Elevated Intracranial Pressures
Last updated: 08/02/2023
- Intracranial pressure (ICP) can fluctuate. An ICP greater than 20-25 mmHg is considered elevated, and an ICP greater than 40 mmHg is severely elevated.
- ICP is mainly affected by the cerebral blood flow, the cerebrospinal fluid volume/flow, and the integrity of the brain parenchyma.
- Acute intracranial hypertension is a neurosurgical emergency, and anesthesiologists can directly employ multiple treatment options for these patients.
- ICP normally ranges from 7 to 15 mmHg. It can fluctuate slightly with day-to-day activities. However, a sustained ICP greater than 20-25 mmHg is associated with poor neurologic outcomes, and an ICP above 40 mmHg is life-threatening.1,2
- Most often, a diagnosis of acute intracranial hypertension is made clinically before the direct measurement of ICP.
- Intracranial compliance is defined as the change in intracranial pressure over the change in intracranial volume.1
Pathophysiology of Intracranial Hypertension
- The importance of ICP was recognized more than 200 years ago and is referred to as the Monro-Kellie doctrine (or hypothesis), which states that4
- the brain is enclosed in a nonexpandable case of bone;
- the brain parenchyma is nearly incompressible;
- the volume of blood in the cranial cavity is therefore, nearly constant; and
- a continuous outflow of venous blood from the cranial cavity is required to make room for incoming arterial blood.
- The intracranial vault is composed of 3 compartments:
- blood volume
- cerebral spinal fluid (CSF)
- brain parenchyma
- Intracranial hypertension and elevated ICP occur when the volume of one of the compartments increases, and further compensation by a decrease in another compartment is no longer possible.
Signs and Symptoms
- Common presenting symptoms of intracranial hypertension include:
- nausea, vomiting, headache, downcast eyes, papilledema, altered mental status, and/or acute focal neurologic deficit
- The concern with acute intracranial hypertension is progression to brain herniation, the symptoms of which would vary depending on the place of herniation.2.3
- The Cushings triad includes hypertension, bradycardia, and irregular respirations. It reflects severe, increased intracranial pressure.1
- The potential sites of brain herniation can be classified into supratentorial and infratentorial (Figure 2).
- Supratentorial: uncal (transtentorial), central, cingulate (subfalcine), transcalvarial, and tectal (posterior)
- Infratentorial: upward cerebellar and tonsillar (downward cerebellar).
Indications for ICP Monitoring
- Several organizations have proposed guidelines for ICP monitoring. Most generally agree that ICP monitoring is indicated for patients with a structural brain abnormality and a Glasgow Coma Scale (GCS) score < 8.
- Other indications exist regardless of GCS score include:5
- acute brain injuries such as subarachnoid hemorrhage;
- brain abnormalities at risk of rapid progression;
- patients with coagulopathies; and
- patients requiring emergent neurologic surgery.
Modalities for ICP Monitoring
- Invasive modalities
- An extraventricular drain (EVD) inserted into the lateral ventricle is the gold standard. It is both diagnostic and therapeutic as it provides a measurement of ICP and can be also be used to drain CSF as necessary (Figure 3).
- Other invasive modalities include fiberoptic monitoring, combination catheters (“Hummingbird Synergy”) and telemetric monitors. Telemetric monitoring allows the opportunity for long-term ICP monitoring since it involves implantation of the device via a burr hole and reading through an external device.
- Noninvasive modalities
- External structures communicate with the subarachnoid space, and can therefore reflect ICP.5
- Eye: use of ultrasonography to measure optic nerve sheath diameter
- Vasculature: external ultransonography of middle cerebral artery, which is based on the principle that increased ICP affects cerebral blood flow; the vessel wall changes based on ICP and acts as “transducer” of ICP.
Management of Elevated Intracranial Pressure by Compartment3
Cerebral Metabolic Rate of Oxygen Consumption and Burst Suppression
- The brain consumes approximately 3 to 4 mL of oxygen per 100g of brain tissue per minute. This is referred to as the cerebral metabolic rate of oxygen consumption (CMRO2).
- Lowering CMRO2 decreases cerebral blood volume through metabolic autoregulation and subsequent vasoconstriction of cerebral arterioles.
- Burst suppression refers to suppression of cortical electrical activity with the presence of intermittent “bursts” of activity alternating with a flat line as seen on the EEG. This offers neuroprotection by reducing the CMRO2.1
Hyperventilation & its Controversies
- Hyperventilation affects ICP by lowering the arterial partial pressure of CO2, which in turn causes vasoconstriction and decreases cerebral blood flow and volume.
- Increasing CO2 results in arterial vasodilation, and the inverse is true. However, there is a limit to the effectiveness of hyperventilation, such that below a PaCO2 of 25 mmHg, cerebral vasoconstriction has been maximized.
- The brain will adjust to the reduced levels of CO2 within 6-18 hours, and hyperventilation may no longer be beneficial.
- Caution must be taken in patients at risk for cerebral ischemia as the cerebral vasoconstriction will incidentally decrease blood flow to at-risk areas of brain parenchyma.7
- Hyperventilation is associated with worse outcomes in traumatic brain injury.
- Hyperventilation should only be used in cases of impending herniation and as a bridge to more definitive therapy, such as surgical decompression or hyperosmolar therapy.
- Bebawy JF, Pasternak JJ. Anesthesia for Neurosurgery. In: Barash PG, et al. Clinical Anesthesia. Eighth Edition. Philadelphia, PA; Wolters Kluwer; 2017.
- Sharma S, Hashmi MF, Kumar A. Intracranial hypertension. In: StatPearls (Internet). Treasure Island, FL. StatPearls Publishing. January 2022. PubMed
- Hararay M, Dolmans RGF, Gormley WB. Intracranial pressure monitoring-review and avenues for development. Sensors (Basel). 2018;18(2): 465. PubMed
- Andrews PJD, Citerio G. Intracranial pressure. Part one: historical overview and basic concepts. Intensive Care Med. 2004; 30:1730-33. PubMed
- DiGiorgio A, Huang MC, Wang VY, et al. Intracranial pressure monitoring. In: Winn HR (ed). Youmans and Winn Neurological Surgery. Philadelphia, PA. Elsevier. 2023. 37, 288-295.
- Anesthesia for Neurosurgery. In: Butterworth IV JF, Mackey DC, Wasnick JD. eds. Morgan & Mikhail’s Clinical Anesthesiology, 7e. McGraw Hill; 2022. Accessed July 18, 2022.
- Monahan C. Intracranial Pressure. In: Freeman BS, Berger JS. Anesthesiology Core Review: Part Two Advanced Exam. McGraw Hill; 2016. Accessed July 19, 2022.
- Ropper A. Hyperosmolar therapy for raised intracranial pressure. N Engl J Med. 2012; 367:746-752. Link
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