Indian J Pediatr DOI 10.1007/s12098-012-0918-2
SYMPOSIUM ON PGIMER MANAGEMENT PROTOCOLS IN EMERGENCY MEDICINE
Approach to a Child with Bleeding in the Emergency Room Deepak Bansal & Sapna Oberoi & R. K. Marwaha & Sunit C. Singhi
Received: 1 June 2012 / Accepted: 26 October 2012 # Dr. K C Chaudhuri Foundation 2012
Abstract A bleeding child is a cause of great concern and often, panic, for parents and pediatricians alike. Causes of bleeding could be trivial or secondary to an underlying bleeding disorder or a potentially serious systemic illness. Based on etiology, they can be categorized into disorders affecting platelets or the coagulation cascade and can be inherited or acquired. A systematic approach with relevant clinical history and examination along with appropriate laboratory investigations aid in reaching the diagnosis promptly. Indication and administration of blood products including fresh frozen plasma, cryoprecipitate, random donor and single donor apheresis platelets is elaborated. Management of hemophilia, Von Willebrand disease, disseminated intravascular coagulation and bleeding in cyanotic congenital heart disease, among other causes is outlined. Role of antifibrinolytic therapy, desmopressin and recombinant factor VIIa is briefly described. The review outlines the approach to a bleeding child in the emergency room. Practical points in history, examination, investigations and management are discussed. Management in resource constraint setting of developing countries is addressed. Keywords DIC . FFP . ITP . RICE . Tranexamic acid . VWD D. Bansal : S. Oberoi : R. K. Marwaha Hematology -Oncology Unit, Department of Pediatrics, Advanced Pediatric Centre, Post Graduate Institute of Medical Education and Research, Chandigarh, India S. C. Singhi (*) Department of Pediatrics and Pediatric Emergency and Intensive Care, Advanced Pediatrics Centre, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India e-mail:
[email protected]
Introduction A child with bleeding is a relatively common hematological emergency encountered by pediatricians in every day practice. Common causes include disorders affecting coagulation or platelets; they could be inherited or acquired. The initial approach, differential diagnosis, investigations and management of children with bleeding are outlined in this review. Bleeding in a neonate and the local causes of bleeding, e.g., trauma, varices, etc. are not dealt here.
Common Causes of Bleeding Broadly, bleeding disorders can be inherited or acquired. Inherited disorders typically present in infancy or early childhood, however, can manifest later in adult life. A contributory family history can often be elicited; pedigree charts with at least three generations should be explored. Common inherited disorders include hemophilia A/B, von Willebrand disease (VWD) and platelet function defects [1]. At presentation, besides bleeding, the children typically appear well. The rare exception is a child with hemodynamic instability resulting from a massive bleed. Common acquired causes of bleeding include immune thrombocytopenic purpura (ITP), liver disease, vitamin K deficiency, disseminated intravascular coagulation (DIC), sepsis, aplastic anemia and leukemia. These children typically present with a relatively short history of bleeding and are comparatively ‘unwell’, except in ITP. A family history of bleeding is lacking. Pallor, lymphadenopathy, organomegaly or other findings of the underlying disease may be evident [1, 2].
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Systemic Bleeding Disorder vs. Local Etiology At the outset, it should be identified whether bleeding is due to a local cause or result of a systemic bleeding disorder. Typically, recurrent bleeding from a single site is likely to have a local etiology (e.g., trauma, tumor, surgery) and concurrent bleeding from multiple sites is usually due to a systemic bleeding disorder. Self-limiting isolated recurrent epistaxis, particularly in young boys is often due to frequent nose picking and detailed investigations are unwarranted. Similarly, it is uncommon for a bleeding disorder to present as recurrent isolated hematuria. Frequent bruises limited to the shin are often physiological, due to susceptibility of the vessels in the region devoid of subcutaneous fat.
The step following the clinical suspicion of a bleeding disorder is to identify whether the bleeding is due to a primary hemostatic defect or a clotting factor deficiency (Table 1) [1, 3]. Bleeding from umbilical stump is typical of factor XIII deficiency, but may occur in deficiencies of fibrinogen or factor X, as well. The common disorders of bleeding are listed in Table 2 [2]. Age and Gender These provide valuable clues towards the diagnosis.
&
&
&
Family History
Type of Bleeding
&
&
in infancy. It is commonly observed in infants who have not received vitamin K prophylaxis at birth, typically in the setting of a home delivery. In older children, it may occur due to underlying liver disease, malabsorption or chronic diarrhea. Acute ITP typically occurs in children 2–6 y of age. Acute onset, widespread mucocutaneous bleeds (petechiae, purpura or epistaxis) in an otherwise well-child, following a viral infection is the typical presentation. Children with severe VWD or platelet function defect usually present with mucocutaneous bleeding in early childhood. Less severe disease may manifest in adolescence with recurrent epistaxis or menorrhagia.
Inherited coagulation disorders typically manifest when a child begins to bear weight in infancy. Infants with Wiskott-Aldrich syndrome, an X-linked recessive immunodeficiency disorder, may present with thrombocytopenic purpura and/or eczema beginning in early infancy. Clinical presentation of Vitamin K deficiency bleeding (VKDB), earlier known as hemorrhagic disease of newborn may range from ecchymosis to an intracranial bleed
X-linked recessive inheritance is observed in factor VIII and IX deficiency. All other coagulation factor deficiencies, e.g., factor V, VII, X, XI or XIII have autosomal recessive inheritance. VWD has an autosomal inheritance. It is classified into three types: Type 1, 2 and 3. Type 1, 2A, 2B and 2 M have autosomal dominant pattern of inheritance, while type 2 N and 3 are inherited recessively. It is important to remember that a negative family history does not rule out the possibility of an inherited disorder. Spontaneous mutation has been observed in up to one third of patients with hemophilia [1].
Medical History A past history of prolonged or difficult to control bleeding during common surgical procedures, viz., dental extraction, circumcision, appendectomy, tonsillectomy or following vaccination should be elicited. A major inherited bleeding disorder is unlikely if patient has had an uneventful surgery in the past. Recent ingestion of drugs that effect platelet function/
Table 1 Clinical manifestations of primary hemostatic defect vs. clotting factor deficiency Clinical characteristic
Primary hemostatic defect (e.g., Quantitative and qualitative platelet defects, VWD or vessel wall defects)
Clotting factor deficiency (e.g., Hemophilia and coagulation disorders)
Site of bleeding Bleeding following minor cuts Petechiae Ecchymosis Hemarthrosis Soft tissue hematomas
Skin, mucous membrane Yesa Present Small, superficial Rare Rare
Soft tissues, muscles, joints Not usualb Absent Large, deeper, palpable Common Characteristic
Bleeding following trauma, surgery
Immediatea
Delayedc
a
Defect in primary phase of hemostasis leads to impaired production of the platelet plug Primary phase of hemostasis is intact c Defect in secondary phase of hemostasis leads to impaired production of fibrin clot b
Indian J Pediatr Table 2 Common platelet and coagulation disorders causing bleeding in children Platelet disorders Thrombocytopenia Decreased platelet survival ● Immune mediated ○ Immune thrombocytopenia ○ Collagen vascular diseases ○ Drug induced ● Disseminated intravascular coagulation ● Hemolytic uremic syndrome ● Thrombotic thrombocytopenic purpura ● Wiskott-Aldrich syndrome Decreased platelet production ● Malignancies (leukemia, neuroblastoma) ● Sepsis: viral and bacterial ● Aplastic anemia Platelet sequestration ● Congestive splenomegaly ● Large hemangiomas (Kasabach-Merritt syndrome) Disorders of platelet function Congenital ● Glanzmann’s thrombasthenia ● Bernard-Soulier syndrome Acquired ● Drug induced: aspirin Coagulation disorders Congenital ● Hemophilia A (Factor VIII), Hemophilia B (Factor IX) and other factor deficiencies ● Von Willebrand disease Acquired ● Disseminated intravascular coagulation ● Vitamin K deficiency ● Liver disease ● Warfarin therapy ● Renal disease ● Cyanotic congenital heart disease
number, including aspirin, valproate, chloramphenicol, or non-steroidal anti-inflammatory drugs, should be explored.
count is normal. Purpura localized to palms and soles may indicate rickettsial infection. Purpuric or ecchymotic lesions that are at unusual site or of unusual shape, particularly in a female child should arouse a suspicion of child abuse. Children with purpura fulminans (thrombotic DIC) may have well-demarcated purple papules with erythematous borders, along with petechiae and ecchymosis. Pallor, jaundice, lymphadenopathy, hepatomegaly or splenomegaly point towards an underlying systemic disorder, including infections, leukemia, infiltrative disorders or liver disease. Presence of splenomegaly typically goes against the diagnosis of ITP or aplastic anemia.
Investigations The initial laboratory evaluation for bleeding disorder includes a complete blood count with review of the peripheral smear, prothrombin time (PT) and activated partial thromboplastin time (aPTT). Complete Blood Count A complete blood count obtained from a well calibrated electronic coulter will promptly identify or refute thrombocytopenia as the cause of bleeding. Uncommonly, spurious thrombocytopenia may result from EDTA induced clumping of platelets; examination of peripheral smear will confirm the presence of platelet clumps. A low hemoglobin may be secondary to the underlying bleed. However, anemia disproportionate to bleeding is ominous and may suggest underlying red cell destruction, bone marrow failure or leukemia. WBC count provides information suggestive of sepsis or leukemia. Peripheral Blood Smear Commonly overlooked, a smear provides valuable information about platelet size, morphology and presence of clumping. Giant sized platelets are commonly observed in ITP or inherited disorders including Bernard-Soulier syndrome. Wiskott-Aldrich syndrome is characterized by microthrombocytopenia. Schistocytes may suggest microangiopathic hemolytic anemia, observed in hemolytic uremic syndrome, thrombotic thrombocytopenic purpura or sepsis.
Examination
Bleeding and Clotting Time
A search for bleeds from head to toe should be performed to look for petechiae, purpura, gingival bleeding, ecchymosis, hematomas, and hemarthrosis. Purpura localized to the lower body (buttocks, legs, ankles), with or without joint swelling suggests a possibility of Henoch-Schönlein purpura (HSP). The rash in HSP results from vasculitis; platelet
Bleeding time is measure of interaction of platelets with the blood vessel wall (primary hemostatic pathway). Clotting time gives a rough estimate of the integrity of intrinsic clotting pathway. Sensitivity and specificity of both is not acceptable, particularly in children. These tests are largely obsolete except in rare situations.
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PT (Prothrombin time) and aPTT (Activated Partial Thromboplastin Time) The sample for coagulation assay must be obtained prior to the administration of a plasma product or any coagulation factor. If a product has been administered in emergency, the lag period required for investigative work-up is dependent on the half-life of the factor under consideration. e.g., for suspected hemophilia A/B, it is reasonable to sample after 10 d. A sample drawn from a clean venepuncture site, without air bubbles or tissue fluid contamination, along with the correct blood to anticoagulant ratio (9:1), is crucial for an accurate result. An incorrectly and hastily collected sample is a common cause for falsely elevated result in the emergency room [4]. The approximate normal values for children are: PT: 10–11 s and aPTT: 26–35 s [1]. Prothrombin time is prolonged due to deficiency of extrinsic pathway (tissue factor, factor VII) or common pathway factors (II, V, X, and fibrinogen). aPTT is prolonged due to deficiency of intrinsic pathway (VIII, IX, XI, or XII), common pathway factors, or in the presence of inhibitors (e.g., lupus anticoagulant and heparin). An approach to a child with bleeding is graphically illustrated in Fig. 1.
Elevated levels are observed in DIC, recent trauma or surgery and venous thromboembolism [4, 6].
Bleeding Child with Normal First Line Investigations In a bleeding child with normal platelet count and PT/aPTT, possible diagnosis include VWD, factor XIII deficiency, platelet function disorder and vascular abnormality. Services of a hematologist may be obtained at this juncture who may order specific tests, including platelet aggregation studies.
Management Initial Stabilization Vitals should be recorded in a bleeding child as the bleeds may be substantial and life threatening. Stabilization of airway, breathing and circulation is the priority in any child in a decompensated state. The severity of bleeds governs the speed/extent of investigations versus administration of treatment. e.g., a coagulation disorder with intracranial bleed will require urgent action vs. a patient with hemarthrosis.
Mixing Studies Specific Management In a child with suspected coagulation disorder, result of an abnormal PT or aPTT should be followed by a mixing study. This aids in differentiating between a clotting factor deficiency and presence of an inhibitor (e.g., lupus anticoagulant or antibodies to factor). Patient's plasma is mixed in a 1:1 ratio with normal pooled plasma, and the abnormal test is repeated. Normalization of clotting test (PT or aPTT) following a 1:1 dilution with normal pooled plasma indicates deficiency of a factor. Majority of inhibitors will not be effectively diluted following the addition of normal pooled plasma. Thus, an abnormal test following dilution indicates the presence of an inhibitor [4, 5].
This is directed towards the underlying etiology.
Undiagnosed Coagulation Disorder In the setting of severe hemorrhage occurring in an undiagnosed coagulation disorder, fresh frozen plasma (FFP) should be administered, as it contains all the clotting factors. The average concentration of factor in FFP is 1 unit/ml; the typical dose is 15 ml/kg.
Hemophilia Coagulation-Factor Assay Acute Hemarthrosis When a factor deficiency is suggested by clinical history or a mixing study, specific coagulation-factor assay is performed to confirm the diagnosis and assess the severity of deficiency. Fibrinogen, Fibrin Degradation Products and D-dimer Normal plasma fibrinogen level is 200–400 g/L. Fibrinogen is decreased in congenital afibrinogenemia, hypfibrinogenemia and in consumption states, e.g., DIC. Fibrin degradation products and D-dimer are indicators of a fibrinolytic state.
In a child presenting with acute hemarthrosis, initial replacement with factor (factor VIII in hemophilia A and factor IX in hemophilia B) should be given to raise the factor level to 40-60 %. A lower goal of 10-20 % may be acceptable if there is resource constraint [7, 8]. If symptoms do not abate, or if the hemarthrosis is severe, a second dose should be given 12–24 h later. Factors are often not an option to a large majority of patients in India due to cost constraints (1 vial of 250 units of factor VIII: ~Rs 2800; 1 vial of 600 units of factor IX: ~Rs 11,000). Thus, FFP or cryoprecipitate are
Indian J Pediatr Petechiae/Purpura/Abnormal bleeding
History and examination to differentiate between primary hemostatic and coagulation disorder (Table 1)
Screening tests • Complete blood count • Peripheral smear: Platelet size/morphology • PT and aPTT
Thrombocytopenia? Yes
No
PT and aPTT
Prolonged PT and aPTT? Yes
• DIC • Sepsis
Abnormal PT and normal aPTT
• Early liver disease • Factor VII deficiency • Warfarin
Abnormal
No
• • • • •
ITP HUS TTP Acute leukemia Aplastic anemia
Normal
• • • • • •
Child abuse HSP Factor XIII deficiency Von Willebrand disease# Platelet function disorder* Vascular disorders e.g., Hereditary hemorrhagic telengiectasia, Ehler- Danlos syndrome
Abnormal PT and aPTT
Normal PT and abnormal aPTT
• Factor VIII, IX, XI deficiency • Moderate to severe VWD
• • • • • •
Liver disease Vitamin K deficiency DIC Deficiency of fact or II, X or V Massive transfusion Excessive heparin
Fig. 1 Step wise approach to a child with bleeding. CBC Complete blood count; PT: Prothrombin time; aPTT Activated partial thromboplastin time; DIC Disseminated intravascular coagulation; ITP Immune thrombocytopenia; HUS Hemolytic uremic syndrome; TTP Thrombotic
thrombocytopenic purpura; HSP Henoch-Schönlein purpura. #Thrombocytopenia is observed in type 2B VWD. *Mild thrombocytopenia can be present in Bernard-Soulier syndrome
often administered as the only feasible, though, inferior alternative. FFP can be administered to patients with hemophilia A as well as B, whereas cryoprecipitate can only be used in hemophilia A, as it does not contain factor IX.
Composition, dose and indications of FFP and cryoprecipitate are illustrated in Table 3. The formula for calculating the replacement dose of factor VIII and IX in patients with haemophilia is outlined below.
Indian J Pediatr Table 3 Composition, dose and indications of plasma derived products in a bleeding child [9–11]
Component
Contents
Indications and Dose
Fresh frozen plasma (1 unit: 150–300 ml)
All coagulation factors: 1 unit of factor/ml of FFP & plasma proteins
● Correction of bleeding due to excess warfarin, vitamin K deficiency, or deficiency of multiple coagulation factors (e.g., DIC, liver disease, massive blood transfusion with coagulopathy) ● For infusion or plasma exchange in TTP-HUS ● Congenital or acquired coagulation factor deficiency; only when virus-inactivated concentrates are unavailable ● Dose: 10–15 ml/kg
Cryoprecipitate (1 unit: 10–20 ml)
1 unit contains: vWF (80 U), factor VIII (80–110 U), factor XIII (40–60 U), fibrinogen (150–250 mg), fibronectin (30–60 mg)
● Factor XIII deficiency ● Congenital or acquired deficiency of fibrinogen ● Hemophilia A and VWD; only when virusinactivated concentrates are unavailable ● Dose: 1–1.5 units/10 kg
Factor VIII One unit of recombinant or plasma derived factor VIII raises the measured factor level by 2 %. Dose of factor VIII ðunitsÞ ¼ Desired rise ðU=dlÞð%Þ weight of the patient ðkgÞ 0:5 Half-life: 10–12 h, Technique: slow IV push at a rate not to exceed 100 units/min Frequency: q 12 hourly, factor is stable at room temperature for 12 h
required dose of recombinant VIII is 200 units (40 units/dL X 10 kg X 0.5). If cost is a limitation, the dose of factor can be reduced to half. One ml of FFP will provide 0.8-1 unit, and 1 unit of cryoprecipitate contains 80–110 units of factor VIII. To raise the factor level by 20 %, the dose of FFP and cryoprecipitate will therefore be 200 ml and 2 units (40 ml), respectively. Cryoprecipitate is preferred over FFP due to lower chances of volume overload. The corresponding dose of recombinant factor IX in a child with hemophilia B, who presents with similar scenario will be 480 units (40 X 10 X 1.2), to raise the factor IX level by 40 U/dl. It is a common practice to round the dose to the nearest vial size, to prevent wastage of the expensive factors.
Factor IX RICE Therapy One unit of plasma derived factor IX raises the measured factor level by 1 %. Dose of factor IX ðunitsÞ ¼ Desired rise ðU=dlÞð%Þ weight of the patient ðkgÞ (*If recombinant factor IX is used, the dose is increased by 1.2-1.5 units, because of the poor recovery of factor IX in some patients) Half-life: 18–24 h. Technique: slow IV push at a rate not to exceed 100 units/min. Frequency: q 24 hourly, factor is stable at room temperature for 12 h Example A 10 kg child with hemophilia A presents with acute hemarthrosis of right knee to the emergency room. What is the dose of Factor VIII or FFP or cryoprecipitate that should be administered? Answer The choice of product is determined by finances and availability. To achieve a factor level of 40 U/dl on day 1, the
Along with the factor replacement, analgesics, Rest, Immobilization, Cold compression and Elevation (RICE) should be advised as well. Rest is done in the position of function (a sling for an upper limb bleed and bed rest or splint for lower limb bleed) for one day, followed by avoidance of weight bearing for next 3–4 d. Application of ice aids by decreasing pain and swelling. It can be performed with crushed ice cubes wrapped in a wet towel or with cold packs, intermittently for a period of 5–15 min over 24–48 h. Ice should not be applied directly to the skin, as prolonged application can lead to skin damage. It is not useful, if applied beyond 48 h [8]. Wrapping the joint gently with bandage or elastic stocking may help in limiting the bleeding and supporting the joint. The application of these adjunctive interventions is not evidence based; however, they are commonly recommended, as they help in reducing pain, swelling and promoting early mobilization [7, 12–14]. In a landmark order, in 2007, the Delhi High Court had directed the Delhi state Government to make factors available to patients with hemophilia [15]. Under the scheme, below-
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poverty-line families are to be supplied factors free of cost. This was followed by a similar ruling in Lucknow, Uttar Pradesh, in response to a public interest litigation [15]. Based on these developments, hospital authorities should be convinced to make factors available in the hospital at least for emergency use.
Intracranial Bleed and Other Hemorrhages In patients with head trauma, a quick neurological examination, followed by CT head should be performed. Factor replacement should not be delayed pending the imaging. Raised intracranial pressure, if any, should be managed with medical measures. Level of the appropriate factor should be immediately raised to 100 % and a level of 50-60 % should ideally be maintained for at least 2 wk. If resources are limited, a dose of 30–50 U/kg of factor VIII or 60–100 U/kg of factor IX may be used for 3–5 d, followed by maintenance with lower doses, depending on the response [7, 14]. In children with known inhibitors to factor VIII or IX, administration of activated prothrombin complex (FEIBA, 1 vial of 500 units costs~Rs 25,000) or activated factor VIIa may be considered, in consultation with a hematologist [1]. Treatment of commonly observed hemorrhages in hemophilia is outlined in Table 4.
Bleeding in Platelet Disorders Platelets are transfused to control bleeding in quantitative or qualitative platelet disorders. Platelets are available as random donor platelets (RDP) or as single donor apheresis platelets (SDAP). The differences are outlined in Table 5. Although both are effective, SDAP is better than RDP in ease of leucoreduction, decreasing risk of septic platelet transfusion reactions, reducing exposures to multiple donors and transfusion frequency, and in treating alloimmunization [17–19]. Indication and dose of platelets is often a dilemma. It is important to remember that transfusion trigger in a thrombocytopenic patient depends not only on the platelet count, but also on its etiology and the clinical condition of the patient. Platelet transfusion is futile and not indicated in majority of patients with ITP as the transfused platelets are quickly destroyed due to circulating antibodies. In stable children with non-immune thrombocytopenia, a transfusion trigger of 10×106/μL is now widely accepted. A few studies have even recommended a lower threshold of 5×106/ μL [20–22]. The common indications for platelet transfusions are listed in Table 6.
Bleeding in Von Willebrand Disease Desmopressin is helpful in controlling mild bleeding in patients with type 1 and 2A VWD, but not in type 2B and
3. It is recommended that every patient with VWD should have therapeutic trial of desmopressin to assess the response at diagnosis or when the patient is not bleeding. In responsive patients, 0.3 μg/kg (maximum 20 μg) of desmopressin diluted in 50 mL saline is administered i.v over 20–30 min. Although i.v route is the most effective, subcutaneous injection or nasal spray (150 μg/puff) can be used as well [23, 24]. The desired concentration of the drug as a nasal spray is not available in India. The commercially available nasal spray (Minirin: 10 μg/puff), indicated for nocturnal enuresis and diabetes insipidus, is too dilute to be used for VWD. Facial flushing, headache, hyponatremia, hypo/hypertension and tachyphylaxis are common adverse effects. VWF concentrate is preferred for major bleeds. High purity VWF concentrate is not available in the market. Hence, intermediate purity factor VIII concentrates containing VWF are used (Immunate: 1 vial0500 units of factor VIII and 290 units of VWF; cost~Rs 3400). Initial dose of 40–60 units/kg followed by 20–40 units/kg q 12–24 h is recommended. Antifibrinolytic agents should be used concomitantly in patients with mucosal bleeds [23, 24].
Disseminated Intravascular Coagulation The cornerstone of treatment of DIC is the aggressive management of the underlying etiology. In some children, this may resolve the DIC, however, in some it may not. Patients with persistent coagulation abnormalities are at risk of hemorrhage or thrombosis and require supportive care, including component replacement and/or anticoagulation. Transfusion of platelets or FFP is not indicated to correct the coagulation abnormalities in a child who is asymptomatic or has minor bleeds (e.g., skin petechiae). It should be reserved for children with active bleeding or prior to invasive procedures, with an aim of maintaining the platelet count above 50×106/μL and fibrinogen concentration above 1 g/L. Clotting factors are replaced by FFP or by cryoprecipitate. The latter is particularly indicated for hypofibrinogenemia (fibrinogen 100 U/dL for 24 h. Subsequently administer 2-3/kg/h for 5–7 d to maintain factor level >50 U/dL. b
To achieve a plasma level of 100 %, administer 80–100 U/kg factor IX concentrate at outset, followed by 20–40 U/kg q 12–24 h to maintain factor IX >30 U/dL for 5–7 d
c
Treat painless hematuria with bed rest and vigorous hydration (3 L/m2 /d) for 48 h. Raise the patient’s factor level if there is pain or persistent gross hematuria. Avoid antifibrinolytics. Rule out other causes if hematuria is persistent. Prednisone (1 mg/kg x 3–5 d) can be used, though the benefit is unclear
d
If bleeding is not controlled by firmly pinching the nose for 15–20 min. and with antifibrinolytic agents
due to DIC. Thus, instead of conventional doses, weight adjusted doses (e.g., 10 U/kg/h) of unfractionated heparin
Table 5 Random donor vs. single donor apheresis platelets [19]
may be administered without the intention of prolonging the aPTT to 1.5-2.5 times the control.
Parameter
Random donor platelets
Single donor apheresis platelets
Method of collection
Prepared from single whole blood unit by plaletet rich plasma or buffy coat centrifugation technique 50-70 ml 5-7×1010/cumm
Collected from a single donor by automated apheresis technique using an apheresis kit 200-300 ml 3-6×1012/cumm (1 bag of SDAP06–8 bags of RDP) Less Difficult Easy Weight 30 kg: one unit More
Volume of one unit Platelet content per unit Donor exposure Donor availability Leucoreduction Dose Cost (Rs)
More Easy Difficult Weight 10 kg: 1 unit/10 kg Less
Indian J Pediatr Table 6 Indications for platelet transfusion in children [17, 18, 21] Indications of prophylactic platelet transfusions ■ Platelet count
