The Central Nervous System in Pediatric Critical Illness and Injury

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Use scientific evidence and methods to investigate, evaluate and improve patient care practices. Demonstrate both an understanding of the contexts and systems in which health care, in particular critical care, is provided, and the ability to apply this knowledge to improve and optimize health care.

Year One Recognize need for, state proper indications for, discuss potential complications of, and demonstrate appropriate initial stabilization of patients requiring Airway management Cardiopulmonary resuscitation Transport intra- and inter-facility Invasive procedures Recognition and initial management of shock Demonstrate appropriate titration of basic life support including Conventional mechanical ventilation Hemodynamic support Explain indications for, and manage, advanced life support technologies under close senior fellow and attending supervision including: Mechanisms and toxicity Infectious diseases Mechanisms of microbial pathogenesis Nutritional and gastrointestinal disorders Fulminant hepatic failure and transplantation Intestinal and multivisceral transplantation Intestinal insufficiency and failure Renal, endocrine, and metabolic disorders Inborn errors of metabolism Year 3 Read and be able to explain principles relevant to pediatric critical care medicine of the following: Provide patient care that is compassionate, appropriate and effective for the promotion of health, prevention or treatment of disease esp associated with actual or threatened organ system failure, and at the end-of-life Objectives: Specifically, this includes understanding the management of pediatric patients with: Specifically, this includes understanding the etiology and pathophysiology as well as the management of pediatric patients with: Anticipate and manage potential complications Initiate and titrate appropriate advanced pharmacologic support for hypertension, hypotension, and arrhythmias, and evaluate the effectiveness of the intervention Competently and proactively manage patients before, during, and after ECMO to minimize complications and demonstrating appropriate judgment in initiating and discontinuing ECMO Order appropriate and timely laboratory tests for ICU patients Demonstrate mature ability to initiate advanced levels of support for acute, life-threatening illnesses in children ranging from newborn to adolescents who do not respond adequately to basic support.

Specifically, this includes generating a complete differential diagnosis addressing the problem, understanding the pathophysiology, and implementing cutting edge approach to management of pediatric patients with: Interpersonal and Communication Skills Goal: We have also shown that samples could reasonably be collected from at least two, and in most cases, all three time points per protocol we did not require a third blood draw in those patients that had improved to the point they no longer were having blood drawn. We have made the necessary modifications to the study design to ensure the integrity of sample identification through the initial processing, shipping, and final testing phases of the study, and have made the necessary label changes during this vanguard phase.

Although small changes were made to the methods and protocols these changes will save a significant amount of money and time in the long run when performed on a larger scale. Although a small number of subjects was included in this pilot study, our patient characteristics reveal a representative panel of pediatric DKA patients indicating, at least in this vanguard phase, a lack of enrollment bias.

This is consistent with recent information that most likely a high percentage of children with DKA have some element of cerebral injury or dysfunction at the time of presentation, albeit frequently subclinical [ 6 — 8 , 22 , 42 ]. This reinforces the importance of identifying patients at risk for cerebral injury, given that the scope of the problem is much larger than that represented by the small percentage of patients with overt cerebral edema.

The elevations we found were modest [ 31 , 36 , 37 , 44 ] and there were no differences noted between those with depressed mental status and those without. However, the small sample size is likely to be underpowered to demonstrate a difference. A larger study may show that these are important markers to distinguish those patients with potential for more significant cerebral injury. This is contrary to previously reported study results revealing elevated levels of GFAP in patients with presumed cerebral inflammation and injury [ 38 , 39 , 44 ].

A limitation of this study is that we have measured GFAP in plasma and not in cerebrospinal fluid and levels may be confounded by non-CNS sources. In addition, we did not compare amounts of fluid resuscitation between patient groups however we did evaluate levels of electrolytes and these were consistent across the two groups making dilution less likely.

Evidence exists for both vasogenic and direct inflammatory injury; a combination of these mechanisms may cause injury and ultimately overt severe cerebral edema in these patients [ 2 , 26 , 44 ]. This pilot study demonstrates the feasibility of exploration of mechanism of injury in these patients.

Our findings indicate that GFAP should be explored further. A tool or scale that encompasses more non-specific evidence of neuronal dysfunction or injury would be useful in identifying patients at risk as GCS is a fairly blunt scale addressing mental status primarily.

Markers of more direct neuronal injury, in addition to glial injury, are of potential interest. In addition, with the evolution in testing availability we will most likely be able to evaluate a wider array of biologic and genetic markers of inflammation and neuronal injury, which will lead to a greater understanding of this complex pathophysiology. These are all potentially important, albeit non-specific, symptoms of cerebral inflammation and injury [ 10 , 11 , 19 , 42 ]. The larger planned study will be designed to have adequate power to explore these symptoms and their correlation with CNS injury and biomarkers and genetic markers.

Upon procurement of the appropriate funding, we will follow at least a subset of patients in order to determine cognitive outcomes over a longer time frame and correlate cognitive impairment with these markers and with evidence of CNS injury at time of presentation with DKA.

For both financial and ethical reasons many would require the use of sedating medications exposing patients to risk versus exposing patient to radiation , obtaining brain imaging for even a subset of patients using magnetic resonance imaging or computed tomography is not feasible. However, technologies such as trans-cranial Doppler or specialized electroencephalogram hold some promise for more sensitive and specific measures of CNS injury and may be possible in the future large trial.

PICU Rotation Goals and Learning Objectives

The specific aims for the larger study will be based on those of the pilot study, which include:. In conclusion, in spite of great gains in the understanding of the pathophysiology of DKA, the mechanism and scope of CNS injury remain unclear. We have performed a complex pilot study demonstrating the feasibility of exploring potential genetic and biochemical markers important in the process of CNS injury in DKA.

We have identified inflammatory markers with potential involvement, and GFAP was specifically identified as a marker that warrants continued exploration. Further work is needed to better understand the extent of CNS injury in DKA as well as the mechanism underlying this injury. We thank all of the patients and ancillary staff for their participation in this study.

National Center for Biotechnology Information , U. J Pediatr Intensive Care. Author manuscript; available in PMC Jun Noble , b Daniel L. Levin , a Natalie Z. Cvijanovich , c Monica S. Vavilala , d J. Dean Jarvis , a and Heidi R. Author information Copyright and License information Disclaimer.

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Abstract Diabetic ketoacidosis DKA is the primary cause of death for children with diabetes, especially when complicated by cerebral edema. Cerebral edema, diabetic ketoacidosis, genetic biomarkers, vanguard, pilot. Introduction Diabetic ketoacidosis DKA complicated by cerebral edema was first identified and described in , and it remains the most common and catastrophic presentation of previously undiagnosed or poorly controlled type 1 diabetes mellitus T1DM in children [ 1 ]. Materials and methods After local institutional review board IRB approvals, consent and assent were obtained, and clinical data were collected using standard case reporting forms.

Procedures for biomarker and gene expression studies Samples were collected during the acute and convalescent phases of DKA. Total volumes were specifically chosen based on weight to minimize blood loss, as follows: Biomarker assays Once samples were received, biomarker assays were completed. Statistical analysis This pilot study was not designed with statistical power sufficient to establish clinically and statistically relevant biomarker and genetic results.

Project feasibility Although the study was designed as a pilot study, a significant goal of the work completed was to determine feasibility and establish effective methodology for the larger, multi-center trial. Table 1 Site activities.

Open in a separate window. Patient characteristics Patient characteristics are shown in table 2 and reflect those of the general pediatric diabetes population [ 35 ].

Table 2 Patient characteristics. Biomarker results As shown in table 3A , levels of IL-6 were moderate initially and generally increased over the next 12 hr to 24 hr as compared with levels that have been reported for healthy children, although the ranges of normal reported are wide [ 36 ] and as compared with young adults with T1DM without DKA, approximately 2. Table 4 Levels of glial fibrillary acidic protein at the three time points in the two patient groups. Discussion The main findings of this pilot study are: The specific aims for the larger study will be based on those of the pilot study, which include: To determine the association between candidate genes involved in inflammation and their biological marker end products with CNS injury associated with DKA.

To establish the infrastructure and collect samples for a specimen repository that will safely allow these data and residual gene and biological marker specimens to be used for further analyses e. Acknowledgments We thank all of the patients and ancillary staff for their participation in this study. Statement on diabetic ketoacidosis in children and adolescents. Predicting cerebral edema during diabetic ketoacidosis. N Engl J Med. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis.

Causes of death in children with insulin dependent diabetes — Diabetic ketoacidosis and memory dysfunction in children with type 1 diabetes. Cognitive dysfunction associated with diabetic ketoacidosis in rats. Risk factors for cerebral edema in children with diabetic ketoacidosis.

Specialist

Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Risk factors for developing brain herniation during diabetic ketoacidosis. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. Cerebral edema in childhood diabetic ketoacidosis: Natural history, radiographic findings, and early identification. Intracerebral crises during treatment of diabetic ketoacidosis.

Cerebral edema in diabetic ketoacidosis: A prospective evaluation of children with diabetic ketoacidosis. The impact of type 1 diabetes on brain development and function. Nat Clin Pract Neurol. Cerebral edema in diabetic ketoacidosis. Pediatr Crit Care Med. Comparisons of patient characteristics, clinical presentations and outcomes today and 20 years ago. Chang Gung Med J.

Economic impact of diabetic ketoacidosis in a multiethnic indigent population: Analysis of costs based on the precipitating cause. Assessing the outcome of pediatric intensive care. Recurrent diabetic ketoacidosis in inner-city minority patients: Behavioral, socioeconomic, and psychosocial factors.

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