Approach to increased intracranial pressure: Clinical sciences

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Introduction0:00–0:44

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.

Unstable Patient 0:44–1:16

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.

Focused H&P 1:16–5:02

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.

Increased ICP5:02–6:32

If there is concern for imminent herniation or herniation has already occurred, be sure to transiently hyperventilate the patient.
Hyperventilation decreases carbon dioxide blood levels and causes vasoconstriction, eventually decreasing blood flow to the brain and lowering ICP.
You should perform hyperventilation only as a bridge to additional therapies because prolonged vasoconstriction and decreased blood flow can cause brain ischemia.
The next steps in order of escalating therapies include analgesia, hyperosmolar therapy, medically-induced coma with anesthesia, and paralysis.
If you are escalating medical treatment without an immediate plan for the operating room, you should place an ICP monitor to track the efficacy of your treatments.
However, depending on the etiology, or if there is already evidence of herniation, such as a blown pupil, you can skip ICP monitoring and proceed straight to surgical treatment.
Surgical options include a decompressive craniectomy, and mass or hemorrhage evacuation. Finally, if there is ventriculomegaly, you may need CSF diversion, such as with an external ventricular device.
Alright, now, your next step is to determine the underlying cause of increased ICP. First, assess the head CT for any hemorrhagic lesions.

Hemorrhagic Lesions 6:32–7:24

If you identify a hemorrhagic lesion, the next step is to determine what type of hemorrhage it is. If you see a biconvex-shaped hyperdensity that does not cross suture lines, diagnose epidural hematoma.
However, if CT shows a crescent-shaped hyperdensity that does cross suture lines, you can be confident it’s a subdural hematoma.
Next, If you visualize hyperdensity within the subarachnoid space, diagnose subarachnoid hemorrhage. Finally, if the CT scan shows hyperdensity within the brain parenchyma itself, diagnose intracerebral hemorrhage.
Now, let’s go back and take a look at individuals with no hemorrhagic lesions on CT. In this case, assess CT findings for signs of infarction.

Non-hemorrhagic Lesions 7:24–8:01

These include loss of gray-white differentiation, which refers to a blurring of the margins between the gray and white matter, and hypodensity within brain parenchyma correlating to a particular vascular territory.
For example, you might see a large area of hypodensity in the area of the brain supplied by the middle cerebral artery. If you see these signs, diagnose ischemic stroke as the cause of elevated ICP.
On the other hand, if there is no infarction, assess the CT for a ring-enhancing mass lesion. If present, diagnose a brain tumor or an abscess as the underlying cause of increased ICP.

Brain abscess/tumor 8:01–8:16

Finally, if there’s no ring-enhancing mass lesion on the head CT, assess for the presence of diffuse edema. If present, consider meningitis or encephalitis as a cause of increased ICP.

Meningitis/Encephalitis8:16–9:19

Next, obtain a CSF sample for analysis. If CSF analysis reveals elevated white blood cell count, elevated protein, and a positive culture or PCR, diagnose meningitis or encephalitis as the cause.
Remember, if there is high ICP in the setting of a mass lesion, a lumbar puncture is contraindicated! Now, here’s a clinical pearl to keep in mind!
Increased ICP is commonly seen in cryptococcal meningitis, which occurs in immunocompromised patients such as those with HIV.
Treatment often requires serial lumbar punctures or even placement of a CSF diversion device, such as an external ventricular drain or lumbar drain.
Alright, as a quick recap… Management of increased intracranial pressure includes tiered medical therapy, as well as ICP monitoring and surgical treatments.

Review 9:19–9:57

To determine the underlying cause, first assess the patient’s head CT for any hemorrhagic lesions such as an epidural hematoma, a subdural hematoma, a subarachnoid hemorrhage, or an intracerebral hemorrhage.
If not found, look for an ischemic stroke. If you rule out a stroke, look for a mass lesion, which could be a tumor or an abscess.
Finally, don’t forget to be on the lookout for diffuse edema, which is typically seen in meningitis or encephalitis.