There are no reliable up-to-date figures for the total denominator of attendees who attend Emergency Departments (EDs) with a head injury (National Institute for Health and Clinical Excellence 2007). The role of ED staff is to diagnose and appropriately treat a large number of patients presenting following a head injury. Neurological damage occurs both at the time of the injury (primary insult) and evolves over the following minutes, hours and days (secondary insult). Patient outcomes improve where secondary insults are treated early, and where successful responses result in limiting and preventing further injury caused by secondary insult. Wyatt et al. (2008) argue that emergency nurses are ‘fundamental to keeping morbidity to a minimum by being vigilant and prevent secondary brain injury.’

While 90 % of traumatic brain injuries (TBIs) are considered mild (Vos et al. 2012), it is the world’s leading cause of morbidity and mortality in individuals under the age of 45 years old (Wilson 2011). It is estimated that the ED attendance rate in the UK for patients with head injuries is close to 700 000 patients (National Institute for Clinical Excellence 2007) and that 20 % of these are admitted to hospital. Half of those who die from TBI do so within the two hours of the injury. Approximately 30 % of admitted patients with a Glasgow Coma Score (GCS) of <13 will die, and if the GCS is <8, this increases to 50% (Wilson 2011).

The most common causes of a minor head injury are falls (22–43 % of injuries), assaults (30–50 % of injuries), and road traffic accidents (25 % of injuries) (Department of Health 2001, National Institute for Health and Clinical Excellence 2007). In the UK, 70–88 % of individuals that sustain a head injury are male, 10–19 % are aged 65 years or greater, and 40–50 % are children. Alcohol may be involved in up to 65 % of adult head injuries and road traffic accidents account for a large proportion of moderate to severe head injuries. Traumatic injury in which severe head injury plays a major role in over 50 % of cases, is a leading cause of death in those aged 25 years or less (Maartens & Lethbridge 2005); 5–10 % of patients who suffer a severe head injury also suffer a cervical spine injury.

It is vital that the emergency department staff caring for patients with head injuries has a good knowledge and understanding of the anatomy and physiology of the skull, the brain and its related structures along with the physiological processes that maintain homeostasis. Such knowledge and understanding allows the nurse to relate the mechanisms of injury to the brain injuries suffered and thus assess, plan, evaluate, and implement the care and management needed by the patient at any particular stage following the injury.

A structured approach to the care of head-injured patients should be initiated based on current valid evidence. The Brain Trauma Foundation has developed recommendations for the management of moderate and severe head injuries (Bratton et al. 2007) in collaboration with the Advanced Trauma Life Support (ATLS) system (American College of Surgeons 2008), providing a mechanism for assessment and immediate management and minimizes the risk of secondary brain injury in adults. For children the Advanced Paediatric Life Support (APLS) system (Advanced Life Support Group 2011) should be employed (National Institute for Health and Clinical Excellence 2007). These guidelines are based on class II (studies based on prospectively collected data and the retrospective analysis of reliable data) and III (studies based on retrospectively collected data) evidence. There is a lack of class I (prospective randomized controlled trials) evidence to support practice.

Anatomy and physiology

The skull

The skull is a rigid bony cavity composed of 29 individual bones: the 8 bones of the cranium, 14 facial bones, the 6 ossicles of the ear, and the hyoid bone. To ensure maximum protection, strength and support, bony capsules surround the brain, the eyes, the nasal passages, and the inner ear; bony buttresses extend upwards from the teeth through the facial bones. To relieve the potential weight, the skull is made lighter by the paranasal sinuses, which also give resonance to the voice.

The cranium is one of the strongest structures in the body and provides the bony protection for the brain. It is composed of the parietal (2), occipital, frontal, temporal (2), sphenoid, and ethmoid bones. Figure 5.1 shows an exploded view of the cranial skull; however, the bones are fused along main sutures, the sagittal, coronal, lambdoidal, and squamosal. The facial bones form the framework for the nasal and oral cavities and include the zygomatic bones (2), palatine bones (2), mandible, maxilla (2), lacrimal bones (2), nasal bones (2), vomer and the inferior nasal concha (2) (Fig. 5.2).

Figure 5.1 Exploded view of the cranial skull.

Figure 5.2 Exploded view of the facial skull.

Figure 5.3 shows the irregular internal surfaces of the skull. These irregular surfaces/bony protrusions account for injury to the brain as it moves within the skull under acceleration/deceleration forces.

Figure 5.3 View of the base of the skull from above.

The surface area of the cerebral cortex (grey matter) on the surface of the brain is much increased by the presence of gyri and sulci (Fig. 5.6), resulting in a 3:1 proportion of grey to white matter. Below the cortex lies the white matter. The cerebral hemispheres are composed of four lobes, the frontal, parietal, temporal and occipital lobes. Box 5.2 summarizes the main functions of these lobes.

Figure 5.6 Gyri, sulci and fissures of the cerebral hemispheres. (A) Superior view. (B) Right lateral view.

The diencephalon is located deep into the cerebrum and consists of the thalamus, hypothalamus, subthalamus and epithalamus. It connects the midbrain to the cerebral hemispheres. The hypothalamus includes several important structures, such as the optic chiasma, the point at which the two optic tracts cross, and the stalk of the pituitary gland (hypophysis).

Cerebellum

The cerebellum is situated behind the pons and attached to the midbrain, pons and medulla by three paired cerebellar peduncles. It consists of three main parts:

• the cortex

• the white matter, which forms the connecting pathways for impulses joining the cerebellum with other parts of the central nervous system

• four pairs of deep cerebellar nuclei.

The cerebellum is the processing centre for coordination of muscular movements, balance, precision, timing, and body positions. It does not initiate any movements and is not involved with the conscious perception of sensations.

Brain stem

The brain stem is the connection between the brain and the spinal cord and is continuous with the diencephalon above and the spinal cord below. Within the brain stem are ascending and descending pathways between the spinal cord and parts of the brain. All cranial nerves except the olfactory (1) and the optic (2) nerves emerge from the brain stem (Fig. 5.7). The brain stem is formed from three main structures:

Figure 5.7 Brain stem (dorsal view).

• midbrain

• pons

• medulla.

The midbrain connects the pons and the cerebellum to the cerebrum. It is involved with visual reflexes, the movement of the eyes, focusing and the dilatation of the pupils. Contained within the midbrain and upper pons is the reticular activating system, which is responsible for the ‘awake’ state.

The pons is located between the midbrain and the medulla and serves as a relay station from the medulla to higher structures in the brain. It is involved with the control of respiratory function.

The medulla connects the pons and the spinal cord. The point of decussation of the pyramidal tract occurs within the medulla. The vital centres associated with autonomic reflex activity are present in its deeper structure. These are the cardiac, respiratory and vasomotor centres and the reflex centres of coughing, swallowing, vomiting and sneezing.

Cerebral circulation

The brain is supplied with blood by four major arteries: two internal carotid arteries, which supply most of the cerebrum and both eyes; and two vertebral arteries, which supply the cerebellum, brain stem and the posterior part of the cerebrum. Before the blood enters the cerebrum it passes through the circle of Willis, which is a circular shunt at the base of the brain consisting of the posterior cerebral, the posterior communicating, the internal carotids, the anterior cerebral and the anterior communicating arteries (Figs 5.8 and 5.9). These vessels are frequently anomalous; however, they allow for an adequate blood supply to all the brain, even if one or more is ineffective.

Figure 5.8 Major arteries of the head and neck.

Figure 5.9 Cerebral circulation.

The venous drainage from the brain does not follow a similar pathway (Fig. 5.10). Cerebral veins empty into large venous sinuses located in the folds of the dura mater. Bridging veins connect the brain and the dural sinuses and are often the cause of subdural haematomas. These sinuses empty into the internal jugular veins, which sit on either side of the neck and return the blood to the heart via the brachiocephalic veins.

Figure 5.10 Major veins of the head and neck.

The brain, especially the grey matter, has an extensive capillary bed, requiring approximately 15–20 % of the total resting cardiac output, about 750 mL/min. Glucose, required for metabolism in the brain, requires about 20 % of the total oxygen consumed in the body for its oxidation. Blood flow to specific areas of the brain correlates directly with the metabolism of the cerebral tissue.

Physiology of raised intracranial pressure

Intracranial pressure (ICP) represents the pressure exerted by the CSF within the ventricles of the brain (Hickey 2009). The exact pressure varies in different areas of the brain. The normal range is 0–15 mmHg in adults, 3–7 mmHg in children, and 1.5–6 mmHg in term babies when measured from the foramen of Munro.

ICP is fundamental in maintaining adequate brain function. The brain lies in the skull, a rigid compartment. The contents of the skull are non-compressible, i.e., brain tissue (80 %), intravascular blood (10 %) and cerebrospinal fluid (10 %). Normally these components maintain a fairly constant volume, therefore creating dynamic equilibrium therein. Should one or more components increase for whatever reason, the Monro-Kellie hypothesis states that another component must decrease in quantity in order to maintain the dynamic equilibrium and thus maintain adequate cerebral blood flow (CBF). If this does not occur, ICP rises, leading to brain injury (Hickey 2009). Dynamic equilibrium is maintained by a number of compensatory mechanisms, these include:

• increasing CSF absorption

• decreasing CSF production

• shunting of CSF to the spinal subarachnoid space

• vasoconstriction – reducing cerebral blood flow.

In severe traumatic brain injury the compensatory mechanisms are rapidly exhausted (Deitch & Dayal 2006). They fail in the healthy adult brain when the ICP reaches 20 mmHg. Once exhausted, small increases in brain mass, blood, or CSF volume have a profound effect on ICP. Chestnut et al. (1993) demonstrated a clear correlation between the length of time patient’s ICP remains greater than 20 mmHg and an increased mortality and morbidity rate.

Maintenance of the dynamic equilibrium in the brain is further aided by autoregulation. Pressure autoregulation is the ability of the brain to maintain a relatively constant CBF over a wide range of cerebral perfusion pressures (50–150 mmHg). Pressure autoregulation is initiated by cerebral perfusion pressure (CPP), which is defined as the blood pressure gradient across the brain and is calculated by subtracting ICP from the systemic mean arterial pressure (MAP):

CPP is used as an indicator of CBF, and therefore oxygen delivery to the brain. Current recommendations suggest that in adults the CPP should lie between 50–70 mmHg, although adults with intact pressure autoregulation may tolerate higher CPP values (Bratton et al. 2007). When the patient’s MAP falls and/or the patient’s ICP increases, there is a risk that the cerebral perfusion pressure will fall to too low a value to maintain adequate CBF. This results in cerebral hypoxia and secondary brain injury in the form of cerebral ischaemia and potentially infarction. Autoregulation fails when CPP falls below 50 mmHg or rises above 150 mmHg, resulting in CPP and CBF become dependent on the systemic blood pressure alone.

Chemo autoregulation is triggered by changes in extracellular pH and metabolic by-products. Changes in PCO₂ or a dramatic reduction in PO₂ (Fig. 5.11) may trigger this. Hypercapnia >45 mmHg (or 6 kPa) (Albano 2005) is a potent vasodilator that induces hyperaemia and cerebral blood volume increases, without an adequate decrease in CSF; as a result of the compensatory response the ICP will rise. Hypocapnia <45–>30 mmHg (or 6–4 kPa) considered a critical low value (Garner & Amin 2007) is a potent vasoconstrictor that reduces brain mass and induces hypoaemia; as a result cerebral blood flow and volume decrease leading to a risk of secondary ischaemia and potentially an infarction if not treated (Albano 2005).

Figure 5.11 Autoregulation of the brain.

Classification of head injuries

Head injuries can be classified under three anatomical sites:

• the scalp

• the skull

• the brain.

Patients often present with a combination of injuries. The pathophysiology of brain injury is multivariate, complex, and evolutionary. Neurological damage occurs both at the time of the injury (primary insult) and evolves over the following minutes, hours and days (secondary insult). Patient outcomes improve where secondary insults are treated early, and where successful responses result in limiting and preventing further injury.

Scalp injuries

There are four types of injury to the scalp:

• abrasion – minor injury that may cause a small amount of bleeding. Treatment may not be required, but ice applied to the area may reduce any haematoma formation (Hickey 2009)

• contusion – no break in the skin, but bruising to the scalp may cause blood to leak into the subcutaneous layer

• laceration – a cut or tear of the skin and subcutaneous fascia that tends to bleed profusely. Bleeding from the scalp alone is unlikely to cause shock in the adult. In small children, a scalp laceration may be sufficient to cause hypovolaemia. Scalp lesions should be explored under local anaesthetic for foreign bodies and/or skull fracture with a skull X-ray if there is any doubt about the diagnosis. Lesion(s) should be sutured or glued according to their depth and position

• subgaleal haematoma – a haematoma below the galea, a tough layer of tissue under the subcutaneous fascia and before the skull. The veins here empty into the venous sinus, and thus any infection can spread easily to the brain, despite the skull remaining intact. There is controversy surrounding the treatment of subgaleal haematomas, due to the risks of infection; therefore some doctors argue that it is best to evacuate the haematoma, while others suggest that it is best to let it reabsorb.

If the scalp injuries are only part of other injuries, it is important they are documented to allow further investigation at a more appropriate time. They may need to be cleaned and dressed or temporarily sutured.

Skull injuries

Skull fractures indicate that the head has suffered a major impact. Patients who suffer skull fractures have a high incidence of intracranial haematoma. Skull fractures are classified into five groups:

• linear – these are the most common types of injury. They usually result from low-velocity direct force. They are usually diagnosed from skull X-ray and need no specific treatment

• depressed – usually evident clinically, but a skull X-ray to discover the full extent of the potential brain damage is usually necessary. Management is dependent on the severity of the fracture and whether there are any accompanying injuries. If there are no other injuries requiring surgical management, they may not be surgically elevated, due to the risks of infection. However, surgical intervention will normally be necessary if there are bone fragments embedded in the brain so as to elevate the bone fragments and manage the brain trauma

• open – usually evident clinically. Usually managed according to the severity of the injury. If debris is dispersed in the brain tissue then surgery will be required and there is a heightened risk of infection

• comminuted – these are detected on skull X-ray. These patients should be closely observed and any neurological deficits managed appropriately. Surgical intervention is usually required. If there are bone fragments imbedded in the brain tissue then surgery will be required to elevate the bone fragments and manage the brain trauma

• basal – these are diagnosed clinically as they are difficult to detect on X-ray. Signs include CSF leakage from the nose (rhinorrhoea) or the ear(s) (otorrhoea). Rhinorrhoea or otorrhoea indicates that a skull base fracture has breached the dura and formed a communication between the intracranial contents and an air sinus. This places the patient at risk of meningitis while the CSF leak continues. If CSF leakage is suspected, the fluid should be tested for glucose and the ‘halo test’ performed, where a small amount of fluid is placed on blotting paper; if CSF is present it will separate from blood and form a yellow ring around the outside of the blood. Patients with a base of skull fracture may also have retroauricular bruising (Battle’s signs) and periorbital bruising (‘panda eyes’ or ‘raccoon eyes’): 80–90 % of cases seal within two weeks and neurosurgical intervention is usually not considered until this time has elapsed. An exception is a fracture of the posterior wall of the frontal sinus, visualized on CT scan, where anterior fossa repair may be undertaken early.

Brain injuries

Severe brain injury is uncommon because the skull and scalp absorb the majority of the impact of the assault. The amount of brain damage suffered is relative to the force/energy of the assault. A high-energy head injury results when: a pedestrian is struck by a motor vehicle, an occupant is ejected from a motor vehicle, a person falls from a height of greater than 1 metre or more than five stairs (a lower threshold for the height of falls should be used when dealing with infants and young children under 5 years old), following a diving accident, following a high-speed motor vehicle collision, following a rollover motor accident, or a bicycle collision (National Institute for Health and Clinical Excellence 2007).

Damage to the brain as a result of trauma includes both the immediate (primary) injury caused at the moment of the impact and the secondary injury that develops during the first few minutes, hours or days after the impact (Box 5.3). These secondary injuries may have extracranial or intracranial causes.

There are no interventions that can prevent the primary brain injury. Secondary brain injuries, which further exacerbate the primary neuronal injury and lead to a worsening outcome depending upon their duration and severity, are largely preventable. The two main causes of secondary injury are delayed diagnosis and treatment of intracranial haematomas, and failure to correct systemic hypoxaemia and hypotension (Fig. 5.12). Brain injuries are usually categorized as either focal or diffuse injuries.

Figure 5.12 Cycle of progressive brain swelling.

Focal injuries

Focal injuries occur in a specific area of the brain. The mechanism of injury is usually blunt injury and acceleration/deceleration injury.

Cerebral contusion (bruising of the surface of the brain) is sustained as the brain hits the bony protuberances of the skull at the site of the impact (coup injury) and at the opposite side of the brain during deceleration (contrecoup injury). Cerebral contusion is a common type of brain injury, which is diagnosed by CT scan, and is most commonly seen at the frontal and temporal lobes as a result of the irregular surfaces/bony protrusions of the skull. The term contusion is used when the pia mater has not been breached. The brain swells around the site(s) of the contusion(s). Bleeding may occur into the contusion(s). If the contusion(s) is (are) large and/or widespread, the swelling may cause the ICP to rise. Nausea, vomiting and visual disturbances are common clinical signs.

Cerebral lacerations of the cortical surface commonly occur in similar locations to contusions, and are most commonly seen at the frontal and temporal lobes as a result of irregular surfaces/bony protrusions of the skull. The term laceration is used when the pia mater is torn.

Haematoma: Extradural haematoma (EDH) is an accumulation of blood in the extradural space between the periosteum on the inner side of the skull and the dura mater (Fig. 5.13). Most are associated with skull fracture and are commonly caused by a laceration to the middle meningeal artery or vein, or less commonly to the dural venous sinus, following an insult to the temporal-parietal region. Consequentially, the parietal and parieto-temporal areas of the brain are affected. In 85 % of patients the EDH will be accompanied by a skull fracture (Hudak & Gallo 1994).

Figure 5.13 Extradural haematoma.

Patients with skull fractures may be neurologically intact on admission and later deteriorate as the EDH develops. Most often the primary brain injury causes some disturbance of consciousness and the developing haematoma results in rapid neurological deterioration (Kwiatkowski 1996). Patients with EDHs most commonly present with a history of transient loss of consciousness, followed by lucidity for a period (hours to days) dependent on the rate of the bleed, irritation and headache. Patients then rapidly lose consciousness and deteriorate very quickly. Late signs are seizures, ipsilateral pupil dilatation, unconsciousness, and contralateral hemiplegia. Surgical treatment is required to evacuate the haematoma and ligate the damaged blood vessel.

Relatives, friends and/or carers often require a great deal of reassurance, as they often feel responsible for not bringing the patient to hospital earlier.

Subdural haematoma (SDH) is an accumulation of blood between the dura mater and arachnoid mater. SDHs are caused by the rupture of bridging veins from the cortical surfaces to the venous sinuses (cortical veins) (Fig. 5.14).

Figure 5.14 Subdural haematoma.

SDHs can be seen in isolation, but more commonly are associated with accompanying brain injury, i.e., cerebral contusions and/or intracerebral haematomas. They are the most common intracranial mass result from head trauma (Maartens & Lethbridge 2005). In most cases a large contusion is found at the frontal or temporal surface of the brain. SDHs are predisposed with increasing age and alcoholism. Both groups can suffer regular falls and have a degree of cerebral atrophy, which puts strain on the bridging veins and coagulopathy. Subdural haematomas are classified as acute, subacute and chronic:

• acute (ASDH) refers to symptoms which manifest before 72 hours post-injury. Most patients harbouring an acute SDH are unconscious immediately following major cerebral trauma. The expanding haematoma then causes additional deterioration (Duffy 2001)

• subacute refers to symptoms which manifest between 72 hours and 3 weeks post-injury

• chronic refers to symptoms which manifest after 3 weeks post-injury. The injury may have been considered as minor and the patient often does not remember a particular predisposing injury.

The most common symptom of a SDH is a headache, which progressively intensifies and is eventually accompanied by vomiting, cognitive impairment(s), a depressed level of consciousness, and a focal deficit, which will vary depending on severity of the injury. Even in the absence of focal deficit, increasing ICP may lead to cognitive impairment and eventually a depressed level of consciousness (Watkins 2000). SDHs are often associated with other injuries, and therefore the symptoms can become confused within a general head injury picture. Small SDHs may be treated conservatively, as they will reabsorb over time. Larger SDHs will require evacuation, due to the secondary damage they cause.

A poor outcome is likely if the SDH is bilateral, it accumulates rapidly or there is a greater than 4-hour delay in the surgical management of an ASDH. Increased patient age and underlying accompanying brain injury also lead to a poor outcome.

Intracerebral haematoma (ICH) is caused by bleeding within the substance of the brain (Fig. 5.15). ICH usually affects the white matter and the basal ganglia found deep within the brain parenchyma. ICHs are related to contusions as a result of a major impact, and are usually found in the frontal, temporal, and parietal lobes. Other causes include penetrating and missile injuries and shearing of blood vessels deep within the brain following an acceleration/deceleration injury. Symptoms include headache, contralateral hemiplegia, ipsilateral dilated/fixed pupil and deteriorating level of consciousness, progressing to deep coma (GCS < 8). Treatment tends to be conservative, due to the difficulties of evacuating haematomas situated so deeply within the brain. Mortality is high within this group of patients.