case study in hematology and coagulation

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Case Studies in Hematology and Coagulation

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This compendium of 200 case studies is the result of a unique collaboration of leading hematologists, hematopathologists, and oncologists. It serves as both a case-based guide to the diagnosis and management of patients suffering from hematologic conditions and a valuable teaching tool.

The editors have compiled an invaluable collection of cases covering common and rare entities—from anemias and acute leukemias to plasma cell, platelet and coagulation disorders. Cases are presented in an easy-to-follow format, grouped by related conditions. The final two sections present 27 self-study challenge cases that include answers (with images) provided by the authors of each case.

A broad range of topics in hematology and coagulation are covered in this CaseSet, including:

• Myeloproliferative Disorders
• Myelodysplastic Syndromes
• Lymphoproliferative Disorders
• Lymphomas and Their Mimicks
• Plasma Cell Disorders
• Platelet Disorders
• Hematologic Infectious Diseases
• Other Hematologic Disorders
• Bleeding Disorders
• Thrombophilias
• Other Hemostasis Disorders

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Case Studies in Hematology and Coagulation, G.L. Gulati, J. Filicko-O'Hara, J.R. Krause (Eds.). American Society of Clinical Pathologists Press (2012), 400, $175

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Case Studies in Hematology and Coagulation Hardcover – January 1, 2012

• Print length 527 pages
• Language English
• Publisher American Society for Clinical Pathology
• Publication date January 1, 2012
• Dimensions 7.36 x 1.38 x 10.43 inches
• ISBN-10 089189585X
• ISBN-13 978-0891895855
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• Publisher ‏ : ‎ American Society for Clinical Pathology; 1st edition (January 1, 2012)
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Case studies in hematology and coagulation - hardcover, gulati gene ed.

• About this edition

This second edition compendium of 250 case studies (adding more than 170 pages over the first edition) is the result of a unique collaboration of 227 leading hematologists, hematopathologists, and oncologists. It will serve as both a case-based guide to the diagnosis and management of patients suffering from hematologic conditions and a valuable teaching tool. The editors have compiled an invaluable collection of cases covering common and rare entities-from anemias through lymphoma to plasma cell, platelet and coagulation disorders. Cases are presented in an easy-to-follow format, grouped by related conditions. The final two sections present 40 self-study challenge cases that provide basic history presentation information and initial workup data with images. The data is followed by questions about differential diagnosis, additional workup, most likely diagnosis, course of management and salient features of the case. Corresponding answers/discussions are provided by the authors of each case. Item Details: A broad range of topics in both hematology and coagulation are covered in this ASCP CaseSet, including: Anemias Leukemias Myeloproliferative Disorders Myelodysplastic Syndromes Lymphoproliferative Disorders Lymphomas and Their Mimics Plasma Cell Disorders Platelet Disorders Hematologic Infectious Diseases Other Hematologic Disorders Bleeding Disorders Thrombophilias Other Hemostasis Disorders

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• Publisher American Society of Clinical Oncology
• Publication date 2019
• ISBN 10  0891896732
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• Binding Hardcover
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• Number of pages 700

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Overview of the coagulation system

Sanjeev palta.

Department of Anaesthesiology and Intensive Care, Government Medical College and Hospital, Chandigarh, India

Richa Saroa

Anshu palta.

1 Department of Pathology, Government Medical College and Hospital, Chandigarh, India

Coagulation is a dynamic process and the understanding of the blood coagulation system has evolved over the recent years in anaesthetic practice. Although the traditional classification of the coagulation system into extrinsic and intrinsic pathway is still valid, the newer insights into coagulation provide more authentic description of the same. Normal coagulation pathway represents a balance between the pro coagulant pathway that is responsible for clot formation and the mechanisms that inhibit the same beyond the injury site. Imbalance of the coagulation system may occur in the perioperative period or during critical illness, which may be secondary to numerous factors leading to a tendency of either thrombosis or bleeding. A systematic search of literature on PubMed with MeSH terms ‘coagulation system, haemostasis and anaesthesia revealed twenty eight related clinical trials and review articles in last 10 years. Since the balance of the coagulation system may tilt towards bleeding and thrombosis in many situations, it is mandatory for the clinicians to understand physiologic basis of haemostasis in order to diagnose and manage the abnormalities of the coagulation process and to interpret the diagnostic tests done for the same.

INTRODUCTION

The concept of blood coagulation dates back to 1960's when Davie, Ratnoff and Macfarlane described the “waterfall” and “cascade” theories outlining the fundamental principle of cascade of proenzymes leading to activation of downstream enzymes.[ 1 ] Haemostasis, defined as arrest of bleeding, comes from Greek, haeme meaning blood and stasis meaning to stop.[ 2 ] This thrombohaemmorhagic balance is maintained in the body by complicated interactions between coagulation and the fibrinolytic system as well as platelets and vessel wall.

Usually, the coagulation process is under the inhibitory control of several inhibitors that limit the clot formation, thus avoiding the thrombus propagation. This delicate balance is interrupted whenever the procoagulant activity of the coagulation factors is increased, or the activity of naturally occurring inhibitors is decreased.[ 3 ] Some of the thrombogenic and antithrombogenic components are listed in Table 1 .

Thrombogenic and antithrombogenic components in the body

It is important for a perioperative physician to understand the intricacies of two systems (more so in a preexisting haematological disorder) that go side by side in maintaining the circulating blood in a fluidic state.

Pathological situations requiring surgery or anaesthesia or any other invasive procedure trigger the haemostatic system. This balance is also disturbed by trauma, cytokines or infectious agents. Thus, the perioperative period is at high risk for both prohaemorrhagic and prothrombotic abnormalities. Hypoxia, hypothermia, metabolic acidosis and extracorporeal circulation may also further aggravate the situation.[ 4 ]

Coagulopathy, may also be encountered by the intensivist due to physiological disturbances, disturbances in the primary haemostasis, abnormalities of blood, plasma or due to disseminated intravascular coagulation (DIC).[ 5 ]

This review aims to simplify the understanding of the coagulation system as a whole as well as discuss various abnormalities of the same, which may have an impact in the perioperative period and ICU. They can be classified as those that affect the primary haemostasis, the coagulation pathways and the fibrinolytic system.

PRIMARY HAEMOSTASIS

Primary haemostasis results from complex interactions between platelets, vessel wall and adhesive proteins leading to the formation of initial ‘platelet plug’. The endothelial cells lining the vascular wall exhibit the antithrombotic properties due to multiple factors viz: negatively charged heparin-like glycosaaminoglycans, neutral phospholipids, synthesis and secretion of platelet inhibitors, coagulation inhibitors and fibrinolysis activators. In contrast, subendothelial layer is highly thrombogenic and contains collagen, Von Willebrand factor (vWF) and other proteins like laminin, thrombospondin and vitronectin that are involved in platelet adhesion. Any vascular insult results in arteriolar vasospasm, mediated by reflex neurogenic mechanisms and release of local mediators like endothelin and platelet-derived thromboxane A2 (TxA2).[ 6 , 7 , 8 ]

Platelets are disc shaped, anucleate cellular fragments derived from megakaryocytes. They have a pivotal role in haemostasis by forming the initial haemostatic plug that provides a surface for the assembly of activated coagulation factors leading to the formation of fibrin stabilized platelet aggregates and subsequent clot retraction. Platelets have two types of granules:

• α granules-contain P-selectin, fibrinogen, fibronectin, factor V, factor VIII, platelet factor IV, platelet-derived growth factor and tumour growth factor-α (TGF-α)[ 9 ]
• δ granules or Dense granules-contain adenosine triphosphate (ATP), adenosine diphosphate (ADP), calcium (Ca), serotonin, histamine and epinephrine.[ 9 ]

Normally platelets do not adhere to intact vascular endothelium. Subsequent to the vascular injury, platelets adhere to collagen and vWF in the subendothelial tissue and undergo a morphological change by assuming irregular surface, forming numerous pseudopods thus drastically increasing their surface area.[ 10 ] The formation of the platelet plug involves a series of steps:

Platelet adhesion

After vascular injury vWf acts as a bridge between endothelial collagen and platelet surface receptors GpIb and promotes platelet adhesion.[ 9 ] The platelet glycoprotein complex I (GP-Ib) is the principal receptor for vWF.

Platelet secretion

After adhesion, degranulation from both types of granules takes place with the release of various factors. Release of calcium occurs here. Calcium binds to the phospholipids that appear secondary to the platelet activation and provides a surface for assembly of various coagulation factors.

Platelet aggregation

Thromboxane A2 produced by activated platelets provide stimulus for further platelet aggregation. TxA2 along with ADP enlarge this platelet aggregate leading to the formation of the platelet plug, which seals off vascular injury temporarily. ADP binding also causes a conformational change in GpIIb/IIIa receptors presents on the platelet surface causing deposition of fibrinogen. Thrombin generation also catalyses the conversion of this fibrinogen to fibrin which adds to the stability of the platelet plug and is now known as secondary haemostasis.[ 9 ]

Prostacyclin inhibits platelet aggregation (platelet anti aggregating effect) and the balance between TxA2 and prostacyclin leads to localized platelet aggregation thus preventing extension of the clot thereby maintaining the vessel lumen patency.[ 6 , 11 ]

COAGULATION DISORDERS INVOLVING PRIMARY HEMOSTASIS

Defects of primary haemostasis may be due to abnormalities of the vessel wall or qualitative/quantitative defects of platelets that may cause bleeding in varying severity.

Thrombocytopenia may be observed secondary to numerous causes listed in Table 2 . The inherited platelet disorders are uncommon and if present, are, usually, diagnosed in childhood and these patients need to be given platelet concentrates before and after surgery.

Disorders of primary haemostasis

High platelet counts may occur in the perioperative period after major bleeding, splenectomy, major reconstruction surgery or may just represent the inflammatory response.

Certain inherited bleeding disorders with platelet glycoprotein deficiency as seen in Glanzmann thromboasthenia (deficiency of IIb/IIIa) or Bernard-Soulier syndrome (deficiency of platelet glycoprotein Ib) may be seen secondary to viral infections and are associated with immediate failure of haemostasis.[ 12 , 13 ]

Massive blood transfusion entails the replacement of one whole blood volume within a period of 24 h with stored blood that is deficient in both functional platelets and coagulation factors. Transfused red cells dilute patient's native coagulation reserve also. All these effects are exacerbated by infusion of fluids especially colloids. Hence, massive blood transfusion may lead to dilutional coagulopathy.

COAGULATION PATHWAYS

The coagulation proteins are the core components of the coagulation system that lead to a complex interplay of reactions resulting in the conversion of soluble fibrinogen to insoluble fibrin strands.

CLOTTING FACTORS (COAGULATION PROTEINS)

Majority of clotting factors are precursors of proteolytic enzymes known as zymogens that circulate in an inactive form. The activation of each zymogen is depicted by suffixing letter “a” to the Roman numeral identifying that particular zymogen. Most of the procoagulants and anticoagulants are produced by liver except factor III, IV and VIII. These proteins undergo a post translational modification (vitamin K dependent ϒ carboxylation of glutamic acid residues) which enables them to bind calcium and other divalent cations and participate in clotting cascade.[ 14 ] Deficiency of vitamin K or administration of vitamin K antagonists (warfarin) lead to anticoagulation.

Nomenclature of coagulation proteins is rather complex [ Table 3 ]. The first 4 of the 12 originally identified factors are referred to by their common names, i.e., fibrinogen, prothrombin, tissue factor (TF), and calcium and are not assigned any Roman numerals. FVI no longer exists. The more recently discovered clotting factors (e.g. prekallikrein and high-molecular-weight kininogen) have not been assigned Roman numerals. Some factors have more than one name. Factors V and VIII are also referred to as the labile factors because their coagulant activity is not durable in stored blood.

Nomenclature of the coagulation proteins/clotting factors

Prothrombin is a plasma protein formed by liver (MW 68700). It is an unstable protein, splitting into smaller proteins one of which is thrombin (MW33700). Thrombin generated from prothrombin also has pro-inflammatory effects which are exerted by the activation of protease activating receptors present on monocytes, lymphocytes, endothelium and dendritic cells.[ 15 ]

Von Willebrand factor is a glycoprotein present in blood plasma and produced constitutively as ultra-large vWf in endothelium, megakaryocytes, and subendothelial connective tissue. It mediates platelet adhesion to subendothelial surface. It also acts as a carrier protein for coagulant activity of Factor VIII and is referred there as VIII: C.[ 16 , 17 ]

Fibrinogen is an essential coagulation protein produced by liver (MW340 kDa) and is the precursor of fibrin that ultimately defines the strength of clot.[ 18 , 19 ]

Factor III or TF is a membrane bound procoagulant glycoprotein (MW47-kDa) present in the subendothelial tissue and fibroblasts and is not exposed to blood until disruption of the vessel wall.[ 14 ] It is the primary initiator of coagulation in vivo . TF is localised predominantly to the tunica media and tunica adventitia of blood vessels and a smaller quantity as circulating TF on monocytes. Tissue factor may be activated by physical injury (activation of Vessel wall TF), by direct vascular injury or functional injury (activation of circulating TF), by hypoxia, sepsis, malignancy, inflammation, etc.[ 20 , 21 ]

Clotting factors can also be classified into three groups [ Table 4 ].

Classification of coagulation factors

• Fibrinogen Family
• Vitamin K dependent proteins
• Contact family.

Hypoxia up regulates the expression of P selectin present in the α granules of platelets on the endothelium leading to recruitment of monocytes containing TF, thus initiating coagulation.[ 22 , 23 ] With the exposure of TF to factor VII/VIIIa in the blood, it allows for the formation of TF-VIIIa complex and thus initiate the coagulation cascade.

NATURALLY OCCURRING ANTICOAGULANTS IN THE BODY

The anticoagulant system exerts a regulatory role over the procoagulant activity in blood thus localizing the thrombus formation.[ 13 ] The main anticoagulant mechanisms naturally present in the body include the following:

Antithrombin

Antithrombin (AT), previously known as AT III is the main inhibitor of thrombin. It is a serine protease inhibitor, which binds and inactivates thrombin, factor IXa, Xa, XIa and XIIa. The enzymatic activity of AT is enhanced in the presence of heparin. However, the plasma concentration of heparin is low and does not contribute significantly to the in vivo activation of AT. AT is activated by binding of heparin sulphate present on endothelial cell surface. AT binds coagulation factors in a ratio of 1:1 and this complex is removed by reticuloendothelial cells. Other thrombin inhibitors are heparin cofactor II, α2 macroglobulin and α1-antitrypsin.[ 24 , 25 ]

Tissue factor plasminogen inhibitor

It is a polypeptide produced by endothelial cells. It acts as a natural inhibitor of the extrinsic pathway by inhibiting TF-VIIa complex.[ 25 , 26 ] Protein S enhances the interaction of factor Xa in the presence of calcium and phospholipids.[ 27 ]

Protein C pathway

The propagation phase of the coagulation is inhibited by the Protein C pathway that primarily consist of four key elements:

• Protein C is a serine protease with potent anticoagulant, profibrinolytic and anti-inflammatory properties. It is activated by thrombin to form activated protein C (APC) and acts by inhibiting activated factors V and VIII (with Protein S and phospholipids acting as cofactors)
• Thrombomodulin - A transmembrane receptor on the endothelial cells, it prevents the formation of the clot in the undamaged endothelium by binding to the thrombin
• Endothelial protein C receptor is another transmembrane receptor that helps in the activation of Protein C
• Protein S is a vitamin K-dependent glycoprotein, synthesised by endothelial cells and hepatocytes. It exists in plasma as both free (40%) and bound (60%) forms (bound to C4b-binding protein). The anticoagulant activity is by virtue of free form while the bound form acts as an inhibitor of the complement system and is up regulated in the inflammatory states, which reduce the Protein S levels thus resulting in procoagulant state. It functions as a cofactor to APC in the inactivation of FVa and FVIIIa. It also causes direct reversible inhibition of the prothrombinase (FVa–FXa) complex.[ 28 ]

Protein Z dependent protease inhibitor/protein Z (PZI)

It is a recently described component of the anticoagulant system that is produced in the liver. It inhibits Factor Xa in reaction requiring PZ and calcium.[ 29 ]

COAGULATION CASCADE

It has been traditionally classified into intrinsic and extrinsic pathways, both of which converge on factor X activation. The classical theory of blood coagulation is particularly useful for understanding the In vitro coagulation tests, but fails to incorporate the central role of cell-based surfaces in In vivo coagulation process.[ 4 ] Interestingly contact activation critical for In vivo haemostasis does not get support from following observations. Persons lacking FXII, prekallikrein, or high-molecular-weight kininogen do not bleed abnormally. Second, patients with only trace quantities of FXI can withstand major trauma without unusual bleeding, and those who completely lack factor XI (haemophilia C) exhibit mild haemorrhagic disorder. Deficiencies of FVIII and FIX (both intrinsic pathway factors) lead to haemophilia A and B, respectively, however the classic description of two pathways of coagulation leave it unclear as to why either type of haemophiliac cannot not simply clot blood via the unaffected pathway.

To answer all this, the modern time-based structuring of blood coagulation provides more authentic description of the coagulation process. It is now appreciated that the classic theories may provide only a reasonable model of in vitro coagulation tests (i.e., aPTT and PT).

Extrinsic pathway

It is considered as the first step in plasma mediated haemostasis. It is activated by TF, which is expressed in the subendothelial tissue.[ 7 ] Under normal physiological conditions, normal vascular endothelium minimises contact between TF and plasma procoagulants, but vascular insult expose TF which binds with factor VIIa and calcium to promote the conversion of factor X to Xa.[ 30 ]

Intrinsic pathway

It is a parallel pathway for thrombin activation by factor XII. It begins with factor XII, HMW kininogen, prekallekerin and factor XI, which results in activation of factor XI. Activated factor XI further activates factor IX, which then acts with its cofactor (factor VIII) to form tenase complex on a phospholipid surface to activate factor X.[ 15 , 31 ]

Common pathway

Activated factor X along with its cofactor (factor V), tissue phospholipids, platelet phospholipids and calcium forms the prothrombinase complex which converts prothrombin to thrombin. This thrombin further cleaves circulating fibrinogen to insoluble fibrin and activates factor XIII, which covalently crosslinks fibrin polymers incorporated in the platelet plug. This creates a fibrin network which stabilises the clot and forms a definitive secondary haemostatic plug[ 15 , 31 ] [ Figure 1 ].

Earlier concept of coagulation

CURRENT CONCEPT OF COAGULATION

Current evidence supports the understanding that intrinsic pathway is not a parallel pathway but indeed it augments thrombin generation primarily initiated by the extrinsic pathway[ 8 ] Newer model describes coagulation with following steps:

It occurs by expression of TF in damaged vessel which binds factor VIIa to activate factor IX and factor X. This activation of factor IX by TF-VIIa complex serves as the bridge between classical extrinsic and intrinsic pathways. Factor Xa then binds to factor II to form thrombin (factor IIa). Thrombin generation through this reaction is not robust and can be effectively terminated by TF pathway inhibitor [ Figure 2 ].

Current concept of coagulation (initiation phase)

Amplification

Since the amount of thrombin generated is not sufficient, therefore numerous positive feedback loops are present that bind thrombin with platelets. Thrombin that is generated in the initiation phase further activates factor V and factor VIII, which serves as a cofactor in prothrombinase complex and accelerates the activation of Factor II by F Xa and of F Xa by F IXa, respectively.

Propagation

The accumulated enzyme complexes (tenase complex and prothrombinase complex) on platelet surface support robust amounts of thrombin generation and platelet activation. This ensures continuous generation of thrombin and subsequently fibrin to form a sufficiently large clot [ Figure 3 ].

Current concepts of coagulation (propagation phase)

Stabilization

Thrombin generation leads to activation of factor XIII (fibrin stabilizing factor) which covalently links fibrin polymers and provides strength and stability to fibrin incorporated in platelet plug. In addition, thrombin activates thrombin activatable fibrinolysis inhibitor (TAFI) that protects the clot from fibrinolysis.[ 4 , 7 ]

DISORDERS OF COAGULATION

A balance between clotting and bleeding is always maintained in the body under normal physiology. However any pathological scenario will tilt this balance to either haemorrhagic or thrombotic complications. Hence as a corollary disorders of haemostasis can be categorised into those that lead to abnormal bleeding and those that lead to abnormal clotting [ Table 5 ].

Classification of disorders of coagulation

BLEEDING DISORDERS

Haemophilias.

Haemophilia A, the most common form of haemophilia is associated with the deficiency of factor VIII and B (Christmas disease) is secondary to deficiency of factor IX. C is only found in 1% of the population and is due to deficiency of factor XI. Haemophilia's are X linked recessive disorders and occur in males. The severity of the bleeding tendency is directly related to the levels of the coagulation factors. The levels of factor VIII need to be assessed in the preoperative period and human or recombinant factor VIII concentrates are transfused to keep the factor VIII levels 100% in the perioperative period.[ 32 ]

Von Willebrand disease is the most common autosomal dominant inherited disorder of coagulation due to abnormality in the production of vWF, which may be qualitative or quantitative. vWF acts as a carrier molecule for factor VIII coagulant protein and the deficiency of former has a profound effect on the stability of latter. The clinical presentation may be variable and complete deficiency, though rare leads to severe bleeding. The diagnosis is usually made by prolonged bleeding time in the presence of adequate platelets. Antifibrinolytic agent and tranexamic acid may be used for minor bleeding. Desmopressin D arginine vasopressin administered in the preoperative period is expected to raise the concentration of factor VIII in patients with quantitative disorders.[ 32 ]

Fibrinogen deficiency

Total or partial is an extremely rare inherited bleeding disorder. Afibrinogenemia is rather well tolerated and may manifest as subcutaneous haematoma or umbilical haematoma at birth. The clinical findings are variable in childhood and adults.[ 33 ] DIC is the most common consumptive coagulopathy that maybe observed secondary to numerous causes. It often presents as diffuse bleeding associated with consumption of coagulation factors and thrombocytopenia secondary to widespread small vessel thrombosis. Common causes include sepsis/infections, obstetric causes, incompatible blood transfusion, shock, trauma and embolism.

Liver disease

Majority of clotting factors are synthesized in liver therefore severe liver disease is associated with coagulopathy. Since liver is also involved in the clearance of activated clotting factors and fibrinolytic products, it may predispose to DIC. Management of bleeding secondary to liver disease is based on the laboratory values of various coagulation tests.

Hypothermia is also associated with anticoagulatory effects, which are more pronounced in the presence of acidosis. The effects may result from platelet dysfunction in mild hypothermia (below 35°C) to decreased synthesis of clotting enzymes and plasminogen activator inhibitors when temperatures is <33°C.[ 34 ]

The availability of newer oral anticoagulants, targeting either thrombin (dabigatran etexilate) or factor Xa (rivaroxaban or apixaban) exhibit rapid onset/offset and minimal drug interactions with more predictable pharmacokinetics thus eliminating the need for frequent coagulation monitoring. All these features give newer oral anticoagulants a major pharmacological benefits over vitamin K antagonists.[ 35 ]

THROMBOTIC DISORDERS

Plasma concentration of certain coagulation factors (factor V, VII, VIII, IX, fibrinogen) increase progressively with age.[ 36 ] Same is true for vWF, a key protein in platelet vessel wall interaction.[ 37 ] High incidence of cardiovascular events seen in elderly may be due to increased levels of plasma fibrinogen, which enhance the bridging of the platelets via glycoprotein IIb-IIIa receptor and act as a direct substrate for clot and/or by increasing the blood viscosity.[ 3 ]

The constitutive or acquired disorders of thrombosis are termed as thrombophillia.

There are number of factors that are associated with the hypercoaguable states. In addition to the genetic and hereditary disorders that predispose to thrombosis, several risk factors such as smoking, obesity, pregnancy, immobility, malignancy, surgery, females on oral contraceptives may also contribute to its development.[ 38 ] Disorders of ATIII deficiency, reduced protein C and Protein S are inherited in autosomal dominant fashion and are associated with increased risk of thrombosis. Acquired Protein C and Protien S deficiency may be observed in vitamin K deficiency, warfarin therapy, pregnancy, liver cirrhosis and sepsis.[ 39 ] Numbers of observational studies have shown decreased levels of APC in critically ill-patients that may have a direct correlation with the mortality.[ 40 ]

The risk of thromboembolism in the perioperative period is well recognized. Therefore, patients with herditary thrombophillia should be given thromboprophylaxis.

During pregnancy stasis due to obstruction of inferior vene cava by gravid uterus along with increase in the majority of clotting factors, fibrinogen and vWF is observed. Activity of Protein S decreases with simultaneous resistance of protein C. In addition, fibrinolytic system is also impaired thus contributing to a hypercoaguable state that makes the parturient more prone to thromboembolism.[ 2 ]

During surgery and trauma, prolonged immobility promotes stasis which results in local hypoxia. Physical disruption leads to exposure of TF thus triggering thrombosis.[ 37 ] Furthermore during the first hours of surgery, there is increase in TF, tissue plasminogen activator (tPA) and vWF, leading to hypercoaguable state thus promoting venous thrombosis. Even a venepuncture cause vascular wall injury thus, predisposing to thrombus formation. Since lower limb is associated with stasis and immobilization during surgery, venepuncture preferably should be avoided in the lower limb.

FIBRINOLYTIC SYSTEM

Fibrinolytic system is a parallel system which is activated along with activation of coagulation cascade and serves to limit the size of clot. Fibrinolysis is an enzymatic process that dissolves the fibrin clot into fibrin degradation products (FDPs) by plasmin originating from fibrin bound plasminogen in liver. This reaction is catalysed by tPA or urokinase plasminogen activator (u-PA) released from vascular endothelium. The release of t-PA is stimulated by tissue occlusion, thrombin, epinephrine, vasopressin and strenuous exercise.

Plasmin activity is tightly regulated by its inhibitor (α-2 antiplasmin) thus preventing widespread fibrinolysis[ 41 ] [ Figure 4 ]. In vivo activity of the fibrinolytic system is assessed clinically by measuring the FDP's. D dimers are produced by digestion of cross linked fibrin and are specific indicators of fibrinolysis used in the assessment and diagnosis of pulmonary embolism, DIC or deep vein thrombosis.[ 13 ]

Regulation of the fibrinolytic system

Since plasmin has the potential to degrade fibrinogen leading to deleterious consequences, the fibrinolytic activity is limited by following factors:

• Plasminogen activator inhibitor - It is the main physiological inhibitor of fibriolysis and acts by inhibiting t-PA and u-PA irreversibly
• TAFI - It is a plasma proenzyme synthesized by liver and activated by thrombin. It decreases the affinity of plasminogen to fibrin and augments the action of anti-trypsin in inhibiting plasmin
• Plasmin inhibitors - α2 antiplasmin and α2Macroglobulin are the glycoproteins that exert action by virtue of plasmin inhibition.[ 25 ]

DISORDERS OF FIBRINOLYSIS

Congenital disorders pertaining to fibrinolytic system are rare. Although the hyperfibrinolytic state is associated with increased tendency to bleed, deficiency of the same predisposes to thromboembolism.[ 42 ] Excessive activation of fibrinolysis may be observed during cardiopulmonary bypass, hence antifibrinolytics have a beneficial role in the prevention of same. Acquired hyperfibrinolysis may be encountered in trauma, liver cirrhosis, amniotic fluid embolism, multiple myeloma, snake bite and conditions associated with massive activation of t-PA, which can lead to DIC and haemorrhage.[ 25 ]

Haemostasis is a complex physiological process, maintaining the fluidity of blood and is regulated by delicate balance existing between thrombogenic and anti thrombogenic mechanisms present in the body. Imbalance between the two components predisposes a patient to either bleed or present with thrombosis. The physiology of the same therefore, needs to be understood to predict the pathological and clinical consequences of the same before implementing any pharmacological interventions.

Source of Support: Nil

Conflict of Interest: None declared

• A to Z Guides

What Are Coagulation Studies?

Coagulation studies help you understand blood disorders, so you can pursue treatment options to improve your blood’s ability to form clots.

How Blood Coagulation Works

Blood coagulation, or blood clotting, is a process in which multiple proteins produced by the liver circulate in the blood and interact with a damaged vessel wall to form a blood clot.

In some cases, you may have too many of these proteins, making your blood clot too easily. A lack of these proteins can lead to unexplained bleeding that isn’t easily stopped.

Most coagulation tests look for activity within your blood rather than specific proteins. While it's easy to determine the amount of coagulation protein in your bloodstream, the test results won’t show if the proteins work correctly. A blood activity test shows the actual function of your blood.

Your blood needs to clot to protect your body from too much blood loss following an injury. When you get hurt, your coagulation system activates and plugs leaking blood vessels to stop active bleeding.‌

Your body’s blood clotting function is dynamic. Once a clot successfully forms, your body begins breaking it down. This process is called fibrinolysis. Eventually, your body dissolves the clot.

If you’ve ever sustained a cut or scrape, you’ve probably noticed a thick patch of blood that forms and dries at the site of the wound. This is a blood clot. It stays in place until the skin heals completely.

If you have a bleeding disorder, your blood doesn’t clot the way it should. Many blood disorders are hereditary, but some form after birth. If you have signs of a bleeding disorder, your doctor can test for specific factors to determine which treatment is right for your specific diagnosis.‌

Coagulation Studies

When you sustain damage, your body depends on specific interactions between the plasma–based coagulation factors, blood platelets, and the endothelium of your blood vessels. Coagulation studies measure these interactions in your blood. Specific types of coagulation tests include:

• Prothrombin time (PT)
• Activated partial thromboplastin time (aPTT)‌
• Thrombin time (TT)

These studies help make sense of unexplained bleeding. They may also provide answers about hereditary risks for blood clotting disorders. However, they won’t predict the severity of a bleed in the future. Once results come back from a testing lab, your blood technician reviews the results with you to provide answers.

Reasons for a Coagulation Study

The obvious reason for a coagulation study is unexplained bleeding or bleeding that doesn’t stop. However, sometimes other health conditions, such as liver disease, lead to poor blood coagulation. Coagulation studies may help doctors follow the progress of the liver disease or diagnose a vitamin K deficiency.‌

If you’re taking a medicine to thin your blood, a coagulation study provides results on how much your blood is affected by the medication. Other reasons for a coagulation study include:

• An injury that causes severe blood loss
• Bruising easily
• Persistent swelling
• Unexplained pain and stiffness

Understanding Coagulation Test Results

If your activity report is normal, that means your blood exhibits normal clotting function. Low activity means you probably bleed easily, while high function means you probably clot easily.‌

For each factor, 100% is considered normal. As your percentage goes up or down, your condition worsens. In some cases, a coagulation study indicates that something is temporarily affecting your blood’s ability to clot. This is good news because it means you may be able to take steps to address concerns.‌

When more than one of your blood’s clotting factors is negatively impacted, your condition is most likely hereditary. Because this may be caused by a chronic health condition, your doctor may suggest additional tests.

Health conditions that decrease clotting factors in your blood include:

• Liver disease
• Venom from a snake bite
• Inability to absorb fat
• Vitamin K deficiency
• Medications, like Warfarin ‌
• Blood transfusions 

It's important to keep your blood’s clotting ability in mind when you're considering medical procedures where blood clotting is important, like a dental excision. Talk to your doctor before undergoing any procedures and ensure other medical professionals know about your condition in advance.

Understanding the impact of hereditary disorders. Hemophilia A and Hemophilia B are commonly passed down through genetics. If you have a family member with one of these blood disorders, you may have it, too.‌

These disorders are linked to the X chromosome in your genetic makeup, which is why men are more likely to suffer from the conditions. Women may carry the genes, passing them down to daughters and sons without ever showing symptoms of the disease.

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• Hematopoiesis Case Studies

A 73-Year-Old Man With Extensive Bruising

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A 73-year-old man presented to his primary care provider for evaluation of easy bruising. He was in his usual state of health until 10 days prior to presentation when he noticed bruising of his bilateral upper extremities associated with mild swelling and discomfort. He initially attributed this to musculoskeletal pain from doing yardwork, but the bruising and pain did not improve.

The patient denied any personal or family history of bleeding disorders. His medical history was otherwise remarkable for osteoarthritis of the bilateral knees and obesity. He underwent a tooth extraction and an inguinal hernia repair several years ago, which were not complicated by bleeding. He reported taking ibuprofen sparingly in the 10 days prior for his upper extremity pain but denied any other new medications. He was not on any prescription medications, other over-the-counter medications, or herbal supplements. He otherwise denied fevers, chills, night sweats, change in weight, shortness of breath, chest pain, abdominal pain, change in urination, new joint pain, skin rashes, and other bleeding symptoms including epistaxis, mucosal bleeding, hematemesis, hemoptysis, melena, hematochezia, and hematuria.

Upon presentation, vital signs were normal. His physical examination was notable for scattered large ecchymoses involving the right upper arm, left upper arm, chest, and abdomen. A comprehensive metabolic panel was within normal limits, and the remainder of the laboratory workup was remarkable for the following:

What is the most appropriate next step in treating this patient?

This patient has acquired hemophilia A due to autoantibodies directed against coagulation Factor VIII. Given the absence of active bleeding, he should be treated with immunosuppression using steroids to eliminate the autoantibody and minimize bleeding risk.

Acquired hemophilia A is an uncommon disorder that most often presents in the elderly with a slight male predominance. While acquired hemophilia A can be associated with pregnancy, autoimmune disorders, and malignancy, approximately half of cases are idiopathic. Most patients present with bleeding symptoms in the absence of a previous history of abnormal bleeding. In contrast to congenital hemophilia, hemarthroses are uncommon, and most patients present with spontaneous subcutaneous bleeding in atypical locations such as the upper extremities, chest, and abdomen. Mucosal bleeding (gastrointestinal, urogenital, and lung) and intracranial bleeding can also occur. A small minority of patients present with isolated laboratory abnormalities and no bleeding. 1

APTT measures the activity of the common and intrinsic coagulation pathways. Isolated elevation in APTT can be caused by factor deficiency (Factors VIII, IX, XI, or XII), exposure to certain medications (such as heparin), or can be acquired due to a lupus anticoagulant or more rarely via a direct Factor VIII inhibitor. An isolated prolonged APTT in a patient without a personal history of bleeding should raise suspicion for acquired Factor VIII deficiency, leading to acquired hemophilia A. To distinguish an acquired inhibitor against Factor VIII from a factor deficiency, a mixing study is performed by combining equal volumes of pooled normal plasma with the patient’s plasma and then repeating the APTT test. An APTT that remains prolonged after mixing with normal plasma suggests the presence of a Factor VIII inhibitor, whereas correction of the APTT after mixing with normal plasma suggests a Factor VIII deficiency. If the APTT is corrected, it is important to incubate the sample for one or two more hours to assess whether APTT would prolong again, indicating a slow inhibitor that had initially corrected. The Bethesda assay can be used to identify and quantify autoantibody titer level. 2

The first step in treating acquired hemophilia A is to identify and manage any acute bleeding. A detailed history, a comprehensive physical exam, and a review of medications, prior surgeries, and recent and chronic medical problems can provide insightful information about the potential causes of the acquired deficiency. Diagnostic laboratory work-up includes CBC and coagulation studies. First-line therapy depends on the degree of illness. In the absence of acute hemorrhage, immunosuppression therapy should be initiated to reduce bleeding risk and induce a remission. First-line therapy should be individualized based on prognostic information at the time of diagnosis. For patients with a Factor VIII activity level higher than 1 percent and titer level lower than 20 Bethesda units, treatment should consist of high-dose steroids for three to four weeks. For patients with a Factor VIII activity level lower than 1 percent or titer level higher than 20 Bethesda units, treatment should consist of steroids plus either cyclophosphamide or rituximab for three to four weeks. 3

More serious bleeding may require bypassing agents, such as recombinant activated Factor VII and activated prothrombin concentration complex, or recombinant factor VIII. Desmopressin is not recommended in the management of bleeding associated with acquired hemophilia A. 3

This patient has no evidence of active bleeding. Thus, recombinant Factor VIII or recombinant activated Factor VII are not indicated at this time. A Factor VIII autoantibody was ultimately detected at a titer level of 10 Bethesda units. The patient should thus be treated with steroid monotherapy for three to four weeks.

• Sborov DW, Rodgers GM. How I manage patients with acquired hemophilia A . Br J Haematol. 2013;161:157-165.
• Franchini M, Lippi G. Acquired factor VIII inhibitors . Blood. 2008;112:250-255.
• Tiede A, Collins P, Knoebl P, et al. International recommendations on the diagnosis and treatment of acquired hemophilia A . Haematologica. 2020;105:1791-1801.

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American Society of Hematology. (1). A 73-Year-Old Man With Extensive Bruising. Retrieved from https://www.hematology.org/education/trainees/fellows/case-studies/a-73-year-old-man-with-extensive-bruising .

American Society of Hematology. "A 73-Year-Old Man With Extensive Bruising." Hematology.org. https://www.hematology.org/education/trainees/fellows/case-studies/a-73-year-old-man-with-extensive-bruising (label-accessed September 14, 2024).

"American Society of Hematology." A 73-Year-Old Man With Extensive Bruising, 14 Sep. 2024 , https://www.hematology.org/education/trainees/fellows/case-studies/a-73-year-old-man-with-extensive-bruising .

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Table of Contents

Explore the latest case studies  and articles  from  Hematopoiesis .

• Announcing Hematopoiesis, Our New ASH Trainee Council Newsletter by Trainees and for Trainees
• A Primer on Advocacy for the Hematology Trainee
• Blood Smear: The Fifth Vital Sign in Hematology
• Chimeric Antigen Receptor T-cell Therapy: What Fellows Need to Know
• The Blood Sisters Project
• Case Study: A 73-Year-Old Man With Extensive Bruising
• Case Study: A 2.5-Year-Old Girl With Fever and Pancytopenia

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The effect of blood flow restriction during low-load resistance training unit on knee flexor muscle fatigue in recreational athletes: a randomized double-blinded placebo-controlled pilot study.

1. Introduction

2. materials and methods, 2.1. ethical considerations, 2.2. study design, 2.3. participants, 2.4. knee flexor muscle maximal isometric torque measurements, 2.5. local muscle fatigue assessment, 2.6. occurrence of adverse events, 2.7. blood flow restriction, 2.8. low-load restriction training, 2.9. statistical analysis, 4. discussion, 5. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.

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Królikowska, A.; Daszkiewicz, M.; Kocel, J.; Avram, G.M.; Oleksy, Ł.; Prill, R.; Witkowski, J.; Korolczuk, K.; Kołcz, A.; Reichert, P. The Effect of Blood Flow Restriction during Low-Load Resistance Training Unit on Knee Flexor Muscle Fatigue in Recreational Athletes: A Randomized Double-Blinded Placebo-Controlled Pilot Study. J. Clin. Med. 2024 , 13 , 5444. https://doi.org/10.3390/jcm13185444

Królikowska A, Daszkiewicz M, Kocel J, Avram GM, Oleksy Ł, Prill R, Witkowski J, Korolczuk K, Kołcz A, Reichert P. The Effect of Blood Flow Restriction during Low-Load Resistance Training Unit on Knee Flexor Muscle Fatigue in Recreational Athletes: A Randomized Double-Blinded Placebo-Controlled Pilot Study. Journal of Clinical Medicine . 2024; 13(18):5444. https://doi.org/10.3390/jcm13185444

Królikowska, Aleksandra, Maciej Daszkiewicz, Julia Kocel, George Mihai Avram, Łukasz Oleksy, Robert Prill, Jarosław Witkowski, Krzysztof Korolczuk, Anna Kołcz, and Paweł Reichert. 2024. "The Effect of Blood Flow Restriction during Low-Load Resistance Training Unit on Knee Flexor Muscle Fatigue in Recreational Athletes: A Randomized Double-Blinded Placebo-Controlled Pilot Study" Journal of Clinical Medicine 13, no. 18: 5444. https://doi.org/10.3390/jcm13185444

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the new old age

Three Medical Practices That Older Patients Should Question

Some treatments and procedures become routine despite lacking strong evidence to show that they’re beneficial. Recent studies have called a few into question.

By Paula Span

An older patient with dementia is in the hospital and has trouble swallowing. A speech pathologist recommends thickening the liquids the patient drinks with starch or gum and specifies how viscous her tea, water or juice should be. Should it resemble honey? Or apricot nectar?

A doctor writes the order, and the discharged patient returns to her home or nursing facility. She may be drinking thickened liquids from then on.

The rationale is that this sludgy stuff prevents patients from drawing liquids into their lungs and from developing aspiration pneumonia. But does the practice work? Some geriatricians have doubted it for years.

Now, a large-scale study from the Feinstein Institutes for Medical Research in Manhasset, N.Y., has found that liquid thickening doesn’t actually help such patients.

This happens with some frequency: Medical practices so commonplace they rarely raise eyebrows turn out, after further investigation, to have scant basis in fact.

“There are plenty of things we do in medicine that have no evidence,” said Dr. Matthieu Legrand, an anesthesiologist and critical care doctor at the University of California, San Francisco.

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