Presentation on theme: "พญ. อิศราภรณ์ พูน สวัสดิ์ พบ. AITSARAPORN PHUNSAWAT MD. DEPARTMENT OF ANESTHESIOLOGY, FACULTY OF MEDICINE NARESAUN UNIVERSITY HOSPITAL."— Presentation transcript:
พญ. อิศราภรณ์ พูน สวัสดิ์ 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) 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 Best Practice & Research Clinical Anaesthesiology.2007;21: 517–38 The normal range for ICP varies with age Age group ICP normal (mmHg) Infant < 7.5 Child < 10 Adult < 15 ( cm H2O)
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 Neurol Clin 2008;26: 521–41 Goal: Keep ICP≤ 20 mmHg
Monro-Kellie Doctrine (Compensatory mechanism) 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. 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
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
Neurogenic Patterns of Respiration Typelocation Cheynes - Stokes RespirationDiffuse forebrain injury Central neurogenic hyperventilation Midbrain,such as thalamus Apneustic (pause at full inspiration) Mid to caudal pontine, brainstem or Basilar a. occlusion Ataxic ( radom deep and shallow breaths) Medulla lesion (terminal stage) Cluster (irregular breaths and pause) Lower medulla
Page 16 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
Powerpoint Templates Page 17 CT-brain MRI
Powerpoint Templates Page 18
Powerpoint Templates Page 19 Measure basal arterial cerebral blood flow, ◦ 40 to 70 cm/s. Diffuse Increase ICPcompress cerebral arteriesincrease flow velocity TCD is insufficiently sensitive and specific to provide a noninvasive alternative to ICP monitoring.
Powerpoint Templates Page 21 Direct ICP Monitoring
Powerpoint Templates Page 22 (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 The goals of ICP treatment 1. Maintain ICP ≤ 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 CPP=MAP-ICP CBF = CPP / CVR
Management of ICP Head elevation 15 ˚ - 30 ˚ Hyperventilation Control BP Hyperosmolar therapy Sedative and paralysis Steroid Decompressive craniectomy and lumbar drainage
Head elevation venous out ﬂow resistance 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 ± 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 intrathoracic pressure are transmitted directly through the neck to the intracranial cavity Increase intrathoracic pressure: increase ICP decreased venous return to the right atrium and a rise in jugular venous pressure, increase in CBV and in ICP Decreased venous return also leads to a drop in cardiac output and blood pressure, thereby reducing CPP PEEP
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 PaCO 2 1 mmHg CBF 2 ml/100g/min In situations of reduced intracranial compliance Increased ICP and reduced CPP In situations of reduced cerebral blood flow and oxygen delivery, where ICH is not a problem improvements in cerebral blood flow
Hyperventilation Hyperventilation PaCO2, which can induce constriction of cerebral arteries Cerebral vasodilate CBF and ICP PaCO 2 1 mmHg CBF 2 ml/100g/min PaCO 2 1 mmHg CBV 0.04 ml/100g/min Aim: Paco mmHg Hyperventilation may produce a decrease in CBF su ﬃ cient 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
Hyperventilation Most e ﬀ ective use of hyperventilation is acutely The vasoconstrictive e ﬀ ect :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 Prophylactic hyperventilation (PaCO 2 of 25 mm Hg or less) is not recommended. 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 decompressive laparotomy 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 e ﬀ ectively reduce ICP (30.0± ±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 normothermic controle Cochrane review in 2004 not 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-effects Although routine induction of hypothermia is not indicated at present,hypothermia may be an e ﬀ ective 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 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 a ﬀ ecting 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-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Dose-dependent CBF and CMRO2 ICP by CBF and CBV Neuroprotective effect Hemodynamic stability is essential before and during barbiturate therapy. Barbiturate coma: EEG shows a burst suppression pattern.
Barbiturate coma Complications 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
Propofol recommended for the control of ICP, but not for improvement in mortality or 6 month outcome. High-dose propofol Hypotension and propofol infusion syndrome
Propofol 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
ICP BloodBrain Mannitol HTS Steroid CSF Drainage Drug
Mannitol onset 1-5 min peak e ﬀ ect min Duration hrs depending on the clinical condition Dose:Bolus g/kg Urgent reduce ICP :initial dose of 1 g/kg Can be repeated g/kg q 2-6 hrs. Neurol Clin 2008;26:521–41
Mannitol Sosm 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 depletion Neurol Clin 2008;26:521–41
Mannitol Osmotic e ﬀ ect of mannitol serum tonicity ( draws edema ﬂuid from cerebral parenchyma) Neurol Clin 2008;26:521–41
Mannitol Mannitol has rheologic ( Hct and blood viscosity ( o 2 delivery to the brain) CSF production, lead to prolonged ICP free radical scavenging e ﬀ ects. Neurol Clin 2008;26:521–41
Loop diuretic Furosemide Dose: mg/kg Synergize with mannitol Greater ICP, less brain edema, prolong elevation of plasma osmolarity Effect from CSF formation via alter Na + transport across choroid plexus
Hypertonic saline Concentration %,
Hypertonic saline Osmotic force to draw water from the interstitial space of the brain parenchyma into the intravascular compartment in the presence of an intact BBB intracranial volume and ICP. augments volume resuscitation circulating BV, MAP,and CPP modulation of the inflammatory response by adhesion of leukocytes to endothelium Effective to reduce refractory increased ICP Anesth Analg 2006;102:1836–46
Hypertonic saline Adverse e ﬀ ects - hematologic and E’lyte abnormalities HypoNa + should be excluded before administering HTS, to reduce the risk for central pontine myelinolysis Serum Na is maintained mmol/L in TBI. repeated until ICP is controlled or Na 155 mmol/L After 3–4 days of HTS therapy, boluses of furosemide to mobilize tissue Na. J Trauma 2001;50:367–83 Anesth Analg 2006;102:1836–46
Steroids Common use for 1° and metastatic brain tumors Decrease vasogenic cerebral edema. ICH decreases in 2-5 days The most commonly used regimen - Dexamethasone 4 mg q 6 hours IV. Other neurosurgical disorders, such as TBI or spontaneous ICH - not have a beneﬁt Curr Opin Oncol2004;16:593–600
CSF drainage Decrease ICP immediately by reducing intracranial volume If brain is di ﬀ use swollen, the ventricles may collapse, limited usefulness Special consideration - large hemispheric mass - infratentorial mass Result in subfalcine herniation, upward trantentorial herniation Neurol Clin 2008;26: 521–41
Surgical interventions Resection of mass lesions Decompressive craniectomy - Failure of medical therapy - Persistent cerebral swelling or increase ICP - Prevent transtentorial herniation Anesthesiology Clin 2007;25:
Prevent secondary brain damaged Avoid hyper or hypoglycemia Maintain glucose level mg/dL A relative reduction in mortality of around 30% in patients with severe HI after the introduction of protocol Correct electrolyte imbalance Infection control Prevent other organs dysfunction