Authors

  1. Laing, Craig MSN, RN, ANP-BC

Article Content

Found unresponsive at a local park, Mr. M, 23, is rushed to the ED by paramedics. En route to the hospital, his Glasgow Coma Scale (GCS) score is assessed as a 10 (E4, V2, M4). Although the paramedics administer a dose of I.V. naloxone, Mr. M's clinical status doesn't improve. (See Using theGCS.)

 

Upon arrival at the ED, his vital signs are core body temperature, 102.4[degrees] F (39.1[degrees] 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 are administered I.V. bolus. An additional dose of naloxone doesn't improve his clinical status. Blood and urine specimens are obtained and sent to the lab, including two sets of blood cultures and a urine culture and sensitivity. A complete blood cell count, comprehensive metabolic panel, lactate level, prothrombin time, and activated partial thromboplastin time are also performed. A 12-lead ECG is done and the patient undergoes computed tomography (CT) of the brain.

 

About 25 minutes after Mr. M'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 diffuse 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

A urinalysis shows no evidence of infection. His ECG shows sinus tachycardia with no significant abnormalities. A broad-spectrum antibiotic is administered, and he's admitted to the medical ICU for suspected sepsis. (See Close-up on abnormal lab values.)

 

That evening, Mr. M'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 systolic dysfunction with a left ventricular ejection 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 the CT of the brain is consistent with systemic septic embolization.

 

What's 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 (S. aureus) is the most common causative organism for infective endocarditis.3 Because many other microorganisms can cause infective endocarditis, blood should be drawn for 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

 

Risk factors

Although anyone can develop infective endocarditis, certain patients are at increased risk. 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

 

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 signs of vegetation, or a mobile mass on the valvular surface that moves independently of the valve.4

  
Table Using the GCS... - Click to enlarge in new windowTable Using the GCS

The American Heart Association/American College of Cardiology guidelines state that a "TTE is recommended 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 completion of antibiotic therapy.3

 

Other indications for surgical valve replacement include congestive heart failure, cardiogenic shock, aortic abscess, atrioventricular (AV) block, systemic embolization, and infection resistant to antibiotic treatment.3 The Modified Duke Criteria for diagnosing infective endocarditis has been established to give clinicians a format for making the correct diagnosis. (See Understanding criteria for diagnosis.)

  
Table Close-up on ab... - Click to enlarge in new windowTable Close-up on abnormal lab values*

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 AV blocks, and pericarditis.3

 

Fatal outcome

Mr. M underwent TEE on his second hospital day. It revealed a 12-mm mobile echodensity on his mitral 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 life-threatening 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.

 

Identifying dermatologic diagnostic clues

When caring for a patient with suspected infective endocarditis, perform a comprehensive skin assessment. Splinter hemorrhages and petechia 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

  
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Figure. No caption a... - Click to enlarge in new windowFigure. No caption available.

* Petechia, 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

 

 

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[degrees] F (38[degrees] 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.

 

 

REFERENCES

 

1. Sexton DJ. Epidemiology, risk factors and microbiology of infective endocarditis. UpToDate. 2013. http://www.uptodate.com. [Context Link]

 

2. Garcia-Cabrera E, Fernandez-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. [Context Link]

 

3. Sabe MA, Shrestha NK, Menon V. Contemporary drug treatment of infective endocarditis. Am J Cardiovasc Drugs. 2013;13(4):251-258. [Context Link]

 

4. Kessenich CR, Flanagan M. Infective endocarditis: beyond TEE. Nurse Pract. 2014;39(9):18-20. [Context Link]

 

5. Olmos C, Vilacosta I, Pozo E, et al. Prognostic implications of diabetes in patients with left-sided endocarditis: findings 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. [Context Link]

 

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. [Context Link]

 

8. Sexton DJ, Fowler VJ. Clinical manifestations and diagnosis of infective endocarditis. UpToDate. 2014. http://www.uptodate.com. [Context Link]