14 Nutrition



Stephanie Dobak and Jacqueline S. Urtecho


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.




14 Nutrition




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





















































































Table 14.1 Intensive insulin therapy (IIT) RCTs

Trial (year)


N


Setting


Primary outcome


IIT group glucose range (mg/dL)


P-value


Van den Berghe (2006)


1,200


MICU


Hospital mortality


80–110


NS


HI-5 (2006)


240


CCU (AMI)


6 m mortality


<180


NS


Glucontrola (2009)


1,101


MICU/SICU


ICU mortality


80–110


NS


Gandhi (2007)


400


OR (cardiac)


30 d mortality/ morbidity


80–100


NS


VISEPb (2008)


537


ICU (severe sepsis)


28 d mortality/ organ failure


80–110


NS


De La Rosa (2008)


504


MICU/SICU


28 d mortality


80–110


NS


Oddo (2008)


20


Neuro-ICU


Cerebral glucose metabolism


80–120


<0.01 (increased cerebral metabolic crisis with IIT)


NICE-SUGAR (2009)


6104


ICU


3 m mortality


81–108


<0.05 (increased mortality with IIT)


Vespa (2012)


13


ICU (TBI)


Brain metabolism


80–110


0.05 (increased cerebral metabolic crisis with IIT)


aTrial stopped early due to high rate of protocol violations.


bTrial ended early due to safety concerns (severe hypoglycemia and SAEs)


Abbreviations: CCU (AMI), coronary care unit (acute myocardial infarction); ICU, intensive care unit; MICU, medical intensive care unit; OR, operating room; RCT, randomized control trial; SAEs, serious adverse events; SICU, surgical intensive care unit; TBI, traumatic brain injury.



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



  • Delayed wound healing



  • Overall increased risk for morbidity and mortality 7 , 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.








































Table 14.2 Criteria for diagnosing malnutrition in acute illness/injury 9 a

Malnutrition severity


Energy intake


% Weight loss


Muscle wasting


Subcutaneous fat wasting


Fluid accumulation


Grip strength


Severe


≤50% kcal of estimated energy requirement for ≥5 days


>2% in 1 week


>5% in 1 month


>7.5% in 3 months


Moderate


Moderate


Moderate to Severe


Measurably reduced


Moderate


< 75% of estimated energy requirement for >7 days


1–2% in 1 week


5% in 1 month


7.5% in 3 months


Mild


Mild


Mild


N/A


atwo criteria must be met to diagnose



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

Fig. 14.1 Measures to prevent refeeding syndrome.



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.








































Table 14.3 Variables affecting indirect calorimetry measurement 10

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.








































Table 14.4 Calorie needs determined by adult weight categories/BMI

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.


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Feb 6, 2021 | Posted by in NEUROLOGY | Comments Off on 14 Nutrition

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