TI M E C R ITICAL
Infective endocarditis: What you need to know By Craig Laing, MSN, RN, ANP-BC
FOUND UNRESPONSIVE at a local park, JM, 23, is rushed to the ED by paramedics. En route to the hospital, his Glasgow Coma Scale score is assessed as a 10 (E4, V2, M4). (See Using the Glasgow Coma Scale.) Although the paramedics administer a dose of I.V. naloxone, JM’s clinical status doesn’t improve. Upon arrival
at the ED, his vital signs are core body temperature, 102.4° F (39.1° C); heart rate, 114; respiratory rate, 26; SpO2 96% on supplemental oxygen at 4 L/minute via nasal cannula; and BP, 84/49. Two large-bore peripheral I.V. catheters are inserted and 2 L of 0.9% sodium chloride solution is administered I.V. bolus. An additional
Using the Glasgow Coma Scale Score Eye opening (E) Spontaneous
4
Response to verbal command
3
Response to pain
2
No eye opening
1
Best verbal response (V) Oriented
5
Confused
4
Inappropriate words
3
Incomprehensible sounds
2
No verbal response
1
Best motor response (M) Obeys commands
6
Localizing response to pain
5
Withdrawal response to pain
4
Flexion to pain
3
Extension to pain
2
No motor response
1
Total The Glasgow Coma Scale (GCS) is scored between 3 and 15. The components of the GCS should be recorded individually; for example, E2, V3, M4 results in a GCS score of 9. A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less represents severe brain injury. Source: UpToDate, 2015.
dose of naloxone doesn’t improve his clinical status. Blood and urine specimens are obtained and sent to the lab, including specimens for lactate level, two sets of blood cultures, and urine culture and sensitivity. About 25 minutes after JM’s arrival to the ED, his BP hasn’t increased significantly despite the fluid challenge. His SpO2 has dropped to 81% on supplemental oxygen at 15 L/ minute via non-rebreather mask, and he’s dyspneic. A stat portable chest X-ray shows bilateral pulmonary edema. Due to his increased work of breathing and hypoxemia, he’s endotracheally intubated and placed on mechanical ventilation. A diuretic can’t be safely administered because of his hypotension. Diagnostic testing See Close up on abnormal lab values for JM’s abnormal blood work results. A urinalysis displays no evidence of infection. A 12-lead ECG shows sinus tachycardia with no significant abnormalities. A broad-spectrum antibiotic is initiated, and he’s admitted to the medical ICU for suspected sepsis. That evening, JM’s parents arrive at the hospital and inform the staff that their son has an ongoing heroin addiction. The nurse relays this information to the healthcare provider and a stat bedside transthoracic echocardiogram (TTE) is ordered. The echocardiogram shows severe left ventricular dysfunction with a left ventricular ejection March l Nursing2015 l 11
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TI M E C R ITICAL
fraction of 25% (normal range, 55% to 65%). A large, mobile echodensity consistent with vegetation is seen on the mitral valve. A stat consult with cardiology is requested for suspected infective endocarditis. The result of a computed tomography scan of the head completed urgently is consistent with systemic septic embolization. Looking into infective endocarditis Infective endocarditis is an infection of the endocardium, caused by bacteria, fungi, or viruses. This may affect not only ventricular function, leading to heart failure, but also the valvular structures. In the United States, 10,000 to 15,000 cases are diagnosed per year.1 Mortality is high, ranging from 20% to 40%.2 Staphylococcus aureus is the most common causative organism for infective endocarditis.3 Because many other kinds of bacteria and fungi can cause infective endocarditis, blood should be drawn for blood cultures before starting antibiotics.3 Fungal infective endocarditis, while extremely rare, has an even higher mortality, more than 50%.3 Proper identification of the causative organism is critical to successful treatment. It allows appropriate pharmacologic therapy and evaluation for valve replacement surgery and helps determine which patients might develop complications.3
Identifying dermatologic diagnostic clues When caring for a patient with suspected infective endocarditis, perform a comprehensive skin assessment. Splinter hemorrhages and petechiae aren’t specific to infective endocarditis, while Osler’s nodes, Roth spots, and Janeway lesions are usually indicative of the disease.8 • Splinter hemorrhages are long striations of blood under the nailbeds.7 • Petechiae, small red or purple spots caused by broken capillaries, are frequently seen, especially on the extremities.1 • Osler’s nodes (top figure) are painful purple nodes on the fingertips, bottoms of the toes, palms of the hands, dorsal aspect of the feet, and the earlobes. They’re caused by septic emboli with inflammatory reactions.9 • Roth spots (bottom figure) are exudative, edematous hemorrhagic lesions of the retina. • Janeway lesions are small nonpainful lesions, typically red, found on the palms of the hands and soles of the feet.9
Risk factors Although anyone can develop infective endocarditis, certain patients are more prone to infection. They include men older than age 60; patients with poor dentition, a history of I.V. drug abuse, or type 2 diabetes; those on hemodialysis; and those with implanted central venous access devices and pacemakers, implantable cardioverter defibrillators, ventricular assist devices, or prosthetic heart valves.4-6 Patients with history of structural heart disease and immunodeficiency are also at an increased risk.1
Close up on abnormal lab values* Lab test
JM’s values
Normal range
Potassium
4.7 mEq/L
3.5-4.5 mEq/L
Total carbon dioxide
36 mEq/L
24-32 mEq/L
Lactate
2.7 mEq/L
0.5-1.5 mEq/L
White blood cell count
22.4 × 103 cells/mm3
3.9-10.6 × 103 cells/mm3
Platelet count
89 × 10 cells/mm
150-400 × 103 cells/mm3
Erythrocyte sedimentation rate
94 mm/hr
0-15 mm/hr
3
3
*Lab values are based on those used by Christiana Care Health System, Wilmington, Del.
Diagnosis A thorough history and physical exam are imperative for an early diagnosis. Nurses must have a high index of suspicion for infective endocarditis when patients present with ongoing fatigue, fever, chills, malaise, a new murmur, stroke signs and symptoms, or congestive heart failure. A dermatologic assessment can assist with clinical decision making. (See Identifying dermatologic diagnostic clues.) While many patients initially undergo a TTE as part of their workup for infective endocarditis, the diagnostic test of choice is the transesophageal echocardiogram (TEE).4 The TEE has been shown to have a sensitivity of 100% for detecting infective endocarditis; the TTE’s sensitivity is much lower.4 When interpreting an echocardiogram, the cardiologist is looking for a signs of vegetation, or a mobile mass on the valvular surface that moves independently of the valve.4 The American Heart Association/ American College of Cardiology guidelines state that a “TTE is recommended March l Nursing2015 l 13
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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
TI M E C R ITICAL
in patients with suspected infective endocarditis to identify vegetations, characterize the hemodynamic severity of valvular lesions, assess ventricular function and pulmonary pressures, and detect complications.”7 They go on further to state that a “TEE is recommended in all patients with known or suspected infected endocarditis when TTE is nondiagnostic, when complications have developed or are clinically suspected, or when intracardiac leads are present.”7 Patients with mechanical heart valves who are being treated for infective endocarditis present a special challenge because their infection almost always requires surgery for valve replacement to completely clear the infection.3 In patients with both prosthetic valve endocarditis and native valve endocarditis, early surgical intervention is recommended instead of delaying surgery for antibiotic therapy.3 Other indications for surgical valve replacement include congestive heart failure, cardiogenic shock, aortic abscess, heart block, systemic embolization, and infection resistant to antibiotic treatment.3 The Modified Duke Criteria for diagnosing infective endocarditis have been established to give clinicians a format for making the correct diagnosis. (See Understanding criteria for diagnosis.) Complications The many complications of infective endocarditis include destruction of cardiac valves, heart failure, systemic embolization, stroke, multisystem organ failure, and cardiac conduction abnormalities, including heart blocks, and pericarditis.3 Fatal outcome JM underwent TEE on his second hospital day. It revealed a 12-mm mobile echodensity on his mitral
Understanding criteria for diagnosis6 The Modified Duke Criteria for diagnosing infective endocarditis include one or more of these pathologic criteria: • microorganism identified by culture or histology in a vegetation, or in an embolized vegetation, or in a cardiac abscess • histological specimen from a vegetation or an intracardiac abscess showing active endocarditis. Additional criteria needed include two major criteria OR one major and three minor criteria, OR five minor criteria. The two major criteria are: • two positive blood cultures from samples drawn at least 12 hours apart • evidence of endocardial involvement (echocardiographic evidence of an oscillating intracardiac mass, abscess, new partial prosthetic valve dehiscence, new valvular regurgitation). The five minor criteria include: • fever greater than 100.4° F (38° C) • vascular phenomena (such as major systemic emboli, Janeway lesions) • immunologic phenomena (such as Osler’s nodes) • predisposition to infective endocarditis (predisposing heart condition or I.V. drug abuse) • microbiologic evidence not meeting major criteria.
valve. Magnetic resonance imaging of the brain performed the same day showed several areas consistent with infarction and early hemorrhagic conversion in the cerebellum and brainstem. His blood cultures were positive for methicillin-resistant S. aureus. After 4 days of antibiotic therapy, he showed no signs of neurologic or hemodynamic improvement. Further testing by the neurologist confirmed brain death, and he was removed from the mechanical ventilator. An autopsy confirmed bacterial endocarditis with septic embolization as the cause of death. Prompt action required Infective endocarditis is a lifethreatening disease that requires prompt assessment and treatment. Practitioners must examine all details of the history and physical exam to make the correct diagnostic and treatment choices when encountering these critically ill patients. ■
REFERENCES 1. Sexton DJ. Epidemiology, risk factors and microbiology of infective endocarditis. UpToDate. 2013. http://www.uptodate.com. 2. García-Cabrera E, Fernández-Hidalgo N, Almirante B, et al. Neurological complications of infective endocarditis: risk factors, outcome, and impact of cardiac surgery: a multicenter observational study. Circulation. 2013;127(23):2272-2284. 3. Sabe MA, Shrestha NK, Menon V. Contemporary drug treatment of infective endocarditis. Am J Cardiovasc Drugs. 2013;13(4):251-258. 4. Kessenich CR, Flanagan M. Infective endocarditis: beyond TEE. Nurse Pract. 2014;39(9):18-20. 5. Olmos C, Vilacosta I, Pozo E, et al. Prognostic implications of diabetes in patients with left-sided endocarditis: fi ndings from a large cohort study. Medicine (Baltimore). 2014;93(2):114-119. 6. Thanavaro KL, Nixon JV. Endocarditis 2014: an update. Heart Lung. 2014;43(4):334-337. 7. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-2492. 8. Sexton DJ, Fowler VJ. Clinical manifestations and diagnosis of infective endocarditis. UpToDate. 2014. http://www.uptodate.com. 9. Servy A, Valeyrie-Allanore L, Alla F, et al. Prognostic value of skin manifestations of infective endocarditis. JAMA Dermatol. 2014;150(5):494-500. Craig Laing is an NP at Christiana Care Cardiology Consultants, Christiana Care Health System, in Newark, Del. The author has disclosed that he has no financial relationships related to this article. DOI-10.1097/01.NURSE.0000460725.56988.a4
14 l Nursing2015 l March
www.Nursing2015.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Infective endocarditis: What you need to know By Craig Laing, MSN, RN, ANP-BC
FOUND UNRESPONSIVE at a local park, JM, 23, is rushed to the ED by paramedics. En route to the hospital, his Glasgow Coma Scale score is assessed as a 10 (E4, V2, M4). (See Using the Glasgow Coma Scale.) Although the paramedics administer a dose of I.V. naloxone, JM’s clinical status doesn’t improve. Upon arrival
at the ED, his vital signs are core body temperature, 102.4° F (39.1° C); heart rate, 114; respiratory rate, 26; SpO2 96% on supplemental oxygen at 4 L/minute via nasal cannula; and BP, 84/49. Two large-bore peripheral I.V. catheters are inserted and 2 L of 0.9% sodium chloride solution is administered I.V. bolus. An additional
Using the Glasgow Coma Scale Score Eye opening (E) Spontaneous
4
Response to verbal command
3
Response to pain
2
No eye opening
1
Best verbal response (V) Oriented
5
Confused
4
Inappropriate words
3
Incomprehensible sounds
2
No verbal response
1
Best motor response (M) Obeys commands
6
Localizing response to pain
5
Withdrawal response to pain
4
Flexion to pain
3
Extension to pain
2
No motor response
1
Total The Glasgow Coma Scale (GCS) is scored between 3 and 15. The components of the GCS should be recorded individually; for example, E2, V3, M4 results in a GCS score of 9. A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less represents severe brain injury. Source: UpToDate, 2015.
dose of naloxone doesn’t improve his clinical status. Blood and urine specimens are obtained and sent to the lab, including specimens for lactate level, two sets of blood cultures, and urine culture and sensitivity. About 25 minutes after JM’s arrival to the ED, his BP hasn’t increased significantly despite the fluid challenge. His SpO2 has dropped to 81% on supplemental oxygen at 15 L/ minute via non-rebreather mask, and he’s dyspneic. A stat portable chest X-ray shows bilateral pulmonary edema. Due to his increased work of breathing and hypoxemia, he’s endotracheally intubated and placed on mechanical ventilation. A diuretic can’t be safely administered because of his hypotension. Diagnostic testing See Close up on abnormal lab values for JM’s abnormal blood work results. A urinalysis displays no evidence of infection. A 12-lead ECG shows sinus tachycardia with no significant abnormalities. A broad-spectrum antibiotic is initiated, and he’s admitted to the medical ICU for suspected sepsis. That evening, JM’s parents arrive at the hospital and inform the staff that their son has an ongoing heroin addiction. The nurse relays this information to the healthcare provider and a stat bedside transthoracic echocardiogram (TTE) is ordered. The echocardiogram shows severe left ventricular dysfunction with a left ventricular ejection March l Nursing2015 l 11
www.Nursing2015.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
TI M E C R ITICAL
fraction of 25% (normal range, 55% to 65%). A large, mobile echodensity consistent with vegetation is seen on the mitral valve. A stat consult with cardiology is requested for suspected infective endocarditis. The result of a computed tomography scan of the head completed urgently is consistent with systemic septic embolization. Looking into infective endocarditis Infective endocarditis is an infection of the endocardium, caused by bacteria, fungi, or viruses. This may affect not only ventricular function, leading to heart failure, but also the valvular structures. In the United States, 10,000 to 15,000 cases are diagnosed per year.1 Mortality is high, ranging from 20% to 40%.2 Staphylococcus aureus is the most common causative organism for infective endocarditis.3 Because many other kinds of bacteria and fungi can cause infective endocarditis, blood should be drawn for blood cultures before starting antibiotics.3 Fungal infective endocarditis, while extremely rare, has an even higher mortality, more than 50%.3 Proper identification of the causative organism is critical to successful treatment. It allows appropriate pharmacologic therapy and evaluation for valve replacement surgery and helps determine which patients might develop complications.3
Identifying dermatologic diagnostic clues When caring for a patient with suspected infective endocarditis, perform a comprehensive skin assessment. Splinter hemorrhages and petechiae aren’t specific to infective endocarditis, while Osler’s nodes, Roth spots, and Janeway lesions are usually indicative of the disease.8 • Splinter hemorrhages are long striations of blood under the nailbeds.7 • Petechiae, small red or purple spots caused by broken capillaries, are frequently seen, especially on the extremities.1 • Osler’s nodes (top figure) are painful purple nodes on the fingertips, bottoms of the toes, palms of the hands, dorsal aspect of the feet, and the earlobes. They’re caused by septic emboli with inflammatory reactions.9 • Roth spots (bottom figure) are exudative, edematous hemorrhagic lesions of the retina. • Janeway lesions are small nonpainful lesions, typically red, found on the palms of the hands and soles of the feet.9
Risk factors Although anyone can develop infective endocarditis, certain patients are more prone to infection. They include men older than age 60; patients with poor dentition, a history of I.V. drug abuse, or type 2 diabetes; those on hemodialysis; and those with implanted central venous access devices and pacemakers, implantable cardioverter defibrillators, ventricular assist devices, or prosthetic heart valves.4-6 Patients with history of structural heart disease and immunodeficiency are also at an increased risk.1
Close up on abnormal lab values* Lab test
JM’s values
Normal range
Potassium
4.7 mEq/L
3.5-4.5 mEq/L
Total carbon dioxide
36 mEq/L
24-32 mEq/L
Lactate
2.7 mEq/L
0.5-1.5 mEq/L
White blood cell count
22.4 × 103 cells/mm3
3.9-10.6 × 103 cells/mm3
Platelet count
89 × 10 cells/mm
150-400 × 103 cells/mm3
Erythrocyte sedimentation rate
94 mm/hr
0-15 mm/hr
3
3
*Lab values are based on those used by Christiana Care Health System, Wilmington, Del.
Diagnosis A thorough history and physical exam are imperative for an early diagnosis. Nurses must have a high index of suspicion for infective endocarditis when patients present with ongoing fatigue, fever, chills, malaise, a new murmur, stroke signs and symptoms, or congestive heart failure. A dermatologic assessment can assist with clinical decision making. (See Identifying dermatologic diagnostic clues.) While many patients initially undergo a TTE as part of their workup for infective endocarditis, the diagnostic test of choice is the transesophageal echocardiogram (TEE).4 The TEE has been shown to have a sensitivity of 100% for detecting infective endocarditis; the TTE’s sensitivity is much lower.4 When interpreting an echocardiogram, the cardiologist is looking for a signs of vegetation, or a mobile mass on the valvular surface that moves independently of the valve.4 The American Heart Association/ American College of Cardiology guidelines state that a “TTE is recommended March l Nursing2015 l 13
www.Nursing2015.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
TI M E C R ITICAL
in patients with suspected infective endocarditis to identify vegetations, characterize the hemodynamic severity of valvular lesions, assess ventricular function and pulmonary pressures, and detect complications.”7 They go on further to state that a “TEE is recommended in all patients with known or suspected infected endocarditis when TTE is nondiagnostic, when complications have developed or are clinically suspected, or when intracardiac leads are present.”7 Patients with mechanical heart valves who are being treated for infective endocarditis present a special challenge because their infection almost always requires surgery for valve replacement to completely clear the infection.3 In patients with both prosthetic valve endocarditis and native valve endocarditis, early surgical intervention is recommended instead of delaying surgery for antibiotic therapy.3 Other indications for surgical valve replacement include congestive heart failure, cardiogenic shock, aortic abscess, heart block, systemic embolization, and infection resistant to antibiotic treatment.3 The Modified Duke Criteria for diagnosing infective endocarditis have been established to give clinicians a format for making the correct diagnosis. (See Understanding criteria for diagnosis.) Complications The many complications of infective endocarditis include destruction of cardiac valves, heart failure, systemic embolization, stroke, multisystem organ failure, and cardiac conduction abnormalities, including heart blocks, and pericarditis.3 Fatal outcome JM underwent TEE on his second hospital day. It revealed a 12-mm mobile echodensity on his mitral
Understanding criteria for diagnosis6 The Modified Duke Criteria for diagnosing infective endocarditis include one or more of these pathologic criteria: • microorganism identified by culture or histology in a vegetation, or in an embolized vegetation, or in a cardiac abscess • histological specimen from a vegetation or an intracardiac abscess showing active endocarditis. Additional criteria needed include two major criteria OR one major and three minor criteria, OR five minor criteria. The two major criteria are: • two positive blood cultures from samples drawn at least 12 hours apart • evidence of endocardial involvement (echocardiographic evidence of an oscillating intracardiac mass, abscess, new partial prosthetic valve dehiscence, new valvular regurgitation). The five minor criteria include: • fever greater than 100.4° F (38° C) • vascular phenomena (such as major systemic emboli, Janeway lesions) • immunologic phenomena (such as Osler’s nodes) • predisposition to infective endocarditis (predisposing heart condition or I.V. drug abuse) • microbiologic evidence not meeting major criteria.
valve. Magnetic resonance imaging of the brain performed the same day showed several areas consistent with infarction and early hemorrhagic conversion in the cerebellum and brainstem. His blood cultures were positive for methicillin-resistant S. aureus. After 4 days of antibiotic therapy, he showed no signs of neurologic or hemodynamic improvement. Further testing by the neurologist confirmed brain death, and he was removed from the mechanical ventilator. An autopsy confirmed bacterial endocarditis with septic embolization as the cause of death. Prompt action required Infective endocarditis is a lifethreatening disease that requires prompt assessment and treatment. Practitioners must examine all details of the history and physical exam to make the correct diagnostic and treatment choices when encountering these critically ill patients. ■
REFERENCES 1. Sexton DJ. Epidemiology, risk factors and microbiology of infective endocarditis. UpToDate. 2013. http://www.uptodate.com. 2. García-Cabrera E, Fernández-Hidalgo N, Almirante B, et al. Neurological complications of infective endocarditis: risk factors, outcome, and impact of cardiac surgery: a multicenter observational study. Circulation. 2013;127(23):2272-2284. 3. Sabe MA, Shrestha NK, Menon V. Contemporary drug treatment of infective endocarditis. Am J Cardiovasc Drugs. 2013;13(4):251-258. 4. Kessenich CR, Flanagan M. Infective endocarditis: beyond TEE. Nurse Pract. 2014;39(9):18-20. 5. Olmos C, Vilacosta I, Pozo E, et al. Prognostic implications of diabetes in patients with left-sided endocarditis: fi ndings from a large cohort study. Medicine (Baltimore). 2014;93(2):114-119. 6. Thanavaro KL, Nixon JV. Endocarditis 2014: an update. Heart Lung. 2014;43(4):334-337. 7. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-2492. 8. Sexton DJ, Fowler VJ. Clinical manifestations and diagnosis of infective endocarditis. UpToDate. 2014. http://www.uptodate.com. 9. Servy A, Valeyrie-Allanore L, Alla F, et al. Prognostic value of skin manifestations of infective endocarditis. JAMA Dermatol. 2014;150(5):494-500. Craig Laing is an NP at Christiana Care Cardiology Consultants, Christiana Care Health System, in Newark, Del. The author has disclosed that he has no financial relationships related to this article. DOI-10.1097/01.NURSE.0000460725.56988.a4
14 l Nursing2015 l March
www.Nursing2015.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
