Presentation is loading. Please wait.

Presentation is loading. Please wait.

Focus on Intracranial Pressure

Similar presentations


Presentation on theme: "Focus on Intracranial Pressure"— Presentation transcript:

1 Focus on Intracranial Pressure
(Relates to Chapter 57, “Nursing Management: Acute Intracranial Problems,” in the textbook) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

2 Intracranial Pressure
{See next slide for figure.} Intracranial pressure is the hydrostatic force measured in the brain CSF compartment. Intracranial Pressure Skull has three essential components: Brain tissue Blood Cerebrospinal fluid (CSF) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 2

3 Components of the Brain
Fig Components of the brain. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 3

4 Intracranial Pressure
Intracellular and extracellular fluids of brain tissues make up 78% of the volume. Blood makes up 12%. Remaining 10% is CSF. Balance of these components maintains the ICP under normal conditions. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 4

5 Intracranial Pressure
The degree to which these factors increase or decrease the ICP depends on the ability of the brain to accommodate to the changes. Intracranial Pressure Factors that influence ICP Arterial pressure Venous pressure Intraabdominal and intrathoracic pressure Posture Temperature Blood gases (particularly CO2 levels) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 5

6 Regulation and Maintenance
This hypothesis is applicable only in situations in which the skull is closed. The hypothesis is not valid in neonates and in adults with displaced skull fractures. Regulation and Maintenance Normal intracranial pressure Modified Monro-Kellie doctrine: describes relatively constant volume within skull structure If volume in any one of the components increases within the cranial vault, and volume from another component is displaced, the total intracranial volume will not change. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 6

7 Regulation and Maintenance
Alterations in intracranial blood volume occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow. Tissue brain volume compensates through distention of the dura or compression of brain tissue. Regulation and Maintenance Normal compensatory adaptations Alteration of CSF absorption or production Displacement of CSF into spinal subarachnoid space Ability to compensate is limited. If volume increase continues, ICP rises. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 7

8 Regulation and Maintenance
Measuring ICP Can be measured in Ventricles Subarachnoid space Epidural space Brain tissue Measured with a pressure transducer Normal ICP: 5 to 15 mm Hg Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 8

9 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
A difference in flow is noted between the white and gray matter of the brain. The white matter has a slower blood flow, approximately 25 mL/min per 100 g, and the gray matter has a faster blood flow, approximately 75 mL/min per 100 g. The brain uses 20% of the body’s oxygen and 25% of its glucose. Cerebral Blood Flow Definition The amount of blood in milliliters passing through 100 g of brain tissue in 1 minute About 50 mL/min per 100 g of brain tissue Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 9

10 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
The lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is a mean arterial pressure (MAP) of 50 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. Cerebral Blood Flow Autoregulation of cerebral blood flow Automatic alteration in diameter of cerebral blood vessels to maintain constant blood flow to brain Ensures a consistent CBF to provide the metabolic needs of brain tissue and maintain cerebral perfusion pressure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 10

11 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
This formula is clinically useful, although it does not consider the effects of cerebral vascular resistance. See example of CPP in Table 57-1. It is important to remember that CPP may not reflect perfusion pressure in all parts of the brain. Local areas of swelling and compression may limit regional perfusion pressure. For example, a patient with an acute stroke may require a higher blood pressure and increasing MAP and CPP to increase perfusion to the brain and prevent further tissue damage. Cerebral Blood Flow Cerebral perfusion pressure (CPP) Pressure needed to ensure blood flow to the brain CPP = MAP – ICP Normal is 60 to 100 mm Hg. <50 mm Hg is associated with ischemia and neuronal death. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 11

12 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
With low compliance, small changes in volume result in greater increases in pressure. Cerebral Blood Flow Pressure changes Compliance is the expandability of the brain. Compliance = Volume/Pressure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 12

13 Intracranial Volume Pressure Curve
The relationship of pressure to volume is depicted in the pressure-volume curve. The curve is affected by the brain’s compliance. Intracranial Volume Pressure Curve Fig Intracranial pressure-volume curve. (See text for descriptions of 1, 2, 3, and 4.) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 13

14 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Stage 4: 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 to occur, brainstem death is imminent. Cerebral Blood Flow Pressure-volume curve represented by stages Stage 1: high compliance Stage 2: compliance ↓, risk for ↑ ICP Stage 3: any small addition in volume causes a great ↑ in ICP, loss of autoregulation Stage 4: ICP rises to lethal levels Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 14

15 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
The partial pressure of carbon dioxide in arterial blood (PaCO2) is a potent vasoactive agent. Cerebral O2 tension < 50 mm Hg results in cerebrovascular dilation. This dilation decreases cerebral vascular resistance, increases CBF, and raises O2 tension. 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. Cerebral Blood Flow Factors affecting cerebral blood vessel tone CO2 O2 Hydrogen ion concentration Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 15

16 Mechanisms of Increased ICP
Elevated ICP is clinically significant because it diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis. Mechanisms of Increased ICP Causes Mass lesion Cerebral edema Head injury Brain inflammation Metabolic insult Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 16

17 Increased Intracranial Pressure
Cerebral insult may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, which promote the formation and spread of cerebral edema. This edema distorts brain tissue, further increasing the ICP, which leads to even more tissue hypoxia and acidosis. Increased Intracranial Pressure Fig Progression of increased intracranial pressure (ICP). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 17

18 Mechanisms of Increased ICP
Herniations force the cerebellum and brainstem downward through the foramen magnum. If compression of the brainstem is unrelieved, respiratory arrest will occur as the result of compression of the respiratory control center in the medulla. {See next slide for figure.} Mechanisms of Increased ICP Sustained increase in ICP results in brainstem compression and herniation of brain from one compartment to another. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 18

19 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Herniation A, Normal relationships of intracranial structures. B, Shift of intracranial structures. Fig Herniation. A, Normal relationship of intracranial structures. B, Shift of intracranial structures. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 19

20 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Cerebral Edema Increased accumulation of fluid in the extravascular spaces of brain tissue Three types of cerebral edema: Vasogenic Cytotoxic Interstitial More than one type may occur in the same patient. {See Table 57-2 for more information.} Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 20

21 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
This edema may produce a continuum of symptoms ranging from headache to disturbances in consciousness, including coma (profound state of unconsciousness) and focal neurologic deficits. It is important to recognize that although a headache may seem to be a benign symptom, in cases of cerebral edema, it can quickly progress to coma and death. Cerebral Edema Vasogenic cerebral edema Most common type Occurs mainly in white matter Associated with changes in the endothelial lining of cerebral capillaries Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 21

22 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Cytotoxic cerebral edema develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia, sodium depletion, and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. In this type of edema, the blood-brain barrier remains intact, with cerebral edema occurring as a result of a fluid and protein shift from the extracellular space directly into the cells, with subsequent swelling and loss of cellular function. Cerebral Edema Cytotoxic cerebral edema Results from local disruption of functional integrity of cell membranes Occurs mainly in gray matter Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 22

23 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Hydrocephalus is a buildup of fluid in the brain and is manifested by ventricular enlargement. It can be due to excess CSF production, obstruction of flow, or an inability to reabsorb the CSF. Hydrocephalus can be communicating or noncommunicating, and treatment typically consists of a ventriculostomy or a ventriculoperitoneal shunt. Cerebral Edema Interstitial cerebral edema Result of rupture of CSF brain barrier Usually a result of obstructive or uncontrolled hydrocephalus Can also be caused by enlargement of the extracellular space as a result of systemic water excess Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 23

24 Clinical Manifestations
Level of consciousness is the most sensitive and reliable indicator of the patient’s neurologic status. Changes in LOC are a result of impaired CBF, which deprives the cells of the cerebral cortex and the reticular activating system of oxygen. Manifestations such as Cushing’s triad may be present but often do not appear until ICP has been increased for some time or is suddenly markedly increased (e.g., head trauma). Compression of cranial nerve (CN) III, the oculomotor nerve, results in dilation of the pupil on the same side as or ipsilateral to the mass lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the eyelid. Clinical Manifestations Change in level of consciousness Change in vital signs Cushing’s triad Ocular signs Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 24

25 Clinical Manifestations
A decerebrate posture results from disruption of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly extended, adducted, and hyperpronated. Hyperextension of the legs with plantar flexion of the feet also occurs. Decorticate posture consists of internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts in the cerebral cortex. Extension of the legs may also be seen. {See next slide for figure.} Clinical Manifestations ↓ In motor function Decerebrate posturing (extensor) Indicates more serious damage Decorticate posturing (flexor) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 25

26 Decorticate and Decerebrate Posturing
A, Decorticate response. Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities. B, Decerebrate response. All four extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet. C, Decorticate response on right side of body and decerebrate response on left side of body. D, Opisthotonic posturing. Decorticate and Decerebrate Posturing Fig Decorticate and decerebrate posturing. A, Decorticate response. Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities. B, Decerebrate response. All four extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet. C, Decorticate response on right side of body and decerebrate response on left side of body. D, Opisthotonic posturing. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 26

27 Clinical Manifestations
Headache Often continuous and worse in the morning Vomiting Not preceded by nausea Projectile Straining, agitation, or movement may accentuate the pain. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 27

28 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Tentorial herniation (central herniation) occurs when a mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brainstem. Uncal herniation occurs with lateral and downward herniation. Cingulate herniation occurs with lateral displacement of brain tissue beneath the falx cerebri. Complications Two major complications of uncontrolled increased ICP Inadequate cerebral perfusion Cerebral herniation Tentorial herniation Uncal herniation Cingulate herniation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 28

29 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Computed tomography (CT) and magnetic resonance imaging (MRI) have revolutionized the diagnosis of increased ICP. These tests are used to differentiate the many conditions that can cause increased ICP and to evaluate therapeutic options. Diagnostic Studies Aimed at identifying underlying cause MRI CT Cerebral angiography EEG Brain tissue oxygenation measurement Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 29

30 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
In general, a lumbar puncture is not performed when increased ICP is suspected because of the possibility of cerebral herniation from the sudden release of pressure in the skull from the area above the lumbar puncture. Diagnostic Studies Aimed at identifying underlying cause (cont’d) ICP measurement Measurement via the LICOX catheter Transcranial Doppler studies Evoked potential studies PET Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 30

31 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Measurement of ICP ICP monitoring used to guide clinical care when at risk for increased ICP Those admitted with a Glasgow Coma Scale of 8 or less Those with abnormal CT scans or MRI Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 31

32 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Measurement of ICP The gold standard for ICP monitoring is the ventriculostomy. Catheter inserted into lateral ventricle Coupled with an external transducer {See next 4 slides for figures.} Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 32

33 Potential Placements of ICP Monitoring Devices
Coronal section of brain showing potential sites for placement of ICP monitoring devices. Potential Placements of ICP Monitoring Devices Fig Coronal section of brain showing potential sites for placement of ICP monitoring devices. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 33

34 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Intracranial pressure monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated, and plateau waves. At high ICP, the P2 peak is higher than the P1 peak, and the peaks become less distinct and plateau. ICP Monitoring Fig Intracranial pressure monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated, and plateau waves. At high ICP the P2 peak is higher than the P1 peak, and the peaks become less distinct and plateau. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 34

35 Ventriculostomy in Place
CSF can be drained via a ventriculostomy when ICP exceeds the upper pressure parameter set by the physician. Intermittent drainage involves opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30 to 120 seconds) until the pressure is below the upper pressure parameters. ICP, Intracranial pressure. Fig Ventriculostomy in place. CSF can be drained via a ventriculostomy when ICP exceeds the upper pressure parameter set by the physician. Intermittent drainage involves opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30 to 120 seconds) until the pressure is below the upper pressure parameters. ICP, Intracranial pressure. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 35

36 Leveling a Ventriculostomy
A, Leveling a ventriculostomy. B, CSF is drained into a drainage system. It is important to make sure that the transducer of the ventriculostomy is level to the foramen of Monro (interventricular foramen) and that the ventriculostomy system is at the ideal height. A reference point for this foramen is the tragus of the ear. When the patient is repositioned, the system needs to be re-zeroed. Fig A, Leveling a ventriculostomy. B, CSF is drained into a drainage system. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 36

37 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Measurement of ICP Fiberoptic catheter Sensor transducer located within the catheter tip Subarachnoid bolt or screw Allows for CSF drainage Ideal for patients with mild or moderate head injury {See next 4 slides for figures.} Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 37

38 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Prophylactic systemic antibiotics may be administered to reduce the incidence of infection. Factors that contribute to the development of infection include ICP monitoring longer than 5 days, use of a ventriculostomy, the presence of a CSF leak, and concurrent systemic infection. Measurement of ICP Infection is always a serious consideration with ICP monitoring. ICP should be measured as mean pressure at the end of expiration. Waveform should be recorded. Shaped similar to arterial pressure trace Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 38

39 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Measurement of ICP Inaccurate readings can be caused by CSF leaks Obstruction in catheter Differences in height of bolt/transducer Kinks in tubing Incorrect height of drainage system relative to patient’s reference point Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 39

40 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
The physician typically will order a specific level to initiate drainage (e.g., if ICP > 15 mm Hg), as well as the frequency of drainage (intermittent or continuously). Two options for CSF drainage are available (intermittent or continuous). Measurement of ICP With catheter, it is possible to control ICP by removing CSF. Careful monitoring of the volume of CSF drained is essential. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 40

41 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Normal range of PbtO2 is 20 to 40 mm Hg. A lower than normal PbtO2 level is indicative of ischemia. Another advantage of the LICOX is the ability to measure brain temperature. A cooler brain temperature (36°C) has been shown to produce better outcomes. The jugular venous bulb catheter is placed in the internal jugular vein and is positioned so that the catheter tip is located in the jugular bulb; placement is verified by an x-ray. This catheter provides a measurement of jugular venous oxygen saturation (SjvO2) that indicates total venous brain tissue extraction of oxygen, which is a measure of cerebral oxygen supply and demand. The normal SjvO2 range is 55% to 75%. Measurement of ICP LICOX brain tissue oxygenation catheter Provides continuous monitoring of pressure of oxygen in brain tissue Jugular venous bulb catheter Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 41

42 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
LICOX catheter The LICOX brain tissue oxygen system involves a catheter inserted through an intracranial bolt (A). The system measures oxygen in the brain (Pbt02), brain tissue temperature, and intracranial pressure (ICP) (B). Fig The LICOX brain tissue oxygen system involves a catheter inserted through an intracranial bolt (A). The system measures oxygen in the brain (PbtO2), brain tissue temperature, and intracranial pressure (ICP) (B). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 42

43 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Collaborative Care Adequate oxygenation PaO2 maintenance at 100 mm Hg or greater ABG analysis guides the oxygen therapy. May require mechanical ventilator Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 43

44 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Collaborative Care Drug therapy Mannitol (Osmitrol) Hypertonic saline Corticosteroids Barbiturates Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 44

45 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Collaborative Care Nutritional therapy Patient is in hypermetabolic and hypercatabolic state. ↑ Need for glucose Keep patient normovolemic. IV 0.9% NaCl Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 45

46 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Nursing assessment Subjective data from patient or family members Glasgow Coma Scale Neurologic assessment Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 46

47 Pupillary Check for Size and Response
Fig Pupillary check for size and response. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 47

48 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Motor strength and response Vital signs BP Pulse Respiratory rate Temperature Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 48

49 Abnormal Respiratory Patterns of Coma
Fig Common abnormal respiratory patterns associated with coma. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 49

50 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Nursing diagnoses Risk for ineffective cerebral tissue perfusion Decreased intracranial adaptive capacity Risk for disuse syndrome Altered family process Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 50

51 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Planning Overall goals Maintain a patent airway ICP within normal limits Normal fluid and electrolyte balance No complications secondary to immobility and decreased LOC Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 51

52 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Nursing implementation Respiratory function Fluid and electrolyte balance Monitoring of intracranial pressure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 52

53 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Management Nursing implementation Body position maintained in head-up position Protection from injury Psychologic considerations Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 53

54 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Audience Response Question Intracranial pressure monitoring is instituted for a patient with a head injury. The patient’s arterial blood pressure is 92/50 mm Hg, and intracranial pressure is 18 mm Hg. Using these values to calculate the patient’s cerebral perfusion pressure (CPP), the nurse determines that: 1. The CPP is adequate for normal cerebral blood flow. 2. To prevent cerebral hypoxemia, the patient’s blood pressure should be increased. 3. The CPP is so low that ischemia and neuronal death are imminent. 4. Lowering the patient’s blood pressure will reduce the intracranial pressure, increasing cerebral blood flow. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 54

55 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Audience Response Question A patient with increased intracranial pressure is placed in a lateral position with the head of the bed elevated 30 degrees. The nurse evaluates the need for lowering the head of the bed when the patient experiences: 1. Ptosis of the eyelid. 2. Unexpected vomiting. 3. A decrease in motor functions. 4. Decreasing level of consciousness. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 55

56 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study 56 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

57 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study A son brings his 68-year-old father to ED with confusion, lethargy, and headache. The son is concerned that the father may be developing dementia. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 57

58 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study He was in a car accident 2 days ago where he hit his head on the windshield. He refused care. He says he “felt just fine.” Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 58

59 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study His vital signs are BP 144/54 Heart rate 76 Respiratory rate 12 Temperature 98.9 CT indicates a subacute subdural hematoma. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 59

60 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Discussion Questions What can you tell the son about the difference between his father’s current condition and dementia? What information can you give the son about the treatment his father will undergo? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 60

61 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Discussion Questions What is the primary nursing management for the father? 3. Monitoring neurologic status and any behavioral manifestations. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 61


Download ppt "Focus on Intracranial Pressure"

Similar presentations


Ads by Google