Transcript Slide 1

Micronutrients in Critical care
BY
Ahmed Salah
Lecturer of anesthesia &critical
care
Micronutrients in the critically ill
patient
• Nutritional support of the critically ill patient
includes the daily provision of vitamins and
trace elements. These compounds, collectively
termed “micronutrients”, are essential not
only as intermediaries in metabolism but also
for their potential roles in cellular immunity,
wound healing and antioxidant activity
Micronutrients in the critically ill
patient
 Any injured patient will develop an acute phase response
(APR) and a systemic infammatory response syndrome
(SIRS) with the production of various mediators, including
cytokines, which modulate the metabolic response. SIRS is
associated with a redistribution of vitamins and trace
elements from the circulating compartment to tissues and
organs, which are involved in protein synthesis and immune
cell production.
 The circulating concentrations of most trace elements
(iron, selenium, zinc) and of their carrier proteins decrease
as do the water-soluble vitamins, whereas copper and
manganese increase,causing a relative defcit in circulating
antioxidants.
Micronutrients in the critically ill
patient
• Critical illness is associated with increased ROS
production (and thus increased oxidative
stress), and on the other hand low levels of
most antioxidant micronutrients (endogenous
antioxidant defenses).
Micronutrients in the critically ill
patient
Oxidative stress is defined as
“a state in which the level of toxic reactive
oxygen intermediates (ROI) /reactive oxygen
species overcome the endogenous
antioxidant defences of the host”
Micronutrients in the critically ill
patient
• Free radicals cause a cascade of intracellular
events resulting in the release of nuclear factorkappa B (NF-Kb) in the cytoplasm, and
subsequently enabling the initiation of the
transcription process. NF-KB controls the
production of acute phase mediators such as
tumour necrosis factor (TNF-a), interleukin 2 (IL2), and IL-2 receptors, which in turn activate NFKB, intensifying the infammatory cascade. In this
regard, selenium has been shown to
downregulate NF-KB,
Pathways leading to activation of NF-KB and the production of adhesion
molecules. (Dinardo et a1,2008)
Vitamin A (retinol, carotene)
Vitamin A is fat-soluble vitamin needed for the normal structure
and functioning of the cells in the skin and body linings, e.g. in
the lungs.
This vitamin also helps with vision in dim light, as well a keeping
the immune system healthy.
It is found in two forms; retinol in foods from animal
sources and carotenoids (the most abundant of which
is the beta-carotene) from plant sources.
Vitamin A – retinol is found in liver and whole milk,
Vitamin A – carotenoids are found in dark green leafy
vegetables, carrots and orange coloured fruits.
Vitamin E (Tocopherol)
Vitamin E is a group of similar molecules with common properties
and functions.
Vitamin E acts as an antioxidant and protects cells in the body
against damage.
Vitamin E is mainly found in vegetable oils, nuts,
seeds and wheat germ.
Thiamin (B1)
Thiamin is needed for the release of energy from carbohydrate. It
is also involved in the normal functioning of the nervous system
and the heart.
Thiamin deficiency can lead to the development of the disease beriberi. Symptoms include fatigue, weakness of the legs and
anorexia.
Vitamin C (Ascorbic acid)
Ascorbic acid is needed to make collagen which is required for the
normal structure and function of body tissues, such as skin,
cartilage and bones.
It also acts as an antioxidant that protects the body from damage
by free radicals.
Sources of ascorbic acid include fresh fruits, especially
citrus fruits and berries, green vegetables, peppers
and tomatoes. Ascorbic acid is also found in potatoes
(especially in new potatoes).
Anti-oxidants
Vitamins A, C and E are anti-oxidants and work together in the
body to protect cells against oxidative damage from free radicals.
This damage to cells can increase the risk of developing diseases
such as heart disease and cancer.
Selenium
• regulates free-radical scavenging systems
• low levels common in normals and ICU
patients
• several small studies inconclusive but suggest
benefit
• one large, flawed recent study showed nonsignificant mortality benefit
ZINC
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Beneficial effect of Zn in critical care:
Repair of damaged tissues
Protect the liver from endotoxin
Co-factor function in acute phase protien
synthesis and increased bacteriocidal
capability after phagocytosis.
• Zn is thought to have benefial effect by
decreasing microbial effect.
ZINC
The decrease in serum Zn is related to
redistribution of Zn to site of tissue injury .
Surgical trauma increases corticosteroid
secretion ,which decreases s.Zn.
Hypermetabolic trauma patient experience
loss Zn through gastrointestinal tract,also loss
throug urine may contribute
Micronutrient Deficiencies - I
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•
Essential Fatty Acids
Zinc
Copper
Chromium
• Molybdenum
Cholestasis
• Selenium
Scaly dermatitis
Growth retardation
Anemia, Leukopenia
Glucose intolerance,
Neuropathy
Confusion,
(Cardio)myopathy
Micronutrient Deficiencies - II
• Vitamin A
• Vitamin D
weakness
• Vitamin E
• Vitamin K
• Biotin
• Carnitine
Night blindness, keratosis
Osteomalacia, Muscle
Retinal & posterior column
nuclei dystrophy,
Bleeding diathesis
Alopecia, Dermatitis, Neuritis
Abnormal LFTs
• Endogenous mechanisms work in a network-like
fashion to neutralise the production of ROS in an
attempt to counteract the deleterious effects thereof.
Intracellular glutathione and nonenzymatic ROS
scavengers (including vitamins such as ascorbic acid,
β-carotene and a-tocopherol) form part of this highly
evolved mechanism. Enzymatic systems [including
superoxide dismutase (SOD), catalase and glutathione
peroxidases (GSHPx)] then work synergistically to
detoxify ROS further. These enzyme systems are
dependant on minerals such as selenium, copper, zinc
and manganese as important cofactors in these
enzymatic reactions.
THEN WHAT TO DO?
EVIDENCE BASED RESULTS
• Mortality
• Fourteen of the 15 trials provided mortality data ,
When the results of all 14 RCTs were aggregated
(n = 1468), overall, micronutrients were
associated with a significant decrease in mortality
(P = 0.0009)
• Six trials in total reported on 28-d mortality, and
when the results of these trials were aggregated
(n = 1194), micronutrient supplementation was
associated with a significant decrease in 28-d
mortality ( P = 0.0006)
EVIDENCE BASED RESULTS
• Infectious complications
• Although 11 of the 15 trials provided infectious
complications data , trials indicated that micronutrient supplements showed no significant
effect on infectious complications ( P = 0.69).
• Length of hospital stay
• When the results of these four trials were pooled
(n = 113), micronutrient supplementation was
not associated with a significant difference in LOS
, P = 0.75).
ENTERAL VS PARENTRAL ROUTE?
• This present review did not find clear evidence that parenteral is superior
to enteral administration in terms of clinical outcomes,. The vast majority
of trials available in the literature delivered micronutrients intravenously,
with the intravenous route seen as the only reliable method by which
micronutrients can be administered in the critically ill . Absorption by the
enteral route in critically ill patients is unpredictable because of bowel
edema, bowel ischemia, hemodynamic instability, fluid resuscitation, and
alterations in blood supply . Conversely, delivering micronutrients to the
gut may be beneficial through the prevention of the local gut
inflammatory response , indicating that the two routes, in theory at least,
do have advantages . Bearing in mind the important role of the
gastrointestinal tract as a source of cytokine and leukocyte activation and
ROS formation, the provision of key nutrients directly to the
gastrointestinal tract makes biological sense . It is thus proposed that
future studies investigate the use of parenteral and enteral
administrations of micronutrients to maximize the opportunity of
demonstrating a treatment effect, if one really exists.
WHEN TO GIVE?
• The timing of micronutrient supplementation
is important and is probably a key factor
because the repletion of micronutrients, and
specifically of antioxidants, would probably
achieve a greater efficacy if given before
massive oxidative injury (e.g., severe sepsis or
septic shock) .
ARTICLES
CONCLUSION
• This show suggests potential benefit of micronutrient
supplementation in critically ill adults by possibly being
associated with a decrease in mortality but highlights
that caution is warranted because nutrient interactions
and risk of toxicity are not clearly defined in critical
illness. Timing, duration, and dosing appear to be key
factors to ensure optimal clinical benefit.
• Still larger studies with greater number of patients are
warranated to determine a clear end of when ,what
and how nutrients are supplemented with other
studies determining the optimum dosages.
Thank you