HEMOSTASIS Three phases

1. Primary hemostasis : (within seconds) 2. Secondary hemostasis: (needs several minutes) 3. Fibrin
Vessel wall injury → release of vasoconstrictors Platelet plug is reinforced by production of fibrin clot stabilization &
• extrinsic pathway: initiation of coagulation in vivo fibrinolysis
→ Blood flow is impeded and platelets come into contact
with damaged vessel wall • intrinsic pathway: amplification once coagulation (resolution)
• Adhesion : to subendothelium with vWF has started
• Activation → release of mediators as ADP & TXA2.
• Aggregation → formation of localized plug
 GENERAL TESTS FOR HEMOSTASIS
COAGULATION SYSTEM PLATELETS
1. COAGULATION TIME: (5-10 minutes) Prolonged in all types of COAGULATION disorders. 1. BLEEDING TIME (2-7 minutes)
2. PROTHROMBIN TIME : (12-14 seconds) It measures PLT plug formation
It measures the function of the extrinsic & common pathways. Prolonged in all diseases causing :
Measured by adding Tissue factor + Ca + Pl to the plasma & measuring the time for clot formation ▪ PLT deficiency
If Prolonged we can consider : ▪ PLT dysfunction
▪ ↓↓ Factors : 7 , 10 , 5 , 2 , 1
▪ Liver cell failure.
▪ Vitamin K deficiency :
o Obstructive jaundice ο Use of oral anticoagulants ο Malabsorption synd.

2. CBC: for
- PLT count
- May reveal the cause as :
▪ Megaloblastic anemia
3. ACTIVATED PARTIAL THROMBOPLASTIN TIME APTT (30 - 40 seconds) ▪ Leukemia
It measures the function of the intrinsic & common pathways.
Measured by adding Kaolin+ Ca + Pl to the plasma & measuring the time for clot formation
If Prolonged we can consider diseases of both the intrinsic & common pathways as
▪ ↓↓ Factors : 11 , 9 , 12 , 8 , 10 , 5 , 2 , 1

4. THROMBIN TIME TT (9-11 seconds)

It measures the ability to convert Fibrinogen to Fibrin.
It is measured by to the plasma & measuring the time for clot formation
If Prolonged we can consider diseases affecting FIBRINOGEN:
▪ Fibrinogen Deficiency (afibrinogenemia). 3. PLATELET FUNCTION TESTS
▪ Fibrinogen Dysfunction (dysfibrinogenemia).
▪ Fibrinogen inhibitors: Drugs as (heparin & oral anticoagulants). 4. BM EXAMINATION
▪ DIC.
 HEMOSTATIC DISORDERS
A. PLATELET DEFECT
THROMBOCYTOPENIA THROMBOCYTOPATHY
Decreased PLTs Diseased PLTs
↓ PLT production ↑ PLT destruction Hereditary Aquired
▪ BM failure ▪ Autoimmune: ▪ Glanzmans dis. ▪ Multiple myeloma
▪ BM infiltration 1ry : ITP ▪ Bernard Soulier ▪ Uremia
▪ Megaloblastic anemia 2ry : Lupus syndrome ▪ Thrombocytosis
▪ Myelodysblastic Synd. Leukemia , CLL ▪ VW disease. ▪ Autoimmune : SLE
( more common among older Lymphoma ▪ Antiplatelets : as
patients ) Drugs as Aldomet Aspirin , clopidpgrel
▪ Drugs as : ▪ Acute infections
(Impipenem & Thiazides) ▪ DIC , HUS , TTP
▪ Congenital conditions that cause ↓ ▪ Hypersplenism
PLTs include: ▪ HELLP synd. , Preeclampsia
amegakaryocytic thrombocytopenia, ▪ Heparin induced thrombocytopenia
the thrombocytopenia-absent radius ▪ Post transfusion purpura
syndrome, and Wiskott-Aldrich
PURPURA

syndrome; ▪ Other conditions :

these disorders usually feature - Gestational thrombocytopenia
isolated thrombocytopenia, whereas
patients with Fanconi anemia and ▪ Infections that causes thrombocytopenia :
dyskeratosis congenita typically - Bacterial : Pseudomonas , Klebsiella
include cytopenias in other blood cell - Viral : EBV , CMV , hepatitis viroses
lineages. Mutations in genes (FLI1, - Fungal : H.encapsulatum
MYH9, GATA1, ETV6, among others) - Parasitic : S.mansoni , Plasmodium falciparum (malaria)
that cause thrombocytopenia are
being identified.

B. VESSEL WALL DISEASE (VASCULAR PURPURA)

▪ Idiopathic ▪ Immune (vasculitis) ▪ Infections : ▪ Iatrogenic :
▪ Purpura Simplex - SLE - SBE Salicylate ,
▪ Senile purpura - PAN - meningococcemia Sulfonamides
- HSP Penicillins
▪ Scurvy Corticosteroids
▪ Cushing’s synd.
▪ Congenital (Hereditary)
Osler-Weber-Rendu
Ehler danlos
 A. HEREDITARY
COAGULOPATHY ▪ Hemophilia A ● Hemophilia B ● Parahemophilia
▪ Fibrinogen defect :
- Fibrinogen Deficiency (afibrinogenemia).
- Fibrinogen Dysfunction (dysfibrinogenemia).
B. AQUIRED
- Liver cell failure. - Nephrotic syndrome
- Vitamin K Deficiency :
o Obstructive jaundice ο Use of oral anticoagulants ο Malabsorption synd.
- Fibrinogen inhibitors: Drugs as (heparin & oral anticoagulants).
- DIC.

CLINICAL PICTURE
▪ A personal history of hemostatic challenges (eg, circumcision, trauma, injury during youth sports, tooth extractions, motor vehicle
accidents, prior surgery, and pregnancy and delivery) and a family history of bleeding are critical when evaluating someone for a
possible bleeding disorder.
I. BLEEDING
In PURPURA In Coagulopathy
SITE ▪ Orificial: epistaxis, melena, Hematochezia, Hematernesis, Hemoptysis, Hematuria.
▪ Cutaneous: petechiae , ecchymosis, excessive bleeding from wounds
▪ Mucos membranes: oral, gingival, conjunctival.
▪ Internal: cerebral ,retinal , cavitary ▪ Internal: Hemarthrosis & muscle hematomas
(serous membranes). + Other sites like in purpura
HESS test Positive Hess test Negative Hess test
MECHANISM spontaneous or post-traumatic
CHARACTER ▪ Immediate bleeding ▪ Delayed bleeding

II. +/- Family history or history of previous bleeding requiring blood transfusion
III. ANEMIA: Acute & chronic post-hemorrhagic anemia may occur.
IV. SHOCK: Severe hemorrhage may lead to hypovolemic shock.
V. MANIFESTATIONS OF THE CAUSE.
 THROMBOCYTOPENIA

❖ The risk of clinically relevant spontaneous bleeding (including petechial hemorrhage and
bruising) does not typically increase appreciably until the platelet count falls below
10,000-20,000/mcL, although patients with dysfunctional platelets or local vascular
defects can bleed with higher platelet counts.

❖ Suggested platelet counts to prevent spontaneous bleeding or to provide adequate

hemostasis around the time of invasive procedures are found in the following table.
However, most medical centers develop their own local guidelines to have a consistent
approach to such complex situations.

❖ MDS also presents as cytopenias and can have pancytopenia, but the marrow typically
demonstrates hypercellularity and dysplastic features.
- The presence of macrocytosis, ringed sideroblasts on iron staining of the bone
marrow aspirate, dysplasia of hematopoietic elements,
- or cytogenetic abnormalities (especially monosomy 5 or 7 and trisomy 8) is more
suggestive of MDS.

Bone Marrow Infiltration

❖ Replacement of the normal bone marrow elements by leukemic cells, myeloma,
lymphoma, or other nonhematologic tumors, or by infections (such as mycobacterial
disease or ehrlichiosis) may cause thrombocytopenia; however, abnormalities in other
blood cell lines are usually present.

❖ These entities are easily diagnosed after examining the bone marrow biopsy and aspirate
or determining the infecting organism from an aspirate specimen, and they often lead to
a leukoerythroblastic peripheral blood smear (left-shifted myeloid lineage cells,
nucleated red blood cells, and teardrop-shaped red blood cells).

❖ Treatment of thrombocytopenia is directed at eradication of the underlying infiltrative

disorder, but platelet transfusion may be required if clinically significant bleeding is
present.
 Chemotherapy & Irradiation
❖ Chemotherapeutic agents and irradiation may lead to thrombocytopenia by direct toxicity
to megakaryocytes, hematopoietic progenitor cells, or both.

❖ Until recovery occurs, patients may be supported with transfused platelets if bleeding is
present or the risk of bleeding is high. Initial studies suggest that that platelet growth
factors, such as eltrombopag and romiplostim may help prevent chemotherapy-induced
thrombocytopenia and allow patients to receive their full chemotherapy doses on
schedule.

Chemotherapy → doesn’t differentiate

Target therapy → differentiates

Nutritional Deficiencies
❖ Thrombocytopenia, typically in concert with anemia, may be observed with a deficiency
of folate (that may accompany alcoholism) or vitamin B12 (concomitant neurologic
findings may be manifest). In addition, thrombocytopenia can occur in very severe iron
deficiency, albeit rarely, whereas thrombocytosis is far more common.

❖ Replacing the deficient vitamin or mineral results in improvement in the platelet count.

Cyclic Thrombocytopenia
❖ Cyclic thrombocytopenia is a rare disorder that produces cyclic oscillations of the platelet
count, usually with a periodicity of 3-6 weeks.

❖ The pathophysiologic mechanism responsible for the condition is unclear.

❖ Severe thrombocytopenia and bleeding typically occur at the platelet nadir.

❖ Oral contraceptive medications, androgens, azathioprine, and thrombopoietic growth

factors have been used successfully in the management of cyclic thrombocytopenia

Immune Thrombocytopenic Purpura (ITP)

ESSENTIALS OF DIAGNOSIS
❖ Isolated thrombocytopenia (rule out pseudothrombocytopenia by review of peripheral
smear).

❖ Assess for any new causative medications and HIV, hepatitis B, and hepatitis C,
Helicobacter pylori infections.

❖ ITP is a diagnosis of exclusion.

General Considerations
o ITP is an autoimmune condition in which pathogenic antibodies bind platelets,
accelerating their clearance from the circulation. Many patients with ITP also lack
appropriate compensatory platelet production, thought, at least in part, to reflect the
antibody’s effect on megakaryocytopoiesis and thrombopoiesis.

o Antiplatelet antibody targets include glycoproteins Ilb/IIIa and Ib/IX on the platelet
membrane, although antibodies are demonstrable in only two-thirds of patients. In
addition to production of antiplatelet antibodies, HIV and hepatitis C virus may lead to
thrombocytopenia

o ITP is primary (idiopathic) in most adult patients, although it can be secondary (ie,
associated with autoimmune disease, such as systemic lupus erythematosus [SLE];
lymphoproliferative disease, such as lymphoma; medications; and infections, such as
hepatitis C virus, HIV, and H pylori infections).

Clinical types
Acute ITP Chronic ITP
CHILD-TYPE ADULT-TYPE
AGE Children (2-6 y.) Young adults & middle age (20-40 y.)
SEX Males = Females Females ˃ Males (3:1)
ONSET Acute Gradual
COURSE ▪ 90% recovers completely within 2 ▪ Prolonged for months to years
weeks to 6 months ▪ With remissions &
▪ 10 % → Chronic ITP exacerbations
▪ may be associated with AIHA
(Evan’s syndrome)
Hx of recent Common Rare
infection
C/P ▪ can present with no symptoms, minimal bruising to a serious bleed
(including GI bleed, skin and mucosal hemorrhage or intracranial
hemorrhage), lethargy, fatigue (see previous page)
▪ generally do not occur until the PLT count has fallen below 10,000-
20,000/mcL.
▪ most common cause of isolated
thrombocytopenia
INV. ▪ CBC: thrombocytopenia
Usually ˂ 20000 Moderate ↓ : usually 20000-100000
▪ Blood film: ↓↓ platelets, giant platelets (to rule out platelet clumping)
▪ BT : Prolonged PT , aPTT , TT : Normal
▪ Hepatitis B and C viruses and HIV infections should be excluded by
serologic testing. H.Pylori can sometimes cause isolated ↓ PLTs.
▪ BM Exam.: should be examined in patients with unexplained cytopenias
in two or more lineages, in patients older than 40 years with isolated
thrombocytopenia, or in those who do not respond to primary ITP-specific
therapy.
- A bone marrow biopsy is not necessary in all cases to make an ITP
diagnosis in younger patients.
- Megakaryocyte morphologic abnormalities and hypocellularity or
hypercellularity are not characteristic of ITP.
▪ Antiplatelet Abs : can be detected

HEMATOLOGY – DR.kamal mokbel 7

TTT ❖ Individuals with platelet counts less than 25,000-30,000/ mcL or those with
significant bleeding should be treated; the remainder may be monitored
serially for progression, but that is a patient-specific decision.

A. Emergency Treatment (active bleeding (CNS, GI or GU) or in need of

emergency surgery)
▪ General measures: stop drugs reducing platelet function, control BP
▪ Corticosteroids: prednisone (1 mg/kg) or methylprednisolone (1 g/dx3d)
▪ IVIG 1 g/kg/d x 2 doses, or 2 g/kg over 5 d
▪ Antifibrinolytic: tranexamic acid if refractory bleeding
▪ Platelet transfusion: for life-threatening bleeding
▪ Emergency splenectomy

B. Non-Urgent Treatment (platelet transfusion does not work )

▪ First Line
- The mainstay of initial treatment of new-onset primary ITP is a short
course of corticosteroids with or without intravenous immunoglobulin
(IVIG) or anti-D (WinRho).
→ Response to corticosteroids is generally seen within 3-7 days of
initiating treatment, with responses to IVIG typically seen in 24-36
hours.

- Adding the anti-B cell monoclonal antibody rituximab to corticosteroids

as first-line treatment may improve the initial response rate, but it is
associated with increased toxicity and is not regarded as standard first-
line therapy in most centers.

- Short course of high-dose dexamethasone is also an option.

▪ Second Line
- Although over two-thirds of patients with ITP respond to initial treatment
with oral corticosteroids, most relapse following reduction of the
corticosteroid dose. Patients with a persistent platelet count less than
30,000/mcL or clinically significant bleeding are appropriate candidates for
second-line treatments

- IVIG or anti-D (WinRho) temporarily ↑ PLT counts (duration, up to 3

weeks), although serial IVIG or anti-D treatment (platelet counts less than
30,000/mcL) may allow adult patients to delay or avoid splenectomy.

- Rituximab (anti-CD 20) : Rituximab leads to clinical responses in about

50% of adults with corticosteroid-refractory chronic ITP, which decreases to
about 20% at 5 years.

- Splenectomy has a durable response rate of over 50% and may be

considered for cases of severe thrombocytopenia that fail to respond
durably to initial treatment or are refractory to second-line agents; patients
should receive pneumococcal, Haemophilus influenzae type b, and
meningococcal vaccination at least 2 weeks before therapeutic
splenectomy. If available, laparoscopic splenectomy is preferred.

- Romiplostim, eltrombopag, or avatrombopag can be taken indefinitely

- The Syk inhibitor fostamatinib represents a novel mechanism of action to

treat ITP patients who do not respond to corticosteroids.

HEMATOLOGY – DR.kamal mokbel 8

 THROMBOTIC MICROANGIOPATHIES (TMAs)
Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS)

Definition Thrombotic microangiopathies (TMAs) are potentially life-threatening conditions

caused by small-vessel platelet microthrombi.

TTP HUS
Age
More in adults More in children
Etiology - Congenital
Shiga toxin (E. coli serotype
- Acquired (drugs, malignancy,
O157:H7)
transplant, HIV-associated,
idiopathic)

In idiopathic TTP, autoantibodies against ADAMTS-13

(a disintegrin and metalloproteinase with
thrombospondin type 1 repeat, member 13), also
known as the von Willebrand factor (vWF) cleaving
protease (vWFCP), lead to accumulation of ultra-large
vWF multimers. The ultralarge multimers bridge and
aggregate platelets in the absence of hemostatic
triggers, which in turn leads to the vessel obstruction
and various organ dysfunctions seen in TTP.

Features 1. Thrombocytopenia 1. Severe thrombocytopenia:

2. MAHA purpura, epistaxis, hematuria,
3. Neurological symptoms: hemoptysis, GI bleed
headache, confusion, focal 2. MAHA
defects, seizures 3. Renal failure: abnormal
4. Renal failure urinalysis, oliguria, acute
5. Fever renal failure

▪ in a subset of patients with HUS, the platelet count remains in the

normal range.

▪ Only approximately 25% of patients with TMA manifest all

components of the original pentad of findings (microangiopathic
hemolytic anemia, thrombocytopenia, fever, kidney disease, and
neurologic abnormalities)
Inv.
▪ CBC and blood film: decreased platelets and schistocytes
▪ PT, aPTT, fibrinogen: normal
▪ Markers of hemolysis: ↑unconjugated bilirubin, ↑LDH, ↓haptoglobin
▪ Negative Coombs’ test

▪ In TTP : ↓↓ activity of ADAMTS-13; inhibitor usually identified

▪ Stool C&S (HUS)

▪ KFTs: to follow renal function

HEMATOLOGY – DR.kamal mokbel 9

 Management ▪ Medical emergency
▪ Plasmapheresis : Plasma exchange usually is administered once daily
until the platelet count and LD have returned to normal for at least 2
days, after which the frequency of treatments may be tapered slowly
while the platelet count and LD are monitored for relapse. In cases of
insufficient response to once-daily plasma exchange, twicedaily
treatments can be considered. Fresh frozen plasma (FFP) may be
administered if immediate access to plasma exchange is not
available or in cases of familial TMA.
▪ Platelet transfusion is contraindicated (↑microvascular thrombosis)
▪ Caplacizumab (selected patients of TTP)
▪ TTP mortality ~90% if untreated

Differential Diagnosis of TTP:

o Sepsis
o DIC
o HELLP
o Antiphospholipid Ab syndrome
o Evans syndrome (AIHA + ITP)

Heparin-Induced Thrombocytopenia (HIT)

Pathophysiology Immune mediated

Heparin-induced thrombocytopenia (HIT) is an acquired disorder that affects
approximately 3% of patients exposed to unfractionated heparin and 0.6% of patients exposed
to low-molecular-weight heparin (LMWH). The condition results from formation of IgG
antibodies to heparin-platelet factor 4 (PF4) complexes; the antibody:heparin-PF4 complex
binds to and activates platelets independent of physiologic hemostasis, which leads to
thrombocytopenia and thromboses.

Diagnosis 50% reduction in platelets while on heparin within 5-15 weeks of initiation
(if previously exposed to heparin, HIT can develop in hours)

Risk of Thrombosis ~30% (25% of events are arterial)

Clinical Features Bleeding complications uncommon
▪ Venous thrombosis: DVT, PE, limb gangrene, cerebral sinus thrombosis
▪ Arterial thrombosis: MI, stroke, acute limb ischemia, organ infarct (mesentery, kidney)
▪ Heparin-induced skin necrosis (with LMWH)
▪ Acute platelet activation syndromes: acute inflammatory reactions (e.g. fever/chills, flushing)
▪ Transient global amnesia (rare)

HEMATOLOGY – DR.kamal mokbel 10

Specific Tests
▪ C serotonin release assay (uses donor platelets with 14C serotonin and heparin with patient’s plasma)
14

▪ ELISA for HIT-Ig (more sensitive, less specific than serotonin assay)
▪ Ultrasound of lower limb veins for DVT
Management
1. Clinical suspicion of HIT should prompt discontinuation of heparin (specific tests take days)
2. Because of 90% cross-reactivity, LMWH should not be substituted
3. Alternative agents include :fondaparinux (treatment dose, not prophylaxis)

Von Willebrand Disease (vWD)

▪ It is the most common inherited bleeding disorder.

▪ usually mild in severity
▪ usually autosomal dominant (type 3 is autosomal recessive)
▪ qualitative or quantitative abnormality of vWF
- vWF needed for platelet adhesion and acts as carrier for Factor VIII;
abnormality of vWF can affect both primary and secondary hemostasis

Classification
1. Type 1: mild quantitative defect (↓amount of vWF and proportional ↓in vWF activity) – 75% of cases
2. Type 2: qualitative defect (vWF activity disproportionally lower than quantity) – 20-25% of cases
3. Type 3: severe total quantitative defect (no vWF produced) – rare

Clinical Features
Consider vWD in all women with menorrhagia.
▪ mild
- asymptomatic
- mucosal and cutaneous bleeding, easy bruising, epistaxis, menorrhagia
▪ moderate to severe
- as above but more severe, occasionally soft-tissue hematomas, petechiae (rare),
GI bleeding, Hemarthroses

Investigations
▪ Type 1: Bleeding time and aPTT are normal or ↑, vWF is normal or ↓.
▪ Type 2: Bleeding time is ↑, aPTT is ↑ or normal, vWF is normal or ↓.
▪ Type 3: Bleeding time and aPTT are very high, vWF is absent.
▪ Ristocetin activity = (cofactor for vWF-Plt binding)

Treatment
▪ Desmopressin (DDAVPR) is treatment of choice for type 1 vWD
- causes release of vWF and Factor VIII from endothelial cells
- variable efficacy depending on disease type; tachyphylaxis occurs
- need good response before using with further bleeding
- caution in children due to hyponatremia

HEMATOLOGY – DR.kamal mokbel 11

 ▪ Tranexamic acid to stabilize clot formation
▪ High-purity Factor VIII concentrate containing vWF in select cases and type
▪ Frozen plasma (FP) is not useful

Henoch-Schönlein Purpura (HSP)

▪ also called IgA vasculitis (IgAV) , is the most common form of systemic vasculitis in children.
▪ Ninety percent of cases occur in the pediatric age group.
▪ the underlying cause of HSP (IgAV) remains unknown. Immunologic, genetic, and
environmental factors all seem to play a role.

▪ Purpura on buttocks and legs, arthralgia and fever

▪ Abdominal pain (& may be melena & hematochezia--- to be differentiated from intusseception)

▪ Glomeruli show varying degrees of mesangial hypercellularity

▪ IgA and C3 staining of mesangium

▪ Treatment
- usually benign, self-limiting course, 10% progress to CKD
- if sever : give steroids

Hemophilia A (Factor VIII Deficiency)

Pathophysiology X-linked recessive ↓ Factor VIII = AHG :Antihemophilic globulin)
Clinical Features
Age : Since birth Sex : Male Family Hx: Positive Bleeding : as before
Investigations
- Prolonged CT , Prolonged aPTT, normal INR (PT)
- decreased Factor VIII (<40% of normal)
- vWF usually normal or increased
Treatment
▪ Avoid: antiplatelet drugs , Trauma
▪ Desmopressin (DDAVPR) in mild hemophilia A
▪ Recombinant Factor VIII concentrate for
- prophylaxis (2-3 times a week at home)
- minor but not trivial bleeding (e.g. hemarthroses)
- major potentially life-threatening bleeding (e.g. multiple trauma)
▪ Anti-fibrinolytic agents (e.g. tranexamic acid)

Hemophilia B (Factor IX Deficiency)

▪ aka Christmas disease ● X-linked recessive
▪ Clinical and laboratory features identical to hemophilia A (except decreased Factor IX)
▪ Treatment: recombinant Factor IX concentrate, anti-fibrinolytic agents

HEMATOLOGY – DR.kamal mokbel 12

 Disseminated Intravascular Coagulation (DIC)

Definition
Uncontrolled release of plasmin and thrombin leading to intravascular coagulation
→ And depletion of platelets, coagulation factors and fibrinogen
→ risk of life-threatening hemorrhage

Etiology Occurs as a complication of many other conditions

widespread endothelial damage → extensive inflammatory cytokine release
OMITS
Obstetric complications
Malignancy :Solid tumours & hematologic malignancies (especially APML)
Infection , Intravascular hemolysis (Incompatible blood)
Trauma, burns, crush injuries
Sepsis , Shock (Acute hypoxia , acidosis) , Stasis (hypotension , hypovolemia , pulmonary embolism)
Splenectomy , Liver disease
Snake venum , heat Stroke

Clinical Features DIC is a spectrum which may include thrombosis, bleeding or both.

Signs of Microvascular Thrombosis Signs of Hemorrhagic Diathesis

- Neurological: multifocal infarcts, Convulsions , - Bleeding from any site in the body
confusion ,coma - Neurologic: intracranial bleeding
- Skin: focal ischemia, superficial gangrene
- Skin: petechiae, ecchymosis, oozing from
- Renal: oliguria, azotemia, cortical necrosis puncture sites
- Pulmonary: ARDS - Renal: hematuria
- GIT: acute ulceration - Mucosal: gingival oozing, epistaxis, massive
- RBC: microangiopathic hemolysis bleeding

Investigations
▪ Blood film : fragmented RBCs (schistocytes)
▪ Primary hemostasis: decreased platelets
▪ Secondary hemostasis: prolonged INR (PT),
▪ aPTT, TT, decreased fibrinogen
▪ Fibrinolysis: increased FDPs or D-dimers

Treatment

HEMATOLOGY – DR.kamal mokbel 13