14 Nutrition
Abstract
Brain injuries alter metabolism making glucose management and nutrient provision challenging. The main nutrition goal is to manage glycemic control and provide adequate nutrients to prevent or treat malnutrition. In this chapter, we will discuss the nutritional challenges of and recommendations for patients with brain injury.
Keywords: glucose, nutrition, enteral nutrition, parenteral nutrition, brain injury
14.1 Glucose Utilization
Hyperglycemia is common after brain injury, resulting from stress, inflammation, corticosteroids, diabetes mellitus, decreased insulin sensitivity, and increased gluconeogenesis from lactate clearance.1 Early profound hyperglycemia is independently associated with poor prognosis after traumatic brain injury (TBI), stroke, and subarachnoid hemorrhage. Hyperglycemia has been associated with increased infection risk and critical illness polyneuropathy. In acute ischemic stroke there is evidence that persistent hyperglycemia is associated with worse outcome.2 Yet hypoglycemia, which has been defined as blood glucose of < 60 or < 80 (mg/dL) depending on the study, also has deleterious effects. There are limited intensive insulin therapy (IIT) studies (blood glucose 80–120 (mg/dL)) specific to the neurologically injured patient population, and many of the most cited studies excluded patients with a neurologic injury. ▶ Table 14.1 summarizes key IIT studies. Of note, though the NICE-SUGAR trial observed more hypoglycemia events with IIT, this was not associated with Glasgow outcome score at 24 months post TBI.3
In summary, IIT may impair cerebral glucose metabolism after brain injury, and more liberal serum glucose goals may be needed. Although the ideal serum glucose target is still under debate, maintaining a range of 140 to 180 mg/dL and avoiding hypoglycemia are recommended.2,4,5,6
14.2 Nutrition in Critical Care
Brain injuries alter the body’s metabolism of nutrients causing a hypermetabolic and hypercatabolic state. Inadequate nutrition leads to malnutrition, which is associated with:
• Increased risk for infectious complications
• Prolonged need for mechanical ventilation
• Longer hospital and intensive care unit (ICU) length of stays
• Overall increased risk for morbidity and mortality7,8
Multiple factors play a role in determining calorie and protein needs and must be considered prior to devising a nutrition regimen:
• Acuity and degree of brain injury
• Medical history (e.g., diabetes, renal disease, heart disease)
• Surgical history (e.g., extensive bowel resection, bariatric surgery)
• Current medications (e.g., phenytoin, fluoroquinolones)
• Nutritional history (recent weight changes, intake, vitamin/mineral/herbal supplements)
14.3 Nutrition Status
14.3.1 Malnutrition
Patients should be evaluated on admission for the presence of malnutrition. Malnutrition should not be based on body mass index (BMI) alone as obese patients can be malnourished. The American Society for Parenteral and Enteral Nutrition (ASPEN)/Academy of Nutrition and Dietetics Malnutrition Consensus suggests using the following criteria to diagnose malnutrition:
• Insufficient energy intake (estimated percentage of usual intake)
• Weight loss ([usual body weight – current weight]/usual body weight × 100)
• Loss of muscle mass (in temples, clavicles, shoulders, scapulae, quadriceps, calves)
• Loss of subcutaneous fat (in orbital fat pads, triceps, over rib cage)
• Localized or generalized fluid accumulation (rule out other causes of edema/ascites)
• Diminished functional status (hand dynamometer strength and overall activity level)
▶ Table 14.2 identifies the criteria for moderate and severe malnutrition.9 Note that there is no definition for mild malnutrition according to the guidelines.
It is important to recognize that patients with certain neurologic injuries remain at high risk for developing malnutrition. Some of these conditions include:
• Stroke
• Aneurysmal subarachnoid hemorrhage
• Brain tumors
• Spinal cord injury
• TBI
• Dementia
• Multiple sclerosis
14.3.2 Refeeding Syndrome
It is important to screen for malnutrition prior to starting nutrition support. Initiating aggressive nutrition in the malnourished patient may result in refeeding syndrome. Refeeding syndrome is the potentially fatal intracellular shifts of fluids and electrolytes caused by the introduction of carbohydrates and subsequent insulin secretion. Measures must be taken to identify patients at refeeding syndrome risk, slowly advance nutrition, closely monitor electrolytes, and provide thiamine supplementation. ▶ Fig. 14.1 provides an algorithm for the prevention of refeeding syndrome.11
14.3.3 Nutrition-Related Laboratory Tests
Due to inflammation, serum protein markers (pre-albumin, albumin, transferrin) do not accurately reflect nutrition status during critical illness and may remain low despite adequate nutrition.12 A 24-hour urine urea nitrogen measurement may help determine daily protein needs.
14.4 Nutrition Assessment
14.4.1 Calorie Needs
Calorie and protein assessments are needed to develop a nutrition plan, especially in the ICU. Indirect calorimetry (IC) is considered the gold standard in measuring resting energy expenditure (REE). IC calculates REE by measuring oxygen consumption and carbon dioxide production. Although considered to be the gold standard, IC is expensive, requires trained personnel, and is contingent on many variables. ▶ Table 14.3 outlines the variables which affect IC.10 Predictive equations (Penn State, Mifflin-St. Jeor, weight-based equations) using dry or usual weight to determine energy requirements are less reliable but often more feasible than IC. Caloric needs by weight category can be found in ▶ Table 14.4. It is important to know that caloric needs may increase from TBI, fever, or wounds and decrease from therapeutic hypothermia, barbiturate coma, paralytics, quadriplegia, or paraplegia, and this should be taken into consideration when determining nutritional goals.
Variable | Suggested limits | Reasoning |
RQ | 0.67–1.2 | Values outside of range suggest technical errors |
FiO2 | ≤ 60% | Elevated FiO2 can increase errors in measured VO2 |
PEEP | < 12 cm H2O; Not on APRV | High PEEP can increase FiO2 variability |
Activity (PT/OT, transport) | Conduct IC 1 to 2 hours after activity | Hyperventilation can lead to increased VCO2, REE, RQ |
Dialysis | Conduct IC ≥ 4 hours after HD N/A while on CRRT, ECMO | Filtration process removes CO2, resulting in inaccurate RQ and underestimation of REE |
Potential air leaks | No bronchopleural fistula or leaks in chest tube, trach, or ETT cuff | Gas losses result in erroneous data via reduced VO2, VCO2, REE measurements |
Abbreviations: APRV, airway pressure release ventilation; CRRT, continuous renal replacement therapy; ECMO, extracorporeal membrane oxygenation; ETT, endotracheal tube; HD, hemodialysis; IC, indirect calorimetry; OT, occupational therapy; PEEP, positive end-expiratory pressure; PT, physical therapy; REE, resting energy expenditure; RQ, respiratory quotient. |
14.4.2 Protein Needs
Protein requirements often increase following neurologic injury due to hypercatabolism. At this time, it is no longer recommended to restrict protein in the critically ill patient with acute kidney injury or liver failure.5 Protein needs are typically calculated based on ideal body weight (as determined by the Hamwi method). ▶ Table 14.5 lists protein needs by clinical condition or therapy.
Weight category | BMI | Calorie needs (kcal/kg) |
Underweight | BMI < 18.5 | 30–40 |
Normal | 18.5–24.9 | 25–30 |
Overweight | 25–29.9 | 20–25 |
Obesity Class I | 30–34.9 | 15–20 |
Obesity Class II | 35–39.9 | 10–15 |
Obesity Class III (Morbid Obesity) | ≥ 40 | 10–15 |
Abbreviation: BMI, body mass index. |
Clinical condition | Protein needs by ideal weight (gm/kg) |
Stroke; AKI; hepatic failure | 1.2–2 |
HD | 1.2–1.5 |
TBI | 1.5–2.5 |
CRRT | 2–2.5 |
Abbreviations: AKI, acute kidney injury; CRRT, continuous renal replacement therapy; HD, hemodialysis; TBI, traumatic brain injury. |
14.4.3 Nutrition Support
Adequate oral intake is always the primary nutritional goal. When not feasible, enteral nutrition (EN) or parenteral nutrition (PN) should be initiated after achieving fluid resuscitation and hemodynamic stability. ▶ Fig. 14.2 lists an algorithm for determining the appropriate nutrition route.
14.4.4 Enteral Nutrition8
For patients with functional guts, the use of EN is currently recommended over PN.
• Early EN initiation (within 24–48 hours of admission) is associated with decreased
◦ Gut permeability (supports intraepithelial cell tight junctions and villi height; stimulates blood flow and release of cholecystokinin, gastrin, and bile salts)