1. Nutritional support Dr. Abdul-Monim Batiha Assistant Professor Critical Care Nursing Philadelphia university

2. Critically ill patients are often unable to eat because of 1- Endotracheal intubation. 2-The need for mechanical ventilation. 3-Altered level of consciousness as a result of severe trauma, major surgery or acute medical condition.

3. lack of nutrients may: 1-Alter the structure and function of the gut. 2-Increase the risk of entry and spread of intestinal bacteria.

4. Early nutritional support for critically ill patients has been advocated to: 1-Promote the immune system recovery 2-prevent as much as tissue breakdown 3-nutritional deficit as possible

5. 4-Improves patient outcomes. 5-Enhances recovery from illness.

6. Nutritional support means the provision of patient's dietary requirements

7. Nutritional support: includes: the use of artificial feeding methods such as tube feeding (enteral feeding), totalparenteral nutrition (TPN)and administration of intravenous fluids

8. Enteral feeding should be prescribed whenever oral intake is inadequate for the patient who has a functional gastrointestinal tract.

9. Enteral feeding has several advantages over total parenteral nutrition: 1-EN has been shown to be easier, safer and cheaper than PN. 2- EF maintains the structure and functional integrity of the gastrointestinal tract by intraluminal delivery of nutrients and preventing atrophic changes.

10. 3-EF preserves the normal sequence of intestinal and hepatic metabolism, fat metabolism, lipoprotein synthesis and prevents cholestasis by stimulating bile flow.

11. 4-Maintains normal insulin / glucagon ratios. 5-Reduction in septic complications with EF compared with PN. 6-EF improves systemic immunity and lower infection risk. 7- Prevents translocation of bacteria into the systemic circulation and reduce the incidence of sepsis.

12. On the other hand, intragastric EN often is complicated by intolerance, as indicated by elevated volumes of aspirated gastric residual. High gastric residual is a return of at least half of the hourly feeding rate. It is commonly accepted that high gastric residual volume enhances regurgitation and increases the risk for aspiration pneumonia.

13. Gastric residual is the amount of previous feeding remaining in the stomach

14. Gastric volume during intragastric feeding is determined by the balance between The amount of infused formula plus The endogenous secretions of saliva And gastric juice and The amount of fluid emptied from the stomach.

15. Fluids that commonly accumulate in the gastrointestinal tract of a tube fed patient include the 1-Feeding formula, 2-Swallowed saliva (> 0.8 L/ day), 3-Gastric secretion (1.5 L/ day), 4-Small bowel secretion regurgitated into the stomach (2.7 – 3 L/ day).

16. Critical care nurses play a crucial role before initiating NS to prevent high residual volume and other complications.

17. Critically ill patients with feeding tubes are therefore at higher risk for adverse outcomes than are other patients with feeding tubes

18. Most complications can be prevented with close monitoring and timely and accurate assessment of a patient’s tolerance to feeding.

19. Nurses are responsible for monitoring tolerance for the duration of therapy. A- Residuals should be checked for color, consistency and amount of last feeding still in the stomach, also for tolerance of enteral feeding.

20. B- Haemodynamic status should be monitored during nasogastric tube feeding.

21. Patients receiving isotonic formulas who are given too much fluid may show signs of fluid excess such as weight gain, edema and may develop dilutional hyponatremia.

22. On the other hand, patients receiving hypertonic, high-protein feedings who do not ingest enough fluid are at risk for life- threatening condition called tube-feeding syndrome, characterized by fluid-volume deficit, hypernatremia, hyperchloremia and azotemia.

23. So it is very important to monitor and assess fluid intake and output such as 1- body weight, 2-edema and respiratory rate, 3-blood urea nitrogen and other electrolytes.

24. The practice that is very important during feeding is measuring the gastric residual volumes: to help the nurse to confirm the placement of the tube, determine the nutritional tolerance and occurrence of gastric delay and if a high gastric residual volume can be detected early, it may be possible to prevent complications.

25. COMPLICATIONS OF EF

26. Mechanical complication Gastrointestinal complications Metabolic complications

27. Mechanical complication

28. Aspiration Tube obstruction Tube displacement

29. Aspiration is the most dangerous mechanical complication associated with EF. Pulmonary aspiration of EF with subsequent pneumonia is a frequent and serious complication of enteral nutrition in critically ill adults despite the presence of cuffed and properly inflated endotracheal tubes.

30. Aspiration pneumonia develops in 43% of patients on nasogastric tube feeding and in 56% of patients with a gastrostomy

31. CAUSES OF ASPIRATION

32. A-When gastric motility is moderately or seriously impaired, feedings accumulate in the stomach along with gastric secretions and predispose to reflux and aspiration. Therefore, if a high gastric residual volume can be detected early, it may be possible to prevent aspiration.

33. Nosocomial pneumonia accounts for 13% to 18% of nosocomial infections and is the leading cause of death. Rates of nosocomial pneumonia and associated mortality are high in patients receiving mechanical ventilation and aspiration is the primary route by which bacteria enter the lung.

34. B-Other common causes of aspiration is tube placed in the trachea and regurgitation, this can be prevented by several techniques such as: 1-Checking the tube position before feeding

35. 2-Elevating head of bed 30-60 degree during feeding and for one hour afterwards and if feeding is given by bolus. 3-No more than 330 ml should be given at one feeding to prevent excessive distension of stomach. 4-Also checking the gastric residual before each feed and if more than 150 ml, feeding should be held to prevent gastric distension.

36. NURSING ROLE

37. Critical care nurses play a vital role in early detection of aspiration of gastric content into the pulmonary bed through the following methods :

38. food coloring method Checking Ph glucose strips

39. Using the food coloring method, by adding blue food coloring to feeding formulas to achieve a visible blue color, then suctioning tracheal secretions into transparent suction trap and examining the specimen for blue discoloration against a white background under full room lighting.

40. Checking pH is another method for detecting aspiration of gastric fluid into the lungs, because pulmonary fluid has a pH of approximately 7.6 while gastric pH is less than 4.

41. Moreover glucose strips can help to identify the fluid aspirated from the nasogastric tube as follows: a positive glucose reading is defined as a tracheal secretion specimen having a glucose concentration of ≥20 mg /dl measured using an automated glucose meter.

42. Presumptive aspiration is defined as having occurred when tracheal secretions showed either a positive glucose reading or observable blue discoloration.

43. On the other hand, measuring the glucose level is considered a more labored intensive technique because nurses should be trained and certified to use the bedside glucose testing equipment, in addition to the costs associated with the glucose strips.

44. Clinically, significant aspiration is defined as the occurrence of objective aspiration combined with one or more signs of systemic inflammation (temperature ≥ 37.8oC; heart rate ≥ 100 beats/min; leukocyte count ≥ 10.000 /cu mm)

45. and one or more signs of respiratory deterioration (respirations ≥ 20/min Pao2 0.50) in addition to X ray

46. So it is very important to observe and measure the vital signs to determine the occurrence of aspiration and any alterations in the haemodynamic status that can lead to increasing the days remaining in the hospital and on nasogastric tube feeding

47. Gastrointestinal complications

48. Nausea and vomiting, Constipation Delayed gastric emptying Distension Diarrhea

49. Nausea and vomiting associated with EF can be caused by the following: 1-Tube migration into the esophagus, 2-Decreased absorption that lead to increase the gastric residual volume and hyperosmolar formula and excessive infusion of air. 3-An excessive accumulation of EF and gastric secretions increases the potential for regurgitation and vomiting.

50. Nursing interventions to reduce this complication include : 1-Checking residuals and holding feeding for one hour and rechecking if high gastric residual is found. 2-The head of the bed should be kept elevated. 3-When giving a bolus feeding, tubing should be pinched off when refilling syringe with formula and when giving continuous feeding, checking that the bag does not empty before closing off tubing is importance.

51. Also when patients experience nausea, it is important to empty the stomach by aspirating the gastric residual volumes through the gastric tube.

52. 4- Other interventions to reduce nausea and vomiting include changing the formula to low- fat formula. 5-Administering prokinetic agent (metoclopramide, cisapride) to stimulate gastrointestinal motility. 6-Positioning the patients on the right side to facilitate the passage of gastric contents through the pylorus. 7-Maintaining the patients head of bed elevated at 30-45 degree angle during feeding and for 30-60 minutes after feeding.

53. Delayed gastric emptying: is also considered among the problems associated with EF. To determine the presence of delayed gastric emptying, measuring gastric residual volumes should be done. Residual volume greater than the hourly rate indicates impairment in gastric emptying.

54. Delayed gastric emptying can be caused by several causes such as critical illness, high density and high lipid content and effect of medication such as narcotic

55. Distension is another gastrointestinal complication associated with tube feeding, causes of distension may include: 1-Poor gastric emptying that lead to increase gastric residual volume. 2-Rapid infusion of feeding and constipation or diarrhea.

56. Air in the tube Cold formula and bolus feeding rapidly administered.

57. Nursing measures to reduce distension include: 1-Reducing the rate of infusion and giving gastric motility agents. 2-If possible encourage mobility and treat constipation or diarrhea. 3-Check the rate and temperature of the formula before administration. 4-Eliminate all air from the delivery system before attaching it to the feeding tube and always keep tube clamped between intermittent feedings.

58. Diarrhea: There are several causes leading to diarrhea namely: Drug therapy Hypoalbuminemia or high osmolarity of the formula, The rapid infusion, bolus feeding, Bacterial-contaminated: feeding which is considered a significant cause of diarrhea. Potential contamination during checking residual volumes can occur, since this is not a sterile procedure.

59. In addition to the formula which can become contaminated at any point in the preparation and delivery process as well as temperature of the formula. However, the cause of diarrhea is often multifactorial, particularly in critically ill patients.

60. When patients have moderate deficits in serum albumin levels indicating malnutrition, possibly this malnutrition leads to less efficient intestinal absorption which predisposes the patient to diarrhea. Also pulmonary patients who are critically ill and require mechanical ventilation may be in catabolic phase of metabolism which may decrease the ability of the gut to absorb.

61. The treatment of diarrhea is based on the cause and is aimed at replacing fluid and electrolytes and decreasing the number, volume and frequency of stools.

62. Nursing management include the following: 1-Evaluating the drug regimen for possible cause of drug-induced diarrhea such as antibiotic, magnesium-containing antacids 2-Checking the serum albumin levels, 3-Administering formula requiring less digestion and by a slow rate, 4-Administering lactose-free formula,

63. 5-Replacing the bag and tubing using aseptic techniques and careful hand washing before formula administration, 6-Changing to high fiber formula. 7-Assessing fluid balance, electrolyte levels 8-As well as checking formula temperature..

64. Metabolic complications

65. Consist of fluid and electrolytes imbalance namely; Hypernatremia, Hhyponatremia, Hhyperkalemia, Hhypokalemia, Overhydration, Dehydration, Hyperglycemia and hypoglycemia.

66. The loss of gastrointestinal secretions by vomiting, diarrhea or nasogastric suctioning may cause sodium, potassium and chloride loss, excessive gastric residual can be reinjected to prevent electrolyte abnormalities and nutrients loss.

67. The basal oral potassium requirement is 5 –6 m mol / kg body weight per day, however, in depleted and catabolic patients this may increase to a maximum of 9 m mol / kg body weight over 24 hours. Intravenous potassium chloride is usually given for correcting potassium deficit and maintaining potassium balance.

68. Hyperkalemia ( ↑ 5.0 m Eq/L) may be caused by: extrarenal causes such as metabolic acidosis, decreased insulin availability/hyperglycemia that is enhancing the delayed gastric emptying and may increase the gastric residual volume, exercise, tissue catabolism, excessive intravenous infusions or oral administration of potassium, blood for transfusion that is two weeks old or more and digitalis overdose.

69. Renal causes include renal failure, renal insufficiency, decreased urine output after surgery, decreased effective arterial blood volume miner alocorticoid deficiency that may result from either the production of aldosterone or the diminished effect of the hormone on the kidney.

70. The nursing management include reducing potassium intake, closely monitoring of serum potassium level, in addition to the flow rate of intravenous fluid with potassium

71. Hypokalemia (↓3.5mEq/L) may be due to extrarenal causes such as gastrointestinal losses namely; vomiting, diarrhea, nasogastric suctioning that lead to decrease the gastric residual volumes, excessive tap water enemas,

72. medications such as potassium-wasting diuretics, insulin which moves glucose and potassium back into cells, steroids and beta-adrenergics promot potassium loss and alkalosis which causes potassium to shift into cells in exchange for the hydrogen ion.

73. Renal causes such as mineralocorticoid excess, nonreabsorbable anions and diuretic phase of acute renal failure.

74. Nursing management: the nurse should Monitor serum potassium daily, Assess patients for signs and symptoms of decreased cardiac output and the development of congestive heart failure because, in hypokalemia, the contractility of the cardiac muscle is impaired, The ECG should be observed for changes indicative of hypokalemia, The emergency resuscitation equipment should be kept readily available,

75. Nurses should provide appropriate support and assistance as necessary because muscle weakness is a common manifestation of hypokalemia and the patients may not have the strength to perform activities.

76. Hypernatremia ( ↑ NA 145 m Eq/L) may be caused by A-hypovolemic hypernatremia such as renal losses (osmotic diuresis, severe hyperglycemia) or extrarenal losses (decreased thirst, diarrhea occurring with inadequate volume replacement or fluid replacement with hyperosmolar solutions)

77. B-Hypervolemic hypernatremia such as the administration of concentrated saline solutions, hypertonic feedings, commercially prepared soups and canned vegetables. C-Euvolemic hypernatremia such as excess fluid losses from the skin and lungs, hypodipsia in the elderly and infants.

78. To decrease the total body sodium and replace fluid loss, either a hypo- osmolar electrolyte solution (NaCL) or D5 W is administered.

79. Nursing management for hypernatremia include: Assess the patients for the following: 1-Signs and symptoms of dehydration namely daily body weight, skin turgor, oral mucous membrane, blood urea nitrogen, central venous pressure, tachycardia and hypotension,

80. 2-Assessment for drugs that contain sodium such as cough medication and corticosteroids, 3-The diet should also be assessed for sodium consumption 4-And the serum sodium level should be checked.

81. Hyponatremia ( ↓ NA 135 m Eq/L), is usually associated with fluid volume status. Hyponatremia may occur when the total body water is decreased Also may result from the kidney's inability to excrete sufficiently diluted urine.

82. Hyponatremia may be caused by: A-Hypovolemic hyponatremia such as: Renal loss of sodium from diuretic use, diabetic glycosuria, intrinsic renal disease. Extrarenal loss of sodium from vomiting, diarrhea, increased sweating and burns.

83. B-Hypervolemic hyponatremia such as: edematous disorders resulting in sodium deficits namely congestive heart failure, acute and chronic renal failure.

84. C-Euvolemic hyponatremia such as sodium deficit. Inappropriate secretion of antidiuretic hormone or the continuous secretion of antidiuretic hormone due to pain. Discarding gastric residual volume can lead to a decrease in the sodium level because of gastrointestinal secretion losses mainly sodium.

85. Nursing management, the nurse should be: Obtain a history of the cause of hyponatremia such as vomiting, diarrhea and decrease intake of sodium. Check serum sodium levels and estimating the serum osmolality. Assess urine output as well as recent fluctuation in body weight. Observe signs and symptoms of hyponatremia (headache, mental status changes, nausea, vomiting and abdominal cramping ).

86. Hyperglycemia, a metabolic complication that can be caused by high carbohydrate formula and Hyperosmolar feeding of fluid overload.

87. Hyperglycemia can be prevented by: 1-Monitoring for fluid balance, urine and blood for glucose. 2-Administering insulin on a sliding scale if necessary 3-Changing the formula to lower calorie content and observing for hypercapnea.

88. hypoglycemia, caused by: Sudden cessation of feeding can be prevented by frequent monitoring of blood sugar if feeding is interrupted.

89. Dehydration caused by: 1-High osmolality formula. 2-Diarrhea and excessive protein intake with inadequate fluid intake. 3-Large amount of fluid that can be lost during prolonged uncorrected vomiting and diarrhea without adequate replacement of fluid and electrolytes.

90. 4-Also it may result if gastric and intestinal suctioning occur without the proper monitoring of intake and output to ensure that fluid and electrolytes losses are adequately replaced.

91. Management of dehydration include: 1-Management of the diarrhea, 2-Decreasing the protein content of the formula 3-The provision of additional water and changing the formula if high osmolality formula is used 4-Also reporting signs and symptoms of dehydration.

92. Overhydration, can be caused by: 1-Fluid overload, 2-When the metabolic demands are high and the organ function is impaired namely cardiac, renal or hepatic.

93. Management of Overhydration include: 1-Restricting free water intake 2-Changing to concentrated formula 3-Administering diuretics 4-Decrease the delivery rate.

94. Body weight alteration, body weight is the most important single indicator of the overall nutritional status in adults. Reasons for weight loss include: Reduced oral intake, patients dislike of the food offered, The wrong timing of meals Medications affecting patient's appetite In addition to the environment.

95. Moreover defective gastrointestinal function can cause poor absorption of nutrients the catabolic effects of disease can accelerate weight loss.

96. On the other hand, rapid excessive weight gain can be caused by: Excess calories, Excess fluid and electrolytes imbalance.

97. Most patients can be weighed on scales, but sometimes it is difficult or impossible to obtain a patient’s weight, because of the patient’s medical conditions, equipment attached to the patient (for example, life support devices, traction equipment.) or lack of a suitable bed or wheelchair scale.

98. FEMALES AgeEquation 19-59(KH X1.01)+(MAC X 2.81)-66.04 60-80 (KH X 1.09)+(MAC X 2.68)-65.51 MALES 19-59 (KH X 1.19)+(MAC X 3.21)-86.82 60-80 (KH X 1.10)+(MAC X 3.07)-75.81 KH knee height MAC mid-arm circumference

99. mechanical complications

100. Tube obstruction Tube displacement Aspiration

101. Tube obstruction, a mechanical complication associated with NGF can be related to 1-The increased frequency of checking residual volume. 2-The use of dense formula or insufficiently crushed medicines

102. Nursing interventions to prevent or decrease tube obstruction: 1-Obtaining liquid medications when possible 2-Flushing feeding tube before and after medication administration 3-And diluting feeding with water if it is dense and straining if necessary.

103. Whenever different types of medications are administered, each type should be given separately using the bolus method that is compatible with its preparation and the tube should be flushed with 15 to 30 ml of water after each dose.

104. Tube displacement, another mechanical complication of NGF, can be detected through aspirating gastric residual volume. Failure to aspirate recognizable gastric contents is an indication that the tube is not in the stomach. However others believe that inability to aspirate fluid through the syringe may merely reflect collapse of the walls of the small-bore feeding tubes.

105. Tube displacement may be caused by excessive coughing, vomiting, tracheal suctioning, air way intubation and this can be managed by checking tube placement before administering feeding.

106. Parenteral Nutrition

107. A variety of locations can serve as sites for catheter insertion including: subclavian, internal jugular, external iliac, and cephalic veins

108. Solutions containing 10% or less dextrose (final concentration) plus amino acids (750-900 mOsm/L).

109. This practice is associated with a high risk of phlebitis and is therefore reserved for short-term therapy in individuals with robust veins

110. Initiating Parenteral Nutrition (PN) 1. Formula Determination Determine energy requirement Determine protein requirements. Determine fluid requirements. Determine the proportion of calories to be provided as intravenous fat

111. Complications of Parenteral Nutrition

112. Technical Septic Metabolic complications

113. Technical complications associated with PN include: Air embolism Subclavi anartery puncture/hemotoma/laceration Pneumothorax, hemothorax Carotid artery injury

114. Thromboembolism Catheter embolism Catheter malposition brachial plexus injury and phrenic nerve paralysis

115. Septic complications associated with PN include: Catheter infection, Catheter tunnel infection, and sepsis.

116. Metabolic complications

117. Possible Cause Complication Inadequate fluid support; unaccounted fluid loss (e.g. diarrhea, fistulae, persistent high fever Dehydration Excess fluid administration; compromised renal or cardiac function Overhydration

118. Inadequate K to compensate for cellular uptake during glucose transport; excessive GI or renal K losses. Inadequate Cl in patients undergoing gastric decompression. Alkalosis Excessive renal or Gl losses of base; excessive Cl in PN Acidosis

119. Excessive PO4salts, low serum albumin. Inadequate Ca in PN Hypocalcemia Excessive Ca in PN or administration of vitamin A in patients with renal failure. Hypercalcemia Inadequate Mg in PN; excessive Mg losses; cellular uptake with induction of anabolism Hypomagnese mia

120. Excess losses (urinary PO4; in alkalosis, diabetes mellitus, steroid and diuretic therapy); cellular uptake with induction of anabolism Hypophosphate mia Sustained untreated glucose intolerance. Easily prevented by frequent glucose monitoring. 40% mortality rate. Hyperglycemic, hyperosmolar nonketonic coma Stress response. Occurs in approximately 25% of cases. Hyperglycemia

121. Sudden withdrawal of concentrated glucose. More common in children. Hypoglycemia Excessive calorie or carbohydrate load Hypercarbia Inadequate provision of linoleic acid in PN; release of linoleic deficiency acid from adipose stores prevented by continuous dextrose infusion and associated hyperinsulinemia. Essential fatty acid

122. Unclear etiology. Maybe be related to excessive glucose or energy administration; Hepatic tissue damage and fat infiltration Lack of GI stimulation. Sludge present in 50% of patients on PN for 406 weeks; resolves with resumption of enteral feeding. Cholestasis