Page 1 Musculoskeletal/Neurological/Psychosocial Study Guide for the CCRN®
This is another wide-ranging area and it is covered by 13% of the CCRN® test questions. You can see that the content ranges from the physical body to the brain’s functions to mental health concerns. Problems with any or all of these could be present in critical care patients, and you not only need to know how the systems work, but what to do if a patient has an emergency in any of these areas. Use this study guide to help you know what to study.
The musculoskeletal system is the primary force behind movement, stability, support and strength of the body. Numerous conditions may affect the musculoskeletal system as primary concerns or secondary injuries. Review the following conditions that involve the musculoskeletal system. Know the premises of the conditions, how to assess these in patient populations, and how to intervene when necessary.
Osteomyelitis is one of the most common and critical musculoskeletal infections. It can occur from a variety of injuries. Other common musculoskeletal infections include cellulitis and septic arthritis. If not treated, these infections can quickly become serious, life-threatening events.
Signs and Symptoms
In the critical care world, osteomyelitis is an infection in the bone that often develops in the site of a large wound or after introduction of bacteria to an open sore. Infection that harbors in the bone can be very difficult to treat. It is more commonly seen in patients with chronic wounds or slow or non-healing ulcerations. Symptoms of this condition include pain, swelling, and erythema around the site. Purulent drainage may also be present if located near an open wound. Depending on the severity of the infection, fever and chills can occur.
Common lab work obtained when there is concern for osteomyelitis includes complete blood count (CBC), erythrocyte sedimentation rate (ESR), blood cultures, and C-reactive protein (CRP). This helps to identify how involved the inflammation and infection are and to determine if the infection has spread to the bloodstream (sepsis). Radiologic imaging may be obtained as well to secure a diagnosis. Osteomyelitis may be seen on CT, MRI, x-ray, and bone scans. In some cases, bone biopsies are indicated to identify the offending organism.
Treatment of osteomyelitis (cellulitis and septic arthritis as well) includes the initiation of antibiotic therapy. Identifying the organism(s) present may become critical to assess the functionality of specific antibiotics and help to determine the course for treatment. Antibiotics must be given intravenously to ensure access to the bone. Oral antibiotics are often not potent enough to treat this type of infection.
In some cases, surgical intervention may be necessary. Depending on the location and severity of the infection, surgical debridement and sterile irrigation may be performed to remove any debris and bacterial toxins from the bone itself. Rarely, limb amputation may be required if the infection has become unmanageable by traditional therapies.
Other than infectious causes, the musculoskeletal system may be affected by a series of functional issues that can cause or complicate critical illness.
Immobile patients are at considerable risk for illness and injury. Some of the most common conditions that plague patients with decreased mobility include skin breakdown, pressure ulcers, decreased muscle mass, decreased coordination, increased risk for falls, deep vein thrombosis, constipation, and depression. Patients should also be monitored for neurologic and cardiovascular decline.
Patients in critical care units are at high risk for decreased mobility and complete immobility due to their primary conditions. In order to avoid severe complications, nurses should turn patients every 1-2 hours, practice passive and active range of motion, encourage patient participation in mobilizing when possible, and implementing protective measures to prevent skin breakdown and ulcerations. All patients should be working toward progressive mobility. Constantly assessing and reassessing a patient’s ability to move about is essential to improved recovery measures without secondary injury or illness.
Falls are the number one adverse event that occurs in the hospital. Many times, falls can be prevented. Patients who are confused and agitated have great risk of falling. Other common patients at increased risk include those with abnormal gait, orthostatic hypotension, and those with a history of falling. Many patients are injured after a fall, complicating their hospital stay and possibly leading to increased morbidity and mortality related to the injury.
Preventing fall events is critical to improving patient outcomes. Nurses should frequently survey their patients’ environments with the objective of removing or at least limiting obstacles. Implementation of bed alarms, gait belts, and progressive mobility goals should be tailored to all patients to reduce their risk of falling. Nurses should also anticipate patient needs such as toileting and easy access to commonly used items. The nurse should attempt to help patients prior to them trying to help themselves. Many facilities have active care plans and standards that are used to identify patients at highest risk for falls and how to prevent these adverse events.
Gait disorders fall along the same line of falls and immobility. Patients with gait disorders have an array of involuntary, abnormal movements that impact how they maneuver. Most gait disorders are poorly understood as to why they occur or how they progress. The most common gait disorder is functional tremor. Elderly patients often develop gait disorders due to decreased mobility in joints or balance. Nurses may assess gait disorders, such as in patients with dragging gait, knee buckling, slow stepping, swaying movements, hesitant gait, and hyperkinetic gait.
Patients with gait disorders should have a complete neurologic workup to determine any underlying causes, especially if the gait change is new. Nurses should implement fall precautions to prevent injury. The need for balancing devices such as canes, walkers, braces, and gait belts should be addressed as well to protect the patient from injury.
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.
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 or 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 least 12 hours apart 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. Testing of primary reflexes is also part of the brain death examination. 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 20 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.
Encephalopathy, with regard to the nervous system, most commonly occurs due to a hypertensive crisis. In patients with chronically elevated blood pressure, the brain adapts to manage the pressures and prevent issues in blood flow. When a patient 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 patient vital signs before it develops into a more severe complication.
Treatment of hypertensive encephalopathy 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 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 patients 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 patient’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 patient positioning to prevent obstruction of cranial venous drainage, frequent vital signs, decreasing the patient’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 patient’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. Patients 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 of 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 patient’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. Patients who have experienced an intracranial hemorrhage often have long-term consequences following the event. Nurses must be aware of the patients’ 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. Patients 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 patient’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, patients 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 patients should be monitored closely to identify early signs of patient decline. Depending on the severity of the subarachnoid hemorrhage, evacuation of the pooling blood may be indicated. Patients 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.