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Energy Expenditure in Patients With Nontraumatic Intracranial Hemorrhage

Posted on: Tuesday, 28 March 2006, 03:03 CST

By Esper, Dema Halasa; Coplin, William M; Carhuapoma, J Ricardo

ABSTRACT. Background: Patients with intracerebral (ICH), intraventricular (IVH) and subarachnoid hemorrhage (SAH) have increased morbidity and mortality compared with other forms of stroke. We postulate that the systemic inflammatory state triggered by these forms of nontraumatic intracranial hemorrhage (IH) translates into higher nutrition requirements than traditionally assumed. In order to test this hypothesis, we performed a retrospective study comparing the resting energy expenditure (REE) of 14 mechanically ventilated IH patients with the REE of 6 severe traumatic brain injury (sTBI) patients (a disease known to induce an increased metabolic state). Methods: Using nonparametric analysis, we compared 2 contemporary cohorts of patients-IH and sTBI-who required mechanical ventilation and who underwent indirect calorimetry (IC) within 7 days after the ictus. Results: Fourteen patients with nontraumatic IH (IVH, 2; SAH, 9; SAH/ICH, 1; ICH/SAH/ IVH, 2) who underwent IC within 7 days from injury were identified; median age: 59 (28-84) years, median admission Glasgow Coma Scale (GCS): 6 (4-9), and median APACHE II: 19.5 (15-28). A control cohort of 6 patients with sTBI was identified; median age: 57.5 (18-80) years, admission GCS: 6.5 (4-8), and APACHE II: 16 (11-31). Sedation was used in 11/14 patients with IH and in 5/6 severe TBI patients. No patient was pharmacologically paralyzed. Median REE was 1810 (1124-2806) and 2238 (1860-2780) kcal/d for the IH and for the sTBI patient cohorts, respectively. Using Wilcoxon signed ranks test, the 2 patient groups were found comparable in regard to baseline clinical variables and disease severity (APACHE II). We did not identify a statistically significant difference in the REE between these 2 cohorts of patients (p = .25). Conclusions: Patients with severe TBI and patients with IH have similar increments in metabolic rate during the initial phase (1 week from onset) of their disease. This information needs to be confirmed in a larger cohort of patients. If reproduced, our results suggest that nontraumatic IH patients are at high risk of inadequate nutrition if their metabolic rate is estimated after conventional nutrition practice. (Journal of Parenteral and Enteral Nutrition 30:71-75, 2006)

Critically ill patients with intracerebral (ICH), intraventricular (IVH) and subarachnoid hemorrhage (SAH) often trigger systemic and intracranial pathophysiologic processes, including elevated intracranial pressure (ICP), reduced cerebral blood flow, decreased tissue oxygen supply, and decreased total systemic blood volume.1 Furthermore, systemic and intracranial inflammatory responses have been identified in patients with intracranial hemorrhage (IH), such as ICH and SAH patients.2-4 These abnormalities are more prevalent in the most severely ill patients, thus increasing their risk for morbidity and mortality. Although guidelines for the management of different forms of IH have been developed in recent years,5 few advances have sufficiently addressed the nutrition needs and metabolic status in this group of potentially critically ill patients.

Hypermetabolism, increased catabolism, and nitrogen loss have been well documented in traumatic events, such as in acute traumatic injury and sepsis.6,7 This response is mediated by a misbalance between modulatory hormones (ie, glucagon, epinephrine, and glucocorticoids), which leads to impaired nitrogen balance and immune function, therefore increasing the risk for poor nutrition and nosocomial infection. Severe traumatic brain injury (sTBI) has been repeatedly associated with an increased metabolic expenditure and negative nitrogen balance, which varies according to the severity of the injury.6 It has been documented that nutrition support appropriate for these increased caloric requirements lessens morbidity and mortality and improves outcome in patients with sTBI.6 Because the metabolic response of IH and other forms of stroke seem to resemble that of moderate to major head injury8'9 and in view of only scarce preestablished criteria to calculate energy requirements in these patients, we tested the hypothesis that the energy requirements in IH patients are underestimated after current clinical methodology. Thus, the objective of this retrospective study was to investigate the metabolic state and energy expenditure of nontraumatic IH patients and to compare them to those of patients with sTBI, a cohort of critically ill patients known to be in a state of increased metabolism.

MATERIALS AND METHODS

Patient Selection

With approval of the Wayne State University investigational review board, medical records of patients admitted to the Neurosciences Critical Care Unit (NCCU) at the Detroit Receiving Hospital from July 2001 to March 2003 after having acute brain injury were screened for study eligibility, review, and for subsequent analysis. Criteria for selection included the following: (1) diagnosis of nontraumatic ICH, SAH, or IVH in the IH patient cohort and admitting diagnosis of sTBI (Glasgow Coma Scale [GCS] score <8 and abnormal head computed tomography [CT] scan) in the control group. Patients in both cohorts required mechanical ventilation; (2) indirect calorimetry (IC) studies performed within the first 7 days after the injury. Exclusion criteria were pregnancy, age <16 years, barbiturate coma, and hemodynamic instability, fraction of inspired oxygen (FIO^sub 2^) ≥60%, positive end-expiratory pressure ≥5 cm H2O, failure to cooperate, agitation, seizure activity, or presence of early spasticity.9 Indirect calorimetry studies were performed in either the fasting or fed state. Fasting state was defined as no nutrition support for at least 6 hours before IC measurement, a frequent scenario within the initial 24 hours of admission to the NCCU. The fed state was defined as continuous enteral nutrition (EN) for at least 4-6 hours before IC measurement.

Nutrition Support

Protein requirements were calculated as 1.5-2.0 g/kg/d of protein.12 This initial delivery of energy provision was further adjusted according to IC results, with caloric goals aimed at matching the measured resting energy expenditure (REE). Degree of hypermetabolism was defined by the following ratio: [measured REE/ Harris Benedict predicted REE] 100.13 Other standard NCCU nutrition practices included the assessment of changes in prealbumin values to determine adequate protein requirement. Nursing staff monitored gastric residuals every 4-6 hours in order to assess gastrointestinal tolerance. Signs of abdominal distention, nausea, and vomiting were also monitored to determine patients' tolerance to nutrition support. Prokinetic agents (enteral/IV metoclopramide, enteral erythromycin) used during the study period were based upon the treating physician's preference.

Equipment

Before initiation of the IC study, calibration was performed every morning according to manufacturer guidelines to ensure accuracy of the oxygen and carbon dioxide sensory equipment. Indirect calorimetry studies were completed when a steady state was achieved, as indicated by the machine (a single 5-minute interval during which average minute VO^sub 2^ and VCO^sub 2^ change by <10% and average RQ changes by <5%). In patients who failed to achieve a steady state, the mean REE and RQ values reported at 30 minutes were used to determine the patient's energy requirements. Also, as per NCCU protocol, the following conditions had to be met before conducting IC studies13,15,16: quiet study environment with no routine nursing intervention or visitors allowed in the room during the IC study, constant FIo^sub 2^, postponing of the IC study for 1- 2 hours if ventilator setting changes were clinically required.

Data Analysis

All study information was entered and recorded in a PowerBook G4 (Apple Computer Inc, Cupertino, CA). Data analysis was performed using SPSS (version 11.0.2 for Mac OS X; SPSS Inc, Chicago, IL). The data collected in this study were deemed to be non-Gaussian in nature; therefore, comparisons between the study groups were performed using nonparametric statistics: Wilcoxon signed ranks test. A p value < .05 was considered statistically significant. Descriptive statistics were used to describe patient clinical characteristics and the specific nutrition variables and endpoints in both patient cohorts. Because of the small sample size of the study cohorts and the known risk of extreme values ("outliers") artificially skewing descriptive statistics in such small patient groups, we decided to use the median to compare the clinical and metabolic variables of the study groups.

TABLE I

Clinical-nutrition characteristics of study cohorts

RESULTS

Demographic and Clinical Characteristics

Fourteen patients with the diagnosis of nontraumatic IH (IVH: 2, SAH: 9, ICH/SAH: 1, SAH/ICH/IVH: 2) and 6 diagnosed with sTBI were enrolled (Table I). Median age of the IH cohort was 59 (28-84) years, median GCS upon admission was 6 (4-9) and median APACHE II score was 19.5 (15-28). The control group of sTBI patients had a median age of 57.5 (18-80) years, median admission GCS of 6.5 (4- 8), and APACHE II score of 17.5 (11-31). Sedation was used in 11/16 (68.8%) patients with IH and in 5/6 (83%) sTBI patients. No patient was pharmacolog\ically paralyzed. In the IH group, 9/14 (64.3%) patients underwent craniotomy for aneurysm clipping. In the sTBI cohort, 4/6 (66.7%) patients had craniotomy performed for subdural hematoma/contusion evacuation. Overall medical management of these IH and sTBI patients followed the standard care recommended by the American Heart Association and the Guidelines for the Management of Severe Head Injury, respectively.5,17-19 In particular, no glucocorticoids were administered to any of the patients enrolled in this study. No evidence of clinical vasospasm was present in any of the SAH patients at the time the IC studies were performed.

Nutrition Characteristics

The median time from injury to IC studies was 2 (1-6) days in the study group (IH) and 2 (1-7) days in the control group (sTBI). The median body mass index (BMI) was 26 (20-39) kg/m^sup 2^ and 25 (20- 33) kg/m^sup 2^ for the IH and sTBI cohorts, respectively. Median time from injury to initiation of EN was 2 (1-7) days in the IH cohort and 1.5 (1-3) days in the sTBI group. Desired enterai caloric supplementation goal was achieved at 2 (1-5) days in the IH cohort and 3 (2-6) days in the sTBI group of patients. Median baseline serum prealbumin concentration was 12 (7-19) g/dL and 12 (4-22) g/ dL in the IH and sTBI cohorts, respectively. The median REE was 1810 (1124-2806) and 2238 (1860-2780) kcal/d in the IH and TBI patients, respectively. The median energy expenditure in the IH group was 126% of BEE (101%-170%), and 147% in the TBI group (114%-176%). Using the Wilcoxon signed ranks test, the 2 patient groups were found comparable with regard to admission GCS (p = .7) and APACHE II score (p = .07). There was no statistically significant difference in REE (p = .2) or in their median increase in BEE between these 2 cohorts of patients (p = .3).

DISCUSSION

We report on the observed increase in REE during the first 7 days after IH in 14 consecutive patients of a similar magnitude to the one observed in a contemporary cohort of 6 sTBI patients. These 2 cohorts had comparable neurologic and acute injury score values, thus indicating that the severity of neurologic and medical illness was similar upon admission.

Early and adequate nutrition intervention improves outcome and lessens morbidity and mortality in stroke and sTBI patients.6'20 Robertson and coworkers21 reported that the severity of neurologic injury damage after sTBI could have a profound effect on REE. In their report, patients with GSC of 4 or 5 had the highest REE levels (168% 53% of that expected), whereas those with GSC of 6 or 7 had lower levels (129% 31% of that expected). Therefore, the thorough assessment of the actual caloric requirements becomes imperative in order to favorably modify in-hospital morbidity/ mortality and possibly neurologic outcomes after acute brain injury. Two widely adopted methods for determining caloric needs are the application formulas to predict caloric requirements, such as the Harris- Benedict equation, and the measured energy expenditure through IC. Current clinical experience seems to support that due to an extremely high variability in the energy expenditure and metabolic response among critically ill patients, routine use of IC should be preferred in order to minimize the risk of under- or overfeeding critically ill patients.13,15,16 The relevance of such a critical aspect in the care of the critically ill patient was underlined when Sunderland and Heilbrun22 demonstrated in a group of sTBI patients that the application of predicting formulas to estimate caloric requirements led to critical discrepancies when matched against IC studies. Furthermore, the actual caloric requirements in other forms of acute brain injury (eg, ischemic and hemorrhagic stroke) are understudied, at best.8

Kasuya and coworkers9 reported that SAH patients treated with early craniotomy for aneurysm clipping experienced a profound increase in metabolic rate, particularly among the most severely ill. Although their investigation excluded patients with surgical complications and those on ventilators, our data share similar conclusions as reported by these authors. The authors reported that percent increase in REE was attributed to concomitant conditions such as cerebral vasospasm. Thus, it seems conceivable that unless patients with IH and reduced level of consciousness are deemed as hypermetabolic as sTBI patients, their caloric requirements within the first week of onset of injury are at high risk of being underestimated. Further prospective studies should be performed to confirm these initial observations. Also, the interaction between inflammatory markers, amount of intraparenchymal, intraventricular, and subarachnoid blood, and the increase in metabolic rate should be studied in these patients.

Limitations of the Study

Although consistent with similar previous observations, the results of our study should be used as hypothesis-generating at this early stage. The following are factors that could limit the generalizability of our observations:

(1) The chosen time interval of 7 days after the ictus limited the inclusion of IC studies performed beyond that time point. Future studies of this nature should include larger study cohorts and prospective IC monitoring in IH patients.

(2) We studied all patients with IH, including SAH, IVH, and ICH. It is conceivable that different forms of IH could have different levels of hypermetabolic response to the initial injury. Future studies should be powered enough to allow subgroup analysis.

(3) A careful analysis between the amount of blood on CT scan in different central nervous system compartments and energy requirements was not performed due to the small sample size of our study cohorts.

(4) Correlation between inflammatory markers in IH patients and the degree of hypermetabolism these patients experience was not carried out due to our small sample size. This form of analysis could help us understand the mechanisms behind the increased caloric requirements after IH.

(5) Although 2 important variables capable of modifying caloric requirements such as craniotomy and sedation were similar between the study cohorts, a prospective study design aimed at balancing these variables and others should be performed in order to strengthen the results of future studies similar to ours.

CONCLUSIONS

There are few data that sufficiently address the nutrition needs of patients with nontraumatic IH. According to the results of our study, we postulate that the metabolic profile of IH patients may be similar to that of sTBI patients, at least during the first week after the ictus. Because complications resulting from inadequate nutrition support can negatively modify the outcome of critically ill patients, it seems that IC monitoring is warranted in this subgroup of critically injured neurologic patients until larger studies can better define the actual magnitude of increased caloric requirements in this and other subsets of acute stroke victims.

ACKNOWLEDGMENTS

The authors thank Nichol McBee, MPH, for her expert statistical assistance during the data management and analysis in this manuscript.

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Dema Halasa Esper, MS, RD, CNSD*; William M. Coplin, MD[dagger][double dagger]; and J. Ricardo Carhuapoma, MD, FAHA||

From the * Department of Nutrition, Detroit Receiving Hospital, Detroit, Michigan; [dagger] Department of Neurology and [double dagger] Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, Michigan; and the Departments of Neurology, Neurological Surgery, and || Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland

Received for publication January 7, 2005.

Accepted for publication November 7, 2005.

Correspondence: J. Ricardo Carhuapoma, MD, FAHA, Division of Neurosciences Critical Care, The Johns Hopkins Hospital, 600 North Wolfe Street/Meyer 8-140, Baltimore, MD 21287. Electronic mail may be sent to jcarhual@jhmi.edu.

Originally presented at Nutrition Week during the Scientific Poster Presentations, Feb. 2003, San Antonio, Texas.

Copyright American Society for Parenteral and Enteral Nutrition Mar/ Apr 2006

Source: JPEN, Journal of Parenteral and Enteral Nutrition

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