Trauma Resuscitation - part 5 pdf

5.5 Summary Injuries to the abdomen and the pelvis can vary immensely in magnitude. The presence of significant injury may not always be obvious on presentation. The clinical signs may add to the confusion. The trauma team leader must be suspicious of the existence of abdominal trauma in all patients of multiple injuries and must have a clear understanding of the mechanism of injury. It is best to assume that abdominal trauma exists unless proven otherwise. The investigations available to establish a diagnosis all have their roles and must be used liberally according to the index of suspicion. Transfer of patients for such investigations must only be done with stable haemodynamically normal patients. Such heightened awareness and a policy of aggressive investigation will help reduce unexpected findings in the abdomen and the avoidable deaths that still occur due to abdominal trauma. Further reading 1.American College of Surgeons Committee on Trauma (1997) Advanced Trauma Life Support for Physicians. Chicago: American College of Surgeons. 124 TRAUMA RESUSCITATION 6 Head trauma D Bryden, C Gwinnutt Objectives In order to care for a patient with a head injury, members of the trauma team must be familiar with: normal anatomy and physiology; the anatomical and physiological changes that may occur following a head injury; the terms commonly used when describing the type of head injury sustained; how to assess the patient with a head injury; how safely to manage a patient with a head injury; when and how to communicate with a neurosurgeon; when to perform investigations or carry out specific treatments. 6.1 Introduction Of all patients attending a UK ED, 11% will have sustained some form of head injury. Only 1% of patients with a head injury will be referred to a specialist neurosurgical unit, and so staff working within the ED must become familiar with managing all forms of head-injured patients, since they represent a large proportion of their workload. As the majority of head injuries occur in younger male age groups, the economic and social consequences of delayed or inadequate treatment can be devastating. Alcohol is a contributory factor in 25% of cases of head injury. 6.2 Anatomy A basic knowledge of neuroanatomy is important in understanding some of the clinical signs that may be seen after a head injury. The scalp is made up of five distinct layers. The subcutaneous layer is very vascular and open scalp wounds that breach this layer can cause considerable blood loss unless the scalp injury is repaired. Scalp haematomas of a considerable size can also develop in the looser areolar layer. The white and grey matter of the brain is contained within the rigid box-like skull and bathed in cerebrospinal fluid (CSF). The interior of the skull base has many bony projections. To prevent brain injury, two perpendicular folds of dura mater prevent excessive movement; the falx cerebri separates the two cerebral hemispheres and the tentorium cerebelli separates the cerebral hemispheres superiorly, from the cerebellum inferiorly. The dura mater is one of three layers of tissue covering the brain, the others being pia and arachnoid. Arteries run between the dural folds and the inner surface of the skull. The most important is the middle meningeal artery, which lies beneath the temporo-parietal area of the skull. Bridging veins also run in the subarachnoid space, which is a CSF-filled space between the pia mater covering the brain and the arachnoid mater. Bridging veins carry blood from the brain to the venous sinuses that run in the dura mater. The midbrain consists of the pons and medulla and passes through an opening in the tentorium cerebelli and continues at the level of the foramen magnum with the spinal cord. The oculomotor (IIIrd) nerves leave the anterior aspect of the midbrain, run forward between the free and attached edges of the tentorium cerebelli and go on to supply many of the extrinsic muscles of the eye. They also contains pre-ganglionic parasympathetic fibres that cause constriction of the ipsilateral pupil (Figure 6.1). The brain is not a solid structure but has spaces (ventricles) within it containing CSF. Two lateral ventricles, one in each cerebral hemisphere, are connected to the third ventricle at the junction of the midbrain and the cerebral hemispheres. The third ventricle is in turn connected to the fourth ventricle at the level of the medulla. The CSF is secreted by the choroid plexus in the lateral ventricles of each hemisphere, and passes through foraminae or channels in the brain before draining into the subarachnoid space at the level of the midbrain. In the healthy person, CSF communicates freely within the skull before being absorbed by folds of arachnoid villi in the walls of the venous sinuses. Figure 6.1 Coronal section of brain showing the folds of the dura mater and IIIrd nerve 126 TRAUMA RESUSCITATION 6.2.1 Anatomical changes following head injury Primary brain injury Damage that is sustained at the time of an accident as a result of either direct injury or inertial forces is termed primary brain injury. Either mechanism may result in many of the changes described below. Direct injuries These result from contact with a hard object. Contact at the point of impact may deform the skull producing a linear fracture, and considerable underlying brain injury. Depressed fractures occur when bone fragments enter the cranial cavity. Compound fractures occur when there is direct communication between an open scalp laceration and the meninges or brain substance. A basal skull fracture is a special form of compound fracture whose presence requires careful treatment (see later). A contusion may develop in an area of brain lying under the impact point of a contact force. The bone is deformed inwards, and shock waves distribute out from the point of impact, producing haemorrhage, brain oedema and neuronal death. This may also occur when the brain contacts the inner aspect of the skull base. Patients usually lose consciousness at the scene of the accident, and focal signs have often developed by the time of arrival in the ED. Inertial injuries Inertial injuries can produce injuries that result in a significantly worse outcome than damage resulting from direct contact. Diffuse axonal injury (DAI) Occurs after a rapid acceleration or deceleration of the head. Is associated with a high transfer of energy, e.g. shaking a child. Causes deformation of the white and grey matter of the brain. Leads to axonal damage, microscopic haemorrhages, tears in the brain tissue and the subsequent development of oedema. Severe DAI can cause immediate coma at the scene of the accident and has an overall mortality of 33– 50%. Concussion May occur after minor inertial forces to the head and is a less severe form of DAI. The patient is always amnesic of the injuring event. There may be amnesia for events before (antegrade amnesia) or afterwards (post-grade amnesia). Consciousness may have been lost for up to 5 min. There may be nausea, vomiting and headaches. The patient rarely has any localizing signs. HEAD TRAUMA 127 Microscopic structural brain damage occurs, and so the effect of numerous episodes can be considerable. Contra coup injuries These are brain injuries that occur away from the site of impact. The head undergoes an acceleration/deceleration force, the skull and brain move in the direction of the force producing injuries opposite the point of impact. Greater damage develops furthest from the impact point as the brain collides with the inner skull or skull base. Haematomas These can occur outside the dura (extradural) or beneath the dura (intradural). Extradural haematoma (EDH) (Figure 6.2) Associated with a fractured skull in 90% of cases. Most often develops in the temporo-parietal area following a tear in the middle meningeal artery (rarely due to a tear in a venous sinus). As the commonest source is arterial, an EDH develops quickly (Box 6.1). The classical presentation of an EDH occurs in only one third of cases. The commonest clinical signs are a loss of consciousness and pupillary changes, although these can develop rapidly and late on. An EDH is a neurosurgical emergency, as early evacuation (within 2–4 h of clinical deterioration) will result in a better patient outcome by reduction of secondary injury. BOX 6.1 THE CLASSIC HISTORY OF AN EXTRADURAL HAEMATOMA Transient loss of consciousness at the time of the injury from a momentary disruption of the reticular formation Patient then regains consciousness for several hours, the lucid period Localizing signs develop, with neurological deficits, headaches and eventually unconsciousness from the developing ECH, which causes the ICP to rise Acute intradural haematomas (IDH) Can be either subdural (SDH) or intracerebral (ICH). Both often coexist in the same patient. Are three to four times more common than extradural haematomas. Are produced by inertial or rotational forces, although considerably more force is needed to produce an ICH. 128 TRAUMA RESUSCITATION Subdural haematomas develop when the bridging veins are torn and blood collects in the subdural space, commonly over the temporal lobe (Figure 6.3). Clinical deterioration of the patient can be very slow (up to several days). This type of haematoma is more common where there is pre-existing cerebral atrophy, e.g. in alcoholics or the elderly, as the bridging veins are more likely to tear and a considerable blood collection can form in the space. Early evacuation within 4 h of deterioration reduces mortality and outcome so early neurosurgical referral is vital. Intracranial haematomas are produced by much larger forces than SDH, and are rarely found in isolation. Cerebral contusions and lacerations are often present and, as a result, mortality is considerably higher than SDH. Patients frequently lose consciousness at the time of injury, or may quickly develop seizures or focal signs. Subarachnoid haemorrhage May occur following head trauma. May be an incidental finding on CT scan following severe trauma. Patients may present with headaches, photophobia or other signs of meningism and with a history of head trauma. Treatment should be as for any other head injured patient. Figure 6.2 CT scan of EDH HEAD TRAUMA 129 Secondary brain injury This is damage that occurs after the primary brain injury as a result of a number of factors (see Box 6.2). It is estimated that up to 30% of deaths after head injury are directly due to secondary injury, many of which are easily preventable or recognizable and treatable within the ED. BOX 6.2 FACTORS IMPORTANT IN GENERATING SECONDARY INJURY Delay in diagnosis Delay in definitive treatment Hypoxia (pO 2 <10 kPa) Hypotension (systolic BP<90 mmHg) Seizures Extremes of arterial pCO 2 Raised ICP Suboptimal management of other injuries Figure 6.3 CT scan of IDH (subdural) 130 TRAUMA RESUSCITATION 6.3 Physiology 6.3.1 Intracranial pressure (ICP) This is determined by the relationship between the skull, a rigid box of fixed volume and the volumes of the brain, CSF and blood. In health, small changes in the volume of CSF and blood occur in order to keep the intracranial pressure within the range of 5–13 mmHg. CSF can be displaced into the spinal CSF space or its absorption by the pia-arachnoid increased, and the volume of blood within the venous sinuses can change. The changes in blood and CSF volume are often referred to as indicative of the compliance, dV/dP (or more strictly elastance, dP/dV) of the intracranial contents. Transient rises in pressure may occur, e.g. due to changes in posture (bending over), sneezing or coughing, but these quickly return to baseline levels. Once the capacity to make these changes has become exhausted, that is, no further CSF or blood can be displaced, or if the volume of one of the contents within the skull rises very rapidly, for example, an expanding intracranial haematoma, the compensatory mechanisms fail and intracranial pressure rises very rapidly. This is the Monro-Kellie principle (Figure 6.4). The rate of rise of ICP is a direct function of the rate of increase in one of the volumes within the skull. 6.3.2 Cerebral perfusion Cerebral neurons require an almost continuous supply of oxygen and glucose. If blood flow is interrupted for as little as 4 min, neurons rapidly fail and die. Perfusion of the brain is dependent upon the pressure gradient across the vasculature and is termed the cerebral perfusion pressure (CPP). This is the difference between MAP and cerebal venous pressure (CVP). The latter is difficult to measure and in health approximates to the more easily measured ICP: Figure 6.4 Diagram of dV/dP, Monro-Kellie principle HEAD TRAUMA 131 Cerebral perfusion pressure is reduced primarily by a reduction in MAP, an increase in ICP or both. Cerebral venous pressure may also play a role in reducing CPP. When venous drainage of the brain is impaired, for example by a tight endotracheal tube tie or a patient coughing, venous pressure will be elevated above ICP and therefore reduce CPP. Under normal circumstances, MAP and hence CPP varies, but blood flow to the brain must remain constant and this is achieved by a process termed autoregulation. The trigger to autoregulation is CPP; as CPP falls the cerebral arterioles dilate to maintain flow, as CPP rises they constrict to reduce flow, so that cerebral blood flow remains constant over a CPP range of 50–150 mmHg (Figure 6.5). As ICP rises, it becomes increasingly important to calculate CPP. An adequate CPP depends not only on a low ICP, but also on an adequate MAP. The threshold for developing cerebral ischaemia varies with the type of neuronal tissue, but on average occurs if the CPP falls to 50 mmHg or less in a normal person. Following a head injury the threshold for developing ischaemia is often much higher and occurs at CPPs of 60–70 mmHg. This is due to a disruption of cerebral autoregulation in the early stages after a head injury. In the first few hours, cerebral blood flow falls although the metabolic requirements of the neurones are unchanged. Consequently, a higher cerebral perfusion pressure is needed to maintain an adequate cerebral blood flow to prevent ischaemia and neuronal death. 6.3.3 Consciousness This is determined by a number of cranial and extracranial factors. Damage to the reticular formation (a neuronal network in the midbrain and brain stem) or either of the cerebral cortices will result in a loss of consciousness. Hypercapnia from any cause will lead to drowsiness and unconsciousness, whilst hypoxia will initially result in restlessness and agitation, but if uncorrected will cause unconsciousness. Other factors which may impair a patient’s level of consciousness are shown in Box 2.4. Figure 6.5 Relationship between cerebral blood flow (CBF) and cerebral perfusion pressure (CPP) in normal and traumatized brain 132 TRAUMA RESUSCITATION 6.4 Signs of a head injury Signs of a head injury may be nonspecific and can develop in an atypical pattern. Practitioners must therefore always have a high degree of suspicion of injury based on the presenting history or information obtained. Unconsciousness is an unreliable sign of the severity of injury, as it may be due to the primary injury or to treatable secondary factors such as hypoxia and hypotension. A patient with multiple injuries may possess false focal signs, e.g. pupillary dilatation due to direct eye trauma. A high degree of vigilance along with continual reassessment of the patient is therefore necessary. Early manifestations of temporal lobe problems (e.g. extradural haematoma) relate to its close proximity to the tentorium, where its medial aspect compresses the IIIrd nerve causing ipsilateral pupillary dilatation. A contra-lateral hemiparesis occurs due to compression of the corticospinal motor tracts crossing over at the level of the midbrain. As intracranial pressure increases signs of a more general nature are apparent, of which Cushing’s response is the most well known. If untreated, the opposite pupil enlarges, the patient becomes apnoeic, cardiovascular instability ensues as a result of brain stem herniation or ‘coning’ followed shortly after by death (Figure 6.6). Recognition of Cushing’s Response is an indication of the need for urgent action to reduce ICP with control of the airway and ventilation, hyperventilation and mannitol, as progression to brain stem herniation can be extremely rapid. Signs of a rise in intracranial pressure within the posterior fossa may be quite subtle, and often initially manifest only as changes in respiratory pattern or activity. It is important therefore to record and observe respiratory pattern in head-injured patients in addition to respiratory rate. Figure 6.6 Coronal section of brain showing herniation of medial temporal lobe. Compare with Figure 6.1 HEAD TRAUMA 133 [...]... injury could still be extensive Resuscitation should be carried out on a trolley capable of head down and head up tilt, in order that once stabilized, the head-injured patient can be managed in a 15 head-up position to reduce ICP 6 .5. 2 Primary survey and resuscitation It is essential that the patient is managed using the approach described in Section 1.6.1 The life-threatening injury may be extracranial... frequent arterial blood sampling Do not forget that extracranial injuries may be the cause of a neurological deterioration HEAD TRAUMA 137 6 .5. 3 Secondary survey A detailed head-to-toe examination is carried out as described in Section 1.6.2 Features specific to patients with head trauma are described below The medical team leader is responsible for ensuring that the examination is completed as fully as... the various sports clubs 148 TRAUMA RESUSCITATION 7.1.1 What are the risks? Spinal cord injury (SCI) affects mainly young adults in the age from 16–30 with almost 80% of them being male Post-mortem studies indicate that the incidence of spinal cord injury in the UK approaches almost 50 per million population per year Of those surviving a spinal injury, approximately 15 20 per million population per... thoracic or 154 TRAUMA RESUSCITATION Figure 7.6 Blood supply of the cord upper lumbar region and sends branches to both anterior and posterior spinal arteries and supplies a significant part of the lower spinal cord As there are no anastamoses between the anterior and posterior circulation, the cord is susceptible to any reduction in blood supply and may result in infarction of the cord, particularly... 48 h The outlook is poor, as there is likely to be little or no further improvement With incomplete injuries there are several well-recognized patterns of injury Anterior cord syndrome Due to the loss of function of the anterior two-thirds of the spinal cord  156 TRAUMA RESUSCITATION Usually the result of a flexion injury or an axial loading leading to a burst fracture and damage to the anterior spinal... wherever possible, treated any factors causing secondary brain damage; they have assessed and treated any associated injuries; any cervical injuries have been detected HEAD TRAUMA 141 6 .5. 5 Definitive care Investigation This is partly determined by the stability of the patient If, for example, hypotension due to a ruptured viscus is detected, it is imperative the patient undergoes a laparotomy to treat... signs present after assessment and resuscitation Deteriorating consciousness or coma after resuscitation Significant head injury, haemodynamically stable, needing anaesthesia Uncertain or difficult diagnosis, e.g alcohol, drugs GCS< 15 at 2 h after injury; suspected open or depressed skull fracture; any signs of a base of skull fracture; vomiting,≥2 episodes; age> 65 years Current UK recommendations... those that do Further reading 1.Stiell IG, Wells GA, Vandemheen K, et al (2001) The Canadian CT Head Rule for patients with minor head injury Lancet 357 :1391 146 TRAUMA RESUSCITATION 2.The Royal College of Surgeons of England (1999) Report of the Working Party on the Management of Patients with Head Injuries The Royal College of Surgeons of England: London 3.Maas AIR, Dearden M, Teasdale GM, et al ((on...134 TRAUMA RESUSCITATION 6 .5 Assessment and management 6 .5. 1 Preparation The medical team leader must: ascertain the mechanism of any injuries; establish the neurological state of the patient at the scene; identify any subsequent changes... between the spinous processes  150 TRAUMA RESUSCITATION Figure 7.2 Lateral view of vertebra and ligaments Cervical spine There are seven cervical vertebra, of which the top two are structurally distinct The 1st cervical vertebra (atlas) has no body but, instead, lateral masses that articulate by synovial joints with the occipital condyles on the base of the skull (the atlanto-occipital joints) These joints . deterioration 136 TRAUMA RESUSCITATION 6 .5. 3 Secondary survey A detailed head-to-toe examination is carried out as described in Section 1.6.2. Features specific to patients with head trauma are described. abdominal trauma. Further reading 1.American College of Surgeons Committee on Trauma (1997) Advanced Trauma Life Support for Physicians. Chicago: American College of Surgeons. 124 TRAUMA RESUSCITATION 6 Head. associated injuries; any cervical injuries have been detected. 140 TRAUMA RESUSCITATION 6 .5. 5 Definitive care Investigation This is partly determined by the stability of the patient. If, for example,