Musculoskeletal/​Neurological/​Psychosocial Study Guide for the CCRN

Neurology

The neurologic system accounts for several conditions, ranging from brain function to nervous system disorders. Numerous conditions may occur in this system that can result in mild to devastating effects on the patients. Understanding early signs and symptoms of many of these conditions helps to implement therapies to reduce complications from the events.

Acute Spinal Cord Injury

Acute spinal cord injury can occur in the event of infection or trauma, such as falls, motor vehicle accidents, blunt trauma, gunshot wounds, or diving accidents. It may range from mild contusion to complete transection. Males and people between 16 to 30 years old more commonly experience this type of injury.

Symptoms of acute spinal cord injury depend on the location and severity of the injury. Injury may occur anywhere along the spine.

• Severe cervical injury can cause quadriplegia, where all four extremities have loss of function and breathing assistance is needed.

• Paraplegia can occur in spinal cord injuries in the lumbar or thoracic spinal region and results in loss of voluntary movement and sensation in the lower half of the body. Voluntary bladder and bowel function may also be lost.

• Following acute injury, patients may experience spinal shock. Spinal shock can cause extensive decreases in feeling, sensation, reflexes, and paralysis. This is due to the swelling surrounding the spinal cord. As the swelling subsides, patient symptoms may improve depending on the severity and location of the injury.

Diagnosis of acute spinal cord injury may be obtained with a thorough patient history and radiologic imaging. If acute injury is suspected, patients must have their spinal cord stabilized with bracing or surgical intervention. Patients will likely spend several days in the intensive care unit for close observation and management of potential spinal and neurogenic shock.

After their intensive care stay, patients often need extensive rehabilitation. Rehabilitation includes preventing complications of immobility. Patients will need education on mobility aids, proper skin care (avoidance of pressure areas), and bladder and bowel management. While some patients may recover their function following recovery from spinal shock, many patients with acute spinal cord injury have prolonged, lifelong complications that need continued management.

Brain Death

Brain death is determined by a series of tests when a patient becomes completely unresponsive due to irreversible damage to the respiratory and circulatory regulation mechanisms. It is diagnosed when there is no longer function of any part of the brain, including the brain stem. By law, patients tested for brain death must have symptoms of lack of responsiveness, apnea without ventilator support, and absence of primary reflexes. Often, it is required for two different physicians at different times to test the patient to ensure the criteria for brain death are met.

Several tests may be used to assist in the diagnosis of brain death. These include cerebral angiograms to determine the rate of intracerebral filling or obstruction (usually delayed), EEG to determine electrical impulse activity (or lack thereof), transcranial ultrasound, and cerebral scintigram. Pupils are fixed, dilated, and nonreactive. Testing of primary reflexes is also part of the brain death examination. This can include basic protective reflexes, such as a gag reflex or a cough. Patients who are brain dead will have absence of the “doll’s eyes” or oculocephalic reflex. Absence of this reflex is defined as fixed eye movement when the head is turned from side to side. Another reflex assessed in the event of brain death is the “cold caloric” or oculovestibular reflex. Absence of this reflex can be determined if the patient does not experience an ocular response to a cold water stimulus inserted into the ear. In order for the “cold caloric” reflex test to be accurate, the patient’s head of bed must be at least 30 degrees.

Patients who are declared brain dead are technically and legally dead regardless of the mechanical devices keeping the body “alive.” Nurses must be prepared to educate the families regarding this condition and how, when mechanical support is removed, the body will proceed to cease functioning.

Delirium

Delirium is an acute condition. Delirium occurs suddenly and can be reversible. In delirium, patients will experience episodes of fluctuating awareness and consciousness. If not treated, delirium has been proven to increase a patient’s morbidity and mortality.

Causes

Causes of delirium may vary among patients. Approximately 10% to 40% of patients, especially older patients, become delirious in a hospital setting. This percentage increases in critically ill patients, especially if sedation and intubation are involved. Approximately 80% of terminally ill patients experience delirium at some point in their illness. Other causes of delirium include toxic drug levels, drug or alcohol withdrawal, vision or hearing loss, pain, dementia, hypoxia, infection, trauma, surgery, fluid/electrolyte imbalance, and malnutrition/dehydration.

Symptoms and Diagnosis

Symptoms of delirium include decreased focusing abilities, difficulty remembering, language disturbances, disorientation, confusion, hallucinations (both auditory and visual), sleep disturbance, and motor disruption. Diagnosis of delirium can be made after thorough patient history, medication review, and laboratory levels to determine if there are any abnormalities.

Treatment

Treatment of delirium primarily focuses on the prevention of delirium. Maintaining a normal day/night wake/sleep cycle, encouraging movement and activity, and providing familiar objects/routines to the patient are critical for improving the patient’s mental health. Patients should have infections treated, dehydration/malnutrition addressed, and be evaluated for the need for changes in medications to prevent escalation of delirium symptoms. In some cases, sitters may be used to ensure patient safety and provide reorientation or redirection when needed.

Treatment of any underlying conditions should be performed to prevent further complications of those conditions. Medications such as trazodone, lorazepam, and haloperidol have been used to help calm patients. These medications should be used with caution in elderly populations, as they can worsen confusion.

Dementia

Dementia is a progressive, irreversible condition of memory loss and decreasing function. Alzheimer’s disease is the most common type of dementia, accounting for the majority of dementia cases. It gradually affects memory, thinking, and the ability to perform everyday activities. Several other types of dementia exist and can be due to a variety of conditions. These include:

• vascular dementia—This is the second most common type of dementia that is caused by impaired blood flow to the brain and often caused by strokes. Symptoms are similar but have a more sudden decline compared to the gradual progression of Alzheimer’s disease.

• mixed dementia—Symptoms involve several types of dementia from a variety of causes.

• frontotemporal dementia—This occurs more frequently at a younger age (45 to 65) than other forms of dementia and has a genetic link. It involves significant changes in personality and behavior, as well as difficulty interpreting language.

• dementia with Lewy bodies—Patients can often present with dementia with Lewy bodies coexisting with Alzheimer’s disease. The symptoms include fluctuating symptoms that include visual hallucinations, muscular tremors, and rigidity.

• Parkinson’s dementia—This occurs in those with long-lasting Parkinson’s disease. Those affected will experience difficulty with decision-making, concentrating, learning new skills, understanding complex language, and sequencing.

• normal pressure hydrocephalus—This is a condition that is caused by the buildup of cerebrospinal fluid in the brain, and unlike other causes of dementia, normal pressure hydrocephalus is potentially reversible. It is characterized by ataxia, memory loss, and loss of urinary continence.

• Creutzfeldt-Jakob disease—This is a rare disease that progresses rapidly, often over a couple of months, and causes dementia due to abnormal prion proteins that cause brain damage. Patients will experience impaired memory, impaired behavioral ability, and muscular incoordination.

Patients who experience dementia will need additional nursing attention. Nurses should provide frequent reorientation to those actively experiencing symptoms of delirium. Nurses should never argue with patients experiencing dementia, as this will exacerbate symptoms and may negatively escalate the situation. Restraints and sedatives may worsen dementia and should be avoided.

Encephalopathy

Encephalopathy is a broad term referring to any diffuse dysfunction to the brain that can result from a variety of causes. It is characterized by alterations in cognition, consciousness, behavior, or neurological function. The severity and course of encephalopathy depend on the underlying etiology, which may include metabolic disturbances, infections, hypertension, toxins, or trauma. Early recognition and understanding of the different types are essential for timely and appropriate management.

• metabolic encephalopathy—caused by systemic metabolic disturbances such as liver (hepatic encephalopathy) or kidney failure (uremic encephalopathy), electrolyte imbalances, hypoxia, or hypoglycemia

• infectious encephalopathy—results from bacteria, fungi, or most commonly, viruses

• hypertensive encephalopathy—occurs when severely elevated blood pressure overwhelms the brain’s regulatory mechanisms and causes cerebral edema

• other types—includes toxic encephalopathy (drugs, toxins), anoxic encephalopathy (lack of oxygen/circulation to the brain), traumatic encephalopathy (head injuries), and prion encephalopathy (Creutzfeldt-Jakob disease)

Signs and Symptoms

Encephalopathy typically presents with altered mental status ranging from mild confusion and irritability to lethargy or coma. Patients may also experience personality changes, disorientation, memory deficits, and impaired attention. Neurological manifestations can include seizures, dysphasia, motor deficits, ataxia, and myoclonus. Other common symptoms include headache, nausea, vomiting, and visual disturbances. The onset may be sudden or gradual, depending on the underlying cause.

Diagnosis

Diagnosis of hypertensive encephalopathy often relies on a combination of clinical assessment, laboratory evaluations, and imaging studies such as CT or MRI to identify an underlying cause. Nurses must be aware of the early signs and symptoms, as timely recognition is critical. If infection is suspected, infectious marker laboratory values or a lumbar puncture may be necessary.

Treatment

Management of encephalopathy depends on the cause. Treatment of metabolic encephalopathy involves identifying and correcting the underlying issue This can include restoring oxygenation for hypoxia, IV dextrose for hypoglycemia, lactulose for hepatic encephalopathy, dialysis for uremic encephalopathy, and vitamin or electrolyte supplementation for any imbalances.

For infectious encephalopathy, the treatment is targeted towards the pathogen. Viral illnesses are generally self-limiting and resolve over several days. Occasionally, antiviral medications may be used to help shorten the duration of symptoms. Bacterial infections require antibiotics. Fungal infections are rare and are treated with systemic antifungals.

For hypertensive encephalopathy, treatment primarily focuses on the lowering of the patient’s blood pressure. Nitroprusside sodium (Nitropress®) is a medication commonly used to help lower blood pressure. It is administered as a continuous intravenous medication. Nurses must be sure to closely monitor the patient’s blood pressure while administering this medication, as blood pressure reduced too quickly may result in cerebral ischemia. Seizure prophylaxis with medications such as phenobarbital or phenytoin may be indicated. In patients with cerebral edema, osmotic and loop diuretics (mannitol and Lasix®) may be used to reduce fluid overload and cerebral edema.

Measures to maintain the patient’s \(\text{PCO}_2\) between \(33\) and \(37 \text{mmHg}\) reduce vasoconstriction of cerebral arteries and prevent further increases of intracranial pressure. Nursing interventions in the event of encephalopathy include maintaining neutral patient positioning to prevent obstruction of cranial venous drainage, frequent monitoring of neurological status and vital signs, reducing metabolic demand through pain control, applying cooling devices to prevent hyperthermia, and reducing incidences of unnecessary suctioning and stimulation.

Intracranial Hemorrhage

Intracranial hemorrhage (ICH) refers to any bleeding within the cranium (skull). Because the cranium is a fixed space, even small amounts of bleeding can rapidly increase intracranial pressure (ICP) and compromise cerebral perfusion. Early recognition and correction of the bleeding source are critical to preventing neurological injury, herniation, and death. While all ICHs involve bleeding within the skull, they differ based on anatomic location. This section focuses on two important subtypes: intraventricular hemorrhage (IVH) and subarachnoid hemorrhage (SAH). Other forms of intracranial bleeding, such as intracerebral hemorrhage are addressed in the hemorrhagic stroke section of this guide.

Intraventricular Hemorrhage (IVH)

IVH occurs when bleeding develops in or around the ventricles of the brain. Although IVH is most commonly associated with neonates, it can occur in adults as well. The hemorrhage may develop quickly or progress over several weeks. Chronic hemorrhages, or the slow leaking of blood into the ventricles, are most common in the elderly population. Acute bleeding may occur due to traumatic injury, blood vessel rupture, brain tumors, or coagulopathies. Because the ventricles are part of the cerebrospinal fluid (CSF) pathway, accumulating blood can further increase pressure, cause hydrocephalus, and lead to rapid deterioration.

Symptoms

Symptoms of intraventricular hemorrhage are similar to those of other intracranial hemorrhages, including headache, nausea, weakness, and decreased level of consciousness, with an increased likelihood of vital sign changes such as bradycardia and bradypnea.

Subarachnoid Hemorrhage (SAH)

SAH occurs when bleeding develops between the meninges and the brain. This can occur due to arteriovenous malformation, trauma, or, most commonly, a ruptured aneurysm. Subarachnoid hemorrhages can cause significant brain injury and death due to compression of the brain as the pooling blood increases pressure inside the skull.

Symptoms

The hallmark symptom of SAH is a sudden, severe “thunderclap” headache, often described as the worst headache of one’s life. Other symptoms include severe headache, nausea, vomiting, nuchal rigidity, partial facial paralysis or palsy due to cranial nerve compression, papilledema, and retinal hemorrhage. If not identified early, patients may become hyponatremic and collect more fluid inside of the ventricles, known as hydrocephalus. A grading system is often used to define the severity of a subarachnoid hemorrhage, ranging from mild headache and stiffness to stupor, coma, decerebrate rigidity, and risk of death.

Diagnosis and Treatment

Diagnosis for both IVH and SAH relies on prompt imaging, with a non-contrast CT scan being the gold standard. MRI and conventional angiography may be used to identify underlying causes. Lumbar puncture may be indicated if SAH is suspected but CT is negative. Treatment focuses first on stabilizing the patient, preventing secondary brain injury, and managing intracranial pressure. Supportive care includes airway management, blood pressure control, seizure prevention with antiepileptics, adequate sedation, pain control, and correction of coagulopathies. For the reduction of intracranial pressure, refer to the increased ICP section down below. Definitive interventions depend on the type and severity of bleeding: SAH may require endovascular coiling or clipping of aneurysms, while IVH may require CSF diversion through a drain or shunt. Further surgical interventions are discussed in the neurosurgery section of this guide. Continuous monitoring is essential to identify early neurologic decline, hydrocephalus, re-bleeding, or electrolyte disturbances. Long-term rehabilitation is often required due to persistent deficits in cognition, mobility, vision, or swallowing.

Increased Intracranial Pressure

In the event of an injury, tumor, bleeding, or structural abnormality in or around the brain, intracranial pressure (ICP) may increase. One common cause of increased intracranial pressure is the accumulation of cerebrospinal fluid in the ventricles of the brain, otherwise known as hydrocephalus.

When the intracranial pressure rises, patients will experience significant symptoms. These include severe headache, confusion, nausea, vomiting, increased blood pressure, double vision, and shallow breathing. As intracranial pressure rises, Cushing’s triad (widened pulse pressure, bradycardia, and irregular respirations) may appear as a hallmark sign of impending herniation. If not corrected, elevated intracranial pressure can cause seizures, coma, and death. An MRI or CT scan is generally used to diagnose this condition.

Treatment of increased intracranial pressure focuses on relieving the pressure. Refer to the neurosurgery section listed below for surgical interventions to relieve increased ICP. External ventricular drains and intracranial pressure monitors (bolt) are also useful for monitoring a patient’s ICP. ICPs greater than \(20\, \text{mm\,Hg}\) will likely require intervention.

Medications such as hypertonic saline (\(3\% \,\text{NS}\)) and mannitol are used frequently to help draw fluid from the brain back into circulation and ultimately eliminate it. Important cautions with hypertonic saline include the need for a central line for infusion (especially for concentrations above 3%) and close monitoring of serum electrolytes. Serum sodium should be checked every \(6\) hours and serum osmolality every \(12\) hours. Sodium levels should be maintained between \(145\) and \(155 mmol/L, and serum osmolality maintained at\)320 \,\text{MOsmol/L}\(to prevent renal failure and cardiac and respiratory complications.\)30 \, \text{mL}\(boluses of hypertonic saline are administered over\)15$$ minutes for acute increases in ICP. Continuous infusion may also be used to maintain ICPs at a specific pressure.

Mannitol also requires close monitoring of lab work and patient status. Mannitol should also ideally be administered through a central line. Typical dosing is \(0.25\) to \(2 \, \text{g/kg}\) over \(30\) minutes to an hour. ICP decrease should be visualized approximately \(15\) to \(20\) minutes following administration of this medication. Higher concentrations of the medication may require in-line filtration because the medication can crystallize when exposed to low temperatures or when stored in polyvinyl chloride bags or tubing. Patients should be monitored closely for fluid and electrolyte shifts, as well as nausea, vomiting, hypotension, tachycardia, fever, and urticaria.

Healthcare providers may work with nurses to help reduce the metabolic demand of patients with elevated intracranial pressure. Agitated patients should be kept calm. They may require the use of pain and sedative medications. Patients may also require mechanical ventilation to help regulate their breathing. Patients’ head of bed should be maintained at 30 to 45 degrees at their neck’s midline position to prevent worsening the pressures within the brain.

Neurologic Infectious Disease and Inflammatory Disorders

Neurologic infectious diseases and inflammatory disorders can have devastating effects for the patient. Early identification of any suspected neurologic involvement is imperative for best long-term outcomes. Neurologic infection can be from viral, bacterial, or fungal components, while inflammatory or immune-mediated conditions may be triggered by an infection elsewhere in the body. These processes most commonly affect the spinal cord and meninges surrounding the brain. Rarely, brain abscesses will form and present similarly to a space-occupying lesion, as described later in this guide.

Meningitis

Meningitis is an inflammation of the meninges, the protective membranes surrounding the brain. Viral meningitis is more common overall but often milder. Bacterial meningitis is more severe with a higher risk of mortality. Streptococcus pneumoniae and Neisseria meningitidis are two of the most common offenders in meningeal infection. Fungal meningitis is uncommon and typically occurs in patients with a compromised immune system, such as those with HIV, cancer, or those on immunosuppressive therapy. The most common organisms that cause this type of fungal infection include Candida albicans and Cryptococcus neoformans. Infection can be from distal infection, surgical site wounds, invasive devices, nasal colonization, or invasive traumas. Pathogens raise havoc in the nervous system by releasing toxins that cause inflammation, WBC accumulation, and exudate formation. This response may quickly cause brain cell damage if not treated.

Symptoms typically progress rapidly and include headache, stiff neck (nuchal rigidity), photophobia, decreasing level of consciousness, agitation, irritability, and seizures. Diagnosis is usually made via lumbar puncture, blood cultures, CT, and/or MRI.

Treatment of meningitis depends on the causative pathogen. Bacterial meningitis is treated with IV antibiotics, corticosteroids, and pain management. Fungal meningitis is treated with antifungal therapy, and viral meningitis is usually mild and self-limiting; treatment is primarily supportive. Patients should be monitored closely for changes in neurologic status, signs of increased ICP (unequal pupils, coma, etc.), and hemodynamic instability.

Inflammatory Disorders

Inflammatory neurologic disorders occur when the body’s immune system causes inflammation within the nervous system. These conditions may develop after an infection or other immune trigger but are not infections themselves. Common examples include Guillain-Barré syndrome and transverse myelitis.

Guillain-Barré Syndrome

An autoimmune disorder, Guillain-Barré syndrome generally occurs when a viral or bacterial infection activates the attack of myelinated structures in the peripheral nervous system. This condition may also occur due to idiopathic causes. The autoimmune reaction to the nervous system most commonly causes ascending paralysis.

Symptoms of this condition include generalized numbness and tingling, increased weakness of lower extremities, loss of deep tendon reflexes, and progressive loss of sensation leading to possible complete paralysis and inability to breathe. Patients may also lose the ability to move their eyes and experience facial weakness. Diagnosis may be made via lumbar puncture, electromyography, and nerve conduction studies.

Treatment for Guillain-Barré is typically supportive. Patients should have their airway maintained with artificial ventilation as needed. Some evidence has shown shorter duration of symptoms when IVIG and plasma exchange are implemented. Overall prognosis of Guillain-Barré is good, and the condition is usually temporary. Most patients will start to regain function around 2 to 4 weeks after initial symptoms. Recovery involves intensive therapy services, as patients will be required to relearn and strengthen many motor skills.

Transverse Myelitis

Transverse myelitis is a condition in which one or both sides of the spinal cord in one or more sections become inflamed and damage the myelin sheaths of the nerve cell fibers. This causes interruption of the nerve transmissions throughout the body. It can be due to viral, bacterial, myelin disorders, or immune responses to illness.

Symptoms of transverse myelitis include muscle weakness, paralysis, decreased sensation, pain, and bladder and bowel dysfunction. Symptoms may develop over the course of a few hours to few days. Usually, with aggressive rehabilitation and therapy, partial to all function is restored after the spinal cord swelling subsides. Diagnosis of transverse myelitis may be determined with MRI, lumbar puncture, and lab work.

Treatment of transverse myelitis includes supportive therapy. If the inflammation affects the cervical spine (C3 to C5), maintaining the patient’s airway is more of a concern. Treatment includes intravenous steroids, plasma exchange therapy, antiviral medication, immunosuppressants, and pain management. Patients will need extensive physical therapy, occupational therapy, and psychotherapy. Most people have at least partial recovery.

Neuromuscular Disorders

Neuromuscular disorders are characterized by weakness and wasting of the muscles. This can be accompanied by nerve damage or miscommunication. Common disorders that fall within this category of disorders include muscular dystrophy, cerebral palsy, and myasthenia gravis.

Muscular Dystrophy

Muscular dystrophy is an inherited disease classified by progressive muscle weakness. The most common type of muscular dystrophy is Duchenne muscular dystrophy, which primarily occurs in young boys. The other types of muscular dystrophy can occur in all races and both sexes. Patients may develop symptoms of muscular dystrophy in childhood, middle age, or as older adults. The muscle loss is progressive, and there is no cure available. Supportive measures such as physical therapy, occupational therapy, speech therapy, and assistive devices can be used to help maximize a patient’s abilities.

Cerebral Palsy

Cerebral palsy is a neuromuscular disorder that affects a patient’s balance and posture. Damage to the immature brain usually occurs before or during birth (gene mutations, maternal infection, trauma, hypoxemia) or in early infancy (infection, trauma, severe jaundice leading to kernicterus). Symptoms of cerebral palsy include altered gait, abnormal reflexes, abnormal posture, a mix of floppiness and/or rigidity, and involuntary movements. Patients with cerebral palsy may have a range of symptoms from mild to severe. Potential complications of cerebral palsy include contractures, osteopenia, heart and lung disease, malnutrition, premature aging, and mental health conditions. It is non-progressive, and the prognosis varies greatly depending on the extent of brain damage. Patients may require varying modifications and medical equipment to improve their symptoms.

Myasthenia Gravis

Myasthenia gravis is the progressive, long-term weakening of muscles, particularly in the face and neck. Patients may struggle with seeing (drooping eyelids), trouble talking and swallowing, and difficulty walking. This condition typically affects women under the age of 40 and men over 60 years old. Myasthenia gravis can be caused by antibody creation that attacks specific nerve receptors or muscle receptors and thus interrupts the communication between the nerves and muscles. It can also be caused in the absence of antibody creation.

Patients with myasthenia gravis have worsening muscle weakness with muscle use. Rest can improve some of the fatigue. Some patients may experience myasthenic crisis when their respiratory muscles become too weak to regulate breathing, and mechanical ventilation is needed. It is commonly triggered by stress or infection. Patients may regain their ability to breathe on their own with blood filtering therapies (plasmapheresis) and other medications (intravenous immunoglobulin, cholinesterase inhibitors, corticosteroids, and immunosuppressants) to help manage their condition. Patients with myasthenia gravis should be screened for a tumor in the thymus gland. Tumors, if identified and removed, may improve some symptoms. It is important to note, though, that there is no cure for myasthenia gravis.

Neurosurgery

Neurosurgery is a vast category of surgical interventions that can be performed on any part of the nervous system. Most commonly, neurosurgery involves surgical intervention of the skull, brain, and/or spinal column and cord.

Neurosurgery will likely be indicated in patients with head trauma or increased intracranial pressure due to infection or cerebral edema. Patients may need to undergo a craniotomy to decompress a swelling brain or have a resection of a tumor that is disrupting the brain structures. Intracranial pressure may be monitored through an external ventricular drain (EVD) placed in the ventricles or a pressure transducer inserted into the brain tissue. Patients with hydrocephalus may require a ventriculoperitoneal (VP) shunt.

Spinal injuries and some congenital conditions may result in spinal cord damage and scarring. Neurosurgery may be indicated to provide detethering of the cord to improve motor skills, gait, bowel and bladder continence, and flexibility.

Nursing Interventions

Several nursing interventions are expected following a neurosurgical event. After brain surgery or placement of an ICP monitor, nurses should maintain neutral patient positioning with the head of the bed elevated between 30 to 45 degrees. After some neurosurgeries, patients may need to be on bed rest for several hours and have activity restrictions to prevent complications following the procedure. Patients should be monitored closely for infection.

Avoidance of increased stimulus can help to reduce increased intracranial pressure. Administration of medications such as corticosteroids, anticoagulants, antibiotics, and antiepileptics may be indicated to reduce complications from the surgery or preceding event. Patient intake and output should be monitored closely. Frequent monitoring of arterial blood gases, pulse oximetry, and lab work (CBC, electrolyte panels, etc.) would also be expected.

Seizure Disorders

Seizure disorders are some of the most common neurologic conditions. Epilepsy can be diagnosed based on a patient’s history of seizure activity with supporting electroencephalogram (EEG) evidence. Several seizure types exist, including generalized, partial, absence, atonic, myoclonic, tonic-clonic, and individual tonic and clonic seizures. Seizures may be congenital, infantile, or acquired later in life. Patients with head trauma and severe illness with electrolyte imbalances are at high risk for seizure activity. Febrile seizures often occur in young children. Many seizures are preceded by an aura.

Treatment

Treatment of seizures generally involves medications. Treatment must be individualized to each person. Medications are often added one at a time so that appropriate doses and management can be maintained. Some medications, such as phenobarbital, require close monitoring of drug levels to optimize therapeutic effects. Patients will also have rescue medications, which are additional, stronger antiepileptics that can be used in the event of breakthrough seizure activity. Benzodiazepines, such as rectal diazepam (Diastat®) and lorazepam (Ativan®), are most commonly administered in an epileptic emergency. Review the common epileptic medications and their effects for this exam.

Medication education regarding common side effects and possible interactions should be provided to patients. Antiepileptic medications may cause symptoms of allergic reactions, skin irritations, severe rash, and hepatotoxicity. Women of childbearing age should understand that some antiepileptic medications are teratogenic and/or may decrease the effectiveness of birth control. Women may need additional or alternative contraception while on these medications.

Status Epilepticus

Patients in the intensive care unit may be admitted due to breakthrough seizures or develop seizures due to their other conditions. Prolonged seizure activity can cause permanent brain changes. Status epilepticus is a medical emergency. It is defined as a seizure lasting more than five minutes or two or more seizures without a return of consciousness between them. This condition is dangerous and often deadly if not treated promptly. Patients may need to be sedated and intubated in the event of uncontrollable status epilepticus.

Nursing Interventions

Nursing interventions for patients with seizures should prioritize patient safety. Patients should have bed alarms notifying nurses of falls. Padding on side rails and flooring surrounding the patient’s bed may be necessary to prevent injury. If a patient begins to convulse, nurses should immediately place the patient on his or her side to prevent aspiration of oral secretions or vomitus. This allows for the protection of the patient’s airway as well. Nurses should note the exact time a seizure occurs and how long it lasts. The first-line medication used for an active seizure within the hospital setting is IV lorazepam (Ativan®).

Brain Tumors

Space-occupying lesions in the brain are most likely the result of a brain tumor, but may also result from a hematoma, abscess, cyst, or swelling. Brain tumors may be benign or malignant. Primary and secondary brain tumors exist. Primary brain tumors result when the lesion begins in the brain or the brain stem. Secondary lesions are usually due to metastasis of other lesions in the body.

Types

There are several types of brain tumors that occur in adults. These include: astrocytoma, glioblastoma, brain stem glioma, craniopharyngioma, meningioma, ganglioglioma, medulloblastoma, oligodendroglioma, and optic nerve glioma. The slow-growing tumors include astrocytoma, low-grade brain stem glioma, craniopharyngioma (congenital and recurrent), meningioma (most often in women ages 40 to 70), ganglioglioma (usually benign), oligodendroglioma (most often in ages 40 to 60), and optic nerve glioma (often occurs with neurofibromatosis type I, NFI). Tumors that are typically fast-growing tumors include glioblastoma (the most common malignant brain tumor; adults aged 45 to 70), high-grade brain stem glioma, and medulloblastoma.

Diagnosis and Testing

Diagnosis for brain tumors is classically made with imaging, particularly CT, MRI, or PET. Patients will also have several lab tests run to determine the type of cancer and possible malignancies. CBC, tumor marker labs, and electrolyte panels are among the many tests that can be run in the event of a suspected brain tumor.

Treatment

Treatment of these space-occupying lesions involves a variety of measures. If possible, many tumors are resected or debulked to reduce the amount of space they occupy and to help treat the lesion. Chemotherapy, immunotherapy, and radiation are used to treat metastatic lesions to prevent or treat the spread of cancer cells.

Stroke

Patients may be admitted to the intensive care unit due to a stroke or may experience a stroke as a complication of other medical conditions. Strokes occur when blood flow to part of the brain is suddenly reduced or interrupted. This can occur due to blood vessel rupture (bleeding) or obstruction (clot). When the blood flow is altered, tissue death occurs.

Symptoms of stroke include difficulty speaking, unilateral paralysis, blurred vision, difficulty walking, and headache. Time from the onset of symptoms to patient treatment is crucial to reducing the burden of the stroke.

Ischemic Stroke

Ischemic strokes occur when blood flow to the brain (or a part of the brain) is obstructed or interrupted. When blood flow cannot reach the distal structures of the vessels, tissue death quickly occurs. Approximately 80% of strokes are due to ischemia. The other 20% are generally a result of hemorrhage.

Ischemic strokes generally occur due to thrombus. A thrombus that occurs in large arteries is usually a result of atherosclerosis. The elderly are most at risk of a large thrombus ischemic stroke. Thrombosis that penetrates into smaller arteries, also known as a lacunar infarct, is most common in patients with diabetes mellitus and hypertension. Another type of ischemic stroke may occur due to embolism that lodges in the brain after traveling through the arterial system. This type of stroke often happens without warning and can be fatal quickly. Occasionally, ischemic stroke occurs with an unidentified cause. This is known as cryptogenic.

Treatment of ischemic stroke must be initiated as quickly as possible to restore perfusion, or at least prevent progression of ischemia, to the distal areas of the blockage. Patients diagnosed with this condition may be eligible for tissue plasminogen activator (tPA, Activase®), which is ideally administered within three hours of symptom onset with an extended window to four and a half hours in some patients. This medication is used to dissolve fibrin clots and is given intravenously at a dose of \(0.9\, \text{mg/kg}\) up to \(90 \, \text{mg}\). Nurses should administer this medication by injecting \(10\%\) of the dose as an initial bolus. The rest of the dose should then be administered over the next \(60\) minutes.

Contraindications to tPA include stroke symptoms lasting longer than five hours, hemorrhage or bleeding in the brain, recent surgery, anticoagulant use with abnormal lab work, uncontrolled hypertension, and severe head injury. If tPA cannot be administered or is ineffective in breaking apart the clot, surgical removal of the clot may be indicated up to 24 hours from the start of stroke symptoms.

Patients should also be placed on antihypertensive medications if their diastolic blood pressure exceeds 110 mmHg or systolic blood pressure exceeds 220 mmHg. This elevation in blood pressure is not an automatic disqualification to tPA if it can be safely lowered. Preferred IV medications include labetolol or nicardipine. Nicardipine is preferred if bradycardia is a concern or if labetolol is contraindicated.

Osmotic diuretics such as mannitol, hypertonic saline, loop diuretics (generally Lasix®), and corticosteroids may be initiated to decrease cerebral edema and intracranial pressure. If the patient’s symptoms are due to embolism, aspirin and anticoagulation may be initiated. However, if the patient received tPA, blood-thinning medication cannot be started immediately to prevent hemorrhage.

Additional measures of care include cooling the patient to avoid hyperthermia and increased metabolic demand, treating hyperglycemia, and doing frequent neurological assessments. Nursing interventions during this time include reducing factors that may increase the patient’s ICP, such as maintaining a neutral head/body position, elevating the patient’s head to 30 degrees, reducing external stimulation, reducing pain, and closely monitoring the patient’s vital signs.

Hemorrhagic Stroke

Hemorrhagic stroke occurs when there is bleeding in or around the brain. When blood vessels burst, the bleeding surrounds and displaces the brain tissue, not only cutting off distal circulation but also causing swelling within the skull. It is less common than ischemic strokes, accounting for only \(15 to 20\%\) of stroke diagnoses. Despite this, the mortality rate is high.

Hemorrhagic stroke can be intracerebral, within the brain, or subarachnoid, between the brain and membranes. The most common cause of hemorrhagic stroke is hypertension. Patients may also develop hemorrhagic strokes from cerebral cavernous malformations or arteriovenous malformations (AVMs). Other risk factors include bleeding disorders, anticoagulant or antiplatelet medication, head trauma, and cerebral aneurysm.

Symptoms of hemorrhagic stroke vary slightly from those of ischemic stroke. One of the hallmark signs of hemorrhagic stroke is sudden, severe headache. Patients may experience balance and coordination changes, vision changes, photophobia, inability to move, unilateral or bilateral numbness, seizures, confusion, difficulty understanding speech, difficulty speaking, nausea, vomiting, and coma. Hemorrhagic stroke can be diagnosed by CT scan, MRI, and/or MRI angiography.

Treatment of hemorrhagic stroke initially focuses on stopping the bleeding and lowering the patient’s blood pressure. Immediate treatment is critical to reducing the impact of the bleeding on the brain. Surgical intervention may be needed to tie off bleeding blood vessels. Pressure of the bleeding must also be relieved from the brain. Patients with a hemorrhagic stroke cannot receive tPA. Long-term rehabilitation of the patient depends on the extent of bleeding damage. Patients will require long-term physical therapy and rehab to help maximize their recovery.

TIA

Transient ischemic attack (TIA) is an event where blood flow is interrupted in the brain for a short period of time. Symptoms are brief, and damage is not permanent. Having a TIA increases a patient’s risk for stroke in the future. It may be viewed as a warning. Treatment focuses on resolving underlying conditions and medications, such as aspirin and antihypertensives, to help prevent future events.

Symptoms of TIA include weakness, slurred speech, blindness or double vision, vertigo, and loss of balance or coordination. Depending on the area of the brain involved, symptoms may vary even if patients have more than one TIA. Risk factors for TIA are the same for stroke. Age greater than 55, male sex, older women, prior TIA, sickle cell disease, and heart disease, including atherosclerosis, are all risk factors. Patients should be educated on factors that can help reduce their risk of TIA and stroke, including managing blood pressure, cholesterol levels, diet, activity, and weight. Patients should stop smoking, limit alcohol intake, and maintain a low-sodium, low-fat diet.

Traumatic Brain Injury

Traumatic brain injury (TBI) is the result of an external force to the head or neck that causes alteration in brain function. Common causes of TBI include car accidents, blunt force trauma, falls, and assault. Non-accidental trauma is an important mechanism of injury, occurring with head trauma results from intentional harm. Head injuries are the leading cause of death in non-accidental trauma cases. There are several types of brain injury. These are addressed below.

• Concussion—Concussion injuries occur due to acceleration-deceleration trauma that causes temporary disruption in brain function. In the grand scheme of traumatic brain injuries, concussions are mild, but they can cause significant symptoms and long-term effects if not treated appropriately. Symptoms of concussion include memory difficulty, confusion, loss of consciousness, drowsiness, dizziness, light sensitivity, nausea, vomiting, decreased reaction times, and changes in vision. Symptoms may begin immediately or several hours to days after the injury. Patients may also experience symptoms of irritability, difficulty concentrating, headaches, and light or noise sensitivity while recovering from the injury.

• Epidural—Epidural hematomas occur between the skull and the dura. They may cross the midline, but not suture lines. It most commonly occurs due to a traumatic head injury that results in skull fracture. Hemorrhage is usually from damage to the middle meningeal artery. The classic presentation is loss of consciousness, temporary improvement, then rapid deterioration. As the hematoma grows, it compresses the brain, causing symptoms of weakness, unilateral pupillary changes, and opposite side eye vision changes. Treatment of epidural hematomas includes evacuation and treatment of the bleeding site. Close monitoring (in mild to moderate cases), burr hole procedures, and craniotomies may all be considered as treatments for an epidural hematoma.

• Subdural—Subdural hematomas occur between the dura and arachnoid space. This bleeding will often be identified on one side of the brain, as it typically does not cross the midline, but it can cross suture lines. This condition usually develops due to the bleeding of veins torn in the initial injury. The onset is typically slower with more gradual worsening of symptoms. Symptoms of subdural hematoma include confusion, slurred speech, headache, seizures, nausea and vomiting, weakness, and vision changes. Brain herniation may occur if the bleeding is not addressed. Treatment is similar to that of an epidural hematoma. Mild to moderate hematomas may be monitored without incision and drainage. More complicated and larger bleeds may need to be managed with a craniotomy or burr hole procedure.

Diagnosis

Diagnosis of TBI may be obtained via CT, MRI, and patient assessment. The Glasgow coma scale can be used to evaluate a patient’s neurologic status and to help support the severity diagnosis and worsening or improving of the injury. Patients should be assessed frequently to identify any worsening of their condition and the need for emergent or additional interventions.

Treatment

Mild forms of TBI, such as concussions, are usually self-limited. They generally do not require treatment besides OTC analgesics, rest, and monitoring for worsening symptoms. Most patients recover fully in days to weeks.

Moderate TBI may require more intensive interventions. Supportive care focuses on maintaining a patent airway, ensuring adequate hemodynamics, and minimizing increased ICP. Medications such as hypertonic saline solution \((3\%)\) and mannitol may be used to help reduce swelling of the brain and provide osmotic diuresis. For more detailed information on these medications, refer to the ICP section of this guide. Seizure prophylaxis and early rehabilitation may also be initiated.

In addition to the interventions stated above, severe TBI requires intensive care with continuous monitoring. Patients may need to be placed in a medically induced coma, during which they are sedated, paralyzed with a neuromuscular blockade, and mechanically ventilated to reduce metabolic demand and provide rest for the brain while treating the injury or injuries. Neuromuscular blockades come in two forms: depolarizing agents and non-depolarizing agents. Succinylcholine is one of the most common depolarizing agents. Non-depolarizing agents have several subcategories and medications that fall within those categories. These include short-acting medications like mivacurium and rapacuronium; intermediate-acting agents like rocuronium, vecuronium, atracurium, and cisatracurium; and long-acting agents such as pancuronium, doxacurium, and pipecuronium.

Nursing Management

Nursing management of patients who require neuromuscular blockade includes maintaining the airway, usually by way of intubation and mechanical ventilation; prevention of contractures and skin breakdown with frequent repositioning; and frequent evaluation of vital signs to identify early changes in blood pressure and heart rate to prevent complications of these medications. Reversal of paralytic agents should be performed as early as deemed medically safe to prevent long-term deconditioning and complications from the medication(s).