Vitamin-A-Deficiency.pptPRESENTATION OF VIT A

vitamin A

1. VitaminVitamin AA
DeficiencyDeficiency

2. Vitamin AVitamin A
Deficiency of vitamin A is the most common cause Deficiency of vitamin A is the most common cause
of non-accidental blindness, worldwideof non-accidental blindness, worldwide
PreformedPreformed
Retinoids (retinal, retinol, retinoic acid)Retinoids (retinal, retinol, retinoic acid)

Found in animal productsFound in animal products
Provitamin AProvitamin A
CarotenoidsCarotenoids
Must be converted to retinoid formMust be converted to retinoid form
Intestinal cells can split carotene in two (molecules of retinoids)Intestinal cells can split carotene in two (molecules of retinoids)
Found in plant productsFound in plant products

3. RolesRoles
Development (growth and cell differentiation) Development (growth and cell differentiation)
and maintenance of epithelial tissueand maintenance of epithelial tissue..
EnamelEnamelانيمانيم
EyesEyes
Genitourinary TractGenitourinary Tract
LungsLungs
SkinSkin
Toxic at high levelsToxic at high levels..
AcuteAcute
Chronic (stored in liver)Chronic (stored in liver)
2

4. Retinoid UptakeRetinoid Uptake
All-trans retinol is produced from carotene by All-trans retinol is produced from carotene by
oxidation in the intestinal epithelium, and from oxidation in the intestinal epithelium, and from
retinyl fatty acid ester by hydrolysisretinyl fatty acid ester by hydrolysis..
Plant Sources
(carotenes)
Animal Sources
(retinyl fatty acid esters)
all-trans
retinol
esterified and
stored all-trans
retinyl fatty acid
esters.
various
uses
bile
salts
intestinal
epithelium
liver
other
tissues
4

5. Transport and Storage of Transport and Storage of
Vitamin AVitamin A
Liver stores 90% of vitamin A in the bodyLiver stores 90% of vitamin A in the body
Reserve is adequate for several monthsReserve is adequate for several months
Transported via chylomicrons from intestinal Transported via chylomicrons from intestinal
cells to the livercells to the liver
Transported from the liver to target tissue as Transported from the liver to target tissue as
retinol via retinol-binding proteinretinol via retinol-binding protein..

6. Vitamin A in FoodsVitamin A in Foods
PreformedPreformed
Liver, fish oils, fortified milk, Liver, fish oils, fortified milk,
eggs, other fortified foodseggs, other fortified foods
Contributes ~70% of vitamin A intake for Contributes ~70% of vitamin A intake for
AmericansAmericans
Provitamin A carotenoidsProvitamin A carotenoids
Dark leafy green, yellow-orange Dark leafy green, yellow-orange
vegetables/fruitsvegetables/fruits

7. Vitamin A was the first vitamin identified Vitamin A was the first vitamin identified
(McCollum, Davis, 1915) and hence given the first (McCollum, Davis, 1915) and hence given the first
letter in the alphabet. Vitamin A (retinol) is a fat-letter in the alphabet. Vitamin A (retinol) is a fat-
soluble vitamin, present in liver, milk and eggssoluble vitamin, present in liver, milk and eggs..
Beta-carotene and other provitamin carotenoids Beta-carotene and other provitamin carotenoids
occur in green leafy and orange/yellow vegetables occur in green leafy and orange/yellow vegetables
and fruits. They are converted and fruits. They are converted to retinal to retinal by small by small
intestine mucosal cells, reduced to intestine mucosal cells, reduced to retinolretinol, then , then
esterified and stored in the liver (as esterified and stored in the liver (as retinylretinyl
palmitate). Vitamin A is transferred round the body palmitate). Vitamin A is transferred round the body
as retinol bound to retinol-binding protein and as retinol bound to retinol-binding protein and
prealbumin (transthyretin). Retinol is converted to prealbumin (transthyretin). Retinol is converted to
rhodopsin (photoreceptor pigment) in the retina, rhodopsin (photoreceptor pigment) in the retina,
and is also used to regulate gene expression and and is also used to regulate gene expression and
guide differentiation guide differentiation

8. Primary vitamin A deficiencyPrimary vitamin A deficiency
This is caused by prolonged dietary This is caused by prolonged dietary
deficiency, particularly where rice is deficiency, particularly where rice is
the staple food (doesn't contain the staple food (doesn't contain
carotenecarotene((. .
Vitamin A deficiency occurs with Vitamin A deficiency occurs with
protein-energy malnutritionprotein-energy malnutrition ))marasmus
oror kwashiorkor(( mainly because of mainly because of
dietary deficiency (but vitamin A dietary deficiency (but vitamin A
storage and transport are also storage and transport are also
impairedimpaired((..

9. Secondary vitamin A deficiencySecondary vitamin A deficiency
This occurs where there are problems This occurs where there are problems
in converting carotene to vitamin A, or in converting carotene to vitamin A, or
reduced absorption, storage, or reduced absorption, storage, or
transport of vitamin Atransport of vitamin A. .
This occurs inThis occurs in coeliac disease, ,
tropical sprue, , giardiasis, , cystic fibrosis, ,
other pancreatic diseaseother pancreatic disease, , cirrhosis, ,
duodenal bypass surgery, and bile duodenal bypass surgery, and bile
duct obstructionduct obstruction..

10. EpidemiologyEpidemiology
it is rare in the UKit is rare in the UK, , but is extremely common in developing but is extremely common in developing
countries, especially Africa, Asia and the Western Pacificcountries, especially Africa, Asia and the Western Pacific. .
Between 100 and 140 million children are vitamin A Between 100 and 140 million children are vitamin A
deficient; 250,000-500,000 of these children become blind deficient; 250,000-500,000 of these children become blind
every year and half of these die within 12 months of losing every year and half of these die within 12 months of losing
their sighttheir sight. .
In pregnant women, vitamin A deficiency occurs especially In pregnant women, vitamin A deficiency occurs especially
in the last trimester (demand by fetus and mother is in the last trimester (demand by fetus and mother is
highesthighest((. .
Other risk factors for vitamin A deficiency includeOther risk factors for vitamin A deficiency include::
FatFat malabsorption, , cholestasischolestasis, ,
inflammatory bowel disease, , cystic fibrosiscystic fibrosis, ,
pancreatic insufficiency or following small-bowel bypass or following small-bowel bypass
surgerysurgery. .
Vegan dietVegan diet. .
Alcoholism. .
Toddlers and preschool children living below the poverty Toddlers and preschool children living below the poverty
lineline. .
Recent immigrants or refugees from developing countriesRecent immigrants or refugees from developing countries..

11. PresentationPresentation
Mild forms of vitamin A deficiency may Mild forms of vitamin A deficiency may
cause no symptoms. However, there may cause no symptoms. However, there may
still be an increased risk of developing still be an increased risk of developing
respiratory infections andrespiratory infections and gastroenteritis, ,
and delayed growth and bone development. and delayed growth and bone development.
There is also a risk of infertility secondary There is also a risk of infertility secondary
to impaired spermatogenesis, and an to impaired spermatogenesis, and an
increased risk ofincreased risk of miscarriage. . Fatigue may Fatigue may
present as a consequence of vitamin A present as a consequence of vitamin A
deficiencydeficiency anaemia..

12. Eye and visionEye and vision: pathognomonic changes occur : pathognomonic changes occur
in the eye (usually bilateral, although may be of in the eye (usually bilateral, although may be of
differing degreesdiffering degrees((: :
Poor adaptation to darknessPoor adaptation to darkness - - night blindness. .
Keratomalacia ( (thinning and ultimately ulceration of thinning and ultimately ulceration of
the cornea - colliquative necrosisthe cornea - colliquative necrosis((. .
. . Conjunctiva dryness, corneal drynessConjunctiva dryness, corneal dryness, ,
xerophthalmia
Bitot's spots ( (areas of abnormal squamous cell areas of abnormal squamous cell
proliferation and keratinisation of the conjunctiva, proliferation and keratinisation of the conjunctiva,
causing oval, triangular or irregular foamy patches causing oval, triangular or irregular foamy patches
on the white of the eyeon the white of the eye((. .
Corneal perforationCorneal perforation. .
Blindness due to structural damage to the retinadue to structural damage to the retina..

15. Skin and hairSkin and hair: :
Dry skin, dry hairDry skin, dry hair, , pruritus. .
Broken fingernailsBroken fingernails. .
Follicular hyperkeratosis secondary to Follicular hyperkeratosis secondary to
blockage of hair follicles, with plugs of blockage of hair follicles, with plugs of
keratinkeratin..
Other less specific changes includeOther less specific changes include: :
Keratinisation of mucous membranesKeratinisation of mucous membranes. .
Increased susceptibility to infection (due to Increased susceptibility to infection (due to
impairment of the humoral and cell-impairment of the humoral and cell-
mediated immunitymediated immunity((. .
Skin changes (follicular hyperkeratosis) are Skin changes (follicular hyperkeratosis) are
also commonalso common..

16. Deficiency of Vitamin ADeficiency of Vitamin A
Most susceptible Most susceptible
populationspopulations::
Preschool children Preschool children
with low F&V intakewith low F&V intake
Urban poorUrban poor
Older adultsOlder adults
AlcoholismAlcoholism
Liver disease (limits Liver disease (limits
storage)storage)
Fat malabsorptionFat malabsorption
ConsequencesConsequences::
Night blindnessNight blindness
Decreased mucus Decreased mucus
productionproduction
Decreased immunityDecreased immunity
Bacterial invasion of the Bacterial invasion of the
eyeeye
Conjunctival xerosisConjunctival xerosis
Bitot’s spotsBitot’s spots
XerophthalmiaXerophthalmia
Irreversible blindnessIrreversible blindness
Follicular hyperkeratosisFollicular hyperkeratosis
Poor growthPoor growth

17. InvestigationsInvestigations
Serum retinol study is costly. Serum retinol-Serum retinol study is costly. Serum retinol-
binding protein study is easier to perform and less binding protein study is easier to perform and less
expensiveexpensive. .
Zinc levelZinc level ))zinc deficiency interferes with production interferes with production
of retinol-binding proteinof retinol-binding protein((. .
Iron studies( ( iron deficiency can affect the can affect the
metabolism of vitamin Ametabolism of vitamin A( (
FBC: : anaemia and infection may occuranaemia and infection may occur. .
Renal function tests, , electrolytes andelectrolytes and LFTs to to
evaluate for nutritional and hydration statusevaluate for nutritional and hydration status. .
In children, X-rays of the long bones may be useful In children, X-rays of the long bones may be useful
to evaluate bone growth and for excessive to evaluate bone growth and for excessive
deposition of periosteal bonedeposition of periosteal bone. .
Dark-adaptation threshold should be testedDark-adaptation threshold should be tested..

18. Differential diagnosisDifferential diagnosis
Hypothyroidism
Zinc deficiencyZinc deficiency

19. ManagementManagement
Treatment for subclinical vitamin A Treatment for subclinical vitamin A
deficiency includes the consumption of deficiency includes the consumption of
vitamin A-rich foods vitamin A-rich foods - for example, liver, - for example, liver,
beef, chicken, eggs, fortified milk, carrots, beef, chicken, eggs, fortified milk, carrots,
mangoes, sweet potatoes and leafy green mangoes, sweet potatoes and leafy green
vegetablesvegetables. .
Good animal sources of vitamin A include Good animal sources of vitamin A include
liver, egg yolks, whole milk, animal butter liver, egg yolks, whole milk, animal butter
and whole small fish (with liver intactand whole small fish (with liver intact((. .
Animal sources, including vitamin A in Animal sources, including vitamin A in
breast milk, are more bioavailable than breast milk, are more bioavailable than
vegetable sources, which include carrots vegetable sources, which include carrots
and other orange/yellow fruits and and other orange/yellow fruits and
vegetables, and dark green leafy vegetables, and dark green leafy
vegetablesvegetables. .

20. For clinically evident vitamin A deficiency, treatment For clinically evident vitamin A deficiency, treatment
includes daily oralincludes daily oral vitamin A supplementsvitamin A supplements
In childreen (2000-9400iu)In childreen (2000-9400iu)::
Children aged 3 years or younger - 600 micrograms Children aged 3 years or younger - 600 micrograms
(2,000 IU(2,000 IU((
Children aged 4-8 years - 900 micrograms (3,000 Children aged 4-8 years - 900 micrograms (3,000
IUIU((. .
Children aged 9-13 years - 1,700 micrograms (5,665 Children aged 9-13 years - 1,700 micrograms (5,665
IUIU((. .
Children aged 14-18 years - 2,800 micrograms Children aged 14-18 years - 2,800 micrograms
(9,335 IU(9,335 IU((. .
All adults All adults - 3,000 micrograms (10,000 IU- 3,000 micrograms (10,000 IU((. .
Therapeutic doses for Therapeutic doses for severe disease severe disease include include
60,000 micrograms 60,000 micrograms (200,000 IU(200,000 IU), which have been ), which have been
shown to reduce child mortality rates by 35-70%shown to reduce child mortality rates by 35-70%..

21. Massive overdose of vitamin A can cause Massive overdose of vitamin A can cause
rough skin, dry hair, anrough skin, dry hair, an enlarged liverenlarged liver, , and a and a
raisedraised erythrocyte sedimentation rateerythrocyte sedimentation rate and and
raised serum calcium and serum alkaline raised serum calcium and serum alkaline
phosphatase concentrationsphosphatase concentrations.5 .5
In view of evidence suggesting that high In view of evidence suggesting that high
levels of vitamin A may cause birth defects, levels of vitamin A may cause birth defects,
women who are (or may become) pregnant women who are (or may become) pregnant
are advised neither to take vitamin A are advised neither to take vitamin A
supplements (including tablets and fish-supplements (including tablets and fish-
liver oil drops), except on medical advice, liver oil drops), except on medical advice,
nor to eat liver or products such as liver nor to eat liver or products such as liver
paté or liver sausagepaté or liver sausage

22. PrognosisPrognosis
Prognosis is good if patients are treated when the Prognosis is good if patients are treated when the
deficiency is subclinical. Morbidity increases once deficiency is subclinical. Morbidity increases once
blindness has progressed. Irreversible conditions blindness has progressed. Irreversible conditions
include punctate keratopathy, keratomalacia, and include punctate keratopathy, keratomalacia, and
corneal perforationcorneal perforation.4.4
For patients with early mild eye problems, prompt For patients with early mild eye problems, prompt
treatment can result in full preservation of sight treatment can result in full preservation of sight
without residual impairment (heals completely without residual impairment (heals completely
within a few weekswithin a few weeks). ).
In the developing world, because a severe degree of In the developing world, because a severe degree of
vitamin A deficiency is often accompanied by vitamin A deficiency is often accompanied by
severe generalisedsevere generalised malnutritionmalnutrition, , death is the most death is the most
likely outcome. Mortality in infants with severe likely outcome. Mortality in infants with severe
vitamin A deficiency is up to 50%vitamin A deficiency is up to 50%. .
Only about 40% of patients with corneal Only about 40% of patients with corneal
xerophthalmia are alive one year later (25% are xerophthalmia are alive one year later (25% are
totally blind, and the remainder partially blindtotally blind, and the remainder partially blind((

23. PreventionPrevention
Liver, beef, chicken, eggs, whole milk, fortified Liver, beef, chicken, eggs, whole milk, fortified
milk, carrots, mangoes, orange fruits, sweet milk, carrots, mangoes, orange fruits, sweet
potatoes, spinach, kale, and other green potatoes, spinach, kale, and other green
vegetables are among foods rich in vitamin Avegetables are among foods rich in vitamin A. .
Eating at least 5 servings of fruits and Eating at least 5 servings of fruits and
vegetables per day is recommended in order to vegetables per day is recommended in order to
provide a comprehensive distribution of provide a comprehensive distribution of
carotenoidscarotenoids. .
A variety of foods, such as breakfast cereals, A variety of foods, such as breakfast cereals,
pastries, breads, crackers, and cereal grain pastries, breads, crackers, and cereal grain
bars, are often fortified with vitamin Abars, are often fortified with vitamin A. .

24. Vitamin A ToxicityVitamin A Toxicity
Vitamin A is an important fat-soluble vitamin. Its Vitamin A is an important fat-soluble vitamin. Its
basic molecule is a retinol, After absorption, retinol basic molecule is a retinol, After absorption, retinol
is transported via chylomicrons to the liver, where is transported via chylomicrons to the liver, where
it is either stored as retinol ester or re-exported it is either stored as retinol ester or re-exported
into the plasma in combination with retinol-binding into the plasma in combination with retinol-binding
protein for delivery to tissue sitesprotein for delivery to tissue sites..
Dietary vitamin A is obtained from preformed Dietary vitamin A is obtained from preformed
vitamin A (or retinyl esters), which is found in vitamin A (or retinyl esters), which is found in
animal foods (liver, milk, kidney, and fish oil), animal foods (liver, milk, kidney, and fish oil),
fortified foods, and drug supplements. Dietary fortified foods, and drug supplements. Dietary
vitamin A is also obtained from provitamin A vitamin A is also obtained from provitamin A
carotenoids from plant sources, principally carrots. carotenoids from plant sources, principally carrots.
Dietary vitamin A is available mainly as preformed Dietary vitamin A is available mainly as preformed
vitamin A in western countries and as provitamin A vitamin A in western countries and as provitamin A
carotenoids in developing countriescarotenoids in developing countries. .

25. PathophysiologyPathophysiology
The recommended daily allowance for The recommended daily allowance for
vitamin A is 5000 international units (IU) for vitamin A is 5000 international units (IU) for
adults and 8000 IU for pregnant or lactating adults and 8000 IU for pregnant or lactating
women. Being fat-soluble, vitamin A is women. Being fat-soluble, vitamin A is
stored to a variable degree in the body, stored to a variable degree in the body,
making it more likely to cause toxicity when making it more likely to cause toxicity when
taken in excess amounts In contrast, water-taken in excess amounts In contrast, water-
soluble vitamins are generally excreted in soluble vitamins are generally excreted in
the urine and stored only to a limited the urine and stored only to a limited
extent; hence, adverse effects occur only extent; hence, adverse effects occur only
when extremely large amounts are takenwhen extremely large amounts are taken..

26. EpidemiologyEpidemiology
FrequencyFrequency
United StatesUnited States
Nutritional surveys indicate that about 35-50% of adults Nutritional surveys indicate that about 35-50% of adults
regularly consume vitamin and mineral supplements. Data are regularly consume vitamin and mineral supplements. Data are
not available for consumption of vitamins in childrennot available for consumption of vitamins in children. .
Mortality/MorbidityMortality/Morbidity
Mortality is rare from vitamin A toxicityMortality is rare from vitamin A toxicity..
Morbidity is evident by the wide range of complications Morbidity is evident by the wide range of complications
observed in this conditionobserved in this condition..
RaceRace
The use of supplements is generally higher in whites, as well The use of supplements is generally higher in whites, as well
as in individuals with higher levels of education and incomeas in individuals with higher levels of education and income. .
SexSex
The use of vitamin supplements is more common among The use of vitamin supplements is more common among
femalesfemales..
AgeAge
Single vitamins are consumed more often by adults, while Single vitamins are consumed more often by adults, while
multivitamins are administered more frequently to childrenmultivitamins are administered more frequently to children

27. HistoryHistory
Carotenemia, the ingestion of Carotenemia, the ingestion of
excessive amounts of vitamin A excessive amounts of vitamin A
precursors in food, mainly carrots, is precursors in food, mainly carrots, is
manifested by a yellow-orange manifested by a yellow-orange
coloring of the skin, primarily the coloring of the skin, primarily the
palms of the hands and the soles of palms of the hands and the soles of
the feet. It differs from jaundice in that the feet. It differs from jaundice in that
the sclerae remain whitethe sclerae remain white

28. In acute vitamin A toxicity, a history of In acute vitamin A toxicity, a history of
some or all of the following may be some or all of the following may be
obtainedobtained: :
NauseaNausea
VomitingVomiting
AnorexiaAnorexia
IrritabilityIrritability
DrowsinessDrowsiness
Altered mental statusAltered mental status
Abdominal painAbdominal pain
Blurred visionBlurred vision
HeadacheHeadache
Muscle pain with weaknessMuscle pain with weakness

29. In chronic vitamin A toxicity, a history of some or all of the In chronic vitamin A toxicity, a history of some or all of the
following may be obtainedfollowing may be obtained: :
AnorexiaAnorexia
Hair lossHair loss
Dryness of mucus membranesDryness of mucus membranes
Fissures of the lipsFissures of the lips
PruritusPruritus
FeverFever
HeadacheHeadache
InsomniaInsomnia
FatigueFatigue
IrritabilityIrritability
Weight lossWeight loss
Bone fractureBone fracture
AnemiaAnemia
Bone and joint painsBone and joint pains
DiarrheaDiarrhea
Menstrual abnormalitiesMenstrual abnormalities
EpistaxisEpistaxis

30. Manifestations of acute toxicityManifestations of acute toxicity
Muscle and bone tenderness, Muscle and bone tenderness,
especially over the long bones of the especially over the long bones of the
upper and lower extremitiesupper and lower extremities
Neurologic manifestations with signs Neurologic manifestations with signs
of increased intracranial pressure (eg, of increased intracranial pressure (eg,
children may have bulging children may have bulging
fontanelles)fontanelles)

31. Manifestations of chronic toxicityManifestations of chronic toxicity
AlopeciaAlopecia
Skin erythemaSkin erythema
Skin desquamationSkin desquamation
Brittle nailsBrittle nails
ExanthemaExanthema
CheilitisCheilitis
ConjunctivitisConjunctivitis

32. PetechiaePetechiae
Liver cirrhosisLiver cirrhosis
Premature epiphysial closure in childrenPremature epiphysial closure in children
HepatosplenomegalyHepatosplenomegaly
Peripheral neuritisPeripheral neuritis
Benign intracranial hypertensionBenign intracranial hypertension
AtaxiaAtaxia
PapilledemaPapilledema
DiplopiaDiplopia
HyperostosisHyperostosis
EdemaEdema
Hepatic hydrothoraxHepatic hydrothorax

33. CausesCauses
Causes of carotenemiaCauses of carotenemia
Carotenemia is the result of excessive intake of Carotenemia is the result of excessive intake of
vitamin A precursors in foods, mainly carrotsvitamin A precursors in foods, mainly carrots. .
Other than the cosmetic effect, carotenemia has no Other than the cosmetic effect, carotenemia has no
adverse consequences because the conversion of adverse consequences because the conversion of
carotenes to retinol is not sufficient to cause carotenes to retinol is not sufficient to cause
toxicitytoxicity. .
Causes of vitamin A toxicityCauses of vitamin A toxicity are generally are generally
categorized into acute and chroniccategorized into acute and chronic. .
Acute toxicity Acute toxicity occurs within a few hours or days occurs within a few hours or days
after a very large intake as a result of accidental after a very large intake as a result of accidental
over-ingestion or inappropriate therapy. The over-ingestion or inappropriate therapy. The
estimated toxic dose is about 25,000 IU/kgestimated toxic dose is about 25,000 IU/kg. .
Chronic toxicity Chronic toxicity appears after ingestion of 25,000 appears after ingestion of 25,000
IU or more daily for prolonged periodsIU or more daily for prolonged periods

34. InvestigationInvestigation
Laboratory StudiesLaboratory Studies
Serum electrolytes, if vomiting or diarrhea is Serum electrolytes, if vomiting or diarrhea is
presentpresent
Serum calcium (hypercalcemia may be Serum calcium (hypercalcemia may be
observedobserved((
Liver function testsLiver function tests
Complete blood count (CBC) for anemia, Complete blood count (CBC) for anemia,
leukopenia, or thrombocytopenialeukopenia, or thrombocytopenia
Vitamin A assessment by serum retinol Vitamin A assessment by serum retinol
concentrations (This may be helpful if the level concentrations (This may be helpful if the level
is markedly high. However, in mild conditions, it is markedly high. However, in mild conditions, it
may not be sensitivemay not be sensitive((

35. Imaging StudiesImaging Studies
Hand radiography for periosteal Hand radiography for periosteal
calcificationscalcifications
Computed tomography (CT) scanning of the Computed tomography (CT) scanning of the
brain in the presence of neurologic brain in the presence of neurologic
abnormalitiesabnormalities
Bone mineral density testing to evaluate the Bone mineral density testing to evaluate the
effect of long-term vitamin A intoxication on effect of long-term vitamin A intoxication on
reducing bone density and causing reducing bone density and causing
osteoporosisosteoporosis
Lumbar puncture may be needed in patients Lumbar puncture may be needed in patients
with increased intracranial pressure to with increased intracranial pressure to
prevent its complications.prevent its complications.

36. TreatmentTreatment
Medical CareMedical Care
Emergency department care includes Emergency department care includes
the followingthe following: :
Supportive careSupportive care
Hydration if vomiting, diarrhea, or Hydration if vomiting, diarrhea, or
hypercalcemia is presenthypercalcemia is present
OxygenOxygen
MonitoringMonitoring
Stopping vitamin A supplementsStopping vitamin A supplements

37. Further Inpatient CareFurther Inpatient Care
Admit patients with the following symptoms to the hospitalAdmit patients with the following symptoms to the hospital: :
Altered mental statusAltered mental status
Severe dehydrationSevere dehydration
Neurologic deficitsNeurologic deficits
Metabolic derangementsMetabolic derangements
Liver toxicityLiver toxicity
Significant hypercalcemia Significant hypercalcemia
Patients with increased intracranial pressure may need therapeutic Patients with increased intracranial pressure may need therapeutic
lumbar punctures or further treatment with medications such as lumbar punctures or further treatment with medications such as
diuretics and mannitoldiuretics and mannitol. .
Patients with symptomatic hypercalcemia require the followingPatients with symptomatic hypercalcemia require the following: :
Close monitoringClose monitoring
Treatment with intravenous fluids and diureticsTreatment with intravenous fluids and diuretics
Additional therapy, including pamidronate, calcitonin, Additional therapy, including pamidronate, calcitonin,
corticosteroids, or mithramycincorticosteroids, or mithramycin
Discontinuation of vitamin ADiscontinuation of vitamin A

38. Further Outpatient CareFurther Outpatient Care
Follow-up is recommended with a Follow-up is recommended with a
primary care physicianprimary care physician..
The pigmentation of carotenemia The pigmentation of carotenemia
usually disappears with the omission usually disappears with the omission
of carrots from the dietof carrots from the diet..
Patients on isotretinoin should be Patients on isotretinoin should be
evaluated by their dermatologist for evaluated by their dermatologist for
consideration of stopping the drugconsideration of stopping the drug

39. PreventionPrevention
Education on the proper required daily Education on the proper required daily
allowance dose of vitamin A should be allowance dose of vitamin A should be
provided to modify the individual's provided to modify the individual's
current use of vitamin supplementscurrent use of vitamin supplements

40. Toxicity of Vitamin AToxicity of Vitamin A
Chronic – long-term megadose; possible Chronic – long-term megadose; possible
permanent damagepermanent damage
Bone and muscle painBone and muscle pain
Loss of appetiteLoss of appetite
Skin disordersSkin disorders
HeadacheHeadache
Dry skinDry skin
Hair lossHair loss
Increased liver sizeIncreased liver size
VomitingVomiting

41. Toxicity of Vitamin AToxicity of Vitamin A
Teratogenic (may occur with as little as 3 x Teratogenic (may occur with as little as 3 x
RDA of preformed vitamin A)RDA of preformed vitamin A)
Tends to produce physical defect on Tends to produce physical defect on
developing fetus as a result of excess vitamin developing fetus as a result of excess vitamin
A intakeA intake
Spontaneous abortionSpontaneous abortion
Birth defectsBirth defects