Neurological injury can cause various gastrointestinal GI and nutritional complications. These problems can often affect recovery of patients with traumatic brain injury (TBI). Appropriate recognition and practices regarding treatment and prevention can help minimize the impact of these complications.
Gastrointestinal complications
Gastrointestinal complications can affect a TBI patient in the acute and chronic phases of injury. These complications often affect the tolerance of feeding and thus the nutritional health of the patient.
Gastritis
Gastritis is the most common GI complication after head injury, with a reported incidence of 74% to 100%. , Head injury has been shown to be an independent risk factor for gastric stress erosions and is shown to be correlated to severity of injury. Erosive gastritis is the most common lesion and is often found in the first week of injury.
There is an elevated risk of gastric ulceration after TBI secondary to gastric acid hypersecretion caused by elevated serum gastrin levels.
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Cushing’s ulcer: gastroduodenal ulcer produced by elevated intracranial pressure (ICP) caused by an intracranial tumor, head injury, or other space-occupying lesion
Prevention
Agents used to control gastric acid hypersecretion:
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Proton pump inhibitors
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Histamine 2 (H2) receptor antagonists
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Higher incidence of aspiration pneumonia thought to be secondary to bacterial overgrowth ,
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Cytoprotectant:
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Sucralfate
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Protects gastric mucosa
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Does not alter the gastric pH
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Gastrointestinal dysfunction
Gastrointestinal motility disturbances are very common in patients with TBI. Dysfunction of the different segments of the GI tract, including prolonged transit and decreased peristalsis, will increase the risk of aspiration and often delay the onset of enteral feedings.
Gastroesophageal reflux
Acute brain injury is associated with low pressure in the lower esophageal sphincter (LES) and reduced LES tone, increasing the rate of regurgitation and aspiration. , Prolonged stays in bed in the supine position and increased abdominal pressure in patients with severe constipation also increase the risk of gastroesophageal reflux disease (GERD).
Symptoms
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Sharp or burning chest pain in the sternal region
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Tightness in the chest or upper abdomen
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Regurgitation
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Nausea
Management
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Proton pump inhibitors, H2-receptor antagonists, sucralfate
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Esophago-gastroduodenoscopic (EGD) examination may be indicated if further evaluation is needed.
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Jejunostomy may be considered in patients with particularly low LES tone and difficulty with feeding tolerance.
Delayed gastric emptying
Traumatic brain injury causes a delayed but significant decrease in intestinal contractile activity leading to delayed transit. A delay in gastric emptying (GE) may be suspected when there is feeding intolerance with high residuals. Feeding intolerance can be manifested by diarrhea, vomiting, abdominal distention, and increased gastric residuals.
Although the exact mechanisms of GI motility disturbances are not fully recognized, several factors have been proposed:
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Suppressed vagal nerve activity caused by elevated ICP inhibits GE.
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Corticotropin-releasing factor (CRF), a hormone involved in response to stress, can significantly inhibit GE and intestinal motility mainly via a CRF2-mediated pathway.
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Changes in the brain-gut peptides such as vasoactive intestinal peptide (VIP) and cholecystokinin (CCK) in both the plasma and small intestine
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Hyperglycemia may alter GE by decreasing vagal efferent activity in the central nervous system (CNS) and releasing nitric oxide from the myenteric plexus.
Management
Prokinetic Agents
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Metoclopramide
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Limited by its potential for CNS side effects because of its central dopaminergic blocking activity
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Erythromycin
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Similar to the GI hormone motilin
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Used effectively as a motility agent
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Combination of erythromycin and metoclopramide therapy exhibited greater benefits—and less tachyphylaxis—than erythromycin or metoclopramide monotherapy. ,
Reduced gut absorption
Many severe TBI patients do not tolerate early enteral nutrition because of reduced gut absorptive capacity (GAC). The reasons for reduced GAC are not completely understood but may be related to delayed gastric emptying, intestinal dysmotility, mucosal villous atrophy, or edema and reduced perfusion. Singh et al found that GAC was severely depressed in trauma patients soon after injury but returned to normal 1 to 3 weeks later.
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Rat studies demonstrated that the absorption of proteins, carbohydrates, and lipids significantly decreased within 2 weeks after TBI. Additionally, animal studies found intestinal mucosal epithelium may develop apoptosis at 3 hours after TBI, and at 24 hours postinjury, the villous height and surface area decreased significantly and further declined to the degree of mucosal atrophy within a week after injury.
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Dehydration and overhydration may potentially hamper the absorptive function of the intestinal mucosa because of splanchnic hypoperfusion or edema of the GI tract.
Bowel complications
Bowel incontinence
Bowel and bladder incontinence have been observed, especially in lesions involving the frontal lobes. Individuals with TBI have a high incidence of fecal incontinence. Volitional control of bowel function is controlled by the frontal lobes.
Incontinence is most often related to cognitive awareness, with control of bowel movements improving as cognition improves. Reflexes, spinal reflex arc, and sensation are typically intact. Decreased awareness of the need to defecate and decreased control of the external sphincter result in the inability to inhibit defecation.
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In one study, using data from the Traumatic Brain Injury Model Systems National Database, the incidences of fecal incontinence were 68% at admission to an inpatient rehabilitation, 12.4% at the time of discharge from rehabilitation units, and 5.2% at 1-year follow-up
Diarrhea
Diarrhea is not a common finding of the TBI population, although with this population, there are multiple causes that should be considered.
Various etiologies
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Prolonged hospitalization and/or concurrent use of antibiotics
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Workup should include stool evaluation, testing for Clostridium difficile
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Diarrhea-inducing medications
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Enteral tube feeding
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Diarrhea is the most common complication of enteral tube feeding
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Formula composition
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Rate infusion
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Enteral formula contamination
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Altered bacterial flora
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Hypoalbuminemia
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Serum albumin level less than 2.6 g/dL is correlated with diarrhea
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Complications
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Electrolyte abnormalities
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Dehydration
Constipation
Constipation often develops in patients who are nonambulatory, who have delayed gastric motility or diabetic autonomic neuropathy, and those who use chronic pain medications such as opioids. It can be a much more serious problem in the TBI and spinal cord injury (SCI) patient population, as it can lead to autonomic dysreflexia, which can be a life-threatening event.
Bowel regimens/programs
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High-fiber diet
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Daily stimulant laxative
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Long-term use of Senna products has been associated with melanosis coli.
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Daily stool softener
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Enema, suppository
Complications
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Poor appetite
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Nausea or vomiting
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Abdominal discomfort
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Bowel obstruction or rupture
Gallbladder disease
Posttraumatic acute acalculous cholecystitis is a potentially serious complication that may develop among patients hospitalized for trauma. The cause is likely multifactorial, often related to hypotension, sepsis, or biliary stasis with subsequent cystic duct obstruction. Most report symptoms usually begin between 1 week and 1 month after trauma.
Suspicion should be raised if patient exhibits:
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Unexplained fever, vomiting, abdominal distention, ileus, right upper quadrant pain, and/or developing intolerance to oral or tube feedings
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Elevated serum bilirubin, alkaline phosphatase, liver enzymes, and leukocytosis
Best diagnosed with:
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Hydroxy iminodiacetic acid (HIDA) scan
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Ultrasound or abdominal computed tomography (CT) scan
Treatment options:
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Cholecystectomy
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Broad spectrum antibiotics
Pancreatitis
Elevations of serum amylase and lipase have been described in patients with head injury.
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Although no clinical signs or symptoms of pancreatitis may be present, hyperamylasemia has been reported in 19% to 41% of patients with severe head injury and in 45% to 60% of patients with intracranial bleeding. ,
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Proposed causes have included vagal stimulation, altered modulation of the central control of pancreatic enzyme release, and release of cholecystokinin from the brain. ,
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Nutritional considerations
Metabolic alterations
Traumatic brain injury can stimulate tremendous changes in metabolism. The degree of this hypermetabolic state is proportional to the severity of injury and motor dysfunction. The result of these alterations is systemic catabolism, which leads to hyperglycemia, protein wasting, and increased energy demand.
The injured brain stimulates the secretion of many hormones that affect metabolic function, including hypothalamic–pituitary axis products such as adrenocorticotrophin releasing hormone (ACTH), growth hormone, prolactin, vasopressin, and cortisol as a natural response to stress. Glucagon and catecholamines are also released in excess.
Additional metabolic demands can be increased by factors such as hyperventilation, increased cardiac output, fever, restlessness, seizures, and infections. Several studies have revealed that patients with head injuries can have an increase of 120% to 200% of resting energy expenditure and twice the normal oxygen consumption.
Hyperglycemia
Catecholamine levels reflect the severity of head injury. Catecholamines help support blood pressure and cardiac output but also increase basal metabolism, oxygen consumption, proteolysis, muscle wasting, glycogenolysis, and hyperglycemia.
Hyperglycemia (>200 mg/dL) is a predictor of poor outcome and is associated with an increased morbidity and mortality in TBI patients. TBI patients, however, have demonstrated some differences in brain glucose metabolism and likely require slightly higher glucose values to ensure appropriate brain metabolism.
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Maintenance of serum glucose values between 80 and 110 mg/dL may result in cerebrospinal fluid (CSF) glucose values below the normal threshold.
The precise goal glucose range is not well defined for TBI patients. In practice, either no guidance at all or excessively aggressive protocols are likely to lead to more hypoglycemia, which may be problematic.
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The American Society for Parenteral and Enteral Nutrition (ASPEN) recommends controlling blood glucose in the range of 100 to 150 mg/dL to improve CSF glucose values and reduce the risk of hypoglycemia. ,
Nutritional support
Nutrition assessment
Brain Trauma Foundation guidelines recommend that moderate to severe TBI patients should receive basal caloric replacement at least by the fifth day and at most by the seventh day postinjury to decrease mortality. Prompt assessment of the nutrition requirements is needed to establish goals for optimal calories, protein, and fluids. The hypermetabolic response can be prolonged and is usually correlated with injury severity, thus the measured resting energy expenditure is higher in those patients with more severe brain injury.
Nutritional assessment: Calories
Accurate assessment of caloric requirements in TBI patients is important in providing adequate nutritional support. Delayed nutritional support may result in negative outcomes such as poor wound healing, malnutrition, impaired organ function, and altered immunological status.
Unfortunately, predicting the nutritional needs of a patient with TBI is not simple. Many of the various equations used to predict energy expenditure are not specific to TBI and have a degree of inaccuracy.
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Indirect calorimetry is the current “gold standard” for determining energy expenditure in TBI patients.
Nutrition status will often fluctuate during recovery and require periodic reassessment of metabolic needs to prevent underfeeding. More calories may also be required if the patient has additional injuries and/or stress, especially long bone fractures or sepsis.
For example:
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Comatose TBI patients have increased resting metabolic expenditure of 120% to 140% because of hypercatabolic response.
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Pharmacologically induced coma patients, however, may have a resting metabolic expenditure as low as 80%.
Close monitoring is also needed to prevent overfeeding. Metabolic needs will often decrease as the patient’s medical stability improves. Prolonged or excessive overfeeding can be harmful as well.
Overfeeding can result in metabolic complications such as :
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Hyperglycemia
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Refeeding-like syndrome with electrolyte derangements
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Hepatic steatosis
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Pulmonary compromise with difficulty weaning from the ventilator
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Obesity
Nutritional assessment: Protein
Inflammatory mediators and catecholamines trigger hypercatabolism in TBI patients, often resulting in protein breakdown. Protein catabolism appears to be related to the severity of injury and appears to peak 8 to 14 days after injury.
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Recommendations suggest protein provision ranging between 1.5 and 2 g/kg per day for acute TBI patients to account for the excess catabolism.
Routine monitoring and adjustment of protein doses should be done during TBI recovery to ensure safety and efficacy.
Nutritional assessment: Fluids and electrolytes
Monitoring of blood pressure and volume status is necessary in patients with moderate to severe TBI. TBI patients often require intravenous fluid resuscitation after injury to maintain adequate mean arterial and cerebral perfusion pressures.
Excessive fluid volumes, however, may also be harmful. Excessive fluid resuscitation may decrease cerebral compliance and increase brain edema Large volumes of salt-free water and other hypotonic fluids should be avoided to prevent exacerbation of cerebral edema and hyponatremia
Enteral versus parenteral nutrition support
Many patients with moderate to severe TBI have feeding intolerance secondary to intubation, dysphagia, or altered mental status and require an alternative means of feeding. Parenteral nutrition (PN) has been associated with increased risk of infection, immunosuppression, hyperglycemia, hepatic steatosis, and diminished gastric mucosa integrity. Enteral nutrition (EN), however, has demonstrated protective effects against infection, a decrease in critical care days, and improved mortality when administered appropriately.
Parenteral nutrition should be considered in those who do not tolerate enteral nutrition or when safe enteral access cannot be achieved.
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Central venous access is required for infusion of the hyperosmolar solutions of parenteral solutions.
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Precaution must be taken to prevent infection and hyperglycemia, particularly in patients receiving PN.
The TBI patient should be reassessed frequently for the ability to swallow and continued need for temporary or longer-term feeding access. The use of a percutaneous endoscopic gastrostomy (PEG) tube is indicated when a patient persists with dysphagia for a prolonged period. TBI patients are likely to tolerate gastric feedings as the acute phase subsides (2–3 weeks). Optimal timing of PEG placement varies pending stabilization of the patient’s clinical status, established feeding tolerance, and demonstration of adequate bowel function.
Timing of nutrition
Early nutritional support is an important goal in treating the TBI patient. The American Society of Parenteral and Enteral Nutrition (ASPEN) and Society of Critical Care Medicine (SCCM) guidelines recommend EN be initiated within 24 to 48 hours for critically ill adults, as long as patients are hemodynamically stable. Early nutritional support can prevent breakdown of protein and fat stores, reduce inflammatory response, decrease infections, and improve neurological outcomes. In addition, early administration of EN promotes gut integrity and motility, whereas a long period of starvation is associated with mucosal atrophy and reduced enzymatic activity.
Feeding to goal within 2 to 3 days has been associated with accelerated neurological recovery and a decreased incidence of death caused by infection. Once feeding access has been established:
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Administer a calorically dense EN product as early as possibe.
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Provide at least 18% to 25% of calories as protein to account for protein catabolism.
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Frequently monitor patient tolerance to EN rate and advance as tolerated.
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Reevaluate metabolic needs of the patient throughout recovery.
Nutrient supplementation
Omega-3
Some animal studies have suggested that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) supplementation may have neuroprotective benefits through inhibition of the central proinflammatory response. However, the role of omega-3 supplementation on the treatment or prevention of the detrimental effects of human neurological injuries is currently undefined.
Zinc
Available clinical data suggest that zinc deficiency should be prevented to enhance the potential for neurological recovery in the acute care setting.
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Moderate to severe TBI
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Acute increases in urinary zinc excretion and significant decreases in serum zinc levels have been shown to be proportional to the severity of injury.
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Zinc supplementation has been associated with increased visceral proteins and improvements in Glasgow Coma Scale (GCS) scores 2 weeks after start of treatment.
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Mild TBI
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There have been no clinical trials to address the efficacy of zinc supplementation in mild TBI.
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Vitamin D
Research findings have suggested that vitamin D supplementation may serve as a role in treatment of TBI as a neuroprotective adjuvant with progesterone.
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Severe TBI
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Treatment with the combination therapy of vitamin D and progesterone demonstrated significantly greater improvements in GCS values and Glasgow Outcome Scale (GOS) values.
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Mild TBI
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No clinical trials have addressed the efficacy of vitamin D supplementation in mild TBI.
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Review questions
- 1.
A 22-year-old man with traumatic brain injury (TBI) and dysphagia was recently started on bolus tube feedings through his percutaneous endoscopic gastrostomy tube. Following the boluses, he complains of burning pain behind his breastbone and associated nausea. He also has associate coughing after the feeds. What is the most likely etiology of his condition?
- a.
Suppressed vagal nerve activity
- b.
Reduced lower esophageal sphincter
- c.
Reduced gut absorptive capacity
- d.
Mucosal villous atrophy
- a.
- 2.
A 53-year-old woman with TBI and a history of diabetes mellitus type 2 has been found to have elevated gastric residual volumes, abdominal distention, and nausea. What treatment options have studies shown to be most beneficial in this condition?
- a.
Metoclopramide
- b.
Erythromycin
- c.
Erythromycin and metoclopramide
- d.
Cisapride
- a.
- 3.
What is the most appropriate approach in attempting to control hyperglycemia during nutritional support for a brain injury patient?
- a.
Blood glucose concentrations should be maintained above 200 mg/dL.
- b.
Blood glucose concentrations should be maintained at 80 to 100 mg/dL.
- c.
Blood glucose concentrations should be maintained at 110 to 180 mg/dL.
- d.
During nutritional support, it is not recommended to monitor blood glucose concentrations.
- a.
Answers on page 390.
Access the full list of questions and answers online.
Available on ExpertConsult.com
- 4.
Which of these statements is correct regarding nutritional assessment and support of the brain-injured patient?
- a.
The measured resting energy expenditure is lower in patients with more severe brain injury.
- b.
Protein catabolism peaks around 3 to 5 days after injury.
- c.
Hypotonic fluids are recommended for fluid resuscitation after injury.
- d.
Comatose TBI patients have increased resting metabolic expenditure.
- a.
- 5.
Which of these statements is true regarding enteral nutrition?
- a.
It promotes gut motility and integrity.
- b.
It is associated with increased risk of infection.
- c.
Guidelines recommend prolonging initiation until day 10 postinjury to improve feeding tolerance.
- d.
It should only be considered in those who cannot tolerate parenteral nutrition.
- a.
References
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