‘The eyes see what the brain knows.’ This old adage, famous in the echelons of medicine, highlights why syncope is important in clinical medicine, for it is often missed while evaluating a patient.
Syncope is a transient loss of consciousness due to cerebral hypoperfusion. In simple terms, it is a brief cut-off from reality, which is accompanied by a loss of tone and posture, and ends with regaining of consciousness once perfusion to the brain is reinstated.
The path to the hospital for syncope is as varied as are its causes. It is the end effect of multiple pathologies – neural, orthostatic hypotension, cardiac, all of which have a peculiar origin – an evolutionary bane.
Humans adopted the upright posture to enable greater range for themselves. However this produced a unique physiologic stress on the body – to maintain constant perfusion pressure against gravity to the brain. Consequently, about 1 litre of blood gets pooled in the vascular plexus in the lower limbs, which draws from the central circulation. The workaround for this is cerebral autoregulation. Cerebral autoregulation refers to the brain’s ability to maintain constant/stable blood despite changes in blood volume of the central circulation.
When this cerebral autoregulation is altered, it leads to the final outcome of syncope, a transient, self-limited loss of consciousness, so brief that the patient or their caretakers might not even recognise it.
Some case studies of syncope
The following case study is one interesting example.
A 27-year-old male had presented to the orthopaedic department multiple times with recurrent fractures of the upper limb over the course of three months, all of which occurred in his washroom. It took a physician friend of the orthopaedic surgeon to link the falls in the washroom to micturition syncope (fainting while urinating), a rare type, where syncope occurs post urination highlighting the importance of interdisciplinary coordination in health.
A vasovagal syncope, also known as a neurally-mediated syncope occurs when the nervous system overreacts to a stimulus – pain, emotion, cough, swallow, anxiety, etc. – which leads to an enhanced parasympathetic out flow and a sympathoinhibition which leads to the final effect – syncope.
Ocular pressure, during ocular examinations, fear and anxiety, recurrent cough, airway instrumentation, post micturition and defecation, glossopharyngeal neuralgia (severe attacks of pain in the mouth) and carotid sinus massage are the more common causes of neural mediated syncope.
It is important to diagnose neural mediated syncope as it can save a lot on unnecessary investigations and loss of time of the patient, as most cases improve with reassurance and awareness of the event, and avoidance of stimuli. First aid measures of isometric counter pressure manoeuvres like hand grip and limb tensing help in aborting the syncope.
Presyncope is lightheadedness, dizziness, and weakness with auditory and visual symptoms. This signifies the onset of decreasing cerebral perfusion pressure where the brain is starting to find it difficult to work with the supply of blood and the pressure at which it is supplied.
In another case, a 78-year-old female was referred to a tertiary care set-up to evaluate for knee buckling for the past three months. The anxiety of knee buckling would not let her go to sleep, as, if she did, it would lead to her falling down after getting up from the bed. This too, was a case of syncope. But how could a person stay awake for three months? The answer was her armchair, where she would sleep comfortably after lunch for three hours until her son came back from work. This turned out to be a simple case of orthostatic hypotension induced syncope, which was treated by asking her to be seated for a few minutes after getting up from a supine position and then getting up, and the knee buckling vanished altogether!
Orthostatic hypotension is the reduction of systolic BP of at least 20 mmHg and diastolic BP of at least 10 mmHg after three minutes of standing up from a supine position. This is a result of sympathetic vasoconstrictor hypoactivity leading to pooling of blood, secondary to gravity. The most common cause is diabetic autonomic dysfunction.
With the increasing geriatric population, synuclienopathies like Parkinson’s Disease and Multisystem Atrophy are witnessing orthostatic hypotension in old age.
As with all conditions in medicine, remove the reversible causes. Non-pharmacological interventions like staged moving to an erect posture, avoidance of large meals, and isometric counter pressure manoeuvres need to be explained to patients.
In a third instance, we examine the case of a 43-year-old female who came to the OPD with complaints of multiple presyncopal episodes which recur every other month. Her neurological and cardiac evaluations were normal and there was no orthostatic hypotension. Multiple investigations were done in vain. It took a keen-eyed physician who glanced at her neck and found a goitre. Her thyroid profile revealed she was hyperthyroid and this led her to have paroxysms of atrial fibrillation which caused the presyncope. Anti-thyroid medications ensured she never had a presyncopal episode again.
Cardiac syncope is caused by arrhythmia or, rarely, due to structural heart disease. The idea is to have a comprehensive look out for the arrhythmia which may be paroxysmal as discussed in the above case. Cardiomyopathies can predispose to arrhythmia which lead to syncope.
So why is syncope still an enigma?
This is primarily due to the multiple differential diagnoses that it throws at the doctor. The physician has to decipher a syncope from a seizure, hypoglycaemia, cataplexy and psychiatric illness like anxiety panic disorders and somatisation disorders.
The thumb rule of a loss of consciousness of more than 5 minutes being a seizure is a good guide. Another guide would be postictal confusion which is conspicuous in its absence in syncope.
Cataplexy is known for intact consciousness with loss of tone and posture. Hypoglycemia is generally identified by the presence of hunger, which is absent in syncope. A medication history of oral hypoglycaemic agents or insulin is of utmost importance in narrowing down the investigations. A low CBG is highly diagnostic.
Patients need to be evaluated on an OPD basis with a detailed yet pointed history with a special focus on psychiatric history, along with a blood pressure for orthostatic hypotension and an ECG to rule out cardiac causes of syncope. Targeted investigations for anemia, thyroid profile, uremia, and hepatic function serve better than a routine baseline blood test. Tests often not performed on a routine basis to evaluate the autonomic nervous system become of extreme importance here.
A detailed cardiovascular evaluation with a Holter monitor for 24-hour ECG and an ambulatory BP monitoring added with a 2D Echocardiography ensures a comprehensive baseline workup. Rare causes can be unearthed with a treadmill test where exercise induced tachyarrhythmia are covered.
Syncope is a common problem that results in about 3% of all hospital admissions. The knowledge of syncope enables early diagnosis, significantly reducing DALY (disability-adjusted life years). While most of the investigations are to be done on an OP basis, some conditions like coronary ischemia, atrial fibrillation, Trifascicular block, and ECG with long QT , and a family history of sudden cardiac deaths warrant in-patient (IP) evaluation.
Syncope is one of those rare presentations that needs a broad-based approach inclusive of all systems in the body.
(Dr. Arvind Radhakrishnan is a final year general medicine postgraduate and simplifies health for all through medical communication. [email protected])
Published – April 20, 2025 02:03 pm IST