Adams–Stokes syndrome |
Classification and external resources |
ICD-10 |
I45.9 |
ICD-9 |
426.9 |
DiseasesDB |
12443 |
MeSH |
D000219 |
Stokes–Adams syndrome (alternative eponyms include Gerbezius-Morgagni-Adams-Stokes syndrome and Gerbec-Morgagni-Adams-Stokes syndrome)[1] refers to a sudden, transient episode of syncope, occasionally featuring seizures. Named after two Irish physicians, Robert Adams (1791–1875)[2] and William Stokes (1804–1877)[3], the first description of the syndrome was published in 1717 by the Carniolan physician of Slovene descent Marko Gerbec, which was 44 years after its publication quoted by Giovanni Battista Morgagni.
Contents
- 1 Signs and symptoms
- 2 Diagnosis
- 3 Causes
- 4 Treatment
- 5 Prognosis
- 6 References
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Signs and symptoms
Prior to an attack, a patient may become pale, their heart rhythm experiences a temporary pause, and collapse may follow. Normal periods of unconsciousness last approximately thirty seconds; if seizures are present, they will consist of twitching after 15–20 seconds. Breathing continues normally throughout the attack, and so on recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.[4]
As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient's position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.[4]
Diagnosis
Stokes-Adams attacks may be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic. The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.
Causes
The attacks are caused by lack of cardiac output due to antimony poisoning, cardiac asystole, heart block, Lev's disease or ventricular fibrillation. The resulting lack of blood flow to the brain is responsible for the faint.
Treatment
Initial treatment can be medical, involving the use of drugs like isoprenaline (Isuprel) and epinephrine (adrenaline). Definitive treatment is surgical, involving the insertion of a pacemaker – most likely one with sequential pacing such as a DDI mode as opposed to the older VVI mechanisms,[4] and the doctor may arrange the patient to undergo Electrocardiography to confirm this type of treatment.[5]
Prognosis
If undiagnosed (or untreated), Stokes–Adams attacks have a 50% mortality within a year of the first episode. The prognosis following treatment is very good.
References
- ^ synd/1158 at Who Named It?
- ^ R. Adams. Cases of Diseases of the Heart, Accompanied with Pathological Observations. Dublin Hospital Reports, 1827, 4: 353–453.
- ^ W. Stokes. Observations on some cases of permanently slow pulse. Dublin Quarterly Journal of Medical Science, 1846, 2: 73–85.
- ^ a b c Katz, Jason; Patel, Chetan (2006). Parkland Manual of Inpatient Medicine. Dallas, TX: FA Davis. p. 903.
- ^ Chart 63: "Faintness and Fainting" ISBN 0-86318-864-8, page 161
Cardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429)
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Ischaemic |
CD/CHD
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CAD · Coronary thrombosis · Coronary vasospasm · Coronary artery aneurysm · Coronary artery dissection · Myocardial Bridge
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Active ischemia
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Angina pectoris (Prinzmetal's angina, Stable angina) · Acute coronary (Unstable angina, Myocardial infarction / heart attack)
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Sequelae
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hours (Myocardial stunning, Hibernating myocardium) · days (Myocardial rupture) · weeks (Aneurysm of heart/Ventricular aneurysm, Dressler's syndrome)
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Layers |
Pericardium
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Pericarditis (Acute, Chronic/Constrictive) · Pericardial effusion (Hemopericardium, Cardiac tamponade)
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Myocardium
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Myocarditis (Chagas disease)
Cardiomyopathy: Dilated (Alcoholic) · Hypertrophic · Restrictive (Loeffler endocarditis, Cardiac amyloidosis, Endocardial fibroelastosis)
Arrhythmogenic right ventricular dysplasia
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Endocardium/
valves
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Endocarditis
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Infective endocarditis (Subacute bacterial endocarditis) · noninfective endocarditis (Nonbacterial thrombotic endocarditis, Libman-Sacks endocarditis)
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Valves
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mitral (regurgitation, prolapse, stenosis) · aortic (stenosis, insufficiency) · tricuspid (stenosis, insufficiency) · pulmonary (stenosis, insufficiency)
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Conduction/
arrhythmia |
Bradycardia
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Sinus bradycardia · Sick sinus syndrome
Heart block: Sinoatrial · AV (1°, 2°, 3°) · Intraventricular (Bundle branch/Right/Left, Left anterior fascicular/Left posterior fascicular, Bifascicular/Trifascicular) · Adams–Stokes syndrome
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Tachycardia
(paroxysmal and sinus)
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Supraventricular
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Atrial (Multifocal) · Junctional (AV nodal reentrant, Junctional ectopic)
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Ventricular
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Torsades de pointes · Catecholaminergic polymorphic · Accelerated idioventricular rhythm
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Premature contraction
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Atrial · Ventricular
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Pre-excitation syndrome
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Wolff-Parkinson-White · Lown-Ganong-Levine
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Flutter/fibrillation
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Atrial flutter · Ventricular flutter · Atrial fibrillation (Familial) · Ventricular fibrillation
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Pacemaker
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Wandering pacemaker · Ectopic pacemaker/Ectopic beat · Parasystole · Multifocal atrial tachycardia · Pacemaker syndrome
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Long QT syndrome
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Romano-Ward syndrome · Andersen-Tawil syndrome · Jervell and Lange-Nielsen syndrome
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Cardiac arrest
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Sudden cardiac death · Asystole · Pulseless electrical activity · Sinoatrial arrest
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Other/ungrouped
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hexaxial reference system (Right axis deviation, Left axis deviation) · QT (Short QT syndrome) · T (T wave alternans) · ST (Osborn wave, ST elevation, ST depression)
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Cardiomegaly |
Ventricular hypertrophy (Left, Right/Cor pulmonale) · Atrial enlargement (Left, Right)
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Other |
Cardiac fibrosis · Heart failure (Diastolic heart failure, Cardiac asthma) · Rheumatic fever
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noco/cong/tumr, sysi/epon, injr
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proc, drug (C1A/1B/1C/1D), blte
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