773CHAPTER 63 Intracranial Hypertension and Monitoring 0 1 2 3 Time (min) IC P (m m H g) A B P (m m H g) 17 5 15 0 12 5 75 70 65 60 80 10 0 20 0 A 12 5 15 0 17 5 20 0 IC P (m m H g) 10 0 PRx 2= 0 4 0[.]
CHAPTER 63 Intracranial Hypertension and Monitoring ABP (mm Hg) 17.5 15.0 12.5 10.0 80 75 ICP (mm Hg) ABP (mm Hg) ICP (mm Hg) 20.0 70 65 60 773 100 95 90 85 80 75 70 20.0 17.5 15.0 12.5 10.0 3 Time (min) Time (min) 20.0 PRx = –0.37 PRx = 0.42 18 17.5 ICP (mm Hg) ICP (mm Hg) 16 15.0 12.5 14 12 10 10.0 70 A ABP (mm Hg) B 80 90 100 ABP (mm Hg) • Fig 63.5 Relation between slow waves of arterial blood pressure (ABP) and intracranial pressure (ICP) (A) Slow waves in ICP and ABP produce a positive correlation (lower left), giving a positive value of the pressure-reactivity index (PRx), which indicates loss of cerebrovascular reserve (B) Coherent waves both in ABP and ICP produced a negative correlation coefficient when plotted on the regression graph (lower right), giving values of PRx that were clearly negative Measurement of Intracranial Pressure Invasive Monitoring Devices ICP monitoring devices can be categorized according to the ana tomic site of placement and how the pressure record is trans duced For example, in infants, surface tonometry applied to the anterior fontanelle was an early method used for noninvasive transduction of the ICP waveform This method, however, is limited because the force of applanation influences the pressure record More standard approaches for the measurement of ICP rely on manometry of catheters placed in the ventricular system or in other CSF space Alternatively, pressure sensors may be placed within the brain The complications of ICP monitoring include infection, hem orrhage, CSF overdrainage, and monitor malfunction The overall incidence of infection for the various forms of ICP monitors is not significantly different regardless of their location, but the se verity of infection may differ slightly depending on the anatomic site of the device Hemorrhage is a rare complication of ICP monitoring and is a direct result of surgical placement of the device Overdrainage of ventricular catheters can result in rapid emptying of the ventricular system and accumulation of subdural hematomas Close attention must be paid to prevent drainage systems from being placed too low or falling to the floor This complication is most serious when intraventricular pressure is monitored in children with hydrocephalus Overdrainage also may result in pneumocephalus Overall, an intraventricular drain connected to an external pressure transducer is still considered the gold standard for mea suring ICP ICP can be controlled by CSF drainage, and the transducer can be zero-calibrated to a point externally (most commonly, the position of the external auditory meatus as a sur rogate for the foramen of Monro) After days of monitoring, however, the risk of infection starts to increase, with an overall risk estimated to be about 5% to 10%.25,26 Insertion of the ventricular catheter may be difficult or impossible in cases of advanced brain swelling As an alternative, modern cathetertipped ventricular, subdural, or intraparenchymal microtrans ducers have been used, and often modern considerations include compatibility with MRI One disadvantage of microtransducer S E C T I O N V I Pediatric Critical Care: Neurologic PRx CPP (mm Hg) 774 90 80 70 60 50 40 30 0.5 –0.5 –1 17/12 17:30 17/12 18:00 17/12 18:30 17/12 19:00 17/12 19:30 17/12 20:00 17/12 20:30 PRx Time/date 0.4 0.2 –0.2 –0.4 < 45 47.50 52.50 57.50 62.50 67.50 72.50 77.50 82.50 87.50 92.50 > = 95 CPP (mm Hg) • Fig 63.6 Example trend chart of spontaneously fluctuating cerebral perfusion pressure (CPP; top, shaded area) and pressure-reactivity index (PRx; middle) data recorded over a 4-hour period and the corresponding error-bar plot of PRx versus CPP with accompanying parabolic regression line The regression line indicates a CPPopt of 70 mm Hg, at which point PRx is approximately –0.4 systems is that they cannot, in general, be readjusted to zero after insertion, and considerable zero drift sometimes can occur in long-term monitoring.26 Regarding other forms of monitoring, contemporary epidural sensors are much more reliable now than they were 10 years ago Lumbar CSF pressure is seldom measured in patients receiving neurointensive care This form of assessment of craniospinal dy namics is more often used in the assessment of hydrocephalus and idiopathic intracranial hypertension It is unreliable if the instan taneous value of the fluid column pressure is recorded; at least 30 minutes averaging in resting conditions (with a period of over night monitoring as the gold standard) is the desired requirement Finally, attempts to monitor ICP noninvasively, although promis ing, need to be evaluated in large series (see earlier discussion) Noninvasive Diagnostic Tests of Intracranial Pressure Over the years, a variety of techniques have been used to assess whether a patient has raised ICP, including TCD pulsatility index of middle cerebral artery velocity, tympanic membrane displace ment, ultrasound time-of-flight techniques, and ONSD measure ments A recent systematic review and meta-analysis of noninva sive diagnostic tests of raised ICP in critically ill adults indicated that clinicians cannot rely on these tests because their accuracy is unknown.27 (An equivalent meta-analysis is not available for critically ill children.) Perhaps the most studied metric is the ONSD As Fernando et al.27 conclude, ONSD “could be an ac curate method of measuring ICP, but no agreed threshold exists, and the method’s accuracy can be influenced by provider exper tise.” There have been a number of studies in children examining normal growth of the ONSD and criteria for identifying raised ICP In general, across the pediatric age range, the threshold may be a diameter greater than 4.0 to 4.5 mm, in infants younger than year and older children, respectively However, these are isolated reports and any conclusion about utility must be the same as that made by Fernando et al.27 (as discussed earlier) Pressure Gradients and Compartments In a fluid-filled container, pressure is the same wherever one chooses to measure it within that space Generally, uniformly distributed ICP can be seen only when CSF is circulating freely among all its natural pools, equilibrating pressure everywhere When little or no CSF volume is left (because of brain swelling), the assumption of one uniform value of ICP is questionable (This is why brain tissue shift and herniation occur: they move down tissue pressure gradients.) It is worth remembering that with the commonly used catheter-tipped, intraparenchymal probes, the measurement of pressure is at a particular point, an area of cortex within a hemisphere, and the ICP may merely reflect pressure in that compartment rather than be representative of pressure within the ventricular system (i.e., real CSF pressure) Clinical Analysis of Intracranial Pressure Normal Values in Intracranial Pressure Establishing a universal normal value for ICP is difficult because it depends on age, body posture, and clinical condition In the horizontal position, a normal ICP value in healthy adults was re ported to be within the range of to 15 mm Hg.28 In the upright position ICP is a negative value, with a mean of around 10 mm Hg but not exceeding 15 mm Hg.29 In infants and children, normal values for ICP, usually taken at the time of a “negative” diagnostic lumbar puncture using the CSF “opening pressure,” indicate that we should not be using different values to those de scribed in adults For example, Avery et al.30 found that the 90th percentile of opening CSF pressure in 197 children aged to 18 years was 21 mm Hg (i.e., 28 cm H2O) Some authorities CHAPTER 63 Intracranial Hypertension and Monitoring Proximal cerebral arteries Distal cerebral arteries CSF formation Cerebral and intracranial veins CSF outflow 775 Extracranial venous CBF BP + – Injection into CSF space ICP 25 25 20 20 15 48 mm Hg 36 mm Hg 10 CBF (mL/s) CBF (mL/s) A 0.0% 10 100.0% 0 B 15 20 40 60 80 100 120 140 160 180 CPP (mm Hg) C 20 40 60 80 100 120 140 160 180 CPP (mm Hg) • Fig 63.7 Electrical circuit equivalent of the lumped compartment model and some baseline physiologic operating characteristics (A) The model includes different segments: proximal and distal cerebral arteries, cerebral and intracranial veins, extracranial venous, and cerebrospinal fluid (CSF) formation and outflow (B) Dependence of CBF on cerebral perfusion pressure (CPP) under steady-state conditions at various Paco2 values (36, 38, 40, 42, and 44 mm Hg) Increasing Paco2 increases CBF at any given CPP (C) Dependence of CBF on CPP when cerebral autoregulation gain varies CPP variation leads to more alteration in CBF as cerebral autoregulation impairment increases (0%, 25%, 50%, 75%, and 100%). BP, Blood pressure; CBF, cerebral blood flow; ICP, intracranial pressure; Paco2, partial pressure of arterial carbon dioxide consider this value too high or reflective only of lumbar fluid pres sure rather than ICP Thus, for example, the definition of a raised ICP in hydrocephalus is a pressure above 15 mm Hg Alterna tively, in severe TBI, various pressure levels have been used as a threshold for treatment5: the protocols referred to in the third edition of the Brain Trauma Foundation guidelines4 used initial ICP target values, from less than 15 mm Hg to less than 20 mm Hg and up to 25 mm Hg Choice of Type of Invasive Intracranial Pressure Monitoring Traditionally, ICP monitoring is performed via a ventriculostomy Newer technologies rely on fiberoptic monitoring, with the cath eter sensor tip placed in the brain parenchyma The potential ad vantage of ventriculostomy is that it enables CSF drainage as a treatment However, it can be difficult to place and maintain function in the child with small, compressed, or distorted ven tricles Also, as the severe TBI treatment protocols5 (referred to in the third edition of the Brain Trauma Foundation guidelines4) have indicated, there is considerable variation in how external ventricular drains are used For example, drainage level is set as low as to cm H2O or up to 27.2 cm H2O above the tragus (2.2–3.7 and 20 mm Hg, respectively) and is used for venting or diverting CSF either continuously or intermittently There are no randomized controls trials on this topic, but a recent retrospective analysis of external ventricular drains versus intraparenchymal ICP monitoring in adults with severe TBI found that the drains were associated with worse functional outcome.31 Hence, the best technique remains elusive Choice of Whether to Use Intracranial Pressure Monitoring Another question is whether to use ICP monitoring at all Many practitioners will be familiar with the idea that in a comatose patient with severe TBI (i.e., Glasgow Coma Scale [GCS] score #8) it is more or less expected that invasive ICP monitoring will 776 S E C T I O N V I Pediatric Critical Care: Neurologic 2.0 140 1.5 1.0 0.5 100 PRx BP (mm Hg) 120 80 –1.0 60 –1.5 –2.0 40 A 0.0 –0.5 50 100 150 200 250 300 40 350 Time (min) B 50 60 70 80 90 100 110 120 130 CPP (mm Hg) • Fig 63.8 Impact of shifting the 6-hour mean arterial blood pressure (BP) profile on PRx when cerebral autoregulation is intact Paired graphs with input BP profiles and output cerebral perfusion pressure (CPP) PRx plots before final curve fitting (A) BP profile shifted either up or down by a fixed amount, giving six inputs differing in mean BP (B) Output PRx plots for profiles show that difference in mean BP, but fixed pattern, results in a shift in the minima in the plots, which would be interpreted as a different optimal CPP PRx, Pressure reactivity index be used However, this approach is by no means universal around the world Even in the United States, there is variation in practice In a large multicenter database (2001 to 2011) of 4667 children with TBI, there was significant between-hospital variation in ICP monitoring.32 Overall, 55% of patients (n 2586) received ICP monitoring Observed hospital ICP monitoring rates were 14% to 83% After adjustment for patient factors, 13% of the ICP monitoring variation was attributable to between-hospital varia tion Hospitals with more observed ICP monitoring, relative-toexpected, and hospitals with higher patient volumes had lower rates of mortality or severe disability After adjustment for be tween-hospital variation and patient severity of injury, ICP monitoring was independently associated with age year and older (odds ratio, 3.1; 95% confidence interval, 2.5–3.8) versus age younger than year Another study using the US National Trauma Data Bank of pediatric TBI cases managed in levels I and II centers (2001 to 2006) found that ICP monitoring was under taken in few pediatric patients with severe TBI.33 Usage of ICP monitoring was associated with decreased mortality rate in only a small subset of the targeted population In addition, children who received a monitoring device had longer hospital stay, longer pe diatric intensive care unit (PICU) stay, and more ventilator days These findings suggest that current use of ICP monitoring does not necessarily identify patients who are most likely to benefit from it.34 It is also true that not all patients undergoing invasive ICP monitoring for severe TBI exhibit raised ICP In a national study in the United Kingdom of all pediatric cases of severe TBI man aged in the PICU (2001–2003), raised ICP was documented in only 49% of cases (98 of 199) undergoing monitoring.35 Forsyth et al.35 found that of the variables significantly associated with raised ICP in univariate analyses (emergency department GCS score, pupil reactivity, age, and the findings on admission cranial computed tomography [CT] scans in relation to presence of sub arachnoid hemorrhage, intracerebral hemorrhage or traumatic axonal injury [TAI], and lateral ventricle appearance), only the presence of TAI retained an independent association with devel opment of raised ICP in multivariate logistic regression GCS of or less predicted raised ICP with a sensitivity of 80% and a specificity of 55% (positive predictive value, 59%; negative predictive value, 77%) “Any abnormality on CT” predicted raised ICP with a sensitivity of 91% and a specificity of 38% (positive predictive value, 58%; negative predictive value, 82%) As also reported by others,36 the presence of raised ICP despite normal radiology and pupil responses likely reflect the known low sensitivity of CT for clinically significant TAI It is now known that, in certain settings, aggressive medical treatment of intracranial hypertension complicating severe TBI can be guided by one of two strategies with no difference in out come: use of ICP monitoring as a guide to therapy, or use of intensive clinical examination and serial CT scans to guide therapy.37,38 In this 2012 study in South America, 324 patients (13 years or older, 25% younger than 22 years ) were randomly assigned to one of two specific protocols: guidelines-based man agement in which a protocol for monitoring intraparenchymal ICP was used or a protocol in which treatment was based on CT scans and clinical examination The primary outcome was a com posite of survival time, impaired consciousness, and functional status at months and months and neuropsychological status at months There was no significant between-group difference in the primary outcome Six-month mortality was no different be tween the groups (39% in the pressure-monitoring group and 41% in the imaging-clinical examination group) The median length of stay was similar in the two groups (12 days in the pressuremonitoring group and days in the imaging-clinical examination group), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyper ventilation) was higher in the imaging-clinical examination group than in the pressure-monitoring group Clearly there is still much to learn in how we select patients for invasive monitoring and how we use the information from moni toring to guide our therapies Even so, it is our practice to use invasive monitoring to guide treatment rather than to rely solely on serial clinical examinations and CT imaging Clinical Targets in Intracranial Pressure and Cerebral Perfusion Pressure Levels In adults, the threshold for initiating treatment of intracranial hypertension is taken as 20 to 25 mm Hg It is likely that the ICP CHAPTER 63 Intracranial Hypertension and Monitoring threshold for poorer outcome is similar across all ages; the “Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Founda tion Guidelines”5,6 concludes that treatment threshold for raised ICP is 20 mm Hg Normal values for mean ABP and, hence, CPP are lower in children, particularly in infants and young children Two assump tions are made when using calculated CPP to guide treatment The first assumption is that the mean ABP is a good reflection of brain surface arteriolar pressure; however, this may not be the case The second assumption is that both pressures contributing to the calculation are calibrated to the same level In the case of ICP monitoring via ventriculostomy, the point for zero calibra tion can be adjusted, although few reports discuss the exact details of calibration and zeroing This adjustment is not possible with fiber-tip intraparenchymal devices, for which the pressure is re corded at the tip of the sensor If, in the case of ventricular moni toring, the zero point for ICP is taken as the level of the external auditory meatus and the conventional zero point for ABP is taken as the level of the right atrium, then the actual CPP driving CBF would be lower than the simply calculated difference between the mean ABP and the mean ICP The magnitude of this difference is related to the product of the sine of the angle of elevation of the bed and the distance between the two calibration points In chil dren, this difference is of the order of mm Hg However, if an intraparenchymal fiber-tip device is used and the bed is elevated beyond 30 degrees, the error could be double Therefore, clini cians should be cautious about how the data reporting exact criti cal CPP values are interpreted, particularly as few reports describe the methods of calibration in their practice The 2019 Brain Trauma Foundation guidelines and consensus for tiered therapies5,6 sup ports the maintenance of a minimum CPP value of 40 mm Hg along with support for consideration of implementing age-specific thresholds between 40 and 50 mm Hg, with infants at the lower end and adolescents at the upper end of this range It should be recognized that these represent minimum acceptable values and that higher values may often be maintained in order to prevent patients from being at risk of falling below these thresholds and the risk of cerebral ischemia This threshold may be achieved by a variety of approaches, including ensuring appropriate intravascu lar volume status with an adequate central venous pressure, generally between and 10 mm Hg; targeting mean ABP normal for age (i.e., 50th percentile); targeting systolic blood pressure below 140 mm Hg, but above 90 mm Hg, or between 100 and 110 mm Hg, or above 70 (2 age in years) mm Hg Supplementing Intracranial Pressure Monitoring With Other Monitoring Modalities The continuous measurement of ICP is an essential modality in most brain monitoring systems After a decade of enthusiastic at tempts to introduce newer modalities for brain monitoring (e.g., brain tissue oxygenation, microdialysis, cortical blood flow, TCD ultrasonography, near infrared spectroscopy, and jugular bulb oxygen saturation) to accompany our use of invasive ICP moni toring, only brain tissue oxygenation monitoring has continued to be used in pediatric practice to a limited extent Brain tissue oxygen monitoring therefore features as a new tier intervention in the 2019 Brain Trauma Foundation guidelines and consensus for tiered therapies.5,6 In centers that use this form 777 of monitoring, there is a minimum target level of tissue oxygen of 10 mm Hg However, the current studies reviewed in the guide lines have generally failed to outline whether the monitor should be inserted into the uninjured or injured brain (obviously influ encing the interpretation of the findings) Interventions that can specifically increase tissue oxygen level include raising fraction of inspired oxygen via the mechanical ventilator, raising mean ABP with vasopressors, increasing Paco2 to increase CBF, and optimiz ing blood hemoglobin concentration Beyond such interventions, further data comparing management with or without such moni toring are required Mechanism of Brain Injury in Intracranial Hypertension In patients with a head injury, cerebral MRI commonly reveals focal lesions within the frontal and temporal lobes, the temporal poles, and the limbic system, including its connections with the orbitofrontal surface of the frontal cortex.39,40 Pathologic change may occur by means of several injurious mechanisms in these re gions In the temporal lobes or its connections, manifestations of the following conditions may be found: • Mechanism 1: Direct high-speed impact injury with or without acceleration-deceleration forces In this instance, the medial temporal lobe is vulnerable to mechanical deformation and contusion.41 • Mechanism 2: Metabolic perturbation resulting from vascular or systemic factors such as hypoxia, ischemia, hypoglycemia, and seizures In these head injury–related insults, there is a predilection for vulnerability within a structure in the tempo ral limbic system, the hippocampus.42 • Mechanism 3: Diffuse axonal injury or TAI as a consequence of rotational forces at the time of injury affecting axonal integrity; thereafter, secondary or postacute deafferentation or deafferen tation of structures such as the hippocampus occurs.43,44 • Mechanism 4: Raised ICP with brain swelling resulting in pres sure necrosis of the main cortical input to the hippocampus, to the parahippocampal gyrus, and against the free edge of the tentorium cerebelli.45 • Mechanism 5: Frontal hemodynamic perfusion failure as a consequence of inadequate local CBF, failed local cerebral au toregulation, raised ICP, or anterior compartment syndrome When consideration is given to monitoring other modalities be sides ICP, two problems are encountered The first problem is understanding the extent to which these mechanisms contribute to the physiologic derangements that can be followed in the in tensive care unit (ICU) The second problem is making a differ ence in patient assessment and outcomes provided that these mechanisms can be influenced Intracranial Pressure Monitoring and the Postinsult Natural History of Injury In a patient with a severe TBI, the value and utility of monitoring may serve a spectrum of functions Given the five potential mechanisms outlined in the previous section (i.e., direct me chanical effect, metabolic perturbation, axonal injury, brain swell ing, and hemodynamic perfusion failure), specific foci, whether for assessment or treatment, can be identified for monitoring The potential for treatment rather than for assessment, however, will ... patients receiving neurointensive care This form of assessment of craniospinal dy namics is more often used in the assessment of hydrocephalus and idiopathic intracranial hypertension It is unreliable... particular point, an area of cortex within a hemisphere, and the ICP may merely reflect pressure in that compartment rather than be representative of pressure within the ventricular system (i.e.,... The magnitude of this difference is related to the product of the sine of the angle of elevation of the bed and the distance between the two calibration points In chil dren, this difference is