Week 4 ICU: Hypermetabolism: Trauma/ICU and Metabolic Phases of Stress

Question 1

Common Medical Issues contributing to Hypermetabolism in the ICU

Answer 1

• Trauma: multiple sites in body.
• Sepsis/Infection
• Burns (extreme case of hypermetabolism)
• Acute Respiratory Distress Syndrome (ARDS)
• End-stage organ failure (e.g liver, heart, lungs)

Question 2

Physiological responses to metabolic stress

Answer 2

Extent depends on EBB vs. FLOW phase
* Hypermetabolism: ↑ O2 consumption
* Hyperglycemia (krebs cycle overwhelmed by AA converting to glucose)
* Hyperlactemia (excess pyruvate converting to lactate)
* Protein catabolism (contributes to hyperglycemia)
* Cardiovasular response (↑ blood flow, tachycardia, tachypnea)
* Perfusion to Gut decreased
* Increase in aldosterone & ADH-promotes fluid & sodium re-absorption in kidneys - protects microvascular volume (important in trauma where hemorrhage possible)
* Get electrolyte disturbances
* If GI trauma; may have losses of GI fluids; important to replace these losses with fluid and electrolytes to ensure hemodynamic stability

Question 3

Common electrolytes disturbances

Answer 3

• sodium
• potassium
• chloride
• calcium
• magnesium
• phosphorous

Question 4

What electrolytes are CRITICAL for normal organ function

Answer 4

• sodium
• potassium
• chloride

Question 5

How are changes in intracranial pressure controlled for?

Answer 5

MD will set a tight TFI to prevent massive edema due to change in organ function
* patients with massive trauma (esp closed head injuries

Question 6

Hormone response disturbances to metabolic stress

Answer 6

Fight or flight response: elevations in glucocorticoids (cortisol); catecholamines (epinephrine ) + increase in insulin & glucagon
* Rise in glucagon supercedes rises in insulin – ie lower insulin to glucagon ratio
* Insulin resistance develops resulting in hyperglycemia (not diabetes, but worse with diabetes)
* High catecholamine + cortisol: favors protein breakdown

Question 7

Carbohydrate metabolism disturbances to stress response

Answer 7

↑ glycolysis, ↓ glycogen production, ↑ insulin resistance, ↑ lactate production, ↑ glucagon + ↑ epinephrine, ↑ gluconeogenesis + ↑ recycling of alanine to pyruvate (via transamination) results in hyperglycemia
* Enhanced peripheral glucose uptake & utilization
* Hyperlactemia
* Increased glucose production with depressed glycogen production, glucose intolerance, and insulin resistance

Question 8

GIR recommendations for stressed adult

Answer 8

GIR: 4-7 mg/kg/min; Recommend 2-4 mg/kg/min due to risk of hyperglycemia esp if pt already has high Blood sugars

Question 9

Protein metabolism disturbances to stress response

Answer 9

• Increase in protein turnover; predominantly protein degradation to supply AA for gluconeogenesis \ Increased need for protein
• Some increase in protein synthesis; diverted towards production of acute phase reactants eg coagulation proteins, immune system proteins
• Laboratory consequences: may see ↑ serum levels of acute phase reactants (eg C-reactive protein), and ↓ serum levels of protein such as albumin, pre-albumin

Question 10

Fat metabolism disturbances to stress response

Answer 10

• lipolysis resulting in ↑ serum concentrations of triglycerides (this is via hormone sensitive lipase; hormones such as glucagon, epinephrine, norepinephrine and adrenocorticotropic hormone (ACTH) stimulate activity of this enzyme)
• Lipid oxidation is not increased (likely due to higher insulin levels and insulin resistance)
• Ketogenesis is inhibited \ gluconeogenesis becomes major energy pathway (resulting in lean body depletion)

Question 11

Nutrient utilization during starvation

Answer 11

• Increase in Fat oxidation and gluconeogenesis
• Decrease protein synthesis
• Liver: get synthesis of ketone bodies (3-OH-butyrate) within 2-3 days
• Brain adapts to use of ketone bodies after levels sufficiently high
• During starvation individuals experience a down regular in REE; and become hypometabolic

Different from metabolic stress response

Question 12

Definition of Trauma

Answer 12

Characterized by Blunt vs Penetrating Injury (with thermal or electrical injuries)
* Blunt Trauma; Severity determined by force of injury (eg MVA)
* Penetrating Trauma (eg stabbing)
* Combination of Both

Question 13

When is nutritional support NOT indicated for trauma patient?

Answer 13

Patients who are able to resume oral intake within 3-5 days of injury do NOT need nutritional support
* unlikely to be those admitted to an ICU; although it is always possible

Question 14

Phases of Metabolic Stress Following Trauma

Answer 14

• Ebb or Shock Phases; decreased metabolic rate
• Flow Phase: Regeneration and repair with increased metabolic rate

[Important to understand as one phase is a hypometabolic/catabolic state which may be influenced by the need for ventilatory support; the other phase is a hypermetabolic/catabolic state which maybe influenced by the need for ventilatory support]

Question 15

Effects of trauma on blood flow to GI

Answer 15

Get ↓ splanchnic blood flow (abdomen organs) and relatively high metabolic demand of the GI tract during stress
* In non-stressed state: viscera (eg GI tract) responsible for about 30% of total circulating blood volume (receive 25% of cardiac output)
* In post-prandial state: have increase of blood flow to viscera (upwards 50%) so very sensitive to ischemic injury

Question 16

Immediate goals following major trauma

Answer 16

• Restore and maintain oxygen delivery; ventilatory support
• Ensure organ function by appropriate fluid and electrolyte rescusitation; goal is to establish hemodynamic stability

Question 17

What is hemodynamic instabilty

Answer 17

A state requiring pharmacologic or mechanical support to maintain a normal blood pressure or adequate cardiac output
* the cardiovascular system is not working.
* Being on mechanical respiratory support does NOT necessarily mean the patient is UNSTABLE

Question 18

Physical signs of hemodynamic instability

Answer 18

Cannot get lab values into equilibrium
* Typical of acute circulatory failure constitute primary references for shock, including hypotension, abnormal heart rates, cold extremities, peripheral cyanosis and mottling together with bedside measurements of right-sided filling pressure and decreased urine flow.
* Need to consider overall perfusion to organs like the GI tract and kidneys severely diminished.

Question 19

What phase is hemodynamic instability typically seen?

Answer 19

Most patients experiencing hemodynamic instability are in the Ebb Phase of the metabolic stress response. However, it is possible for this to occur later in the Flow Phase as well.
* Flow phase: acute insult occurs such as bleeding during operation

Question 20

Hormone response during ebb phase

Answer 20

• Get some surges of counter-regulatory hormones such as cortisol, catecholamines, glucagon: all result in lean body tissue breakdown.
• Insulin resistance may occur due to changes in insulin secretion. Hyperglycemia often occurs as a result.
• May have low levels of TSH, lower body temperature (due to hypo-perfusion)
• CRP increased (but not as high as flow)

Question 21

How long does the Ebb phase last?

Answer 21

Typically shorter phase; but if prolonged due to major organ damage; then patient at high risk for ++ inflammation.
* Ebb response to metabolic stress; 1-7 days but usually under 48 hrs
* Body trying to respond to a ‘physiological shock’; get major shifts in cardiovascular function. Patient may be hemodynamically unstable

Question 22

Metabolic response during ebb phase

Answer 22

Hypometabolism
* Period of Hypoperfusion
* Decrease blood perfusion to other organs may be due to sustained organ damage.
* Medical therapy during Ebb Phase may contribute to hypometabolism

Question 23

Energy requirements during ebb phase

Answer 23

80-90% of basal metabolic rates OR 10-20 kcal/kg
* Period of Hypoperfusion of organs results in ↓ energy requirements

Question 24

How does medical therapy contribute to hypometabolism in the ebb phase?

Answer 24

• Ventilation
• Medications (barbituates) may inhibit Central nervous system (sedatives, analgesics, narcotics, hypnotics) and lead to hypometabolism → e.g Codeine, morphine, propofol, haldol
• Autonomic agents (neuromuscular blocking agents that are needed for optimal ventilation) or cardiovascular agents (eg B-adrenergic receptor antagonists such as propranolol).

Question 25

How do energy requirements change transitioning from ebb to flow phase?

Answer 25

1. ebb: 0.8-0.9 x REE
2. transition: REE
3. flow: REE x AF

Question 26

Energy requirements in flow phase with REE

Answer 26

BMR x SF: To predict TEE add on activity/injury factor of 1.2-1.8 (depending on severity and nature of injury)
* Multiple Injuries
* Degree of Injury & Inflammation
* Body Temperature
* Ventilation

Question 27

Energy requirements in flow phase with kcal/kg

Answer 27

• ≤ 25 kcal/kg for patients on propofol infusion (or rocuronium/pancuronium)
• 25 kcal/kg for single system organ failure
• 25-30 kcal/kg for double system organ failure
• 30-35 kcal/kg for multisystem organ failure
• 27-30 kcal/kg for CRRT

Question 28

protein needs in flow phase

Answer 28

1.5-2.5 g/kg/d
* most patients 1.5-2 g/kg for protein.

Question 29

Describe what happens in the flow phase

Answer 29

Period of hypermetabolism; catabolism
* lean body tissue breakdown due to high levels of catecholamines, glucagon, etc (can be higher than in Ebb Phase). Insulin resistance ++ /++ CRP (due to inflammation)
* Wound healing is the number one priority
* Increase in cardiac output, BMR, body temperature, muscle wasting, weight loss
* ++ gluconeogenesis/++ lipolysis/++ proteolysis; increases in urinary nitrogen excretion; ++ insulin resistance (caused by +++ up regulation of counter regulatory hormones).
* Increased synthesis of acute phase reactants; such as CRP; down regulation of hepatic proteins such as albumin

Question 30

Summary of Metabolic Changes in Ebb vs Flow Phase

Answer 30