Approach to increased intracranial pressure: Clinical sciences

Increased intracranial pressure, or increased ICP for short, refers to intracranial pressure greater than 20 millimeters of mercury, which can occur due to an increase in the blood, brain, or cerebrospinal fluid compartment. According to the Monroe-Kellie doctrine, the total volume of these three compartments is constant, meaning a volume increase in one compartment should cause a decrease in the others.

Common causes of increased ICP include intracranial hemorrhage, ischemic stroke, brain tumors or abscesses, or meningitis or encephalitis.

Now, if your patient presents with a chief concern suggesting increased ICP, first, perform an ABCDE assessment. You should consider all patients with increased ICP as unstable, so be sure to stabilize their airway, breathing, and circulation. Sometimes, you might even need to intubate the patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry.

Once you have initiated the acute management, your next step is to obtain a focused history and physical exam and get a head CT. Your patient, or their family member or friend, will typically report symptoms, such as headache, and in some cases, nausea and vomiting. On the exam, your patient will present with an altered mental status, more specifically a decrease or even loss of consciousness.

Moreover, be sure to use the Glasgow Coma Scale, or GCS, to assess the patient’s level of consciousness by evaluating eye-opening, verbal, and motor responses to varying levels of stimulation. The scale goes from 3 to 15, with a lower number indicating a worse level of consciousness.

A patient with a GCS score of 3 will have no eye-opening, verbal, or motor response to even the most noxious stimulation, such as sternal rub or nail bed pressure. On the other hand, a patient with a GCS score of 15 will have normal eye-opening, verbal, and motor responses to verbal commands.

Additionally, increased intracranial pressure can trigger a physiological response known as the Cushing triad, which consists of bradycardia, irregular breathing, and hypertension.

Other important findings include a dilated pupil from uncal herniation and papilledema from swelling of the optic discs.

Next, a downward pressure of the brain on cranial nerve six over the petrous ridge of the temporal bones can result in their stretching and eventual bilateral sixth cranial nerve palsies.

Finally, depending on the location of the pathology, you might see focal neurologic deficits. For example, you might see right hemiparesis from a left frontal lobe bleed or a left visual field cut from a right occipital lobe ischemic stroke.

Finally, the head CT will reveal edema, possibly in combination with focal lesions, such as a mass, hemorrhage, or infarction. You might also see an enlargement of brain ventricles, called ventriculomegaly, due to obstruction of CSF outflow. This might occur when blood inside the ventricles blocks CSF reabsorption at the arachnoid villi, or if there’s a mass compressing the ventricular system. In severe cases, these pathologies can cause a severe increase in ICP and eventually cause brain herniation.

Now, here’s a clinical pearl to keep in mind! There are several important types of brain herniation, which can be supratentorial or infratentorial in origin!

First, let’s focus on supratentorial ones, which include uncal, central, and subfalcine herniation! In uncal herniation, a portion of the inferior medial temporal lobe, known as the uncus, slips downward toward the midbrain, causing a decrease in consciousness. In addition, this places pressure on cranial nerve 3 called the oculomotor nerve, causing an ipsilateral dilated nonreactive pupil and impaired oculomotor movements; as well as the cerebral peduncle, which results in contralateral hemiparesis.

Next, in central herniation, the diencephalon, which includes the thalamus and hypothalamus, slips through the tentorial notch and causes downward compression of the brainstem, while in subfalcine herniation, the cingulate gyrus herniates under the falx cerebri, eventually compressing anterior cerebral arteries.

On the flip side, one important infratentorial herniation is cerebellar tonsillar herniation through the foramen magnum, which can also cause compression of the brainstem.

With these findings, you can diagnose increased ICP and proceed with tiered medical management.

Start by placing the head of the bed at 30 to 45 degrees, and ensure the patient’s head is midline to optimize venous outflow.