ICP elevation

Physiologic principles of ICP:

3 main factors of volume within the cranium of the normal adults: The intracranial volume is ~1900/cm3. Brain: 89%, blood: 10%, and CSF: 10%.

• Brain, 1400. 

• Blood, 150 mL

• CSF, 150 mL.

Normal intracranial pressure in adults: 5 - 20 cm H20 (4 - 15 mmHg). (1 cm H2O = 0.735 mm Hg); 1 mm Hg = 1.36 cm H2O).

Control of ICP-compliance: Ability of brain to accommodate changes in the intracranial volume without significant changes in ICP. Compliance: change in volume/change in pressure.

As per Monroe-Kellie doctrine: if the volume of one of the three compartments increases, the volume of another must decrease to maintain normal ICP (0-20 mm Hg).

Intracranial compliance. As the intracranial vault is a rigid fixed container, any ▲ intracranial volume →→ ▲ ICP.  Initially, as volume is added to the intracranial space, increases in pressure are minimal because of the highly compliant nature of the intracranial contents; as intracranial volume increases, CSF is displaced through the foramen magnum into the paraspinal space, and blood is displaced from compressed brain tissue. When these mechanisms are exhausted, however, intracranial compliance decreases, and further increases in intracranial volume lead to dramatic elevations of ICP. The brain may then begin to herniate because of increasing ICP, or if ICP increases above mean arterial pressure, then cerebral perfusion pressure will drop and ischemia result.

Autoregulation of blood flow:  The ability of brain to develop a mechanism to maintain blood flow over and fairly wide range of BP as a consequence of cerebrovascular resistance. Changes in cerebral perfusion pressure between 60 and 100 mm Hg do not alter cerebral blood flow because of autoregulation. Above or below these pressures, flow is related to pressure.

• CSF is produced at a rate of 20 mL/hr, resulting in the formation of ~500 mL/day.

• Normal Cerebral Blood Flow (CBF): 50 - 60 ml/100 g of brain tissue/min

• CBF: 20 ml/100 g/min – neuronal tissue is impaired, but salvageable if blood flow is restored.

• CBF: < 10 ml/100 g/min – neuronal tissue becomes irreversibly damaged.

  • Brain receives 15% of the cardiac output uses 20% oxygen consumed by the body.

Principal factors affecting CBF:

• Cerebral perfusion pressure (CPP)

• CPP = MAP – (ICP or CVP, whichever is greater)

• CPP: 50 – 150 mm Hg (>70)

• ICP: <20 mm Hg

• CBF increased in metabolic acidosis and hypercapnea.

• CBF decreased in metabolic alkalosis and hypocapnea.

▼ SABP - 2° to dehydration, pharmacologic, mechanical →→ ▼ CPP →→  ▲ Vasodilation →→ ▲ CBV →→ ▲ ICP →→▼ CPP

Fundamental mechanism of 2° ischemic brain injury:

CSF and CBV can be redistributed initially.  By the time ▲ ICP occurs, intracranial compliance is severely impaired.  Any small ▲ CSF volume, edema, mass lesion or ▲ CBV →→ significant ▲ ICP and ▼ CPP.

Common signs and symptoms of ▲ ICP:  Headache, altered mental status, especially irritability and depressed level of alertness and attention, nausea, vomiting, papilledema, visual loss, diplopia, Cushing’s triad: hypertension, bradycardia, and irregular respirations.

Conditions Associated with Increased ICP

• Intracranial mass lesions

  • SDH, EDH, ICH, brain tumor, brain abscess

• Increased CSF volume (or resistance to outflow)

  • Hydrocephalus

  • Benign Intracranial HTN (pseudotumor cerebri)

• Increased brain volume (cytotoxic cerebral edema)

  • Cerebral infarction

  • Global hypoxia-ischemia

  • Reye's syndrome

  • Acute hyponatremia

• Increased brain and blood volume (vasogenic cerebral edema)

  • Head trauma

  • Meningitis

  • Encephalitis

  • Lead encephalopathy

  • Eclampsia

  • HTN encephalopathy

  • Dural sinus thrombosis

  • SAH

Vascular: ICH, EDH, SAH, malignant stroke, venous thrombosis, jugular vein ligation (radical neck dissection), SVC syndrome.

Infectious: Abscess or empyema with mass effect. Any meningitis or encephalitis (especially

brucellosis, Lyme disease, cryptococcosis)

Inflammatory: Behçet’s syndrome, SLE, sarcoidosis

Toxic:  Vitamin A intoxication

Trauma: TBI with edema

Metabolic/endocrine: adrenal insufficiency, hyper- or hypoparathyroidism, hyperthyroidism, hepatic encephalopathy.

Neoplastic: mass lesion, carcinomatous meningitis

Medications that raise ICP:

Amiodarone, cytarabine, cyclosporine, tetracylines, vitamin A, retinoic acid, lithium carbonate, sulfa antibiotics, and nalidixic acid. Anabolic steroids.

Succinylcholine may raise intracranial pressure (do not use in intubation)

Other: Hydrocephalus, Pseudotumor cerebri, Reye’s syndrome, eclampsia

ICP monitoring required:

• Stroke, TBI GCS 3 to ≤8 or less, and abnormal CT.

• Also indicated in patients with severe TBI who have normal CT if they have 2 of the following characteristics:

  • Age >40 years

  • Unilateral or bilateral posturing

  • SBP <90 mmHg.

• Altered level of consciousness with multiple system trauma.

• Brain imaging shows intracranial mass effect or global brain edema.

  • Patients with large hemispheric infarction (greater than 50% middle cerebral artery territory)

  • High-grade (Hunt and Hess grade greater than 2)

  • Subarachnoid hemorrhage(SAH) with radiologic evidence of hydrocephalus

  • Intraparenchymal hemorrhage with poor neurologic examination (GCS less than 9) or with intraventricular hemorrhage and risk of developing obstructive hydrocephalus

  • Sagittal sinus thrombosis with poor neurologic examination

  • Fulminant hepatic failure

  • DKA

• Prognosis is such that aggressive treatment in the ICU is indicated.

Clinical features of raised ICP:

• Depressed level of consciousness (lethargy, stupor, coma)

• HTN, with or without bradycardia

• Decreased RR

• Headache

• Vomiting

• Papilledema

• CN VI palsies

• Signs of brain stem compression: unreactive pupils, loss of EOM, hyperventilation, motor posturing (flexion or extension)

Dx is confirmed only with ICP measurement /monitoring:

• GCS <8

• Severe head trauma

Intraventricular catheter: Once inserted, a ventricular catheter is connected to both a pressure transducer and an external drainage system via a 3-way stopcock.  The major advantage to ventricular catheters is that they allow treatment of increased ICP via drainage of CSF.  The main disadvantage is the high infection rate (10% - 20%), which increased dramatically after 5 days. Best method of measuring ICP.

Intraparenchymal probe (Camino, Codman): These devices are easy to insert and very accurate, and the infection rate is exceedingly low (~1%).

Subacrachnoid

Epidural transducer (Gaeltec): These devices are inserted deep in the inner table of the skull and superficial to the dura.  They are associated with a minimal infection rate but have a tendency to malfunction and to have a baseline drift (>5 - 10 mm Hg) after more than a few days of use.

Pathological ICP waves:

1. Lundberg A wave (plateau waves).  These are dangerous elevations of ICP; they can reach levels of 50-80 mm Hg and generally last from 5 min - 20 min in duration.  When severe, they are associated with reduced CPP (less than 60 mmHg) and CBF, with global hypoxic-ischemic injury. Presence of A waves suggests failing compliance of the brain to ICP and risk for global cerebral ischemia

2. Lundberg B waves.  These are lesser in amplitude (20-50 mmHg) and duration 1-2 min and therefore less dangerous than Lundberg A waves.  Clinically, they are a useful marker of abnormal autoregulation and reduced intracranial compliance.

3. Lundberg C waves. Normal, last 4-5 min, amplitude <20 mm Hg. 

Complications: 

• Herniation syndromes.

  • Duret’s hemorrhages of brainstem: result from shearing and traction on the basilar perforators and compression of their intramedullary portions. 

  • Pituitary stalk shearing (diabetes insipidus)

  • Bilateral occipital infarctions from compression of posterior cerebral artery.

  • Tentorial (uncal): Uncus is displaced over edge of tentorium cerebelli, trapping ipsilateral CN III (dilation of pupil) and compressing midbrain. If herniation continues, both central and tonsillar herniation may occur. Ipsilateral CN III palsy usually is first sign, followed by loss of consciousness and brainstem findings. Uncal herniation may also compress posterior cerebral artery, resulting in infarction. 

  • Infratentorial: 

    • Upward cerebellar: cerebellar vermis ascends rostral to tentorium cerebelli, compressing the midbrain, may compress the cerebral aqueduct

    • Tonsillar: Cerebellar tonsils herniate through foramen magnum, compressing the medulla.

Treatment measures for elevated intracranial pressure:

1. Elevate head of bed 30° - 45°, if spine cleared.

2. Consult NS: EVD, Lumbar drain, shunt.

3. Insert ICP monitor - ventriculostomy vs parenchymal device vs epidural monitor.

   • Ventriculostomy is preferable to ICP monitoring devices placed in brain parenchyma because it allows CSF drainage as a method of ▲ ICP.

   • Parenchymal ICP monitoring is appropriate for Pts with diffuse edema and small ventricles, making placement of ventriculostomy difficult, or if coagulopathy precludes ventriculostomy due to increased H'gic complications.

4. General goals:  maintain ICP <20 mmHg and CPP ≥60 mmHg.  For ICP >20-25 mmHg for >10 min:

• 1. Drain CSF via ventriculostomy, 5-10 mL of CSF should be removed. If blocked - Consider repeat CT scan  of head. Emergent craniotomy or hemicraniectomy is the ultimate intervention for an ICP crisis.

  2. Sedation patient in a quiet and motionless state. 

     • Morphine 2-5 mg IVP q1h

     • Fentanyl (50 mcg/mL) 25-100 mcg IVP. For sustained sedation, give fentalyl IV infusion 4 mg/250 mL NS. Start at 5 mL/hr (1.33 mcg/min); the range is 8 - 23 mL/hr (2-6 mcg/min).

     • Propofol IV (10 mg/mL) is powerful, sedative-hypnotic, rapidly reversible than fentanyl. 5-50 mcg/kg/min (0.3 - 3 mg/kg/hr); this translates into 2-20 mL/hr for a 70 kg person.

  3. CPP opitimization: vasopressors to maintain >70 mmHg or anti-HTN to lower <120 mmHg. Optimum range: 60 - 90 mmHg

     • If CPP >120 mmHg and ICP >20 mmHg, BP should be lowered. However, CPP should not be allowed to fall to <70 mmHg. Control HTN by the following:

       • Labetalol IV (5 mg/mL) is a combination of alpha-1 and beta-1 blocker.  20 - 80 mg IVP q10-20 mins.  Once desired BP is attained, start drip 200 mg/200 mL NS (1 mg/mL) at 2 mg/min (120 mL/hr) and titrate.

       • Nicardipine IV, 25 mg/250 mL NS at 5 mL/hr (8 mcg/min) and titrate.

     • If CPP <70 mmHg and ICP >20 mmHg, BP should be elevated and CPP should be raised >70 mmHg; this can lead to a reflex reduction in ICP by reducing the cerebral vasodilation that occurs in response to inadequate perfusion. Pressor agents used:

       • Norepinephrine (4 mg/250 mL NS), start at 8 mcg/min (30 mL/hr), adjusted to maintain desired target CPP (2-12 mcg/min)

       • Phenylephrine (10 mg/250 mL) is a pure alpha agonist. Start at 15 mL/hr (10 mcg/min) and titrate it upward to a maximum of 200 mcg/min.

  4. Intubate and hyperventilation - to PaCO2 30 mmHg

  5. Pressor therapy - phenylephrine, dopamine, or norepinephrine to maintain adequate MAP to ensure CPP ≥60 mmHg (maintain euvolemia to minimize deleterious systemic effects of pressors)

  6. I/O, foley cath.

  7. Osmotherapy:

     • Mannitol (20%) 0.25 - 1 g/kg IV rapid infusion bolus (maintain serum Osm ~310 mOsm), follow up doses 0.25 g/kg IV q8hr; or hypertonic saline (30 mL, 23.4% NaCl bolus x 30 min via CVC

     • When the osmolar gap is above the baseline or extremely high (greater than 15 mOsm/L), the mannitol dose should be lowered or maintained to prevent renal toxicity.

     • Because mannitol is a potent diuretic agent, intravascular volume must be vigilantly monitored and replaced with isotonic fluid to maintain euvolemia.

     • If the patient is in complete renal failure, mannitol is of little value, and the patient should be dialyzed to a higherosmolarity using continuous dialysis.

     • Hypertonic saline can be administered as a continuous infusion, typically with 3% NaCl at the rate of 10 mL/h to 40 mL/h, or as bolus administration, with either 3% NaCl (250 mL to 300 mL bolus over 20minutes every 4 to 6 hours as needed) or 23.4% NaCl (typically 30 mL of 8008 mOsm/L solution every 4 to 6 hours as needed).

     • In addition to reducing the brain volume by creating an osmotic gradient, hypertonic saline also expands intravascular volume and increases cardiac output without significant nephrotoxicity or diuretic effect.

     • To prevent rebound cerebral edema, hypertonic saline should be tapered slowly after prolonged use.

  8. NS at 100 mL/hr

  9. Prevent seizures. Fosphenytoin 10-20 mg/kg loading dose, than 3-5 mg/kg/day is the preferred agent for seizure prophylaxis.

  10. Arctic sun cooling. Treat fever aggressively. APAP, 650 mg PO q4hr, indomethacin, 25 mg PO q6hrs, or a cooling blanket or arctic sun cooling to maintain euthermia 35.5°C can be effective.

  11. Glucocorticoids - dexamethasone 4 mg q6h for vasogenic edema from tumor, abscess (avoid glucocorticoids in head trauma, ischemic and H'gic stroke)

  12. Consider 2nd tier therapies for refractory elevated ICP

      • High-dose barbiturate therapy ("pentobarb coma"). Loading dose of pentobarbital, 10-20 mg/kg, repeat 5 mg/kg boluses, until a state of flaccid coma is attained (pupillary reactivity is intact). Dopamine, phenylephrine should be ready at hand at bedside to maintain BP and CPP.

        • It uses a physiologic flow-metabolic feedback mechanism called neurovascular coupling, which regulates CBF to match the demand of the cerebral metabolism.

        • If this coupling mechanism is intact, lowering the cerebral metabolism will eventually reduce CBF by vasoconstricting the small arterioles until the blood flow matches the metabolic demand.

      • Maintenance dose of pentobarbital, 1-8 mg/kg/hr (500 mg/250 NS), starting at 35 mL/hr. Continuous EEG monitoring should be used, with the infusion titrated to a burst-suppression pattern.

        • Minimal dose of barbiturates should be used to avoid hypotension, sepsis, renal and hepatic dysfunction, negative cardiac inotropic effect (vasopressor are needed to counter this side effect). The vasopressor should be norepinephrine (both alpha and beta agonist properties, conferring positive cardiac inotropic effect and peripheral vasoconstriction).

        • If adequate MAP and CPP cannot be maintained, barbiturate induced coma should not be attempted as this could result in cerebral ischemia.

      • If ICP is adequately maintained for 24-48 hrs. It can be d/c abruptly, with a washout period lasting from 24-96 hrs.

      • Failure of ICP to respond to pentoparbital is an ominous sign.

      • Aggressive hyperventilation to PaCO2 <30 mmHg

      • Hypothermia 32°C to 34°C  can reduce ICP that is refractory. it can at most decrease ICP by 10 mmHg. Not found to improve outcome.

      • Decompressive Hemicraniectomy

      • Mass resection

  13. Throughout ICP treatment, consider repeat head CT to identify mass lesions amenable to surgical evaluation.

Kjelberg ("shellberg): is decompressive bifrontal craniectomy with removal of frontal bone placed in a freezer for possible later replacement.

GCS <8 = abnormal CT = ICP monitoring

GCS <8 or less, normal CT = ICP monitoring

Becker’s drain: tap CSF in a safe and sterile fashion

P1>P2>P3 - normal

P2 < P1 = not good, compromised cerebral compliance.

Lundberg A wave = ▲ 20 - 100 mm Hg

Lundberg B wave = 5 - 20

CPP = (MAP - ICP). 60-100

Trauma: CPP <70.

Treatment of ▲ ICP: hyerosmolar Tx with hypertonic saline.  Mannitol goes out of the BBB and crystalizes, latches on the brain parenchyma and causes more cytotoxic edema.

Hypothermia, sedation

If needed hyperventilate to reduce ICP by vasconstriction.  Prolonged hyperventilation → global ischemia.  Use only as rescue therapy.

Mannitol, 20%, 1 g/kg bolus, f/up 0.5 g/kg q4-6h. Keep Sr. Osm: 320, check q6h.

Hypertonic saline 23.4% or 14.6%.  c/w sodium acetate. 1 cc/kg/h. Check Na (150-155) q6h.  Problems increases chloride level in renal failure.