1. NUTRITION IN CRITICAL CARE
BY DR JYOTI KHARE
FCCCM PART II
PSRI NEW DELHI

2. Introduction
Nutritional Support refers to enteral, parenteral, provisions of calories, proteins, electrolytes, vitamins, minerals, trace elements and fluid.
These are hyper metabolic and have increased nutritional requirements.
In critically ill patients malnutrition develop rapidly due to the presence of acute phase responses, which not only promote catabolism but also alter the response to nutritional support. Malnutrition once established exerts well-known deleterious effects by altering immunity, increasing susceptibility to nosocomial infections, decreasing wound healing and by altering the function of vital organ and promoting organ failure.

3. Nutrition in critical illness
What ?
And whom ?
How ?
When ?

4. A Practical Approach During Nutrition
Supplementation should be based on the following consideration –
When should nutrition supplementation be initiated in a particular patient ?
Which route should be used for the delivery of nutrient delivery ?
What special precaution should be taken before initiating supplementation in the patients (Diabetic background, Cardiac Diseases, Chronic Renal Failure), which may necessitate appropriate modification in both nutrient contents delivery ?
Termination of Parenteral Nutrition.
Nutritional support Support has become a routine part of the care of critically ill patients and now widely accepted for the treatment and prevention of malnutrition and specific nutrient deficiencies.

5. Assessment of Nutritional Status
Nutritional assessment in critically ill patient is very difficult. These are summarized as – A, B, C, D. Anthropometric Measurements: It measures the current nutritional status Body weight: 10% loss is considered SIGNIFICANT 20% loss is considered CRITICAL 30% loss is considered LETHAL Mid-Arm Circumference Skinfold thickness Head Circumference Head Chest Ration Nutritional Indices: Body Mass Index (BMI) BMI = Weight in Kg/ Height in m2 It is frequently used tool and has been shown to be an independent predictor of mortality in seriously ill patients.

6. Biochemical tools:
Hemoglobin
Albumin
Transferrin
Pre-albumin
Lymphocyte Count
Clinical assessment: Simplest and most practical method
Good nutritional History
General physical examination
loss of subcutaneous fat (chest & triceps)
Oedema
Ascitis
Dietary Assessment: It can be assessed by 24 hrs dietary recall
Food frequencies
Food daily technique
Observed food consumption

7. Why Supplement Weakness, fatigue Infection
Impaired wound healing (impaired cellular & humoral immunity)
Diminished organ function
Death
Increase weight

8. Natural History of Starvation

9. Energy Expenditure Energy Expenditure Basal Metabolic Rate (BMR)
Basal Energy Expenditure (BEE)
Resting Energy Expenditure (REE)
Activity Level
Thermic Effect of Food
Energy Expenditure

10. Illness Acute phase response
Altered amino acis distribution and metabolism
Inc Globulin synthesis
Inc Gluconeogenesis
Dec. S. Iron and Zn
Inc. S. Cu & ceruloplasmin
Catabolism and inc. UUN
D/t inc. protein breakdown
1g UUN = N2 iin 6.25 g protein
Normal: 10 – 12 gm
Critically ill pts: 16 – 20 gm
Hormonal changes
Insulin resistance
Rise in S. Cortisol, Cas, Glucagon and GH
Dec. glucose oxidation, inc. hepatic glucose production rate
Inc. FA oxidation rates
Sick euthyroid syndrome
Inc. T4 to rT3 thus causing low T3 (Energy saving response)

11. When to start ??
Previously good nutritional status and moderately severe catabolic state:
Less than 60 yrs – 14 days
60 – 70 yrs – 10 days
>70 yrs – 7 days
Nutritional support should be started before effects of starvation appear.
In acute hypercatabolic critical illness, stabilization of hemodynamics and correction of fluid, electrolytes and acid base status takes precedence over nutrition.

12. Role of components CARBOHYDRATES FATS PROTEINS WATER/ ELECTROLYTES
MINERALS

13. Carbohydrates
Ready fuel for energy, less expensive and Nitrogen sparing effect.
RBCs, WBCs and renal medulla require glucose and brain prefers glucose as fuel.
Disadvantages –
Excess carbohydrates increase NE, Glucagon secretion and insulin resistance.
Severe hyperglycemia in sepsis (impaired utilization)
Excessive glucose  fat  Hapatic Steatosis
Excess glucose inc. CO2 production  pulmonary work load

14. Fats Provide energy Regulation of cardiovascular tone (PGs)
Components of cell membranes (Phospholipids)
Cellular messengers (Phosphoinositides)
Linoleic acid: essential fatty acid
should provide 4% of total calorie intake.

15. Proteins Minimum intake: 0.5 g/ Kg/ day
Intact digestion: intact protein diet
Impaired digestion: peptides (< 10 amino acids) based diet advantageous (dec. diarrhoea, improved wound healing and inc. protein synthesis).
Restrict protein if BUN > 100 mg/ dl and rising or elevated NH3 associated with encephalopathy.

16. Indications of amino acids plus dextrose containing solutions:
Patient needs PN, but needs it for short period (< 2 wk)
Patient is not malnourished, stable and total caloric requirement is not high.
Patients where lipids are contraindicated (i.e. hyper troglyceridemia)
Essential fatty acid deficiency prevented by infusing lipid emulsion once a week.

17. Modes of administration
Bolus feeding: administration of 200 – 400 ml of feed over 20 – 30 minutes several times a day.
Intermittent feeding: Administration of 300 – 400 ml of feed over 30 – 60 minutes several times a day.
Continuous feeding: Feed given at continuous rate over 16 – 24 hrs per day. It is preferred for small intestine feeding.

18. Feeding Formulas for enteral Feeding
There are many commercially prepared feeds available:
Polymeric Preparation: These contain intact proteins, fat and carbohydrate which requires digestion prior to absorption, in addition to electrolytes, trace elements, vitamins and fibers. These feed tend to be lactose free as lactose intolerance is common in unwell patients. Different patients vary in their osmolality, calorie:nitrogen ratio, carbihydrate:lipid ratio and can provide 0.5 – 2.0 Kcal/ ml
Elemental Preparation: These preparations contain the macronutrients in absorbable form (i.e. proteins as peptides or amino acids, lipids as medium chain triglycerides and carbihydrates as mono and disaccharides. They are expensive and indicated in severe malabsorption or pancreatic insufficiency.

19. Methods of enteral feeding
Nasogastric Tube: Most common method
Naso-duodenostomy tube
Naso-jejunal tube
Percutaneous feeding gastrostomy
Jejunostomy tube

20. Monitoring of gastric residual volume every 2 – 4 hrs mandatory
Gastric feeding
Advantages:
Stomach initiates digestion
Gastric acid secretion sterilizes gastric contents (risk of bacterial contamination reduced)
Stomach protects gut from osmotic load (mortility reduced in presence of hyperosmolar fluid and diluted till is oosmolar)
Disadvantages:
Development of gastric atony
Risk of aspiration of gastric contents
Monitoring of gastric residual volume every 2 – 4 hrs mandatory

21. Complications of enteral feeding
Gastric retention, vomiting and aspiration: more often with gastric feeding. Incidence varies from 1 – 44%
Mechanical problems:
Feeding tube obstruction (10%)
Flush the tube with water before and after infusion of nutrients.
if tube is blocked and can’t be flushed with water  flush tube with warm solution of 7.5% sodium bicarbonate.
` If unsucessful, replace the feeding tube.

22. Complications Tube position in the GIT should be confirmed.
Malposition: associated with blind bedside tube placement. (Altered mental status due to injury or sedation, absence of gag reflex, inability to cough, dysphagia or endotracheal intubation)
Dislodgement
Tube position in the GIT should be confirmed.
(Radiographic, assessment of myoelectric activity, aspiration of gastric contents or aspiration of bile and direct laryngoscopy).
Note: Auscultation findings can be misleading (Tube placed in base of left lung can produce sounds similar to tube placed in stomach).

23. ESPEN Recommendation
In ICU setting, evidence of bowel motility (presence or absence of bowel sounds or passage of flatus and stools) is not required to initiate EN in ICU Holding EN for GRV< 500 ml in absence of signs of intolerance should be avoided.

24. Parenteral Nutrition
Pharmacological therapies where nutrients, vitamins, electrolytes and medications are delivered via venous route to those patients whose GIT is not functioning and are unable to tolerate enteral nutrition.

25. Indications of parenteral nutrition
Inadequate oral or enteral nutrition for atleast 7 – 10 days.
ESPEN: initiate within 24 – 48 hrs of ICU pts who can’t be fed enterally
Pre existing severe malnutrition with inadequate oral or enteral nutrition.
Conditions that impair absorption of nutrients:
Enterocutaneous fistula
Short bowel syndrome
Small bowel obstruction
Effects of radiation or chemotherapy
Need for bowel rest:
Severe pancreatitis, inflammatory bowel disease, Ischemic bowel Peritonitis, Pre and post op status.
Motility disorders: Prolonged ileus

26. Inability to achieve or maintain enteral access:
Haemodynamic instability
Massive GI bleeding
Unacceptable aspiration risk
Hyperemesis gravidarum, eating disorders
Significant multi organ system disease
Renal, hepatic or pulmonary disease
Multiorgan failure, severe head injury, burns etc.

27. Central parenteral nutrition
Most efficient way to deliver all the nutrients by central venous catheter inserted in SVC or IVC.
Composition: varied composition
Conc. Forms of dextrose (50-70%) and amino acids (8.5 – 10%)
Osmolarity 1000 – 1900 mosm/l
Selection of catheter for CPN: Polyurethane (for short term use) or silicon rubber ( months to years)

28. Complication of TPN
Catheter related: Pneumothorax, Hemothorax, Chylothorax, Air embolism, Cardiac Tamponade, Catheter sepsis.
Metabolic: Azotemia, Hepatic Dysfunction, Cholestasis, Hyperglycemia/ Hypoglycemia, excessive CO2 production, metabolic acidosis/ alkalosis, electrolyte imbalances.
Refeeding Syndrome
Overfeeding

29. Clinical data monitored daily
History: fever, h/s/o fluid overload or glucose and electrolyte imbalance.
Vital signs: Temp, HR, BP, RR
Fluid balance: input/ output chart, weight
Local care: inspection and dressing of site of vascular access.
Delivery system: inspection of solution for contamination and functioning of infusion pump.

30. Disease specific formulae
These are usually polymeric and feed designed for:
Liver diseases: Low sodium and altered amino acids contents ( to reduce encephalopathy)
Renal diseases: Low phosphate and Potassium 2 Kcal/ ml (to reduce fluid intake)
Respiratory disease: High fat content reduce CO2 production.
Seizures disorder: Ketogenic diet emerging nonpharmacological treatment of refractory status.

31. Conclusion
Malnutrition is associated with a poor outcome in critical illness. Enteral nutrition is mainstay of nutritional support and should be started early in all patients in whom it is safe to do so. Parenteral nutrition has definite role but only in selected patients. In all patients receiving nutritional support it is vital to achieve glucose control with insulin therapy and important not to overfeed.

32. THANK YOU