Nursing Management: Acute Intracranial Problems

Chapter 57


Nursing Management


Acute Intracranial Problems


Meg Zomorodi





Reviewed by Sarah Livesay, RN, DNP, ACNP, CNS-A, System Director of Service Line Development, St. Luke’s Episcopal Health System, Houston, Texas; Molly M. McNett, RN, PhD, Director, Nursing Research, MetroHealth Medical Center, Cleveland, Ohio; and Susan Yeager, RN, MS, CCRN, ACNP, Neurocritical Care Nurse Practitioner, The Ohio State University Medical Center, Columbus, Ohio.


Acute intracranial problems include diseases and disorders that can increase intracranial pressure (ICP). This chapter discusses the mechanisms that maintain normal ICP and increase ICP. In addition, head injury, brain tumors, and cerebral inflammatory disorders are discussed.



Intracranial Pressure


Understanding the dynamics associated with ICP is important in caring for patients with many different neurologic problems. The skull is like a closed box with three essential volume components: brain tissue, blood, and cerebrospinal fluid (CSF) (Fig. 57-1). The intracellular and extracellular fluids of brain tissue make up approximately 78% of this volume. Blood in the arterial, venous, and capillary network makes up 12% of the volume, and the remaining 10% is the volume of the CSF.




image eNursing Care Plan 57-1   Patient With Increased Intracranial Pressure




Patient Goals














Outcomes (NOC) Interventions (NIC) and Rationales




Cerebral Edema Management


• Monitor vital signs and neurologic status closely and compare with baseline to evaluate patient’s response to treatment and enable immediate reporting and modification of treatment if necessary.


• Monitor respiratory status: rate, rhythm, depth of respirations; PaO2, PaCO2, pH, bicarbonate because low PaO2 and a high hydrogen ion concentration (acidosis) are potent cerebral blood vasodilators that increase cerebral blood flow and may increase ICP.


• Analyze ICP waveform to provide an accurate indicator of ICP.


• Monitor patient’s ICP and neurologic responses to care activities.


• Position with head of bed up 30 degrees or greater to promote venous drainage from head, reducing ICP.


• Limit suction passes to <10 sec to prevent increased ICP.


• Allow ICP to return to baseline between nursing activities to prevent sustained increases in ICP.


• Maintain normothermia as elevated temperature increases cerebral metabolism and causes increased ICP.


• Give sedation to decrease agitation and hyperactivity that cause increased ICP.


• Decrease stimuli in patient’s environment to prevent increases in ICP



image





Patient Goal


Maintains cerebral perfusion within normal parameters












Outcomes (NOC) Interventions (NIC) and Rationales





Cerebral Perfusion Promotion


• Consult with physician to determine hemodynamic parameters, and maintain hemodynamic parameters within this range.


• Induce hypertension with volume expansion or inotropic or vasoconstrictive agents, as ordered, to maintain hemodynamic parameters and maintain/optimize cerebral perfusion pressure (CPP).


• Consult with physician to determine optimal head of bed placement (e.g., 0, 15, or 30 degrees) and monitor patient’s responses to head positioning.


• Monitor determinants of tissue oxygen delivery (e.g., PaCO2, SaO2, and hemoglobin levels and cardiac output), if available, to ensure adequate oxygenation to support brain function.


• Calculate and monitor CPP to evaluate adequacy of cerebral blood perfusion.


• Monitor neurologic status to determine hemodynamic status.


• Monitor intake and output to assess effects of diuretic and corticosteroid therapy.




image




Patient Goal


Experiences no complications of immobility












Outcomes (NOC) Interventions (NIC) and Rationales









image


ICP, Intracranial pressure; PaCO2, partial pressure of carbon dioxide in arterial blood; PaO2, partial pressure of oxygen in arterial blood; ROM, range of motion; SaO2, oxygen saturation of arterial blood.



*Nursing diagnoses listed in order of priority.



image eNursing Care Plan 57-2   Patient With Bacterial Meningitis





Patient Goals














Outcomes (NOC) Interventions (NIC) and Rationales






Delirium Management


• Monitor neurologic status on an ongoing basis to determine extent of problem.


• Administer PRN (as needed) medications for anxiety or agitation to reduce fear and anxiety.


• Provide a low-stimulation environment for patient in whom disorientation is increased by overstimulation.


• Approach patient slowly and from the front to avoid stimulating or frightening patient.


• Provide appropriate level of supervision/surveillance to monitor patient and to allow for therapeutic actions.


• Reorient the patient to the health care provider with each contact to assist with orientation and reduce anxiety.


• Communicate with simple, direct, descriptive statements to avoid overstimulation.


• Assist with needs related to nutrition, elimination, hydration, and personal hygiene because the patient may lose awareness of the needs.



image




Patient Goal


Maintains body temperature within normal range





Patient Goals







*Nursing diagnoses listed in order of priority.


Because cerebral edema and increased intracranial pressure may occur with bacterial meningitis, see the related nursing care plan, eNCP 57-1, for these nursing diagnoses.


Primary versus secondary injury is another important concept in understanding ICP. Primary injury occurs at the initial time of an injury (e.g., impact of car accident, blunt-force trauma) that results in displacement, bruising, or damage of the three components. Secondary injury is the resulting hypoxia, ischemia, hypotension, edema, or increased ICP that follows the primary injury. Secondary injury, which could occur several hours to days after the initial injury, is a primary concern when managing brain injury. Nursing management of the patient with an acute intracranial problem must include management of secondary injury, and thus increased ICP.



Regulation and Maintenance of Intracranial Pressure


Normal Intracranial Pressure.


Intracranial pressure (ICP) is the hydrostatic force measured in the brain CSF compartment. Under normal conditions in which intracranial volume remains relatively constant, the balance among the three components (brain tissue, blood, CSF) maintains the ICP. Factors that influence ICP under normal circumstances are changes in (1) arterial pressure; (2) venous pressure; (3) intraabdominal and intrathoracic pressure; (4) posture; (5) temperature; and (6) blood gases, particularly carbon dioxide levels. The degree to which these factors increase or decrease the ICP depends on the brain’s ability to adapt to changes.


The Monro-Kellie doctrine states that the three components must remain at a relatively constant volume within the closed skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change.1 This hypothesis is only applicable in situations in which the skull is closed. The hypothesis is not valid in persons with displaced skull fractures or hemicraniectomy.


ICP can be measured in the ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer.2 Normal ICP ranges from 5 to 15 mm Hg. A sustained pressure greater than 20 mm Hg is considered abnormal and must be treated.



Normal Compensatory Adaptations.


In applying the Monro-Kellie doctrine, the body can adapt to volume changes within the skull in three different ways to maintain a normal ICP. First, compensatory mechanisms can include changes in the CSF volume. The CSF volume can be changed by altering CSF absorption or production and by displacing CSF into the spinal subarachnoid space. Second, changes in intracranial blood volume can occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow. Third, brain tissue volume compensates through distention of the dura or compression of brain tissue.


Initially an increase in volume produces no increase in ICP as a result of these compensatory mechanisms. However, the ability to compensate for changes in volume is limited. As the volume increase continues, the ICP rises and decompensation ultimately occurs, resulting in compression and ischemia.



Cerebral Blood Flow


Cerebral blood flow (CBF) is the amount of blood in milliliters passing through 100 g of brain tissue in 1 minute. The global CBF is approximately 50 mL/min/100 g of brain tissue.3 The maintenance of blood flow to the brain is critical because the brain requires a constant supply of oxygen and glucose. The brain uses 20% of the body’s oxygen and 25% of its glucose.4



Autoregulation of Cerebral Blood Flow.


The brain regulates its own blood flow in response to its metabolic needs despite wide fluctuations in systemic arterial pressure. Autoregulation is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP). The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits.


The lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is a mean arterial pressure (MAP) of 70 mm Hg. Below this, CBF decreases, and symptoms of cerebral ischemia, such as syncope and blurred vision, occur. The upper limit of systemic arterial pressure at which autoregulation is effective is a MAP of 150 mm Hg.3 When this pressure is exceeded, the vessels are maximally constricted, and further vasoconstrictor response is lost.


The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. CPP is equal to the MAP minus the ICP (CPP = MAP − ICP) (see example in Table 57-1). This formula is clinically useful, although it does not consider the effect of cerebrovascular resistance. Cerebrovascular resistance, generated by the arterioles within the cranium, links CPP and blood flow as follows: CPP = Flow × Resistance.



When cerebrovascular resistance is high, blood flow to brain tissue is impaired. Transcranial Doppler is a noninvasive technique used in intensive care units (ICUs) to monitor changes in cerebrovascular resistance.


As the CPP decreases, autoregulation fails and CBF decreases. Normal CPP is 60 to 100 mm Hg. A CPP of less than 50 mm Hg is associated with ischemia and neuronal death. A CPP of less than 30 mm Hg results in ischemia and is incompatible with life.


Normally, autoregulation maintains an adequate CBF and perfusion pressure primarily by adjusting the diameter of cerebral blood vessels and metabolic factors that affect ICP. It is critical to maintain MAP when ICP is elevated.


Remember that CPP may not reflect perfusion pressure in all parts of the brain. There may be local areas of swelling and compression limiting regional perfusion pressure. Thus a higher CPP may be needed for these patients to prevent localized tissue damage. For example, a patient with an acute stroke may require a higher BP, increasing MAP and CPP, in order to increase perfusion to the brain and prevent further tissue damage.



Pressure Changes.


The relationship of pressure to volume is depicted in the pressure-volume curve (Fig. 57-2). The curve is affected by the brain’s compliance. Compliance is the expandability of the brain. It is represented as the volume increase for each unit increase in pressure. With low compliance, small changes in volume result in greater increases in pressure.



MAP  =  DBP  +  1/3 (SBP    DBP) or  =  SBP+2 (DBP)3


image

The concept of the pressure-volume curve can be used to represent the stages of increased ICP. At stage 1 on the curve, there is high compliance. The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (in brain tissue, blood, or CSF) does not increase the ICP.


At stage 2, the compliance is beginning to decrease, and an increase in volume places the patient at risk of increased ICP and secondary injury. At stage 3, there is significant reduction in compliance. Any small addition of volume causes a great increase in ICP. Compensatory mechanisms fail, there is a loss of autoregulation, and the patient exhibits manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness).


With a loss of autoregulation, the body attempts to maintain cerebral perfusion by increasing systolic BP. However, decompensation is imminent. The patient’s response is characterized by systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations. This is known as Cushing’s triad and is a neurologic emergency.


As the patient enters stage 4, the ICP rises to lethal levels with little increase in volume. Herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. In this situation, intense pressure is placed on the brainstem, and if herniation continues, brainstem death is imminent.



Factors Affecting Cerebral Blood Flow.


Carbon dioxide, oxygen, and hydrogen ion concentration affect cerebral blood vessel tone. An increase in the partial pressure of carbon dioxide in arterial blood (PaCO2) relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, and increases CBF. A decrease in PaCO2 constricts cerebral vessels, increases cerebrovascular resistance, and decreases CBF.


Cerebral oxygen tension of less than 50 mm Hg results in cerebrovascular dilation. This dilation decreases cerebrovascular resistance, increases CBF, and increases oxygen tension. However, if oxygen tension is not increased, anaerobic metabolism begins, resulting in an accumulation of lactic acid. As lactic acid increases and hydrogen ions accumulate, the environment becomes more acidic. Within this acidic environment, further vasodilation occurs in a continued attempt to increase blood flow. The combination of a severely low partial pressure of oxygen in arterial blood (PaO2) and an elevated hydrogen ion concentration (acidosis), which are both potent cerebral vasodilators, may produce a state where autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.


CBF can be affected by cardiac or respiratory arrest, systemic hemorrhage, and other pathophysiologic states (e.g., diabetic coma, encephalopathies, infections, toxicities). Regional CBF can also be affected by trauma, tumors, cerebral hemorrhage, or stroke. When regional or global autoregulation is lost, CBF is no longer maintained at a constant level but is directly influenced by changes in systemic BP, hypoxia, or catecholamines.



Increased Intracranial Pressure


Any patient who becomes unconscious acutely, regardless of the cause, should be suspected of having increased ICP.



Mechanisms of Increased Intracranial Pressure


Increased ICP is a potentially life-threatening situation that results from an increase in any or all of the three components (brain tissue, blood, CSF) within the skull. Elevated ICP is clinically significant because it diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis.5 Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation).


These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema. This edema distorts brain tissue, further increasing the ICP, and leads to even more tissue hypoxia and acidosis. Fig. 57-3 illustrates the progression of increased ICP.


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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Acute Intracranial Problems

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