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CHAPTER9 Cardiology and vascular disease
Aneurysms
An arterial aneurysm forms when there is a 50% i in normal diameter of
the vessel. Aneurysms may aect any medium/ large artery— aorta/ iliac arteries > popliteal > femoral > carotid. FH of aneurysm is a risk factor.
Causes Atheroma (most common); injury; infection (e.g. endocarditis,
syphilis— mycotic aneurysms).
Abdominal aortic aneurysm (AAA) Prevalence is 74% in men aged
65– 74y (♂:♀ 76:1). Acute rupture of AAA in the community has 790%
mortality accounting for 2% of deaths in ♂ aged >65y. Elective surgical
repair has 75– 7% mortality.
Risk factors Smoking; i BP; family history (risk i ×4– 10 if there is an af-
fected 1st- degree relative).
Factors predisposing torupture ofAAA
• Diameter (risk i with diameter)
• COPD
• Smoking
• i diastolic BP
• FH
Presentation Often discovered as an incidental nding on abdominal examination, X- ray (calcication of aneurysm wall in 50% cases) or USS (75%
asymptomatic at diagnosis). Otherwise presents with:
• Local symptoms Vague abdominal or back pain
• Distant symptoms Embolization / acute ischaemia of a limb. Multiple
small infarcts (e.g. of toes) with good peripheral pulses suggests an
aneurysm proximally
• Collapse due to rupture Hypovolaemic shock ± pulsatile abdominal
mass ± abdominal or back pain— E p. 1060
Investigation USS conrms diagnosis, diameter, site, and extent.
Screening In the UK, all men aged 65y are oered aneurysm screening with
a single abdominal USS. Men >65y can self- refer. Screening d death from
AAA by 44% over 4y. Possible screening results— Figure 9.4.
Management ofabdominal aorticaneurysm
• Acute rupture E p. 1060
• Elective surgery Refer if risk of rupture > risk elective repair. The
greater the diameter, the more the risk (5.5cm diameter 810% 1y
rupture rate; 10cm diameter >75% 1y rupture rate). AAAs >5.5cm
are routinely repaired except if other factors i risk of surgery; there
is no survival benet from treating smaller aneurysms. Refer urgently if
symptomatic— may indicate rapid expansion, or inammation— both
risk factors for rupture
• USS surveillance Patients with AAAs <5.5cm diameter are screened
at least annually. Routine repair takes place when and if the aneurysm
expands to >5.5cm. 3 in 5 eventually warrant surgery
Inammatory aneurysms Characterized by inammatory inltrate in the
aneurysm wall. May be adherent to surrounding structures. Presentation:fever,
malaise, and abdominal pain. Associated with i mortality at operation.
• Fast rate of expansion
• Inammation within the aneurysm
wall
• Thrombus free surface area of
aneurysm sac
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ANEURYSMS
Single abdominal USS screen aged 65y
NORMAL
Aortic
diameter
<3cm
No further
USS needed
SMALL
ANEURYSM
Aortic
diameter
3–4.4cm
Oered
further
USS in 1y
Advice on CVD risk factor
management
SMALL
ANEURYSM
Aortic
diameter
4.5–5.5cm
Oered
further
USS in 3mo
LARGE
ANEURYSM
Aortic
diameter
>5.5cm
Referred to
vascular
surgery
Figure9.4 Possible AAA screening results
Thoracoabdominal aneurysm Involves thoracic and abdominal
aorta— including the origins of the visceral and renal arteries. Surgery is
more complex and carries higher mortality.
Dissecting thoracic aortic aneurysm E p. 1060
Popliteal aneurysm 80% peripheral aneurysms. Most are >2cm diam-
eter; 50% are bilateral. Associated with AAA (40%). Presents with acute
below knee ischaemia secondary to aneurysm thrombosis or embolization.
Popliteal pulses are pronounced. Diagnosis is conrmed on USS.
Management
• Acute ischaemia— E p. 1108
• Elective surgery (popliteal bypass)— when aneurysm >2.5cm diameter
Femoral artery aneurysm Presentation : local pressure symptoms,
thrombosis, or distal embolization. Surgical treatment:bypass surgery.
Carotid artery aneurysm Rare. Presents with pulsatile lateral neck
swelling ± carotid territory TIAs. Rarely can rupture. Refer to vascular surgery for surgical treatment.
Carotid body tumour Slow- growing tumour arising in the carotid
body at the carotid bifurcation. Presents with a slowly enlarging mass which
transmits carotid pulsation. Refer to vascular surgery for angiographic conrmation of diagnosis. Treatment is with surgical excision. If untreated, becomes locally invasive and may eventually metastasize.
Cerebral artery aneurysm E p. 534
Further information
National Screening Aneurysm Screening Programme M www.gov.uk/
topic/ population- screening- programmes/ abdominal- aortic- aneurysm
Patient information and support
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
Circulation Foundation M www.circulationfoundation.org.uk
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CHAPTER9 Cardiology and vascular disease
Chronic peripheralischaemia
Peripheral vascular disease (normally atherosclerotic) commonly aects arteries supplying the legs.
Prevalence 20% patients age >60y. Assess for the presence of periph-
eral arterial disease if:
• Symptoms suggestive of peripheral arterial disease or
• DM, non- healing wounds on the legs or feet or unexplained leg pain or
• Being considered for interventions to the leg or foot or
• Need to use compression hosiery
Natural history Most remain stable. A minority (20% over 10y) pro-
gress from intermittent claudication to critical limb ischaemia. Management
of CVD risk factors is essential.
Intermittent claudication Restriction of blood ow causes pain on
walking. Risk factors:
• ♂ > ♀
• Smoking
• Obesity
Presentation Presents with muscular, cramp- like pain in the calf, thigh or
buttock on walking that is rapidly relieved on resting. The leg is cool and
white with atrophic skin changes and absent pulses (Table 9.9):
• Disease in the supercial femoral artery Absent popliteal and foot
pulses. Causes calf claudication
• Disease of the aorta or iliac artery Weak or absent femoral pulse ±
femoral bruit. Causes calf, thigh, or buttock claudication
Dierential diagnosis Nerve root compression, e.g. sciatica; spinal stenosis—
usually bilateral pain which may occur after prolonged standing as well as
exercise— not rapidly relieved by rest.
Investigation
• Blood FBC, U&E, Cr, eGFR (peripheral vascular disease is associated
with renal artery stenosis— E p. 417), HbA1c, lipids
• Ankle– brachial systolic pressure index (ABPI) Good history + ABPI
<0.95 conrms diagnosis; 0 do not exclude peripheral arterial disease
in people with DM based on normal or i ABPI
• Duplex USS Used to determine site of disease (may only be available
via secondary care referral)
Management
• Exercise Oer a supervised programme (ideally 2h/ wk for 3mo) to all
patients; encourage to exercise to the point of maximal pain
• d risk factors Patients with claudication have a 3× i risk of death from
MI/ stroke. Advise to stop smoking, moderate alcohol, and lose weight.
Ensure optimum treatment of i BP, lipids, and DM
• Antiplatelet agents Treat all patients with aspirin 75mg od (or
clopidogrel 75mg od if aspirin- intolerant)
• Foot care Regular chiropody
Referral tovascularsurgery
E=Emergency admission; U=Urgent; S=Soon; R=Routine
• Critical limb ischaemia— E/ U
• Severe symptoms— S
• i BP
• Hyperlipidaemia
• DM
• Uncertainty about diagnosis— R
• No better after exercise training— R
• Physical inactivity
• Hypercoagulable states
• Postmenopausal
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CHRONIC PERIPHERALISCHAEMIA
Table9.9 Location ofthe pulses ofthe lower limbs
Pulse Location
Femoral Below inguinal ligament; ⅓ of the way up from pubic tubercle
Popliteal With knee exed at right angles palpate deep in the midline
Posterior tibial 1cm behind medial malleolus
Dorsalis pedis Variable—on the dorsum of the foot just lateral to the tendons
to the big toe. 0 Many healthy people have only 1 foot pulse
Critical limbischaemia
Presentation Deteriorating claudication and nocturnal rest pain (usually
just after fallen asleep— hanging the foot out of bed improves the pain).
Ulceration or gangrene results from minor trauma.
Examination Look for:
• Atrophic skin changes— pallor, cool to the touch, hairless, shiny
• On lowering the leg turns a dusky blue- red colour; on elevation— pallor
and venous guttering
• Ulceration— check under the heel and between the toes
• Swelling suggests the patient is sleeping in a chair to avoid rest pain or,
rarely, pain from deep infection
• Absent foot pulses— if present consider alternative diagnosis
• ABPI <0.5— 0 arterial calcication can result in falsely high readings
Management Analgesia (often requires opioid); refer for urgent vascular
surgical assessment.
The diabetic foot E p. 330
Specialist management ofperipheral arterialdisease
• Angiography to assess extent and position of disease
• Percutaneous transluminal angioplasty ± stenting Most suitable for
short occlusions/ stenoses of the iliac and supercial femoral vessels. 1y
patency rate 80– 90%
• Surgery Most suitable for longer occlusions/ multiple stenoses—
aortobifemoral bypass grafts have 5y patency rates >90%;
femoropopliteal bypass grafting gives 5y patency rates of <70%. Aspirin
d risk of re- occlusion. Amputation is a last option
Drug treatment of intermittent claudication Naftidrofuryl i
walking distance but it is unclear whether it inuences outcome. Consider
only if supervised exercise has not led to improvement and the person does
not want or is unsuitable for angioplasty or bypass surgery. Reassess after
3– 6mo. Discontinue if no improvement.
Acute limb ischaemia E p. 1108
Further information
NICE (2012, updated 2018)Lower limb peripheral arterial disease:diagnosis and management. M www.nice.org.uk/ guidance/ cg147
Patient information and support
Circulation Foundation M www.circulationfoundation.org.uk
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CHAPTER9 Cardiology and vascular disease
Varicoseveins
Tortuous, twisted, or lengthened veins. Prevalence:17– 31%. ♂ > ♀ (85:4).
The vein wall is inherently weak leading to dilatation and separation of the
valve cusps so they become incompetent. Blood ows backwards from
the deep to supercial venous system, causing back pressure and further
dilatation.
Most varicose veins are primary. Risk factors:age, parity, occupations requiring a lot of standing, obesity (women only). 2° causes:DVT, pelvic tumour, pregnancy, or AV stula.
Types
• Trunk Varicosities of the long or short saphenous vein or their
branches. May be symptomatic
• Reticular Usually asymptomatic. Dilated tortuous subcutaneous veins
not belonging to the main branches of the long or short saphenous vein
• Telangiectasia Intradermal venules <1mm— spider veins, thread veins,
star bursts, matted veins. Unsightly but otherwise asymptomatic
Presentation Consider:
• Why is the patient consulting now? Patients are often worried about
appearance of varicose veins or prognosis if left untreated but have no
other symptoms (1 in 3 consultations)
• Symptoms Heaviness, tension, aching (worse on standing and in the
evening; improved by elevating the leg and support stockings), itching
• Complications
• PMH Previous surgery or injection for varicose veins; pregnancy; past
history of DVT or thrombophlebitis; CHC or HRT
• FH Varicose veins or DVT
Examination
• Abdominal examination To exclude secondary causes
• Veins With the patient standing, inspect distribution of the veins and any
secondary skin changes. Patterns of distribution:
• Long saphenous distribution:thigh and medial aspect of the calf
• Short saphenous distribution:below the knee on the posterior and
lateral aspects of the calf
Management Reassurance is often all that is needed.
• If symptoms are troublesome Advise support stockings; avoid standing
for prolonged periods and if standing do not stand still; walk regularly; d
weight (if obese)
• If any complications or severe symptoms Refer for vascular surgical
assessment. In general, patients with purely cosmetic problems are not
treated under the NHS
• Check ABPI to exclude signicant arterial disease before recommending
compression hosiery (ABPI should be >0.8).
Bleeding varicose veins Bleeding can be stemmed by raising the foot
above the level of the heart and applying compression. If the patient is t
for surgery, refer for surgical assessment. Once recovered from the bleed,
advise compression hosiery if ABPI >0.8.
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VARICOSEVEINS
Complications
• Haemorrhage
• Varicose eczema
• Skin pigmentation
• Thrombophlebitis
• Lipodermatosclerosis— brosis of the
dermis and subcutis around the ankle
resulting in rm induration
• Oedema
• Venous ulceration— 40%
do not have visible varicose
veins.
• Atrophie blanche— white,
lacy scars
CHC and HRT Women with varicose veins taking CHC or HRT are not
at i risk of DVT but are at i risk of thrombophlebitis.
Saphena varix Dilatation of the saphenous vein at its conuence with
the femoral vein which transmits a cough impulse. May have bluish tinge
and disappears on lying down. Acause of a lump in the groin. Action only
needed if symptomatic.
Thrombophlebitis Presents as severe pain, erythema, pigmentation
over, and hardening of the vein. Thrombophlebitis in varicose veins results
from stasis. Consider underlying malignancy or thrombophilia if thrombophlebitis occurs in normal veins or there is recurrent thrombophlebitis in
varicose veins.
Management 0 There is no indication for antibiotics.
• Crepe bandaging to compress vein and minimize propagation of
thrombus (if ABPI >0.8)
• Analgesia— preferably NSAID
• Ice packs and elevation
• Low- dose aspirin— 75– 150mg od
• If phlebitis extends up the long saphenous vein towards the saphenofemoral junction, refer for urgent duplex scanning— saphenofemoral ligation may be indicated if thrombus extends into the femoral vein.
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Follow- up If the patient is t for surgery, refer for surgical assessment as
thrombophlebitis tends to recur if the underlying venous abnormality is not
corrected.
History of thrombophlebitis is a relative contraindication to CHC (E
p. 731). Evidence regarding HRT is less clear.
Thrombophlebitis migrans Recurrent tender nodules aecting veins
throughout the body. Associated with carcinoma of the pancreas.
Patient information
Circulation Foundation M www.circulationfoundation.org.uk
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CHAPTER9 Cardiology and vascular disease
Deep veinthrombosis
DVT may be proximal— involving veins above the knee— or isolated to the
calf veins. It may also occur in the cerebral sinus, and veins of the arms,
retina, and mesentery. Incidence:1 in 1000 people/ y. Riskfactors:
• Age >40y
• Smoking
• Obesity
• Immobility
• Recent long- distance
travel
• Pregnancy
0 Central venous catheters are a common cause of upper limb DVT.
Presentation Unilateral leg pain, swelling, and/ or tenderness ± mild
fever, pitting oedema, warmth, and distended collateral supercial veins.
Dierentialdiagnosis
• Cellulitis
• Arthritis/ muscle tear
• Ruptured Baker’s cyst
• Supercial
thrombophlebitis
Immediate action Clinical diagnosis is unreliable. <50% with clinically
suspected DVT have diagnosis conrmed on diagnostic imaging. In most
areas in the UK, rapid access DVT assessment clinics operate.
• If there will be a delay in investigation to exclude DVT, provide
anticoagulation with a direct oral anticoagulant (DOAC) or lowmolecular- weight heparin (LMWH) in the interim.
• Puerperium
• CHC/ HRT use
• Surgery
• Recent trauma
• Malignancy
• Heart failure
• Nephrotic syndrome
• Chronic venous
insuciency
• Venous obstruction
• Post- thrombotic
syndrome
• Inammatory bowel
disease
• PMH of venous
thromboembolism
• Inherited thrombophilic
clotting disorders
• Other chronic illness
• Acute arterial
ischaemia
• Lymphoedema
• Fracture
• Hypoproteinaemia
Clinical prediction rules (e.g. Wells’ score— Box 9.2) are used to decide
whether patients fall into high or low probability groups for DVT.
• If low probability Do a blood D- dimer. If −ve, DVT is excluded. If +ve,
assess the patient as if medium/high probability
• If medium/ high probability Compression USS assessment is undertaken
± D- dimer. If USS is negative and low probability or −ve D- dimer, DVT
is excluded. If USS is +ve, diagnosis of DVT is conrmed. If USS is −ve
and medium/ high probability or +ve D- dimer, USS is repeated after
1wk or the patient is assessed with venography, CT, or MRI
D- dimer testing Detects a degradation product of fresh venous thrombus.
It may be available as a near- patient test with a result in <15min in some
practices— do not delay referral to await result if near- patient testing is
not available. Anormal D- dimer result has a high negative predictive value
making DVT unlikely. However, raised D- dimer levels are not specic for
venous thromboembolism. Other causes of i D- dimer include:
• Malignancy
• Pregnancy
• Wound healing
• Recent trauma
• Inammation
• Anticoagulant use
• Sepsis
• Liver impairment
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DEEP VEINTHROMBOSIS
Management ofpatients withconrmedDVT
• Initial anticoagulation is as an outpatient with either a direct oral
anticoagulant (e.g. rivaroxaban, apixaban) or LMWH followed by oral
anticoagulation (usually warfarin). If anticoagulating with warfarin,
LMWH should be continued for at least 4d and until INR is in
therapeutic range (target INR 2.5; range 2– 3) for ≤2d
• Oral anticoagulants d risk of further thromboembolism and should be
continued for 3– 6mo after a single DVT (E p. 648)
• Graduated elastic compression stockings— should be worn for >2y as
they d risk post- thrombotic leg syndrome by 12– 50%
0 If a patient has a DVT and there is no obvious cause:if <45y, consider
thrombophilia; if >45y, consider undiagnosed cancer.
Management duringpregnancy E p. 802
Complications ofDVT
• Pulmonary embolus Without treatment 20% with proximal DVT
develop PE (E p. 1070)
• Post- thrombotic syndrome Occurs after DVT. Results in chronic venous
hypertension causing limb pain, swelling, hyperpigmentation, dermatitis,
ulcers, venous gangrene, and lipodermatosclerosis
• Recurrent venous thromboembolism Patients with history of DVT or
PE have i risk of recurrence in high- risk situations (trauma, surgery,
immobility, pregnancy) and should receive prophylaxis with heparin/ oral
anticoagulants in such situations
Box 9.2 Wells’ diagnosticalgorithm
Score 1 point if:
• Active cancer (ongoing treatment or treatment in the past 6mo, or
palliative care)
• Paralysis, paresis, or recent plaster immobilization of the legs
• Recently bedridden for ≥3d, or major surgery in the past 12wk (GA
or regional anaesthesia)
• Localized tenderness along the distribution of the deep vein system
(e.g. back of the calf )
• Entire leg swelling
• Calf diameter of aected leg (measured 10cm below the tibial
tuberosity) >3cm greater than that of the unaected leg
• Pitting oedema of aected but not unaected leg
• Collateral supercial veins (non- varicose)
• Previous DVT
Take away 2 points if:
An alternative cause is as/ more likely than DVT.
Interpretation
• If score is <2— DVT is unlikely
• If DVT is ≥2— DVT is likely
Source:data from Wells PS etal., Value of assessment of pretest probability of deep- vein thrombosis in clinical management, The Lancet, 350, 1795– 8.
Further information
NICE (2012, updated 2015)Venous thromboembolic diseases. M www.
nice.org.uk/ guidance/ cg144
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Chapter10
Respiratorymedicine
Breathlessness 264
Cough 266
Chest signs 268
Other signs of respiratory disease 270
Respiratory investigations 272
Bronchodilators and steroids 276
Asthma in adults 278
Asthma management in practice 280
Drug treatment of asthma 282
Chronic obstructive pulmonary disease 284
Management of COPD 286
Acute exacerbations of COPD 288
Lung cancer 290
Colds and inuenza 292
Pneumonia in adults 294
TuberculosisND 296
Other respiratory infections 298
Cystic brosis and Kartagener syndrome 300
Interstitial lung disease 302
Occupational lung disease 306
Snoring and obstructive sleep apnoea 308
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