Raised ICP measures

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Raised Intracranial Pressure (ICP) - Management

Physiology Recap

The Monro-Kellie doctrine states the skull is a rigid compartment containing brain tissue (~80%), CSF (~10%), and blood (~10%). Any additional volume initially displaces venous blood and CSF. Once this compensation is exhausted, ICP rises exponentially - small further increases cause rapid deterioration and herniation.

Normal ICP: 5-15 mmHg

Key equation:

CPP = MAP - ICP Normal CPP = 75-105 mmHg (MAP 90-110 minus ICP 5-15)

Monro-Kellie ICP curve showing compensation, decompensation, and herniation

Figure: As mass lesion size increases, ICP remains near-normal during compensation, then rises exponentially past the point of decompensation, culminating in herniation. (Bailey & Love, p. 382)

Indications for ICP Monitoring

ICP monitoring is recommended in:

Severe TBI (GCS ≤ 8) with an abnormal CT scan
Severe TBI with normal CT if ≥ 2 of: age >40 years, unilateral/bilateral motor posturing, systolic BP <90 mmHg
Acute subarachnoid hemorrhage with coma or neurological deterioration
Intracranial hemorrhage with intraventricular blood
Ischemic MCA stroke (malignant)
Fulminant hepatic failure with coma and cerebral edema on CT
Global cerebral ischemia/anoxia with cerebral edema on CT

ICP > 20 mmHg is associated with unfavorable outcomes in TBI. Treatment threshold is generally ICP > 20-22 mmHg or CPP < 50-60 mmHg.

ICP monitors: Ventriculostomy (gold standard - allows CSF drainage + measurement), parenchymal, subdural, or epidural transducers.

Treatment Protocol

The measures below should be administered simultaneously, not sequentially.

Figure: ICP treatment protocol - Plum & Posner's Diagnosis and Treatment of Stupor and Coma, p. 541

Step 1 - Immediate Stabilization (All Patients)

Measure	Detail
Airway/C-spine	Rapid sequence intubation (RSI) with IV lidocaine premedication
Head positioning	HOB elevated to 30 degrees, head midline (optimizes jugular venous drainage)
Hyperventilation	Target PCO2 26-30 mmHg - vasoconstrictive, temporizing measure only. Never let PCO2 drop below 25 mmHg
Oxygenation	Maintain SpO2 >95%, confirm with ABG
MAP maintenance	Target MAP ≥ 80 mmHg using isotonic fluids (0.9% NaCl 100-150 cc/hr); vasopressors if needed (phenylephrine 10-1000 mcg/min or norepinephrine 2-100 mcg/min)
Avoid hypotonic fluids	Worsens cerebral edema
Pain control	Fentanyl 20-200 mcg/hr IV (short-acting, least BP effect); morphine 2-4 mg IV q2-4h as alternative
Sedation/agitation	Propofol 0.1-5 mg/kg/hr or benzodiazepines
Fever control	Antipyretics (acetaminophen); cooling devices if needed (control shivering)
Seizure control	Treat promptly
Steroids	Only for vasogenic edema (brain tumors, abscess) - NO role in TBI or cytotoxic edema

Step 2 - Head CT and Surgical Options (Definitive Treatment)

Get urgent CT head for all patients with suspected raised ICP.

Intervention	Indication
External ventricular drain (EVD)	Hydrocephalus, intraventricular hemorrhage - allows CSF drainage + ICP monitoring
Mass/hematoma evacuation	Space-occupying lesions, especially cerebellar hemorrhages
Decompressive craniectomy	Refractory raised ICP, malignant MCA infarct

Do not delay empiric pharmacological treatment while awaiting imaging when herniation is clinically suspected.

Step 3 - Osmotherapy

Used when general measures are insufficient.

Mannitol (first-line osmotic agent):

Dose: 0.5-1 g/kg (some sources: 1-2 g/kg) IV over 15 minutes as bolus
Replaces urinary losses with normal saline
Monitor serum osmolality - caution if >330 mOsm/kg; osmol gap should stay ≤ 55 mOsm/kg
Mechanism: osmotic gradient draws water from brain into vasculature; also reduces blood viscosity

Hypertonic saline (alternative):

23.4%: 0.5-1 mL/kg IV bolus over 15-20 minutes via central line
3%: 500 mL IV if only peripheral access
Caution in: chronic hyponatremia, cardiac instability, pulmonary edema
Target serum sodium <160 mEq/L
Check serum Na+ and osmolality regularly for both agents

Step 4 - Refractory ICP (Last Resort)

Barbiturate coma:

Pentobarbital: load 20 mg/kg IV over 60 minutes, then 1 mg/kg/hr maintenance
Titrate up to 3 mg/kg/hr to achieve burst suppression on EEG (4-6 bursts/min)
Major side effect: hypotension - monitor closely
Alternative: thiopental

Hypothermia: Role in TBI is unclear; not routinely recommended.

Brain Herniation Syndromes (Consequence of Uncorrected Raised ICP)

Figure: Brain herniation. (1) Subfalcine - cingulate gyrus under falx. (2) Midline shift. (3) Uncal - temporal lobe over tentorium, compresses CN III (pupil dilation). (4) Central herniation. (5) Tonsillar - cerebellar tonsils through foramen magnum, compresses medullary vasomotor and respiratory centres. (Bailey & Love, p. 382-383)

Syndrome	Location	Key Sign
Subfalcine	Cingulate under falx	Midline shift
Uncal (transtentorial)	Temporal lobe over tentorium	Ipsilateral dilated pupil (CN III palsy)
Central	Downward displacement	Bilateral signs, Cushing's triad
Tonsillar	Cerebellar tonsils through foramen magnum	Cushing's triad: hypertension + bradycardia + irregular respiration

Cerebral Perfusion Pressure (CPP) Targets

Target CPP 50-70 mmHg (exact target debated; Brain Trauma Foundation recommends 60-70 mmHg)
Can increase CPP by raising MAP (vasopressors) or by reducing ICP (measures above)
CPP <50 mmHg = cerebral ischemia risk
Cerebral autoregulation normally maintains constant CBF with MAP 50-150 mmHg, but this is impaired in trauma

Sources: Plum & Posner's Diagnosis and Treatment of Stupor and Coma (pp. 541-543); Bailey & Love's Short Practice of Surgery, 28th ed. (pp. 382-383); Schwartz's Principles of Surgery, 11th ed. (pp. 475-476)

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