatty liver disease?
1. Referred to a liver specialist
2. Have a liver biopsy to stage the disease more accurately
213
What is the management for patients with non-alcoholic fatty liver disease with no advanced fibrosis?
1. Mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring
2. Consider pharmacological agents or surgery (Orlistat is an enteric lipase inhibitor that prevents the absorption of fats from the GI tract/ bariatric surgery)
3. Treatment of insulin resistance and diabetes (metformin)
4. If presence of end-stage liver failure:
a. Transjugular intrahepatic portosystemic shunt (TIPS)
b. Liver transplantation
214
What are the complications of Non-alcoholic steatohepatitis (NASH)?
1. Ascites
2. Cirrhosis
3. Variceal haemorrhagae
4. Portosystemic encephalopathy
5. Hepatocellular carinoma
6. Hepatorenal syndrome
7. Hepatopulmonary syndrome
8. Death: result of the increased risk of coronary artery disease
215
What is the prognosis of Non-alcoholic steatohepatitis (NASH)?
1. Independent predictors of fibrosis progression include:
a. Diabetes mellitus
b. A low initial fibrosis stage
c. Higher BMI
2. Patients who have NASH progress to cirrhosis 9% to 20% of the time: up to 1/3 of these patients will die from liver failure or require liver transplantation
3. Recurrent NAFLD following liver transplantation is now a well-recognised phenomenon
216
What is oesophageal cancer?
A malignant tumour arising in the oesophageal mucosa. There are two major histological types:
1. Squamous cell carcinoma
2. Adenocarcinoma (now most common)
217
What is oesophageal adenocarcinoma?
1. Most common type of oesophageal cancer
2. More likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's
3. Majority are located near the gastroesophageal junction in the lower third of oesophagus
218
What is oesophageal squamous cell carcinoma?
1. Most common type of oesophageal cancer in the developing world
2. Associated with alcohol and smoking
3. Located in the upper 2/3rds of the oesophagus
219
What are the risk factors for oesophageal cancer?
1. Male sex, 7:1
2. Squamous cell carcinoma:
a. Alcohol
b. Tobacco
c. FH of oesophageal, stomach, oral or pharyngeal cancer
d. Achalasia
3. Adenocarcinoma:
a. GORD
b. Barrett's oesophagus
c. Obesity
220
What are the features of oesophageal cancer?
1. Dysphagia: the most common presenting symptom
2. Anorexia and weight loss
3. Vomiting
4. Other possible features include:
a. Odynophagia: painful swallowing
b. Hoarseness: may indicate recurrent laryngeal nerve palsy
c. Melaena
d. Cough
221
What is the initial and best investigation for oesophageal cancer?
Upper GI endoscopy with biopsy:
1. Mucosal lesion
2. Histology shows squamous carcinoma or adenocarcinoma
222
What are the other useful investigations for staging of oesophageal cancer?
1. Endoscopic ultrasound: is the preferred method for locoregional staging
2. CT scanning of the chest, abdomen and pelvis: is used for initial staging
3. FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans
4. Laparoscopy is sometimes performed to detect occult peritoneal disease
223
What is the management of oesophageal cancer?
Operable disease is best managed by surgical resection with adjuvant chemotherapy
224
What is the most common surgical procedure of oesophageal cancer?
Ivor-Lewis type oesophagectomy
225
What is the biggest risk of surgical resection management of oesophageal cancer?
Anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
226
What is pancreatic cancer?
1. Malignancy arising from the exocrine or endocrine tissues of the pancreas
2. Refers to primary pancreatic ductal adenocarcinoma, which accounts for >80% of all pancreatic neoplasms (head of pancreas)
227
What is the aetiology of pancreatic cancer?
1. Pancreatic cancer is a disease of older people, with a peak incidence in people 65 to 75 years of age
2. The only consistently reported exogenous risk factor for pancreatic cancer is cigarette smoking
3. 5-10% have a familial component
4. Weak risk factors:
a. Obesity
b. Diabetes Mellitus
c. Dietary factors ( high in meats and fat, and low serum folate)
228
What are the associations of pancreatic cancer?
1. Increasing age
2. Smoking
3. Diabetes
4. Chronic pancreatitis (alcohol does not appear an independent risk factor though)
5. Hereditary non-polyposis colorectal carcinoma
6. Multiple endocrine neoplasia
7. Genetics: BRCA2 gene, KRAS gene mutation
229
What is the main problem with the presentation of pancreatic cancer?
Pancreatic cancer is often diagnosed late as it tends to present in a non-specific way
230
What are the early/ initial symptoms of pancreatic cancer?
Initial symptoms (often non-specific):
a. Anorexia
b. Malaise
c. Weight loss
d. Nausea
Later symptoms: jaundice, epigastric pain
231
What is the main presenting symptom that often occurs later in pancreatic cancer?
Painless jaundice: pale stools, dark urine, and pruritus
232
What are the signs of pancreatic cancer of physical examination?
1. Courvoisier's law: states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
2. migratory thrombophlebitis (Trousseau sign): is more common than with other cancers
233
What is Courvoisier's law?
In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
234
What are associated features of pancreatic cancer?
1. Loss of exocrine function (e.g. steatorrhoea)
2. Loss of endocrine function (e.g. diabetes mellitus)
235
What is the initial investigation for pancreatic cancer?
Ultrasound: has a sensitivity of around 60-90%
236
What is the investigation of choice for pancreatic cancer?
High-resolution CT scanning:
imaging may demonstrate the 'double duct' sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
237
What are the other investigations alongside imaging for pancreatic cancer?
Bloods:
1. Tumour marker CA19-9 can be elevated (specific, but not diagnostic)
2. If causing obstructive jaundice: bilirubin, alkaline phosphatase, and gamma glutamyl transpeptidase elevated
238
What is the management of pancreatic cancer?
Less than 20% are suitable for surgery at diagnosis:
1. Surgery
2. Palliation (± ERCP stenting)
239
What is the surgical management of pancreatic cancer?
Whipple's resection (pancreaticoduodenectomy):
1. Performed for resectable lesions in the head of pancreas
2. Side-effects of a Whipple's include dumping syndrome and peptic ulcer disease
3. Adjuvant chemotherapy following surgery
240
What is acute pancreatitis?
An acute inflammatory process of the pancreas and is associated with acinar cell injury with local and systemic inflammatory responses (self-limiting and reversible pancreatic injury)
241
What are the two most common causes of acute pancreatitis?
Gallstones and alcohol
242
What are the other causes of acute pancreatitis?
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hypercalcemia
Hypertriglyceridemia
ERCP
Drugs: furosemide, azathioprine, thiazide diuretics, sulfonamides, tetracyclines, sodium, mesalazine, oestrogen
243
What is the epidemiology of acute pancreatitis?
1. Common- the most common cause worldwide is alcohol consumption
2. Peak age is 60 years
3. In males, alcohol-induced is more common while in females, principal cause is gallstones
244
What is the pathophysiology of acute pancreatitis?
Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
245
What are the presenting symptoms of acute pancreatitis?
1. Severe epigastric or abdominal pain:
a. radiating to back
b. relieved by sitting forward
c. aggravated by movement
2. Associated with anorexia, nausea and vomiting
246
What are the signs of acute pancreatitis on examination?
1. Epigastric tenderness
2. Ileus
3. Low-grade fever
4. Rarer signs:
a. periumbilical discolouration (Cullen's sign)
b. flank discolouration (Grey-Turner's sign)
247
What are the investigations for acute pancreatitis?
1. Bloods:
a. Amylase (>3 times of normal)
b. Lipase
c. FBC: neutrophilia
d. U&Es: hypocalcaemia
e. Hyperglycaemia
f. LDH and AST (LFTs): raised
2. Imaging: ultrasound e.g. for gallstones
248
What is the role of serum amylase and lipase in the investigation of acute pancreatitis?
1. Amylase:
a. Raised in 75% of patients - typically > 3 times the upper limit of normal
b. Levels do not correlate with disease severity
2. Lipase:
a. More sensitive and specific than serum amylase
b. Has a longer half-life than amylase and may be useful for late presentations > 24 hours
249
What conditions could lead to a raised amylase?
1. Pancreatitis
2. Pancreatic pseudocyst
3. Mesenteric infarct
4. Perforated viscus
5. Acute cholecystitis
6. Diabetic ketoacidosis
250
When is imaging not needed in the diagnosis of acute pancreatitis?
If there is characteristic pain + amylase/lipase > 3 times normal level
251
What are some of the scoring systems for acute pancreatitis?
Ranson score, Glasgow score and APACHE II. Factors for severe pancreatitis include:
1. Age > 55 years
2. Hypocalcaemia
3. Hyperglycaemia
4. Hypoxia
5. Neutrophilia
6. Elevated LDH and AST
252
How can acute pancreatitis be stratified?
1. Mild: no organ failure, no complications
2. Moderately severe: no/ transient (<48 hours) organ failure, possible complications
3. Severe: persistent (> 48 hours) organ failure, possible complications
253
What is the key aspect of care in the management of acute pancreatitis?
Fluid resuscitation:
1. Aggressive early hydration with crystalloids
2. In severe cases 3-6 litres of third space fluid loss may occur
3. Aim for a urine output of > 0.5mls/kg/hr
4. May also help relieve pain by reducing lactic acidosis
254
What are the other aspects of managing acute pancreatitis?
1. Analgesia: IV opioids are normally required to adequately control the pain
2. Nutrition: not routinely be made 'nil-by-mouth' unless there is a clear reason e.g. the patient is vomiting, enteral nutrition offered if there is moderately severe pancreatitis within 72 hours of presentation
3. Antibiotics: not prophylactic, potential indications include infected pancreatic necrosis
4. Surgery e.g. urgent early cholecystectomy for gallstones, ERCP for obstructed biliary system
255
What is the surgical management of pancreatitis?
1. Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
2. Patients with obstructed biliary system due to stones should undergo early ERCP
3. Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some
4. Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy
256
What are the complications of acute pancreatitis?
Local:
1. Peripancreatic fluid collection
2. Psuedocyst
3. Pancreatic necrosis
4. Pancreatic abscess
5. Haemorrhage
Systemic: ARDS (high mortality rate around 20%)
257
What are peripancreatic fluid collections?
1. Complication of acute pancreatitis
2. Occur in 25% cases
3. Located in or near the pancreas and lack a wall of granulation or fibrous tissue
4. May resolve or develop into pseudocysts or abscesses
5. Since most resolve aspiration and drainage is best avoided as it may precipitate infection
258
What are pancreatic pseudocysts?
1. Result from organisation of peripancreatic fluid collection
2. They may or may not communicate with the ductal system
3. The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after an attack of acute pancreatitis
4. Most are retrogastric
75% are associated with persistent mild elevation of amylase
5. Investigation is with CT, ERCP and MRI or endoscopic USS
6. Treatment is either with endoscopic or surgical cystogastrostomy or aspiration
259
What is Pancreatic necrosis?
1. May involve both the pancreatic parenchyma and surrounding fat
2. Complications are directly linked to extent of parenchymal necrosis and extent of necrosis overall
3. Early necrosectomy is associated with a high mortality rate (should be avoided)
4. Sterile necrosis should be managed conservatively (at least initially)
260
What are pancreatic abscesses?
1. Complication of acute pancreatitis
2. Intraabdominal collection of pus associated with pancreas but in the absence of necrosis
3. Typically occur as a result of infected pseudocyst
4. Transgastric drainage is one method of treatment, endoscopic drainage is an alternative
261
What is usually the timeline of complications of acute pancreatitis?
1. Peripancreatic fluid collections → pseudocyst → abscess
2. Necrosis → infected → haemorrhage
262
What is pancreatic haemorrhage following acute pancreatitis?
1. Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de novo or as a result of surgical necrosectomy
2. When retroperitoneal haemorrhage occurs Grey Turner's sign may be identified
263
What is the Glasgow criteria scoring system for assessing the severity of acute pancreatitis?
Modified Glasgow criteria (3 or more indicates severe disease):
(P) pO2 < 7.9 kPa
(A) Age > 55
(N) WCC > 15x109/L
(C) Ca2 þ < 2 mmol/L
(uR) Urea > 16 mmol/L
(Enz) LDH > 600
(A) Albumin > 32 g/L
(Sugar) Glucose > 10 mmol/L
264
What is chronic pancreatitis?
Chronic inflammatory disease of the pancreas characterized by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain
265
What is the main cause of chronic pancreatitis?
Alcohol (80% of cases)
266
Other than alcohol, what are the causes of chronic pancreatitis?
1. Genetic: cystic fibrosis, haemochromatosis
2. Ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas
267
What are the features of chronic pancreatitis?
1. Pain: typically worse 15 to 30 minutes following a meal
2. Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
3. Diabetes mellitus develops in the majority of patients, typically occurs more than 20 years after pain begins
268
What are the investigations of chronic pancreatitis?
1. Abdominal x-ray shows pancreatic calcification in 30% of cases
2. CT is more sensitive at detecting pancreatic calcification
3. Functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
269
What is the best investigation for chronic pancreatitis?
CT: Sensitivity is 80%, specificity is 85% for pancreatic calcification
270
What is the management of chronic pancreatitis?
1.Pancreatic enzyme supplements
2. Analgesia
3. Treat DM
4. Antioxidants: limited evidence base - one study suggests benefit in early disease?
271
What are the complications of chronic pancreatitis?
1. Local: Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites
Important: pancreatic cancer
2. Systemic: Diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes and dependence on strong analgesics
272
What is the prognosis of chronic pancreatitis?
1. Difficult to predict as pain may improve, stabilise or worsen (generally, pain decreases or disappears over time, regardless of aetiology)
2. Surgery improves symptoms in 60–70% but results are often not sustained
3. Life expectancy can be reduced by 10–20 years
273
What is Peptic ulcer disease?
A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa, most commonly gastric and duodenal
274
What are the risk factors for Peptic ulcer disease?
1. Helicobacter pylori is associated with the majority of peptic ulcers:
a. 95% of duodenal ulcers
b. 75% of gastric ulcers
2. Drugs:
a. NSAIDs
b. SSRIs
c. corticosteroids
d. Bisphosphonates
275
What is the epidemiology of Peptic ulcer disease?
1. Common
2. More common in males
3. Duodenal ulcers have a mean age in 30s while gastric ulcers have a mean age in 50s
4. H. pylori is usually acquired in childhood
276
What type of peptic ulcer disease is more common?
Duodenal ulcers
277
What are the features of peptic ulcer disease?
1. Epigastric pain: depends on gastric (worsened by eating), or duodenal (worse when hungry, relieved by eating)
2. Nausea
278
What is the pattern of epigastric pain in gastric ulcers?
Epigastric pain worsened by eating
279
What is the pattern of epigastric pain in duodenal ulcers?
Epigastric pain when hungry, relieved by eating
280
How else can peptic ulcer disease present?
Complicated:
1. Acute bleeding
2. Perforation
281
What are the investigations for peptic ulcer disease?
1. History of drugs e.g. NSAID use
2. Helicobacter pylori should be tested for via either a Urea breath test or stool antigen test (first line)
282
What is the the management of uncomplicated peptic ulcer disease?
1.If Helicobacter pylori is negative then proton pump inhibitors (PPIs) should be given until the ulcer is healed
2. If Helicobacter pylori is positive then eradication therapy should be given:
a. PPI + amoxicillin + (clarithromycin OR metronidazole)
b. If penicillin-allergic: a PPI + metronidazole + clarithromycin
283
What is the most common complication of peptic ulcer disease?
Bleeding
284
What is the aetiology of acute bleeding in peptic ulcer disease?
The gastroduodenal artery can be the source of a significant gastrointestinal bleed
285
What is the main feature of acute bleeding secondary to peptic ulcer disease?
1. Haematemesis
2. Other features include:
melaena, hypotension, tachycardia
286
What are the investigations and management of acute bleeding secondary to peptic ulcer disease?
1. ABC approach as with any upper gastrointestinal haemorrhage
2. IV proton pump inhibitor
3. First line treatment: endoscopic intervention
4. If this fails (approximately 10% of patients) then either:
urgent interventional angiography with transarterial embolization or surgery
287
What is the first line management for acute bleeding secondary to peptic ulcer disease?
Endoscopic intervention
288
What is a less common complication of peptic ulcer disease?
Perforation:
1. Typically develops sudden epigastric pain, later becoming more generalised
2. Patients may describe syncope
289
What are the investigations of perforation secondary to peptic ulcer disease?
First: plain x-rays:
1. Upright ('erect') chest x-ray is usually required when a patient presents with acute upper abdominal pain
2. This is a useful test, as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm
290
What is the management of perforation secondary to peptic ulcer disease?
Acute:
a. Resuscitation if perforated or bleeding (IV colloids/crystalloids)
b. Close monitoring of vital signs
c. Proceed to endoscopic or surgical treatment: Truncal vagotomy (reduce acid production) and pyloroplasty (reconstruct the lining lost)
291
What is the prognosis of Peptic ulcer disease?
1. Overall lifetime risk is 10%
2. Generally good prognosis as peptic ulcers associated with H. pylori can be cured by eradication (or NSAID discontinuation)
3. With proton-pump inhibitor (PPI) therapy, duodenal ulcers typically heal within 4 weeks and gastric ulcers within 8 weeks
292
What is gastritis?
The histological presence of gastric mucosal inflammation
293
What are the two main causes of gastritis?
H. pylori and NSAID use (can be alcohol too)
294
What are the presenting symptoms/signs of Gastritis?
1. Dyspepsia (indigestion)/epigastric discomfort
2. Nausea and vomiting
3. Loss of appetite
4. Absence of malignancy features
295
What are the investigations for Gastritis?
§. Helicobacter pylori urea breath test or stool antigen: positive result if H pylori present
2. FBC: may show reduced Hb and HCT and increased MCV in autoimmune gastritis; leukocytosis in phlegmonous gastritis (caused by numerous bacterial agents)
3. Consider endoscopy:
a. For patients 60 years of age or older presenting with dyspepsia
b. Only on a case-by-case basis in younger patients with dyspepsia who have red flag features (weight loss, anaemia, dysphagia and persistent vomiting)
296
What is the management of Gastritis?
1. Helicobacter pylori gastritis:
a. Triple therapy for 1–2 weeks, PPI and two antibiotics (e.g. clarithromycin + amoxicillin, metronidazole + tetracycline)
2. Erosive gastritis:
a. Reducing exposure to the associated agent is essential e.g. alcohol and NSAID discontinuation
b. Symptomatic therapy with either H₂ antagonists or a PPI
297
What are Perineal abscesses and fistulae?
1. Perineal abscess: is a collection of pus resulting from an infection in the perineum
2. Perineal fistula: an abnormally chronically infected tract communication between the perineal skin and the anal canal or rectum
298
What is the aetiology of Perineal abscesses and fistulae?
1. Abscess: Bacterial infection
2. Fistulae are often a complication of an abscess
3. RF for fistulae:
a. IBD (especially Crohn's)
b. DM
c. Malignancy
299
What are the presenting symptoms of Perineal abscesses and fistulae?
1. Throbbing pain in the perineum
2. Intermittent discharge near the anal region (mucus or faecal)
3. PMH or FH of IBD
300
What are the signs of Perineal abscesses and fistulae on physical examination?
1. Localised tender perineal mass
2. Small skin lesion near the anus - opening of the fistula
3. On DRE: thickened area over the abscess or fistula may be felt
301
What is Goodsall's law regarding perineal fistulas?
Correlate the location of the internal fistula opening based on the location of the external fistula opening:
1. If external opening is anterior to anal canal, the fistula runs radially and directly into anal canal
2. If external opening lies posterior to the transverse anal line, it will follow a curved path and open internally in the posterior midline
302
What are the appropriate investigations for Perineal abscesses and fistulae?
1. Bloods:
a. FBC: leukocytosis
b. CRP/ESR: inflammation
2. Blood culture: positive for causative organism
3. Imaging: MRI
303
What is the management of Perineal abscesses and fistulae?
1. Medical: antibiotics
2. Surgical treatment:
a. Open drainage of abscess
b. Laying open if fistula, investigate via probe or dye
c. LOW fistula: fistulotomy, care taken to prevent damage to anal sphincter
d. HIGH fistula: seton- non-absorbable suture that is threaded through the fistula and allows drainage (fistulotomy would cause incontinence)
304
What are the complications of Perineal abscesses and fistulae?
1. Recurrence (high rate if abscess not completely excised)
2. Damage to internal anal sphincter
3. Incontinence
4. Persisting pain
305
What is Peritonitis?
1. Inflammation of the peritoneum usually caused by infection from bacteria or fungi
2. Left untreated, peritonitis can rapidly spread into the blood (sepsis) and to other organs, resulting in multiple organ failure and death
306
What is the aetiology of peritonitis?
The two main types:
1. Primary spontaneous peritonitis: an infection that develops in the peritoneum
2. Secondary peritonitis: usually develops when an injury or infection in the abdominal cavity allows infectious organisms into the peritoneum
307
What is the epidemiology of peritonitis?
1. Both types of peritonitis are life-threatening
2. The death rate from peritonitis depends on many factors, but can be as high as 40% in those who also have cirrhosis
308
What are the risk factors for primary spontaneous peritonitis?
1. Liver disease with cirrhosis: buildup of abdominal fluid (ascites) that can become infected
2. Kidney failure getting peritoneal dialysis
309
What are the causes for secondary peritonitis?
1. Ruptured appendix, diverticulum, or stomach ulcer
2. Digestive diseases such as Crohn’s disease and diverticulitis
3. Pancreatitis
4. Pelvic inflammatory disease
5. Perforations of the bowel, stomach, intestine, gallbladder, or appendix
6. Surgery/ trauma
310
What are the presenting symptoms of peritonitis?
1. Abdominal pain or tenderness
2. Rigors , fever
3. Not passing any urine (or passing less volume than usual)
4. Difficulty passing gas or having a bowel movement
5. Vomiting
6. May have ascites if SBP
311
What are the signs of peritonitis on physical examination?
1. Abdominal pain or tenderness
2. Signs of ascites:
a. flank dullness
b. shifting dullness
c. fluid wave, and auscultatory percussion
3. Signs of sepsis may be present:
a. Hypothermia
b. Hypotension
c. Tachycardia
312
What are the appropriate investigations for peritonitis?
1. Bloods:
a. FBC: leukocytosis, anaemia (if worsens may be a GI bleed)
b. Creatinine: elevated hepatorenal syndrome may be present
c. LFTs: May be useful in determining if patient has liver disease
d. Blood cultures: growth of causative organism
2. Paracentesis: analysis of peritoneal fluid for culture and neutrophil count
3. Imaging: CT scan
a. Demonstrate diffuse ascites
b. Can exclude pneumoperitoneum in patients with secondary peritonitis
313
What is the management for peritonitis?
1. Patients who appear otherwise well (no signs of sepsis, encephalopathy, or GI bleeding): started on oral antibiotics: quinolone or a cephalosporin such as cefixime, continue for 5 to 10 days
2. Patients who have signs of sepsis, encephalopathy, or GI bleeding: started on empirical broad-spectrum antibiotics e.g cephalosporin, ciprofloxacin
3. Surgery: necessary to remove infected tissue, treat the underlying cause of the infection, and prevent the infection from spreading, especially if peritonitis is due to a ruptured appendix, stomach or colon
314
What are the possible complications of peritonitis?
1. High risk of sepsis/septic shock
2.High risk of renal dysfunction/impairment
3. Medium risk of worsening ascites
315
What is spontaneous bacterial peritonitis?
A form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis
316
What are the features of spontaneous bacterial peritonitis?
1. Ascites
2. Abdominal pain
3. Fever
4. May be signs of sepsis
317
How is SBP diagnosed?
1. A to E approach
2. Bloods
3. Paracentesis
a. neutrophil count > 250 cells/ul
b. Culture: E. coli
318
What is the best investigation for SBP?
Paracentesis:
1. Neutrophil count > 250 cells/ul
2. Most common organism found on ascitic fluid culture is E. coli
319
What is the management of SBP?
IV cefotaxime is usually given
320
When should antibiotic prophylaxis be given to patients with acites secondary to liver cirrhosis?
1. Patients who have had an episode of SBP
2. Patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
3. NICE: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved'
321
What is a marker of poor prognosis of SBP?
Alcoholic liver disease
322
What is Pilonidal sinus disease?
A relatively common condition where sinuses and cysts form near the upper part of the natal cleft of the buttocks
323
What is the epidemiology of pilonidal disease?
More common in men and typically presents around the age of 20 years
324
What is the pathophysiology of pilonidal disease?
1. Thought to develop as a result of hair debris collecting in intergluteal pores that become stretched when a person sits or bends
2. Over a period of time, this may lead to sinus formation, with further hairs become trapped within the sinus
3. The opening of the sinus is lined by squamous epithelium, but most of its wall consists of granulation tissue
325
What are the clinical features of pilonidal disease?
1. Typically sinus presents when acute inflammation occurs, leading to an abscess:
a. pain (may be severe)
b. purulent discharge
c. fluctuant swelling at the site
2. Patients may describe cycles of being asymptomatic and periods of pain and discharge from the sinus
326
What is the management of asymptomatic pilonidal disease?
May be managed conservatively, with a focus on local hygiene
327
What is the management of symptomatic pilonidal disease?
1.If acute: then incision and drainage, allowing the wound to close by secondary intention
2. If chronic/recurrent: then surgical options including excision of the pits and obliteration of the underlying cavity
328
What is the prognosis of Pilonidal sinus?
1. Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%
2. Less likely to occur after healing by secondary intention
3. Small risk of pilonidal abscess or necrotising fascitis: presence of fever and toxaemia should raise suspicion for severe skin infection
329
What is ascites?
Tthe abnormal accumulation of fluid in the abdomen
330
How can the causes of ascites be grouped?
Serum-ascites albumin gradient (SAAG):
1. SAAG > 11g/L
(indicates portal hypertension)
2. SAAG <11g/L
331
What are the causes of serum ascites albumin gradient > 11g/L?
1. Liver disorders (most common cause):
a. cirrhosis/alcoholic liver disease
b. acute liver failure
c. liver metastases
2. Cardiac:
a. right heart failure
b. constrictive pericarditis
3. Other causes:
a. Budd-Chiari syndrome
b. portal vein thrombosis
332
What are the causes of serum ascites albumin gradient < 11g/L?
1. Hypoalbuminaemia:
a. nephrotic syndrome
b. severe malnutrition (e.g. Kwashiorkor)
2. Malignancy: peritoneal carcinomatosis
3. Infections: tuberculous peritonitis
4. Other causes:
a. pancreatitisis
b. bowel obstruction
c. biliary ascites
333
What is the general management of ascites?
1. Reducing dietary sodium
2. Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
3. Aldosterone antagonists: e.g. spironolactone
4. Drainage if tense ascites (therapeutic abdominal paracentesis)
5. Consider prophylactic antibiotics to prevent SBP
