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Critical care management of Increase Intracranial Pressure. พญ.อิศ รา ภรณ์ พูนสวัสดิ์ พบ. Aitsaraporn Phunsawat MD. Department of anesthesiology, Faculty of medicine Naresaun University Hospital. Anatomy of the cranium. Cranium is a rigid box containing 1. brain 80% (1300 ml)
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Critical care management of Increase Intracranial Pressure พญ.อิศราภรณ์ พูนสวัสดิ์ พบ. AitsarapornPhunsawat MD. Department of anesthesiology, Faculty of medicine Naresaun University Hospital
Anatomy 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)
Intracranial pressure The normal range for ICP varies with age Best Practice & Research Clinical Anaesthesiology.2007;21: 517–38
Intracranial pressure • Transient elevation with straining, coughing, or trendelenberg position • Sustained ICP ≥20: abnormal • ICP 20-40mmHg : moderate ICH (intracranial hypertension) • Sustained ICP ≥ 40 mm Hg indicate severe, life-threatening ICH Goal: Keep ICP≤ 20 mmHg Neurol Clin 2008;26: 521–41
Monro-KellieDoctrine(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.
Brain • displaced to moderate degrees to accommodate an expanding mass. • Slow expansion • Rapid expansion • Cerebral herniation • 1.Subfalcine 2.Uncal transtentorial 3.Tonsillar 4.Trancalvarial 5.Transtentorial(Central) 6.Upward transtentorial
Adverse effect of ICH • Decreased CPP • Brain ishemia brain edema increase ICP • Brain herniation
Conditions Associated with Increased ICP Intracranial mass lesions Increased brain volume (cytotoxic edema) • Subdural hematoma • Epidural hematoma • Brain tumor • Cerebral abscess • Intracerebral hemorrhage • Cerebral infarction • Global hypoxia-ischemia • Reye's syndrome • Acute hyponatremia
Conditions Associated with Increased ICP Increased blood and brain volume (vasogenic edema) Increased CSF volume • Hepatic encephalopathy • Traumatic brain injury • Meningitis • Encephalitis • Hypertensive encephalopathy • Eclampsia • Subarachnoid hemorrhage • Dural sinus thrombosis • Altitude-related cerebral edema • Communicating hydrocephalus • Noncommunicating hydrocephalus • Choroid plexus papilloma
Extracranial cause (secondary) Prevent cause, Prevent ICH
Clinical Signs of Increased ICP • Signs which are almost always present • Depressed level of consciousness (lethargy, stupor, coma) • Hypertension, with or without bradycardia • Cushing triad: hypertension, bradycardia, and respiratory depression • Symptoms and signs which are sometimes present • Headache • Vomiting • Papilledema • Sixth cranial nerve palsies
ICP Monitoring Powerpoint Templates
Indirect Monitoring Techniques • Monitoring Clinical Status 1. 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; and 7. Current vital signs and the recent course. Best to Correlate with ICP
Neuroimaging • CT-brain • MRI
Transcranial Doppler ultrasonography(TCD) • Measure basal arterial cerebral blood flow, • 40 to 70 cm/s. • Diffuse Increase ICP compress cerebral arteries increase flow velocity • TCD is insufficiently sensitive and specific to provide a noninvasive alternative to ICP monitoring.
Direct ICP Monitoring 1. Fontanometry 2. Epiduralpressuremonitoring 3. Subduralpressuremonitoring 4.Parenchymalmeasuring 5. Ventricularpressuremonitoring 6.Lumbar pressure monitoring Neurol Clin 2008;26: 521–41
Indications for ICP monitoring • (1) the condition leading to ICP elevation • is 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. Neurol Clin 2008;26: 521–41
Treatment of increased ICP CPP=MAP-ICP CBF = CPP / CVR The goals of ICP treatment 1. Maintain ICP ≤ 20-25 mmHg. 2.Maintain CPP ≥ 60 mmHg by maintaining adequate MAP. 3. Avoid factors that aggravate or precipitate elevated ICP. Neurol Clin 2008;26: 521–41
Management of ICP • Head elevation 15 ˚ - 30˚ • Hyperventilation • Control BP • Hyperosmolar therapy • Sedative and paralysis • Steroid • Decompressivecraniectomy and lumbar drainage
Head elevation • venous out flowresistance • CSF from intracranial spinal compartment • Position 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. 19.7 ± 8.3 mm Hg). J Neurosurg 1992;76:207–11.
Head elevation • The anesthetized or hypovolemic pts may response to head elevation by developing systemic hypotension • Must treat to avoid adverse impact to CPP Neurol Clin 2008;26: 521–41
Oxygenation and Ventilation • Respiratory dysfunction is common esp in head trauma. • Hypoxia and hypercapnia can ICP • Adequate ventilation: Pao2 ≥60 mmHg Paco2:30-35 mmHg Neurol Clin 2008;26: 521–41
Oxygenation and Ventilation PEEP • intrathoracicpressurearetransmitteddirectlythroughthenecktotheintracranialcavity Increase intrathoracicpressure: increase ICP • decreasedvenousreturntotherightatriumand a riseinjugularvenouspressure, increaseinCBVandinICP • Decreasedvenousreturnalsoleadsto a dropincardiacoutputandbloodpressure, therebyreducingCPP
Oxygenation and Ventilation • The consequences of PEEP on ICP depend on • lung compliance, • ICP • MAP Minimal consequences for ICP are usually observed when lung compliance is low J Trauma 2005;58:571–6.
Hypercapnia and hypocapnia • Hypercapnia • Cerebral vasodilate CBF and ICP • PaCO2 1 mmHg CBF 2 ml/100g/min • In situations of reduced intracranial compliance • Increased ICP and reduced CPP • In situations ofreducedcerebralbloodflowandoxygendelivery, where ICH isnot a problem • improvementsincerebralbloodflow
Hyperventilation • Hyperventilation PaCO2, which can induce constriction of cerebral arteries • Cerebral vasodilate CBF and ICP • PaCO2 1 mmHg CBF 2 ml/100g/min • PaCO2 1 mmHg CBV 0.04 ml/100g/min • Aim: Paco2 30-35 mmHg • Hyperventilation may produce a decrease in CBF sufficientto induce ischemia. • Hyperventilationshouldbeavoidedduringthefirst24hoursafterinjurywhencerebralbloodflow (CBF) isoftencriticallyreduced. Neurol Clin 2008;26: 521–41
Hyperventilation • Most effective use of hyperventilation is acutely • The vasoconstrictiveeffect :11-20 hours • When hypocarbia is induced and maintained for several hours, it should be reversed slowly, over several days, to minimize this rebound hyperemia Prophylactichyperventilation (PaCO2of25mmHg orless) isnotrecommended. Crit Care Clin 1997;13:163–84.
Decompressive Abd Pressure • intra-abdominal P.(abdominal compartment syndrome), can ICP by obstructing cerebral venous outflow. • Immediate reductions in ICP with decompressivelaparotomy Neurol Clin 2008;26: 521–41
Decompressive Abdominal Pressure • 17 pts with intractable ICH that is refractory to medical treatment (abdominal compartment syndrome is not present) • abdominal fascial release can effectivelyreduce ICP (30.0±4.0 17.5±3.2) J Trauma 2004;57:687–93.
Hyperthermia • metabolic rate 10-13% per 1°C and is a potent vasodilator. • Induce dilation of cerebral vessels can CBF and ICP. • Fever during the post injury period worsens neurologic injury in TBI Neurosurgery 1996;38:533–41
Hypothermia • Prophylactic hypothermia • Not significantly associated with decrease mortality when compare with normothermiccontrole • Cochranereviewin 2004 • notfindanyevidencesupportingtheuseofhypothermiaduringthetreatmentofTBI, • a statisticallysignificantincreasedriskofpneumoniaandotherpotentiallyharmfulside-effects Although routine induction of hypothermia is not indicated at present,hypothermia may be an effective adjunctive treatment of increased ICP refractory to other medical management
Hypertension • Common in pts who have ICH • Esp 2° to HI • Characterize by a SBP increase greater than diastolic increase. • Associate with sympathetic hyperactivity Neurosurgery 1996;38:533–41.
Hypertension • Not reduce BP in HT pts associated with untreated intracranial mass lesions • cerebral perfusion maintain by the higher BP. • In the absence of an intracranial mass lesion, controversy to treat HT Neurol Clin 2008;26:521–41
Hypertension • When autoregulation is impaired, common after TBI, • HT may CBF and ICP,cerebral edema ,risk for post-op intracranial hemorrhage • Keep SBP 120-150 mmHg Neurol Clin 2008;26:521–41
Hypertension • Vasodilating drugs e.g. nitroprusside,NTG, and nifedipine, can ICP and catecholamines • Sympathomimetic-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
Treatment of anemia • Mechanism: 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
Prevention of seizures • Seizure occur 15-20% in severe HI. • Seizures can CMR and ICP • In severe TBI, 50% of seizures may be subclinical and can be detected only with continuous EEG monitoring J Neurosurg 1999;91:750–60
Prevention 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 years Neurol Clin 2008;26:521–41
Barbiturates • High-dosebarbiturateadministration isrecommendedtocontrolelevatedICPrefractorytomaximumstandardmedicalandsurgicaltreatment. • Dose-dependent CBF and CMRO2 • ICP by CBF and CBV • Neuroprotective effect • Hemodynamicstabilityisessentialbeforeandduringbarbituratetherapy. • Barbiturate coma: EEG shows a burst suppression pattern.
Barbiturate coma • Complicationsduring 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
Propofol • recommendedforthecontrolofICP, butnotforimprovementinmortalityor6monthoutcome. High-dosepropofol • Hypotension and propofol infusion syndrome
Propofol infusion syndrome Acuterefractorybradycardialeadingtoasystole, inthepresenceofoneormoreofthefollowing: • metabolicacidosis(basedeficit>10mmol/l), • rhabdomyolysis, • hyperlipidaemia, • enlargedorfattyliver. propofolinfusionsatdoseshigherthan4mg/kg/h forgreaterthan48 h duration