Anemia sem / dental implant courses by Indian dental academy

INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
Leader in continuing Dental EducationLeader in continuing Dental Education
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ContentsContents
• Introduction
• Common hematological terminologies
• Red blood cell indices
• Normal values of hematological measurements
• Causes of anemia
• Classification of anemia
• Iron deficiency anemia
• Megaloblastic anemia
• Hemolytic anemias
• Hereditary spherocytosis
• Glucose 6 phosphate dehydroginase deficiency

• Sickle cell anemia
• Thalassemia syndromes
• Auto immune hemolytic anemia
• Anemia of chronic disease
• Anemia due to bone marrow failure
• Aplastic anemia
• Sideroblastic anemia
• Anemic issues in older people
• Dental considerations for anemic patients
• Polycythemia
• conclusion

INTRODUCTIONINTRODUCTION
• Blood is described as a
specialized connective tissue
accounts for 5-7% of the total
body weight and is composed
of two major elements
Cellular elements (RBCs,
WBCs, Platelets)
Fluid elements (plasma –
water, electrolytes,
proteins

• Red blood cell are the cells responsible for
carrying oxygen and carbondioxide between the
lungs and the tissues via the hemoglobin
content in cytoplasm
• It has no nucleus and no mitochondria.The
normal red cell life span is about 120 days and
in this time it will travel approximately 300 miles
around the circulation.
• Red cell has to pass through the smallest
capillaries in the circulation and their membrane
structure is adapted to be a deformable

• HEMOGLOBIN:
• A hemoglobin molecule contains two
ingredients, haem and globin
• The haem is the iron containing
compound belonging to the class of
compounds called protoporphyrins. Globin
belongs to the class of protein called
globulins hemoglobin thus is a conjugated
protein

HEMATOLOGICAL TERMINOLOGIESHEMATOLOGICAL TERMINOLOGIES
• Hematology : is the study of the blood forming
and circulating blood components
• Red cell count or RBC count : number of RBCs
present in one cubic millimeter of blood
• Hemoglobin concentration : the amount of Hb in
gms in 100 ml of whole blood.
• Packed cell volume or Hematocrit: refers to the
proportion of the volume of red cells relative to
the total volume of the blood

• Red cell indices : are measurements that
indicate size and hemoglobin content of red
cells. These values can be calculated
quantitatively from the hemoglobin
concentration,red cell counts and PCV
• Mean corpuscular volume: refers to the average
volume of the individual red cells.
MCV = PCV / 1000ml blood
red cell count (millions/mm3
)

• Mean corpuscular hemoglobin (MCH): refers to
the hemoglobin content per red cell.
MCH = Hemoglobin (g/ 1000ml blood)
red cell count (millions /mm3
)
 Mean corpuscular hemoglobin concentration
(MCHC):refers to the hemoglobin concentration
of the red cells
MCHC = Hemoglobin (g/ 1000ml blood) 100
pcv (%)

• Normocyte: RBCs are of normal size
• Macrocyte : RBCs are bigger than normal
• Microcyte : RBCs are size less than normal
• Normochromic: the brightness of the RBCs are
normal intensity indicating normal Hb
concentration
• Hypochromic: pale RBCs
• Anisocystosis: size of RBCs variation is too
much
• Spherocyte:round RBCs
• Burr cells: containing spiky projections in the
RBC

WHAT IS ANEMIA?WHAT IS ANEMIA?
 Anemia is defined as a reduction in the oxygen
carrying capacity of the blood and usually is
related to a decrease in the number of
circulating RBCs or to an abnormality in the HB
contained with in RBCs.
 Globally 30% of the total world population are
anemic and half of these, some 600 million
people have iron deficiency.

CAUSES OF ANEMIACAUSES OF ANEMIA
 Poor intake of haematinics (uncommon)
Socioeconomic reasons
Dietary fads
Dysphagia
 Impaired absorption of haematinics
Disease of small intestine
 Increased demands of haematinics
Pregnancy and haemolysis

 Haemolytic anemias
sickle cell and thalassaemia
 Blood loss (most common cause)
Menorrhagia
Any gastro intestinal lesions
Lesions of urinary tract
Trauma
 Impaired erythropoiesis
Aplastic anemia
Drugs
Chronic disease
Viral infections

CLINICAL FEATURES OF ANEMIACLINICAL FEATURES OF ANEMIA
• Some times none
• General lassitude
• Cutaneous
Pallor of oral mucosa, conjunctiva or
palmar creases
Brittle nails
Koilonychia (iron deficiency)
 cardiorespiratory

 Cardiorespiratory
Dyspnoea
Cardiac failure
Murmurs
Angina pectoris
 Oral
Sore mouth
Oral ulceration
Angular stomatitis
Glossitis

NORMAL VALUES OFNORMAL VALUES OF
HEMATOLOGICAL MEASUREMENTSHEMATOLOGICAL MEASUREMENTS

CLASSIFICATION OF ANEMIACLASSIFICATION OF ANEMIA

DIAGNOSISDIAGNOSIS
• The diagnosis of anemia must not only
include the assessment of its clinical
severity. But also define the underlying
cause. This results on the clinical history
and examination assessment of the full
blood count and blood film and further
appropriate investigation

IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
• Most common of all anemia's
• Increased prevalence is seen individuals of
south east asian background
• Importance of iron:
• Normally the total body iron content is in range
of 2gm in women and up to 6gm in men
• Iron required for hemoglobin synthesis is
derived from two sources
 From ingestion of foods containing iron such
as leafy vegetables, beans, meat, liver
 By recycling of iron from senescent red cells

• Iron is distributed in the body as
 Functional form
 Nonfunctional form
Functional form of iron:
Hemoglobim – most of the body iron (65%)
Myoglobin – present in muscles (35%)
Enzymes such as cytochrome, catalase,
peroxidase (0.5%)
Transferrin bound iron – circulates in plasma (0.5%)

Non functional form of iron/ storage form of iron:
Ferritin and hemosiderin are storage forms of
excess of iron comprise up to 35% are stored in
mononuclear phagocytic cells of spleen, liver,
bone marrow and in the parenchymal cells of liver
• Absorption: the most active site of iron absorption
is the duodenum, but the stomach, ileum and
colon may also participate to some degree

• The amount of iron lost per day is 0.5 – 1mg
independent of iron intake while in menstruating
women this is nearly thrice
• Iron is lost from the body as a result of
desquamation of epithelial cells from the
gastrointestinal tract
• Excretion in urine and sweat via hair and nails.
All of this makes a daily requirement of 1mg/day
for males and 1.5 mg/day for females.

Causes of iron deficiency of anemiaCauses of iron deficiency of anemia
• Low dietary intake
• Poor absorption
• Chronic blood loss
• Excessive demand

• During pregnancy the mother requires additional
iron for the fetus, placenta and her own red cell
mass and blood loss at parturition. This results
in an additional requirement of 2.5 mg totalling
to 3.5 mg per day thus iron deficiency is more in
females than in males during the reproductive
years.

Clinical features:
• Symptoms such as weakness fatigue, dyspnoea
on exertion, palpitations, pallor of skin and
mucosa membrane
• Loss of papillae on the lateral aspect of the
tongue
• Cracking at the corners of the mouth
• Older patients may develop angina and
congestive cardiac failure
• Menorrhagia is a common symptom in iron
deficient women.

Long standing iron
deficiency causes:
• Koilonychia
• Atrophic glossitis
• glossodynia

Plummer vinson syndrome:Plummer vinson syndrome:
Oral manifestation of iron deficiency anemia first described
by plummer in 1914 and by vinson in 1922 under the
term “hysterical dysphagia”
• Characterized by
• Dysphagia
• Microcytic hypochromic anemia
• Atrophic tongue
• Xerostomia
• Koilonychia and angular stomatitis
• Atrophy of pharynx, oesophagus and vulua due to which
tissues are inelastic and dry.
• Occurrence of oral and pharyngeal carcinoma.

• Investigations:
• Hemoglobin – reduced
• Mean cell volume – reduced
• Erythrocyte count –normal/ reduced
• Blood film shows microcytic hypochromic
cells with anisocytosis and poikilocytosis
• Leucocyte count – usually normal
• Platelet count – usually normal

• Bone marrow finding shows increased
cellularity due to erythroid hyperplasia and
deficient iron stores.
• Plasma transferrin – raised
• Plasma iron – raised
• Serum ferritin - reduced

Management:
 Correction of disorder
 Correction of deficiency
Oral therapy:
 Ferrous sulphate 200mg thrice daily to be given
for 3 months
 Ferrous gluconate can be given 250 mg/ day if
ferrous sulphate is not tolerated
 Parentral therapy involves intramuscular
injections of iron dextran (imferon) single Inj/day
or iron sorbitol citrate (jectofer) multiple Inj/ day.

MEGALOBLASTIC ANEMIAMEGALOBLASTIC ANEMIA
• Caused by impaired DNA synthesis due to
which the maturation of nucleus is delayed
relative to that of cytoplasm.
• The defective DNA synthesis is due to
Deficiency of vitamin B12
Deficiency of folic acid

VITAMIN BVITAMIN B1212 DEFICIENCY ANEMIADEFICIENCY ANEMIA
(PERNICIOUS ANEMIA)(PERNICIOUS ANEMIA)
• The therapeutic vitamin B12 preparation is
called cynocobalamin
• Dietary source of vitamin B12 include
kidney, liver, heart, meat, fish, eggs,
cheese and milk.
• Vegetables contain no vitamin B12
• Average daily requirement of vitamin B12 is
2-4 micrograms

Absorption utilization and storage:
 After ingestion vitamin B12 released from the
food binds to a glycoprotein called R-binder
which is found in various secretions such as
saliva, milk, gastric juice, bile.
 In duodenum, the vitamin B12 – R binder complex
splits and then the vitamin B12 binds to the
intrinsic factor (IF). The intrinsic factor is a
glycoprotein produced by parietal cells of
stomach.

• The vitamin B12- IF complex on reaching
the distal ileum binds to the specific
receptor on the mucosal border, there by
enabling the vitamin to be absorbed. The
intrinsic factor therefore acts as a carrier
protein within the mucosal cells. The
vitamin binds to transcobalamin to form vit
B12 – TC complex to be secreted into the
portal circulation from where it is taken to
liver.

• Principle storage of vitamin B12 is liver .
Other tissues that store vitamin B12 include
kidney, heart and brain
• The vitamin B12 is mainly essential for
general cell metabolism, hematopoiesis
and for maintenance of the integrity of the
nervous system

• Cause of vitamin B12 deficiency:
 Lack of intrinsic factor
Pernicious anemia
Gastrectomy
 Dietary deficiency
Strict vegetarian diet
 Impaired absorption
Regional ileitis, ileal resection
sprue (tropical)
 Drugs
Alcohol, neomycin and paraaminosalicylic
acid

Biologic competition
Small bowel bacterial overgrowth
Diverticulosis
Anastomosis and fistulas
Blind loop strictures
Scleroderma

• Clinical features of vitamin B12 deficiency:
 Developmental delay
 Weakness
 Irritability and failure to thrive
 neurological manifestations
 Glossodynia
 Glossitis
 Atrophic tongue due to loss of filiform papillae
 Tongue appears to be ‘beefy red’

Dysphagia and taste abnormalities
Oral mucosa becomes thin and may
cause discomfort to denture wearers
Abnormal skin pigmentation, anorexia,
vomiting and diarrhoea

FOLIC ACID DEFICIENCY ANEMIAFOLIC ACID DEFICIENCY ANEMIA
• Dietary sources of folic acid include fresh
green leafy vegetables, fruits, liver ,kidney,
muscle meat, cereals, and milk
• Average daily requirement – 100 –200micro
grams
• Folates exist in polyglutamate form.
Metabolic actions occurs only after reduction
to dihydro and tetra hydro forms

• Importance of folic acid:
• The folic acid accepts and transfers one
carbon fragment.
• It causes conversion of formimino
glutamic acid (FIGlu) to glutamic acid by
accepting one carbon fragment (FIGlu is
formed due to metabolism of histidine).
Tetrahydro folate so formed donates one
carbon fragment for synthesis of
biologically active molecules

Causes of folate deficiency:
 Dietary deficiency
Water and toast diet
 Malabsoption
Sprue
Jejunal resection
 Drugs
Alcohol
Methotrexate
Trimethoprim
Triamterene

Increased requirement
Pregnancy
Chronic hemolytic anemia
Hyperthyroidism
Neoplasms
Exfoliative dermatitis
Long- term hemodialysis

Clinical features of folic acid deficiency
anemia:
• Neural tube defects including spina bifida,
anencephaly and Downs syndrome
• Pharyngitis
• Ulcerative stomatitis and angular cheilitis
The history and physical examination often
provides important clues for differentiating
folate deficiency and vitamin B12

INVESTIGATIONSINVESTIGATIONS
General laboratory findings:
• Hemoglobin –often reduced
• Mean cell volume – usually raised
• Erythrocyte count – low to normal
• Blood film – macrocytosis, anisocytosis, poikilocytosis,
red cell fragmentation and neutrophil hyper
segmentation
• Reticulocyte count – low to normal
• Leucocyte count –normal or reduced
• Serum iron – normal / elevated
• Serum ferritin - elevated

• Bone marrow finding shows –
• Hypercellular marrow
• Megaloblastic changes in erythroid series,
dysplastic megakaryocytes and increased
iron stores

• TESTS FOR VITAMIN B12 :
 Schillings test
 Serum vitamin B12 assay
Normal serum vitamin B12 - 200 – 900 picogm/ml
Less than 100 pg/ml indicates deficiency
Schillings test:
In this test the patient is given a small amount of
radioactive vitamin B12 orally followed by a large
dose of parentral non radioactive vit B12. The
excess of vitamin B12 causes an over load of
kidneys and the excess will appear in urine with
in 24 hours. The amount of radioactive vitamin
B12 in the urine will be proportional to the amount
administered orallywww.indiandentalacademy.comwww.indiandentalacademy.com

• In a normal patient 7% to 30% of
radioactive vitamin B12 will be seen in
urine, whereas in patients with pernicious
anemia only 3% is excreted ( indicating
defective absorption of vitamin B12)

Tests for folate deficiency:
• FIGlu (formamino glutamic acid)
excretion test: Urinary excretion of
FIGlu is increased if folate deficiency is
present.
• Serum folate assay:
normal range is 6 –12mg/ml
Less than 4mg/ml indicates folate
deficiency

TREATMENTTREATMENT
• It is with replacement therapy
For vitamin B12 deficiency:
 Parentral administration of hydroxycobalamin
1000 micro grams every 2-3 days for 5 doses
followed with maintenance therapy 1000
micrograms every 3 months
 Nitrous oxide sedation should be avoided in
patients with vitamin B12 deficiency anemia as
nitrous oxide depletes the bioavailable
cobalamin and may precipitate acute
neurologic decompensation and
pancytopenia.

Treatment for folic acid deficiency:
 Oral folic acid 5mg tablets daily for 4 months
followed by maintenance therapy with once
weekly
 Prophylactic folic acid in pregnancy will
prevent megaloblastosis in women at risk
 Folate supplements of 350 micro gram daily
should be given to all pregnant woman. This
reduces the occurrence of neural defects

HEMOLYTIC ANEMIASHEMOLYTIC ANEMIAS
• The cause of excessive hemolysis may lie
Outside the erythrocyte
With in the erythrocyte
In hemolytic anemia RBC count is low, PCV
is low MCV is usually low. But may be
normal and reticulocyte count is high.

Hereditary spherocytosisHereditary spherocytosis
Is an autosomal dominant disorder characterized by an
intrinsic defect in the red cell membrane that renders
erythrocytes spheroidal, less deformable and vulnerable
to splenic sequestration and destruction
• It appears that fundamental defect is in the skeleton of
the red cell membrane
• The characteristic clinical features are anemia,
splenomegaly, jaundice and presence of gallstones
• Blood film will show spherocytes
• Management: Folic acid prophylaxis 5mg once daily
should be given life long

Glucose -6 phosphate dehydroginaseGlucose -6 phosphate dehydroginase
deficiencydeficiency
• Glucose 6 phosphate dehydroginase is a crucial enzyme
because it initiates the first reaction in the shunt pathway
and generates nicotinamide- adenine dinucleotide
phosphate. (NADPH) required as a cofactor in the
maintenance of glutathione.
• G6PD deficiency causes hereditary, sex linked hemolytic
anemia apparent mainly during stressful conditions.
• The compounds induce hemolysis in persons with G6PD
deficiency
 Antibacterial - chlormphenical, isoniazid
 Antimalarials - chloroquine, quanine
 aspirin, dapsone
Management : stop any precipitant drugs or deal with
underlying infection
Auto transfusion may be life saving

Sickle cell anemiaSickle cell anemia
• Occurs almost exclusively in blacks and in
whites of Mediterranean.
• Normal adult hemoglobin (HbA) is genetically
altered to Produce sickle hemoglobin (HbS) by
substitution of valine for glutamine at the sixth
position of the beta globin chain
• In heterozygotes, only about 40% of hemoglobin
is HbS, so the individual has only sickle cell trait
and manifests clinical evidence of sickling only
under conditions of severe hypoxia
• In homozygotes, nearly all hemoglobin is HbS
and the individual suffers from sickel cell anemia

• Features of sickle cell anemia:
• Anemia
• Hemolysis
jaundice
gallstones
reticulocytosis
• Crises
painful crises
Aplasitic crisis
Dactylitis
Infracts of lungs, kidney, spleen, bone, skin.
• Impaired growth
• Skeletal deformities
• Susceptibility to infections

• Oral manifestations:
• Exhibit significant bone changes in dental
radiographs
• Mild to severe generalized osteoporosis
• Loss of trabeculations of the jaw bones
• Irregular marrow spaces
• Investigations:
• Anemia with a hemoglobin level often as low as
5.9gm/dl is the main cause of death in sickle cell
anemia
• Target cells and reticulocytosis is seen
• Sickled erythrocytes are seen in stained blood film

• Management:
• All patients with sickle disease should
receive prophylaxis with daily folic acid
and penicillin v to protect against
pneumococcal infections
• Blood transfusions

Dental management of patients withDental management of patients with
sickle cell anemiasickle cell anemia
• Confirm the patients physician the condition is
stable
• Arrange short appointments
• Avoid long and complicated procedures
• Institute aggressive preventive dental care
• Avoid oral infections; treat aggressively
• Use local anesthesia without epinephrine for
routine dental care; for surgical procedures use
1: 100, 000 epinephrine in local anesthesia
• Use prophylactic antibodies for major surgical
procedures
• Avoid liberal use of salicylates; pain control with
acetaminophen

Autoimmune haemolytic anemiaAutoimmune haemolytic anemia
• Increased red cell destruction due to red cell auto
antibodies i.e IgG or IgM or more rarely IgE.
• The optimum temperature at which the antibody is
active is used to classify immune haemolysis
 Warm antibodies bind best at 370
c and account for 80%
of cases
 Cold antibodies bind best at 40
c but can bind up to 370
c
in some cases
Investigations : spherocytes on the blood film
Diagnosis is confirmed by the direct coombs or
antiglobulin test
Management : transfusion support can be given for life
threatening problems

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ThalassaemiasThalassaemias
• Group of anemias characterized by a lack of
or decreased synthesis of either alpha or
beta globin chain of hemoglobin A
 Alpha thalassaemia
 Beta thalassaemia
In heterozygotes, the disease is mild and is
called thalassaemia minor or trait
Homozygotes may exhibit a severe form of the
disease that is called thalassaemias major

Clinical features:
 Yellowish pallor of the skin and exhibits fever,
chills, malaise and generalized weakness
 Splenomegaly, hepatomegaly
 The face often develops mongoloid features due
to the prominence of the cheek bones,
protrusion or flaring of maxillary anterior teeth
 Prominence of premaxilla

• Laboratory findings :
• Hypochromic and microcytic anemia
• Red cells exhibt poikilocytosis and anisocytosis
• The presence of typical ‘ saftey-pin’ cells and
of normoblasts or nucleated red blood cells in
circulating blood.
• WBC count frequently elevated
• Bone marrow smear shows cellular hyperplasia
with large number of immature, primitive and
stem forms of red blood cells all indicating
maturation arrest.
• Serum bilurubin - elevated

• Radiographic feature:
• In skull there is extreme thickening of the
dipole the inner and the outer plates become
poorly defined and the trabeculae between the
plates become elongated, producing bristle
like ‘crew-cut’ or ‘hair on end appearance’
Management:
Blood transfusions and folic acid supplements

ANEMIA OF CHRONIC DISEASEANEMIA OF CHRONIC DISEASE
• Most commonly seen in hospitalized patients
• Systemic illness especially those characterized
by chronic inflammation. These include lung
abscess, ostemyelitis pneumonia, bacterial
endocarditis.
• The anemia of chronic disease is characterized
by a hemolytic component manifest as a slight
shortening of red blood cell survival, inadequate
marrow compensatory response to the RBC
survival and low serum iron level and decreased
total iron binding capacity

• Laboratory findings:
• Hemoglobin levels between 9 and 11g/dl is
typically normochromic and normocytic
• Reticulocyte count is low
• Low serum accompanied by a low total iron
binding capacity
• Management:
• Underlying disease should be treated

ANEMIAS DUE TO BONE
MARROW FAILURE

APALSTIC ANEMIAAPALSTIC ANEMIA
• Aplastic anemia is defined as pancytopenia i.e,
simultaneous presence of anemia, leucopenia
and thrmobocytopenia resulting from aplasia of
the bonemarrow. The defect occurs due to
reduction in the number of pleuripotent
hemopoietic stem cells.
 Primary aplastic anemia
a) congenital form called fanconi s anemia
b) immunologically mediated
 Secondary aplastic anemia:
usually caused by chemical substances like
paints, solvents, benzol, exposure to high levels of
x – ray radiation, chemotherapy

• Clinical features:
• Mild progressive weakness and fatigue
• Due to thrombocytopenia hemorrhage from
various sites such as skin, nose, gums,
vagina. Bowel, and retina
• Oral petechiae and gingival hyperplasia
• Bacterial sepsis , fungal infections and
herpetic lesions occur due to absence of
neutrophils
• Brown discoloration of skin, hyperplasia of
kidney and spleen, microcephaly, mental and
sexual retardation. This changes occur if the
person is affected during fetal development an
infancy

• Investigations:
• Hemoglobin level - moderately reduced
• Reticulocyte count – reduced
• Leucocyte count – very low less than1500/
microliter
• Platelet count – reduced
• Blood film shows –shows normocytic
normochromic anemia
• Bone marrow findings –include acellular marrow
and replacement with fat

Aplastic anemiaAplastic anemia

Treatment:
• immunosuppressive therapy
• Bone marrow transplantation
• Oral infections should be treated aggressively
• Antibiotic prophylaxis and platelet transfusions may
be needed depending on the severity of
pancytopenia
• Systemic agents such as aminocaproic acid and
tranexamic acid and local hemostatic agents may be
require to control gingival bleeding
• Intraligamentary injections are safe. IM injections
and nerve blocks should be avoided

SIDEROBLASTIC ANEMIASIDEROBLASTIC ANEMIA
• Sideroblastic anemias are a group of
disorders of varying etiology in which the
marrow spaces show marked
dyserythropoiesis and an abnormal
intramitochondrial accumulation of iron in
erythroid precursors
• Increase in RBC precursors called
sideroblasts that contain excess stainable
iron granules around the cell nucleus.

• Classification of sideroblastic anemias
• Hereditary
• Acquired
Drugs and chemicals – lead, isoniazid,
ethonal
Inflammatory disease – rheumatoid disease
hematological disorders – acute leukemia,
• polycythemia vera, hodgkins disease

• Diagnostic feature is demonstration
of ringed sideroblasts in bone
marrow
• Management: patient require
maintenance transfusions.
• The use of iron chelators may be
necessary to avoid iron over load

ISSUES IN OLDER PEOPLEISSUES IN OLDER PEOPLE
ANEMIAANEMIA
• Although the mean hemoglobin falls with
age in both sexes, it remains well with in the
normal range
• When a low hemoglobin does occur, it is
generally due to disease. Anemia can never
be considered ‘normal’ in old age
• Symptoms may be subtle and of insidious
onset, but cardiovascular features such as
dyspnoea and edema and cerebral features
tend to predominate
• Iron deficiency results almost exclusively
from gastro intestinal blood loss

• Anemia of chronic disease is frequent
in old age because older people are
prone to those diseases that reduce
erythropoiesis
• Vitamin B12 is most commonly due to
pernicious anemia as the prevalence
of chronic atrophic gastritis raises in
older people

D e n t a l c o n s i d e r a t i o n s f o r a n e m i cD e n t a l c o n s i d e r a ti o n s f o r a n e m i c
p a t i e n t sp a t i e n t s
• D e n t al p ati e n t s p r e s e n ti n g wit h s y m p t o m s o f
a n e m i a s h o u l d h a v e r o u ti n e bl o o d t e st s. If
s i g n ific a n t d e c r e a s e h e m o g l o b i n l e v e l s ar e
o b t ai n e d , r ef e r t h e p ati e n t t o hi s / h e r p h y si ci a n
f o r t h r o u g h m e d i c al c h e c k u p .
• G e n e r al a n e st h e si a s h o u l d n ot b e a d m i n i st e r e d
u n l e s s t h e H b i s at l e a st 1 0 g / dl
• N e v e r tr e at t h e p ati e n t wit h ir o n u n til t h e c a u s e
o f t hi s m i c r o c yti c h y p o c h r o m i c a n e m i a is f o u n d
a n d c o r r e ct e d o r t h r o u g h s e a r c h f o r c a u s e i s
d o n e

• I n h e m o l ytic a n e m i a s t h e s e v e rit y of a n e m i a a n d
it s c o rr e cti o n s h o u l d b e e v a l u at e d b e f o r e m a j o r
d e n t al i nt er v e n ti o n s, b e c a u s e t h e d e cli n e i n H b
c a n r e a c h u p t o 3 t o 4 m g / dl d u ri n g i n f e c ti o n s .
• B l o o d tr a n s f u si o n s m a y b e u s e d p ri o r t o d e n t al
tr e at m e n t i n s e v e r e c a s e s .
• D r u g s t h at i n d u c e h e m o l y si s s h o u l d b e a v o i d e d ,
a n a l g e s i c s a n d a n ti bi oti c s c a n b e s af el y g i v e n i n
t h e r a p e u tic d o s e s e g : a s p iri n.

polycythemiapolycythemia
• Polycythemia is defined as an abnormal
increase in the number of red blood cells
in the peripheral blood usually with an
increased hemoglobin level.
• Relative polycythemia – occurs as a
result of loss of blood fluid.
• Primary polycythemia or polycythemia
rubra vera – true idopathic increase in
RBCs.
• Secondary polycythemia – due to bone
marrow anoxia or production of
erythropoietic stimulators

• Clinical features: manifests primarily by
headache or dizziness, weakness and lassitude,
tinnitus, visual disturbances, mental confusion,
slurring of the speech and inability to
concentrate
• Splenomegaly
• Gastric complaints such as gas pains, belching
and peptic ulcers are common
• The gingivae are often engorged and swollen
and bleeding up on slight provocation
• Submucosal petechiae are common

• Laboratory findings:
• RBC count is elevated more than10 lakh cells
per cubic millimeter
• The hemoglobin content also increased often
high as 20gm/dl
• Specific gravity and viscosity are increased
• Bleeding and clotting times are normal
Treatment : No specific treatment is known
In recent years radioactive isotope of
phosphorus is used

conclusion

REFERENCES :
 Robins pathologic basis of disease – Cotran, Kumar,
Robbins – 4th
edition
 Concise medical physiology – Chaudhri -2nd
edition
 internal medicine for dentistry – Rose , kaye – 2nd
edition
 Principles and practice of medicine – Davidson's – 19th
edition
 Dental management of medically compromised patient
– James , Donald, Craig , Nelson
 Medical problems in dentistry - Scully, Cawson -4th
edition
 Text book of oral pathology – shafer - 4th
edition
 Practical hematology - Lewis

Anemia sem / dental implant courses by Indian dental academy

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