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Introduction   

Intracranial hypertension, more commonly referred to as increased intracranial pressure (ICP), is elevated pressure within the cranium. Left untreated elevated ICP can lead to brain tissue ischemia and brainstem herniation. Management of elevated ICP focuses on ensuring enough perfusion to the brain tissue ensuring enough oxygen and nutrients without worsening the intracranial volume and pressure.  

The etiology of elevated ICP is distinguishable by the physiologic component of the brain affected, which includes the brain tissue, cerebrospinal fluid (CSF), and blood. This continuing education module emphasizes an understanding of the Monro-Kellie Doctrine, which is a cornerstone in recognizing the clinical manifestations, medical management, and nursing implications in the setting of cerebral edema. 

Epidemiology and Etiology 

The actual incidence of intracranial hypertension is unknown because the exact epidemiology of intracranial hypertension depends on its etiology, which is numerous (2). Intracranial hypertension results from anything that creates increased pressure within the cranium, including cerebral edema. The most basic definition of cerebral edema is swelling of the brain tissue from neurologic or non-neurologic causes. Brain parenchyma refers to the functional tissue in the brain (1). 

Pathophysiology 

Intracranial hypertension results from anything that creates increased pressure within the cranium.  

Cerebral Edema  

Intracranial hypertension can result from cerebral edema. The most basic definition of cerebral edema is swelling of the brain tissue from neurologic or non-neurologic causes. There are four categories of cerebral edema:  

Vasogenic cerebral edema, most commonly caused by tumors, occurs due to a breakdown of the blood-brain barrier which leads to an osmotic draw of fluid into the brain (3).  

Cellular (cytotoxic) edema occurs from cerebral ischemia which leads to failure of the sodium-potassium pump resulting in an accumulation of sodium within the cell. The accumulation of intracellular sodium creates an osmotic gradient drawing water into the cell. Traumatic brain injury (TBI) and stroke are causes of cellular cerebral edema (5,2).  

Interstitial cerebral edema occurs from an overflow CSF due to obstruction from the intraventricular space into the interstitial spaces and settling into the brain parenchyma. Hydrocephalus and meningitis are causes of interstitial cerebral edema (5,1).  

Osmotic cerebral edema results from differing solute concentrations between the brain parenchyma and blood plasma. This gradient leads to a fluid flowing from the serum into the brain (4). Pathologies that contribute to the differing solute concentrations include diabetic ketoacidosis, hyponatremia, and hepatorenal failure (2). 

Monro-Kellie Doctrine  

Familiarity with the Monro-Kellie Doctrine is important to understand how cerebral edema impacts ICP. The human skull holds a fixed volume between 1400-1700 mL of three main physiologic components: brain (80%), CSF (10%), and blood (10%) (6). Since the skull has an unchangeable volume, any increase in three components requires a decrease in another, otherwise, increased intracranial pressure (ICP) occurs. The normal range for ICP is 5-15 mmHg.   

Prolonged elevated ICP, greater than 20 mmHg, has serious consequences on brain function, in particular cerebral tissue perfusion and brainstem herniation. Increased ICP essentially compresses the brain, which in turn compresses blood vessels bringing oxygen to the brain resulting in cerebral hypoxia. A catastrophic consequence of increased ICP is brain herniation, which occurs when the brain is displaced (7).  

Cerebral Perfusion Pressure 

Normal body functions such as coughing, and hyperthermia can transiently elevated ICP without harming cerebral perfusion. Persistently elevated ICP poses a risk of injury from direct brainstem compression or decreased cerebral blood flow resulting in ischemia. Adequate cerebral blood flow is determined by cerebral perfusion pressure (CPP). Normal CPP ranges from 60-80 mmHg. This is the necessary amount of blood flow to adequately supply oxygen and nutrients for neurons to survive. The CPP is calculated by subtracting mean arterial pressure (MAP) from the intracranial pressure (ICP) (8).  

CPP = MAP – ICP 

ICP is a direct measurement from a device placed directly into the brain. A normal MAP ranges from 70-100 mmHg. A minimum MAP of 60 mmHg is necessary for vital organ perfusion. The MAP is a calculation of the amount of pressure in the arteries during a single cardiac cycle​ and is the force that pushes blood into the brain​.  

The MAP is provided from either an arterial line or from non-invasive blood pressure (NIBP) values. An arterial line catheter can provide continuous BP and MAP readings, necessary to monitor critically ill patients requiring continuous hemodynamic monitoring and/or frequent lab draws. The following equation is a common way to determine the MAP through NIBP monitoring (8,9). 

MAP = SBP + (2 x DBP) 

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Example: A 15-year-old is admitted to the PICU after an eight-foot fall while climbing a tree. Based on GCS 7 and evidence of intracranial bleeding on head CT, the decision is made to intubate and place an ICP probe. Upon transfer to the PICU, his current BP is 110/72 and his ICP is 12. Let’s determine if the patient has adequate CPP at this time. 

Step 1: First calculate the MAP  

110 + (2 x 72) 

                  3 = 84 mmHg 

Step 2: The ICP 12 is provided from a direct measurement.  

Step 3: Calculate CPP   

84 mmHg – 12= 72 mmHg 

The patient has a CPP of 72 mmHg, which falls within the normal range for CPP indicating adequate blood perfusion to the brain.  

Clinical Manifestations 

This section covers the clinical manifestation of increased ICP and reviews the contributing pathophysiology. Cerebral edema can begin within the first few hours after brain injury and peaks between 48 to 72 hours (10). Early symptoms of cerebral edema or increased ICP include altered mental status, headaches, and emesis. The late signs include Cushing Triad, fixed and dilated pupils, Babinski reflex, and abnormal posturing.  

Altered mental status occurs due to cerebral hypoxia. Signs of altered mental status include irritability, restlessness, change in level of consciousness (LOC), and sleepiness (10).  

The Glasgow Coma Scale (GCS) is a scale that evaluates and trends a patient’s level of consciousness. The GCS assesses three aspects of LOC: eye-opening, motor, and verbal responses. The highest score is fifteen indicating normal LOC. A GCS score of eight or below indicates severe brain injury.  

Headaches are a result of the increased pressure within the cranium. The headache is likely worse upon waking due to fluid accumulation from recumbent positioning while asleep. The headache may improve with upright positioning because gravity drains accumulated fluid from the brain. 

Emesis occurs because of the increased pressure on the vagus nerve. Emesis as a result of increased ICP is characterized as sudden, projectile, and without nausea. The vagus nerve innervates the parasympathetic nervous system, specifically the stomach causing vomiting.  

Increased ICP compromises venous drainage from the eye leading to swelling of the optic disk, more commonly referred to as papilledema (11). Papilledema typically affects both eyes and results in vision problems, including blurred or double vision and loss of visual fields. Untreated papilledema can cause blindness. 

The Cushing (Reflex) Triad is composed of three components; hypertension with widened pulse pressure, bradycardia, and irregular respirations (i.e. Cheyney-Stokes). When the ICP increases leading to decreased CPP, the sympathetic nervous system is stimulated by the hypothalamus, and the peripheral vascular system vasoconstricts, increasing the blood pressure (particularly the systolic blood pressure) to increase cerebral blood flow.  

The body attempts to compensate for the increased BP by decreasing heart rate (bradycardia). This steadies diastolic pressure; however, the systolic blood pressure continues increasing leading to a widened pulse pressure.  The respiratory center is in the medulla at the base of the brain. The pressure placed on the medulla alters respiratory pattern and rate. Cheney-Stokes respirations are a noteworthy irregular respiratory pattern from increased ICP. Cheyney-Stokes respirations are characterized by alternating periods of shallow breathing with deeper, rapid breathing followed by a brief apneic period (6).  

On physical assessment, the healthcare provider may witness changes in pupils, abnormal posturing, and abnormal reflexes when the ICP is severely elevated (6,10). Pupillary abnormalities include fixed, dilated, and possibly unequal size pupils. Fixed means that the pupils are not reactive to light and dilated means the pupils measure eight millimeters (normal two to six millimeters). Decorticate (arms flexed and fixed at the chest) and decerebrate posturing (all limbs are hyperflexed) are abnormal posturing that are signs of severe brain damage. Additionally, Seizures and coma are complications of severely elevated ICP.  

Evaluation  

Head computerized tomography (CT) is a crucial part of the initial evaluation for increased ICP.  Head CT is preferred over magnetic resonance imaging (MRI) in acute emergency settings because it is faster and more convenient. Head CT can show signs of ICP including enlarged ventricles, herniation, or mass effect, and can reveal possible causes such as evidence of bleeding, tumors, and abscesses. MRIs provide more sensitive anatomic details and may be utilized once the patient is stabilized (6).  

A complete blood count (CBC), electrolytes, liver function, and blood gas are initially collected to check for infection and electrolyte abnormalities that contribute to or exacerbate cerebral edema and monitor responsiveness to therapies.  

A lumbar puncture is sometimes necessary for diagnosis if an infectious process like meningitis is suspected. Lumbar puncture also provides opening pressure, a one-time measurement of intracranial pressure. Due to the risk of brainstem herniation from a sudden decrease in intracranial pressure from a lumbar puncture, a head CT should be evaluated before the procedure (6).  

Management 

The management goals for elevated ICP are to ensure adequate CPP, lower ICP, and treat the underlying cause. Ensuring adequate breathing and circulation is the priority. Measures including sedation, pain and temperature control, seizure prophylaxis, venous drainage promotion, and osmotic agents are crucial in maintaining a balance between lowering ICP and maintaining adequate cerebral perfusion.  

Endotracheal intubation and mechanical ventilation are indicated for patients with a GCS 8 or lower due to severe brain injury and loss of protective airway reflexes (i.e. cough), a risk for aspiration. Hypoxia and hypercarbia (elevated CO2) cause vasodilation leading to increased cerebral blood flow therefore cerebral pressure. Mechanical ventilation can help lower ICP by maintaining oxygenation and controlling hypercarbia with temporary hyperventilation to decrease CO2 (6). 

Temperature and pain control are important to minimize increases in ICP. Fever increases brain metabolic demand and vasodilates contribute to increased ICP. Antipyretics, cooling blankets, and identifying infectious sources are measures to minimize elevated body temperature. Induced hypothermia has no significant benefit and therefore is not a mainstay treatment for elevated ICP (2). 

Agitation and pain increase blood pressure and therefore ICP. Sedation and analgesia are necessary adjunctive treatments in the management of elevated ICP. Propofol and barbiturates are options for the management of patients with elevated ICP. Their mechanisms of action allow for increased comfort, decreased agitation, and seizure prevention, which are all important factors to address in controlling intracranial hypertension (12). 

Analgesic and sedation medications have many side effects that need to be monitored, specifically hypotension. MAP requires close monitoring to ensure adequate CPP (13). Hypovolemia can exacerbate hypotension from analgesic and sedation medications, therefore fluid status also requires close monitoring and correction.  

Hyperosmolar therapy, particularly with mannitol or hypertonic saline, is the mainstay treatment for elevated ICP. Both agents decrease ICP by removing water from the brain thereby reducing the volume and pressure within the skull. Both medications are given intravenously. Central venous access is the preferred route for hypertonic saline due to concerns for extravasation injuries. However, peripheral intravenous administration is acceptable if it is the only available route (14).  

Adverse effects of mannitol include hypotension with rapid administration, systemic volume overload, and electrolyte imbalances (7). Adverse effects of hypertonic saline include hyperchloremic metabolic acidosis, coagulation abnormalities, and hypernatremia. Cautious administration of hypertonic saline should be used in the setting of hyponatremia. A rapid increase in serum sodium can lead to osmotic demyelination syndrome (7).  

Glucocorticoids are another medication used to decrease swelling in vasogenic cerebral edema from brain tumors. Steroids are contraindicated in patients with cerebral edema from traumatic brain injury and intracerebral hemorrhage (6,7). 

Proper head positioning is important to help alleviate fluid accumulation within the brain. Maintain the head of the bed (HOB) at 30 degrees (semi-Fowler’s) with the head in a neutral position to promote venous drainage. Ensure any circumferential devices around the neck such as tracheostomy or endotracheal ties and cervical collars fit correctly for safety yet are not too tight to compress the jugular veins. Increased intraabdominal pressure (e.g. Straining or coughing) also hinders venous drainage from the head (7, 10). 

Surgical measures to treat causes of or for refractory cases include resection of mass lesions, CSF drainage through extra-ventricular drain (EVD), and decompressive craniotomy for patients with widespread cerebral edema (6).  

Implications for Nurses 

Changes in neurologic status are sometimes subtle. Nurses caring for patients with or at risk for cerebral edema have an important role in identifying early and sometimes subtle changes in neuro exams. A thorough neurologic exam starts with an assessment of mental status, specifically alertness, orientation, and GCS. Slight changes in mental status are often the first sign of increasing ICP. Additional components of the neurologic exam include assessing motor coordination and strength, presence of pain, and pupillary exam.  

Early intervention with neurologic deterioration is vital to maintaining adequate airway, breathing, and circulation to ensure cerebral perfusion. The nurse should promptly notify the need for escalation in care (e.g. activating rapid response). The responsibilities nurses play in providing the best outcome for patients with increased ICP are expansive, ranging from monitoring cerebral perfusion to sedation and analgesia.  

Conclusion

Careful monitoring and early intervention can minimize complications for patients with cerebral edema and elevated ICP. Diligent monitoring and frequent neurological checks are necessary for identifying worsening cerebral edema that could lead to brainstem herniation.  

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