Gastrointestinal emergencies Flashcards
1
Q
Cardiovascular causes of the acute abdomen?
A
- Acute coronary syndrome
- Acute mesenteric ischaemia
- Ruptured AAA
- Aortic dissection
2
Q
Gastrointestinal causes of the acute abdomen?
A
- GI tract perforation
- Mechanical bowel obstruction
- Acute appendicitis
- Peptic ulcer disease
- Diverticulitis
- Constipation
*
3
Q
Biliary and pancreatic causes of the acute abdomen?
A
- Acute pancreatitis
- Gallstones
- Acute cholecystitis
- Ascending cholangitis
4
Q
Genitourinary causes of the acute abdomen?
A
- Ruptured ectopic pregnancy
- Ovarian torsion
- Testicular torsion
- Acute pyelonephritis
- Kidney stones
5
Q
Presentation of ruptured AAA?
A
- Sudden, severe chest/abdominal pain, radiates to the back
- Hypotension/shock
- Pulsatile mass in abdomen
6
Q
Diagnosis of ruptured AAA?
A
- If the patient is unstable, diagnosis should not delay management.
- If the patient is hemodynamically stable, abdominal ultrasound can confirm diagnosis.
- CT/MR angiography can be used to localise rupture site and plan surgical management.
7
Q
Presentation of oesophageal rupture?
A
- Mackler’s triad:
- Vomiting and/or retching
- Severe retrosternal pain that radiates to the back
- Subcutaneous/mediastinal emphysema
- Crackling sound when auscultating mediastinal region (Hamann sign)
8
Q
What is Boerhaave syndrome?
A
- Transmural oesophageal rupture secondary to severe vomiting/coughing
- Risk factors include chronic cough, alcoholism, repeated episodes of vomiting
9
Q
Diagnosis of oesophageal rupture?
A
- Chest x-ray
- Widened mediastinum
- Pneumomediastinum
- Pleural effusion
- CT scan
- Same findings as CXR
10
Q
What is shown on this x-ray?
A
- Pneumomediastinum (shown in green)
- This patient has Boerhaave syndrome (oesophageal rupture)
11
Q
Management of oesophageal rupture?
A
- ABCDE approach
- Nil-by-mouth
- Broad-spectrum IV antibiotic prophylaxis
- Non-surgical (expectant) management:
- Small, contained perforation
- Surgical management:
- Haemodynamic instability or larger perforation
- Surgical closure of the rupture
12
Q
Complications of peptic ulcer disease?
A
- Gastrointestinal bleeding
- Gastric ulcers of the lesser curvature may cause bleeding from the left gastric artery
- Posterior duodenal arteries may cause bleeding from the gastroduodenal artery
- Perforation
13
Q
Presentation of a perforated peptic ulcer?
A
- Sudden, diffuse abdominal pain
- Peritonism (guarding and rebound/percussion tenderness)
- Fever, tachycardia, hypotension
- Shoulder-tip pain (irritation of the phrenic nerve)
14
Q
Diagnosis of a perforated peptic ulcer?
A
- Upright chest x-ray
- 75% will have free air under the diaphragm
- Diagnosis is usually clinical
15
Q
Management of a perforated peptic ulcer?
A
- ABCDE
- Fluid resuscitation
- Nil-by-mouth
- Surgical repair using a patch of omentum
16
Q
Presentation of GI perforation?
A
- Sudden-onset diffuse abdominal pain
- Constipation/obstipation
- Nausea/vomiting
- Peritonism
- Guarding, rebound tenderness
17
Q
Diagnosis of GI perforation?
A
- Chest x-ray:
- Free air under the diaphragm
- Patient must be sat upright
- Can be done quickly in A&E, with much lower radiation dose than an abdominal x-ray
- Abdominal x-ray:
- Pneumoperitoneum
- CT with contrast
- Most sensitive investigation
- Shows pneumoperitoneum
18
Q
What does this x-ray show?
A
Pneumoperitoneum (shown in green)
19
Q
Management of GI perforation?
A
- Supportive care
- Stable patient
- IV PPI
- Opioid analgesics (unless also bowel obstruction)
- Antiemetics
- Surgical management
- Most patients require an urgent exploratory laparotomy
20
Q
Commonest causes of small bowel obstruction?
A
- Bowel adhesions
- Commonest cause
- History of GI surgery
- Incarcerated hernias
- Second commonest cause
21
Q
Commonest causes of large bowel obstruction?
A
- Malignancy
- Commonest cause of LBO
- Diverticulitis
- Volvulus
22
Q
Presentation of mechanical bowel obstruction?
A
- Colicky abdominal pain
- Obstipation
- Abdominal distension
- Progressive nausea and (bilious) vomiting
- Tinkling bowel sounds
- History of abdominal surgery
23
Q
Diagnosis of mechanical bowel obstruction?
A
- Abdominal x-ray
- Distended loops of bowel proximal to the obstruction
- Air-fluid levels
- CT abdomen with contrast
- Similar findings
- Transition point at site of obstruction
24
Q
How to differentiate between SBO and LBO?
A
- The folds in the bowel on AXR
- Small bowel folds (valvulae conniventes) = visible across the whole width of the bowel
- Large bowel folds (haustra) = don’t completely transverse the bowel
- Rule of thumb - haustra can sometimes appear to cross the full width of the large bowel.
- The anatomical position of the distended bowel loops
- The history
- SBO = early vomiting, late obstipation
- LBO = early obstipation, late vomiting
25
Q
What is the 3/6/9 rule?
A
- Upper limits of normal for the diameter of bowel segments are as follows:
- Small bowel = 3cm
- Large bowel = 6cm
- Caecum = 9cm
26
Q
Management of mechanical bowel obstruction?
A
- Nil-by-mouth
- “Drip and suck”
- IV fluids
- Nasogastric tube decompression
- Most will require surgical management
27
Q
Causes of paralytic ileus (functional bowel obstruction)
A
- Intraabdominal surgery
- Intraabdominal infection/inflammation
- Medications (e.g. anticholinergics, opioids)
- Hypokalaemia
- Sepsis
The 5 P’s: Peritonitis, Postoperative, low Potassium, Painkillers (opioids), Pelvic/spinal fractures are some of the common causes
28
Q
Presentation of paralytic ileus?
A
- Constipation and reduced flatulence
- Continuous (non-colicky) abdominal pain
- Abdominal distention
- Nausea and vomiting
- Decreased or absent bowel sounds
29
Q
Diagnosis of paralytic ileus?
A
- CT abdomen
- Gold standard
- Diffuse small and/or large bowel distention
- Abdominal x-ray
- Less sensitive than CT
- Same findings as CT
- Abdominal ultrasound
- Not routinely used in adults, but is the investigation of choice in children
30
Q
Management of paralytic ileus?
A
- Nil-by-mouth
- “Drip and suck”
- IV fluids
- NG tube decompression
- Correct underlying cause if possible
- Avoid opiate analgesia
31
Q
Presentation of acute appendicitis?
A
- Abdominal pain
- Initially central/diffuse
- Eventually localises to RIF
- Fever
- Tachycardia
- Nausea/anorexia
Examination
- Rosving’s sign - palpation of LIF causes RIF pain
- Psoas sign - extension of right leg (in L lateral position) causes RIF pain
32
Q
Diagnosis of acute appendicitis?
A
- FBC
- Neutrophilic leukocytosis
- Abdominal ultrasound
- Distended, aperistaltic appendix
- Abdominal CT scan
- Periappendiceal fat stranding
- Distended appendix
33
Q
Management of acute appendicitis?
A
- Laparoscopic appendicectomy
- Prophylactic IV antibiotics
- If the appendix has perforated then patients will need a peritoneal lavage
34
Q
Causes of intussusception?
A
- No identifiable cause in 75%
- Meckel’s diverticulum (commonest cause found in children)
- Polyps/malignancy (commonest cause found in adults)
- Enlarged Peyer’s patches
- Lymphoid patches on the wall of the ileum
- Can become hypertrophied after infection/vaccination
35
Q
Presentation of intussusception?
A
- Acute colicky abdominal pain
- Infants often draw legs up during episodes
- Sausage-shaped RUQ mass
- Vomiting
- “Redcurrant jelly” stools (due to PR bleeding)
36
Q
Diagnosis of intussusception?
A
- Abdominal ultrasound (best initial investigation)
- Target sign - telescoping section of bowel appears as rings on a target
- Contrast enema with ultrasound/fluoroscopy (best confirmatory test)
- Abdominal CT
- Used if the diagnosis is equivocal after ultrasound and AXR
37
Q
Management of intussusception?
A
- NGT decompression and fluid resuscitation if needed
- Non-surgical
- Air enema is the treatment of choice
- Surgical management
- Indicated if the patient is unstable (e.g. perforation) or if a pathological lead point is suspected (e.g. malignancy)
38
Q
Presentation of acute mesenteric ischaemia?
A
- Age > 60, VTE risk factors (usually have AF).
- Severe pain out of proportion to examination findings (often normal BP, HR etc.)
- Diffuse abdo pain and distension
- Nausea and vomiting
39
Q
Diagnosis of acute mesenteric ischaemia?
A
- Lactic acidosis
- Abdominal x-ray: normal early on, progressing to pneumatosis (gas in the walls of the intestines).
- CT angiography gold standard
40
Q
Management of acute mesenteric ischaemia?
A
- ABCDE
- NGT decompression
- IV fluid resuscitation
- Prophylactic IV antibiotics
- Emergency laparotomy and resection of necrotic bowel preferred in most
- If the patient is stable revascularization may be attempted
- Optimise AF treatment if appropriate to reduce the risk of recurrence
41
Q
Types of volvulus and malrotation?
A
- Sigmoid colon - commoner in the elderly
- Caecal volvulus - commoner in 40-60 year-olds
- Midgut volvulus and malrotation - commoner in children
42
Q
Presentation of volvulus?
A
- Abdominal pain
- Episodic
- Relieved by the explosive passage of stool/gas
- Distension
- Vomiting & constipation
- Peritonitis if the bowel perforates
43
Q
Diagnosis of volvulus?
A
- Abdominal x-ray
- Sigmoid volvulus: large bowel obstruction with ‘coffee bean sign’
- Caecal volvulus: small bowel obstruction
44
Q
What is shown on this x-ray?
A
Sigmoid volvulus with the coffee bean sign
45
Q
Management of volvulus?
A
- Sigmoid volvulus
- Rigid/flexible endoscopic decompression, detorsion, and reduction
- Surgery if bowel perforates
- Caecal volvulus
- Typically requires surgical management
- Right hemicolectomy is often needed
46
Q
What is acute megacolon?
A
- Imbalance in parasympathetic and sympathetic nervous system → progressive abdominal distention
- Often occurs in seriously ill patients who have undergone major surgery
47
Q
Management of acute megacolon?
A
- Supportive measures
- NGT decompression
- Nil-by-mouth
- IV fluids
- Neostigmine
- Surgery
- Indicated if conservative measures fail
48
Q
What is toxic megacolon?
A
- A form of megacolon occurring as a result of infective/inflammatory colitis
- Commonly secondary to C. difficile infection
- May also occur secondary to IBD
49
Q
Presentation of toxic megacolon?
A
- Bloody diarrhoea
- Vomiting
- Abdominal distention and pain
- Signs of sepsis
50
Q
Diagnosis of toxic megacolon?
A
- Abdominal x-ray
- Dilated colon
- Loss of haustration
- Multiple air-fluid levels
51
Q
Management of toxic megacolon?
A
- Supportive care
- Will likely need escalating to HDU/ICU
- Nil-by-mouth
- NGT
- IV fluid
- Surgery
- If no improvement within 24-72 hours or the development of complications
52
Q
Presentation of a strangulated abdominal hernia?
A
- Acute abdominal pain localising to the site of the hernia
- Features of bowel obstruction (if bowel is part of hernial contents)
- Tender, irreducible hernia
- Toxic appearance, fever, signs of sepsis
53
Q
Management of a strangulated abdominal hernia?
A
- ABCDE and resuscitation
- Surgical hernia repair
- Do not attempt manual reduction as this can cause generalised peritonitis
54
Q
Presentation of acute cholecystitis?
A
- Right upper quadrant pain
- Typically more severe and prolonged (> 6hrs) than biliary colic
- Positive Murphy’s sign
- Sudden pausing during inspiration on deep palpation of the RUQ due to pain.
- Fever, anorexia
- Guarding
55
Q
Diagnosis of acute cholecystitis?
A
- Blood tests to support clinical diagnosis
- Raised WCC and CRP
- LFTs - transaminitis
- RUQ ultrasound scan if the diagnosis is uncertain
- Shows gallbladder wall thickening
56
Q
Management of acute cholecystitis?
A
- Elective laparoscopic cholecystectomy (within 1 week)
- Prophylactic IV antibiotics
57
Q
Pathophysiology of acute cholecystitis?
A
- Biliary tract obstruction → bile stasis → ascending bacterial infection
- May be iatrogenic through the introduction of GI contents into bile ducts e.g. ERCP, biliary stenting, or liver transplantation
58
Q
Presentation of ascending cholangitis?
A
- Charcot’s triad (present in up to 70%)
- RUQ pain
- Jaundice
- Fever
- Reynold’s pentad
- Charcot’s triad
- Mental status changes
- Hypotension
59
Q
Diagnosis of ascending cholangitis?
A
- Laboratory tests to confirm clinical diagnosis
- FBC → raised WCC
- CRP → raised
- LFT → cholestasis (raised ALP, bilirubin, GGT, ALT)
- RUQ ultrasound scan if diagnosis is uncertain
- Shows dilated common bile duct
60
Q
Management of ascending cholangitis?
A
- IV antibiotics
- ERCP after 24-48 hrs to relieve any obstruction
61
Q
Risk factors for spontaneous bacterial peritonitis?
A
- Liver disease and ascites
- Upper GI bleeding
- Previous SBP
62
Q
Presentation of spontaneous bacterial peritonitis?
A
- Diffuse abdominal pain and tenderness
- Fever and rigors
- Worsening ascites
- New-onset or worsening encephalopathy
63
Q
Diagnosis of spontaneous bacterial peritonitis?
A
- Paracentesis and M, C & S of ascitic fluid
- Commonest organism found is E. coli
64
Q
Management of spontaneous bacterial peritonitis?
A
- IV antibiotics (usually cefotaxime)
- Antibiotic prophylaxis is given if a patient with ascites:
- Has had a previous episode of SBP
- Has fluid protein < 15g/L
65
Q
Causes of acute pancreatitis?
A
I GET SMASHED
- I - iatrogenic
- G - gallstones
- E - ethanol (alcohol intoxication)
- T - trauma
- S - steroids
- M - mumps
- A - autoimmune
- S - scorpion venom
- H - hyperlipidaemia, hypercalcaemia
- E - ERCP
- D - drugs (e.g. azathioprine, loop diuretics, anticonvulsants)
66
Q
Clinical features of acute pancreatitis?
A
- Constant, severe epigastric pain
- Classically radiates to the back
- Nausea, vomiting
- Fever
- Signs of shock: hypotension, tachycardia, oliguria/anuria
- Cullen’s sign - periumbilical bruising
- Gray-Turner’s sign - flank bruising
67
Q
Diagnosis of acute pancreatitis?
A
- Early ultrasound scan important to assess whether gallstones are involved as this affects management
- Serum markers to aid clinical diagnosis
- Serum amylase raised in 75% of patients
- Serum lipase - longer half-life so may be useful for later presentation
68
Q
What scoring system is used to assess severity?
A
Glasgow score
69
Q
Management of acute pancreatitis?
A
- Aggressive fluid resuscitation
- Analgesia - IV opioids
- Don’t need to be nil-by-mouth unless they are vomiting
- Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
- Patients with biliary obstruction should undergo early ERCP
70
Q
What scoring system is used to assess acute upper GI bleeding?
A
The Glasgow-Blatchford scale. Variables included are:
- Urea
- Haemoglobin
- Systolic BP
- The presence of:
- Syncope
- Malaena
- Tachycardia
- Hepatic failure
- Cardiac failure
A score of 0 indicates a patient can be considered for early discharge
71
Q
Resuscitation of a patient with an acute upper GI bleed?
A
- ABCDE
- Wide-bore IV access (e.g. 2 x grey cannulas)
- Platelet transfusion
- Actively bleeding and platelets < 50 x 109
- Fresh frozen plasma
- Fibrinogen < 1g/L
- APTT or PT > 1.5 x normal
- Prothrombin complex concentrate
- Taking warfarin and bleeding
72
Q
Investigation of patients with acute upper GI bleeding?
A
- Upper GI endoscopy
- Should be offered immediately after resuscitation if severe bleeding
- All patients should have endoscopy within 24 hours
73
Q
Management of variceal bleeding?
A
- Terlipressin and prophylactic antibiotics should be given at presentation
- Before endoscopy if known history of varices
- Elastic band ligation of oesophageal varices is first line
- If vessels can’t be visualised (too much blood) or elastic band ligation fails to control bleeding, a Sengstaken-Blakemore tube can be inserted
- Expands against the walls of the oesophagus and physically tamponades the vessels
- Mustn’t be left in longer than 2 days as can cause oesophageal necrosis
- Definitive management of varices is a transjugular intrahepatic portosystemic shunt (TIPS) procedure that relieves backpressure in the portal vein.
74
Q
Management of non-variceal bleeding?
A
- Endoscopy to look for cause
- IV PPIs
- Only given after endoscopy if confirmed non-variceal bleed
75
Q
Priorities in assessment and management of a lower GI bleed?
A
- Consider (and exclude by urgent endoscopy) an upper GI source of bleeding
- Urgent involvement of surgical teams if there is major blood loss and/or haemodynamic instability
- Consider and correct clotting abnormalities
- Consider reversing anticoagulation
-
Blood transfusion
- Transfuse when Hb < 80g/L if bleeding has stopped
- Threshold is Hb < 100g/L if ongoing bleeding
-
Admit or discharge?
- Minor lower GI bleeding that stops spontaneously → early outpatient sigmoidoscopy
- Admit if moderate/severe bleeding or significant comorbidities
76
Q
Investigation of a suspected acute flare-up of IBD?
A
- Abdominal x-ray to rule-out toxic dilatation (megacolon) or proximal constipation
- Blood tests:
- FBC
- CRP (raised in 90%)
- In patients with normal CRP platelets can be a marker of disease severity
- U&Es
- Dehydration indicates late presentation and a severe flare
- Stool sample
- Infection can trigger flares
- Rule-out C. difficile → pseudomembranous colitis
77
Q
Management of an acute flare-up of ulcerative colitis?
A
- Drug therapy
- Oral prednisolone (poorly absorbed in severe flare → IV hydrocortisone)
- Ciclosporin/infliximab if poor response to steroids
- Surgery
- If medical management fails
- Crohn’s disease must be definitively ruled-out
- Colectomy/hemicolectomy depending on how diffuse the illness is
78
Q
Management of an acute flare-up of Crohn’s disease?
A
- Drug management
- Glucocorticoids (PO or IV) are first-line to induce remission
- Azathioprine or mercaptopurine may be used second-line
- TPMT levels must be measured before starting these
- Methotrexate is an alternative second-line drug
- Infliximab can be used in refractory cases
- Surgical management
- Reserved for when medical management fails
- Recurrence within one year in 80% of cases
- Aims to remove as little of the gut as possible
- May end up with a short gut/ileostomy
79
Q
Causes of acute liver failure?
A
- Hepatotoxic substances
- Drugs: paracetamol
- Alcohol
- Cocaine (causes vasoconstriction → hepatic hypoperfusion)
- Infections
- Hepatitis A, B, E (or superinfection with B & D)
- Vascular
- Budd-Chiari syndrome (hepatic vein thrombosis)
- Pregnancy-related
- HELLP syndrome, acute fatty liver of pregnancy
- Autoimmune hepatitis
80
Q
Clinical features of acute liver failure?
A
- Hepatic encephalopathy
- Altered consciousness
- Asterixis
- Jaundice
- Pruritis
- Abdominal pain
- Nausea and vomiting
- Anorexia
81
Q
Definition of acute liver failure?
A
ALF is defined as:
- Severe acute liver injury
- Encephalopathy
- Impaired liver synthetic function (prothrombin time/international normalized ratio 1.5)
- In the absence of pre-existing liver disease
82
Q
Investigation of suspected acute liver failure?
A
- Detailed drug history (including any herbal and over-the-counter medications) from the patient or family members
- If ALF is suspected to be due to paracetamol poisoning start NAC without delay
- Arrange urgent investigations:
- PT, APTT, INR
- FBC
- Blood glucose
- U&Es - ?hepatorenal syndrome
- LFT
- ABG if reduced consciousness
- Culture and microscopy of ascitic fluid
- Liver ultrasound
83
Q
Management of acute liver failure
A
- Seek hepatology advice
- Escalate to HDU (or ITU if encephalopathy is severe)
- Manage complications (e.g. AKI, sepsis, SBP)
- Liver transplantation
- Indications vary depending on pathology
- Generally require deranged INR (> 6.5)
84
Q
What is decompensated liver disease?
A
- Background of chronic liver disease
- Acute hepatic decompensation → liver failure
- Jaundice
- Prolongation of the prothrombin time/international normalized ratio
- Extrahepatic organ failure
85
Q
Management of decompensated chronic liver disease?
A
- Fluid and electrolyte balance
- Thromboprophylaxis - LMWH
- Increased risk of thromboembolism despite prolonged PT/APTT
- Drugs
- IV vitamin K & oral folic acid once daily
- Avoid opioids and sedatives
- Nutritional support
86
Q
What is hepatorenal syndrome?
A
- AKI in the context of acute, severe liver failure when other causes of AKI have been excluded
- Low albumin → low oncotic pressure → ascites → hypovolemia → renal hypoperfusion → activation of RAA system → renal artery constriction → further renal hypoperfusion and AKI
87
Q
LFT results in alcoholic hepatitis?
A
- Gamma-GT characteristically raised (Gin and Tonic → gGT raised in ALD)
- Transaminitis
- AST:ALT normally > 2, ratio > 3 → suggests severe alcoholic hepatitis
88
Q
Management of alcoholic hepatitis?
A
- Supportive care (e.g. nutritional support, fluid balance etc.)
- Glucocorticoids is sometimes beneficial
- “Discriminant function” is a score used to determine this
- Calculation involves PT and bilirubin levels
- Improves symptoms but increases the risk of infection and doesn’t improve prognosis
- Pentoxyphylline sometime used
89
Q
Clinical features of hepatic encephalopathy?
A
- Confusion, altered GCS
- Asterixis - “liver flap”
- Apraxia (e.g. can’t draw a 5-pointed star)
- Likely jaundiced
90
Q
Investigation and diagnosis of hepatic encephalopathy?
A
- Investigations
- Check for infection (e.g. FBC)
- Abdominal x-ray (?constipation)
- PR examination & stool sample (?GI bleed)
- EEG
- Diagnosis
- Usually clinical diagnosis, investigations help identify precipitating factor
91
Q
Grading of hepatic encephalopathy?
A
- Irritability
- Confusion, inappropriate behaviour
- Incoherent, restless
- Coma
92
Q
Management of hepatic encephalopathy?
A
- Lactulose 1st line - increases GI clearance of ammonia, decreasing absorption
- Rifaximin - antibiotic that alters gut fauna, decreasing ammonia production
- Liver transplantation if the above fail
93
Q
What is Budd-Chiari syndrome?
A
- Hepatic vein thrombosis
- Causes triad of symptoms:
- Abdominal pain: sudden onset, severe
- Ascites → abdominal distension
- Tender hepatomegaly
94
Q
Diagnosis of Budd-Chiari syndrome?
A
Ultrasound with doppler flow studies
