Anemia - Sem

8/8/2019 Anemia - Sem

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ANEMIA


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Definition

According to Cawson Scully, Anemia is

not a disease in itself and may be a

feature of many diseases but the

different type of anemia have many

clinical features in common


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CLASSIFICATION

(Based on the pathogenesis)

Blood loss anemia Iron deficiency anemia; Plummer Vinsonsyndrome

Hemolytic anemia Glucose 6 Phosphate Dehydrogenase; druginduced; immune mediated

Hemoglobinopathies or disorders of hemoglobin Sickle cellanemia; Thalassemia; Cooleys anemia

Hypoproliferative anemia Vitamin B12 deficiency;

Pernicious anemia; Folic acid deficiency; Aplastic anemia


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Causes ofanemia Blood loss Menorrhagia, Any gastrointestinal lesion (e.g. ulcer

or carcinoma), lesion of the urinary tract, trauma

Impaired absorption of hematinics

Increased demands for hematinics especially pregnancy

Poor intake of Hematinics Aplastic anemia and Leukemia

Hemolytic anemias

Miscellaneous mechanisms, including drugs and chronic disease


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Clinical features of anemia

Sometimes none

General lassitude

Cardiorespiratory

DyspnoeaCongestive cardiac

failure

Murmurs

Angina pectoris

Cutaneous

Pallor

Brittle nails

Koilonychia (irondeficiency)

Oral

Sore mouth

Oral ulceration

Angular stomatitis

Glosstitis


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In general anesthetic

The main danger is when a general anesthetic is

given, as it a vital to ensure full oxygenation

Myocardium may be unable to respond to the

demands of anesthesia Whenever possible therefore the cause of the

anemia should be corrected preoperatively, but at

least the hemoglobin level must be raised, if

necessary by transfusion.


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Elective operations under general anesthesia

should not usually be carried out when the

hemoglobin is less than 10 g/dl


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In an emergency, anemia can be corrected

by whole blood transfusion, but this should

only be given to a young and otherwise fit

patient

Transfusion risks include fluid overload, and

viral infections such as hepatitis and HIV


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Packed red cells avoid the risk of fluid

overload and can be given in emergency to

the elderly patient or those with incipient

congestive cardiac failure. A diuretic given at

the same time further reduces the risk of

congestive cardiac failure.


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The patient should be stabilized at least 24

hours preoperatively and it should be noted

that hemoglobin estimation are unreliable for

12 hours post-transfusion. Nitrous oxide is

possibly contraindicated in vitamin B12,

deficiency


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Iron Deficiency Anemia

Women of child bearing age and older are

therefore mainly affected

Excessive menstrual losses or

gastrointestinal blood loss are the main

causes. Very many children are mildly iron

deficient because of the high demands for

growth, especially during adolescence.


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Iron Deficiency Anemia

By contrast, iron deficiency in an adult male

almost invariably indicates blood loss, usually

from the gastrointestinal or genitourinary

tracts. The same holds true for post-

menopausal women

Symptoms ascribed to iron deficiency do not

always respond to iron replacement


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IRONDEFICIENCY ANEMIA


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Laboratory findings during the development of iron deficiency anemia

MCVHb MCHC Serum

ferriti

n

Transferrinsaturation*

Marrow ironstores

Normal N N N N 33% N

Mild iron deficiency anaemiaq

N orq

Nq

>16%


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Treatmentofiron deficiency

The best treatment of iron deficiency is an

iron salt by mouth but the cause of the

deficiency should be found and eliminated

Ferrous gluconate 250 mg/day can be given

if ferrous sulphate is not tolerated

FeSO4200mg 3 times/ day


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Treatmentofiron deficiency

Oral iron may need to be given for 3 months

or more to replenish marrow iron stores

Parenteral iron has no advantages except,

for example, when inflammatory bowel

disease is aggravated by oral iron


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PLUMMERVINSONSYNDROME

Dysphagia; Xerostomia

Depapillated tongue

Koilonychia

Angular stomatitis

Pallor and fatigue dyspnea


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Vitamin B12 Deficiency

Pernicious (Addisonian) anemia is the most

common type of macrocytic anemia and

typically affects women in the middle age or

over particularly of Northern Europeandescent


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Pernicious anemia

It is caused by a specific defect of absorption of

Vitamin B12 not by malnutrition

Autoantibodies against gastric parietal cells and / or

intrinsic factor or both are found and the disease issometimes seen with other autoimmune diseases,

especially hypothyroidism, or less often, diabetes,

mellitus, vitiligo, Addisons disease or

hypothyroidism


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Causes of vitamin B12 deficiency

Poor intake

Poverty

Strict vegetarians


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Malabsorption

Defect in intrinsic factor production Congenital

Autoimmune (pernicious anemia)

Gastrectomy

Illeal diseaseCoeliaa disease

Tropical sprue

Crohns disease

Blind loop syndrome

Resections

Fish tapeworm

Transcobalamin II deficiency


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DrugsColchicine

Neomycin

Nitrous oxide


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Causes of folate deficiency

Poor intake

Poverty

Old age Alcoholism


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Malabsorption

Coeliac disease

Crohns disease Other malabsorption states


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Increased demandsInfancyPregnancyChronic

hemolysisMalignant diseaseExfoliative skin

lesionsChronic dialysis


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Increased demands

Infancy

Pregnancy Chronic hemolysis

Malignant disease

Exfoliative skin lesions

Chronic dialysis


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Oral aspects of the deficiency anemias

sore or burning, but otherwise normal tongue

Atrophic glossitis

Moellers glossitis and other colour changes

Candidosis

Angular stomatitis (cheilitis)

Aphthous stomatitis

PatersonK

elly syndrome (Plummer

Vinson)


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Anemia associated with systemic disease

Chronic inflammation (infections or

connective tissue disease).

Neoplasms including leukaemia. Acute

leukaemia is an important cause of

anaemia and should always be considered

when anaemia is seen in a child.

Liver disease.


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Anemia associated with systemic disease

very rarely : Hypothyroidism

Hypopituitarism Hypoadrenocorticis

Uraemia

HIV infection


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Aplastic Anemia

Bone-marrow aplasia is a rare disease

causing refractory normochromic, normocytic

anemia, leucopenia and thrombocytopenia

Drugs are an important cause but many

cases are idiopathic, though probably viral or

immunologically mediated


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Aplastic Anemia

The prognosis is poor and 50

per cent of patients die within 6

months usually fromhemorrhage or infection


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Causes of aplastic anaemia

Idiopathic

Genetic

Fanconis anaemia

Dyskeratosis congenita

Drugs

Phenylbutazone

Chloramphenicol

Sulphonamides

Gold Penicillamine

Anticonvulsants

Cytotoxic agents

Chemicals

Benzene

Toluene

Heavy metals

Glue-sniffing Viruses

Hepatitis


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Principles ofmanagement

Removal of the cause. Even when this isdecoverable, as in the case of drugs, such aschloramphenicol, marrow damage may still beirreversible

Isolation and antibiotics to control infection Androgenic steroids. (Corticosteroids are of

questionable benefit)

Bone marrow transplantation after intenseimmunosuppression. This in turn may cause graft-

versus-host disease (GVHD) which is often lethal


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Oral manifestations ofAplastic anemia

and managementare somewhat similar to those of leukemia, namely;

Anemia

Hemorrhagic tendencies

Susceptibility to infections Effects of corticosteroid therapy

Hepatitis B and other viral infections

Oral lichenoid lesions, or a Sjogren like syndrome may developif there is graft-versus-host disease if marrow transplantation hasbeen carried out to relieve the anemia. Gingival hyperplasia may

develop if cyclosporin is used.


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Fanconis anemia

a rare autosomal recessive syndrome characterized by:

skeletal defects

hyperpigmentation

pancytopenia &

other congenital anomalies

It is associated with an increased susceptability to

oral or other head and neck carcinomas at an early

age, as is dyskeratosis congenital


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Bone-marrowtransplantation

is increasingly used, particularly in

the treatment of aplastic anemia,

leukemia and some immunedeficiencies


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Bone-marrowtransplantation

Patients are usually prepared for transplantwith cyclophosphamide, with or without totalbody irradiation, such that they will accept

donor bone-marrow with minimal chance orrejection. Recipients are then, aftertransplantation, treated with methotrexate ormore usually cyclosporin for 6 months or

more to prevent or ameliorate graft-versus-host disease


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Genetherapy

Gene therapy clinical trials that could lead to

a cure for children


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Oral symptoms

are the main complaint in patients after bone-

marrow transplantation and consist of

mucositis, dry mouth, sinusitis,parotitis and otherinfections, pain orbleeding

These develop usually within the first month of the transplant and are

exacerbated by chemotherapy and immunosuppressive treatment.

Cyclosporin may induce gingival hyperplasia


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Management problems caninclude

Oral complications of cytotoxic treatment and

radiotherapy, particularly oral herpetic and

fungal infections which are now recognized

as the main causes of death

Immunosuppressive therapy

Graft-vesus-host disease


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Anaemia caused bymarrowinfiltration

Replacement of haemopoietic marrow by abnormal cells

(metastases, leukaemias, myeloma or myelofibrosis) causes

normocytic anaemia and often leucopenia or thrombocytopenia

with a leucoerythroblastic peripheral blood picture. There may be

extramedullary haemopoiesis in other organs

Dental care may be complicated by

susceptibility to infections, haemorrhage

(as in aplastic anaemia) or the

underlying disease


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Hemolytic anemias

Worldwide, malaria is the most common

cause of hemolytic anemia


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Hemolytic anemia mayalsoresultfrom

manyothercauses

Abnormal hemoglobin (the

hemoblobinopathies)

Abnormal structure or function of the

erythrocyte

Damage to erythrocytes (autoimmune or

infective)


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Congenital Hemolytic Anemias

Hemoglobinopathies

sickling disorders

Thalassaemias


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Sickling disorders include

Heterozygoous sickle cell trait (HbAS)

Homozygous sickle cell anaemia or disease

(HbSS)

Heterozygous sickling trait associated with

another hemoglobinopathy


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Disorder Haemoglobin typeOrigins of predominant racial groups

affectedClinical features

Sickle cell trait S A Africa, West Indices, Mediterranean, India Usually asympotomatic

Sickle cell anaemia S-S Africa, West Indices, Mediterranean, India Severe anaemiaJaundice

Impaired growthCrises

InfarctsInfections

Sickle cell HbC disease S-C West Africa, South East Asia Variable anaemia

Sickle cell HbD disease S-D Africa, India, Pakistan Moderately severe anaemia

Sickle cell HbE disease S-E South East Asia Moderately severe anaemia

Sickle cell thalassaemia S-A-F Mediterranean, Africa, West Indices Moderately severe anaemia


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Sickle cell trait (HbAS)

The sickling trait is frequently

asymptomatic, but sickle cell crises can be

caused by reduced oxygen tension (general

anesthesia, high altitudes or unpresurizedaircraft). At times such patients may have

renal complications causing hematuria or

splenic infarcts


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Features of sickle cell anemia

Anemia

Jaundice

Impaired growth

Dactylitis

Skeletal deformities Painful crises

Aplastic crises

Susceptability to infections

Infarcts of CNS, lungs, kidney, spleen

Skin ulcer

Gall stone


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Painful crises

Infection

Dehydration

hypoxia

acidosis or

cold and cause severe bone pain and pyrexia


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Hematological crises

These are often causes by parvovirus

infections and can be of three types, namely :

Hemolytic

Aplastic

Sequestration crises


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main cause of death in sicklecell anemia is infection,

particularly by pneumococci,meningococci and salmonellae,because of an associated

immune defect mainly as aresult of splenic dysfunction.


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Laboratoryinvestigations in sickling

disorders

In sickle cell disease there is anemia and

reticulocytosis; sickled erythrocytes are

sometimes seen in a stained blood film

By contrast, hematological findings are often

normal in sickle cell trait


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Laboratoryinvestigations in sickling

disorders

Sickling may be demonstrated in both sickle cell

anemia and trait, by tests relying on the decreased

solubility of HbS (Sickledex) or by the additionof a reducing agent (such as 10 per cent sodiummetabisulphate or dithionite) to a blood sample

Hemoglobin electrophoresis shows HbS and upto 15

per cent HbF, but no HbA in sickle cell anemia


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Nowadays an increasing number of patientswith sickle cell disease survive into latemiddle age; infections and thromboses are

the main cause of death If the sickle cell test is positive, hemoglobin

electrophoresis is required to establish thediagnosis, but if the hemoglobin is less than

11 g/dl sickle cell anemia is probable


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Sickle cell trait (HbAS)

Patients with the common sickle cell trait

cause few problems in management but if

general anesthesia is necessary full

oxygenation must be maintained throughout.Respiratory infections must be treated

vigorously as they can cause a crisis


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Sickle cell anemia (HbSS)

oral mucosa may be pale or jaundiced and

there may be a susceptability to dental

infection

Hard tissue changes are conspicuous:hypercementosis may develop and there is

bone-marrow hyperplasia with apparent

osteoporosis of the jaw. Skeletal but notdental maturation is delayed


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The lamina dura is distinct and dense and the

permanent teeth may be hypomineralized,

though neither caries nor periodontal disease

is more severe


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The skull is thickened but osteoporotic with a

hair on end pattern to the trabeculae.The dipole are thickened, especially in the

parietal regions giving a tower skull form Lesions suggestive of bone infarction

dense radio-opacities may be seen in the

skull and / or jaws


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Patients with sickle cell anemia must bemanaged with the help of a hemotologist

Pulpal symptoms are common in the absence

of any obvious dental disease Acute infections should be treated

immediately, since they may precipitate asickling crisis

Surgical procedures should have antibioticcover


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Alpha thalassaemias

Beta thalassaemias


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Cooleys anemia most serious type and is characterized by failure to

thrive, increasingly severe anemia,hepatosplenomegaly and skeletal abnormalities

Affected children are susceptible to folate deficienc(as in other chronic hemolytic states) and also to

infection

Discolouration of teeth


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Patients with homozygous beta-

thalassaemia become overloaded with iron

and hemosiderosis damages the heart, liver,

pancreas, skin and sometimes the salivary

glands, causing a sicca syndrome


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major oral changes in thalassaemia are

enlargement of the maxilla caused by bone

marrow expansion (chipmunk facies) Alveolar bone rarefaction produces a chicken

wire appearance on radiography Pneumatization of the sinuses may be delayed

Expansion of the dipole of the skull causes a

hair-on-end appearance that is frequentlyconspicuous on lateral skull radiographs


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Less common oral complications include

painful swelling of the parotids and

xerostomia caused by iron deposition, and a

sore of burning tongue related to the folatedeficiency

difficulties in intubation


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G6PDDEFICIENCY

Icteric sclera skin, soft palate

and floor of the mouth


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G6PDDEFICIENCY

Apart from the problems of anemia it is vital to avoid

oxidant drugs such as the sulphonamids (including

co-trimoxazole) or menadiol (water soluble vitamin K)

which can precipitate hemolysis

Aspirin can be safely used in G6PD deficiency

Metabolic acidosis also causes hemolysis and must

be avoided during general anesthesia


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Acquired hemolytic anemia

Intravascular destruction of erythrocytes can

caused by factors such as gross trauma,

complement mediated lysis, toxins and

malaria These diseases are rare but may

occasionally have dental relevance because

of anemia, corticosteriod treatment orhemorrhagic tendencies


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Ch l l P


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Chronic Renal FailurePatients

Administration of PROCRIT is an increasein the reticulocyte count within 10 days,followed by increases in the red cell count,

hemoglobin, and hematocrit, usually within 2to 6 weeks

PROCRIT, at a dose of100 Units/kg TIW,

is effective in decreasing the transfusionrequirement and increasing the red bloodcell level of anemic


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CONCLUSION

The existence of anemia in surgical patients

has implications that are brief consideration.

Anemia has a number of pathophysiological

consequences of decreased oxygen carryingcapacity of the blood.

CONC S ON


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CONCLUSION

Cardiorespiratory problems

Impaired wound healing

Precipitation of hemolysis


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CONCLUSION


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CONCLUSION

Wound healing:

Relative hypoxia impairs tissue

healing and increases the risk of infection.

CONCLUSION


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CONCLUSION

Precipitation of Hemolysis:

Hypoxia of anesthesia can induced

hemolysis crises in certain hereditary

hemolytic anemias such as sickle celldisease. Preoperative planning with or

without transfusion and careful anesthesia

aim to prevent this

CONCLUSION


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CONCLUSION

Operating on a background of anemia will

result in the patient having fewer reserves to

compensate for operative blood loss. There

might be associated depletion of other bloodcells, including WBC, which increases

susceptibility to infection and platelets which

increases the bleeding tendency.


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CONCLUSION


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CONCLUSION

Oxygen carrying capacity of the transfused

blood is lowered by the presence of high

concentration of2,3 Di Phosho Glycerate

(DPG) and H+ ions which sift the oxygen hemoglobin dissociation curve to the

right.(known as Bohr effect)

CONCLUSION


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CONCLUSION

According to the principles of radiation

oncology, a patient with significant anemia

has been suggested to adversely effect the

efficacy of radiation therapy in patients withhead and neck cancer and therefore patients

being treated with curative intent should have

a hematocrit more than 30%

REFERENCE


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REFERENCE

CAWSON & SCULLY

DAVIDSON

DAVID WRAY JATIN SHAH

OOO/FEB2003/SCOTT

NCCN

ROSSERT www.goggle.com

www.yahoo.com

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Anemia - Sem