This document discusses sepsis, septic shock, and their management. Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is a subset of sepsis with profound circulatory and cellular abnormalities that increase mortality. The goals of treatment are early recognition, reversal of hemodynamic compromise, and infection control. Initial management involves aggressive fluid resuscitation and vasopressors if needed to maintain blood pressure and tissue perfusion. Norepinephrine is the first-line vasopressor for refractory hypotension in septic shock.
Shock is a life-threatening condition defined as inadequate tissue perfusion and cellular respiration. The document discusses the pathophysiology, classification, signs, and management of shock. Shock can be caused by hemorrhage, sepsis, anaphylaxis, or trauma. Early recognition and treatment is critical to prevent multiple organ failure and death. Fluid resuscitation is initially used but controlling any hemorrhage is paramount to recovery. Monitoring for signs of persistent or worsening shock is also important.
Pathophysiology of shock and its managementBipulBorthakur
This document discusses different types of shock including distributive, cardiogenic, obstructive, hypovolemic, and stages of shock. It provides details on sepsis and septic shock including pathogenesis, diagnostic criteria, and elements of care. Specific types of shock like neurogenic shock, anaphylactic shock, and cardiogenic shock are also summarized. The document emphasizes early recognition and treatment of shock.
Approach to Sepsis & Septic Shock in Emergency Medicine.AngelGovekar
Sepsis and septic shock result from a dysregulated host response to infection. Sepsis criteria include suspected or proven infection and an increase in the SOFA score of 2 or more, while septic shock requires sepsis with vasopressor need to maintain blood pressure and elevated lactate. Treatment involves early recognition, source control with antibiotics, initial fluid boluses of 1-2L for hypotension or elevated lactate, vasopressors if needed, and lactate clearance-guided resuscitation.
Hyperviscosity syndrome (HVS) occurs when increased levels of proteins, cells, or other components in the blood cause it to become abnormally viscous or thick. This leads to reduced blood flow and organ damage. HVS is diagnosed based on clinical signs and symptoms along with laboratory tests showing elevated blood viscosity. Treatment involves reducing the cause of viscosity, typically through plasmapheresis to remove excess proteins in multiple myeloma or Waldenstrom macroglobulinemia. Prompt treatment is needed to prevent organ damage and vision loss from HVS.
Sepsis in surgical patients and its biomarkers.pptxsamrat277229
The document discusses sepsis in surgical patients and biomarkers for diagnosis. It defines sepsis and outlines the Surviving Sepsis Campaign guidelines for treatment, including early antibiotic therapy, source control, and hemodynamic support. Biomarkers like lactate, C-reactive protein, and procalcitonin are described as potential diagnostic tools, though each has limitations. Procalcitonin in particular increases significantly in response to bacterial infection and can help differentiate between infectious and non-infectious causes of inflammation. The document concludes that while biomarkers show promise in rapid sepsis diagnosis and treatment monitoring, further research is still needed.
This document discusses adrenal insufficiency and its causes, presentation, diagnosis, and management. It can be primary or secondary. Primary adrenal insufficiency, also known as Addison's disease, is caused by destruction of the adrenal cortex leading to deficiencies in glucocorticoids, mineralocorticoids, and sex steroids. Its hallmark symptoms include fatigue, gastrointestinal issues, hyperpigmentation, and electrolyte abnormalities. Secondary adrenal insufficiency spares mineralocorticoid function and can result from pituitary or hypothalamic disease. Diagnosis involves ACTH and cortisol testing, and treatment is glucocorticoid and mineralocorticoid replacement.
The document discusses different types of shock including their causes, pathogenesis, and management. It defines shock as an imbalance between oxygen supply and demand resulting in organ dysfunction. The main types are distributive, cardiogenic, obstructive, and hypovolemic shock. Septic shock is discussed in depth including its pathogenesis involving an inflammatory response to infection, diagnostic criteria using SOFA and qSOFA scores, and elements of care including resuscitation, infection control, and supportive therapies. Cardiogenic shock is defined as a low cardiac output state resulting from various cardiac causes such as myocardial infarction. Hypovolemic shock reduces cardiac output through a decrease in preload from losses such as hemorrhage.
This document provides an overview of sepsis and septic shock, including definitions, epidemiology, pathogenesis, clinical features, investigation, treatment, complications, and prognosis. It defines sepsis as infection plus SIRS, and septic shock as sepsis that is not responsive to fluid resuscitation and requires vasopressors. The pathogenesis involves an initial inflammatory response to infection that can become dysregulated and lead to organ dysfunction. Treatment involves prompt resuscitation, antibiotics, source control, and organ support. Outcomes depend on factors like age, immune status, pathogen, and need for prolonged vasopressor support.
Shock is a life-threatening condition defined as inadequate tissue perfusion and cellular respiration. The document discusses the pathophysiology, classification, signs, and management of shock. Shock can be caused by hemorrhage, sepsis, anaphylaxis, or trauma. Early recognition and treatment is critical to prevent multiple organ failure and death. Fluid resuscitation is initially used but controlling any hemorrhage is paramount to recovery. Monitoring for signs of persistent or worsening shock is also important.
Pathophysiology of shock and its managementBipulBorthakur
This document discusses different types of shock including distributive, cardiogenic, obstructive, hypovolemic, and stages of shock. It provides details on sepsis and septic shock including pathogenesis, diagnostic criteria, and elements of care. Specific types of shock like neurogenic shock, anaphylactic shock, and cardiogenic shock are also summarized. The document emphasizes early recognition and treatment of shock.
Approach to Sepsis & Septic Shock in Emergency Medicine.AngelGovekar
Sepsis and septic shock result from a dysregulated host response to infection. Sepsis criteria include suspected or proven infection and an increase in the SOFA score of 2 or more, while septic shock requires sepsis with vasopressor need to maintain blood pressure and elevated lactate. Treatment involves early recognition, source control with antibiotics, initial fluid boluses of 1-2L for hypotension or elevated lactate, vasopressors if needed, and lactate clearance-guided resuscitation.
Hyperviscosity syndrome (HVS) occurs when increased levels of proteins, cells, or other components in the blood cause it to become abnormally viscous or thick. This leads to reduced blood flow and organ damage. HVS is diagnosed based on clinical signs and symptoms along with laboratory tests showing elevated blood viscosity. Treatment involves reducing the cause of viscosity, typically through plasmapheresis to remove excess proteins in multiple myeloma or Waldenstrom macroglobulinemia. Prompt treatment is needed to prevent organ damage and vision loss from HVS.
Sepsis in surgical patients and its biomarkers.pptxsamrat277229
The document discusses sepsis in surgical patients and biomarkers for diagnosis. It defines sepsis and outlines the Surviving Sepsis Campaign guidelines for treatment, including early antibiotic therapy, source control, and hemodynamic support. Biomarkers like lactate, C-reactive protein, and procalcitonin are described as potential diagnostic tools, though each has limitations. Procalcitonin in particular increases significantly in response to bacterial infection and can help differentiate between infectious and non-infectious causes of inflammation. The document concludes that while biomarkers show promise in rapid sepsis diagnosis and treatment monitoring, further research is still needed.
This document discusses adrenal insufficiency and its causes, presentation, diagnosis, and management. It can be primary or secondary. Primary adrenal insufficiency, also known as Addison's disease, is caused by destruction of the adrenal cortex leading to deficiencies in glucocorticoids, mineralocorticoids, and sex steroids. Its hallmark symptoms include fatigue, gastrointestinal issues, hyperpigmentation, and electrolyte abnormalities. Secondary adrenal insufficiency spares mineralocorticoid function and can result from pituitary or hypothalamic disease. Diagnosis involves ACTH and cortisol testing, and treatment is glucocorticoid and mineralocorticoid replacement.
The document discusses different types of shock including their causes, pathogenesis, and management. It defines shock as an imbalance between oxygen supply and demand resulting in organ dysfunction. The main types are distributive, cardiogenic, obstructive, and hypovolemic shock. Septic shock is discussed in depth including its pathogenesis involving an inflammatory response to infection, diagnostic criteria using SOFA and qSOFA scores, and elements of care including resuscitation, infection control, and supportive therapies. Cardiogenic shock is defined as a low cardiac output state resulting from various cardiac causes such as myocardial infarction. Hypovolemic shock reduces cardiac output through a decrease in preload from losses such as hemorrhage.
This document provides an overview of sepsis and septic shock, including definitions, epidemiology, pathogenesis, clinical features, investigation, treatment, complications, and prognosis. It defines sepsis as infection plus SIRS, and septic shock as sepsis that is not responsive to fluid resuscitation and requires vasopressors. The pathogenesis involves an initial inflammatory response to infection that can become dysregulated and lead to organ dysfunction. Treatment involves prompt resuscitation, antibiotics, source control, and organ support. Outcomes depend on factors like age, immune status, pathogen, and need for prolonged vasopressor support.
The study randomized 1554 ICU patients with septic shock to either a restrictive or standard IV fluid therapy strategy. The restrictive group could only receive IV fluids if certain criteria for hypoperfusion were met, while the standard group had no limits. The primary outcome of death within 90 days was 42.3% in the restrictive group and 42.1% in the standard group, indicating no significant difference. Serious adverse events and other secondary outcomes were also similar between the two groups, suggesting that a restrictive IV fluid strategy for septic shock is not inferior to standard therapy.
This document provides an overview of shock in pediatrics, including epidemiology, classification, pathogenesis, clinical manifestations, and principles of management. It begins with an introduction defining shock and its causes. It then discusses the main types of shock - hypovolemic, cardiogenic, distributive, and septic shock. The document reviews the epidemiology of shock in developing countries and the United States. It also provides details on the pathophysiology, clinical features, diagnosis, and management approaches for different shock types. The goals of treatment are outlined as restoring circulatory volume and blood flow while monitoring the patient.
Shock is a state of low tissue perfusion resulting in inadequate cellular respiration. With reduced oxygen and glucose delivery, cells switch from aerobic to anaerobic metabolism, producing lactic acid and risking cell death if perfusion is not restored. Shock is classified as hypovolemic, cardiogenic, obstructive, distributive, or endocrine/neurogenic and ranges from compensated to severe.
Blood transfusion involves transfusing blood products intravenously to replace lost components. Whole blood is now rarely used, with components like red blood cells, platelets, plasma, and cryoprecipitate being transfused individually. Testing and compatibility checks are done prior to transfusion to reduce risks of reactions or infections
- Acute liver failure (ALF) is characterized by rapid loss of liver function and development of hepatic encephalopathy, coagulopathy, and multi-organ failure within 26 weeks. Common causes include drug overdoses, viruses, and inherited metabolic disorders.
- Management involves global organ support, with a focus on circulatory resuscitation, renal replacement therapy, respiratory support, infection prophylaxis, and gastrointestinal protection. Cerebral protection measures aim to prevent intracranial hypertension through temperature control, normocapnia, mannitol, hypernatremia, and hypothermia if needed.
- Patients meeting criteria for liver transplantation should be transferred urgently to a specialized liver unit for assessment
Sepsis and septic shock definitions have evolved over time. Sepsis is now defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock presents as circulatory and metabolic abnormalities with fluid-refractory hypotension requiring vasopressors and signs of hypoperfusion. The pathophysiology involves an excessive inflammatory response and imbalance between coagulation and fibrinolysis. Treatment involves early antibiotics, fluid resuscitation, vasopressors if needed, and source control. Scoring systems like SOFA and qSOFA can help identify those at highest risk.
Cerebral malaria is the most severe complication caused by Plasmodium falciparum infection. It is characterized by coma and occurs when infected red blood cells sequester in the brain's microvasculature. Sequestration is mediated by cytoadherence of parasite proteins on infected cells to endothelial receptors and results in reduced blood flow and organ damage. Diagnosis involves identifying the parasite on blood smears with treatment consisting of intravenous artesunate or quinine along with supportive care. Prompt and complete antimalarial therapy is needed to prevent relapses.
The document provides information on sepsis epidemiology, pathogenesis, diagnosis, management and prognosis. Some key points:
- Sepsis cases and deaths are increasing worldwide, with the highest incidence among Black males, older adults, and in winter months. Regional disparities exist with most cases in low-income countries.
- Common infectious organisms include gram-positive bacteria and opportunistic fungi/viruses in immunocompromised patients. Culture-negative sepsis occurs in around half of cases.
- Sepsis diagnosis is based on life-threatening organ dysfunction caused by infection, as indicated by a SOFA score ≥2. Septic shock requires vasopressors to maintain blood pressure.
- Management
This document provides guidelines for monitoring patients with septic shock and surviving sepsis. It defines key terms like sepsis, severe sepsis, septic shock, and refractory septic shock. It discusses the pathophysiology of sepsis and how it leads to organ dysfunction. It also outlines the Surviving Sepsis Bundle care guidelines for initial resuscitation and infection management, including measuring lactate levels, administering antibiotics and fluids, and achieving hemodynamic and tissue perfusion targets within 3-6 hours. The guidelines recommend protocolized, quantitative resuscitation for sepsis-induced hypoperfusion.
This document provides information on the adrenal gland and adrenal disorders including:
1) The adrenal gland is a paired organ that produces hormones important for stress response and electrolyte balance. Diseases include primary adrenal insufficiency (Addison's disease) and Cushing's syndrome.
2) Pheochromocytoma is a rare catecholamine-producing tumor that causes symptoms of headache, sweating, and palpitations. Preoperative management with alpha-blockade is important to prevent postoperative hypotension.
3) Adrenocortical carcinoma is a rare malignant tumor most commonly presenting as Cushing's syndrome or virilization in adults. Surgical resection is the main treatment when possible
1. The document discusses sepsis, including definitions, pathogenesis, clinical manifestations, treatment goals and guidelines. It provides an example case of a patient presenting with sepsis from an infected wound.
2. Key treatment guidelines include administering IV fluids and antibiotics within 1 hour, maintaining a MAP of 65 mmHg with vasopressors if needed, identifying and treating the infection source, and supporting failing organs like the lungs and kidneys.
3. Sepsis results from the body's immune response to infection causing organ dysfunction. Timely treatment of the infection and its symptoms is important for recovery.
This document discusses complications that can occur from blood transfusions. It describes various types of immunologic reactions like acute and delayed hemolytic reactions, febrile non-hemolytic reactions, allergic reactions, transfusion-related acute lung injury, transfusion-associated circulatory overload, and post-transfusion purpura. It also discusses infectious complications from transfusions like viruses, bacteria, and other pathogens. Massive blood transfusions are outlined as carrying additional risks such as acidosis, hyperkalemia, citrate toxicity, hypocalcemia, metabolic alkalosis, iron overload, fluid overload, and hypothermia. Prevention strategies and treatment approaches for various complications are provided.
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
The document contains medical bullet points about various clinical topics including:
- Hypokalemia can cause muscle weakness and cardiac arrhythmias.
- During cardiac arrest, epinephrine can be administered endotracheally if IV access is unavailable.
- Pernicious anemia results from vitamin B12 absorption failure in the GI tract and causes GI and neurological signs and symptoms.
- A pressure ulcer patient should consume a high-protein, high-calorie diet unless contraindicated.
A condition affecting the blood's ability to clot and stop bleeding.
In disseminated intravascular coagulation, abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood's clotting factors, which can lead to massive bleeding in other places. Causes include inflammation, infection and cancer.
The document provides an overview of the management of sepsis and septic shock. It discusses that early goal-directed therapy within the first 6 hours including antibiotics, fluids, vasopressors and inotropes if needed can significantly improve outcomes. Other key points covered include the definitions and diagnostic criteria for sepsis; appropriate antibiotic therapy and vasopressor use; importance of lung-protective ventilation; role for activated protein C, steroids, tight glucose control and renal replacement therapy. Prognosis depends on early recognition and treatment as mortality increases significantly with delayed or inadequate care.
Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.
The document discusses sepsis and septic shock. It defines shock and classifies different types including cardiogenic, hypovolemic, anaphylactic, septic, and neurogenic shock. It describes the systemic inflammatory response syndrome (SIRS) criteria. Non-infective processes like trauma or surgery can also cause SIRS. Investigations for sepsis may include blood cultures, imaging, and biomarkers like procalcitonin. Positive findings include leukocytosis/leukopenia, thrombocytopenia, organ dysfunction, hyperglycemia, and hyperlactatemia. Early goal-directed resuscitation including antibiotics, fluid resuscitation, and inotropes can improve outcomes in septic shock.
This document discusses massive or large volume blood transfusions. It defines massive transfusion as replacing a patient's total blood volume within 24 hours, which is 70 mL/kg in adults and 80-90 mL/kg in children. While administering large volumes can cause complications like acidosis, hypokalemia, and coagulation issues, the main risks are from the underlying trauma causing blood loss. The document provides guidelines for managing potential complications and recognizing acute transfusion reactions from mild to life-threatening.
1. Shock is defined as a state where the delivery of oxygen to tissues is inadequate to meet metabolic demands, resulting in cellular dysfunction.
2. Shock is classified into five main types: hypovolemic, cardiogenic, obstructive, distributive, and endocrine.
3. Treatment for shock involves rapid fluid resuscitation to restore circulating volume, with vasopressors or inotropes as needed depending on the type of shock. Ongoing monitoring of vital signs and urine output is also critical.
MENINGITIS IN CHILDREN-1.pptx by John wambugu clinical officer paediatricsJohnMainaWambugu
This document provides an overview of meningitis, including its definition, causes, pathogenesis, clinical manifestations, diagnosis, treatment, and prevention. Key points include:
- Meningitis is an inflammation of the meninges that surround the brain and spinal cord. It can be caused by bacterial, viral, or fungal infections.
- Bacterial meningitis requires urgent treatment with antibiotics as it can be fatal if untreated. Common bacterial causes include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b.
- Symptoms may include fever, headache, stiff neck, nausea, confusion, and seizures. Diagnosis involves examination of cerebrospinal fluid
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
The study randomized 1554 ICU patients with septic shock to either a restrictive or standard IV fluid therapy strategy. The restrictive group could only receive IV fluids if certain criteria for hypoperfusion were met, while the standard group had no limits. The primary outcome of death within 90 days was 42.3% in the restrictive group and 42.1% in the standard group, indicating no significant difference. Serious adverse events and other secondary outcomes were also similar between the two groups, suggesting that a restrictive IV fluid strategy for septic shock is not inferior to standard therapy.
This document provides an overview of shock in pediatrics, including epidemiology, classification, pathogenesis, clinical manifestations, and principles of management. It begins with an introduction defining shock and its causes. It then discusses the main types of shock - hypovolemic, cardiogenic, distributive, and septic shock. The document reviews the epidemiology of shock in developing countries and the United States. It also provides details on the pathophysiology, clinical features, diagnosis, and management approaches for different shock types. The goals of treatment are outlined as restoring circulatory volume and blood flow while monitoring the patient.
Shock is a state of low tissue perfusion resulting in inadequate cellular respiration. With reduced oxygen and glucose delivery, cells switch from aerobic to anaerobic metabolism, producing lactic acid and risking cell death if perfusion is not restored. Shock is classified as hypovolemic, cardiogenic, obstructive, distributive, or endocrine/neurogenic and ranges from compensated to severe.
Blood transfusion involves transfusing blood products intravenously to replace lost components. Whole blood is now rarely used, with components like red blood cells, platelets, plasma, and cryoprecipitate being transfused individually. Testing and compatibility checks are done prior to transfusion to reduce risks of reactions or infections
- Acute liver failure (ALF) is characterized by rapid loss of liver function and development of hepatic encephalopathy, coagulopathy, and multi-organ failure within 26 weeks. Common causes include drug overdoses, viruses, and inherited metabolic disorders.
- Management involves global organ support, with a focus on circulatory resuscitation, renal replacement therapy, respiratory support, infection prophylaxis, and gastrointestinal protection. Cerebral protection measures aim to prevent intracranial hypertension through temperature control, normocapnia, mannitol, hypernatremia, and hypothermia if needed.
- Patients meeting criteria for liver transplantation should be transferred urgently to a specialized liver unit for assessment
Sepsis and septic shock definitions have evolved over time. Sepsis is now defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock presents as circulatory and metabolic abnormalities with fluid-refractory hypotension requiring vasopressors and signs of hypoperfusion. The pathophysiology involves an excessive inflammatory response and imbalance between coagulation and fibrinolysis. Treatment involves early antibiotics, fluid resuscitation, vasopressors if needed, and source control. Scoring systems like SOFA and qSOFA can help identify those at highest risk.
Cerebral malaria is the most severe complication caused by Plasmodium falciparum infection. It is characterized by coma and occurs when infected red blood cells sequester in the brain's microvasculature. Sequestration is mediated by cytoadherence of parasite proteins on infected cells to endothelial receptors and results in reduced blood flow and organ damage. Diagnosis involves identifying the parasite on blood smears with treatment consisting of intravenous artesunate or quinine along with supportive care. Prompt and complete antimalarial therapy is needed to prevent relapses.
The document provides information on sepsis epidemiology, pathogenesis, diagnosis, management and prognosis. Some key points:
- Sepsis cases and deaths are increasing worldwide, with the highest incidence among Black males, older adults, and in winter months. Regional disparities exist with most cases in low-income countries.
- Common infectious organisms include gram-positive bacteria and opportunistic fungi/viruses in immunocompromised patients. Culture-negative sepsis occurs in around half of cases.
- Sepsis diagnosis is based on life-threatening organ dysfunction caused by infection, as indicated by a SOFA score ≥2. Septic shock requires vasopressors to maintain blood pressure.
- Management
This document provides guidelines for monitoring patients with septic shock and surviving sepsis. It defines key terms like sepsis, severe sepsis, septic shock, and refractory septic shock. It discusses the pathophysiology of sepsis and how it leads to organ dysfunction. It also outlines the Surviving Sepsis Bundle care guidelines for initial resuscitation and infection management, including measuring lactate levels, administering antibiotics and fluids, and achieving hemodynamic and tissue perfusion targets within 3-6 hours. The guidelines recommend protocolized, quantitative resuscitation for sepsis-induced hypoperfusion.
This document provides information on the adrenal gland and adrenal disorders including:
1) The adrenal gland is a paired organ that produces hormones important for stress response and electrolyte balance. Diseases include primary adrenal insufficiency (Addison's disease) and Cushing's syndrome.
2) Pheochromocytoma is a rare catecholamine-producing tumor that causes symptoms of headache, sweating, and palpitations. Preoperative management with alpha-blockade is important to prevent postoperative hypotension.
3) Adrenocortical carcinoma is a rare malignant tumor most commonly presenting as Cushing's syndrome or virilization in adults. Surgical resection is the main treatment when possible
1. The document discusses sepsis, including definitions, pathogenesis, clinical manifestations, treatment goals and guidelines. It provides an example case of a patient presenting with sepsis from an infected wound.
2. Key treatment guidelines include administering IV fluids and antibiotics within 1 hour, maintaining a MAP of 65 mmHg with vasopressors if needed, identifying and treating the infection source, and supporting failing organs like the lungs and kidneys.
3. Sepsis results from the body's immune response to infection causing organ dysfunction. Timely treatment of the infection and its symptoms is important for recovery.
This document discusses complications that can occur from blood transfusions. It describes various types of immunologic reactions like acute and delayed hemolytic reactions, febrile non-hemolytic reactions, allergic reactions, transfusion-related acute lung injury, transfusion-associated circulatory overload, and post-transfusion purpura. It also discusses infectious complications from transfusions like viruses, bacteria, and other pathogens. Massive blood transfusions are outlined as carrying additional risks such as acidosis, hyperkalemia, citrate toxicity, hypocalcemia, metabolic alkalosis, iron overload, fluid overload, and hypothermia. Prevention strategies and treatment approaches for various complications are provided.
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
The document contains medical bullet points about various clinical topics including:
- Hypokalemia can cause muscle weakness and cardiac arrhythmias.
- During cardiac arrest, epinephrine can be administered endotracheally if IV access is unavailable.
- Pernicious anemia results from vitamin B12 absorption failure in the GI tract and causes GI and neurological signs and symptoms.
- A pressure ulcer patient should consume a high-protein, high-calorie diet unless contraindicated.
A condition affecting the blood's ability to clot and stop bleeding.
In disseminated intravascular coagulation, abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood's clotting factors, which can lead to massive bleeding in other places. Causes include inflammation, infection and cancer.
The document provides an overview of the management of sepsis and septic shock. It discusses that early goal-directed therapy within the first 6 hours including antibiotics, fluids, vasopressors and inotropes if needed can significantly improve outcomes. Other key points covered include the definitions and diagnostic criteria for sepsis; appropriate antibiotic therapy and vasopressor use; importance of lung-protective ventilation; role for activated protein C, steroids, tight glucose control and renal replacement therapy. Prognosis depends on early recognition and treatment as mortality increases significantly with delayed or inadequate care.
Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.
The document discusses sepsis and septic shock. It defines shock and classifies different types including cardiogenic, hypovolemic, anaphylactic, septic, and neurogenic shock. It describes the systemic inflammatory response syndrome (SIRS) criteria. Non-infective processes like trauma or surgery can also cause SIRS. Investigations for sepsis may include blood cultures, imaging, and biomarkers like procalcitonin. Positive findings include leukocytosis/leukopenia, thrombocytopenia, organ dysfunction, hyperglycemia, and hyperlactatemia. Early goal-directed resuscitation including antibiotics, fluid resuscitation, and inotropes can improve outcomes in septic shock.
This document discusses massive or large volume blood transfusions. It defines massive transfusion as replacing a patient's total blood volume within 24 hours, which is 70 mL/kg in adults and 80-90 mL/kg in children. While administering large volumes can cause complications like acidosis, hypokalemia, and coagulation issues, the main risks are from the underlying trauma causing blood loss. The document provides guidelines for managing potential complications and recognizing acute transfusion reactions from mild to life-threatening.
1. Shock is defined as a state where the delivery of oxygen to tissues is inadequate to meet metabolic demands, resulting in cellular dysfunction.
2. Shock is classified into five main types: hypovolemic, cardiogenic, obstructive, distributive, and endocrine.
3. Treatment for shock involves rapid fluid resuscitation to restore circulating volume, with vasopressors or inotropes as needed depending on the type of shock. Ongoing monitoring of vital signs and urine output is also critical.
MENINGITIS IN CHILDREN-1.pptx by John wambugu clinical officer paediatricsJohnMainaWambugu
This document provides an overview of meningitis, including its definition, causes, pathogenesis, clinical manifestations, diagnosis, treatment, and prevention. Key points include:
- Meningitis is an inflammation of the meninges that surround the brain and spinal cord. It can be caused by bacterial, viral, or fungal infections.
- Bacterial meningitis requires urgent treatment with antibiotics as it can be fatal if untreated. Common bacterial causes include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b.
- Symptoms may include fever, headache, stiff neck, nausea, confusion, and seizures. Diagnosis involves examination of cerebrospinal fluid
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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2. SEPSIS
Life-threatening organ dysfunction caused by a dysregulated host
response to infection
Criteria
- The Third International Consensus
Definition
I. Suspected or proven infection and
II. Increase in SOFA score of 2 or more from baseline
3. Septic shock
A subset of sepsis in which underlying circulatory and cellular metabolism
abnormalities are profound enough to substantially increase mortality
Criteria
Third international Consensus Definition
I. Sepsis
II. Vasopressor therapy required to maintain a MAP
of ≥65 mm Hg
III. Lactate >2 mmol/L despite adequate fluid
therapy
6. Why qSOFA?
● Rapid identification of high-risk patients immediately upon presentation
● Lower Sensitivity - Many who might benefit from early aggressive treatment
are negative according to qSOFA So full SOFA score is to be used on
patients with infection requiring hospital admission
7. Pathology of sepsis
Imbalance in procoagulant
and anticoagulant
functioning
• DIC causes micro- and
macrovascular clot formation and
impaired microvascular tissue
perfusion.
• Microvascular ischemia adds to
organ failure
The host develops a
hyperinflammatory
response
Blunted immune
response
• Increased risk of secondary
hospital-acquired infections
• Programmed death of key
immune, epithelial, and endothelial
cells, leading to tissue injury and
multiorgan dysfunction
…….There are no current specific therapies to remedy microvascular dysfunction
8. CLINICAL FEATURES
● Vital sign abnormalities—notably fever, hypotension, and/or tachycardia—are a hint
to sepsis.
● In ED patients with undifferentiated hypotension, 40% will ultimately have an
infectious cause of symptoms.
9. ● ED patients with sepsis are often volume-depleted from decreased intake and
increased fluid losses
● Classically sepsis is distributive shock with warm peripheries
intravascular volume depletion + septic cardiomyopathy = “cold shock,”
(impaired peripheral perfusion and cool extremities)
10. PULMONARY INJURY
● Widespread inflammation secondary to sepsis can affect pulmonary function even in
the absence of pneumonia.
● Acute lung injury is common and may result in ARDS
11. ● New bilateral pulmonary infiltrates on chest
radiographs not explained by effusions, lung
collapse, or nodules and not fully explained by
heart failure or volume overload.
● Clinically, severe refractory hypoxemia,
noncompliant lungs noted on mechanical
ventilation, and a chest radiograph showing
bilateral pulmonary alveolar infiltrates suggest the
diagnosis.
12. RENAL INJURY
AKI can present with azotemia, oliguria, or anuria.
Factors increasing acute kidney injury risk:
● Pre existing kidney dysfunction
● Depth and duration of hypotension
● Dehydration
● Nephrotoxic substances .
13. HEPATIC INJURY
● Marked elevations of ALT,AST, ALP are less common unless shock is present-
consider a biliary source of infection.
● Lessor elevations in LFTs can result from hypoperfusion and ischemia or be
secondary to direct endotoxin, cytokines, or immune complex damage.
● RBC hemolysis from microvascular coagulation can cause jaundice.
14. GI CHANGES
● The most common GI manifestation of sepsis is ileus, which may persist for days
after shock resolves.
● Minor GI blood loss within 24 hours of developing severe sepsis can result from
painless erosions in the mucosal layer of the stomach or duodenum.
15. HEMATOLOGIC CHANGES
● Neutropenia or neutrophilia, thrombocytopenia, or DIC
● Neutropenia occurs rarely and is associated with increased mortality.
● Neutropenia creates a relative immunosuppression, particularly later in
patients’ course.
● Both red cell production and survival decrease
16. HEMATOLOGIC CHANGES
● Thrombocytopenia may be from DIC but is present in >30% of cases of sepsis even in
the absence of DIC.
● Lower platelet levels are associated with worse outcomes.
● Fulminant DIC ( clinical clotting and bleeding coexist) , is rare but associated with a
very poor prognosis.
17. LABORATORY STUDIES SUGGESTING DIC
● Thrombocytopenia
● Prolonged PT and aPTT
● Decreased fibrinogen and antithrombin III levels
● Increased fibrin monomer, fibrin split products, and d-dimer levels.
18. METABOLIC CHANGES
● Abnormalities in lactate metabolism come from tissue hypoperfusion
● Hyperglycemia in patients without a history of diabetes is associated with a
worse prognosis
● Hypoglycemia( uncommon) may result due to depletion of hepatic glycogen
and inhibition of gluconeogenesis or adrenal insufficiency
19. ADRENAL INSUFFICIENCY
● Hypoperfusion of the adrenal glands
● Adrenal or pituitary hemorrhage
● Cytokine dysfunction of the adrenals
● Drug-induced hypermetabolism
● Inhibition of steroidogenesis by drugs
● Desensitization of glucocorticoid responsiveness at the cellular level.
20. SKIN
● Direct bacterial involvement of the skin and underlying soft tissues
● Hematogenous seeding of the skin or the underlying tissue
● Lesions from hypotension and/or DIC (acrocyanosis and necrosis of
peripheral tissues);
● Lesions from intravascular infections (microemboli and/or immune complex
vasculitis)
● Lesions caused by toxins (toxic shock syndrome).
● Look for any necrotizing or surgical source of sepsis
23. “Sepsis is a clinical diagnosis predicated on suspicion or confirmation of infection,
systemic inflammation, and evidence of new organ dysfunction and/or tissue
hypoperfusion”
24. Sepsis triggers
● Acute bacterial pneumonia(MC)
● Acute pyelonephritis
● Cholecystitis and cholangitis – Rare but severe
● Acute abdomen perforated viscous, appendicitis, diffuse colitis, or intra-
abdominal abscesses.
● In women of childbearing age, septic abortion and postpartum endometritis
or myometritis are unusual etiologies of septic shock
25. ……Sepsis triggers
● Acute pancreatitis can result in a presentation identical to that of septic shock
due to widespread inflammation
● Necrotizing soft tissue infections can occur in immunocompromised patients,
diabetic patients, or patients with a history of poor vascular circulation
● Elderly and Bedridden Consider decubitus ulcers and necrotizing infection
such as Fournier’s gangrene.
27. …..Sepsis triggers
● In female patients, particularly those with a rash, a pelvic exam
including an assessment for a retained foreign body or tampon
responsible for
toxic shock syndrome is important
● Those without an obvious source of septic shock may have primary
bacteremia or endocarditis.
28. Sepsis source could be indwelling medical devices
Dialysis
catheters
Chemotherapy ports
Peripherally inserted central
catheters
Ventriculoperitoneal
shunts
Pacemaker/Defibrillato
rs
29. ● Acute bacterial meningitis – rare but devastating cause of septic shock.
● Brain and spinal abscesses, subdural or epidural empyemas, and viral CNS infections
are seldom associated with shock on the initial presentation.
● Shock is unusual in neurosurgical patients secondary to neurosurgical procedure or
skull fracture.
30. INVESTIGATIONS
● CBC with platelet count
● serum electrolytes (including calcium and glucose)
● RFT
● lactic acid level;
● LFT
● URE
● ABG - the metabolic, ventilatory, and oxygenation assessment in select
patients.
● ? DIC -PT, aPTT, fibrinogen, and d-dimer.
31. The cornerstones of the initial treatment and
stabilization of severe sepsis are…….
1.Early recognition
1.Early reversal of
hemodynamic
compromise
Early infection control
32. SEPTIC SHOCK RESUSCITATION
1. Administering fluids
2. Frequently assessing response
3. Adding adjunct therapies including vasopressors based on response.
The specific method of titrating resuscitation is less important than treating
early and aggressively
……………………do not delay vasopressors when blood pressure does not respond to volume or if volume
overload seems likely.
33. The goals of resuscitation are to improve preload, tissue perfusion, and oxygen delivery.
34. VOLUME RESUSCITATION
● First assess and replenish circulating volume, typically with an
initial 20 - 30 mg/kg crystalloid bolus.
● 1- to 2-L bolus of RL or NS in a 70-kg adult
● Give more fluids if not clinically better and there is no evidence of volume overload.
● Often, 3 to 5 L are needed in the first 6 hours.
● Use balanced fluids after 2 to 3 L when possible.
35. ● Saline can produce a hyperchloremic metabolic acidosis if used in large-volume
resuscitation.
● Balanced fluids(Like RL) is preferable, particularly among critically ill patients or
those receiving large volumes of fluids.
36. Determine whether a patient is volume responsive
● Stroke volume variation - lift the legs of a supine patient for 60 seconds
improved blood pressure identifies a volume-responsive patient who will likely
benefit from more fluid.
● If these tools are unavailable - empiric crystalloid boluses until the patient fails to
demonstrate a response.
37. VASOPRESSORS
● Once the patient fails to respond to further IV volume expansion, aid perfusion with
vasoactive agents.
● Target a MAP goal of 65 mm Hg.
● Systolic pressure is commonly used in practice, seeking a goal of 90 mm Hg or higher.
● Administer norepinephrine as the first-line vasopressor to patients with refractory
hypotension
39. “In septic shock, norepinephrine, 0.5 to 30 micrograms/min, is the best first choice since
the dual α- and β-adrenergic effects result in peripheral vasoconstriction and cardiac
inotropy”
40. Vasopressin
● Vasopressin is a second-line agent and may allow for the down titration of
the norepinephrine dose.
● Give vasopressin as a constant infusion at a rate of 0.03 or 0.04 U/min.
● Do not titrate the dose, because higher rates are associated with vasospasm
and high morbidity.
41. ● Epinephrine at a dose of 1 to 20 micrograms/min is an option instead of
norepinephrine when dosed appropriately
● the risk of medication dosing errors related to epinephrine concentration may make
norepinephrine a superior choice.
● If tachydysrhythmias are a problem, phenylephrine is an option as a pure α-
adrenergic agonist.
42. CENTRAL VENOUS OXYGENATION
● After volume repletion and perfusion pressure optimization, if tissue perfusion is
compromised (cool extremities, poor pulses, worsening organ function), assess
oxygen balance.
● Although not needed routinely, measuring continuous SCVO2 with a catheter can aid
additional therapy
● An SCVO2 <70% implies a relative oxygen supply and demand mismatch
43. LACTATE CLEARANCE
● A decrease in lactate over time suggests a restoration of adequate tissue
perfusion.
● Measure lactate using the same method 1 to 2 hours apart
● Improvement of 10% or more is associated with improved clinical outcomes.
● Larger reductions in lactate are associated with even better outcomes
44. TREAT INFECTION
● Give broad-spectrum antibiotics as early as possible for severe sepsis.
● Combination antibiotic therapy leads to improved outcomes, potentially due to
higher rates of bactericidal activity.
45. ANTIBIOTIC OF CHOICE
In Adults (non- neutropenic) without an obvious source of infection
● Imipenem, 500 mg Q6H to 1 g IV Q8H OR
● Meropenem, 1 g IV every Q8H OR
● Doripenem, 500 mg IV Q8H OR
● Ertapenem*, 1 g IV OD
plus
● Vancomycin, 15 mg/kg loading dose
46. Adults (Nonneutropenic) - Suspected Pneumonia
● Ceftriaxone, 1–2 grams IV Q12H
● Azithromycin, 500 mg IV, then 250 mg IV OD
+
● Levofloxacin, 750 mg IV OD or moxifloxacin, 400 mg IV OD
● Vancomycin†, 15 milligrams/kg loading dose
50. Recommend against using qSOFA as a single screening tool for sepsis or septic
shock.
Septic shock on vasopressors an initial target MAP of 65 mm Hg is
recommended over higher MAP targets
Use crystalloids as first-line fluid for resuscitation.
Use norepinephrine as the first-line agent over other vasopressors.
51. Sepsis induced ARDS
Use a low tidal volume ventilation strategy (6 mL/kg), over a high tidal volume strategy (> 10
mL/kg
Use an upper limit goal for plateau pressures of 30 cm H2O, over higher plateau pressures.
For moderate-severe ARDS use prone ventilation for greater than 12 hours daily.
52. PROPHYLAXIS
If risk factors for GI bleeding, use stress ulcer prophylaxis
Use pharmacologic venous thromboembolism prophylaxis unless a contraindication to
such therapy exists.
Use low-molecular-weight heparin.
53. COMORBIDITIES
● Sepsis or septic shock and acute kidney injury, use either continuous or intermittent
renal replacement therapy.
● Initiate insulin therapy at a glucose level of ≥ 180mg/dL (10mmol/L).
● For severe metabolic acidemia (pH ≤ 7.2) and acute kidney injury (AKIN score 2 or 3),
use sodium bicarbonate therapy.
● Early (within 72 hours) initiation of enteral nutrition.