Stage I prevention of intracranial hypertension general medical and nursing care avoidable factors

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This section lists simple preventive measures and interventions that should be used in all patients who are either at risk of developing intracranial hypertension or have raised ICP (Box 7.4).965

The position of the patients' head should minimise any obstruction to cerebral venous drainage. Many units use head up tilt to improve venous drainage from the head. Relevant obstruction to venous outflow can also be caused by lateral head tilt, neck collars used for stabilisation of the cervical spine, tight bands used for the fixation of endotracheal tubes, or inappropriate amounts of positive end expiratory pressure (PEEP). There is a certain reluctance to use a PEEP greater than 5 cm H2O in head-injured patients, but PEEP needs to be selected based on individual patient characteristics and by optimising the effects on intracranial pressure and arterial partial pressure of oxygen. When patients are nursed in a head up position, care must be taken that

Box 7.4 Potential problems exacerbating raised intracranial pressure

Incorrect calibration of intracranial pressure and arterial blood pressure transducers and monitors

- check calibration and proper position of arterial transducer reference point

Obstruction of venous drainage from the head

- inappropriate position of head and neck

- avoid constricting tape/tube fixations around neck Cardiovascular problems

- inadequate cerebral perfusion pressure (too low (hypovolaemia?) or too high)

- cerebral vasodilating drugs Respiratory problems

- hypercapnia/hypoxia

- inappropriate positive end expiratory pressure

- secretions, bronchospasm, etc.

Metabolism: fever, hyperglycaemia, infusion of hypo-osmotic fluids Insufficient analgesia, insufficient sedation

- consider using muscle relaxants if analgesia and sedation are adequate


Developing or new space occupying lesions cerebral perfusion pressure is maintained. Direct measurement of global cerebral blood flow and cerebral perfusion pressure suggests that a head up tilt of up to 30 degrees is safe but cerebral perfusion pressure needs to be monitored carefully in individual patients.69-72 Ideally the transducer of the arterial pressure monitor should be zeroed at the level of the external acoustic meatus, which approximates the zero point for ICP, and not the right atrium, to measure true cerebral perfusion pressure.

Maintaining adequate perfusion pressure is critical. Low cerebral perfusion pressure will lead to ischaemia and consequently increase cytotoxic oedema. However, moderately low cerebral perfusion pressure can also increase intracranial pressure due to autoregulation: in patients with intact autoregulation, decreases in cerebral perfusion pressure will lead to vasodilatation which, especially in patients with low intracranial compliance, leads to an increase in ICP. In patients with lost autoregulation, increases in cerebral perfusion pressure will be mirrored by increases in ICP. Excessively high cerebral perfusion pressure will increase vasogenic oedema. There is no consensus as to the level of cerebral perfusion pressure which is appropriate in an individual patient. For head-injured adults values ranging from 50 to > 90 mmHg are found in the literature.73-76 The guidelines of the Brain Trauma Foundation list a cerebral perfusion pressure target of 70 mmHg as an option, other authors suggest 60 mmHg as a target. In this context the "Lund concept" needs to be mentioned. This concept is based on the assumption that vasogenic oedema is the major cause of post-traumatic brain oedema and focuses on prevention and reduction of oedema. Therefore cerebral perfusion pressure is not augmented but arterial blood pressure is normalised with metoprolol and clonidine. A cerebral perfusion pressure as low as 50 mmHg is tolerated. Plasma oncotic pressure is corrected through administration of albumin. Dihydroergotamine is used to further reduce the intracerebral blood volume.73 Good results have been reported with this approach.77 However, there has never been a controlled trial in which this concept was directly compared to a more traditional approach, and possibly the fact that contusions are removed surgically whenever possible may confound the issue. Irrespective of the targeted cerebral perfusion pressure, hypovolaemia must be corrected. The evidence for this is most clear cut in patients after head injury and subarachnoid haemorrhage: a negative fluid balance exceeding -594 ml during the first 96 hours after head injury was associated with an adverse effect on outcome.78 Patients with CT evidence of raised ICP are at greater risk of hypovolaemia after subarachnoid haemorrhage,79 and hypovolaemic patients after subarachnoid haemorrhage, particularly when coupled with hyponatraemia, have an increased risk of cerebral infarction.80 Hypovolaemia may be revealed only when the patient is given a sedative agent such as propofol. A stable circulation must be maintained, with normal saline, colloids, and if necessary vasoactive drugs. In this context it is useful to briefly comment on hyponatraemia, which is a frequent finding in patients with brain injury and is associated with extracellular volume depletion and cerebral ischaemia. Most neurosurgical patients with hyponatraemia do not have inappropriate secretion of antidiuretic hormone (SIADH), which is characterised by a hypervolaemic or euvolaemic state. Cerebral salt wasting, defined as the loss of sodium during intracranial disease leading to hyponatraemia and volume depletion, is the alternative cause of hyponatraemia. Possible mechanisms leading to this syndrome are secretion of atrial and brain natriuretic peptides as well as ouabain-like compounds. The two syndromes are differentiated by the volume status of the patient. Cerebral salt wasting is treated with fluid and sodium substitution (for a detailed review see Harrigan81). Overenthusiastic hypertensive-hypervolaemic therapy remains very controversial, especially in the context of head injury with its multiple pathology and uncertainty over the integrity of the blood-brain barrier.82-84 It carries the risk of development of vasogenic oedema but also of adult respiratory distress syndrome85 and cardiac dysfunction.86 The question whether systemic hypertension should be treated in the context of appropriate cerebral perfusion pressure remains controversial and there are no recommendations. In stroke patients it has been suggested that arterial hypertension should be treated if mean arterial pressure exceeds 130 mmHg or systolic pressure exceeds 220 mmHg.87 If arterial blood pressure is to be lowered vasodilators such as sodium nitroprusside or nitroglycerine are to be avoided. All cerebral vasodilators will increase ICP and some such as sodium nitroprusside impair autoregulation, and this drug has also been shown to increase the risk of boundary zone infarction.88 If easily corrected causes for hypertension such as pain or urinary retention are excluded and the decision to treat hypertension is made, labetalol, esmolol, or other short acting beta-blockers or clonidine are potentially useful drugs.

Adequate ventilation is critical. Hypoxia must be avoided, as it is one of the most important secondary insults to the injured brain.89 There is no role for prophylactic hyperventilation and Paco2 should be kept in the normal range. Chest infections are a common complication in patients on a neurointensive care unit. Typically they are either a consequence of aspiration or are associated with mechanical ventilation (ventilator associated pneumonia), especially if neuromuscular blockers are used.

Pyrexia not only increases cerebral metabolism and hence cerebral blood volume but also cerebral oedema. Patients should be kept normothermic either by the administration of paracetamol, non-steroidal anti-inflammatory drugs, or surface cooling. It is important to note that brain temperature is approximately 0 5°C higher than core temperature.

Hyperglycaemia should be treated aggressively. There is considerable evidence that cerebral ischaemia and infarction are made worse by hyperglycaemia and the use of high concentration glucose solutions is contraindicated unless there is significant evidence of benefit in a particular metabolic encephalopathy.90,91 Glucose containing solutions should also be avoided because they are hypo-osmotic once the glucose has been metabolised. Because of concerns about increasing brain oedema by infusing fluids with low osmolarity most units also avoid Ringer's lactate in brain-injured patients and use normal saline as a maintenance fluid.

Adequate sedation and analgesia are essential to control ICP. Coughing, straining, and "fighting the ventilator" all lead to considerable increases in ICP. Sedation not only alleviates stress but also suppresses cerebral metabolism, therefore improving the supply-demand balance. Propofol is widely used because of its cerebral vasoconstrictor effect and its relatively short duration of action. Care has to be taken to avoid hypotension which is likely to occur in hypovolaemic patients due to the propofol induced reduction in preload. An interesting and potentially beneficial side effect of propofol is its free radical scavenging effect.92 There is some concern about the long term use of propofol for sedation, and it should not be used for this purpose in children as deaths have been linked to long term infusions of this drug ("propofol infusion syndrome").93 This syndrome has recently also been reported in adults.94 Furthermore, a substantial amount of long chain fatty acids is infused with propofol and, especially in hypothermic patients, lipid levels need to be checked at regular intervals. Alternatively, midazolam or lorazepam can be used for sedation.

Epilepsy has long been known to raise ICP and increase the risk of cerebral ischaemia as a result of a massive increase in cerebral electrical activity and oxidative metabolism, resulting in an increase in oxygen demand and at the same time a cerebral perfusion pressure decrease. Seizures must be treated aggressively but may be difficult to recognise when the patient is paralysed and ventilated. Episodes of pupillary dilatation with increases in arterial blood pressure and intracranial pressure are suggestive. Some units use continuous EEG monitoring to detect occult seizures. Prophylactic administration of anticonvulsants has been advocated for patients with large haemorrhagic strokes involving the cortex, cortical tumours, and head-injured patients with acute subdural haematomas (evacuated and non-evacuated), depressed skull fractures, and penetrating missile injuries.95 In this context it should be noted that many antibiotics including carbapenems, fluoroquinolones, and metronidazole have proconvulsant properties through GABA antagonism.

If despite these measures ICP exceeds 20-25 mmHg active treatment should be instigated. If no CT scan has been performed recently, a repeat scan is advisable to exclude conditions that are amenable to surgical interventions.

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Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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