Traumatic head Injury is the most common cause of death and disability in the UK (National Institute of Clinical Excellence (NICE), 2014) and is the world’s leading cause of morbidity and mortality of those under the age of 45 (Wilson, 2011). A head injury has an impact in epidemiological and economic terms as well as loss in quality of life (Mar et al. 2011). Approximately 700,000 people per year in England and Wales attend an emergency department for head injury, with almost half being the result of falls (NICE, 2007 & Clinical Knowledge Summary, 2009). The vast majority of patients (90%) will have minor head injuries (Vos et al. 2012) and be discharged, however many patients will need to be admitted for definitive care and treatment. The most common cause of head injury is from falls, assaults and road traffic accidents (Department of Health, 2001 & NICE, 2007) with 70-88% of those head injuries occurring in the male population (Dolan & Holt, 2013).

This essay aims to explore the physiological and psychosocial impact of sustaining a head injury. This will include normal physiology of the brain, along with the altered physiology and signs and symptoms as a result of the injury. Advanced interpersonal skills required by the nurse to care for the patient or their family will also be examined. To achieve this, the author will analyse and evaluate types of head injury and their classification, whilst also considering the social and psychological consequences faced by patient and their family. The discussion will be in relation to a 45 year old male who for the purpose of this essay will be referred to as Sam, who has sustained a traumatic head injury through a fall.

In order to understand injuries and to assess and implement care, it is important that the nurse has knowledge, awareness and be able to comprehend the anatomy and normal physiology of the skull and brain, in conjunction with the physiological processes that allow homeostasis and how injury/illness can affect this (Dolan & Holt, 2013).

The brain can be divided into three areas; the hindbrain (cerebellum), the midbrain (pons varolii, medulla oblongata and brain stem) and the forebrain (Cerebrum) (Porth, 2011). Within the brain there is a ventricular system containing four connected cavities which contain cerebrospinal fluid (CSF). The CSF is a clear fluid of water, protein, oxygen, carbon dioxide, sodium, potassium, chloride and glucose, (Dolan & Holt, 2013) that enables the brain to float within the cavity of the bony structure of the rigid skull. Between the skull and the brain there are three membranes; dura, arachnoid and pia mater collectively known as meninges, which also provide protection and cushioning of the brain (Porth, 2011).

The brain has high energy requirements and in normal conditions, mostly provided by adenosine triphosphate (ATP) from the circulation (Belanger et al. 2011). ATP is produced by the metabolic degradation and oxidative phosphorylation of glucose (Hall et al. 2012). Oxygen is required via the cerebral circulation to facilitate this metabolism. Depletion of ATP causes neuron depolarisation which in turn leads to failure of membrane ion-transport systems (Guyton, 2010). Although the brain makes up only 2% of the body’s weight, about 20% of the oxygen and 25% of the glucose consumed by the body are dedicated to cerebral functions (Porth, 2011 & Belanger et al. 2011).

The brain occupies about 80% of the space within the cranial cavity, the remaining 20% being occupied by cerebrospinal fluid (CSF) and blood, occupying 10% each. The volume of these contributes to the Intracranial Pressure (ICP) which is normally maintained within a range of 0 to 15mmHg (Porth, 2011). ICP represents the pressure exerted by the CSF within the ventricles of the brain (Hickey, 2009). If the volume of one component increases, the other two components can compensate by displacement of CSF from the intracranial compartment to the spinal subarachnoid space, increased rate of CSF absorption and reduction of cerebral blood volume by displacement of venous cerebral blood into the venous sinuses, without causing changes in the ICP. This is known as Monro-Kellie hypothesis (Porth, 2011).

Severe head injury can affect the compensatory mechanisms resulting in them becoming rapidly exhausted (Deitch & Dayal, 2006) and failing.

If Sam was showing symptoms such as confusion, memory loss and reduced ability to move his body this would be indicative of cerebral hypoxia, which could be a result of ICP increasing above 20 mmHg (Brain Trauma Foundation, 2007). If ICP increases and unrelieved, compression of the brainstem could occur, causing Sam to become bradycardia, hypertensive and have a decreased respiratory rate, known as the Cushing’s response.

The brain is dependent on blood flow to provide oxygen and nutrients to the neurones and remove waste products. The cerebral blood flow (CBF) is generally constant 700ml/min, approximately 15% of total cardiac output due to the brains ability to autoregulate, by the cerebral arterioles vasoconstricting/vasodilating, in response to cerebral perfusion pressure (CPP) (Porth, 2011). CPP represents the blood pressure gradient across the brain and can be calculated by subtracting ICP from systemic mean arterial pressure (MAP). Normal CPP ranges from 50 – 70mmHg with a CPP below 30mmHG incompatible with life (Adam, 2009). It is when CPP falls below 50mmHG or rises above 150mmHG that autoregulation fails and CBF becomes dependent on systemic blood pressure alone (Dolan & Holt, 2013). It is the chemoreceptors that detect changes in the pH levels, which are based on the amounts of carbon dioxide, hydrogen ions and bicarbonate ions in the CSF. Changes in PaO2 or PO2 may trigger chemo autoregulation (Dolan & Holt, 2013). Hypercapnia causes cerebral vasodilation resulting in hyperaemia, whereas hypocapnia causes vasoconstriction inducing hypoaemia. Sam maybe observed to be hypertensive, 140/90mmHg or higher (NICE, 2011) and have increased respiratory rate which can be an indicator of hypercapnia. To prevent secondary injuries, the goal is to achieve and maintain normocapnia, a PaO2 greater than 13kPa and PaCO2 4.5 – 5.0 kPa (Dolan & Holt, 2013).

Head injuries can by classified under three anatomical sites; scalp, skull and brain, with brain injuries further categorised as focal or diffuse injuries (Dolan & Holt, 2013).
The skull is particularly vulnerable to injury as the brains first line of defence. It is the irregular internal surface and bony protrusions of the skull that can account for injury when the brain moves as a result from an impact. Skull fractures can be classified as; linear, depressed, open, comminuted and basal (Dolan & Holt, 2013).

Focal injury occurs in specific area of the brain and is usually caused by direct force resulting in a coup injury whereby damage is caused as a result of impact or contrecoup when the impact causes the brain to be thrown against the opposite side of skull. Contusions, laceration and intracranial haemorrhage could occur as a result of this type of injury. Trauma to the head can cause the head to turn or twist with the force of the impact causing the brain to rotate inside the skull, subjecting to acceleration/deceleration rotational forces causing stretching and shearing of the nerve fibres (Dawson & Shah, 2005). This type of injury is known as a Diffuse Axonal Injury (DAI).

Head injuries can be further classified into primary (immediate) and secondary (delayed). Primary head injury is damage which results from the causative event, causing damage to neurones, blood vessels, cell structure and function (Porth, 2011), whereas, secondary injuries occur as a response to damage of primary injury and is a result from the subsequent brain swelling, infection or cerebral hypoxia (Hickey, 2009).

When assessing Sam, this should involve taking a careful history of the mechanism of injury as this will provide a good understanding of the likely injury. History can be obtained from witnesses, paramedics and also family. Thierauf (2010) noted the severity and type of injury sustained depends upon the height and objects encountered during the fall. When treating a head injury it is suggested to suspect a neck/spinal injury and to imobilse patient (NICE 2014) until this is ruled out.

Alcohol could be a contributing factor to the mechanism of the injury and is also associated with an increased chance of sustaining head injury. If Sam consumed alcohol, assessing the severity of head injury would be difficult due to the effects alcohol has on the conscious state. It is important to note that alcohol has been consumed, but to ignore its contribution to clinical state of patient as stated in NICE guidelines (2007). Alcohol consumption can induce hypoglycaemia which alters conscious state and therefore capillary blood test should be carried out to plan treatment.

Due to not having a complete history of mechanism of fall, it could be Sam may have suffered a fracture to his skull. External assessment of Sam’s head for any lacerations and observations for signs indicative of fractures such as; depressed area, indicating depressed fracture of skull, bilateral periorbital ecchymoses (raccoon eyes), retroauricular ecchymosis (battle sign, bruising behind ear) and also loss of cerebral fluid from ears (otorrhea) and nose (rhinorrhoea) which can indicate a basilar skull fracture (Parry, 2014). If Sam had a depressed fracture it is important to note that the brain may be exposed which could lead to infection and appropriate treatment commenced.

Sam may report; a period of unconsciousness at the time of injury, headache exacerbated by bright lights, feelings of dizziness and nausea and may also vomit, which are all signs of a concussion. Concussion can result from any direct force to the body and is a form of diffuse injury (Dolan & Holt, 2013). The impact starts the complex pathophysiological process; transmitting biomechanical forces to the brain, initiating neurochemical and neurometabolic events. Brain function relies on electrochemical signals that are transmitted via neurones to other cells. The dendrites of the neurone form specialised junctions which are known as synapses from which the signals are transmitted.

When a signal is received positive ions pass the neurone membrane because the membrane is more permeable to K+ than to Na+, this causes a voltage difference so that the intracellular fluid is more positive than the extracellular fluid which forms the basis for depolarisation of action potential. It is when the potassium channels are activated that homeostasis is restored within the cell (Guyton, 2010). It is through these neurotransmitters that neurones drive functions within the body. As a result of the fall, the stretching of neuronal and axonal membranes enables a flux of ions to pass through previously regulated ion channels. Impaired energy metabolism may trigger excitotoxicity. Glutamate is the principal excitatory neurotransmitter in the brain. It is with interaction with specific receptors that glutamate is responsible for memory, cognition and movement (Porth, 2011).

Following head injury, interstitial glutamate concentration increases, this may be caused from damage to parenchymal cells, damage to the blood brain barrier and damage to the cell membranes. The increase in glutamate forces the opening of N-methyl-D-aspartate (NMDA) receptor channels allowing influx of calcium activating degenerative enzymes which destroy cell membranes and other neuronal structures, causing mitochondrial injury and eventually cell death (Porth, 2011).

If Sam developed symptoms such as headache, vomiting, ipsilateral (same side as injury) dilated pupil, contralateral (opposite side of injury) hemiparesis altered level of consciousness, flexor or extensor posturing the cause maybe due to a haematoma.
Haematoma is an accumulation of blood and be classed according to where it occurs: epidural, subdural and intracerebral. Epidural haematoma forms outside of the dura and are usually caused by bleeding from an artery, subdural form beneath the dura and are usually from veins and intracerebral within brain parenchyma (Huether, 2012)

Haematoma’s can deform and displace the brain tissue, causing herniation. Depending on where the displacement occurs and the structure which it is under defines the type of herniation. Different types of herniation are subfalcine under the falx cereri, transtentorial through the tentorial notch or incisura of the tentorium cerebelli and tonsillar through the foramen magnum (Cottrell, 2010). Signs and symptoms that Sam may develop are as a result of the brain shifting away from the skull, becoming compressed and herniation occurring.

Cerebral oedema is a consistent reaction following brain injury. It is an increase in tissue volume secondary to abnormal fluid accumulation of water and fluid within the intracellular and extracellular spaces (Porth, 2011). It is associated with two pathophysiological processes based on Klatzo’s (1994) classification of cellular oedema (cytotoxic) and transcapillary flux (vasogenic). Cytotoxic oedema is where the intracellular fluid increases due to the failure of the ATPase pump, resulting in cellular retention of sodium and water and subsequent swelling of the cells. Whereas vasogenic occurs when the blood brain barrier is impaired, allowing transfer of water and proteins from vascular into interstitial space. The primary force for driving vasogenic fluid into the extracellular space is the hydrostatic pressure gradient (systemic arterial pressure minus ICP). Oedema formation is accompanied by a local inflammatory response leading to an increase in neutrophils, T-Cells and macrophages; it is presumed that the response of these inflammatory reactions can also contribute to neurone damage and vascular dysfunction (Ladecola, 2011; Kleinschnitz, 2010).

All brain injuries can lead to altered levels of consciousness. Often people who have received a brain injury suffer disorders of consciousness as a result of a breakdown in cortical connectivity (Leon-Carrion et al. 2012). Consciousness comprises of two components; cognitive and content, and arousal and wakefulness. Cognitive and content depends upon the function of the ascending reticular activating system (ARAS).

Arousal and wakefulness is dependent on cognitive and content but is the function of the cerebral hemisphere with support from the basal ganglia, thalamus and (ARAS). When a person is fully conscious they are aware of their surroundings and able to react to the environment. At present the gold standard to assess the level of consciousness is behavioural assessment (Boly, 2014). However it is becoming increasingly evident that limited evidence of behavioural response does not accurately predict underlying brain function (Schiff, 2010). Early signs Sam would demonstrate in level of consciousness would be mild confusion, disorientation and becoming withdrawn.

Brain injury sets in motion a cascade of pathophysiologic processes that can persist after the initial impact. The process of brain damage and the subsequent physiological changes are a dynamic process that continues for some time following the actual injury (Stavinoha, 2005). The care and management of Sam revolves around accurate neurological assessment and the skills of the nurse to be alert to the potential problems that may be encountered and the risk of sudden deterioration at any time.

Nursing and Midwifery Council (2008) state that nurses are to provide both social and psychological support along with a duty of care to their patients and to be empathetic in their manner. It is recognised nurse’s focus on the patient as a whole person and their individual response to experiences of health, illness and disability (Royal College of Nursing, 2003). For nurses to care for patients with a head injury more effectively, they need to have an understanding of the pathological basis of the injury together with the psychological consequences that may occur.

Engel (1980) proposed the biopsychosocial model, suggesting that in order to understand the disease within a person; you have to encompass the persons mind, body and spirit. This is further supported by Helmchen (2013) who states that the biopsychosocial model of health provides a framework for understanding some of the variables that may contribute to the development of psychosocial problems following brain injury. Mortality rates due to brain injury have decreased in recent years due to advances in life support procedures. However it is recognised by Selassie (2008) that long term physical and cognitive difficulties may be faced by the patient.

Recovery from a head injury can be lengthy, uneven and unpredictable. It could be said that health care professionals are reluctant to discuss prognosis due to the uncertainty of the outcome and this could be perceived by the family as incompetence (Botlorf et al. 1998). When it comes to informing patients of diagnosis and prognosis, it is the doctor’s legal responsibility (Kalber, 2009). This is important for Sam and his family as following a head injury uncertainty about the future compounds the suffering already experienced. Cappa (2011) found that families identified information with regard to prognosis as one of their most important needs following head injury. When giving Sam a prognosis or giving information with regard to his injury this could be regarded as bad news. Bad news may be defined as “any information which adversely and seriously affects an individual's view of his or her future” (Buckman, 1992).

Effective inter-personal skills are required to deliver bad news appropriately, effectively and in a manner in which the patient can understand. Higgins (2002) report nurses are in a more pivotal position to carry this out, due to a patient, nurse relationship being formed. According to nursing theorist Peplau (1952), nurse’s interpersonal skills should be interchangeable in order to meet the patients’ individual needs and should include teaching, counselling and leadership skills. Furthermore, he is of the opinion that an effective nurse-patient relationship can contribute towards the enhancement of patient wellbeing.

Recent literature claims that basic skills required in interpersonal communication include listening, questioning, encouraging/reinforcing, giving information, responding and comforting and reassuring (Spouse et al. 2008). Nurses working within an emergency department are faced with challenges such as; busy environment, distractions, limited time, overstressed patients/relatives and consequently the nurse/patient relationship can suffer. Creswick et al (2009) report that poor communication is a contributing factor to 12% of errors made in emergency department. For Sam and his family the setting of an emergency department in itself can be frightening, seem chaotic and could cause feeling of anxiousness and distress. Arnold and Undermann (2011) suggest that to develop and enhance the nurse patient relationship non-verbal communication such as touching a person’s hand, providing eye contact is an expressive way of showing empathy, feelings, care and understanding towards the patient, which could alleviate Sam’s anxiety.

Kaplan (2010) suggests that when delivering bad news, the use of structured series of steps should be followed. Arguably Watson et al (2011), state that all patients receive and respond to bad news in different ways, and communication of bad news should be tailored to the individual patient. Sam has suffered a head injury and may be finding it difficult to understand and retain information, therefore written documentation could be provided.

The model most widely used for breaking bad news is that of six steps; setting, perception, invitation, knowledge, empathy and summary (SPIKES) as developed by Buckman (1992). A basic strategy for giving bad news is that it is given in a planned and co-ordinated way. Using the Spikes approach the room would be prepared, where no interruptions would be anticipated and where the patient would feel comfortable.

A study conducted by Peteet et al (1991), identified that the majority of their patients (75%) were given their bad news in a private room, however in a more recent study (Loge et al (1997) only 52% were given their bad news in the privacy of a doctor’s office. In a hospital setting and in an emergency department, it is not always possible to arrange a private room and Sam may receive bad news at the trolley side or even in a corridor.

Step two, three and four is where Sam’s perception with regard to his illness would be broached and what information would be given. Ponsford et al (2001) showed that information giving can minimise stress for individuals and their families. It is highlighted by Snell et al (2011) the importance of the patients perception of their illness in the recovery process. It is useful for the nurse to ask Sam to repeat what he had been told, thus analysing what has been understood. Step five and six is where the nurse would be empathetic in discussing any concerns raised and clarifying what has been discussed and any further care needed.

Faced with the uncertainty of prognosis and the length of recovery, Sam may encounter a number of stages in relation to grief and loss before he is able to reach acceptance and cope with his situation. Grief is more often associated with death, however today’s society is beginning to acknowledge there are other losses in life that need to be grieved. Dikmen et al (2009) reports that cognitive deficit is a common consequence following brain injury. Deficits such as memory, attention, depression, communicative impairments decreased social contact, and loneliness can occur within days to months following injury. Sam may be faced with losses of previous abilities, changes to personality, unable to return to work, which may result in financial difficulties.

Adjustment to loss generally involves a grieving process. Grieving can be different for each individual and is mostly a private experience. Many theorists have revised the course of loss and grief and concluded a series of behaviours which are commonly experienced. Early 20th century, Freud (1917) and Linderman (1944) concentrated on the psychodynamics and expectations of loss and grief. It was not until Kubler-Ross (1969) that a model for grief was developed comprising five stages; denial, anger, bargaining, depression and acceptance. However these stages have been an issue of conflict by Friedman & James (2008) who are of mind that more harm than good can be as a result.

Adjustment to loss will not only affect Sam, but also affect those who are close to him, such as partners, family, and friends. Sam may have lost confidence which may have led to a decrease in social interaction. However, it is noted by Weiten et al (2012) that society has become more accepting of diverse and changing life events. The problems of social isolation and decrease in previous activities may create a renewed dependence of Sam on his family to meet these needs. Kniepmann (2012) report females who care for their partners’, feel occupational loss and a decrease in quality of life, through the change in roles.

Buckman (1992) reports denial is the refusal to believe bad news. For Sam, it may be he is not aware of his awareness deficits also known as Anosognosia. The term anosognosia was first introduced by Babinski (1914) and is shown it can increase the emotional and interpersonal impact of brain injury. Hardy (2009) noted that the normal justification of denial is often a method of disavowal. It is stated by Freud (1927) that disavowal allows for patients to accept the information they have received, but find ways to lessen its impact. An example of this could be that Sam may be told that it could take a few months to recover and then imply he will return to work in a few days. Sam may have noticed a change in himself, and deny these changes for fear of admitting something is wrong.

The Transactional Model of Stress and Coping (Lazarus and Folkman 1984) has been utilised to explain adjustment to illness. Patients can cope with their diagnosis and prognosis by adopting a dual way of thinking. Sam may see this as an effective coping mechanism. According to Prigatano (1996) denial is a positive symptom in that patients are aware of the problem and reflects their attempts to cope. Conversely Herrmann (2000) highlighted evidence that suggests that denial or avoidance strategies may be detrimental with regard to successful rehabilitation and readjustment. For Sam to be concordant with his rehabilitation and treatment, agreed goals need to be set, if Sam is in denial this cannot be achieved. It is important for the nurse when caring for Sam to assess his progress and that time is given if he appears to be struggling to come to terms with his prognosis, especially if they know the ‘denial’ that patients are experiencing is disavowal and is normal for their condition.

Having sustained a brain injury, Sam may experience surges of anger about the injury; why me? Or problems that may have come with the injury such as time off work, loss of money and control of his life. As Sam is 45 years old he may have a young family dependent on him and become angry that he is unable to provide for them for a period of time. Anger is a difficult emotion to deal with for patients, family and nurses. It is important for the nurse to be aware that underneath the anger, Sam maybe feeling scared and reassurance should be given.

The bargaining stage implies some degree of acceptance; however it also highlights traces of denial. This stage may indicate that Sam has acknowledged the reality of his illness, but does not accept the limitations the injury may have caused, for example he may want to return to work but may not be able to do the job he used to do. Sam may revert back to anger as he realises that the outcome he wanted or bargained for does not happen.

According to Bombardier et al (2010) and Lin et al (2010) depressive symptoms are more prevalent in early stages after an injury, which could be from the result of physiological damage. Furthermore Rao et al (2010) report that depressive symptoms occur in the long term recovery, suggesting that the challenges Sam may be facing, could lead to him becoming depressed if he was not coping well.

Acceptance is the final stage of Kubler-Ross model. Acceptance following a head injury can be a long process with patients confronted with both physical and psychological challenges. Acceptance for Sam is coming to terms with suffering from a head injury and the realisation that his situation has changed post injury. It is reported by Ropaki et al (2014) that acceptance benefits the progress of rehabilitation and for Sam and his family this could be feeling realistic and hopeful about the future.

In conclusion, due to advances in life support procedures, the number of people surviving and living with a brain injury is increasing. From the literature reviewed, it is identified that the care and treatment of a person having suffered a brain injury is complex in that the prevention of secondary injury is paramount for the survival of patient. It is evident that both the social and psychological issues need to be addressed to provide holistic care. It is therefore imperative for nurses to have a clear understanding of brain injury and to have effective communicative skills to be able to provide individualised care for each patient and their family.