Elevated Intracranial Pressures

Introduction

• 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

1. the brain is enclosed in a nonexpandable case of bone;
2. the brain parenchyma is nearly incompressible;
3. the volume of blood in the cranial cavity is therefore, nearly constant; and
4. 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).

ICP Monitoring

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

Hyperosmolar Therapy⁸

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.