Exam revision Flashcards
What is a TIA?
TIA is defined as transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction. It is a medical emergency
What is is risk of a patient developing stroke following a TIA?
within the first week following a TIA, the risk of stroke is up to 10%. The estimated incidence of TIA within the UK is 50 per 100,000 people per year.
What is the diagnostic criteria for TIA?
Traditionally, transient neurological dysfunction with resolution within 24 hours was diagnostic of TIA. However, up to a third of patients whose symptoms have resolved within 24 hours have evidence of infarction on imaging. Consequently, the definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.
What is the aetiology of TIA?
TIA is caused by temporary blockage to blood flow, which leads to ischaemia.
Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.
Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell). Listen for bruits
Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease. valve disease prosthetic valves
Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.
Hyperviscosity-polycythemia,sickle cell,myeloma
Vasculitis-SLE,PAN,syphilis
During a TIA, there is a transient reduction in blood flow to an area of cerebral tissue that causes neurological symptoms. TIA commonly occurs secondary to embolisation from atrial fibrillation or carotid artery disease.
What are the risk factors for TIA?
TIA is a cardiovascular disease, and as such, it shares many common risk factors with conditions such as ischaemic heart disease and peripheral vascular disease.
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity Atrial fibrillation Carotid artery disease Age Thrombophilic disorders (e.g. antiphospholipid syndrome) Sickle cell disease Family history
How does TIA present?
A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.
Neurological deficit
Unilateral weakness or sensory loss
Dysphasia
Ataxia, vertigo, or incoordination
Amaurosis fugax: see below
Homonymous hemianopia: visual field loss on the same side of both eyes
Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits
What are the differentials for amaurosis fugax
Amaurosis fugax
This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.
The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.
How can TIA be diagnosed?
Diagnosis
Any patient with ongoing symptoms requires urgent referral to a stroke unit.
TIA is a clinical diagnosis based on the history as the majority of patients will have complete resolution of symptoms. Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
Key aspects to making the diagnosis of TIA include:
Onset & duration of symptoms: collateral history may be needed
Associated symptoms (suggest alternative diagnosis): headache, vomiting, syncope, seizures
Neurological deficit: see clinical features
Cardiovascular risk factors: hypertension, diabetes, smoking, high cholesterol, family history
Co-morbidities: heart disease, atrial fibrillation, carotid disease, previous stroke/TIA
Anticoagulation history
Clinical examination: cardiovascular exam including BP, neurological examination, fundoscopy
NOTE: patients on anticoagulation with new neurological deficits require urgent admission and exclusion of intracerebral bleeding
The Face Arm Speech Time Test (FAST test)
A rapid diagnostic screen to assess for features of TIA/stroke used in the community. Anyone with a positive screen should be assessed urgently at a stroke unit. The test is positive if any of the following are met:
New facial weakness
New arm weakness
New speech difficulty
What are the differentials for TIA and
Numerous conditions can present similarly to TIA, which are collectively referred to as ‘stroke mimics’.
Toxic/metabolic: hypoglycaemia, drug and alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, consider causes of syncope
When would you refer patient with TIA?
All patients with a suspected TIA should be referred to a specialist TIA clinic and be seen within 24 hours.
At the TIA clinic, patients should have a comprehensive medical assessment including blood tests, electrocardiogram (ECG) and imaging. If the episode occurred > 1 week ago, the assessment should be within 7 days.
The ABCD2 is a prognostic score that was traditionally used to identify people at high risk of stroke after a TIA score. It was originally used to triage the urgency of TIA referrals and treatment with aspirin. NICE no longer recommend its use.
What investigations are done for TIA?
Investigations
MRI is the key investigation in a patient with suspected TIA.
Bloods
Haematology: full blood count (FBC), HbA1c +/- haemoglobin electrophoresis
Routine biochemistry: Urea & electrolytes (U&Es), bone profile, liver function tests (LFTs), lipid profile
Coagulation: routine clotting
Special (as indicated): ‘young stroke screen’ (e.g. thrombophilia screen, Fabry’s)
Cardiac investigations
ECG: assessment for arrhythmias, especially atrial fibrillation
Echo: not routinely offered unless suspicion of heart disease or confirmed stroke
Imaging
MRI head with diffusion-weighted imaging (DWI): preferred to CT unless alternative diagnosis suspected that CT could detect. Enables detection of small infarcts.
Carotid dopplers: all patients who are candidates for carotid endarterectomy.
When is urgent admission warranted?
Certain features warrant urgent admission to hospital because of the high risk of stroke, bleeding or deterioration.
≥1 suspected TIA (crescendo TIA): typically within the last 7 days
Suspected cardioembolic source or severe carotid stenosis
Vulnerable patient: lack of reliable observer at home to monitor for worsening symptoms
Bleeding disorder or taking an anticoagulant
Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
ABCD2 SCORE 4 HIGH RISK,greater than 6 very high risk
How can TIA be managed?
Management
Any patient with a suspected TIA should be treated with 300 mg of aspirin unless contraindicated.
The management of TIA can be divided into acute treatment, secondary prevention and lifestyle measures.
Acute treatment
The principle management for TIA is 300 mg of aspirin that is usually continued for two weeks. This is followed by treatment with 75 mg of clopidogrel as long-term vascular prevention.
Patients with atrial fibrillation or significant carotid artery disease require a different treatment pathway.
Atrial fibrillation (AF): should be offered and counselled about starting an oral anticoagulant
Carotid artery disease (CAD): urgent referral for consideration of carotid endarterectomy if significant disease. Based on NASCET or ECST criteria for stenosis.
NASCET: 50-99% stenosis
ECST: 70-99% stenosis
Secondary prevention
Patients with a TIA should be offered secondary prevention treatments to optimise their cardiovascular risk
Anti-hypertensives: as per hypertension guidelines (tolerate higher if significant bilateral CAD)
Lipid modification: offer high-dose statin therapy unless contraindication.
Diabetic control: treat any new diagnosis of diabetes and optimise control of pre-existing disease
Obstructive sleep apnoea: referral to specialist sleep medicine/respiratory clinic if suspected
Pre-menopause: use of combined oral contraceptive pill contraindicated.
Lifestyle measures
Basic advice on physical activity, smoking cessation, diet optimisation and alcohol intake should be given to all patients
What is recommended for driving with TIA?
Driving
It is vital to advise all patients to stop driving if they have had a suspected, or confirmed, TIA.
Patients should always be advised to check the DVLA for the most up to date recommendations on driving.
Cars and motorcycles: stop driving one month, do not need to inform DVLA Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
When should aspirin not be given?
Immediate antithrombotic therapy:
give aspirin 300 mg immediately, unless
1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team
When should carotid endarterectomy be done in TIA?
With regards to carotid artery endarterectomy:
recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
should only be considered if carotid stenosis > 70% according ECST* criteria or > 50% according to NASCET** criteria
within 2 weeks
What is aspirin is contraindicated?
aspirin 75mg od with dipyridamole
What are the most common sites of crescendo attacks?
critical intracranial stenosis-superior division of MCA
What are the stroke mimics?
Differential diagnosis
M8S:
Migraine
Sugar: hypoglycaemia.
Seizures, especially Todd’s palsy.
Sepsis, encephalitis.
Syncope
SDH
Space occupying lesion.
OldStrokes with intercurrent illness.
Somatisation
Where is asbestos found?and how can it affect the lung?
Asbestos widely used to construct ceiling, walls and flooring of houses/ buildings
Provide insulation and fire protection
Latency period
Several years before pleural thickening develops
>20 years for fibrosis & plaque
Asbestos is a fibre-like material that was once used in buildings for insulation, flooring and roofing. Its use has been fully banned in the UK since 1999.
While asbestos can be dangerous, it’s not harmful if left alone. But if material containing asbestos is damaged, it can release a fine dust that contains asbestos fibres.
When the dust is breathed in, the asbestos fibres enter the lungs and can gradually damage them over time.
What are the different lung presentations of asbestos?
Asbestos can cause a variety of lung disease from benign pleural plaques to mesothelioma.
Pleural plaques
Pleural plaques are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis. As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
Lung cancer
Asbestos exposure is a risk factor for lung cancer and also has a synergistic effect with cigarette smoke.
What is asbestosis?
Asbestosis is a diffuse interstitial lung fibrosis that manifests in patients with pleural plaque disease ≥10 years following exposure to asbestos.
What are the CXR findings for asbestosis?
Takes >10 years for radiographic changes to develop
Small, irregular, oval opacities
Diffuse interstitial fibrosis
“Shaggy heart border” sign
Cardiac silhouette ill-defined on chest radiograph
Implies pleural disease on mediastinal interface
How can asbestosis be diagnosed?symptoms,signs,examination and investigation findings?
History of asbestos exposure, typically 20 or more years prior
Symptoms: dyspnoea, cough
Signs: crepitations on auscultation, finger clubbing, cyanosis, reduced chest expansion
Chest x-ray: linear interstitial fibrosis, pleural plaques, pleural thickening, atelectasis
Pulmonary function tests: may be normal or show a restrictive pattern (reduced forced vital capacity (FVC) and total lung capacity (TLC) with a normal FEV1/FVC ratio) or obstructive pattern (reduced FEV1).
High resolution CT: pleural thickening, pleural plaques
Bronchoscopy + biopsy: limited use as normally cannot sample enough tissue for a diagnosis
Open lung biopsy: for definitive diagnosis if cancer is suspected
How can asbestosis be managed?
Management
Smoking cessation Pulmonary rehabilitation Bronchodilators Oxygen therapy if SpO2 ≤89% Lung transplant If a death occurs due to asbestosis, this must be reported to the coroner Compensation
see a GP to have the flu vaccination and the pneumococcal vaccination – your lungs will be more vulnerable to infections like flu and pneumonia
How to get compensation?
Patients who develop asbestos related lung disease following occupational exposure may be eligible to claim compensation
If you’ve been diagnosed with asbestosis, you may be able to claim compensation through:
industrial injuries disablement benefit
a civil claim for compensation against previous employers
a claim for governmental compensation under the Pneumoconiosis etc. (Workers’ Compensation) Act 1979
Find out about industrial injuries disablement benefit on GOV.UK. You can also get advice on benefits and compensation on the British Lung Foundation website.
Support for people with asbestosis
Asbestosis can have a big impact on your life, but help is available. Support services include:
Asbestos Victims Support Groups Forum
British Lung Foundation – helpline 03000 030 555
Cancer Research UK: mesothelioma – helpline 0808 800 4040
Mesothelioma UK – helpline 0800 169 2409
What are the complications of asbestosis?
People with asbestosis also have a higher risk of developing other serious conditions, such as:
pleural disease – thickening of the lining covering the lungs (pleura)
mesothelioma – cancer that affects the lining of the lungs, tummy, heart or testicles
lung cancer
What are the different types of gall stones?
Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation.
Gallstones form as a result of supersaturation of the bile. There are three main types of gallstones:
Cholesterol stones – composed purely of cholesterol, from excess cholesterol production
There is a well recognised link between poor diet, obesity, and cholesterol stones
Pigment stones – composed purely of bile pigments, from excess bile pigments production
Commonly seen in those with known haemolytic anaemia
Mixed stones – comprised of both cholesterol and bile pigments
What are the risk factors for gall stones?
Classically the common risk factors for gallstone disease are colloquially described as the “5 F’s”: Fat, Female, Fertile, Forty, and Family history.
Other recognised risk factors include pregnancy and oral contraceptives*, haemolytic anaemia (specifically for pigment stones), and malabsorption (such as previous ileal resection or Crohn’s disease).
*Oestrogen causes more cholesterol to be secreted into bile
How to differentiate biliary colic and acute cholecystitis?
Biliary Colic
Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain.
The pain is typically sudden, dull, and colicky in nature. It is often focused in the right upper quadrant although it may radiate to the epigastrium and/or back. The pain may be precipitated by the consumption of fatty foods* and the patient often complains of nausea / vomiting. In general, once pain relief has been started, symptoms often settle quickly.
*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.
Acute Cholecystitis
Patients with acute cholecystitis will report a constant pain in the RUQ or epigastrium, associated with signs of inflammation, such as fever or lethargy.
Patients with acute cholecystitis will be tender in the RUQ and may demonstrate a positive Murphy’s sign. Ensure to check for any guarding (may suggest a gallbladder perforation) and for features of sepsis.
What is Murphy’s sign?
Murphy’s Sign
Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder. This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.
What. are the differentials for RUQ pain?
There are a wide variety of pathologies that can present with RUQ pain. However, differentials to consider include gastro-oesophageal reflux disease, peptic ulcer disease, acute pancreatitis, or inflammatory bowel disease.
How can RUQ be investigated in suspected biliary colic?
Laboratory Test
Certain blood tests can help in the initial evaluation of suspected cases:
FBC and CRP – assess for the presence of any inflammatory response, which will be raised in cholecystitis
LFTs – biliary colic and acute cholecystitis are likely to show a raised ALP (indicating ductal occlusion), yet ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome, discussed below)
Amylase (or lipase) – to check for any evidence of pancreatitis
A urinalysis, including a pregnancy test if relevant, should be performed to exclude any renal or tubo-ovarian pathology.
What imaging techniques are used in biliary colic?
Imaging
A trans-abdominal ultrasound (Fig. 2) is one of the most sensitive modalities for visualising gallstone disease and is typically used first line to investigate suspected gallstone pathology.
Three specific areas are often visualised on US:
The presence of gallstones or sludge (the start of gallstone formation)
Gallbladder wall thickness (if thick walled, then inflammation is likely)
Bile duct dilatation (indicates a possible stone in the distal bile ducts)
If results from US scans are inconclusive, further imaging options are available. The gold standard investigation* for gallstones is Magnetic Resonance Cholangiopancreatography (MRCP), largely replacing ERCP for diagnostic purposes (Fig. 3). MRCP can show potential defects in the biliary tree caused by gallstone disease, with a sensitivity approaching 100%.
How can biliary colic be managed?
Biliary Colic
Patients with biliary colic should be prescribed analgesia (regular paracetamol +/- NSAIDs +/- opiates analgesia).
The patient should be advised about lifestyle factors that may help control symptoms (and help with future surgery), such as a low fat diet, weight loss, and increasing exercise.
Following first presentation of biliary colic, there is a high chance of symptom recurrence or the development of complications of gallstones, therefore an elective laparoscopic cholecystectomy* (Fig. 4) is warranted and should be offered within 6 weeks of first presentation.
*The laparoscopic route is preferred for cholecystectomy but is not always possible
By User:Pschemp [CC-BY-SA-3.0], via Wikimedia Commons
How can acute cholecystitis be managed?
Acute Cholecystitis
Patients with acute cholecystitis should be started on appropriate intravenous antibiotics (such as co-amoxiclav +/- metronidazole). Concurrent analgesia and antiemetics should also be prescribed.
A laparoscopic cholecystectomy is indicated within 1 week of presentation, as per NICE guidance, however this ideally should be done within 72hrs of presentation for a likely simpler procedure*.
For those not fit for surgery and not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection (although as the gallstones remain in-situ, the risk of recurring disease remains).
*A Cochrane review previously demonstrated that earlier cholecystectomies are safe and reduce overall hospital stay
Any patient readmitted with RUQ pain post-cholecystectomy, it is important to exclude a retained CBD stone post-operatively. US abdomen scan may be useful, yet if this is unremarkable, then further investigation via MRCP imaging is warranted.
What are the complications of gallstones?
Mirizzi Syndrome
A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.
This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy.
Gallbladder Empyema
A gallbladder empyema is when the gallbladder becomes filled with pus (Fig. 6). Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis. They are associated with significant morbidity and mortality.
The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy* (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).
*There is a higher rate of conversion to open cholecystectomy with emypema than with uncomplicated acute cholecystitis
Chronic Cholecystitis
Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall. Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting.
It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy. Its main complications are gallbladder carcinoma and biliary-enteric fistula.
Bouveret’s Syndrome and Gallstone Ileus
Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel (Fig. 7), termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)
As a consequence, bowel obstruction can occur:
Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone Ileus*– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction
*The term ileus is misleading, as it is actually a bowel obstruction
By Thomas Newman, TeachMeSurgery [CC-BY-NC-ND 4.0]
How does fatty food trigger biliary colic?
*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.
What is Cholangitis and what are the causes?
Cholangitis refers to infection of the biliary tract. It is associated with high morbidity and mortality when left untreated, and therefore is an important condition to recognise and manage.
It is caused by a combination of biliary outflow obstruction* and biliary infection. During an obstruction, stasis of fluid combined with elevated intraluminal pressure allows the bacterial colonisation of the biliary tree to become pathological.
*In patients without outflow obstruction, a bacterial colonisation is unlikely to cause cholangitis
Causes
Any condition which causes occlusion of the biliary tree has the potential to cause cholangitis.
The most common causes are gallstones, ERCP (iatrogenic), and cholangiocarcinoma. Rarer causes include pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections.
The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%).
What are the clinical features of cholangitis?
The common presenting symptoms of cholangitis are right upper quadrant pain, fever,and jaundice (when bilirubin >50 μmol/L). The patient may also complain of pruritus (itching), as a result of bile accumulation, and pale stool with dark urine, from the obstructive jaundice.
The patient’s past medical history may include gallstones, recent biliary tract instrumentation (i.e. ERCP/cholecystectomy), or previous cholangitis. Medication including oral contraceptive pill and fibrates can increase the risk, and a lipid-rich diet may be indicative of gallstones (as a potential underlying cause).
On examination, patients may have pyrexia (in 90% of cases), rigors, jaundice, right upper quadrant tenderness, confusion, hypotension, and tachycardia may be present.
Two common eponymous syndromes associated with cholangitis are:
Charcots Triad: Jaundice, Fever, and RUQ Pain
Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion
How is cholangitis investigated?
Laboratory Tests
Routine bloods should be taken, especially FBC (leucocytosis is found in the vast majority of patients) and LFTs (showing a raised ALP ± GGT with a raised bilirubin).
Blood cultures should always be taken in suspected cases, despite only being positive in 20% of cases. The best opportunity to obtain a positive blood culture is early, before the start of broad spectrum antibiotics.
Imaging
An ultrasound scan of the biliary tract will show bile duct dilation. The common bile duct is usually less than 6mm in size (it may be greater in the elderly and those who have had previous cholecystectomy), so any diameter larger than this suggests dilatation. Ultrasound imaging may also demonstrate the presence an underlying cause (e.g. gallstones).
The gold standard investigation for cholangitis is ERCP, as it is both diagnostic and therapeutic. Many endoscopists may require an MRCP prior to intervention, however to obtain detailed imaging of the biliary system prior to scoping.
How is cholangitis managed?
Management
Immediate Management
Patients with cholangitis may present with sepsis, so should be managed promptly, appropriately and often in a higher level of care. Ensure IV access is gained with sufficient fluid resuscitation, routine bloods, and blood cultures taken early, with broad spectrum IV antibiotic therapy instigated (e.g. co-amoxiclav + metronidazole), as per local guidelines.
Definitive Management
The definitive management of cholangitis is via endoscopic biliary decompression, removing the cause of the blocked biliary tree. For patients who are deteriorating, this may need to be done earlier than those who are responding well to antibiotic therapy.
ERCP, with or without a sphincterotomy and stenting, should clear any obstruction. In patients who may be too sick to tolerate ERCP, percutaneous transhepatic cholangiograpy (PTC) is the second line intervention.
In the long-term, patients may require a cholecystectomy if gallstones were the underlying cause. Any other cause for the cholangitis identified should also be managed as appropriate.
It is important to remember that there are significant complications of ERCP, including repeated cholangitis, pancreatitis (in 3-5% of patients), bleeding (more common when a sphincterotomy is performed), and perforation (a rare complication yet requires urgent surgical intervention if present)
What is the prognosis of cholangitis and what factors determine this?
The mortality of cholangitis is around 5-10% in those who are given antibiotic therapy. Early ERCP and early antibiotic therapy have both been found to improve patient outcomes.
Factors which increase the mortality rate include delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female gender, and >50yrs.
What causes acute pancreatitis?
Aetiology
The majority of acute pancreatitis cases occur secondary to gallstone disease or excess alcohol consumption. However, causes are wide ranging and a popular mnemonic is ‘GET SMASHED’:
Gallstones
Ethanol (Alcohol)
Trauma
Steroids
Mumps
Autoimmune disease, such as SLE
Scorpion venom (a rare and unlikely cause in most countries)
Hypercalcaemia
Endoscopic retrograde cholangio-pancreatography (ERCP)
Drugs, such as Azathioprine, NSAIDs, or Diuretics
Unfortunately, no evident cause will be found in 10-20% of patients with acute pancreatitis
What is acute pancreatitis and pathophysiology?how is it different to chronic?
Acute pancreatitis refers to inflammation of the pancreas. Its incidence is increasing, with around 30 per 100,000 cases each year in the UK. Mortality figures can range between 5-30%, depending on severity.
It can be distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland, with no gross structural damage developing. Repeated episodes of acute pancreatitis can eventually lead to chronic pancreatitis.
Pathogenesis
Each cause described above will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).
Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.
Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas.
What are the clinical features of acute pancreatitis?
Patients will classically present with a sudden onset of severe epigastric pain, which can radiate through to the back, with nausea and vomiting.
On examination, there is often epigastric tenderness, with or without guarding. In severe cases, there may be haemodynamically instability, due to the inflammatory response occurring.
Less common signs that are often described are Cullen’s sign (bruising around the umbilicus, FIg. 2A) and Grey Turner’s sign (bruising in the flanks, Fig. 2B) , representing retroperitoneal haemorrhage. Tetany may occur from hypocalcaemia (secondary to fat necrosis) and, in select cases, gallstone aetiology may also cause a concurrent obstructive jaundice.
What are the differentials for acute pancreatitis?
There are a wide variety of causes of an acutely painful abdomen, as discussed elsewhere. However causes specifically resulting in abdominal pain that radiates through to the back include abdominal aortic aneurysm, renal calculi, chronic pancreatitis, aortic dissection, or peptic ulcer disease.
What investigations are done for acute pancreatitis?
Laboratory Tests
Routine blood tests, as per investigation of any acute abdomen, are required. Specifically for acute pancreatitis, it is important to consider:
Serum amylase – diagnostic of acute pancreatitis if 3x the upper limit of normal*
Amylase can also be marginally raised in pathologies such as bowel perforation, ectopic pregnancy, or diabetic ketoacidosis
LFTs – assess for any concurrent cholestatic element to the clinical picture
Patients with acute pancreatitis noted that an alanine transaminase (ALT) level >150U/L has a positive predictive value of 85% for gallstones as the underlying cause
Serum lipase – A raised serum lipase is more accurate for acute pancreatitis (as it remains elevated longer than amylase), yet it is not available or routinely performed in every hospital
*Serum amylase levels do not directly correlate with disease severity
Imaging
An abdominal ultrasound scan may be requested if the underlying cause is unknown; it is typically used to identify any gallstones (as a potential underlying cause) and any evidence of duct dilatation
Whilst not routinely performed for acute pancreatitis, an AXR can show a ‘sentinal loop sign’. This is a dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to localised inflammation. A CXR should be undertaken to look for pleural effusion or signs of ARDS.
A contrast-enhanced CT scan (Fig. 3) may be required if the initial assessment and investigations prove inconclusive. If performed after 48hrs from initial presentation, it will often show areas of pancreatic oedema and swelling, or any non-enhancing areas suggestive of pancreatic necrosis.
Current UK guidelines state that any CT scan used to assess for severity of disease should only be performed 6-10 days after admission in patients with features of persistent inflammatory response or organ failure*.
*Prior to this time frame, CT-based severity scoring systems have been shown to be equivocal to clinical scoring systems in predicting severity, whilst increasing length of hospital stay with no improvement in clinical outcome
By Hellerhoff (Own work) [CC BY-SA 3.0], via Wikimedia Commons
What scoring systems can be used for acute pancreatitis?
The modified Glasgow criteria is used to assess the severity of acute pancreatitis within the first 48 hours of admission. Any patient scoring with ≥3 positive factors within the first 48hrs should be considered to have severe pancreatitis and a high-dependency care referral is warranted.
Helpfully, the mneumonic to remember the score is PANCREAS: pO2 <8kPa, Age >55yrs, Neutrophils (/WCC) >15×109/L, Calcium <2mmol/L, Renal function (Urea) >16mmol/L, Enzymes LDH>600U/L or AST>200U/L, Albumin <32g/L, Sugar (blood glucose) >10mmol/L
Other risk stratification scores that can be used scoring severity of acute pancreatitis include the APACHE II score, the Ranson Criteria, and Balthazar score (CT scoring system).
