A. Neurologic Intensive Care
[Figure] "Intracranial Pressure"

1. Mostly management of increased Intracranial Pressure (ICP)
2. Includes brain tumors, aneurysms, trauma, encephalitis, stroke, near-drowning
3. ICP increase is a problem due to brain compression, ischemia, herniation

B. Normal Contents of Intracranial Vault

1. Brain
2. Cerebrospinal fluid (CSF)
3. Blood
4. All contained within a non-compliant skull (Vault)

C. Increased Intracranial Pressure (ICP)

1. CSF production increased
2. Increased blood flow (eg. fever, seizures)
3. Hemorrhage
4. Tumors
5. Foreign bodies
6. Cerebral edema (eg. due to trauma or infection)

D. Cerebrospinal Fluid (CSF)

1. Approximately 5% of intracranial volume (75mL)
2. Approximately 10% of total CNS volume (150mL)
3. Produced by choroid plexus 14-36mL/hour
4. Reabsorption
   1. Arachnoid villi
   2. Superior surfaces of ceregral hemispheres
   3. Base of the brain, around spinal nerve roots

E. Blood Volume

1. Cerebral Blood Volume Determinants
   1. Cerebral blood flow (CBF)
   2. Size of capacitance vessels within the brain.
2. CBF is determined primarily by CPP (cerebral perfusion pressure).
3. CBF = CPP/Resistance. CPP = MAP - ICP (or Central Venous P, whichever is higher)
4. CPP ~ 90 - 15 mm Hg = 75 mm Hg (range 70-80) normally
5. Major capacitance vessels, veins and sinuses, contain 80% of cranial blood

F. Types of Edema

1. Vasogenic
   1. Permeability of brain capillary endothelial cells increases
   2. Seen in brain tumors, abscess or hemorrhage
   3. Reponds well to glucocorticoids
2. Cytotoxic
   1. Failure of intracellular ATP dependent pumps
   2. Hypoxic ischemia (e.g. stroke, vascular sludging), Head trauma
   3. Poor response to glucocorticoids
3. Interstitial: Hydrocephalus

1. Normally, brain can tolerate small increase in intracranial volume without affecting ICP
2. In abnormal states, ICP can increase rapidly within small change in Intracranial volume
3. Slow, but fairly large, increase in volume can often be tolerated better than more moderate rapid increase, eg. the case with slow growing brain tumors

B. Intracranial Pressure and Blood Flow (CBF)

1. As described above, blood flow depends on cerebral perfusion pressure
   1. This is determined by systemic mean arterial pressure (MAP) - downstream P
   2. This downstream pressure is the greater of either CVP or ICP
2. Over a range of MAPs, CBF is maintained at fairly constant levels
3. This includes an ~100 mmHg range from 60-160 mmHg
4. Increases in IBP from any cause may compromise CBF
5. ICP Relationships
   [Figure] "Intracranial Pressure"

C. Other Determinants of Cerebral Blood Flow

1. Increased PaCO2 will increased CBF. This is the main determinant of CBF
   1. Note that medullary receptors detect CSF CO2 levels
   2. CO2 from blood freely diffuses across medulla to CSF where CSF pH is sensed
   3. Hyperventillation, which decreases PaCO2 will decrease CBF (and ICP)
   4. Levels of PaCO2 around 25-30mmHg are recommended for decrease of ICP
2. Increased PaO2 will decrease CBF
   1. Increased Brain metabolism will increase O2 demand and increase CBF
   2. Siezures and infection both increase O2 demand

1. Length of hypoxia
2. Duration of coma

B. Headache

1. Subacute or chronic increased ICP: bifrontal or bioccipital
2. Accompanied by Nausea and/or vomiting

C. Cushing Triad (Usually Late Signs)

1. Systemic hypertension
2. Bradycardia
3. Abnormal Respiration

D. Long Term Chronic ICP Increases

1. Bilateral frontal lobe dysfunction: inattentive, distraction, cannot plan or sustain
2. Cranial nerve syfunction
   1. CN VI (Abducens) usually first affected due to long course and proximity to Clivas bone
   2. CN VI symptoms include crossed eyes, usually seen in children and lateral gaze diplopia
   3. CN III also affected early in course of increased ICP
   4. Symptoms of ptosis and decrease pupillary reflex or "blown" pupil

E. Herniation

1. Subfalcial herniation
2. Temporal lobe-tentorial herniation
3. Cerebellar-foramen magnum herniation
4. Assess for signs of cerebral herniation
   1. Signs include: fixed, dilated or asymmetric pupils OR
   2. Asymmetric motor responses or extensor posturing OR
   3. No movement on administration of noxious stimuli
   4. In the field, these signs should prompt immediate hyperventilation

F. Brain Oxygen Utilization

1. Place jugular Oxygen sensor or take blood sample from internal jugular
2. Determine arteriolar pO2, look at brain extraction of oxygen

G. Edema

1. Trauma, ischemia, hydrocephalus, and infection can lead to edema in brain
2. Changes in endothelial cells lead to vasogenic edema
3. Cytotoxic edema from ischemia, and interstitial edema from hydrocephalus
4. Vasogenic edema from trauma

H. Treatment of Increased ICP Overview

1. Mechanical Ventilation - Iatrogenic Hypocapnia (not generally recommended)
2. Medications to reduce ICP
3. Medications or cerebrospinal fluid drainage to reduce edema
4. Maintain mean arterial blood pressure >90mmHg
5. Goal is to maintain cerebral perfusion pressure >70 mmHg

I. Mechanical Ventilation

1. Hyperventilation
   1. Reduction of PaCO2 will reduce CBF and therefore reduce ICP
   2. However, CSF pH will be adjusted over the next 4-6 hours
   3. Thus, hyperventilation will only work for 4-6 hours
   4. Hypocapnia causes vasoconstriction and may exacerbate brain injury [4]
2. Patient must be weaned slowly from hyperventilation, or:
   1. PaCO2 will increase
   2. Brain CSF (now with a normal pH) will become acidic
   3. CBF will increase tremendously, even fatally
3. Hypothermia
   1. Keep core temperature > 30°C
   2. Reduces cerebral metabolism, particularly important in fever
4. Pleural Pressure
   1. Important to realize that increased pleural pressures can increase ICP
   2. Especially important in PEEP assisted ventillation for chest trauma
5. Utility of Iatrognic Hypocapnia [4]
   1. In vast majority of patients, iatrogenic hypocapnia is detrimental
   2. Causes vasoconstriction and increased pulmonary shunting
   3. Exacerbates tissue hypoxia and cell death
   4. Increases metabolic demands on cells to counteract pH changes
6. Hypocapnia should only be induced after careful consideration of risks and benefits

J. Pharmacologic Agents [3]

1. Reduction of arteriolar and cerebral PaCO2
   1. Acetazolamide (Diamox®)
   2. Blocks excretion of bicarbonate (HCO3-)
2. Treatment of fevers
   1. Fever increase cerebral metabolism and blood flow
   2. Antibiotics, antipyretics
3. Seizure medication
   1. Seizures increase cerebral metabolism and blood flow
   2. Phenytoin (Dilantin®) - standard 1.0gm load (maximal rate 50mg/minute)
4. Barbiturates
   1. Decrease brain metabolism, thus decrease CBP
   2. Significant respiratory depression and autonomic instability
   3. Generally use only on patients on ventilator
   4. Intensive hemodynamic monitoring required
   5. Pentobarbital may be used
5. Nimodipine indicated for subarachnoid hemorrage
6. Blood pressure control as needed (hypotension increases cerebral perfusion)
7. Control of edema
   1. Vasogenic: tumors and some abscesses will respond to glucocorticoid therapy
   2. Cytotoxic and Interstitial edema do not respond well to glucocorticoids
   3. Dexamethasone (Decadron®): 4-10mg iv q4-6 hours may be used in some situations
8. Use of diuretics is may be indicated
   1. Mannitol: may cause transient rise in ICP; dose is 0.5-1gm/kg over 20 minutes
   2. Furosemide (Lasix®) or other loop agent may also be used
   3. Conern for reduction in blood pressure - may require vasoconstrictive agents
9. Ultrafiltration to Remove Plasma Volume
   1. 500cc of plasma may be removed in a session
   2. Probably most useful in patients with poor renal function (poor diuretic response)
10. Transient Hypothermia [3]
    1. Hypothermia for 10-14 hours with core body temperature down to 32-33°C
    2. May be effective, particularly in elevated ICP associated with severe liver failure

K. Intracranial Hypotension [2]

1. Present with postural headaches
2. Etiology
   1. Spontaneous
   2. After lumbar puncture
   3. Head trauma
   4. Shunt placement
   5. Dural tears
3. Pathophysiology
   1. Decreased intracranial volume leads to reduced pressure
   2. Reduced pressure leads to increased dural venous blood volume
   3. Nerve palsy may occur due to downward displacement of the brain stem
   4. Subdural hygroma may form
4. Diagnosis
   1. Rule out other causes is critical: AIDS, Lyme Disease, Neurosyphilis, meningitis, etc.
   2. Retinal venous pulsations may be seen
   3. Headache is usually relieved by recumbancy
   4. Diffuse dural enhancement with gadolinium on MRI scans
   5. Small subdural collections of fluid may also be present on MRI
   6. CSF opening pressure on lumbar puncture is <60mm H20, may be unmeasurable
   7. CSF protein level is usually elevated, lymphocytes usually present
5. Draining subdural fluid collections may improve symptoms
6. Bedrest, caffeine, and/or oral acetaminophen (Tylenol®) may relieve symptoms

References

1. Cody CM. 1992. Am Fam Physician. 45(4):1671
2. Jalan R, Damink SWMO, Deutz NEP, et al. 1999. Lancet. 354(9185):1164
3. Ghajar J. 2000. Lancet. 356(9233):923
4. Laffey JG and Kavanagh BP. 2002. NEJM. 347(1):43