Increased Intracranial Pressure

Etiology

The causes of increased ICP can be divided based on the intracerebral components causing elevated pressures, including:

• Increase in brain volume: Generalized swelling of the brain or cerebral edema from a variety of causes:
  • Hypoxic-ischemic injury
  • Trauma
  • Hypertensive encephalopathy
  • Infection
    • Meningitis
    • Encephalitis
  • Metabolic derangement or toxin
    • Hyponatremia
    • Diabetic ketoacidosis
    • Dialysis disequilibrium syndrome
    • Reye syndrome
    • Fulminant hepatic encephalopathy
    • Pulmonary insufficiency with hypercarbia
    • Lead intoxication
• Mass effect
  • Hematoma
  • Tumor
  • Abscess
  • Inflammatory mass
  • Arterial ischemic stroke with edema
  • Cerebral venous sinus thrombosis
  • Cyst
• Increase in cerebrospinal fluid
  • Increased production of cerebrospinal fluid
  • Choroid plexus tumor
• Decreased reabsorption of cerebrospinal fluid
  • Obstructive hydrocephalus
  • Meningeal inflammation or granulomas
• Increase in blood volume
  • Increased cerebral blood flow during hypercarbia, aneurysms
  • Venous stasis from venous sinus thromboses, elevated central venous pressures, eg, heart failure
• Other causes
  • Idiopathic or benign intracranial hypertension may result secondary to drugs, withdrawal of long-term steroid administration, endocrinologic disturbance, and obesity.[2] Please see StatPearls' companion resource, "Pseudotumor Cerebri," for further information.
  • Skull deformities (eg, craniosynostosis)
  • Drugs, eg, hypervitaminosis A, tetracyclines, recombinant growth hormone, lithium [3]

Epidemiology

The true incidence of intracranial hypertension is unknown. The Centers for Disease Control and Prevention (CDC) estimates that in 2010, 2.5 million people sustained a traumatic brain injury (TBI), which is associated with increased ICP. ICP monitoring is recommended for all patients with severe TBI. Studies of American-based populations have estimated that the incidence of idiopathic intracranial hypertension ranges from 0.9 to 1.0 per 100,000 in the general population, increasing in women who are overweight.[4]

Pathophysiology

The harmful effects of intracranial hypertension are primarily due to brain injury caused by cerebral ischemia. Cerebral ischemia is the result of decreased brain perfusion secondary to increased ICP. CPP is equal to the pressure gradient between mean arterial pressure (MAP) and intracranial pressure (CPP = MAP - ICP).[5] When central venous pressure (CVP) exceeds ICP, the formula adjusts to CPP = MAP - CVP. This adjustment is not routinely used unless the ICP is very low or the CVP is abnormally elevated (eg, in high PEEP ventilation or venous outflow obstruction). In most clinical contexts, the CPP = MAP - ICP formula remains the standard. The CPP target for adults following severe traumatic brain injury is recommended at greater than 60 to 70 mm Hg, and a minimum CPP greater than 40 mm Hg is recommended for infants, with minimal data on normal CPP targets for children in between.

Cerebral autoregulation refers to the brain's ability to maintain consistent cerebral blood flow despite fluctuations in systemic blood pressure. When MAP increases, cerebral vasoconstriction limits blood flow to preserve stable perfusion. In contrast, hypotension prompts vasodilation within the cerebral vasculature to enhance blood flow and maintain adequate CPP. This adaptive mechanism plays a critical role in protecting the brain from ischemic injury during changes in systemic circulation.

History and Physical

Clinical Features

Clinical suspicion for intracranial hypertension should be raised if a patient presents with the following signs and symptoms: headaches, vomiting, and altered mental status varying from drowsiness to coma. Visual changes can range from blurred vision and double vision resulting from cranial nerve defects to photophobia, optic disc edema, and ultimately, optic atrophy. Infants with an open anterior fontanelle may exhibit a bulge overlying the area.

Clinical features of herniation

Cushing triad is a clinical syndrome consisting of hypertension, bradycardia, and irregular respiration, and is a sign of impending brain herniation. This occurs when the ICP is significantly elevated, and the elevation of blood pressure is a reflex mechanism to maintain CPP. High blood pressure can cause reflex bradycardia and compromise of the brain stem, which in turn affects respiration. Ultimately, the contents of the cranium are displaced downwards due to the high ICP, causing a phenomenon known as herniation, which can be potentially fatal.[6]

The different types of herniation include:

• Subfalcine (cingulate) herniation: involves the cingulate gyrus and pericallosal arteries, producing leg weakness
• Lateral (uncal) herniation affects several structures, including:
  • Oculomotor nerve causing ptosis and ipsilateral mydriasis
  • Cerebral peduncle causing contralateral hemiparesis
  • Posterior cerebral artery leading to decreased consciousness
• Posterior (tectal) herniation compresses the superior colliculi, resulting in bilateral ptosis and upward gaze paralysis
• Central (axial) herniation involves
  • Perforating branches of the basilar artery resulting in depressed consciousness and impaired eye movement
  • Midbrain, pons, and medulla causing respiratory irregularity or apnea
  • Reticular formation causing hypertension and bradycardia
• Tonsillar herniation compresses the medulla, resulting in apnea

Close monitoring of neurological status plays a crucial role in the timely detection of neurological issues. Typical clinical findings include altered mental status and the emergence of a fixed, dilated pupil, both of which often indicate worsening intracranial pressure and potential impending herniation. A funduscopic exam can reveal papilledema, which is a tell-tale sign of raised ICP, as the cerebrospinal fluid is in continuity with the fluid around the optic nerve.

Evaluation

Evaluation of increased ICP requires appropriate ancillary studies in addition to a thorough medical history and a comprehensive physical examination. Early recognition of elevated ICP remains critical for preventing brain herniation and death.

Imaging Studies

Computed tomography (CT) of the head or magnetic resonance imaging (MRI) can detect signs of elevated ICP, eg, ventricular enlargement, brain herniation, or mass effect resulting from tumors, abscesses, hematomas, and other space-occupying lesions. Patients with clinical findings indicative of cerebral injury should undergo a noncontrast CT scan of the brain, which may reveal cerebral edema characterized by low-density regions and loss of gray-white matter differentiation.

Additional findings may include obliteration of the basal cisterns and sulcal spaces. CT imaging can also help identify the underlying cause of increased ICP. The presence of flattened gyri, narrowed sulci, or ventricular compression further supports a diagnosis of elevated ICP. Serial CT scans provide a valuable means of monitoring the progression or resolution of cerebral edema over time.[7][8]

Lumbar Puncture

The opening pressure can be measured with a lumbar puncture. In this procedure, a needle is introduced into the subarachnoid space. This can be connected to a manometer to give the pressure of the CSF before drainage. A measurement >20 mm Hg is suggestive of raised ICP. Brain imaging should precede a lumbar puncture because a lumbar puncture can cause a sudden and rapid decrease in ICP, and the sudden change in volume can lead to herniation.

Intracranial Pressure Monitoring

Multiple devices assist in the direct monitoring of ICP.[9] A fiber optic catheter inserted into the brain parenchyma allows continuous measurement of pressure transmitted through the brain tissue. This method provides real-time data, which is crucial for clinical decision-making in critical care settings. Devices for direct ICP monitoring include: 

• External ventricular drain (EVD): A drain placed directly into the lateral ventricles can be connected to a manometer to give a reading for the pressure in the ventricles.
• Optic nerve sheath diameter (ONSD): Ultrasound measurement of the optic nerve sheath diameter has emerged as a noninvasive tool for detecting elevated ICP. Measurements are taken 3 mm behind the globe, with 2 to 3 readings obtained from each eye. A sheath diameter between 0.48 cm and 0.63 cm often indicates raised ICP.[10]
• Additional studies: Noninvasive tools, eg, quantitative pupillometry and transcranial Doppler ultrasonography, may serve as useful adjuncts in assessing ICP and guiding management.[11][12]

Treatment / Management

Increased Intracranial Pressure Management

The management of elevated ICP is a critical component of care in patients with acute neurological deterioration. Such patients should be managed in an intensive care unit. Continuous neuro-observation, vigilant monitoring of vital signs, and timely interventions can prevent secondary brain injury and potentially fatal herniation syndromes.

All interventions should be viewed as temporizing measures aimed at preventing or reversing cerebral herniation until the underlying disease is treated or resolves. While recovery is possible with prompt and appropriate treatment, the prognosis is poor once there is evidence of uncal or tonsillar herniation accompanied by bilateral fixed pupils and loss of brainstem reflexes.

Ventilation and circulatory interventions

The primary goals of care include stabilizing the airway, ensuring adequate ventilation and oxygenation, and maintaining systemic circulation.[13] Once cardiopulmonary stability has been achieved, specific steps should follow. The neck should remain in a neutral midline position, avoiding flexion or rotation to prevent restriction of jugular venous outflow. Elevating the head of the bed to approximately 30 degrees promotes venous drainage and lowers cerebral blood volume.

Endotracheal intubation is indicated if the Glasgow Coma Scale (GCS) score is 8 or lower, when consciousness deteriorates, when airway reflexes are lost, or when impending herniation is suspected. Controlled ventilation may then be used to reduce ICP, with temporary targeting of a PaCO2 not lower than 35 mm Hg to induce cerebral vasoconstriction. Aggressive hyperventilation, targeting a PaCO2 below 30 mm Hg, should be reserved for acute herniation, as prolonged vasoconstriction can impair cerebral perfusion and precipitate ischemia.[14][15]

Pharmacologic interventions 

Pharmacologic interventions play a central role in reducing ICP, with osmotherapy using mannitol or hypertonic saline (HTS) serving as the most widely employed approach. Mannitol, administered intravenously at a dose of 0.25 to 1 g/kg, creates an osmotic gradient that shifts fluid from the brain parenchyma into the intravascular space. Additionally, mannitol reduces blood viscosity, thereby enhancing cerebral perfusion. Close monitoring of serum osmolality remains critical, as levels above 320 mOsm increase the risk of renal injury and dehydration.[16]

Hypertonic saline, often administered as a 3% solution either as a bolus (5 mL/kg) or through continuous infusion, provides an alternative with strong efficacy. Clinicians typically maintain serum sodium below 160 mEq/L and osmolality below 340 mOsm to reduce complications.[17] Comparative studies indicate that hypertonic saline can be as effective as mannitol in lowering ICP and reversing transtentorial herniation.[18] Higher concentrations, eg, 23.4% HTS, may be used for rapid ICP reduction in select cases. Unlike mannitol, HTS does not cause rebound edema and carries a lower risk of renal injury; however, its use requires central venous access and vigilant monitoring because of potential electrolyte disturbances.[19][20](A1)

Corticosteroids play only a limited role in managing raised ICP. Their use remains primarily indicated for vasogenic edema caused by intracranial tumors or abscesses, while they remain contraindicated in traumatic brain injury and most other causes of elevated ICP. Acetazolamide, a carbonic anhydrase inhibitor, decreases CSF production and provides benefit in conditions, eg, idiopathic intracranial hypertension and postinfectious hydrocephalus.

Intravenous glyburide, an experimental agent targeting the SUR1 receptor, shows potential in reducing cerebral edema following large hemispheric infarction.[21] When conventional measures fail, induction of a barbiturate coma may be employed to reduce cerebral metabolic demand and lower ICP, with pentobarbital serving as the most frequently used agent.[22] In addition, vasopressor support may be required to maintain adequate MAP and ensure CPP remains within the target range of 50 to 70 mm Hg.(A1)

Invasive interventions

Invasive interventions are often required when medical management fails.

Lumbar puncture

A lumbar puncture can provide a temporary reduction of ICP in cases without mass effect. Clinicians must avoid the procedure in the presence of midline shift or obstructive hydrocephalus, as the sudden alteration in pressure may trigger brain herniation.

External ventricular drain 

Placement of an external ventricular drain (EVD) offers both diagnostic and therapeutic advantages by permitting continuous or intermittent cerebrospinal fluid (CSF) drainage while simultaneously monitoring ICP.

Optic nerve sheath fenestration and CSF diversion procedures

In carefully selected patients, surgeons may also perform optic nerve sheath fenestration to relieve pressure and preserve vision, particularly in those with chronic idiopathic intracranial hypertension.[23] When elevated ICP results from hydrocephalus, surgical interventions, eg, ventriculoperitoneal or lumboperitoneal shunting, provide long-term CSF diversion.

Decompressive craniectomy

Malignant intracranial hypertension that fails to respond to standard measures may require decompressive craniectomy to lower ICP by creating space for cerebral expansion. The procedure involves removing a portion of the skull and opening the dura to alleviate pressure on the brain. Decompressive craniectomy can be life-saving in critical situations, but the intervention carries significant risks. Potential complications include infection, hematoma formation, and the possibility of long-term functional disability. Careful patient selection and ongoing interprofessional management remain crucial to strike a balance between the benefits of pressure relief and the risks of adverse outcomes.[24]

Therapeutic hypothermia

Therapeutic hypothermia, with a target temperature of 32 °C to 35 °C, may also reduce ICP by lowering cerebral metabolism and inflammation. Current evidence regarding its efficacy remains inconclusive, and its application is generally reserved for select patients treated in specialized centers.

Supportive Care

Fever requires aggressive management, particularly in patients with intracerebral or intraventricular hemorrhage, where central fever frequently develops. Hyperthermia raises the cerebral metabolic rate and amplifies neurological injury. Treatment should include antipyretics, surface cooling methods, eg, cooling blankets, and thorough evaluation for potential infectious causes.

Glycemic control remains equally important, as both hyperglycemia and hypoglycemia contribute to worsened neurological outcomes. Continuous monitoring of serum electrolytes and fluid balance helps detect complications, eg, syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting, allowing for timely intervention to prevent further deterioration.

Differential Diagnosis

Differential diagnoses that should be considered when evaluating increased intracranial pressure include:

• Blood dyscrasias and stroke
• Hydrocephalus
• Intracranial hemorrhage
• Intracranial epidural abscess
• Lyme disease
• Meningioma
• Migraine variants
• Subarachnoid hemorrhage

Prognosis

Prognosis depends on the underlying etiology and severity of the presentation. Benign intracranial hypertension does not increase the risk of death by itself; rather, the death rate is increased by morbid obesity, which is a common association with benign intracranial hypertension. Visual loss is a significant morbidity in idiopathic intracranial hypertension.

Complications

ICP can lead to a range of serious, often life-threatening complications if not promptly recognized and managed. One of the most critical outcomes is brain herniation, a condition in which brain tissue is displaced due to excessively high pressure within the rigid cranial vault. This can compress vital structures in the brainstem, resulting in loss of consciousness, impaired respiration, and ultimately death. Cushing triad—characterized by hypertension, bradycardia, and irregular respirations—is a late and ominous sign of impending herniation. Elevated ICP also compromises CPP, leading to global or focal ischemia, which can cause irreversible brain damage. Neurological deficits, ranging from cognitive impairments and motor dysfunction to vision loss from optic atrophy, may persist even after pressure normalization.

Secondary complications can arise from both the underlying cause of ICP and the interventions used to manage it. For instance, osmotic therapies, eg, mannitol, may result in electrolyte imbalances, dehydration, or renal injury if serum osmolality exceeds safe thresholds. Hypertonic saline can also cause hypernatremia if not carefully monitored. Invasive procedures, eg, external ventricular drains, carry risks of infection or hemorrhage. Additionally, lumbar puncture in the presence of a mass effect can precipitate herniation by rapidly altering pressure dynamics. Long-term complications include chronic hydrocephalus, requiring permanent cerebrospinal fluid diversion through shunting, and potential neurocognitive decline, necessitating ongoing rehabilitation and support. Without proper interprofessional coordination and vigilant monitoring, the risks of long-term disability or mortality remain significant.