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Stokes-Adams Attacks
A classic Stokes-Adams attack is a collapse without warning, associated with loss of consciousness for a few seconds.1 Typically, complete (third degree) heart block is seen on the ECG during an attack (but other ECG abnormalities such as tachy-brady syndrome have been reported).1,2
Cardiologists, and other doctors specialising in syncope, do not use the term 'Stokes-Adams attack' as often these days. The development of investigation techniques and improvements in the understanding of the physiology of the cardiovascular system have meant that there has been a move away from clinical diagnoses to a more rigid diagnostic classification.1
Various synonyms include Adams-Stokes, Morgagni, Morgagni-Adams-Stokes and Spens syndrome.
- The condition is usually associated with ischaemic heart disease and so tends to occur in the elderly.
- Stokes-Adams attacks have been reported in much younger age groups, including those with congenital heart block. With congenital heart block, it has been described as being precipitated by bradycardia or tachycardia.3
- Heart block may result from:4,5,6
- Myocardial infarction
- Fibrosis (usually associated with ischaemia)
- AV-nodal disease
- Structural or valvular heart disease
- Myocarditis
- Electrolyte disturbance
- Drugs
- Rheumatic diseases including ankylosing spondylitis, Reiter syndrome, rheumatoid arthritis, scleroderma
- Infiltrative processes including amyloidosis, sarcoidosis, tumours, Hodgkin disease, multiple myeloma
- There may be a familial tendency to Stokes-Adams attacks (recognised by William Osler in 1903; the family concerned was his own).7
- Stokes-Adams attacks have been described as due to:
- Chronic or paroxysmal atrio-ventricular (AV) block in 50 to 60% of patients
- Sino-atrial (SA) block in 30 to 40%
- Paroxysmal supraventricular tachycardia or atrial fibrillation in up to 5%2
- There is collapse, usually without warning.
- Loss of consciousness is usually between about 10 and 30 seconds.
- Pallor, followed by flushing on recovery can be reported.
- Some seizure-like activity sometimes occurs if the attack is prolonged.1
- If anyone manages to check the pulse during an episode, it will be slow, usually less than 40 beats per minute.
- Recovery is fairly rapid although the patient may be confused for a while after.
- Typically complete (third degree) heart block is seen on the ECG during an attack but other ECG abnormalities such as tachy-brady syndrome have been reported.1,2 (A separate article ECG Identification of Conduction Disorders describes complete heart block in more detail.)
- Attacks can happen a number of times in one day.
- They are not posture related.
A separate article entitled Syncope details the assessment of a patient with a syncopal episode. Briefly, this should include:
- History of other episodes
- Past medical history, including history of heart disease
- Drug history: could medication be contributing?
- Blood pressure examination (supine and standing)
- Cardiovascular examination
- 12-lead ECG: this may be normal by the time the patient is seen or may show heart block or ischaemic changes; 24-hour ECG may show changes during attacks
- Routine haematological and biochemical investigations
- If underlying heart disease is suspected, this should be investigated appropriately.
- If seizure activity has been witnessed, the possibility of epilepsy should be investigated.
This is the differential diagnosis of syncope (further detailed in the separate article) and includes the following:
- Epilepsy (if convulsions occur)
- Vaso-vagal fainting
- Carotid sinus hypersensitivity
- Orthostatic hypotension
- A fast tachyarrhythmia (may also reduce cardiac output but does not usually have the same brief but dramatic effect)
- Drop attacks
- Transient ischaemic attack
- Syncope due to hypoperfusion (e.g. due to hypovolaemia)
- Reversible causes such as drug toxicity should be addressed.
- Underlying heart disease should be managed appropriately.
- A cardiac pacemaker may be required.
- If a person is susceptible to syncope with little or no warning then driving must be forbidden, at least until a diagnosis is made and a pacemaker is working well.
- Other behaviours in which sudden loss of consciousness may pose a risk also need to be addressed. These may include cycling, swimming and operating machinery.
- William Stokes (1804-1877) and Robert Adams (1791-1875) were both Irish physicians.
- Adams description of syncope associated with bradycardia dates back to 182712 and Stokes described the same association in 1846.13 (Stokes is also remembered for Cheyne-Stokes breathing.)
- Thomas Spens (1764-1842), a Scottish physician, also described a similar syndrome.
- Although Adams, Stokes, and Spens all described the syndrome independently in the early 19th century, the first description was recorded in 1761 by Morgagni.
- Giovanni Battista Morgagni (1682-1771) was an Italian anatomist and pathologist. He was a great scholar and teacher and a number of anatomical landmarks bear his name.
Document references
- Harbison J, Newton JL, Seifer C, et al; Stokes Adams attacks and cardiovascular syncope. Lancet. 2002 Jan 12;359(9301):158-60.
- Sigurd B, Sandoe E; Management of Stokes-Adams syndrome.; Cardiology. 1990;77(3):195-208. [abstract]
- Pearl W; Stokes-Adams attacks in congenital complete heart block.; Pediatr Cardiol. 1988;9(2):125-6. [abstract]
- Levine M, Brown D; Heart Block, First Degree. eMedicine, 2006.
- Levine M, Brown D; Heart Block, Second Degree. eMedicine, 2006.
- Levine MD, Brown DFM; Heart Block, Third Degree. eMedicine, 2006.
- Wooley CF, Bliss M; William Osler: slow pulse, stokes-adams disease, and sudden death in families.; Am Heart Hosp J. 2006 Winter;4(1):60-5. [abstract]
- William Stokes; on whonamedit.com
- Robert Adams; on whonamedit.com
- Thomas Spens; on whonamedit.com
- Giovanni Battista Morgagni; on whonamedit.com
- Adams R.; Cases of disease of the heart, accompanied with pathological observations. Dublin Hospital Reports 1827; 4:353-453.
- Stokes W.; Observations in some cases of permanently slow pulses. Dublin Quarterly Journal Medical Science 1846; 2:73-85.
DocID: 1119
Document Version: 22
DocRef: bgp1962
Last Updated: 3 Oct 2008
Review Date: 3 Oct 2010
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