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Ambo University 
Collage Of Medicine & Health Sceince 
Department Of Medicine 
Seminar Presentation on; 
Approach to Bleeding Disorders In 
Pediatrics Patient 
By 
Alemu A, Amdu T & Aregahegn T 
Sep,10/2014
Outline 
 Over view of homeostasis and the blood 
clotting process. 
Over view of some bleeding disorders in 
pediatrics patient 
Approach to a child with bleeding disorder. 
Lab investigations 
Interpretation of lab. tests & clinical
Introduction 
Normal hemostasis 
 Mechanism by which bleeding from an injured vessel is arrested by 
formation of a thrombus. 
• Functions 
 To maintain the blood in fluid state 
 To prevent clots in intact vessels 
 To arrest bleeding in injured vessels 
• Components 
 Blood vessels 
 Platelets 
 Plasma coagulation factors 
 Fibrinolytic system
STAGES OF HEMOSTASIS 
INJURY 
VESSEL WALL+PLATELET 
FORMATION OF PLT PLUG 
ACTIVATION OF PLASMA COAGULATION 
FACTORS 
FORMATION OF STABLE FIBRIN CLOT 
DISSOLUTION OF FIBRIN CLOT BY FIBRINOLYSIS 
PRIMARY 
SECONDARY
Cont’d 
PRIMARY 
 Platelet & vessel wall 
mediated 
 Occurs within seconds of 
injury 
 Forms Platelet plug 
 Prevent blood loss from 
capillary , arterioles and 
venules 
SECONDARY 
 Coagulation factors mediated 
 Takes several minutes for 
completion 
 Forms stable fibrin plug 
 Prevents blood loss from large 
vessels
Cont’d
Cont’d
Cont’d
Cont’d
Bleeding 
 Bleeding or hemorrhaging, is the escape of blood from the circulatory 
system. 
 Bleeding can occur 
– internally, where blood leaks from blood vessels inside the body, or 
– externally, either through a natural opening such as the mouth, nose, 
ear, urethra, vagina or anus, or through a break in the skin. 
 It is then inferred that the bleeding is due to a 
functional impairment of the normal hemostatic 
process.
Cont’d 
This impairment may be due to 
1. A functional deficiency in the procoagulant 
mechanism. This may involve 
a. The platelets 
b. The procoagulant plasma components
Cont’d 
2. A functional excess in anticoagulant 
mechanisms. 
a. Anticoagulant drugs 
b. Natural anticoagulants 
3. A functional excess in the fibrinolytic 
mechanism.
CAUSES OF BLEEDING 
Vessel wall disorders 
Platelet disorders: quantitative or 
functional. 
Coagulation factor: deficiency or inhibitors. 
Combination of these.
VASCULAR DISORDERS 
ACQUIRED CONGENITAL 
•Senile purpura 
•Vascular purpura 
•Henoch schonlein 
purpura 
•Hereditary 
hemorrhagic 
telengiectasia 
•Ehlers danlos 
syndrome
telengiectasia
Senile purpura
PLATELET ABNORMALITIES 
QUALITATIVE QUANTITATIVE 
•THROMBASTHENIA 
•BERNARD-SOULIER 
SYNDROME 
•DRUGS(ASPIRIN,IND-OMATHACIN 
•THROMBOCYTOPENIA 
•THROMBOCYTHEMIA
Petechia 
•
Purpura
DISORDERS OF COAGULATION F 
Hereditary 
 haemophilia A (factor VIII deficiency) 
 haemophilia B (factor IX deficiency) 
 von will brand disease 
 Disorders of fibrinogen- 
Hereditary afibrinogenaemia 
hypofibrinogenaemia 
Dysfibrinogenaemia 
Acquired 
 Disseminated intravascular coagulation(DIC) 
 Liver disease 
 Vit k deficiency 
 Massive transfusion of stored blood 
 Acquired inhibitors of coagulation 
 Heparin or oral anticoagulant therapy 
 Renal disease
Hemophilia A 
Massive hemorrhage in the 
area of right buttock
Hemophilia A 
Gross swelling from acute 
haemarthroses of the 
knee joints
DIC
Classification of Disorders of Hemostasis 
Major Types Disorders Examples 
Acquired Thrombocytop 
enia's 
Autoimmune and alloimmune, drug-induced, 
hypersplenism, hypoplastic (primary, myelosuppressive 
therapy, myelophthisic marrow infiltration), 
disseminated intravascular coagulation (DIC), 
thrombotic thrombocytopenic purpura, hemolytic-uremic 
syndrome 
Liver diseases Cirrhosis, acute hepatic failure, liver transplantation , 
Vitamin K 
deficiency 
Malabsorption syndrome, hemorrhagic disease of the 
newborn, prolonged antibiotic therapy, malnutrition, 
prolonged biliary obstruction 
Hematologic 
disorders 
Acute leukemia's , myelodysplasias, monoclonal 
gammopathies, essential thrombocythemia
Major Types Disorders Examples 
Acquired Acquired 
antibodies 
against 
coagulation 
factors 
Neutralizing antibodies against factors V, VIII, and XIII, 
accelerated clearance of antibody-factor complexes, 
e.g., acquired von Willebrand disease, 
hypoprothrombinemia associated with 
antiphospholipid antibodies 
DIC Acute (sepsis, trauma, obstetric complications) and 
chronic (malignancies, giant hemangiomas, retained 
products of conception) 
Drugs Antiplatelet agents, anticoagulants, antithrombins, and 
thrombolytic, hepatotoxic, and nephrotoxic agents 
Vascular Non-palpable purpura ("senile," solar, and factitious 
purpura), use of corticosteroids, vitamin C deficiency, 
thromboembolic 
Palpable-purpura -Henoch-Schönlein, vasculitis
Aproach to bleeding disorder in Pediatrics
Clinical features 
• Epistaxis-symptoms of platelet disorders & vWD 
• Gingival hemorrhage- platelet disorders & vWD 
• Oral mucous membrane bleeding- severe 
thrombocytopenia 
• Skin hemorrhage ( petechiae and ecchymoses)- 
common manifestations of hemostatic & non-hemostatic 
disorders 
• Hemarthroses- hallmark abnormality in the 
hemophilia’s, severe factor VII deficiency and type 3 
von Willebrand disease
Cont’d 
• Easy bruising- Ehlers-Danlos syndrome 
• Excessive bleeding in response to razor nicks =platelet 
disorders or von Will brand disease. 
• Hemoptysis- haemostatic disorders in URT. 
• Hematemesis- haemostatic disorders in upper GI 
• Hematuria- hemophilia's & haemostatic disorders 
• Rectal bleeding -in normal-hemorrhoids- von 
Willebrand disease and platelet disorders 
• Melena 
• Postpartum hemorrhage -DIC 
• Habitual spontaneous abortions- quantitative or 
qualitative abnormality of fibrinogen.
DIAGNOSIS OF BLEEDING DISORDERS 
• HISTORY 
• CLINICAL EXAMINATION 
• LABORATORY INVESTIGATIONS
History taking 
On Hx 
– Site or sites of bleeding, 
– The severity and duration of hemorrhage, and 
– The age at symptom onset. 
– Spontaneous or after trauma? 
– Does bruising occur spontaneously? 
– Previous personal or family history of similar 
problems? 
– Recent transfusion?
Cont’d 
– A history of anemia and/or previous treatment 
with iron 
– Joint pain, swelling or limitation of movement 
– Bleeding from umbilical stump 
– Previous surgery or significant dental procedures, 
was there any increased bleeding? 
– Delayed or slow healing of superficial injuries 
suggest a hereditary bleeding disorder
Cont’d 
– Menstrual history (in post pubertal females) 
– Medications ( NSAIDs, anticonvulsant , anti TB, 
antihistamin, or herbal medications 
cause thrombocytopenia 
– Nutritional Hx to assess the likelihood of vt k & C 
deficiency and general malnutrition and/or 
malabsorption
Physical Examination 
On PH/E 
• We can look for the presence of 
– Petechiae , ecchymoses , hematomas, 
hemarthroses, or mucous membrane bleeding. 
 defects in platelet/blood vessel wall interaction 
– fixed drug eruption, erythema nodosum, viral 
exanthem and mosquito bites
Cont’d 
• Look for hepatosplenomegaly 
• Do a rectal exam for evidence of GI bleeding 
• Look for physical signs and symptoms of diseases 
related to capillary fragility: 
– Petechiae secondary to coughing, sneezing, Valsalva 
maneuver, blood pressure measurement
Cont’d 
• If there is bleeding is it localized or 
generalized? 
– Localized- single site 
– Generalized 
• Is it platelet type or coagulation type of bleeding? 
• Is it congenital/hereditary or acquired disorder? 
• Symptoms of a longer duration are indicative of a congenital 
disorder such as von Will brand Disease (vWD) or 
coagulation-factor deficiencies
Cont’d 
36
Cont’d 
37
Cont’d 
38
Cont’d 
NB. 
– Petechiae are pathognomonic of platelet-related 
bleeding 
– Deep tissue and intramuscular bleeds should 
prompt the diagnosis of a coagulation factor 
deficiency 
– Patient with a clotting factor VIII or factor IX 
deficiency have deep bleeding into muscles and 
joints with much more extensive ecchymoses and 
hematoma formation.
Aproach to bleeding disorder in Pediatrics
Laboratory Evaluation 
1st line investigation 
– Test for platelets 
• Platelet count 
• Bleeding Time(BT) 
– Test for coagulation factors 
• Prothrombin Time(PT) 
• Activated Partial Thromboplastin Time(aPTT) 
• Thrombin Time(TT) 
• Fibrinogen assay
Lab. exam 
Bleeding Time (BT) 
Significance 
• Assess primary haemostatic defect 
– vessel wall or platelet interaction. 
• Dependent on adequate functioning of 
– Platelets 
– Blood Vessels. 
Range 
• 4-8 min
Cont’d 
Interpretation 
Causes of prolonged BT 
• Thrombocytopenia 
• VWD 
• Platelet function disorder 
• Disorder of blood vessels.
Cont’d 
Prothrombin Time(PT) 
Significance 
• Reflects overall activity of the Extrinsic Pathway. 
• Most sensitive to changes in Factor V,VII,X. 
• Lesser to Factor I & II. 
Principle 
• Platelet poor plasma + Tissue Thromboplastin + Calcium 
• In Presence of F VII Extrinsic pathway is activated & clot 
formed 
Normal Range 
• 10-12 seconds (with human thromboplastin)
Cont’d 
Interpretation 
 Causes of prolonged PT 
1. Deficiency of Factor VII,X,V,II,I 
2. Vit K deficiency 
3. Liver disease 
4. Oral anticoagulants
Cont’d 
Activated Partial Thromboplastin Time (aPTT) 
Significance 
• Reflects efficiency of Intrinsic Pathway. 
• Sensitive to changes in Factor VIII,IX,XI,XII. 
• Also sensitive to heparin & circulating anticoagulants. 
 The test measures the clotting time of plasma after the 
activation of contact . 
 So it indicates the overall efficiency of the Intrinsic 
pathway 
Normal range 
26 to 40 seconds.
Cont’d 
Interpretation 
 Causes of prolonged aPTT 
1. Deficiency of Factor VIII (Haemophilia A). 
2. Deficiency of Factor IX (Haemophilia B). 
3. Heparin therapy. 
4. Circulating anticoagulants. 
5. Liver disease.
Cont’d 
Thrombin Time(TT) 
Significance 
• Asses the final step of coagulation, i.e. conversion of fibrinogen to 
fibrin in presence of thrombin. 
• Bypasses Extrinsic & Intrinsic pathway. 
Principle 
• Thrombin is added to plasma and the clotting time is 
measured. 
• TT is affected by the concentration and reaction 
of fibrinogen and by the presence of inhibitory substances. 
Normal range 
• 15–19 sec, Times of 20 s and longer are definitely abnormal.
Cont’d 
Interpretation 
 Causes of prolonged TT 
1. Disorders of fibrinogen- 
Afibrinogenaemia. 
Hypofibrinogenaemia 
Dysfibrinogenaemia. 
2. Liver disease. 
3. heparin therapy
Cont’d 
2nd line investigations 
Carried out with each of the patterns of 
abnormalities in first line tests 
1. Mixing test. 
2. Factor VII assay. 
3. Liver function test.
Cont’d 
Mixing test 
– If prolong. PT, PTT, or TT 
 Normal plasma + patient's plasma, and the PT or PTT 
is repeated. 
• Correction of PT or PTT => def. of a clotting factor, 
(because a 50% level of individual clotting proteins is 
sufficient to produce normal PT or PTT.)
Cont’d 
• If the clotting time is not corrected or only partially 
corrected, an inhibitor 
– chemical similar to heparin that delays coagulation or 
– an antibody directed against a specific clotting 
factor.(MC- VIII, IX, or XI, may be present) or 
– the phospholipids used in clotting tests is usually 
present
Summary of Interpretation of lab. tests & 
clinical 
• Intrinsic
Interpretation cont’d 
• Extrinsic
Interpretation cont’d 
• Common
Reference 
Nelson textbook of pediatrics ,19th edition 
Current diagnosis and treatment in 
pediatrics,20th edition 
Pediatrics and child health lecture note for 
health sceince students ,jimma university
Aproach to bleeding disorder in Pediatrics

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Aproach to bleeding disorder in Pediatrics

  • 1. Ambo University Collage Of Medicine & Health Sceince Department Of Medicine Seminar Presentation on; Approach to Bleeding Disorders In Pediatrics Patient By Alemu A, Amdu T & Aregahegn T Sep,10/2014
  • 2. Outline  Over view of homeostasis and the blood clotting process. Over view of some bleeding disorders in pediatrics patient Approach to a child with bleeding disorder. Lab investigations Interpretation of lab. tests & clinical
  • 3. Introduction Normal hemostasis  Mechanism by which bleeding from an injured vessel is arrested by formation of a thrombus. • Functions  To maintain the blood in fluid state  To prevent clots in intact vessels  To arrest bleeding in injured vessels • Components  Blood vessels  Platelets  Plasma coagulation factors  Fibrinolytic system
  • 4. STAGES OF HEMOSTASIS INJURY VESSEL WALL+PLATELET FORMATION OF PLT PLUG ACTIVATION OF PLASMA COAGULATION FACTORS FORMATION OF STABLE FIBRIN CLOT DISSOLUTION OF FIBRIN CLOT BY FIBRINOLYSIS PRIMARY SECONDARY
  • 5. Cont’d PRIMARY  Platelet & vessel wall mediated  Occurs within seconds of injury  Forms Platelet plug  Prevent blood loss from capillary , arterioles and venules SECONDARY  Coagulation factors mediated  Takes several minutes for completion  Forms stable fibrin plug  Prevents blood loss from large vessels
  • 10. Bleeding  Bleeding or hemorrhaging, is the escape of blood from the circulatory system.  Bleeding can occur – internally, where blood leaks from blood vessels inside the body, or – externally, either through a natural opening such as the mouth, nose, ear, urethra, vagina or anus, or through a break in the skin.  It is then inferred that the bleeding is due to a functional impairment of the normal hemostatic process.
  • 11. Cont’d This impairment may be due to 1. A functional deficiency in the procoagulant mechanism. This may involve a. The platelets b. The procoagulant plasma components
  • 12. Cont’d 2. A functional excess in anticoagulant mechanisms. a. Anticoagulant drugs b. Natural anticoagulants 3. A functional excess in the fibrinolytic mechanism.
  • 13. CAUSES OF BLEEDING Vessel wall disorders Platelet disorders: quantitative or functional. Coagulation factor: deficiency or inhibitors. Combination of these.
  • 14. VASCULAR DISORDERS ACQUIRED CONGENITAL •Senile purpura •Vascular purpura •Henoch schonlein purpura •Hereditary hemorrhagic telengiectasia •Ehlers danlos syndrome
  • 17. PLATELET ABNORMALITIES QUALITATIVE QUANTITATIVE •THROMBASTHENIA •BERNARD-SOULIER SYNDROME •DRUGS(ASPIRIN,IND-OMATHACIN •THROMBOCYTOPENIA •THROMBOCYTHEMIA
  • 20. DISORDERS OF COAGULATION F Hereditary  haemophilia A (factor VIII deficiency)  haemophilia B (factor IX deficiency)  von will brand disease  Disorders of fibrinogen- Hereditary afibrinogenaemia hypofibrinogenaemia Dysfibrinogenaemia Acquired  Disseminated intravascular coagulation(DIC)  Liver disease  Vit k deficiency  Massive transfusion of stored blood  Acquired inhibitors of coagulation  Heparin or oral anticoagulant therapy  Renal disease
  • 21. Hemophilia A Massive hemorrhage in the area of right buttock
  • 22. Hemophilia A Gross swelling from acute haemarthroses of the knee joints
  • 23. DIC
  • 24. Classification of Disorders of Hemostasis Major Types Disorders Examples Acquired Thrombocytop enia's Autoimmune and alloimmune, drug-induced, hypersplenism, hypoplastic (primary, myelosuppressive therapy, myelophthisic marrow infiltration), disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome Liver diseases Cirrhosis, acute hepatic failure, liver transplantation , Vitamin K deficiency Malabsorption syndrome, hemorrhagic disease of the newborn, prolonged antibiotic therapy, malnutrition, prolonged biliary obstruction Hematologic disorders Acute leukemia's , myelodysplasias, monoclonal gammopathies, essential thrombocythemia
  • 25. Major Types Disorders Examples Acquired Acquired antibodies against coagulation factors Neutralizing antibodies against factors V, VIII, and XIII, accelerated clearance of antibody-factor complexes, e.g., acquired von Willebrand disease, hypoprothrombinemia associated with antiphospholipid antibodies DIC Acute (sepsis, trauma, obstetric complications) and chronic (malignancies, giant hemangiomas, retained products of conception) Drugs Antiplatelet agents, anticoagulants, antithrombins, and thrombolytic, hepatotoxic, and nephrotoxic agents Vascular Non-palpable purpura ("senile," solar, and factitious purpura), use of corticosteroids, vitamin C deficiency, thromboembolic Palpable-purpura -Henoch-Schönlein, vasculitis
  • 27. Clinical features • Epistaxis-symptoms of platelet disorders & vWD • Gingival hemorrhage- platelet disorders & vWD • Oral mucous membrane bleeding- severe thrombocytopenia • Skin hemorrhage ( petechiae and ecchymoses)- common manifestations of hemostatic & non-hemostatic disorders • Hemarthroses- hallmark abnormality in the hemophilia’s, severe factor VII deficiency and type 3 von Willebrand disease
  • 28. Cont’d • Easy bruising- Ehlers-Danlos syndrome • Excessive bleeding in response to razor nicks =platelet disorders or von Will brand disease. • Hemoptysis- haemostatic disorders in URT. • Hematemesis- haemostatic disorders in upper GI • Hematuria- hemophilia's & haemostatic disorders • Rectal bleeding -in normal-hemorrhoids- von Willebrand disease and platelet disorders • Melena • Postpartum hemorrhage -DIC • Habitual spontaneous abortions- quantitative or qualitative abnormality of fibrinogen.
  • 29. DIAGNOSIS OF BLEEDING DISORDERS • HISTORY • CLINICAL EXAMINATION • LABORATORY INVESTIGATIONS
  • 30. History taking On Hx – Site or sites of bleeding, – The severity and duration of hemorrhage, and – The age at symptom onset. – Spontaneous or after trauma? – Does bruising occur spontaneously? – Previous personal or family history of similar problems? – Recent transfusion?
  • 31. Cont’d – A history of anemia and/or previous treatment with iron – Joint pain, swelling or limitation of movement – Bleeding from umbilical stump – Previous surgery or significant dental procedures, was there any increased bleeding? – Delayed or slow healing of superficial injuries suggest a hereditary bleeding disorder
  • 32. Cont’d – Menstrual history (in post pubertal females) – Medications ( NSAIDs, anticonvulsant , anti TB, antihistamin, or herbal medications cause thrombocytopenia – Nutritional Hx to assess the likelihood of vt k & C deficiency and general malnutrition and/or malabsorption
  • 33. Physical Examination On PH/E • We can look for the presence of – Petechiae , ecchymoses , hematomas, hemarthroses, or mucous membrane bleeding.  defects in platelet/blood vessel wall interaction – fixed drug eruption, erythema nodosum, viral exanthem and mosquito bites
  • 34. Cont’d • Look for hepatosplenomegaly • Do a rectal exam for evidence of GI bleeding • Look for physical signs and symptoms of diseases related to capillary fragility: – Petechiae secondary to coughing, sneezing, Valsalva maneuver, blood pressure measurement
  • 35. Cont’d • If there is bleeding is it localized or generalized? – Localized- single site – Generalized • Is it platelet type or coagulation type of bleeding? • Is it congenital/hereditary or acquired disorder? • Symptoms of a longer duration are indicative of a congenital disorder such as von Will brand Disease (vWD) or coagulation-factor deficiencies
  • 39. Cont’d NB. – Petechiae are pathognomonic of platelet-related bleeding – Deep tissue and intramuscular bleeds should prompt the diagnosis of a coagulation factor deficiency – Patient with a clotting factor VIII or factor IX deficiency have deep bleeding into muscles and joints with much more extensive ecchymoses and hematoma formation.
  • 41. Laboratory Evaluation 1st line investigation – Test for platelets • Platelet count • Bleeding Time(BT) – Test for coagulation factors • Prothrombin Time(PT) • Activated Partial Thromboplastin Time(aPTT) • Thrombin Time(TT) • Fibrinogen assay
  • 42. Lab. exam Bleeding Time (BT) Significance • Assess primary haemostatic defect – vessel wall or platelet interaction. • Dependent on adequate functioning of – Platelets – Blood Vessels. Range • 4-8 min
  • 43. Cont’d Interpretation Causes of prolonged BT • Thrombocytopenia • VWD • Platelet function disorder • Disorder of blood vessels.
  • 44. Cont’d Prothrombin Time(PT) Significance • Reflects overall activity of the Extrinsic Pathway. • Most sensitive to changes in Factor V,VII,X. • Lesser to Factor I & II. Principle • Platelet poor plasma + Tissue Thromboplastin + Calcium • In Presence of F VII Extrinsic pathway is activated & clot formed Normal Range • 10-12 seconds (with human thromboplastin)
  • 45. Cont’d Interpretation  Causes of prolonged PT 1. Deficiency of Factor VII,X,V,II,I 2. Vit K deficiency 3. Liver disease 4. Oral anticoagulants
  • 46. Cont’d Activated Partial Thromboplastin Time (aPTT) Significance • Reflects efficiency of Intrinsic Pathway. • Sensitive to changes in Factor VIII,IX,XI,XII. • Also sensitive to heparin & circulating anticoagulants.  The test measures the clotting time of plasma after the activation of contact .  So it indicates the overall efficiency of the Intrinsic pathway Normal range 26 to 40 seconds.
  • 47. Cont’d Interpretation  Causes of prolonged aPTT 1. Deficiency of Factor VIII (Haemophilia A). 2. Deficiency of Factor IX (Haemophilia B). 3. Heparin therapy. 4. Circulating anticoagulants. 5. Liver disease.
  • 48. Cont’d Thrombin Time(TT) Significance • Asses the final step of coagulation, i.e. conversion of fibrinogen to fibrin in presence of thrombin. • Bypasses Extrinsic & Intrinsic pathway. Principle • Thrombin is added to plasma and the clotting time is measured. • TT is affected by the concentration and reaction of fibrinogen and by the presence of inhibitory substances. Normal range • 15–19 sec, Times of 20 s and longer are definitely abnormal.
  • 49. Cont’d Interpretation  Causes of prolonged TT 1. Disorders of fibrinogen- Afibrinogenaemia. Hypofibrinogenaemia Dysfibrinogenaemia. 2. Liver disease. 3. heparin therapy
  • 50. Cont’d 2nd line investigations Carried out with each of the patterns of abnormalities in first line tests 1. Mixing test. 2. Factor VII assay. 3. Liver function test.
  • 51. Cont’d Mixing test – If prolong. PT, PTT, or TT  Normal plasma + patient's plasma, and the PT or PTT is repeated. • Correction of PT or PTT => def. of a clotting factor, (because a 50% level of individual clotting proteins is sufficient to produce normal PT or PTT.)
  • 52. Cont’d • If the clotting time is not corrected or only partially corrected, an inhibitor – chemical similar to heparin that delays coagulation or – an antibody directed against a specific clotting factor.(MC- VIII, IX, or XI, may be present) or – the phospholipids used in clotting tests is usually present
  • 53. Summary of Interpretation of lab. tests & clinical • Intrinsic
  • 56. Reference Nelson textbook of pediatrics ,19th edition Current diagnosis and treatment in pediatrics,20th edition Pediatrics and child health lecture note for health sceince students ,jimma university