Presión intracraneal elevada

What is raised intracranial pressure?

Normal intracranial pressure in adults ranges from 7 to 15 mmHg when lying flat. Values above 20 to 25 mm Hg are generally considered pathological.

Raised intracranial pressure (ICP) can arise as a consequence of intracranial mass lesions, disorders of cerebrospinal fluid (CSF) circulation and more diffuse intracranial pathological processes. Its development may be acute or chronic.

The causes of raised intracranial pressure can be divided as:

• Increase in brain volume (generalised cerebral oedema) due to:

  • Hypoxic ischaemic injury.

  • Trauma.

  • Hypertensive encephalopathy.

  • Infection - meningitis or encephalitis.

  • Metabolic derangement - hyponatraemia, cetoacidosis diabética, Reye syndrome, hepatic encephalopathy, pulmonary insufficiency with hypercarbia, dialysis disequilibrium syndrome.

  • Toxins - lead poisoning.

• Mass effect due to:

  • Haematoma.

  • Tumour.

  • Abscess.

  • Ischaemic cerebrovascular accident with localised oedema.

  • Cerebral venous sinus thrombosis.

  • Cyst.

• Increase in cerebrospinal fluid due to:

  • Increased production of cerebrospinal fluid.

  • Choroid plexus tumour.

• Decreased reabsorption of cerebrospinal fluid due to:

  • Obstructive hydrocephalus.

  • Meningeal inflammation.

• Increase in blood volume due to:

  • Increased cerebral blood flow eg, due to hypercarbia.

  • Venous stasis from venous sinus thromboses, heart failure etc.

• Other causes:

  • Skull anomalies eg, craniosynostosis.

  • Drugs eg, lithium or tetracyclines

• Idiopathic or benign intracranial hypertension can be caused by obesity, withdrawal of long-term steroid treatment or by other drugs.

The combination of headache, papilloedema and vomiting is generally considered indicative of raised intracranial pressure, although there is no consistent relation between the severity of symptoms and the degree of hypertension.

Clinical suspicion should be raised if a patient presents with headache, vomiting and altered mental state.²

A 2021 study exploring the diagnostic accuracy of clinical signs as indicators of a raised ICP found that relying on them alone may lead to undertreatment.⁴

A headache is more worrying when it is nocturnal, present on waking, worse on coughing or moving the head, and associated with altered mental state.⁵

Early changes in mental state include lethargy, irritability, slow decision making and abnormal social behaviour. Untreated, this can deteriorate to stupor, coma and death.

Vomiting often occurs in the early stages without nausea and can progress to projectile vomiting with rising intracranial pressure.

Pupillary changes may include irregularity or dilatation in one eye. Fundoscopy shows blurring of the disc margins, loss of venous pulsations, disc hyperaemia and flame-shaped haemorrhages. In later stages, obscured disc margins and retinal haemorrhages may be seen. There may be unilateral ptosis or third and sixth nerve palsies. In later stages, there may be ophthalmoplegia and the loss of vestibulo-ocular reflexes.

Late signs include motor changes (hemiparesis), raised blood pressure, widened pulse pressure and a slow irregular pulse.

In an acute situation:

• Head injury and obtundation: bleeding can form a rapidly expanding haematoma leading to rapidly rising ICP if not treated promptly.

• Síncope, headache and meningismus: abrupt onset of headache with these symptoms suggests ruptured cerebral aneurysm or vascular lesion.

• Focal deficit followed by convulsiones: focal deficit can be associated with a mass lesion or with cerebral oedema or haemorrhage. Intracranial compartment shift can cause increased ICP within minutes or hours; status epilepticus can cause decompensation of cerebral volume regulation.

• CT/MRI scanning to determine any underlying lesion.

• Lumbar puncture can be used to measure the opening pressure.

• Blood pressure, blood glucose, renal function, electrolytes and osmolality should all be checked.

Monitoring intracranial pressure ⁶

• Intracranial pressure monitoring is:

  • Used either as a guide to treatment or as a diagnostic test. The most common use of continuous ICP monitoring is in the management of severe closed head injury.

  • Appropriate in patients with severe head injury (Glasgow Coma Score between 3 and 8 after cardiopulmonary resuscitation) and an abnormal CT scan (haematomas, contusions, oedema or compressed basal cisterns).

  • Appropriate in patients with severe head injury and a normal CT scan if two or more of the following features are noted on admission: age over 40 years, unilateral or bilateral motor posturing, systolic blood pressure <90 mm Hg.

  • Not routinely indicated in patients with mild or moderate head injury; however, a clinician may choose to monitor ICP in certain conscious patients with traumatic mass lesions.

• Other conditions in which intracranial pressure monitoring is used include:

  • Hemorragia subaracnoidea with associated hydrocephalus: ventriculostomy allows therapeutic drainage and ICP monitoring.

  • Reye's syndrome: active treatment of raised ICP decreases mortality.

  • Brain tumours: may be of value in selected patients deemed at high risk of swelling or obstructive hydrocephalus - eg, following posterior fossa surgery.

  • .

  • Decompensated hydrocephalus: can be a valuable diagnostic tool in complex cases.

  • Idiopathic intracranial hypertension: as both a diagnostic test and to monitor response to treatment.

  • Other potential indications include hypoxic brain swelling after drowning, meningitis, encephalitis, venous sinus thrombosis and hepatic encephalopathy.

In the acute emergency situation the priority is maintaining adequate arterial oxygen tension and ensuring normal vascular volume and normal osmosis. It is also essential to maintain normoglycaemia. Patients with raised ICP who have neurological deterioration should be managed in an intensive care unit. ²

Subsequent treatment, which may include medication, sedation, hyperventilation or neurosurgery, will depend on the underlying pathology. ²