BMJ: Blackouts and collapse

Question 1

What is a transient loss of consciousness?

Answer 1

Spontaneous loss of consciousness with complete recovery of consciousness without any residual neurological deficit

Question 2

Which major categories can TLOC be caused by?

Answer 2

Causes of TLOC may be cardiovascular, neurological, or psychogenic

Question 3

Are witness reports of seizure duration reliable?

Answer 3

No

Question 4

What is the most urgent investigation to be performed following TLOC?

Answer 4

A 12-lead ECG would be the most urgent investigation, as it would be necessary to exclude any immediate life threatening causes of TLOC

Question 5

History taking in a patient with suspected seizure

Answer 5

• Pre-seizure:
  Circumstances of the collapse/loss of consciousness
  Posture just before the event
  Prodromal symptoms, such as sweating, feeling hot, aura (“warning signs”)
• Seizure:
  Duration of the event
  Whether the patient experienced any movement, limb jerking, bit their tongue or sustained any other injuries, or was incontinent
  Bystander accounts (colour of the patient, were their eyes shut?)
  Presence or absence of confusion during the recovery period
• Post-seizure:
  What the patient can remember from during the seizure
  Are they confused afterwards?
  Any weakness down one side of the body?
  Any injuries including tongue biting
• Risk factors
  Any history of blank spells or previous TLOC
  Any history of head injury, early childhood convulsion, serious childhood illness
  Birth history (eg prematurity or birth injury), birth weight, and development
  Family history of similar events, or sudden death
  Does the patient have diabetes?

Question 6

What is the most common type of idiopathic generalised epilepsy? How much does it account for epilepsy disorders?

Answer 6

Juvenile myoclonic epilepsy, occurs in about 5% of patients who attend epilepsy clinics

Question 7

Characteristics of juvenile myoclonic epilepsy

Answer 7

• It is characterised by generalised tonic-clonic seizures, commonly on waking or within a few hours of getting up, as well as myoclonic jerks that occur during full consciousness, with a predilection for the morning, evening, or when the patient is tired
• The name juvenile myoclonic epilepsy is misleading, as the disorder is not confined to the juvenile years; instead, it is often a lifelong disorder, which usually starts around puberty.

Question 8

Treatment of juvenile myoclonic epilepsy

Answer 8

It is a condition with a high risk of recurrent seizures, so you may consider treatment with an antiepileptic drug (AED

Question 9

What is something that would make you less likely to think TLOC was caused by a vasovagal episode?

Answer 9

Confusion after the event

Question 10

What are absence seizures?

Answer 10

Absence seizures are generalised seizures where there is brief loss of consciousness, typically with no subsequent postictal state. These may be associated with myoclonic jerks

Question 11

What are functional neurological symptoms

Answer 11

• Functional neurological symptoms are emotionally generated physical symptoms
• Such symptoms can mimic physical disorders, and the differentiation from physical illness can be challenging.

Question 12

What are clinical features strongly suggestive of epilepsy?

Answer 12

• A bitten tongue
• Head turning to one side during the transient loss of consciousness (TLOC)
• No memory of abnormal behaviour that was witnessed before, during, or after the TLOC by someone else
• Unusual posturing
• Prolonged limb jerking (note that brief seizure like activity can often occur during uncomplicated faints)
• Confusion following the event
• Prodromal déjà vu, or jamais vu

Question 13

Triggers of vasovagal syncope

Answer 13

• Posture: prolonged standing, or similar episodes that have been prevented by lying down
• Provoking factors: such as pain or a medical procedure
• Prodromal symptoms: such as sweating or feeling warm/hot before TLOC

Question 14

Mrs P, a 70 year old woman with type 2 diabetes mellitus controlled with insulin, presents to the ward with fainting episodes. As Ms P speaks little English, she is able to give you only a limited history. She says the attacks are happening about once a month, and she can be sitting or standing when they occur. She reports that she faints with no warning, and thinks she briefly loses consciousness but is able to get up soon afterwards. Her lying and standing blood pressure measurements are normal. A CT scan of her head is reported as showing some early diffuse ischaemic changes but no discrete lesions.
Which two of the following are the most likely differential diagnoses?

Atonic seizure
Hypoglycaemic episode
Cardiac dysrhythmia
Vasovagal syncope
Poor mobility

Answer 14

The correct answers are:
Cardiac dysrhythmia
Vasovagal syncope

The lack of prodromal symptoms and rapid recovery after loss of consciousness (“drop attack”) suggests that cardiac dysrhythmia may be a cause. Vasovagal syncope is more common, and the standing posture of the patient could precipitate this; however, the fact that Mrs P has also experienced episodes while sitting makes this less likely. Additionally, there is no postural drop in blood pressure.

Diabetic autonomic neuropathy can predispose to postural hypotension and fainting. As this is variable in nature though often worse after meals, a normal lying and standing blood pressure does not confidently exclude this possibility.

Epilepsy is likely to produce prolonged confusion after the event, which is not consistent with Mrs P’s presentation.

Hypoglycaemia is unlikely as she recovers quickly, and without requirement for glucose treatment.

There is no evidence in the history to suggest Mrs P has poor mobility, and this would not explain the possible loss of consciousness reported.

Question 15

When is title table testing considered and its main use?

Answer 15

• Tilt table testing is useful in patients with unexplained syncope, or where there is significant occupational or personal risk to the patient.
• However, the test has a high false positive rate, and should not be used to diagnose syncope.
• Its main use is to determine whether syncope is accompanied by significant bradycardia, and therefore might respond to pacing.

Question 16

When is cardiac pacing used?

Answer 16

Pacing in the acute setting is usually used when a patient has a symptomatic bradyarrhythmia associated with adverse features, such as dizziness, syncope and/or fluid overload.

Question 17

What is the treatment for symptomatic bradycardia?

Answer 17

• Atropine as first line treatment for patients with symptomatic bradyarrhythmias (eg if there is shock, syncope, myocardial ischaemia, or heart failure)
• If symptoms do not satisfactorily respond to the treatment with atropine, you should consider giving second line drugs such as isoprenaline or adrenaline.
• If there is no response, or if medical treatment is unlikely to be effective, transcutaneous pacing under sedation should be considered.
• This is often an interim measure to facilitate transvenous pacing or a permanent pacing device.

Question 18

Dose of atropine for bradycardia

Answer 18

Atropine is given intravenously in 500 microgram doses every three to five minutes until a dose of 3 mg is reached

Question 19

Why shouldn’t atropine be given to patients with cardiac transplants?

Answer 19

Do not give atropine to patients with cardiac transplants, as it can cause high degree AV block or sinus arrest.

Question 20

What are features suggestive of cardiac dysrhythmia following TLOC?

Answer 20

Lack of prodromal symptoms and rapid recovery after TLOC (“drop attack”) are suggestive of cardiac dysrhythmia

Question 21

What is orthostatic hypotension also known as?

Answer 21

Postural hypotension

Question 22

What is orthostatic hypotension?

Answer 22

• Drop in systolic blood pressure of at least 20 mmHg, or diastolic drop of 10 mmHg, within three minutes of standing
• Also valid if a fall in systolic blood pressure to under 90 mmHg after three minutes of standing is seen

Question 23

Symptoms associated with postural hypotension

Answer 23

Associated with light-headedness and recovery is generally prompt

Question 24

Cause of orthostatic hypotension

Answer 24

• Usually secondary to failure of the autonomic reflex, volume depletion, or adverse reaction to a medication particularly in the case of polypharmacy in the elderly
• Orthostatic hypotension can be caused by both neurogenic and non-neurogenic etiologies and can also be related to medications.
• The most common causes of orthostatic hypotension are medications and conditions that cause hypovolaemia

Question 25

Neurogenic conditions that can lead to orthostatic hypotension

Answer 25

• Neurodegenerative diseases - Parkinson disease, Parkinson-plus syndromes, pure autonomic failure,
• Peripheral neuropathy - Diabetes, vitamin B12 deficiency, amyloidosis, renal failure, autoimmune, rheumatological, and paraneoplastic condition

Question 26

Non-neurogenic causes of orthostatic hypotension

Answer 26

• Most commonly due to volume depletion (e.g. Anemia, dehydration, hemorrhage, hyperglycemia)
• Cardiovascular diseases - Aortic stenosis, hypertension, atherosclerosis, heart failure, vascular stiffening, or arrhythmias
  Other - Adrenal insufficiency, physical deconditioning, aging
• Alcohol consumption
  Short term: diuretic effect, impairment of vasoconstriction[16]
  Long term or chronic: neurotoxic effects

Question 27

Medications that can lead to orthostatic hypotension

Answer 27

Alpha-blockers, antihypertensive, diuretics, nitrates, tricyclic antidepressants, selective serotonin reuptake inhibitors, antipsychotics, beta-blockers

Question 28

Which patients is lying standing blood pressure done for?

Answer 28

Usually those with syncope and pre-syncope

Question 29

How is lying standing blood pressure performed?

Answer 29

• Measure blood pressure when patient is lying down for at least 5 minutes
• Ask patient to stand up and measure blood pressure after 1 minute, then again after 3 minutes
• If after 3 minutes there is a drop in blood pressure, then positive

Question 30

What should you consider if patient during lying standing blood pressure is symptomatic after standing up, but blood pressure doesn’t drop?

Answer 30

Consider alternative diagnoses such as panic attacks, postural tachycardia syndrome, cerebrovascular disease, or hypoventilation

Question 31

Diagnosis of vasovagal syncope

Answer 31

Vasovagal syncope is a clinical diagnosis. Uncomplicated vasovagal syncope is diagnosed when:
- There are no features in the history suggestive of an alternative diagnosis, and
The three Ps are present, suggestive of uncomplicated faint:
- Posture: prolonged standing
- Provoking factors (eg pain)
- Prodromal symptoms (eg sweating or feeling hot).
*Brief convulsive activity can occur during uncomplicated faints and is not uncommon and not diagnostic of epilepsy.

Question 32

How does diabetes mellitus affect blood pressure?

Answer 32

• Diabetes mellitus can precipitate orthostatic hypotension in many ways. In hyperglycaemia, the osmotic diuresis caused by glycosuria can cause hypovolaemia.
• It can also cause autonomic neuropathy to develop as a microvascular complication. This is where the autonomic nervous system fails to respond to change in posture and increase the blood pressure on standing

Question 33

Mr T is prescribed intravenous fluids and the amlodipine is crossed off his drug chart temporarily. On further review, he reports to you that he has had loose stools for five days and is not drinking very much.

Mr T is isolated in a side room due to infection control measures and blood tests are performed, including a full blood count, and urea and electrolytes. The initial creatinine and urea are 150 micromol/L and 15 mmol/L respectively, but within 24 hours of slow intravenous fluids these results normalise. You decide to review the drug chart and notice that prior to admission he was taking 20 mg of furosemide once a day. You ask Mr T why he takes this and he tells you it is for water retention in his legs.

Which one of the following is the most appropriate action for Mr T?

• Prescribe the furosemide as blood tests have now normalised
• Stop the furosemide indefinitely
• Stop the furosemide for the time being and explain the reasons for this in the discharge summary to the GP
• Stop the furosemide, perform an urgent inpatient echocardiogram, and inform the GP of the results
• Halve the dose of the furosemide and ask the GP to consider increasing the dose back to the patient’s original dose of 20 mg when discharged

Answer 33

The most appropriate action to take in this case is to stop the diuretic due to Mr T’s acute kidney injury during this hospital admission, and to inform the GP of the change in medication. The furosemide may be exacerbating his acute kidney injury and may have contributed to his hospital admission, so continuing it at this stage is not appropriate.

An urgent inpatient echocardiogram is not needed as Mr T has no overt signs of cardiac failure. As he reports peripheral oedema, an echocardiogram may need to be considered in the future, but will not change management during this admission.

Peripheral oedema is also a known adverse effect of amlodipine so the oedema may or may not have been due to this medication. The amlodipine has already been discontinued.

Mr T should be advised to make an appointment with his GP one or two days after discharge since the GP will need to monitor Mr T’s general condition and manage his blood pressure.

Question 34

What is non-epileptic attack disorder?

Answer 34

• A psychological condition that is thought to be precipitated by psychological factors (often serious emotional trauma)
• The episodes are usually dissociative attacks, which can be seen as enabling the patient to avoid recalling traumatic episodes in their lives, or helping to cope with very strong emotions

Question 35

What is Non-epileptic attack disorder (NEAD) also known as?

Answer 35

Psychogenic seizures, dissociative seizures, or pseudoseizures

Question 36

How to differentiate between NEAD and epileptic seizures

Answer 36

• NEAD can be very difficult to differentiate from epilepsy on history alone
• The scope of functional disease (ie emotionally generated) is very wide, with symptoms including seizures, weakness, sensory change, fatigue, and concentration impairment
• Epileptic seizures rarely stop and start, except in the context of serial seizures and status epilepticus, which would be associated with a sicker patient
• Resistance to eye opening is characteristic of psychogenic (dissociative) seizures
• Raised lactate is also another indicator of true seizure

Question 37

Why is a patient resisting eye opening in an apparent “seizure” an indication that it is not a true seizure?

Answer 37

If a patient is resisting eye opening during the attack, this suggests they are not unconscious

Question 38

How to handle NEAD?

Answer 38

• When assessing people with a non-epileptic attack an ABCDE approach should be used, as in any other medical situation. Consciousness levels are assessed for NEAD in the same way as for any other type of blackout (see box below).
• If a patient is resisting eye opening during the attack, this suggests they are not unconscious. A Glasgow coma scale assessment can be done, but is often misleading due to the dependence of the scale on eye opening and speech. After the attack, patients with NEAD can appear drowsy but repeated assessment of consciousness level is not required unless you suspect an alternative cause for the drowsiness.
• Medical intervention should be considered only if there is evidence of respiratory compromise, which is not a feature of non-epileptic seizures. However, witnesses often report that the patient stops breathing for a short while. Non-epileptic seizures often respond to distraction and psychotherapy techniques. [18]
• You should try to reassure partner/family member that this is an emotional attack and she is in no imminent danger. Explain to them that it will soon pass, and perhaps suggest that she tries to concentrate on something else. Ensure that she is monitored to avoid risk of injury from falling.
• If there are persistent concerns about the nature of the seizure, a neurology opinion is advised.

Question 39

Assessment of TLOC

Answer 39

• Most patients who present with a history of TLOC will recover in the short term, which allows you to take your time with a history and examination (eg those with vasovagal syncope or hyperventilation). However, some will not, and will need you to assess and treat them urgently to prevent deterioration.
• This is best achieved using an ABCDE approach:
  Airway: Airway obstruction prevents air from entering the lungs and ultimately stops oxygen being transported to the brain. This leads to TLOC. Unless this obstruction is removed or bypassed quickly, the patient is likely to deteriorate quickly and possibly progress to cardiac arrest.

Breathing: If the patient is tachypnoeic with low peripheral oxygen saturations following an acute TLOC, you should have a high suspicion for a pulmonary embolism. If these features have a more progressive onset then pulmonary hypertension may be considered (which is often associated with peripheral oedema and a raised jugular venous pressure). A TLOC may also be triggered by raised intrathoracic pressure, which is commonly secondary to coughing or sneezing (also known as cough syncope), but you should also examine the chest for conditions such as a tension pneumothorax.

Circulation: If the patient is bradycardic (ie a heart rate of less than 60 beats per minute), then a bradyarrhythmia may be the cause of the TLOC. Hypotension (whether postural or not) is a common cause of TLOC secondary to shock, which may require urgent fluid resuscitation. You should also auscultate the heart for murmurs, as aortic stenosis and hypertrophic cardiomyopathy can both cause TLOC because of impairment of the left ventricular outflow tract. However, they can also precipitate malignant arrhythmias, so an ECG should also be performed.

All patients who are unwell following a TLOC should have a 12-lead ECG and be connected to a cardiac monitor to rule out and monitor for any possible arrhythmias.

Disability: You should start by measuring the glucose level, as hypoglycaemia may be the cause of the TLOC in someone with diabetes on treatment. Care should be taken in interpreting blood glucose, as physiological hypoglycaemia related to fasting is not generally a cause of loss of consciousness. If there is any focal neurology that persists after the TLOC then you may consider a stroke or transient ischaemic attack. Abnormal movements during a TLOC may suggest a seizure, but the differential is wide (including non-epileptic attacks and vasovagal episodes).

Exposure: Full exposure of the patient may help you to identify active haemorrhage, which may be the underlying cause of any hypotension. In addition, an urticarial rash or facial angioedema may suggest anaphylaxis as the underlying cause of the blackout.

Question 40

How common are psychogenic seizures?

Answer 40

• Psychogenic seizures are remarkably common, and may sometimes coexist with epilepsy in the same patient
• About 30% of all patients who present to neurology services in the UK having a functional disorder

Question 41

Treatment of NEAD

Answer 41

• Non-epileptic seizures often respond to distraction and psychotherapy techniques
• In patients who accept a diagnosis of NEAD, psychotherapy (including CBT) can have beneficial results
• Medical intervention should be considered only if there is evidence of respiratory compromise, which is not a feature of non-epileptic seizures
• Treatment usually involves a series of six to 12 sessions of therapy with a specialist psychotherapist.
• The treatment aims to stabilise the patient emotionally, help them understand the nature of dissociation, and help them with traumatic memories and the emotional consequences.