bubble_chart Overview

Acute intracranial hypertension is a common syndrome caused by various diseases, which can rapidly progress to brain herniation in severe cases, posing a life-threatening risk.

bubble_chart Etiology

(1) Increase in brain tissue volume

1. Diffuse cerebral edema
   1. Infection: Encephalitis, meningitis (especially epidemic cerebrospinal meningitis), severe pneumonia, toxic dysentery, sepsis, etc., leading to toxic encephalopathy.
   2. Cerebral hypoxia: Severe cerebral edema caused by asphyxia, drowning, cardiac arrest, carbon monoxide poisoning, status epilepticus, etc.
   3. Traumatic brain injury, Reye's syndrome, etc.
2. Focal cerebral edema
   1. Brain tumors: Especially rapidly progressing brain tumors.
   2. Intracranial hemorrhage: Neonatal intracranial hemorrhage, hematologic diseases (hemophilia, leukemia, thrombocytopenic purpura, etc.).
   3. Cerebral edema adjacent to lesions such as cerebral cysticercosis or cysts.

(2) Disorders of cerebrospinal fluid dynamics

1. Communicating hydrocephalus: Obstruction of cerebrospinal fluid outside the ventricular system, seen in traumatic brain injury, infections, congenital malformations, etc.
2. Obstruction of cerebrospinal fluid flow within the ventricular system, such as congenital malformations, infections, tumors, etc.
3. Excessive secretion or impaired absorption of cerebrospinal fluid.

(3) Increase in cerebral blood volume

1. Impaired venous return: Superior vena cava syndrome.
2. Increased cerebral blood flow due to metabolic disorders.
   For example, cerebral vasodilation caused by hypoxia or hypercapnia due to various reasons.
3. Hypertension or hypervolemia, and water-electrolyte imbalances, etc.
4. Failure of vascular autoregulation reflexes: Such as trauma, tumors, cerebral ischemia, severe hypertension or hypotension.

Under normal circumstances, the brain parenchyma, cerebral blood flow, and cerebrospinal fluid volume within the cranial cavity remain relatively constant, maintaining intracranial pressure within the normal range of 0.59–1.57 kPa (60–160 mmH₂O). When the volume of any one or two of these three components increases, the other two or one component compensatorily decreases to balance intracranial pressure. However, the actual adjustable range of cranial cavity volume is very small. When the increased volume exceeds compensatory limits, it inevitably leads to increased intracranial pressure. In children, when cerebrospinal fluid pressure is measured in the lateral decubitus position under quiet conditions and is ≥1.96 kPa (200 mmH₂O), it indicates increased intracranial pressure; if ≥4.9 kPa (500 mmH₂O), it signifies severe increased intracranial pressure. This often leads to brain tissue herniation into foramina, forming brain herniation.

bubble_chart Clinical Manifestations

(1) Increased Intracranial Pressure

Headache, vomiting, and optic disc edema are the three main signs of intracranial hypertension in older children. The headache is severe, especially in the morning, and worsens with coughing, sneezing, or changes in head position. Newborns often exhibit wide-eyed wakefulness, high-pitched crying, and bulging, tense anterior fontanelles. In infants and toddlers, due to compensatory mechanisms like cranial suture separation and open anterior fontanelles, headaches are less pronounced than in older children. Instead, they may display restlessness, nose-rubbing, or ear-picking. Vomiting is often projectile and usually not accompanied by nausea, becoming more severe in cases of posterior fossa tumors. Bilateral optic disc edema is a key indicator of intracranial hypertension, with possible signs such as small, flickering pulses, dilated veins, or even retinal edema. A few cases may experience diplopia due to oculomotor or abducens nerve palsy. Compression of the midbrain and damage to the reticular formation can lead to impaired consciousness, apathy, sluggish responses, lethargy, or agitation, with severe cases progressing to unconsciousness. Increased muscle tone may occur, and seizures can arise if the motor cortex is irritated. When the medulla oblongata is stimulated, compensatory blood pressure elevation and slowed pulse may occur. If the respiratory center is damaged, breathing initially accelerates, followed by irregular rhythms or even apnea. Infants and toddlers may show a full anterior fontanelle, separated cranial sutures, increased head circumference, recurrent seizures, and central respiratory failure.

(2) Brain Herniation

1. Tentorial Herniation (Uncal Herniation) In cases of supratentorial intracranial hypertension, the affected temporal lobe herniates through the tentorial notch. Symptoms include initial constriction or fluctuating size of the ipsilateral pupil, followed by dilation. Unequal pupil size is characteristic of tentorial herniation. Light reflexes weaken or disappear, unconsciousness sets in, accompanied by central respiratory failure and contralateral or bilateral limb paralysis.
2. Tonsillar Herniation (Foramen Magnum Herniation) In posterior fossa lesions, the cerebellar tonsils herniate through the foramen magnum. Symptoms include neck stiffness, head retraction, and tonic spasms in the limbs. Pupils are initially symmetrically constricted, then dilate, with loss of light reflexes. Pupils and eyeballs become fixed, unconsciousness deepens, breathing becomes irregular, heart rate first accelerates then slows, blood pressure first rises then falls, until respiratory and cardiac arrest occurs.

bubble_chart Diagnosis

Early diagnosis is extremely important. The typical manifestations of headache, vomiting, and optic disc edema make diagnosis straightforward. Once confirmed, the underlying disease cause should be identified. Depending on the patient's condition, selective examinations such as cerebral ultrasound, skull transillumination, CT scans, skull X-rays, subdural or lumbar puncture, etc., should be performed to establish the cause of the disease. Lumbar puncture must be approached with caution in cases of increased intracranial pressure to avoid inducing brain herniation. If puncture is necessary for definitive diagnosis, intravenous mannitol should be administered preoperatively, cerebrospinal fluid flow rate and volume should be controlled during the procedure, Queckenstedt's test (jugular compression) must be avoided, and the patient should remain supine for 2–4 hours postoperatively under close observation.

bubble_chart Treatment Measures

1. Reducing intracranial pressure: Closely monitor the patient's condition and remain vigilant for cerebral herniation. The preferred treatment is hypertonic dehydrating agents, such as 20% mannitol at 1–2 g/kg, administered intravenously over 30–60 minutes, repeated every 4–6 hours. Once symptoms improve, reduce the frequency to every 8–12 hours. In cases of acute cerebral herniation, prompt intervention is critical to prevent fatal outcomes. Administer 20% mannitol via rapid intravenous drip or push, completing the infusion within 10–30 minutes. The hypotensive effect typically begins within 10–20 minutes, peaking at 30 minutes. If no improvement is observed after half an hour, repeat the dose.
2. Diuretics: The first-line choice is furosemide at 1–2 mg/kg per dose or sodium ethacrynate at 0.5–1 mg/kg per dose, dissolved in 10% glucose and administered intravenously 2–3 times daily. Intramuscular injection is also an option. To reduce cerebrospinal fluid volume, oral acetazolamide (Diamox) can be used, which not only acts as a diuretic but also inhibits cerebrospinal fluid production. The dose is 10–30 mg/kg per dose, once daily.
3. Adrenocortical hormones: These have nonspecific anti-inflammatory and antitoxic effects, reducing vascular and blood-brain barrier permeability to prevent and treat cerebral edema. Administer dexamethasone at 0.25–0.5 mg/kg once daily via intravenous drip.
4. Fluid therapy: The principle is to "balance rehydration and dehydration," emphasizing fluid restriction. Avoid excessive fluid administration; generally, maintain intake at 30–60 ml/kg per day, keeping the child in a grade I dehydration state. In cases of cerebral herniation, prioritize rapid dehydration followed by slow rehydration. For cerebral edema complicated by heart or kidney failure or pulmonary edema, administer diuretics first, then proceed with slow dehydration and rehydration. For cerebral edema with shock, simultaneously rehydrate and dehydrate or rehydrate first before dehydrating. Correct acidosis and electrolyte imbalances as needed, and consider blood or plasma transfusion if necessary.
5. Prevent and treat respiratory failure.
6. Etiological treatment: Provide targeted therapy based on the underlying cause of the disease.