The effect of nutritional support on outcome from severe head injury

1987 ◽  
Vol 67 (5) ◽  
pp. 668-676 ◽  
Author(s):  
Byron Young ◽  
Linda Ott ◽  
Diana Twyman ◽  
Jane Norton ◽  
Robert Rapp ◽  
...  

✓ Fifty-one brain-injured patients with peak 24-hour admission Glasgow Coma Scale (GCS) scores of 4 to 10 were prospectively randomly assigned to receive total parenteral (TPN) or enteral (EN) nutrition. Patients were studied from hospital admission to 18 days postinjury. Outcome was assessed by the Glasgow Outcome Scale at 3 months, 6 months, and 1 year postinjury. The TPN group received a significantly higher cumulative mean intake of protein than the EN group (mean ± standard error of the mean: 1.35 ± 0.12 vs. 0.91 ± 0.9 gm/kg/day; p = 0.004). Mean cumulative caloric balance was also significantly higher in the TPN than in the EN group (75.6% ± 5.13% vs. 59% ± 4.26%; p = 0.02). Nitrogen balance was significantly more negative in the EN group during the 1st week postinjury (p = 0.002). The incidence of pneumonia, urinary tract infections, septic shock, and infections was not significantly different between groups. Classic nutritional assessment parameters such as anergy screens, total lymphocyte counts, and albumin levels were not significantly different between groups. The 11 patients in the EN group who did not tolerate tube feedings for 1 week postinjury had a significantly higher incidence of septic shock (p = 0.008). The change over time in GCS scores between groups was significantly different, with the TPN group showing a mean four-point increase in GCS score compared with a three-point increase in the EN group (p = 0.02). At 3 months the TPN group had a significantly higher percentage of favorable outcomes (43.5% vs. 17.9%, respectively; p = 0.05). At 6 months, 43.5% of the TPN group had a favorable outcome while 32.1% of the EN group had a favorable outcome (p = 0.29). By 1 year, 47.8% of the TPN group and 32.1% of the EN group had a favorable outcome (p = 0.20). In conclusion, more calories and protein usually can be administered to acute brain injury patients via the TPN route than by EN feedings via nasogastric or nasoduodenal routes. Traditional parameters for nutritional assessment are not useful in studying the efficacy of nutritional support during the first 2 weeks after head injury. Neurological recovery from head injury occurs more rapidly in patients with better early nutritional support.

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.


1982 ◽  
Vol 56 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Thomas A. Gennarelli ◽  
Gerri M. Spielman ◽  
Thomas W. Langfitt ◽  
Philip L. Gildenberg ◽  
Timothy Harrington ◽  
...  

✓ Recent studies attempting to define the outcome from severe head injury have implied, directly or indirectly, that the severity of injury (as determined by the Glasgow Coma Scale (GSC)) is the sole determinant of outcome. Little attention has been focused on the type of lesion that causes the low GCS score, and there exists an unstated hypothesis that the lesion type is not an important determinant of outcome. No attempt has been made to determine whether patients who have the same GCS score caused by different lesions have the same or different outcomes. Since this is impossible to test without a large number of cases, data were obtained from seven head-injury centers on patients who fulfilled the Glasgow criteria for severe head injury (GCS ≤ 8 for at least 6 hours). Patients were categorized according to a simple classification system comprising seven lesion types, each of which was further subdivided into two GCS score ranges (3 to 5 and 6 to 8). Of 1107 patients, the overall mortality was 41%, but ranged from 9% to 74% among the different lesion categories. Conversely, 26% had good recovery (at 3 months), but among the different lesion groups the range was 6% to 68%. Acute subdural hematoma with GCS scores of 3 to 5 was uniformly the worst problem (74% mortality and 8% good recovery), whereas diffuse injury coma of 6 to 24 hours with GCS scores of 6 to 8 had 9% mortality and 68% incidence of good recovery. Results of this study demonstrate marked heterogeneity within this severe head-injury group and point out that patients with the same GCS score have markedly different outcomes, depending on the causative lesion. The type of lesion is thus as important a factor in determining outcome as is the GCS score, and both must be considered when describing severely head-injured patients.


1996 ◽  
Vol 85 (5) ◽  
pp. 762-771 ◽  
Author(s):  
Daniel F. Kelly ◽  
Rouzbeh K. Kordestani ◽  
Neil A. Martin ◽  
Tien Nguyen ◽  
David A. Hovda ◽  
...  

✓ The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 ± 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 ± 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all ≤ 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.


1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.


1991 ◽  
Vol 75 (Supplement) ◽  
pp. S28-S36 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Theresa Gautille ◽  
Melville R. Klauber ◽  
Howard M. Eisenberg ◽  
John A. Jane ◽  
...  

✓ The outcome of severe head injury was prospectively studied in patients enrolled in the Traumatic Coma Data Bank (TCDB) during the 45-month period from January 1, 1984, through September 30, 1987. Data were collected on 1030 consecutive patients admitted with severe head injury (defined as a Glasgow Coma Scale (GCS) score of 8 or less following nonsurgical resuscitation). Of these, 284 either were brain-dead on admission or had a gunshot wound to the brain. Patients in these two groups were excluded, leaving 746 patients available for this analysis. The overall mortality rate for the 746 patients was 36%, determined at 6 months postinjury. As expected, the mortality rate progressively decreased from 76% in patients with a postresuscitation GCS score of 3 to approximately 18% for patients with a GCS score of 6, 7, or 8. Among the patients with nonsurgical lesions (overall mortality rate, 31%), the mortality rate was higher in those having an increased likelihood of elevated intracranial pressure as assessed by a new classification of head injury based on the computerized tomography findings. In the 276 patients undergoing craniotomy, the mortality rate was 39%. Half of the patients with acute subdural hematomas died — a substantial improvement over results in previous reports. Outcome differences between the four TCDB centers were small and were, in part, explicable by differences in patient age and the type and severity of injury. This study describes head injury outcome in four selected head-injury centers. It indicates that a mortality rate of approximately 35% is to be expected in such patients admitted to experienced neurosurgical units.


1988 ◽  
Vol 69 (3) ◽  
pp. 386-392 ◽  
Author(s):  
Craig J. McClain ◽  
Bernhard Hennig ◽  
Linda G. Ott ◽  
Simeon Goldblum ◽  
A. Byron Young

✓ Severely head-injured patients are hypermetabolic/hypercatabolic and exhibit many aspects of the postinjury acute-phase response. These patients have hypoalbuminemia, hypozincemia, hypoferremia, hypercupria, fever, and increased synthesis of acute-phase proteins such as ceruloplasmin and higher C-reactive protein levels. It has been suggested that increased interleukin-1 (IL-1) in the ventricular fluid may be responsible, at least in part, for these metabolic abnormalities. In the present study, serum albumin levels were evaluated throughout an 18-day study period in 62 head-injured patients receiving aggressive nutritional support. Hypoalbuminemia (mean ± standard error of the mean 3.10 ± 0.2 gm/dl; normal value 3.5 to 5 gm/dl) was observed upon hospital admission; these albumin levels continued to decrease until 2 weeks postinjury, despite aggressive nutritional support. This hypoalbuminemia may be mediated via altered endothelial permeability properties due to endothelial cell dysfunction caused by cytokines such as IL-1. Transendothelial movement of albumin was assayed using a pulmonary artery endothelial cell culture system. Both a crude macrophage supernatant derived from a murine P388D cell line having IL-1 activity (mIL-1) and human recombinant IL-1 (rIL-1) were tested. The amount of albumin transferred was time- and concentration-dependent, with maximal transfer at 24 hours and 20 U of mIL-1 per 0.5 ml of culture medium. Endothelial permeability changes observed after incubation with mIL-1 were confirmed using rIL-1. Compared to control cultures, 20 U of rIL-1 and 20 U of mIL-1 increased albumin transfer across endothelial monolayers 205% and 459%, respectively. These findings suggest that the mechanism of hypoalbuminemia seen after severe head trauma can be explained in part by IL-1-induced endothelial cell injury, resulting in enhanced endothelial permeability to albumin.


1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.


2003 ◽  
Vol 99 (4) ◽  
pp. 661-665 ◽  
Author(s):  
Sergey Spektor ◽  
Samuel Agus ◽  
Vladimir Merkin ◽  
Shlomo Constantini

Object. The goal of this paper was to investigate a possible relationship between the consumption of low-dose aspirin (LDA) and traumatic intracranial hemorrhage in an attempt to determine whether older patients receiving prophylactic LDA require special treatment following an incidence of mild-to-moderate head trauma. Methods. Two hundred thirty-one patients older than 60 years of age, who arrived at the emergency department with a mild or moderate head injury (Glasgow Coma Scale [GCS] Scores 13–15 and 9–12, respectively), were included in the study. One hundred ten patients were receiving prophylactic LDA (100 mg/day) and these formed the aspirin-treated group. One hundred twenty-one patients were receiving no aspirin, and these formed the control group. There was no statistically significant difference between the two groups with respect to age, sex, mechanism of trauma, or GCS score on arrival at the emergency department. Most of the patients sustained the head injury from falls (88.2% of patients in the aspirin-treated group and 85.1% of patients in the control group), and had external signs of head trauma such as bruising or scalp laceration (80.9% of patients in the aspirin-treated group and 86.8% of patients in the control group). All patients underwent similar neurological examinations and computerized tomography (CT) scanning of the head. The CT scans revealed evidence of traumatic intracranial hemorrhage in 27 (24.5%) patients in the aspirin-treated group and in 31 patients (25.6%) in the control group. Surgical intervention was required for five patients in each group (4.5% of patients in the aspirin-treated group and 4.1% of patients in the control group). A surprising number of the patients who arrived with GCS Score 15 were found to have traumatic intracranial hemorrhage, as revealed by CT scanning (11.5% of patients in the aspirin-treated group and 16.5% of patients in the control group). Surgery, however, was not necessary for any of these patients. Conclusions. There was no statistically significant difference in the frequency or types of traumatic intracranial hemorrhage between patients who had received aspirin prophylaxis and those who had not. The authors conclude that LDA does not increase surgically relevant parenchymal or meningeal bleeding following moderate and minor head injury in patients older than 60 years of age.


1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.


Neurosurgery ◽  
1985 ◽  
Vol 16 (3) ◽  
pp. 309-313 ◽  
Author(s):  
Howard H. Kaufman ◽  
Brian J. Rowlands ◽  
Debra K. Stein ◽  
Dennis R. Kopaniky ◽  
Philip L. Gildenberg

Abstract This study measured the nutritional status of eight spine-injured patients during their first 10 to 14 days in the hospital. Initial and follow-up nutritional assessment showed that their nutritional status deteriorated at least partly due to an inadequate supply of protein and calories. Infective complications and prolonged respiratory support were common and may have been caused in part by impaired nutrition. This suggests that a prospective study of aggressive nutritional support for patients with spinal cord transection should be initiated to determine whether this acquired malnutrition and its associated complications can be prevented.


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