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11. Ilkin Cankayali 6 Turkish Journal of Trauma & Emergency Surgery Ulus Travma Acil Cerrahi Derg 2009;15(1):39-44 Original Article Klinik Çal›flma Thermogenic and metabolic response to amino acid solution in brain-dead patients Beyin ölümü hastalar›nda aminoasit solüsyonlar›na metabolik ve termojenik yan›t ‹lkin ÇANKAYALI, Kubilay DEM‹RA⁄, Seden KOCABAfi, Ali Reflat MORAL BACKGROUND AMAÇ There is a strong correlation between amino acid infusion and Aminoasit infüzyonu ile enerji tüketimi ve termojenezdeki increase in energy expenditure and thermogenesis. In this art›fl aras›nda güçlü bir ilinti vard›r. Bu çal›flmada, yo¤un study, the effects of amino acid solutions on thermogenesis bak›mda beyin ölümü tan›s› alm›fl hastalarda termojenez ve and energy expenditure were investigated in intensive care enerji tüketimindeki art›fla aminoasit solüsyonlar›n›n etkisi patients who were diagnosed as brain death. araflt›r›ld›. METHODS GEREÇ VE YÖNTEM Twenty-six brain-dead patients were included in the study. Çal›flmaya 26 beyin ölümü olgusu dahil edildi. Hastalara The patients received a 4 h infusion of standard amino acid dört saat boyunca aminoasit solüsyonu verildi. ‹stirahat solution. Energy expenditure was measured by indirect enerji tüketimleri endirekt kalorimetrik yöntemle ölçüldü. calorimetric method. A N O VA and Bonferroni tests were used ‹statistiksel analizler için AN O VA ve Bonferroni testleri kul- for statistical analysis. lan›ld›. RESULTS BULGULAR The predicted energy expenditure (PEE) values were higher Yirmi dört hastada, tahmin edilen (hesaplanan) enerji tüketimi than the resting energy expenditure (REE) values in 24 de¤erleri (TET) ölçülen istirahat enerji tüketimi (‹ET) de¤er- patients. The mean REE/PEE value in all patients indicated lerinden daha yüksek bulundu. TET ile karfl›laflt›r›ld›¤›nda, that there was a 29% decrease in REE when compared to PEE. tüm hastalar›n ortalama ‹ET/TET de¤erleri, ‹ET’de %29 de¤e- Body temperature and energy expenditure values were not rinde bir azalma oldu¤unu gösterdi. Vücut ›s›s› ve enerji tüke- increased during the parenteral infusion of amino acid solu- timi de¤erleri parenteral aminoasit infüzyonu s›ras›nda artma- tions. There was no statistically significant difference between d›. Çal›flma boyunca herhangi bir zamanda, metabolik ölçüm- mean metabolic measurements and basal values at any time ler ve bafllang›ç de¤erleri aras›nda istatistiksel herhangi bir interval during the study period. fark bulunmad›. CONCLUSION SONUÇ We conclude that the stimulatory effect of amino acid solution Aminoasit solüsyonlar›n›n enerji tüketimi ve termojeneze on energy expenditure and thermogenesis is abolished in olan uyar›c› etkilerinin beyin ölümü olgular›nda görülmedi¤i brain-dead patients. This result may indicate a possible central (yok oldu¤u) kan›s›na var›ld›. Bu sonuç, enerji tüketimi ve ter- pathway responsible for the increase in energy expenditure mojenezdeki art›fltan merkezi yollar›n sorumlu olabilece¤ini and thermogenesis. göstermektedir. Key Words: Amino acid; brain death; e n e rgy expenditure; Anahtar Sözcükler: Amino asit; beyin ölümü; enerji tüketimi; termo- thermogenesis. jenez. Department of Anesthesiology and Intensive Care Unit, Ege Üniversitesi T›p Fakültesi, Anesteziyoloji ve Reanimasyon Ege University Faculty of Medicine, Izmir, Turkey. Anabilim Dal›, ‹zmir. Correspondence (‹letiflim): ‹lkin Çankayal›, M.D. Department of Anesthesiology and ICU, Ege University School of Medicine, 35100 Bornova, ‹z m i r , T u r k e y . Tel: +090 - 232 - 390 21 42 Fax ( F ak s ): +090 - 2 3 2 - 339 7 6 8 7 e -m a i l ( e -p o s t a) : i l k i n . c a n k a y a l i @ e g e . e d u . t r 39 Ulus Travma Acil Cerrahi Derg Possible protein energy malnutrition and related according to the diagnosis and clinical stiation of the functional disorders may only be prevented by opti- patient (Table 1). The appropriate exogenous calories mal nutritional support and positive nitrogen bal- were replaced, using a standard enteral nutrition prod- ance. Amino acid (AA) solutions are one of the com- uct (Osmolite, Abbott Laboratories, North Chicago, ponents of parenteral nutrition for multidisciplinary IL, USA) via nasogastric tube. Enteral nutrition was intensive care patients. There is a strong correlation given continuously using an enteral infusion pump between AA infusion and increase in energy expen- (Kangaroo 624 Enteral Feeding Pump, Ty c o diture (EE) and thermogenesis.[1-4] It was reported Healthcare Group LP, Mansfield, MA, USA) before that AA infusion-related EE increase depends on the and during the study according to the PEE. Patients composition of the AA solution, as well as the clini- were randomly assigned to receive a 4-hour (h) infu- [2,4-6] cal condition of the patient. This hypothesis is sion of 0.4 g/kg protein as A A solution. Brain-dead also supported by a study indicating that there was patients received standard A A solution (FreAmine an increase in thermogenesis and EE during the par- 8.5%, Eczac›bafl ›- B a x t e r, Istanbul, Turkey) using an enteral infusion of the AA solutions in unconscious [4] infusion pump (Life Care Pump - Model 5000, intensive care patients. The mechanism of this Abbott Laboratories, North Chicago, IL, USA). T h e increase has not been completely explained. In spite composition of the A A solutions infused is presented of this knowledge, the effects of AA solutions in in Table 2. Enteral nutrition was continued during the brain death, in which there is irreversible destruction 4-h A A infusion period without subtracting the addi- of the brain with the resulting total absence of all tional energy derived from the A A s o l u t i o n . cortical and brainstem functions, have not been investigated before. Table 1. Etiology of the brain-dead patients In this study, the effects of AA solutions on thermogenesis and EE were investigated in intensive Patient No Diagnosis care patients who were diagnosed as brain death. 1 1 + 2 2 1 + 2 MATERIALS AND METHODS 3 3 Patients 4 4 After obtaining Institutional Ethics Committee 5 5 approval and written informed consent, the study 6 1 was carried out at the Department of Anesthesiology 7 6 8 1 + 7 and Intensive Care Unit, Ege University Faculty of 9 8 Medicine. A total of 26 mechanically ventilated 10 9 patients who were diagnosed as brain death were 11 1 included in this prospective study. Brain death was 12 5 determined according to the criteria of the Ministry 13 1 + 10 of Health and the protocol of the university hospital. 14 5 All patients included in this study were hemodynam- 15 1 ically and metabolically stable and had normal labo- 16 1 ratory values. 17 8 18 11 Study design 19 12 + 7 Predicted energy expenditure (PEE) was calculat- 20 11 ed using the Harris-Benedict (HB) equation for all 21 1 patients. PEE was calculated as follows: Male PEE- 22 1 HB (kcal/day) = 66.473 + (13.7516 * W) + (5.0033 23 1 24 1 * H) - (6.755 * A); Female PEE-HB (kcal/day) = 25 10 + 12 655.0955 + (9.5634 * W) + (1.8496 * H) - (4.6756 * 26 1 A). For both equations, W is body weight in kilo- Subarachnoid hemorrhage 1; Intracerebral hemorrhage 2; Cranial aneurysm 3; grams, H is height in centimeters and A is age in Cardiopulmonary resuscitation, hypoxic encephalopathy 4; Brain tumor 5; Intracerebral hematoma 6; Skull fracture 7; Intraventricular hemorrhage 8; years. PEE was then multiplied by an activity factor Polytrauma (cerebral infarction) 9; Subdural hematoma 10; Cranial arteriove- of 1.2 (bed rest) and corresponding stress factor nous malformations 11; Epidural hematoma 12. 40 Ocak - January 2009 Thermogenic and metabolic response to amino acid solution in brain-dead patients Table 2. The composition of the amino acid solution (Datex-Engstrom Division, Instrumentarium Corp, FreAmine 8.5% Finland) was used to measure the resting energy expenditure (REE), oxygen consumption (VO2) and Essential AA carbon dioxide production (VCO2). The Deltatrac II L- Isoleucine 0.59 g Metabolic Monitor is an open system device that L- Leucine 0.77 g L- Valine 0.56 g measures VO2 and VCO2 in both mechanically and Total amount of BCAA 1.92 g spontaneously breathing patients. This system uses a L- Lysine 0.62 g fast differential paramagnetic oxygen analyzer to L- Methionine 0.45 g measure a different signal between inspired and L- Threonine 0.34 g expired gases, an infrared CO2 analyzer to measure L- Tryptophan 0.13 g the CO2 in the inspired and expired gases, and a gas L- Phenylalanine 0.48 g dilution system to measure flow. This monitor has Non-essential AA L- Alanine 0.60 g been previously validated and tested in vitro for [7] L- Arginine 0.81 g accuracy and reproducibility. L- Histidine 0.24 g Before the measurements, the O2 and CO2 ana- L- Proline 0.95 g lyzers were calibrated with a precise mixture con- L- Serine 0.50 g Glycine 1.19 g taining 95% oxygen and 5% CO2 (Deltatrac High- Accuracy Calibration Gas, Datex Instrumentation, L-Cysteine HCl H2O <0.02 g Sodium bisulfide NF <0.10 g Helsinki, Finland) according to the manufacturer’s Phosphoric acid 0115 g guidelines. Basal metabolic data (REE, VO2, VCO2 pH 6.5 and respiratory quotient [RQ]) were measured dur- Osmolarity 810 mOsm/L ing 20 min before the start of AA infusion. Then Sodium 10 mEq/L metabolic data were recorded every 30 min during Phosphate 20 mEq/L Chloride <3 the 4-h infusion period and at 30, 60, 120 and 180 Acetate 72 min after the infusion ended. We recorded the data from the Metabolic Monitor by using the long-trend BCAA: Branched-chain amino acid.
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