Chapter 23: Sepsis & Critical Illness

Question 1

Define sepsis.

Answer 1

• Life-threatening organ dysfunction caused by a dysregulated host response to infection.
• The systemic response to infection

Question 2

Define septic shock.

Answer 2

• Refers to a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone
• Associated with hemodynamic instability, which is primarily refractory hypotension with systolic peak pressure less than 90 mmHg, mean arterial pressures less than 65 mmHG or a drop of greater than 40 mmHg from baseline.

Question 3

The metabolic response to sepsis is in many ways similar to the response that follows major surgery or trauma. What are both responses characterized by?

Answer 3

• Increases in energy expenditure
• Protein catabolism
• Oxidation of stored lipids alson with significant alterations in the body’s ability to metabolize CHOs

Question 4

In what ways is appropriate nutrition therapy during sepsis and severe infections essential?

Answer 4

• Plays a key role in modulating the inflammatory response
• Maintaining immune function
• Abrogating skeletal muscle catabolism
• Improving wound healing
• Maintaining GI and pulmonary mucosal barrier function

Question 5

What is the glucose target for patients with sepsis?

Answer 5

No greater than 180 mg/dL.

Question 6

(TRUE/FALSE)

Following the onset of sepsis, glycogen stores are depleted within hours and endogenous lipid and protein become the major source of oxidative energy substrate.

Answer 6

TRUE.

Related to catabolic hormones stimulating glycogenolysis and gluconeogenesis.

However, oxidation of lipid from endogenous adipose stores is impaired during sepsis.

Question 7

Why does sepsis result in hyperglycemia?

Answer 7

Sepsis results in hyperglycemia secondaryto alterations in:

• Endogenous glucose production
• Decreased glucose uptake
• Insulin resistance

Gluconeogenesis increases with progressive organ failure

Question 8

(TRUE/FALSE)

Although protein breakdown and synthesis both continue to occur at acclerated rates during sepsis, patients remain in generalized net-negative N balance for variable periods even after the inciting insult has been resolved.

Answer 8

TRUE.

The acceleration of peripheral muscle protein breakdown noted in sepsis is accompanied by diminished AA uptake by muscle. Excreted in increased amounts in the urine during sepsis.

Question 9

(TRUE/FALSE)

Mammalian species have no “storage” of protein and that any protein utilized during catabolic stress of any kind comes at the expense of other tissues that are more labile.

Answer 9

TRUE.

Question 10

Explain hepatic reprioritization.

Answer 10

• During sepsis, hepatic uptake of AAs and hepatic protein synthesis are increased, which allows a substrate for gluconeogenesis and production of acute-phase protein.
• However, the increase in hepatic protein synthesis is NOT uniform
• Although serum concentrations of positive acute-phase proteins (such as haptoglobin and CRP), increase in response to stress, synthesis of negative acute-phase proteins, such as albumin and prealbumin, falls.

Question 11

(FILL IN THE BLANK)

As the systemic response to sepsis progresses, protein catabolism XXXX, and the failure of synthetic processes to keep up with the breakdown rate results in XXXX of skeletal protein.

Answer 11

• INCREASES
• SEVERE LOSSES

Question 12

What does prolonged catabolism of skeletal protein result in?

Answer 12

• Compromises respiratory function
• Impaires wound healing
• Exacerbates immunosuppression
• Accelerates the loss of strength and endurance necessary for recovery
• Increases ventilator-dependent time and ICU stay
• Increases thromboembolic disease
• Increase recovery time
• Increases mortality incidence.

Question 13

(TRUE/FALSE)

**SCCM/ASPEN recommend that clinicians evaluate weight loss and nutrition history prior to admission, level of disease severity and GI function.

Answer 13

**TRUE

Question 14

(TRUE/FALSE)

Practitioners are often concerned that EN may increase ischemic injury during states of decreased perfusion of the splanchnic organs in septic patients, especially if the patient is receiving vasoactive medications.

Answer 14

TRUE.

Lab evidence provides support for the OPPOSING VIEW: namely that EN provides protection and even enhances perfusion during septic states.

Question 15

What are some approaches to maintaining visceral perfusion?

Answer 15

• Adequate resuscitation
• Glycemic control
• Correction of acidosis
• Correction of electrolyte abnormalities
• Minimizing the use of anticholinergic medications, narcotics and other medications that decrease intestinal motility
• Instituting EN, even at low rates, within the first 24 to 48 hours of the onset of SIRS or sepsis

Question 16

**What are SCCM/ASPEN recommendations related to nutrition support in a critically ill septic patient?

Answer 16

**ASPEN/SCCM guidelines recommend trophic feeding (10 to 20 kcal/hr or 500 kcal/d) for the initial phase of sepsis, advancing as tolerated after 24 to 48 hours to greater than 80% of target energy goal over the first week.

Question 17

**What are the SCCM/ASPEN recommendations related to PN in a critically ill septic patient?

Answer 17

**When a patient is in the acute phase of severe sepsis, the ASPEN/SCCM guidelines suggest NOT using exclusive PN or supplemental PN in conjunction with EN regardless of patient’s degree of nutrition risk.

Obviously, if the gut is deemed unreliable, PN may be selected.

Question 18

What is the 3-armed approach to management of sepsis?

Answer 18

1. Source control
2. Early antibiotic administeration
3. Resuscitation

Question 19

Define hypotensive.

Answer 19

Mean arterial pressure less than 65 mmHg

Question 20

(TRUE/FALSE)

There is a single laboratory/hemodynamic parameter signaling the successful resuscitation of the critically ill patient in shock.

Answer 20

FALSE.

There is NOT; Generally, clinicians use the trends in hemodynamic parameters, including mean arterial pressures, central venous pressures, and vasopressor requirements, in conjunction with urine output, arterial base deficit, serum lactate and venous oxygen saturations, to determine the relative success of resuscitation.

Question 21

Define NMI (nonocclusive mesenteric ischemia.

Answer 21

• A uncommon compklication following the early initiation of enteral feeding in the underresuscitated patient
• It is a low flow state that most commonly affects the distribution of the superior mescenteric artery, which can result in irreversible ischemia and necrosis of the associated small and large bowel.

Question 22

**When does SCCM/ASPEN recommend initiation of enteral support in critically ill septic patients?

Answer 22

**SCCM/ASPEN guidelines recommend that critically ill patients receive EN therapy within 24 to 48 hours of making the diagnosis of severe sepsis/septic shock, as soon as resuscitation is complete and the patient is hemodynamically stable.

Feeding immediately after the initial dx of sepsis yields a distinct set of problems.

Question 23

How should GI intolerance be continually reassessed?

Answer 23

• Abdominal distention
• Increased gastric residual volumes
• Increased NG output
• Abdominal pain
• Diarrhea

Question 24

(TRUE/FALSE)

Impaired gastric and proximal GI motility can be addressed efficiently through the placement of postpyloric feeding tubes.

Answer 24

TRUE.

They can be done successfully at bedside in more than 80% of patients.

Question 25

What are two prokinetic agents?

Answer 25

1. Erythromycin: acts on motilin receptors, resulting in increased motility, although its use may be limited by tachyphylaxis (short/rapid drug intolerance)
2. Metoclopramide: a 5-HT(4) receptor agonist, works via cholinergic stimulation and is most effiacious in the proximal gut

No single prokinetic agent will have uniform success in the ICU, and the factors contributing to GI dysmotility in each patient must be considered.

Question 26

**What are the energy requirements for patients with sepsis/septic shock?

Answer 26

• **Increases of 20 to 60% over basal expenditure
• Range of 20 to 30 kcal/kg/d is considered safe for critically ill patients (excluding the morbidly obese)

Question 27

**What are the CHO recommendations related to energy expenditure in critically ill septic patients?

Answer 27

• **CHO administeration should supply 50 to 60% of the total energy prescription to avoid exceeding the maximum contribution of glucose oxidation and contributing to excess lipogenesis.
• Glucose admin. rates greater than 4 to 6 mg/kg/min result in excess lipogensis and lead to hyperglycemia.

Question 28

**In critical care and sepsis patients, the amount of ILES should not exceed XXXXX, if XXXX.

Answer 28

• **1.0 g/kg/d
• if soybean oil is the source of lipid.

Guidelines for enteral lipid delivery are similar to those for parenteral lipid provision. The usual lipid goal of 1.0 g/kg/d can be liberalized when enteral lipids include lipid substrates containing omega-3 FAs, MCTs, and SCFA. And a mixture of lipid fuels should be delivered whenever possible.

Question 29

(TRUE/FALSE)

**Conflicting data prevented the ASPEN/SCCM guidelines from making a recommendation for use of anti-inflammatory lipid formulas at this time.

Answer 29

TRUE.

Question 30

**What are the SCCM/ASPEN guidelines for protein in sepsis?

Answer 30

** 1.5 to 2.0 g/kg/d (possibly even up to 2.5 g/kg/d in selected cases).

Question 31

(TRUE/FALSE)

**ASPEN/SCCM guidelines recommend use of an arginine/fish oil formula only in surgical ICU patients and do NOT recommend their routine use in patients with sepsis alone.

Answer 31

**TRUE.

Question 32

(TRUE/FALSE)

**SCCM/ASPEN guidelines recommend that clinicians supplement severely ill ICU patients with enteral or parenteral glutamine.

Answer 32

FALSE.

It is NOT recommended.

Question 33

**Does SCCM/ASPEN have specific guidelines for supplementing zinc, selenium, or antioxidants in sepsis?

Answer 33

**NO

There is not a definitive recommendation.

The literature suggests clinicians provide at least the RDA of antioxidants vitamins and trace elements to critically ill patients throughout hospitalization.