Resting energy expenditure in brain death

Resting energy expenditure in brain death free pdf ebook was written by on September 01, 1999 consist of 7 page(s). The pdf file is provided by www.rtjournalonline.com and available on pdfpedia since May 16, 2011.

in brain dead patients and to inves- tigate the hypothesis that the reduc- tion in ree of a tertiary…...

x
send send what is readshare?


Thank you for helping us grow by simply clicking on facebook like and google +1 button below ^^

Resting energy expenditure in brain death pdf




Read
: 1356
Download
: 1
Uploaded
: May 16, 2011
Category
Author
: anonymous
Total Page(s)
: 7
Resting energy expenditure in brain death - page 1
Intensive Care Med (1999) 25: 970±976 Ó Springer-Verlag 1999 O R I GI N A L M. Bitzani D. Matamis V. Nalbandi A. Vakalos A. Karasakalides D. Riggos Resting energy expenditure in brain death Received: 7 October 1998 Accepted: 23 June 1999 M. Bitzani ( ) ´ D. Matamis ´ V. Nalbandi ´ A. Vakalos ´ A. Karasakalides ´ D. Riggos Intensive Care Unit, ªG. Papanikolaouº General Hospital, Exohi, Thessaloniki, Greece e-mail millybi@rincewind.biotrast.gr Tel. + 30(31)31 51 83 Fax + 30(31)35 09 37 ) Abstract Objective: To evaluate resting energy expenditure (REE) in brain dead patients and to inves- tigate the hypothesis that the reduc- tion in REE results from a decrease in cerebral blood flow. Design: Prospective, open labeled, control study. Setting: General intensive care unit of a tertiary referral teaching hospi- tal. Patients: 30 critically ill patients with isolated head injury divided in two groups: group 1 patients (n = 10) with a Glasgow Coma Scale (GCS) score of 4 to 8 and group 2 patients (n = 20), in whom the final outcome was brain death (GCS = 3). Group 2 patients were divided into two sub- groups: Group 2 a (n = 11) were ad- mitted as brain dead (GCS = 3) and group 2 b (n = 9) were admitted with a GCS > 3 and progressed to brain death. Interventions: Clinical and instru- mental, using transcranial Doppler sonography (TCD), diagnosis of brain death. Cerebral blood flow studies of the middle cerebral artery bilaterally by bidimensional TCD and measurement of REE using in- direct calorimetry. Measurements and results: Measure- ments of REE and TCD studies were performed simultaneously on admis- sion and after hemodynamic and neurologic stabilization. In cases with progressive neurologic deterio- ration, serial measurements were performed REE values were ex- pressed as percentage of basal meta- bolic rate (%BMR), which were estimated according to each patient's gender, age, height, and weight. Group 1 patients, had normal TCD patterns throughout their hospital- ization and their REE value was 21  11 % higher than BMR. Group 2 patients demonstrated TCD patterns compatible with brain death and their REE value was 24.5  11 % lower than BMR (p < 0.01). Group 2 a patients, who were admitted as brain dead and re- mained brain dead, had REE values 30  11 % lower than BMR (p < 0.01). Group 2 b patients, who were not brain dead on admission but progressed to brain death, in serial measurements revealed a significant relationship between REE and TCD findings (R = ±0.77, p < 0.0001). In this subgroup of patients, with multi- ple regression analysis a significant relationship was found only between REE and the TCD pattern, but not with body temperature. Conclusions: In brain dead patients, REE decreases to values lower than BMR. This can be attributed to the cessation of cerebral blood flow and consequently cerebral metabolism and not to hypothermia. Key words Brain death ´ Head injury ´ Resting energy expenditure ´ Basal metabolic rate ´ Transcranial Doppler sonography
You're reading the first 7 out of 7 pages of this docs, please download or login to readmore.
Resting energy expenditure in brain death - page 2
971 Introduction The diagnosis of brain death is based on a series of clin- ical as well as instrumental criteria. The clinical criteria rely on the findings of absent brain stem reflexes and a positive apnea test. Besides the clinical criteria, some authors advocate an isoelectric electroencephalogram [1]. However, in cases of hypothermia or overdose with central nervous system depressant drugs, these criteria are unreliable and considered insufficient. Therefore, other confirmatory tests are required to establish accu- rately the diagnosis of brain death, tests that can either document the absence of neuronal activity or the ab- sence of cerebral blood flow or perfusion. Abolition of neuronal activity in brain death can be documented with brain stem auditory evoked responses [2±4]. The absence of cerebral blood flow/perfusion can be docu- mented via selective cerebral angiography, radionuclide computed tomography (CT), xenon CT measurements, radioisotope bolus technique, as well as transcranial doppler sonography (TCD), [5±8]. In certain countries, such as Norway and Switzerland, clinical criteria alone are considered insufficient to diagnose brain death and therefore cerebral angiography is required as the final confirmatory test, especially if these patients are consid- ered for organ procurement [1, 9]. Basal metabolic rate (BMR) represents the metabol- ic rate of the patient while awake, at rest, without physi- cal or psychological stress, and at least 12 h after the last meal. It is dependent on age, weight, height, and sex. Resting energy expenditure (REE) represents the met- abolic rate of the patient while awake, at rest, and in the postabsorptive state. Various disease processes in- fluence the REE, modifying the patient's metabolic re- quirements. Traumatic brain injury induces a hypermet- abolic-hypercatabolic state, with an increase in REE up to 125±165 % of the predicted BMR [10±12]. On the contrary, several investigators have reported a reduc- tion in the REE in brain dead patients [13±16]. This re- duction in REE is considered by some to be due to hy- pothermia [13, 16]. We designed this study in order to investigate whether, once brain death is established, REE is indeed reduced to values lower than BMR, and whether this reduction is mainly due to decreased cere- bral blood flow, and consequently decreased cerebral metabolism, and not to hypothermia. were divided into two groups according to their initial Glasgow Coma Scale score (GCS), and the evolution of their neurologic state and TCD pattern during hospitalization. Group 1 consisted of 10 patients with severe head injury (GCS 4±8), clinically con- firmed neurologic activity, and normal TCD findings after hemo- dynamic stabilization. Group 2 consisted of 20 patients in whom the final outcome was brain death. This group was further divided into two subgroups. Group 2 a (n = 11) consisted of patients who, on admission, met the clinical criteria and TCD findings of brain death (GCS = 3) as well as after 24 h of resuscitation. Group 2 b (n = 9) consisted of patients who, on admission, had a GCS of 4±8; however, despite medical and/or surgical treatment, they pro- gressed to brain death. Medical treatment in both groups consisted of hemodynamic support with fluid administration and inotropic drugs to preserve the cerebral perfusion pressure, treatment of in- tracranial hypertension with mannitol and/or hypertonic saline (7.5 %), and treatment of hyperthermia with cooling blankets. Mild hypothermia ³ 35 C presenting on admission was considered therapeutic and not treated, since hypothermia decreases the cere- bral metabolic needs. Midazolam and fentanyl were administered to groups 1 and 2 b to keep them sedated while on the ventilator. Group 2 a was neurologically unresponsive on admission and therefore did not require sedation. In all patients, the following parameters were continuously monitored: heart rate, invasive blood pressure, arterial oxygen sat- uration via pulse oximetry, central body temperature, and intracra- nial pressure (ICP) where applicable. Postcraniectomy patients did not receive an ICP device because the validity of the measure- ments are questionable. Central body temperature was recorded with a temperature probe inserted into the esophagus or via the thermistor of the pulmonary artery catheter which was inserted in some patients with hemodynamic instability for guidance of hemo- dynamic support. The diagnosis of brain death was established clinically (based on absent brain stem reflexes and a positive apnea test) as well as on their TCD flow patterns (see below). These patients had no ma- jor metabolic disorder, no major hypothermia (tempera- ture ³ 35 C), and were hemodynamically stable for at least 24 h and after cessation of sedation for at least 48 h. Methods In all patients, estimation of BMR and measurements of REE and cerebral blood flow velocities in the middle cerebral artery (MCA) were performed as described below. BMR BMR was estimated according to the Harris-Benedict equation [17]. Men: BMR(kcal) = 66.5 + (13.75 ´ weight) + (5.003 ´ height) ± (6.775 ´ age). Women: BMR (kcal) = 655.1 + (9.63 ´ weight) + (1.50 ´ height)±(4.76 ´ age) REE REE was measured by indirect calorimetry using the Deltatrac II metabolic computer (Datex, Finland) connected to the ventilator. This method calculates REE based on the measurement of oxygen consumption (VO 2 ) and carbondioxide production (VCO 2 ) in the expired gases, according to the Weir equation [18]. REE = (3.14 ´ VO 2 ) + (1.106 ´ VCO 2 ) ´ 1.44 Patients and methods Patients We included 30 patients admitted to the intensive care unit of our institution over a period of 2 years with the diagnosis of isolated traumatic brain injury. All patients were under controlled mechan- ical ventilation in order to maintain normal arterial carbondioxide tension (PaCO 2 ) and arterial oxygen tension (PaO 2 ). Patients
Resting energy expenditure in brain death - page 3
972 a c b Fig. 1 From top to the bottom: TCD patterns showing a progres- sive decrease in cerebral blood flow. a Normal pattern, b ischemic pattern, c flow reversal, d early systolic spikes d Patients with no TCD signal on admission were excluded from the study, since this absence cannot be attributed to the inability to obtain an acoustic window or loss of cerebral blood flow. All groups had one set of TCD and REE measurements on ad- mission, which were not taken into account for statistical analysis because on admission patients were hemodynamicaly and neuro- logically unstable; however, they were used to guide medical treat- ment. Group 1 patients had a second set of measurements within 48 h (10 patients:10 paired REE and TCD measurements, Ta- ble 1), once hemodynamic stabilization was obtained. Group 2 a patients also had a second set of measurements within 48 h (11 pa- tients: 11 paired REE and TCD measurements, Table 2), once brain death was confirmed (based on clinical and TCD criteria). We chose these sets of measurements for statistical analysis be- cause they were performed after hemodynamic and neurologic sta- bilization and before other factors, like nosocomial infection, could influence REE. Group 2 b patients, despite medical and/or surgical treatment, clinically deteriorated from an initial GCS of 4±8 to brain death. These patients had multiple REE and TCD measurements (once on admission, after hemodynamic stabiliza- tion, and after deterioration of the neurologic status). Of these multiple measurements, we used for statistical analysis those which corresponded to the TCD patterns compatible with a graded re- duction in cerebral blood flow. The TCD patterns which we took into account were: (1) normal pattern (pulsatility index: 0.8 < PI < 1.6), (2) high resistance pattern (PI > 1.6), (3) diastolic flow reversal pattern, and (4) early systolic spikes or absence of flow signal (Fig. 1). The total number of paired REE and TCD measurements in this group (2 b) was 34 because of two missing REE data (Table 4). Before each REE measurement, the metabolic computer was calibrated for 30 min. After this calibration period, 28 measure- ments of VO 2 and VCO 2 were performed at 1 min intervals for each patient using the formula above; we obtained 28 serial mea- surements of REE. The mean value of these 28 serial measure- ments represents the REE for each patient. The overall standard deviation in REE measurements for the entire series of patients was 4.29  1.8 % (Table 2). Each patient's calculated REE value was compared to his other BMR and expressed as a percentage of BMR (% BMR). TCD TCD was performed simultaneously with REE measurements over a period of 30 min using a 2-MHZ 2D ultrasound probe (Computer Sonography Accuson 128 XP/10 c, USA). MCAs were identified bilaterally with the two-dimensional color-flow map- ping, and pulse-wave Doppler signals with angle correction ob- tained using the transtemporal approach and insonating to a depth of between 40 and 60 mm. Early systolic spikes, and loss of a preex- isting TCD signal are findings which were considered compatible with brain death if they persisted for more than 24 h (Fig. 1). These findings are typical when the ICP exceeds the arterial blood pres- sure, resulting in cessation of cerebral blood flow and perfusion.
Resting energy expenditure in brain death - page 4
973 Table 1 Demographic and measurement data for group 1 (non-brain dead) patients. Values are means Group No 1 Patient No. 1 2 3 4 5 6 7 8 9 10 Mean ± SD Sex M M M F M M M F M M Age (years) 25 31 45 45 18 23 69 56 72 66 45 ± 20 BMR 1790 1790 1530 1760 1880 1930 1610 1460 1380 1600 1673 ± 184 REE 2420 2100 1620 2130 2400 2540 2240 1580 1610 1870 2051 ± 361 REE (% BMR) 1.35 1.17 1.06 1.21 1.27 1.31 1.39 1.08 1.16 1.17 1.21 ± 0.11 % of increase 35.2 17.3 6 21 27.6 31.6 39 8.2 16.6 16.9 21 ± 11 Temperature (C) 39 37.5 38 39.3 36 38.6 37.9 38 39 38.5 38.18 ± 0.95 It is well recognized that there is no absolute correlation be- tween cerebral flow velocities (measured with TCD) and cerebral blood flow. This lack of absolute correlation can be attributed to the possible changes in cerebral blood vessel diameter or changes in PaCO 2 . In our study, PaCO 2 was kept within the normal range during the TCD measurements. In addition, when there was dete- rioration of the normal TCD pattern (high resistance, flow rever- sal, or absence of flow), we assumed this to be due to a relative de- crease in cerebral blood flow. Mean velocity, pulsatility index, and other TCD findings were not used for statistical analysis, because these findings are considered meaningless when the TCD pattern shows diastolic flow reversal or early systolic spikes. Statistics Data were expressed as mean  SD. The Kolmogorov-Smirnov Goodness of Fit test was used for normal distribution pattern anal- ysis of age, REE, BMR, and temperature for all patients as well as between group 1 and 2, and between group 2 a and 2 b. Data analy- sis between groups 1, 2, 2 a and 2 b was performed using the one way analysis of variance with the Duncan test. One-way ANOVA, simple regression with the Spearman test for nonparametric data, and multiple stepwise regression analysis were also used for the se- rial measurements of temperature, REE, and TCD patterns in pa- tients in group 2 b. A p value < 0.05 was considered significant. For statistical analysis, the SPSS for windows (Student's version) software was used. Results The Kolmogorov-Smirnov Goodness of Fit test indicat- ed a normal distribution pattern for all variables. Ta- ble 1 summarizes the individual data and the mean val- ues  standard deviation for age, temperature, BMR, REE, and REE expressed as a percentage of BMR in group 1. Table 2 summarizes these data for group 2 as well as for subgroups 2 a and 2 b. There was no significant difference in age or BMR between group 1 and group 2 (45  20 vs 47.8  18 years, and 1673  184 vs 1561  206 kcal, respectively) (Ta- ble 3). Group 1 patients had a higher body temperature than those in group 2. (38.2  0.9 vs 36.5  1.37 C, p < 0.01). Group 2 a had a significantly lower temperature than groups 1 and 2 b (35.8  1.1 vs 37.2  1.2 C and 38.18  0.95 C, respectively, p < 0.01). Furthermore, REE values were higher in group 1 than in group 2 pa- tients (2051  361 vs 1170  193 kcal/day, or 121.5  11 vs 75  11 % of BMR (p < 0.01) (Table 3). All group 1 patients had normal TCD patterns of the MCA bilaterally, on admission, and during their hospi- talization. Among group 2 patients, 11 (group 2 a) had on admission a TCD pattern compatible with brain death and 9 (group 2 b) were admitted with a normal TCD pattern but became brain dead during hospitaliza- tion. Serial TCD studies in group 2 b patients revealed TCD patterns compatible with progressive deteriora- tion of cerebral perfusion. In this last group of patients we observed a significant decrease in REE (p < 0.01, ANOVA) as the TCD pattern deteriorated from normal to early systolic spikes or no flow (Table 4). In addition, a highly significant correlation was found between REE values (expressed as % BMR) and TCD findings (R = ±0.77, p < 0.0001) (Fig. 2). Concerning the relation- ship between TCD pattern, REE, and temperature, multiple stepwise regression analysis revealed a strong relationship only between the worsening of the TCD pattern and the decrease in REE (multiple R = 0.77, F = 46.5, p < 0.01). On the contrary, no relationship was found between TCD patterns and temperature, or REE and temperature (Table 4). Discussion The metabolic changes accompanying brain death have not been studied extensively. Pevsner et al. [14], were the first to indicate that cerebral metabolism decreases in brain death and suggested that this could be a reliable prognostic finding. Subsequent studies reported that in brain death REE is decreased to levels ranging from 50
Resting energy expenditure in brain death - page 5
974 Table 2 Demographic and measurement data for group 2 (brain dead) patients. Values are means Patient No. Group 2 a 1 2 3 4 5 6 7 8 9 10 11 Mean ± SD (n = 11) Group 2 b 12 13 14 15 16 17 18 19 20 Mean ± SD (n = 9) Mean ± SD (n = 20) M M F F M M M M M Sex Age (years) 37 47 15 43 73 64 32 60 56 48 65 49 ± 16 17 32 61 34 17 68 56 66 65 46.2 ± 21 47.8 ± 18 BMR REE REE SD (%) 3.6 4.4 4.6 6.2 3.7 3.7 4.9 2.4 1.5 2.2 2.3 3.5 ± 1.4 7.5 8 2.3 4.4 3.9 4 5 3.7 7.5 5.14 ± 2 4.29 ± 1.8 REE (% BMR) 0.61 0.502 0.605 0.689 0.798 0.727 0.735 0.761 0.714 0.926 0.618 0.7 ± 0.1 0.789 0.814 0.857 0.935 0.768 0.746 0.893 0.673 0.93 0.82 ± 0.08 0.75 ± 0.11 % of decrease 39 49.7 39.4 31 20.1 27.2 26.5 23.8 28.5 7.33 38.1 30 ± 11 21 18.5 14.2 6.5 23.1 25.3 10.6 32.6 6.94 17.68 ± 8.8 24.5 ± 11.8 Temperature (C) 35 35 35.8 37.5 35 36 35 38 35.2 37 35 35.8 ± 1.1 38.6 37.8 35.7 35.6 36 37.5 39.3 37.3 37.8 37.2 ± 1.2 36.5 ± 1.37 M M M M M F F M F F M 1820 1910 1420 1450 1440 1360 1510 1720 1330 1500 1600 1550 ± 190 1850 1830 1330 1230 1860 1660 1500 1470 1440 1574 ± 235 1561 ± 206 1110 960 860 1000 1150 990 1110 1310 950 1390 990 1074 ± 160 1460 1490 1140 1150 1430 1240 1340 990 1340 1286 ± 168 1170 ± 193 Table 3 Statistical analysis by one-way ANOVA with the Duncan test between groups 1, 2, 2 a, and 2 b. Values are means ± SD Group 1 Age (years) BMR REE REE (% BMR) Temperature (C) 45 ± 20 1673 ± 184 2051 ± 361 1.21 ± 0.11 38.18 ± 0.95 Group 2 47.8 ± 18 1561 ± 206 1170 ± 193* 0.75 ± 0.11* 36.5 ± 1.37* Group 2 a 49 ± 17 1550 ± 191 1074 ± 160* 0.7 ± 0.1* 35.8 ± 1.1* Group 2 b 46.2 ± 21 1574 ± 235 1286 ± 168* $ 0.82 ± 0.08* $ 37.2 ± 1.2* $ NS NS p < 0.01 p < 0.01 p < 0.01 * Significant differences between groups 2, 2 a, 2 b and group 1 $ Significant difference between groups 2 a and 2 b to 80 % of BMR [13, 15, 16, 19]. After head injury, REE usually increases [10, 11], and this is mainly attributed to high levels of endogenous catecholamines. However, the decrease in REE during brain death remains un- clear. Few investigators have addressed this issue, and the decrease in REE has been attributed to hypother- mia [13, 16]. Dominguez-Roldan et al. [13] observed a significant correlation between REE and temperature, thus emphasizing the influence of core temperature on REE values. Body temperature is considered normal in the range 36.5±37.5 C. Usually within 24 h after head injury, the body temperature increases, probably as a result of a change in the hypothalamic thermoregulatory set-point, mediated by interleukin-1, a product of macrophages af- ter tissue damage [20]. This was also the case in our pati- ents in group 1 in whom the temperature increased to 38.1  0.95. There is a positive correlation between tem- perature and REE in non-brain dead, head injured pati- ents [20]. Sztark et al. [21] demonstrated a 10 % increase in REE per 1 C increase in body temperature. An in- crease in REE up to 21  11 % was also found in our group 1 patients, and this increase was in accordance with the increase in body temperature up to 38.18  0.95 C. Although the effect of increased tem- perature on REE is proven, there are conflicting data
Resting energy expenditure in brain death - page 6
975 Table 4 Statistical analysis of group 2 b patients by one-way ANOVA with Duncan test between REE values (expressed as % of BMR) and temperature, as TCD pattern worsens from the normal to now-flow conditions Patient No. TCD 1: Normal pattern REE (% BMR) Temp. (C) 12 13 14 15 16 17 18 19 20 Mean ± SD Missing 31 Ÿ1 16 Missing 14 15 18 65 22.5 ± 20 Missing 36.8 35 36 Missing 37.5 38.8 37.9 39 37.2 ± 1.4 TCD 2: Ischemic pattern REE (% BMR) Temp. (C) Ÿ4 8 Ÿ1 8 Ÿ1 2 Ÿ4 12 35 6.1 ± 12.2* 38 36.6 35.7 35.8 36 37.3 38 37.8 39 37.1 ± 1.1 TCD 3: Reverse flow REE (% BMR) Temp. (C) Ÿ 16 ± 10 Ÿ4 Ÿ1 Ÿ8 Ÿ 12 Ÿ 15 Ÿ 16 4 Ÿ 8.6 ± 7* $ 38.6 35.8 36 35.8 35.8 37 36.2 37.3 37.8 36.7 ± 1 TCD 4: Systolic spikes or absence of flow REE (% BMR) Ÿ 22 Ÿ 18.5 Ÿ 14.2 Ÿ7 Ÿ 23 Ÿ 25 Ÿ 11 Ÿ 33 Ÿ7 Ÿ 17.68 ± 8.8* $ Temp. (C) 38.6 37.8 35.7 35.6 36 37.5 39.3 37.3 37.8 37.2 ± 1.2 * Significant differences in REE between normal TCD pattern and the other TCD patterns (p < 0.01) $ differences between TCD patterns 3 and 2 as well as 4 and 2 (p < 0.05) Fig. 2 Individual REE changes as TCD pattern deteriorates from normal to no-flow pattern. Letters A±I represent the 9 patients in group 2 b reported in Table 4. The equation represents the linear correlation between TCD pattern and REE concerning the influence of hypothermia. Some investi- gators have demonstrated a decrease in cerebral meta- bolic rate of oxygen and REE during hypothermia [20, 22±24], while others have found an increase in REE and suggested that this may be due to either catechol- amine-mediated non-shivering thermogenesis or hypo- thalamus-mediated shivering thermogenesis [24]. A sig- nificant but transient increase in catecholamine levels has been demonstrated during brain death [25]. Howev- er, it remains unknown if catecholamine-mediated non- shivering thermogenesis ceases immediately after the onset of brain death. Hypothalamic, mesencephalic, and bulbar failure result in cessation of central tempera- ture regulation, leading to poikilothermy [26]. This could possibly explain the low temperatures observed in most of the brain dead patients. In the context of our results, as well as in the above mentioned reports, we believe that hypothermia must be considered very care- fully as being the major determinant of a decrease in REE during brain death. In our study, in 20 brain dead patients (group 2) we found that REE decreases to a mean value of 24.5 % lower than BMR when brain death is established. This decrease in REE correlates with the reduction of cere- bral blood flow as indicated by TCD patterns. Of the 20 brain dead patients, 11 met the clinical and TCD criteria of brain death on admission and after 24 h of resuscita- tion (group 2 a) and their REE values were 30  11 % lower than BMR. Furthermore, 9 patients (group 2 b), who were admitted as non-brain dead and became brain dead during hospitalization, had REE values that gradu- ally decreased from 22.5  20 % above BMR to 17.68  8.8 % lower than BMR. This REE decrease was in accordance with the cerebral blood flow changes indi- cated by the TCD pattern (Fig. 2 and Table 4) which evolved from normal to ischemic, to reverse flow, to ear- ly systolic spikes, or to a no-flow pattern (Fig. 1). In this group of patients (2 b), multiple regression stepwise sta- tistical analysis demonstrated that between TCD pat- tern, temperature, and REE, only the TCD pattern was responsible for the decrease in REE. Given the coupling of cerebral blood flow and metabolism, these findings suggest that the decrease in REE is the result of the re- duction of cerebral metabolism. Approximately 20 % of cardiac output is directed to the brain, which, despite its small volume, has high energy requirements, consum- ing up to 20 % of the total body REE [13±15]. There- fore, we can assume that during brain death, the arrest of cerebral blood flow is accompanied by a drop in cere- bral energy consumption. This most likely accounts for a significant proportion of the 24.5 % decrease in REE we observed. However, the decrease in REE beyond the
Resting energy expenditure in brain death - page 7
976 level expected to result from lack of cerebral perfusion, observed in patients in group 2 a (30  11 % of BMR) could be attributed to other factors, such as mild hypo- thermia (35.8  1.1 C), absence of regulatory/anabolic functions of the brain, hormonal changes, and the lack of specific dynamic action of food. Other factors, such as hypermetabolic hormones (thyroid hormones and catecholamines), have been ana- lyzed in brain death. Low levels of triiodothyronine are a common finding [27]. In addition, in an experimental study Cooper et al. [28] showed that 3 h after the onset of brain death adrenaline and dopamine levels were normal and only noradrenaline levels were significantly below normal values. Consequently, the early decrease in energy expenditure observed in brain dead patients cannot be attributed to low thyroid hormones or cate- cholamine levels. We conclude that the onset of brain death is accom- panied by a decrease in REE to values lower than BMR. This is mainly due to the decrease in cerebral blood flow and, consequently, metabolism. However, in some cases variations in temperature may influence this decrease in REE to levels higher (patients 1, 2, 3, 5, 7, 11, Table 2) or lower than can be expected (patients 12, 13, 18, 20, Table 4). Further, larger scale studies are required to confirm and validate our findings and to clarify the time-course between brain death and changes in REE due to changes in cerebral metabolism. References 1. Paolin A, Manuali A, Di Paola F, Boc- caleto F, Caputo P, Zanata R, Bardin GP, Simini G (1995) Reliability in diag- nosis of brain death. Intensive Care Med 21: 657±662 2. Firsching R, Frowein RA, Wilhelms S, Buchholz F (1992) Brain death: practi- cability of evoked potentials. Neuro- surg Rev 15: 249±254 3. Erbengi A, Erbengi G, Cataltepe O, Topcu M, Erbas B, Aras T (1991) Brain death: determination with brain stem evoked potentials and radionuclide studies. Acta Neurochir Wien 112: 118±125 4. Roosen K, Tonn JC, Burger R, Schlake HP (1992) Diagnosis of brain death. Zentralbl Chir 117: 632±636 5. Bonetti MG, Ciritella P, Valle G, Per- one E (1995) 99mTc HM-PAO brain perfusion SPECT in brain death. Neu- roradiology 37: 365±369 6. Lemmon GW, Franz RW, Roy N, Mc- Carthy MC, Peoples JB (1995) Deter- mination of brain death with the use of color duplex scanning in the intensive care setting. Arch Surg 130: 517±520 7. Jalili M, Crade M, Davis AL (1994) Ca- rotid blood flow velocity changes de- tected by Doppler ultrasound in deter- mination of brain death in children. A preliminary report. Clin Pediatr Phila 33: 669±674 8. Pistoia F, Johnson DW, Darby JM, Hor- ton JA, Applegate LJ, Yonas H (1991) The role of xenon CT measurements of cerebral blood flow in the clinical deter- mination of brain death. AJNR Am J Neuroradiol 12: 97±103 9. Wilkening M, Louvier N, D'Athis P, Freysz M (1995) Validity of cerebral an- giography via venous route in the diag- nosis of brain death. Bull Acad Natl Med 179: 41±48 10. Charlin V, Carrasco F, Ferrer L, Brito A, Poblete R (1993) Protein and energy requirements in patients with severe head injury. Rev Med Chil 121: 626±632 11. Chiolero RL, Thoin D, Schutz Y, Je- quier L (1990) Energy metabolism and craniocerebral injury. Ann Fr Anesth Reanim 9: 169±175 12. Raurich JM, Ibanez J (1994) Metabolic rate in the severe head trauma. JPEN J Parenter Enteral Nutr 18: 521±524 13. Dominguez-Roland JM, Murillo-Cabe- zas F, Santamaria-Mifsat JL, Munoz- Sanchez A, Villen-Nieto J (1995) Chan- ges in resting energy expenditure after development of brain death. Transplant Proc 27: 2397±2398 14. Pevsner H, Blushan S, Ottesen O, Earl Walker A (1971) Cerebral blood flow and oxygen consumption. Johns Hop- kins Med J 128: 134±140 15. Langeron O, Couture P, Mateo J, Riou B, Pansard L, Coriat P. (1996) Oxygen consumption and delivery relationship in brain dead organ donors. Br J Ana- esth 76: 783±789 16. Bursztein S, Elwyn D, Askanazi J, Kin- ney J (1989) Guidelines for parenteral and enteral nutrition. In Grayson HT (ed) Energy metabolism, indirect calo- rimetry and nutrition. Williams &Wil- kins, Baltimore, p 238 17. Harris J, Benedict F (1979) Standard basal metabolic constants for physiolo- gists and clinicians; a biometric study of basal metabolism in man. Lippincott, Philadelphia 18. Weir JB (1949) New methods for calcu- lating metabolic rate with special refer- ence to protein metabolism. J Physiol 109: 1±9 19. Depret J, Teboul JL, Benoit G, Mercat A, Richard C (1995) Global energetic failure in brain dead patients. Trans- plantation 60: 966±971 20. Matthews DSF, Bullock RE, Matthews JNS, Aynsley-Green A, Eyre JA (1995) Temperature response to severe head injury and the effect on body energy ex- penditure and cerebral consumption. Arch Dis Child 72: 507±515 21. Sztark F, Thicoipe M, Mason F, Lassie P, Faravel-Garrigues JF, Petit-Jean ME (1993) Metabolic status of brain dead patients managed for organ procure- ment. Transplant Proc 25: 3171±3172 22. Manthous K, Hall J, Olson D, Singh M, Chatila W, Rohlman A, Kushner R, Schmidt G, Wood L (1995) Effect of cooling on oxygen consumption in fe- brile critically ill patients. Am J Respir Crit Care Med 151: 10±14 23. Lanier W (1995) Cerebral metabolic rate and hypothermia: their relation- ship with ischemic neurologic injury. J Neurosurg Anesth 7: 216±221 24. Nemoto E, Klementavicious R, Melick J, Yonas H (1994) Effect of mild hypo- thermia on active and basal cerebral ox- ygen metabolism and blood flow. In: Hogan MC et al. (eds) Oxygen trans- port to tissue, vol 16. Plenum, New York 25. Biancolini C, Del Bosco C, Jorge M, Po- deroso J, Capdevila A (1993) Active core rewarming in neurologic, hypother- mic patients: effects on oxygen-related variables. Crit Care Med 21: 1164±1168 26. Pia HW (1986) Brain death. Acta Neu- rochir 82: 1±6 27. Westenskow D, Schipke C, Raymond J, Saffle J, Becker J, Young E, Cutler C (1988) Calculation of metabolic expen- diture and substrate utilisation from gas exchange measurements JPEN J Parenter Enteral Nutr 12: 20±24 28. Cooper DK, Novitzky D, Wicomb WN (1989) The pathophysiological effects of brain death on potential donor organs, with particular reference to the heart. Ann R Coll Surg Engl 71: 261Ð266
You're reading the first 7 out of 7 pages of this docs, please download or login to readmore.

People are reading about...