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| Postoperative Complications | Respiratory Care| Cardiovascular Therapy| Fluid Management| Nutrition in Critical Patients |Traumatic Brain Injury-Stroke-Brain Death |

The goals of nutritional support in patients who are critically ill are to provide protein and caloric replacement while attenuating a negative nitrogen balance. It is estimated that 50% of hospitalized patients and 60% to 80% of patients in the intensive care unit (ICU) are malnourished. Delays in the initiation of nutritional support may result in muscle and gastrointestinal (GI) atrophy, inability to be weaned from ventilatory support, heart failure, impaired immunity, and an increase in the incidence of sepsis, length of hospital stay, and morbidity and mortality.
There is no doubt that effective nutritional support coupled with appropriate monitoring improves patient outcome. Since the early 1980s, the importance of nutritional support in patients who have severe neurologic injury has been appreciated. Recent studies have also documented the same nutritional and metabolic requirements in patients who have acute ischemic injury and other critical neurologic illnesses. Compelling evidence now exists that strict glycemic control in critically ill patients reduces morbidity and mortality.

I. Pathophysiology

The effects of elective operations, trauma, and critical illness activate the neural and endocrine systems. The resultant increase in sympathetic outflow leads to lipolysis, proteolysis, and decreased glucose uptake owing to the antagonism of insulin by growth hormone and epinephrine. This sympathetic surge increases energy expenditure (EE), tissue catabolism, and mobilization of protein, fat, and carbohydrates. Immobility and delays in the administration of nutritional support exacerbate these effects of increased sympathetic outflow. Other untoward effects include hyperglycemia, poor wound healing, decreased serum proteins, increased carbon dioxide (CO2) production, release of inflammatory mediators, and depressed immune function.
After neurologic injury, the ensuing state of cardiac hyperdynamism increases oxygen consumption and caloric requirements. Studies using indirect calorimetry demonstrate that patients with severe head injury are hypermetabolic and hypercatabolic. The resting energy expenditure (REE) can increase 40% to 165%. This increase has been demonstrated in patients who are treated both with and without steroids. In addition, delayed gastric emptying, bacterial translocation, and altered vascular permeability with resultant intestinal edema and malabsorption also occur.
Patients with neurologic injury. Patients who have head injury exhibit changes consistent with hypermetabolism, hypercatabolism, hyperglycemia, suppressed immunity, and a generalized inflammatory response. Nutritional support should satisfy these physiologic demands.
Patients who have suffered a stroke. These patients also exhibit hypermetabolic physiology. Although it has been suggested that protein supplementation beyond normal nutritional support after stroke may improve outcome, recent trials have not supported this strategy.
Patients who are obese. Recent estimates indicate that approximately 40% of adults in the United States are overweight. Patients who are obese are more likely to manifest comorbid medical conditions including hypertension, coronary artery disease, diabetes mellitus, pulmonary disease, and gout. Critical illness is likely to result in protein malnutrition, inhibition of lipolysis, and preferential use of carbohydrate substrate for gluconeogenesis. It has been suggested that patients who have actual body weight (ABW) in excess of 125% of ideal body weight (IBW) may benefit from diets that are hypocaloric and high protein in structure. The goal for obese patients is to provide adequate protein intake to meet but not exceed metabolic demands. Ideally, the nutritional supplementation will contain enough protein to keep the patient in a positive nitrogen balance, but sufficient relative calorie deficit to encourage a net increase in lean body mass (LBM) and a loss of total body fat.

II. Nutritional assessment

Delivery of appropriate metabolic support begins with an assessment of the patient's nutritional status. It is important to identify patients who present with subtle signs of deficiencies in caloric, protein, vitamin, or trace metal intake. These patients should be considered candidates for earlier and more aggressive support.
Definitions. The malnourished state exists when intake does not meet nutritional demands. When approximately 10% of LBM is lost, moderate protein energy malnutrition exists. A loss of 20% of LBM indicates severe protein malnutrition and describes a severely underweight patient. When more than 35% of LBM is lost, it is likely that irreversible changes leading to death have occurred.
History. In most cases, a history of recent unintentional weight loss (5% LBM in 1 month or 10% LBM in 6 months) raises the possibility of malnutrition. A careful social history may demonstrate vitamin or mineral deficiencies associated with alcoholism or other substance abuse. Patients who have renal failure lose amino acids, vitamins, and trace metals during dialysis. Patients who have cancer may have deficiencies owing either to the underlying disease or to chemotherapy (e.g., methotrexate). Other risk factors for malnutrition include age >75 years, homelessness, nothing by mouth for more than 3 days, major surgery, corticosteroid administration, renal dialysis, malabsorption syndromes, and chronic disease states, especially cancer, stroke, and acquired immunodeficiency disease.
Physical examination. Caloric intake can be assessed by the amount of fat in the extremities, buttocks, and buccal fat pad. The adequacy of protein intake can be evaluated from the bulk of the extremity muscles, grip strength, and size of the temporal muscle. Vitamin deficiencies may manifest themselves as changes in skin texture and hair quality and texture, cheilosis, glossitis, or loss of vibration and position sense. Examination of the head and neck may reveal xerostomia, malocclusion, odynophagia, dysphagia, esophagitis, or other findings suggestive of difficulty with eating.
Anthropometrics. Measurements are used to estimate the stores of body fat and protein. Body fat is approximated by the thickness of the triceps skin fold (TSF), and protein status is estimated by the mid-arm muscle circumference (MAMC).
MAMC = mid-arm circumference - fat
MAMC = mid-arm circumference - (0.314 x TSF)
These data are then compared with normal values to determine the patient's nutritional status. Two possibly incorrect assumptions are that body fat is uniformly distributed and that population standards apply to patients who are critically ill. In fact, anthropometric measurements are generally invalid in patients who are critically ill owing to anasarca. Adjustments in the estimations can be based on IBW calculated from the measurements of height and weight.
Biochemical measurements. Various biochemical and metabolic measurements have been studied as potential indices of nutritional status. Although many of these tests have significant value in assessing either stable patients who are scheduled for elective surgery or those well on the way to recovery, their applicability to patients who are critically ill has not been demonstrated. Trends between the same patient's measurements taken on different days can be used if other factors are relatively stable.
Plasma proteins. Plasma protein levels depend on hepatic synthetic function and the availability of substrate. Unfortunately, a decrease in level is not specific because the biologic half-life, the catabolic rate, and a variety of nonnutritional factors can alter plasma protein levels. For example, expansion of the extracellular fluid compartment results in a reduction in albumin concentration. In addition, some serum protein levels decrease promptly in response to trauma, sepsis, or severe illness as a result of fluid shifts, alterations in capillary permeability, and changes in rates of synthesis and degradation. Liver disease, nephrotic syndrome, eclampsia, and protein-losing enteropathies are additional causes of hypoproteinemia.
a. Albumin has a half-life of approximately 18 days. It is the most commonly used test to diagnose protein-calorie undernutrition. Depending on measured albumin alone, however, can lead to delays in treating nutritional deficits because plasma levels can be maintained for a long time owing to the long half-life. In critical illness, albumin may also remain low until the remission of the inflammatory response despite adequate nutritional intake. Serum albumin levels have been shown to be good predictors of sepsis and major infection in surgical patients. However, serum albumin has not been correlated with either morbidity or mortality in the setting of severe neurologic injury.
b. Transferrin has a half-life of approximately 8 days. Therefore, transferrin levels reflect acute changes in nutritional status more accurately than albumin. Low serum transferrin is indicative of protein malnutrition. Iron deficiency, pregnancy, and hypoxia stimulate synthesis of transferrin whereas chronic infection, sepsis, and iron overload decrease transferrin levels.
c. Thyroxine-binding prealbumin and retinol-binding protein (RBP) have a half-life of 2 to 3 days and 8 to 12 hours, respectively. RBP complexes with prealbumin in the circulation. The resultant compounds are much more sensitive to short-term alterations in protein and total caloric intake; low levels can return to normal after only 3 days of adequate nutritional support. While serum levels of the RBP-prealbumin complex reflect acute changes in nutritional status and indicate the adequacy of nutritional supplementation, many nonnutritional factors can affect these levels as well. Infection and trauma depress prealbumin levels. Stress and vitamin A deficiency decrease the concentration of RBP; renal failure can cause erroneous elevation of RBP. The short half-lives and the myriad of factors influencing their serum concentrations have limited the clinical significance and usefulness of these proteins.
Immunologic functions. Total lymphocyte count (TLC) and reactivity to skin test antigens are immunologic functions that can assess nutritional status, but they are not routinely used in patients who are critically ill. Any stressful situation, especially any disease process that requires a stay in the ICU, can depress cellular immunity, leading to a nonspecific test result.

III. Estimation of energy requirements

Because all of the previously mentioned tests measure nutritional status indirectly, other more sensitive and specific techniques have been developed to assess nutritional status.
Predictive equations
Harris-Benedict equation. REE is the energy requirement at rest and can be estimated using the Harris-Benedict equation as follows:
Women: REE (kcal/day) = 65 + 9.6W + 1.8H - 4.7A
Men: REE (kcal/day) = 66 + 13.7W + 5H - 6.8A
where W = ABW in kilograms or IBW in kilograms if the patient is edematous; H = height in centimeters; and A = age in years. If the patient is obese, an adjusted IBW should be used as follows:
Adjusted IBW = IBW + 0.25 (ABW - IBW)
Adjustments to REE. EE can vary greatly from daily resting energy requirement in active subjects. Hospitalized patients typically require 30 kcal/kg/day in the absence of severe illness or obesity. Fever increases the REE by approximately 10% above baseline for each degree Celsius rise in temperature. Brain injury induces a hyperdynamic state. Elevated EE is usually associated with total body surface area burns of 20% to 40%. Figure 21-1 shows the EE as the percentage above normal for several disease states. A common practice is to adjust the estimated REE for the state of hypermetabolism that characterizes patients who are critically ill. Usual correction factors are as follows:
Fever: REE × 1.1 (for each 1C above normal)
Mild stress: REE 7times; 1.2 - 1.3
Moderate stress: REE 7times; 1.4 - 1.5
Severe stress: REE 7times; 1.6 - 1.8
Using predictive equations in patients who are critically ill has a potential limitation. The Harris-Benedict equation was determined using healthy volunteers as test subjects. The validity of applying this equation to patients who are critically ill has been questioned.
Indirect calorimetry. Indirect calorimetry relies on the measurement of oxygen consumption (Vco2) and the production of carbon dioxide (Vco2). The oxygen consumed in a given period of time is the amount required for oxidation of carbohydrate, fat, and protein.
Simultaneously, CO2 is produced from the oxidation of carbohydrate, fat, and protein. If the patient inspires a known concentration of O2 and CO2, measurements of Vco2 and Vco2 can be made. A metabolic computer can then calculate the REE and the respiratory quotient (RQ). Normal RQ is 0.8. An elevated RQ indicates overfeeding or excess carbohydrate in the diet.

Figure-1. Energy expenditure as a percentage above normal in several disease states

Usually, measurements taken over a minimum period of 20 to 30 minutes generate better baseline values. Indirect calorimetry can be performed only on patients who have fraction of inspired oxygen (Fio2) requirements of 50% or less. To account for sedation, ICU activity, dietary-induced thermogenesis, anabolism, and the work of breathing, an extra percentage is added to the measured EE. Examples of usual correction factors are as follows:
Thermogenesis: 5% to 10%
ICU activity: 10%
Anabolism: 5% to 10%
Sedation: 0% to 30%
REE can be calculated using indirect calorimetry:
REE (kcal/day) = (3.9 x [Vo2] + 1.1 x [Vco2]) x 1.44
The Fick equation and mixed venous oxygen content (Cvco2). The 24-hour EE for an ICU patient is approximately 7 times the Vco2, calculated using measured arterial oxygen content (Caco2), mixed venous oxygen content (Cvco2), and the cardiac output (CO). The arterial oxygen saturation (Sao2) and mixed venous oxygen saturation (Svco2) should be measured at the same time that CO is measured.
Cao2 - Cvo2 = Hb (g/dL) x1.39 x (Sao2 - Svo2)
Vo2 (mL/minute) = (Cao2 - Cvo2)x 10 x CO (L/minute)
24-hour EE (kcal/day) = 7 x Vo2
These "spot" measurements should be performed for several days in succession to establish an accurate trend.

IV. Estimation of protein requirements

The daily protein requirements are usually estimated first and measured later.
Predictive equations. The goal of protein supplementation is to decrease the degree of loss of LBM because there are no protein stores in the body. Approximate protein requirements can be estimated on the basis of the patient's weight, degree of illness, and extent of organ system failure. High-dose steroids, which are often given to patients after neurologic insult, also increase protein requirements because of catabolism.
Normal protein requirement: 0.8 to 1 g protein/kg/day
Mild stress requirements: 1 to 1.2 g protein/kg/day
Moderate stress requirements: 1.2 to 1.4 g protein/kg/day
Severe stress requirements: 1.4 to 1.6 g protein/kg/day
Patients in renal failure on hemodialysis: 1.2 g protein/kg/day
Patients who have encephalopathy: 0.8 g protein/kg/day
Studies of patients with head injury receiving 1 to 1.5 g protein/kg/day have still reported negative nitrogen balances. Current recommendations are to provide 2 g protein/kg/day if renal function is normal and to reassess the nitrogen balance in a few days.
Postsurgical patients typically require 2 g protein/kg/day.
Nitrogen balance. Nitrogen balance is used to assess the adequacy of caloric and/or protein intake and whether the anabolic state has been achieved as a result of nutritional therapy. Nitrogen balance equals nitrogen intake minus nitrogen output. Total nitrogen output equals urine urea nitrogen from a 24-hour urine collection and 2 to 4 g/day of nonurinary losses. In patients who are critically ill, this may be as much as 6 g/day owing to blood loss, increased mucosal sloughing, and increased fecal nitrogen loss from diarrhea. Because protein is 16% nitrogen, each gram of urinary nitrogen represents 6.25 g of degraded protein.
Nitrogen balance = (protein intake/6.25) - (urine urea nitrogen + [2 or 4])
Measurements of nitrogen balance may not be reliable in patients who have renal and hepatic failure owing to altered protein synthesis and clearance. For patients who are in renal failure, the creatinine (Cr) clearance must be >50 mL/minute to achieve a valid result.

V. Macronutrients

Carbohydrates. As long as the diet provides adequate energy and protein, there is no specific requirement for dietary carbohydrate, but current recommendations are to provide 50% to 60% of total calories as carbohydrates. Much of this is used by the central nervous system, which relies on glucose as its primary fuel source.
Fat. The goals of lipid supplementation include providing for essential fatty acids, promoting nitrogen sparing, and offering a balanced approach to fulfilling energy requirements. Increased fat decreases the incidence of hepatic steatosis and the production of CO2 from a high-carbohydrate diet. Lipid oxidation as an energy source is increased in the patient who is critically ill. The recommendation is therefore to provide 30% to 40% of the total calories as lipid. A minimum of 3% of the kilocalories delivered as fat should be linoleic acid to prevent a deficiency of essential fatty acids.
Protein. The goal of protein supplementation is to provide substrate for cellular protein synthesis and the maintenance of LBM. Protein requirements increase if excessive losses from the GI tract, skin, or draining wounds occur. It is often difficult to achieve positive balance in patients who are critically ill, but the effort to minimize negative nitrogen balance should be made.
Fluid. Nonhospitalized patients consume approximately 1 mL of free water/kcal ingested. With a normal diet, this is approximately 30 to 50 mL/kg of body weight per day. Patients who are hospitalized typically require 30 to 35 mL/kg/day. The patients' underlying medical condition and comorbidities must be considered when replacing fluids. Patients should be adequately volume resuscitated before initiating parenteral nutrition.
When calculating free water replacement in patients receiving enteral nutrition, it is important to remember to subtract the free water in the enteral formula from the total daily volume of free water.

VI. Micronutrients

Because the response to injury is characterized by greatly increased energy demands and clinical malnutrition, appropriate nutritional support might prevent the multisystem organ failure that often occurs in patients who are critically ill. The gut is now being seen as an important metabolic organ that has a critical need for certain substrates. Clinical trials are being conducted to evaluate diets enriched with immunomodulatory components. Although the use of these components has been advocated, currently their benefits remain controversial.
Vitamins. Vitamins are involved in metabolism, wound healing, and immune function. They are essential and cannot be synthesized by the body. The 12 essential vitamins that should be supplied daily are divided into fat- and water-soluble categories. Recommended dietary allowances of vitamins are listed in Table-1.
Trace nutrients. Deficiencies in the nine essential trace elements can lead to problems in several organ systems including insulin resistance, myopathy, increased susceptibility to infections, and pancytopenia. Recommended dietary allowances of trace elements are listed in Table-2.

Table-1. Recommended dietary allowance of vitamins for a healthy 25- to 50-year-old man
Vitamin Amount Vitamin Amount
Vitamin A 1,000 mcg Vitamin D 5 mcg
Vitamin E 10 mg Vitamin K 80 mcg
Vitamin C 60 mg Thiamine 1.5 mg
Riboflavin 1.7 mg Niacin 19 mg
Vitamin B6 2 mg Folate 200 mcg
Vitamin B12 2 mcg    

For patients in renal failure, zinc and chromium should be either reduced or omitted because they are excreted in the urine. Similarly, in the presence of biliary tract obstruction, the intake of copper and manganese is either reduced or omitted because both are excreted primarily in the bile.
Decreased serum zinc levels and increased urinary zinc losses have been reported after a head injury, although the mechanism and clinical significance are unknown. No other specific changes in vitamin and mineral metabolism have been identified after neurologic injury.
Glutamine. The primary fuel for the intestine, glutamine is important in maintaining intestinal structure and function, preventing mucosal atrophy during starvation, decreasing bacterial translocation, and stimulating the intestinal immune system in sepsis and stress. Glutamine may also decrease intestinal injury during ischemia by preserving the level of glutathione in the gut.

Table-2. Recommended dietary allowance of trace elements for a healthy 25- to 50-year-old man
Element Oral Intravenous
Zinc 10-15 mg 2.5-4.0 mg
Chromium 50-290 mcg 10-15 mcg
Copper 1.2-3 mg 0.5-1.5 mg
Manganese 0.7-5 mg 0.15-0.8 mg
Selenium 50-200 mcg 40-120 mcg
Molybdenum   200 mcg

Arginine. Arginine improves wound healing, stimulates immune function by increasing the production of natural killer and helper T cells, and enhances intestinal absorption and proliferation. Arginine is also responsible for the synthesis of nitric oxide, which maintains the integrity of microvascular structure in the gut after injury.
Omega-3 fatty acids. The omega-6 fatty acids have been shown to impair the immune response by generating degradation products that suppress T cell and macrophage activity. Replacement of dietary omega-6 fatty acids with omega-3 fatty acids might down regulate several aspects of the inflammatory response and thereby improve immune function. A few reports have indicated, however, that omega-3 fatty acids may interfere with wound healing. Balance should therefore be maintained between the two fatty acids.
Dietary nucleotides. Dietary nucleotides are important for intestinal structure and function. In animals, the addition of dietary nucleotides to total parenteral nutrition (TPN) diminishes the intestinal mucosal atrophy. Ribonucleic acid nucleotides have also been shown to stimulate the immune system by promoting the development of T lymphocytes.
Growth hormone. In patients who are critically ill, growth hormone has beneficial anabolic effects. It is associated with the mobilization of fat stores as an energy source and the enhancement of whole-body protein stores in trauma patients. TLC and serum albumin and transferrin levels have also increased after the administration of growth hormone. Intestinal function is also enhanced directly by the binding of growth hormone to growth hormone receptors in the gut and indirectly by the growth hormone's stimulation of insulin-like growth factor.
Anabolic steroids. Anabolic steroids are sometimes used as a replacement for growth hormone because of their beneficial effect on the deposition of lean tissue. They cause less hyperglycemia than growth hormone and also cost substantially less.

VII. Timing and route of feeding

Although some patients can safely tolerate protein and calorie deprivation for several days, nutritional support should not be delayed in patients who are critically ill and are not expected to have any oral intake for a prolonged period. Nutritional support should also be administered promptly to patients who will have huge caloric requirements from burns, sepsis, trauma, or head injury. The decision as to which route (enteral or parenteral) to use involves assessing the functional capacity of the gut. It is important to remember that enteral feeding and parenteral feeding are not mutually exclusive; combinations are often appropriate. Each has specific advantages and complications, but overall, it appears that early nutritional support is more important than the route chosen.
Enteral feeding. If the GI tract is functional, enteral feeding is preferred because it is easier, safer, and less expensive. Auscultation of the abdomen for bowel sounds as an indication of bowel function can be misleading. The absence of bowel sounds does not mean the absence of bowel function. If no air is present, there will be no bowel sounds, but the small bowel will likely still have peristalsis and absorptive function. Contraindications for the use of tube feedings include ileus, intestinal obstruction, and the need for total bowel rest. Studies in animals have shown that villus atrophy increases intestinal permeability, and bacterial translocation occurs after parental nutrition and gut disuse. Although this has yet to be demonstrated in humans, the occurrence of the sequence has been extrapolated from clinical cases in which bacteria from the gut have been cultured in patients who are critically ill and had no clear focus of abdominal infection.
Types of formulas. The selection of an enteral formula is based on the patient's digestive capacity and specific nutritional needs. Table-3 lists some enteral formulas and their nutritional components.
Polymeric contains intact nutrients and requires normal digestion and absorption.
Fiber enriched is frequently used in patients who have diarrhea or constipation.
Calorically dense is used in patients who have cardiac, renal, or hepatic failure and when fluid restriction is required.
Elemental contains one or more partially digested macronutrients and is used in patients who have compromised GI function.
Modular is composed of individual nutrient modules to produce a formula customized to meet a patient's specific needs. These formulations have increased caloric and protein concentrations. They can also be used to modify a preexisting commercial formula to add to the caloric and/or protein density.
There has been a great deal of interest in the immunomodulating potential of nutrients such as omega-3 fatty acids, branched-chain amino acids, nucleotides, arginine, and glutamine. While these nutrients do change the intermediate metabolic pathways that affect cellular survival invitro, thus far randomized trials have not demonstrated any difference in length of hospital stay, morbidity, or mortality.

Table-3. Enteral formulas and their components

        Composition per liter (g)
Product Formula type kcal/mL mosmol Protein Fat CHO
Osmolite Polymeric 1.06 300 37 38 145
Osmolite HN Plus   1.2 360 56 39 158
Jevity Fiber-enriched 1.06 300 44 36 151
Jevity Plus   1.2 450 56 39 175
Glucerna   1 375 42 56 94
Two Cal HN Calorically dense 2 690 84 91 217
Peptamen Peptide-based (semielemental) 1 270 40 39 127
Peptamen VHP   1 300 62 39 104
Crucial   1.5 490 94 68 135
Vivonex Plus Elemental 1 650 45 6.7 189

CHO, carbohydrate.

Routes of enteral feeding
Gastric. Gastric feeding can be established either by the insertion of a feeding tube through the nose to the stomach or by the surgical insertion ("open" or laparoscopically) of a gastrostomy tube. This method takes advantage of the reservoir capacity of the stomach, but many patients, especially those who have elevated intracranial pressure, might not tolerate this owing to delayed gastric emptying, impaired gag reflex, and/or gastric atony.
Duodenal. The proposed advantage is that there is reduced risk of reflux and aspiration, but, unfortunately, there is no evidence to support this hypothesis. Patients can still aspirate, even with jejunal feeds. Feedings given into the duodenum must be as continuous infusions because large boluses are not tolerated.
Percutaneous enteral tubes. Gastric (percutaneous endoscopic gastrostomy [PEG]) and jejunal (percutaneous endoscopic jejunostomy [PEJ]) tubes can be inserted percutaneously under either fluoroscopic or endoscopic guidance. PEG tubes allow enteral feeding of patients who have dysphagia or altered mental status. PEJ tubes allow enteral nutrition with a reduction in gastric residuals. Neither PEG nor PEJ feeding prevents aspiration.
Initiation and advancement. Before initiating enteral feeding, proper placement of the enteral tube should be ascertained radiographically. An abdominal radiograph is performed to locate the distalmost portion of the enteral tube.
Isotonic solutions can be started slowly at full strength and then the rate advanced as tolerated until the goal rate is achieved. Hypertonic solutions should be diluted to isotonicity and the concentration advanced to full strength before the infusion rate is increased. These strategies help guard against diarrhea and electrolyte disturbances.
Enteral feeding through the stomach (nasogastric or PEG) is typically advanced while monitoring gastric residuals. Patients requiring intensive care often have delayed gastric emptying and gastric distention, which predispose them to aspiration. Enteral feeding may begin at 10 to 15 mL/hour; and the rate is increased by 10 to 15 mL/hour every 8 hours until a predetermined goal rate is reached. If the feeds are delivered to the stomach, gastric residuals should be checked every 6 hours and infusions held for residuals of >200 mL.
Emesis, gross abdominal distention with absent bowel sounds, and radiographic evidence of bowel obstruction necessitate alterations in feeding.
Complications of enteral feeding
Mechanical. Misplaced nasal feeding tubes might end up in the bronchus or in the brain in patients who have fractures of the cribriform plate. There is also a higher incidence of epistaxis and sinusitis because the tube passes through the nares.
GI. Nausea and vomiting might occur from postinjury ileus and gastric atony. Diarrhea can be a problem because of the concentration, osmolarity, or volume of the administration of the tube feeds; the presence of lactose, fat, or gluten; low residue; or bacterial contamination. Diarrhea may also be caused by either the lack of fiber or an intestinal obstruction and may lead to either free water deficits or dehydration.
Pulmonary. Pulmonary aspiration is probably the most common serious, potentially fatal complication of enteral nutrition. The reported incidence is highly variable (0% to 95%), depending on the population of patients studied and the definition of aspiration because chemical evidence of aspiration is more common than clinically diagnosed aspiration pneumonia. The presence of tube feeds in the pulmonary secretions can be detected by checking for glucose or adding food coloring to the feeds and checking the secretions for a color change.
Metabolic. Osmolarity and volume status must be carefully monitored to avoid hyperosmolarity and volume overload. Electrolyte imbalance (e.g., hyponatremia) is common, especially in patients who have a head injury and are at risk for the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or diabetes insipidus. Hypophosphatemia, hypokalemia, and hypomagnesemia occur commonly when feeding is begun again.
Parenteral feeding. TPN should be initiated when gut failure is demonstrated. Before initiating parenteral nutrition, the patient's total energy requirements, total protein requirements, daily fluid requirements, and the proportion of calories to be delivered as fat must be determined.
Parenteral solutions. There are three elemental nutrients in parenteral nutrition.
1. Dextrose is available in concentrations ranging from 10% to 70%. The higher the percentage of dextrose, the higher the osmolarity and the greater the need for central access. Only solutions with <10% dextrose are considered safe for peripheral venous administration because solutions with an osmolarity of >900 mOsm/L can cause either sclerosis or phlebitis.
2. Amino acids provide for protein requirement.
3. Fat emulsions are rich in linoleic acid. The infusions are given over several hours, and the rate of infusion should be adjusted for patients receiving propofol for sedation. Propofol is in a fat emulsion and provides the equivalent of 1.1 kcal/mL of fat calories.
4. Additives such as electrolytes, vitamins, and trace elements are added directly to the dextrose and amino acid infusion.
Routes of parenteral feeding. Intravenous calories can be given peripherally or centrally.
1. Peripheral access for administration of TPN should be used only for short-term nutritional support. The hyperosmolarity and low pH of TPN predispose small veins to thrombophlebitis. It is also difficult to provide the necessary caloric requirements by way of this route owing to the limitations imposed by dextrose (maximum 10%) and amino acid concentrations. Long peripheral lines that extend into a central vein can be used as a central line and do not have the same limitations from the dextrose and amino acid concentrations.
2. Central access should be used when longer periods of parenteral feeding are necessary or if the patient is seriously ill.
Initiation and advancement. Parenteral nutrition is usually started at a slow rate of infusion and then the rate is advanced every 12 to 24 hours until the goal rate is achieved. When the infusion is discontinued, the rate should be tapered so that hypoglycemia does not result from the increase in insulin production stimulated by the parenteral nutrition.
Mechanical. Significant venous thrombosis, which can usually be diagnosed by ultrasound or the injection of radiopaque contrast, requires the removal of the catheter and heparinization. Catheter infections must always be suspected. Meticulous catheter care, a high index of suspicion, and a low threshold for removal are essential.
GI. Elevated transaminases are common at the beginning of the administration of TPN, but they should not persist for long. Fatty liver might develop from the excess carbohydrates or total calories in the diet. Cholelithiasis or gall bladder sludge might be secondary to changes in bile composition as well as the decreased frequency of gallbladder contractions. These usually resolve after enteral alimentation has been initiated.
Metabolic. Elevations in glucose can occur early from relative insulin resistance and might require an infusion of insulin. Hypercapnia can result from refeeding a malnourished patient who cannot adequately increase minute ventilation. Decreasing the daily calories or replacing dextrose with fat can reduce carbon dioxide production. Any electrolyte abnormality can occur, so that daily adjustments must be made in conjunction with the laboratory results. Suggested laboratory monitoring guidelines are listed in Table 21-4. Vitamin K is the most common vitamin deficiency, because it is not contained in multivitamin preparations.
Monitoring. While receiving enteral or parenteral nutrition, the patient must be monitored for changes in body composition, blood chemistry, blood glucose, triglycerides, and protein synthesis.

Table-4. Suggested monitoring guidelines for enteral and parental nutrition

Schedule Enteral Parenteral
Baseline Electrolytes, BUN, Cr, Ca, Mg, PO4, glucose, albumin Electrolytes, BUN, Cr, Ca, Mg, PO4, glucose, liver function tests, triglycerides, cholesterol, albumin
Daily Intake and output, weight Intake and output, weight
Daily until stable; then 2 to 3 times/week Electrolytes, BUN, Cr, glucose Electrolytes, BUN, Cr, glucose
Every other day until stable; then 1 to 2 times/week Ca, Mg, PO4 Ca, Mg, PO4
Every 10-14 days Albumin Liver function tests, albumin, triglycerides
Weekly PT, prealbumin PT, prealbumin
BUN, blood urea nitrogen; PT, prothrombin time; Cr, creatinine; PO4, phosphate.

Daily weight and the total volume of the patient's intake and output need to be monitored in addition to assessing other markers of hydration and volume status.
Electrolytes (Na, K, Cl, Mg, Phosphate, and Ca) and markers of renal function (blood urea nitrogen and creatinine) should be monitored routinely.
Intensive glycemic therapy in patients who are critically ill has been shown to reduce morbidity and mortality to a significant extent. Maintaining blood glucose levels of 80 to 110 mg/dL in all patients who are critically ill, regardless of preexisting diabetes mellitus, resulted in a relative morbidity and mortality risk reduction of approximately 40%. Recent studies also suggest that tight glycemic control in patients who have isolated severe brain injury may reduce secondary central and peripheral neurologic injury.
Hypertriglyceridemia is a potential complication of sedation with continuous infusion of propofol because of the lipid carrier solution. Escalating or preexisting elevated triglyceride levels may predispose patients to pancreatitis and therefore necessitate alternate sedation strategies.
Refeeding syndrome. Patients who are severely malnourished could have a physiologic response to carbohydrate utilization. During starvation, insulin production decreases in the absence of carbohydrates. Protein and fat are preferentially used to meet metabolic demands. As a result, intracellular electrolytes are depleted, especially phosphate. When carbohydrates are administered, insulin causes electrolyte and fluid shifts. This results in hypokalemia, hypomagnesemia, hypophosphatemia, and fluid retention. Without phosphate, adenosine triphosphate cannot be generated. In the most severe cases, arrhythmias, heart failure, respiratory failure, seizures, or death may occur. Prolonged fasting, prolonged intravenous hydration, chronic malnutrition, chronic alcoholism, and anorexia nervosa are a few of the risk factors for the refeeding syndrome. Closely monitoring electrolytes and vital signs can prevent a potentially fatal complication of refeeding patients who are severely malnourished.


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