Presentation on theme: "Critical care management of Increase Intracranial Pressure"— Presentation transcript:
1Critical care management of Increase Intracranial Pressure พญ.อิศราภรณ์ พูนสวัสดิ์ พบ.Aitsaraporn Phunsawat MD.Department of anesthesiology, Faculty of medicineNaresaun University Hospital
2Anatomy of the cranium Cranium is a rigid box containing 1. brain 80% (1300 ml)2. blood 12% (110 ml)3. CSF 8% (65 ml)All of these contents are maintained a balanced pressure referred to as intracranial pressure (ICP)
3Intracranial pressure The normal range for ICP varies with ageAge groupICP normal (mmHg)Infant< 7.5Child< 10Adult< 15( cm H2O)Best Practice & Research Clinical Anaesthesiology.2007;21: 517–38
4Intracranial pressure Transient elevation with straining, coughing, or trendelenberg positionSustained ICP ≥20: abnormalICP 20-40mmHg : moderate ICH (intracranial hypertension)Sustained ICP ≥ 40 mm Hg indicate severe, life- threatening ICHMild 20-29,moderate 30-40,severe_> 40,persist>_5 minGoal: Keep ICP≤ 20 mmHgNeurol Clin 2008;26: 521–41
5Monro-Kellie Doctrine (Compensatory mechanism) The skull is a rigid bowl that offers little flexibility for changes in the size of the three intracranial components. To maintain normal pressure in the skull, any increase in the size of one component initially will lead to a compensatory decrease in one or both of the other two.
6Brain displaced to moderate degrees to accommodate an expanding mass. Slow expansionRapid expansionCerebral herniation1.Subfalcine2.Uncal transtentorial3.Tonsillar4.Trancalvarial5.Transtentorial(Central)6.Upward transtentorial
7Adverse effect of ICH Decreased CPP Brain herniation Brain ishemia brain edema increase ICPBrain herniation
12Clinical Signs of Increased ICP Signs which are almost always presentDepressed level of consciousness (lethargy, stupor, coma)Hypertension, with or without bradycardiaCushing triad: hypertension, bradycardia, and respiratory depressionSymptoms and signs which are sometimes presentHeadacheVomitingPapilledemaSixth cranial nerve palsies
14Neurogenic Patterns of Respiration TypelocationCheynes - Stokes RespirationDiffuse forebrain injuryCentral neurogenic hyperventilationMidbrain ,such as thalamusApneustic(pause at full inspiration)Mid to caudal pontine, brainstem or Basilar a. occlusionAtaxic(radom deep and shallow breaths)Medulla lesion (terminal stage)Cluster(irregular breaths and pause)Lower medulla
16Indirect Monitoring Techniques Monitoring Clinical Status1. Level of alertness and GCS;2. Pupillary examination;3. Ocular motor examination (with special attention to the third and sixth cranial nerves);4. Motor examination with special attention for hemiparesis;5. Presence of nausea or vomiting;6. Complaints of headache; and7. Current vital signs and the recent course.Best to Correlate with ICP
19Transcranial Doppler ultrasonography (TCD) Measure basal arterial cerebral blood flow,40 to 70 cm/s.Diffuse Increase ICP compress cerebral arteries increase flow velocityTCD is insufficiently sensitive and specific to provide a noninvasive alternative to ICP monitoring.
22Indications for ICP monitoring (1) the condition leading to ICP elevationis amenable to treatment(2) ongoing direct assessment of ICP will be of consequence in decisions regarding treatment interventions(3) the risks of device placement do not outweigh the potential benefits.Brain trauma foundation 2007Neurol Clin 2008;26: 521–41
26Management of ICP Head elevation 15 ˚ - 30˚ Hyperventilation Control BPHyperosmolar therapySedative and paralysisSteroidDecompressive craniectomy and lumbar drainage
27Head elevation venous out ﬂow resistance CSF from intracranial spinal compartmentPosition above heart and prevent kinking or compression of jugular v.(c-spine precaution)The mean ICP was significantly lower when the patient's head was elevated at 30° than at 0° (14.1 ± 6.7 mm Hg vs ± 8.3 mm Hg).J Neurosurg 1992;76:207–11.
28Head elevationThe anesthetized or hypovolemic pts may response to head elevation by developing systemic hypotensionMust treat to avoid adverse impact to CPPNeurol Clin 2008;26: 521–41
29Oxygenation and Ventilation Respiratory dysfunction is common esp in head trauma.Hypoxia and hypercapnia can ICPAdequate ventilation: Pao2 ≥60 mmHgPaco2:30-35 mmHgNeurol Clin 2008;26: 521–41
30Oxygenation and Ventilation intrathoracic pressure are transmitted directly through the neck to the intracranial cavityIncrease intrathoracic pressure: increase ICPdecreased venous return to the right atrium and a rise in jugular venous pressure,increase in CBV and in ICPDecreased venous return also leads to a drop in cardiac output and blood pressure, thereby reducing CPPPEEP
31Oxygenation and Ventilation The consequences of PEEP on ICP depend onlung compliance,ICPMAPMinimal consequences for ICP are usually observed when lung compliance is lowJ Trauma 2005;58:571–6.
32Hypercapnia and hypocapnia Cerebral vasodilate CBF and ICP PaCO2 1 mmHg CBF 2 ml/100g/minIn situations of reduced intracranial complianceIncreased ICP and reduced CPPIn situations of reduced cerebral blood flow and oxygen delivery, where ICH is not a problemimprovements in cerebral blood flow
33Hyperventilation Cerebral vasodilate CBF and ICP Hyperventilation PaCO2, which can induce constriction of cerebral arteriesCerebral vasodilate CBF and ICPPaCO2 1 mmHg CBF 2 ml/100g/minPaCO2 1 mmHg CBV 0.04 ml/100g/minAim: Paco mmHgHyperventilation may produce a decrease in CBF suﬃcient to induce ischemia.Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often critically reduced.Neurol Clin 2008;26: 521–41
34Hyperventilation Most eﬀective use of hyperventilation is acutely The vasoconstrictive eﬀect :11-20 hoursWhen hypocarbia is induced and maintained for several hours, it should be reversed slowly, over several days, to minimize this rebound hyperemiaProphylactic hyperventilation (PaCO2 of 25 mm Hgor less) is not recommended.Crit Care Clin 1997;13:163–84.
36Decompressive Abd Pressure intra-abdominal P.(abdominal compartment syndrome), can ICP by obstructing cerebral venous outﬂow.Immediate reductions in ICP with decompressive laparotomyNeurol Clin 2008;26: 521–41
37Decompressive Abdominal Pressure 17 pts with intractable ICH that is refractory to medical treatment (abdominal compartment syndrome is not present)abdominal fascial release can eﬀectively reduce ICP (30.0± ±3.2)J Trauma 2004;57:687–93.
38Hyperthermiametabolic rate 10-13% per 1°C and is a potent vasodilator.Induce dilation of cerebral vessels canCBF and ICP.Fever during the post injury period worsens neurologic injury in TBINeurosurgery 1996;38:533–41
39Hypothermia Prophylactic hypothermia Cochrane review in 2004 Not significantly associated with decrease mortality when compare with normothermic controleCochrane review in 2004not find any evidence supporting the use of hypothermia during the treatment of TBI,a statistically significant increased risk of pneumonia and other potentially harmful side-effectsAlthough routine induction of hypothermia is not indicated at present,hypothermia may be an eﬀective adjunctive treatment of increased ICP refractory to other medical management
40Hypertension Common in pts who have ICH Esp 2° to HI Characterize by a SBP increase greater than diastolic increase.Associate with sympathetic hyperactivityNeurosurgery 1996;38:533–41.
41HypertensionNot reduce BP in HT pts associated with untreated intracranial mass lesionscerebral perfusion maintain by the higher BP.In the absence of an intracranial mass lesion, controversy to treat HTNeurol Clin 2008;26:521–41
42Hypertension When autoregulation is impaired, common after TBI, HT may CBF and ICP,cerebral edema ,risk for post-op intracranial hemorrhageKeep SBP mmHgNeurol Clin 2008;26:521–41
43HypertensionVasodilating drugs e.g. nitroprusside, NTG, and nifedipine, can ICP and catecholaminesSympathomimetic-blocking antiHT drugs,β-blocking drugs ( esmolol)α-central acting receptor agonists (clonidine)are preferred ( reduce BP without aﬀecting the ICP)Agents with a short half-life have an advantage when BP is labile.Neurol Clin 2008;26:521–41
44Treatment of anemiaMechanism: CBF for maintain cerebral oxygen delivery when severe anemia.Anemia has not been clearly shown to exacerbate ICP after TBI,a common practice is to maintain Hb ≥ 10 g/dL.Neurol Clin 2008;26:521–41
45Prevention of seizures Seizure occur 15-20% in severe HI.Seizures can CMR and ICPIn severe TBI, 50% of seizures may be subclinical and can be detected only with continuous EEG monitoringJ Neurosurg 1999;91:750–60
46Prevention of seizures Signiﬁcant risk factors for later seizures- brain contusion- subdural hematoma- depressed skull fracture- penetrating head wound- loss of consciousness or amnesia ≥1 day- age ≥ 65 yearsNeurol Clin 2008;26:521–41
47Barbiturates Dose-dependent CBF and CMRO2 ICP by CBF and CBV High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment.Dose-dependent CBF and CMRO2ICP by CBF and CBVNeuroprotective effectHemodynamic stability is essential before and during barbiturate therapy.Barbiturate coma: EEG shows a burst suppression pattern.
48Barbiturate comaComplications during treatment with barbiturate coma include- hypotension in 58%of patients- hypokalemia in 82%- respiratory complications in 76%- infections in 55%- hepatic dysfunction in 87%- renal dysfunction in 47%Acta Neurochir 1992;117:153–9
49Propofolrecommended for the control of ICP, but not for improvement in mortality or 6 month outcome.High-dose propofolHypotension and propofol infusion syndrome
50Propofol infusion syndrome Acute refractory bradycardia leading to asystole, in the presence of one or more of the following:metabolic acidosis (base deficit > 10 mmol/l),rhabdomyolysis,hyperlipidaemia,enlarged or fatty liver.propofol infusions at doses higher than 4 mg/kg/h for greater than 48 h duration
53Mannitol onset 1-5 min peak eﬀect 20-60 min Duration hrs depending on the clinical conditionDose:Bolus g/kgUrgent reduce ICP :initial dose of 1 g/kgCan be repeated g/kg q 2-6 hrs.Neurol Clin 2008;26:521–41
54MannitolSosm optimal is mOsm and should ≤ 320 mOsm to avoid S/E e.g. hypovolemia, hyperosmolarity, and renal failure.Attention to replacing ﬂuid that is lost because of mannitol-induced diuresis, or intravascular volume depletionNeurol Clin 2008;26:521–41
55MannitolOsmotic eﬀect of mannitol serum tonicity ( draws edema ﬂuid from cerebral parenchyma)Neurol Clin 2008;26:521–41
56Mannitol Mannitol has rheologic ( Hct and blood viscosity ( o2 delivery to the brain)CSF production, lead to prolonged ICPfree radical scavenging eﬀects.Neurol Clin 2008;26:521–41
57Loop diuretic Furosemide Dose: 0.5-1 mg/kg Synergize with mannitol Greater ICP, less brain edema, prolong elevation of plasma osmolarityEffect from CSF formation via alter Na+ transport across choroid plexus
59Hypertonic salineOsmotic force to draw water from the interstitial space of the brain parenchyma into the intravascular compartment in the presence of an intact BBBintracranial volume and ICP.augments volume resuscitationcirculating BV, MAP,and CPPmodulation of the inflammatory response by adhesion of leukocytes to endotheliumEffective to reduce refractory increased ICPAnesth Analg 2006;102:1836–46
60Hypertonic saline Adverse eﬀects - hematologic and E’lyte abnormalitiesHypoNa+ should be excluded before administering HTS, to reduce the risk for central pontine myelinolysisSerum Na is maintained mmol/L in TBI.repeated until ICP is controlled or Na 155 mmol/LAfter 3–4 days of HTS therapy, boluses of furosemide to mobilize tissue Na.J Trauma 2001;50:367–83Anesth Analg 2006;102:1836–46
61Steroids Common use for 1° and metastatic brain tumors Decrease vasogenic cerebral edema.ICH decreases in 2-5 daysThe most commonly used regimen- Dexamethasone 4 mg q 6 hours IV.Other neurosurgical disorders, such as TBI or spontaneous ICH- not have a beneﬁtCurr Opin Oncol2004;16:593–600
62CSF drainage Decrease ICP immediately by reducing intracranial volume If brain is diﬀuse swollen, the ventricles may collapse, limited usefulnessSpecial consideration- large hemispheric mass- infratentorial massResult in subfalcine herniation, upward trantentorial herniationNeurol Clin 2008;26: 521–41
63Surgical interventions Resection of mass lesionsDecompressive craniectomyFailure of medical therapyPersistent cerebral swelling or increase ICPPrevent transtentorial herniationAnesthesiology Clin 2007;25:
64Prevent secondary brain damaged Avoid hyper or hypoglycemiaMaintain glucose level mg/dLA relative reduction in mortality of around 30% in patients with severe HI after the introduction of protocolCorrect electrolyte imbalanceInfection controlPrevent other organs dysfunction