Intracranial Pressure Management



Fig. 11.1
Intracranial compliance curve. Initial increases in intracranial volume are well tolerated. Continued increase in intracranial volume results in loss of compliance and rapid elevations in ICP. Sustained increases can lead to secondary brain injury and herniation syndromes (No re-print premission needed)



Cerebral edema is a common cause of elevated ICP and is classified in two categories: vasogenic and cytotoxic. Vasogenic cerebral edema is characterized by an increase of fluid in the extracellular space and occurs when there is a breakdown in the blood brain barrier. Trauma, brain tumors, infection, hemorrhage and surgical procedures are common causes. Cytotoxic cerebral edema is characterized by an excess of fluid within the intracellular space. Sodium and water shift into the cell, causing swelling and, eventually, cell death [1, 2, 5]. This type of cerebral edema is typically seen in acute hypoxic injury, cerebral ischemia, and hypo-osmolality, but can also occur in trauma, inflammation, and hemorrhage. Both types of cerebral edema, if not managed effectively, can lead to herniation syndromes (see Table 11.1).


Table 11.1
Signs of increased ICP

































Changes in level of consciousness:

 Confusion

 Lethargy

 Agitation

Changes in vital signs:

 Hypertension

 Bradycardia

 Widening pulse pressure

 Irregular respiratory pattern

Headache

Visual disturbances

Nausea and vomiting

Pupillary changes

Hemiplegia/hemiparesis

Herniation syndromes include uncal, transtentorial, subfalcine, and cerebellar [5] (See Fig. 11.2). Each is related to mass effect and compartmental pressure changes because of the rigid intracranial boundaries. The brain tissue herniates from an area of increased pressure to an area of lesser pressure causing clinical exam changes leading to poor outcomes if not treated immediately. Patients with herniation syndrome will present with progressive somnolence, decreased respirations and Cushing’s Triad of symptoms: sudden hypertension, bradycardia, and respiratory irregularities.

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Fig. 11.2
Herniation Syndromes. The brain tissue herniates from an area of increased pressure to an area of lesser pressure causing clinical exam changes leading to poor outcomes if not treated immediately. The different types of herniation syndromes are illustrated below (Retrieved from Wikimedia Commons, a free medical repository. No re-print permission needed)



11.2 Case Presentation


A 23-year-old male with no past medical history was brought to the emergency department following a motor vehicle collision (MVC). He was an unrestrained driver T-boned by another vehicle at approximately 50 mph. Extrication from the vehicle was required. He was unresponsive in the field and immediately intubated upon arrival of EMS in the field for airway protection. Trauma scans revealed a right tentorial subdural hematoma with mild mass effect, a right pontine/midbrain intraparenchymal hemorrhage, fracture of the right occipital condyle, and fracture of the eighth tooth. No other injuries were identified. An external ventricular drain (EVD) and intraparenchymal ICP monitor, temperature, and brain tissue oxygen probes via a triple lumen intracranial bolt were placed. He was admitted to the Neuro ICU in hemodynamically stable condition. Proper positioning, sedation, analgesia, and seizure prophylaxis were immediately implemented. Because of ICP elevations to 55 mmHg sedation was increased; a paralytic administered, and 3% hypertonic saline was started. The patient subsequently had a temperature spike and surface cooling with a goal of normothermia was initiated. Acetaminophen was given and empiric antibiotics began to prevent further fever. The paralytic was gradually weaned off. Over the course of a week, his ICP was maintained <20 mmHg and the intracranial bolt was removed. EVD was removed on hospital day 13.


11.3 Initial Evaluation


It is the role of the neurocritical care clinician to recognize physiologic signs of elevated ICP and take any necessary steps to prevent secondary brain injury and herniation. Initial evaluation should include baseline vital signs and a complete neurologic exam. Symptoms to be evaluated include changes in vital signs, mental status, and pupil size; in addition to headache, visual disturbances, vomiting and motor function abnormalities (see Table 11.2). If there is sudden or unexplained ICP elevation, the patient must be examined immediately. Interventions to lower the ICP must be initiated urgently prior to any diagnostic studies. Head CT should be repeated to rule out new mass lesion that may require surgical evaluation such as new subdural hematoma, epidural hematoma, or hemorrhagic transformation of stroke.


Table 11.2
Common causes of increased ICP

































Primary causes

Edema

Trauma

Brain tumors

Infection/inflammation

Hemorrhage

Ischemic injury/infarction

Hypoxic injury

Hydrocephalus

Secondary causes

Agitation

Hypertension

Seizures

Fever

Most ICP lowering therapies are effective for variable amounts of time and early management goals should include placement of an ICP monitoring device. The purpose of ICP monitoring is to improve the clinician’s ability to maintain adequate cerebral perfusion pressure and oxygenation to the brain. The diagnosis of elevated ICP is made from clinical findings based on the patient’s exam, imaging, and past medical history.

Any patient that is suspected to be at risk for elevated ICP should be considered for placement of an ICP monitoring device. There are four common sites used for ICP measurements; intraventricular, intraparenchymal, subarachnoid, and epidural. Intraventricular monitors are the gold standard of ICP monitoring catheters. They are placed through the skull into the ventricular system and attached to a pressure transducer with collection bag (See Fig. 11.3 for example). The major advantage of an intraventricular system is that CSF can be drained. Disadvantages are infection and potential hemorrhage during placement. Intraparenchymal devices are built around a thin cable with a fiber optic transducer at the tip. These devices are inserted through the skull directly into the brain parenchyma. Their main disadvantage is the lack of ability to drain CSF; advantages include ease of placement and lower risk of infection. Subarachnoid bolts are fluid filled systems within a hollow screw that are placed through the skull adjacent to the dura. The dura is punctured and the CSF communicates with the fluid column and the transducer. Advantages of subarachnoid monitors are low rates of infection and hemorrhage. The major disadvantage is frequent clogging of the system, which renders the measurements unreliable. Epidural ICP monitors contain and optical transducer that rests against the dura once passed through the skull. They are often inaccurate and have limited use clinically.

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Fig. 11.3
Extraventricular drain (EVD). This is a temporary method to reduce ICP that can be regulated manually. The drain is attached to a bag that is transduced to atmospheric pressure and leveled to the midbrain. The drain can then be raised or lowered to different anatomical reference points to facilitate drainage (Photo courtesy of University of Pittsburgh Medical Center)

Once ICP monitors are in place, the waveforms can be easily accessed to help the clinician evaluate intracranial compliance. There are three peaks to the waves that are referenced for clinical significance. P1 is the percussion wave, which reflects arterial pulsation. P2 (tidal wave) represents intracranial compliance and P3 is the dicrotic wave signaling closure of the aortic valve [1, 2]. Normal intracranial compliance is depicted by a sharp, high P1, followed by a P2 that is lower than P1, followed by an even lower P3 wave. Poor intracranial compliance is seen as a P2 wave that is equal to or higher than that of P1 (See Fig. 11.4).
Jan 31, 2018 | Posted by in NEUROSURGERY | Comments Off on Intracranial Pressure Management
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