2.1 - increased intracranial pressure

45
Patricia Ann D. Canto, MD Adult Neurology

Upload: rose-ann-mecija

Post on 20-Nov-2015

20 views

Category:

Documents


4 download

DESCRIPTION

ICP

TRANSCRIPT

  • Patricia Ann D. Canto, MD

    Adult Neurology

  • OBJECTIVES

    Review the Ventricular System and CSF Pathway.

    Identify common manifestations of patients with increased intracranial pressure (ICP).

    Evaluate and correlate history and examination in localization of possible neurological lesion.

    Discuss the pathophysiology of each clinical condition that result to increased ICP.

  • OBJECTIVES

    Discuss the appropriate ancillary procedures and lab examination that would aid in differential diagnoses.

    Discuss the treatment and therapeutic/non-therapeutic options including surgical approach.

    Review the pharmacodynamics and pharmacokinetics of appropriate medicines.

  • CEREBROSPINAL FLUID Function:

    Mechanical protection by bouyancy

    Provides a constant chemical environment for neuronal activity

    Important for acid-base regulation for control of respiration

    Rate of production: 500mL/day (0.3-0.4mL/min)

    CSF formation is dependent on cerebral perfusion

  • VENTRICULAR SYSTEM

  • THE CSF PATHWAY

  • INTRACRANIAL PRESSURE (ICP)

    Pressure within the skull Cranium is similar to a closed box with 3 volume

    components Brain Tissue (intra/extracellular fluids): 78% Blood: 12% Cerebrospinal fluid: 10%

    Each of the 3 components contributes to the total pressure exerted within the skull ICP

    Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium.

    Normal ICP: 0-20 mmHg

  • THE MONROE-KELLIE HYPOTHESIS

  • RELATIONSHIP BETWEEN CEREBRAL PERFUSION PRESSURE AND INTRACRANIAL PRESSURE

    FORMULA NORMAL

    ICP 0-20 mmHg (adult)

    CPP = MAP - ICP 70-100 mmHg (adult)

    CBF = CPP CVR

    20-70 mL/100g tissue/min

    MAP = DBP + 1/3 (SBP-DBP) 70-110 mm Hg (adult)

  • CEREBRAL AUTOREGULATION

  • CAUSES Obstructed to CSF flow

    and/or absorption

    Increase CSF production/CSF volume expansion

    Generalized Cerebral Edema Cytotoxic, Vasogenic or

    Interstitial

    Cerebral or Extracerebral mass

    Increase in Venous pressure

  • OBSTRUCTED CSF FLOW

    Obstruction at ventricles or in the subarachnoid space at the base of the brain

    Ventricle closest to the obstruction enlarges the most

  • OBSTRUCTED CSF ABSORPTION

    Obstruction of the basal cisterns

    Extensive meningeal disease

    At absorptive sites adjacent to cerebral convexities and SSS: ventricles are normal in size

  • INCREASE CSF PRODUCTION

    Rare Choroid plexus papilloma increased ICP and

    hydrocephalus

  • SPACE OCCUPYING LESIONS

    Brain Tumors

    Massive Infarction with edema

    Extensive Traumatic Contusion

    Parenchymal, Subdural or extradural hematoma

    Abscess

  • GENERALIZED CEREBRAL EDEMA

    Ischemic-anoxic states, acute hepatic failure, hypertensive encephalopathy, hypercarbia, Reye hepatocerebral syndrome

    Increased pressure reduces CPP Cytotoxic

    Fluid accumulation within cells

    Vasogenic Proteinaceous fluid leaks into

    extracellular space from capillaries

    Interstitial CSF pushed into the extracellular space

    in periventricular white matter in hydrocephalus

  • INCREASED VENOUS PRESSURE

    Impairs CSF Reabsorption

  • CLINICAL PRESENTATION

    Headache

    Vomiting

    Papilledema

    Ocular Palsies

    Altered Level of consciousness

    Herniation Syndromes

    Cushings Triad: increased systolic BP with widened pulse pressure, bradycardia and abnormal breathing pattern

    Anisocoria

  • SUPRATENTORIAL HERNIATION SYNDROMES

    Subfalcine Herniation of brain tissue under

    falx cerebri Unilateral space occupying

    lesion

    Central (diencephalic) Dencephalon is displaced

    downward through tentorium cerebelli resulting in rostrocaudal deterioration

    Duret hemorrhages, pituitary stalk shearing, bilateral occipital infarctions

    Reduced level of consciousness appears early

  • SUPRATENTORIAL HERNIATION SYNDROMES

    Tentorial (Uncal)

    Uncus is displaced over edge of tentorium cerebelli and traps ipsilateral CN III

    If it continues, central and tonsillar herniation may occur

    Ipsilateral CN III palsy: 1st sign

    Can compress PCA

  • INFRATENTORIAL HERNIATION SYNDROMES

    Upward cerebellar

    Cerebellar vermis ascends rostral to tentorium cerebelli

    Compressing the midbrain may compress cerebral aqueduct

    Tonsillar Herniate through foramen

    magnum compressing medulla

    Occur with supratentorial or infratentorial lesions or with increased ICP

  • CASE 1 A 62 year-old male right-handed male was

    brought in due to progressive holocranial headaches with a VAS of 8-9/10 accompanied by fever, projectile vomiting and diplopia.

    Physical Examination findings were unremarkable.

    Pertinent Neurologic Examination findings: Drowsy and disoriented with bilateral papilledema, bilateral lateral rectus palsies, bilateral extensor toe sign and positive meningeal signs.

  • LOCALIZATION

    Headache

    Fever

    Projective vomiting

    Diplopia

    Drowsy

    Disoriented

    Bilateral papilledema

    Bilateral LR palsy

    Bilateral Extensor toe sign

    (+) Meningeal Sign

  • LOCALIZATION

    Is there a lesion?

    Upper Motor Neuron

    Lower Motor Neuron

  • LOCALIZATION

    Upper Motor Neuron

    Supratentorial

    Cortical Subcortical

    Infratentorial

    Brainstem Cerebellum

    Spinal Cord

  • LOCALIZATION

    Lower Motor Neuron

    Anterior Horn Cell

    Peripheral Nerve

    Neuromuscular Junction

    Muscle

  • LOCALIZATION

    1 YES There is a Lesion!!!

    2 Upper Motor Neuron

    3 Supratentorial

    4 Diffuse Cortical and Subcortical

  • DIFFERENTIAL DIAGNOSIS Vascular

    Intracerebral or epidural hemorrhage with mass effect, SAH, large hemispheric stroke, venous thrombosis, jugualr vein ligation, SVC syndrome

    Infectious Abscess or empyema,

    meningitis or encephalitis

    Trauma Autoimmune

    Behcets syndrome, systemic lupus erythematosus, sarcoidosis

    Metabolic Endocrine disturbances

    (parathyroid, thyroid, adrenal), hepatic encephalopathy

    Iatrogenic Vitamin A intoxication,

    medications (anabolic steroids, tetracycline, cyclosporine)

    Neoplastic Mass lesion, carcinomatous

    meningitis

    Degenerative Congenital

  • DO NOT MISS!!!

    Herniation

    Acute Hydrocephalus

    Surgical Mass Lesions

  • ANCILLARY PROCEDURES Neuroimaging

    Find the cause!!!

    Check for mass effect, midline shift, effacement of the basal cisterns and sulci, global or focal edema, acute/subacute hemorrhage/infarction

    10-15% TBI patients have elevated ICP despite normal CT

    33% comatose TBI patients with normal head CT and 2 of the following will have increased ICP >40 years old

    Posturing

    SBP

  • ANCILLARY PROCEDURES ICP Monitoring indications

    GCS < 8 with abnormal CT GCS < 8 with normal CT if 2/3 of

    the following risk factors are present

    Age >40 years Posturing SBP

  • INTRACRANIAL PRESSURE MONITORS

  • INTRACRANIAL PRESSURE MONITORS TYPE OF MONITOR PRO CON

    Intraventricular Gold standard, more global ICP measurement, allows for diagnosis

    and treatment

    Highest infection rate (5-20%), risk of hemorrhage (2%)

    Intraparenchymal Infection and hemorrhage rate low (1%), easy to place

    Measures regional ICP, cannot recalibrate placement, drift

    (reading may vary by 3 mmHg)

    Subarachnoid/Subdural Infection and hemorrhage rate low Unreliable measurements, not often used

    Epidural Low risk of hemorrhage compared to Intraventricular and

    intraparenchymal monitors, occasional use with coagulopathic

    liver patients

    Unreliable measurements

  • ANCILLARY PROCEDURES

    Lundberg Waves Marker of critically low intracranial compliance

    Result from: Spiral tissue hypoperfusion

    Progressive arteriolar dialtion

    Increased cerebral blood volume

    Termination spike serves to restore brain perfusion and break cycle of cerebral vasodilation

    Pressure gradients between brain compartments can cause shift and herniation even when the absolute ICP in any given compartment is

  • LUNDBERG WAVES

    Lundberg A (plateau waves): sudden increases in ICP of 20-

    100mm Hg

    Minutes to hours

    Cause reduced CBF/CPP and brain ischemia

    Treat aggressively by increasing CPP and decreasing ICP

    Lundberg B Increases of 5-20 mmHg

    Lasts 1-5 minutes

    Related to respiratory variation

    Characterized by sharpened waveform

  • ANCILLARY PROCEDURES

    Microdialysis technology Placed intracranially in an at-risk

    area

    Measure tissue levels of lactate, pyruvate and glucose

    Brain tissue oxygen monitoring

    Multimodality monitoring Combination of microdialysis

    technology with a brain tissue oxygen sensor, ICP and CBF monitoring

    Offers a biochemical profile of the regional brain environment

  • PREVENTION OF ELEVATED ICP IN BRAIN-INJURED PATIENTS AT RISK

    Elevate the head of the bed to 30-45 degrees.

    Keep head midline to promote venous drainage

    Avoid all free water and maintain normal or elevated serum osmolarity

    Place a central venous catheter to infuse vasoactive or hyperosmolar medications as needed

    Hypotension will exacerbate increased ICP

  • PREVENTION OF ELEVATED ICP IN BRAIN-INJURED PATIENTS AT RISK

    Avoid fever and treat shivering

    Prevent seizures

    Control pain and agitation

    Consider lidocaine 1% 10cc into ETT before suctioning

    Maintain Normocarbia

    Maintain euvolemia with normal saline or albumin

  • TREATMENT OF ELEVATED ICP Consider Urgent Neurosurgical referral

    Evacuation

    Ventricular Drainage

    Decompressive Hemicraniectomy

    Lumbar-Peritoneal Shunting

  • TREATMENT OF ELEVATED ICP

    Optimize CPP Vasopressors

    Isotonic Fluids

    Reducing blood pressure

  • TREATMENT OF ELEVATED ICP: OSMOTIC TX

    Hypertonic saline

    Loading dose: 30mL 23% saline over 10-20mins via central line

    Maintenance dose: 3% saline 1mg/kg/h titrate to a serum Na of 150-155 mEq/h

    Mannitol 20% Loading dose: 1g/kg (or 100g if wt unknown) Maintenance dose: 0.5g/kg ever 4-6 hours titrated

    to a serum osmolarity of 300-320 mOsm or osmololal gap (measure Osm-calculated Osm) of 50 mOsm/kg

    Half-life: 0.16 hour Efficacy: 15-30 minutes Duration of effect: 90 minutes 6 hours

  • TREATMENT OF ICP Mannitol

    Major osmotic diuretic Elevates blood plasma osmolality flow of water from tissues into interstitial fluid and plasma

    Expands circulating volume and decreases blood viscosity increase CBF and cerebral oxygen delivery

    Hypertonic Saline Dehydration of brain tissue,

    reduce viscosity, increase plasma tonicity and regional brain tissue perfusion, increase CO and MAP, decreased inflammatory response to brain injury, restoration of normal membrane potentials, and reduction of extravascular lung volume

  • TREATMENT OF ICP

    Carbonic Anhydrase Inhibitors Acetazolamide 500 mg BID

    or TID Reduce CSF formation

    Loop Diuretic Furosemide 0.5-1.0 mg/kg

    alone 0.15-0.30mg/kg in

    combination with Mannitol Block Na/K/Cl symporter in

    the ascending limb of the loop of Henle

  • OSMOTIC THERAPY

    PROS CONS USE IF AVOID IF

    Hypertonic Saline

    1. Can be given as continuous infusion

    2. Ease of titration 3. Improves CPP 4. Volume expands 5. Effective in lowering ICP in

    patients refractory to Mannitol

    1. Volume Overload 2. Flash pulmonary edema 3. Extreme hypernatremia 4. Rebound cerebral edema

    upon tapering 5. Renal insufficiency (less

    common ) 6. Single report of CPM

    when used in chronic hyponatremia

    Want to volume expand or improve CPP

    Decompensated CHF, care if baseline hyponatremia >24 hours (risk of CPM

    Mannitol 1. Can use through a peripheral line

    2. Bolus dosing

    1. Volume depletion 2. Must replete UO ml/ml

    with saline especially in TBI and SAH

    3. Hypotension 4. Rebound cerebral edema 5. Hypernatremia 6. Renal insufficiency

    (reversible, seen if >200g used daily or osmolal gap >60-75 mOsm/kg)

    Want to diurese, no central line access

    Renal failure, hypotension

  • TREATMENT OF ELEVATED ICP

    Short-term hyperventilation to PaCO2 of 25-30 mmHg.

    Barbiturates Pentobarbital: 5-20 mg/kg bolus followed by 1-4

    mg/kg/h titrated to burst suppression on EEG

    Can be used in patients refractory to ICP treatments

    Induced hypothermia to 32 to 340C

    Steroids

    Paralytics