Loss of Consciousness History Taking – OSCE guide

---

Taking a history from a patient presenting after an episode of loss of consciousness (LOC) is an important skill that is often assessed in OSCEs. This guide provides a structured approach to taking a LOC history in an OSCE setting.

---

Background

Syncope

Syncope occurs due to global cerebral hypoperfusion which can itself have a variety of underlying causes which are discussed below.

Reflex syncope (a.k.a. neurally mediated syncope)

Reflex syncope involves a neurally mediated sudden decrease in blood pressure and heart rate in response to a trigger.

Vasovagal syncope is a form of reflex syncope which can be triggered by:

• Emotional distress (e.g. fear, pain, instrumentation, blood phobia, enclosed space)
• Orthostatic stress (e.g. prolonged standing)

Situational syncope is a form of reflex syncope which can be triggered by coughing, sneezing, defecating, urinating, exercising and eating (post-prandial).

Carotid sinus hypersensitivity is another form of reflex syncope which can be triggered by sudden head-turning, wearing a tight collar and shaving.

Cardiovascular syncope

Cardiovascular syncope involves sudden decreased cardiac output secondary to pathology within the cardiovascular system such as:

• Arrhythmias
• Structural cardiovascular disease (e.g. coronary artery disease, valve disease, cardiac tamponade, hypertrophic cardiomyopathy and aortic dissection)
• Structural pulmonary disease (e.g. pulmonary embolism)

Orthostatic hypotension

Orthostatic hypotension involves a sudden drop in blood pressure after standing upright.

Causes of orthostatic hypotension include:

• Hypovolaemia (e.g. haemorrhage, diarrhoea, vomiting)
• Iatrogenic (e.g. beta-blockers, diuretics, alcohol, vasodilators, antidepressants, phenothiazines)
• Autonomic failure (e.g. diabetic neuropathy, Parkinson’s disease, spinal cord injury)

Seizure

Seizures are caused by abnormal excessive neuronal activity in the brain, leading to impairment of normal cognitive function. Seizures that involve a complete loss of consciousness are known as generalised seizures (either convulsive or non-convulsive).

Causes of generalised seizures include:

• Metabolic disturbances (e.g. hypoglycaemia, electrolyte abnormalities, drug or alcohol intoxication and adrenal insufficiency)
• Space-occupying lesions (e.g. brain metastases, primary brain tumour, cerebral abscess)
• Head trauma
• Stroke
• Medication: some medications lower the seizure threshold (e.g. nefopam).
• Epilepsy: spontaneous abnormal excessive neuronal activity in the brain.

---

Opening the consultation

Wash your hands and don PPE if appropriate.

Introduce yourself to the patient including your name and role.

Confirm the patient’s name and date of birth.

Explain that you’d like to take a history from the patient.

Gain consent to proceed with history taking.

---

Presenting complaint

Use open questioning to explore the patient’s presenting complaint:

• “What’s brought you in to see me today?”
• “Tell me about the issues you’ve been experiencing.”

Provide the patient with enough time to answer and avoid interrupting them.

Facilitate the patient to expand on their presenting complaint if required:

• “Ok, can you tell me more about that?”
• “Can you explain what that pain was like?”

---

History of presenting complaint

A comprehensive history is essential to effectively narrow the differential diagnosis in patients presenting with loss of consciousness. A collateral history from someone who witnessed the episode is often required to gain accurate details about what happened during and immediately after the loss of consciousness.

Before the loss of consciousness

Triggers

It is important to explore potential triggers for the loss of consciousness as they may provide insight into the likely underlying pathology:

• “Was there any obvious trigger that preceded your loss of consciousness?”
• “What were you doing just before you lost consciousness?”

Reflex syncope is often associated with a trigger:

• Vasovagal syncope: triggers include emotional distress (e.g. fear, pain, instrumentation, blood phobia) and orthostatic stress (e.g. prolonged standing).
• Situational syncope: triggers include cough, sneeze, defecation, micturition, exercise and eating (post-prandial).
• Carotid sinus hypersensitivity: triggers include shaving, tight-fitting collars and sudden turning of the head.

Triggers in other types of loss of consciousness can include:

• Physical exertion: associated with cardiovascular syncope (e.g. aortic stenosis, arrhythmia).
• Standing from sitting: associated with orthostatic hypotension (e.g. hypovolaemia, autonomic failure).
• Working with arms elevated above head: associated with subclavian steal syndrome.
• Exposure to rapidly flickering light source: associated with photosensitive epilepsy.

Prodromal symptoms including aura

Vasovagal syncope is often preceded by prodromal symptoms such as:

• Progressive light-headedness
• Visual disturbances (dimming of vision or loss of vision)
• Weakness or sensory disturbances of the extremities
• Sweating
• Nausea
• Tinnitus

The patient also typically demonstrates a slow, controlled collapse towards the ground (unlike cardiovascular syncope which typically involves a sudden uncontrolled fall to the ground).

Cardiovascular syncope often lacks any prodromal symptoms, with the patient feeling ok and then losing consciousness suddenly with no warning. Sometimes patients with cardiovascular syncope may experience palpitations or chest pain prior to the loss of consciousness (secondary to an arrhythmia). You should, therefore, consider the possibility of an underlying arrhythmia or structural heart disease if the patient reports palpitations, chest pain or a complete absence of prodromal symptoms. Chest pain is also associated with pulmonary embolism and aortic dissection, both of which can cause syncope.

Ask the patient if they experienced any prodromal symptoms:

• “Did you have any symptoms before you lost consciousness?”
• “Did you notice any visual changes before your lost consciousness?”
• “Did you feel nauseated or sweaty before you lost consciousness?”
• “Did you notice any changes to your hearing before you lost consciousness?”
• “Did you notice any weakness or changes in sensation before you lost consciousness?”
• “Did you notice that your heartbeat became more prominent before you lost consciousness?”
• “Did you experience any chest pain before you lost consciousness?”

Generalised seizures can begin with epileptic auras or focal motor/sensory seizures causing symptoms such as:

• Olfactory or gustatory hallucinations (e.g. a specific smell or taste)
• Visual hallucinations (e.g. flashing lights or blurring of vision)
• A sense of déjà-vu
• Sensory disturbances (e.g. numbness, tingling)
• Motor weakness (e.g. unilateral limb weakness, twitching)

Ask the patient if they experienced any focal motor/sensory or aura-like symptoms:

• “Did you notice any unusual smells or tastes prior to losing consciousness?”
• “Did you experience any visual hallucinations prior to losing consciousness?”
• “Did you experience a sense of déjà-vu prior to losing consciousness?”
• “Did you experience any changes to the sensation of your body prior to losing consciousness?”
• “Did you notice any twitching or weakness or your arms, legs or face prior to losing consciousness?”

During the period of unconsciousness

Motor symptoms

Ask the person providing the collateral history if the patient’s muscles appeared stiff or flaccid and if they noticed any jerking movements:

• “Did the patient’s muscles appear stiffened or flaccid during the episode?”
• “Did you notice any jerking movements during the episode?”

During a syncopal episode, most patient’s muscles will become flaccid secondary to cerebral hypoperfusion. In cases where a patient has a syncopal episode which results in them remaining upright (e.g. against a wall), they may then develop stiffening of the muscles and jerking movements as a result of a secondary anoxic seizure due to prolonged cerebral hypoperfusion.

Initial tonic stiffening, followed by clonic (jerking) movements of the extremities is typically associated with generalized tonic-clonic seizures.

Duration

Ask the person providing the collateral history how long the episode of LOC lasted:

• “How long did the episode last in total?”
• “Was the episode seconds or several minutes long?

Episodes of syncope typically last less than 20 seconds.

Seizures typically last longer than 20 seconds, although it is possible to have seizures of a shorter duration.

Other clinical features

Ask the patient or the person providing the collateral history if they noticed any other clinical features during the episode:

• “Did you notice any evidence of tongue biting during the episode?”
• “Was there loss of continence during the episode?”
• “Did the patient appear blue in colour during the episode? Was this immediate or did it develop after a while?”

Tongue biting (typically the lateral aspect) is more commonly associated with generalized tonic-clonic seizures.

Urinary or faecal incontinence is more commonly associated with seizures than syncope (although it can occur in either).

Cyanosis caused by cardiorespiratory arrest is typically associated with arrhythmias, structural cardiac disease and pulmonary embolism.

Cyanosis can also occur in the context of a prolonged seizure, however tonic-clonic movements will typically precede the development of cyanosis.

After the loss of consciousness

Time to full recovery

Ask the person providing the collateral history how long it took for the patient to regain consciousness and if they were confused initially:

• “How long did it take for the patient to be back to their usual self?”
• “Did they seem confused after the loss of consciousness?”
• “Did they appear drowsy after the loss of consciousness?”

Patients experiencing a syncopal episode will typically regain consciousness and full lucidity within 20-30 seconds.

Patients experiencing a seizure will have a post-ictal period after the seizure in which they may be drowsy, confused and agitated. The post-ictal period can last for several minutes to hours and is often not remembered by the patient.

Relieving factors

Ask if there was anything that seemed to quickly resolve the episode of loss of consciousness:

• “Was there anything that seemed to help bring the patient around?”

Patients experiencing an episode of orthostatic hypotension may improve suddenly once laid flat on the ground and may lose consciousness again if sat back up.

Patients experiencing a seizure may stop seizing upon administration of a benzodiazepine.

Further questions

Ask the patient or person providing the collateral history if they think any injuries have occurred as a result of the episode:

• “Did you see any evidence of injuries during or after the period in which they lost consciousness?”
• “Did they fall as a result of the loss of consciousness?”
• “Have you got any pain anywhere at the moment?”

Ask specifically about whether the patient incurred any head trauma and airway issues during the episode:

• “Did the patient hit their head at any point during the episode?”
• “Did the patient vomit whilst unconscious and was there evidence of any loose objects within their mouth during or immediately after the episode?”

Ideas, concerns and expectations

A key component of history taking involves exploring a patient’s ideas, concerns and expectations (often referred to as ICE) to gain insight into how a patient currently perceives their situation, what they are worried about and what they expect from the consultation.

The exploration of ideas, concerns and expectations should be fluid throughout the consultation in response to patient cues. This will help ensure your consultation is more natural, patient-centred and not overly formulaic.

It can be challenging to use the ICE structure in a way that sounds natural in your consultation, but we have provided several examples for each of the three areas below.

Ideas

Explore the patient’s ideas about the current issue:

• “What do you think the problem is?”
• “What are your thoughts about what is happening?”
• “It’s clear that you’ve given this a lot of thought and it would be helpful to hear what you think might be going on.”

Concerns

Explore the patient’s current concerns:

• “Is there anything, in particular, that’s worrying you?”
• “What’s your number one concern regarding this problem at the moment?”
• “What’s the worst thing you were thinking it might be?”

Expectations

Ask what the patient hopes to gain from the consultation:

• “What were you hoping I’d be able to do for you today?”
• “What would ideally need to happen for you to feel today’s consultation was a success?”
• “What do you think might be the best plan of action?”

Summarising

Summarise what the patient has told you about their presenting complaint. This allows you to check your understanding of the patient’s history and provides an opportunity for the patient to correct any inaccurate information.

Once you have summarised, ask the patient if there’s anything else that you’ve overlooked. Continue to periodically summarise as you move through the rest of the history.

Signposting

Signposting, in a history taking context, involves explicitly stating what you have discussed so far and what you plan to discuss next. Signposting can be a useful tool when transitioning between different parts of the patient’s history and it provides the patient with time to prepare for what is coming next.

Signposting examples

Explain what you have covered so far: “Ok, so we’ve talked about your symptoms, your concerns and what you’re hoping we achieve today.”

What you plan to cover next: “Next I’d like to quickly screen for any other symptoms and then talk about your past medical history.”

---

Systemic enquiry

A systemic enquiry involves performing a brief screen for symptoms in other body systems which may or may not be relevant to the primary presenting complaint. A systemic enquiry may also identify symptoms that the patient has forgotten to mention in the presenting complaint.

Deciding on which symptoms to ask about depends on the presenting complaint and your level of experience.

Some examples of symptoms you could screen for in each system include:

• Systemic: fevers (e.g. cerebral abscess, meningitis), weight change (e.g. malignancy)
• Cardiovascular: palpitations (e.g. arrhythmia), chest pain (acute coronary syndrome), shortness of breath (e.g. heart failure)
• Respiratory: dyspnoea, cough (e.g. pneumonia), pleuritic chest pain (e.g. pulmonary embolism)
• Gastrointestinal: diarrhoea, vomiting (e.g. dehydration/hypotension)
• Genitourinary: oliguria (e.g. dehydration/hypotension)
• Neurological: visual symptoms (e.g. pre-syncope), headache (e.g. brain tumour), motor or sensory disturbances (e.g. stroke)
• Musculoskeletal: trauma (e.g. secondary to syncope)
• Dermatological: rashes (e.g. meningococcal sepsis)

---

Past medical history

Ask if the patient has any medical conditions: 

• “Do you have any medical conditions?”
• “Are you currently seeing a doctor or specialist regularly?”

If the patient does have a medical condition, you should gather more details to assess how well controlled the disease is and what treatment(s) the patient is receiving. It is also important to ask about any complications associated with the condition including hospital admissions.

Ask if the patient has previously undergone any surgery or procedures (e.g. coronary artery bypass grafts, pacemaker insertion):

• “Have you ever previously undergone any operations or procedures?”
• “When was the operation/procedure and why was it performed?”

Allergies

Ask if the patient has any allergies and if so, clarify what kind of reaction they had to the substance (e.g. mild rash vs anaphylaxis).

---

Drug history

Ask if the patient is currently taking any prescribed medications or over-the-counter remedies:

• “Are you currently taking any prescribed medications or over-the-counter treatments?”

If the patient is taking prescribed or over the counter medications, document the medication name, dose, frequency, form and route.

Ask if the patient has recently started any medications which may have precipitated a seizure (e.g. nefopam) or caused a syncopal episode (e.g. antihypertensive):

• “Have you recently started any new medications?”

Ask the patient if they’re currently experiencing any side effects from their medication:

• “Have you noticed any side effects from the medication you currently take?”

Ask the patient if they’ve recently stopped any medications or had any doses changed as this may have precipitated a seizure (e.g. gabapentin withdrawal) or resulted in hypotension (e.g. corticosteroid withdrawal causing adrenal insufficiency):

• “Have you recently stopped any medications?”

---

Family history 

Ask the patient if there is any family history of cardiovascular disease or seizures:

• “Do any of your parents or siblings have any heart problems or have they experienced seizures in the past?” 

Clarify at what age the disease developed (disease developing at a younger age is more likely to be associated with genetic factors):

• “At what age did your father suffer his first heart attack?”

If one of the patient’s close relatives are deceased, sensitively determine the age at which they died and the cause of death:

• “I’m really sorry to hear that, do you mind me asking how old your dad was when he died?”
• “Do you remember what medical condition was felt to have caused his death?”

If the patient reports unexplained sudden deaths in young relatives, consider the possibility of cardiac channelopathies (e.g. Brugada syndrome, long QT syndrome).

---

Social history

Explore the patient’s social history to both understand their social context and identify potential risk factors.

General social context

Explore the patient’s general social context including:

• the type of accommodation they currently reside in (e.g. house, bungalow) and if there are any adaptations to assist them (e.g. stairlift)
• who else the patient lives with and their personal support network
• what tasks they are able to carry out independently and what they require assistance with (e.g. self-hygiene, housework, food shopping)
• if they have any carer input (e.g. twice daily carer visits)

Understanding the patient’s daily activities allows you to consider the risk posed by further episodes of LOC.

Smoking

Record the patient’s smoking history, including the type and amount of tobacco used.

Calculate the number of ‘pack-years‘ the patient has smoked for to determine their cardiovascular risk profile:

• pack-years = [number of years smoked] x [average number of packs smoked per day]
• one pack is equal to 20 cigarettes

Alcohol

Record the frequency, type and volume of alcohol consumed on a weekly basis.

Patients drinking significant volumes of alcohol regularly are at increased risk of seizures, particularly if they suddenly stop drinking (i.e. alcohol withdrawal seizures). Patients who binge drink are also at increased risk of seizures secondary to acute intoxication.

Recreational drug use

Ask the patient if they use recreational drugs and if so determine the type of drugs used and their frequency of use. Recreational drugs can cause seizures and syncope.

Fluid intake

Patients with poor fluid intake are at increased risk of syncopal episodes (e.g. secondary to hypotension).

Occupation

Ask about the patient’s current occupation:

• Explore what tasks the patient performs at work to identify high-risk activities (e.g. working at heights, operating heavy machinery).
• If the patient is experiencing episodes of LOC and works with heavy machinery or at heights, it is important to advise them to take time off work until they have been fully investigated.

Driving

If the patient drives and has presented with LOC it is important to advise them not to drive until they have been fully investigated and to inform the relevant driving authority (e.g. DVLA) of their current medical issues.

---

Closing the consultation

Summarise the key points back to the patient.

Ask the patient if they have any questions or concerns that have not been addressed.

Thank the patient for their time.

Dispose of PPE appropriately and wash your hands.

---

References

1. Developed in collaboration with, European Heart Rhythm Association (EHRA), Heart Failure Association (HFA), et al. Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). European Heart Journal. 2009;30(21):2631-2671. doi:10.1093/eurheartj/ehp298.
2. Seizures & Syncope. In: Aminoff MJ, Greenberg DA, Simon RP. eds. Clinical Neurology, 9e New York, NY: McGraw-Hill; 2015. Accessed June 28, 2017.
3. Syncope. In: Stern SC, Cifu AS, Altkorn D. eds. Symptom to Diagnosis: An Evidence-Based Guide, 3e New York, NY: McGraw-Hill; 2014. Accessed June 28, 2017.
4. The Nervous System. In: LeBlond RF, Brown DD, Suneja M, Szot JF. eds. DeGowin’s Diagnostic Examination, 10e New York, NY: McGraw-Hill; 2014. Accessed June 28, 2017.
5. Benditt D. Syncope in adults: Clinical manifestations and diagnostic evaluation. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed on June 30, 2017.
6. Dhileepan V. Syncope – Causes and history taking. Geeky Medics. Available from: [LINK]. Accessed on June 15^th 2017.
7. Dirk PS, Gert van Dijk J. Classifying syncope. Autonomic Neuroscience. 2014;184:3-9.
8. Egedy M, Fournier A. Syncopes. In: Dictionnaire de pédiatrie Weber. Montreal, QC: Chenelière education; 2015:1069-1070.
9. Hatoum T, Sheldon R. A practical approach to the investigation of syncope. Can J
10. Cardiol. 2014 Jun;30(6):671-4. PubMed PMID: 24882540.
11. Khan T, Stecker M, Stecker M. Evaluating the patient with loss of consciousness. Surgical Neurology International. 2015;6(Suppl 6): S262-S265. doi:10.4103/2152-7806.157615.
12. Letendre J. Syncope et lipothymie. In: Guide pratique de médecine Clinique. Ville Mont-Royal, QC: Décarie Éditeur inc.; 2004:329-334.
13. Morin G, Lacroix G, Baraboi E. Petit guide de l’entrevue médicale. Québec, QC: GPHC; 2016:155-158.
14. Sirven JI, Britton JW, Cascino GD, et al. Epilepsy. New York, NY: American Academy of Neurology; 16, 47.

---