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RBCs & Its Clinical 
Implications 
Dr. Amit T. Suryawanshi 
Oral and Maxillofacial Surgeon 
Pune, India 
Contact details : 
Email ID - amitsuryawanshi999@gmail.com 
Mobile No - 9405622455
Contents 
1. Introduction. 
2. History. 
3. Erythropoiesis. 
4. Morphology of RBCs. 
5. Properties of RBCs. 
6. Functions of RBCs. 
7. Lifespan & Fate of RBCs. 
8. Hemoglobin & Iron Metabolism. 
9. Blood tests & Blood indices . 
10. Clinical implications of RBCs. 
11. Conclusion.
Introduction 
• Blood is connective tissue of the body in fluid form. 
• Blood is a specialized body fluid 
in humans that delivers oxygen and nutrients to 
the cells and transports carbon dioxide and 
metabolic waste products away from the cells. 
Hence it is called as a “ River of Life ” 
• Blood and Blood related disorders has got very 
much importance in patients life ,making it 
mandatory to learn for Oral Surgeons .
Composition of Blood 
Blood Cells 45.7 % Plasma 54.3% 
Solid 
6-7% 
Water 
92-93 % 
Gases 
<1 % 
Organic 
Substances 
Inorganic 
Substances 
Erythrocytes 
45 % 
Leucocytes 
0.6 % 
Thrombocytes 
0.1 %
Blood is considered as a fluid of life. Because it 
carries Oxygen from lungs to all parts of the body 
and Carbon dioxide from all parts of the body to the 
lungs. 
This function of the blood is performed by RBCs. 
i.e. Red blood Cells which are also known as 
Erythrocytes . ( Erythros - Red , Cytes – Cells )
Introduction of RBCs 
• RBCs- Red Blood Cells .They are also known as 
Erythrocytes. 
• Red colour of RBCs is due to presence of coloring 
pigment Hemoglobin. 
• RBCs play important role in transport of Oxygen 
from lungs to the tissues and carbon dioxide 
from tissues to lungs.
History 
• The first person to describe red blood cells was the 
young Dutch biologist Jan Swammerdam, who had 
used an early microscope in 1658 to study the 
blood. 
• In 1959, Dr. Max Perutz was able to reveal 
the structure of hemoglobin .
Normal RBC Count - 
• Avrg RBC count = 4 - 5.5 millions / mm3 
• RBC count in adults male – 5- 5.5 millions /mm3 
• RBC count in adults female – 4 – 4.5 millions /mm3 
• RBC count in infants - 6-7 million/mm3
Erythropoiesis 
• Haematopoiesis is the process which includes 
origin, development & maturation of all blood 
cells. 
• Whereas the process by which origin , 
development and maturation of erythrocytes 
occur is known as Erythropoiesis.
Stages & Sites of Erythropoiesis 
• In Fetal life - 
Mesoblastic 
stage 
• First 2 
months of 
i.u. 
• From 
mesenchyme 
of yolk sac 
Hepatic 
stage 
• From 2-6 
months 
• Liver, spleen 
& lymphoid 
organs 
Myeloid 
stage 
• From 7-9 
month 
• Red bone 
marrow, 
Liver
In post natal life 
• Upto 5-6 years : Red bone 
marrow of all bones. 
• From 6-20 years : Red 
bone marrow of long 
bones & all flat bones . 
• After 20th year : almost 
red bone marrow of all 
the long bones is replaced 
by yellow bone marrow.
In post natal life 
• Only the upper ends of 
the femur & humerus 
contain red bone marrow. 
• Vertebras , ribs, sternum 
scapula ,iliac bone also 
produce red cells 
continuously. 
• In case of Bone disorders, 
RBCs are produced in 
spleen, liver
Erythropoiesis - 
o Blood cells are derived from Pluripotent 
Hemopoetic Stem Cells (PHSC) 
o Growth inducers (GI) like interleukin-3 and 
differentiation inducers (DI) play an important 
role. 
o Few PHSC are retained throughout life as they 
are.
Erythropoietin dependent stages
Iron dependent stages 
CELL 
DIAMETER 
NUCLEUS CYTOPLASM 
15-20 ÎĽm Big Very Scanty & basophilic. 
No Hb 
11-16ÎĽm Smaller Still Scanty & basophilic. 
No Hb 
10-12ÎĽm Smaller & 
denser 
Hb starts to appear, 
cytoplasm polychromatic 
8-10ÎĽm Ink spot nucleus Plentiful, eosinophilic 
cytoplasm. Increase in 
Hb 
8-10ÎĽm Absent Some RNA still present 
7.2 ÎĽm Absent Hb is present in large 
amount .
RBC Maturation factors 
1. Vitamin B12 (Extrinsic factor) – 
• Essential for maturation of RBCs 
• Deficiency of Vitamin B12 causes Pernicious Anemia. 
So it is also called as antipernicious factor . 
2. Intrisic Factor of castle- 
• Produced in Gastric mucosa 
• Essential for absorption of Vit.B 12
3. Folic acid – 
• Essential for synthesis of DNA in RBCs. 
• Absence of folic acid causes failure of 
maturation of cells leading to 
Megaloblastic anemia.
Morphology 
• Size : 7.2 μ 
• Shape : Circular , Biconcave 
• Thickness : 2.2 μ, 1 μ 
• Surface area : 120 μm2 
• Volume : 85-90 μm3
Advantages of bi-concave shape: 
1. provides large surface area for 
absorption and removal of 
respiratory gases and other 
substances. 
2. Cells can easily squeeze through 
while passing through capillaries
Composition 
• Water - 62.5% 
• Hemoglobin - 35% 
• Others - 2.5% 
(glucose, lipids, 
proteins, enzymes, 
vitamin, ions) 
others 
water 
haemoglobin
Properties of RBCs 
Rouleaux formation Packed cell volume
Specific gravity- 
1.092 – 1.101 
Suspension stability
Functions of RBCs - 
1. Transport of OXYGEN from lungs to the tissues 
2. Transport of CARBON DIOXIDE from tissues to 
the lung 
3. Buffering action in blood
5. Blood group determination. 
6. Help to maintain the viscosity of blood.
LIFE SPAN AND FATE OF RBC’S 
• Average life span -- 100-120 days. 
• Spleen -- Graveyard of red blood cells. 
• Daily 10% red blood cells, which are senile, get 
destroyed in normal young healthy adults.
Hemoglobin 
• Hemoglobin is an oxygen carrying pigment of 
the RBCs. 
• It is a conjugated protein which consists of 
protein combined with an iron containing 
pigment.
Functions of Hemoglobin 
1. Transport of OXYGEN from lungs to the 
tissues 
2. Transport of CARBON DIOXIDE from tissues 
to the lung 
3. Buffering action in blood
HAEMOGLOBIN 
NORMAL VALUES 
• Average hemoglobin (Hb) -- 14 to 16 gm%. 
• At different ages: 
– At birth : 22 – 25 gm% 
– After 3 months : 18 – 20 gm% 
– After1 year : 17 gm% 
– In adult males : 14 – 17 gm% 
– In adult females : 12 – 16 gm%
Iron Metabolism- 
• Iron is absorbed for small intestine and 
transported to blood . 
• In blood , Iron combines with β globulin to 
form Transferrin 
• Iron is stored in large quantities in 
RE cells and Hepatocytes as Ferritin. 
• In RBCs , Iron is stored in Fe++ form .
Synthesis of hemoglobin 
A. 2 succinyl-CoA + 2 glycine Pyrole compund 
B. 4 pyrrole compunds Protoporphyrin IX 
C. Protoporphyrin IX + Fe++ Heme 
D. Heme + globin Hemoglobin
Factors for Hemoglobin synthesis 
• Proteins 
• Iron 
• Vitamin C, Riboflavin ,Nicotinic acid , Pyridoxine 
• Copper 
• Cobalt and nickel
Structure of Hemoglobin 
• It is a conjugated protein 
• It consists of 
1. Heme - An Iron containing pigment. 
2. Globin- Protein
Heme part- Structure 
• It consists of 
1. Iron – Ferrous form(Fe++) 
2. Porphyrin – Pigment part
Globin -Structure 
It consists of 4 polypeptide chains 
1. Two α chains 
2. Two β chains
Types of Normal Hemoglobin 
• There are 2 types of hemoglobin . 
1. Adult Hemoglobin (HbA)- 
- It contains 2 α and 2 β chains 
2. Fetal Hemoglbin (HbF)- 
-It contains 2 α and 2 γ chains
DESTRUCTION OF HEMOGLOBIN 
– Occurs in Phagocytes of Spleen. 
– Globin is broken into amino acid and 
reused. 
– Heme – Its tetrapyrrole ring is opened up 
to form BILIVERDIN. 
– Its oxidation produces BILIRUBIN
CLINICAL 
IMPLICATIONS OF RBC
Clinical disorders related to RBCs 
Broadly classified into 
1. Anemia – Decrease in RBC count and 
Hemoglobin level. 
2. Polycythemia – Increase in RBC count and 
Hemoglobin level.
ANEMIA 
• It is defined as a blood cell disorder 
characterized by decreased oxygen carrying 
capacity of blood caused by reduction in red 
blood cell count or hemoglobin content or 
both.
Classification 
Etiological (Whidby's) classification 
A. Deficiency anemias - 
1. Iron deficiency anemia 
2. Megaloblastic anemia 
3. Pernicious anemia 
B. Blood loss anemias - 
1. Acute post- hemorrhagic anemia 
(accidents) 
2.Chronic post- hemorrhagic anemia
C. Haemolytic anemias ( increased destruction of 
rbc) 
1. Hereditary heamolytic anemias 
a. Thalassemia 
b. Sickle cell anemia 
c. Hereditary spherocytosis 
d. Glucose 6-phosphate dehydrogenase 
deficiency (G6PD)
• Acquired haemolytic anemias 
- Due to direct toxic effect ( eg snake venom, drugs 
, chemicals, etc) 
- In splenomegaly 
- In paroxysmal nocturnal haemoglobinuria( PNH) 
D. APLASTIC ANEMIA (failure of bone marrow) 
E. Anemia due to chronic diseases 
(tuberculosis, chronic infections, malignancies )
Morphological (Wintrobe’s) classification 
1.Normocytic normochromic anemias 
• Acute post-haemorrhagic anemia 
• Haemolytic anemias 
• Aplastic anemia 
• Anemia in chronic diseses. 
2.Macrocytic normochromic anemia 
• Pernicious anemia (Addison’s anemia)
3. Macrocytic hypochromic anemias- 
• Protein deficiency anemia 
• Megaloblastic anemia 
2.Microcytic hypochromic anemias 
• Iron deficiency anemia 
• Chronic post-haemorrhagic anemia 
• Thalassemias
SIGN & SYMPTOMS 
Considered in two broad categories: 
1. Clinical features common to all anemias. 
2. Certain special clinical features for different 
types of anemias.
Common Clinical features 
• Typically none in early stages 
• General lassitude 
Cardio-respiratory - 
1. Dyspnoea 
2. Tachycardia 
3. Murmurs 
4. Palpitations 
5. Angina Pectoris
Oral – 
1. Sore mouth 
2. Oral ulceration 
3. Angular stomatitis 
4. Glossitis 
5. Burning mouth syndrome 
Cutaneous - 
1. Pallor 
2. Brittle Nails 
3. Koilonychia
Iron deficiency anemia 
• Most common type of anemia 
• It Develops due to inadequate availibity for 
iron for hemoglobin synthesis . 
• Causes – 
1. Loss of blood 
2. Decreased intake or poor absorption of iron 
3. Increased demand in conditions like growth 
and pregnancy
Clinical features 
PALLOR KOILONYCHIA 
ANGULAR CHEILITIS PAPILLARY ATROPHY OF TONGUE
Megaloblastic anemia 
• Megaloblastic anemia is due to deficiency of 
Maturation factor of RBC i.e. folic acid. 
• DNA synthesis is impaired so cells are 
megaloblastic but immature .
Oral manifestations 
1. Atrophic glossitis 
2. Patchy erythema 
3. Taste alterations 
4. Dysphagia 
5. Burning mouth 
Atrophic glossitis
Pernicious anemia 
• Cause – 
• It occurs due to atrophy of gastric mucosa 
because of autoimmune destruction of 
parietal calls. 
• Hence , it leads to decreased production of 
intrinisic factor and poor absorption of 
vitamin B12 .( Maturation factor )
Oral manifestations 
1. Atrophic glossitis 
2. Patchy erythema 
3. Taste alterations 
4. Dysphagia 
5. Burning mouth 
Atrophic glossitis
SICKLE CELL ANEMIA 
•It is a congenital anamaly occurs 
due to abnotmal Hb called Hb–S. 
•Molecules of Hb-S polymerize 
into long chains and precipitate 
inside the cell. 
•Hence RBCs attain “ Sickle” or 
“Crescent” shape & become 
more fragile leading to hemolysis
Hemolysis in Sickle cell anemia
Oral 
Manifestations 
Pallar of mucosa Delayed erruption of teeth
Other clinical features - 
Jaundice Hand & Foot 
syndrome
THALASSEMIA 
• It is also known as “Cooley’s anemia” . 
• It is caused by inherited anomalies of hemoglobin 
• It is of 2 types 
1. α thalesemia 
2. Î’ thalesemia
Clinical features 
1. Saddled nose 
2. Prominent malar 
bone 
3. Retracted upper 
lip 
4. Bimaxillary 
protrusion 
5. Chipmunk facies
Radiographic feature 
HAIR ON END APPEARENCE
APLASTIC ANEMIA 
• Aplastic anemia is due to failure of red bone 
marrow . 
• Red bone marrow is replaced by fatty tissues 
• Causes – 
1. Repeated exposure to X-rays & Gamma rays 
2. Due to bacterial toxins , quinine , gold salts
Oral manifestations 
ORAL PETECHIAE 
GINGIVAL HYPERPLASIA
Blood Tests
Blood tests 
The routine blood tests are 
1. Complete blood count 
I. RBC count 
II. Blood indices – 
PCV , MCV, MCH, MCHC 
2. ESR 
3. Blood smear 
4. Retuculocyte count
ERYTHROCYTE SEDIMENTATION RATE 
• It is commonly used blood test and is also called 
as a sed rate or BIERNACKI’s REACTION. 
• Procedure – 
1. Blood is mixed with an anticoagulant and 
allowed to stand on a vertical tube. 
2. RBCs settle down due to gravity leaving 
supernatant layer of clear plasma above .And 
the rate at which RBCs settle down is called as 
ESR . 
• It is the length of clear supernatant plasma 
measured in mm at the end of 1 hr.
• Determination by 
1. Westergreen’s Method 
2. Wintrobe’ s Method 
• Normal Values of ESR 
– Westergreen's Method 
• Adult Males = 
0 – 15 mm in 1 hr 
• Adult Females= 
0 - 20 mm in 1 hr
• Variations of ESR 
Pathological - 
• ESR increases in - 
– All Anemias, 
except sickle cell anemia . 
• ESR decreases in - 
– Polycythemia 
– Sickle cell anemia
BLOOD INDICES 
• Importance – Help in diagnosis & typing of Anemias. 
• Different Blood Indices 
1. Packed Cell Volume (PCV) 
2. Mean Corpuscular Volume (MCV) 
3. Mean Corpuscular Hemoglobin (MCH) 
4. Mean Corpuscular Hemoglobin Concentration 
(MCHC)
PACKED CELL VOLUME 
• Also called as HEMATOCRIT value 
• It is the fraction of blood composed of 
RBC 
• Procedure- 
• Blood is mixed with anticoagulant & filled in 
wintrobe’s tube upto 100mm mark . 
• And tube is typically centrifuged at 3000 RPM 
for 30 minutes OR at 10,000 rpm for 1 minute
• NORMAL VALUES OF PCV – 
Males = 40 to 45%. 
Females = 38 to 42% 
• VARIATIONS IN PCV 
1. PCV increases in 
- Polycythemia 
2. PCV decreases in 
-All types of anemia.
HEMATOCRIT VALUES
MEAN CORPUSCULAR VOLUME (MCV) 
Average volume of a single red blood cell 
– Normal MCV = 85 - 90 μm3 . 
– VARIATIONS IN MCV- 
• Increases in (Macrocyte anemia ) - 
1. Pernicious anemia 
2. Megaloblastic anemia
• Decreases in (Microcyte anemia ) 
1. Iron deficiency anemia 
2. Chronic post-haemorrhagic anemia 
3. Thalassemias
MEAN CORPUSCULAR HEMOGLOBIN 
(MCH) 
• Quantity or amount of Hb present in one RBC 
– Normal value of MCH is 30 pg (27 -32pg) 
–Increases or remains normal in 
1. Pernicious anemia
• Decreases in (Hypochromic anemia). 
1. Protein deficiency anemia 
2. Megaloblastic anemia 
3. Iron deficiency anemia 
4. Thalassemia
MEAN CORPUSCULAR HEMOGLOBIN 
CONCENTRATION (MCHC) 
• It is the amont of Hb expressed in relation to volume of 
single RBC . 
• Normal value of MCHC is 30 % 
• Increases in (Macrocyte anemia ) - 
1. Megaloblastic anemia
• Decreases in ( Microcyte anemia ) 
1. Iron deficiency anemia 
2. Chronic post-haemorrhagic anemia 
3. Thalassemias
Peripheral blood smear (PBS) 
o A well prepared & correctly read smear gives 
vast amount of information of RBC 
morphology. 
o They are stained by polychromatic stain such 
as Wright’s stain 
o Variation in shape, size & Hb concentration & 
the presence of abnormal cells is noted
Management of 
anemia 
Oral Surgeon’s Perspective
Pre operative – 
When patient has to undergo surgery , following 
preoperative measures should be carried out. 
1. Complete blood count with differential 
2. Consultation with physician if lower values of Hb 
are obtained . (<10gm/dL ) 
3. Severity of anemia & its correction should be 
evaluated before surgical intervention. 
4. Possible blood tranfusions , if severe.
5. Drugs that induce Hemolysis should be avoided. 
6. Avoidance of elective surgical treatment in patients 
in “crisis” (sickle cell anemia) 
7. Elimination of oral sources of infection should be 
done. 
8. Administration of antibiotic prophylaxis , if 
necessary 
9. GA should be administered only when Hb is 10 
gm/dL or more . 
10. Short appointments should be given and that too in 
the morning (Sickle cell anemia)
11. Thorough oral examination of teeth , 
periodontium ,soft tissues should be conducted 
to correct the cause of infection .(Aplastic 
anemia ) 
12. Oral rinses with chlorhexidene 0.2% in aquous 
solution will reduce the chances of infection.
Intra operative - 
1. Gingival bleeding , if present , can be controlled 
with antifibrinolytic agents. 
2. Intramuscular inj. and Nerve blocks should be 
avoided because of risk of bleeding. 
3. Intraligamantary anesthesia can be used safely in 
extraction procedures .
4. GA should be used in caution 
Mostly N2 O + O2 is safe to use. 
(Sickle cell anemia & vitamin B12 
deficiency ). 
5. Prevent dehydration using Normal saline I.V. 
during operation. 
Primary closure
Post operative - 
1. Avoidance of drugs that can cause hemolysis in 
patients with hemolytic anemias 
2. Oral hygiene techniques have to be done. 
3. Recommendation of prophylactic antibiotics if poor 
wound healing 
4. Prescribe Acetaminophen , codein , oxycodone as an 
analgesics because salicylates can induce acidosis.
Treatment of Anemia 
Physician’s perspective
Treatment of Anemia 
1. Exclude the possibility of hemoglobinopathy 
2. Correct any identified cause of blood loss 
3. Give oral iron therapy 
4. Correct identified vitamin deficiency with oral folic acid & 
Vit. B12 by injection. 
5. Treat malaria with effective antimalarial drugs( in sickle 
cell anemia & thalessemia ) 
6. If evidence of hemolysis, review the drug treatment, & 
stop the drugs if possible 
7. Check if the patient is on marrow suppressing drugs and 
stop if possible
Polycythemia 
• It is a general term used for 
1. Increased red blood cell count 
2. Increased Hb level. 
Causes- 
1. chronic hypoxia 
2. smoking 
3. fluid loss 
4. hypertension & obesity
• Classified as 
1. Primary polycythemia (Polycythemia vera) 
2. Secondary Polycythemia
Signs & symptoms 
1. Lassitude 
2. Dyspnoea 
3. Dizziness 
4. Headache ,Body 
ache 
5. Itching 
,numbness, 
burning and 
weakness in 
hands, feet. 
Facial plethora 
• Urticaria
Oral manifestations 
Purplish mucosa Edematous gingiva
Treatment of Polycythemia 
1. Oral surgical procedures in patients with 
polycythemia, should be avoided. 
2. Patient should have CBC with differential 
before surgery. 
3. If Hb levels are found increased , 
Physician’s concern should be taken and 
patient should undergo treatment for the 
same.
1. Before performing surgery , threshold levels should 
be obtained .. 
a. Hb = < 16 g/ dL 
b. Hematocrit value = < 47% 
2. Intraoperatively, patients require special 
attention to hemostasis. 
3. If emergency surgery is required venesection is 
performed & blood is replaced with equal amount 
of colloid until a satisfactory hematocrit is reached.
Conclusion 
It is necessary for the oral surgeon to 
have knowledge about RBC related disorders . 
Because , it is mandatory to find the 
etiology of the RBC disorders by letting the 
patient undergo Blood tests or by consulting with 
General physician for medicinal treatments 
before performing any surgical procedure to 
prevent further complications during & after 
surgery .
References 
• Medical Physiology : 11th edition GYTON & 
HALL. 
• Davidson : General Medicine . 
• Burket’s Principle of medicine . 
• Articles- 
1. Dental managemenotf idiopathic aplastic 
anemia: report of a case . 
2. Managing the dental patient with sickle cell 
anemia: a review of the literature 
• Tuft university manual – Rx of Medically 
compromised patients
Thank you

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Rbcs & its clinical implications by Dr. Amit T. Suryawanshi, Oral Surgeon, Pune

  • 1. RBCs & Its Clinical Implications Dr. Amit T. Suryawanshi Oral and Maxillofacial Surgeon Pune, India Contact details : Email ID - amitsuryawanshi999@gmail.com Mobile No - 9405622455
  • 2. Contents 1. Introduction. 2. History. 3. Erythropoiesis. 4. Morphology of RBCs. 5. Properties of RBCs. 6. Functions of RBCs. 7. Lifespan & Fate of RBCs. 8. Hemoglobin & Iron Metabolism. 9. Blood tests & Blood indices . 10. Clinical implications of RBCs. 11. Conclusion.
  • 3. Introduction • Blood is connective tissue of the body in fluid form. • Blood is a specialized body fluid in humans that delivers oxygen and nutrients to the cells and transports carbon dioxide and metabolic waste products away from the cells. Hence it is called as a “ River of Life ” • Blood and Blood related disorders has got very much importance in patients life ,making it mandatory to learn for Oral Surgeons .
  • 4. Composition of Blood Blood Cells 45.7 % Plasma 54.3% Solid 6-7% Water 92-93 % Gases <1 % Organic Substances Inorganic Substances Erythrocytes 45 % Leucocytes 0.6 % Thrombocytes 0.1 %
  • 5. Blood is considered as a fluid of life. Because it carries Oxygen from lungs to all parts of the body and Carbon dioxide from all parts of the body to the lungs. This function of the blood is performed by RBCs. i.e. Red blood Cells which are also known as Erythrocytes . ( Erythros - Red , Cytes – Cells )
  • 6. Introduction of RBCs • RBCs- Red Blood Cells .They are also known as Erythrocytes. • Red colour of RBCs is due to presence of coloring pigment Hemoglobin. • RBCs play important role in transport of Oxygen from lungs to the tissues and carbon dioxide from tissues to lungs.
  • 7. History • The first person to describe red blood cells was the young Dutch biologist Jan Swammerdam, who had used an early microscope in 1658 to study the blood. • In 1959, Dr. Max Perutz was able to reveal the structure of hemoglobin .
  • 8. Normal RBC Count - • Avrg RBC count = 4 - 5.5 millions / mm3 • RBC count in adults male – 5- 5.5 millions /mm3 • RBC count in adults female – 4 – 4.5 millions /mm3 • RBC count in infants - 6-7 million/mm3
  • 9. Erythropoiesis • Haematopoiesis is the process which includes origin, development & maturation of all blood cells. • Whereas the process by which origin , development and maturation of erythrocytes occur is known as Erythropoiesis.
  • 10. Stages & Sites of Erythropoiesis • In Fetal life - Mesoblastic stage • First 2 months of i.u. • From mesenchyme of yolk sac Hepatic stage • From 2-6 months • Liver, spleen & lymphoid organs Myeloid stage • From 7-9 month • Red bone marrow, Liver
  • 11. In post natal life • Upto 5-6 years : Red bone marrow of all bones. • From 6-20 years : Red bone marrow of long bones & all flat bones . • After 20th year : almost red bone marrow of all the long bones is replaced by yellow bone marrow.
  • 12. In post natal life • Only the upper ends of the femur & humerus contain red bone marrow. • Vertebras , ribs, sternum scapula ,iliac bone also produce red cells continuously. • In case of Bone disorders, RBCs are produced in spleen, liver
  • 13. Erythropoiesis - o Blood cells are derived from Pluripotent Hemopoetic Stem Cells (PHSC) o Growth inducers (GI) like interleukin-3 and differentiation inducers (DI) play an important role. o Few PHSC are retained throughout life as they are.
  • 14.
  • 16. Iron dependent stages CELL DIAMETER NUCLEUS CYTOPLASM 15-20 ÎĽm Big Very Scanty & basophilic. No Hb 11-16ÎĽm Smaller Still Scanty & basophilic. No Hb 10-12ÎĽm Smaller & denser Hb starts to appear, cytoplasm polychromatic 8-10ÎĽm Ink spot nucleus Plentiful, eosinophilic cytoplasm. Increase in Hb 8-10ÎĽm Absent Some RNA still present 7.2 ÎĽm Absent Hb is present in large amount .
  • 17. RBC Maturation factors 1. Vitamin B12 (Extrinsic factor) – • Essential for maturation of RBCs • Deficiency of Vitamin B12 causes Pernicious Anemia. So it is also called as antipernicious factor . 2. Intrisic Factor of castle- • Produced in Gastric mucosa • Essential for absorption of Vit.B 12
  • 18. 3. Folic acid – • Essential for synthesis of DNA in RBCs. • Absence of folic acid causes failure of maturation of cells leading to Megaloblastic anemia.
  • 19. Morphology • Size : 7.2 ÎĽ • Shape : Circular , Biconcave • Thickness : 2.2 ÎĽ, 1 ÎĽ • Surface area : 120 ÎĽm2 • Volume : 85-90 ÎĽm3
  • 20. Advantages of bi-concave shape: 1. provides large surface area for absorption and removal of respiratory gases and other substances. 2. Cells can easily squeeze through while passing through capillaries
  • 21. Composition • Water - 62.5% • Hemoglobin - 35% • Others - 2.5% (glucose, lipids, proteins, enzymes, vitamin, ions) others water haemoglobin
  • 22. Properties of RBCs Rouleaux formation Packed cell volume
  • 23. Specific gravity- 1.092 – 1.101 Suspension stability
  • 24. Functions of RBCs - 1. Transport of OXYGEN from lungs to the tissues 2. Transport of CARBON DIOXIDE from tissues to the lung 3. Buffering action in blood
  • 25. 5. Blood group determination. 6. Help to maintain the viscosity of blood.
  • 26. LIFE SPAN AND FATE OF RBC’S • Average life span -- 100-120 days. • Spleen -- Graveyard of red blood cells. • Daily 10% red blood cells, which are senile, get destroyed in normal young healthy adults.
  • 27. Hemoglobin • Hemoglobin is an oxygen carrying pigment of the RBCs. • It is a conjugated protein which consists of protein combined with an iron containing pigment.
  • 28. Functions of Hemoglobin 1. Transport of OXYGEN from lungs to the tissues 2. Transport of CARBON DIOXIDE from tissues to the lung 3. Buffering action in blood
  • 29. HAEMOGLOBIN NORMAL VALUES • Average hemoglobin (Hb) -- 14 to 16 gm%. • At different ages: – At birth : 22 – 25 gm% – After 3 months : 18 – 20 gm% – After1 year : 17 gm% – In adult males : 14 – 17 gm% – In adult females : 12 – 16 gm%
  • 30. Iron Metabolism- • Iron is absorbed for small intestine and transported to blood . • In blood , Iron combines with β globulin to form Transferrin • Iron is stored in large quantities in RE cells and Hepatocytes as Ferritin. • In RBCs , Iron is stored in Fe++ form .
  • 31. Synthesis of hemoglobin A. 2 succinyl-CoA + 2 glycine Pyrole compund B. 4 pyrrole compunds Protoporphyrin IX C. Protoporphyrin IX + Fe++ Heme D. Heme + globin Hemoglobin
  • 32. Factors for Hemoglobin synthesis • Proteins • Iron • Vitamin C, Riboflavin ,Nicotinic acid , Pyridoxine • Copper • Cobalt and nickel
  • 33. Structure of Hemoglobin • It is a conjugated protein • It consists of 1. Heme - An Iron containing pigment. 2. Globin- Protein
  • 34. Heme part- Structure • It consists of 1. Iron – Ferrous form(Fe++) 2. Porphyrin – Pigment part
  • 35. Globin -Structure It consists of 4 polypeptide chains 1. Two α chains 2. Two β chains
  • 36. Types of Normal Hemoglobin • There are 2 types of hemoglobin . 1. Adult Hemoglobin (HbA)- - It contains 2 α and 2 β chains 2. Fetal Hemoglbin (HbF)- -It contains 2 α and 2 Îł chains
  • 37. DESTRUCTION OF HEMOGLOBIN – Occurs in Phagocytes of Spleen. – Globin is broken into amino acid and reused. – Heme – Its tetrapyrrole ring is opened up to form BILIVERDIN. – Its oxidation produces BILIRUBIN
  • 39. Clinical disorders related to RBCs Broadly classified into 1. Anemia – Decrease in RBC count and Hemoglobin level. 2. Polycythemia – Increase in RBC count and Hemoglobin level.
  • 40. ANEMIA • It is defined as a blood cell disorder characterized by decreased oxygen carrying capacity of blood caused by reduction in red blood cell count or hemoglobin content or both.
  • 41. Classification Etiological (Whidby's) classification A. Deficiency anemias - 1. Iron deficiency anemia 2. Megaloblastic anemia 3. Pernicious anemia B. Blood loss anemias - 1. Acute post- hemorrhagic anemia (accidents) 2.Chronic post- hemorrhagic anemia
  • 42. C. Haemolytic anemias ( increased destruction of rbc) 1. Hereditary heamolytic anemias a. Thalassemia b. Sickle cell anemia c. Hereditary spherocytosis d. Glucose 6-phosphate dehydrogenase deficiency (G6PD)
  • 43. • Acquired haemolytic anemias - Due to direct toxic effect ( eg snake venom, drugs , chemicals, etc) - In splenomegaly - In paroxysmal nocturnal haemoglobinuria( PNH) D. APLASTIC ANEMIA (failure of bone marrow) E. Anemia due to chronic diseases (tuberculosis, chronic infections, malignancies )
  • 44. Morphological (Wintrobe’s) classification 1.Normocytic normochromic anemias • Acute post-haemorrhagic anemia • Haemolytic anemias • Aplastic anemia • Anemia in chronic diseses. 2.Macrocytic normochromic anemia • Pernicious anemia (Addison’s anemia)
  • 45. 3. Macrocytic hypochromic anemias- • Protein deficiency anemia • Megaloblastic anemia 2.Microcytic hypochromic anemias • Iron deficiency anemia • Chronic post-haemorrhagic anemia • Thalassemias
  • 46. SIGN & SYMPTOMS Considered in two broad categories: 1. Clinical features common to all anemias. 2. Certain special clinical features for different types of anemias.
  • 47. Common Clinical features • Typically none in early stages • General lassitude Cardio-respiratory - 1. Dyspnoea 2. Tachycardia 3. Murmurs 4. Palpitations 5. Angina Pectoris
  • 48. Oral – 1. Sore mouth 2. Oral ulceration 3. Angular stomatitis 4. Glossitis 5. Burning mouth syndrome Cutaneous - 1. Pallor 2. Brittle Nails 3. Koilonychia
  • 49. Iron deficiency anemia • Most common type of anemia • It Develops due to inadequate availibity for iron for hemoglobin synthesis . • Causes – 1. Loss of blood 2. Decreased intake or poor absorption of iron 3. Increased demand in conditions like growth and pregnancy
  • 50. Clinical features PALLOR KOILONYCHIA ANGULAR CHEILITIS PAPILLARY ATROPHY OF TONGUE
  • 51. Megaloblastic anemia • Megaloblastic anemia is due to deficiency of Maturation factor of RBC i.e. folic acid. • DNA synthesis is impaired so cells are megaloblastic but immature .
  • 52. Oral manifestations 1. Atrophic glossitis 2. Patchy erythema 3. Taste alterations 4. Dysphagia 5. Burning mouth Atrophic glossitis
  • 53. Pernicious anemia • Cause – • It occurs due to atrophy of gastric mucosa because of autoimmune destruction of parietal calls. • Hence , it leads to decreased production of intrinisic factor and poor absorption of vitamin B12 .( Maturation factor )
  • 54. Oral manifestations 1. Atrophic glossitis 2. Patchy erythema 3. Taste alterations 4. Dysphagia 5. Burning mouth Atrophic glossitis
  • 55. SICKLE CELL ANEMIA •It is a congenital anamaly occurs due to abnotmal Hb called Hb–S. •Molecules of Hb-S polymerize into long chains and precipitate inside the cell. •Hence RBCs attain “ Sickle” or “Crescent” shape & become more fragile leading to hemolysis
  • 56. Hemolysis in Sickle cell anemia
  • 57. Oral Manifestations Pallar of mucosa Delayed erruption of teeth
  • 58. Other clinical features - Jaundice Hand & Foot syndrome
  • 59. THALASSEMIA • It is also known as “Cooley’s anemia” . • It is caused by inherited anomalies of hemoglobin • It is of 2 types 1. α thalesemia 2. Î’ thalesemia
  • 60. Clinical features 1. Saddled nose 2. Prominent malar bone 3. Retracted upper lip 4. Bimaxillary protrusion 5. Chipmunk facies
  • 61. Radiographic feature HAIR ON END APPEARENCE
  • 62. APLASTIC ANEMIA • Aplastic anemia is due to failure of red bone marrow . • Red bone marrow is replaced by fatty tissues • Causes – 1. Repeated exposure to X-rays & Gamma rays 2. Due to bacterial toxins , quinine , gold salts
  • 63. Oral manifestations ORAL PETECHIAE GINGIVAL HYPERPLASIA
  • 65. Blood tests The routine blood tests are 1. Complete blood count I. RBC count II. Blood indices – PCV , MCV, MCH, MCHC 2. ESR 3. Blood smear 4. Retuculocyte count
  • 66. ERYTHROCYTE SEDIMENTATION RATE • It is commonly used blood test and is also called as a sed rate or BIERNACKI’s REACTION. • Procedure – 1. Blood is mixed with an anticoagulant and allowed to stand on a vertical tube. 2. RBCs settle down due to gravity leaving supernatant layer of clear plasma above .And the rate at which RBCs settle down is called as ESR . • It is the length of clear supernatant plasma measured in mm at the end of 1 hr.
  • 67. • Determination by 1. Westergreen’s Method 2. Wintrobe’ s Method • Normal Values of ESR – Westergreen's Method • Adult Males = 0 – 15 mm in 1 hr • Adult Females= 0 - 20 mm in 1 hr
  • 68. • Variations of ESR Pathological - • ESR increases in - – All Anemias, except sickle cell anemia . • ESR decreases in - – Polycythemia – Sickle cell anemia
  • 69. BLOOD INDICES • Importance – Help in diagnosis & typing of Anemias. • Different Blood Indices 1. Packed Cell Volume (PCV) 2. Mean Corpuscular Volume (MCV) 3. Mean Corpuscular Hemoglobin (MCH) 4. Mean Corpuscular Hemoglobin Concentration (MCHC)
  • 70. PACKED CELL VOLUME • Also called as HEMATOCRIT value • It is the fraction of blood composed of RBC • Procedure- • Blood is mixed with anticoagulant & filled in wintrobe’s tube upto 100mm mark . • And tube is typically centrifuged at 3000 RPM for 30 minutes OR at 10,000 rpm for 1 minute
  • 71. • NORMAL VALUES OF PCV – Males = 40 to 45%. Females = 38 to 42% • VARIATIONS IN PCV 1. PCV increases in - Polycythemia 2. PCV decreases in -All types of anemia.
  • 73. MEAN CORPUSCULAR VOLUME (MCV) Average volume of a single red blood cell – Normal MCV = 85 - 90 ÎĽm3 . – VARIATIONS IN MCV- • Increases in (Macrocyte anemia ) - 1. Pernicious anemia 2. Megaloblastic anemia
  • 74. • Decreases in (Microcyte anemia ) 1. Iron deficiency anemia 2. Chronic post-haemorrhagic anemia 3. Thalassemias
  • 75. MEAN CORPUSCULAR HEMOGLOBIN (MCH) • Quantity or amount of Hb present in one RBC – Normal value of MCH is 30 pg (27 -32pg) –Increases or remains normal in 1. Pernicious anemia
  • 76. • Decreases in (Hypochromic anemia). 1. Protein deficiency anemia 2. Megaloblastic anemia 3. Iron deficiency anemia 4. Thalassemia
  • 77. MEAN CORPUSCULAR HEMOGLOBIN CONCENTRATION (MCHC) • It is the amont of Hb expressed in relation to volume of single RBC . • Normal value of MCHC is 30 % • Increases in (Macrocyte anemia ) - 1. Megaloblastic anemia
  • 78. • Decreases in ( Microcyte anemia ) 1. Iron deficiency anemia 2. Chronic post-haemorrhagic anemia 3. Thalassemias
  • 79. Peripheral blood smear (PBS) o A well prepared & correctly read smear gives vast amount of information of RBC morphology. o They are stained by polychromatic stain such as Wright’s stain o Variation in shape, size & Hb concentration & the presence of abnormal cells is noted
  • 80. Management of anemia Oral Surgeon’s Perspective
  • 81. Pre operative – When patient has to undergo surgery , following preoperative measures should be carried out. 1. Complete blood count with differential 2. Consultation with physician if lower values of Hb are obtained . (<10gm/dL ) 3. Severity of anemia & its correction should be evaluated before surgical intervention. 4. Possible blood tranfusions , if severe.
  • 82. 5. Drugs that induce Hemolysis should be avoided. 6. Avoidance of elective surgical treatment in patients in “crisis” (sickle cell anemia) 7. Elimination of oral sources of infection should be done. 8. Administration of antibiotic prophylaxis , if necessary 9. GA should be administered only when Hb is 10 gm/dL or more . 10. Short appointments should be given and that too in the morning (Sickle cell anemia)
  • 83. 11. Thorough oral examination of teeth , periodontium ,soft tissues should be conducted to correct the cause of infection .(Aplastic anemia ) 12. Oral rinses with chlorhexidene 0.2% in aquous solution will reduce the chances of infection.
  • 84. Intra operative - 1. Gingival bleeding , if present , can be controlled with antifibrinolytic agents. 2. Intramuscular inj. and Nerve blocks should be avoided because of risk of bleeding. 3. Intraligamantary anesthesia can be used safely in extraction procedures .
  • 85. 4. GA should be used in caution Mostly N2 O + O2 is safe to use. (Sickle cell anemia & vitamin B12 deficiency ). 5. Prevent dehydration using Normal saline I.V. during operation. Primary closure
  • 86. Post operative - 1. Avoidance of drugs that can cause hemolysis in patients with hemolytic anemias 2. Oral hygiene techniques have to be done. 3. Recommendation of prophylactic antibiotics if poor wound healing 4. Prescribe Acetaminophen , codein , oxycodone as an analgesics because salicylates can induce acidosis.
  • 87. Treatment of Anemia Physician’s perspective
  • 88. Treatment of Anemia 1. Exclude the possibility of hemoglobinopathy 2. Correct any identified cause of blood loss 3. Give oral iron therapy 4. Correct identified vitamin deficiency with oral folic acid & Vit. B12 by injection. 5. Treat malaria with effective antimalarial drugs( in sickle cell anemia & thalessemia ) 6. If evidence of hemolysis, review the drug treatment, & stop the drugs if possible 7. Check if the patient is on marrow suppressing drugs and stop if possible
  • 89. Polycythemia • It is a general term used for 1. Increased red blood cell count 2. Increased Hb level. Causes- 1. chronic hypoxia 2. smoking 3. fluid loss 4. hypertension & obesity
  • 90. • Classified as 1. Primary polycythemia (Polycythemia vera) 2. Secondary Polycythemia
  • 91. Signs & symptoms 1. Lassitude 2. Dyspnoea 3. Dizziness 4. Headache ,Body ache 5. Itching ,numbness, burning and weakness in hands, feet. Facial plethora • Urticaria
  • 92. Oral manifestations Purplish mucosa Edematous gingiva
  • 93. Treatment of Polycythemia 1. Oral surgical procedures in patients with polycythemia, should be avoided. 2. Patient should have CBC with differential before surgery. 3. If Hb levels are found increased , Physician’s concern should be taken and patient should undergo treatment for the same.
  • 94. 1. Before performing surgery , threshold levels should be obtained .. a. Hb = < 16 g/ dL b. Hematocrit value = < 47% 2. Intraoperatively, patients require special attention to hemostasis. 3. If emergency surgery is required venesection is performed & blood is replaced with equal amount of colloid until a satisfactory hematocrit is reached.
  • 95. Conclusion It is necessary for the oral surgeon to have knowledge about RBC related disorders . Because , it is mandatory to find the etiology of the RBC disorders by letting the patient undergo Blood tests or by consulting with General physician for medicinal treatments before performing any surgical procedure to prevent further complications during & after surgery .
  • 96. References • Medical Physiology : 11th edition GYTON & HALL. • Davidson : General Medicine . • Burket’s Principle of medicine . • Articles- 1. Dental managemenotf idiopathic aplastic anemia: report of a case . 2. Managing the dental patient with sickle cell anemia: a review of the literature • Tuft university manual – Rx of Medically compromised patients

Editor's Notes

  1. Nutrient function Respiratory function Excretory function Transport of hormones & enzymes Regulation of water balance Regulation of acid- base balance Regulation of body temperature Storage function Defensive function
  2. RBCs being produced in spleen, liver is know as Extramedullary erythropoiesis.
  3. ESR depends on rouleaux formation and Suspension stability PCV – Proportion of blood volume that is occupied by RBC It is volume of RBCs packed at the bottom of hematocrit tube when blood is centrifuged ast 3000rpm for 30 mins
  4. ESR depends on rouleaux formation and Suspension stability Suspension stability – physiological property of rbc to remain suspended in blood ..
  5. Hb in RBCs combines with O2 to form oxyhemoglobin .97% of O2 is transported in this form . Hb in RBCs combines with CO2 to form Carbhemoglobin .30% of CO2 is transported in this form . rbcs contain carbonic anhydrase which forms bicarbonate from CO2 and water .63 % of co2 is transported in this form 3. Hb regulates H ion concentrn and hence maintains acid base balance . 4.
  6. Cross matching ( blood typing )- Is done by mixing serum of recipient and RBCs of donar. To chech agglutination b4 transfusion. Blood group determination – RBCs determine the blood group Bl group A == Antigen A in RBC and anti B in serum Bl group B == Antigen B in RBC and anti A in serum Bl group AB == Antigens AB in RBC and no antibodies in serum Bl group o == no antigen in RBC and antibody A &B in serum Blood transfusion – Antigen of donar and antibody of the recipient are considered. Donar of O has no antigen ..so no agglutination with any blood group. Recpn has no antibdies hence no agglutination with any blood group. Plasma – clotting factors = serum
  7. Hb in RBCs combines with O2 to form oxyhemoglobin .97% of O2 is transported in this form . Hb in RBCs combines with CO2 to form Carbhemoglobin .30% of CO2 is transported in this form . rbcs contain carbonic anhydrase which forms bicarbonate from CO2 and water .63 % of co2 is transported in this form 3. Hb regulates H ion concentrn and hence maintains acid base balance . 4.
  8. bile is essential for absorption of iron . RE cells are monocytes and macrophages of spleen.
  9. Hb synthesis starts in Proerythroblastic stage and Hb appears first in Intermediate normoblati stage . Continued till reticulocyte . Heme is synthesized in mitochondria & Globin is synthesized in Ribosomes ! Globin molecule = 2 alpha and 2 beta chains
  10. Riboflavin -B2 nicotinic acid –B3 pyridoxine-B6
  11. Bile pigments help in absorption of iron from small intestine.
  12. Iron poor blood or tired blood
  13. The surgical significance is, the chronic anemia tend to tolerate surgical and anesthetic procedures more satisfactorily than those with acute anemia.
  14. Murmurs -, a soft-sound and quiet utterance/talking "under breath" so it is hard to understand what the speaker is saying Palpitations - is an abnormality of heartbeat often accompanied by difficulty breathing
  15. Angular cheilitis -is an inflammatory lesion at the labial commissure, or corner of the mouth, 
  16. Hemolysed sickle cells aggregate and block the blood vessels leading to infarction .common in small bones.
  17. Hand & foot syndrome -Hemolysed sickle cells aggregate and block the blood vessels leading to infarction in small bones of hands and feet resulting in varying length in digits ..and jaundicen can also occur in these children …
  18. α thalesemia - occurs in fetal life ..alpha chains are less or absent –- more gamma chains ---precptn of gamma chains ---defectv erythrpsis –hemolysis. infants may be stillborn or die immedtly aftr birth. Β thalesemia –b chains are less or absent –- more alpha chains ---precptn of alpha chains ---defectv erythrpsis –hemolysis.
  19. Saddle nose- It is characterized by a loss of height of the nose, because of the collapse of the bridge.
  20. Lateral ceph showing hair on end appearance .it has the appearance of long, thin vertical striations that look like hair standing on end.
  21.  red or purple spot on the body, caused by a minor hemorrhage (broken capillaryblood vessels).[1]
  22. Mean corpuscular volume
  23. Newborn 0-2 mm in 1 hr 3yrs to puberty – 3-13 mm in 1hr ..
  24. Most important value in diagnosis of anemia
  25. Patient should be refered to physician for medical history , dignosis and treatment . When Hb level falls below 10gm/dL low oxygen tension affects rheological interactions betwn cellular componants of blood ,mainly platelet and endothelium ,decreasing their ability to clot . Hence increased bleeding and poor wound healing occurs. in Hemolytic anemia Decline in Hb can be upto 3-4 g/dL hence blood transfusion should be given prior to surgery. Hemolytic episodes are self limiting .most patients recover immedietly after treatment . Blood transfusion--pRBC approx 300 +/- 25 mL     - hematocrit: 70 +/- 5%; duration - 4hrs , first 5-10 mins .patient shounld be observed and then examined frequently for sighns if fuid overload.     - one unit of pRBCs should increase hemoglobin by approximately 1 gm/dl; Cross matching ( blood typing )- Is done by mixing serum of recipient and RBCs of donar. To chech agglutination b4 transfusion. Blood group determination – RBCs determine the blood group Bl group A == Antigen A in RBC and anti B in serum Bl group B == Antigen B in RBC and anti A in serum Bl group AB == Antigens AB in RBC and no antibodies in serum Bl group o == no antigen in RBC and antibody A &B in serum Blood transfusion – Antigen of donar and antibody of the recipient are considered. Donar of O has no antigen ..so no agglutination with any blood group. Recpn has no antibdies hence no agglutination with any blood group. Plasma – clotting factors = serum
  26. 5. Drugs that induce hemolysis are NSAIDs, (Dapsone malaria,peumonia and leprosy), Sulphasalazine (Rh arthritis ), Phenacetin(analgesics,antipyretic) Prescribe Acetaminophen , codein , oxycodone as an analgesics because salicylates can induce acidosis. 7. Because infection can precipitate aplastic crisis. 9. And if it is < 10g/dL then optimum levels should be obtained using blood transfusion before 10-15 days in sickle cell anemia. 10. It is imperative to avoid episodes of hypoxia because cerebral or myocardial thrombosis can result. Less chances of hypoxia and stress in the morning .
  27. 11.In patients with aplastic anemia , two consequences can occur which should be taken care of 1. Infection 2. Bleeding infection can have a fatal course hence should be treated. 14.
  28. In Aplstic & sickle cell anemia 1 . Antifibrinolytic agents – Aminocaproic acid , tranexamic acid . Tranexamic acid – 20 mg/kg body weight QID, 24 hrs before procedure .and continued for 3-4 days after surgery. Aminocaproic acid-
  29. 4.In sickle cell anemia it is imperative to avoid episodes of hypoxia because cerebral or myocardial thrombosis can result. Sufficient Oxygenation and body temprature should be maintained. Stress management using n2o +o2 & not diazepam.because diazepam decreases respiratory centre. 5. Ringer lactater should be avoided in sickle cell anemia as it can cause lactic acidosis in these patients .
  30. Drugs that induce hemolysis are NSAIDs, (Dapsone malaria,peumonia and leprosy), Sulphasalazine (Rh arthritis ), Phenacetin(analgesics,antipyretic) Penicillins are safe to use .clindamycin , cephalosporin. Also can be used .
  31.  1. Polycythemia vera (PCV), occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow.[3] Often, excess white blood cells and platelets are also produced 2. Secondary polycythemia is caused by increases in the production of erythropoietin due to physiological or pathological cause. It resolvs when underlying cause is treated .. Causes –high altitude ,obstructive lung diseases , obstructive sleep apnea,patients using steroids
  32. Urticaria or Hives are raised, often itchy, red welts on the surface of the skin. Dizziness—impairment of spatial perception or stability.
  33. Oral surgical procedures in patients with polycythemia presents a risk because of possibilities bleeding and thrombosis
  34. Complications – 3. surgical incision into a vein; used to treat hemochromatosis It is a myeloproliferative disorder which leads to raised blood viscosity, increased risk of thrombotic events & bleeding problems