Medical Nutrition Therapy for Metabolic Stress and Critical Care

Medical Nutrition Therapy for Metabolic Stress and Critical Care... • Describe the metabolic response to critical illness • Describe role of nutrition therapy for critically ill patien

Medical Nutrition Therapy for Metabolic Stress and Critical Care

• Describe the metabolic response to

critical illness

• Describe role of nutrition therapy for

critically ill patients

• Describe how to assess nutrient

needs for a critically ill patient

Metabolic Stress

• Stressors:

– Sepsis

– Surgery

– Trauma (includes burns)

• These stressors activate a particular

systemic response, leading to a

number of physiologic and metabolic changes

What happens during metabolic stress?

• Metabolic alterations to meet the body’s

needs for survival

– hypermetabolism

– hypercatabolism

– hyperglycemia

– sodium & water retention

– increased heart rate & cardiac output

– hypercoagulability & increased platelet

aggregation

– increased sympathetic tone

• controls “fight or flight” response

Metabolic Response to Stress

• Involves most metabolic pathways

• Accelerated metabolism of lean body

mass

• Negative nitrogen balance

• Muscle wasting

Hypercatabolism!

Ebb Phase

• Usually restricted to the first 24-48 hours

• Immediate response

– Hypovolemia and tissue hypoxia

– Decreased cardiac output

– Decreased oxygen consumption

– Lowered body temperature

– Decreased insulin and increased glucacon

levels

Flow Phase

• Follows fluid resuscitation and improved

O2 transport

• Increased cardiac output begins

• Increased body temperature

• Increased energy expenditure

• Total body protein catabolism begins

•  glucose production, free fatty acids,

circulating insulin, catecholamines,

glucagon, & cortisol

Figure 89.2 Neuroendocrine and metabolic consequences of

Perez JM The hypercatabolic state In Shils ME, et al (eds) Modern Nutrition in Health & Disease Lippincott, Williams & Wilkins, 2006.

Metabolic Responses During Sepsis

Organ Response

 Amino acid uptake

 Acute-phase protein synthesis

 Trace metal sequestration Central nervous system Anorexia, fever

Metabolic Responses During Sepsis

Intestine  Amino acid uptake from both luminal and

circulating sources, leading to gut mucosal atrophy

Endocrine  Adrenocorticotropic hormone

 Insulin initially, then  levels & insulin resistance

From Michie HR: Metabolism of sepsis and multiple organ failure, World J Surg 20:461, 1996

Hormonal and Cell-Mediated Response

• Causes energy metabolism to shift to protein

Skeletal Muscle Proteolysis

Hormonal Stress Response Specifics

• Conserve fluid & sodium to maintain

blood volume:

– Aldosterone

• Corticosteroid that causes the kidney to retain

sodium – Antidiuretic hormone

• Stimulates renal tubular water absorption

Hormonal Stress Response Specifics

(continued)

• Simulate metabolism:

– Adrenocorticotropic hormone (ACTH)

• Acts on adrenal cortex to release cortisol

• Mobilize amino acids from skeletal muscle

– Catecholamines

• Epinephrine & norepinephrine from renal medulla

• Stimulate hepatic glycogenolysis, fat

mobilization, gluconeogenesis

From: http://health-pictures.com/gland/adrenal-gland.htm accessed 2/28/09

Acute Phase Response

• Occurs when a patient is very stressed

• See increased production of cytokines

– Protein mediators secreted by

macrophages in response to tissue

damage, infection, inflammation, and some drugs and chemicals

– Hormone regulators of the immune system – Stimulate production of inflammatory

mediators associated with shock & sepsis

Actions of Specific Cytokines

• Tumor necrosis factor (TNF)

– Increased catabolism of lean body mass – Causes anorexia

– Activates the

hypothalamic-pituitary-adrenal axis

• Interleukin-1

– Mediates the acute phase response

– Associated with fever, hypotension,

inflammation, protein catabolism

• Interleukin-6

– Release of hepatic acute phase proteins

Response at the Cellular Level

• Eicosanoids are produced in response

Immune Cell Saturated with

omega-6 Fat

Phospholipid Membrane AA

AA

AA

AA

AA AA

AA AA

AA Proinflammatory compounds

Slide courtesy Abbott Nutrition

• Prostaglandins

– Modulate intensity & duration of inflammatory &

immune responses

– 2 series derived from arachidonic acid (n-6)

– PGE 2 has significant pro-inflammatory function

• Induction of fever & erythema

• Increased vascular permeability

(continued)

• The 3 series is less inflammatory

– Derived from omega-3 fatty acids:

eicosapentaenoic acid (EPA) and

docosahexaenoic acid (DHA)

– Thromboxanes are derived from PGH

• These are similar to PG in that

– 2 series is pro-inflammatory – 3 series is much less active

• Primary mediators of inflammation &

allergic reactions

• Also increase microvascular permeability

• Promote arteriolar constriction

• Promote bronchoconstriction and

increase bronchial mucous production

(continued)

• The 4 series, derived from AA, is

proinflammatory

• LTB 4 has the most significant action

– Potent chemoattractant & chemokinetic action

toward leukocytes

– Inhibition of T-cell mitogenesis

– Stimulation of PMN cells to aggregate & adhere to

• Similar function to leukotrienes

• Derived from PGH

• Involved in platelet aggregation

• TXA2 stimulates formation of derived growth factor

platelet-– Stimulates blood clotting

• 2-series is inflammatory & 3-series is

less so

Influencing Eicosanoid Production

• Arachidonic acid comes from omega-6 fatty

acids

– Example: corn oil is high in omega-6 fatty acids

• Feeding more omega-3 fats may help push

production of the anti-inflammatory (or less active) eicosanoids

– Example: enteral formulas with fish oil are

promoted as “immune modulating”

Metabolic Response in Starvation vs Stressed

State

Starvation vs Stress

• Metabolic response to stress differs from the

responses to starvation

• Starvation = decreased energy expenditure,

use of alternative fuels, decreased protein

wasting, stored glycogen used in 24 hours

• Late starvation = fatty acids, ketones, and

glycerol provide energy for all tissues

except brain, nervous system, and RBCs

Metabolic Changes

in

Starvation

Comparison of Starvation and Stress

Starvation

Stress Hypermetabolism

From Barton RG: Nutrition support in critical illness, Nutr Clin Pract 9:127, 1994 Modified from the American Society for

Parenteral and Enteral Nutrition (ASPEN).

*Patients fall in a continuum between the extremes of starvation and stress hypermetabolism

Complications Associated with Critical Illness

Etiology of the Hypermetabolic

Response

From Krause, 11 th edition

Systemic Inflammatory Response Syndrome

(SIRS)

• SIRS describes the inflammatory

response that occurs in:

Diagnosis of SIRS

• Site of infection established and at least

two of the following are present

– Body temperature >38° C (100.4 F) or <36° C (96.8  F)

– Heart rate >90 beats/minute

– Respiratory rate >20 breaths/min (tachypnea) – PaCO 2 <32 mm Hg (hyperventilation)

– WBC count >12,000/mm 3 or <4000/mm 3

– Bandemia: presence of >10% bands (immature

neutrophils) in the absence of induced neutropenia and leukopenia

• SIRS criteria plus the organism

causing the infection is identified

SIRS/Sepsis Complications

• Multiple organ dysfunction syndrome

is common

• Ileus (lack of peristalsis)

– Enteral feeding may preserve gut function – Tube feeding may help prevent bacterial

translocation

• Hypermetabolism & hypercatabolism

Multiple Organ Dysfunction Syndrome

• Hematologic and cardiac failure

• CNS changes occur at any time

Bacterial Translocation across Microvilli and How It

Spreads into the Bloodstream

Respiratory Failure

Respiratory Failure

• Impairment in respiration in response to

– Trauma

– Surgery

– Critical illness (MODS)

• The patient needs oxygen therapy

– Nasal cannula

– Face mask

– Noninvasive positive pressure ventilation – Mechanical ventilation

Nasal Cannula

From http://www.frankshospitalworkshop.com/equipment/oxygen_concentrators_equipment.html accessed 9/4/12

Face Mask

From http://nursingcrib.com/nursing-notes-reviewer/oxygen-therapy/ accessed 9/4/12

Noninvasive Positive Pressure

Ventilation

From http://www.itamar-medical.com/WatchPAT/Patient/Sleep_Apnea_Treatment/CPAP.html accessed 9/4/12

Mechanical Ventilation

From

http://www.bluegrass.kctcs.edu/en/AH/Respiratory_Care/Respiratory_Care_Treatm ent_and_Management.aspx accessed 9/4/12

Acute Respiratory Distress Syndrome

• Occurs as a result of pulmonary injury

or severe infection

• Or as part of the multi-organ

dysfunction syndrome (MODS)

• Starts out as acute lung injury (ALI),

then progresses into ARDS

• Alveolar membrane produces exudate,

leaks into the interstitial space

ALI vs ARDS

Bilateral infiltrates on CXR  

Pulmonary-artery wedge pressure «18 mm

Hg or the absence of clinical evidence of

left atrial hypertension

NEJM, 2000; 342:1334- 1349

Impact of Malnutrition on

Respiratory Status

• Decreased

– Vital capacity (lung volume)

– Minute ventilation (volume

Impact of Malnutrition on

Respiratory Status

(continued)

• Increased pulmonary edema

– Decreased oxygen transport

– Decreased respiratory muscle strength – Decreased energy substrates in the cell – Decreased ventilator drive with hypoxia – Decreased immune function

Feeding the Hemodynamically Unstable

Patient

• All of the mechanisms that keep blood

flowing

• When a patient is hemodynamically

unstable, blood flow is impaired

• Nutritional concern: is there adequate

blood flow to the intestine?

What is shock?

• Shock: insufficient tissue perfusion that

results in cellular hypoxia

Characteristics of Shock

• Pulmonary artery catheter measurements are

helpful to determine type of shock

• The characteristics will vary depending on the

type of shock, but often you will see:

– Hypotension

– Low mean arterial pressure

• Need a mean arterial pressure (MAP) > 60 mm Hg to

perfuse coronary arteries, brain, & kidneys

Pulmonary Artery Catheter

From http://www.healthdataintl.com/ABOUTUS.html accessed 02/28/09

• Induce vasoconstriction to elevate MAP

• Examples: phenylephrine (Neosynephrine), norepinephrine

(Levophed), epinephrine, vasopressin

– Inotropic agents

• Increase cardiac contractility

• Examples: dobutamine, isoproterenol

– Some medications have both vasopressor or inotropic

activity, depending on the dose

• Example: dopamine

Enteral Feeding During Shock

• Consider:

– What is the blood flow to the gut & other

organs if a patient is severely hypotensive?

– Enteral feeding causes “hyperemia” of the

intestine

• Blood flow is diverted from the extremities to the

intestine

– There may be inadequate diversion of blood

flow to the intestine, which can lead to bowel ischemia during feeding

Is it safe to enterally feed during

shock?

• Evaluate the clinical status

– What is the trend of the vasopressor dose?

– How is the patient doing overall?

• If the vasopressor requirement is increasing

and the patient is getting sicker, hold on

enteral feeding

• If the vasopressor dose is decreasing and the

patient is getting better, start tube feeding

slowly

Other Considerations

• Is the fluid resuscitation phase complete?

• Evaluate end-organ function

– Renal function

• What is the creatinine doing?

• Trending up may suggest poor blood flow – Liver function

• What is the bilirubin doing?

• Trending up may suggest poor blood flow

• Consider monitor serum lactate

– High level is suggestive of ischemia

When it’s (relatively) safe to feed:

• Start low & go slow!

– It’s ok to start with a very low rate and

advance slowly

• Monitor carefully for abdominal

distention, pain, ileus

– If any of these symptoms occur—STOP

– May be a sign of small bowel ischemia or

necrosis

– This can lead to patient death!

Nutrition Intervention in

the ICU

Screening the ICU Patient

• Preadmission nutritional status

• Current organ function/dysfunction

• Use of pharmacologic agents,

vasopressors, paralytic agents

• Ability to predict clinical course

– Duration of mechanical ventilation

• Need for enteral/parenteral nutrition

Surgery-Specific ICU Issues

• Elective vs emergency surgery

• Preoperative nutritional status

• Intraoperative complications

• Postop cardiopulmonary status

• SIRS or Sepsis

• GI function

– Ability to predict return of GI function

• Nutrition support access options

Complexity in Nutrition Assessment

• Weight history and diet history are an

important part of your assessment

– Interview family, read old medical record if

you can’t talk to the patient

• Be careful with interpreting circulating

proteins

– Albumin & prealbumin are negative acute

phase proteins

•  as a result of the acute phase response

• Monitor C-reactive protein—it’s a good

indicator of inflammation

Enteral vs Parenteral?

• If the gut works and can be used

safely, use it!

• Enteral nutrition is the best and

should be your first choice

• Parenteral is second choice after

making every effort to maximize enteral nutrition

When to Feed in the ICU

Well-nourished patient

Anticipate intubation for >72 hours, start within 24-48h

Parenteral nutrition Inability to tolerate

enteral nutrition by ICU day 7-10

Inability to tolerate enteral nutrition (no specific timeline in American ICU

guidelines)

Energy Requirements

• For the metabolically stressed:

– Consider Ireton-Jones or Penn State equation for

vent-dependent patients

– Some references say 25-35 kcal/kg

– Ideal: measure resting energy expenditure

• Consider 1.05-1.1 activity factor

• It’s important to avoid overfeeding

– Watch out for medications that may decrease

energy expenditure

– Watch for therapies that provide calories

Energy Requirements:

1992 Ireton-Jones Equation

• RMR = 1925 – (age x 10) + (wt x 5) + (sex x 281) + (trauma x 292) + (burn x 851)

– wt, weight in kg

– age in years

– sex, male =1, female = 0

– trauma, present = 1, absent, 0

– burn, present = 1, absent = 0

24 hours in degrees Celsius

– VE = minute ventilation in L/min;

– Adjusted weight for obesity is used for patients

>25% above IBW

Nitrogen Balance

• Nitrogen output can help you determine a

patient’s stress:

• 24 hour urine collection for urea nitrogen

– For each gram of nitrogen lost, ~ 30 g lean

body mass is lost

• Mild catabolism: 5-10 g urinary urea nitrogen/24 hrs

• Moderate catabolism: 10-15 g urinary urea

nitrogen/24 hrs

• Severe catabolism: > 15 g urinary urea nitrogen/24

hrs

Nitrogen Balance Equation

• Calculating nitrogen balance:

– Grams nitrogen in – (g urinary urea

nitrogen + 2 to 4 g insensible losses)

– Urinary urea nitrogen is obtained from a 24

hour urine collection and is usually

• Keep parenteral carbohydrate  5

mg/kg/minute

• Typical carbohydrate delivery: 50-70% of kcals

• Glucose control is important

• Hyperglycemia increases the risk of infectious

complications

• New literature suggests optimal blood glucose

for the ICU is < 150 mg/dL

– For cardiac surgery, still 80-110 mg/dL

(continued)

• Use of fiber in the ICU

– Soluble fiber may be used for patients

who have diarrhea

– Avoid use of insoluble fiber

• Theoretical risk of bowel obstruction

– Avoid any type of fiber in

hemodynamically unstable patients, those

at risk for intestinal ischemia, or those at risk for intestinal dysmotility

• Can be immunosuppressive, so don’t

overfeed

– Especially IV fat emulsion

• Provide anywhere between 15-40% of