Critical Care Guidelines Flashcards

1
Q

Which of the following characterizes the current understanding of the inflammatory response?
A) Overstimulated immune system
B) Mixture of immune stimulation and suppression
C) Initial immune suppression followed by stimulations
D) Immune suppression

A

B

-There is a compensatory action which will cause immune metabolic suppression, and decreased immunity sometimes pre-dominates depending on source of inflammation, timing, and clinical status of the patient.

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2
Q

Why is hemodynamic stability an important consideration before initiating enteral nutrition?

A

As gastrointestinal perfusion may be compromised

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3
Q

When is GI perfusion compromised?

A
  • In septic states, particularly in the context of hemodynamic instability
  • Feeding into the GI tract may elicit an ischemia event
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4
Q

What is the best reason to conservatively prescribe energy in nutrition support regimens?

A

For glycemic control

  • Hyperglycemia is associated with adverse outcomes, such as increased incidence of infections.
  • Conservative prescriptions and a gradual increase of infusion rates to goal energy req. can assist in controlling BG levels
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5
Q

What are the most common sources of sepsis for adult hospital admission?

A
  • Lung
  • Urinary tract
  • GI system
  • Skin
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6
Q

What is sepsis?

A

No longer considered a disease, but a group of diseases based on the patient, severity of insult, response of host and number of organs involved.

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7
Q

Define sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to the infection

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8
Q

Define septic shock

A

Subset of sepsis in which profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than sepsis itself. Associated with hemodynamic unstability

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9
Q

(T/F) Sepsis requires an infectious agent

A

F

-Severe trauma, pancreatitis, burn injury etc can produce the same clinical findings without an infectious source

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10
Q

What are the two phases of sepsis?

A

Inflammatory and anti-inflammatory in the later phase

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11
Q

When is nutritional support optimized in the septic patient?

A

During the later immuno-suppressed phase

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12
Q

How does nutrition therapy play a key role in sepsis and in severe infections?

A
  • Modulate the inflammatory response
  • Maintain immune function
  • Abrogating skeletal muscle catabolism
  • Improving wound healing
  • Maintaining GI and pulmonary mucosal barrier function
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13
Q

Discuss the dysregulation of CHO metabolism during sepsis

A

Pro-inflammatory cytokines will potentiate the release of catabolic hormones (glucagon, catecholamines, cortisolP) to mobilize glucose, inducing hyperglycemia and insulin resistance.
–> Onset of sepsis will use up glycogen stores within hours, and lipid and protein will predominate as energy sources.

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14
Q

_____ increases with progressive organ failure, and _____ will impair blood flow to liver, leading to hepatic dysfunction, hypoglycemia and end of live.

A
  • Gluconeogenesis

- Reduced splanchnic blood flow

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15
Q

Discuss the dysregulation of protein metabolism during sepsis

A
  • Protein breakdown and synthesis increases, however remain in a net-negative nitrogen balance.
  • Decreased AA uptake and accelerated peripheral muscle protein breakdown, which results in a flux of AA to the liver, increasing production of creatinine, uric acid and ammonia which are excreted in high amounts.
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16
Q

Discuss hepatic re-prioritization in septic patients

A
  • Hepatic uptake of AA increases and hepatic protein synthesis increases, which will allow for the production of glucose via gluconeogenesis and APP
  • Liver will prioritize synthesizing positive acute phase proteins, such as CRP at the expense of negative acute phase proteins, such as albumin and pre-albumin
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17
Q

In an unfed, stressed up to ____ of lean body mass will be broken down each day

A

250 g

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18
Q

Consequences of prolonged catabolism of skeletal muscle protein?

A
  • Compromises respiratory function
  • Impairs wound healing
  • Exacerbates immunosuppression
  • Accelerates the loss of strength and endurance needed for recovery
  • Increases ventilator time and ICU stay
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19
Q

Discuss the dysregulation of lipid metabolism during sepsis

A
  • Catabolic hormones epinephrine, norepinephrine and glucagon are the predominant stimulators if the hydrolysis of TG by stimulating HSL
  • Impaired acyl-carnitine carrier which will decrease FFA uptake
  • Accumulation of FFA in the cell, and can result in intracellular acidosis and accumulation of lactate and pyruvate –> Results in impaired ketogenesis but high-levels of B-hydroxybutyrate
  • Inactivation of LPL, which causes hyperlipidemia
20
Q

Energy expenditure changes in sepsis?

A

Significant increase of 20-60% above the basal energy expenditure.

21
Q

What may attenuate the anti-inflammation in sepsis?

A

-EN and use of anti-inflammatory lipids (EPA and DHA) can attenuate the catabolic response to stress.

22
Q

(T/F) PN is preferable in the septic patient

A

F

EN is associated with better outcomes

23
Q

Susceptibility to ischemia in EN and sepsis?

A

GI tract and liver associated with ischemia risk secondary due to shunting of blood flow away from the splanchnic bed.
-EN may enhance perfusion during septic states

24
Q

What must be considered amongst EN delivery and vasopressors during the critically ill?

A

-Vasopressors may prevent a normal increase in splanchnic blood flow associated with EN, therefore aggravating necrosis

25
Q

ASPEN guidelines for feeding the septic patient?

A

10-20 kcal/h or 500kcal/day for initial phase of sepsis, advancing as tolerated after 24-48 hours to greater than 80% of EE requirements in one week

26
Q

What is the best approach to EN feeding in an acutely ill ventilated septic patient?

A
  • Cannot initiate feeding until the patient is stable
  • Start tube feeding at a low rate, with immune-enhancing formula
  • Use PENN state formula due to ventilator
27
Q

What is the best approach to PN in an acutely ill septic patient? The patient is hyperglycemic with an intestinal fistula and is malnourished

A
  • Use mixed-fuel formula as the patient was hyperG, thus dextrose infusion alone is sufficient
  • Increase proportion of formula from fat and protein, especially due to malnutrition and impaired PO intake
28
Q

Benefits of EN in the septic patient?

A
  • Prevention of adverse structural and functional alterations in the mucosal barrier
  • Augmentation of visceral blood flow
  • Enhancement of local and systemic immune response
29
Q

What is the 3-armed approach to sepsis management? in which arm should NS be initiated?

A

1) Source control
2) Early antibiotic administration
3) Resuscitation
- -> EN feeding should not be undertaken until resuscitation is complete

30
Q

What is non-occlusive mesenteric ischemia?

A
  • Uncommon complication following the early initiation of EN
  • Low-flow state, affecting the superior mesenteric artery and can result in irreversible ischemia and and necrosis of the small or large bowel
31
Q

(T/F) we must wait until active bowel sounds and function to initiate EN

A

F

May delay feedings

32
Q

APEN recommendations of initiating nutrition therapy for sepsis/septic shock?

A

Within 24-48 hours of of making the diagnosis, and as soon as resuscitation is complete and the patient is hemodynamically stable

33
Q

What are the 3 common GI dysfunctions in ICU patients?

A
  • Mucosal barrier disruption
  • Altered motility
  • Atrophy of mucosa and GALT
34
Q

What causes mucosal barrier disruption? What are the net results?

A
  • Often caused by reduced splanchnic hypo-perfusion

- Results in reduced mucosal blood flow, barrier disruption, altered GI motility, and changes in gut microflora.

35
Q

Bottom-line recommendations to maintain gut function in post-operative care in ICU settings?

A
  • Maintain visceral perfusion, glycemic control and electrolytes
  • Early EN
  • Minimize medications that alter GI function, including anti-cholinergic agents, narcotics and vasopressors.
36
Q

What is the paradox of the increase in energy expenditure in septic patients?

A
  • Their energy expenditure will increase 20-60%

- Cannot efficiently utlize increases in energy during the first phase of sepsis

37
Q

CHO administration in septic patients?

A

50-60% of energy

-Avoid excess hyperglycemia and lipogenesis

38
Q

Two characteristics which make lipids a valuable source of energy for septic patients?

A
  • Energy dense, 9kcal/g with less volume

- Lipid oxidation produces less CO2, and may reduce blood concentrations of CO2

39
Q

ILE infusions for ICU septic patients?

A

Should not exceed 1.0g/kg/day

40
Q

Why should MCT and SCFA be beneficial for septic patients?

A
  • MCT is not carnitine dependant

- SCFA from fermentation of soluble fibres can maintain GI mucosa and immune function

41
Q

Omega-3 FA down-regulate the ______ to stressful stimuli and can enhance ______ & _______

A
  • pro-inflammatory response
  • respiratory function
  • resistance to gram - pathogens
42
Q

What may be the optimal lipid blend for ICU patient with sepsis?

A

A mix of omega-3 and omega-6

43
Q

Why may arginine have potential to benefit the septic ICU patient?

A
  • Arginine is critical in the nitric oxide production, and nitric oxide can decrease hepatic and splanchnic injury following ischemia
  • ASPEN recommends use in surgery ICU patients only
44
Q

Why may glutamine have potential to benefit the septic ICU patient?

A
  • Glutamine is associated with increasing production of HSP proteins, which enhances the ability of of cells to protect themselves from stress.
  • APSEN does NOT recommend use in ICU patients due to RCT showing increased mortality
45
Q

The development of malnutrition is rapid in the ICU and septic patient due to the _____

A

complex metabolic changes induced by cytokine and catabolic hormones

46
Q

If appropriate NS is not administered in the septic ICU patient, what can happen?

A
  • The gut can fail
  • Proximal bacterial colonization is associated with septic mortality.
  • We need to maintain host immunity, through the gut