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Intracranial Pressure Monitoring and Assessing Intracranial Compliance in Brain Injury
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Neurotrauma
lntracranial Pressure Monitoring and Assessing lntracranial Compliance in Brain Injury Karen March, MN, RN, CNRN, CCRN
The goal of care following a traumatic brain injmy is to prevent secondary injury by maintaining adequate perfusion. Inadequate cerebral perfusion resulting in cerebral ischemia may be caused by a reduction in perfusion pressure (increased intracranial pressure or decreased blood pressure), an increase in vascular resistance ( vasospasm), or decrease in oxygen or glucose supply (hypoxia or hypoglycemia). Intracranial pressure (ICP) monitoring is a tool used to assess the balance of the components of the cranial contents, blood, brain, and cerebrospinal fluid (CSF).
Principles of nntracranial Dynamics Compliance The skull is a rigid container that holds the intracranial contents at a relative fixed volume; the brain comprises 80%, blood 10%, and CSF 10% of the intracranial contents. According to the Monroe-Kellie doctrine, as one of the intracranial contents increases there is
From the Harborview Medical Center; and Department of Biobehavioral Nursing, School of Nursing, University of Washington, Seattle, Washington
a reciprocal decrease in the other contents so that pressure remains constant and within normal levels, which is an ICP of less than 20 mm Hg (Fig. 1). If the increase in volume exceeds the adaptive capacity, pressure increasesn Another term for the adaptive capacity of the contents is compliance. Compliance can be measured using the pressure-volume index (PVI). 3 When compliance is exhausted, ICP will increase (volumepressure relationship). The magnitude of the response to an increase in volume, the volume-pressure response (VPR) is a reflection of the brain elastance (Table 1). 22
Cerebral Blood Flow and Cerebral Blood Volume Compliance and elastance can be assessed using the CSF system; however, the CSF system cannot assess the role of cerebral blood flow (CBF) and cerebral blood volume in intracranial pressure. CBF is a function of the influx (systemic arterial pressure) and efflux pressure (venous pressure), vascular radius (vessel diameter), and blood viscosity. Normal CBF within the brain (average between gray and white matter) is 50 mL per 100 g brain tissue. 20
CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 /Number 4 /December 2000
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50
Compliance Blood
~ Brain
40
El
Ci J:
Mass (edema, hematoma)
E
30
sa. !::2
El
CSF
20 10 2
0
3
4
5
6
7
Volume (ml) Figure 1
Volume pressure relation and compliance. ICP
Cerebral blood volume (CBV) is a function of vascular capacitance (vessel diameter). A constant CBF is maintained through autoregulation when mean systemic arterial blood pressure (MSABP) is 60 to 160 mm Hg. As MSABP falls, vessels dilate, thus increasing CBV; as MSABP increases, vessels constrict, thus decreasing CBV. This mechanism is known as myogenic or adrenergic autoregu-
lation.
=
intracranial pressure; CSF
=
cerebrospinal fluid.
There are two other mechanisms that affect cerebrovascular resistance (vessel diameter), flow-metabolism coupling and metabolic autoregulation. Flow coupling is the matching of CBF to tissue demand. Metabolic autoregulation is the response of the cerebrovasculature to changes in hydrogen ion content (pH) (Table 2). If these mechanisms are impaired, cerebrovasodilitation and vascular congestion may result, leading to increased CBV and increased ICP. 3· 10· 25
ICP Monitoring Pressure Volume Index (PVI)
Volume Pressure Index (VPI) VPI
=
~p ~v
Rise in ICP produced by injecting 1 ml of fluid in 1 s Normal = 1-2 mm Hg/ml After surgery for head trauma = 3-4 mm Hg/ml Mass lesion = 1020 mm Hg/ml ICP = intracranial pressure
PVI
I Final ICP og Initial ICP Volume of saline injected or withdrawn that produces a 10fold increase in ICP Normal volume = 25 ml =
Since the works of Guillaume and Janny in 1951 and Lundberg in 1960 first described the use of intraventricular cerebral spinal fluid pressure monitoring, ICP monitoring has become commonplace. No longer is the intraventricular catheter the only method for monitoring ICP. 8• 21 Devices used include subarachnoid screws, epidural and subdural catheters, and intraparenchymal catheters that use strain gauge transducers and fiberoptic technology. 18 Some devices do more than monitor pressure; they monitor temperature and tissue Po 2 as well as allow for sampling of tissue substrates. Controversy exists about which technique provides the more accurate and safe method
INTRACRANIAL PRESSURE MONITORING AND ASSESSING INTRACRANIAL COMPLIANCE
Vasoconstriction Myogenic or adrenergic Flow coupling Metabolic
t BP 1 metabolic
demand (i.e., coma, sedation, hypothermia) Alkalosis-hypocapnia, hyperoxygenation
431
Vasodiiatation
I BP I metabolic
demand (i.e., seizures, agitation, fever) Acidosis-hypercapnia, hypoxia
BP = blood pressure
of monitoring. Each system has advantages and disadvantages to its use (Table 3). When choosing a system, several questions should be asked. Why is ICP being monitored? What compartment is involved (e.g., basilar system, posterior fossa, CSF, cerebral hemispheres)? Can CSF be drained or does that matter? How easy and safe is it to insert? What is the incidence of complications with insertion of the device and why do they occur? What is the
ease of setting up the system once it has been inserted? What is the accuracy of the device (drift) and can it be rezeroed? What is the infection rate (colonization of bacteria) and what are the contributing factors to infections? What is the breakage or pull-out rate of the device requiring replacement? Will the system provide a waveform? 2· 5· 18· 22 • 30 To minimize the complications from ICP, a trained, experienced physician should per-
Monitoring Device
Transducer Type
Ventriculostomy
External strain gauge (ESG) Internal strain gauge (ISG) Fiberoptic ( F)
Gold standard Allows CSF drainage 1%-10% colonization 1. 1% hematomas Good waveform
Parenchymal
Internal strain gauge Fiberoptic
Quick insertion 2.8%-5.1 % hematomas Good waveform
Subarachnoid screw
External strain gauge Fiberoptic
Quick insertion 1%-10% colonization 0% hematomas
Epidural
External strain gauge Fiberoptic
Subdural
External strain gauge Internal strain gauge Fiberoptic
Extradural Easy insertion Low colonization 0% hematomas 1%-10% colonization 0% hematomas
CSF
= cerebrospinal fluid
Advantages
Disadvantages Most difficult to insertsmall ventricle or ventricle shift May occlude (6 3%) F-may malfunction F-catheter breakage Needs close monitoring of CSF drainage-may overdrain ISG and F-unable to rezero to correct drift F-catheter breakage ISG-catheter displacement 0.7%-16.7% colonization ISG and F-unable to rezero to correct drift Fair waveform 16% occlusion rate-debris in device (e.g., brain, dura, clot) CSF leak Indirect measure Poor waveform Poor accuracy Poor waveform Poor accuracy May be compressed as brain swells (10.5%)
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form monitoring insertion using sterile technique. Maintenance involves minimal manipulation, maintenance of a closed system, and use of an occlusive dressing. Frequently opening the system to rezero, sampling CSF, and flushing the system increases the risk of infection. Bacterial colonization of monitoring devices increases when the device is left in for more than 5 days. Care must be taken when moving the patient to avoid breaking fiberoptic catheters or dislodging the catheter. 2, 4
ICP Waveforms Trends Lundberg in 1960 described three basic waveform trends: A, B, and C waves. 8 • 21 C waves are reflections of arterial pulsation and are not pathologic. B waves are fluctuations in ICP to 20 mm Hg or higher of short duration (0.52 waves/min). A waves or plateau waves are fluctuations in ICP that may exceed 50 to 80 mm Hg and last for 15 minutes or more. These latter waves result in secondary injury. s, 22, 32
Pulse Wave-P1, P2 Bering first described CSF pulsation in 1955, but the implications of these pulsations gained interest in the 1980s and 1990s. 1 Hamer et al 21 in 1977 described the influence of systemic and cerebral vascular factors on the CSF pulsation. Hamer recognized that as cerebrovascular resistance decreased, as with vasodilatation during hypoxia and hypercapnia, the CSF pulse waveform became more evident. 21 The ICP waveform is composed of several components, the most significant being Pl,
Figure 2
P2, and P3. Pl represents the transmission of the blood being ejected from the heart and is transmitted through the choroid plexus and other intracranial conductive vessels. Pl is known as the percussion wave. P2, known as the tidal wave, represents the intracranial brain bulk. Intracranial compliance, microcirculatory vasomotor paralysis, cerebral swelling, and edema influence P2. P3 is called the dicrotic wave. The dicrotic wave follows the dicrotic notch, which represents the closures of the aortic valve (Fig. 2). The most significant of the waves are Pl and P2. A patient with ICP and good compliance will have a waveform demonstrating that Pl is greater than P2 with a ratio of less than or equal to 0.8. 33 As ICP increases, P2 may become equal to or greater than Pl, which may represent decreased compliance (Fig. 3). An increase in the pulse amplitude is thought to indicate cerebral vasodilatation (Fig. 4). A loss of autoregulation results in an ICP waveform that looks like the arterial waveform (Fig. 5). 6• 8• 13 · 17 A dampened waveform (Fig. 6) requires an evaluation of the system and questions the reliability of the data. If the device is occluded or improperly placed, an inadequate waveform will be seen. Air in the cranium or the transducer will dampen the waveform. The patient who has undergone a craniectomy will also exhibit a dampened wavefonn. 2
Using ICP Waveform to Predict Disproportionate Increases
in ICP In a study by Mitchell et al2 9 looking at the reliability of using the ICP waveform to predict which patients will have disproportionate increases in ICP in response to nursing care
Normal waveform with components P1, P2, and P3.
INTRACRANl,ll.L PRESSURE IV!ONITORING AND ASSESSING INTRACRANIAL COIV!PUfa,NCE
Figure 3
Figure 4
Poor compliance.
Increased pulse amplitude.
A
B Figure 5
Autoregulation. A, Arterial line; B, ICP.
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Figure 6
Dampened waveform.
actlv1tles, the authors found that abnormal waveforms were predictive. 29 This study monitored 37 neurologic and neurosurgical critical care patients using ICP, arterial blood pressure, cerebral perfusion pressure, and transcranial doppler ultrasonography simultaneously for 1 hour. Cerebral autoregulation was calculated at that time using the dynamic method. An abnormally low autoregulation index was defined as 0 to 3. Disproportionate increases in ICP were defined as ICP increases of greater than 10 mm Hg above baseline for greater than 5 minutes, or ICP increases sufficient to trigger ventriculostomy drainage from the 24-hour trend recordings. Contingency tables were used to evaluate the predictive value of the presence of abnormal ICP waveforms and of low autoregulation value for greater than five or greater than 15 episodes of disproportionate increases in ICP in the subsequent 24 hours. Spectral analysis using Fast Fourier Transform and KarhunenLoeve expansion: joint spectral properties of ICP and arterial blood pressure were described by the cohesion function. Outcome at discharge was categorized using the Glasgow Outcome Scale. Thirty-seven patients ranging in age from 22 to 92 years were monitored. Incidence of disproportionate increases in ICP, abnormally low autoregulation value, or elevated P2 ICP waveform did not differ significantly by diagnostic category. P2 elevation was predictive of increased frequency of disproportionate increases in ICP with an odds ration of 7.2 for greater than five episodes in 24 hours, 11 for greater than 15 episodes, with a sensitivity of 99% for both, and a predictive value of a positive test of 88% and 75%, respectively, and an overall accuracy of 86% for episodes greater than fn1 e episodes, 76% for greater than 15 episodes. Specificity, however, was only 17% and 10%, respectively. Elevated P2 had low specificity in distinguishing patients with fewer episodes of disproportionate in-
creased ICP; however, several spectral indices were significantly different between those with more and less disproportionate increases in ICP Clower mean ICP, higher low frequency spectral mean, larger high frequency centroid, and greater coherence between arterial blood pressure and ICP spectra). Those with the poorest outcome at discharge had greater than 15 episodes of disproportionate increases in ICP. The authors concluded that an elevated P2 ICP waveform, which can be easily determined visually, was a rough estimate of patients at risk for elevations in ICP during care-related activities. Increases in episodes of disproportionate increases in ICP in combination with spectral indices of poor autoregulation were related to poor outcomes. There were normal ICP values in over 40% of patients who had abnormal waveforms and increased frequency of disproportionate increases in ICP. 29
Implication for Practice This study tells practitioners that by monitoring the ICP pulse wave, they can anticipate when patients are developing decreased compliance and therefore will develop increased ICP. 6· 13• 28 Nurses can alter their care activities to improve the patient's adaptive capacity. Adjusting the elevation of the head of the bed can improve CSF and venous outflow while closely monitoring cerebral perfusion. 14• 15 • 23 • 27 · 31 If the patient has impaired autoregulation, is dehydrated, or hypotensive, lying flat may be the better position to promote cerebral perfusion.11i, 16 · 27 Ensuring that the neck is not flexed, extended, or rotated will facilitate venous outflow. 26 When positioning the patient ia the bed, be sure that flexion occurs at the hips, not in the abdomen, to decrease intraabdominal pressure. Monitor the patient's bowel routine and avoid constipation, which may increase intra-
INTRACRANIAL PRESSURE MONITORING AND ASSESSING INTRACRANIAL COMPLIANCE
abdominal pressure. 28 Positive end expiratory pressure can increase ICP by impeding venous outflow. 12 • 16 Maintain normothermia. Fever and agitation increase metabolic demand and will increase CBF in patients with intact autoregulation. 7· 9· 16 Suctioning is also an excitatory stimulus that increases CBF and therefore ICP. Sedation before suctioning may decrease the effect. 16• 19•24 It is important to monitor and minimize noxious environmental stimuli. Nurses can monitor and positively influence the external influences on ICP dynamics. 26
Future Direction Monitoring ICP gives practitioners only partial insight into the dynamics of the intracranial contents and does not provide the details of the status of CBF, cerebral blood volume, autoregulation, cerebral metabolism, tissue oxygenation, and other factors. Multimodality monitoring will help to put the picture together. Current research is focused on tissue
435
oxygenation, tissue substrates such as excitatory amino acids, and temperature.11 Methods of testing cerebral autoregulation using the transcranial doppler exist but currently are cumbersome and require constant attention. Little is known about how long impaired autoregulation lasts, whether it is a static or a dynamic process, and whether practitioners can facilitate its recovery. Intermittent or continual monitoring of autoregulation may aid in the management of the cerebrovascular factors, which influence ICP and perfusion. Currently, monitoring ICP is an invasive procedure. In the future, noninvasive forms of monitoring will exist. Transcranial doppler ultrasound can currently be used as an indirect measure of the effects of ICP on perfusion. Near infrared spectroscopy allows for noninvasive measurement of tissue oxygenation, hemoglobin content, and measures of mitochondrial function. In the future, similar technologies may allow for noninvasive measurement of ICP.
SUMMARY Caring for the patient with a brain injury is a dynamic process with the goal of providing therapy to prevent secondary injury. Until practitioners have a better understanding of the pathophysiology of ischemia and the response of therapies for treating increased ICP, they must use the tools that exist. ICP monitoring gives a rough index of the relationships and the response of the intracranial contents to changes in volume that may produce increases in pressure and further damage. Understanding the information supplied by ICP monitoring is imperative to successful management of increased ICP.
REFERENCES 1. Adolph R, Fukusumi H, Fowler N: Origin of cerebrospinal fluid pulsation. Am ] Physiol 212:840-846, 1967 2. American Association of Neuroscience Nurses: Intracranial Pressure Monitoring: Clinical Guideline Series. Chicago, IL, American Association of Neuroscience Nurses, 1997 3. Avellino A, Lam A, Winn R: Management of acute head injury. In Ablin M Ced): Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. New York, McGraw-Hill, 1996 4. Bader MK, Littlejohns L, Palmer S: Ventriculostomy and intracranial pressure monitoring M: In search of a 0% infection rate. Heart Lung 24:166-172, 1995 5. Brain Trauma Foundation and the Joint Section on Neurotrauma and Critical Care of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons: Guidelines for the Man-
6. 7. 8.
9.
10.
11.
agement of Severe Head Injury. Park Ridge, IL, The Brain Trauma Foundation, 1995 Cardoso E, Rowan ], Galbraith S: Analysis of the cerebrospinal fluid pulse wave in intracranial pressure.] Neurosurg 59:817-821, 1983 Chestnut R: Secondary brain insults after head injury: Clinical perspectives. New Horizons 3:366-375, 1995 Chestnut R, Marshall L: Treatment of abnormal intracranial pressure. Neurosurg Clin N Am 2:267-284, 1991 Clifton G, Allen S, Barrodale P: A phase II study of moderate hypothermia in severe brain injury. ] Neurotrauma 10:263-271, 1993 DeWitt D,Jenkins L, Prough D: Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury. New Horizons 3:376-383, 1995 Doberstein C, Hovda D, Becker D: Clinical considerations in the reduction of secondary brain injury. Ann Emerg Med 22:993-997, 1993
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12. Domino K: Pathophysiology of head inju1y: Secondary systemic effects. In Lam A ( ed): Anesthetic Management of Acute Head lnjmy. New York, McGrawHill, 1995 13. Doyle DJ, Mark PW: Analysis of intracranial pressure. J Clin Monit 8:81-90, 1992 14. Durward Q, Amacher A, DelMaestro R, et al: Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension. J Neurosurg 59:938-944, 1983 15. Feldman Z, Kanter M, Robertson C: Effect of head elevation on intracranial pressure, cerebral perfusion pressure and cerebral blood flow in head injury patients.] Neurosurg 76:207-211, 1992 16. Frank J: Management of intracranial hypertension. Med Clin N Am 77:61-76, 1993 17. Germon K: Interpretation of pulse waves to determine intracerebral compliance. ] Neurosci Nurs 20:344-349, 1988 18. Ghajar J: Intracranial pressure monitoring techniques. New Horizons 3:395-399, 1995 19. Grady M, Lam A: Management of acute head injury: Initial resuscitation. In Lam A (ed): Anesthetic Management of Acute Head Injury. New York, McGrawHill, 1995 20. Grady M, Shapira Y: Pathophysiology of head inju1y: Central nervous system effects. In Lam A Ced): Anesthetic Management of Acute Head Injury. New York, McGraw-Hill, 1995 21. Hamer], Alberti E, Hoyer S, et al: Influences of systemic and cerebral vascular factors on the cerebrospinal fluid pulse waves.] Neurosurg 46:36-45, 1977 22. Kanter M, Narayan R: Intracranial pressure monitoring. Neurosurg Clin N Am 2:257-265, 1991 23. Kenning], Toutant S, Sunders R: Upright patient positioning in the management of intracranial hypenension. Surg Neurol 15:148-152, 1981
24. Kerr M, Rudy E, Bmcia J, et al: Head injured adults: Recommendations for endotracheal suctioning. ] Neurosci Nurs 25:86-91, 1993 25. Lang EW, Chestnut RM: Intracranial pressure and cerebral perfusion pressure in severe head injury. New Horizons 3:400-409, 1995 26. Lipe H, Mitchell P: Positioning the patient with intracranial hypertension: How turning and head rotation affect the internal jugular vein. Heart Lung 9: 10311037, 1980 27. March K, Mitchell P, Grady M, et al: Effect of backrest position on intracranial and cerebral perfusion pressures.] Neurosci Nurs 22:375-381, 1990 28. Mitchell P: lntracranial hypertension: Influence of nursing care activities. Nurs Clin N Am 21:563576, 1986 29. Mitchell P, Kirkness C, Burr R, et al: Intracranial pressure and transcranial doppler waveform analysis. Jn Marmarou A, Bullock R, Avezaat C, et al (eds): Intracranial Pressure and Neuromonitoring in Brain Injrny. New York, Springer Wien, 1997, p 420 30. Munch E, Weigel R, Schmiedek P, et al: The Camino intracranial pressure device in clinical practice: Reliability, handling characteristics and con1.pl_ications. Acta Neurochir (Wien) 140:1113-1120, 1998 31. Simmons BJ: Management of intracranial hemodynamics in the adult: A research analysis of head positioning and recommendations for clinical practice and future research.] Neurosci Nurs 28:44-49, 1997 32. VanTanenhove J: Neurodiagnostic tests and procedures. Jn Melander S, Bucher L (eds): Critical Care Nursing. Philadelphia, WB Saunders, 1999, pp 824-842 33. Willis M: Interpretation of intracranial pressure waveforms: The predictive value of P2 elevation in the diagnosis of decreased adaptive intracranial capacity [master's thesis]. Seattle, University of Washington (unpublished), 1991
Address reprint requests to Karen March, MN, RN, CNRN, CCRN 8545 166th Avenue NE, E107 Redmond, WA 98052
+ 00
Neurotrauma
lntracranial Pressure Monitoring and Assessing lntracranial Compliance in Brain Injury Karen March, MN, RN, CNRN, CCRN
The goal of care following a traumatic brain injmy is to prevent secondary injury by maintaining adequate perfusion. Inadequate cerebral perfusion resulting in cerebral ischemia may be caused by a reduction in perfusion pressure (increased intracranial pressure or decreased blood pressure), an increase in vascular resistance ( vasospasm), or decrease in oxygen or glucose supply (hypoxia or hypoglycemia). Intracranial pressure (ICP) monitoring is a tool used to assess the balance of the components of the cranial contents, blood, brain, and cerebrospinal fluid (CSF).
Principles of nntracranial Dynamics Compliance The skull is a rigid container that holds the intracranial contents at a relative fixed volume; the brain comprises 80%, blood 10%, and CSF 10% of the intracranial contents. According to the Monroe-Kellie doctrine, as one of the intracranial contents increases there is
From the Harborview Medical Center; and Department of Biobehavioral Nursing, School of Nursing, University of Washington, Seattle, Washington
a reciprocal decrease in the other contents so that pressure remains constant and within normal levels, which is an ICP of less than 20 mm Hg (Fig. 1). If the increase in volume exceeds the adaptive capacity, pressure increasesn Another term for the adaptive capacity of the contents is compliance. Compliance can be measured using the pressure-volume index (PVI). 3 When compliance is exhausted, ICP will increase (volumepressure relationship). The magnitude of the response to an increase in volume, the volume-pressure response (VPR) is a reflection of the brain elastance (Table 1). 22
Cerebral Blood Flow and Cerebral Blood Volume Compliance and elastance can be assessed using the CSF system; however, the CSF system cannot assess the role of cerebral blood flow (CBF) and cerebral blood volume in intracranial pressure. CBF is a function of the influx (systemic arterial pressure) and efflux pressure (venous pressure), vascular radius (vessel diameter), and blood viscosity. Normal CBF within the brain (average between gray and white matter) is 50 mL per 100 g brain tissue. 20
CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 /Number 4 /December 2000
429
430
MARCH
• •
50
Compliance Blood
~ Brain
40
El
Ci J:
Mass (edema, hematoma)
E
30
sa. !::2
El
CSF
20 10 2
0
3
4
5
6
7
Volume (ml) Figure 1
Volume pressure relation and compliance. ICP
Cerebral blood volume (CBV) is a function of vascular capacitance (vessel diameter). A constant CBF is maintained through autoregulation when mean systemic arterial blood pressure (MSABP) is 60 to 160 mm Hg. As MSABP falls, vessels dilate, thus increasing CBV; as MSABP increases, vessels constrict, thus decreasing CBV. This mechanism is known as myogenic or adrenergic autoregu-
lation.
=
intracranial pressure; CSF
=
cerebrospinal fluid.
There are two other mechanisms that affect cerebrovascular resistance (vessel diameter), flow-metabolism coupling and metabolic autoregulation. Flow coupling is the matching of CBF to tissue demand. Metabolic autoregulation is the response of the cerebrovasculature to changes in hydrogen ion content (pH) (Table 2). If these mechanisms are impaired, cerebrovasodilitation and vascular congestion may result, leading to increased CBV and increased ICP. 3· 10· 25
ICP Monitoring Pressure Volume Index (PVI)
Volume Pressure Index (VPI) VPI
=
~p ~v
Rise in ICP produced by injecting 1 ml of fluid in 1 s Normal = 1-2 mm Hg/ml After surgery for head trauma = 3-4 mm Hg/ml Mass lesion = 1020 mm Hg/ml ICP = intracranial pressure
PVI
I Final ICP og Initial ICP Volume of saline injected or withdrawn that produces a 10fold increase in ICP Normal volume = 25 ml =
Since the works of Guillaume and Janny in 1951 and Lundberg in 1960 first described the use of intraventricular cerebral spinal fluid pressure monitoring, ICP monitoring has become commonplace. No longer is the intraventricular catheter the only method for monitoring ICP. 8• 21 Devices used include subarachnoid screws, epidural and subdural catheters, and intraparenchymal catheters that use strain gauge transducers and fiberoptic technology. 18 Some devices do more than monitor pressure; they monitor temperature and tissue Po 2 as well as allow for sampling of tissue substrates. Controversy exists about which technique provides the more accurate and safe method
INTRACRANIAL PRESSURE MONITORING AND ASSESSING INTRACRANIAL COMPLIANCE
Vasoconstriction Myogenic or adrenergic Flow coupling Metabolic
t BP 1 metabolic
demand (i.e., coma, sedation, hypothermia) Alkalosis-hypocapnia, hyperoxygenation
431
Vasodiiatation
I BP I metabolic
demand (i.e., seizures, agitation, fever) Acidosis-hypercapnia, hypoxia
BP = blood pressure
of monitoring. Each system has advantages and disadvantages to its use (Table 3). When choosing a system, several questions should be asked. Why is ICP being monitored? What compartment is involved (e.g., basilar system, posterior fossa, CSF, cerebral hemispheres)? Can CSF be drained or does that matter? How easy and safe is it to insert? What is the incidence of complications with insertion of the device and why do they occur? What is the
ease of setting up the system once it has been inserted? What is the accuracy of the device (drift) and can it be rezeroed? What is the infection rate (colonization of bacteria) and what are the contributing factors to infections? What is the breakage or pull-out rate of the device requiring replacement? Will the system provide a waveform? 2· 5· 18· 22 • 30 To minimize the complications from ICP, a trained, experienced physician should per-
Monitoring Device
Transducer Type
Ventriculostomy
External strain gauge (ESG) Internal strain gauge (ISG) Fiberoptic ( F)
Gold standard Allows CSF drainage 1%-10% colonization 1. 1% hematomas Good waveform
Parenchymal
Internal strain gauge Fiberoptic
Quick insertion 2.8%-5.1 % hematomas Good waveform
Subarachnoid screw
External strain gauge Fiberoptic
Quick insertion 1%-10% colonization 0% hematomas
Epidural
External strain gauge Fiberoptic
Subdural
External strain gauge Internal strain gauge Fiberoptic
Extradural Easy insertion Low colonization 0% hematomas 1%-10% colonization 0% hematomas
CSF
= cerebrospinal fluid
Advantages
Disadvantages Most difficult to insertsmall ventricle or ventricle shift May occlude (6 3%) F-may malfunction F-catheter breakage Needs close monitoring of CSF drainage-may overdrain ISG and F-unable to rezero to correct drift F-catheter breakage ISG-catheter displacement 0.7%-16.7% colonization ISG and F-unable to rezero to correct drift Fair waveform 16% occlusion rate-debris in device (e.g., brain, dura, clot) CSF leak Indirect measure Poor waveform Poor accuracy Poor waveform Poor accuracy May be compressed as brain swells (10.5%)
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form monitoring insertion using sterile technique. Maintenance involves minimal manipulation, maintenance of a closed system, and use of an occlusive dressing. Frequently opening the system to rezero, sampling CSF, and flushing the system increases the risk of infection. Bacterial colonization of monitoring devices increases when the device is left in for more than 5 days. Care must be taken when moving the patient to avoid breaking fiberoptic catheters or dislodging the catheter. 2, 4
ICP Waveforms Trends Lundberg in 1960 described three basic waveform trends: A, B, and C waves. 8 • 21 C waves are reflections of arterial pulsation and are not pathologic. B waves are fluctuations in ICP to 20 mm Hg or higher of short duration (0.52 waves/min). A waves or plateau waves are fluctuations in ICP that may exceed 50 to 80 mm Hg and last for 15 minutes or more. These latter waves result in secondary injury. s, 22, 32
Pulse Wave-P1, P2 Bering first described CSF pulsation in 1955, but the implications of these pulsations gained interest in the 1980s and 1990s. 1 Hamer et al 21 in 1977 described the influence of systemic and cerebral vascular factors on the CSF pulsation. Hamer recognized that as cerebrovascular resistance decreased, as with vasodilatation during hypoxia and hypercapnia, the CSF pulse waveform became more evident. 21 The ICP waveform is composed of several components, the most significant being Pl,
Figure 2
P2, and P3. Pl represents the transmission of the blood being ejected from the heart and is transmitted through the choroid plexus and other intracranial conductive vessels. Pl is known as the percussion wave. P2, known as the tidal wave, represents the intracranial brain bulk. Intracranial compliance, microcirculatory vasomotor paralysis, cerebral swelling, and edema influence P2. P3 is called the dicrotic wave. The dicrotic wave follows the dicrotic notch, which represents the closures of the aortic valve (Fig. 2). The most significant of the waves are Pl and P2. A patient with ICP and good compliance will have a waveform demonstrating that Pl is greater than P2 with a ratio of less than or equal to 0.8. 33 As ICP increases, P2 may become equal to or greater than Pl, which may represent decreased compliance (Fig. 3). An increase in the pulse amplitude is thought to indicate cerebral vasodilatation (Fig. 4). A loss of autoregulation results in an ICP waveform that looks like the arterial waveform (Fig. 5). 6• 8• 13 · 17 A dampened waveform (Fig. 6) requires an evaluation of the system and questions the reliability of the data. If the device is occluded or improperly placed, an inadequate waveform will be seen. Air in the cranium or the transducer will dampen the waveform. The patient who has undergone a craniectomy will also exhibit a dampened wavefonn. 2
Using ICP Waveform to Predict Disproportionate Increases
in ICP In a study by Mitchell et al2 9 looking at the reliability of using the ICP waveform to predict which patients will have disproportionate increases in ICP in response to nursing care
Normal waveform with components P1, P2, and P3.
INTRACRANl,ll.L PRESSURE IV!ONITORING AND ASSESSING INTRACRANIAL COIV!PUfa,NCE
Figure 3
Figure 4
Poor compliance.
Increased pulse amplitude.
A
B Figure 5
Autoregulation. A, Arterial line; B, ICP.
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MARCH
Figure 6
Dampened waveform.
actlv1tles, the authors found that abnormal waveforms were predictive. 29 This study monitored 37 neurologic and neurosurgical critical care patients using ICP, arterial blood pressure, cerebral perfusion pressure, and transcranial doppler ultrasonography simultaneously for 1 hour. Cerebral autoregulation was calculated at that time using the dynamic method. An abnormally low autoregulation index was defined as 0 to 3. Disproportionate increases in ICP were defined as ICP increases of greater than 10 mm Hg above baseline for greater than 5 minutes, or ICP increases sufficient to trigger ventriculostomy drainage from the 24-hour trend recordings. Contingency tables were used to evaluate the predictive value of the presence of abnormal ICP waveforms and of low autoregulation value for greater than five or greater than 15 episodes of disproportionate increases in ICP in the subsequent 24 hours. Spectral analysis using Fast Fourier Transform and KarhunenLoeve expansion: joint spectral properties of ICP and arterial blood pressure were described by the cohesion function. Outcome at discharge was categorized using the Glasgow Outcome Scale. Thirty-seven patients ranging in age from 22 to 92 years were monitored. Incidence of disproportionate increases in ICP, abnormally low autoregulation value, or elevated P2 ICP waveform did not differ significantly by diagnostic category. P2 elevation was predictive of increased frequency of disproportionate increases in ICP with an odds ration of 7.2 for greater than five episodes in 24 hours, 11 for greater than 15 episodes, with a sensitivity of 99% for both, and a predictive value of a positive test of 88% and 75%, respectively, and an overall accuracy of 86% for episodes greater than fn1 e episodes, 76% for greater than 15 episodes. Specificity, however, was only 17% and 10%, respectively. Elevated P2 had low specificity in distinguishing patients with fewer episodes of disproportionate in-
creased ICP; however, several spectral indices were significantly different between those with more and less disproportionate increases in ICP Clower mean ICP, higher low frequency spectral mean, larger high frequency centroid, and greater coherence between arterial blood pressure and ICP spectra). Those with the poorest outcome at discharge had greater than 15 episodes of disproportionate increases in ICP. The authors concluded that an elevated P2 ICP waveform, which can be easily determined visually, was a rough estimate of patients at risk for elevations in ICP during care-related activities. Increases in episodes of disproportionate increases in ICP in combination with spectral indices of poor autoregulation were related to poor outcomes. There were normal ICP values in over 40% of patients who had abnormal waveforms and increased frequency of disproportionate increases in ICP. 29
Implication for Practice This study tells practitioners that by monitoring the ICP pulse wave, they can anticipate when patients are developing decreased compliance and therefore will develop increased ICP. 6· 13• 28 Nurses can alter their care activities to improve the patient's adaptive capacity. Adjusting the elevation of the head of the bed can improve CSF and venous outflow while closely monitoring cerebral perfusion. 14• 15 • 23 • 27 · 31 If the patient has impaired autoregulation, is dehydrated, or hypotensive, lying flat may be the better position to promote cerebral perfusion.11i, 16 · 27 Ensuring that the neck is not flexed, extended, or rotated will facilitate venous outflow. 26 When positioning the patient ia the bed, be sure that flexion occurs at the hips, not in the abdomen, to decrease intraabdominal pressure. Monitor the patient's bowel routine and avoid constipation, which may increase intra-
INTRACRANIAL PRESSURE MONITORING AND ASSESSING INTRACRANIAL COMPLIANCE
abdominal pressure. 28 Positive end expiratory pressure can increase ICP by impeding venous outflow. 12 • 16 Maintain normothermia. Fever and agitation increase metabolic demand and will increase CBF in patients with intact autoregulation. 7· 9· 16 Suctioning is also an excitatory stimulus that increases CBF and therefore ICP. Sedation before suctioning may decrease the effect. 16• 19•24 It is important to monitor and minimize noxious environmental stimuli. Nurses can monitor and positively influence the external influences on ICP dynamics. 26
Future Direction Monitoring ICP gives practitioners only partial insight into the dynamics of the intracranial contents and does not provide the details of the status of CBF, cerebral blood volume, autoregulation, cerebral metabolism, tissue oxygenation, and other factors. Multimodality monitoring will help to put the picture together. Current research is focused on tissue
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oxygenation, tissue substrates such as excitatory amino acids, and temperature.11 Methods of testing cerebral autoregulation using the transcranial doppler exist but currently are cumbersome and require constant attention. Little is known about how long impaired autoregulation lasts, whether it is a static or a dynamic process, and whether practitioners can facilitate its recovery. Intermittent or continual monitoring of autoregulation may aid in the management of the cerebrovascular factors, which influence ICP and perfusion. Currently, monitoring ICP is an invasive procedure. In the future, noninvasive forms of monitoring will exist. Transcranial doppler ultrasound can currently be used as an indirect measure of the effects of ICP on perfusion. Near infrared spectroscopy allows for noninvasive measurement of tissue oxygenation, hemoglobin content, and measures of mitochondrial function. In the future, similar technologies may allow for noninvasive measurement of ICP.
SUMMARY Caring for the patient with a brain injury is a dynamic process with the goal of providing therapy to prevent secondary injury. Until practitioners have a better understanding of the pathophysiology of ischemia and the response of therapies for treating increased ICP, they must use the tools that exist. ICP monitoring gives a rough index of the relationships and the response of the intracranial contents to changes in volume that may produce increases in pressure and further damage. Understanding the information supplied by ICP monitoring is imperative to successful management of increased ICP.
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