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Biomedical subjects

L Ott

Publications and source records attributed to L Ott.

At least 19 recordsLinked to original sources

Postpyloric enteral feeding costs for patients with severe head injury: blind placement, endoscopy, and PEG/J versus TPN.

This study describes the advantages and disadvantages of several forms of enteral nutrition for patients with severe head injury (Glasgow Coma Scale Score [GCS], <12). Included in the study are nasoenteric nutrition delivery using blind, endoscopic, percutaneous endoscopic gastrostomy (PEG) and PEG with jejeunostomy (PEG/J), and open jejeunostomy tube placement methods. These methods are compared with parenteral delivery of nutrition. The study constituted a retrospective analysis of the success rate of early enteral feedings by blind, endoscopic PEG and PEG/J and by open jejeunostomy placement of small-bowel feeding tubes for 57 patients with severe head injury. The delivery cost of enteral nutrition per intensive care unit day was compared to the delivery cost of parenteral nutrition per intensive care unit day in the same group of patients. Fifty-three percent of patients were adequately maintained nutritionally with nasoenteric delivery alone and did not require parenteral feeding. The average number of days for initiation of either enteral or parenteral feedings was 1.8 +/- 0.2 days from injury [standard error of mean (SEM); range, 0-10 days]. An average of 3.3 days (range, 0-23 days) was required for feeding tube placement in all patients. For 70% of patients, tube placement was completed within 48 h after injury. Full-strength, full-rate enteral feedings were achieved by a mean of 4.9 days after injury. A total of 128 feeding tubes were placed while the patients were in the intensive care unit (ICU; 2.2 +/- 0.2 tubes per patient). Blind placement of feeding tubes into the small bowel was rarely achieved without repositioning. Endoscopic tube placement into the duodenum was achieved in 50% of patients, into the jejunum for 33% of patients, and into the stomach for 18% of patients. While in the intensive care unit, patients received an average of 77 +/- 2% of their measured energy expenditure (range, 57-114%). Eleven percent of patients experienced severe gastrointestinal problems. Other problems were associated with the inability to achieve or maintain access: dislodged tubes (30%), clogged or kinked tubes (21%), and mechanical access problems (7 %). Seventy-one percent of patients in barbiturate coma were able to tolerate early nasoenteric feedings. Aspiration pneumonitis occurred equally among patients fed nasogastrically and those fed nasoenterically. The overall aspiration rate was 14%. The cost of acute enteral feeding was $170 per day and that for parenteral feeding, $308 per day. We conclude that blind transpyloric feeding tube placement is difficult to achieve in patients with severe head injury; endoscopically guided placement is a better option. Endoscopic feeding tube placement most consistently allows for early enteral nutritional support in severe head injured patients. Limitations include the inability to establish and/or maintain enteral access, increased intracranial pressure, unstable cervical spinal injuries, facial fractures, and dedication of the physician to tube placement and monitoring.

Adult↗

Zinc supplementation is associated with improved neurologic recovery rate and visceral protein levels of patients with severe closed head injury.

Sixty-eight patients were entered into a randomized, prospective, double-blinded controlled trial of supplemental zinc versus standard zinc therapy to study the effects of zinc supplementation on neurologic recovery and nutritional/metabolic status after severe closed head injury. One month after injury, the mortality rates in the standard zinc group and the zinc-supplemented group were 26 and 12%, respectively. Glasgow Coma Scale (GCS) scores of the zinc-supplemented group exceeded the adjusted mean GCS score of the standard group at day 28 (p = 0.03). Mean motor GCS score levels of the zinc-supplemented group were significantly higher on days 15 and 21 than those of the control group (p = 0.005, p = 0.02). This trend continued on day 28 of the study (p = 0.09). The groups did not differ in serum zinc concentration, weight, energy expenditure, or total urinary nitrogen excretion after hospital admission. Mean 24-h urine zinc levels were significantly higher in the zinc-supplemented group at days 2 (p = 0.0001) and 10 (p = 0.01) after injury. Mean serum prealbumin concentrations were significantly higher in the zinc-supplemented group (p = 0.003) at 3 weeks after injury. A similar pattern was found for mean serum retinol binding protein level (p = 0.01). A significantly larger number of patients in the standard zinc group had craniotomies for evacuation of hematoma; thus a bias may have been present. The results of this study indicate that zinc supplementation during the immediate postinjury period is associated with improved rate of neurologic recovery and visceral protein concentrations for patients with severe closed head injury.

Adolescent↗

Cytokines and metabolic dysfunction after severe head injury.

Patients with head injury must overcome central as well as peripheral metabolic insults. In addition to specific tissue damage to the brain, a cellular biochemical cascade occurs that can negatively affect organ function, cause a systemic response to injury, and may cause secondary tissue injury. The metabolites involved in this cascade are numerous and complex. Cytokines are important cell-to-cell communication mediators during injury. It is speculated that cytokines, such as interleukin 1 (IL-1), interleukin 6 (IL-6), tumor necrosis factor (TNF), and interleukin 8 (IL-8), which are found in elevated amounts in both human and basic trials after head injury, play a role in the cellular cascade of injury. Some of the metabolic events produced by small doses of cytokine infusion in animals, as well as humans, include fever, neutrophilia, muscle breakdown, altered amino acid metabolism, depression of serum zinc levels, production of hepatic acute phase reactants, increased endothelial permeability, and expression of endothelial adhesion molecules. These are all known sequelae of severe head injury. Cytokines have also been implicated in organ failure. Infusion of cytokines in basic science trials revealed that organ functions of the gut, liver, and lung are negatively altered by high-dose cytokine infusion. Infusion of certain cytokines has been shown to cause death of brain cells, increase blood-brain barrier permeability, and cause cerebral edema. This suggests that cytokines may also play a role in the sequelae of organ demise. These effects of cytokines have been attenuated in basic trials by blocking the initial signaling system of cytokines or by decreasing serum cytokine activity. We hypothesize that cytokines that are elevated after head injury play a role in the pathology of injury, including altered metabolism and organ demise.

Animals↗

Nutritional and metabolic variables correlate with amino acid forearm flux in patients with severe head injury.

OBJECTIVE: To measure the arterial-venous amino acid flux across the forearm muscle in patients with severe head injury. DESIGN: Prospective, interventional study. SETTING: Level I trauma hospital in the neurosurgery intensive care unit (ICU) at a university medical center. PATIENTS: Eight nonsteroid-treated patients with severe head injury. INTERVENTIONS: Patients were prospectively randomized to receive either standard or supplemental intravenous zinc therapy. MEASUREMENTS AND MAIN RESULTS: Net forearm alanine, glutamine, tyrosine, phenylalanine, and branch-chain amino acid forearm flux were measured and compared with metabolic markers of energy expenditure and nitrogen excretion. There was a significant inverse relationship between the measured energy expenditure/predicted energy expenditure ratio and glutamine flux (r2 = .62; p < .05). The patients with the highest measured energy expenditure/predicted energy expenditure ratio had the greatest release of glutamine from forearm muscle. Nitrogen balance was significantly correlated with leucine flux (r2 = .53; p < .05) and with isoleucine flux (r2 = .67; p < .05). The patients with the most positive nitrogen balance had the least release of branch-chain amino acids from skeletal muscle. Tyrosine flux was highly correlated with net amino acid flux (r2 = .76; p < .01). Tyrosine flux was therefore indicative of overall muscle catabolism. Four patients had an overall negative flux of amino acids from skeletal muscle. Three patients had an overall negative flux of branch-chain amino acids. CONCLUSIONS: This preliminary descriptive report suggests that increased skeletal muscle efflux of amino acids correlates significantly with metabolic variables of hypermetabolism and hypercatabolism in nonsteroid-treated, head-injured patients.

Adult↗

Institutional respite care: benefits and risks for dementia patients and caregivers.

Thirty-seven dementia patients and their caregivers were studied before and after a two-week in-hospital respite stay. Institutional respite care did not alter behavior problems in dementia patients, nor did changes in performance of activities of daily living (ADLs) by Alzheimer's disease (AD) patients exceed those expected from disease progression. Caregivers exhibited an improvement in burden and depression during the respite study, but levels returned to baseline following the patient's return home.

Activities of Daily Living↗

The MEE/PEE ratio as a predictor of excess weight loss for up to 1 year after vertical banded gastroplasty.

Thirteen morbidly obese individuals were studied prospectively for 1 year after vertical banded gastroplasty (VBG) to determine the relationships between energy balance equation parameters and excess weight loss. The measured energy expenditure (MEE), as determined by indirect calorimetry, was not correlated with weight loss. However, when this parameter was expressed as a ratio to the predicted energy expenditure (PEE), the ratio was significantly correlated with the postoperative excess weight loss at 2, 6, and 12 months. The mean daily energy intake after the VBG was 2715 +/- 865 kJ. The postoperative energy intake was not correlated with the excess weight loss. Diet-induced thermogenesis was studied in eight patients. The mean diet-induced thermogenesis was 10.31% +/- 13.92%. The diet-induced thermogenesis was not correlated with the postoperative excess weight loss. The preliminary findings of this trial suggest that the MEE/PEE ratio is useful in predicting excess weight loss after VBG.

Adult↗

Nutrition and brain injury.

The patient with head injury must overcome central and systemic insults. In addition to the head injury itself, the patient suffers a systemic metabolic response to injury. Both of these insults can affect the patient's ability to survive and recover. During the past decade, investigators have described the systemic metabolic result identified by hypermetabolism, hypercatabolism, the acute-phase response, decreased immunocompetence, hyperglycemia, increased counterregulatory hormone levels, increased ventricular fluid and serum cytokine levels, and altered gastric function. During the next decade, investigators will attempt to modulate this response by manipulating the types of nutrients administered, use of pharmacologic and physiological agents, and administration of growth factors.

Brain Injuries↗

Altered gastric emptying in the head-injured patient: relationship to feeding intolerance.

Most patients with moderate to severe head injury initially do not tolerate enteral feedings postinjury. This intolerance is more prolonged than that found in patients suffering other types of trauma. The authors prospectively evaluated 12 patients with moderate to severe head injury (Glasgow Coma Scale score between 4 and 10) throughout their hospitalization for liquid gastric emptying as a possible mechanism for intolerance to enteral feeding. During Week 1, the majority of patients displayed a delay in gastric emptying. Patients also displayed an abnormal biphasic response (gastric emptying faster than normal during the early stage but prolonged later). By Week 2, many patients still had delayed and abnormal biphasic responses to gastric emptying. By Week 3, an improvement was observed with the majority of patients exhibiting rapid gastric emptying, but delays and abnormal biphasic responses were still seen. Patients who initially had rapid or normal gastric emptying tolerated full-strength full-rate feedings significantly earlier compared with those who experienced delayed gastric emptying (8.5 +/- 0.5 days vs. 13.7 +/- 3.2 days, p less than 0.001). All patients tolerated full-strength full-rate feedings by Day 16 postinjury (range 7 to 16 days) except the two patients who displayed delayed gastric emptying for prolonged periods of time (mean 25 days). This is the first study to longitudinally evaluate gastric emptying following head injury. The authors suggest that patients with moderate to severe head injury often experience alterations in gastric emptying which may affect their ability to tolerate enteral feedings.

Adolescent↗

Metabolic management of the patient with head injury.

Patients with severe head injury have a disruption in metabolic homeostasis that includes increased energy expenditure and increased protein catabolism. These changes have been suggested to occur secondary to steroid administration, immobility, and other factors. A review of investigations indicates that the head injury itself causes these metabolic changes, although steroid administration can further alter plasma amino acid changes. Altered plasma amino acid profiles after head injury may have an effect on substrate availability to the brain, bacterial translocation, and overall nitrogen balance. Patients with severe head injury have increased skeletal muscle efflux of amino acids. Lack of nutrient supplementation in these patients is associated with increased morbidity and mortality. Enteral nutrition is the preferred mode of feeding but often is not tolerated in the patient with head injury. Parenteral nutritional support can be given to these patients without worsening cerebral edema.

Amino Acids↗

Increased plasma and ventricular fluid interleukin-6 levels in patients with head injury.

The cytokine interleukin-6 (IL-6) plays a major role in initiating the acute phase response, especially in the production of acute phase reactants such as C-reactive protein. The objectives of this study were to determine whether plasma or ventricular fluid IL-6 levels were elevated at time of admission after head injury and whether plasma IL-6 levels related temporally to clinical improvement of levels of acute phase reactants. Thirty patients with Glasgow Coma Scale (GCS) scores of 3 through 10 were observed for 15 days after head injury. Peak elevation of plasma IL-6 occurred on admission (85 +/- 12 U/ml; normal level is less than 2 U/ml) and then decreased during the hospital course to a level of 29 +/- 4 U/ml on day 15. Plasma IL-6 levels decreased significantly faster in patients with admission peak 24-hour GCS scores of 8 through 10 compared with patients with GCS score less than 8 (p less than 0.01). Patients had markedly elevated and variable ventricular fluid IL-6 levels on admission (mean 3880 +/- 2022 U/ml; normal, less than 2 U/ml). A temporal relationship was found between plasma IL-6 levels and multiple acute phase reactants thought to be mediated by IL-6. We conclude that plasma and ventricular fluid levels of IL-6 are elevated after head injury and that plasma IL-6 level is temporally related to acute phase reactants and clinical improvement. We suggest that IL-6 may play an etiologic role in many of the metabolic or nutritional sequelae of head injury.

Adolescent↗

Brain injury and nutrition.

This review has discussed the current status of metabolic alterations and demands, nutrient administration, and nutritional assessment of the head-injured patient. More work is necessary in all areas to further describe and ascertain the nutritional requirements of these patients. Future research in this area should involve specific nutrient requirement, modification of the acute-phase response, and possibly administration of growth factors.

Brain Injuries↗

Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients.

Severe head injury is associated with a stress response that includes hyperglycemia, which has been shown to worsen outcome before or during cerebral ischemia. To better define the relationship between human head injury and hyperglycemia, glucose levels were followed in 59 consecutive brain-injured patients from hospital admission up to 18 days after injury. The patients who had the highest peak admission 24-hour serum glucose levels had the worse 18-day neurologic outcome (p = 0.01). Patients with peak 24-hour admission glucose levels greater than 200 mg/dL had a two-unit increase in Glasgow Coma Scale score while patients with admission peak 24-hour serum glucose levels less than or equal to 200 mg/dL had a four-unit increase in Glasgow Coma Scale score during the 18-day study period (p = 0.04). There was a significant relationship between 3-month and 1-year outcome and peak admission 24-hour serum glucose level (p = 0.02 and p = 0.02, respectively). Those patients with admission peak 24-hour serum glucose levels less than or equal to 200 mg/dL had a greater percentage of favorable outcome at 18 days, 3 months, and 1 year than those with admission peak 24-hour glucose levels greater than 200 mg/dL (p = 0.0007, p = 0.03, and p = 0.005, respectively). A significant relationship between admission peak 24-hour Glasgow Coma Scale score and 18-day, 3-month, and 1-year outcomes was found (p = 0.0001, p = 0.0002, and p = 0.0002, respectively). Patients with mean admission peak 24-hour Glasgow Coma Scale scores of 3.5, 6, and 10 had mean admission 24-hour peak serum glucose levels of 252 +/- 23.5, 219.1 +/- 19, and 185.8 +/- 21, respectively (p = 0.05). These relationships were not significantly altered when confounding variables such as the amount of glucose given over the initial 24-hour postinjury period, the presence of diabetes or multiple injuries, and whether patients were given steroids, dilantin, or insulin were statistically incorporated. These data suggest that admission hyperglycemia is a frequent component of the stress response to head injury, a significant indicator of severity of injury, and a significant predictor of outcome from head injury.

Analysis of Variance↗

Relationship of visceral proteins to nutritional status in chronic and acute stress.

Visceral protein levels are used as indicators of prognosis, severity of injury, and nutritional status in hospitalized patients. Clinicians often use visceral protein levels to assess efficacy of nutritional support. The purpose of this study was to test the validity of such practices. Visceral protein levels were determined in patients in a medical ICU, head injury unit, and burn unit. The serum albumin and thyroxine-binding prealbumin (TBPA) levels correlated significantly with mortality in the medical ICU patients. Burn patients had depressed albumin and TBPA concentrations over the duration of hospitalization that related to the severity of thermal injury but not to adequacy of nutritional support. Head-injured patients had depressed admission albumin and TBPA levels, with neither protein level adequately related to caloric or protein supplementation. We conclude that visceral proteins may reflect severity of injury and prognosis in critically ill hospitalized patients, but they often do not accurately reflect nutritional status or adequacy of nutritional support.

Adult↗

The effect of total parenteral nutrition on vasogenic edema development following cold injury in rats.

Total parenteral nutrition (TPN) has been shown to decrease mortality and to increase the rate of recovery in head-injured patients. However, a recent short-term animal experiment has raised concern over the potential enhancement of vasogenic edema by TPN. The experiment described here was undertaken to examine longer-term effects of TPN infusion on vasogenic edema development. Twenty-four rats received an infusion of a TPN solution (35% glucose) or 0.9% saline at 4 ml/kg/hr for 4 or 26 hours following cold injury. In the 4-hour experiment, TPN increased the serum glucose level to 772 +/- 57 mg/dl compared to 160 +/- 14 mg/dl in the saline-treated animals (p = 0.0001) and increased serum osmolality to 312 +/- 3 mOsm/kg compared to 291 +/- 3 mOsm/kg in the saline-treated group (p = 0.0006). In the 26-hour experiment, TPN-infused rats were also hyperglycemic and hyperosmotic by 4 hours postinjury and remained hyperglycemic at 26 hours postinjury (serum glucose level 374 +/- 97 mg/dl compared to 141 +/- 3 mg/dl in saline-treated animals; p = 0.0371). Although by 26 hours the TPN-infused rats appeared hyperosmotic compared to the saline-treated rats, high variability in the TPN group prevented statistical confirmation of this observation (serum osmolality 337 +/- 35 mOsm/kg in the TPN group compared to 287 +/- 6 mOsm/kg in the saline group). A three-way analysis of variance with repeated measures was used to analyze the effect of infusion (saline vs. TPN), time (4 vs. 26 hours), and cold injury on the specific gravity of the five brain regions studied. Cold injury significantly increased edema development in the injured versus uninjured hemisphere for every region studied (p less than or equal to 0.0034, all five regions), and edema development increased significantly between 4 and 26 hours in three of the five regions (p less than or equal to 0.0207, all three regions). The infusion fluid was not a significant factor in any of the analyses. In conclusion, TPN infusion produced hyperglycemia and hyperosmolality in cold-injured rats but did not enhance vasogenic edema development in any brain region studied.

Analysis of Variance↗

Effect of total parenteral nutrition upon intracranial pressure in severe head injury.

Animal investigations suggest that administration of hyperosmolar total parenteral nutrition (TPN) solutions may potentiate cerebral edema following head injury. Intravenous nutrition (TPN) is often required after head injury due to intolerance to enteral feeding (EN). This study evaluates the effect of TPN on intracranial pressure (ICP) measurements in severely brain-injured patients. Ninety-six severely brain-injured patients were randomly assigned to receive TPN or EN and were studied from hospital admission until 18 days postinjury. The TPN was started within 48 hours postinjury and the EN was started when tolerated. Peak daily ICP was not significantly different on admission and over time (overall mean +/- standard error of the mean 32.01 +/- 1.62 for TPN versus 32.5 +/- 1.25 for EN). Intracranial pressure was greater than 20 mm Hg in 75% of TPN patients and 73% of EN patients. Conventional therapy failed to control elevated ICP in 36% of TPN patients and 38% of EN patients. Of these patients, subsequent barbiturate therapy failed to control ICP in 56% of TPN patients and 64% of EN patients. Serum osmolality was not significantly different between groups at admission or over the course of the study. The TPN group tended to have higher mean serum glucose levels for the first 13 days postinjury, while the EN group had a higher mean serum glucose content thereafter, but these differences were not statistically significant. This study shows that TPN can be given safely to the severely brain-injured patient without causing serum hyperosmolality or affecting ICP levels or ICP therapy.

Brain Injuries↗

The effect of nutritional support on outcome from severe head injury.

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.

Craniocerebral Trauma↗

Nutritional support and measured energy expenditure of the child and adolescent with head injury.

Energy expenditure, nitrogen excretion, and serum protein levels were studied from the time of hospital admission until 2 weeks after severe head injury in eight adolescents and four children with peak 24-hour Glasgow Coma Scale scores ranging from 3 to 8. The mean measured energy expenditure (MEE) was 1.3 times Harris and Benedict's predicted value for energy expenditure. Seventy percent of the patients achieved caloric balance (MEE X 1.2) by 4 to 14 days after injury, but balance was not consistently maintained. Five of the 12 patients had intermittent diarrhea, and two had increased gastric residuals. In five patients fluid restrictions were imposed due to either the syndrome of inappropriate secretion of antidiuretic hormone, pulmonary complications, or intracranial pressure complications. For the adolescents (aged 11 to 17 years) the mean calorie intake during the 1st week was 752 kcal/day and for the children (aged 2 to 5 years) it was 340 kcal/day. During the 2nd week the mean calorie intake for the adolescents was 1671 kcal/day and for the children was 691 kcal/day. Mean urinary nitrogen excretion was 307 mg/kg/day for the adolescents and 160 mg/kg/day for the children. The calculated mean nitrogen balance for the eight adolescents and the four younger children was -13.6 and -4.1, respectively. Mean albumin levels decreased from 2.9 gm/dl during the 1st week to 2.4 gm/dl during the 2nd week (normal 3.5 to 5.0 gm/dl). Mean total protein level during the 1st week was 5.4 gm/dl and increased to a mean of 6.0 gm/dl during the 2nd week (normal 6.0 to 7.8 gm/dl). Weight loss ranged from 2 to 26 lb during the 2-week period. From these studies it can be concluded that head injury in the child and adolescent induces a metabolic response that includes increased energy expenditure and decreased serum albumin levels similar to those observed for head-injured adults. Mean nitrogen excretion values are less than those in adults with a severe head injury.

Adolescent↗