Rapid Medicine

Amir H. Sam, James T. H. Teo

• Publisher: Wiley-Blackwell
• Year: 2011
• ISBN:
  9781118293638
• Edition: 2
• Topic: Medicine
• Subtopic: Internal Medicine & Diagnosis

This pocket reference and revision guide is a must for all medical students and junior doctors preparing for major exams in clinical medicine or needing a rapid reminder of essential facts during a clinical attachment. Now thoroughly updated, this new edition combines the first editions of Rapid Medicine and Rapid Differential Diagnosis and contains reference to over 200 common medical conditions and diseases and 350 signs and symptoms encountered on a daily basis on the wards, in clinics and in exams.

This concise, no-nonsense reference is presented in an A-Z format for easy access to information, and includes a thematic index with conditions sorted by speciality making it an ideal companion in any clinical situation.

Medical Conditions

CARDIOLOGY

Aortic dissection

DEFINITION

A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen.

AETIOLOGY

Degenerative changes in the smooth muscle of the aortic media are the predisposing event. Common causes and predisposing factors are:

• hypertension;
• aortic atherosclerosis;
• connective tissue disease (e.g. SLE, Marfan’s, Ehlers–Danlos);
• congenital cardiac abnormalities (e.g. aortic coarctation);
• aortitis (e.g. Takayasu’s aortitis, tertiary syphilis);
• iatrogenic (e.g. during angiography or angioplasty);
• trauma;
• crack cocaine.

Stanford classification divides dissection into:

• type A with ascending aorta tear (most common);
• type B with descending aorta tear distal to the left subclavian artery.

Expansion of the false aneurysm may obstruct the subclavian, carotid, coeliac and renal arteries.

EPIDEMIOLOGY

Most common in

between 40 and 60 years.

HISTORY

Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI). Aortic dissection can lead to occlusion of the aorta and its branches:

Carotid obstruction: Hemiparesis, dysphasia, blackout.

Coronary artery obstruction: Chest pain (angina or MI).

Subclavian obstruction: Ataxia, loss of consciousness.

Anterior spinal artery: Paraplegia.

Coeliac obstruction: Severe abdominal pain (ischaemic bowel).

Renal artery obstruction: Anuria, renal failure.

EXAMINATION

Murmur on the back below left scapula, descending to abdomen.

Blood pressure (BP): Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure. If hypotensive may signify tamponade, check for pulsus paradoxus.

Aortic insufficiency: Collapsing pulse, early diastolic murmur over aortic area.

Unequal arm pulses.

There may be a palpable abdominal mass.

INVESTIGATIONS

Bloods: FBC, cross-match 10 units of blood, U&E (renal function), clotting.

CXR: Widened mediastinum, localized bulge in the aortic arch.

ECG: Often normal. Signs of left ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery.

CT-thorax: False lumen of dissection can be visualized.

Echocardiography: Transoesophageal is highly specific.

Cardiac catheterization and aortography.

MANAGEMENT

Acute: If suspected, CT-thorax should be performed urgently concurrent to resuscitation. Resuscitate and restore blood volume with blood products. Monitor pulse and BP in both arms, central venous pressure monitoring, urinary catheter. Best managed in ITU setting.

Type A dissection: Treated surgically. Emergency surgery because of the risk of cardiac tamponade. Affected aorta is replaced by a tube graft. Aortic valve may also be replaced.

Type B dissection: Can be treated medically, surgically or by endovascular stenting. Control BP and prevent further dissection with IV nitroprusside and/or IV labetalol (use calcium channel blocker if β-blocker contraindicated). Surgical repair may be appropriate for patients with intractable or recurrent pain, aortic expansion, end-organ ischemia or progression of dissection, and has similar outcome rates. Endovascular repair is a newer technique using endovascular stents and is available in some centres, although evidence of benefit is still lacking (ADSORB trial results pending).

COMPLICATIONS

Aortic rupture, cardiac tamponade, pulmonary oedema, MI, syncope, cerebrovascular, renal, mesenteric or spinal ischaemia.

PROGNOSIS

Untreated mortality: 30% at 24 h, 75% at 2 weeks.

Operative mortality of 5–10%. A further 10% have neurological sequelae.

Prognosis for type B better than type A.

Aortic regurgitation

DEFINITION

Reflux of blood from aorta into left ventricle (LV) during diastole. Aortic regurgitation (AR) is also called aortic insufficiency.

AETIOLOGY

Aortic valve leaflet abnormalities or damage: Bicuspid aortic valve, infective endocarditis, rheumatic fever, trauma.

Aortic root/ascending aorta dilation: Systemic hypertension, aortic dissection, aortitis (e.g. syphilis, Takayasu’s arteritis), arthritides (rheumatoid arthritis, seronegative arthritides), Marfan’s syndrome, pseudoxanthoma elasticum, Ehlers–Danlos syndrome, osteogenesis imperfecta.

Reflux of blood into the LV during diastole results in left ventricular dilation and ↑ end-diastolic volume and ↑ stroke volume. The combination of ↑ stroke volume and low end-diastolic pressure in the aorta may explain the collapsing pulse and the wide pulse pressure. In acute AR, the LV cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.

EPIDEMIOLOGY

Chronic AR often begins in the late 50s, documented most frequently in patients >80 years.

HISTORY

Chronic AR: initially asymptomatic. Later, symptoms of heart failure: exertional dyspnoea, orthopnoea, fatigue. Occasionally angina.

Severe acute AR: sudden cardiovascular collapse.

Symptoms related to the aetiology, e.g. chest or back pain in patients with aortic dissection.

EXAMINATION

Collapsing ‘water-hammer’ pulse and wide pulse pressure. Thrusting and heaving (volume-loaded) displaced apex beat.

Early diastolic murmur at lower left sternal edge, better heard with the patient sitting forward with the breath held in expiration. An ejection systolic murmur is often heard because of ↑ flow across the valve.

Austin Flint mid-diastolic murmur: Over the apex, from turbulent reflux hitting anterior cusp of the mitral valve and causing a physiological mitral stenosis.

Rare signs associated with a hyperdynamic pulse:

Quincke’s sign: Visible pulsations on nail-bed.

de Musset s sign: Head nodding in time with pulse.

Becker s sign: Visible pulsations of the pupils and retinal arteries.

Müller’s sign: Visible pulsation of the uvula.

Corrigan’s sign: Visible pulsations in neck.

Traube’s sign: ‘Pistol shot’ (systolic and diastolic sounds) heard on auscultation of the femoral arteries.

Duroziez’s sign: A systolic and diastolic bruit heard on partial compression of femoral artery with a stethoscope.

Rosenbach’s sign: Systolic pulsations of the liver.

Gerhard s sign: Systolic pulsations of the spleen.

Hill’s sign: Popliteal cuff systolic pressure exceeding brachial pressure by >60 mmHg.

INVESTIGATIONS

CXR: Cardiomegaly. Dilation of the ascending aorta. Signs of pulmonary oedema may be seen with left heart failure.

ECG: May show signs of left ventricular hypertrophy (deep S wave in V_1–2, tall R wave in V_5–6, inverted T waves in I, aVL, V_5–6 and left-axis deviation).

Echocardiogram: 2D echo and M-mode may indicate the underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or the effects of AR (left ventricular dilation/dysfunction and fluttering of the anterior mitral valve leaflet). Doppler echocardiography for detecting AR and assessing severity. Periodic (annual) follow-up echocardiogram for serial measurements of LV size and function.

Cardiac catheterization with angiography: If there is uncertainty about the functional state of the ventricle or the presence of coronary artery disease.

MANAGEMENT

Aortic valve replacement: In patients with symptoms of ventricular decompensation, or LV dysfunction: ejection fraction <50%, LV enlargement (end-systolic dimension >55 mm; end-diastolic dimension >75 mm).

Vasodilators (ACE inhibitor or nifedipine): In patients with LV systolic dysfunction (left ventricular ejection fraction (LVEF) <50%), or progressive LV dilatation. Vasodilators ↓ systemic vascular resistance and the afterload, i.e. the burden on the volume-loaded LV. Treat the complications (e.g. heart failure).

COMPLICATIONS

Left ventricular failure and pulmonary oedema.

PROGNOSIS

Chronic AR is often well tolerated for many years without symptoms.

Prognosis depends on the underlying aetiology. Acute AR caused by aortic dissection or infective endocarditis is fatal if not treated urgently.

Aortic stenosis

DEFINITION

Narrowing of the left ventricular outflow at the level of the aortic valve.

AETIOLOGY

1. Stenosis secondary to rheumatic heart disease (commonest worldwide);

2. calcification of a congenital bicuspid aortic valve;

3. calcification/degeneration of a tricuspid aortic valve in the elderly.

EPIDEMIOLOGY

Prevalence in ~3% of 75-year-olds.

>

. Those with bicuspid aortic valve may present earlier (as young adults).

HISTORY

May be asymptomatic initially.

Angina (because of “ oxygen demand of the hypertrophied ventricles).

Syncope or dizziness on exercise.

Symptoms of heart failure (e.g. dyspnoea).

EXAMINATION

BP: Narrow pulse pressure.

Pulse: Slow-rising.

Palpation: Thrill in the aortic area (if severe). Forceful sustained thrusting undisplaced apex beat.

Auscultation: Harsh ejection systolic murmur at aortic area, radiating to the carotid artery and apex. Second heart sound (A2 component) may be softened or absent (because of calcification). A bicuspid valve may produce an ejection click.

Distinguish from aortic sclerosis¹ and hypertrophic obstructive cardiomyopathy (HOCM).²

INVESTIGATIONS

ECG: Signs of left ventricular hypertrophy (deep S wave in V_1–2, tall R wave in V_5–6, inverted T waves in I, aVL, V_5–6 and left-axis deviation), LBBB.

CXR: Post-stenotic enlargement of the ascending aorta, calcification of aortic valve.

Echocardiogram: Visualizes structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar). Estimation of aortic valve area and pressure gradient across the valve in systole and left ventricular function may be assessed.

Cardiac angiography: Allows differentiation from other causes of angina, and to assess for concomitant coronary artery disease (50% of patients with severe aortic stenosis have significant coronary artery disease).

MANAGEMENT

General principle is surgical management unless contraindicated.

Surgical: Valve replacement is recommended if valve pressure difference is >50 mmHg in a symptomatic patient. If unfit for surgery, balloon dilation (valvoplasty) may be performed but this is considered to be a palliative procedure due to high rate of complications (e.g. MI, myocardial perforation, severe AR).

Medical: Manage left ventricular failure (see Cardiac failure); ACE inhibitors and vasodilators should be used very cautiously in aortic stenosis. Antibiotic prophylaxis against infective endocarditis.

COMPLICATIONS

Arrhythmias, Stokes–Adams attacks, MI, left ventricular failure and sudden death.

PROGNOSIS

Survival differs according to symptoms. In symptomatic patients with severe aortic stenosis causing left ventricular failure, average survival 50% at 18 months without surgery. Average survival with angina 5 years; syncope 3 years; dyspnoea 2 years.

Atrial fibrillation

DEFINITION

Characterized by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: ‘permanent’, ‘persistent’ and ‘paroxysmal’.

AETIOLOGY

There may be no identifiable cause (‘lone’ atrial fibrillation (AF)). Secondary causes lead to abnormal atrial electrical pathways that result in AF.

Systemic causes: Thyrotoxicosis, hypertension, pneumonia, alcohol.

Heart: Mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, sick sinus syndrome,¹ atrial myxoma.

Lung: Bronchial carcinoma, pulmonary embolism.

EPIDEMIOLOGY

Very common in the elderly (~5% of those >65 years). May be paroxysmal.

HISTORY

Often asymptomatic. Some patients experience palpitations or syncope. Symptoms of the cause of the AF.

EXAMINATION

Irregularly irregular pulse, difference in apical beat and radial pulse. ...