45

PART 2

Trauma care

PART CONTENTS

4. Head injuries 47

5. Skeletal injuries 79

6. Spinal injuries 123

7. Thoracic injuries 135

8. Abdominal injuries 153

9. Facial injuries 171

10. Burns 185

CHAPTER CONTENTS

Introduction 47Anatomy and physiology 48Physiology of raised intracranial pressure 54Classification of head injuries 55Management 62Admission to hospital 67Management of minor head injury 67Management of serious head injury 68Management of intracranial complications 71Brain stem death testing 76Conclusion 76

INTRODUCTION

Onemillion patients attend emergency departments inthe UK each year with head injuries. For mosttheir head injury is minor. Nine out of ten people seenin hospital have aminor head injury and are not admit-ted to hospital. Of those admitted to hospital, most willbe able to go home after 48 hours (NICE 2003).

There are many causes of head injuries, with roadtraffic accidents (RTAs) being the single largest cause.Other common causes include falls, assaults andsports injuries. There is an increased incidence ofhead injuries in young males and children (NICE2003). Eighty per cent of head injuries in the UK areminor (Glasgow Coma Scale (GCS) 13–15), 10% aremoderate (GCS 9–12) and 10% are severe (GCS lessthan 8). Severe head injuries account for 50% oftrauma-related deaths in the UK. Five to ten per centof patients who suffer a severe head injury also suffera cervical spine injury.

Severe head injuries, i.e. brain injuries, are uncom-mon because the skull and scalp absorb most of theimpact of the assault. The amount of damage sufferedis relative to the power of the assault. A high-energyhead injury results from the following circumstances:when a pedestrian is struck by a motor vehicle, anoccupant is ejected from a motor vehicle, a personfalls from a height of greater than 1 metre or morethan five stairs (a lower threshold for the height offalls should be used when dealing with infants andyoung children under 5 years old), following a divingaccident, following a high-speed motor vehicle colli-sion, following a rollover motor accident or a bicyclecollision (NICE 2003).

It is vital that the emergency nurse caring forpatients with head injuries has a good knowledgeand understanding of the anatomy and physiology

47

Chapter 4

Head injuriesKaren Lesley Sanders

of the skull, the brain and its related structures alongwith the physiological processes that maintainhomeostasis. Such knowledge and understandingallows the nurse to relate the mechanisms of injuryto the brain injuries suffered and thus assess, plan,evaluate and implement the care and managementneeded by the patient at any particular stage follow-ing the injury.

A structured approach to the care of head-injuredpatients should be initiated. The system advocated bythe Advanced Trauma Life Support (ATLS) system(American College of Surgeons 2004) provides amechanism for assessment and immediate manage-ment and minimizes the risk of secondary brain injuryin adults. For children the advanced paediatric life sup-port (APLS) system should be employed (NICE 2003).

ANATOMY AND PHYSIOLOGY

The skull

The skull is a rigid bony cavity composed of 29 indi-vidual bones: the 8 bones of the cranium, 14 facialbones, the 6 ossicles of the ear and the hyoid bone.To ensure maximum protection, strength and sup-port, bony capsules surround the brain, the eyes, thenasal passages and the inner ear; and bony buttresses

extend upwards from the teeth through the facialbones. To relieve the potential weight, the skull ismade lighter by the paranasal sinuses, which alsogive resonance to the voice.

The cranium is one of the strongest structures in thebody and provides the bony protection for the brain. Itis composed of the parietal (2), occipital, frontal, tem-poral (2), sphenoid and ethmoid bones. Figure 4.1shows an exploded view of the cranial skull; however,the bones are fused along main sutures, the saggital,coronal, lambdoidal and squamosal. The facial bonesform the framework for the nasal and oral cavitiesand include the zygomatic bones (2), palatine bones(2), mandible, maxilla (2), lacrimal bones (2), nasalbones (2), vomer and the inferior nasal concha (2)(see Fig. 4.2).

Figure 4.3 shows the irregular internal surfaces ofthe skull. These irregular surfaces/bony protrusionsaccount for injury to the brain as it moves within theskull under acceleration/deceleration forces.

The meninges

The brain and the spinal cord are encased by threelayers of membrane – the dura mater, the arachnoidmater and the pia mater known collectively as themeninges (see Fig. 4.4).

Parietal bone (2)

Sagittal suture

Squamosalsuture

Coronal suture

Frontal bone

Ethmoid bone

Sphenoid bone

Temporal bone (2)Mastoid process of

temporal bone

Occipital bone

Cra

nial

sku

ll (8

bon

es)

Lambdoidalsuture

Figure 4.1 Exploded view of the cranial skull.

48 TRAUMA CARE

Faci

al s

kull

(14

bon

es)

Malleus (2)Stapes (2)

Incus (2)

Ossicles of ear (6)

Zygomatic bone(malar) (2)

Palatine bone (2)

Mandible

Maxilla (2)

Inferior nasalconcha (2)

Vomer

Nasalbone (2)

Lacrimalbone (2)

Hyoid bone

Figure 4.2 Exploded view of the facial skull.

Frontal bone

Crista galli

Cribriform plateof ethmoid bone

Optic foramen

Internal acoustic

Sella turcica

meatus

Foramen magnum

Frontal sinus

Small wing of sphenoid

Great wing of sphenoid

Petrous portionof temporal bone

Parietal bone

Occipital bone

Figure 4.3 View of the base of the skull from above.

Head injuries 49

The dura mater

The duramater consists of two layers: the outer layer isthe periosteal layer of the skull, which terminates at theforamenmagnum, and the inner layer is a strong, thickmembrane that is continuous with the spinal duramater. There is a potential space between the two dura,except at the falx cerebri, which divides the left andright hemispheres of the cerebrum; the tentorium cere-belli, which divides the cerebrum and cerebellum; thefalx cerebelli, which divides the lateral lobes of the cer-ebellum; and the diaphragm sellae. The dura creates aroof for the sella turcica (which houses the pituitarygland). These compartments provide support andprotection for the brain and form the sinuses, whichdrain venous blood from the brain (Lindsey et al.2004, Crossman & Neary 2000).

The arachnoid materThe arachnoid mater is fine serous membrane thatloosely covers the brain. There is a potential spacebetween this and the inner dura mater, known as thesubdural space. Between the arachnoid mater and thepia mater is an actual space, known as the subara-chnoid space, which contains the arachnoid villi, cere-brospinal fluid (CSF) and small blood vessels.

The pia materThe pia mater follows the convolutions and isattached to the surface of the brain. It consists of fine

connective tissue, housing the majority of the bloodsupply to the brain.

The ventricles and cerebrospinal fluid

Within the brain there are four connected cavities calledventricles, which contain cerebrospinal fluid (CSF).These are the left and right lateral ventricles, the thirdventricle and the fourth ventricle. The lateral ventricleslie in the cerebral hemispheres, the third in the dien-cephalon and the fourth in the brain stem. The lateralventricles are connected to the third ventricle by theinterventricular foramen, sometimes known as theforamen of Munro, and the third ventricle is connectedto the fourth by the cerebral aqueduct, sometimesknown as the aqueduct of Sylvius (see Fig. 4.5).

CSF is a clear, colourless fluid composed of water,some protein, oxygen, carbon dioxide, sodium, potas-sium, chloride and glucose. Its purpose is to protectthe brain from injury by providing a cushioning effect.The major source of CSF is from the secretions of thechoroid plexus, found in the ventricles. The choroidplexus produce approximately 500 ml of CSF daily;however, the average adult brain only holds between125 and 150 ml. CSF is renewed and replaced approxi-mately three times daily, being reabsorbed through thearachnoid villi, which drain into the superior saggitalsinus, when the CSF pressure exceeds the venous pres-sure. Normal CSF pressure is 60–180 mmH2O in thelumbar puncture position (lateral recumbent) and200–350 mmH2O in the sitting position.

Subarachnoid space

Subdural space

Superior sagittal sinusArachnoid villi

Skin

Periosteum

Bone

Dura mater

Arachnoid

Pia mater

Falx cerebri

Figure 4.4 The cranial meninges.

50 TRAUMA CARE

The brain

The brain consists of three main areas:

� cerebrum

� cerebellum

� brain stem.

The major structures within the brain are summar-ized in Box 4.1.

CerebrumThe cerebrum consists of two cerebral hemispheres,which are partially separated by the longitudinal fissureand connected at the bottomby the corpus callosum. It isgenerally accepted that one hemisphere (usually theleft) is more highly developed than the other. The leftside of the brain has been shown to control the right sideof the body, spoken and written language, scientificreasoning and numerical skills, whereas the right sideis more concerned with emotion and artistic and crea-tive skills. However, at birth, the hemispheres are ofequal ability and very early injury to one side or anotherusually results in skills being acquired by the oppositeside of the brain. Each cerebral hemisphere has an areaof grey matter called the basal ganglia, which assists inthe motor control of fine body movements.

The surface area of the cerebral cortex (grey matter),on the surface of the brain is much increased by thepresence of gyri and sulci (see Fig. 4.6), resulting in a3:1 proportion of grey towhite matter. Below the cortexlies the white matter. The cerebral hemispheres arecomposed of four lobes, the frontal, parietal, temporaland occipital lobes. Box 4.2 summarizes the mainfunctions of these lobes.

The diencephalon is located deep into the cere-brum and consists of the thalamus, hypothalamus,

Subarachnoid space

Arachnoid villus

Superior saggital sinusChoroid plexus of third ventricle

Choroid plexus of lateral ventricle

Interventricularforamen

Lateral ventricle

Third ventricle

Cerebral aqueduct

Fourth ventricle

Choroid plexus offourth ventricle

Subarachnoid space

Cisterna magna(cerebellomedullary cistern)

Straight sinus

Confluence ofthe sinuses

Figure 4.5 Ventricles of the brain and circulatory path of cerebrospinal fluid through the cranial pathways.

Box 4.1 The major structures of the brain

Cerebrum

� Cerebral hemispheres

� Corpus callosum

� Basal ganglia

� Diencephalon

� Hypophysis

Brain stem

� Midbrain

� Pons

� Medulla

Cerebellum

Head injuries 51

sub-thalamus and epithalamus. It connects the mid-brain to the cerebral hemispheres. The hypothalamusincludes several important structures, such as the opticchiasma, the point at which the two optic tracts crossand the stalk of the pituitary gland (hypophysis).

CerebellumThe cerebellum is situated behind the pons and attachedto the midbrain, pons and medulla by three-pairedcerebellar peduncles. It consists of three main parts:

� the cortex

� the white matter, which forms the connectingpathways for impulses joining the cerebellum withother parts of the central nervous system

� four pairs of deep cerebellar nuclei.

The cerebellum is the processing centre for co-ordi-nation of muscular movements, balance, precision,timing and body positions. It does not initiate any

Longitudinal fissure

Left hemisphere

Precentral gyrus

Central sulcus

Post central gyrus

Parieto-occipital line

Occipital lobe(a)

Parietal lobe

Frontal lobe

Right hemisphere

Parieto-occipital line

Central sulcus

Frontal lobe

Supramarginal gyrus

Insula

Lateral cerebral fissure

Temporal lobe

Transverse cerebral fissure

Angular gyrus

(b)

Occipital lobe

Figure 4.6 a, b Gyri, sulci and fissures of the cerebral hemispheres. A: Superior view. B: Right lateral view.

Box 4.2 The functions of the cerebral cortexby lobe

Frontal

� Motor

� Expression

� Moral

Parietal

� Sensation

� Spatial

Temporal

� Auditory

� Equilibrium

� Interpretive

� Intellectual

Occipital

� Visual

52 TRAUMA CARE

movements and is not involved with the consciousperception of sensations.

Brain stemThe brain stem is the connection between the brain andthe spinal cord and is continuous with the diencepha-lon above and the spinal cord below. Within the brainstem are ascending and descending pathways betweenthe spinal cord and parts of the brain. All cranial nervesexcept the olfactory (1) and the optic (2) nerves emergefrom the brain stem (see Fig. 4.7). The brain stem isformed from three main structures:

� Midbrain connects the pons and the cerebellum tothe cerebrum. It is involved with visual reflexes,the movement of the eyes, focusing and thedilatation of the pupils. Contained within themidbrain and upper pons is the reticular activatingsystem, which is responsible for the ‘awake’ state.

� Pons is located between the midbrain andthe medulla and serves as a relay station fromthe medulla to higher structures in the brain. It isinvolved with the control of respiratory function.

� Medulla connects the pons and the spinal cord.The point of decussation of the pyramidaltract occurs within the medulla. The vital centres

associated with autonomic reflex activity arepresent in its deeper structure. These are thecardiac, respiratory and vasomotor centres andthe reflex centres of coughing, swallowing,vomiting and sneezing.

Cerebral circulation

The brain is supplied with blood by four majorarteries: two internal carotid arteries, which supplymost of the cerebrum and both eyes; and two vertebralarteries, which supply the cerebellum, brain stem andthe posterior part of the cerebrum. Before the bloodenters the cerebrum it passes through the circle ofWillis, which is a circular shunt at the base of the brainconsisting of the posterior cerebral, the posterior com-municating, the internal carotids, the anterior cerebraland the anterior communicating arteries (see Fig. 4.8and Fig. 4.9). These vessels are frequently anomalous;however, they allow for an adequate blood supply toall the brain, even if one or more is ineffective.

The venous drainage from the brain does not fol-low a similar pathway (Fig. 4.10). Cerebral veinsempty into large venous sinuses located in the foldsof the dura mater. Bridging veins connect the brainand the dural sinuses and are often the cause of

Diencephalon

Midbrain

Pons

Cerebellarpeduncles

Medullaoblongata

Spinal cord

SuperiorMiddleInferior

Tuberculumcuneatus

OliveTuberculum

gracilis

Third ventricle

Pineal body

Superior colliculus

Inferior colliculus

Trochlear nerve (IV)

Trigeminal nerve (V)

Vestibulocochlear nerve (VIII)

Facial nerve (VII)

Fourth ventricle

Glossopharyngeal nerve (IX)

Vagus nerve (X)

Accessory nerve (XI)

C1

C2

Hypoglossal nerve (XII)

Thalamus

Figure 4.7 Brain stem (dorsal view).

Head injuries 53

subdural haematomas. These sinuses empty into theinternal jugular veins, which sit on either side ofthe neck and return the blood to the heart via thebrachiocephalic veins.

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

PHYSIOLOGY OF RAISED INTRACRANIALPRESSURE

Intracranial pressure (ICP) represents the pressureexerted by the cerebrospinal fluid (CSF)within the ven-tricles of the brain (Hickey 1997). The exact pressurevaries in different areas of the brain. Its normal rangeis 0–15 mmHg in adults, 3–7 mmHg in children and

1.5–6 mmHg in term babies when measured from theForamen of Munro.

ICP is fundamental in maintaining adequate brainfunction. Thebrain lies in the skull, a rigid compartment.The contents of the skull are non-compressible, i.e. braintissue (80%), intravascular blood (10%) and cerebrospi-nal fluid (10%). Normally these components maintain afairly constant volume, therefore creatingdynamic equi-librium therein. Shouldone ormore component increasefor whatever reason the Monro-Kellie hypothesis statesthat another component must decrease in quantity inorder to maintain the dynamic equilibrium and thusmaintain adequate cerebral blood flow (CBF). If thisdoes not occur, ICP rises, leading to brain injury (Hickey1997). Dynamic equilibrium is maintained by a numberof compensatory mechanisms: these include

� increasing CSF absorption

� decreasing CSF production

� shunting of CSF to the spinal subarachnoid space

� vasoconstriction – reducing cerebral blood flow.

Middle cerebral artery

Superficial temporal artery

Basilar artery

Occipital artery

Maxillary artery

Post auricular artery

Internal carotid artery

External carotid artery

Vertebral artery

Costocervical trunk

Right subclavian artery

Anterior cerebral artery

Ophthalmic artery

Internal carotid artery

Facial artery

Lingual artery

Superior thyroid artery

Right common carotid artery

Thyrocervical trunk

Clavicle

Brachiocephalic trunk

First rib

Aortic arch

Figure 4.8 Major arteries of the head and neck.

54 TRAUMA CARE

Maintenance of the dynamic equilibrium in thebrain is further aided by autoregulation. Autoregula-tion is the ability of the brain to maintain a relativelyconstant CBF over a wide range of perfusion pres-sures (60–160 mmHg). Autoregulation is initiated bycerebral perfusion pressure (CPP), which is definedas the blood pressure gradient across the brain andis calculated by subtracting ICP from the systemicmean arterial pressure (MAP)

CPP ¼ MAP � ICP

In healthy adults CPP is 60–70 mmHg. Shouldthe patient’s MAP fall and/or the patient’s ICPincrease, there is a risk that the cerebral perfusion pres-sure will fall to too low a value to maintain adequatecerebral blood flow. This will result in hypoxia andcerebral ischaemia, causing secondary brain injury.CPP should bemaintained between 70 and 100 mmHg.Autoregulation fails should the CPP fall below60 mmHg or rise above 160 mmHg. It is raised ICP,decreased MAP or reduced CPP, which is responsiblefor most secondary brain injury.

Chemoregulation is triggered by changes in extra-cellular pH and metabolic by-products. Changes inPCO2 or a dramatic reduction in PO2 (see Fig. 4.11)may also trigger it. In the head-injured patient, main-taining adequate oxygenation is vital, because allowing

the PCO2 to rise initiates chemoregulation, which inturn increases ICP, because it increases overall brainmass due to the resulting vasodilatation. Cerebralvasoconstriction reduces brain mass, and it is for thisreason that ventilated head-injured patients are hyper-ventilated, as this reduces PCO2 and activates chemor-egulation, thus inducing vasoconstriction which helpsto reduce ICP.

The mechanisms which compensate for rises in ICPin the healthy adult brain fail as ICP reaches 20 mmHg.From then on, small increases in brain mass, blood vol-ume or CSF have a profound effect on ICP. Chestnut(1993) demonstrated a clear correlation between thelength of time the patient’s ICP remains greater than20 mmHg and an increased mortality and morbidityrate.

CLASSIFICATION OF HEAD INJURIES

Head injuries can be classified under three anatomicalsites:

� the scalp

� the skull

� the brain.

Patients often present with a combination ofinjuries.

Anterior communicating artery

Middle cerebral artery

Internal carotid artery

Posterior cerebral artery

Basilar artery

Occipital lobe of cerebrum

Frontal lobe of cerebrum

Anterior cerebral artery

Temporal lobe of cerebrum

Cerebral arterial circle(circle of Willis)

Posterior communicating artery

Pons

Medulla

Vertebral artery

Cerebellum

Figure 4.9 Cerebral circulation.

Head injuries 55

Scalp injuries

There are four types of injury to the scalp:

� Abrasion – minor injury that may cause a smallamount of bleeding. Treatment may not berequired, but ice applied to the area may reduceany haematoma formation.

� Contusion – no break in the skin, but bruising tothe scalp may cause blood to leak into thesubcutaneous layer.

� Laceration – a cut or tear of the skin andsubcutaneous fascia that tends to bleed profusely.Bleeding from the scalp alone is unlikely to causeshock in the adult. In small children, a scalp

Superior sagittal sinus

Inferior sagittal sinus

Straight sinus

Right transverse (lateral) sinus

Right sigmoid sinus

Right posterior auricular vein

Right retromandibular vein

Right external jugular vein

Right internal jugular vein

Right vertebral vein First rib

Right subclavian vein

Right facial vein

Right thyroid vein

Clavicle

Figure 4.10 Major veins of the head and neck.

PCO2extracellular pHmetabolic by-products Cerebral perfusion pressure

Cerebral perfusion pressure

Cerebral vasodilation

Cerebral vasoconstriction

(chemoregulation)

(autoregulation) (chemoregulation) (autoregulation)

PO2 PCO2extracellular pHmetabolic by-products

Figure 4.11 Chemoregulation of the brain.

56 TRAUMA CARE

laceration may be sufficient to cause hypovolaemia.Scalp lesions should be explored under localanaesthetic for foreign bodies and/or skull fracturewith a skull X-ray if there is any doubt about thediagnosis. Lesion(s) should be sutured or gluedaccording to their depth and position.

� Subgaleal haematoma – a haematoma below thegalea, a tough layer of tissue under thesubcutaneous fascia and before the skull. The veinshere empty into the venous sinus, and thus anyinfection can spread easily to the brain, despite theskull remaining intact. There is controversysurrounding the treatment of subgalealhaematomas, due to the risks of infection; thereforesome doctors argue that it is best to evacuate thehaematoma, while others suggest that it is best tolet it reabsorb.

If the scalp injuries are only part of other injuries, itis important they are documented to allow furtherinvestigation at a more appropriate time. They mayneed to be cleaned and dressed or temporarily sutured.Abrasions may not require any treatment, but iceapplied to the area may reduce any haematoma forma-tion (Hickey 1997). Lacerations can bleed extensively;however, bleeding from the scalp alone is unlikely tocause shock in the adult patient.

The skull

Skull fractures indicate that the head has suffered amajor impact. Patients who suffer skull fractures havea 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 andneed no specific treatment.

� Depressed. Usually evident clinically, but a skull X-ray to discover the full extent of the potential braindamage is usually necessary. Management isdependent on the severity of the fracture andwhether there are any accompanying injuries. Ifthere are no other injuries requiring surgicalmanagement, they may not be surgically elevated,due to the risks of infection. However, surgicalintervention will normally be necessary if there arebone fragments imbedded in the brain so as toelevate the bone fragments and manage the braintrauma.

� Open. Usually evident clinically. Usually managedaccording to the severity of the injury. If debris isdispersed in the brain tissue then surgery will berequired and there is a heightened risk of infection.

� Comminuted. These are detected on skull X-ray.These patients should be closely observed and anyneurological deficits managed appropriately.Surgical intervention is usually required. If thereare bone fragments imbedded in the brain tissuethen surgery will be required to elevate the bonefragments and manage the brain trauma.

� Basal. Are diagnosed clinically as they are difficultto detect on X-ray. Signs include CSF leakage fromthe nose (rhinorrhoea) or the ear(s) (otorrhoea).Rhinorrhoea or otorrhoea indicates that a skull basefracture has breached the dura and formed acommunication between the intracranial contentsand an air sinus. This places the patient at risk ofmeningitis while the CSF leak continues. If CSFleakage is suspected, the fluid should be tested forglucose and the ‘halo test’ performed, where asmall amount of fluid is placed on blotting paper; ifCSF is present it will separate from blood and forma yellow ring around the outside of the blood.Patients with a base of skull fracture may also haveretroauricular bruising (Battle’s signs) and peri-orbital bruising (‘panda eyes’ or ‘raccoon eyes’):80–90% of cases seal within 2 weeks and usuallyneurosurgical intervention is not considered untilthis time has elapsed. An exception is a fracture ofthe posterior wall of the frontal sinus, visualized onCT scan, where anterior fossa repair may beundertaken early.

Patients with CSF leakage are usually prescribedprophylactic antibiotics, because of the high risk ofbacterial meningitis. The available evidence, however,does not support the use of prophylactic antibiotics(Watkins 2000). If gastric decompression is indicated,the orogastric route should be used, as the nasogastricroute carries the risks of trauma to the brain and theintroduction of infection.

The brain

Damage to the brain as a result of trauma includesboth the immediate (primary) injury which is thedamage caused at the moment of the impact and thesecondary injury that develops during the first fewhours or days after the impact (Box 4.3). These sec-ondary injuries may have extracranial or intracranialcauses.

There are no interventions that can prevent the pri-mary brain injury. Secondary brain insults, which fur-ther exacerbate neuronal injury and lead to aworsening outcome depending on their duration andseverity, are largely preventable. The two main causesof secondary injury are delayed diagnosis and treat-ment of intracranial haematomas and failure to correct

Head injuries 57

systemic hypoxaemia and hypotension. Over one thirdof all patients who suffer a severe head injury appear toexperience either hypoxia or hypotension or both dur-ing the acute post-injury period and these secondaryinsults correlate with a doubling of mortality and anincrease in morbidity (Chesnut 1995) (see Fig. 4.12).

Brain injuries are usually categorized as eitherfocal or diffuse injuries.

Focal injuries

Focal injuries occur in a specific area of the brain. Themechanism of injury is usually blunt injury and accel-eration/deceleration injury.

Cerebral contusion – bruising of the surface of thebrain is sustained as the brain hits the bony protuber-ances of the skull at the site of the impact (coup

injury) and at the opposite side of the brain duringdeceleration (contrecoup injury). Cerebral contusionis a common type of brain injury, which is diagnosedby computed tomography (CT) scan, and is mostcommonly seen at the frontal and temporal lobes asa result of the irregular surfaces/bony protrusions ofthe skull. The term contusion is used when the piamater has not been breached. The brain swells aroundthe site(s) of the contusion(s). Bleeding may occur intothe 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 com-mon clinical signs.

Cerebral lacerations – of the cortical surface com-monly occur in similar locations to contusions andare most commonly seen at the frontal and temporallobes as a result of irregular surfaces/bony protru-sions of the skull. The term laceration is used whenthe pia mater is torn.

HaematomaExtradural haematoma (EDH) is an accumulation ofblood in the extradural space between the periosteumon the inner side of the skull and the dura mater (seeFig. 4.13). Most are associated with skull fracture andare commonly caused by a laceration to the middlemeningeal artery or vein, or less commonly to thedural venous sinus, following an insult to the

Cerebralvasodilationand oedema

PCO2pH

Tissuehypoxia

CBF

ICP

Figure 4.12 Cycle of progressive brain swelling.

Box 4.3 Types of brain injury

Primary brain injury

� Disruption of brain vessels

� Haemorrhagic contusion

� Diffuse axonal injury

Secondary brain injuryExtracranial insults

� Systemic hypotension

� Hypoxaemia

� Hypercarbia

� Disturbances of blood coagulation

Intracranial insults

� Haematoma (extradural, subdural, intracerebral)

� Cerebral oedema (see Fig. 4.12)

� Infection

Extra duralhaematoma

Duramater

Figure 4.13 Extradural haematoma.

58 TRAUMA CARE

temporal-parietal region. Consequentially the parietaland parieto-temporal areas of the brain are affected.In 85% of patients the EDH will be accompanied bya skull fracture (Hudak & Gallo 1994).

Patients with skull fractures may be neurologicallyintact on admission and later deteriorate as the EDHdevelops. Most often the primary brain injury causessome disturbance of consciousness and the develop-ing haematoma results in rapid neurological deterio-ration (Kwiatkowski 1996). Patients with EDHs mostcommonly present with a history of transient loss ofconsciousness, followed by lucidity for a period(hours to days) dependent on the rate of the bleed,irritation and headache. Patients then rapidly loseconsciousness and deteriorate very quickly. Late signsare seizures, ipsilateral pupil dilatation, unconscious-ness and contralateral hemiplegia. Surgical treatmentis required to evacuate the haematoma and ligatethe damaged blood vessel.

Relatives, friends and/or carers often require agreat deal of reassurance, as they often feel respon-sible for not bringing the patient to hospital earlier.

Subdural haematoma (SDH) is an accumulation ofblood between the dura mater and arachnoid mater.SDHs are caused by the rupture of bridging veinsfrom the cortical surfaces to the venous sinuses (corti-cal veins) (see Fig. 4.14).

SDHs can be seen in isolation, but more commonlyare associated with accompanying brain injury, i.e.cerebral contusions and/or intracerebral haematomas.They are the most common intracranial mass resultfrom head trauma (Maartens & Lethbridge 2005). Inmost cases a large contusion is found at the frontal ortemporal surface of the brain. SDHs are predisposedwith increasing age and alcoholism. Both groups cansuffer regular falls and have a degree of cerebralatrophy, which puts strain on the bridging veins andcoagulopathy. Subdural haematomas are classified asacute, subacute and chronic:

– Acute (ASDH) refers to symptoms which mani-fest before 72 hours post-injury. Most patients har-bouring an acute SAH are unconscious immediatelyfollowing major cerebral trauma. The expanding hae-matoma then causes additional deterioration (Duffy2001).

– Subacute refers to symptoms which manifestbetween 72 hours and 3 weeks post-injury.

– Chronic refers to symptoms which manifest after 3weeks post-injury. The injury may have been consid-ered as minor and the patient often does not remembera particular predisposing injury.

Themost common symptomof a SDH is a headache,which progressively intensifies and is eventuallyaccompanied by vomiting, cognitive impairment(s), adepressed level of consciousness and a focal deficit,which will vary depending on severity of the injury.Even in the absence of focal deficit, increasing ICPmay lead to cognitive impairment and eventually adepressed level of consciousness (Watkins 2000). SDHsare often associated with other injuries, and thereforethe symptoms can become confused within a generalhead injury picture. Small SDHsmay be treated conser-vatively, as they will reabsorb over time. Larger SDHswill require evacuation, due to the secondary damagethey cause.

A poor outcome is likely if the SDH is bilateral, itaccumulates rapidly or there is a greater than 4 hourdelay in the surgical management of an acute sub-dural haematoma. Increased patient age and underly-ing accompanying brain injury also lead to a pooroutcome.

Intracerebral haematoma (ICH) is caused by bleedingwithin the substance of the brain (see Fig. 4.15). ICHusually affects the white matter and the basal gangliafound deep within the brain parenchyma. ICHs arerelated to contusions as a result of a major impact,which are usually found in the frontal, temporaland parietal lobes. Other causes include penetratingand missile injuries and shearing of blood vesselsdeep within the brain following an acceleration/deceleration injury. Symptoms include headache,

Dura mater

Pia arachnoid

Subdural haematoma

Figure 4.14 Subdural haematoma

Head injuries 59

contralateral hemiplegia, ipsilateral dilated/fixedpupil and deteriorating level of consciousness, pro-gressing to deep coma (Glasgow coma scale < 8).Treatment tends to be conservative, due to the diffi-culties of evacuating haematomas situated so deeplywithin the brain. Mortality is high within this groupof patients.

Subarachnoid haemorrhage (SAH) is seen in 30–40% ofpatients following severe traumatic brain injury.Mortality and morbidity is double in these patientscompared to those with similar injury without theSAH component (Dearden 1998). The patient eithersuffered the SAH prior to the insult and thus theSAH is possibly the cause of the incident (Sakas et al.1995), or the vessels in the subarachnoid space aredamaged by the shearing forces at the time of the insult.

Diffuse injuries

Diffuse injuries occur throughout the brain ratherthan in a specific area of the brain. They result ingeneralized dysfunction. Diffuse injuries range fromconcussion, with no residual damage, to diffuse axonalinjury and persistent vegetative state. Diffuse injuryoccurs in 50–60% of patients with severe head traumaand is the commonest cause of unconsciousness, thevegetative state and subsequent disability (Graham1995).

Concussion – This is a transient form of diffuseinjury, which occurs following blunt trauma. It causesa temporary neuronal dysfunction because of tran-sient ischaemia or neuronal depolarization. Thismanifests as a headache, dizziness, inability to con-centrate, disorientation, irritability and nausea. Con-cussion can occur with or without memory loss.Concussion is graded in line with the severity ofsymptoms (see Box 4.4).

Recovery is usually rapid, but if neurologicalsymptoms persist, a CT scan should be performed torule out more severe injuries. Skull X-ray should onlybe performed if the mechanisms of injury or existingclinical findings are suggestive of a skull fracture.Most patients with concussion can be discharged withan accompanying adult. If there has been a loss ofconsciousness greater than 10 minutes, the patientshould be admitted for observation even if he appearsfully recovered.

Approximately one-third of patients with head inju-ries who are discharged from emergency departmentshave persistent post-concussion-type symptoms, suchas headache, fatigue, inability to concentrate, irritabil-ity and anxiety, persisting for several months due tomild diffuse axonal injury (Jackson 1995). The majorityof these patients will have been knocked out for a shorttime and may have other mild neurological signs. Asthere is no treatment for mild diffuse axonal injury,and recovery is usually spontaneous, reassurance andpsychological support are vital to the patient’s recovery(see Box 4.5).

Acute axonal injury – This is usually the result of anacute rotation/deceleration injury, typically followinga road traffic accident (Fig. 4.16). The patient usuallybecomes unconscious rapidly after injury, due to theshearing injury to the brain. Mortality is high in thispatient group, and those who do survive usually suf-fer severe neurological dysfunction.

Initially a CT scan may show little abnormality, butgraduallywith repeated scans,many small diffuse hae-morrhagic areas will begin to appear, commonly in the

Box 4.4 Grading concussion

Grade I No loss of consciousness, transientconfusion and rapid return to normalfunction

Grade II Confusion and mild amnesiaGrade III Profound confusion with pre- and post-

traumatic amnesiaGrade IV Loss of consciousness, variable confusion,

amnesia

Intracerebralhaemorrhage

Figure 4.15 Intracerebral haematoma.

60 TRAUMA CARE

corpus callosum, often associated with traumatic intra-ventricular haemorrhage and the brain stem. As aresult of these injuries the patient may also developautonomic dysfunction and exhibit symptoms such asexcessive sweating, hyperpyrexia and hypertension.Severe generalized cerebral oedema usually accompa-nies such injuries.Management and treatment involvesmaximizing cerebral perfusion and the prevention ofsecondary brain injury.

Cerebral oedema – This is a consistent reaction of thebrain to an insult and it usually develops during thefirst 3–5 days following the insult causing an increasein ICP. Cerebral oedema following severe traumaticbrain injury affects almost all patients to a greater orlesser degree. The opening of the blood brain barrieris a central prerequisite to the development of cere-bral oedema (Fernandex & Landolt 1996). Four patho-physiological mechanisms of cerebral oedema havebeen proposed (Box 4.6).

Cerebral ischaemia – This occurs whenever the deliv-ery of oxygen and substrates to the brain falls belowits metabolic needs, as a result of hypoxia (cardiacarrest, obstructive airway, cervical spinal injury andprolonged epileptic-type seizures), hypotension and/or intracranial hypertension (raised ICP).

Blood flow in and around areas of brain tissuedamaged by trauma may be abnormal. Vasomotorparalysis also occurs in and around areas of brain tis-sue damaged by trauma. Blood vessels lose the ability

Acceleration

Deceleration

Corpus callosum

Dorsolateral quadrant of the midbrain

Central white mater

Midbrain at level of superiorcerebellar peduncles

Figure 4.16 Diffuse axonal injury.

Box 4.5 Symptoms of mild diffuse axonal injury

� Headache

� Fatigue

� Irritability

� Poor concentration

� Dizziness

� Poor balance

� Depression

Box 4.6 Types and causes of cerebral oedema

Types of oedema Cause

VasogenicBlood vessel damageExtends slowly over a

period of 72 hours

Contusion

CytotoxicCell membrane pump

failure

Hypoxaemia/ischaemia

HydrostaticHigh vascular transmural

pressure

Loss of autoregulationPost brain decompression

Hypo-osmoticLow plasma osmotic

pressure(serum sodium

< 120 mEq/l)

Hyponatraemia (dilutional/mannitol)

Head injuries 61

to control their own resistance actively withsubsequent loss of blood pressure autoregulationand reactivity to CO2. Cerebral blood flow thusbecomes pressure dependent, rendering these areasof brain more susceptible to ischaemia at lower bloodpressures and more likely to sustain injury at higherpressures.

Cerebral ischaemia may be global or focal, completeor incomplete. Incomplete ischaemia differs from com-plete ischaemia in that there is a continuing supply ofglucose to the brain tissue despite tissue hypoxia. Theglucose sustains anaerobic metabolism, whichincreases the brain lactic acid level. Neuronal damageoccurs above a certain threshold. This effect is the basisfor concern that increased peri-ischaemia glucoselevels may increase and/or hasten the ischaemia tissuedamage. Ischaemia leads instantly to cerebral oedema,which in turnworsens ischaemia (Farnsworth& Sperry1996).

As the PaCO2 increases, unaffected normal bloodvessels dilate, however blood is shunted away fromthe abnormal areas of the brain that do not respond toCO2 and is known as the ‘steal phenomenon’. Aninverse steal (Robin Hood Phenomenon) occurs whenthe PaCO2 is reduced and the unaffected, normal bloodvessels vasoconstrict, shunting blood to the abnormalareas of the brain that do not constrict (Darby et al.1988).

The concept of ischaemia penumbra states that thearea of the brain around an ischaemic brain, whereblood flow is providing sufficient oxygenation for thecells to survive, but insufficient oxygenation for thecells to maintain normal neuronal function, can re-establish normal function if blood flow and oxygena-tion to this area is rapidly improved. Cerebral ischae-mia is the single most important factor in determiningoutcome in severe traumatic brain injury: ischaemialesions are found in 90% of patients at post-mortem(Dearden 1998).

MANAGEMENT

Patients who have sustained a head injury shouldinitially be assessed and managed according to clearprinciples and standard practice as embodied in theadvanced trauma life support (ATLS) system (Ameri-can College of Surgeons 2004) and for children theadvanced paediatric life support (APLS) system(Bavetta & Benjamin 2002, NICE 2003). The mainfocus of the assessment should be the risk of clinicallyimportant brain and cervical spine injuries. Dueattention should also be paid to co-existing injuriesand other concerns the healthcare team may have,e.g. non-accidental injury.

External referrals

Community health services, e.g. general practice,paramedics, NHS walk-in centres, dental practitionersand NHS minor injury clinics and telephone adviceservices, e.g. NHS Direct, should refer people whohave sustained a head injury to the ambulance ser-vices for emergency transport to ED if they haveexperienced any of the following:

� GCS less than 15 at any time since the injury

� any loss of consciousness as a result of the injury

� any focal neurological deficit since the injury, e.g.problems understanding, speaking, reading orwriting, loss of sensation in a part of the body,problems balancing, general weakness, problemswalking and any changes in eyesight

� any seizure since the injury

� any suspicion of a skull fracture or penetratinghead injury, e.g. CSF leakage from the nose(rhinorrhoea) or the ear(s) (otorrhoea), black eye(s)with no associated damage around the eye(s),bleeding from one or both ears, new deafness inone or both ears, bruising behind one or both ears,penetrating injury signs or visible trauma to thescalp or skull

� a high-energy head injury

� or the injured person or their carer is incapable oftransporting the injured person safely to thehospital emergency department without the use ofambulance services, providing any other riskfactors indicating emergency department referralare present (NICE 2003).

Telephone advice services, e.g. NHS Direct, shouldrefer people who have sustained a head injury to anhospital emergency department if the related historyindicates any of the following risk factors:

� amnesia for events before or after the injury: theassessment of amnesia will not be possible in pre-verbal children and is unlikely to be possible in anychild under 5 years old

� persistent headache since the injury

� any loss of consciousness as a result of theinjury from which the injured person hasnow recovered

� any vomiting episode since the injury: clinicaljudgement should be used regarding the cause ofvomiting in those aged less than or equal to 12years and whether referral is necessary

� any previous cranial neurosurgical intervention

� history of bleeding or clotting disorders

� current anticoagulant therapy such as warfarin

� current drug or alcohol intoxication

� age greater than or equal to 65 years

62 TRAUMA CARE

� suspicion of non-accidental injury

� irritability or altered behaviour particularly ininfants and young children

� continuing concern by the Helpline’s personnelabout the diagnosis (NICE 2003).

In the absence of the factors listed above the tele-phone advice services should advise the injured per-son to seek medical advice from community healthservices, e.g. general practice and NHS walk-in cen-tres if any of the following factors are present:

� adverse social factors, e.g. no one able to supervisethe injured person at home

� continuing concern by the injured person or theircarer about the diagnosis (NICE 2003).

History

Accurate history-taking gives vital clues to the typeand potential severity of the head injury (Shah 1999)(see Box 4.7). This may have to be obtained from awitness or paramedic. If the history is obtained fromthe patient, it should be corroborated by a witness/relative if possible.

AssessmentManagement of head injury in the emergency depart-ment revolves largely around the assessment of therisks of, and the prevention or limiting of secondarybrain injury (the causation of secondary brain injury isshown in Box 4.8) and of injury to the cervical spine,whilst the patient awaits definitive treatment such assurgery to evacuate haematoma. Due attention shouldalso be paid to co-existing injuries.

Patients presenting to the emergency departmentwith a GCS less than or equal to 8 should be assessedearly by an anaesthetist or critical-care physician toprovide appropriate airway management and to assistwith resuscitation (NICE 2003). The recommended pri-mary investigation of choice for the detection of acuteclinically important brain injuries is CT imaging (NICE

2003). MRI for safety, logistic and resource reasons isnot currently indicated as the primary investigation,although additional information of importance to thepatient’s prognosis can sometimes be detected usingMRI. MRI is contraindicated unless there is certaintythat the patient does not harbour an incompatibledevice, implant or foreign body. Skull X-ray(s) are therecommended primary investigation of choice for skullfractures (see Box 4.9). If CT scanning is not availablethen skull X-rays alongwith high quality patient obser-vations have a vital role. Early imaging, rather thanadmission and observation for neurological deteriora-tion, reduces the time needed to detect life-threateningcomplications and is associated with a better outcome(NICE 2003). Indications for CT scanning are listed inBox 4.10.

Neurological assessmentFull neurological assessment forms part of the sec-ondary survey, as should thorough examination ofthe scalp for lacerations, haematomas or evidence ofa depressed skull fracture. The assessment and classi-fication of patients who have suffered a head injuryshould be guided primarily by the adult (16 years orolder) and paediatric versions of the Glasgow Coma

Box 4.8 Causes of secondary brain injury

� Hyperpyrexia

� Cerebral ischaemia

� Cerebral oedema

� Raised intracranial pressure

� Infection

� Metabolic disorder

� Evolving intracranial bleed

� Hypotension

Box 4.7 History-taking in head injury

� Mechanism of injury

� Time elapsed

� Period of loss of consciousness

� Any pre/post-traumatic amnesia

� Condition since injury, such as nausea, vomiting,confusion, visual disturbance, lethargy ordizziness

Box 4.9 Indications for skull X-ray

� Suspected penetrating injury

� Decreased consciousness (if GCS below 8/15, CT isindicated)

� Altered neurology

� CSF from nose or ear

� Significant scalp bruising or swelling

� Difficulty in clinical examination, where mechanismof injury is suggestive of fracture

Head injuries 63

Scale (GCS) and its derivative the Glasgow ComaScore (NICE 2003). The paediatric version shouldinclude a ‘grimace’ alternative to the verbal score tofacilitate assessment in the pre-verbal or intubatedpatients (NICE 2003).

TheGlasgowComa Scale (GCS), developed by Teas-dale & Jennett (1974), provides an objective, standar-dized and easily interpreted tool for neurologicalassessment without relying on subjective terminologysuch as ‘stupor’, ‘semi-coma’ and ‘deep coma’ (seeBox 4.11 and Fig. 4.17). The GCS records what you see,measuring arousal, awareness and activity, by asses-sing eye opening, verbal response and motor ability.Each activity is allocated a score, therefore enablingobjectivity, ease of recording and comparison betweenrecordings. It also provides useful information forpatient outcome prediction. The score should be basedon the sum of 15 and to avoid confusion this denomina-tor should be specified, e.g. 13/15 (NICE 2003). Whenrecording the GCS it is important to record the threeseparate response scores as well as the total GCSscore, i.e. E2, V3, M4. GCS ¼ 9 (NICE 2003)

When applying verbal stimulus, it is good practiceto commence with normal voice and then increasevolume to elicit a response. It is important to ascertain

whether the patient is deaf, wears a hearing aid andwhether English is the patient’s spoken language.When applying a painful stimulus, it is good practiceto commence with light pressure and then increase toelicit a response. When assessing motor function,always record the response from the best arm. Thereis no need to record left and right differences, as theGCS does not aim to measure focal deficit. It is notappropriate to measure leg response unless unavoid-able, i.e. injury to both arms, as a spinal reflex ratherthan a brain-initiated response might be initiated(Teasdale & Jennett 1974).

The GCS may be misleading in patients who havea high cervical injury, or brain stem lesion, and inthose who are hypoxic, haemodynamically shockedfitting or post-ictal. These patients may be unable tomove their limbs or may show no responses at all. Itis important to attempt to assess the spinal patientusing facial movements, being aware of the possibilityof a combined head and neck injury. Patients whoshow no response should be re-evaluated followingcorrection of any shock or hypoxia (NICE 2003).

The GCS assessment should be accompanied by anassessment of pupil size and reactivity, limb move-ment and vital signs observations:

Box 4.10 Indications for urgent CT scanning following a head injury

� GCS less than 13 at any point since the injury

� GCS 13–14, two hours after the injury

� Suspected open or depressed skull fracture

� Clinical symptoms of basal skull fracture

� Post-traumatic seizure

� Focal neurological deficit(s)

� More than one episode of vomiting (clinicaljudgement should be used regarding the cause ofvomiting in those children 12 years or younger, andwhether imaging is necessary)

� Amnesia for greater than 30 minutes of events prior tothe assault. This assessment is not possible in children5 years or younger.

CT should be immediately requested in patients withany of the following risk factors, providing they haveexperienced some loss of consciousness or amnesiasince the assault.

� Age 65 years or older

� Coagulopathy (clotting disorder or current treatmentwith warfarin)

� A high-energy head injury

CT Scanning and the results should be analysed withinone hour of the request having been received by the radiologydepartment in patients with the following risk factors

� GCS less than 13 at any point since the injury

� GCS 13–14, 2 hours after the injury

� Suspected open or depressed skull fracture

� Any signs of basal skull fracture

� Post-traumatic seizure

� Focal neurological deficit(s)

� More than 1 episode of vomiting (clinical judgementshould be used regarding the cause of vomiting inthose children 12 years or younger, and whetherimaging is necessary)

� Amnesia for greater than 30 minutes of events prior tothe assault. This assessment is not possible in children5 years or younger.

� Age 65 years or older providing that loss ofconsciousness or amnesia has been experienced.

� Coagulopathy (history of bleeding, clotting disorder orcurrent treatment with warfarin) providing that loss ofconsciousness or amnesia has been experienced.

� A high-energy head injury (NICE 2003).

64 TRAUMA CARE

� blood pressure

� respiration rate

� heart rate

� temperature

� blood oxygen saturation.(NICE 2003).

As well as providing a baseline for assessing thepatient’s progress, vital signs give important informa-tion about potential secondary brain injury, e.g. respi-ration rate and cerebral hypoxia. When assessing vitalsigns in conjunction with GCS, it is important toremember the following:

� Hypotension is only of neurological origin in end-stage brain injury or spinal shock. Other causes ofhypotension, such as hypovolaemia, should beinvestigated.

� Cushing’s triad (hypertension, bradycardiaand bradypnoea) indicates a life-threateningrise in ICP.

� Pyrexia with hypertension may indicate autonomicdysfunction.

Limbmovement is useful to assess for focal damage.However, although it is usual for a hemiparesis orhemiplegia to occur on the contralateral side to thelesion, it may occur on the ipsilateral side. This is dueto indentation of the contralateral cerebral peduncleand is known as a false localizing. Spontaneous move-ments are observed for equality. If there is little or nospontaneous movement, then painful stimuli must beapplied to each limb in turn, comparing the result. Itis most appropriate to complete this while assessingthe motor component of the GCS.

Box 4.11 Adult and Paediatric Glasgow Coma Scale

Adult (16 years and older)

Eye opening Motor response Verbal response

Spontaneous 4 Obeys 6 Orientated 5To speech 3 Localizes 5 Confused 4To pain 2 Normal flexion 4 Inappropriate 3None 1 Abnormal flexion 3 Incomprehensible 2

Extensor response 2 None 1None 1

Child

Eye opening Motor response Verbal response

Spontaneous 4 Obeys commands or performsnormal spontaneous movements 6

Alert, babbles, coos, words or sentences to usualability 5

To speech 3 Localizes to painful stimuli orwithdraws to touch 5

Less than usual ability and/orspontaneous irritable cry 4

To pain 2 Withdrawal to painful stimuli 4 Cries inappropriately 3None 1 Abnormal flexion 3 Occasionally whimpers and/or moans 2

Abnormal extension 2 None 1None 1

Pre-verbal child or intubated patient

Eye opening Motor response Grimace response

Spontaneous 4 Obeys commands or performsnormal spontaneous movements 6

Spontaneous normal facial/oro-motoractivity 5

To speech 3 Localizes to painful stimuli orwithdraws to touch 5

Less than usualSpontaneous ability or only responseto touch stimuli 4To pain 2 Withdrawal to painful stimuli 4

None 1 Abnormal flexion 3 Vigorous grimace to pain 3Abnormal extension 2 Mild grimace to pain 2None 1 None 1

Head injuries 65

(mm)

RespirationICP x

NAMED.O.BDATE

TIME

Eyesopen

Verbalresponse

Best motorresponse(Recordbest arm)

SpontaneouslyTo speechTo painNoneOrientatedSentencesWordsSoundsNoneObey commandsLocalize painNormal flexionAbnormal flexionExtensionNone

432154321654321

240230220210200190180170160150140130120110100

908070605040353025201510

5

Bloodpressureand pulse

Pupildiameter

guide

Right

Left

Size (mm)ReactionSize (mm)ReactionNormal powerMild weaknessSevere weaknessFlexionExtensionNo responseNormal powerMild weaknessSevere weaknessFlexionExtensionNo response

LIMBMOVEMENT

ARMS

LEGS

Bowels

WARD:REFERRING HOSPITAL:

UNIT NO:WEIGHT:

CONSULTANT:

C = Eyes closed by swelling

T = Endotrachealtube ortracheostomy

D = Dysphasia

P = Paralysed

40.039.539.038.538.037.537.036.536.035.535.034.534.033.533.032.532.0

Temp. (°C)

+ = reacts– = no reactionSL = sluggish

Recordright (R)and left (L)separatelyif there is adifferencebetween thetwo sides

P = Paralysed# = Fracture

1

2

3

4

5

6

7

8

PUPILS

Figure 4.17 Glasgow Coma Scale.

66 TRAUMA CARE

Pupils are assessed for their reaction to light, sizeand shape, i.e. cranial nerves II (optic) and III (oculo-motor) activity. Each pupil needs to be assessed andrecorded individually. Pupils are measured in milli-metres, the normal range being 2–6 mm in diameter.They are normally round in shape and abnormalitiesare described as ovoid, keyhole or irregular (Hickey1997). A bright light is shone into the side of each eyeto assess the pupils’ reaction to light. This should pro-duce a brisk constriction in both pupils, the consensuallight reaction. Herniation of the medial temporal lobethrough the tentorium directly damages the oculomo-tor (IIIrd) nerve, resulting in dilation of the pupil andan impaired reaction to light. The pupil dilates on theside of the lesion.

Patients with head injuries can be classified intothree groups depending on their GCS:

� A score of 13–15 is indicative of a minor headinjury. In some patients, a one-point drop in theirGCS can be alcohol- or drug-induced. Thisnecessitates extra vigilance from nursing staff asalcohol and/or drugs may mask subtle changes inthe patient’s cognition or conscious level.

� A GCS of 9–12 suggests a moderate head injury,or a more serious injury evolving. Any changesin the patient’s condition should be closelymonitored.

� A severe head injury is classed by a GCS of 8 orless. These patients are potentially at risk ofsecondary brain injury, and their GCS and vitalsigns should be monitored at frequent intervals.

ADMISSION TO HOSPITAL

Patients should be admitted if

� they have suffered a new surgically significantabnormality on imaging

� the patient has not returned to a GCS equal to 15after imaging, regardless of the imaging results

� they fulfil the criteria for CT scanning but this cannotbe done within the appropriate period, eitherbecause CT is not available or because the patient isnot sufficiently co-operative to allow scanning

� the patient has continuing worrying signs ofconcern to the clinicians, e.g. persistent vomitingand severe headache

� the patient has received sedation or generalanaesthetic during CT imaging

� the patient has other sources of concern to theclinicians, e.g. drug or alcohol intoxication, otherinjuries, shock, suspected non-accidental injury,meningism and cerebrospinal fluid leak(NICE 2003).

Urgent re-assessment by the clinician in chargeof the case

Anyof the following shouldprompt anurgent response:

� development of agitation or abnormal behaviour.

� a sustained (at least 30 minutes) drop of one pointin GCS level (greater weight should be given to adrop of one point in the motor score of the GCS).

� any drop of greater than two points in GCS levelregardless of duration or GCS sub-scale.

� development of severe or increasing headache orpersisting vomiting.

� new or evolving neurological symptoms or signssuch as pupil inequality or asymmetry of limb orfacial movement (NICE 2003).

MANAGEMENT OF MINOR HEAD INJURY

The majority of patients treated in emergency depart-ments with head injury will have a ‘minor’ headinjury. Some 92% of these patients will have normalneurology (Klauber 1993) and the majority will be dis-charged home. A thorough assessment of the patient’scondition should be performed, which should includepulse, respiration, blood pressure, pupil size andreaction, and the patient’s GCS. Although only 1%of head-injured patients have skull fractures (Ramra-kha & Moore 1997), there are certain circumstanceswhere a skull X-ray is appropriate (see Box 4.9).

The key to managing minor head injury is givingadequate information and advice to the patient andhis carer. The patient should be advised to rest quietly,avoid stressful situations, should be discouraged fromtaking part in strenuous activities and from undertak-ing long periods of VDU work or watching TV whichwill exacerbate any headache. The patient should notstay at home alone for the first 48 hours after leavinghospital. Simple analgesia should be suggested, suchas paracetamol, which should be sufficient to alleviateheadaches without masking other signs of deteriora-tion. The patient should be discouraged from takingalcohol or drugs until symptoms have subsided. Thepatient should not play any contact sport for at least 3weeks after the injury without talking to their doctoror other appropriately qualified clinician first. Writtenadvice should always be given to the patient/carer toreinforce any verbal information (Box 4.12). (See alsoChapter 33 – Health Promotion.)

When discussing the outcomes of a minor headinjury, it is important that the emergency nurse explainspost-concussion-type symptoms to the patient. Head-injured patients should be discharged into the care of aresponsible adult. Not all patients with minor headinjury are appropriate for discharge (see Box 4.13).

Head injuries 67

Particular care is needed with patients who are intoxi-cated and/or have taken drugs where neurologicalassessment is unreliable.

MANAGEMENT OF SERIOUS HEADINJURY

Despite the fact that patients who have suffered severeinjury to the brain may recover completely if they aretreated quickly and appropriately, it is also possiblethat the patient may suffer serious disability or evendeath (NICE 2003). Age is a significant factor in deter-mining outcome, especially in patients who becomedeeply unconscious. Mortality is 19% in patients aged20, but 71% in those aged 60 and over (Hickey 1997).

The aimofmanagement of thehead-injuredpatient isto prevent and treat secondary physiological insults.There is a developing base of evidence to guide theman-agement of patients with traumatic brain injury (TBI)but a study carried out by Matta & Menon (1996) sug-gests that there is considerable room for improvement,with many centres not following basic recommen-dations for monitoring and principles of treatment.A study by Patel et al. (2002) looked at the effect ofneurocritical care, delivered by specialist staff andbased onprotocoldriven therapy. They found improvedoutcomes, supporting, though not proving, the notionthat treatment directed at ICP and CPP improvesoutcome.

It is universally accepted that initial managementof severe TBI requires urgent cardiopulmonary resus-citation, emergency CT scan, transfer to a neurosurgi-cal centre and appropriate surgical intervention, andguidelines covering this initial care are generally wellestablished (McNaughton & Harwood 2002, IntensiveCare Society 1997). Monitoring of ECG, direct arterialblood pressure, central venous pressure and pulseoximetry is mandatory in all patients. Regular arterialblood gas analysis, measurement of blood glucoseand sodium and core temperature monitoring are alsorequired to optimize treatment strategies.

In an attempt to address variability in practice, theEuropean Brain Injury Consortium (EBIC) set out todefine general standards of severe TBI management(Maas et al. 1997). The resulting guidelines were pub-lished in 1997 and were based on consensus andexpert opinion (see Box 4.14). In 1996 the AmericanBrain Injury Consortium (ABIC) had produced evi-dence-based guidelines for the management of severeTBI (Brain Trauma Foundation 1996). Despite the dif-ferent approaches used in formulating the guidelines,the conclusions and recommendations of both theABIC and EBIC guidelines are similar, reflecting theconsensus that exists in many countries on the man-agement of severe TBI.

Extracranial complications of severe TBIand treatment

Extracranial complications occur frequently in severeTBI and studies suggest that some complications arehighly influential in determining patient outcome.

RespiratoryIn patients with isolated head injury, acute lung injury(ALI) is common. Studies show ALI occurrence in 20%of patients with a post-resuscitative GCS of 8 or less.ALI is an additional marker of the severity of brain

Box 4.13 Indications for hospital admission

� Decreased consciousness

� Neurological deficit

� Severe headache and persistent vomiting

� Confusion

� Intoxification rendering clinical assessmentunreliable

� Coexisting conditions such as clotting disorders

� Social circumstances making discharge unwise

Box 4.12 Typical head injury advice sheet

� General advice about observing a patient every2 hours; ensure he wakes easily and is orientatedwhen awake. Ensure the patient is able to move alllimbs

� You should return to hospital if any of the followingoccur:– persistent vomiting– confusion– excessive sleeping; difficulty in rousing patient– severe headache– double vision– limb weakness– convulsions or ‘passing out’– discharge of blood/fluid from nose/ears

� You should not drink alcohol until all symptomshave subsided

� The name and telephone of the hospital should beincluded

68 TRAUMA CARE

injury and is associated with an increased risk ofmorbidity andmortality (Bratton &Davis 1997). Neuro-genic pulmonary oedema (NPE) represents the mostsevere form of ALI and is typically reported in cases offatal or near fatal head injuries (Bratton & Davis 1997).The exact mechanism responsible for this acute condi-tion seen after severe TBI and after abrupt elevations inICP is unclear. It is generally accepted that there is a neu-rological pathway following central nervous systeminjury and that it is the result of massive sympatheticoutflow, possibly mediated by the hypothalamus.

The pathophysiological changes result in the rapiddevelopment of interstitial oedema and subsequentincreased pulmonary shunt, decreased complianceand loss of lung volume. Signs and symptoms include

dyspnoea, cyanosis, pallor, sweating, a weak rapidpulse and the production of pink frothy sputum.The development of neurogenic pulmonary oedemacan be remarkably rapid and is usually associatedwith an acute and significant rise in ICP. The classicform appears early, within minutes to a few hours,after injury while the delayed form progresses slowlyover a period of 12 to 72 hours (Durieux 1996). Pri-mary treatment consists of employing therapeuticinterventions aimed at reducing ICP and providingappropriate ventilation support and management,increasing inspired oxygen concentration, controllingcarbon dioxide levels and increasing positive trachealend pressure (PEEP) to maximize oxygenation withminimal effect on ICP and cardiac output.

Box 4.14 EBIC guidelines for management of severe head injury in adults (Maas et al. 1997)

Monitoring and general care

� Minimal monitoring requirements include ECG,Sp02 invasive arterial BP, temperature and endtidal CO2

� Maintain SpO2 > 95%, MABP > 90 mmHg

� Central venous pressure monitoring to ensurenormovolaemia

� If ICP monitored – continuous monitoring of arterialblood pressure (ABP) and calculation of cerebralperfusion pressure (CPP)

Ventilatory parameters

� Adjust ventilation to maintain PaO2 > 13 kPa(100 mmHg) and PaCO2 4.0–4.5 kPa (30–35 mmHg)

Management of ICP and CPP

� Treat ICP elevations above 20–25 mmHg.

� Maintain CPP 60–70 mmHg

� There is no consensus whether patients should benursed flat or with the head up to a maximum of 30�

elevation

Accepted methods of management of ICP and CPP

� Sedation

� Analgesia

� Mild to moderate hyperventilation (PaCO2 4.0–4.5 kPa,30–35 mmHg)

� Volume expansion and inotropes or vasopressor whenABP insufficient to maintain CPP in a normovolaemiapatient

� Osmotic therapy – preferably mannitol, repeated inbolus infusions, maintaining serum osmolarity >315

� If osmotherapy has insufficient effect, frusemide canbe given additionally

� CSF drainage

� If these methods fail, more intensive hyperventilation(PaCO2 < 4.0 kPa or 30 mmHg), preferably withmonitoring by jugular oxymetry of cerebraloxygenation to detect ischaemia

� Alternatively, the use of barbiturates, inducingincreased sedation, may be considered

� There is no established indication for steroids in themanagement of acute head injury

Timing and indications for operative therapy

� A surgically significant EDH or ASDH should beevacuated immediately upon detection.

� For small haemorrhagic contusions or other smallintracerebral lesion, a conservative approach isgenerally adopted, but operation should be consideredurgent for large intracerebral lesions with high ormixed density on CT scan

� Depressed skull fracture: operation is definitelyindicated only if it is a compound (open) fracture (notover sagittal sinus) or if the fracture is so extensivethat is causes mass effect

� Closed depressed skull fractures are usually treatedconservatively, but operation may be appropriate inselected cases to reduce mass effect or correctdisfigurement

� Decompressive craniotomy may be considered inexceptional situations.

Head injuries 69

The development of non-cardiogenic pulmonaryoedema complicates the management of severe TBIbecause many of the therapies used to protect thelungs causes a rise in ICP or decreased CPP. The ven-tilatory strategies used to protect the lungs, e.g.reduced tidal volume, permissive hypoxia and hyper-carbia, increased levels of PEEP, and prone lying,pose management problems during the managementof the acute head injury when intracranial hyperten-sion may be high and delay the early rehabilitationtherapy which is essential to maximize recovery(Robertson et al. 1999).

Some studies have shown a link between CPP man-agement and acute respiratory distress syndrome(ARDS) (Contant et al. 2001, Robertson 2001). Inducedhypertension to raise CPP can cause increased pulmo-nary hydrostatic pressures and thereby increase theamount of water accumulating within the lungs. Theresults of a randomized trial comparing two headinjury management strategies, one ICP targeted andthe other CPP targeted, showed a fivefold increase inthe incidence of ARDS in the CPP targeted groupwhere CPP was maintained > 70 mmHg (Robertson2001). Approximately 60% of patients with severe TBIbecome hypoxaemic without ventilatory support oradded oxygen and require advanced ventilatorysupport within a short period of time.

Management should follow the sequence laiddown by ATLS (American College of Surgeons2004). Airway management is paramount in prevent-ing hypoxia and therefore secondary brain injury.Oedema and/or debris following injury, loss of thegag reflex and/or vomiting may threaten airwaypatency. If a clear airway cannot be maintained withsimple aids, such as a guedal or oro-pharyngeal air-way then intubation should be performed. Cervicalspine immobilization should be maintained until afull risk assessment (and imaging if deemed neces-sary) has been undertaken and the possibility of aneck injury has been excluded. Suctioning should bekept to a minimum as it raises ICP.

The neurophysiology of breathing is complex andinvolves several areas of the brain. Following headinjury the normal pattern of breathing is easily dis-rupted, leading to hypoxia. It is important to maintainadequate oxygenation, as a rise in PCO2 levels initi-ates autoregulation, causing cerebral vasodilatationand a rise in ICP. If unchecked, this can lead to sec-ondary brain injury. As good oxygenation is impera-tive, head-injured patients should be given oxygenvia a facemask and reservoir bag: if bradypnoeic, thisshould be assisted by mechanical ventilation as soonas possible following the severe TBI. Induced

hyperventilation should be used to reduce PCO2

levels, but this should be discussed with a neurosur-geon first (Bullock & Teasdale 1996).

If urgent intubation is indicated, it should beassumed that the patient has a full stomach, and cri-coid pressure should be applied to prevent vomitingor gastric regurgitation. In adults, this should bemaintained until the cuff of the ET tube is inflated,creating a secure airway. Short-acting sedatives andmuscle relaxants should always be used for intuba-tion, to minimize the impact on the brain. Hypoxiais a major cause of cerebral ischaemia and care shouldalways be taken to maintain adequate oxygenationlevels by monitoring respiratory effort closely witharterial blood gases (ABGs) and O2 saturation mea-surement and intervening with supportive therapyat an early stage.

Intubation and ventilation should be implementedimmediately in the following circumstances:

� GCS less than or equal to 8

� loss of protective laryngeal reflexes

� ventilatory insufficiency as judged by arterial bloodgases:– hypoxaemia (PaO2 less than 9 kPa on air or lessthan 13 kPa on oxygen) or

– hypercarbia (PaCO2 greater than 6 kPa)

� spontaneous hyperventilation (causing PaCO2 lessthan 3.5 kPa)

� respiratory arrhythmia (NICE 2003).

Intubation and ventilation should be implementedbefore the start of a transfer in the following circum-stances in addition to the above:

� significantly deteriorating conscious level

� bilateral fractured mandible

� copious bleeding into the mouth, e.g. base of skullfracture

� seizures (NICE 2003).

Cardiovascular complicationsHigh levels of sympathetic activity and of circulatingcatecholamines after severe TBI can have an adverseeffect on cardiac function, basal metabolic rate andvascular and neuronal function in the central nervoussystem (Clifton et al. 1983). The magnitude of thishyperdynamic cardiovascular state occurring aftersevere head injury does not necessarily correlate withICP, GCS or CT findings (Clifton et al. 1981). There isboth clinical and experimental evidence that cerebralneurogenic factors cause arrhythmias in normal hearts,with fatal arrhythmias being reported in otherwisehealthy brain-injured patients (McLeod 1982,

70 TRAUMA CARE

Oppenheimer et al. 1990). A wide variety of atrial andventricular arrhythmias, abnormalities of the QRScomplex, T-wave and ST segment andQTprolongationhave been documented and occur most commonly inpatients with diffuse injury, oedema and contusions.In two seminal studies, 31% of patients admitted withhead injury exhibited some form of cardiac arrhythmia(Hersch 1961) and cardiac arrhythmias were observedin 41 of 100 patients admitted with acute subduralhaematoma, with more than half of these showingventricular arrhythmias ranging in severity frompremature ventricular contractions to ventriculartachycardia and ventricular fibrillation (Van der Ark1975). Elevations of pulse greater than 120 beatsper minute have been found in one third of patientswith severe TBI.

It is generally accepted that hypotension related totrauma is not caused by head injury, although it canbe related to head injury per se in children. However,there is some evidence that episodes of hypotensionfollowing severe TBI may be of neurogenic origin ina small proportion of patients, and that this is notsimply attributable to devastating, unsurvivable braininjury (Chesnut 1998).

Hypotension is usually a result of systemic hypo-volaemia following multiple traumas. Causes ofhypotension should be identified and fluid resuscita-tion is imperative to prevent a drop in cerebral ischae-mia and secondary brain injury. In the late stages ofhead injury, hypertension occurs with bradycardiaand bradypnoea. Hypertension is a late sign of pend-ing brain injury. Arterial blood pressure increases inan attempt to maintain the cerebral perfusion pres-sure in the brain. The decreases in respiration andheart rate are due to pressure on the medulla. Thesesigns often precede death. This is referred to asCushing’s triad.

CoagulopathySevere TBI can be complicated by the development of acoagulopathy that can worsen blood loss and delayinvasive neurosurgical treatment. Studies havereported a positive correlation between the presenceand severity of disseminated intravascular coagulation(DIC) and the degree of brain injury, assessed byplasma fibrinogen degradation product levels.Although most of the acute coagulopathies associatedwith brain injury are not preventable, prompt treat-ment can be effective in reducing morbidity. Clottingstudies at the time of admission to ED can be valuablein predicting the occurrence of delayed injury andearly follow-upCT scanning is advocated in the patientwith coagulopathy (Piek et al. 1992, May et al. 1997).

MANAGEMENT OF INTRACRANIALCOMPLICATIONS

Raised intracranial pressure

Uncontrolled elevation in ICP is the most commoncause of mortality, morbidity and secondary braininjury after severe TBI. More than one third of patients’ICP exceeds 20 mmHg at some stage (Chan et al. 1995).This is because it alters tissue perfusion, causing cere-bral ischaemia. It is therefore important to ensure thatsigns of raised ICP are noted and treated early. Disor-ientation, irritation, headache, seizures, nausea andvomiting are all possible indicators of raised ICP, andlater signs include deterioration in the GCS, limband pupil changes and finally alteration in the vitalsigns (Cushing’s triad).

Hypercapnia can cause secondary brain injury,which results from either inadequate ventilation or aresponse to hypermetabolism following trauma. HighPCO2 levels result in cerebral vasodilation in anattempt to increase oxygenation. This increases cere-bral blood flow and, therefore, intracranial pressure.Hyperventilation is controversial (Harrahill 1997), butis the most common treatment for inducing vasocon-striction, and reduces PCO2 and thus intracranial pres-sure. Arterial blood gas analysis should be frequentlyrecorded in-patients being artificially hyperventilated/ventilated.

While it has never been shown definitively thatlowering ICP in patients with raised ICP improvesoutcome, an ICP > 20 mmHg has been shown to bethe fourth most powerful predictor of outcome afterage, admission GCS and pupillary signs (Marmarouet al. 1991) and there is evidence to suggest that treat-ment should be initiated if the ICP is 20–25 mmHg(Lang & Chesnut 1995). Both ICP and CPP correlatestrongly with outcome after TBI with the worse out-comes occurring in patients with an ICP > 20 mmHgand/or a CPP < 60 mmHg (Chesnut 1995). One study,which examined early versus late treatment of raisedICP, reported that early aggressive managementbased on ICP monitoring significantly reduced theoverall mortality rate from 84% to 69% without caus-ing a disproportionate number of severely disabledor vegetative patients (Rosner et al. 1995).

Focal increases of ICP lead to distortion of brainparenchyma and secondary ischaemic damage, whilediffusely raised ICP leads to tentorial hemiation andbrain stem death. Early intracranial hypertension isconfirmed as a sign of poor prognosis. The ABICand EBIC guidelines recommend that ICP be main-tained ICP < 20–25 mmHg during the acute course ofhead injury. They also advise that treatment for raised

Head injuries 71

ICP should only be continued if it is effective indecreasing ICP and/or increasing CPP (Maas et al.1997, Brain Trauma Foundation 1996).

Maintenance of cerebral perfusion pressure

One of the most controversial areas in the manage-ment of severe TBI is the level of CPP required to ade-quately perfuse the brain, and to date no study hasshown that any one approach with a particular CPPthreshold improves clinical outcome more than anyother. Substantial clinical and experimental evidenceshows that hypotension following TBI has an adverseeffect on outcome, and particularly so if it occurs inthe first few hours after injury. Hypotension (definedas a systolic BP < 90 mmHg) has been uniformly iden-tified as the most predominant factor in secondarybrain injury and has the highest correlation with mor-bidity and mortality (Chesnut et al. 1993).

There is general agreement on the need to maintainCPP between 60 and 70 mmHg, either by reducingICP or by elevating MAP. Aggressive fluid replace-ment and cardiovascular support with vasopressorsand inotropes to increase MAP and maintain CPP>70 mmHg has been associated with a reduction inthe incidence of secondary ischaemic events by approx-imately 50% (Rosner et al. 1995). However, this treat-ment has been shown to lead to a fivefold increase inthe incidence of acute ARDS. Robertson (2001) advo-cates a target CPP of 60 mmHg, with higher CPP levelsbeing reserved for patients who demonstrate a specificindication for induced raised ICP such as regional orglobal ischaemic.

TheABIC and EBIC guidelines recommend that epi-sodes of hypotension be avoided whenever possible,or if they do occur, corrected immediately to maintaina mean arterial blood pressure (MABP) >90 mmHg ora systolic BP >120 mmHg (Maas et al. 1997, BrainTrauma Foundation 1996).

Blood haemoglobin concentration

CBF can be influenced by blood viscosity, ofwhich hae-matocrit is the single most important determinant.Blood viscosity increases logarithmically with increas-ing haematocrit and the optimal level is probably about35%. Cerebral blood flow is reduced by haematocritlevels over 50% and increased with haematocrit levelsbelow 30%. This compensatory mechanism allowssufficient oxygen delivery in healthy individuals evenwith haematocrit levels of 20%.

Studies suggest that a haematocrit of 30–34% mayresult in optimal oxygen delivery to brain tissue.However, if maximum vasodilatation already exists,haemodilution may decrease oxygen delivery and

lead to increases in cerebral blood volume (CBV)and therefore ICP (Cesarini 1996).

Control of ICP

Mannitol is an effective agent to reduce cerebraloedema and ICP (Bullock 1995). In addition to itsosmotic effects, mannitol may also reduce ICP byimproving cerebral microcirculatory flow and oxygendelivery. However, repetitive administration canpotentially increase ICP since mannitol accumulateswithin brain tissue, reversing osmotic shift andincreasing cerebral oedema. The peak effect of manni-tol on ICP occurs within 15 minutes of administration,but its effects on serum osmolarity last 2 to 6 hours,depending on the dose and clinical condition of thepatient. Adverse effects of mannitol include:

� opening of blood-brain barrier – this effect maybecome harmful after multiple doses and actuallyexacerbate ICP by increasing brain swelling

� accumulation of mannitol in the brain is mostmarked when mannitol is in the circulation for longperiods as occurs with continuous infusionadministration, therefore mannitol should beadministered in repeat boluses

� mannitol is excreted entirely by the urine,therefore there is increased risk of acute renalfailure (acute tubular necrosis) if administeredin large doses, particularly if serum osmolarity is> 320 mosmol/l)

� increased serum sodium levels

� mannitol raises urine osmolarity and specificgravity, therefore these variables cannot be used todiagnose diabetes insipidus.

The ICP-lowering effect of bolus administration ofmannitol appears to be equal over the range 0.25 to1.0 g/kg, although the duration of activity may besomewhat shorter with the lower dose. Under mostcircumstances, the lower dose should be used in orderto minimize the risk of hyperosmolality and avoid anegative fluid balance. The ABIC and EBIC guidelinesrecommend mannitol 20% be given as an intravenousinfusion over 15 to 20 minutes, and repeated as neces-sary. Blood osmotic pressure must be monitored andserum osmolarity kept below 315 mosmol/l. Theyalso recommend that if mannitol has insufficienteffect then frusemide can be given additionally (Maaset al. 1997, Brain Trauma Foundation 1996).

Drugs

It is common practice for severe TBI patients to beempirically managed with a protocol that includes theroutine use of sedatives, analgesics and neuromuscular

72 TRAUMA CARE

blocking agents to facilitate mechanical ventilation andto treat intracranial hypertension.

Intravenous anaesthetic agents cause a dose-depen-dent reduction in cerebral metabolism, CBF and ICPwhile maintaining pressure autoregulation and CO2

reactivity. The use of barbiturates in TBI is controver-sial and has largely been replaced by propofol, whichhas similar cerebrovascular effects but a more favour-able pharmacological profile. Propofol has become thesedative of choice but care must be taken to avoidhypotension (Kelly 2000, Kelly et al. 1999).

Fentanyl andmorphine are frequently administeredto limit pain, facilitate mechanical ventilation andpotentiate the effect of sedation. Neuromuscular block-ing drugs have no direct effect on ICP but may preventrises produced by coughing and straining on the endo-tracheal tube. However, such agents are not associatedwith improved outcome and their use is the subject ofmuch debate (Prielipp & Coursin 1995).

The ABIC and EBIC guidelines suggest that seda-tion and neuromuscular blocking drugs can be usefulin optimizing transport of the head-injured patient. Inthe absence of outcome-based studies the choice ofsedative is left to the physician, and neuromuscularblocking agents should only be employed when seda-tion alone proves inadequate (Maas et al. 1997, BrainTrauma Foundation 1996).

Hyperventilation

The aim is to reduce PCO2, cerebral blood volume andthus ICP; it also causes a significant reduction in CBF.Hyperventilation only has a short-lived effect on ICP.The ABIC and EBIC guidelines advocate that, in theabsence of increased ICP, prolonged prophylactichyperventilation should be avoided. Prophylactichyperventilation should be reserved for only brief per-iods in the event of acute neurological deterioration, orfor longer periods when intracranial hypertension isunresponsive to sedation, paralysis, CSF drainage andosmotic diuretics (Maas et al. 1997, Brain Trauma Foun-dation 1996).

Temperature control

Following TBI, temperature regulation may be dis-rupted as a result of damage to the hypothalamus.Injury to the CNS is temperature dependent. Fevercan make an existing neurological dysfunction moreapparent and may worsen an ongoing insult. Thebrain’s metabolic rate for oxygen increases by 6–9%for every degree Celsius rise in temperature. In theacute phase of head injury, therefore, hyperthermiashould be treated since it will exacerbate cerebralischaemic and adversely affect outcome.

Hypothermia as a treatment in severe TBI has beena major area of research during the last decade. Theinterim results of a large multicentre study showedthat cooling to 32–33�C within 10 hours of injuryimproved neurological recovery in patients present-ing with head injury and a GCS of 5–7 but not thosewith a lower GCS. However, this study was termi-nated early with no clear benefit established (Marionet al. 1997).

Some studies suggest that while hypothermia maynot attenuate damage from the primary injury, it pro-vides protection against secondary injury, specificallyhypotension and hypoxia, and that there may bea therapeutic window for neuroprotection in the earlystages following injury (Yamamoto et al. 1999).Whether this protection can be sustained over longerperiods remains to be determined.

A randomized trial evaluating the use of mild hypo-thermia during intracranial aneurysm surgery foundthat, compared with normothermic patients, morepatients in the hypothermic group had good outcomesand fewer of these patients had neurological deficits atthe time of discharge (Hindman 1999). In a furtherstudy on CBF and oxygen metabolism during mildhypothermia (33–34�C) in elective aneurysmal surgery,positron emission tomography (PET) showed luxuryperfusion in almost all cases, providing the first PETevidence of decreased CBF and metabolic rate of O2

during hypothermia in humans (Kawamura 2000).There is some evidence of increased mortality in the

general trauma population for patients admitted withhypothermia and at least one early study demonstratedan increased incidence of infection in head injuredpatients subjected to hypothermia (Sutcliffe 2001). Boththe ABIC and EBIC guidelines, while recognizing theneed to treat pyrexia after severe TBI, consider thera-peutic hypothermia as experimental at present (Maaset al. 1997, Brain Trauma Foundation 1996).

Seizure activity

This reflects disordered electrical discharges in thedamaged brain and results in local loss of autoregula-tion, increased metabolic activity in the brain with con-comitant increases in cerebral blood flow and tissuelactacidosis, which may aggravate ICP. Seizures arecommon after TBI in 5–15% of patients, especially inthose who have suffered a haematoma, penetratinginjury, including depressed skull fracture with duralpenetration, and focal neurological signs or intracranialsepsis (Watkins 2000, Dunn 1996).

If seizure activity is continuous, i.e. status epilepti-cus or serial fitting, severe cerebral oedema may occur.Patients having seizures should be protected from

Head injuries 73

harm, but if they are not in any danger then they shouldnot be handled. The seizure should be observed fororigin, sequence of events and time of start/finish.This information should be clearly recorded in thepatient’s notes. In the conscious patient a single seizurerequires only supportive treatment, but in the coma-tose patient every seizure can threaten life or neurolog-ical function and should be treated appropriately.Anticonvulsants should be used if two ormore seizuresoccur (Watkins 2000). Both the post-ictal state andmedication may alter the neurological observations,so extra vigilance is required. Regular GCS observa-tions should be completed until the pre-seizure stateis regained.

No generally accepted classification of seizuresexists, but it is useful to distinguish between non-focalseizures, where loss of consciousness is the primaryevent, followed by convulsions affecting all four limbs,and focal or partial seizures, where activity is confinedto one area of the cerebral cortex. The continuous neu-ronal firing, which occurs during non-focal seizureactivity, causes a massive increase in the brain’srequirement for oxygen. As these demands can rarelybe met by a corresponding increase in the supply ofoxygen, ischaemia and neuronal death may occur.

Neuroprotective drugs

Corticosteroids have been used in the treatment ofcertain neurological conditions since the 1950s. Thereis no doubt about their value in producing rapidimprovement in patients with brain tumours asso-ciated with oedema and there is evidence of benefitin the early administration of high-dose methylpred-nisolone in spinal cord injury.

CRASH Trial collaborators (2004, 2005) state, aftera major study involving over 10 000 adults, thatpatients with head injuries should not be given corti-costeroids, as they increase the risk of death or severedisability. The ABIC and EBIC guidelines also do notrecommend steroids in the treatment of severe TBI.

Fluid management

Fluid management is crucial to ensuring adequatemaintenance of ICP. As previously stated, patientsshould have adequate fluid resuscitation to ensurethey are normotensive. Several factors need to be con-sidered in the fluid management of patients followingsevere TBI:

� clinical and laboratory assessment of volumestatus

� the effects of different fluids on CPP and cerebraloedema

� osmotic therapy

� water and electrolyte disturbances.

Following TBI the blood-brain barrier (BBB) islikely to be disrupted, and different solutions canhave an effect on cerebral oedema. If the serum osmo-larity falls, water moves across the BBB along thealtered osmotic gradient, causing cerebral oedema,increased ICP and decreased CPP. The use of hypo-tonic fluids should, therefore, be avoided.

Since 0.9% saline is isotonic, with an osmolarity of308 mosm/l, it has a negligible effect on brain waterand has become the crystalloid of choice in the man-agement of TBI. Resuscitation with 0.9% salinerequires 4 times the volume of blood lost to restorehaemodynamic parameters; therefore, blood loss fromother injuries should be replaced with blood products(Spiekermann & Thompson 1996).

The use of hypertonic saline solutions (7.5%) hasrecently been studied in the context of fluid resuscita-tion in TBI. Theoretically, hypertonic saline, like man-nitol, through its osmotic effect on the brain shoulddecrease brain oedema and potentially decrease ICPwhen used for volume resuscitation. This assumptionis supported by several laboratory studies and oneclinical study that reported improved survival whenhypertonic saline was compared to isotonic crystal-loid for initial fluid replacement in patients withsevere TBI. A decrease in CSF production with theuse of hypertonic saline has also been reported.Hypertonic saline solutions may improve outcomein patients with multiple trauma because of a favour-able effect on ICP; however, further studies areneeded before they can be used routinely in clinicalpractice (Spiekermann & Thompson 1996)

Based on data from various studies, it is widelyaccepted that glucose-containing solutions shouldnot be used in the fluid management of patients fol-lowing severe TBI unless specifically indicated tocorrect hypoglycaemia. The mechanism by which glu-cose worsens neurological injury is not fully under-stood; however, it is believed that, in the presence ofischaemia, glucose is metabolized anaerobically lead-ing to an accumulation of lactic acid. Increased lacticacid is thought to decrease intracellular pH, compro-mise cellular function and ultimately cause cell death.An alternative explanation proposes that hypergly-caemia worsens ischaemia by decreasing CBF. Otherstudies suggest that hyperglycaemia decreases cere-bral adenosine levels, and adenosine is an inhibitorof the release of excitatory amino acids that arethought to play a major role in ischaemic cell death(Spiekermann & Thompson 1996). Accurate fluidinput and output observations are essential. For this

74 TRAUMA CARE

reason, because of diuretic therapy (mannitol) and toreduce discomfort, patients should have a urinarycatheter.

Positioning

Many studies have been undertaken to determine theinfluence of body position on ICP and CPP and estab-lish the best practices for positioning of severe TBIpatients (Sullivan 2000). It has been demonstrated thathead elevation decreases ICP and that head rotationand neck flexion are associated with increased ICP,decreased jugular venous return and localized changesin cerebral blood flow. In the light of these findings, it iscommon practice to position head-injured patients inbed with the head elevated above the heart to varyingdegrees (0–30�) provided they have an adequate bloodpressure and there are no contraindications, in neutralalignment with the trunk, in order to reduce ICP.

Referral to a neurosurgeon

Patients should be referred where

� a new surgically significant abnormality onimaging is seen

� a persisting coma (GCS less than or equal to 8) afterinitial resuscitation

� unexplained confusion, which persists for morethan 4 hours

� deterioration in GCS score after admission. Greaterattention should be paid to motor responsedeterioration

� progressive focal neurological signs

� a seizure without full recovery

� definite or suspected penetrating injury

� a cerebrospinal fluid leak (NICE 2003).

Transfer to a specialist neurosurgical unit

The most common reason for interhospital transferin the head-injuredpatient is the need for surgical inter-vention, such as evacuation of haematoma or treatmentof a depressed skull fracture. Once the decision totransfer has been made, it is imperative that the patientis thoroughly resuscitated and stabilized prior totransfer to avoid complications during the journey.

The neck should be fully examined to identify orexclude cervical injury (see also Chapter 6). Chestor abdominal injuries (Chapters 7 and 8) should betreated if potentially life-threatening and fracturessplinted where appropriate (see Chapter 5). Airwaymanagement is a major cause for concern during

transfer. Unconscious patients, those who are vomitingor those whose condition appears to be deteriorating(GCS less than 8) should be intubated and ventilatedprior to transfer (NICE 2003).

Any patient being transferred should be accompa-nied by a clinician with at least 2 years experience inan appropriate specialism, e.g. anaesthesia, or a pae-diatrician and one who has received supervised train-ing in the transfer of patients with a severe headinjury, along with a competent nurse escort (NICE2003). During transfer, the patient should be carefullyobserved and ECG, oxygen saturation levels andblood pressure should be monitored continuously(Parkins 1998). All patients with a GCS less than orequal to 8 requiring transfer should be intubatedand ventilated. If the patient is not sedated, pupil sizeand reaction and GCS should be recorded. All docu-mentation and results of clinical investigations, suchas CT, should accompany the patient (Jones 1993).

Surgical treatment

Delay in surgical treatment of TBI has been shown tobe a major preventable cause of morbidity and mor-tality. In a typical series of patients who had surgeryfor acute sub-dural haematoma (ASDH), more than70% had a functional recovery, that is, good recoveryor moderate disability, if the delay from injury tooperation was less than 2 hours. Where the delaywas 2–4 hours, just over 60% made a functional recov-ery. Where the delay was more than 4 hours after theinjury, fewer than 10% made a functional recovery(Watkins 2000). The Royal College of Surgeons ofEngland recommends that, in all circumstances, life-saving decompressive surgery must be available, toall patients who require it, within 4 hours of the injury(Royal College of Surgeons 1999, Flannery & Buxton2001).

Some lesions may be inaccessible to the neurosur-geon or be in such sensitive areas of the brain that therisks of surgery are too great. Alternatively, brain injurymay be diffuse and surgical intervention inappropriate.Whether all haematomasmust be removed remains con-troversial and this is particularly so in the managementof intracerebral haematomas and haemorrhagic contu-sions. While some surgeons advocate early surgery insuch cases, experience has shown that despite surgicaltreatment, post-operative intracranial hypertensioncontinues to occur in virtually all patients. The ABICand EBIC guidelines outline specific indications forsurgery based on biological and pathophysiologicalprinciples, published evidence and practical experience(Maas et al. 1997, Brain Trauma Foundation 1996).

Head injuries 75

Indications for decompressive surgery:� intracranial mass lesions with > 5 mmmidline shift

or basal cistern compression on CT scan

� a surgically significant (1 cm thick) EDH or ASDHneeds evacuation within 2–4 hours of injury toachieve optimal chance of recovery

� for small haemorrhagic contusions or other smallintracerebral lesions a conservative approach isgenerally adopted but operation should beconsidered urgent for a large ICH (> 20–30 ml)based on position, clinical condition and ICP

� skull fracture depressed greater than the thicknessof the skull or compound fractures with a torn durarequire surgery (Maas et al. 1997, Brain TraumaFoundation 1996).

Decompressive craniectomy/craniotomy

The practice of wide bone removal for the treatment ofintracranial hypertension due to cerebral oedema,refractory to medical management, has a long historyand remains controversial. Polin et al. (1997) concludedthat provided surgery was performed before ICPexceeded 40 mmHg for a sustained period and within48 hours of injury, decompressive craniectomy showeda statistical advantage over medical treatment.

Surgical excision of a contused lobe to give theswelling brain more space is also a controversial issue.It has been shown to produce a worthwhile outcome insome cases and seems to be indicated especially inyoung patients with deteriorating coma scores and CTevidence of widespread bilateral swelling. Contraindi-cations are primary brainstem injury or establishedsigns of herniation, that is, bilateral dilated and unreac-tive pupils. Decompressive craniectomy, which canalso increase oedema formation, is usually reserved asa last resort (Maas et al. 1997).

BRAIN STEM DEATH TESTING

The diagnosis of brainstem death is usually made inthe intensive care unit.

Preconditions� Diagnosis compatible with brainstem death

� Presence of irreversible structural brain damage

� Presence of apnoeic coma preconditions

Exclusions� Therapeutic drug effects (sedatives, hypnotics,

muscle relaxants)

� hypothermia (temp >35�C)

� metabolic abnormalities

� endocrine abnormalities

� intoxication

Clinical tests1. Confirmation of absent brain stem reflexes

� no pupillary response to light

� absent corneal reflex

� no motor response within cranial nervedistribution

� absent gag reflex

� absent cough reflex

� absent vestibulo-ocular reflex

2. Confirmation of persistent apnoea

� pre-oxygenation with 100% oxygen for10 minutes

� allow PaCO2 to rise above 5.0 kPa before test

� disconnect from ventilator

� maintain adequate oxygenation during test

� allow PaCO2 to climb above 6.65 kPa

� confirm no spontaneous respiration

� reconnect ventilator

3. Two experienced practitioners should performclinical tests

� at least one should be a consultant: both must becompetent to perform the tests, i.e. intensivists/neurologists/neurosurgeons

� neither should be part of the transplant team

� the tests should be performed on two separateoccasions

� there is no necessary prescribed time intervalbetween the tests.

These conditions limit the probability of the fulltesting occurring in the emergency department; how-ever, some or all of the tests may be performed, eitherto complete a clinical picture or to reach an endpointin an inevitable situation. This is a very difficult situ-ation to manage, even in the intensive care unit, whenthe nurse may be familiar with the patient’s familyand friends.

CONCLUSION

Head trauma can have a devastating effect on a per-son’s life and some mortality and morbidity are inev-itable. The emergency nurse is fundamental tokeeping morbidity to a minimum by being vigilantand preventing secondary brain injury

76 TRAUMA CARE

References

American College of Surgeons (2004) Advanced Trauma

Life Support, 7th edn. Chicago: American College ofSurgeons.

Bavetta S, Benjamin JC (2002) Assessment and managementof the head-injured patient. Hospital Medicine, 63,289–293.

Brain Trauma Foundation (1996) American Association ofNeurological Surgeons’ Joint section on neurotrauma andcritical care guidelines for the management of severehead injury. Journal of Neurotrauma 13, 641–734

Bratton Sl, Davis RL (1997) Acute lung injury in isolatedtraumatic brain injury. Neurosurgery 40(4), 707–712

Bullock R (1995) Mannitol and other diuretics in severeneurotrauma. New Horizons 3(3), 443–452.

Bullock R, Teasdale G (1996) Head injuries. In: Skinner D,Driscoll R, Earlam R (eds), ABC of Trauma. London: BMJPublishing Group.

Cesarini KG (1996) Pathophysiology of cerebral ischaemia.In: Palmer JD (ed.), Manual of Neurosurgery. London:Churchill Livingstone

Chan K, Dearden NM, Miller JD, Andrews PJD, Midgley S(1995) Multimodality monitoring as a guide to treatmentof intracranial hypertension after severe brain injury.Neurosurgery 32(4), 547–553.

Chesnut RM, Marshall LF, Klauber MR (1993) The role ofsecondary brain injury in determining outcome fromsevere head injury. Journal of Trauma 34, 216–222.

Chesnut RM (1995) Secondary brain insults after injury:clinical perspectives. New Horizons 3, 366–375.

Chesnut RM, Gautille T, Blunt BA, Kaluber MR, Marshall LF(1998) Neurogenic hypotension in patients with severehead injuries. Journal of Trauma 44(6), 958–963.

Clifton GL, Ziegler MG, Grossman A (1981) Circulatingcatecholamines and sympathetic activity after headinjury. Neurosurgery 8, 10–14.

Clifton GL, Robertson CS, Kyper K et al. (1983)Cardiovascular response to severe head injury. Journalof Neurosurgery 3, 447–454.

Contant CF, Valadka AB, Shankar MD et al. (2001) Adultrespiratory distress syndrome: a complication of inducedhypertension after severe head injury. Journal ofNeurosurgery, 95, 560–568.

CRASH Trial collaborators (2005) Final results of MRCCRASH, a randomized placebo-controlled trialof intravenous corticosteroid in adults with headinjury – outcomes at 6 months. The Lancet 365 (9475),1957–1959.

CRASH Trial collaborators (2004) Effects of intravenouscorticosteroids on death within 14 days in 10 008 adultswith clinically significant head injury (MRC CRASHTrial): randomized placebo-controlled trial. Lancet 364(9442), 1321–1328.

Crossman AR, Neary D (2000) Neuroanatomy – An Illustrated

Colour Text, 2nd edn. Edinburgh: Churchill Livingstone.Darby J, Yonas H., Marion DW et al. (1998) Local ‘inverse

steal’ induced by hyperventilation in head injury.Neurosurgery, 23, 84.

Dearden NM (1998) Mechanism and prevention ofsecondary brain damage during intensive care. ClinicalNeuropathology 17(47), 221–228.

Duffy C (2001) Anaesthesia for head injury. In: Gupta AKand Summors A (eds), Notes in Neuroanaesthesia and

Critical Care. London: Greenwich Medical Media.Dunn LT (1996) Post-traumatic epilepsy. In: Palmer JD (ed),

Manual of Neurosurgery. London: Churchill Livingstone.Durieux ME (1996) Anaesthesia for head trauma. In: The

Neuroanaesthesia Handbook (eds. Stone DJ et al.). St. Louis:Mosby

Farnsworth ST, Sperry RJ (1996) Neurophysiology. In: StoneJD, Sperry RJ et al. (eds), The Neuroanaesthesia Handbook, StLouis: Mosby.

Fernandes C, Landolt H (1996) Blood brain barrier andcerebral oedema. In: Palmer JD (ed.), Manual of

Neurosurgery. London: Churchill Livingstone.Flannery T, Buxton N (2001) Modern management of head

injuries. Journal of the Royal College of Surgeons (Edinburgh)46, 150–153.

Graham DI, Hume Adams J, Nicoll JAR, Maxwell WL,Gennarelli TA (1995) The nature, distribution andcauses of traumatic brain injury. Brain Pathology 5,397–406.

Harrahill M (1997) Management of severe head injury: newdocument provides guidelines. Journal of Emergency

Nursing 23(3), 282–283.Hersch C (1961) Electrocardiographic changes in head

injuries. Circulation 23, 853–860.Hickey JV (1997) The Clinical Practice of Neurological and

Neurosurgical Nursing, 4th edn. Philadelphia: JBLippincott.

Hindman BJ, Todd MM, Gelb AW et al. (1999) Mildhypothermia as a protective therapy during intracranialaneurysm surgery: a randomized prospective pilot trial.Neurosurgery 44, 23–33.

Hudak CM, Gallo BM (1994) Critical Care Nursing, 6th edn.Philadelphia: JB Lippincott.

Intensive Care Society (1997) Guidelines for the transport ofthe critically ill adult. London: Intensive Care Society.

Jackson S (1995) Not so minor head injuries? Emergency

Nurse 3(1), 19–22.Jones H (1993) Safe transfer. Nursing Times 89(41), 31–33.Kawamura S, Suzuki A, Hadeishi H et al. (2000) Cerebral

blood flow and oxygen metabolism during mildhypothermia in patients with subarachnoid haemorrhage.Acta Neurochir (Wein) 142(10), 1117–1121.

Kelly DF, Goodale DB, Williams J, Herr DL et al. (1999)Propofol in the treatment of moderate and severe headinjury: a randomized prospective double-blind trial.Journal of Neurosurgery 90(6), 1042–1052.

Kelly DF (2000) Sedation after severe head injury: beneficialto final outcome? European Journal of Anaesthesiology 17

Suppl. 18, 43–54.Klauber K (1993) Rehabilitation of the trauma patient. In:

Neff JA, Kidd PS, eds. Trauma Nursing: the Art and Science.St Louis: Mosby Year Book.

Head injuries 77

Kwiatkowski S (1996) Traumatic acute intracranialhaematoma. In: Palmer JD, ed. Manual of Neurosurgery.London: Churchill Livingstone.

Lang EW, Chesnut RM (1995) Intracranial pressure andcerebral perfusion pressure in severe head injury. New

Horizons 3, 400–409Lindsey KW, Bone I, Callander R (2004) Neurology and

Neurosurgery Illustrated, 4th edn. Edinburgh: ChurchillLivingstone.

Maartens N, Lethbridge G (2005) Head and neck trauma. In:RA O’Shea, ed. Principles and Practice of Trauma Nursing.

Edinburgh: Elsevier Churchill Livingstone.Maas AIR, Dearden M, Teasdale GM, Braakman R,

Cohadon F, Lannotti F et al. (1997) European BrainInjury Consortium Guidelines for management ofsevere head injury in adults. Acta Neurochir (Wien),139, 286–294.

Marion DW, Penrod, LE, Kelsey SF et al. (1997) Treatment oftraumatic brain injury with moderate hypothermia. New

England Journal of Medicine 336(8), 560–566.Marmarou A, Anderson RL, Ward JD et al. (1991) Impact of

ICP instability and hypotension on outcome in patientswith severe head trauma. Journal of Neurosurgery 75,559–566.

Matta BF, Menon DK (1996) Severe head injury in the UnitedKingdom and Ireland: a survey of practice andimplications for management. Critical Care Medicine 24,1743–1748

May AK, Young JS, Butler K et al. (1997) Coagulopathy insevere closed head injury: is empiric therapy warranted?American Journal of Surgery 63(3), 233–236.

McLeod AA, Neil-Dwyer G, Meyer CHA et al. (1982)Cardiac sequelae of acute head injury. British HeartJournal 47, 221–226

McNaughton H, Harwood M (2002) Traumatic brain injury:assessment and management. Hospital Medicine 63, 8–12.

National Institute for Clinical Excellence [NICE] (2003)Head Injury Triage, Assessment, Investigation and Early

Management of Head Injury in Infants, Children and Adults.London: NICE.

Oppenheimer SM, Cochetto DF, Hachinski VC (1990)Cerebrogenic cardiac arrhythmias. Acta Neurology 47, 513-519

Parkins DR (1998) Transportation of the injured: headinjuries. Pre-hospital Immediate Care 2, 25–26.

Patel HC, Menon DK, Tebbs S et al. (2002) Specialistneurocritical care and outcome from head injury. IntensiveCare Medicine 28, 547–553

Piek J, Chesnut RM, Marshall LF et al. (1992) Extracranialcomplications of severe head injury. Journal ofNeurosurgery 77, 901–907.

Polin S, Shaffrey ME, Bogaev CA et al. (1997) Decompressivecraniectomy in the treatment of severe refractorypost-traumatic cerebral oedema. Neurosurgery 41, 84–94.

Prielipp RC, Coursin DB (1995) Sedative and neuromuscularblocking drug use in critically ill patients with headinjuries. New Horizons 3(3), 456–468.

Ramrakha P, Moore K (1997) Oxford Handbook of AcuteMedicine. Oxford: Oxford University Press.

Robertson CS, Valadka AB, Hannay HJ et al. (1999)Prevention of secondary insults after severe head injury.Critical Care Medicine 27, 2086–2095.

Robertson CS (2001) Management of cerebral perfusionpressure after traumatic brain injury. Anaesthesiology95(6), 15, 13–17.

Rosner MJ, Rosner SD, Johnson AH (1995) Cerebralperfusion pressure – management protocol and clinicalresults. Journal of Neurosurgery 83, 949–962.

Royal College of Surgeons (1999) Report of the Working Party

on the Management of Patients with Head Injury. London:Royal College of Surgeons.

Sakas DE, Dias LS, Beale D (1995) Subarachnoidhaemorrhage presenting as a head injury. British MedicalJournal 310, 1186–1187.

Shah S (1999) Neurological assessment. Nursing Standard 13

(22), 49–56.Spiekermann BF, Thompson SA (1996) Fluid management.

In: Stone D and Sperry RJ et al. (eds) The Handbook of

Neuroanaesthesia. St Louis: Mosby.Sullivan J (2000) Positioning of patients with severe

traumatic brain injury: research based practice. Journal ofNeuroscientific Nursing 32(4), 204–209.

Sutcliffe A (2001) Hypothermia (or not) for the managementof head injury. Care of the Critically Ill 17(5), 162–165.

Teasdale G, Jennett B (1974) Assessment of coma andimpaired consciousness: a practical scale. The Lancet,2 (7872), 81–84.

Van der Ark GD (1975) Cardiovascular changes with acutesubdural haematoma. Surgical Neurology, 5(3), 305–308.

Watkins LD (2000) Head injuries: general principles andmanagement. Surgery 18(7), 219–224.

Yamamoto M, Marmarou CR, Stiefel MF et al. (1999)Neuroprotective effect of hypothermia on neuronalinjury in diffuse traumatic brain injury coupled withhypoxia and hypotension. Journal of Neurotrauma, 16(6),487–499.

78 TRAUMA CARE