Heparin Induced Thrombocytopeia (HIT)
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This document provides information about heparin-induced thrombocytopenia (HIT). It begins by introducing HIT as an immune-mediated reduction in platelet count that occurs in 3-5% of patients receiving unfractionated heparin for 5 days or more, and less than 1% for low molecular weight heparin. It then describes HIT as characterized by a platelet decrease of over 50% from baseline 5-10 days after starting heparin, along with hypercoagulability and heparin-dependent antibodies. The document outlines the pathogenesis of HIT and differences between type I and type II, reviews potential clinical complications, diagnostic methods, and emphasizes the need to promptly discontinue heparin and
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HEPARIN INDUCED THROMBOCYTOPENIA
This document discusses heparin-induced thrombocytopenia (HIT). HIT is an immune-mediated reaction to heparin that results in platelet activation and thrombocytopenia. It can lead to thrombotic complications in 20-50% of patients. The document reviews the pathophysiology of HIT, defines its criteria, discusses diagnostic assays and algorithms, and outlines treatment and management approaches including alternative anticoagulants like lepirudin, argatroban, and danaparoid. Early recognition and treatment are important to prevent life-threatening thrombotic events associated with HIT.
Transfusion related acute lung injury
Transfusion-related acute lung injury (TRALI) is a potentially fatal syndrome characterized by acute respiratory distress within 6 hours of blood transfusion. It is believed to be caused by anti-leukocyte antibodies in plasma products that cause leukocyte aggregation in the lungs, inflammatory injury, and non-cardiogenic pulmonary edema. TRALI has an incidence of 1 in 5000 transfusions and mortality rate of 5-25%. Risk factors include plasma-rich products, multiparous donors, and underlying patient conditions. Diagnosis involves new pulmonary edema within 6 hours of transfusion in the absence of circulatory overload. Treatment focuses on supportive care, with most patients recovering within 72 hours. Prevention strategies include leukoreduction of blood products
Heparin induced thrombocytopenia
Heparin-induced thrombocytopenia (HIT) is defined as a decrease in platelet count occurring 5-10 days after starting heparin treatment along with hypercoagulability and the presence of heparin-dependent antibodies. There are two main types of HIT - type 1 is a mild transient decrease while type 2 is an antibody-mediated thrombocytopenia associated with high thrombosis risk. Diagnosis involves clinical features and platelet factor 4 antibody testing, with a strongly positive test supporting HIT. Treatment involves stopping heparin
Massive transfusion
Massive transfusion protocols aim to standardize the resuscitation of patients experiencing severe bleeding through the early administration of blood products. The key aspects of such protocols discussed in the document include:
- Definitions of massive transfusion as the replacement of over 50% of total blood volume within 3-4 hours or transfusion of over 10 units of packed red blood cells within 24 hours.
- Common clinical conditions requiring massive transfusion include severe trauma, ruptured aortic aneurysms, and obstetric or surgical complications.
- Current concepts favor permissive hypotension and minimal crystalloid resuscitation to control bleeding before aggressively restoring blood pressure and volume.
- Blood products administered according to protocols include packed red blood
Heparin induced thrombocytopaenia: HIT
Heparin-induced thrombocytopenia (HIT) is a complication of heparin treatment where antibodies form against platelet factor 4-heparin complexes, activating platelets and potentially causing thrombosis. It typically occurs 5-14 days after starting heparin and is treated by discontinuing heparin and using alternative anticoagulants like argatroban. A case example is presented of a woman who developed deep vein thrombosis and arterial thrombosis after gallbladder surgery treated with heparin, and was diagnosed with HIT when her platelets dropped and she tested positive for HIT antibodies.
Hepatorenal Syndrome
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Hepatorenal syndrome
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
TEG - Thromboelastography
TEG - Thromboelastography
Thromboelastography is a viscoelastic hemostatic assay that measures the global visco-elastic properties of whole blood clot formation under low shear stress
it shows the interaction of platelets with the coagulation cascade (aggregation, clot strengthening, fibrin cross linking and fibrinolysis)
does not necessarily correlate with blood tests such as INR, APTT and platelet count (which are often poorer predictors of bleeding and thrombosis)
Recommended
HEPARIN INDUCED THROMBOCYTOPENIA
This document discusses heparin-induced thrombocytopenia (HIT). HIT is an immune-mediated reaction to heparin that results in platelet activation and thrombocytopenia. It can lead to thrombotic complications in 20-50% of patients. The document reviews the pathophysiology of HIT, defines its criteria, discusses diagnostic assays and algorithms, and outlines treatment and management approaches including alternative anticoagulants like lepirudin, argatroban, and danaparoid. Early recognition and treatment are important to prevent life-threatening thrombotic events associated with HIT.
Transfusion related acute lung injury
Transfusion-related acute lung injury (TRALI) is a potentially fatal syndrome characterized by acute respiratory distress within 6 hours of blood transfusion. It is believed to be caused by anti-leukocyte antibodies in plasma products that cause leukocyte aggregation in the lungs, inflammatory injury, and non-cardiogenic pulmonary edema. TRALI has an incidence of 1 in 5000 transfusions and mortality rate of 5-25%. Risk factors include plasma-rich products, multiparous donors, and underlying patient conditions. Diagnosis involves new pulmonary edema within 6 hours of transfusion in the absence of circulatory overload. Treatment focuses on supportive care, with most patients recovering within 72 hours. Prevention strategies include leukoreduction of blood products
Heparin induced thrombocytopenia
Heparin-induced thrombocytopenia (HIT) is defined as a decrease in platelet count occurring 5-10 days after starting heparin treatment along with hypercoagulability and the presence of heparin-dependent antibodies. There are two main types of HIT - type 1 is a mild transient decrease while type 2 is an antibody-mediated thrombocytopenia associated with high thrombosis risk. Diagnosis involves clinical features and platelet factor 4 antibody testing, with a strongly positive test supporting HIT. Treatment involves stopping heparin
Massive transfusion
Massive transfusion protocols aim to standardize the resuscitation of patients experiencing severe bleeding through the early administration of blood products. The key aspects of such protocols discussed in the document include:
- Definitions of massive transfusion as the replacement of over 50% of total blood volume within 3-4 hours or transfusion of over 10 units of packed red blood cells within 24 hours.
- Common clinical conditions requiring massive transfusion include severe trauma, ruptured aortic aneurysms, and obstetric or surgical complications.
- Current concepts favor permissive hypotension and minimal crystalloid resuscitation to control bleeding before aggressively restoring blood pressure and volume.
- Blood products administered according to protocols include packed red blood
Heparin induced thrombocytopaenia: HIT
Heparin-induced thrombocytopenia (HIT) is a complication of heparin treatment where antibodies form against platelet factor 4-heparin complexes, activating platelets and potentially causing thrombosis. It typically occurs 5-14 days after starting heparin and is treated by discontinuing heparin and using alternative anticoagulants like argatroban. A case example is presented of a woman who developed deep vein thrombosis and arterial thrombosis after gallbladder surgery treated with heparin, and was diagnosed with HIT when her platelets dropped and she tested positive for HIT antibodies.
Hepatorenal Syndrome
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Hepatorenal syndrome
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
TEG - Thromboelastography
TEG - Thromboelastography
Thromboelastography is a viscoelastic hemostatic assay that measures the global visco-elastic properties of whole blood clot formation under low shear stress
it shows the interaction of platelets with the coagulation cascade (aggregation, clot strengthening, fibrin cross linking and fibrinolysis)
does not necessarily correlate with blood tests such as INR, APTT and platelet count (which are often poorer predictors of bleeding and thrombosis)
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Massive Blood Transfusion
This document defines massive blood transfusion as replacing over half the patient's blood volume within 24 hours or transfusing over 10 units of packed red blood cells within a few hours. It indicates massive transfusion is used for hemorrhagic shock, trauma, or critical illness. Complications discussed include acute reactions, infections transmission, coagulopathy, hypothermia, electrolyte abnormalities, and volume overload. Guidelines recommend considering multiple factors like physiological status and oxygen needs rather than single transfusion thresholds.
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Sepsis and septic shock guidelines 2021. part 1
1. Sepsis is a critical imbalance between oxygen supply and demand that can affect any system. Serum lactate levels rise in response to tissue hypoxia and higher levels correlate with poorer outcomes.
2. Guidelines recommend screening high-risk patients for sepsis and using standard treatment protocols. Blood lactate should be measured in suspected cases and treatment begun immediately.
3. Fluid resuscitation of at least 30mL/kg should begin within 3 hours, guided by dynamic measures over static parameters alone. Antimicrobial therapy should also begin immediately or within 1-3 hours depending on risk level and presence of shock.
Heparin induced thrombocytopenia.
Heparin induced thrombocytopenia (HIT) is a life-threatening complication that occurs in up to 5% of patients exposed to heparin. There are two types - HIT type I is a mild transient platelet count drop within 2 days, while HIT type II is immune-mediated and occurs 4-10 days later, carrying risks of thrombosis, amputation and death for 20-50% of patients. Diagnosis involves a presumptive 4Ts assessment and laboratory tests detecting HIT antibodies. Treatment discontinues all heparin and starts alternative anticoagulants like argatroban or danaparoid along with warfarin. Careful monitoring is needed due to risks of further thrombosis.
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This document provides information about platelet transfusion. It discusses what platelets are, their role in hemostasis, normal platelet counts, causes of thrombocytopenia, indications for platelet transfusion, contraindications, donor criteria, preparation of platelet concentrates, dosing, response to transfusion, complications including immunological and non-immunological issues, and methods to reduce complications like use of leukoreduced products. The document contains detailed information about platelet immunology, causes of refractoriness, its management, and methods to improve safety and availability of platelet transfusion like use of matched donors and crossmatching.
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This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
Heparin induced thrombocytopenia hit
This document defines and describes heparin-induced thrombocytopenia (HIT), a condition where heparin triggers the immune system to produce antibodies that activate platelets and cause thrombocytopenia and blood clots. It notes that HIT can develop 5-15 days after starting heparin treatment and discusses the two types of HIT - type I is a mild reaction while type II is immune-mediated and carries a higher risk of blood clots. It also outlines the diagnostic criteria and testing for confirming HIT through platelet counts, coagulation studies, antigen and functional assays. Treatment involves non-heparin anticoagulants until platelet counts recover above 150,000.
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The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
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- ECMO is a form of extracorporeal life support that oxygenates blood and removes carbon dioxide outside of the body, then returns the blood to the patient. It has been used since the 1950s and is now standard treatment for some cardiac and respiratory conditions.
- The basic ECMO circuit includes a blood pump, membrane oxygenator, heat exchanger, cannulas, and tubing. There are various configurations depending on whether it is used for respiratory (VV ECMO) or cardiac (VA ECMO) support.
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This document provides an overview of heparin-induced thrombocytopenia (HIT). It discusses the history, pathogenesis, frequency, clinical features, diagnosis, and treatment of both type 1 and type 2 HIT. Type 2 HIT is an immune-mediated reaction, where antibodies form against the platelet factor 4-heparin complex, leading to platelet activation and thrombosis. The document outlines various laboratory tests used to diagnose HIT, including functional assays measuring platelet activation and immunoassays detecting antibodies.
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- The pathophysiology involves an initial infection that triggers a systemic inflammatory response and release of cytokines and mediators, leading to endothelial damage, coagulation abnormalities, hypotension, and ultimately multiple organ dysfunction if not treated.
- Treatment involves early goal-directed therapy within 3-6 hours including antibiotics, fluid resuscitation, vasopressors, inotropes, and measures to optimize
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This document discusses thrombocytopenia (low platelet count) and its causes and evaluation. It describes the normal physiology of platelets and hemostasis. Common causes of thrombocytopenia include decreased platelet production (bone marrow problems), increased platelet destruction (immune mechanisms like ITP), and increased consumption (DIC). Evaluation involves history, exam, blood smear review, and identifying potential causes like drugs, infections, malignancies or autoimmune disorders. Specific conditions discussed in detail include ITP, HIT, DIC, and thrombocytopenia in cardiac patients.
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(1) Bleeding disorders refer to functional impairments in the normal hemostatic process that result in bleeding even without an anatomical cause.
(2) Common signs of bleeding disorders include petechiae, purpura, hemarthrosis, ecchymoses, and hematomas. Coagulation disorders particularly present with hemarthrosis.
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Massive Blood Transfusion
This document defines massive blood transfusion as replacing over half the patient's blood volume within 24 hours or transfusing over 10 units of packed red blood cells within a few hours. It indicates massive transfusion is used for hemorrhagic shock, trauma, or critical illness. Complications discussed include acute reactions, infections transmission, coagulopathy, hypothermia, electrolyte abnormalities, and volume overload. Guidelines recommend considering multiple factors like physiological status and oxygen needs rather than single transfusion thresholds.
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1. Sepsis is a critical imbalance between oxygen supply and demand that can affect any system. Serum lactate levels rise in response to tissue hypoxia and higher levels correlate with poorer outcomes.
2. Guidelines recommend screening high-risk patients for sepsis and using standard treatment protocols. Blood lactate should be measured in suspected cases and treatment begun immediately.
3. Fluid resuscitation of at least 30mL/kg should begin within 3 hours, guided by dynamic measures over static parameters alone. Antimicrobial therapy should also begin immediately or within 1-3 hours depending on risk level and presence of shock.
Heparin induced thrombocytopenia.
Heparin induced thrombocytopenia (HIT) is a life-threatening complication that occurs in up to 5% of patients exposed to heparin. There are two types - HIT type I is a mild transient platelet count drop within 2 days, while HIT type II is immune-mediated and occurs 4-10 days later, carrying risks of thrombosis, amputation and death for 20-50% of patients. Diagnosis involves a presumptive 4Ts assessment and laboratory tests detecting HIT antibodies. Treatment discontinues all heparin and starts alternative anticoagulants like argatroban or danaparoid along with warfarin. Careful monitoring is needed due to risks of further thrombosis.
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This document provides information about platelet transfusion. It discusses what platelets are, their role in hemostasis, normal platelet counts, causes of thrombocytopenia, indications for platelet transfusion, contraindications, donor criteria, preparation of platelet concentrates, dosing, response to transfusion, complications including immunological and non-immunological issues, and methods to reduce complications like use of leukoreduced products. The document contains detailed information about platelet immunology, causes of refractoriness, its management, and methods to improve safety and availability of platelet transfusion like use of matched donors and crossmatching.
Hyperkalemia 160108171542
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
Heparin induced thrombocytopenia hit
This document defines and describes heparin-induced thrombocytopenia (HIT), a condition where heparin triggers the immune system to produce antibodies that activate platelets and cause thrombocytopenia and blood clots. It notes that HIT can develop 5-15 days after starting heparin treatment and discusses the two types of HIT - type I is a mild reaction while type II is immune-mediated and carries a higher risk of blood clots. It also outlines the diagnostic criteria and testing for confirming HIT through platelet counts, coagulation studies, antigen and functional assays. Treatment involves non-heparin anticoagulants until platelet counts recover above 150,000.
Inotropes and vasopressors
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is a syndrome characterized by widespread activation of coagulation that can occur as a result of various underlying conditions. It results from an imbalance between coagulation and anticoagulation processes in the body. DIC can be acute, with bleeding and shock being dominant symptoms, or chronic, where thrombosis and clotting may predominate. The most common triggers of DIC are infectious diseases, cancer, obstetric complications, and severe tissue injury. Diagnosis involves identifying symptoms of bleeding and thrombosis, abnormal laboratory coagulation test results, and ruling out other conditions. Treatment focuses on treating the underlying cause, replacing coagulation factors, platelets, and fibrinogen, and
ECMO - extracorporeal membrane oxygenation
This document provides an overview of extracorporeal membrane oxygenation (ECMO), including its history, principles, components, indications, and complications. Some key points:
- ECMO is a form of extracorporeal life support that oxygenates blood and removes carbon dioxide outside of the body, then returns the blood to the patient. It has been used since the 1950s and is now standard treatment for some cardiac and respiratory conditions.
- The basic ECMO circuit includes a blood pump, membrane oxygenator, heat exchanger, cannulas, and tubing. There are various configurations depending on whether it is used for respiratory (VV ECMO) or cardiac (VA ECMO) support.
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2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
Heparin induced thrombocytopenia(hit)
This document provides an overview of heparin-induced thrombocytopenia (HIT). It discusses the history, pathogenesis, frequency, clinical features, diagnosis, and treatment of both type 1 and type 2 HIT. Type 2 HIT is an immune-mediated reaction, where antibodies form against the platelet factor 4-heparin complex, leading to platelet activation and thrombosis. The document outlines various laboratory tests used to diagnose HIT, including functional assays measuring platelet activation and immunoassays detecting antibodies.
Sepsis – pathophysiology and management
- Sepsis is a systemic inflammatory response caused by infection that can progress to severe sepsis and septic shock. Severe sepsis is defined as sepsis with organ dysfunction, while septic shock involves hypotension refractory to fluid resuscitation along with lactate levels over 2 mmol/L despite fluid resuscitation.
- The pathophysiology involves an initial infection that triggers a systemic inflammatory response and release of cytokines and mediators, leading to endothelial damage, coagulation abnormalities, hypotension, and ultimately multiple organ dysfunction if not treated.
- Treatment involves early goal-directed therapy within 3-6 hours including antibiotics, fluid resuscitation, vasopressors, inotropes, and measures to optimize
An approach to a patient with Thrombocytopenia
This document discusses thrombocytopenia (low platelet count) and its causes and evaluation. It describes the normal physiology of platelets and hemostasis. Common causes of thrombocytopenia include decreased platelet production (bone marrow problems), increased platelet destruction (immune mechanisms like ITP), and increased consumption (DIC). Evaluation involves history, exam, blood smear review, and identifying potential causes like drugs, infections, malignancies or autoimmune disorders. Specific conditions discussed in detail include ITP, HIT, DIC, and thrombocytopenia in cardiac patients.
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Hypokalemia
Hypokalemia, or low potassium levels, can have significant effects on muscles, the cardiovascular and nervous systems. It is defined as a potassium level below 3.5 mEq/L. The majority of potassium is found inside cells and is essential for various cellular functions through membrane pumps and channels. Causes of hypokalemia include reduced intake, redistribution into cells, and increased losses through the kidneys or gastrointestinal tract. Treatment focuses on replacing potassium stores through oral or intravenous supplementation, addressing the underlying cause, and preventing further losses and complications like cardiac arrhythmias.
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Approach to patient with platelet disorders
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and lab diagnosis
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Treatment of acute pulmonary embolism (PE) involves risk stratification and both primary therapy and secondary prevention. For massive PE with hypotension, resuscitation with fluids, oxygen, and empiric anticoagulation is critical. Primary therapy may include thrombolysis or embolectomy to reduce clot burden. Secondary prevention focuses on anticoagulation to prevent recurrence, using unfractionated heparin, low molecular weight heparin, warfarin or newer oral anticoagulants. Duration of anticoagulation depends on provoking factors and bleeding risk. Prevention of venous thromboembolism involves assessing risk and providing appropriate prophylaxis for moderate to high risk patients, especially with surgery
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Drug-induced blood disorders can affect red blood cells, white blood cells, and platelets. Common types include thrombocytopenia, hemolytic anemia, megaloblastic anemia, and aplastic anemia. Symptoms depend on the specific disorder but may include fatigue, bleeding, and infections. Causative agents include certain medications like sulfonamides, quinine, and chemotherapy drugs. Diagnosis involves blood tests and bone marrow biopsy. Treatment focuses on removing the offending drug, blood transfusions, and immunosuppressive therapy. Drug-induced hematological disorders are rare but potentially life-threatening, so monitoring patients on high-risk medications is important.
medicine.Bleeding disorders.(dr.sabir) (new powerpoint)
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Detaield aggregation of notes about blood transfusion reactions in human body along with the precations and management.
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Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, occurring in approximately 1 in 3,000 live births. It involves four abnormalities - a ventricular septal defect, right ventricular outflow tract obstruction, right ventricular hypertrophy, and overriding of the aorta. Without surgical repair, only 10% of patients survive beyond 20 years of age. Clinical manifestations include cyanosis, clubbing of the fingers and toes, and hypoxic spells in infants. Diagnosis is made through echocardiography, chest x-ray, and cardiac catheterization. Treatment involves palliative shunt procedures for infants or complete repair surgery to close the ventricular septal defect and widen the right ventricular
Ventricular Septal Defect
A ventricular septal defect (VSD) is a hole in the septum separating the left and right ventricles of the heart. VSDs are the most common type of congenital heart defect, occurring in about 2 out of every 1000 live births. They can range from small to large in size. Echocardiography is the primary way to diagnose a VSD and determine its location and size. Small VSDs may close on their own, but larger defects often require surgery to repair.
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Coarctation of the aorta is a narrowing of the aorta that occurs most commonly near the ligamentum arteriosum. It affects 8-10% of congenital heart disease cases and is more common in males. If unrepaired, complications can include heart failure, aortic rupture, and hypertension. Treatment involves opening the coarctation through surgery or catheterization to restore blood flow to the lower body and reduce blood pressure in the upper body.
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- An atrial septal defect (ASD) is an opening in the wall separating the left and right atria of the heart that was not present at birth.
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This document discusses hypertension during pregnancy and classifies it into four categories: chronic hypertension, gestational hypertension, preeclampsia-eclampsia, and preeclampsia superimposed on underlying hypertension. It defines each category and discusses their causes, symptoms, and management. Chronic hypertension is defined as hypertension before or after pregnancy. Gestational hypertension occurs after 20 weeks without proteinuria. Preeclampsia-eclampsia includes new hypertension and proteinuria after 20 weeks. It affects 5% of pregnancies and risks maternal and fetal health. The document recommends treating chronic hypertension if blood pressure is above 160/110 mmHg and below 140/90 mmHg if there is end-organ damage. First-line treatment includes
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This document discusses anticoagulation options during pregnancy for conditions requiring it, such as mechanical heart valves or blood clotting disorders. It describes that warfarin, unfractionated heparin, and low-molecular weight heparin are the three most common agents considered. While warfarin is very effective, it can harm the fetus if used in early pregnancy. Unfractionated heparin and low-molecular weight heparin do not cross the placenta and are safer options for early pregnancy, with low-molecular weight heparin requiring anti-Xa level monitoring. The document provides guidelines for using warfarin or heparins based on the trimester and any needed dose
Cardiac resynchronization therapy
This document provides an overview of cardiac resynchronization therapy (CRT). It discusses how conduction delays can lead to electromechanical dyssynchrony and impair the heart's function. CRT aims to improve this synchrony and thereby improve systolic and diastolic function. The document outlines different types of dyssynchrony and methods to assess it, including echocardiography. Current guidelines recommend CRT for symptomatic heart failure patients with low ejection fraction and wide QRS duration. The implantation procedure involves placing right atrial/ventricular leads and a left ventricular lead via the coronary sinus.
Stent Thrombosis
Stent thrombosis is a rare but serious complication of percutaneous coronary intervention (PCI) with mortality rates between 25-40%. It is classified based on timing (acute, subacute, late, very late) and etiology (primary, secondary). Risk factors include premature discontinuation of dual antiplatelet therapy, smoking, diabetes, chronic kidney disease, acute coronary syndrome, and high platelet reactivity. Strategies to minimize stent thrombosis involve careful patient selection, optimal stent deployment, adherence to potent dual antiplatelet regimens, and treatment involving emergent thrombectomy with escalated antiplatelet therapy.
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Heparin Induced Thrombocytopeia (HIT)
- 1. HEPARIN INDUCED THROMBOCYTOPENIA (HIT) Dr. Sayeedur Rahman Khan Rumi Dr.rumibd@gmail.com MD Cardiology Final Part Student NHFH & RI
- 2. Introduction • Heparin is a widely used anticoagulant drug for the treatment and prevention of thromboembolic disorders • Heparin may cause immune thrombocytopenia (a reduction in platelet count), or HIT • HIT occurs in approximately 3%-5% of patients during or after UFH treatment for 5 days or more. • The incidence is much lower, less than 1% during and after LMWH therapy. • HIT can cause life- or limb-threatening thromboses
- 3. Heparin Induced Thrombocytopenia • Heparin induced thrombocytopenia (HIT) is characterized by a decrease in the platelet count of more than 50% from the highest platelet count value after the start of heparin, an onset 5 to 10 days after the start of heparin, hypercoagulability, and the presence of heparin dependent, platelet activating IgG antibodies. • HIT is an immune-mediated potentially fatal syndrome in which the heparin-induced immunoglobulins bridge platelets causing both thrombocytopenia and thrombosis. • HIT does not induce bleeding but rather results in a paradoxical prothrombotic state. • HIT is more common in surgical than medical patients (especially cardiac and orthopaedic patients).
- 4. 1. Increased platelet destruction • Non-immune • Septicemia/Inflammation • Disseminated intravascular coagulation • Thrombotic thrombocytopenic purpura • Immune • Autoimmune: idiopathic or secondary immune thrombocytopenia • Alloimmune: post-transfusion purpura • Drug-induced: prothrombic (heparin), prohemorrhagic (quinine, quinidine, gold, sulfa antibiotics, rifampin, vancomycin, NSAIDs, many others) Clinical Conditions/Causes of Thrombocytopenia
- 5. Clinical Conditions/Causes of Thrombocytopenia (Cont‘d ) 2. Decreased platelet production • Alcohol, cytotoxic drugs • Aplastic anemia • Leukemia, myelodysplasia • Metastatic invasion of marrow • Certain infections 3. Hypersplenism 4. Hemodilution (infusion of blood products, colloids, or crystalloids)
- 6. TYPES OF HIT
- 7. Parameter Type I HIT (non-immune mediated) Type II HIT (immune –mediated) Epidemiology 10-30% of UFH treated patients 1-5% of UFH-treated patients Less common with LMWH Temporal pattern Between days 1-4 of initiating UFH Between days 4-16 of initiating UFH/LMWH Severity of thrombocytopenia Mild, usually platelet counts remain > 100,000 Moderate to severe, mean platelet count 60,000 Antibody-mediated No Yes Thrombosis common No yes Management Observe Discontinue heparin/LMWH and start treatment with DTI Outcome Self-limited Death, arterial and venous thromb-osis are potential complications Immune vs Non Immune-Mediated HIT
- 9. Clinical events/Complications associated with HIT Possible complications of HIT include the following: • Deep venous thrombosis • Pulmonary embolism • Myocardial infarction • Occlusion of limb arteries (possibly resulting in amputation) • Transient ischemic attack and stroke • Skin necrosis • End-organ damage (eg, adrenal, bowel, spleen, gallbladder, or hepatic infarction; renal failure) • Death
- 10. Clinical signs of HIT Erythematous plaques Skin necrosis Deep venous thrombosis Venous gangrene
- 11. DIAGNOSIS OF HIT
- 13. Treatment of HIT • The prompt cessation of heparin. • As the condition is prothrombotic, these patients require alternative anticoagulation (In the United States, lepirudin, argatroban, and bivalirudin are licensed for HIT therapy) • Prophylactic platelet transfusions should be avoided in patients with HIT. The risk of bleeding is very low, and such transfusions can increase the risk of thrombosis. • The British Society of Haematology advises that all patients receiving prolonged heparin of any sort should have platelet counts on day 1 and every 2-4 days.
- 14. Thank you