Management of Increased Intracranial Pressure and Intracranial Shunts

Brain

Brain volume can be increased by edema, idiopathic intracranial hypertension (IIH), tumor, or bleeding. The three types of edema are vasogenic, cytotoxic, and interstitial. Vasogenic edema results from increased permeability of the capillaries, which leads to passage of excess fluid into the extracellular space. Cytotoxic edema is due to accumulation of intracellular fluid in brain tissue (neurons and glia) secondary to dysfunction of the adenosine triphosphatase pump. Interstitial edema occurs when fluid accumulates as a result of blockage of CSF absorption.

IIH, formerly known as pseudotumor cerebri or benign intracranial hypertension, is a chronic condition characterized by increased CSF pressure not caused by a tumor, edema, hydrocephalus, or change in CSF composition. It occurs most frequently in obese women. Symptoms may include headache, nausea, and blurry vision. The headache is typically worse on waking or with exertion. In general, patients with IIH have normal findings on neurologic examination except for the frequent presence of papilledema. The precise pathophysiology behind IIH remains unclear, with several proposed etiologies, including: cerebral venous outflow abnormalities (e.g., venous stenosis); increased CSF outflow resistance at either the level of the arachnoid granulations or CSF lymphatic drainage sites; obesity-related increased abdominal and intracranial venous pressure and obesity-related chronic inflammation; altered sodium and water retention mechanisms; abnormalities of vitamin A metabolism; and sex hormone dysfunction. Severe and untreated cases of IIH can lead to permanent vision loss. There appears to be some crossover with the more serious and life-threatening diagnosis of cerebral venous thrombosis (CVT), and therefore magnetic resonance (MR) (ideally with venography) or computed tomography (CT) venography of the cerebral venous system is recommended in patients with presumed IIH to rule out CVT. Other commonly associated conditions are listed in Box 59.1 .

Brain tumors encompass neoplasms that originate in the brain itself (primary brain tumors) or involve the brain as a metastatic site (secondary brain tumors). Primary brain tumors include tumors of the brain parenchyma, meninges, cranial nerves, and other intracranial structures (the pituitary and pineal glands) ( Fig. 59.4 ). Primary central nervous system lymphoma refers to high-grade B-cell non-Hodgkin's lymphoma confined to the central nervous system. Secondary brain tumors, the most common type, originate elsewhere in the body and metastasize to the intracranial compartment.

Bleeding in the brain can occur spontaneously (as in the case of hemorrhagic stroke or spontaneous subarachnoid hemorrhage) or can be a result of trauma. In addition to the mass effect of the blood itself, the associated edema contributes to further increases in ICP. Diffuse axonal injury (DAI) may occur in isolation or in conjunction with intracerebral bleeding. With DAI, it is believed that the axons are not actually torn, but instead suffer significant injury that may lead to edema (shearing effect).

CSF

CSF is produced by the choroid plexus at a daily rate of 400 to 600 mL (~ 20 mL per hour) with complete turnover of total volume occurring four to five times per day in young adults ( Fig. 59.5 ). It flows from the ventricles into the cisternae of the subarachnoid space and is drained by the arachnoid villi of the dural sinuses to maintain a constant volume of 100 to 150 mL. Obstructive hydrocephalus occurs when flow is blocked at any point in the ventricular system by clotted blood, tumor, colloid cyst, edema, or primary stenosis. Communicating hydrocephalus is due to impedance of flow beyond the ventricular system at the level of the basal cisternae or lack of absorption by the arachnoid villi. Communicating hydrocephalus can occur with both infection and subarachnoid hemorrhage ( Fig. 59.6 ).

Blood

Up to a certain range, cerebral blood flow (CBF) is maintained by an autoregulatory mechanism despite fluctuations in cerebral perfusion pressure (CPP) ( Fig. 59.7 ). Constant CBF can typically be maintained at any CPP between 60 and 160 mm Hg. Once CPP is out of the autoregulatory zone, CBF is linearly related to CPP. CPP lower than 60 mm Hg can lead to ischemia, whereas CPP higher than 160 mm Hg can result in hypertensive encephalopathy.

Oxygenation

Management of the airway and breathing is paramount in patients with brain injury. If the patient is hypoxic, supplemental oxygen is critical in preventing further ischemia. Patients with a Glasgow Coma Scale (GCS) score of 8 or lower or with impending signs of inadequate respiratory status should undergo rapid-sequence intubation (RSI) to protect their airway and better control blood levels of oxygen and carbon dioxide (partial pressure of oxygen [P o ₂ ] and partial pressure of carbon dioxide [P co ₂ ]). Apneic patients should receive bag-valve-mask ventilation while preparing for intubation, with specific avoidance of hyperventilation, and apneic oxygenation via a high-flow nasal cannula (rate of 15 L/min or higher) during airway securement.

Sedation and Paralytics

A rapid neurologic examination that assesses the patient's pupillary reflexes, motor response to voice and painful stimuli, and the ability to interact with his/her surroundings should be performed before sedation and RSI. To blunt the hemodynamic response to intubation, fentanyl, at an intravenous (IV) dose of 2 to 5 µg/kg, can be given over 30 to 60 seconds while preoxygenating the patient. Fentanyl is an excellent drug for control of pain, which if untreated, can lead to increased ICP. Fentanyl can also be given during the pretreatment phase of RSI (3 minutes before administration of the paralytic agent) if time allows. Caution should be exercised, however, to avoid precipitous drops in blood pressure, which can threaten CBF and exacerbate brain injury. Therefore it should be avoided in hypotensive patients and hypovolemic patients. We also recommend caution in brain-injured patients with concomitant trauma, who may have exaggerated episodes of hypotension with narcotics and sedatives. Pretreatment lidocaine, which was traditionally believed to decrease the sympathomimetic response to intubation, is no longer recommended as multiple studies have shown conflicting and insufficient evidence to support its use. A defasciculating dose (typically 1/10 the intubating dose) of a nondepolarizing neuromuscular blocking agent given prior to intubation has also fallen out of favor as no sufficient evidence has supported its use.

In patients who are normotensive or hypotensive, etomidate (0.3 mg/kg IV) is the induction agent of choice due to its minimal effect on systemic blood pressure and its lowering of ICP. Ketamine, at a dose of 1 to 2 mg/kg IV, can also be used as it does not appear to increase ICP, as previously believed, and should be strongly considered in severely hypotensive patients due to its ability to increase blood pressure and its analgesic effects that minimize the adverse sympathetic stimulation of laryngoscopy. In hypertensive patients, thiopental (50 to 100 mg IV or 3 to 5 mg/kg IV) or propofol (1 mg/kg IV) can be used for induction. Propofol has gained acceptance as a sedative in patients with increased ICP because of its short duration of action and depression of cerebral metabolism and oxygen consumption. This may have a neuroprotective effect. However, with higher doses propofol can cause profound decreases in systemic blood pressure and extended periods of use can be associated with significant morbidity.

Succinylcholine (1.5 mg/kg in adults and up to 2.5 mg/kg in pediatric patients) is the ideal paralytic agent in patients with increased ICP due to its rapid onset, short duration of action, and consistent and reliable effects. Nondepolarizing agents (e.g., rocuronium) are appropriate when contraindications to succinylcholine exist (see Chapter 5 ). Sedatives and paralytics should be short-acting to facilitate close monitoring of the patient's neurologic status.

Oxygenation and Hyperventilation

As the airway is secured, adequate supplemental oxygen should be provided, with titration down rapidly from the initial fraction of inspired oxygen of 1.0 used for RSI to ensure oxygen saturation greater than 90%.

In general, avoid hyperventilation in patients with brain injury as low P co ₂ levels cause cerebral vasoconstriction, resulting in decreased CBF in the critical hours following injury. Hyperventilation is also associated with poor survival and neurologic outcomes. For the majority of brain-injured patients, the target is thus eucapnia with a P co ₂ of 35 to 40 mm Hg. Nevertheless, if a patient displays evolving signs of brain herniation (e.g., anisocoria, hemiparesis, asymmetric posturing, Cushing's reflex, or rapid deterioration in GCS score), hyperventilation may be necessary to arrest the process. Current recommendations target a P co ₂ of 28 to 35 mm Hg in these scenarios as a temporizing measure until surgical or other interventions to lower ICP can occur.