Heparin has an immediate effect on

blood clotting but acts for only 46 hours

and no specific treatment is therefore
needed to reverse its effect.
The effect of heparin is best assessed
by the APTT.
In an emergency, anticoagulation can be
reversed by intravenous protamine
sulfate given in a dose of 1 mg per 100 IU
heparin, but a medical opinion should be
sought first.

ANAEMIA

General aspects
Anaemia is defined as an Hb level below the
norm for the age, gender and ethnic background
of the individual and may be due to:
insufficient red blood cell (RBC) numbers or Hb
content.
Up to puberty, an Hb level below 11.0 g/dL is
the hallmark of anaemia;
the corresponding figure in :
adult females is below 11.5 g/dL, and
in adult males below 13.5 g/dL.
The effect of anaemia is to lower the oxygencarrying capacity of the blood.

 Anaemia is classified on the basis of:

red-cell size as microcytic (small),
macrocytic (large) or normocytic
(normal-size erythrocytes).

Normocytic anaemia (MCV between

79 and 98 fl) may result from
chronic diseases such as leukaemia,
chronic inflammatory disease, liver
disorders, renal failure, infection,
malignancy and sickle cell disease.

Microcytic anaemia
is the most common and is usually
due:
to iron deficiency, or
occasionally to thalassaemia or
chronic diseases.
The mean corpuscular (cell) volume
(MCV) falls below 78 fl.

Macrocytic anaemia
is caused usually by:
vitamin B12 or folate deficiency (not
infrequently in alcoholics); sometimes
by the consumption of folate and vitamin B12 in
chronic haemolysis, pregnancy or malignancy;
and sometimes by drugs
(methotrexate,prazathioprine, cytosine or
hydroxycarbamide).
Macrocytic anaemia may also be caused by liver
disease, myxoedema or, sometimes, aplastic
anaemia.
MCV more than 99 fl.

Elective operations
under GA should not usually be carried out when the Hb is less
than
10 g/dL (male).

Blood
transfusions should be used only when absolutely necessary, if the Hb
concentration has fallen below 7 g/dL, since they may carry the risk of
infection, circulatory overload and allergic reactions.

DEFICIENCY ANAEMIAS
Iron-deficiency anaemia
Vitamin B12 (cobalamin)
deficiency
Folate (folic acid)
deficiency

HAEMOLYTIC ANAEMIAS

The sickling disorders

The thalassaemias

Iron-deficiency anaemia

Dental aspects
LA is satisfactory for pain control.
Atrophic glossitis soreness of the
tongue with depapillation or colour
change.
PatersonBrown-Kelly (Plummer
Vinson) syndrome.
Angular stomatitis.
Aphthous-like ulceration.
Staining of the teeth by iron.
Some iron preparations can cause tooth
erosion, as can chewable vitamin C.

The PatersonBrown-Kelly (Plummer

Vinson) syndrome
glossitis and dysphagia with hypochromic
(iron-deficiency) anaemia is uncommon.
Women are mainly affected and the
prevalence appears to be highest in
northern Europe.
There is a substantial risk of carcinoma in
the postcricoid(a membrane on the anterior
esophageal wall) region or in the mouth.
Koilonychia.
Angular stomatitis .

Treatment
The cause of the iron deficiency
must be sought and treated.
The best treatment for iron
deficiency is an iron salt such as:
ferrous sulfate 200 mg three
times daily orally, which is better
absorbed than ferric salts.
Ferrous gluconate 250 mg/day
can be given if ferrous sulfate is
not tolerated.

 Nausea or constipation is fairly common.

The stools are black whilst on oral iron
therapy and this should not be mistaken
for melaena.
Oral iron may need to be given for 3
months or
more after the Hb has reached normal
levels stores.
Parenteral iron does not raise the Hb
level more rapidly than oral iron;
it must be given intramuscularly

Vitamin B12 (cobalamin) deficiency

General aspects:
Vitamin B12 is needed by the body to synthesize
and break down amino acids, and to synthesize
deoxyribonucleic acid/ribonucleic acid (DNA/
RNA).
This is needed to build new cells, especially
blood, skin and mucosal cells.
Vitamin B12 is found in the diet in meat,
especially liver.
It is stored in the liver and is
necessary for development and myelination of
the central nervous system as well as for the
maintenance of its normal function.

General management
The diagnosis of B12 deficiency
depends on the clinical findings
and low serum B12 levels, together
with autoantibodies against gastric
parietal cells and/or intrinsic factor.
If the patient consumes adequate
vitamin B12 but has clinically
confirmed B12 deficiency,
malabsorption must be present.

 The Schilling test for impaired vitamin B12

absorption is obsolete.
Measurement of the raised serum levels of
methylmalonic acid and homocysteine seen in B12
deficiency appears to be more sensitive and specific
for deficiency than assay of serum vitamin B12 .
Most patients with vitamin B12 deficiency have
malabsorption and
will require parenteral or high-dose oral
replacement.
Pernicious anaemia is treated for life with
intramuscular hydroxycobalamin 1 mg five times at
3-day intervals to replete liver stores, and then at
about 3-monthly intervals.

Dental aspects
LA is satisfactory.
A physically normal but sore or burning tongue can
be caused by early vitamin B12 deficiency, often
with normal Hb levels.
It is important for these patients to undergo
haematological examination.
As Deficiency of vitamin B12 develops slowly since
liver stores last up to 3 years.
In addition to the usual signs and symptoms of
anaemia, neurological symptoms particularly
paraesthesiae of the extremities develop in about
10%. Early signs include loss of toe positional sense
and diminished perception of the vibration of a
tuning fork. These early neurological changes are
reversible with treatment.

 In early B12 deficiency, the tongue, rather than being

sore, may show a pattern of red lines without
depapillation; alternatively, red sore patches may form.
These may come and go, and range from pinhead red
spots to circular areas up to a centimetre across, which
may resemble erythroplasia clinically; though they
resolve with treatment of the anaemia, they may show
dysplasia histologically.(raw, beefy tongue)
PatersonBrown-Kelly syndrome is rarely associated with
a macrocytic anaemia.
Candidosis can be aggravated or precipitated by
anaemia and may be the presenting feature. Angular
stomatitis is uncommon.
Aphthous stomatitis is occasionally the presenting
feature and pernicious anaemia should be considered
when ulceration starts in middle age or later.

Folate (folic acid) deficiency

General aspects:
Folic acid is needed by the body to
synthesize and break down amino
acids, and to synthesize DNA/RNA,
needed to build new cells, especially:
blood, skin and mucosal cells.
There are virtually no body stores of
folic acid.

Dental aspects
LA is satisfactory for pain control.
Soreness of the tongue without depapillation
or colour change can be caused by early
deficiencies, often with normal Hb levels.
Atrophic glossitis is the best-known effect of
severe anaemia.
Angular stomatitis is also a well-known sign
but affects only a minority.
Aphthous stomatitis is sometimes.

 Folic acid deficiency in pregnancy

appears to predispose to neural tube
defects or cleft lippalate in the
fetus. Folic acid prophylaxis is thus
recommended.
treatment with folic acid (5 mg daily
by mouth) rapidly restores the
normal blood picture.
Treatment is usually given for at least
4 months.

HAEMOLYTIC ANAEMIAS
General aspects:
Haemolytic anaemia may result from:
inherited abnormalities of Hb formation (the
haemoglobinopathies);
inherited abnormalities of erythrocyte structure or
function (spherocytosis; glucose-6-phosphate
dehydrogenase [G6PD] deficiency); or
from damage to erythrocytes (autoimmune,
druginduced or infective).
Worldwide, malaria is the most common
cause.

The sickling disorders

General aspects:
gross distortions in the shape of
erythrocytes, with impaired
deformability and membrane
damage.
The erythrocytes cause vascular
occlusions in the microcirculation.

The sickling disorders include:

the sickle cell anaemia or disease,
and sickle cell trait.
Inheritance in the sickling disorders
is autosomal.
Sickle cell trait is many times more
common than sickle cell anaemia.

 Sickle cell anaemia or disease (HbSS is

present in erythrocytes) is homozygous
and is usually a serious disease with
widespread complications.It frequently
becomes apparent in about the third
month of life.
Sickle cell trait (HbSA is present) is
heterozygous and at least ten times as
common. Sickle cell trait is frequently
asymptomatic, but sickle cell crises can be
caused by low O2 tension .At times, such
patients may have renal complications
causing haematuria or splenic infarcts.

Dental aspects
The main principles in patients with sickle cell
disease are to prevent:
trauma, infection, hypoxia, acidosis or dehydration,
all of which can precipitate a crisis.
Infections must be treated early.
Painful crises should be treated promptly with
analgesics, such as diamorphine or pethidine, and
hydration.
Patients with sickle cell anaemia are treated with
hydroxycarbamide (hydroxyurea), which raises the
levels of HbF and iron-chelating agents
(desferrioxamine, deferasirox or deferiprone).

 Orofacial manifestations of sickle cell disease

include painful infarcts in the jaws (which may be
mistaken for toothache) or osteomyelitis.
Pulpal symptoms are common in the absence of
any obvious dental disease and pulpal necrosis has
sometimes resulted.
Lesions suggestive of bone infarction (dense radioopacities) may be seen in the jaws and/or skull.
Bone scans using technetium diphosphonate show
stronger uptake in these areas.
Radiographic findings include a stepladder
trabeculae pattern.
Some patients have such severe painduring crises
that they abuse analgesics and become addicts.

 Hypercementosis may be seen.

Bone marrow hyperplasia leads to an enlarged
haemopoietic maxilla with excessive overjet, and
overbite.
Skeletal but not dental maturation is delayed.
The skull is thickened but osteoporotic with a hairon-end pattern to the trabeculae.
The diplo are thickened, especially in the parietal
regions, giving a tower skull appearance.
Enamel hypomineralization and calcified pulp
canals may be seen.
The lamina dura is distinct and dense, and the
permanent teeth may be hypomineralized, though
neither caries nor periodontal disease is more
severe.

The thalassaemias
Thalassaemias are autosomally dominant
inherited disorders in which either alphaor beta-globin chains are synthesized at a
low rate,
thereby lessening the production of HbA.
Cause excessive erythrocyte fragility and
haemolysis .
Thalassaemias are characterized by a
hypochromic microcytic anaemia.

thalassaemia major
Clinical features Homozygotes for
thalassaemia major suffer from
chronic anaemia, marrow
hyperplasia, skeletal deformities,
splenomegaly, cirrhosis, gallstones
and iron overload.

 Patients with homozygous beta-thalassaemia

become overloaded with iron
(haemosiderosis) from high gut absorption
and from repeated transfusions.
The iron damages the heart (cardiac
haemosiderosis), causing cardiomyopathy
and arrhythmias, which often result in death
in early adult life.
Iron deposits lead to liver and pancreas
dysfunction, and deposits in salivary glands
can cause a sicca syndrome.
Some patients survive, probably because
they have a milder variant, such as betathalassaemia with high levels of HbF.

thalassaemia minor
Heterozygous beta-thalassaemia
(thalassaemia minor or thalassaemia
trait) is common and usually
asymptomatic, except for mild
hypochromic anaemia. Anaemia may
be aggravated by pregnancy or
intercurrent illness.

 General management:
Diagnosis of beta-thalassaemia is
confirmed by finding severe
microcytic hypochromic anaemia with
gross aniso- and poikilocytosis,
normal or raised serum iron and
ferritin, and normal TIBC.
There is a great increase in HbF and
some increase in HbA2.
The main treatment measures in betathalassaemia are blood transfusions,

 folic acid supplements and

iron-chelating agents (desferrioxamine,
deferasirox or deferiprone) and ascorbic acid.
Hydroxycarbamide is now used but the sideeffects can be a significant disadvantage.
Splenectomy may be required if there is
hypersplenism causing greater blood
destruction, which leads to accumulation of
iron elsewhere and other complications.

Dental aspects
Hepatitis B or C, or HIV carriage, may be a complication
in repeatedly transfused patients.
Since splenectomy results in an immune defect, it may
be prudent to cover surgical procedures with
prophylactic antimicrobials.
LA is safe.
CS may be given with oxygen levels not less than 30%.
GA induction may be complicated by enlargement of
the maxilla, which may cause difficulties in intubation,
but in any event,
the chronic severe anaemia and often cardiomyopathy
are contraindications.

 Orofacial manifestations include expansion of the diplo

of the skull, causing a hair-on-end appearance that is
frequently conspicuous on lateral skull radiographs.
Enlargement of the maxilla is caused by bone marrow
expansion (chipmunk facies);
there is often spacing of the teeth and forward drift of the
maxillary incisors, so that orthodontic
treatment may be indicated.
Alveolar bone rarefaction produces a chicken-wire
appearance on radiography.
Pneumatization of the sinuses may be delayed.
Less common oral complications include painful swelling
of the parotids and hyposalivation caused by iron
deposition,
and a sore or burning tongue related to the folate
deficiency.