A lady presenting with loss of consciousness

Presenting complaint

Mrs Johnson, a 42-year-old game developer, has just arrived in A&E. Today, whilst working, she suddenly collapsed onto her desk. A colleague witnessed the collapse, describing the lady holding her head briefly, then losing consciousness, hitting the front of her face against the desk. The colleague explains that her whole body began jerking and he was unable to rouse her. The jerking stopped after a few minutes and she remained very drowsy, localising to pain, making incomprehensible sounds and not opening her eyes.

On arrival of the paramedics, Mrs Johnson’s level of consciousness had improved and she was reported as being able to follow commands and open her eyes spontaneously, despite still appearing disorientated in place and time.

As you enter Mrs Johnson’s hospital room, she appears alert, with eyes opening spontaneously. She is now orientated in time, place and person and is able to follow commands.

  • Eyes – 1
  • Voice – 2
  • Pain – 5
  • Total GCS – 8
  • Eyes – 4
  • Voice – 4
  • Pain – 6
  • Total GCS – 14
  • Eyes – 4
  • Voice – 5
  • Pain – 6
  • Total GCS – 15

History

  • Does the patient have any memory of the event?
  • Did the patient experience any prodromal symptoms (e.g. headache, nausea, vomiting, visual disturbance, confusion)?
  • Prodromal symptoms (e.g. headache, nausea, vomiting, visual disturbance, confusion)?
  • Did the patient experience any weakness or sensory disturbance before or after the event?
  • Did the patient develop incontinence during the episode?
  • Has the patient experienced a loss of consciousness or seizures in the past?
  • Did the patient experience any dizziness or palpitations before or after the episode?
  • Had the patient sustained any head trauma prior to the episode?

Patient answer

“I don’t recall much of the episode, other than a terrible headache that was worse than anything I’ve ever experienced. It came on very suddenly. The headache felt like it was everywhere, rather than in one particular spot on my head. I don’t recall any palpitations, weakness or numbness, however, I did notice that I’d lost control of my bladder afterwards. I’ve never had seizures or episodes of losing consciousness in the past. I haven’t recently hurt my head and I woke up this morning feeling fine, I even biked to work.”

  • Is the headache still present?
  • Is the headache worsening or improving?
  • Does the patient have any nausea or vomiting?
  • Is the patient experiencing any ongoing visual disturbances (e.g. diplopia, decreased acuity, tunnel vision)?
  • Does the patient have any current weakness (e.g. limbs/face) or sensory disturbances?
  • Does the patient have any neck stiffness or photophobia?
  • Is the patient experiencing fevers or rigors?
  • Is the patient orientated in time, place and person?

Patient answer

“I still have a mild generalised headache and nausea. I’ve vomited twice, but the nurses have just given me some anti-sickness medication, so hopefully, that’ll stop now. My neck does feel a little stiff, but that might just be because of been lying in an awkward position. I haven’t noticed any visual problems, fever, weakness or numbness. I’m in the hospital, it’s 2 pm and my name is Claire Johnson.”

Past medical history

  • Has the patient previously experienced dizziness or loss of consciousness (e.g. syncope/pre-syncope)?
  • Relevant medical conditions (e.g. epilepsy, arrhythmias, myocardial infarction, postural hypotension, stroke, intracranial haemorrhage, malignancy)

 

Medications

Prescribed medications:

  • Pay particular attention to any that might cause syncope (e.g. antihypertensives) or alter seizure threshold (e.g. Nefopam).
  • Anticonvulsant medication(s) – if the patient has a diagnosis of epilepsy, ask if they have been taking the medication reliably
  • Antiplatelets and anticoagulants – increased risk of intracranial haemorrhage

Recreational drug use:

  • Cocaine/amphetamines can cause seizures and intracranial haemorrhage

 

Family history

  • Epilepsy
  • Cardiac arrhythmias
  • Intracranial haemorrhages
  • Polycystic kidney disease (increased risk of berry aneurysms)

 

Social history

  • Occupation (particularly relevant in the context of loss of consciousness, as if the job involves working at heights, driving or operating heavy machinery, may not be able to return for work until investigations completed)
  • Accommodation
  • Alcohol history (if the patient normally drinks alcohol most days, they may have had an alcohol withdrawal seizure)
  • Smoking history (relevant if considering malignancy)

 

Systemic enquiry

  • It’s important to briefly screen for other symptoms in other body systems that may be relevant to the presenting complaint (e.g. weight loss in the context of malignancy).

Patient answer

“I don’t have any medical problems, I take no medications and I don’t have any family history of medical problems. I’ve smoked ten cigarettes a day for the last 20 years, but I don’t drink alcohol. I live in a house with my husband and I’m fully independent.”

 


Examination

Clinical findings

General examination:

  • Bruising is noted on the patient’s forehead
  • There is dried blood in her nostrils
  • A small laceration is present on her left cheek
  • Neck stiffness is noted, with the patient struggling to touch her chin to her chest due to pain
  • Otherwise, there appear to be no other significant injuries

 

Cardiovascular examination:

  • Capillary refill time <2 seconds
  • Regular pulse at a rate of 76 beats per minute
  • Auscultation reveals normal heart sounds with no added sounds

 

Respiratory examination:

  • Respiratory rate: 16 breaths per minute
  • Auscultation reveals normal air entry in both lungs with no added sounds

 

Neurological examination

Upper and lower limbs:

  • Tone – normal in all 4 limbs
  • Power – MRC grade 5/5 power in all 4 limbs
  • Reflexes – normal in all 4 limbs
  • Coordination – normal
  • Sensation – normal
  • No pronator drift

Cranial nerves:

  • Pupils equal and reactive to light
  • No other deficits noted

 


Bedside investigations

Vital signs

  • BP – hypotension may have caused collapse or hypertension may have caused an intracranial bleed
  • Pulse rate – useful for identifying tachy- or bradyarrhythmias
  • Temperature – fever may suggest an infection (e.g. encephalitis)
  • SpO2 and respiratory rate – hypoxia may have preceded a collapse or seizure

 

Blood tests

  • FBC – raised WCC may suggest an underlying infection or thrombocytopaenia may have contributed to an intracranial bleed
  • U&Es – to rule out any electrolyte imbalance that may have caused the seizure
  • CRP – useful when considering infective or inflammatory cause for headache/seizure
  • Blood culture – only to be performed if the patient is pyrexial

 

Urine tests

  • If considering infective cause this could potentially be a source.
  • A urine dipstick would provide immediate information as to the likelihood of infection.
  • Sending an MSU (mid-stream specimen of urine) may allow identification of a particular organism.

 

Investigation results

  • Vital signs are all normal
  • Blood tests reveal no abnormalities
  • Urine dipstick is negative

Imaging

CT head

A CT head would be the most appropriate initial imaging choice, given the history of headache and loss of consciousness.

 

CT Head
CT head 1

 

The CT head is unremarkable:

  • No evidence of intracranial haemorrhage
  • No space-occupying lesions
  • No evidence of ischaemia

Lumbar puncture

To rule out a diagnosis of subarachnoid haemorrhage (SAH), a lumbar puncture should be performed (CT head is negative in 2% of patients with SAH).

Around 3% of patients with a negative CT scan will prove, on lumbar puncture, to have had a SAH.4 Lumbar puncture is therefore advised to be performed in all people with suspected subarachnoid haemorrhage (SAH) if imaging is negative (and there is no evidence of raised intracranial pressure on imaging or clinically). 3

The process of ruling out SAH via LP involves the following:

  • Multiple tubes of CSF are taken and labelled in order of removal.
  • Red cell count (RCC) is calculated for each tube.
  • A consistently raised RCC in all bottles is suggestive of SAH.

 

Xanthochromia can also be assessed

The CSF sample is also examined for xanthochromia—the yellow appearance of centrifuged fluid. This can be determined by spectrophotometry (measuring the absorption of particular wavelengths of light).

  • Xanthochromia remains a reliable way to detect SAH several days after the onset of headache.
  • An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the haemoglobin from the red blood cells to be metabolised into bilirubin.

Lumbar puncture results

The lumbar puncture was delayed until 13 hours after the onset of the patient’s headache. The results are shown below.

  • The RCC was consistently raised in all tubes:
    • Tube 1 – RCC 400
    • Tube 2 – RCC 412
    • Tube 3 – RCC 409
  • Xanthochromia was positive

 


Diagnosis

Subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) involves haemorrhage into the subarachnoid space — the area between the arachnoid membrane and the pia mater surrounding the brain. SAH is usually the result of bleeding from a berry aneurysm in the Circle of Willis. Symptoms of SAH include a severe headache with a rapid onset (“thunderclap headache”), vomiting, confusion, reduced level of consciousness and sometimes seizures. Neck stiffness or neck pain are also relatively common. 3

 


Further investigations

CT angiogram of the cerebral vessels

After a subarachnoid haemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as in this case given the absence of any trauma), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain’s vasculature) and CT angiography (visualising blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm at the time of identification. 3

CT angiogram results:

  • The CT angiogram (CTA) reveals a small berry aneurysm in the anterior communicating artery.

 

Cerebral angiography

This confirms the CT angiogram result of an anterior communicating artery aneurysm.

GDCcoilAneurysm - no coil

 

Anterior communicating artery anatomy

  • The anterior communicating artery connects the left and right anterior cerebral arteries.
  • The anterior communicating artery is the most common location for aneurysms within the circle of Willis.
  • These aneurysms can sometimes present pre-rupture with visual field defects due to compression of the optic chiasm.
Circle of Willis
Circle of Willis

 


Management

Coiling

  • Coiling involves inserting a catheter into the femoral artery under x-ray guidance, which is then guided through the aorta, carotid vessels and into the cerebral circulation.
  • Once the aneurysm is reached, platinum coils are released into it, causing coagulation within the aneurysm, obliterating it.

 

Clipping

  • Clipping is more invasive, requiring a craniotomy to access the aneurysm.
  • It is often used for aneurysms that have a wide neck and are therefore unsuitable for coiling.
  • The aneurysm is located visually and a clip is placed around the neck of the aneurysm.
  • This method is often not possible for aneurysms of vessels that are difficult to access surgically (e.g. posterior circulation).

 

The outcome for Mrs Johnson

  • The interventional neuroradiologists felt that coiling of this aneurysm was possible.
  • They performed this at the same time as they were performing the cerebral angiography.
  • It was successful and the patient was left with no residual neurological deficit.

 

Anterior communicating aneurysm (Before/After coiling)
Anterior communicating aneurysm (before and after coiling) 2

 


References

1. Dr Aaron G. Filler, MD, PhD, FRCS. CT Head image. Licence CC BY-SA 3.0. Available from: [LINK]

2. J Neal Rutledge. Anterior communicating artery coiling image. Licence CC BY-SA 3.0. Available from: [LINK]

3. Van Gijn J, Kerr RS, Rinkel GJ (2007). “Subarachnoid haemorrhage”. Lancet. 369 (9558): 306–18. Available from: [LINK]

4. Dr Sarah Jarvis MBE. Patient.info. Subarachnoid haemorrhage. Updated November 2019. Available from: [LINK]


 

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