Nutrition in palliative care

Nutrition in trauma
Nutrition in burns
MOHAMED YASSIN
P H A R M D, E S P E N L L L S , C P H Q , E U S O P, H E A LT H C A R E M A N A G E M E N T D I P LO M A
M E M B E R O F E U R O P E A N S O C I E T Y O F O N C O LO GY P H A R M A C I S T S ( E S O P )
MEMBER OF EGYPTIAN SOCIETY OF NUTRITION PHARMACISTS (ESNP)

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Nutrition in palliative care

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What is palliative care?
WHO definition of palliative care is an approach that improves the quality of life
of patients (adults and children) and their families who are facing problems
associated with life-threatening illness.
It has developed primarily in areas of health care such as cancer although does
also encompass other life-threatening diagnoses.
Palliation may be either the primary focus of care, or it may be provided
concurrently with life-prolonging treatment.
Goal of palliative care is improving the quality of life of patients and their
families.
Palliative care vs Hospice care

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Focuses of palliative care
1. Pain management.
2. Nutritional support.
3. Psychological support.
4. Relaxation techniques.
5. Spiritual support.
6. Support for caregivers and families.

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The role of the dietitian in palliative care

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Prevalence of Nutritional Impact Symptoms

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Managing nutritional problems in palliative care

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 Cachexia and weight loss
Etiology Nutritional management
• Anorexia leading to inadequate nutrient intake. • Individualized nutritional counseling.
• Metabolic disturbances. • Food fortification and appetizers.
• Presence of inflammatory and other humoral • Oral nutrition supplements containing
factors. eicosapentaenoic acid (EPA) led to weight
• Cytokine-induced hypothalamic resistance—the stabilization, gains in lean body mass, reversal of
inability of the hypothalamus to respond negative nitrogen balance, prolonged survival,
appropriately to signals that indicate an energy and improved or stabilized QoL.
deficit. • Pharmacological management including
• Psychological factors. progesterones, corticosteroids, prokinetics
• Intestinal obstruction. (metoclopramide), cannabinoids, melatonin,
• Radiotherapy and chemotherapy. erythropoietin and nonsteroidal anti-
inflammatory drugs (indomethacin).

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 Early satiety
Etiology Nutritional management
• Decreased gastric motility due to • If impaired gastric motility is a known or
paraneoplastic syndrome or chemotherapy. suspected cause, prokinetic agents may be
• Dysfunction of the autonomic nervous system. beneficial.
• Medications (opioids, chemotherapy). • Eating small, frequent, and nutrient-dense
• Gastric surgery. meals or snacks.
• Fibrosis • Avoid consumption of foods that have very high
• Gastritis. fat content.
• Drinking liquids between meals.
• limit intake of gas-forming foods.
• Consider light activity to help stimulate
digestion.

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 Nausea and Vomiting
Etiology Nutritional management
• Mechanical issues (impaired gastric emptying, GI • Avoidance of strong odors.
obstructions). • Keeping foods cold or at room temperature.
• Chemical sources (cytotoxic agents, opioids, • Eating dry, starchy, or salty foods.
NSAIDs). • Eating ginger or peppermint candies.
• Therapeutic side effects (as in palliative radiation • Avoiding liquids on an empty stomach.
therapy). • Avoiding lying down for at least one hour after
• Metabolic factors (infections, comorbidities, eating.
renal or hepatic failure). • Increasing fluid intake to thin secretions.
• Pain, fear, anxiety, and unpleasant odors or • Frequent rinsing and gargling with a baking
tastes. soda solution (1 tablespoon baking soda in 1
quart of water).
• Eating fresh pineapple to thin oral and
pharyngeal secretions.

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Medical management of Nausea and Vomiting
Impaired gastric emptying: prokinetics.
Bowel obstruction: surgery, nasogastric suction, self-expanding metallic stents,
venting gastrostomy, and bowel rest with total parenteral nutrition (TPN) or
hydration.
Drug-induced nausea and vomiting: antiemetics, rotation (in the case of
opioids), steroids, mucosal protectants (in the use of NSAIDs), and changing,
reducing dosage of, or discontinuing use of the causal agent.
Nausea and vomiting related to radiation therapy: serotonin-receptor
antagonists, dopamine-receptor agonists, or dexamethasone.
Metabolic causes: hydration (uremia) or bisphosphonates for hypercalcemia

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 Xerostomia
Etiology Nutritional management
• Opioids. • Both fluid intake and good oral hygiene should
• Antibiotics. be encouraged.
• Antiemetics. • Cool, smooth liquids or suck on ice chips.
• Tricyclic antidepressants. • Avoid highly acidic juices.
• Anticholinergics. • Soft, moist food with dressings.
• Antihistamines. • Avoid alcohol, tobacco and spicy foods.
• Dehydration. • Chew sugar-free gums.
• Mouth breathing. • Pharmacological treatment options include
• Anxiety. pilocarpine, cevimeline, sodium fluoride,
• Advanced age (age > 65 chlorhexidine, and nicotinamide.
years).
• Smoking.

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Constipation
Etiology Nutritional management
• Medications in particular opioids, but also • If impaired motility is suspected, prokinetic
antiemetics, antidepressants, agents may prove useful.
anticholinergics and vinca alkaloids. • Consumption of a high-fiber diet and use of
• Dehydration. bulking agents (methylcellulose, psyllium).
• Hypokalemia. • Adequate fluid intake (minimum 2–3 L/day).
• Hypercalcemia . • If adding wheat germ, bran, or flaxseed to
• Neurogenic (spinal cord compression, foods, begin with 2 tsp and build up to 2
neurotoxicity). tbsp. per day.
• Poor intake. • Limiting gas-forming foods

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Protein requirements
Protein provides the building blocks for repairing damaged tissues, maintaining
muscle and maintaining a healthy immune system.
Due to the increased demands of illness, protein needs are often increased..
Increase to as much as 1.5 to 2.0 gram per kilogram for those suffering from
advanced disease and include foods high in protein at every meal and snack.
Foods rich in protein includes meat, fish, poultry, dairy products, beans,
legumes, nuts, grains chocolate, and oral nutrition supplements that are protein
dense.

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Omega 3 fats
Inflammation in the body is common in cancer and chronic diseases. The omega
3 fatty acids found in fish oils have been shown to slow down loss of muscle
tissue, and the tiredness that goes with it.
Taking 2.0 grams per day of marine omega 3’s (fish oils) can help. This is
equivalent to:
➢2 teaspoons of liquid fish oil.
➢Around 150 to 200 grams of oily fish such as sardines or salmon.
Fish oil is safer than cod liver oil, because cod liver oil contains vitamin A, which
is harmful in large amounts.

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Artificial Nutrition and hydration (ANH)
The decision as to whether palliative care patients may benefit from artificial
nutrition support is difficult and needs to be considered on an individual patient
basis.
The provision of artificial nutrition support in the form of enteral or parenteral
nutrition must be considered as a medical treatment and considered if the
perceived benefits are to outweigh the burdens of providing nutrition support.
Enteral and parenteral nutrition may help improve survival, functional status and
quality of life, but these benefits appear to be limited to patients with good
functional status and with head and neck or gastrointestinal disease affecting
dietary intake.

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Benefits versus burdens of artificial nutrition
support

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Dehydration in terminal illness
Effects of intravenous hydration on the terminal patient including increased
gastrointestinal fluids, which leads to vomiting and need for nasogastric
suctioning, respiratory distress with choking and drowning sensations resulting
from fluid retention in the lungs, peripheral edema, and increased urine
production (if the kidneys have not shut down) leading to a requirement for
catheterization in a patient too weak to ambulate.
The state of dehydration in such a patient results in relief from the previous
symptoms plus increase in endorphins secretions so, there is no feeling of pain.
The only annoying symptom is a dry mouth, which is perceived as thirst easily
ameliorated with meticulous mouth care, sips of tolerated beverages, and/or ice
chips.

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Nutrition in trauma

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Trauma
Trauma is defined as any physical damage to the body and often occurs in young
patients, who have little or no protein-depletion. It includes an immediate
cardiovascular response, an inflammatory response occurring several hours after
the injury, and finally a metabolic response, which has to be taken into account,
particularly during recovery.

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Pathophysiology

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Cardiovascular response
First, heart rate and total peripheral vascular resistance increase to maintain blood pressure.
After a loss of a third of blood volume, blood pressure falls and is accompanied by bradycardia
and syncope. When about 44% of blood is lost, heart rate increases again massively.
Tissue damage alone induces tachycardia, increased blood pressure, increased sympathetic
efferent activity and redistribution of blood flow to skeletal muscle while hemorrhage, which
results in diversion of blood flow to vital organs.
When hemorrhage and tissue damage coexist, as in trauma, the response to tissue damage
prevails.
During the cardiovascular phase, priority is given to resuscitation and maintenance of vital
functions over nutrition support.

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 Inflammatory response
During the inflammatory response there is an increased production of cytokines
(TNF-a, IL-1, IL-6, IL-10) from the gut and wounded tissue.
This change in cytokine secretion may be related to the development of multiple
organ failure (MOF).
Two models explaining early and late MOF are:
1. The first model describes a systemic inflammatory response syndrome (SIRS)
followed by a phase of immunosuppression.
2. Another model hypothesizes a ‘‘one-hit’’ or ‘‘two-hit’’ insult. The ‘‘one-hit’’
insult represents the MOF occurring immediately after severe trauma and the
‘‘two-hit’’ insult represents the MOF triggered by a secondary insult, as
surgery, infection or ischemia a few days after trauma.

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Metabolic response
The metabolic response consists mainly of hypermetabolism, mediated by the
stimulation of catabolic hormones (glucagons, catecholamines and corticoids)
and insulin resistance.
Associated with inadequate nutrition, the administration of drugs as
glucocorticoids and physical immobilization, this neuroendocrine response leads
to protein breakdown to amino acids which are used to produce de novo
glucose in the liver (gluconeogenesis).
Hyperglycemia and increase in endogenous glucose production occurs at this
stage.

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Wound healing and nutrition
Protein intake is essential for wound healing as protein deficiency interferes with
new capillary formation, fibroblastic proliferation, production of proteoglycans,
and collagen synthesis.
Arginine enhances wound healing and immune function. It acts by increasing
growth hormone secretions and nitric acid production which plays important
role in decreasing hepatic and splanchnic injury following ischemic insult.
Other nutrients involved in the complex mechanism of wound healing include
vitamins A, C, and E as well as trace elements (zinc, copper, selenium,
manganese).
Iron indirectly affects wound healing as its deficiency causes anemia which
delays wound healing.

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Timing and route of feeding
Early nutritional support (within 72 h) is more beneficial than delayed feeding in patients with
blunt or penetrating trauma because it leads to a threefold decrease in sepsis.
Total enteral nutrition (TEN) is preferred to total parenteral nutrition (TPN) because it allows
better utilization of nutrients, prevents gut mucosa atrophy, preserves gut flora, reduces stress
response and maintains immunocompetence.
Patients with an Abdominal Trauma Index >15 and fed by TEN show reduced septic
complications from intra-abdominal abscesses and pneumonias compared to those fed by TPN.
After shock resuscitation, enteral nutrition should be started at 15 ml/h and advanced to 25
ml/h eighth to 12 h later. A daily increase of 25 ml/h to goal depending upon tolerance is
advised.

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Routes of feeding

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Small bowel feeding
Small bowel feeding (naso-duodenal tube or jejunostomy) is recommended in:
➢Severe trauma (Injury Severity Score> 18 and Abdominal Trauma Index > 20).
➢Trauma with flail chest.
➢Spinal cord injury.
➢Severe pelvic fracture.
➢Major soft tissue injury.
➢Closed head injury.
About 40%-80% of patients cannot tolerate oral intake during the first 3-4 days
due to delayed gastric emptying rate and gastroparesis.
If a laparotomy is performed, a fine-bore jejunostomy is preferred to a
nasogastric tube.

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Small bowel feeding
Contraindications:
➢Full shock.
➢Sepsis.
➢Incomplete resuscitation causing reduced splanchnic blood flow, which may
then cause non-occlusive bowel necrosis.
The small bowel requires an increased blood flow to absorb nutrients. This
cannot be achieved by the shocked patient.

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Total parenteral nutrition
Total parenteral nutrition should be given in cases of:
➢Prolonged gastrointestinal dysfunction, e.g. massive small bowel resection
➢High-output fistulae
➢Intolerance to enteral feeding
➢High risk of non-occlusive small bowel necrosis (shock resuscitation, high dose
of alpha-agonists and intermittent hemodialysis with hemodynamic instability).

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Transition to oral intake
Clinicians should strive to transition patient to partial or full oral nutrition
whenever the patient’s clinical outcome will permit.
It is important to consider nighttime cycling of enteral nutrition when patients
are meeting > 60% of target calories by oral route before discontinuing EN.
Oral dietary restrictions should be discouraged to maximize intake.

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Energy needs and delivery
Moderate trauma:
Patients with moderate trauma need about 25–30 non-protein kcal/kg/day
(NPC) with 1.0–1.5 g/kg/d protein and a NPC: Nitrogen ratio of 80–120.
With resolving stress, the energy requirements remain the same but the protein
needs decrease to 1.0–1.2 g kg1, leading to a NPC: Nitrogen ratio of 130–160.
Immune-enhancing diets are not recommended for these patients while fibers-
enriched polymeric diets undergoes intracolonic fermentation of fibers and
liberates energy-rich precursors, such as butyrate, mimic the physiologic feed
profile and should therefore be used.

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Energy needs and delivery
Severe trauma:
(Abdominal Trauma Index > 20 or Injury Severity Score >18) or less severe
trauma with complications.
The caloric needs from non-protein resources remain the same but an increased
intake of protein (2.2-2.5 g/kg/d) may be beneficial.
Immune-enhancing Diets, which are enriched in L-arginine, glutamine, u-3 fatty
acids and/or nucleotides may be useful since they induce fewer infections, less
MOF, decreased use of antibiotics and shorter length of hospital stay than
polymeric diets.
These diets should be continued for 7–10 days only and changed to standard
diets thereafter since, in the long term, they induce an energy deficit.

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Nutrition in burns

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Introduction
Although the incidence of burn injury has decreased in Western countries, it still
remains a common problem throughout the World.
Overall, the metabolic responses of burn patients are qualitatively similar to
those of other trauma patients, but often of greater magnitude with an intense
acute phase response.
The resuscitation of burn patients requires massive quantities of sodium
containing fluids.
They suffer cutaneous exudative losses of fluids containing large quantities
proteins, minerals and micronutrients, causing acute deficiency syndromes.
Venous access is more difficult due to the destruction of the skin at the puncture
sites and the surface needing repair is extensive.
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Pathophysiology
1. Increased Permeability:
In the early phase of burns involving > 20% of body surface (BSA), there is a
transient massive increase in capillary permeability.
The most frequent formula used in the fluid resuscitation of burned patients is
the Parkland formula, which is based on lactated Ringer’s solution: Fluid
requirement (ml) = 4 x body weight (kg) x total burn BSA (%)
One half of this fluid is administered as crystalloid over the first 8 hours after
injury and the rest over the next 16 hours.
Fluid resuscitation of major burns, though vital, also has also side effects which
start with the creation of generalized edema.

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Pathophysiology
2. Exudates and Evaporation:
Until surgical closure, the burn wounds lose about 1 liter of fluid per 10% BSA
per day. In addition, there are evaporative water losses, which are increased by
fever and worsened using fluidized beds.

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Pathophysiology
3. Fluid Resuscitation:
All resuscitation formulae deliver roughly 0.5 mmol sodium /kg body weight/%burned
area, creating a large positive sodium balance. Colloids may be started after about 12
hours when capillary leakage is beginning to lessen, allowing a greater proportion of the
infused colloid to be retained within the intravascular space.
Albumin should only be considered with major burns > 40% BSA, and when
albuminemia is < 18 g/L.
The patients to be weighed every day, since weighing is the only accurate way of
measuring water balance
After initial resuscitation, free water requirements may remain high for many days,
especially when patients are nursed on fluidized beds. Water losses may be sufficient to
cause hypernatremia, unless matched by intake.

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Metabolic Response
The metabolic response to trauma is essentially biphasic and is followed by a
late recovery phase.
1. Ebb Phase:
Immediately after injury, there is a period of hemodynamic instability with
reduced tissue perfusion, and release of high levels of catecholamines.
This has classically been called the «ebb phase». Its is characterized by lowered
total oxygen consumption (VO2), and low metabolic rate.
It may be extremely short-lived and last a few hours or persist for a few days
depending on the severity of injury and the quality of resuscitation.

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Metabolic Response
2. Flow Phase:
It is characterized by high VO2, elevated resting energy expenditure (REE) and
accelerated potassium and nitrogen losses.
Visceral blood flow and splanchnic O2 consumption increase, the body’s
temperature is generally increased, and central thermoregulation is shifted
upward, especially in severe burns.
The largest increase in REE is during the first weeks, the duration of this change
depending on the burns size and reverting slowly to normal during the following
months whatever the age of the patient.
Skeletal muscle protein catabolism is markedly increased, and synthesis may be
impaired with extensive losses from the skin.
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Metabolic Response
3. Recovery:
This phase starts when the flow phase declines, the burned surface is covered,
and the patient starts to mobilize.
It requires high levels of energy with hypermetabolism lasting up to a year post-
injury, to restore lost tissue, to fuel physical rehabilitation, and to complete the
process of wound healing.
After major burns, this phase may last up till 2 years.

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Nutrition screening and assessment
The 2016 Society of Critical Care Medicine (SCCM)/ASPEN guidelines recommend assessment
using the Nutrition Risk Screening (NRS-2002) or Nutrition Risk in Critically ill (NUTRIC) scoring
systems to identify patients who would benefit from nutrition therapy.
NRS-2002 attempts to account for both preexisting malnutrition (e.g., weight loss, decreased
food intake) and severity of illness(i.e., type of injury, APACHE II score), whereas NUTRIC focuses
on severity of illness.
Assessment including BMI, anthropometrics and biochemical markers such as such as albumin,
prealbumin, transferrin.

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Energy Requirements
The gold standard for measuring REE is indirect calorimetry.
Both underfeeding and overfeeding have deleterious consequences:
Overfeeding particularly with carbohydrate, not only further increases energy
expenditure through diet induced thermogenesis but, by raising the respiratory
rate, increases CO2 production and hence the gas exchange load on lungs. It also
increases catecholamines production, increasing energy expenditure.
Underfeeding causes unnecessary loss of tissue, particularly lean mass.

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Estimating energy requirements
The modern Toronto equation is the only one to integrate all the factors which
affect requirements such as sex, weight, height, burned BSA, fever, previous
days’ caloric intake and time elapsed since injury. It is the most precise, being
closest to calorimetric determinations especially in burns up to 60% BSA.
For larger burns > 60% BSA, indirect calorimetry remains the optimal tool for
ensuring intake is adapted accurately to changing metabolic requirements.
In absence of indirect calorimeter, give 30-35 kcal/kg/d for burns < 40 % BSA
and 35-50 kcal/kg/d for burns ≥ 40% BSA.

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Equations to estimate TEE

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Proteins
Over the first 21 days after injury, critically ill trauma patients lose up to 16 % of their total body
protein content despite full nutrition support. Nirtogen loss is approximately 10 g per 10 %
burned BSA during the first week and cannot be compensated by nutrition in larger burns.
ESPEN guidelines:
1.3-1.5 g/kg/d (0.2-0.25 g N/kg/d) is recommended.

ASPEN guidelines:
1.5-2.0 g/kg/d for small burns
2.0 g/ kg of ideal body weight for obese patients.
3.0-4.0 g/kg/d may be required for larger burns.
Higher intakes are oxidized, increasing urea production and causing azotemia.

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Fats
As a result of elevated catecholamines, glucagon and cytokines levels, increased
lipolysis occurs giving high free fatty acids levels for oxidation and increasing
glycerol levels for gluconeogenesis.
It is recommended that fat supply doesn't exceed 30% of energy.
Omega-3 fatty acids have anti-inflammatory, antithrombotic and
immunomodulating effect and recommended at dose of 3-5 g/d according to
ESPEN guidelines.
Medium-chain triglycerides are attractive because they are small and water-
soluble and can be absorbed without requiring bile salts.
New lipid emulsions such as mixtures of soybean, olive, and fish oils are widely
used around the world as enteral nutrition formula and have favorable effects.
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Carbohydrates
Glucose is the primary fuel for the central nervous system and blood cells, with a
minimum of about 120 g/d necessary to maintain central nervous system
function. It also serves as a fuel for healing wounds and inflammatory tissues.
In the metabolically stressed adult, the maximum rate of glucose oxidation is 4
to 7 mg/kg/min, roughly equivalent to 400 to 700 g/d in a 70-kg person and
exogenous glucose intake fails to suppress endogenous production .
ESPEN recommendations not to exceed 5g/kg/d and maintain glucose levels <
145 mg/dl using insulin.
ASPEN recommends glucose levels < 180 mg/dl.

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Micronutrient Requirements
During the hypermetabolic phase, the metabolism of micronutrients is increased
in parallel with that of glucose, protein and fat, and there are increased losses
from the burn area.
In addition, some of the micronutrients have antioxidant functions, which are of
utmost importance to burned patients in order to counteract the increase in
free radical production observed in burns.
These nutrients include selenium and zinc, and the vitamins B, C, E and ß-
carotene.
Supplementation has been assessed in various conditions with beneficial clinical
results. To achieve antioxidant effects, the supplements should be provided
early on, starting during the first hours after injury.

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Trace Elements and Minerals
Copper is of special importance for collagen maturation. Copper deficiency has been
associated with fatal arrhythmias. Selenium is essential for glutathione peroxidase
activity and zinc for immunity and cell replication.
Sodium requirements vary while intake is necessarily high during the resuscitation
phase (up to 150 g sodium in 48 hours in burns > 50% BSA), requirements decrease
thereafter.
Hypernatremia is frequently observed during the remobilization of edema between
days 5 and 15, as well as during severe sepsis and should be managed is by
increasing free water intakes either by the enteral route (preferred) or intravenously
(glucose 5%).
Current recommendations: supplement with Dietary Reference Intakes (DRIs) for
vitamins and minerals.

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Vitamins
The water-soluble vitamins of the B complex are rapidly depleted. Their
requirements are greatly increased, being important cofactors for carbohydrate
metabolism (vit. B1).
Vitamin C is crucial in collagen synthesis in addition to its antioxidant effect.
Therefore, a total daily intake of 1-2 g is highly recommended.
The fat-soluble vitamins D, and K are stored in fat deposits and are slowly
depleted during prolonged diseases.
Vitamins A and E have antioxidant function and are involved in tissue repair.
There are reports of late deficiencies of vitamin D after major burns. The
deficiency is probably multifactorial: loss of the skin’s capacity to synthesize
Vitamin D in burned areas, and limited exposure to sun.
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Route of Feeding
The benefits of enteral nutrition are high in burned patients. Oral feeding is only
used in minor burns or in the recovery period: early on, it exposes the patient to
the risk of underfeeding.
Although the fluid shifts that occur in the shock-phase following severe burn
cause significant edema in the gut wall and favor gastrointestinal paresis; using
the gastric route during the first 24 hours after injury, even in patients with
major burns, is associated with a high success rate.
It is contraindicated by abdominal problems (abdominal trauma, electrical injury
or bowel ischemia).

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Enteral Nutrition
Early enteral administration of polymeric, and fiber containing can improve
splanchnic perfusion (animal trials), blunt the hypermetabolic response,
stimulate intestinal IgA production, and maintain intestinal mucosal integrity as
well as gut motility.
Post-pyloric feeding solves the problem of delayed gastric emptying rate caused
by heavy sedation and analgesia and has the benefit of being continued during
long surgical procedures.
Diarrhea is a frequent complication. The causes of this complication are several,
but antibiotic therapy is the most frequent, followed by excessive rate of
administration (>200 ml/hour), or hyperosmolar feeds.
Continuous intake is preferred over bolus and supplementary parenteral feeding
may be required in some conditions.
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Enteral Access
A study, performed in 106 burned patients, showed that gastric feeding initiated
within 6 hours of injury was adequate in a large proportion of patients.
Nasogastric feeding tubes are the simplest to place, but also the easiest to pull
out.
Nasoduodenal tubes are generally well tolerated, and enable feeding round the
clock, reducing the durations of fasting required by the frequent interventions.
With severe burns to the face, it may be very difficult for surgical reasons to
leave a tube through the nostrils, and percutaneous endoscopic gastro- or
jejunal feeding tubes (PEG or PEJ) may be an appropriate alternative.

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Immunomodulating Diets (IMD)
Their use is controversial in critically ill patients. There may be a role for these
diets which combine glutamine, arginine with other micronutrients, but
conclusive trials are lacking.
IMD may be used as starting diet for a maximum of 7-10 days, and at a maximal
volume of 1000 ml/day, in combination with other fiber containing and high
nitrogen polymeric diets .

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Parenteral Route
Parenteral nutrition (PN) is a second choice for nutritional support in burns but
may prove life saving to prevent or correct malnutrition in cases of insufficient
energy delivery by the enteral route or of gastrointestinal complications.
There is no place for peripheral nutrition in the burned patient and central
venous access is used though it carries risk of infection, thrombosis and sepsis.
The intravenous route is the only way to deliver excessive caloric, carbohydrate
intake and the large amounts of micronutrients that are required during the first
2 weeks after injury.
Nevertheless, this supplementation is only considered in burns > 20% BSA
requiring central venous lines for other purpose.

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