Raised intracranial pressure

Raised intracranial pressure

1. Raised intracranial pressure Dr. Sachit Koirala Resident, 2 nd Year Department of Surgery, KISTMCTH

2. Intracranial hypertension is found in 40% to 60% of severe head injuries and is a major factor in death in 50% of all fatalities. The end point of unchecked ICP elevation is a positive feedback loop terminating in herniation and brain death.

3. Physiology of CSF and intracranial pressure

4. The Monro -Kellie doctrine V2(CSF) + V2(BLOOD) + V2(BRAIN) + V2(OTHER) V (INTRACRANIAL SPACE) V1(CSF) + V1(BLOOD) + V1(BRAIN) + V1(OTHER) = = 9% 87% 4% 0% 1500mL

5. If one of 3 compartments increases or a fourth one is created (by a mass-effect lesion such as tumor or hematoma), one or more of the other compartments must necessarily shrink to avoid an increase in ICP. Under normal circumstances, these variations are immediately compensated by means of CSF displacement into the lumbar cistern. Then cerebral blood flow (CBF) decreases. Then parenchyma changes shape as it loses part of extracellular water, and even neurons and glial cells.

6. In case of a slow-growing cerebral lesion, the parenchymal compartment undergoes deformation or remodeling to compensate for increased ICP (loss of extracellular water, glial cells, and even neurons). It is clear that elderly patients tolerate the mass effect of a lesion better than younger patients, given that brain atrophy is natural in advanced age. However, the parenchymal compartment cannot compensate for an abrupt increase in ICP, and therefore CBV and CSF will be responsible for absorbing that increase.

7. ICP is functionally equivalent to CSF pressure. ICP is therefore reflective of the balance among: CSF formation Volume storage or compliance Fluid absorption.

8. In the steady state, intracranial pressure (ICP) is mainly dependent on CSF volume and cerebral blood volume. CSF volume is dependent on the dural venous sinus pressure. Cerebral blood volume is dependent on cardiac parameters and cerebral autoregulation

9. Pressure volume index (PVI) Calculated in milliliters (mL) Volume that would need to be added to the intracranial volume to increase ICP by a factor of 10. Reduced intracranial compliance lowers the PVI  Smaller changes in volume result in greater changes in pressure. Added intracranial volume can be compensated for initially by reduction of one of the other elements, until this compensation is overwhelmed. Thereafter PVI is reduced and elevations in ICP are more pronounced.

10. In case of a slow-growing cerebral lesion, the parenchymal compartment undergoes deformation or remodelling to compensate for increased ICP (loss of extracellular water, glial cells, and even neurons). It is clear that elderly patients tolerate the mass effect of a lesion better than younger patients, given that brain atrophy is natural in advanced age

11. Normal ICP Normal values for ICP depend on age, body posture, and clinical conditions In the supine position, ICP in healthy adults is reported as 7 to 15 mm Hg. In the vertical position, it may become negative (as low as –15 mm Hg). Transient physiologic changes resulting from coughing or sneezing often produce pressures exceeding 30 to 50 mm Hg, but ICP returns rapidly to baseline levels. Upper limit of normal ICP in adults and older children is given as 15 to 20 mm Hg.

12. ICP waveform

13. Baseline pressure level is affected by rhythmic components caused by cardiorespiratory activity. Fluctuation of mean arterial pressure with heart rate causes small amplitude rapid pulsation (high frequency). Respiration causes larger amplitude fluctuations of lower frequency. Percussion wave (W1): derives from pulsations in large intracranial arteries Tidal wave (W2): arise from brain elastance Dicrotic wave (W3): The tidal wave and the dicrotic wave are separated by the dicrotic notch, which corresponds to the dicrotic notch in the arterial pulse waveform

14. Physiology of CSF Mean cranial CSF volume: 164.5 mL [Range 62.2 to 267 mL] Produced principally by the choroid plexuses, which are invaginations of the pia mater into the ventricular cavities. Specifically in the roofs of the third and fourth ventricles and the walls of the lateral ventricles. Fronds of densely branching blood vessels are invested by pia mater and covered by specialized ependymal cells, the choroidal epithelium. Second site of CSF production is the ventricular ependyma, the proportional contribution of which arguably ranges from 50% to 100%.

15. Rate of CSF production Examination of the clearance or turnover of injected substances/ marker dilution techniques/ ventriculocisternal perfusion : 0.35 to 0.37 mL/min Estimates of the flow of CSF through the aqueduct in humans (with flow voids in MRI signals), which should in principal equate to the flow of CSF secretion in the lateral and third ventricles : 0.48 mL/min Diurnal variation: Peak production rates in the late evening and early morning

16. CSF drainage CSF circulates from its origin, through the ventricles, to the cisterna magna, basal cisterns and subarachnoid space. The principal site of physiologic CSF drainage is into the dural venous system through the dural venous sinuses. Evaginations of the arachnoid membrane protrude into the lumens of the dural veins and form the arachnoid granulations or villi. This arrangement forms a valvular connection between the subarachnoid space and the dural sinus so that blood cannot reflux into the CSF. A higher hydrostatic pressure in the subarachnoid space drives the bulk flow of fluid in the forward direction, therefore draining CSF volume,

17. Effects of elevated intracranial pressure Continued perfusion of the brain relies on a cerebral arteriovenous pressure gradient to maintain circulation. ICP is transmitted to the compliant cerebral veins. CPP=Arterial inflow pressure – ICP Decreased CPP  Decreased CBF  Ischemia  More swelling

18. Autoregulatory reserve Lower limit of autoregulation : 50-70 mm Hg Autoregulatory reserve = CPP – Lower limit of autoregulation If CPP is 90, autoregulatory reserve = 20-40 mm Hg

19. A waves, or plateau waves , are prolonged stable increases in ICP that spontaneously recover to a new higher baseline. B waves are short, modest elevations in ICP C waves are rapid sinusoidal fluctuations. It is important to note that these waves do not represent part of steady-state ICP dynamics. Their pathologic significance remains to be defined.

20. Second problem with increased ICP arises from the generation of pressure gradients within the skull. CSF conducts the pressure generated by an increased volume in one region of the brain to others. There are specific anatomic sites where such pressure gradients may cause movement of brain tissue into an abnormal anatomic location, resulting in brain herniation.

21. Central transtentorial herniation Downwardly shifted hemisphere and basal ganglia compress and displace the diencephalon through the tentorial incisura. Subsequent displacement of the brainstem  stretching of the paramedian branches of the basilar artery  marked diencephalon and brainstem dysfunction. Altered levels of consciousness and abnormal respiration. Pupils become small with poor reactivity to light. A unilateral lesion can cause contralateral hemiparesis, with ipsilateral flexor and decorticate responses. With progressive midbrain involvement, respiration becomes tachypneic and the pupils fall into a midline fixed position.

22. Central transtentorial herniation With progressive bilateral involvement, internuclear ophthalmoplegia may arise and motor examination may show bilateral decerebrate posturing. As the pons becomes involved, respiration remains rapid and shallow. Motor examination demonstrates flaccid extremities with bilateral extensor plantar responses. With progressive medullary involvement, respiration slows and becomes irregular with prolonged sighs or gasps. As hypoxia ensues the pupils dilate, and brain death follows shortly thereafter.

23. Uncal herniation Uncus and hippocampal gyrus shift medially into the tentorial notch  distortion of the brainstem and significant dysfunction. One pupil may become dilated and poorly reactive, even in the presence of a normal conscious level. The pupil then fully dilates with external oculomotor ophthalmoplegia. If midbrain compression progresses to this point, consciousness may be impaired, followed by contralateral decerebrate posturing. Occasionally, posturing or hemiparesis may occur ipsilateral to the lesion as a result of pressure on the contralateral cerebral peduncle on the edge of the tentorium cerebelli. If the uncal syndrome is allowed to progress, extensor plantar responses appear bilaterally, along with dilation of the contralateral pupil. Finally, patients have hyperpnea, midposition pupils, impaired oculovestibular response, and bilateral decerebrate rigidity. From this point, progression is as for the central syndrome.

24. Subfalcine herniation Subfalcine herniation of the cingulate gyrus is caused by expansion of one hemisphere that causes movement of the cingulate gyrus under the falx cerebri. Cingulate herniation may compress the internal cerebral veins and/or the ipsilateral anterior cerebral artery, resulting in ischemia and impaired venous drainage. Lesions in the posterior fossa differ slightly in that they may cause upward transtentorial herniation as well as downward transforaminal herniation.

25. Symptoms and signs of raised ICP The cardinal symptoms: Headache, vomiting, and papilledema. Vomiting without any associated nausea is especially suggestive of intracranial disease. Varying degrees of cranial nerve palsies may arise as a result of pressure on brainstem nuclei (in particular, abducens nerve palsies). Papilledema is a reliable and objective measure of raised ICP, with good specificity. However, its sensitivity is observer-dependent, and symptoms suggestive of intracranial disease in the absence of papilledema should not be ignored.

26. Symptoms and signs of raised ICP The Cushing response is defined as arterial hypertension and bradycardia that arise from either generalized CNS ischemia or from local ischemia caused by pressure on the brainstem. Bradycardia is possibly mediated by the Vagus nerve and can occur independently of hypertension. Abnormal respirations may also occur depending in part on the anatomic location of any lesion. Cheyne-Stokes respirations arise from damage to the diencephalic region, and sustained hyperventilation occurs in patients with dysfunction of the midbrain and upper pons. Midpontine lesions cause slow respirations, pontomedullary lesions result in ataxic respirations, upper medullary lesions cause rapid shallow breathing, and with greater medullary involvement, ataxic breathing predominates.

27. Symptoms and signs of raised ICP The Cushing response is defined as arterial hypertension and bradycardia that arise from either generalized CNS ischemia or from local ischemia caused by pressure on the brainstem. Bradycardia is possibly mediated by the Vagus nerve and can occur independently of hypertension. Abnormal respirations may also occur depending in part on the anatomic location of any lesion. Cheyne-Stokes respirations arise from damage to the diencephalic region, and sustained hyperventilation occurs in patients with dysfunction of the midbrain and upper pons. Midpontine lesions cause slow respirations, pontomedullary lesions result in ataxic respirations, upper medullary lesions cause rapid shallow breathing, and with greater medullary involvement, ataxic breathing predominates.

28. Intracranial pressure monitoring Several published clinical trials show that monitoring ICP under situations in which ICP may be high either facilitates treatment or promotes aggressive management. High-quality clinical data have not been able to make the link between ICP monitoring and improved outcomes, however, and some studies have questioned the clinical utility of ICP monitoring. A recent meta-analysis of 14 studies could not demonstrate significant mortality benefits related to ICP monitoring.

29. There is, however, a large body of data implicating the potential positive impact of ICP monitoring, and therefore ICP monitoring remains a useful component of clinical management. Data from the Traumatic Coma Data Bank have shown that the proportion of hourly ICP recordings greater than 20 mm Hg is highly significant in predicting outcome after severe head injury. Mean ICP increases of 10 mm Hg in the first 48 hours after injury have been associated with an adjusted odds ratio of 3.12 for mortality. The role of monitoring in metabolic encephalopathies, cerebral infarction, or diffuse cerebritis is less clear and warrants restraint and further investigation.

30. Management of severe TBI patients using information from ICP monitoring is recommended to reduce in-hospital and 2-week post-injury mortality. Recommendations from the Prior (3 rd Edition) not Supported by Evidence meeting current standards Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe traumatic brain injury (TBI) (GCS 3-8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns. ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission: age over 40 years unilateral or bilateral motor posturing systolic blood pressure (BP) <90 mm Hg

31. Ventriculostomy coupled with a pressure transducer remains the “gold standard” for monitoring ICP because of accuracy and ease of calibration. Disadvantages catheter placement can be difficult when the ventricles are small or shifted from the midline. risk for infection rises in ventriculostomies after 5 days, although this risk can be lessened by tunneling of the catheter under the skin.

32. Prophylactically changing the catheter at regular intervals does not appear to reduce the infection rate and is not recommended currently. Alternative invasive methods of monitoring ICP have used different anatomic locations including brain parenchyma and epidural, subdural, and subarachnoid spaces. Microtransducers are used to determine ICP by several different techniques including a diaphragm to sense light signal intensity, pneumatic strain gauge technology in a balloon tipped catheter, and piezoelectric strain gauge technology. There is no defined reference level for the use of a transducer in the ICU, although the device is typically zeroed at the level of the foramen of Monro , with use of the external acoustic meatus as an anatomic landmark.

33. Non-invasive ICP monitoring Attempts have also been made to measure ICP either noninvasively or in a more continuous fashion without the need for external or invasive equipment. The most promising of these has been sonographic measurement of the optic nerve sheath diameter (ONSD). The intracranial cavity is in communication with the CSF-filled subarachnoid space between the optic nerve and its enclosing sheath. Increasing CSF pressure will expand the sheath and increase the ONSD. A linear ultrasound transducer probe can be placed over the closed eyelid and the optic nerve diameter measured 3 mm deep to the posterior pole of the eyeball. ONSD of 4.5 to 5.5 mm is indicative of raised ICP.

34. Changes in intraocular pressure or pupil reactivity have also been linked with elevations in ICP. Transcranial Doppler ultrasonography has been utilized as a marker of ICP109 and also to gauge CPP. Other technologies include: Tympanic membrane displacement MRI CT EEG Near-infrared spectroscopy Visual evoked responses Experimental

35. Intracranial hypertension therapy

36. There is no uniform agreement about the critical level of ICP beyond which treatment is mandatory. Saul and Ducker demonstrated benefits of treating ICP above 15 mm Hg in comparison with 25 mm Hg. Marmarou and colleagues examined data from 428 patients and calculated the ICP threshold most predictive of 6-month outcome using logistic regression analysis. Threshold that correlated best was 20 mm Hg. Current Brain Trauma Foundation guidelines recommend some form of treatment for persistent ICP above 22 mm Hg. Current opinion regards CPP as a second important variable that should be considered together with ICP, with a recommended target of 60 to 70 mm Hg.

37. V(CSF) Treatment of VCSF is typically mechanical. When obstruction of the CSF pathways by a tumor or other mass causes the hydrocephalus: treat the obstruction in an effort to open the CSF pathways. When hydrocephalus causes ICP elevation and its etiology cannot be eradicated, temporary or permanent CSF diversion may be necessary. If CSF diversion is required, options are: Temporary external drainage (ventriculostomy), temporary internal drainage ( ventriculosubgaleal shunt [VSGS]) Permanent internal drainage (ventriculoperitoneal/atrial/pleural shunt or third ventriculostomy)

38. External ventriculostomy has value as a method for both measuring and controlling ICP. The technique can be especially helpful in the decision whether permanent internal drainage procedure would be of benefit. One approach consists of CSF drainage against minimal resistance early on with eventual elevation of the drip chamber to a level commensurate with physiologic ICP. Pressure is monitored continuously, and CSF is allowed to escape when threshold ICP levels are exceeded. Maintenance of normal ICP with minimal volumes of CSF drainage usually indicate that a permanent shunt will not be needed.

39. VSGS provides continuous ventricular decompression for several weeks to months without the need for percutaneous aspiration of the reservoir. Permanent internal CSF diversion by a ventriculoperitoneal shunt (VPS) is attended by a full array of indications, technical considerations, and risk. Third ventriculostomy with or without choroid plexus ablation using an endoscopic technique can be effective under appropriate clinical conditions, particularly in select cases of obstructive hydrocephalus. It has the benefit of avoiding the inherent risks associated with implanted hardware. Mechanistically, third ventriculostomy tries to reestablish CSF flow and therefore bypass obstruction.

40. When mechanical methods of CSF diversion are not possible or desirable: Adjunctive therapy with Acetazolamide transiently decrease CSF production inhibits carbonic anhydrase–mediated CSF production reduces CSF production by 16% to 66%. Synergy of treatment has been reported when acetazolamide is combined with furosemide. BUT, Acetazolamide has a cerebral vasodilator effect, which may transiently worsen ICP elevations. Other medications such as furosemide and corticosteroids are more controversial in their efficacy and safe applications.

41. V(Blood) The role of VBLOOD in the pathology of ICP is complicated. Excess amounts of intracranial blood (hyperemia) can clearly contribute to reduced compliance and elevations in ICP. Other causes of ICP elevation, however, can occur at the expense of V(Blood) and can in turn cause ischemia and brain edema. There is no absolute CBV or CBF value that is normal per se These parameters are rather defined by the metabolic activity of the brain itself. For example, the mean absolute CBF in normal subjects, 53 mL/100 g per minute, may be considered hyperemic in the anesthetized brain or ischemic in a portion of brain with elevated metabolic need.

42. Generally, CBF tends to stabilize by 36 to 48 hours after injury. Complex interplay of factors affecting V(Blood) makes rational treatment difficult. As ICP increases, arteriovenous oxygen difference usually rises as a result of reductions in venous PO2 caused by greater oxygen extraction. CBV increases with vasodilation in response to lowered CPP, or a rise in PaCO2. Hyperventilation therefore reduces total intracranial blood volume as hypocapnic vasoconstriction moves blood from the pial circulation to the veins and sinuses.

43. The most efficacious methods for reducing blood volume are hyperventilation and elevation of the head. If the patient has any constrictions to jugular outflow such as a cervical collar, these can be loosened or removed in the appropriate context. Hyperventilation causes constriction of pial vessels when blood vessels have retained CO2 reactivity. Pressure autoregulation is frequently lost following head injury, but CO2 reactivity can be preserved in the absence of pressure autoregulation.

44. However, the benefits of hyperventilation may be short-lived. Higher levels can cause vasoconstriction sufficient to produce cerebral ischemia. Only mild or moderate prolonged hyperventilation is used (30 to 35 mm Hg), which is thought to be sufficient to avoid ischemic effects. When hyperventilation is discontinued, it should be tapered over 24 to 48 hours. Abrupt discontinuation can cause vasodilatation as the extracellular pH falls, resulting in ICP elevations.

45. Inverse steal Damaging effects of hyperventilation. In patients with intact or supersensitive CO2 reactivity, hypocapnia can lead to shunting of blood from high-resistance, maximally constricted vessels to low-resistance, dilated vessels that have lost CO2 response. These areas may be so badly damaged as to have low oxygen demand, so hyperventilation may tend to redistribute oxygenated blood from viable tissue into nonviable tissue.

46. Elevation of the head to 30 degrees decreases ICP by facilitating adequate venous drainage and possibly CSF drainage also if mild obstruction is present. This degree of elevation does not alter CPP. Feldman and coworkers demonstrated the beneficial effects of head elevation on ICP clinically. In this study, CPP and CBF seemed unaffected by head position until the head was elevated to 60 degrees. Rotation of the head or flexion of the neck can also impair jugular venous flow and raise ICP. Therefore, an effort should be made to keep the head in a neutral position.

47. An intuitive mechanism by which CBV could be lowered is reduction of CPP. This principal, coupled with a reduction of hydrostatic forces in damaged capillary beds, underlies the Lund protocol for raised ICP. This protocol originally advocated reduced CPP, precapillary vasoconstriction with dihydroergotamine, and maintenance of plasma osmolarity with albumin infusion.

48. This protocol, however, contrasts starkly with the general principles of CPP management and with recommendations of the Brain Trauma Foundation. Maintenance or elevation of CPP in the range of 60 to 70 mm Hg. It is thought that in addition to risk for ischemia, low CPP can stimulate arteriolar vasodilation, causing increases in both CBV and ICP. An opposing theory to the Lund concept argues that with elevation of the CPP with vasopressors, the blood vessel is stimulated by the mechanisms of pressure autoregulation to vasoconstriction, consequently reducing CBV and ICP.

49. V(Brain) Increases in VBRAIN occur most frequently as a result of cerebral edema, which is a nonspecific reaction to a variety of processes. Traditionally edema has been divided into cytotoxic and vasogenic types. The type of edema in traumatic brain injury remains debated, although a body of evidence has accrued supporting cytotoxic edema. BBB disruption can likely occur by both mechanical means at the time of injury and also by a biochemical process (destruction of tight junction protein complexes, integrins etc.) that disrupts endothelial tight junctions and by cytotoxic injury at the level of the endothelial cells and astrocytes.

50. The choice of fluid resuscitation in the head-injured patient is critical. Approximately 10% to 15% of head-injured patients are hypotensive as a result of either the injury itself or associated injuries. Aggressive correction of shock and targeting euvolemia improves survival and clinical outcome, but the osmolality of the blood will have important implications for ICP. Use of hypotonic solutions has the potential to worsen cerebral edema, and hypertonic solutions have been advocated as a possible therapy for elevated ICP. Bolus doses of hypertonic saline appear to be beneficial as osmotic agents. Ongoing fluid replacement therapy with hypertonic saline has been shown to be both beneficial and detrimental for ICP in different studies. Use of albumin is not recommended in traumatic brain injury because it has been linked with worsened outcome.

51. Barbiturates are useful in a wide range of situations because they decrease the cerebral metabolic rate of oxygen, thus permitting tolerance of a degree of ischemia/anoxia not otherwise acceptable on the cellular level. This tolerance in turn can lower demand for CBF, which therefore tends to lower CBV and, consequently, ICP. Barbiturates seem to have maximum effect in situations in which CBF is greater than required by metabolic demand

52. Barbiturates are effective at reducing ICP through an action on V(Brain), but in many studies they have not been shown to improve outcome. Even prophylactic use of barbiturates has not improved outcome or led to easier control of ICP. Considering the risks associated with high-dose barbiturates, their application is most appropriate for patients in whom conventional measures to control ICP have failed. Usually a bolus of pentobarbital (5 to 10mg/kg) is administered over 30 minutes followed by a continuous hourly maintenance infusion of 1 to 5 mg/kg to achieve a serum concentration of 3.5 to 4.5 mg/100 mL153 or 10 to 20 seconds of burst suppression monitored by bedside EEG.

53. Prophylactic anticonvulsants such as phenytoin and levetiracetam, should be given except in limited circumstances such as severe liver conditions or allergies. The incidence of seizures after injury is 4% to 25% and after penetrating injuries is 50%. Seizures may increase ICP through several means, including an increased metabolic demand, Valsalva maneuver, and release of excitotoxins. Prevention of seizures can therefore indirectly treat ICP.

54. Steroids worsen outcome in cerebral ischemia, either by means of direct glucocorticoid toxicity or as a consequence of elevated serum glucose values, which exacerbate ischemic lactic acidosis.

55. V(Brain) can be reduced by increasing the rate of clearance of edema. Both osmotic and loop diuretics are widely used and can treat both vasogenic edema and cytotoxic edema. Osmotic agents raise serum osmolality and create an osmotic gradient between the serum and brain. This effect draws free water from the brain into the intravascular compartment along the osmotic gradient, a process thought to both prevent edema formation and speed clearance. The agents used most commonly for increasing intravascular osmolality are mannitol, hypertonic saline, urea, and glycerol. Mannitol (20% solution) or hypertonic saline (23.4%, 2%, 3%) are usually the agents of choice; hypertonic saline has gained significant popularity in recent years. Mannitol has a rapid effect on ICP, and it is therefore thought that a second mechanism of action, in addition to its osmotic effects, may involve its effects on rheologic characteristics of blood. Mannitol increases plasma volume and decreases both hematocrit and blood viscosity, effects that can cause vasoconstriction and a drop in ICP.

56. Mannitol (0.25 to 1.0 g/kg) can be given as a repeated bolus or as a continuous infusion. Complications of its use in osmotic therapy are dehydration, electrolyte imbalance, and, with extreme hyperosmolarity, renal failure. Fluid replacement is aimed at preserving isovolemia while increasing serum osmolality. Osmolality should not exceed 320 mOsm /kg because the renal tubule can be easily injured, especially if other nephrotoxic drugs are used concomitantly. Maintenance of high serum mannitol levels can lead to penetration of mannitol into injured brain, especially in areas of BBB deficiency. In this case, the osmolality of brain tissue could theoretically draw water into the tissue and worsen edema.

57. Studies have not demonstrated a significant difference in effect between mannitol and hypertonic saline for ICP reduction. Mannitol and hypertonic saline have been shown to be equivalent in treating intracranial hypertension related to subarachnoid hemorrhage. Clinically significant differences between mortality and neurological outcomes have also not been readily identified. Mannitol and hypertonic saline can be used with equivalent effect for management of raised ICP.

58. Loop diuretics such as furosemide and ethacrynic acid can be used in conjunction with mannitol to control ICP associated with edema. Furosemide works synergistically with mannitol to remove free water and is most appropriate in patients with fluid overload.

59. Another approach to limit edema formation and therefore reduce V(Brain) is therapeutic hypothermia. Reports have have suggested a beneficial effect on ICP. Use of hypothermia in a group of severely injured patients with intracranial hypertension refractory to other treatment, including barbiturates, has been shown to reduce ICP. Use of hypothermia to reduce ICP has also been shown to improve patient outcome at 3 and 6 months after injury. The ability of hypothermia to lower ICP probably relates to a depression of cerebral metabolic requirements, as with barbiturates, coupled with a slowing of injurious cellular events (e.g., lipid peroxidation). A large number of studies have confirmed the beneficial physiologic effects and neuroprotective effects of hypothermia.

60. The National Acute Brain Injury Study: Hypothermia (NABIS : H), a large randomized study of 392 patients, did not demonstrate any outcome benefit of hypothermia after severe traumatic brain injury. There was a trend toward ICP reduction with hypothermia but a higher rate of other complications. Hypothermia raises the risks for infection, electrolyte abnormalities, clotting disorders, cardiac arrhythmias, and depression of myocardial function. There can also be problems during the attempt to rewarm patients, and delayed brain swelling can occur at that time. NABIS:H II : Terminated due to futility Eurotherm 3235: Reduced ICP but worsened neurological outcomes and increase in mortality

61. V(Other) The most effective treatment of VOTHER consists of surgical resection. When a definable, abnormal mass (e.g., tumor, abscess, or hematoma) is responsible for severe or refractory intracranial hypertension, consideration should be given to safe removal of the mass. All other therapy should be considered adjunctive and supportive in this case.

62. The entire Monro -Kellie doctrine is based on the concept of a rigid enclosure of the intracranial contents. Reduction in size of this enclosure also affects the ICP-volume relationship. Equally, expansion of the space could theoretically provide increased volume, which will in turn lower pressure. This is the basis of the use of decompressive craniectomy as a treatment for raised ICP.

63. Clinical trials have been very varied in their reporting of benefit for this technique. Randomized controlled Decompressive Craniectomy in Diffuse Traumatic Brain Injury (DECRA) trial used decompressive craniectomy in 155 patients (15 to 59 years of age) to treat ICP. Demonstrated an ability to reduce both ICP and length of ICU stay, but there was no survival benefit, and the unfavorable outcome rate was higher than for standard care. The RESCUEicp trial examined 408 patients with ages ranging from 10 to 65 years and found that decompressive craniectomy for refractory ICP elevations resulted in higher rates of survival, but higher rates of vegetative state and severe disability compared with medically managed patients

64. Recent consensus statement: Supports the use of decompressive craniectomy for ICP control in carefully selected patients with the understanding that underlying brain pathology significantly contributes to outcome.

65. Thank you