Page 2 - Musculoskeletal/Neurological/Psychosocial Study Guide for the CCRN
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 clients. 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 16-30 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. Voluntary bladder and bowel function may also be lost.
Following acute injury, clients 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, client symptoms may improve depending on the severity and location of the injury.
Diagnosis of acute spinal cord injury may be obtained with a thorough client history and radiologic imaging. If acute injury is suspected, clients must have their spinal cord stabilized with bracing or surgical intervention. Clients 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, clients often need extensive rehabilitation. Rehabilitation includes preventing complications of immobility. Clients will need education on mobility aids, proper skin care (avoidance of pressure areas), and bladder and bowel management. While some clients may recover their function following recovery from spinal shock, many clients with acute spinal cord injury have prolonged, life-long complications that need continued management.
Brain death is determined by a series of tests when a client becomes completely unresponsive due to irreversible damage to the respiratory and circulatory regulation mechanisms or when there is no longer function of any part of the brain, including the brain stem. By law, clients 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 least 12 hours apart to test the client 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. Testing of primary reflexes is also part of the brain death examination. Clients 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 client 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 client’s head of bed must be at least 20 degrees.
Clients 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 is an acute condition. Delirium occurs suddenly and can be reversible. Delirium may precede dementia. In delirium, clients will experience episodes of fluctuating awareness and consciousness. If not treated, delirium has been proven to increase a client’s morbidity and mortality.
Causes of delirium may vary among clients. Approximately 10-40% of clients, especially older clients, become delirious in a hospital setting. This percentage increases in critically ill clients, especially if sedation and intubation are involved. Approximately 80% of terminally ill clients 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 client history, medication review, and laboratory levels to determine any elevated or low balances.
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 client are critical for improving the client’s mental health. Clients should have infections treated, dehydration/malnutrition addressed, and be evaluated for the need for changes in medications to prevent escalation of delium symptoms. In some cases, sitters may be used to ensure client 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 clients. These medications should be used with caution in elderly populations, as they can worsen confusion.
Dementia is a progressive, irreversible condition of memory loss and decreasing function. Several types of dementia exist and can be due to a variety of conditions. These include:
Creutzfeld-Jakob disease— happens rapidly and clients will experience impaired memory, behavior lability, and muscular incoordination
Dementia with Lewy bodies— closely associated with Alzheimer’s disease; includes fluctuating symptoms that include visual hallucinations, muscular tremors, and rigidity
Fronto-temporal dementia— involves significant changes in personality and behavior; difficulty interpreting language
Mixed dementia— symptoms involve several types of dementia from a variety of causes
Normal pressure hydrocephalus— characterized by ataxia, memory loss, and loss of urinary continence
Parkinson’s dementia— those affected will experience difficulty with decision making, concentration, learning new skills, understanding complex language, and sequencing
Vascular dementia— symptoms are similar but less severe than Alzheimer’s disease
Clients 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 clients experiencing dementia, as this will exacerbate symptoms and may negatively escalate the situation. Restraints and sedatives may worsen dementia and should be avoided.
Encephalopathy, with regard to the nervous system, most commonly occurs due to a hypertensive crisis. In clients with chronically elevated blood pressure, the brain adapts to manage the pressures and prevent issues in blood flow. When a client then develops a hypertensive crisis, the adaptations cannot support the severely increased pressures. This causes the capillaries to leak fluid, causing cerebral edema. Middle-aged males with chronic hypertension are at the highest risk for hypertensive encephalopathy.
Signs and Symptoms
Signs of hypertensive encephalopathy can develop over the course of a few days. Symptoms include nonspecific neurologic concerns, changes in mental status, visual abnormalities, weakness, constant headache, nausea, vomiting, seizures, and coma. Cerebral edema may develop quickly, increasing intracranial pressure and causing severe brain damage if not treated promptly.
Diagnosis of hypertensive encephalopathy is often subjective in nature. Nurses must be aware of the symptoms of early onset of hypertensive crisis to address and correct client vital signs before it develops into a more severe complication.
Treatment of hypertensive encephalopathy primarily focuses on the lowering of the client’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 client’s blood pressures while administering this medication to prevent a too quick decrease rate. Blood pressures reduced too quickly may result in cerebral ischemia. Phenobarbital and/or phenytoin may be used to prevent seizures in clients with cerebral edema. Osmotic and loop diuretics (mannitol and Lasix®) may be used to reduce cerebral edema by reducing fluid overload and cerebral edema.
Measures to maintain the client’s \(PaCO_2\) between 33-37 mmHg are required to maintain vasoconstriction of cerebral arteries and prevent further increases of intracranial pressure. Nursing interventions in the event of encephalopathy include maintaining neutral client positioning to prevent obstruction of cranial venous drainage, frequent vital signs, decreasing the client’s metabolic demand by reducing pain, applying cooling devices to prevent hyperthermia, and reducing incidences of unnecessary suctioning and stimulation.
While hypertensive encephalopathy occurs most commonly, other types of encephalopathy include metabolic and infectious encephalopathy. Metabolic encephalopathy occurs when a client’s metabolism is altered to the extent that bodily toxins cannot be filtered from the blood. Hepatic failure is the primary cause for metabolic encephalopathy. Symptoms of metabolic encephalopathy include irritability, agitation, changes in level of consciousness, dysphonia, spasticity, seizures, and disorientation that could progress to coma. Treatment of metabolic encephalopathy involves identifying and correcting the underlying cause.
Infectious encephalopathy occurs when the brain is impacted by infection via bacteria, virus, or prion. Symptoms of infectious encephalopathy include changes in consciousness, personality changes, decreased cognition, and lethargy. Clients may also experience seizures, dysphagia, dysphonia, and neuromuscular decline. Bacterial infections usually respond to antibiotics. Prions have no treatment available. Viral illnesses are generally self-limiting and resolve over several days. Occasionally, antiviral medications may be used to help shorten the duration of symptoms. Treating the underlying cause of infectious encephalopathy is required to address the secondary brain involvement.
Hemorrhage anywhere in the body can be devastating. Hemorrhage around the brain or critical nervous system hubs can be deadly. Early recognition and correction of the hemorrhage are essential to preventing significant consequences from the bleeding.
Intracranial hemorrhage occurs when bleeding begins inside the cranium. The bleeding surrounding the brain can cause increasing pressure and brain death if the pressure is not relieved. These events can occur suddenly or gradually depending on the offending injury. Common causes of intracranial hemorrhage include head trauma, such as a fall, car accident, or sports injury; hypertenive crisis; thrombus formation; ruptured cerebral aneurysm; cerebral amyloid angiopathy; arteriovenous malformation; anticoagulant therapy; tumors; and excessive use of drugs, tobacco, or alcohol.
Intracranial hemorrhaging may also result in hemorrhagic stroke. Hemorrhagic strokes generally occur due to intracerebral bleeding due to rupture of an artery, changes due to atherosclerosis, hypertension, brain tumors, excess anticoagulation therapy, or illicit drug misuse.
Symptoms and Diagnosis
Symptoms of intracranial hemorrhage include sudden tingling, weakness, hemiparesis, sudden and severe headache, difficulty swallowing, blurred vision, unequal pupils, loss of balance, slurred speech, and decreased level of consciousness. Diagnostic testing includes evaluating symptoms, CT scan, MRI, CBC, lumbar puncture, and conventional angiography.
Immediate decompression of intracranial hemorrhage must be done to release the pooled blood and decrease the pressure on the brain. This may be completed by burr hole procedure, craniectomy incision, or craniotomy. Removing small pieces or partial sections of the cranium allows for evacuation of the excess fluid while also providing a window to allow brain swelling without compression of the organ. Once the immediate pressure is relieved, the source of bleeding must be addressed. If the bleeding is from an aneurysm, angiography may be performed to allow for coiling and cauterization of the ruptured vessels.
Note that during this time, basic needs must also be met to help minimize the body’s metabolic demand. This includes maintaining the client’s airway, usually with artificial ventilation to maintain appropriate oxygenation; avoiding hypotension; and providing pain relief and sedation to lower intracranial pressure.
Medications that may be prescribed or administered in the event of an intracranial hemorrhage include antihypertensives, anti-anxiety medications, anti-epileptic medications, pain medications, and IV fluid support. Clients who have experienced an intracranial hemorrhage often have long-term consequences following the event. Nurses must be aware of the clients’ increased risk for falls, confusion, vision changes, decreased mobility, and increased difficulty swallowing.
Intraventricular hemorrhage occurs when bleeding develops in or around the ventricles of the brain. Hemorrhage may develop quickly or over several weeks. Chronic hemorrhages, 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 tumor, or coagulopathies.
Symptoms and Diagnosis
Symptoms of intraventricular hemorrhage are similar to those of intracranial hemorrhage. Additional symptoms may include bradycardia or tachycardia, hypertension, and decreased level of consciousness. Diagnosis of intraventricular hemorrhage may be obtained via CT scan, MRI, and conventional angiography.
Treatment of intraventricular hemorrhages ultimately focuses on finding the source of the bleeding and stopping it. Clients should be monitored for decreasing level of consciousness, changes in respiratory patterns, and hemodynamic instability. Antiepileptics and antihypertensives may be used to prevent seizures and hypertension, which can both complicate and worsen the client’s condition and neurologic status. Surgical intervention may be indicated depending on the severity and source of the bleeding. Older children and the elderly are more likely to have surgical intervention of both intraventricular and intracranial hemorrhage.
Subarachnoid hemorrhage occurs when bleeding develops between the meninges and the brain. This can occur due to arteriovenous malformation, trauma, or aneurysm. Subarachnoid hemorrhages can cause significant brain injury and death due to compression of the brain as the pooling blood demands the space inside the skull.
Symptoms and Diagnosis
Symptoms of subarachnoid hemorrhage 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, clients may become hyponatremic and collect more fluid inside of the ventricles, known as hydrocephalus.
A grading system has been implemented to define the severity of a subarachnoid hemorrhage. There are five steps of the grading process. These include:
- Grade I— no symptoms to slight headache with nuchal rigidity
- Grade II— moderate to severe headache, nuchal rigidity, and cranial nerve palsy
- Grade III— drowsy to confused, possible mild focal deficits
- Grade IV— stupor, hemiparesis that is moderate to severe, early decerebrate rigidity, difficulty maintaining the basic functions of life (vegetative disturbances)
- Grade V— coma, decerebrate rigidity, may progress to death
Treatment of subarachnoid hemorrhages are similar to other intracranial and intraventricular hemorrhages. Treating any underlying causes of pressure and bleeding must be addressed to prevent progression of the condition. Re-bleeding is not uncommon and clients should be monitored closely to identify early signs of client decline. Depending on the severity of the subarachnoid hemorrhage, evacuation of the pooling blood may be indicated. Clients will likely be prescribed anti-epileptic medications, such as levetiracetam (Keppra®) or phenytoin, to reduce the risk (or treat) seizures. Antihypertensives are also commonly prescribed in the event of a subarachnoid hemorrhage to maintain optimal hemodynamics.
Increased Intracranial Pressure (Hydrocephalus)
In the event of an injury, tumor, bleeding, or structural abnormality in or around the brain, intracranial pressure 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, clients will experience significant symptoms. These include severe headache, confusion, nausea, vomiting, increased blood pressure, double vision, and shallow breathing. If not corrected, elevated intracranial pressure can cause seizures, coma, and death (herniation). MRI or CT scan are generally used to diagnose this condition.
Treatment of increased intracranial pressure focuses on relieving the pressure. Clients may require a burr hole or decompressive craniectomy to relieve pressure alone. Clients with hydrocephalus may benefit from an external ventricular drain to help slowly reduce the excess fluid accumulation in the ventricles. External ventricular drains and intracranial pressure monitors (bolt) are also useful for monitoring a client’s ICP. ICPs greater than 20 mmHg will likely require intervention. Medications such as hypertonic saline (3% NS) and mannitol are used frequently to help draw fluid from the brain back into circulation and ultimately eliminate it.
Healthcare providers may work with nurses to help reduce the metabolic demand of clients with elevated intracranial pressure. Agitated clients should be kept calm. They may require the use of sedative medications. Clients may also require mechanical ventilation to help regulate their breathing. Clients’ head of bed should be maintained at greater than 30 degrees and their necks midline to prevent worsening the pressures within the brain.
Neurologic Infectious Disease
Infectious disease, when involving the neurologic system, can have a series of devastating effects for the client. Early identification of any suspected neurologic infection is imperative to best long-term outcomes. Neurologic infection can be from viral, bacterial, or fungal components. Neurologic involvement can also be secondary to an infection elsewhere in the body. The most common sources of neurologic infection are within 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.
When a client has viral neurologic infectious disease, the client often has symptoms due to effects such as inflammation or auto-immune activation that react because of the viral presence. Two of the more common conditions related to this event are Guillain-Barre՛ syndrome and transverse myelitis.
An autoimmune disorder, Guillain-Barre՛ syndrome generally occurs when a viral illness 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 causes both ascending and descending paralysis.
Symptoms of this condition include generalized numbness and tingling, increasing weakness of lower extremities, loss of deep tendon reflexes, and progressing loss of sensation leading to possible complete paralysis and inability to breathe. Clients 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-Barre՛ is typically supportive. Clients should have their airways 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-Barre՛ is good. Most clients will start to regain function around 2-4 weeks after initial symptoms. Recovery involves intensive therapy services, as clients will be required to relearn and strengthen many motor skills.
Transverse myelitis is a condition when one or both sides of the spinal cord in one or more sections becomes inflamed and damages 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, maintaining the client’s airway, intravenous steroids, plasma exchange therapy, antiviral medication, immunosuppressants, and pain management. Clients will need extensive physical therapy, occupational therapy, and psychotherapy.
Bacterial infection of the nervous system is known as bacterial meningitis. Streptococcus pneumoniae and Neisseria meningitidis are two of the most common offenders in meningeal infection. Infection of the spinal cord or meninges can be from distal infection, surgical site wounds, invasive devices, nasal colonization, or invasive traumas. Bacteria then raise havoc in the nervous system by releasing toxins that cause inflammation, WBC accumulation, and exudate. The bacteria and their toxins may quickly cause brain cell damage if not treated.
Meningitis spreads quickly among the central nervous structures and causes headache, nuchal rigidity, decreasing level of consciousness, agitation, irritability, and seizures. Diagnosis is usually made via lumbar puncture, blood cultures, CT, and/or MRI.
Treatment of bacterial meningitis includes supportive therapy, IV antibiotics, corticosteroids, and pain management. Clients should be monitored closely for changes in neurologic status, signs of increased ICP (unequal pupils, coma, etc.), and hemodynamic instability. Mortality of this condition may reach up to 34%.
Fungal meningitis is a fungal infection of the meninges and surrounding nervous system structures. It is relatively uncommon and can only occur when a fungal organism enters the subarachnoid spaces or cerebrospinal fluid. Clients with immune deficiencies (HIV, cancer, autoimmune) are at highest risk of developing fungal meningitis. Clients with ventricular shunts are also at increased risk for fungal infection after shunt placement or revision.
The most common organisms that cause this type of fungal infection include Candida albicans and Cryptococcus neoformans. Candida albicans is seen more often in clients who have recently undergone spinal/spinal cord surgery, lumbar puncture, or brain surgery. Cryptococcus neoformans is usually seen in clients with HIV/AIDS.
Symptoms and Diagnosis
Symptoms of fungal meningitis are similar to bacterial meningitis symptoms. These include headache, stiff neck, photophobia, fever, nausea and vomiting, and mental changes. Diagnosis can be obtained with a culture of cerebrospinal fluid obtained by a lumbar puncture, blood cultures, and CT.
Treatment of fungal meningitis includes long-term antifungal medications such as amphotericin B, flucytosine, and fluconazole. Clients should be monitored closely for decline in respiratory function, increased ICP, and seizures. Anticonvulsants may also be administered to prevent seizure activity due to the inflamed and infected tissues.
Neuromuscular disorders are characterized by weakness and wasting of the muscles. This can be accompanied with nerve damage or miscommunication. Common disorders that fall within this category of disorders include muscular dystrophy, cerebral palsy, and myasthenia gravis.
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. Clients may develop symptoms of muscular dystrophy in childhood, middle age, or as older adults. The muscle loss is progressive and there is no treatment available. Supportive measures such as physical therapy, occupational therapy, speech therapy, and assistive devices can be used to help maximize a client’s abilities.
Cerebral palsy is a neuromuscular disorder that affects a client’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, jaundice). Symptoms of cerebral palsy include altered gait, abnormal reflexes, abnormal posture, a mix of floppiness and/or rigidity, and involuntary movements. Clients 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. Clients may require varying modifications and medical equipment to improve their symptoms.
Myasthenia gravis is the progressive, long-term weakening of muscles, particularly in the face and neck. Clients 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 absence of antibody creation.
Clients with myasthenia gravis have worsening muscle weakness with muscle use. Rest can improve some of the fatigue. Some clients may experience myasthenic crisis when their respiratory muscles become too weak to regulate breathing and mechanical ventilation is needed. Clients may regain their ability to breathe on their own with blood filtering therapies and other medications (cholinesterase inhibitors, corticosteroids, and immunosuppressants) to help manage their condition. Clients 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 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 clients with head trauma or increased intracranial pressure due to infection or cerebral edema. Clients may need to undergo a craniotomy to decompress a swelling brain or a have a resection of a tumor that is disrupting the brain structures. Intracranial pressure may be monitored through a ventricular drain or transducer placed into the brain. Clients with hydrocephalus may require an internalized ventricular-peritoneal (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.
Several nursing interventions are expected following a neurosurgical event. After brain surgery or placement of an ICP monitor, nurses should maintain neutral client positioning with head of bed elevated between 30-45 degrees. After a lumbar puncture, clients will need to be on bed rest for several hours and have activity restrictions to prevent complications following the procedure. Clients should be monitored closely for infection.
Avoidance of increased stimulus can help to reduce increased cranial pressure. Administration of medications such as corticosteroids, anticoagulants, antibiotics, and antiepileptics may be indicated to reduce complications from the surgery or preceding event. Client intake and output should be monitored closely. Frequent monitoring of arterial blood gasses, pulse oximetry, and lab work (CBC, electrolyte panels, etc.) would also be expected.
Seizure disorders are some of the most common neurologic conditions. Epilepsy can be diagnosed based on a client’s history of seizure activity with supporting electroencephalogram (EEG) evidence. Several seizure types exist, including generalized, partial, absence, atonic, myoclonic, tonic-clonic, and individually tonic and clonic seizures. Seizures may be congenital, infantile, or acquired. Clients with head trauma and severe illness with electrolyte imbalances are at high risk for seizure activity. Febrile seizures often occur in young childhood. Many seizures are preceded by an aura.
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. Clients will also have rescue medications, which are additional, stronger antiepileptics that can be used in the event of breakthrough seizure activity. Barbiturates, 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 clients. Antiepileptic medications may cause symptoms of allergic reactions, skin irritations, severe rash, and hepatotoxicity. Women of childbearing age should understand that most antiepileptic medications are teratogenic. Women may need to provide two types of birth control while on these medications.
Clients in the intensive care unit may be admitted due to breakthrough seizures or develop seizures due to their other conditions. Chronic seizure activity can cause permanent brain changes. Status epilepticus is a medical emergency. It is defined as a seizure lasting more than 30 minutes or two or more seizures without a break between them. This condition is dangerous and often deadly if not treated in a short period of time. Clients may need to be sedated and intubated in the event of uncontrollable status epilepticus.
Nursing interventions for clients with seizures should prioritize client safety. Clients should have bed alarms notifying nurses of falls. Padding on side rails and flooring surrounding the client’s bed may be necessary to prevent injury. If a client begins to convulse, nurses should immediately place the client on his or her side to prevent aspiration of oral secretions or vomitus. This allows for the protection of the client’s airway as well. Nurses should note the exact time a seizure occurs and how long it lasts. Often seizures lasting greater than 5 minutes will need pharmacologic intervention.
Space-occupying lesions in the brain are most likely the result of a brain tumor. 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 brain stem. Secondary lesions are usually due to metastasis of other lesions in the body.
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, brain stem glioma, craniopharyngioma (congenital and recurrent), meningioma (most often in women ages 40-70), ganglioglioma (usually benign), oligodendroglioma (most often in ages 40-60), 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 age 45-70), brain stem glioma, and medulloblastoma.
Diagnosis and Testing
Diagnosis for brain tumors is classically made with imaging, particularly CT or MRI. Clients 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 suspected brain tumor.
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.
Clients may be admitted to the intensive care unit due to a stroke or experience a stroke as a complication of other medical conditions. Strokes occur when blood flow to part of the brain is interrupted or slowed. 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 client treatment is crucial to reducing the burden of the stroke. The most beneficial treatments work best if given within three hours from symptom onset.
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. Thrombus that occurs in large arteries is usually a result of atherosclerosis. The elderly are most at risk for a large thrombus ischemic stroke. Thrombosis that penetrates into smaller arteries, also known as lacunar infarct, are most common in clients 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. Clients diagnosed with this condition should have tissue plasminogen activator (tPA, Activase®) initiated within 3 hours of symptom onset. This medication is used to dissolve fibrin clots and is given intravenously at a dose of 0.9 mg/kg up to 90 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 5 hours, hemorrhage or bleeding in the brain, recent surgery, anticoagulant use, 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 start of stroke symptoms.
Clients should also be placed on antihypertensive medications if their MAP exceeds 130 mmHg or systolic blood pressure exceeds 220. 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 client’s symptoms are due to embolism, aspirin and anticoagulation may be initiated.
Additional measures of care include cooling the client to avoid hyperthermia and increased metabolic demand; treating hyperglycemia; and surgical intervention to manually remove the obstruction if all else fails. Nursing interventions during this time include reducing factors that may increase the client’s ICP, such as maintaining a neutral head/body position, elevating the client’s head to 30 degrees, reducing external stimulation, reducing pain, and closely monitoring the client’s vital signs.
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% of stroke diagnoses. Despite this, 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. Clients may also develop hemorrhagic strokes from cerebral cavernous malfunctions or arteriovenous malformations (AVMs). Other risk factors include bleeding disorders, anticoagulant or antiplatelet medication, head trauma, and cerebral aneurysm.
Symptoms of hemorrhage stroke vary slightly from ischemic stroke. One of the hallmark signs of hemorrhagic stroke is sudden, severe headache. Clients 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. It can be further confirmed with lumbar puncture (bloody CSF) or electroencephalogram (EEG).
Treatment of hemorrhagic stroke initially focuses on stopping the bleeding and lowering the client’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. Long-term rehabilitation of the client depends on the extent of bleeding damage. Clients will require long-term physical therapy and rehab to help maximize their recovery.
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 client’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 brian involved, symptoms may vary even if clients 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 arterosclerosis are all risk factors. Clients 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. Clients 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. There are several types of brain injury. These are addressed below.
Epidural— Epidural hematomas occur outside of the dura. They may cross the midline suture. Hemorrhage usually occurs due to a shearing, acceleration-deceleration trauma. Bleeding is usually from the damage to an artery. 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 only be identified on one side of the brain, as it is unable to cross the midline suture. This condition usually develops due to the bleeding of veins torn in the initial injury. 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 craniotomy or burr hole procedure.
Concussion— Concussion injuries occur due to acceleration-deceleration trauma. 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. Clients may also experience symptoms of irritability, difficulty concentrating, headaches, and light or noise sensitivity while recovering from the injury. Pain relief may be provided with mild analgesics. Clients should be instructed on rest and activity restrictions that may last several weeks to months following the injury.
Non-accidental trauma— This type of trauma occurs due to abuse and/or assault injury. Head injuries are the leading cause of death in non-accidental trauma events. Depending on the severity of the trauma, management of TBI may fall in any of the previous categories.
Diagnosis and Management
Diagnosis of TBI may be obtained via x-rays of the spine, CT, MRI, and client assessment. The Glascow coma scale can be used to evaluate a client’s neurologic status and to help support the severity diagnosis and worsening or improving of the injury. Clients should be assessed frequently to identify any worsening of their condition and need for emergent or additional interventions.
TBI treatment includes close client monitoring of vital signs, intracranial pressure, and fluid balance. In clients with intracranial pressure monitoring devices, ICP should be maintained between 7-15 mmHg (up to 20-25 mmHg being the upper limit). Clients may undergo neurosurgery to relieve brain swelling and evacuate hematomas.
Medications such as hypertonic saline solution (3%) and mannitol may be used to help reduce swelling of the brain and provide osmotic diuresis to reduce a client’s ICP. Important cautions with hypertonic saline include the necessity of having a central line for infusion and close monitoring of sodium (every 6 hours) and serum osmolality levels (every 12 hours). Sodium levels should be maintained between 145-155 mmol/L and serum osmolality maintained at 320 MOsmol/L to prevent renal failure and cardiac and respiratory complications. 30 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 client status. Mannitol should be administered through a central line. Typical dosing is 0.25-2 g/kg over 30 minutes to an hour. ICP decrease should be visualized approximately 15-20 minutes following administration of this medication. Higher concentrations of the medication may require filtration prior to administration. This is due to the medication’s ability to crystallize when exposed to low temperatures and polyvinyl chloride bags or tubing. Clients should be monitored closely for swings in electrolyte balances, nausea, vomiting, hypotension, tachycardia, fever, and urticaria.
In some events, clients may need to be placed in a medically induced coma via neuromuscular blockade to reduce the body’s metabolism and provide rest for the brain while treating the injury(ies). 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 of clients 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).