Transcript ภาพนิ่ง 1
พญ.อิศราภรณ์ พูน สวัสดิ ์ พบ.
A I T S A R A P O R N P H U N S AWA T M D .
D E PA R T M E N T O F A N E S T H E S I O L O G Y, FA C U L T Y O F M E D I C I N E N A R E S A U N U N I V E R S I T Y H O S P I T A L
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 Age group ICP normal (mmHg) Infant Child
Adult
< 7.5
< 10
< 15 (7.5 -20 cm H2O)
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 threatening ICH indicate Goal: Keep ICP≤ 20 mmHg severe , life Neurol Clin 2008;26: 521–41
Monro-Kellie Doctrine (Compensatory mechanism)
The skull is a rigid bowl that offers little flexibility for changes in the size of the three intracranial components.
other two.
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
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 herniation brain edema increase ICP
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)
Hepatic encephalopathy Traumatic brain injury Meningitis Encephalitis Hypertensive encephalopathy Eclampsia Subarachnoid hemorrhage Dural sinus thrombosis Altitude-related cerebral edema
Increased CSF volume
Communicating hydrocephalus Noncommunicating hydrocephalus Choroid plexus papilloma
Extracranial cause
(
secondary
) Prevent cause, Prevent ICH
Clinical Signs of Increased ICP
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
Type
Cheynes - Stokes Respiration
location
Diffuse forebrain injury Midbrain ,such as thalamus Central neurogenic hyperventilation Apneustic ( pause at full inspiration ) Ataxic ( radom deep and shallow breaths ) Cluster ( irregular breaths and pause ) Mid to caudal pontine, brainstem or Basilar a. occlusion Medulla lesion (terminal stage) Lower medulla
Powerpoint Templates
Monitoring Clinical Status
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.
Powerpoint Templates Page 16
CT-brain MRI Powerpoint Templates Page 17
Powerpoint Templates Page 18
◦ Measure basal arterial cerebral blood flow, 40 to 70 cm/s.
Diffuse Increase ICP arteries compress cerebral increase flow velocity
TCD is insufficiently sensitive and specific to provide a noninvasive alternative to ICP monitoring.
Powerpoint Templates Page 19
1
.
Fontanometry 2
.
Epidural pressure monitoring 3
.
Subdural pressure monitoring 4
.
Parenchymal measuring 5
.
Ventricular pressure monitoring 6.
Lumbar pressure monitoring Powerpoint Templates – 41 Page 20
Direct ICP Monitoring
Powerpoint Templates Page 21
(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.
Powerpoint Templates 41 Page 22
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 MAP.
mmHg by maintaining adequate 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 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 . 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 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
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 PaCO 2 1 mmHg CBF and ICP 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 cerebral arteries Cerebral vasodilate PaCO 2 1 mmHg PaCO 2 1 mmHg CBF and ICP CBF 2 ml/100g/min of CBV 0.04 ml/100g/min Aim: Paco 2 30-35 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 (30.0
± 4.0 17.5
± 3.2) reduce ICP J Trauma 2004;57:687–93 .
Hyperthermia
metabolic rate 10-13% vasodilator . per 1 ° C and is a potent 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
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 controversy to treat HT lesion, 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 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 delivery for maintain cerebral when severe anemia. oxygen 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 monitoring subclinical and can be detected only with continuous EEG 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 coma include hypotension during treatment with barbiturate in 58%of patients hypokalemia in 82% respiratory complications infections in 55% in 76% hepatic dysfunction renal dysfunction in 87% 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
HYPEROSMOLAR THERAPY
Mannitol
onset 1-5 min peak e ff ect 20-60 min Duration 1.5-6 hrs depending on the clinical condition Dose:Bolus 0.25-1 g/kg Urgent reduce ICP :initial dose of 1 g/kg Can be repeated 0.25 - 0.5 g/kg q 2-6 hrs. Neurol Clin 2008;26:521–41
Mannitol
Sosm optimal is 300-320 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 edema fluid from cerebral parenchyma) ( draws 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: 0.5-1 mg/kg Synergize with mannitol Greater ICP, less brain edema, prolong elevation of plasma osmolarity Effect from CSF formation across choroid plexus via alter Na + transport
Hypertonic saline
Concentration 3-29.2%,
Hypertonic saline
Osmotic force to draw water from the interstitial space brain parenchyma into the intravascular compartment in the presence of an intact BBB of the 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 J Trauma 2001;50:367–83 Serum Na is maintained 145-155 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.
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: 579-603
Prevent secondary brain damaged
Avoid hyper or hypoglycemia Maintain glucose level 90-150 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