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The differential of syncope or a brief loss of consciousness is best developed with the use of physiology and, to a lesser extent, anatomy. Like convulsions , syncope is due to a diminished supply of oxygen and glucose in the brain cell. Anything that produces hypoglycemia may lead to episodes of syncope, but the most common cause is overdose of insulin. It is also important to include insulinomas and overdose of oral hypoglycemic agents (Table 55). Reduced delivery of oxygen to the brain cell accounts for most cases of syncope. Oxygen must get into the body through the lungs with adequate ventilation. It must then be absorbed through the alveolar–capillary membrane, picked up by an adequate number of red cells, and delivered to the brain by a good functioning heart and unobstructed carotid and vertebral–basilar system. Retracing the above physiology and anatomy will develop the disease entities that must be considered in the differential diagnosis of syncope.
SYNCOPE
I C A T E Intoxication Congenital Autoimmune Trauma Endocrine Allergic Tolbutamide Hypoglycemic drugs and insulin Insulinoma Addison disease HypopituitarismPneumoconiosis Cystic fibrosis Sarcoidosis AnemiaPneumothorax Drug-induced anemia Sickle cell anemia Hemolytic anemia Idiopathic thrombocytopenic purpura Blood loss Cardiac arrhythmias from drugs and alcohol Rheumatic valvular disease Drug-induced postural hypotension Anomalous circle of WillisMigraine Vasculitis Purpura
Thus, mechanical obstructions of the larynx (foreign body), the bronchi, bronchioles (asthma and emphysema), or alveolar–capillary membrane (pulmonary fibrosis, sarcoidosis, or pulmonary embolism) may cause anoxia and syncope. Severe anemia prevents the adequate transport of oxygen. Oxygen transport from the heart to the brain may be obstructed mechanically or functionally. It is functionally obstructed by CHF of Stokes–Adams syndrome (heart block) and other arrhythmias, particularly ventricular tachycardia and sick sinus syndrome. Functional obstruction may result from a drop in blood pressure from carotid sinus syncope, postural hypotension , and vasovagal syncope. True vertigo may lead to syncope by way of the latter mechanism. Mechanical obstruction may occur at the aortic valve (aortic stenosis or insufficiency), at the carotid arteries (thrombi or plaques), or focally in the smaller arteries from ischemia due to arterial thrombi or emboli. Less commonly, mechanical obstruction may occur from ball–valve thrombi in the mitral or tricuspid valve, large pulmonary emboli, or cough syncope in which poor venous return to the heart is the cause.
Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.