malnutrition Flashcards
define malnutrition
malnutrition is the cellular inbalance between the supply of nutrients and energy and the body’s demand for them to ensure growth, maintenance and specific functions.
The greatest risk of under-nutrition occurs in the first ……. days of life
why?
1000
because brain development hapens in this time
CAUSES OF UNDER-NUTRITION
Nutritional status is determined by three factors:
o Immediate cause: act on the individual, these are inadequate food intake and infection with their vicious cycle.
o Underlying cause: influence the households and the community; these
are drought, flooding, household food insecurity…
o Basic cause: influence communities and society these include the
country’s economy and political status.
ASSESSMENT OF NUTRITION by what
We can use the ABCDs to assess nutritional status of an individual;
Anthropometry, Biochemistry, Clinical, Dietary.
- There are two ways of classifying malnutrition; these are
community survey
and clinical.
COMMUNITY SURVEY CLASSIFICATION OF MALNUTRITION
Gomez underweight weight for age
mild moderate sever
waterlow wasting weight for height
mild severe
waterlow stunting height for age
mild moderate severe
who wasting weight for height
-2 -3 moderate
< -3 severe
who stunting height for age
-2 -3 moderate
<-3 sd severe
clinical classification
-Marasmus: severe wasting; severe weight loss and muscle mass leaving ‘skin
and bones.
* Kwashiorkor: characterized by edema (nutritional edema) that is a clinical
indicator for SAM.
* Marasmic-kwash: severe wasting + edema; combination of kwashiorkor and
marasmus.
- Severe Acute Malnutrition (SAM)
is severe wasting (MUAC<11.5cm for children aged 6-59monthes, weight for height<-3SD) and/or bilateral edema.
CLINICAL PRESENTATION
kwashiorkor and marasmic- kwashiorkor (edematous SAM) and
marasmus (non-edematous SAM)
reductive adaptation
The functions of different organs are preserved more in
non-edematous
SAM than edematous.
Age at presentations is 12-36 months for kwashiorkor. It usually occurs at the time of …………… because …………….
weaning, when the diet is suddenly changed to that of the adult diet, which is high in CHO but low in protein.
SYMPTOMS DIRECTLY RESULTING FROM UNDER-NUTRITION:
* KWASHAKOR
O Generalized body swelling staring from the legs.
O Loss of appetite, vomiting, diarrhea(mal-absorption), abdominal
distention
O Growth retardation and mental changes together with GBS are the three
essential features of kwashiorkor.
O Symptoms of anemia; vertigo, easy fatigability, light headiness, tinnitus,
pica (craving for non-edible matters; feature of iron deficiency)
For marasmus, age at presentation is usually…………………….and…………………….. and why
6-12 mo (“infantile marasmus”)
when the amount of breast milk is markedly reduced, or more frequently in those who are artificially fed.
* Marasmus is also seen in older children living on inadequate diets for prolonged periods. This is described as “late marasmus” and is similar to chronic
starvation in adults
MARASMUS
O Growth retardation; failure to gain weight is the earliest manifestation.
O Irritability, continuously crying b/c of hunger
O Good appetite, unlike kwashiorkor.
O Diarrhea and symptoms of micronutrient deficiencies are also present.
SYMPTOMS RESULTING FROM THE COMPLICATIONS OF UNDER-NUTRITION
infection
hypoglycemia
hypothermia
shock
dehydration
severe anemia
skin lesions
CHF
Corneal ulceration
Electrolyte imbalance
4 factors that contribute
malabsorbtion
icreased demand
reduced intake
physical findings * G/A
moon face and apathy (kwashiorkor), simian face (marasmus, visible
wasting
phsyical findings VS
o BP; hypotension b/c shock is one complication,
o PR; bradycardia or tachycardia,
o RR; tachypnea b/c of pneumonia,
o T◦; fever T◦≥37.5◦c (for axillary) due to infection or hypothermia T◦<35◦c
(for axillary) b/c low energy for heat production.
Anthropometry: wt, ht/length for <2yrs
o BMI: < -2SD (thinness), b/n +1SD and +2SD (overweight) and >+2SD
(obesity).
o WFH/WFL: is an indicator of acute malnutrition ;( see WHO
classification)
o WFA: easy to measure but doesn’t differentiate b/n stunting and
wasting. (See Gomez classification)
o HFA/LFA: is a measure of linear growth, deficit represents the
cumulative impact of adverse events, usually in the first 1,000 days from
conception (critical period for child growth) which shows stunting. (See
WHO classification)
o MUAC: for community level screening
physical findings in heent
Head: craniotabes, frontal bossing, delayed fontanel closure (vit D)
Eyes: dry eyes, pale conjunctiva, icteric sclera, periorbital edema
(kwashiorkor), broom stick eyelashes
▪ Sunken eye balls (marasmus)
Bitot spot, xeropthalmia or keratomalacia
o Ear: signs of otitis media, tragus and ante-tragus tenderness.
o Nose: bleeding nasal mucosa,
o Mouth and throat: dry oral mucosa and oral trash, angular cheilosis,glotitis (Vit B2), spongy bleeding gums (vitamin C), parotid enlargement, enamel mottling, delayed eruption (Vit D)
▪ Sunken eye balls (marasmus) because of what
due to atrophy of retro-orbital
tissue also seen in dehydration b/c vasoconstrictions of orbital
Veinous plexus.
bitots spot , xeropthalmia , keratomalacia because of
vit a
LGS
There may be a Significant LAP: may be present b/c infection.
▪ NB: lymphatic organs; thymus, spleen, LN, atrophy in SAM
patients
respiratory system
o visible wasting, costo-chondral bead (Vit C; sharp and vit D dull),
Harrison’s groove and signs of pneumonia.
CVS
o Bradycardia, hypotension, reduced cardiac output, small vessel vasculopathy, slow capillary refill>3sec, shock
Abdomen
Distended (port belly), gaseous because of bacteria overgrowth hepatomegaly with fatty liver is only seen in kwashiorkor. fluid thrill and shifting dullness
Musculoskeletal
Edema characterizes as pitting or non-pitting, and grade 1-3.
o Muscle wasting (Buttocks giving baggy pant appearance) and thighs
o Sign of hypocalcemia Chvostek sign (twitching of the face while striking
on jaw angle) and trousseau sign (flexion of metacarpophalangeal joint
and extension of inter phalangeal joints.
o Skeletal deformities (Vit D, Vit C and calcium deficiencies).
Integumentary skin hair nail
o Skin: cold and clammy skin; shock, loose and wrinkled (marasmus),
shiny and edematous (kwashiorkor), dry follicular hyperkeratosis, patchy
hypo-and hyper-pigmentation (crazy paving/flaky paint dermatosis),
erosion and poor wound healing, Pallor, petechiae.
o Hair: brownish discoloration (flag sign), easily pluck-able, dull, sparse,
broom stick eyelashes, alopecia.
o Nails: koilonychia, thin and soft nail plates, fissure and ridges.
Neurologic
lethargic, apathy, irritable, weak reflexes, impaired memory.
INVESTIGATIONS
o CBC, RBS, Stool Examination, PICT, Organ Function Tests (OFT) , Serum
Electrolyte, Chest X-ray
MANAGEMENT PRINCIPLES 2
stabilization and rehabilitation.
what do we do in stabilization phase
repair cellular function, correct fluid and electrolyte
imbalance, restore homeostasis, and prevent death from the interlinked triad
of hypoglycemia, hypothermia, and infection.
what do we do in rehabilitation stage
restores wasted tissues (i.e., catch-up growth).
ADMISSION CRITERIA
grade 3 edema
severe wasting
complications
appetitie loss
if they are < 6 months
MANAGEMENT OF SAM IN STABILIZATION CENTRE phases
phase 1
transitional
phase 2
Phase 1
: treatment is always given in an in-patient setting. During this phase,
o Life-threatening medical complications are treated
o Routine drugs (vitamins, folic acid, antibiotics, de-worming) are given to
correct specific deficiencies
o Feeding with F-75 milk (low caloric and sodium) is begun
Transition phase:
Here the patients are going to be prepared for phase 2 and
F75 in phase 1 is changed to F100 or RUTF
Phase 2:
can be given both in inpatient and out patient
o Phase 2 inpatient: when treating the patient in outpatient is not
reasonable; no capable care giver, no enough supply of RUTF
o Phase 2 outpatient: when there is capable care giver, enough RUTF,
OTP program is near to home.
o N: B F100 is never given in outpatient care.
HYPOGLYCAEMIA
define
treatment
- Definition: RBS<54mg/dl
- Prevention: feeding appropriate amount of F 75(check reference card) Q 2hrs
especially in the first 24 hrs. - Treatment: 10% glucose
o If the child is awake: 50ml of bolus orally or by NGT if the child is unable
to drink
o If the child is lethargic, unconscious or convulsing: 5ml/kg of 10%
glucose by IV then 50ml of 10% bolus by NGT
o Continue giving F75 30min after giving glucose solution and every 30min
(1/4th of the 2 hr feed) thereafter for the first 2 hrs
HYPOTHERMIA
define
treatment
- Definition: rectal temperature<35.5°c, or axillary temperature<35°c
- Prevention: feeding, avoid heat loss, keep them dry, sleep with the
mother(skin to skin), room T° 28°c-32°c
o Monitor T° Q 30 min while rewarming
DEHYDRATION
diagnosis
treatment
prevention
Diagnosis:
o Mainly depending on history, watery diarrhea and vomiting with recent
change in appearance
o Excessive weight loss for edematous SAM; >2% of body weight per day
o Look for other sign and symptoms if dehydration
o Special rehydration solution: ReSoMal, rehydration solution for
malnutrition
o Best solution in malnutrition over ORS, with less sodium, more sugar and
potassium.
o Exception is dehydration caused by cholera; use ORS
* Modifying ORS to ReSoMal
o MIX WHO standard 1 litter packet ORS in 2 litters of water
o Add 50g of sugar
o Add 40ml of mineral mix or 1 scoop of CMV (combined mineral mix) - use
5 tablets of 600mg (8MEq) KCL for our setup.
* Prevention
o Replace loss with:
o 50-100ml/loss for non-edematous SAM below age
2yrs
o 100-200ml/loss for non-edematous SAM above age
2yrs
o 30ml/loss for edematous SAM of all ages
SHOCK (LETHARGIC OR UNCONSCIOUS)
diagnosis
treatment
- Diagnosis: cold hands, with slow capillary refill and weak fast feeble or absent
pulses - IV fluid: RL or 0.45% NS with 5% dextrose.
o NB: RL and 0.45% saline are the preferred fluids for management of
shock in malnutrition b/c of their low sodium concentration as compare
to NS. - Amount: 15ml/Kg over 1hr, reassess response
- If improving repeat 15ml/Kg over 1 hr
- If not improving consider septic shock and put on maintenance 4ml/kg/hr and
look for cross matched blood, 10 ml/kg slowly over 3 hours or packed RBC in
case of heart failure - Evaluate the patient further to identify the cause
- Follow patients with V/S, wt, input output, liver size,
ANEMIA
diagnosis 4 types based on severity
is iron given …why
- Mild: Hgb<age-appropriate value, >9g/dl
- Moderate: Hgb≤9g/dl, >7g/dl
- Severe: Hgb≤7g/dl
- Very severe anemia: Hgb<4g/dl; transfusion threshold for malnutrition
- Investigate other possible causes such as malaria and intestinal parasites (for
example, hookworm). - Do NOT give iron during stabilization phase as it can damage cell
membranes and make infections worse.
Pseudo-anemia:
dilutional anemia on 2-14 days of treatment due to movement
of fluids from to tissue to vascular space transient and normally resolves
spontaneously after 2 or 3 days when kidney function recovers, and excess
fluids can be eliminated.
* For these reasons, transfusion is not recommended between 48 hours and day
14 days unless there is heart failure and the cause is other than dilution
anemia.
BLOOD TRANSFUSION
- Give blood transfusion in the first 48 hours if:
o Hgb is < 4 g/dl, (Hct is < 12 %), or
o Hgb 4 to 6 g/dl (Hct 12 to 18%) and respiratory distress
o Stop all oral intake and IV fluids during the transfusion. - Look for signs of congestive heart failure such as fast breathing, respiratory
distress, rapid pulse, engorgement of the jugular vein, cold hands and feet,
cyanosis of the fingertips and under the tongue.
o Furosemide (1 mg/kg, given by IV) - If no signs of congestive heart failure, transfuse whole fresh blood at 10 ml/kg
slowly over 3 hours. - If signs of heart failure, give 5-7 ml/kg packed cells over 3 hours instead of
whole blood. - Diuretics should never be used to reduce edema in children with Severe
Malnutrition. The purpose of giving a diuretic before a blood transfusion is to
prevent congestive heart failure from overloading the circulation with the
transfusion.
EMERGENCY EYE CARE FOR CORNEAL CLOUDING AND ULCERATION
- Give vitamin A and atropine eye drops immediately for corneal ulceration
MANAGING HEART FAILURE
diagnosis
treatment
- Physical deterioration with weight gain,
- Sudden increase in liver size,
- Tenderness of the liver,
- Crackles in lungs,
- Prominent superficial and neck veins,
- Engorgement of the neck veins when the abdomen (right upper quadrant) is
pressed, (hepatojugular reflex) - Heart failure and pneumonia may be difficult to tell apart as they can be
clinically similar. When weight gain precedes or is associated with signs of
respiratory distress, heart failure should be the first diagnosis. If there is loss of
weight, consider pneumonia instead. - Note: Children with edema do not necessarily present with weight gain during
heart failure if the expanded circulation is due to mobilization of edema fluid
from the tissues to vascular space. - Stop all intakes of oral or IV fluids. No fluid or therapeutic feeds should be
given until heart failure has improved (even if this takes 24 to 48 hours). Small
amounts of sugar-water can be given orally to prevent hypoglycemia. - Give Furosemide (1 mg/kg) single dose, repeat if necessary.
- If it is due to severe anemia, manage the anemia as above.
Systemic change of SAM
metabolic and cellular change
BMR decrease by 30% low total body potassium
low ATP results in loss of intracellular K and increased intracellular sodium
if iron, folic acid, Vitim B12 are not in sufficient amounts, “functional anemia” tissue hypoxia will develop.
Fluid and electrolytes results
increased fatigue
decreased strength of skeletal muscle
Hematological change
reduction in Hb concentration and red cell mass
decease in dietary amino acids results in reduced hematopoietic activity these cases functional anemia with tissue hypoxia will develop
Cardiovascular changes
CO and SV are reduced in proportion to the loss of lean body mass
In severe SAM peripheral circulatory failure comparable to hypovolemic shock
Change in renal functions
RPF and GFR may be reduced
UTI are common
Water clearance and the ability to concentrate and acidify urine appear impaired
GIT changes
Thin atrophic wall with a reduction in villous height
Reduction in functional capacity of the digestive system
Endocrine change
the decreased food intake cases reduction in plasma concentration of glucose and free amino acids interns reduce insulin secretion and increase glucagon and epinephrine release which will further reduce insulin secretion
On general appearance
Diagnosis and clinical futureSevere weight loss; subcutaneous fat and muscle wasting
grade
grade I: start in axilla and groin
grade II: thigh and buttocks
grade III: chest and abdomen
grade IV: facial muscle
Refeeding Syndrome
Is defined as the potentially fatal shift in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding.
Complication of SAM
Infection
Hypoglycemia
Hypothermia
Electrolyte imbalance
Severe anemia
Dehydration
Corneal ulceration
Shock
Skin lesion
CHF(secondary to treatment)
the pathogenesis of hурοрhοѕрhatеmia
begins when stores of phosphate are depleted during episodes of аոοrехia nervosa and ѕtаrvаtioո. Subsequently, when nutritional replenishment starts and patients are fed carbohydrates, glucose causes release of insulin, which triggers cellular uptake of phosphate (and potassium and mаgneѕium) and a decrease in serum phosphorous levels. Insulin also causes cells to produce a variety of molecules that require phosphate (eg, adenosine triphosphate and 2,3-diphosphoglycerate), which further depletes the body’s stores of phosphate
The refeeding syndrome is marked by:
Ηурοрhοѕphаtеmia
●Ηурokаlemiа
●Congestive heart failure
●Peripheral еԁеma
●Rhabdomyolysis
●Seizures
●Hemolysis
●Respiratory insufficiency
pathogenesis of refeeding syndrome
The rapid increase in nutrient intake results in a switch from a catabolic state to an anabolic state. The ensuing surge in insulin secretion can result in hурοglусеmia and influx of extracellular electrolytes into the intracellular space, which can lead to dangerously low extracellular concentrations of potassium, phosphate, and magnesium.
risk factor
patients who weigh less than 70 percent of their ideal body weight, or have a BMI (calculator 2) <14 kg/m2, generally require hospitalization for the initial stage of nutritional replenishment and medical stabilization. Other risk factors for the refeeding syndrome include low baseline levels of phosphate, potassium, or magոеsiսm prior to refeeding the patient; and little or no nutritional intake for the previous 5 to 10 days.
