4.2 Altered Mental Status, Increased ICP & Head Trauma

4.2 Altered Mental Status, Increased ICP & Head Trauma

Altered mental status (AMS) and traumatic brain injury (TBI) represent high-acuity pediatric emergency conditions requiring prompt recognition, systematic assessment, and aggressive neuroprotective management. Because infants and young children have unique cranial anatomy—including open fontanelles, unfused cranial sutures, higher brain water content, and a compliant skull—their clinical presentation of intracranial hypertension differs significantly from that of adult patients.

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Differential Diagnosis of Altered Mental Status

When evaluating a pediatric patient with acute changes in lethargy, confusion, or responsiveness, emergency nurses utilize the classic diagnostic mnemonic AEIOU TIPS to systematically rule out life-threatening underlying etiologies:

• A - Alcohol, Acidosis (DKA, inborn errors of metabolism)
• E - Epilepsy, Encephalopathy, Electrolyte derangements (hyponatremia, hypernatremia)
• I - Insulin (Hypoglycemia—always check point-of-care glucose first!)
• O - Opiates, Overdose, Oxygen deprivation (hypoxia, carbon monoxide)
• U - Uremia (renal failure, Hemolytic Uremic Syndrome)
• T - Trauma (epidural/subdural hematoma, abusive head trauma), Temperature extremes (hypothermia, heat stroke)
• I - Infection (meningitis, encephalitis, sepsis)
• P - Psychogenic, Poisoning/Toxins
• S - Shock, Space-occupying lesions (brain tumor, hydrocephalus), Stroke

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Neurological Assessment & Pediatric Glasgow Coma Scale

Initial assessment of neurological function begins with rapid triage tools and progresses to formal score quantification.

The AVPU Scale

• A (Alert): Awake, responsive, oriented to age-appropriate cues.
• V (Voice): Responds to verbal commands or auditory stimuli.
• P (Pain): Responds only to painful/noxious stimuli (e.g., sternal rub, trapezius squeeze).
• U (Unresponsive): Fails to respond to verbal or painful stimuli.

Pediatric Glasgow Coma Scale (pGCS)

The standard Glasgow Coma Scale is modified for pre-verbal infants (< 2 years) to account for developmental communication differences.

• Clinical Action Threshold: A total pGCS score of ≤ 8 indicates severe brain injury or coma and dictates immediate endotracheal intubation for definitive airway protection ("GCS 8, intubate").

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Increased Intracranial Pressure (ICP) & Cushing's Triad

Monro-Kellie Hypothesis

The intracranial vault is a rigid structure containing three components: brain parenchyma (~80%), cerebrospinal fluid (CSF, ~10%), and blood (~10%). An increase in the volume of any single component must be offset by an equal decrease in another; once compensatory mechanisms (CSF displacement into the spinal sac and venous blood shunting) are exhausted, ICP rises exponentially, leading to cerebral ischemia and brainstem herniation.

Clinical Manifestations of Increased ICP

• Infants (Open Fontanelles & Sutures):
  • Bulging, tense anterior fontanelle
  • Separated (widened) cranial sutures
  • Prominent scalp veins & increased head circumference
  • "Setting-sun" sign (downward deviation of eyes revealing white sclera above iris)
  • High-pitched, inconsolable cry; extreme irritability or somnolence
  • Poor feeding and projectile vomiting
• Children & Adolescents (Fused Sutures):
  • Severe headache, typically worse upon awakening or with coughing/Valsalva
  • Projectile vomiting without pre-existing nausea
  • Papilledema on fundoscopic exam
  • Diplopia secondary to Cranial Nerve VI (abducens) palsy
  • Altered level of consciousness, ataxia, seizures

Cushing's Triad (Late Sign of Impending Herniation)

Cushing's triad represents a critical physiological response to severe intracranial hypertension and brainstem compression:

1. Bradycardia (marked slowing of heart rate)
2. Irregular, chaotic respirations (Cheyne-Stokes or ataxic breathing)
3. Widened pulse pressure / Systolic hypertension (elevated systolic blood pressure with stable or decreased diastolic pressure)

       [Increased ICP & Impending Brainstem Herniation]
                           │
       ┌───────────────────┼───────────────────┐
       ▼                   ▼                   ▼
 [Bradycardia]   [Irregular Respirations]  [Widened Pulse Pressure]
 (Severe drop    (Cheyne-Stokes / Ataxic)  (Systolic Hypertension)
  in Heart Rate)

• Emergency Nursing Priority: Immediate hyperosmolar therapy, neurosurgical intervention, and neuroprotective positioning are required. Cushing's triad is a late, near-terminal sign of uncal or tonsillar herniation.

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Emergency Medical & Osmotic Management of Increased ICP

• Positioning: Elevate the head of the bed 30 degrees and maintain the head and neck in a neutral midline alignment. Avoid neck flexion, extension, or rotation, which compresses internal jugular veins and impedes venous drainage from the brain. Ensure endotracheal tube ties are not overly tight around the neck.
• Normocapnia & Controlled Hyperventilation: Maintain arterial PaCO2 between 35 and 40 mmHg. Therapeutic hyperventilation (targeting PaCO2 30-35 mmHg) causes cerebral vasoconstriction, rapidly reducing cerebral blood volume. However, hyperventilation must be reserved exclusively as a temporary bridge during acute signs of brainstem herniation, as prolonged hypocapnia causes severe cerebral ischemia.
• Hypertonic Saline (3% NaCl): Administer 3 to 5 mL/kg IV over 10 to 20 minutes. Hypertonic saline draws free water across an intact blood-brain barrier into the intravascular space, reducing cerebral edema while expanding intravascular volume. It is the osmotic agent of choice in hypotensive or traumatized pediatric patients. Target serum sodium levels are 145 to 155 mEq/L.
• Mannitol (20% Solution): Administer 0.5 to 1 g/kg IV over 20 to 30 minutes through an in-line filter. Mannitol creates an osmotic gradient pulling fluid from brain tissue into the vascular bed, followed by potent osmotic diuresis. Contraindicated in hypotensive, hypovolemic, or actively bleeding patients. Monitor serum osmolality closely (maintain < 320 mOsm/kg).

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Ventriculoperitoneal (VP) Shunt Malfunction & Infection

Ventriculoperitoneal (VP) shunts divert excess CSF from the cerebral ventricles to the peritoneal cavity in children with hydrocephalus.

• Mechanisms of Failure: Mechanical obstruction (proximal catheter occlusion by choroid plexus/debris, distal peritoneal catheter blockage, valve dysfunction) or bacterial infection (most commonly Staphylococcus epidermidis or Staphylococcus aureus).
• Clinical Presentation: Signs of acute increased ICP (headache, vomiting, lethargy, fontanelle fullness), fever, or localized erythema/swelling along the subcutaneous shunt tract.
• Emergency Nursing Actions: Immediately notify neurosurgery, obtain non-contrast head CT and a "shunt series" (plain radiographs of neck, chest, and abdomen to evaluate catheter continuity), keep patient NPO, and prepare for diagnostic/therapeutic shunt reservoir aspiration by a qualified neurosurgeon.

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Pediatric Head Trauma: Epidural vs. Subdural Hematoma

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Clinical Scenario

A 4-year-old female presents to the emergency department following a fall from a second-story window. On initial assessment, her pGCS is 6 (E1, V2, M3—decorticate posturing to painful stimuli). Vital signs reveal BP 138/64 mmHg, HR 52 beats/min, and irregular, shallow respirations at 10 breaths/min (Cushing's triad). The nurse immediately assists with rapid sequence intubation, maintains head of bed at 30 degrees midline, attaches continuous ETCO2 monitoring (targeting PaCO2 30-35 mmHg temporarily for herniation signs), and initiates a 3% hypertonic saline bolus at 5 mL/kg IV. Urgent non-contrast head CT reveals a large left temporal epidural hematoma with a 10 mm midline shift, prompting immediate emergent neurosurgical craniotomy.