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Complication of brain resection procedure and treatment.
What is vasogenic edema, in which the blood–brain barrier becomes increasingly permeable. This type of edema is most common after brain tumor resection and is secondary to changes to the usually tightly controlled blood–brain barrier that becomes inflamed and more permeable in the area of the tumor and surgical resection. The time course for cerebral edema after brain tumor resection is variable and is associated with the type of tumor.
Serial neurological assessments are used to monitor a patient’s response to the surgical procedure, and deterioration of that assessment can be caused by cerebral edema. The edema can be located in and around the area where the tumor was resected or can be located along the path taken by the surgeons to expose and resect the tumor.
Emergent treatment for cerebral edema includes osmotic diuretics, hyperventilation, and head positioning (head of bed elevated greater than 30 degrees). Management of cerebral edema regarding brain tumors often includes increasing the dose of glucocorticoids as these medications decrease the inflammatory process associated with damage in and around the tumor.
Nursing actions for a client with rib fractures.
What is apply oxygen as ordered, anticipate and prepare for intubation, elevate the head of the bed, encourage deep breathing and coughing, every 1 to 2 hours and incentive spirometry use every hour while awake, encourage ambulation as soon as possible, chest tube management, administer pain medications; encourage the use of patient-controlled analgesia before ambulation and pulmonary toileting.
Cause of atelectasis include.
Damage to the alveolar cells that produce surfactant. Surfactant is responsible for maintaining alveolar surface tension. Alveolar surface tension keeps the alveoli from fully collapsing at the end of expiration. If alveolar surface tension is lost, then the alveoli collapse. This is referred to as atelectasis.
Contraindications for Tissue Plasminogen Activator (rt-PA)
What is evidence of intracranial hemorrhage on pre-treatment CT scan, minor or rapidly improving clinical manifestations, clinical manifestations of subarachnoid hemorrhage even with normal head CT, Active internal bleeding: gastrointestinal or urinary bleeding within last 21 days or known bleeding risk (platelets less than 100,000, heparin within 48 hrs., taking oral anticoagulants, major surgery or trauma in prior 14 days, stroke, head trauma, intracranial surgery), history of intracrnial hemorrhage, recent acute MI.
Interpret
pH: 7.58, PaC02: 26, HCO3: 30, PaO2: 99
What is happening to the client?
The ABG result shows respiratory alkalosis and is typically caused by hyperventilation.
Medications that should be held prior to a neurological assessment.
What are sedatives.
Monitoring and maintenance of chest tubes include.
What is maintain a closed chest tube system, keep drainage system below the chest level, monitor amount and color of chest tube drainage, attach to wall suctiong as ordered (usually 20mmHg)monitor water-seal chamber (initially, there is bubbling on expiration, indicating air removal from the pleural space. Later, after the air has escaped from the pleural space, the water level fluctuates with respiratory effort. When the pleural-wall disruption is healed, the water fluctuation may no longer be present. At that point, the patient should be evaluated for chest-tube removal.
Continuous bubbling in the water-seal chamber is an indication of an air leak), never clamp the chest tube, if the chest tube becomes disconnected from the drainage system, immediately submerge the end of the chest tube in sterile water to preserve the water seal, if the chest tube becomes dislodged from the chest, apply a vaseline gauze dressing and notify the provider immediately, and prepare for insertion of a new chest tube.
Medications expected for a client in acute respiratory distress syndrome.
What are antibiotics, Corticosteroids, Neuromuscular blocking agents or paralytics, pain and sedative medication.
Teaching for right and left homonymous hemianopia.
What is:
Right homonymous hemianopia (loss of vision in the right temporal field of vision and left nasal field of vision, requiring patients to scan an area in order to visualize objects on their right side)
Left homonymous hemianopia (loss of vision in the left temporal field of vision and right nasal field of vision, requiring patients to scan an area in order to visualize objects on their left side)
Clinical manefestations of a client with a brain tumor.
What is changes in level of consciousness and cognition secondary to pressure on the frontal lobe, decreased hearing on one side, dysphagia, clinical manifestations of increased ICP include papilledema (swelling of the optic disk), headache, nausea, and vomiting, decreased alertness, cognitive impairment, personality changes, ataxia, hemiparesis, abnormal reflexes, and cranial nerve palsies.
Purpose of ventriculostomy (intaventricular catheter (IVC).
The intraventricular catheter (IVC) with external ventricular drain (EVD), or ventriculostomy, is used for monitoring ICP and draining CSF.
Clinical manifestions of pneumothorax and management.
What is agitation and anxiety, tachypnea/hyperventilation, Tachycardia, pain, shortness of breath, decreased oxygenation, decreased LOC, decreased or absent lung sounds on affected side, asymmetrical chest excursion, and subcutaneous emphysema.
Management includes chest tube insertion for lung re-expansion.
What dooes the acronym B.E.F.A.S.T. stand for?
What is Balance, Eyes, Face, Arm, Speech, Time
Clinical manefestations and medication management for increased intracranial pressure (ICP).
Increased ICP is detected by performing serial neurological assessments, including the elements of wakefulness, arousal, cranial nerves, and motor function. The most sensitive indicator of ICP is a decrease in level of consciousness.
The initial approach to the emergency management of increased ICP consists of airway management and therapies to decrease intracranial contents, such as administration of mannitol (Osmitrol) and high-concentration sodium chloride solutions (e.g., 3%) are used to increase the osmolality in the blood in order to pull water from the interstitial space of the brain and other tissues into the vascular space.
Complications Associated With Mechanical Ventilation.
Complications that are associated with mechanical ventilation include hypotension, infection, barotrauma, tracheal deviation, aspiration, and ventilator-associated pneumonia (VAP), and possible pressure ulcers.
Clinical manifestations of Guillain-Barre Syndrome and diagnostic procedure.
Patient with GBS develop a symmetrical ascending motor weakness and paralysis that usually starts in the feet and extends to the trunk and arms. (Note: there is an easy way to remember the pattern of weakness in GBS: it starts in the toes, and up it goes.) There may be sensory involvement, and patients may complain of paresthesias and pain that involves the shoulders, back, buttocks, and upper legs. After the first few days of weakness, neurological assessment demonstrates diminished or absent deep tendon reflexes (areflexia). Areflexia is recognized as a key finding in GBS. Up to 40% of patients with GBS develop respiratory impairment. Respiratory failure is caused by weakness of the diaphragm and intercostal muscles, and the patient may require intubation and mechanical ventilation to provide respiratory support.
Established diagnostic criteria for GBS include progressive weakness of two or more limbs caused by neuropathy, areflexia, and history of recent viral or bacterial infection. Additionally, a lumbar puncture is performed to obtain cerebrospinal fluid (CSF). Cerebrospinal fluid findings include elevated protein and normal cell count. Electromyography results reveal slowed nerve conduction velocity soon after the patient develops paralysis.
Indications for mechanical ventilation and nursing actions for a client receiving mechanical ventilation include.
Indications for mechanical ventilation include acute respiratory failure; heart failure; exacerbation of COPD; protection of the airway due to cardiac arrest or smoke inhalation, drug overdose, or respiratory depression; and spinal cord or neurological trauma.
What is HOB elevation between 30 and 45 degrees unless contraindicated, clear airway secretions with suctioning, CPT, frequent position changes or prone positioning (reduces mortality), and increasing activity, daily “sedation vacation” and a readiness-to-wean assessment, peptic ulcer disease prophylaxis, deep vein thrombosis (DVT) prophylaxis, daily oral care with chlorhexidine, Weaning From Mechanical Ventilation (patient is monitored for stable vital signs/ABGs, minimal secretions, adequate oxygenation, and spontaneous breathing and is free of sedation medications).
Positioning to promote lung healing.
What is proning and positioing client with affected side up (or dependent).
Bipap vs. CPAP
What is noninvasive positive-pressure ventilation (NPPV), such as bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP), administered via a tight-fitting face mask, can be used to help increase oxygenation. In BiPAP, the patient receives two different pressures. A higher pressure during inhalation assists with the opening of the alveoli, and a lower pressure during exhalation keeps the alveoli from collapsing during/at the end of exhalation but also allows ease of exhalation. In contrast, CPAP maintains one continuous pressure throughout the respiratory cycle to help keep the alveoli open through inspiration and expiration.
Clinical manifestation of herniation can include
Abnormal flexion or extension (posturing)
• Bilateral pupillary dilation
• Abnormal eye movements such as downward and outward eye movements as cranial nerves controlling eye movements are compressed
• Positive Babinski reflex
• Coma
• Cushing’s triad (increased systolic blood pressure, bradycardia, and irregular respiratory pattern)
Unilateral dilated pupil
• Contralateral motor weakness or flexion/extensor posturing
• Positive Babinski reflex
• Coma
Cushing’s triad (increased systolic blood pressure, bradycardia, and irregular respiratory pattern)
Clinical manifestations of amyotrophic lateral sclerosis (ALS) and client teaching.
Patient clinical manifestations are often described first as general complaints of muscle cramps or stiffness, muscle weakness on one part of the body first, slurred speech, and difficulty swallowing (dysphagia). While the disease progresses, the patient experiences weakness and atrophy in other parts of the body. To be diagnosed with ALS, patients must have clinical manifestations of both upper and lower motor neuron damage that cannot be attributed to other causes. Upper motor neuron damage is associated with spasticity, while lower motor neuron damage is characterized by flaccidity.
Airway, because motor weakness involves muscles of the face, mouth, and neck, maintaining an intact airway is compromised. Airway compromise is greater as the patient demonstrates weakened cough and impaired swallowing.
Client teaching include: report increased difficulty swallowing or breathing, disease prognosis and process: need for ventilator, and skin precautions related to decreased mobility.
Cause of high and low pressure alarm on the ventilator.
High pressure - Mucous plug or increased secretions, Patient biting the ETT, Pneumothorax, Patient anxious and fighting the ventilator, Kink in the tubing, Water collected in the ventilator tubing
Low pressure - Cuff leak, Leak in the ventilator circuit, patient stops breathing in the pressure support modes or SIMV
Clinical manifestations and treat for tension pneumothroax.
Tension pneumothorax may occur if air or blood collects in the pleural space and is not removed. If this is left untreated, the positive pressure in the pleural cavity increases, and the affected lung collapses. As the positive pressure increases, it may cause a mediastinal shift toward the unaffected side. This can result in compression of the heart, vena cava, aorta, and contralateral (unaffected) lung. Tracheal deviation toward the unaffected side is a hallmark sign of tension pneumothorax.
In emergent cases of tension pneumothorax, a needle decompression, performed to remove the air from the pleural space, may be required. A large-bore needle (14- or 16-gauge) is inserted between the ribs at the second intercostal space at the midclavicular line to allow for rapid evacuation of air or blood. This is immediately followed by chest tube insertion.
Pathophysiology of pulmonary embolism.
When a blood clot or other particulate matter travels to the lungs, it lodges in the pulmonary artery and blocks blood flow. This obstruction results in an impaired ventilation-to-perfusion ratio (V/Q ratio) described as decreased or blocked blood flow or perfusion to functioning alveoli. This is called a ventilation–perfusion mismatch (V/Q mismatch), a decreased blood flow to functioning alveoli or areas of the lung where gas exchange can take place if perfusion is adequate. A PE results in a high-ventilation/low-perfusion scenario—a high V/Q mismatch. This prevents gas exchange at the alveolar level, leading to hypoxemia (low blood oxygen levels) and local vasoconstriction in the affected pulmonary vascular bed. The PE also results in an increase in pulmonary vascular resistance (PVR) because blood flow cannot move past the venous obstruction. If the right ventricle cannot overcome this increased PVR, then left ventricular preload (blood flow to the left ventricle) is reduced. This leads to decreased oxygenation, decreased cardiac output, and hypotension. The combination of decreased oxygenation and reduced cardiac output results in inadequate tissue perfusion and hypoxia (inadequate oxygenation at the cellular level). The increased PVR also leads to pulmonary hypertension (high pressures in the pulmonary vasculature), causing a backflow of blood into the right ventricle and right heart failure. This can exacerbate if the vascular obstruction continues to grow.
A client weighing 70kg is receiving dopamine at 12 mL/hr. The concentration of dopamine is 200 mg in 250 mL of 0.9% NS. How many mcg/kg/minute is the client receiving? Round the answer to the nearest tenth.
What is 2.3 mcg/kg/min