Raised ICT

Raised intracranial pressure (ICP) is a critical neurological emergency in pediatrics. It is a common complication in critically ill children, potentially arising from traumatic brain injury (TBI), central nervous system (CNS) infections, mass lesions, or metabolic disorders. The prompt recognition and management of elevated ICP are vital to prevent secondary brain injury, herniation, and death.

Normal Values: ICP is the pressure exerted by the brain tissue, blood, and cerebrospinal fluid (CSF) within the cranial vault.

• Newborns: Normal ICP is approximately 6 mm Hg (8 cm H2O).
• Children: Normal ICP ranges between 6–15 mm Hg.
• Threshold for Treatment: A sustained ICP >20 mm Hg (27 cm H2O) for longer than five minutes is generally considered the threshold for initiating treatment.

Pathophysiology

The pathophysiology of raised ICT is governed by the fixed volume of the cranial vault and the dynamic relationship between its contents.

1. The Monro-Kellie Doctrine

The cranium is a rigid, non-expansile box (after suture closure). The total volume within the cranium is constant and consists of three compartments:

• Brain parenchyma (~80%)
• Blood (~10%)
• CSF (~10%)

According to the Monro-Kellie doctrine, an increase in the volume of one compartment (e.g., cerebral edema, hematoma) must be compensated by a decrease in the volume of another compartment to maintain normal pressure. Compensation typically occurs initially by the displacement of CSF into the spinal sac and venous blood into the systemic circulation. Once these compensatory mechanisms are exhausted, even small increases in volume lead to exponential rises in ICP (compliance failure).

2. Cerebral Perfusion Pressure (CPP)

The primary danger of raised ICP is the compromise of cerebral blood flow (CBF). CPP is the driving force for CBF and is defined as: $$CPP = MAP - ICP$$ (MAP: Mean Arterial Pressure)

As ICP rises, CPP decreases. If CPP falls below a critical threshold, cerebral ischemia and infarction ensue. In children, maintaining adequate CPP is crucial for oxygenation.

3. Autoregulation

Cerebral autoregulation is the physiological capability of the brain to maintain constant CBF across a range of systemic blood pressures (typically MAP 60–150 mm Hg in adults) by altering cerebrovascular resistance.

• Intact Autoregulation: Vasoconstriction occurs during hypertension, and vasodilation occurs during hypotension to maintain steady flow.
• Impaired Autoregulation: In trauma or severe ischemia, autoregulation may fail. CBF becomes "pressure-passive," meaning it rises linearly with MAP. In this state, systemic hypotension causes ischemia, while hypertension can worsen cerebral edema and ICP,.

4. Cerebral Herniation Syndromes

When ICP increases significantly, brain tissue shifts from high-pressure compartments to low-pressure compartments, leading to herniation. This can compress the brainstem and vascular structures.

• Subfalcine Herniation: Medial displacement of the cingulate gyrus under the falx cerebri. It may compress the anterior cerebral artery.
• Uncal (Lateral Transtentorial) Herniation: The uncus of the temporal lobe shifts medially, compressing the third cranial nerve (causing ipsilateral dilated pupil/ptosis) and the brainstem (causing contralateral hemiparesis and altered consciousness),.
• Tonsillar Herniation: Downward displacement of cerebellar tonsils through the foramen magnum, compressing the medulla. This leads to respiratory irregularity, apnea, bradycardia, and death,.

Etiology

The causes of raised ICP can be categorized by the compartment affected:

1. Increased Brain Volume:
   • Cerebral Edema: Cytotoxic (e.g., Hypoxic-ischemic encephalopathy, Reye’s syndrome) or Vasogenic (e.g., Tumors, abscesses, meningitis).
   • Space-occupying lesions: Brain tumors, hematomas (epidural, subdural), abscesses, tuberculomas.
2. Increased Blood Volume:
   • Hyperemia (vasodilation due to hypercarbia or hypoxia).
   • Venous obstruction (e.g., Cerebral sinovenous thrombosis).
3. Increased CSF Volume:
   • Hydrocephalus: Obstructive (aqueductal stenosis) or communicating (post-meningitic).
   • Choroid plexus papilloma (overproduction).

Clinical Features

The clinical presentation varies by age and the rate of ICP rise.

Infants (Open Sutures)

• Head: Increased head circumference, tense/bulging anterior fontanelle, separated cranial sutures.
• Eyes: Setting sun sign (downward gaze due to pressure on the tectal plate),.
• General: Irritability, high-pitched cry, lethargy, poor feeding, dilated scalp veins.

Older Children (Closed Sutures)

• Symptoms: Headache (worse in the morning or with coughing/Valsalva), projectile vomiting (often without nausea), diplopia, lethargy,.
• Signs: Papilledema (may be absent in acute rise), sixth nerve palsy (false localizing sign), focal neurological deficits,.
• Cushing’s Triad: A late sign of impending herniation characterized by:
  1. Systemic Hypertension
  2. Bradycardia
  3. Irregular respirations,.

Assessment and Monitoring

1. Neuroimaging

• CT Scan: The primary modality for acute assessment. Findings suggestive of raised ICP include midline shift, effacement of basilar cisterns and sulci, and ventricular compression,.
• MRI: More accurate for detecting etiology but requires sedation and time.
• Ocular Ultrasound: Measurement of optic nerve sheath diameter is a reliable non-invasive bedside tool. In children >1 year, a diameter >5.8 mm correlates with ICP >20 mm Hg.

2. Invasive ICP Monitoring

• Indications: Severe TBI (GCS 3–8) with abnormal CT, or normal CT with hypotension/posturing.
• Methods: External Ventricular Drain (EVD) is the gold standard as it is both diagnostic and therapeutic (allows CSF drainage). Parenchymal monitors (fiberoptic) are alternatives.
• Waveform Analysis:
  • P2 > P1: Suggests reduced intracranial compliance.
  • Lundberg A Waves (Plateau waves): Steep increases in ICP (50–100 mm Hg) lasting 5–20 minutes, indicating critically low compliance and risk of herniation.

Management of Raised ICP

The goal is to maintain CPP and prevent secondary brain injury. Management is graded into tiers, moving from general measures to aggressive interventions for refractory cases.

A. General Stabilization (Tier 0)

1. Airway and Breathing:
   • Secure airway (intubation) if GCS <8 or if there are signs of herniation.
   • Maintain Oxygenation (SpO2 >92%, PaO2 >75 mm Hg) and Normocapnia (PaCO2 35–40 mm Hg). Hypoxia and hypercapnia cause vasodilation and increase ICP,.
2. Circulation:
   • Maintain euvolemia and normotension. Hypotension is detrimental to CPP.
   • Fluids: Use Isotonic fluids (Normal Saline). Avoid hypotonic fluids (e.g., Dextrose 5%) as they exacerbate cerebral edema,.
3. Positioning:
   • Elevate the head end by 30° and keep the head in the midline to facilitate jugular venous drainage. Ensure the neck is not flexed or compressed.
4. Sedation and Analgesia:
   • Pain and agitation increase ICP. Use short-acting agents like Fentanyl and Midazolam. Lidocaine can be used prior to suctioning to blunt ICP spikes,.
5. Seizure Control:
   • Seizures increase metabolic demand and ICP. Prophylactic anticonvulsants (Levetiracetam or Phenytoin) are recommended in high-risk TBI.
6. Temperature Control:
   • Treat fever aggressively with antipyretics, as hyperthermia increases cerebral metabolic rate and blood flow.

B. First-Tier Medical Management

If general measures fail or signs of herniation appear, initiate specific therapy:

1. Osmotherapy:
   • Mannitol (20%):
     • Dose: Bolus 0.25–1 g/kg (approx. 2.5–5 mL/kg) over 20 mins.
     • Mechanism: Creates an osmotic gradient drawing water out of the brain parenchyma. Also improves blood rheology.
     • Monitoring: Maintain serum osmolality <320 mOsm/kg. Avoid in hypovolemia,.
   • Hypertonic Saline (3%):
     • Dose: Bolus 2–5 mL/kg, followed by continuous infusion (0.1–1 mL/kg/hr).
     • Target: Serum Sodium 145–155 mEq/L (up to 160 mEq/L).
     • Advantage: Preferable in hypotensive patients as it acts as a volume expander. Maintains efficacy longer than mannitol,,.
2. CSF Drainage:
   • If an EVD is in place, draining CSF is an immediate and effective method to lower ICP,.
3. Steroids:
   • Indication: Effective only for vasogenic edema (e.g., brain tumors, abscesses, TBM).
   • Contraindication: Not recommended for TBI or ischemic stroke as they do not improve outcomes and may be detrimental.
   • Agent: Dexamethasone,.

C. Second-Tier (Refractory) Management

For ICP that remains elevated despite Tier 1 measures:

1. Hyperventilation:
   • Mechanism: Hypocapnia causes cerebral vasoconstriction, reducing cerebral blood volume and ICP.
   • Protocol: Mild hyperventilation (PaCO2 30–35 mm Hg). Aggressive hyperventilation (PaCO2 <30 mm Hg) creates a risk of cerebral ischemia and should only be used as a temporary measure for impending herniation,.
2. Barbiturate Coma:
   • Pentobarbital or Thiopental infusions reduce cerebral metabolic rate and blood volume. Requires continuous EEG monitoring (burst suppression) and hemodynamic support due to the risk of hypotension,.
3. Decompressive Craniectomy:
   • Surgical removal of a portion of the skull to allow the swollen brain to expand outward, preventing compression of the brainstem. Considered when medical management fails.
4. Hypothermia:
   • Therapeutic hypothermia (32–34°C) is a salvage therapy option but evidence for routine use in pediatric TBI is weak and it carries risks of coagulopathy and infection,.

D. Etiology-Specific Management

• Hydrocephalus: Ventriculoperitoneal (VP) shunt or Endoscopic Third Ventriculostomy (ETV).
• Space Occupying Lesion: Surgical resection or evacuation of hematoma/abscess,.
• Idiopathic Intracranial Hypertension: Acetazolamide, weight loss, or optic nerve sheath fenestration.

Summary

The management of raised intracranial tension requires a systematic, algorithmic approach. The primary objective is to maintain cerebral perfusion pressure by reducing ICP while simultaneously supporting systemic hemodynamics. While osmotherapy and sedation form the cornerstone of medical management, surgical interventions like CSF diversion or decompressive craniectomy are life-saving in selected refractory cases. Continuous monitoring and rapid escalation of therapy are essential for favorable neurological outcomes.