Editorials 2. Hogue C W Jr, Stearns JD, Colantuoni E, et al: The impact of obe­ sity on outcomes after critical illness: A meta-analysis. Intensive Care Med 2009; 3 5 :1 1 5 2 -1 1 7 0

6. Wunsch H, Angus DC: The puzzle of long-term morbidity after critical illness. Crit Care 2010; 14:121

3. Wacharasint P, Boyd JH, Russell JA, et al: One size does not fit all in severe infection: Obesity alters outcome, susceptibility, treatment, and inflammatory response. Crit Care 2013; 17:R122

7. Padkin A, G oldfrad C, Brady AR, et al: Epidem iology of severe sepsis occurring in the first 24 hrs in intensive care units in England, Wales, and Northern Ireland. Crit Care Med 2003; 3 1 :2 3 3 2 -2 3 3 8

4. Schweickert W D, Pohlman MC, Pohlman AS, et al: Early physical and occupational therapy in mechanically ventilated, critically ill patients: A randomised controlled trial. Lancet 2009; 3 7 3:18 74 -188 2

8. Curtis JP, Selter JG, Wang Y, et al: The obesity paradox: Body mass index and outcomes in patients with heart failure. Arch Intern Med 2005; 16 5:55-61

5. Prescott HC, Virginia CW, O ’Brien Jr JM, et al: Obesity and 1-Year Outcomes in Older Americans W ith Severe Sepsis. Crit Care Med 2014; 42:176 6-1 774

9. Uretsky S, Messerli FH, Bangalore S, et al: Obesity paradox in patients with hypertension and coronary artery disease. Am J Med 2007; 12 0 :8 6 3 -8 7 0

Raised Intracranial Pressure During CNS Infection: What Should We Do About It?* Robert C. Tasker, MBBS, MD, FRCP Departments of Neurology and Anesthesia (Paediatrics) Harvard Medical School Boston Children's Hospital Boston, MA ormal cerebrospinal fluid (CSF) pressure in children at the time of lumbar puncture is positive in relation to atmospheric pressure, with 10th-90th percentile of 11.5-28 cm H^O or 8.7-21.2 mm Hg, respectively (1). Intracra­ nial pressure (ICP) is the pressure of CSF inside the cerebral ventricles, which is determined by cerebral blood flow (CBF) and CSF circulation. The Davson equation describes this rela­ tionship and states that ICP is the sum of sagittal sinus pres­ sure and the product of CSF formation rate and resistance to CSF outflow (2). Normal values for sagittal sinus pressure, CSF formation rate, and resistance to CSF outflow are 5-8 mm Hg, 0.3-0.4mL/min, and 6-10m m Hg/mL/min, respectively. Mea­ sured ICP is often greater than the calculated value because of a vascular component, which is probably a result of pulsation in the arterial bed and the interaction between pulsatile arterial inflow and venous outflow curves, cardiac function, and cere­ bral vasomotor tone (3). All of these interrelationships may be altered in critically ill comatose patients with CNS infection.

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*See also p. 1775. Key Words: child; encephalitis; intracranial pressure; meningitis; outcome Dr. Tasker has received support for travel when he lectured on traumatic brain injury for the Miami Children's Hospital and when he attended the Guidelines Specialist Panel committee for the Brain Trauma Foundation. He also receives support from the National Institutes for Health (NIH) (U01 NS081041) and the American Epilepsy Society. He is employed by the Boston Children’s Hospital, received royalties from the Oxford Uni­ versity Press (Handbook of Paediatrics), and received support for article research from NIH. Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins

These abnormalities may also be compounded by brain swell­ ing, edema and increased cerebral blood volume (CBV), focal cerebral perfusion deficits and variable levels of CBF and cere­ brovascular Co2 reactivity, and cerebral vasculitis (4-7). The net result is raised ICP along with significant risk of brain tis­ sue herniation and ischemic syndromes and death (8-10). In this issue of Critical Care Medicine, Kumar et al (11) report a study from Chandigarh, India, in comatose children (aged 1-12 yr) with acute CNS infection undergoing invasive ICP monitoring. The authors addressed the pragmatic ques­ tion of whether to target level of ICP (< 20 mm Hg) or whether to target level of cerebral perfusion pressure (CPP > 60 mm Hg, the difference between mean arterial blood pressure [BP] and mean ICP) with ICU therapies. The authors’ conclusion from this randomized controlled trial (RCT) is that the CPP goal, rather than ICP goal, is superior and results in better rates of morbidity and mortality. This study has significant bearing on both adult and pediatric critical care practice. However, there are important considerations that warrant further discussion. First, there were major therapeutic consequences of the dif­ ferent strategies used in this RCT. The primary aim of targeting level of CPP meant that systolic BP was targeted to the 95th percentile for age, and hence, there was more frequent use of inotropes. The primary aim of targeting level of ICP meant that any systolic BP more than 5th percentile was considered acceptable, and as a consequence, these patients had lower BP. In addition, the ICP group was exposed to hyperventilation and osmotherapy more frequently than the CPP group. At the start of experimental interventions, both groups had similar level of mean BP, around the 90th percentile for age. Yet, over subsequent hours, the ICP group had mean BP that decreased to the 50th percentile, whereas the CPP group had mean BP that increased to the 95th percentile. Over this same period, the mean ICP in all patients fell to a level within the normal range (1), albeit lower in the ICP group. We need to learn more from these observations by Kumar et al (11) and what they tell us about life-threatening CNS infection. For example, in relation

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to the age- and sex-specific standards in BP in healthy children, these patients were nearly “hypertensive” at presentation. Bet­ ter outcomes were observed in those where this “near-hyper­ tensive” level was maintained. Perhaps, then, higher targets for mean BP and systolic BP should be used in these critically ill children (12). Perhaps, too, this near-hypertensive BP at pre­ sentation is a response to lower than normal cerebral oxygen delivery and perfusion deficits (5, 6), and we would do well not to ignore the apparent target that homeostasis is setting. Second, we need to reconsider whether the ICP-directed therapies—mannitol and hyperventilation—lack benefit or are potentially detrimental. In regard to osmotic therapy for menin­ gitis, to date, there have been four RCTs (comprising 1,091 adult and pediatric participants) comparing glycerol with a control. Collective data from the trials do not demonstrate any ben­ efit on death or on death and neurologic disability combined; the Cochrane review in 2013 concluded that osmotic diuretics should not be given to adult and pediatric patients with bacte­ rial meningitis (13). In the report by Kumar et al (11), a greater proportion of the ICP group received mannitol, which may also have resulted in BP lowering and potential detrimental effects (see above). Whether the more frequent and greater duration of hyperventilation in the ICP group was also potentially detri­ mental is unknown. For example, at presentation, most patients with acute bacterial meningitis hyperventilate spontaneously (14), and we do not know what level in arterial Co2partial pres­ sure should be targeted during mechanical ventilation in those with baseline hypocapnia (15). Normally, acute hyperventilation reduces CBF and CBV. In life-threatening CNS infection, this response is used to reduce ICP, but the associated fall in CBF and CBV will only render the brain at risk of focal or global ischemia if cerebrovascular Co2 reactivity is intact. Two studies in adults with acute bacterial meningitis have demonstrated that short­ term hyperventilation does not enhance regional abnormalities in CBF nor does it alter cerebral metabolic rate for oxygen (5, 6). Taking all this evidence together, there is little to support the routine use of mannitol and hyperventilation in neurocritical care for life-threatening CNS infection. Last, it might appear from the current report (11) that all unconscious pediatric patients with CNS infection should now undergo ICP monitoring so that we can target CPP with our therapies. In 2006, a large secondary analysis of administrative data for hospitalized children with meningitis in the United States revealed no association between patient survival and the use of ICP monitors (16). In March 2009, U.S. adult and pedi­ atric neurosurgeons appeared skeptical of the evidence to use ICP monitors in children with meningitis; of 420 respondents to a survey sent to 728 neurosurgeons, only one-third felt there was sufficient evidence to monitor ICP (17). Will the current report by Kumar et al (11) add weight to the clinical decision to place an ICP monitor in a comatose child with acute CNS infection? The reason now for requesting such monitoring is in order to target CPP more than 60 mm Hg with the use of inotropes. However, one could equally argue that what is actu­ ally needed is BP monitoring and targeting systolic BP at the 95th percentile for age and sex. Such an approach is more likely Critical Care Medicine

to be achieved worldwide and implemented in settings with limited resources (18). The quandary that we are left with is reminiscent of the resource issues (19) surrounding a recent RCT of ICP monitoring in traumatic brain injury (20). In that study from South America, intensive care focused on main­ taining monitored ICP at less than or equal to 20 mm Hg was not shown to be superior to intensive care based on serial cra­ nial CT scans and clinical examination. Do we really need an ICP monitor in comatose patients with acute CNS infection or would an arterial catheter alone be as effective, since that is what is actually determining changes in treatment? In conclusion, Kumar et al (11) are to be commended on conducting an informative and instructive study that will reinvigorate this field of neurocritical care. The implications of other important observations will need further study: the range of CT findings in those with raised ICP; over the first 24 hours, the similarity in pattern in mean CPP and mean ICP in both the ICP group survivors and the CPP group nonsurvi­ vors, yet profound difference in outcome; and the time course of lack of responsiveness to therapies in the CPP group non­ survivors in the period 24-48 hours.

REFERENCES 1. Avery RA, Shah SS, Licht DJ, et al: Reference range for cerebrospinal fluid opening pressure in children. N Engl J Med 2010; 363:891 -8 9 3 2. Davson H, Hollingsworth G, Segal MB: The mechanism of drainage of the cerebrospinal fluid. Brain 1970; 9 3 :6 6 5 -6 7 8 3. Tasker RC: Intracranial pressure: Influence of head-of-bed elevation, and beyond. Pediatr Crit Care Med 2012; 1 3 :116 -11 7 4. Quagliarello V, Scheld W M: Bacterial meningitis: Pathogenesis, pathophysiology, and progress. N Engl J Med 1992; 3 2 7 :8 6 4 -8 7 2 5. Moller K, Hogh P, Larsen FS, et al: Regional cerebral blood flow dur­ ing hyperventilation in patients with acute bacterial meningitis. Clin Physiol 2000; 2 0 :3 9 9 -4 1 0 6. Moller K, Strauss Gl, Thomsen G, et al: Cerebral blood flow, oxidative metabolism and cerebrovascular carbon dioxide reactivity in patients with acute bacterial meningitis. Acta Anaesthesiol Scand 2002; 4 6 :5 6 7 -5 7 8 7. Vergouwen MD, Schut ES, Troost D, et al: Diffuse cerebral intravas­ cular coagulation and cerebral infarction in pneumococcal meningitis. Neurocrit Care 2010; 1 3 :2 1 7 -2 2 7 8. Durand ML, Calderwood SB, Weber DJ, et al: Acute bacterial men­ ingitis in adults. A review of 493 episodes. N Engl J Med 1993; 3 2 8 :2 1 -2 8 9. Goitein KJ, Tamir I: Cerebral perfusion pressure in central nervous sys­ tem infections of infancy and childhood. J Pediatr 1983; 1 0 3 :4 0 -4 3 10. Tasker RC, Matthew DJ, Helms P, et al: Monitoring in non-traumatic coma. Part I: Invasive intracranial pressure measurements. Arch Dis Child 1988; 6 3 :8 8 8 -8 9 4 11. Kumar R, Singhi S, Singhi P, et al: Randomized Controlled Trial Comparing Cerebral Perfusion Pressure-Targeted Therapy Versus Intracranial Pressure-Targeted Therapy for Raised Intracranial Pressure due to Acute CNS Infections in Children. Crit Care Med 2014; 42 :177 5-1 787 12. Haque IU, Zaritsky AL: Analysis of the evidence for the lower limit of systolic and mean arterial pressure in children. Pediatr Crit Care Med 2007; 8 :1 3 8 -1 4 4 13. Wall EC, Ajdukiewicz KM, Heyderman RS, et al: Osmotic thera­ pies added to antibiotics for acute bacterial meningitis. Cochrane Database Syst Rev 2013; 3:C D 00 880 6 14. Hansen EL, Kristensen HS, Brodersen P, et al: Acid-base pattern of cerebrospinal fluid and arterial blood in bacterial meningitis and in encephalitis. Acta Med Scand 1974; 196:431 -4 3 7

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Editorials 15. Tasker RC, Lutman D, Peters MJ: Hyperventilation in severe diabetic ketoacidosis. Pediatr Crit Care Med 2005; 6 :4 05-4 11 16. Odetola FO, Tilford JM, Davis MM: Variation in the use of intracranialpressure monitoring and mortality in critically ill children with meningi­ tis in the United States. Pediatrics 2006; 1 1 7 :1 8 9 3 -1 9 0 0 17. Odetola FO, Clark SJ, Lamarand KE, et al: Intracranial pressure in childhood meningitis with coma: A national survey of neurosurgeons in the United States. Pediatr Crit Care Med 2011; 12 :e 3 5 0 -e 3 5 6

18. World Health Organization: Pocket book of hospital care for children: Guidelines for the management of common illnesses with limited resources. 2013. Available at: http://www.who.int/child_adolescent_ health/docum ents/9241546700/en/. Assessed March 20, 2014 19. Mukherjee D, Sarmiento JM, Patil CG : Intracranial-pressure monitor­ ing in traumatic brain injury. N Engl J Med 2013; 3 6 8 :17 48 -174 9 20. Chesnut RM, Temkin N, Carney N, et al; Global Neurotrauma Research Group: A trial of intracranial-pressure monitoring in trau­ matic brain injury. N Engl J Med 2012; 367:24 71 -248 1

Further Reduction in Door-to-Balloon Times: Diminishing Marginal Productivity in Search of Perfection?* Ian C. Gilchrist, MD, FCCM Heart & Vascular Institute Pennsylvania State University, College of Medicine Hershey, PA

onsiderable resources have been expended in improv­ ing the delivery of acute cardiac care in the setting of acute myocardial infarction (MI). The heart is very sensitive to ischemic time, and reversal of the thrombotic occlusion in the coronary artery can stop the ischemia and modify the resulting infarction. So compelling is the data for rapid reperfusion that door-to-balloon times are reported to regulators in the United States and displayed publically on the Centers for Medicare and Medicaid Services website (1). Similar statutory reporting is done in other countries with advanced cardiovascular capabilities. The public health efforts to shorten the door-to-balloon time have been very successful in delivering more efficient care of MI and have raised the logi­ cal extension of this effort to whether even further shortening the time to treatment should be advocated beyond the present maximum of 90 minutes suggested by practice guidelines (2). An example of a population-based improvement project to improve MI reperfusion times in Taiwan is described by Ho et al (3) in this issue of Critical Care Medicine. A natural experiment occurred when the Taiwanese implemented a policy to encour­ age improved door-to-balloon times. Using January 2010 as the

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*See also p. 1788. Key Words: coronary artery disease; guidelines; health policy; myocardial infarction; reperfusion The author has disclosed that he does not have any potential conflicts of interest. Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins

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inflection point of this statutory change, 266 patients with acute MI before and 293 patients after this date were compared for outcomes and treatment times. With this emphasis on short­ ening treatment times, door-to-balloon times dropped with more than 50% of patients in the later cohort receiving reper­ fusion within 60 minutes of presentation versus 12% in the period before enhanced attention to treatment time metrics. Despite this significant improvement in efficiency of healthcare delivery, there was no significant difference in left ventricular ejection fraction, prevalence of 30-day mortality, or 30-day combined endpoint (30-day death or class >3 congestive heart failure) between the two groups. While on the surface this may seem to be counterintuitive, it is a finding that has recently been seen in another study (4). Evaluating data from the National Cardiovascular Data Registry between July 2005 and June 2009, a net 16-minute reduction in door-to-balloon time was noted in a cohort of over 95,000 patients, yet no significant change in mortality could be ascertained. Perhaps, we need to reconsider the push for shorter door-to-balloon times as we may be climb­ ing the wall of marginal cost or diminishing marginal produc­ tivity in search of perfection. Other investment of resources may serve us better in improving outcome. Damage from MI is higJdy time dependent, but not all tis­ sue damage occurs along the same temporal course. MRI stud­ ies (5) and nuclear studies (6) indicate that the primary insult to the myocytes has occurred by 90 minutes from the onset of symptoms. Treatment within this 90-minute window appears to affect ejection fraction, whereas therapy after this point appears to offer little to muscle salvage. Despite this, there is evidence from multiple clinical trials that some benefit exists for reperfusion out to 12 hours after the onset of symptoms (7). Part of this beneficial effect may represent variability in the extent of collateral support from the contralateral arterial sys­ tem found in the population. But even without collaterals, ben­ efit to reperfusion after irreversible changes to myocytes may be due to differential effects on heart cell types other than the myocytes that may be more resistant to ischemia. Likewise, the August 2014 • Volume 42 • Number 8

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Raised intracranial pressure during CNS infection: what should we do about it?*.

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