Hematological disordes

HEMATOLOGICAL
DISORDERS IN
PEDITRIC DENTISTRY
DR. KOMAL GHIYA
MDS –PEDODONTICS AND PREVENTIVE DENTISTRY

INDEX
 DISEASES RELATEDTO RBC
 DISEASES RELATEDTOWBC
 DISEASES RELATEDTO PLATELET

DISEASES RELATEDTO RBC
ANEMIA
IRON DEFICIENCY ANEMIA
HEMOLYTIC ANEMIA
PERNICIOUS ANEMIA
THALESSEMIA
APLATIC ANEMIA

ANEMIA
Anemia is defined as an abnormal reduction in the
number of circulating red blood cells, the quantity of
hemoglobin and the volume of packed red cells in the
given unit of blood.
A hemoglobin level of 13.5 gm/dl or less is usually
regarded as anemia in adult males and less than
11gm/dl is taken as anemia in females.
Classification of anemia:
ETIOLOGICAL CLASSIFICATION
MORPHOLOGICAL CLASSIFICATION
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Burket’s book of oral medicine 10th
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ETIOLOGICAL CLASSIFICATION OF ANEMIA:
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Shafer’sTextbook of oral pathology 6th
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MORPHOLOGICAL CLASSICATION OF ANEMIA:
6
TYPES EXAMPLES
MICROCYTIC HYPOCHROMIC IRON DEFICIENCY
THALESSEMIA
MACROCYTIC VITAMIN B12 DEFICIENCY
FOLATE DEFICIENCY
HAEMOLYSIS
HYPOTHYROIDISM
LIVER DISEASE
APLASTICANEMIA
NORMOCYTIC ANEMIA CHRONIC DISEASE
RENAL FAILURE
HAEMOLYSIS
HYPOTHYROIDISM
C SCULLY,R CAWSON, MEDICAL PROBLEMS IN DENTISTRY,5TH ED

DENTAL MANAGEMENT
 LOCALANESTHESIA IS USUALLY SATISFACTORY FOR PAIN
CONTROL
 CONCIOUS SEDATIONGIVENONLY IFTHERE IS SUPPLEMENTAL
OXYGEN
 DEEPER LEVELSOF SEDATIONARE MORE LIKELYTO LEADTO
HYPOXIA
 GENERALANESTHESIA ,ENSURE FULL OXYGENATION.SICKLE
SELL DISEASE;CONTRAINDICATED
 PACKED RED CELLAVOIDTHE RISK OF FLUIDOVERLOADAND
CAN BE GIVEN IN EMERGENCY .

IRON
DEFICIENCY
OFANEMIA &
PLUMMER –
VINSON
SYNDROME
Iron deficiency is an exceedingly prevalent form
of anemia, particularly in females.
Many older children are mildly iron deficient
because of high demands for growth ,especially
during adolescence.
Iron deficiency anemia is the most prevalent
single deficiency state on a worldwide base
Persistent errors in iron balance lead to either
iron deficiency anemia or hemosiderosis.
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Burket's book of oral medicine 10th
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CAUSES OF IRON DEFICIENCY
BLOOD LOSS
POOR INTAKE
POVERTY
DIETARY IGNORANCE
OLD AGE
MALABSORPTION
ACHLORHYDRIA

CLINICAL FEATURES
TYPICALLY NONE INTHE EARLY STAGES,INCHILDREN PREDISPOSETO DEVELOPMENTALOR
BEHAVIOURAL DISORDERS
GENERAL LASSITUDE
CARDIORESPIRATORY
DYSPNOEA
TACHYCARDIA
CONGESTIVECARDIAC FAILURE
MURMURS
PALPITATIONS
ANGINA PECTORIS
CUTANEOUS
PALLOR
BRITTLE NAILS
KOILONYCHIA
ORAL
SORE MOUTH
ORAL ULCERATION
ANGULAR STOMATITIS
GLOSSITIS
BURNING MOUTH SYNDROME

GENERAL
MANAGEMENT
 FERROUS SULPHATE 200 mgTHREETIMES DAILY ORALLY
 FERROUS GLUCONATE 250 mg /day
 Maximum:3 months
 Parental iron does not raise hemoglobin level more rapidly
than oral iron ,it must be given intramuscularly if needed
DENTAL MANAGEMENT
 LOCAL ANESTHESIA IS SATISFACTORY FOR PAIN CONTROL
 GENERAL ANESTHESIA:SAMEASANEMIA
 STAINING OF IRON IN CHILDREN CAN BE PREVENTED BY USING
SODIUM IRONEDETATEAS IRON SOURCE ,AS IT IS ALSO SUGAR
FREE AND MORE PALATATBLETHAN FERROUS SULPHATE

PLUMMER –VINSONSYNDROME
Also known as Paterson – Kelly syndrome,
sideropenic dysphagia
It is manifestations of iron – deficiency anemia
It is triad of,
Dysphagia
Iron deficiency anemia
Upper esophageal webs or stricture
It is usually associated with middle aged women[4th
to 7th decayed]
It is also associated with upper elementary tract
cancer
Other symptoms are same as iron deficiency anemia
Radiographic examination of pharynx shows webs
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Burket's book of oral medic
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TREATMENT:
The anemia respond well to iron therapy and a high
protein diet
Oral iron supplements are most commonly used
Doses : 325mg (60 mg iron) orally 3 times a day
In cases when patient is unable to take oral iron,
parenteral iron preparation can be given.
Iron dextran is most commonly used parenteral iron
preparation.
In Plummer –Vinson syndrome treatment is same as
iron deficiency anemia
In case of cricoid webs rupture or mechanical dilation
may be required.
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Burket's book of oral medicine 10th edition

PERNICIOUS ANEMIA:
Also known asVitamin B12 deficiency, Addisonian anemia,
Biermer anemia, magaloblastic anemia
It is relatively common chronic hematologic disorder disease.
It is an adult form of anemia that is associated with:
Gastric atrophy
Loss of intrinsic factor production in gastric secretions
A rare congenital autosomal recessive form in which intrinsic
factor production is lacking without gastric atrophy.
Intrinsic factor is necessary for absorption of vita. B12 from GIT.
Vita B12 is erythrocyte – maturating factor
Shafer’sTextbook of oral pathology 6th edition 15

ETIOLOGY:
It is probably an autoimmune disorder with a genetic
predisposition .
Disease Is associated with human leukocyte
antigen (HLA) types A2, A3, & B7 AND A blood
group.
Antiparietal cell antibodies occur in 90% of patients
with pernicious anemia.
A greater association than anticipated exists
between pernicious anemia and other autoimmune
disease:
Thyroid disorders
Type I diabetes mellitus
 ulcerative colitis
Addison disease
Acquired agammaglobulinemia & H pylori infection. 16

 CLINICAL FEATURES:
 It is rare before age of 30 yrs and increases in frequency with advancing age.
 Females > males
 The disease is characterized by triad of symptoms:
1. Generalized weakness
2. A sore, painful tongue
3. Numbness & tingling of the extremities
 Other typical complaints are:
 Easy fatigability, headache, dizziness
 Nausea, vomiting, diarrhea
 Loss of appetite, shortness of breath, loss of weight
 Pallor and abdominal pain
 Patient with sever anemia exhibit a yellowish tinge of the skin & sometimes the sclera.The skin is
usually smooth & dry.
 Nervous system involvement in present over 75% of the cases.
17

Oral Manifestations:
Glossitis is one of the most common symptoms of pernicious anemia.
Patients complain of pain painful and burning lingual sensation
The tongue is generally inflamed either entirely or patches scattered
over the dorsum and lateral borders
In some cases small and shallow ulcers – resembling aphthous ulcer
Characteristically with glossitis, glassodynia, glassopyrosis
There is gradually atrophy of papillae of the tongue causes smooth or
“bald” tongue.
It is also called Hunter’s glossitis or Moeller’s glossitis.
Inflammation and burning sensation extend over the entire oral mucosa,
rest of the oral mucosa exhibits pale yellowish ting like the skin.
Diagnosis :
Schilling test : measures vita B12 (cynocobalamin) absorption by
increasing urine radioactivity after an oral dose of radioactive
cynocobalamin .
18

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Basic pathology Kumar, Cortan, Robin, 6th
edition

TREATMENT:
The treatment of pernicious anemia consists of the
administration of vitamin B12 & folic acid.
Early recognition and treatment of pernicious
anemia provides, normal and usually uncomplicated,
life span.
Delayed treatment permits progression of the
anemia and neurological complications
The mental and neurological damage can become
irreversible without therapy.
20

DENTAL
MANAGEMENT
 LOCALANESTHESIA CAN BE GIVEN
 CONCIOUS SEDATION:HEMOGLOBIN LEVELARE MODERATELY
DEPRESSEDAND O2 LEVELSTO BE MAINTAINED
 GENERALANESTHESIATO BE POSTPONED

HEMOLYTIC
ANEMIAS
QUANTITATIVE
DEFECTS
THALESSEMIA
QUALITATIVE DEFECTS
VARIANT HEMOGLOBIN
SICKLE CELL DISEASE

CAUSES
INHERITED ABNORMALITIES OF HEMOGLOBIN FORMATION
HEMOGLOBINOPATHIES
INHERITED ABNORMAL STRUCTURE OR FUNCTION OF ERYTHROCYTES
SPHEROCYTOSIS,G6PD DEFICIENCY
DAMAGETO ERYTHROCYTES
AUTOIMMUNE,DRUG INDUCED OR INFECTIVE
CLINICAL FEATURES
ACCLERATED ERYTHROCYTE DESTRUCITION LEADSTO BILLIRUBINOVERPRODUCTION
AND SOMETIMES JAUNDICE
SPLENOMEGALY
INCREASE IN RETICULOCYTE COUN,PLAMA LACTAE DEHYDRGENASEAND URIC ACID

SICKLECELLANEMIA
It is a hereditary type of chronic hemolytic anemia
transmitted as a mendelian dominant, non gender linked
characteristic.
It is characteristics by sickle – shaped of RBCs.
Alpha chains are normal and beta chains are abnormal
It is characteristics hemoglobin gene mutation, consisting
of replacement of the amino acid glutamine acid so that
valine is encoded instead in the sixth position on the beta –
hemoglobin chain.
This type of hemoglobin called as HbS
The RBCs with sickle shape become much less deformable,
causes obstructing the microcirculation , cause hypoxia
In children hemolyzed sickle cells aggregate and block the
blood vessels, leading to infraction
24

Sickle cell crisis
 Caused by low o2 tension
 General anesthesia
 High altitudes
 At times patient may have renal complications causing hematuria
or splenic infarcts.O2 and bicarbonates to be given.
PAINFUL CRISIS
CAUSED
:INFECTION,DEHYDRATION,HYPOXIA,
ACIDOSISOR COLD
BONE INFARCTS,PULMONARY
INFARCTS,OCULAR DEFECTS
HEMATOLOGICAL CRISIS
CAUSED:PARVOVIRUS
INFECTION
CHRONIC ANEMIA:HB:5-9 g/dl

FEATURES
ANEMIAS
HAEMOLYSIS
JAUNDICE
GALLSTONES
RETICULOCYTOSIS
IMPAIRED GROWTH
SKELETAL DEFORMITIES
SUSCEPTIBILTYTO INFECTION
SEQUESTERATION SYNDROME
26

Oral manifestations:
Sickle cell anemia exhibit significant bone changes in the dental
radiograph.
Radiographic features are:
Stepladder trabecule pattern(70%)
Enamel hypomineralization (24%)
Calcified canals(5%)
Increased overjet(56%)
Generalized osteoporosis, enlarged marrow spaces.
Hypercementosis
Patients may also have pallor of the oral mucosa and delayed
eruption of the teeth
These involvement of maxillofacial bone leads to infraction of
the vessels to that region leads to facial pain and sensory
changes in the distribution of the inferior alveolar nerve
Burket's book of oral medicine 10th edition 27

DENTAL
MANAGEMENT
 GENERALANESTHESIA:RELATIVELYCONTRAINDIICATED
 IF NECESSARYTHEN FULL OXYGENATION IS REQUIRED
 LOCAL ANESTHESIA:PREFERRED MODE
 PRILOCAINEAVOIDED:CAUSES METHEMOGOBINEMIA
 ASPIRIN:ACIDOSISAND PRECIPITATES CRISIS
 ALTERNATIVE:ACITOAMINOPHEN,CODIENE
 CONCIOUS SEDATION: AT LEAST 30% O2 is NEEDEDAND PROVIDED
 BENZODIAZEPINESTO BE AVOIDED
GENERAL
MANAGEMENT
 REGULAR BLOOD PICTURES
 TESTS:HEMOLYTIC ELECTROPHORESIS
 SICLEDEX:REDUCINGAGENT :10% SODIUM BISULPHITEOR DITHIONITE
 FOLIC ACID
 IF NEEDED BLOODTRANSFUSION

29
DIPLOIC,HAIRON END APPEARANCE
STEP LADDER PATTERN

THALASSEMIAS
Also known as Cooley’s anemia, Mediterranean anemia
It is disorder of hemoglobin synthesis with decreased production of either
alpha or beta polypeptide chains.
Unaffected excess chains precipitate within erythrocytes to cause excessive
erythrocyte fragility and hemolysisi
Many more peoples are carriers [they have the thalassemia trait with only
one beta gene affected or one to two alpha genes affected]
And they usually have no symptoms and need no treatment
Microcytic, hypochromic anemia
30

Alpha thalassemia
Hrmoglobin H and Barts
Ineffective O2 carrier
Lethal inutero BetaThalessemia
Delta and gamma chains increases
Raised level of hemoglobin A2 and F

CLINICAL FEATURES
Chronic anemia,marrow hyperplasia,skeletal deformities,splenomegaly,gall stones,iron
overload,no pubertal growth spurt
Affected children are susceptible to folate deficiency and also to infection
DENTAL FEATURES
Expansion of diploe of skull causes a hair on end appearance
Enlargement of maxilla is caused by bone marrow expansion (chipmunk faces)
Spacing of teeth and forward drift of maxillary incisors
Alveolar bone rarefaction produces a chicken wire appearance
Pnuematization of sinuses may be delayed
Painful swelling of parotis and xerostomia,sore burning tongue

GENERAL MANAGEMENT
 BLOODTRANSFUSIONS
 FOLICACID SUPPLEMENTS
 IRON CHELATINGAGENTS
 ASCORBICACIDS
 SPLENECTOMY IF REQUIRED
DENTAL MANAGEMENT
PROPHYACTICANTIBIOTICS
LOCAL ANESTHESIA:SAFE
CONCIOUS SEDATION: 30% O2
GENERAL ANESTHESIA:CONTRAINDICATED DUETO
CARDIOMYOPATHIESAND CHRONIC ANEMIAAND LARGE MAXILLA
CAUSES PROBLEM IN INTUBATION

APLASTICANEMIA
Aplastic anemia is rare blood dyscrasia in which
peripheral blood pancytopenia results from reduced or
absent blood cell production
in the bone marrow.
Normal hematopoietic tissue in the bone marrow has
been replaced by the fatty marrow.
The disorder can be inherited, idiopathic, or acquired
35

Environmental exposures, such as drugs, viruses and
toxins are thought to trigger the aberrant immune
response in some patients, but most of the cases
classified as idiopathic
Most cases of idiopathic and acquired AA are
immune mediated with activated type I cytotoxicT
cells implicated.
CLINICAL FEATURES:
same as anemia
Abnormal susceptibility to to infection and bleeding
Purpura is often the first manifestaton
36

ORAL MANIFESTATIONS:
Patachie purpuric spots or frank hematomas of the
oral mucosa may occur at any site.
Hemorrhage into the oral cavity, especially
spontaneous gingival hemorrhage
Such findings are related to the blood platelet
deficiency
Because of the neutropenia leads to ulcerative lesions
of the oral mucosa and pharynx
Second and third most common oral manifestations
are candidiasis and viral infections.
37
edition

GENERAL MANAGEMENT
Patients with aplastic anemia require transfusion
support until the diagnosis is established and
specific therapy can be instituted.
Infections should be treated appropriately with
antibiotics
Other treatment options are bone marrow
transplantation & immunosuppressive therapy.
DENTAL MANAGEMENT
Local anesthesia: satisfactory
Concious sedation: avoided
General anesthesia: avoided
38

DISEASES RELATED
TOWBC
LEUKEMIA

LEUKEMIA
 The leukemia are a group of disorder characterized by the
accumulation of immature (malignant) white blood cells in the
bone marrow and blood.
40
edition

CLASSIFIED
AS:
 Lymphoid ( lymphoblastic, lymphocytic)
 Myeloid ( myelogenous)leukemia: inovolving progenitor cell
41
edition

 CLASSIFICATIONOF LEUKEMIA:
 ACUTE:
Acute myeloid leukemia
Acute lymphoblastic leukemia
 CHRONIC:
Chronic myeloid leukemia
Chronic lymphoid leukemia
42

CLINICAL
FEATURES
Acute leukemia Chronic leukemia
 More common in - More common in
children and young middle aged and elders
adults - insidious onset
 Sudden onset - Protracted course
 Fatal short course
45

 COMMON FEATURES:
 Generalized constitutional symptoms
 Signs of anemia
 Infections
 Subcutaneous and submucosal
hemorrhages:Thrombocytopenia
 Generalized lymphadenopathy
46

ORAL MANIFESTATIONS
 Oral bleeding and petechiae
 Gingival ulceration and enlargement
 Herpetic oral and perioral infection is very common
 Candidiosis
 Bone changes seen on radiograph may include
destruction of crypts of developing tooth .these
bony changes may be reversible with chemotherapy
47

ACULTE
LYMPHOBLASTIC
LUEKEMIA:
ASPECTSAND
MANAGEMENT
 CONSULT PHYSICIAN
 PREVENTIVE ORAL HEALTH CARE AND CONSERVATIVE DENTAL
TREATMENT
 ISOLATION:LAMINAR FLOW ROOM ,WHEN STRIC ASEPSIS IS
INDICATED
 ANTIMICROBIAL COVER IS NEEDED FOR ANY SURGERY
 PREOPERATIVE PRECAUTIONS
 INCLUDE SCREENING OF HEPATITIS B OR C
 LOCAL ANESTHESIA CONTRAINDICATED DUETO BLEEDING
TENDENCIES
 CONCIOUS SEDATION IS USUALLY POSSIBLE
 ANEMIA MAY BE CONTRAINDICATION TO GENERAL ANESTHESIA
 INTRAVENOUS SEDATION AND RELATIVE ALGESIA MAY BE
ALTERNATIVES
 ASPIRIN CONTRAINDICATED

CHRONIC
LEUKEMIA:
DENTAL
ASPECTSAND
MANAGEMENT
 ROUTINE DENTALTREATMENT
 CLOSECOOPERATIONWITH HEMATOLOGIST
 ADVERSE EFFESTS OFTREATMENT INCLUDE PULMONARY
FIBROSISAS A RESULT OF BUSULPHAN
 AMPICILLINANDAMOXICILLIN MAY CAUSE IRRITATING
RASHES
 INTERFERONALPHA MAY CAUSETASTE AND CAUSE
XEROSTOMIA
 ORAL HAMEEROHAGE CAN BE SEEN DUETO DRUGS
 LEUKEMIC INFILTRATIONCAN CAUSE SWELLINGOF LACRIMAL
AND SALIVARY GLANDS

DISEASES RELATED
TO PLATELET
HEMOPHILLIA
PURPURA

PURPURA
Purpura is defined as a purplish discoloration of the
skin and mucous membranes due to spontaneous
extravasation of blood, and in itself, is a symptom
rather than a disease entity.
Classification:
1. Nonthrmbocytopenic purpura
2.Thrombocytopenic purpura
(a) Primary or “essential” purpura
(b) Secondary or symptomatic purpura
edition

NONTHROMBOCYTOPENIC PURPURA
This type of purpura is not mediated through
changes in blood platelets.
Caused by alteration in the capillaries themselves
that results in many instances in increased
permeability.
Causes are autoimmune, infections, structural
malformations like hereditary hemorrhagic
telangiectasia & miscellaneous.
edition

PRIMARYTHROMBOCYTOPENIC PURPURA
It is autoimmune disorder in which antiplatelet
globulin is formed which results in decrease the
circulating platelets.
The acute form of disease commonly occurs in
children with viral infections
The chronic form of disease occurs in adults, especially
women of childbearing age.
80% of cases of primary thrombocytopenic purpura
occur before age of 30 years, with greatest incidence
before 10 years
edition

 CLINICAL FEATURES:
Spontaneous appearance of purpuric or hemorrhagic
lesions of the skin which vary in size from tiny, red
pinpoint petechiae to large purplish ecchymosis and
even massive hematomas
Epistaxis is common finding of disease
Bleeding from urinary tract, resulting in hematuria.
Bleeding in GI tract producing melena or hematemesis
A possible complication is intracranial hemorrhage,
which may result in hemiplegia.
edition

ORAL MANIFESTATIONS
Oral manifestations are sever and often profuse
gingival hemorrhage which occurs in majority of cases.
This hemorrhage may be spontaneous and often arises
in the absence of skin lesions.
Petechiae occurs on oral mucosa, commonly on palate,
and appear as numerous tiny, grouped clusters of
reddish spot only a mm or less in diameter
Tendency for excessive bleeding contraindication for
any oral surgical procedures.
edition

LABORATORY FINDINGS
Platelet count is below 60,000/cu mm.
BT is prolonged often an hour or more and CT is
normal
Capillary fragility is increased (also known as
RUMPEL-LEEDE FRAGALITYTEST)
Tourniquet test is strongly positive
Giant platelets on peripheral smear suggest
congenital thrombocytopenia.
edition

TREATMENTAND PROGNOSIS
Splenectomy probably has proved more beneficial
than any other form of therapy.
Symptomatic relief is done by bed rest and
transfusions.
Corticosteroids have been used in many cases with
excellent results.
The prognosis is disease Is fairly good, since remissions
are common.
edition

SECONDARYTHROMBOCYTOPENIA
It is similar to primary thrombocytopenia in that it is
characterized by reduced platelet production or
increased platelet destruction resulting in platelet
levels<60,000/micro L.
Thrombocytopenia can occur from secondary causes
associated with:
Chronic disorders
Chronic infections
Myeloproliferative disorders
Lymphoproliferative disorders
Pregnancy
Autoimmune disorders
edition

DENTAL MANAGEMENT
 REGIONAL LOCALANETSHESIA BLOCK INJECTIONSCAN BE GIVEN
IF PLATELET LEVELSARE ABOVE 30* 10 9/L
 PLATELETTRANSFUSIONS
 LOCAL HEMOSTATICAGENTS:DESMOPRESSINANDTRANSXEMIC
ACID OR CELLULOSE,SYNTHETICCOLLAGEN OR
MICROCRYSTALLINECOLLAGEN
 CONCIOUS SEDATIONCAN BE GIVEN
 GENERALANESTHESIA GIVEN BUT EXPERT INTUBATION
 ASPIRINCONTRAINDICATED
 COX 2 INHIBITORS DO NOT HAVE ANY EFFECT ON PLATELET SO
CAN BE GIVEN

COAGULATIONAND ITS DISORDERS
HEMOSTATIC PROCESS
3 MAIN STEPS:
Primary hemostasis : local vasoconstriction and platelet
plug formation
Coagulation cascade
Fibrinolysis

COAGULATION FACTORS
 PROTEINC is also known as AUTOPROTHROMBIN IIA and blood
COAGULATION FACTOR XIV.

HEMOPHILIA
It is characterized by a prolonged coagulation time
and hemorrhagic tendencies.
X- linked recessive disorder
Types:
Hemophilia A: due to factor VIII deficiency
Hemophilia B: due to factor IX deficiency
Hemophilia C: due to factor XI deficiency

CLINICAL FEATURES
Persistent bleeding either spontaneous or on mild
trauma that produces the mildest of abrasions or cuts.
Hemorrhage into
the subcutaneous tissues,
 internal organs, and
 joints it is also a common feature and may result in
massive hematomas.
The disease is usually present from birth
Approx. 30-50% patient with sever hemophilia shows
bleeding from umbilical cord
Spontaneous cyclic remissions and exacerbations of
hemophilia are common
In Hemophilia C absence of bleeding into joint and
muscles.

CLASSIFICATI
ONOF
HEMOPHILIA
CLASSIFICATI
ON
%FACTORVIII
MILD >5-25
MODERATE 1-5
SEVERE <1
VERY MILD >25

ORAL MANIFESTATIONS
Hemorrhage from many sites into the oral cavity
Gingival hemorrhage may be massive and
prolonged
Physiological processes of tooth eruption and
exfoliation may be attended with severe prolonged
hemorrhage.
Mandibular ‘pseudotumor’ of hemophilia has been
reported due to sub periosteal bleeding, with
reactive bone formation
The problem of dental extraction is a difficult one in
hemophilias.
Without proper premedication, even a minor
surgical procedure may result in death.
Rubber band extraction has often used in
hemophilic patient.

LABORATORY FINDINGS
Bleeding time is normal
Clotting time and aPTT is prolonged

TREATMENTAND PROGNOSIS
PREVENTIVE DENTISTRY
LOCALANESTHETIC INJECTIONSOR SURGERY CAN BE
FOLLOWED BY PROLONGED BLEEDING
NSAIDS:BLEEDINGTENDENCIESAGGRAVATE
LOCALANESTHETICS+FACTORVIII REPLACEMENTS
INTRALIGAMENTARYAND INTRAOSSEOUS INJECTIONSARE
SAFER
CONSERVATIVETREATMENT:
PAPILLARYOR INTRALIGAMENTARY INFILTRATION
ELECTRONIC DENTALANAESTHESIA
MATRIX BAND:PREVENTGINGIVAL LACERATION

 COTTON ROLLSTO BEWETTED
 RUBBER DAM CLAMP
 HIGH SPEED SALIVA EJECTORSTO BE AVOIDEDTO AVOID
HEMATOMA
 ENDODONTICTREATMENT
 AVOIND OVERINSTRUMENTATION
 TOPICALAPPLICATIONOF COCCAINETO EXPOSED PULP IS
RECOMMENDED FORVITAL PULP EXTIRPATION
 INTRACANAL INJECTIONOF LA SOLUTIONCONTAINING
EPINEPHRINEORTOPICALAPPLICATIONOF EPINEPHRINE1:1000
 ORTHODONTICTREATMENT
 NO CONTRAINDICATION

 EXTRACTIONS:
 FACTOR LEVEL 50-75%
 SUTURING IS DESIRABLE:NONTRAUMATIC NEEDLE
 OXIDISEDCELLULOSE SOAKED INTRANSXEMICACID PLACED
INTOTHE BASE OF SOCKET OR COLLAGEN OR CYNOACRYLATE
OR FIBRIN GLUES
 FIBRIN SEALANT:PROVIDES RAPID HEMOSTASIS
 ANTIBIOTIC PROPHYLAXIS

vonWillbrand's Disease
Also called pesudohemophilia
Disease is characterized by the tendency to
excessive bleeding in patients, who have normal:
platelet count
clotting time
Serum fibrinogen
Prothrombin time
The bleeding time is prolonged.
Most common congenital disorder, more common
in female
These disease is characterized by abnormal vWF.

TYPES
Type 1: most common from,
Partial quantitative deficiency of vWF.
Autosomal dominant
Mucocutaneous bleeding
Hematology consult prior to surgery
Prolonged BT, normal platelet
Type 2: qualitative alterations in the vWF structure
and function
Type 3: most severe and rarest form
Marked deficiency in vWF & factorVIII in the plasma
Autosomal recessive

CLINICAL FEATURES
Prevalence is 0.9-1.3%
Many children with vWD are asymptomatic but
have positive parental history.
Excessive bleeding is most common feature
Most common site of bleeding is nose, skin and
gingiva
Bleeding into GI tract and severe menorrhagia are
common

ORAL
MANIFESTATIOS Gingival bleeding is most common
It is spontaneous or occur after brushing
Mostly the disease is discovered after extraction
because of prolonged and excessive bleeding

DENTAL
MANAGEMENT
 DESMOPRESSINGIVENAS NASAL SPRAY USED INTYPE 1 ONLY
 IMMEDIATE PURITY FACTORVIII ,CRYOPRECIPITATEAND
FRESH FROZEN PLASMA
 ASPIRINAND NSAIDS SHOULD BE AVOIDED
 LOCAL INFILTRATIONANESTHESIA SHOULD BE USED
 CONCIOUS SEDATION USED BUTWITH CARE NOTTO DAMAGE
THEVEIN
 GENERALANESTHESIA MUST BE GIVEN IN HOSPITAL SETTING
ONLY,INTUBATION IS DANGEROUS

INCREASEAND
DECREASE INCELL
COUNT

1.NEUTROPHILIA
 Increase in neutrophil count above normal
Conditions:
Acute pyogenic infection
Acute hemorrhage or hemolysis
Tissue damage: trauma or infarction
Metabolic: uremia, gout or eclampsia
Malignant neoplasm
Physiologic in the newborn, during labor, after
strenuous exercise, repeated vomiting, convulsions,
paroxysmal tachycardia, after epinephrine injection
Myelocytic leukemia, polycythemia, myelofibrosis and
myeloid metaplasia
79

2. EOSINOPHILIA
Increase eosinophil count above normal
Conditions:
Allergic diseases: bronchial asthma, urticaria,
angioneurotic edema, hay fever, certain drug allergy
Parasitic infections: pemphigus and dermatitis
herpetiformis
Recovery from acute infection
Polyarthritis nodosa, vasculitis , serum sickness
Graft versus host disease
Hypereosinophilic syndrome
Following irradiation
Hodgkin's disease
Chronic Eosinophilic leukemia
idiopathic
80

3. BASOPHILIA
Increase in basophil count above normal
Condition :
Blood disease: chronic anemia, CML, Hodgkin's
disease,
Splenectomy
Infections: chronic inflammation of accessory sinuses,
small pox, chicken pox
After injection of foreign proteins
Myxedema
81

4. LYMPHOCYTOSIS
Increase in lymphocyte count above normal
Conditions:
Chronic bacterial infections likeT.B, secondary &
congenital syphilis,
Certain acute infections like pertussis,
infectiousmononeucleosis, acute infectious
lymphocytosis
Lymphocytic leukemia acute and chronic,
Hodgkin's disease
Hemopoietic disorders: chronic neutropenia,
measles, mumps , exanthemas
82

5. MONOCYTOSIS
Increase in monocyte count above normal
Conditions:
Certain bacterial infections likeT.B., SABE, syphilis
, rarely in typhoid
Connective tissue disease
Protozoal infection
Recovery from active infection
Lymphoma, leukemia, multiple myeloma,
Myeloproliferative disorders
Collagen vascular diseases
Gauchers disease
Rheumatoid arthritis, systemic lupus
erythematous, sarcoidosis
Chronic high dose steroid therapy
83

AGRANULOCYTOSIS
The term agranulocytosis are commonly used to
interchangeably for reduced number of
leukocytes
Clinical symptoms of agranulocytosis include
sudden onset of fever, rigors, and sore throat
Leukocytopenia (decrease count) in different
leukocyte known as:
1) Neutropenia
2) Eosinopenia
3) Basopenia
4) Lymphocytopenia
5) Monocytopenia
84

1.
NEUTROPENIA
 Decrease in neutrophil count below normal
CONDITIONS:
Bone marrow disorders
Tuberculosis
Typhoid
Autoimmune diseases
85

2.
EOSINOPENIA
Decrease in count of eosinophil below normal
CONDITIONS:
Cushing’s syndrome
Bacterial infections
Stress
Prolonged administration of steroids, ACTH &
epinephrine
86

3.
BASOPENIA
Decrease in basophil count below normal
CONDITIONS:
Urticaria
Stress
Prolonged exposure to chemotherapy or
radiation therapy
87

4.
LYMPHOCYTOP
ENIA
Decrease in lymphocyte count below normal
CONDITIONS:
AIDS
Malnutrition
Radiation therapy
Steroid administration
Hodgkin’s disease
Chronic uremia
Blood diseases: e.g. myelocytic leukemia
88

5. MONOCYTO
PENIA
Decrease in monocyte count below normal
CONDITIONS:
Autoimmune diseases
Prolonged use of steroids
Radiation therapy
89

 PLATELET:Ranges between 2,50,000 to 4,00,000/cu mm of blood.
Increase in platelet count is known as thrombocytopenia.
Decrease in platelet count is known as thrombocythemia or
thrombocytosis
Age: less in infants(1,50,000 to 2,00,000/cu mm), and reaches normal
level at 3rd month after birth.
Sex: in females, its reduced during menstruation
High altitude: count increases
After meals: after taking food, count increases

 RBC
NORMALVALUE:
Range between 4 & 5.5 million/cu mm
Adult male: 4.5 to 5.5 million/cu mm
Adult female: 4.5 to 5.0 million/cu mm
Physiological :
Diurnal variation : lowest during sleep; maximum in evening
Muscular exercise: increases
High Altitude : increases
Pregnancy: decreases
Pathological :
Hypoxia
Shock
Dehydration

 REFERENCES:
 Text book of medical physiologyGuyton and Hall 12th edition
 Shafer’sTextbook of oral pathology 6th edition
 Burket’s book of oral medicine 10th edition
 Basic Pathology Kumar, Cortan, Robin 6th edition
 White and PharaohTextbook of oral radiology
 C Scully ,Rcawson,Medical problems in dentistry,5 edition
92

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