If you'd like to support us and get something great in return, check out ourOSCE Checklist Booklet containing over 120 OSCE checklists in PDF format. We've also just launched an OSCE Flashcard Collection which contains over 1500 cards.
Table of Contents
Suggest an improvement
Head injury is defined as any trauma to the head regardless of mechanism or presence of neurological symptoms.1
This guide provides an overview of the recognition and immediate management of a traumatic head injury using an ABCDE approach.
The ABCDE approach can be used to perform a systematic assessment of a critically unwell patient. It involves working through the following steps:
Each stage of the ABCDE approach involves clinical assessment, investigations and interventions. Problems are addressed as they are identified and the patient is re-assessed regularly to monitor their response to treatment.
This guide has been created to assist students in preparing for emergency simulation sessions as part of their training, it is not intended to be relied upon for patient care.
The severity of head injuries can vary from minor head injuries to life-threatening traumatic brain injury (TBI) and/or intracranial haemorrhage.
Traumatic head injuries are a common presentation, with 1.4 million patients attending emergency departments in the United Kingdom every year.1
Although the incidence of death from head injuries overall is low (0.2%), the consequences of missing major pathology can be catastrophic. Head injuries are the most common cause of death and disability in those under the age of 40 in the UK.1
The Monro-Kellie doctrine
The Monro-Kellie hypothesis describes the relationship between the contents of the skull and intracranial pressure (ICP).
The skull is a closed rigid box with a fixed capacity (after the sutures have closed).
Within the skull there are three main substances:
Cerebrospinal fluid (CSF)
If the volume of one of these substances increases, to maintain a constant ICP, the volume of one of the others must decrease. Initially, this can be achieved through a process referred to as compliance.
An increase in the amount of blood in the skull leads to a compensatory decrease in the amount of CSF and normal ICP is maintained (Figure 1).
Once the compensatory compliance mechanism is overwhelmed, small increases in the volume of any one of the three substances will lead to dramatic increases in ICP (Figure 2). In head injuries, the volume of brain tissue or blood within the skull can increase secondary to swelling (i.e. oedema) or haemorrhage. If left untreated, rising ICP leads to a progressive reduction in cerebral perfusion, herniation of the brainstem and ultimately death.
Clinical features of raised ICP
Clinical features of raised ICP can include:
Nausea and vomiting
Restlessness, agitation or drowsiness
Slow slurred speech
Ipsilateral sluggish dilated pupil which then becomes fixed (“blown pupil”)
Cranial nerve palsy (e.g. CN III palsy with ‘down and out’ pupil)
Abnormal posturing, initially decorticate and then decerebrate
Cushing’s reflex is a physiological response to raised ICP which attempts to improve perfusion. It leads to a triad of hypertension, bradycardia, and an irregular breathing pattern (Figure 3).
Cerebral Perfusion Pressure (CPP)
Cerebral perfusion pressure is the pressure driving blood through the brain tissue, allowing the delivery of oxygen and nutrients. CPP can be calculated using the equation below:
CPP = Mean Arterial Pressure (MAP) – ICP
A rise in ICP will reduce CPP. If CPP drops too low for a significant amount of time, ischaemia occurs.
Herniation can be defined as the movement of brain structures from one cranial compartment to another. Herniation of different brain structures leads to different clinical features.
Herniation of the cerebellar tonsils through the foramen magnum leads to compression of the brainstem and respiratory arrest. This is often referred to as ‘coning’.
Herniation of the uncus of the temporal lobe through the tentorial notch often leads to compression of cranial nerve three (oculomotor nerve) leading to the classical “blown pupil” that is often assessed for in TBI patients.
Primary and secondary brain injury
Primary brain injury is the initial injury caused to brain tissue from the forces of the traumatic event itself. This may be focal (e.g. skull fractures, blood vessel injury and haematoma formation) or diffuse (e.g. contusion).
Secondary brain injury is indirect damage to brain tissue that that occurs after the primary insult, worsening the original injury. Common causes include inadequate perfusion of the brain causing cerebral hypoxia, acidosis, hypoglycaemia and cerebral oedema leading to raised ICP.
Primary brain injury has already occurred in patients who present with a head injury. A key part of head injury management is to minimise secondary brain injury.
Table 1. Factors that may contribute to secondary brain injury, and the interventions to try to limit them.
Hypoxia and hypercapnia
Oxygen to maintain saturations of 94-98%
Intubation in patients unable to protect their airway or with poor respiratory effort
Hypovolaemia and hypotension
Resuscitate with intravenous fluids or blood products
Cerebral oedema and raised ICP
Avoid tight C-spine collars
Position the patient at 30° to aid venous drainage
Mannitol or hypertonic saline to reduce ICP
Intubation and hyperventilation strategies
Reverse clotting abnormalities
Consider the use of tranexamic acid if < 3 hours since injury
Hypoglycaemia or hyperglycaemia
Maintain blood glucose within normal range with insulin or dextrose as required
Increased metabolic demand (e.g. hyperthermia or seizures)
Anti-convulsant medications if seizure activity
Patients who have sustained a head injury may not be able to provide an accurate history as a result of the injury itself (e.g. due to reduced consciousness).
Where possible, obtain a collateral history. If the patient was bought in by ambulance, try to gather a detailed history and description of the scene from the paramedics.
In the context of acute severe head trauma, taking a history should not delay performing an urgent ABCDE assessment to identify and address serious pathology.
A more detailed history can be obtained once the patient is stable.
Typical symptoms of a traumatic head injury include:
Pain localised to the area of trauma
Drowsiness or loss of consciousness
Nausea and vomiting
Confusion or irritability
Changes in hearing (ringing in ears, hearing loss) or vision (double vision, blurring, visual field loss)
Memory loss (amnesia) or concentration difficulties
Weakness or sensory changes such as numbness or paraesthesia
Difficulties with speech (e.g. slurring)
Dizziness or issues with balance
Other important areas to cover in the history include:
A detailed account of the event. This includes when the head injury occurred, how it occurred, and which part of the head took the impact. Find out if the patient was intoxicated or taking any illicit drugs at the time.
Establishing if the patient has any neurological symptoms. This includes seizure activity, weakness, sensory or visual changes.
Whether there was any loss of consciousness after the injury and establishing if the patient has any amnesia.
Whether the patient has any symptoms that may be due to raised ICP (covered previously).
Drug history: establish whether the patient is taking any anticoagulants and if they have any drug allergies.
A focused past medical history: establish if the patient has a bleeding disorder; has previously had brain surgery or sustained a significant head injury.
A focused social history: establish the patient’s baseline functioning and what their home situation is. Take a brief alcohol and drug history.
Whether the patient has sustained any other injures. Specifically, ask about pain in the cervical spine. NICE have guidelines on when c-spine immobilisation should be performed.3
If the head injury was due to a fall, then this should be explored further, and the cause of the fall should be sought. See our article on falls assessment and management.
Typical clinical signs associated with a traumatic head injury include:
Lacerations, abrasions, bruising and swelling over the area of the head that has sustained trauma
Decreased consciousness (GCS) or drowsiness
Focal neurological signs such as weakness or sensory loss
Abnormal findings on cranial nerve examination such as visual field loss; abnormally shaped or sized pupils; and speech difficulties
Impaired coordination on examination
Signs of basal skull fracture: this includes CSF tracking from the nose or ears and bruising around the eyes or behind the ears
Impairments in memory
Tips before you begin
General tips for applying an ABCDEapproach in an emergency setting include:
Treat all problems as you discover them.
Re-assess regularly and after every intervention to monitor a patient’s response to treatment.
Make use of the team around you by delegating tasks where appropriate.
All critically unwell patients should have continuous monitoring equipment attached for accurate observations.
Clearly communicate how often would you like the patient’s observations relayed to you by other staff members.
If you require senior input, call for help early using an appropriate SBARR handover
Make use of your local guidelines and algorithms in managing specific scenarios (e.g. acute asthma).
Any medications or fluids will need to be prescribed at the time (in some cases you may be able to delegate this to another member of staff).
Your assessment and management should be documented clearly in the notes, however, this should not delay initial clinical assessment, investigations and interventions.
Acute scenarios typically begin with a briefhandover from a member of the nursing staff including the patient’s name, age, background and the reason the review has been requested.
You may be asked to review a patient with a traumatic head injury in the emergency department or following a fall on the wards.
Introduceyourself to whoever has requested a review of the patient and listencarefully to their handover.
Introduceyourself to the patient including your name and role.
Ask how the patient is feeling as this may provide some useful information about their current symptoms.
In the context of a head injury, this may not be possible due to impaired consciousness.
Make sure the patient’snotes, observationchart and prescriptionchart are easily accessible.
Ask for another clinicalmember of staff to assist you if possible.
If the patient is unconscious or unresponsive, start the basic life support (BLS) algorithm as per resuscitation guidelines
In patients with head injuries, the airway may be compromised due to a number of factors such as:
Blood or swelling in the airway
Vomit or secretions
Reduced consciousness (from the head injury itself or other factors e.g. intoxication)
Can the patient talk?
Yes: if the patient can talk, their airway is patent and you can move on to the assessment of breathing.
Look for signs of airwaycompromise: these include cyanosis, see-saw breathing, use of accessory muscles, diminished breath sounds and added sounds.
Open the mouth and inspect: look for anything obstructing the airway such as secretions or a foreign object.
Regardless of the underlying cause of airway obstruction, seek immediate expert support from an anaesthetist and the emergency medical team (often referred to as the ‘crash team’). In the meantime, you can perform some basic airway manoeuvres to help maintain the airway whilst awaiting senior input.
Head-tilt chin-lift manoeuvre
The head tilt-chin lift manoeuvre should be avoided if there is any concern of a spinal injury.
If the patient is suspected to have suffered significanttrauma with potential spinal involvement, perform a jaw-thrust rather than a head-tilt chin-lift manoeuvre:
1. Identify the angle of the mandible.
2. With your index and other fingers placed behind the angle of the mandible, apply steady upwards and forward pressure to lift the mandible.
3. Using your thumbs, slightly open the mouth by downward displacement of the chin.
Oropharyngeal airway (Guedel)
Airway adjuncts are often helpful and, in some cases, essential to maintain a patient’s airway. They should be used in conjunction with the manoeuvres mentioned above as the position of the head and neck need to be maintained to keep the airway aligned.
An oropharyngeal airway is a curved plastic tube with a flange on one end that sits between the tongue and hard palate to relieve soft palate obstruction. It should only be inserted in unconscious patients as it is otherwise poorly tolerated and may induce gagging and aspiration.
To insert an oropharyngealairway:
1. Open the patient’s mouth to ensure there is no foreign material that may be pushed into the larynx. If foreign material is present, attempt removal using suction.
2. Insert the oropharyngeal airway in the upside-down position until you reach the junction of the hard and soft palate, at which point you should rotate it 180°. The reason for inserting the airway upside down initially is to reduce the risk of pushing the tongue backwards and worsening airway obstruction.
3. Advance the airway until it lies within the pharynx.
4. Maintain head-tilt chin-lift or jaw thrust and assess the patency of the patient’s airway by looking, listening and feeling for signs of breathing.
Nasopharyngeal airway (NPA)
A nasopharyngeal airway is a soft plastic tube with a bevel at one end and a flange at the other. NPAs are typically better tolerated in patients who are partly or fully conscious compared to oropharyngeal airways.
The use of nasopharyngeal airways in head injury is controversial. They are generally better tolerated than oropharyngeal airways in patients who are partially or fully conscious and may be the only option in severe facial fractures or trismus. However, the general consensus is that they should not be used if there is any concern that the patient may have a basal skull fracture.
Basal skull fracture
Signs suggestive of a basal skull fracture include:
CSF (clear fluid) leaking from nose or ear
Raccoon eyes: bruising around the eyes
Battle sign: bruising behind the ear over the mastoid process
Haemotympanum: blood noted behind the tympanic membrane on otoscopy
If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.
Make sure to re-assess the patient following any intervention.
Ventilation must be sufficient to prevent secondary brain injury from cerebral hypoxia and hypercapnia. Abnormalities in the patient’s respiratory pattern may indicate raised ICP.
Review the patient’s respiratoryrate:
A normal respiratory rate is between 12-20 breaths per minute.
Bradypnoea may be secondary to raised ICP and is seen as part of the Cushing’s reflex. Consider other causes of a reduced RR such as opioid toxicity.
Tachypnoea may be due to pain or agitation, acidosis or due to the presence of respiratory pathology.
Review the patient’s oxygen saturations (SpO2):
A normal SpO2 range is 94-98% in healthy individuals and 88-92% in patients with COPD who are at high-risk of CO2 retention.
Hypoxaemia may occur due to associated injuries or respiratory issues and can contribute to secondary brain injury.
Administer oxygen to all critically unwell patients during your initialassessment. This typically involves the use of a non-rebreathe mask with an oxygen flow rate of 15L. You can then trial titrating oxygen levels downwards after your initial assessment.4
If the patient has COPD and a history of CO2 retention you should switch to a venturi mask as soon as possible and titrate oxygen appropriately.
If your patient is unconscious and their respiratory rate is inadequate (too slow or irregular with big pauses), you can provide assisted ventilation through a bag-valve-mask (BVM): ventilate at a rate of 12-15 breaths per minute (roughly one every 4 seconds).
Other interventions may be appropriate depending on examination findings (e.g., aspiration of tension pneumothorax).
Make sure to re-assess the patient following any intervention.
In patients with TBI, it is important to maintain an adequate mean arterial pressure to ensure adequate cerebral perfusion.
Mortality is significantly increased in patients with TBI who have periods in which their systolic blood pressure is less than 90mmHg.
Aim for a MAP > 90mmHg or systolic BP > 110mmHg. A lower BP may sometimes be permitted in patients with multiple injuries or major haemorrhage.
Review the patient’s heart rate:
Causes of tachycardia (HR>99) in the context of head injury include hypovolaemia, arrhythmia, pain or drugs.
Causes of bradycardia (HR<60) in the context of head injury include Cushing’s reflex and opioid use.
Review the patient’s bloodpressure:
A normal blood pressure (BP) range is between 90/60mmHg and 140/90mmHg but you should review previous readings to gauge the patient’s usual baseline BP.
Causes of hypertension in the context of acute head injury include pain and Cushing’s reflex.
Causes of hypotension in the context of acute head injury include haemorrhage from other injuries, and drugs (e.g. opiates).
A new neurological deficit suggests intracranial injury.
Measure the patient’s capillary blood glucose level to screen for causes of a reduced level of consciousness (e.g. hypoglycaemia or hyperglycaemia). The normal reference range for capillary blood glucose is 4.0-11.0 mmol/L.
A blood glucose level may already be available from earlier investigations (e.g. ABG, venepuncture).
Alert a senior immediately if you have any concerns about the consciousness level of a patient. A GCS of 8 or below warrants urgent expert help from an anaesthetist. In the meantime, you should re-assess and maintain the patient’s airway as explained in the airway section of this guide.
If opioid toxicity is suspected as the cause for the patient’s reduced level of consciousness (e.g. pinpoint pupils) interventions such as naloxone should be considered.