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