Too much pressure on the brain.
The bones of the skull form a rigid box within which the brain is confined. An increase in the volume of contents of the cranial cavity causes pressure on brain structures with potentially devastating consequences.
Each year in New Zealand, 760 out of 100,000 people suffer traumatic brain injury (most commonly from falls and road accidents) and about five per cent of these are moderate to severe. (1) Increased intracranial pressure (ICP) occurs in up to 75 per cent of people who receive a severe traumatic brain injury (TBI) and it is associated with up to 95 per cent mortality. (2,3)
Besides accidents, other factors that may lead to a rise in ICP include:
* Stroke or intracranial haemorrhage.
* Brain tumours.
* Right-sided heart failure.
* Abnormalities in production, circulation or reabsorption of cerebrospinal fluid (CSF).
* Oedema of the brain arising from hypoxic injury, inflammation or infection.
Brain tissue, blood volume and CSF are the three main elements contributing to the generation of ICP. The Monroe-Kellie doctrine (11) says an increase in the volume of one of these must be countered by a decrease in the other components to maintain normal ICP. The volume of brain tissue in a healthy adult is constant, while volumes of blood and CSF within the cranial cavity are tightly controlled to prevent fluctuations in ICP. Damage arises when the regulatory mechanisms designed to protect the brain and maintain normal ICP become overwhelmed. Aside from the initial injury, secondary damage occurs, due to hypoxia and displacement of brain structures.
Any event with the potential to increase the volume of tissue within the cranial cavity requires careful assessment and monitoring. The more rapid the increase in ICP, the more likely serious damage will occur. Close neurological monitoring with prompt recognition of raised ICP are essential to successfully manage and prevent, or minimise, damage. (4)
The brain makes up only about two per cent of the body's weight but receives 15 per cent of cardiac output and consumes 20 per cent of oxygen and 25 per cent of glucose, when the body is at rest. (5) Stored glucose is very limited in the brain, as is the ability to use alternative energy pathways in the absence of oxygen. A continuous blood supply is therefore essential to maintain neurological function. In most circumstances, interruption to blood flow causes irreversible damage within three to eight minutes. (6) The brain has numerous physiological mechanisms to maintain blood flow to meet metabolic demand, without jeopardising the delicate balance of factors that maintain ICP. Appreciating these factors can help nurses understand the rationales for therapies used to prevent neurological damage following an increase in ICP.
Anatomy of the cranium
Of the 22 bones making up the human skull, eight form the cranium, which encloses the brain. In early life, these bones are separated by tough membranes--sutures and fontanelles--which allow the skull to compress and flex during birth, and the brain to grow during early childhood. Fontanelles normally close by about two years of age , while the sutures between the bones may persist into early adolescence.7 Before the cranium fuses completely, increases in the volume of cranial contents, if slow, may cause deformation of the cranium and no change in ICP. Following cranial fusion (or an acute event in an infant or young child), any increase in volume within the cranial cavity will generate a corresponding increase in pressure.
The cranium forms a smooth outer surface for attachment of the scalp but internally it is not as uniform: the cranial floor has ridges and numerous bony projections. These may cause extra trauma to the brain if it moves abruptly within the skull. The base of the cranium contains the foramen magnum--the hole through which the brain, brainstem and cerebellum communicate with the spinal cord.
The brain is suspended and separated into anatomical regions by infolding of the dura mater--the tough outermost layer of the meninges, the membranes that enclose the brain and spinal cord. These folds include the falx cerebri (separating the left and right cerebral hemispheres), and the tentorium, which separates the cerebral hemispheres from the cerebellum (see Box 1, p23). Movement of brain tissue against or within these compartments may also contribute to traumatic damage. Raised ICP may cause compression and herniation (displacement) of brain tissue, giving rise to a variety of neurological symptoms. The most common forms of herniation are shown in Box 1, p23. Severe herniation through the foramen magnum (coning) is irreversible and fatal.
The three volumes that contribute to ICP are brain tissue (~80 per cent), blood (~10 per cent) and the CSF (~10 per cent). ICP remains relatively constant, between five and 15mmHg, despite changes in blood and CSF flow related to posture, exercise and metabolic demand. The brain tissue is relatively incompressible, so first CSF and then blood flow are altered when ICP increases.
Cerebral blood flow (CBF) is affected by conditions that alter cerebral perfusion pressure and the diameter of the cerebral blood vessels. Tight regulation of CBF is necessary to maintain normal ICP: if the amount of blood in the brain increases abnormally, ICP will rise.
Cerebral perfusion pressure
The difference in pressure between blood in the cerebral arteries and in the veins is the cerebral perfusion pressure (CPP). This is the pressure that determines blood flow, and therefore nutrient and oxygen delivery, through the brain. Cerebral arterial pressure is the same as the mean arterial pressure in the body (calculated by adding 2/3 diastolic pressure plus 1/3 systolic pressure). In a person with normal blood pressure, the mean arterial pressure is around 90mmHg. The venous pressure is the same as the ICP--about 10mmHg. Thus CPP is the mean arterial pressure less the ICP, or about 80mmHg. Alterations in mean arterial pressure or in ICP will affect the CPP. Most catastrophic would be hypotension combined with raised ICP. This is the reason close monitoring and maintenance of blood pressure is essential to limit secondary brain damage with raised ICP. A CPP of greater than 70mmHg is necessary to maintain oxygenation of brain tissue. In severe TBI, systolic blood pressures of below 90mmHg (or PaO2 below 60mmHg) should be avoided. (10)
In the healthy brain, CBF can be kept constant across a wide range of values in CPP (see Figure 1, below). This is due to autoregulation of blood vessel diameter in the brain. Increased CPP will cause reflex contraction of arteries and arterioles of the brain, while lowered CPP causes reflex relaxation.6 In up to 50 per cent of patients with severe TBI, autoregulation mechanisms are impaired, increasing the risk of cerebral ischaemia and secondary damage. (11) This may also be an underlying mechanism in secondary damage, following haemorrhage or inflammation. (12)
Once blood vessel walls are maximally relaxed or constricted, autoregulation fails. At this point (CPP of <50mmHg or >150mmHg), for any minor change in CCP there is a rapid disruption of CBF (see Fig 1).
Another factor influencing CBF, particularly regional flow, is neuronal activity. Increased metabolic demand in a region of the brain generates a rise in blood-flow, known as reactive hyperaemia. This may be due to high consumption of oxygen and glucose in the area, the generation of metabolic waste products, or the release of the neurotransmitter glutamate from active neurons.13 If the whole brain becomes hypoxic, increased build-up of metabolic waste products can cause widespread reactive hyperaemia and increased CBF, leading to a rise in ICP and secondary damage.
The concentration of carbon dioxide (CO2) in cerebral blood is significant in the treatment of raised ICP. When CO2 concentration is decreased, eg through hyperventilation, arteriolar vasoconstriction occurs. This causes reduced CBF and can help reduce ICP. However, it carries the risk of causing or aggravating cerebral hypoxia and ischaemia. In parallel with this effect, high CO2 concentrations should be avoided because they induce vasodilation and increase ICP. (6)
Blood vessels are more or less compressible, depending on the thickness of their walls. A consequence of increasing ICP is compression of blood vessels in the brain. Initial compression of veins and venous sinuses helps to compensate for the raised ICP (as per the Monroe-Kellie doctrine). However, as ICP increases, arteriolar and finally arterial blood supply may be compromised, causing ischaemia, cerebral oedema and necrosis, and leading to further increases in ICP and secondary damage to the brain.
Intracranial hypertension is divided into stages: (9,14)
1. Increase in tissue volume in the cranium. Compensatory mechanisms triggered: CSF displaced, arterial vasoconstriction, compression of venous sinuses and displacement of venous volume. ICP not raised or raised transiently, with slowed return to baseline. Clinical signs or symptoms absent, or subtle and transient (brief episodes of confusion, drowsiness, slight pupil or respiratory changes).
2. Compensatory mechanisms become exhausted. ICP increases and CPP is compromised, causing mild hypoxia and impaired neurological function. Systemic blood pressure begins to rise. Clinical signs and symptoms include headache and drowsiness.
3. ICP approaches CPP with consequent hypoxia and hypercapnia. Condition rapidly deteriorates--decreasing consciousness and respiratory changes accompany systemic hypertension, widening pulse pressure and slowed heart rate (bradycardia). Autoregulation mechanisms fail, vasodilation throughout cranium causing rapid fall in CPP. Herniation of brain structures occurs along with obstruction of CSF and small haemorrhages. ICP approaches systemic systolic pressure and cerebral perfusion ceases. Coma, fixed dilated pupils and death ensue.
The third component of the Monroe-Kellie doctrine is cerebrospinal fluid (CSF). This fluid is derived from blood and circulates in the subarachnoid space around the brain and spinal cord, providing these structures with cushioning and buoyancy. About 120ml of CSF is in circulation at any time, and the body produces about 600ml per day. (15) CSF is reabsorbed into the venous blood via the pressure-sensitive one-way valves of the arachnoid villi. So if ICP rises, CSF is reduced due to increased reabsorption and by displacement from the cranial cavity into the spinal column.
Accumulation of CSF (hydrocephalus) may cause raised ICP. Rarely, this may be due to an epithelial tumour causing increased production of CSF; more commonly it is caused by obstruction to flow or impaired reabsorption. Obstructed flow may occur where there is a congenital abnormality or in the presence of a tumour or haemorrhage that blocks circulation. Decreased reabsorption of CSF will occur where inflammation or infection (eg following subarachnoid haemorrhage or with meningitis), tumours or raised venous pressure prevent normal function of the drainage valves.
Normal values for ICP vary with age. In the fused cranium, ICP is normally <10-15mmHg. In young children, the value is less well-established but considered normal at 3-7mmHg, or 1.5-6mmHg in newborn, full-term infants. (11)
Close and careful monitoring of ICP increases the ability to:16
* Maintain CPP.
* Detect early and respond rapidly to compromised cerebral perfusion.
* Detect early deterioration in the status of sedated, intubated or difficult to assess patients.
* Prevent or monitor for increases in ICP during care episodes.
* Provide prognostic information.
* Monitor response to treatment.
AN ICP of 20-25mmHg is associated with a higher risk of death following TBI. (17) Recent research on the use of ICP monitoring following TBI has questioned its worth, (18) but commentators have questioned the validity of this research and still strongly recommend the use of ICP monitoring following severe TBI. (17)
The gold standard for ICP monitoring requires insertion of an intraventricular catheter that allows measurement of pressure, monitoring of waveforms and CSF drainage. (10) While invasive monitoring of ICP is associated with infection or haemorrhage on rare occasions, the benefits outweigh risks, at least for severe TBI.
Monitoring ICP should be accompanied by close monitoring of mean arterial blood pressure. This allows assessment of CPP and thus CBF. CPP is normally maintained at 60-70mmHg, with mean arterial pressure of >90mmHg. (10) Monitoring of cerebral oxygen demand, using a jugular venous bulb catheter, also helps evaluate cerebral perfusion.
Monitoring neurological function
Neurological function is an important indicator of altered ICP, in conjunction with, or in the absence of, monitoring CBF and ICP. Early signs of raised ICP may include headache, vomiting (with no associated nausea), motor impairment and visual disturbances. Neurological function is assessed in five categories: level of consciousness, pupil size/reactivity; eye position and reflexes, respiratory pattern and motor responses.
Level of consciousness
Consciousness--the awareness of self and environment--is a complex entity and terminology surrounding it may be ambiguous or vague. Essentially there are two components to the conscious state: alertness/ wakefulness and awareness or cognition.19 Alterations in these components are often the first sign of impaired neurological function. The anatomical basis of consciousness is widely distributed throughout the cortex, midbrain and brainstem, so altered levels of consciousness (LOC) are not indicative of specific regional damage in the brain. Changes in LOC may be abrupt or subtle, emphasising the importance of routine reliable assessment for comparison.
There is no universal set of terms to describe LOC, leading to some unreliability in interpretation. The Glasgow Coma Scale (GCS) assesses LOC through two means: eye opening and best verbal response, although there are conditions and therapies that may interfere with GCS assessment (intubated patients, aphasia following stroke). The GCS was developed to provide some consistency in evaluation of neurological function, but inter-rater reliability (consistency of judgment among human raters) and precision are not high, leading to debate about its utility in practice. (20,21,26)
The reaction of pupils to light tests for midbrain and third cranial nerve function. A mid-size pupil that constricts spontaneously to light indicates normal function. However, response to light is difficult to assess in a small pupil or brightly lit room. Sluggish or absent responses and enlarged or reduced pupil size indicate midbrain damage. Abnormal responses on one side only (ipsilateral) may indicate compression of the third cranial nerve. Bilateral, dilated, unreactive pupils indicate severe midbrain damage. (9,10)
Abnormally large pupils may occur with amphetamines, anticholinergic drugs or eye drops, or direct trauma to the eyes. Abnormally small pupils are seen with opioid or barbiturate overdose.
Ocular deviation and reflex movements of the eyes in response to head movement can be used to assess damage to the pons (a part of the brainstem that communicates between brain and spinal cord and also controls many autonomic functions), although these are also affected by cortical damage. If the head is moved, reflex responses cause the eyes to move in the opposite direction. In a conscious person, these reflexes are suppressed. Presence of the reflex indicates cortical damage, but complete absence in a comatose patient is due to pons damage. (9)
Box 1. Brain herniation This diagram shows common forms of herniation due to raised intracranial pressure: 1. Cingulate or subfalcine herniation. Unilateral expansion of a cerebral hemisphere displaces the cingulate gyrus (part of the cerebral cortex) and also may cause compression of the anterior cerebral artery. (8) 2. Central herniation. Injury to, or tumour growth within, the cerebral cortex causes direct downward displacement of the thalamic structures onto the brainstem, heralded by constricted pupils and decreased level of consciousness. There follows rapid loss of consciousness, Cheynes-Stokes respirations progressing to apnoea, and fixed, dilated pupils. (9) 3. Uncal herniation. Displacement of the temporal lobe or hippocampus causes compression of the third cranial nerve, causing sluggish and then fixed dilated pupils (initially on the same side as the herniation--'blown pupil'). Compression of other structures may cause an ipsilateral hemiparesis, and Cheynes-Stokes respiration, progressing to a neurogenic hyperventilation (8,9). 4. Tonsillar herniation arises when the lower parts of the cerebellum (the 'tonsils') are compressed downward through the foramen magnum. Brainstem respiratory and cardiac centres are affected, causing life-threatening disruption of heart and lung function. (8)
Absence of the corneal reflex (bilateral blinking in response to gentle stimulation of the cornea) also indicates pons damage. This reflex may be absent when CNS depressant drugs such as opioids, benzodiazepines, barbiturates and anaesthetics have been administered.
Disrupted breathing patterns can occur with a variety of conditions independent of altered neurological function (eg Kussmaul respirations in metabolic acidosis) but changing patterns of respiration (rate, rhythm and depth) in a neurologically vulnerable patient are important. Yawning, hiccoughs and vomiting may be early signs indicating compression on brainstem structures. (9)
Cheynes-Stokes respirations (cyclic, waxing-waning breathing pattern with apnoea episodes) can indicate global cerebral damage or bilateral thalamic damage. (9)
Neurogenic hyperventilation (deep respirations at greater than 25 breaths per minute) may be due to loss of inhibitory reflexes within the brainstem, especially due to damage in the midbrain and pons. This pattern of breathing should be distinguished from Kussmaul respirations and may cause respiratory alkalosis. (9,19)
Apneustic breathing involves a prolonged inspiratory gasp followed by a pause at full inhalation than release. The respiratory rate is very low --often only two to three breaths per minute and arises as a result of damage to the lower pons. (19)
Cluster breathing occurs with midbrain and pontine damage--respirations are irregular and rapid, grouped between periods of apnoea. Ataxic breathing (due to medullary dysfunction)involves less predictable variations in depth and rate of breathing, combined with periods of apnoea. (19)
Providing a person is able to obey commands, differences in motor function between sides of the body (eg weakness) can be important in localising brain damage. Otherwise, response to stimulation is described as purposeful (defensive or withdrawal movements in response to pain) or nonpurposeful.
Nonpurposeful movement is an indication of damage to the corticospinal system and may include grimacing, groaning, generalised body movements and posturing.
Posturing is further divided into decorticate posturing (flexion of upper limbs, extension of legs) and decerebrate posturing (extension of upper and lower extremities). Decerebrate posturing occurs where damage has extended into the brainstem. The absence of purposeful movement indicates damage extending throughout the corticospinal system.9
Managing raised ICP
Regardless of the underlying cause, raised ICP increases the risk of hypoxic damage secondary to the initial injury, in a cycle of events depicted in Figure 2 (p24). Treatment of acute brain injuries seeks to prevent or minimise this secondary damage by reducing intracranial hypertension, maximising oxygen and nutrient delivery while reducing demand, thus preventing or reducing acidosis. (22)
Reducing intracranial hypertension
Head elevation: Patients with increased ICP are normally positioned at 30deg in bed to promote venous drainage and CSF circulation. There has been some concern that this increases the risk of impaired CPP, but research supports use of 30 degree elevation, based on individual responses. (22,23)
Prevention of iatrogenic activities that increase ICP: Nursing a person with raised ICP must be managed to minimise care-induced increases in ICP. Venous drainage from the brain is vulnerable to anything that increases intra-abdominal or intra-thoracic pressures, as these are transmitted to the central venous pressure and then the ICP. Ventilator-associated procedures such as use of positive end expiratory pressure (PEEP) or uncoordinated use of ambubag with respirations will increase intrathoracic pressure. (24)
Venous drainage may also be affected by positioning, such as neck flexion or extension, or flexed hips. The patient should avoid the Valsalva manoeuvre, for example during position changes; straining at stool; sneezing or coughing, all of which raise intra-abdominal or intra-thoracic pressure.
Muscle contraction that raises blood pressure also raises ICP. This may occur with isometric contraction, such as the patient pushing against the bed or pulling on a restraint, or with shivering. A passive range of motion exercises will not have the same effect. Seizures or hyperthermia may contribute to this effect but also increase cerebral metabolism, increasing CBF. (24)
Other factors that might increase blood pressure include pain, suctioning, other noxious stimuli and stressful care activities. Clustering of care activities may cause prolonged elevation in ICP. Spacing them allows ICP to lower after brief elevations. (19,13) Osmotherapy: Infusion of a concentrated fluid draws excess water from the tissues into the bloodstream for removal. Manntiol and hypertonic saline have been used in this way to acutely reduce ICP. Mannitol is thought to confer additional benefits by increasing cerebral perfusion (through reducing plasma viscosity). (10,24)
Maximising oxygen and nutrient delivery
Haemodynamic management: Adequate CPP depends on maintenance of systemic blood pressure. Protocols suggest maintaining a mean arterial pressure of >70mmHg is sufficient if ICP is kept below 20mmHg. This decreases the need for fluid resuscitation and vasopressor drugs that increase the risk of adult respiratory distress syndrome and other systemic complications. (10,24)
Hyperventilation and hypoxia: High levels of [CO.sub.2] in the blood cause vasodilation and increase ICP, while low [CO.sub.2] decreases ICP through vasoconstriction. But the possibility of hypoperfusion and resultant hypoxia-ischaemia must also be considered if hyperventilation is used to lower arterial [CO.sub.2] content. (22) Therefore hyperventilation is not universally recommended. (10) Managing ventilation to prevent hypercapnia or hypoxia, including careful suctioning technique and rapid intubation, is essential. Use of vasodilating drugs, including inhaled anaesthetic agents and antihypertensives, must be carefully considered.
Blood glucose concentration: Hyperglycaemia is associated with brain injury and other critical illnesses. It is linked with poorer outcomes in raised ICP, contributing to acidosis and cerebral oedema. (24) However, strict control of blood glucose increases the risk of hypoglycaemia, which also has adverse effects but does not increase mortality. (25) Recent recommendations are toward less strict glycaemic control with low tolerance for hyperglycaemia. This includes adequate, appropriate nutrition, use of insulin infusions rather than bolus doses and frequent accurate monitoring of blood glucose concentrations. (24,25)
Reducing metabolic demand
Hypothermia: Cooling the brain reduces damage by decreasing metabolic demand, decreasing inflammation and reducing the release of glutamate and free radicals that compound ischaemic damage. (22) However, systemic hypothermia is associated with increased morbidity, eg via sepsis and pneumonia. Selective brain cooling is associated with less risk. In the absence of hypothermia as a therapy, it is important hyperthermia be avoided, as it increases metabolic demand: for every one degree above normal body temperature, oxygen use in the brain increases by seven per cent. (24) Fever should be treated promptly and aggressively, while avoiding shivering.
Sedation and barbiturate coma: The use of sedation and barbiturates to decrease metabolic demand and, in the case of barbiturates, control intracranial hypertension, is not well-supported by evidence.10 Sedation can interfere with assessment of neurological function, even some time after the drug has been stopped. Barbiturates are associated with hypotension--affecting CPP--as well as hypothermia and decreased respiratory drive. (24)
Anticonvulsant prophylaxis: Development of seizures is unpredictable in raised ICP but leads to worsened outcomes. Increased metabolic demand and elevation of ICP during a seizure, as well as the potential for physical injury, suggest prevention of seizures is beneficial. Early seizures (within seven days of initial injury) can be prevented or reduced by using phenytoin, but late seizures are not as easily prevented.10
Managing raised ICP is complex. An understanding of the physiological mechanisms involved in maintaining normal ICP, as well as the goals of therapy, enable nurses to support coherent monitoring and therapy practices. Essential for patients with raised ICP, or with conditions that have that potential, is consistent and close monitoring of neurological signs and symptoms that may indicate worsening ICP.
* References for this article can be found at www.cpd4nurses.co.nz.
THE ADULT brain is encased in a rigid box--the cranium--that restricts any increases in volume. If the volume of the brain increases due to trauma, haemorrhage or intracranial tumour, pressure rises. Increased intracranial pressure has two major effects in the brain: intracranial hypertension which impairs blood flow, and displacement of brain structures causing impaired function.
Treatment aims to maintain existing cerebral function, prevent secondary damage to the brain from hypoxia and, where possible, reverse or alleviate underlying causes. Careful observation of neurological function and purposeful nursing interventions are essential.
After reading this article and completing the accompanying online learning activities, you should be able to:
* Describe normal controls of blood flow and intracranial pressure in the brain.
* Discuss factors that lead to raised intracranial pressure and its adverse outcomes.
* Outline therapies used to prevent primary and secondary brain injury in relation to raised intracranial pressure.
* Discuss specific nursing activities associated with monitoring and therapy for patients experiencing, or at risk of, raised intracranial pressure.
Ear two hours of CPD
By reading this article and doing the associated online learning activities, you can receive a certificate for two hours of continuing professional development (CPD).
Go to www.cpd4nurses.co.nz to complete the learning activities for this article. The online service costs $19.95 per article.
These articles are supplied by CPD4nurses, an independent education company. CPD4nurses is not an NZNO service.
Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
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|Title Annotation:||CPD + nurses; traumatic brain injury|
|Publication:||Kai Tiaki: Nursing New Zealand|
|Date:||Apr 1, 2013|
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