In the final part of our series, Nicola Cooper focuses on the D for disability in the ABCDE system of managing acutely ill patients
How to manage the unconscious patient
The most common reason for a reduced conscious level is critical illness--not necessarily a primary brain problem. Patients who have a serious problem with A (airways), B (breathing), or C (circulation) can be drowsy or unresponsive--for example, obstruction of the airway, any severe lung problem, or shock from any cause.
Coma, by definition, is when the Glasgow coma score is less than 9 (box 1). This is associated with potentially life-threatening complications which require urgent intervention. Such patients have reduced airway reflexes and are considered unable to protect their own airway from aspiration of obstruction. Intubation with a cuffed endotracheal tube is the definitive method of protecting the airway.
Box 1: Glasgow coma score
Eye opening:
Spontaneous--4
To speech--3
To pain--2
Nil--1
Best motor response
Obeys commands--6
Localises pain--5
Withdraws to pain--4
Abnormal flexion to pain--3
Extensor response to pain--2
Nil--1
Best verbal response
Orientated--5
Confused conversation--4
Inappropriate words--3
Incomprehensible sounds--2
Nil--1
Head injury is a common cause of coma. In non-trauma patients who have been unconscious for six hours, 40% will have taken some form of sedative and of the remaining 60%, about a third have hypoxic brain injury (for example, after cardiac arrest), a third have a cerebrovascular cause (infarct or haemorrhage), and a third have a metabolic cause for coma (for example, in diabetes or liver disease). Coma has many causes, and no history is available from the patient. A systematic approach is therefore required:
- A (airway)--Ensure patient airway (airway manoeuvres, suction, and adjuncts may be required)
- B (breathing)--Ensure adequate breathing (treat any problems as you find them)
- C (circulation)--Ensure adequate circulation (treat any problems as you find them)
- D (disability)--Assess Glasgow coma score, pupils, and bedside glucose measurement
- E (examination)--Do an examination (including notes, eye witnesses, and charts for clues to the diagnosis). You can ask for help at any stage, but do it now if not already.
If the patient is stable and not intubated, do not forget the recovery position. If you have a diagnosis, consider which is the best area in which to nurse the patient. If you do not have a diagnosis, consider asking for a computed tomography brain scan. Certain clusters of signs point towards certain diagnoses (box 2).
Box 2: Clusters of signs in coma
(1) Are there any focal neurological signs (FNS)?
(2) Is there meningism?
FNS but no meningism--stroke or space occupying lesion (including haematoma)
Meningism but no FNS--subarachnoid bleed or meningitis
No meningism and no FNS--hypoxic brain injury, drugs and alcohol, metabolic problems, fitting, critical illness
Primary brain injury and secondary brain injury
Primary brain injury has already happened: a stroke, head injury, meningitis, or subarachnoid haemorrhage. Secondary brain injury is the thing you can do something about, so it is important to understand it. Specific cells around the primary brain injury are rendered dysfunctional although not mechanically destroyed. If
the subsequent environment is favourable they can recover. Hypoxaemia or ischaemia, however, facilitate irreversible damage. To understand the factors that influence secondary brain injury, you need to know about cerebral blood flow.
Cerebral blood flow is around 15% of cardiac output. It is affected mainly by Paco2, Pao2, and mean arterial pressure (figure). Also, the brain's metabolic rate is increased by fever and reduced by hypothermia (which is why hypothermia has been used experimentally in the past for treatment of head injury).
The brain autoregulates its own blood flow so that there is a constant flow between a mean arterial pressure of 60 and 150. (Mean arterial pressure is the average blood pressure throughout the cardiac cycle and is roughly ²/3 systolic blood pressure). At higher levels, there is increased blood flow and at lower levels, there is reduced blood flow. Injured brains are not as good at autoregulation as healthy brains. An increased cerebral blood flow might lead to oedema; a reduced cerebral blood flow might lead to ischaemia.
Hypoxaemia and hypotension are commonly found at the scene of head injury and are associated with
a statistically significant worse outcome.
As well as damage limitation, we are also concerned with preventing raised intracranial pressure. This is the most common cause of death after head injury or intracerebral haemorrhage. The skull is a rigid box. At first, any change in intracranial blood volume is accompanied by an opposite change in cerebrospinal fluid volume, but brainstem herniation will eventually occur because this compensatory mechanism is limited.
The signs of acute raised intracranial pressure are confusion and a reduced conscious level (nausea and early morning headaches are seen in patients with a subacute onset
of raised intracranial pressure). Intracranial pressure depends on the volume of the intracranial contents--5% blood, 5-10% cerebrospinal fluid, and 85% brain tissue. Treatment of raised intracranial pressure therefore consists of trying to reduce the volume of these three components (table).
| Reducing intracranial pressure |
| Blood volume |
Cerebrospinal fluid volume |
Brain tissue (oedema) |
| Maintain normal PaCO2 |
Surgical drainage |
Mannitol |
Encourage venous
drainage by:- Nurse head up 15
- Keep head in midline
(to avoid kinking the neck veins) - Avoid coughing and straining
|
| Steroids for tumour related oedema |
It may also be possible to remove the cause of raised intracranial pressure--for example, haematoma.
Consider the history and apply your knowledge to preventing secondary brain injury in this patient (box 3).
Box 3: Case history
A 24 year old man was found to be confused and agitated by his parents, who brought him to the Emergency Department. He was found to be disorientated, but the physical examination (including neurology) was otherwise normal.
What are your thoughts so far?
He was transferred to the ward where he became unresponsive on arrival. The senior doctor assessed him according to the ABCDE system and found the following:
A--snoring relieved by head tilt-chin lift, oxygen administered
B--respiratory rate, oxygen saturations, and chest sounds normal
C--blood pressure 150/80 mm Hg, pulse 100 beats/min, normal capillary refill time
D--unresponsive, bedside glucose 6 mmol/l, left pupil fixed and dilated
E--history reviewed with parents. He was holding his head in the ambulance, he had been perfectly well the day before, no history of drug taking or alcohol
What is your next course of action?
This man needs a computed tomography brain scan, but your immediate priority is to ensure he can be transferred there safely and to prevent secondary brain injury. The anaesthetist was "fast bleeped" (that means he gets a message to attend the ward immediately) and the radiologist was put on standby.
The patient was sedated and intubated. His blood pressure, pulse, oxygen saturations, end tidal CO2, and pupils were continuously monitored. He was nursed with his head in the midline position and the bed tilted head upwards by 15°. He briefly developed hypotension which
was treated with a colloid fluid challenge. He was also given 200 ml of 20% mannitol to treat presumed raised intracranial pressure.
Young people are not like elderly people, in whom confusion can result from almost any systemic illness. If a young person is confused, there is a primary brain problem.
For the patient in box 3, the doctors ensured airway protection, normal Pao2, Paco2, and mean arterial pressure. They would have treated any fever with paracetamol via the rectum and a fan. This patient had a large intracerebral haematoma and was transferred from the computed tomography scanner to the neurosurgical theatre. The apparently simple manoeuvres by the attending doctors would have bought him valuable time and minimised secondary brain injury as far as possible pending definitive treatment.
During cardiac arrest there is complete global ischaemia. The chance of brain recovery is thought to be small after 4-5 minutes. Prognosis after cardiac arrest has been extensively studied. Unlike on television, the reality is that only about one in 10 people survive to discharge after cardiopulmonary resuscitation. This includes all types of cardiorespiratory arrest--in patients with sepsis, multiorgan failure, and poor function before the arrest the results are closer to zero. The UK national guidelines on cardiopulmonary resuscitation make the point that cardiorespiratory function ceases as a part of dying, so cardiopulmonary resuscitation can theoretically be attempted on every individual. However, it is essential to differentiate between patients who are dying and patients who have a reversible cause of cardiac arrest.
This brings us back to the first article in this series.1 Recognising critical illness is one of the most important skills you will need as a doctor. Nearly 85% of in-hospital cardiorespiratory arrests are predictable in the 12 hours beforehand because there is documented serious abnormal physiology. The fact that the patient is sitting up in bed talking to you is irrelevant. The clues are in the vital signs. Hypoxaemia, hypotension, and acidosis may be treated but cardiac arrest usually cannot. So whenever you see a patient, think of ABCDE before history and examination--and you will not go far wrong.
