general Flashcards
what information would you want from a pt presenting with leg pain associated with walking?
- onset of symptoms
- exacerbating and relieving factors
- presence of pain at rest, or any ulcers or foot wounds
- associated conditions and risk factors: smoking Hx, ischaemic heart disease, diabetes, stroke, family history, hypertension
- other conditions associated with leg pain: back problems, arthritis, previous DVT??
what is intermittent claudication?
- a symptom that describes muscle pain on mild exertion, classically in the calf muscles, which occurs during exercise and relieved by rest (secondary to PAD and atherosclerosis)
- aching or burning in leg muscles
- reliably reproduced at a set distance of walking
- relieved with rest
- never present at rest
- not exacerbated by position
how does a normal artery compare to artherosclerotic artery with heamodynamic stenosis
in a normal a., as metabolic demand increases with exercise, vasodilation occurs which allows distal perfusion to be maintained. in an a. affected by PAD, collateral vessels around a significant atherosclerotic stenosis may maintain limb perfusion at rest or on mild to moderate exercise. however, as exercise increases, the abnormal vessel is unable to vasodilator to allow increased flow, and therefore impaired tissue oxygenation leads to anaerobic respiration in muscles distal to the stenosis. this leads to lactic acid accumulation, causing the discomfort of intermittent claudication. with rest, the metabolic demand decreases quickly and the discomfort dissipates within 1/2mins
what is the initial management of intermittent claudication?
- smoking cessation
- anti-platlet agent
- statin (atorvastatin)
- exercise
- management of HTN and diabetes
(artherosclerois is a systemic disease and is likely to also affect coronary and cerebral aa., putting the pt at risk of heart attach and stroke. treatment is to improve life expectancy)
what is the treatment most likely to improve walking distance?
exercise, pushing into the discomfort to increase tolerance to ischaemia, which will increase the distance the pt can walk before rest (i.e supervised exercise programme)
which pt;s with claudication do you think might benefit from referral for further investigation?
- deterioration in symptoms despite best medical management and despite supervised exercise programme
- lifestyle limiting claudication, particularly if threat to employment, which has not improved with supervised exercise programme
- sudden onset claudication (may be due to thrombosis in situ which may require anticoagulation or further Ix)
- uncertain diagnosis: if a diagnosis is unclear, referral to vascular surgery for a specialist opinion may be useful
what is chronic limb-threatening ischaemia?
the presence of ischaemic rest pain, necrosis, or ulceration, in the presence of peripheral arterial disease for more than 2 weeks.
it occurs when peripheral arterial disease is so severe that tissue perfusion is not sufficient to maintain adequate oxygenation, even at rest. although it is principally caused by peripheral arterial disease, symptoms may be worsened by anaemia or cardiac dysfunction, both of which also decreased tissue oxygen delivery.
unless treated with revascularisation, the likely outcome is eventual deterioration and need for amputation
what is buergers test?
- assessment of arterial sufficiency
- elevate foot to 45 degrees, and keep there for 1-2mins
- pallor indicated ischemia of the leg because arterial pressure in the led is insufficient to overcome gravity
- next, ask the pt to hang the foot over the side of the couch or chair
- +ve test if the foot initially becomes dusky purple (due to deoxygenated blood passing through ischaemic tissue) then red (reactive hyperaemia because of post-hypoxic vasodilation)
what is the initial management of chronic limb-threatening ischamia?
analgesia - long acting opiates (e.g. MST or oxycodone MR) may be resquired, with breakthrough short-acting opiate in addition
referral - urgent referral to vascular surgery service
podiatry - can be very useful in managing wounds on the foot and helping prevent deterioration, but should not delay referral to secondary care
what imaging modalities are available to assess circulation?
- duplex ultrasound
- magnetic resonance angiography (MRA)
- computed tomography angiography (CTA)
what options are available with regards to improving the blood supply to the lower limb?
endovascular treatment (angioplasty or stunting)
- percutaneous access to artery under LA, with iodinated contrast injected into an artery to delineate blockages and stenosis
- wires can be used to pass through occlusions or stenoses, which can be dilated with balloons and stents
- generally more suitable for short stenoses or occlusions, or disease very distal in small calf vessels
- less periprocedural cardiac risk for frail patients with extensive womorbidities, but less durable
open surgery:
- open surgical bypass of occlusions, or endarterectomy of atherosclerosis in regions less suited to bypass
- required healthy vessels proximal and distal to the bypass to allow good flow
- if possible, the pt’s native vein (great saphenous) is used as a conduit
- suitable for long occlusions or disease over multiple levels
- higher periprocedural risk (e.g. MI, chest infection, mortality) than endovascular treatment, but when successful, more durable
describe the macrovascular complications of diabetes
tends to be cardiovascular disease:
- coronary artery disease
- stroke
- peripheral arterial disease
- hyperglycaemia damages blood vessels through a process called atherosclerosis, or clogging of aa. this narrowing of aa. can lead to decreased blood flow to heart muscle (causing heart attack), brain (stroke) or to extremities (leading to pain and decreased healing of infections)
- Sx vary: ranging from chest to leg pain, confusion and paralysis
- Dx early detection of these complications can delay progression, but early detection of other risk factors such as smoking, HTN, high serum cholesterol and obesity is even more important
- Tx = controlling risk factors along with blood glucose can prevent or delay CV complications
describe the microvascular complications of diabetes
- retinopathy:
- leading cause of blindness and visual disability
- caused by small blood vessel damage to the retina leading to progressive loss of vision
- usually pt complains of blurred vision
- Dx of early changes in the blood vessels of the retina can be made through regular eye examinations
- Tx = good metabolic control can delay the onset and progression of diabetic retinopathy. early detection and Tx of vision-threatening retinopathy can prevent or delay blindness - nephropathy:
- diabetic kidney disease caused by damage to small blood vessels in the kidneys. this can cause kidney failure and eventually lead to death
- pt’s usually have no symptoms early on, but as the disease progresses, they may feel tired, become anaemic, not think clearly, even develop dangerous electrolyte imbalances
- early diagnosis can be made by a simple urine test for protein as well as a blood test for kidney function
- retard the progression to kidney failure if diagnosed early e.g. control blood glucose, HTN, intervention with medication in the early stage of kidney damage, and restriction of dietary protein - neuropathy:
- nerve damage through different mechanisms, including direct damage by the hyperglycaemia and decreased blood flow to nn. by damaging small blood vessels
- can lead to sensory loss, damage to limbs, and impotence in diabetic men
- symptoms can be many, depending on which nerves are affected: e.g. numbness in extremities, pain in extremities, and impotence
- decreased sensation to feet 🦶 can lead to pts not recognising cuts and developing foot infections. if not treated early can –> amputation
- Dx = early recognition of symptoms by pt and HCPs
- Tx = if detected early, control of blood glucose could prevent or delay these complications
define mourning, grief, bereavement and their relationship
grief = primarily emotional/affective process of reacting to the loss of a loved one through death. internal intrapsychic process of the individual) common grief reactions may include: numbness and disbelief; anxiety from the distress of separation; process of mourning often accompanied by symptoms of depression…eventual recovery
mourning = public display of grief. emphasises the external or public expressions of grief. it is influenced by one’s beliefs, religious practices and cultural context
bereavement =objective situation one faces after having lost an important person via death
*overlap with grief and mourning with each influencing each other i.e. the public expression (mourning) of the emotional distress over the loss of a loved one (grief) is influenced by culturally determined beliefs, morals and values
relate the key effects of bereavement on the person
bad news includes situations where there is a threat to a persons mental or physical wellbeing
a risk of upsetting an established lifestyle or
where a message is given which conveys to an individual fewer choices in his or her life
understand the different between grief and depression
- in grief painful feelings come in waves, lessen in intensity and frequency over time, and are often intermixed with positive memories of the deceased
BUT in depression, moods and ideation are constantly negative - in grief the prevailing affect is one of emptiness
BUT in major depression, it a long, sustained, depressed mood and an inability to expect pleasure or happiness - in grief, self-esteem is usually preserves
BUT in major depression, feelings of worthlessness and self-loathing are common - in grief, while symptoms such as suicidal ideation can occur, they are generally focused on he deceased, such as a wish to join the deceased in death or feelings of guilt toward certain gaps or failures in the relationship with deceased
BUT in major depression, suicidal ideation is more likely directed at self only
outline the key arguments often cited for/against the use of animals in research
- risk/benefit analysis
- moral agency (can you justify it)
- is it an appropriate model for the questions you are answering
- is it a sentient animal and can you then justify what you are doing?
- argue for on the basis of value
explain the 3 principles governing the current use of animals in research Animals (Scientific Procedures) Act 1986 (ASPA)
- replacement - e.g. alternative technologies (in vitro, biochemical, mathematical and computer models); use lower organisms
- reduction - e.g better study design to allow use of fewer animals; better storage of data
- refinement - e.g. improve housing, minimise pain; improve welfare
outline the regulatory role of the home office in animal research, and the national research ethics service and local ethics committees in human research
home office - review and monitor all eligible research (animal)
research ethics - same for humans. nuremberg code (1947), a set of research ethics principles for human experimentation created as a result of the Nuremberg trials at the end of the Second World War. focuses on human rights of research subjects
discuss the importance of the declaration of Helsinki (2013) in human research
like the nuremebrge code, the declaration of Helsinki (developed by the world medical association) was to prevent human subjects from being mistreated. focuses on guidance for physicians who were conducting clinical research and focused on researchers’ roles and responsibilities when it comes to protecting human subjects.
explain why informed consent is important in research and some of the difficulties that can arise from the process
- adequately informed
what are the 4 criteria for valid consent ( in clinical practice)
- pt must have capacity
- pt must give consent voluntarily
- pr must be informed
4 consent must be continuing
demonstrate knowledge of the main ways on which infectious diseases are transmitted
food borne infection - e.g. salmonella, shigella, listeria. food handlers spreading infection
aerosol - e.g. influenza virus
sexual - e.g. T, pallidum
foecal-oral - e.g. hepatitis
direct contact - e.g. staph aureus
waterborne - e.g. cholera
zoonosis (direct or via vector)
define the terms epidemic, endemic and pandemic
endemic
- a disease that is constantly present in a community
- the numbers of cases may fluctuate from time to time
- often sustained by a complex interaction between hosts, environment and ecosystems
- can be eradicated with complex interventions (e.g. vaccines)
- e.g. malaria, influenza, meningococcal disease
epidemic:
- occur when the number of cases is very large and significantly exceed the background (e.g. always a background level of influenza. surges at different points of the year to endemic level)
- can spread widely and rapidly
- drifts antigenic structure as it circulates in human population, but occasionally undergo significant antigenic change
pandemic:
- infection spreads globally
- this can be rapidly (COVID, influenza) or slowly (HIV or TB)
explain why new infections emerge
- we discover/ detect them (e.g. new molecular or serological technique). previously unrecognised pathogens
- generally new infections because a pathogen has jumped from one species into human species
why pathogens emerge?
- depends on the interaction of microorganisms and the human population
- microbial change (emergence of a new pathogenicity factor, resistance or mutation to vaccine)
- ecological change (changing land use (e.g. agriculture, forest clearance, dam building), climate change (vector range - mosquitos))
- human demographics and behaviour (population pressures on food resources, bush meat, migration to towns, war, increasing global tourism/ extreme holidays)
- technological changes (food process, refrigeration and microwaves, immunosuppression, blood transfusion)
- increase in susceptibility to infection (breakdown in public health measures, increasing immunocompromised population)
describe the systems in place for surveillance of infectious disease and the way in which physicians participate in the process
- statutory notification (e.g. notifiable disease like measles, rubella, meningococcal septicaemia)
- specific surveillance schemes e.g. ‘flu and RCGP’
- laboratory reporting
- mandatory reporting of specific hospital infections e.g. MRSA and Ecloi
- death certificate
*emerging infections are the business of all medical practitioners. we need to be aware of them and understand our obligations in surveillance and reporting
explain important emerging diseases and appropriate methods to control them
- sufficient water and sewage seperation
- purify water
- isolate using appropriate methods
what is the pharmacological management of glycemic control?
- insulin always required in T1 diabetes
- oral hypoglycaemic agents (e.g. metformin, gliclazide, sitagliptin, empagliflozin) and injectable therapies (GLP-1 agonists and insulin) can be used in type 2 diabetes
what is the treatment ladder used to control blood glucose in Type 2 diabetes?
- diet and activity
- diet and activity + tablets for insulin resistance (metformin)
- diet and activity + tablets for insulin resistance (metformin) + tablets for increased insulin production (sulfonylureas) +tablets for increased glucose excretion (SGLT2)
- diet and activity + tablets for insulin resistance + insulin
Using the example of diabetes, describe the role of the multiprofessional team in managing long-term health conditions
- achieve treatments aims via pt centred care planning
- education (food, Glycaemic index, activity and the benefits)
- motivation
- facilitate behaviour change
what are the normal fasting glucose levels?
3-5.5mmol/l
(>7mmol/l = diabetes; 5.6-6.9 = impaired fasting Glycaemia and high cardiovascular risk)
compare insulin and glucagon
insulin
- secreted by Beta cells
- removes glucose from the circulation after meals into tissues for energy use or into body stores
glucagon
- secreted by Alpha cells
- facilitates the release of glucose (from liver, muscle, fat) and into the circulation during the fasting state
discuss the clinical features of type II diabetes
- sub acute presentation (same symptoms as type I but less marked and extending over several months)
- polydipsia
- polyuria
- lack of energy
- visual problems
- candida infections
- or asymtomatic and diagnosed on routine bloods
discuss the assessment and diagnosis of type II diabetes
made by demonstrating:
- fasting plasma glucose is >7mmol/l
- random plasma glucose is >11mmol/l
- only one is needed in a pt with typical hyperglycaemic symptoms. both needed in asymptomatic pt
- HAB1c (used to diagnose T1 or gestational diabetes) is an integrated measure of an individuals prevailing blood glucose concentration over several weeks… result over 48mmol/mol or above would be considered diagnostic of diabetes
- type II diabetic is usually older, overweight, onset is over months to years, no HLA links
how is diabetes type 2 managed
- Multidiciplinary approach
- education at diagnosis and continuing - essential that the pt understands the risks of diabetes, the potential benefits of good glycemic control and the importance of maintaining a lean weight, stopping smoking and taking care of the feet
- management involves:
i) achieving good Glycaemic control
ii) advice regarding regular physical activity and reduction of body weight in the obese, with of which improve Glycaemic control in type 2
iii) aggressive treatment of HTN and hyperlipidaemia
iv) regular checks of metabolic control and physical examination for evidence of complications
differentiate between type 1 and type 2 diabetes
- clinical presentation e.g. presence of ketones, weight loss more marked in type 1 (also more acute)
- antibody testing (T1 is autoimmune aetiology)
- FHx of diabetes or autoimmune conditions
type 1
- acute symptoms
- polyphasic, polydipsia, polyuria
- weight loss
- ketonaemia/ketonuria
- fatigue
- visual changes
- dehydration/electrolyte imbalance
- cause and vomiting
- abdominal pain
type 2
- symptoms usually more insidious
- often incidental detection during routine checks
- recurrent infections/delayed wound healing/ recurrent candidiasis
- tiredness/lethargy
- visual disturbance
how are complications of diabetes managed?
GOOD GLYCAEMIC CONTROL for all
retinopathy - annual eye screening, good blood pressure control, laser treatment
nephropathy (hyperglycaemia and HTN damages glomerular basement membrane and causes micro aneurysm formation)- annual urine screen and blood pressure control
neuropathy - annual foot screen for pulses and sensations
erectile dysfunction - phosphodiesterase inhibitors
CVD (fatty deposits in the blood vessels can damage the heart and blood circulation) - managing RFs associated with atherosclerosis, regular cholesterol and BP checks (target 130/80), cholesterol lowering drugs (large <4mmol)
define acute limb ischaemia
sudden decrease in limb perfusion that causes a potential threat to limb viability. will lead to extensive tissue necrosis within 6 hours if not revascularised!
causes: embolus (most common), thrombosis (second most common), trauma, dissection
discuss embolus and thrombosis
embolus:
- often cardiac cause e.g AF, valvular disease , endocarditis
- anything that moves through blood vessels(piece of a blood clot, foreign object)
- embolism is when the thing blocks a blood vessel/flow)
thrombus
- blood clot in vein
- thrombosis = thrombus grows and blocks vessel blood flow
what is the presentation of acute limb ischaemia?
- 6P’s!!
pain ->perishingly cold -> pallor -> pulseless -> paraethesia -> paralysis - don’t need all P’s for diagnosis
- elderly
- Hx of background claudication/PVD
- often new AF, or not on anticoagulants (risk of falls or GI bleed)
how is acute limb ischaemia assessed?
- Hx (risk factors)
- pulses
- cap refil
- sensation
- motor function
- squeeze calf (look at tenderness - if soft and non-tender then that is a good sign, muscles not involved yet. if tender and hard then the muscles are involved and risk of compartment syndrome when reperfused)
- doppler USS
- CT angiography is the gold standard
- check both legs! cardiac cause may chuck clots down both legs
- Ix the cause
- assess severity using Rutherford classification:
I - Viable: small acute embolus but cap refill is maintained and normal motor and sensory signs
IIa - Threatened: salvageable if prompt treated. doppler signal is abnormal or absent. start to get sensory deficit/ numbness and tingling in toes. cap refill slows
IIb - Threatened: salvageable with immediate reconstruction. absent cap refill, numbness, motor deficit in hands and feet.
III- irreversible: major tissue loss or permanent nerve damage inevitable. essential dead leg. if try to perfuse -> reperfusion injury -> hyperkalaemia -> death. Tx is amputation or palliative care.
how is acute limb ischaemia managed
- analgesia
- high flow O2
- hydration (risk of renal failure - will get breakdown of muscle as it becomes more ischamic. high levels of CK, myoglobin in the blood stream)
- LMWH or IV UF heparin (prevent propagating further)
- intervention:
1. endovascular options (class I and IIa) - thrombolysis and angioplasty or stent. risk of distal embolisation
2. fem-pop/ fem-distal bypass - urgent bypass
palliative care or amputation irreversible
what is chronic limb ischamia?
decrease in limb perfusion which may (or may not) threaten viability of the limb, but duration is >2weeks
peripheral arterial disease that results in symptomatic reduced blood supply to the limb
-> cause = atherosclerosis
discus atherosclerosis in the context of chronic limb ischemia
- build up of lipid, calcium and fibrous tissue within the intimate of the arterial wall
- once >50% of the arterial cross section diameter is occupied with atheromatous plaque, this becomes flow limiting and may lead to symptoms
- fibrous plaque is vulnerable to rupture - if the endothelium is exposed, thrombosis may cause an acute deterioration in symptoms
PAD = progressive disorder characterised by stenosis or occlusion of large and medium sized aa. –> increased risk of cardiovascular mortality (around 5% risk of mortality, myocardial infarction or stroke per year)
what are the risk factors for chronic limb ischaemia?
smoking diabetes HTN hyperlipademia age male FHx obesity and physical inactivity
what are the clinical features of chronic ischaemic limb?
depend on severity: I - asymptomatic II - intermittent claudication III - ischaemic rest pain IV - ulceration, gangrene or both
+ve Buergers teat
Buergers angle <20 degrees indicates severe ischaemia
discus the assessment and management of intermittent claudication
IC:
- pain or tightness, often in the calves, on walking (muscle group that is painful will be that supplied by the occluded artery)
- usually occurs after the same distance on the flat, but worse on hills
- ease after resting for 1-2mins
examination:
- inspection (scars; ulceration; colour; venous guttering)
- palpation (temp; cap refill time; pulses; remember aortic pulse)
Ix:
- ankle brachial pressure index (ratio of the ankle to the brachial occlusion pressure). normal = 0.8-1.2. low ABPI usually due to lower limb peripheral arterial disease. elevated usually due to calcified vessel (not reliable in diabetes)
- Dx is clinical but if required -> duplex USS, MR angiography +/or CT angiography
Mx:
- CV risk factor modifications…
- manage RFs (stop smoking, HTN control, diabetic control)
- medications (spirit/clopidogrel and statin)
- supervised exercise
- reassure - very small % deteriorate to limb threatening ischaemia
- referral if pts likely to benefit from intervention i.e. short distance claudicants (<100m), sudden onset symptoms, lifestyle limits, threatening employment
discuss the assessment and management of chronic limb threatening ischaemia (stages III and IV)
- chronic (>2weeks) ischaemic rest pain, necrosis or ulceration, as a result of proven arterial disease
- high mortality rate (approx 50% 4yrs)
presentation:
- ischaemic rest pain
- hang foot out bed at night
- gangrene, ulcers, non healing wounds
- may have background of claudication
assessment: same as IC (ABPI, doppler US, CT angiogram or MR angiogram)
initial management:
- address risk factors
- analgesia
- consider gabapentin or prefab for neuropathic pain
- refer early as possible
- urgent referral for inpatient treatment: extensive tissue loss; sepsis associated with necrosis or ulceration; uncontrolled pain
- podiatry can be very useful to help with wounds - in addition to referral to vascular surgery
management:
- aim is to revascularise the limb
what are the interventional management options of chronic limb ischeamia?
- primary amputation:
- sepsis, tissue los, unreconstrctable disease
- can be minor or major - revascularisation:
- > claudication - revascularisation aims to increase QoL
- > Chronic limb threatening ischeaia - revascularisation aims to prevent limb loss
i) open surgery (endarterectomy or bypass)
ii) endovascular (angioplasty or stenting)
iii) combination of the 2
discuss endovascular treatment
- angiography allows accurate diagnostic imaging, and if appropriate, direct progression to angioplasty or stenting
- direct arterial puncture, with introduction of a sheath, and then injection of iodinated contrast to opacify vessels
- stenoses or occlusions identified and can be crossed with a wire and balloon, and opened uo and or stented
pros and cons:
- lower morbidity and mortality
- lower longterm potency rates
- main immediate complications: groin puncture (pseudo aneurysm or bleeding), thrombosis, dissection, embolus
- longterm complications: stent stenosis and thrombosis
discuss open surgical reeves
- usually surgical bypass
- uses conduit such as native vein (GSV) or prosthetic graft or biological graft to bypass occluded segments of artery
- requires good ‘inflow’ good conduit, and good ‘runoff’ to maintain graft patency
- frequently combines with endovascular procedures to achieve this result
pros and cons:
- difficult operation in comorbid population - specialist anaesthetic team
- higher immediate morbidity and mortality
- higher longterm patent rates
- common complications: infection, bleeding, MI, graft failure, nerve damage
- long term complications: graft thrombosis
what is Leriche’s Syndrome
associated with occlusion in the distal aorta or proximal common iliac artery
A clinical triad:
- Thigh / buttock claudication
- Absent femoral pulses
- Male impotence
define aneurysm
a full thickness dilation of an artery by more than 50% of its normal diameter (normally 2cm so occurs when >3cm. 2-3cm is referred to as “ectatic”)
true aneurysm = involves dilation of all the layers of the arterial wall e.g. atherosclerotic aneurysms
false/pseudo aneurysm = do not involve all the layers of the arterial wall. involve a collection of blood in the outer layer (adventitia) which communicates with the lumen e.g. trauma
causes: atheroma, trauma, infection (mycotic in endocarditis), CT disorders (Marfans), inflammation (Takayasu’s aortitis)
complications: rupture, thrombosis, embolism, fistulae, pressure on other structures
what is the incidence, risk factors and natural Hx of aortic aneurysms
incidence = 4% of men aged 65-74 in UK
RFs: age sex HTN FHx (some AD collagen disorders -Marfans) smoking (not associated with diabetes)
natural history - gradual expansion. as it gets bigger, more at risk of rupture
what is the clinical presentation and diagnosis of AAA
CP:
- can be asymptomatic (found as pulsating mass on abdominal examination or via screening program)
- symptoms due to pressure effects (epigastric or back pain)
- other symptoms = pain (without evidence of rupture on CT), acute limb ischaemia (due to thrombus inside aneurysm embossing distally into lower limbs), inflammatory aneurysms (may cause pain, and other local symptoms such as hydronephrosis due to ureteric involvement within inflammation)
- or rupture symptoms (intermittent or continuous abdominal pain radiating to back + iliac fossa or groin; hypovolaemic shock; expansile abdominal mass)
Dx:
- US
- CT angiogram - to outline anatomy and clarify what options are available
what is the management of asymtpmatic aneurysm (>5.5cm)
- clinical appointment for CT angiography after US diagnosis
- preserve treatment for >5.5cm (or symptomatic)
- anaesthetic assessment (including echo and PFTs
- MDT discussion
- surgery or stunning (EVAR)
- more likely to rupture if ^BP, smoker, male, +ve FHx
what is the management of symptomatic aneurysm
- indications for repair = if locally tender and can’t find any other cause -> sign it is going to burst; if embolising; persistent pain; local effects on other organs such as hydronephrosis
- endovascular repair (EVAR) or open surgical repair
how would you manage a rupture AAA?
- have a high index of suspicion as mortality and morbidity is high
- back pain, abdominal pain, hypotension, collapse
- ABCD approach
- call for help - senior support, vascular team early (to alert theatre and anaesthetics early)
- oxygen
- IV access - bloods, G+S, major haemorrhage protocol
- ? fluids
- CT angiogram
what is the aneurysm screening programme?
- all men invited 65-74
- abdominal US to look at aorta
- if >3cm, ongoing follow up of aorta
- if >5.5cm, referred to surgical clinic for Ix and Tx
- target of 2weeks from diagnosis to clinic appointment, and 40 days from diagnosis to treatment
what can be an atypical presentation of rAAA?
left renal angle pain radiating to groin “first presentation of renal colic in a man over 60”
- RIF pain
- back pain
why should you think carefully about giving fluids in a rAAA case?
permissible hypotension
- in the setting of intraabdominal bleeding, hypotension can be helpful
- if BP is increased rapidly, then this may destabilise retroperitoneal haematoma, and cause bleeding to worsen
- aim whilst organising surgery is to perfuse brain - if the pt is orientated and able to talk, the blood pressure is sufficient to do this
- transfuse if disorientated and confused
- aim 90mmHg
further explore the 2 interventional treatment options for AAA (asymptomatic or ruptured - urgencies differ)
- endovascular repaik (EVAR):
- avoid major surgery by inserting an endovascular stent via the femoral artery
- need to have at least 1.4cm parallel aorta and iliac vessel to get seal at both ends
- pros = lower operative mortality (1%), shorter anaesthetic time, shorter hospital stay
- cons = anatomical restrictions, higher reintervention rate, no long term mortality benefit, need for surveillance - open surgical repair:
- clamp on aorta
(- if planned, heparin)
- open up aneurysm
- sew synthetic graft into vessel
- pros = less anatomical restrictions, low reintervention rate, no need for surveillance
- cons = higher operative mortality (4%)
- longer anaesthetic time
- longer hospital stay
define aortic dissection
results from tear in the intima allowing blood to enter the media of the aortic wall –> sudden tearing chest pain radiating to the back.
this can propagate proximally and distally, ‘dissecting’ the layers of the wall apart and causing a false lumen or channel to form with blood flowing within the wall
involvement of the branch aa. may produce neurological signs, absent pulses and unequal BP in the arms
diagnosed via CT
what are the risk factors of aortic dissection?
hypertension (poorly controlled)
sex of (M)
age (65-75)
also associated with genetic conditions such as Marfan’s syndrome
discuss type A and type B aortic dissection (Stanford classification)
type A:
- 70%
- ascending aorta; may or may not involve descending aorta
- present with sudden onset ‘tearing’ anterior chest pain
- cardiac complications include acute mitral regurgitation, MI (blood flow to coronary aa is restricted), cardiac tamponade (bleeding around the heart and into pericardium) and stroke (propagates into carotid vessels)
- urgent transfer to cardiothoracics for surgical arch replacement if pt is fit - no role for medical management
type B
- 30%
- purely involves the descending aorta
- presents with sudden onset intrascapular pain
- vascular surgery and cardiology joint management
- conservative Tx = pain control and urgent BP control (aiming for <110mmHg)
- indications for surgery = uncontrolled pain, end organ hypo perfusion, ongoing dilation and dissection despite BP control
