Management of Severe Brain Injury

Volume-Pressure Curve (Monro-Kellie Hypothesis)

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  Skull is a rigid compartment and contains three components:

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    Brain

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    Blood

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    Cerebrospinal fluid (CSF)

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  Average adult skull contains a total volume of 1475 mL:

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    Brain: 1300 mL

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    CSF: 65 mL

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    Arterial and venous blood: 110 mL

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  An increase in the volume of one component, the volume of one or more of the another components must decrease to maintain the normal intracranial pressure (ICP). Failure of this compensatory mechanism result in an increase in ICP.

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  An increase in ICP results in a decrease in cerebral perfusion leading to cerebral ischemia.

Autoregulation of Cerebral Perfusion

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  Pressure autoregulation

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    Intrinsic ability of brain to maintain a normal CBF with a CPP ranging from 50–110 mm Hg despite change in systolic blood pressure (SBP)

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    CPP <50 mm Hg may cause cerebral hypoperfusion, and >110 mm Hg may result in cerebral hyperperfusion leading to cerebral edema.

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    Increase in ICP increases MAP primarily through a rise in cardiac output, to maintain a steady CPP.

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    Change in MAP is regulated by reflex construction or dilation of precapillary vasculature to maintain a constant CPP, CBF, and ICP.

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    Intact autoregulation

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      Increase in MAP causes increase in CBF, CPP, and ICP. Intact autoregulation causes cerebral vasoconstriction resulting in decrease in CBF, CPP, and ICP.

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      Decrease in MAP causes decrease in CBF, CPP, and ICP. Intact autoregulation causes cerebral vasodilation leading to increase in CBF, CPP, and ICP.

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    Impaired autoregulation

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      Severe traumatic brain injury (TBI) can result in impaired autoregulation.

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      Increase in MAP causes:

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        increase in CBF, CPP, and ICP.

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        cerebral edema.

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      Decrease in MAP results in decrease in CPP leading to brain ischemia and infarction.

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  Chemical autoregulation

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    Change in CBF in response to change in partial pressure of oxygen (PaO ₂ ) and partial pressure of carbon dioxide (PaCO ₂ ) regulates the CPP and ICP.

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    Acute hypoxia

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      It is a potent cerebral vasodilator and results in an increase in CBF.

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      CBF does not change until tissue PaO ₂ falls below approximately 50 mm Hg.

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      Increases in CBF do not change cerebral metabolism but affect oxygen saturation of cerebral hemoglobin.

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    Hypercapnia

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      Causes dilation of cerebral arteries and arterioles resulting in increased blood flow

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    Hypocapnia

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      Causes constriction of cerebral arteries and arterioles resulting in decreased blood flow

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    Brain injury

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      Can cause impaired chemical autoregulation

Causes of Elevated Intracranial Pressure

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  Mass effect in head injury due to:

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    Epidural hematoma (EDH).

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    Subdural hematoma (SDH).

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    Hemorrhagic contusion.

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    Depressed skull fractures.

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  Diffuse brain edema

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  Hyponatremia

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  Hyperemia due to loss of autoregulation

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  Disturbance of CSF circulation

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    Obstructive hydrocephalus

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    Subarachnoid hemorrhage (SAH)

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  Hypoventilation

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  Cerebral vasospasm

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  Cerebral venous outflow obstruction

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    Increased intrathoracic pressure

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    Increased intraabdominal pressure

Effects of Elevated Intracranial Pressure

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  Normal ICP: 5–15 mm Hg in lateral ventricles or lumbar subarachnoid space in supine position

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  Effects of elevated ICP

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    Decrease in CPP leading to low CBF and cerebral ischemia

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    Severe increase in ICP triggers the cerebral ischemic response, also known as the Cushing reflex, which include:

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      Increase in sympathetic response leading to elevated MAP to increase CPP.

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      Reflex bradycardia.

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      Seen in late phase of intracranial hypertension (ICH), such as near brain dead/herniation syndrome.

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  Sustained ICP >40 mm Hg results in life-threatening IH.

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    May cause a shift in brain parenchyma causing cerebral herniation syndrome

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    Results in irreversible brain damage and death

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  Manifestations of elevated ICP

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    Headache

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    Vomiting, with or without nausea

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    Mental status changes

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      Decrease in level of consciousness

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      Restlessness

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      Agitation

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      Confusion

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    Tachycardia

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    Dysrhythmias

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    Cushing’s triad: due to pressure on medullary center

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      Increase in SBP and pulse pressure

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      Bradycardia

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      Cheyne-Stokes breathing: irregular respiration characterized by periods of slow, deep breaths followed by periods of apnea

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    Pupillary changes

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      Anisocoria (unequal pupils)

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      Sluggish reaction to light

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      No reaction to light

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      Papilledema is a reliable sign of IH but is uncommon after head injury.

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      Pupillary dilation can occur in the absence of IH.

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    Motor changes

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      Asymmetrical weakness

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      Bilateral weakness

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      Posturing

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      Flaccidity

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      Decerebrate posturing can occur in the absence of IH.

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    Brain herniation

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      Manifestation depends on the location of brain herniation.

Brain Herniation

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  Displacement of brain into nearby compartments due to local ICP gradients.

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  Types of brain herniation

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    Subfalcine herniation

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      Most common type of brain herniation

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      Usually due to convexity (frontal or parietal) mass lesion

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      Manifestation

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        Strangulation of the anterior cerebral artery due to movement of brain underneath the falx cerebri

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        Asymmetric (contralateral more than ipsilateral) motor posturing

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        Preserved oculocephalic reflex

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    Transtentorial herniation

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      Temporal lobe (uncal) herniation (lateral descending transtentorial hernia)

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        Usually seen due to mass lesion in the temporal lobe

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        The uncus of the temporal lobe shifts downward into the posterior fossa.

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        Manifestations

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          Ipsilateral pupillary dilation due to compression of cranial nerve III (oculomotor nerve) from herniation of the medial temporal lobe under the tentorium cerebelli causing displacement of the midbrain

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          Contralateral hemiplegia/posturing

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          Bilateral motor posturing

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      Central herniation (central descending transtentorial herniation)

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        Downward displacement of the entire brainstem through the tentorial notch due to diffuse cerebral edema

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        Manifestations:

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          Bilateral pupillary dilatation due to cranial nerve III palsy

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          Lateral gaze palsy: due to cranial nerve VI (Abducens nerve) compression leading to lateral rectus muscle palsy

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          Bilateral decorticate to decerebrate posturing

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          Decorticate posturing: stiffness of the extremities with legs held out straight, clenched fists, and bent arms on the chest

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          Decerebrate posturing: straight and rigid arms and legs, toes pointed downward, and head arched backward

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          Loss of brainstem reflexes

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        Obliteration of the suprasellar cistern in imaging

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      Ascending transtentorial herniation

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        Upward herniation of posterior fossa contents (cerebellum and brainstem) through the tentorium cerebelli.

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        Typically seen after excessive CSF ventricular drainage

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        Manifestations

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          Bilateral pupillary dilation

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          Extensor posturing

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    Cerebellar/tonsillar herniation

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      Downward displacement of cerebellar tonsils through the foramen magnum due to cerebellar mass lesion resulting in compression of the medulla

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      Manifestations

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        Episodic extensor posturing

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        Cardiac dysrhythmias

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        Pupillary dilatation

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        May result in cardiopulmonary arrest

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    Extracranial herniation

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    Brain herniation through a traumatic or post craniotomy skull defect

MRI and CT Scan

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  Qualitative information about ICP can be obtained with CT and MRI of the brain.

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  Features suggestive of increased ICP include:

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    midline shift and compression of the ventricles due to mass occupying lesion.

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    enlarged ventricles due to hydrocephalus.

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    loss of grey and white matter junction due to cerebral edema.

Electroencephalography

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  Triphasic wave in continuous electroencephalography (EEG) monitoring is a prognostic marker in patients with IH.

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  It also is a predictor for improving cortical function in patients with elevated ICP.

Intracranial Pressure Monitoring

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  Indications

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    Severe brain injury (Glasgow Coma Scale [GCS] <8) with initial CT evidence of:

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      structural brain damage such as hematoma or contusion.

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      increased ICP as suggested by compressed or absent basal cisterns.

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    Severe brain injury (GCS <8) with normal initial CT with two or more of the following:

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      Patient >40 years of age

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      Hypotension: SBP <90 mm Hg

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      Bilateral motor posturing

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    Brain injury with GCS >8 with computerized tomography (CT) scan evidence of structural brain damage with high risk of progression

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      Large or multiple contusions or hematoma

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      Coagulopathy

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    Brain injury with GCS >8 and extracranial injuries

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      Need for urgent surgery for extracranial injuries

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      Need for ventilation for extracranial injuries

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      Progression of pathology in CT imaging

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      Clinical deterioration

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  Methods of ICP monitoring

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    External ventricular drain (EVD)

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      A catheter is placed in the lateral ventricle through a burr hole at Kocher’s point (10.5 cm posterior to the nasion and 3.5 cm lateral on the midpupillary line).

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      Traditionally, the right lateral ventricle is preferred.

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      Catheter is tunneled and connected to a pressure transducer via a fluid-filled tubing at the level of the ear.

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      EVD is considered the most accurate method of ICP measurement.

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      Disadvantages

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        Catheter placement into a compressed or displaced ventricle may be difficult.

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        Risk of cerebral parenchymal bleeding during insertion of the catheter.

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        Risk of infection, such as potentially life-threatening ventriculitis

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      Advantages

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        EVD is a preferred method of ICP monitor because it is both diagnostic (measures ICP) and therapeutic (drains CSF).

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        It measures the global brain pressure.

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        It can be recalibrated after placement.

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  Nonventricular devices

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    Useful when access to the ventricle is difficult

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    Less risk of infection

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    Techniques

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      Fiberoptic transducers/pressure microsensors placed outside the ventricles. Locations include:

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        Epidural

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        Intraparenchymal

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        Subarachnoid

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        Subdural

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      Subarachnoid screw

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        A catheter inserted into subarachnoid space through a hole drilled in the skull and connected to a pressure transducer

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    Disadvantages

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      No therapeutic drainage

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      Reflects regional pressure rather than global brain pressure

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      Subarachnoid, subdural, and epidural ICP devices are less accurate.

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      Fiberoptic systems need external calibration to ensure constant accuracy.

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  ICP waveform

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  Three components of ICP waveforms:

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    W-1:

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      Pulse pressure waveforms

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    W-2:

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      Respiratory waveforms due to respiratory cycle

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    Lundberg A, B, and C waves

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      Slow vasogenic waveforms

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  Pulse pressure (W-1) waveforms:

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    Intracranial pulse waveforms are generated by arterial pulses transmitted to brain.

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    These correlate to the arterial pressure.

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    Frequency is equal to heart rate.

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    Elevated ICP affects the characteristics of the waveform.

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    Subdivided into three waves: P1, P2, and P3

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      P1 wave

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        Also called percussion wave.

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        Due to transmitted arterial pulse through the choroid plexus into the CSF

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        High-amplitude P-wave is seen in patients with high SBP.

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        Low-amplitude P-wave is seen in low SBP.

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      P2 wave

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        Called elastance or tidal wave

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        Results from a restriction of ventricular expansion by a closed rigid skull

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        Represents cerebral compliance

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        Amplitude of P2 is increased due to decrease in brain compliance and increase in ICP.

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      P3 wave

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        Also called dicrotic wave

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        Correlates with closure of the aortic valve, equivalent of the dicrotic notch

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    Under normal circumstances: P1 > P2 > P3

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    In brain injury leading to reduced brain compliance:

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      P2 > P1

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      Sensitive predictor of poor outcome

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  Lundberg waves

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    A-wave (plateau wave)

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      Sustained and severe elevation in ICP

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      5–20 minutes long

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      High amplitude (50–100 mm Hg)

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      Suggestive of decreased intracranial compliance, compromised cerebral perfusion pressure, and global cerebral ischemia

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      Considered a high risk for further (or ongoing) brain injury, with critically reduced perfusion due to a prolonged period of high ICP

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      Considered pathognomonic of ICH

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    Lundberg B-wave and C-wave

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      B-waves and C-waves are of less clinical significance.

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    B-wave

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      Lasts for <5 minutes (usually 1–2 minutes) with 20–50 mm Hg in amplitude

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      Does not represent any pathological disturbance

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      Usually associated with Cheyne-Stokes respiration

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      May reflect vasodilatation due to respiratory fluctuation in PaCO ₂

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      May be due to intracranial vasomotor waves causing variation of CBF

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    C-wave

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      Last for 4–5 minutes

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      <20 mm Hg in amplitude

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      No pathological consequence

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      Associated with BP-associated hemodynamic changes

Advanced Neuromonitoring Techniques

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  ICP monitoring alone cannot detect all potential insults; additional monitoring may be required for the management of severe TBI.

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  CBF and cerebral oxygenation are important for outcomes in severe TBI.

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  Low brain tissue oxygen tension (PbO ₂ ) has been seen in patients with normal ICP and CPP.

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  Techniques

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    Cerebral autoregulation measurement

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      Can be monitored by measuring cerebrovascular pressure reactivity index (PRx)

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      PRx is calculated from the MAP and ICP within a frequency range of 0.003–0.05 Hz.

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      PRx varies with the concurrent CPP in a U-shape.

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      Impaired autoregulation is characterized by PRx slope of >0.13 and lower CPP (50–60 mm Hg), and it is associated with poor outcome in TBI.

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      CPP with the lowest PRx is optimal (CPPopt) and is associated with better outcome after severe head injury with elevated ICP.

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      CPP values above CPPopt can cause hyperemia due to high CBF leading to cerebral edema and ICH.

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      CPP values below CPPopt can cause cerebral hypoperfusion and cerebral ischemia.

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      PRx can be used to guide the management of CPP and CBF in severe brain injury.

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  Brain tissue oxygen tension

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    PbO ₂ can be measured using near-infrared spectroscopy (NIRS).

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    NIRS provides continuous PbO ₂ and ICP monitoring.

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    Low PbO ₂ (<15 mm Hg) is associated with poor outcome.

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    Management utilizing ICP and PbO ₂ showed a 10% reduction in mortality and improved neurological outcome in severe TBI.

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  Jugular venous oxygen saturation (SjvO2) measurement

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    SjvO ₂ <50% associated with poor outcome in severe TBI

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  Transcranial doppler ultrasonography (TCD)

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    Provides real-time monitoring of ICP and CPP

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    CBF is measured by mean blood-flow velocity (MFV), and ICP is measured by pulsatility index (PI) values of the middle cerebral artery (MCA) and the other major intracranial vessels.

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    TCD can be used to assess autoregulation with hemodynamic challenges.

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    TCD-based assessment of CBF and autoregulation has been more reliable than TCD-based ICP measurement.

Recommendations (American College of Surgeons Committee on Trauma, 2015)

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  Clinical parameters

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    SBP ≥100 mm Hg

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    Temperature: 36°C–38°C (96.8°F–100.4°F)

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  Monitoring parameters

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    CPP ≥60 mm Hg

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    ICP 20–25 mm Hg

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    Pulse oximetry ≥95%

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    Partial pressure of brain tissue oxygen (PbtO ₂ ) ≥15 mm Hg

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  Laboratory parameters

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    Glucose: 80–180 mg/dL

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    Hemoglobin: ≥7 g/dL

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    International normalized ratio (INR): <1.4

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    Sodium: 135–145 mg/dL

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    PaO ₂ : ≥100 mm Hg

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    PaCo ₂ : 35–45 mm Hg

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    pH: 7.35–7.45

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    Platelets: ≥75 × 10 ³ /mm ³

Management of Airway, Breathing, and Circulation

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  Important to prevent hypoxia, hypercapnia, and hypotension in order to prevent secondary brain injury

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  Hypercarbia is a potent cerebral vasodilator causing increase in cerebral blood volume and ICP.

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  High positive end-expiratory pressure (PEEP) can increase ICP by impeding venous return and increasing central venous pressure (CVP).

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  Hypotension will result in decreased CPP

Management of Hypertension

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  Hypertension is common in patients with head injury with ICH due to sympathetic hyperactivity.

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  Systolic hypertension is greater than diastolic hypertension.

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  Elevated BP may exacerbate cerebral edema.

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  Correction of systolic hypertension before treating the ICH in patients with mass lesion may result in reduction of CPP.

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  In patients with severe head injury with impaired autoregulation:

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    hypertension may increase CBF, CPP and ICP.

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    hypotension may decrease CBF, CPP, and ICP.

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  Goal: SBP ≥100 mm Hg

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  Medication for hypertension

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    Sedation may resolve hypertension.

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    Vasodilating drugs such as nitroprusside, Hydralazine, and nitroglycerin should be avoided as these can increase ICP.

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    Antihypertensives of choice include:

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      Beta-blocking drugs (labetalol, esmolol), and Nicardipine

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      Central acting alpha-receptor agonists: clonidine