Causes of Increased ICP

• Trauma, tumors, hemorrhage.
• Inflammation or infection.
• Obstruction of cerebrospinal fluid (CSF) drainage:
  • CSF is produced in the brain’s ventricles and drains into the jugular vein.
  • Blockage causes CSF accumulation, increasing volume and pressure.

Pathophysiology of ICP

• Normal: Brain, blood, and CSF are within a rigid skull.
• Increase in fluid (blood, CSF, edema) raises pressure.
• Brain tissues are pressure-sensitive and can become ischemic if pressure cuts off blood flow.

Body’s Compensation for Increased ICP

• Initial response:
  • Shifting CSF from ventricles into the spinal canal to reduce intracranial volume.
  • Results in ventricle shrinking.
• Cerebrovascular Vasodilation:
  • Local hypoxia causes nitric oxide release, dilating vessels.
  • Temporarily increases blood flow to brain to compensate.
• Vasoconstriction:
  • Increased volume and pressure lead to pinching off of brain capillaries.
  • Reduced cerebral blood flow, worsening ischemia.

Worsening Condition

• Persistent ICP causes capillary constriction, decreasing oxygen supply.
• Brain becomes hypoxic.
• The medulla oblongata triggers Cushing’s reflex.

Cushing’s Reflex (Triad)

• Triggered by brain ischemia.
• Goal: Maintain blood flow to brain but often worsens ICP.

Cushing’s Triad: Classic Signs of Increased ICP:

1. Systemic hypertension:
   • Increased systolic blood pressure (fight or flight response).
2. Bradycardia:
   • Slowed heart rate (baroreceptor reflex in carotid arteries).
3. Reduced respiration rate:
   • Hypoxia and low CO₂ levels reduce respiratory drive.
   • Leads to hypoventilation, hypoxia, hypercapnia exacerbates injury.

Pathophysiology of Cushing’s Triad

• Brain ischemia triggers sympathetic activation → vasoconstriction → high blood pressure.
• Baroreceptors detect high pressure → reflex bradycardia.
• Increased ICP reduces CO₂ levels (hypocapnia) → respiratory depression.

Outcomes and Risks

• Temporary increase in blood flow relieves ischemia briefly.
• Vicious cycle:
  • Increased pressure → more ischemia → further brain damage.
• Progression:
  • Decreased neuronal function.
  • Unresponsive coma.
  • Potential brain death if ICP persists.

Consequences of Unmanaged ICP

• Progressive hypoxia:
  • Neurons require oxygen (survive 3-5 mins without it).
  • Prolonged ischemia leads to neuronal death.
• Herniation syndromes:
  • Displacement of brain tissue within cranium and/or through skull openings (e.g., foramen magnum).
  • Dangerous and often fatal.

Brain Herniation Types and Effects

Types

• Supratentorial herniation:
  • Downward movement of brain tissue over the tentorial notch.
• Uncal herniation:
  • Displacement of the uncus of the temporal lobe.
  • Compresses cranial nerve III → fixed dilated pupil, eye deviation.
  • Can impair RAS → coma.
• Tectal (midbrain) herniation:
  • Causes altered consciousness and posturing.
• Infratentorial herniation:
  • Downward herniation through the foramen magnum.
  • Compresses brainstem, leading to cardiovascular and respiratory arrest.

Effects

• Compression of vital centers.
• Loss of motor and sensory function depending on herniation site.
• Deep coma and death if untreated.

Signs and Symptoms of Elevated ICP

Key Signs

• Systemic hypertension:
  • High systolic blood pressure.
  • Increased pulse pressure (systolic – diastolic).
• Altered consciousness:
  • Progress from lethargy and confusion to unresponsiveness.
  • Decreased responsiveness often indicates worsening ICP.

Eye and Reflex Signs

• Dilated, fixed pupils (blown pupils):
  • No response to light due to cranial nerve III (oculomotor) compression.
  • Unilateral or bilateral dilation depending on lesion location.
• Visual changes:
  • Swelling optic disc (papilledema).
• Abnormal eye movements:
  • Oculocephalic (Doll’s eyes) reflex: eyes move opposite to head movement if brainstem intact.
  • Oculovestibular (caloric) reflex: eyes gaze toward cold water, away from warm.

Headache and Vomiting

• Severe headache due to meningeal stretching.
• Projectile vomiting caused by pressure on vomit center in medulla.

Diagnostic Methods for Elevated ICP

Imaging

• CT scans: Detect tumors, hemorrhages, swelling.
• MRI: Detailed brain structure, edema, herniation.
• Angiography: Visualize blood flow and vessel integrity.
• Ultrasound: Transcranial, when feasible.

Lumbar Puncture

• Measures CSF pressure:
  • Normal: <20 mm Hg.
  • Elevated >20 mm Hg indicates increased ICP.
• CSF analysis:
  • Blood (hemorrhage).
  • White blood cells (infection).
  • Protein (tumor, inflammation).
  • Color (pink for hemorrhage).

Additional Tests

• EEG: Brain activity monitoring.
• Monitoring:
  • Frequent assessment of vital signs.
  • Ophthalmic exam for papilledema.

Treatments

• Treatment Goals:  Reduce ICP:
  • Diuretics.
  • Steroids.
  • Surgical decompression (craniectomy).
  • Drain CSF via ventriculostomy if necessary.

Summary

• ICP increases due to fluid buildup or bleeding; causes neuronal ischemia.
• The body’s compensation mechanisms can become self-perpetuating, worsening injury.
• Cushing’s reflex signals a critical, life-threatening escalation.
• Care requires prompt intervention to reduce ICP and restore blood flow.
• Imaging, CSF analysis, and clinical signs guide management.
• Rapid identification and treatment are vital.