Critical care management of

Increase Intracranial Pressure

พญ.อิศราภรณ์ พูนสวสัดิ์ พบ.A I T S A R A P O R N P H U N S AW A 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

Best Practice & Research Clinical Anaesthesiology.2007;21: 517–38

The normal range for ICP varies with ageAge group ICP normal (mmHg)

Infant < 7.5Child < 10Adult < 15

(7.5 -20 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)

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 herniation1.Subfalcine 2.Uncal transtentorial3.Tonsillar4.Trancalvarial5.Transtentorial(Central)6.Upward transtentorial

Adverse effect of ICH

Decreased CPP Brain ishemia brain edema

increase ICP Brain herniation

Conditions Associated with Increased ICP

Subdural hematoma Epidural hematoma Brain tumor Cerebral abscess Intracerebral

hemorrhage

Cerebral infarction Global hypoxia-

ischemia Reye's syndrome Acute hyponatremia

Intracranial mass lesions

Increased brain volume (cytotoxic edema)

Conditions Associated with Increased ICP

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

Increased blood and brain volume

(vasogenic edema)Increased CSF volume

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 ofRespiration

Type locationCheynes - Stokes Respiration Diffuse 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

Powerpoint Templates

ICP Monitoring

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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.

Indirect Monitoring Techniques

Best to Correlate with ICP

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CT-brain MRI

Neuroimaging

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Neuroimaging

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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.

Transcranial Doppler ultrasonography

(TCD)

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Direct ICP Monitoring

Neurol Clin 2008;26: 521–41

1. Fontanometry2. Epidural pressure monitoring 3. Subdural pressure monitoring 4. Parenchymal measuring5. Ventricular pressure monitoring6. Lumbar pressure monitoring

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Direct ICP Monitoring

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(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.

Indications for ICP monitoring

Neurol Clin 2008;26: 521–41

MANAGEMENT OF INCREASED

ICP

Treatment of increased ICP

The goals of ICP treatment1. 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

CPP=MAP-ICPCBF = 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. 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

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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 cavityIncrease 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 PaCO2 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 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

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

Hyperventilation Most effective use of hyperventilation is

acutely The vasoconstrictive effect :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 (PaCO2 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

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Decompressive 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±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 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 ective ff

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

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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-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

HYPEROSMOLAR THERAPY

Mannitol onset 1-5 min peak effect 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 effect of mannitol serum

tonicity ( draws edema fluid from cerebral parenchyma)

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Mannitol Mannitol has rheologic ( Hct and blood viscosity ( o2 delivery

to the brain) CSF production, lead to prolonged

ICP free radical scavenging effects.

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Loop diureticFurosemide Dose: 0.5-1 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 3-29.2%,

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 effects

- hematologic and E’lyte abnormalities HypoNa+ should be excluded before

administering HTS, to reduce the risk for central pontine myelinolysis

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.

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 diffuse 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

THE END !!