155: The Skin in Infective Endocarditis, Sepsis, Septic Shock, and Disseminated Intravascular Coagulation Flashcards
What is the definition of infective endocarditis?
Infective endocarditis is the inflammation of the endocardial lining of the heart caused by infection from bacteria or fungus.
What are the common clinical features of infective endocarditis?
The most common clinical features include fever and a new cardiac murmur.
What are the cutaneous findings associated with infective endocarditis?
Cutaneous findings include splinter hemorrhages, petechiae/purpura, Janeway lesions, and Osler nodes.
What are splinter hemorrhages?
Red-brown or black streaks under the nail plate.
What are petechiae/purpura?
Small red or purple spots on the skin.
What are Janeway lesions?
Painless, irregular, nonblanchable erythematous maculopapules on palms and soles.
What are Osler nodes?
Painful red papulonodules with a pale center on fingertips.
What are the risk factors for developing infective endocarditis?
Risk factors include history of infective endocarditis, diabetes, cancer, congenital heart disease, dental procedures, HIV disease, and intravenous drug abuse.
What are the complications associated with infective endocarditis?
The most concerning complications are neurologic, including ischemic lesions, hemorrhagic strokes, transient ischemic attacks, brain abscesses, and meningitis.
What is the etiology of infective endocarditis?
Infective endocarditis is classified based on valve type (native vs. prosthetic) and source of infection (community-acquired vs. health care-acquired).
What is the most common cause of infective endocarditis in high-income countries?
Staphylococcus aureus for both naive and prosthetic valves.
What is the male-to-female ratio for infective endocarditis cases?
2:1.
What is the significance of splinter hemorrhages in infective endocarditis?
They are longitudinal streaks under the nail plate and can indicate small capillary vasculitis or microemboli.
What is the recommended management for infective endocarditis?
The management focuses on eliminating infection with appropriate antibiotics, early surgical intervention, and treatment of complications.
What are the diagnostic methods used for infective endocarditis?
Diagnostic methods include bacterial cultures, echocardiography, EKG baseline, and cardiac CT.
What is the mortality rate associated with right-sided infective endocarditis in IV drug users?
5% to 9% mortality rate.
What are the most common causes of death in infective endocarditis patients?
Cerebral embolic disease and congestive heart failure.
What is the significance of vegetations larger than 10 mm in infective endocarditis?
Vegetations larger than 10 mm are associated with a greater embolic risk.
What are the poor prognostic indicators for infective endocarditis?
Poor prognostic indicators include left-sided infective endocarditis, vegetation size greater than 10 mm, prosthetic valves, older age, diabetes, immunosuppression, heart failure, renal failure, septic shock, and brain hemorrhage.
What is the recommended treatment duration for infective endocarditis?
Long-term parenteral antibiotics for 4 to 6 weeks.
What is the goal of surgical intervention in infective endocarditis?
To eliminate infection and reduce the risk of death, especially when vegetations are larger than 10 mm.
What are the rare causes of infective endocarditis associated with HACEK organisms?
Rare causes may include HACEK organisms: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella, and other organisms like Bartonella, Brucella, Coxiella species, and fungi like Candida.
What is the embolic risk associated with vegetations larger than 10 mm?
Vegetations larger than 10 mm are associated with a greater embolic risk, leading to complications such as emboli to the CNS, resulting in stroke, brain abscess, and meningitis, which can be identified with MRI.
How does the prognosis of infective endocarditis vary based on clinical factors?
The prognosis varies based on infecting organisms and associated clinical comorbidities. Poor prognostic indicators include left-sided infective endocarditis, vegetation size greater than 10 mm, presence of prosthetic valves, older age, diabetes, immunosuppression, heart failure, renal failure, septic shock, brain hemorrhage, and infections from MRSA, fungi, or polymicrobial sources.
What is the 5-year mortality rate of infective endocarditis?
The 5-year mortality rate of infective endocarditis is approximately 40%.
What are the recommended management strategies for infective endocarditis?
Management strategies include eliminating infection with appropriate antibiotics, early surgical intervention, and treatment of complications. Long-term (4 to 6 weeks) parenteral antibiotics, typically penicillin derivatives, are recommended. Surgical intervention is recommended within 48 hours of diagnosis if vegetations are larger than 10 mm to decrease the risk of death.
What diagnostic tests are essential for detecting infective endocarditis?
Essential diagnostic tests include bacterial cultures (3 sets prior to antibiotics), echocardiography, EKG baseline, and imaging such as cardiac CT and F-fluorodeoxyglucose positron emission tomography CT.
What are the key preventive measures for patients at risk of infective endocarditis (IE)?
Key preventive measures include good oral, dental, and skin hygiene, and IE prophylaxis for patients with a high risk of adverse outcomes associated with IE who are undergoing procedures involving contaminated or infected wounds, or surgery on oral or nasal mucosa.
What defines sepsis?
Sepsis is defined as a life-threatening organ dysfunction resulting from a dysregulated host response to infection.
What is septic shock?
Septic shock is a subset of sepsis where vasopressor therapy is required to maintain a mean arterial pressure of 65 mm Hg or greater, and there is a serum lactate level greater than 2 mmol/L persisting after fluid resuscitation.
What are the clinical features of cutaneous findings in septic patients?
Clinical features include erythroderma, pustules, purpura, necrotizing fasciitis, and ecthyma gangrenosum.
What are the noncutaneous findings associated with sepsis?
Noncutaneous findings include fever, prostration, oliguria, tachycardia, and tachypnea, with signs of pneumonia, meningitis, or peritonitis.
What are the potential complications of sepsis?
Potential complications include death, loss of limbs due to hypoperfusion, and permanent organ dysfunction.
What is the diagnosis for a patient with sepsis who has a serum lactate level of 3 mmol/L and requires vasopressors?
The diagnosis is septic shock.
What is the most likely cause of erythematous papules that progress to purpuric lesions in an immunocompromised host?
The most likely cause is an opportunistic fungal infection, such as Aspergillus spp., Fusarium spp., or Candida spp.
What are the risk factors for higher mortality in necrotizing fasciitis?
Risk factors include hospital-acquired infections, age >75 years, severe peripheral vascular disease, and coexistent sepsis or septic shock.
What does a qSOFA score of 3 indicate?
A qSOFA score of 3 indicates a high risk of poor outcomes.
What is the most common causative organism of ecthyma gangrenosum?
The most common causative organism is Pseudomonas aeruginosa, typically seen in neutropenic patients.
What is the most likely causative organism for hemorrhagic bullous cellulitis in a patient with liver disease?
The most likely causative organism is Vibrio vulnificus.
What is the most likely underlying infection in a patient with splenectomy who develops purpura fulminans?
The most likely underlying infection is Streptococcus pneumoniae.
What should be avoided for 3 weeks if infective endocarditis is complicated by hemorrhagic strokes?
Surgery.
What is the role of stress-responsive transcription factors in the pathogenesis of septic shock?
They activate inflammatory genes, leading to a ‘genomic storm’ characterized by increased production of mediators such as tumor necrosis factor-α, IL-6, IL-8, and nitric oxide.
What are the key components of the SOFA score used in diagnosing septic shock?
The SOFA score includes components such as partial pressure arterial oxygen/fraction of inspired oxygen, mean arterial pressure, platelet count, bilirubin levels, Glasgow coma scale score, urine output, and creatinine levels.
What does hyperbilirubinemia indicate in septic patients?
Hyperbilirubinemia indicates hepatic dysfunction and is associated with a worse prognosis.
What is the significance of early goal-directed therapy in the management of septic shock?
It aims to improve blood volume, cellular hypoxia, and tissue and organ perfusion within the first 6 hours, which is crucial for reducing mortality and improving outcomes.
What is disseminated intravascular coagulation (DIC)?
DIC is an acquired syndrome characterized by consumptive hypercoagulation and insufficient anticoagulation, often triggered by infections and sepsis.
What is the relationship between sepsis and septic shock?
Sepsis precedes septic shock in up to 50% of affected patients.
What are common imaging techniques used in septic shock?
Common imaging techniques include chest radiography, ultrasonography, CT, and MRI.
What is the mortality risk associated with septic shock?
In-hospital mortality has ranged from 15% to 30%, with septic shock associated with a higher risk of mortality (up to 50%).
What are some basic infection control measures to prevent sepsis?
Routine hand washing and the minimization and regular replacement of indwelling catheters.
How does age affect the incidence of DIC?
The incidence of DIC increases with age in both men and women, with men having a greater incidence than women.
What are the key factors involved in the pathogenesis of septic shock?
Key factors include infectious agents, cytokines, transcription factors, microvascular dysfunction, and hypotension.
What are cytokines involved in inflammatory responses?
Cytokines include interleukins (IL-1, IL-18) and Toll-like receptors that activate inflammatory responses.
What role do transcription factors play in sepsis?
Transcription factors like nuclear factor κB lead to a genomic storm, increasing mediators such as tumor necrosis factor-α, IL-6, and nitric oxide.
What causes microvascular dysfunction in sepsis?
Microvascular dysfunction results from injury and apoptosis, leading to organ dysfunction.
What is hypotension in the context of sepsis?
Hypotension is caused by overproduction of cyclooxygenase-2 and nitric oxide, contributing to septic shock.
What laboratory findings indicate poor prognosis in septic patients?
Laboratory findings indicative of poor prognosis include thrombocytopenia, hyperbilirubinemia, renal insufficiency, elevated serum lactate, and abnormal WBC count.
What is the significance of the SOFA score in septic patients?
The SOFA score assesses the severity of sepsis and predicts outcomes, with scores greater than 2 suggesting a 10% mortality risk.
What are primary management strategies for septic shock within the first 6 hours?
Primary management strategies include early goal-directed therapy, timely hemodynamic support, blood transfusion, adequate antibiotic administration, and continuous monitoring.
How does disseminated intravascular coagulation (DIC) relate to sepsis?
DIC is a serious complication of sepsis characterized by consumptive hypercoagulation, leading to organ dysfunction and potential outcomes like organ failure and death.
What is the most characteristic cutaneous finding in DIC?
Purpura fulminans is the most characteristic cutaneous finding in DIC, presenting as diffuse noninflammatory retiform purpura.
What are noncutaneous findings associated with DIC?
Noncutaneous findings in DIC include chest pains, shortness of breath, headache, speech changes, paralysis, and bleeding diathesis.
What complications are associated with DIC?
Complications of DIC include tissue necrosis, multiorgan failure, and development of Waterhouse-Friderichsen syndrome.
What is the role of tissue factor in DIC?
Tissue factor binds to factor VIIa, activating downstream coagulation cascades and leading to systemic activation of coagulation.
What laboratory findings are indicative of DIC?
Laboratory findings indicative of DIC include decreased platelet count, prolonged prothrombin time, elevated fibrin degradation products, and decreased protease inhibitors.
What are management strategies for DIC?
Management strategies for DIC include platelet and plasma transfusion, anticoagulation, fibrinolytics, and possible excision of necrotic tissue.
What is the significance of thrombocytopenia in DIC?
Thrombocytopenia in DIC is an independent predictor for organ failure and mortality.
What causes purpura fulminans in sepsis?
Purpura fulminans is caused by extensive microvascular occlusion due to systemic activation of the coagulation cascade.
What laboratory findings are characteristic of DIC?
Characteristic findings include decreased platelet count, prolonged prothrombin time, elevated D-dimer, and decreased fibrinogen.
What is the most characteristic cutaneous finding in DIC?
The most characteristic cutaneous finding in DIC is purpura fulminans.
What mechanisms lead to low antithrombin levels in DIC?
Low antithrombin levels result from continuous consumption, degradation by neutrophil elastase, and impaired synthesis due to liver failure.
What does elevated D-dimer levels indicate in DIC?
Elevated D-dimer levels indicate increased fibrin degradation, reflecting ongoing coagulation and fibrinolysis.
What coagulation abnormalities are typically seen in DIC?
Other abnormalities include prolonged activated partial thromboplastin time and decreased fibrinogen.
What is the underlying cause of ischemic digits in DIC?
The underlying cause is extensive microvascular occlusion due to fibrin deposition.
What is the role of protein C in coagulation?
Protein C is an anticoagulant that inhibits factors Va and VIIIa, and its deficiency contributes to hypercoagulability in DIC.
What does elevated plasmin-antiplasmin complex levels indicate?
Elevated plasmin-antiplasmin complex levels indicate increased fibrinolytic activity.
What is the significance of decreased ADAMTS13 activity in DIC?
Decreased ADAMTS13 activity contributes to microvascular thrombosis and is associated with thrombotic microangiopathy.
What are common noncutaneous findings in DIC?
Common noncutaneous findings include chest pains, shortness of breath, headache, and paralysis.
What complications can arise from DIC?
Complications of DIC include tissue necrosis, multiorgan failure, and death.
What is the role of tissue factor in DIC?
Tissue factor activates downstream coagulation cascades, leading to systemic activation of the coagulation cascade.
What laboratory findings are indicative of DIC?
Laboratory findings indicative of DIC include decreased platelet count, prolonged prothrombin time, and elevated fibrin degradation products.
What is a significant risk factor for mortality in patients with DIC?
Thrombocytopenia (<50 × 10^9/L) increases the risk of bleeding and is an independent predictor for organ failure and mortality.
What management strategies are used for DIC?
Management strategies for DIC include platelet and plasma transfusion, anticoagulation, and possible excision of necrotic tissue.
What is the importance of prompt diagnosis in DIC?
Prompt diagnosis and treatment of causes can prevent severe complications and improve outcomes.
What are the clinical features of purpura fulminans in DIC?
Purpura fulminans is characterized by diffuse noninflammatory retiform purpura, which can progress to gangrene if untreated.
What complications can arise from DIC?
Complications of DIC include tissue necrosis, multiorgan failure, and death, potentially leading to Waterhouse-Friderichsen syndrome.
How does systemic activation of the coagulation cascade contribute to DIC?
Systemic activation leads to fibrin deposition in the vasculature, causing organ ischemia and death.
What management strategies are recommended for patients with DIC?
Management strategies for DIC include platelet and plasma transfusion, anticoagulation, and possible excision of necrotic tissue.
What are the major criteria for a clinically definite case of infective endocarditis?
Major criteria include microbiologic evidence and evidence of endocardial involvement.
What are the minor criteria for diagnosing infective endocarditis?
Minor criteria include predisposition, fever, vascular phenomena, immunologic factors, and serologic evidence.
What are some differential diagnoses for splinter hemorrhages?
Differential diagnoses include atopic dermatitis, endocarditis, and vasculitis.
What are some settings in which DIC can occur?
Settings include hepatic failure, sepsis, transfusion reactions, and vascular abnormalities.
What is one of the major microbiologic criteria for infective endocarditis?
Two separate blood cultures positive for typical microorganisms.
What is a minor criterion for infective endocarditis related to predisposition?
Predisposition to infective endocarditis.
What are the major criteria for a clinically definite diagnosis of infective endocarditis?
- Microbiologic: Two separate blood cultures positive for typical microorganisms, or persistently positive blood culture for typical microorganisms, or single positive blood culture for Coxiella burnetii or a Phase I immunoglobulin G antibody titer greater than 1:800. 2. Evidence of endocardial involvement: New valvular regurgitation, or positive echocardiogram showing oscillating echogenic intracardiac mass at the site of endocardial injury, a periannular abscess, or new dehiscence of a prosthetic valve.
What are the minor criteria for diagnosing infective endocarditis as per the Modified Duke Criteria?
- Predisposition to infective endocarditis 2. Fever 3. Vascular phenomena such as Osler nodes or Roth spots 4. Immunologic factors such as a positive rheumatoid factor or glomerulonephritis 5. Serologic evidence of active infection not meeting microbiologic major criteria.
What are some differential diagnoses for splinter hemorrhages?
Differential diagnoses for splinter hemorrhages include: Atopic dermatitis, Cryoglobulinemia, Drug-induced, Vascular endothelial growth factor receptor inhibitors, Tetracyclines, Endocarditis, Idiopathic, Internal malignancy, Psoriasis, Scurvy, Thyrotoxicosis, Trauma, Trichinosis, Vasculitis.
In which settings can disseminated intravascular coagulation (DIC) occur?
DIC can occur in the following settings: Hepatic failure, Immunologic reaction to drugs or toxins, Malignancy, Obstetrical complications (e.g., amniotic fluid embolism, placental abruption), Protein C or protein S deficiency, Sepsis, Transfusion reactions, Transplant reactions, Trauma, Vascular abnormalities (e.g., aortic aneurysm, cardiac arrest).
What are Janeway lesions?
Painless, irregular, nonblanchable, erythematous maculopapules that appear on the palms and soles and last days to weeks seen in infective endocarditis (IE).
What are Osler nodes?
Painful red papulonodules with a pale center on the fingertips lasting days to weeks seen in infective endocarditis (IE).
What are the most concerning and severe complications of infective endocarditis (IE)?
Heart failure, embolic events, and abscess formation.
What is the most common cause of infective endocarditis (IE) in high-income countries for both naïve and prosthetic valves?
Staphylococcus aureus.
What begins as an erythematous papule that expands and eventually becomes a necrotic bulla, most commonly seen between the umbilicus and the knees?
Ecthyma gangrenosum.
What is Disseminated Intravascular Coagulation (DIC)?
The acquired reactive syndrome of consumptive hypercoagulation, insufficient anticoagulation, hemorrhage, systemic vascular inflammation, and endothelial dysfunction.
What is the most characteristic cutaneous finding in Disseminated Intravascular Coagulation (DIC)?
Diffuse noninflammatory retiform purpura from extensive microvascular occlusion.
Early goal-directed therapy in sepsis focuses on improving blood volume, cellular hypoxia, and tissue and organ perfusion within the first how many hours?
6 hours.
What does DIC in the neonatal period suggest?
Infection or congenital abnormalities.
Vegetations larger than how many mm are associated with a greater embolic risk?
3 mm.
