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Cerebral mycotic aneurysm and infective endocarditis: a case study.

ABSTRACT

Neurologic complications occur in 20%-40% of patients with infective endocarditis. Mycotic aneurysms are one example of these complications, and although rare, they can confound a patient's recovery and increase morbidity and mortality. This article will examine one patient's experience and the devastating effects that this complication had on his life. The information in this article will help to support neurological nurses in refining care and facilitating the best possible recovery for patients who develop this condition.

Keywords: complication, endocarditis, mycotic aneurysm

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A woman calls emergency medical services because her 42-year-old husband is exhibiting a sudden onset of change in mental status. By the time paramedics arrive and assess the patient, he is unresponsive and has to be intubated. He is air lifted to the hospital and has an immediate head computed tomography (CT) that shows a large left frontal intracerebral hemorrhage with a 10-mm left-to-right midline shift and hydrocephalus. The patient's medical history consists of mitral valve prolapse; gastroesophageal reflux disease; and depression with no history of smoking, alcohol, or drug use. In his family history, both his father and paternal grandfather had mitral valve replacements. Three and one-half weeks before this event, he had "flulike" symptoms and was diagnosed with subacute bacterial endocarditis based on positive blood cultures for Streptococcus viridans and Streptococcus gordonii. He is currently on his third week of antibiotic therapy. Within 12 hours of admittance to the emergency department, the patient is taken to the operating room for an evacuation of hematoma via craniotomy and the insertion of a ventriculostomy tube. Several days later, a cerebral angiogram shows multiple mycotic aneurysms (MAs), which the neurosurgeon suspects derived from his endocarditis.

Background: Infective Endocarditis

Infective endocarditis (IE) is diagnosed when there is an infection of the endocardium or the lining layer of the heart (Lester & Wilansky, 2007). It can be acute or subacute, but many studies dealing with diagnosis and treatment do not differentiate between the two types because most of the principles of management are the same. According to the American Heart Association, there are about 10,000-20,000 new cases of IE annually in the United States (Luttenberger & DiNapoli, 2011). The incidence of the disease has remained relatively constant with 0.16-5.4 cases per 1000 hospital admissions; however, the mortality can be up to 75% in high-risk groups (Mocchegiani & Nataloni, 2009). Patients who already have underlying heart disease such as aortic valve disease, mitral regurgitation, or congenital heart disease are at higher risk. Other risk factors include prior history of endocarditis, invasive procedures, prosthetic valves, drug abuse, and chronic medical conditions such as diabetes or end-stage renal disease (Luttenberger & DiNapoli, 2011). Although heart disease is a big risk factor, surprisingly about 10%--20% of adults diagnosed with IE have no clear underlying heart disease (Lester & Wilansky, 2007).

IE is a complex disease that can have nonspecific symptoms (Mocchegiani & Nataloni, 2009). The infection mainly forms along the edges of the valves of the heart and produces lesions (vegetations) that consist of the infecting organisms plus fibrin and platelets. Presentation varies between patients (Luttenberger & DiNapoli, 2011). Signs and symptoms can include fever/chills, fatigue, joint/muscle pain, chest pain, new-onset or changing heart murmur, night sweats, cough, shortness of breath, weight loss, headache, confusion, petechiae, hematuria, enlarged spleen, and edema in the abdomen or lower extremities (National Heart, Lung, and Blood Institute, 2014). Patients can develop red or purple tender areas under the skin of their hands or feet, also known as Osier's nodes, named for the physician who first described endocarditis in 1885.

The gold standard for diagnosis of IE is blood cultures correlated with presenting signs and symptoms (Luttenberger & DiNapoli, 2011). Although IE can have a number of causative organisms, most cases are triggered by staphylococci and streptococci (Lester & Wilansky, 2007). Other studies that may show abnormalities include chest x-ray and transesophageal echocardiogram (TEE) or transthoracic echocardiogram. The echocardiograph studies allow visualization of endocardial lesions (Lester & Wilansky, 2007). Transthoracic echocardiogram can detect 85% of vegetations; however, TEE is more sensitive if the patient has a prosthetic valve (Luttenberger & DiNapoli, 2011). An electrocardiogram may also be ordered. This is not usually used to diagnose IE, but it is sometimes done to determine if the infection is affecting the heart's electrical activity (National Heart, Lung, and Blood Institute, 2014).

The main goals of treatment for IE are to eliminate the infectious agent, prevent additional complications, and manage those complications already present (Luttenberger & DiNapoli, 2011). Timely antimicrobial treatment is necessary to prevent embolic events (Mocchegiani & Nataloni, 2009).

Neurologic Complications

In a prospective, multicenter study, Sonneville et al. (2011) discovered that neurologic complications occur in 20%-40% of patients with IE. Vegetation fragments can embolize and cause infarct. Septic emboli can also cause injury and inflammation such as erosive arteritis and weakening of the vessel wall (Aziz, Perwaiz, Penupolu, Doddi, & Gongireddy, 2011). A study of 218 patients with IE at Massachusetts General Hospital found that 38% of these patients developed some type of neurologic complications (Ahmed, 2013). Symptomatic neurologic complications include ischemic stroke, meningitis, brain abscess, cerebral hemorrhage, and intracranial MA.

MAs are also called infective or microbial aneurysms. Endocarditis is the most frequent cause of MA (Dhomne, Rao, Shrivastava, Sidhartha, & Limaye, 2008). About 2%-3% of patients with IE are diagnosed with MAs, but the incidence as determined on autopsy approaches 10% (Ahmed, 2013). Although rare, these inflammatory neurovascular lesions can complicate a diagnosis of IE and increase morbidity and mortality for these patients (Allen et al., 2013; Mocchegiani & Nataloni, 2009). This high mortality is related to the fact that MAs can enlarge, rupture, and cause subarachnoid and intracerebral hemorrhage, many times without warning (Kuo et al., 2010).

The middle cerebral artery (MCA) is the most common location for cerebral MAs; this area is involved in 50%-70% of these patients (Allen et al., 2013). Because the size of MAs is variable, it is difficult to predict the outcome. A rupture increases the risk of mortality. A rupture can occur weeks to months after the initial diagnosis or treatment of IE (Aziz et al., 2011). The incidence of rupture has been debated but can be up to 80% because many patients present clinically after rupture has occurred (Allen et al., 2013). In their study of patients with IE, Okazaki et al. (2011) showed a relationship between asymptomatic cerebral microbleeds and increased incidence of intracranial hemorrhage.

If MA is suspected, several diagnostic tests are warranted. CT alone can be within normal limits so cerebral angiogram should be recommended in any patient with IE who exhibits mental status changes and/or neurological deficits (Ahmed, 2013; Allen et al., 2013). In the past, digital subtraction angiography was the gold standard in the diagnosis of intracranial aneurysm. Current CT angiogram technology has increased resolution and lower risk; therefore, it has replaced digital subtraction angiography as the best tool for diagnosis of MA (Kuo et al., 2010). Magnetic resonance imaging/angiogram is also useful to visualize areas of ischemia or detect aneurysms, but CT angiography is more sensitive for aneurysms that are less than 3 mm in size (Allen et al., 2013). A study by Duval et al. (2010) indicated that early magnetic resonance imaging identified cerebral lesions even in patients with IE who did not have specific neurologic symptoms.

As mentioned, the biggest complication that can occur during the management of MA is rupture. If MA is recognized and treated early, rupture can be prevented. Unfortunately, there are no widely accepted guidelines for treatment of infective intracranial aneurysm. There are three main treatment options: medical management, endovascular, and surgical treatment. The choice of treatment is dependent on various factors such as patient's age and neurological condition (Hickey, 2009). If medical management is used, antibiotic therapy should be given a minimum of 6 weeks with close monitoring by angiography to evaluate the size and resolution of the aneurysm (Kuo et al., 2010). Unruptured MAs can fully heal with antimicrobial therapy, so this course of treatment can be appropriate for patients with unruptured MAs that remain stable (Aziz et al., 2011; Dhomne et al., 2008). The downside to medical treatment alone is that it takes longer to resolve and carries a higher risk of mortality. Some clinicians recommend endovascular repair as the treatment of choice (Allen et al., 2013). This treatment option continues to evolve, but recent studies support it as a reliable and safe technique with minimal risk (Dhomne et al., 2008). The most popular endovascular treatment is coiling. Neurosurgical options include clipping, clot removal, or excision with vessel grafting. Because surgery carries increased risks, it is usually reserved for patients with hemorrhage from a ruptured aneurysm or increasing intracranial pressure (Kuo et al, 2010).

One additional surgical consideration is whether the patient should have a valve repair to remove the source of cerebral emboli; however, there is no agreement as to when this should be done (Kuo et al., 2010). Cardiac surgery will be required in about 40% of patients with endocarditis, and heart failure is the primary indication for this option (Ahmed, 2013).

Nursing Care: Implications for Practice

Because rupture of MA carries increased mortality, nurses need to be able to recognize potential signs/symptoms early and notify the physician promptly for any changes in neurological status especially in a patient who has or is recovering from IE. Signs of rupture may include changes in level of consciousness, "explosive" headache, cranial nerve deficits, nausea/vomiting, neck stiffness, visual changes, stroke symptoms, and signs of cerebral edema and/or increasing intracranial pressure (Hickey, 2009). Frequent neurological assessments are prudent especially if the patient has other comorbidities. These checks should include level of consciousness and cranial nerve assessment with close attention to pupil reaction/vision, muscle strength, speaking/swallowing, and pain (Hickey, 2009). Pain in the head, neck, or face with or without nuchal rigidity is cause for concern. When assessing the patient's vital signs, be especially alert for acute changes in blood pressure. As with any patient who has an injury to the brain, it is also important to monitor laboratory values paying particular attention to the serum sodium level. A careful cardiac assessment is needed being especially attune to any existing or new-onset heart murmurs.

Close attention to standard nursing care prevents additional complications related to falls, immobility, skin breakdown, constipation, and atelectasis. To coordinate care for patients who develop neurological complications with IE, nurses need to collaborate with other members of the healthcare team including infectious disease specialists, neurologist/neurosurgeon, internists, cardiologist, pharmacist, physical/occupational therapists, speech language pathologists, and social services/care management (Ahmed, 2013).

Complications, most notably rupture, can occur weeks after the initial IE diagnosis; therefore, comprehensive patient/family teaching at discharge is imperative. This teaching needs to cover the signs/symptoms of neurological complications and the importance of notifying the physician promptly if the patient develops any of these. Because prevention of IE will prevent complications such as MA, teaching should also include topics such as antibiotic prophylaxis before invasive procedures like dental work.

Summary of Case Study Patient's Course of Treatment and Outcomes

The case study patient had a prolonged course of treatment, which greatly affected his lifestyle. Immediately postoperatively, he went to the intensive care unit; he was purposeful with the left side and minimally responsive with his right. He was placed on a nicardipine drip to maintain systolic blood pressure between 110 and 140 mm Hg. He had self-extubated over the first night. On postoperative day 1, a head CT scan was obtained, which showed improved midline shift and markedly decreased mass effect of ventricles. On physical examination, the patient had right hemiparesis with a questionable right field cut and was purposeful with the left side. Pupils were equal, round, and reactive to light. He was noted to have receptive and expressive aphasia and very minimal speech. Intracranial pressure ranged from 7 to 15 mm Hg, so the external ventricular drain was clamped. Ceftriaxone (Rocephin) was initiated. The neurologist's differential diagnosis was ischemic event with hemorrhagic transformation versus MAs.

By postoperative day 2, the patient was moving his left side purposefully and would move his right side slightly to noxious stimuli but was not following commands. He would open his eyes to stimulation. The patient was found to have a systolic murmur. Echocardiogram was performed and showed bileaflet mitral valve prolapse with an echodensity noted at the tip of the posterior leaflet of the mitral valve. Cardiology was consulted for echocardiogram results, and the patient was weaned off the nicardipine (Cardene) drip and placed on labetalol (Trandate) as needed. Infectious disease was also consulted for antibiotic management.

The next day, the patient was taken for a cerebral angiogram, which showed multiple MAs. There was a multilobulated aneurysm seen on the right cerebral artery (MCA) measuring 3.9 mm x 2.7 mm x 2.3 mm. There was a 5.1 mm x 5.3 mm x 6 mm saccular aneurysm seen on the right posterior cerebral artery (PCA). Diffuse vasospasm was seen throughout the left cerebral vasculature, namely, in the MCA distribution. On postoperative day 5, the patient pulled out his external ventricular drain. TEE showed mitral valve prolapse with severe mitral regurgitation. There was no clear vegetation on the valve, but the leaflets tips did appear to be thickened. On physical examination, the patient was following commands with his left arm and leg, answering yes and no, but remained with only movement of the right side to painful stimuli. Physical/occupational therapy and speech language pathology were consulted.

By postoperative day 6, the patient was tolerating a pureed diet. The infectious disease physician increased the ceftriaxone to every 12 hours instead of daily. It was decided that cardiothoracic surgery would wait to do a mitral valve repair/replacement for at least 3-4 weeks because of the patient being at high risk for hemorrhage. At 1 week postoperatively, the patient was more alert and oriented to person/place. He remained aphasic with simple one syllable words and had moderate word finding difficulty. He was able to feed himself but still had decreased sensation on the right side. A brace was ordered for right hand drop.

On the eighth postoperative day, a head CT showed further reduction of residual intraparenchymal hemorrhage. Midline shift was resolved, and he had normal ventricular size. The patient was moved out of the intensive care unit to a medical-surgical unit. The patient was getting out of bed to the chair with therapy. At postoperative day 10, a repeat cerebral angiogram was performed, which showed a slightly larger right MCA aneurysm off the inferior division, a new left MCA inferior saccular aneurysm, and an unchanged right saccular PCA aneurysm. It was decided to continue with the course of antibiotics and manage conservatively with a repeat cerebral angiogram in 1 week. Over the next several days, the patient remained stable. The repeat cerebral angiogram showed that the three MAs were essentially unchanged from the previous examination.

On the 20th day after admission, the patient was transferred to a rehabilitation facility. The antibiotic was decreased to once a day and was to continue for 3 months. When the patient left the hospital, his left arm/leg were 5 of 5 strength, and his right arm/leg remained 0 of 5. His speech showed apraxia, dysarthria, and expressive aphasia. While at rehabilitation, the patient had right hemiparesis with the upper extremity mostly involved. He had motor and verbal apraxia. In the beginning, he was able to ambulate 100 feet using a quad cane with moderate assistance. He could transfer from wheelchair to bed with moderate assistance. He also needed moderate assistance to negotiate four stairs for advancement of his right leg.

After 1 month in the rehabilitation facility, the patient was transferred to a skilled nursing facility. At discharge from rehabilitation, the patient could ambulate 165 feet using a quad cane with minimal assistance. He could perform self-care and toileting with close supervision/contact guard but still had moderate-to-severe expressive aphasia and perseverated when performing complex tasks. Another cerebral angiogram showed that the right MCA aneurysm remained unchanged and the left MCA aneurysm was resolved. The right PCA aneurysm was smaller.

At his 6-week follow-up with the neurosurgeon, the patient still had significant right-sided weakness and a significant component of expressive aphasia. His right upper extremity remained plegic. However, he had regained more movement in his right lower extremity. He was conversive and seemed to understand; however, he was unable to say more than 1-word answers and mainly said "yeah" or "no." The patient had a follow-up appointment with cardiothoracic surgery and was scheduled for a repeat TEE. The repeat TEE showed myxomatous changes of the mitral valve with prolapse of the posterior leaflet of the mitral valve, predominantly involving the P2 with severe mitral regurgitation. It was decided that the patient will need to have his mitral valve repaired.

This patient and his family decided to move in with his parents from a different state and were planning to continue his recovery and follow-up there. The final contact with this patient was at his discharge from the skilled nursing facility. At that time, he had progressed quite a long way from the initial injury but still had significant changes to his lifestyle. He was able to shower using a shower bench and with moderate assistance. He also still needed assistance with other activities of daily living such as dressing, bathing, and toileting. He was able to follow commands but continued with expressive aphasia. His speech was dysarthric. His motor examination showed 5 of 5 muscle strength on the left side with 3 of 5 in the right upper extremity, 0 of 5 in the right hand, 4 of 5 at the right hip flexor, and 1 of 5 in the right distal extremity. The plan was to continue with his therapies at his parents' home and to consult with a cardiac surgeon for mitral valve repair.

Conclusion

Neurologic complications, such as MA, after IE can significantly impact the patient's course of recovery. Nurses caring for any patient at risk for these conditions must be vigilant to any signs and symptoms that may indicate that the patient is deteriorating neurologically. Education of patients and families about these signs and symptoms is also important because problems can occur after discharge. Prompt intervention and treatment of any complications will improve the patient outcomes overall.

References

Ahmed, A. (2013). Neurological sequelae of infectious endocarditis. Medscape Reference, Retrieved from http://emedicine. medscape.com/article/1165712-overview#aw2aab6b3

Allen, L. M., Fowler, A. M., Walker, C., Derdeyn, C. P., Nguyen, B. V., Hasso, A. N., ... Moran, C. J. (2013). Retrospective review of cerebral mycotic aneurysms in 26 patients: Focus on treatment in strongly immunocompromised patients with a brief literature review. American Journal of Neuroradiology, 34, 823-827. doi:10.3174/ajnr.A3302

Aziz, F., Perwaiz, S., Penupolu, S., Doddi, S., & Gongireddy, S. (2011). Intracranial hemorrhage in infective endocarditis: A case study. Journal of Thoracic Disease, 3, 134-137. doi:10. 3978/j.issn.2072-1439.2010.11.13

Dhomne, S., Rao, C., Shrivastava, M., Sidhartha, W., & Limaye, U. (2008). Endovascular management of ruptured cerebral mycotic aneurysms. British Journal of Neurosurgery, 22, 46-52. doi: 10.1080/02688690701593561

Duval, X., lung, B., Klein, I., Brochet, E., Thabut, G., Amoult, F., ... IMAGE (Resonance Magnetic Imaging at the Acute Phase of Endocarditis) Study Group. (2010). Effect of early cerebral magnetic imaging on clinical decisions in infective endocarditis: A prospective. Annals of Internal Medicine, 152, 497-504.

Hickey, J. (2009). The clinical practice of neurological and neurosurgical nursing (6th ed.). Philadelphia, PA: Lippincott, Williams & Wilkins.

Kuo, I., Long, T., Nguyen, N., Chaudry, B., Karp, M., & Sanossian, N. (2010). Ruptured intracranial mycotic aneurysm in infective endocarditis: A natural history. Case Reports in Medicine, 2010, 168408. doi: 10.1155/2010/168408

Lester, S. J., & Wilansky, S. (2007). Endocarditis and associated complications. Critical Care Medicine, 35, S384-391. doi: 10. 1097/01.CCM.0000270275.89478.5F

Luttenberger, K., & DiNapoli, M. (2011). Subacute bacterial endocarditis: Making the diagnosis. Nurse Practitioner, 36, 31-38. doi: 10-1097/01.NPR.0000393971.15598.0c

Mocchegiani, R., & Nataloni, M. (2009). Complications of infective endocarditis. Cardiovascular and Hematological Disorders Drug Targets, 9, 240-248.

National Heart, Lung, and Blood Institute. (2014). What is endocarditis? Retrieved from http://www.nhlbi.nih.gov/health/ health-topics/topics/endo/

Okazaki, S., Sakaguchi, M., Hyun, B., Nagano, K., Tagaya, M., Sakata, Y., ... Kitagawa, K. (2011). Cerebral microbleeds predict impending intracranial hemorrhage in infective endocarditis. Cerebrovascular Diseases, 32, 483-488. doi: 10. 1159/000331475

Sonneville, R., Mirabel, M., Hajage, D., Tubach, F., Vignon, P., Perez, P., ... ENDOcardite en REAnimation Study Group. (2011). Neurological complications and outcomes of infective endocarditis in critically ill patients: The ENDOcardite en REAnimation prospective multicenter study. Critical Care Medicine, 39, 1474-1481. doi:10.1097/CCM.0o013e3182120b41

Questions or comments about this article may be directed to Melissa A. Schneider, RN-BC DNP ONC CNRN, at mschneider@ wellspan.org. She is a Clinical Nurse Educator, York Hospital, York, PA, and Nursing Faculty, York College of Pennsylvania, York, PA.

Michelle A. Pomidor, RN CRNP, is Neurosurgical Nurse Practitioner, York Hospital, York, PA.

The authors declare no conflicts of interest.

DOI: 10.1097/JNN.0000000000000188
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Author:Schneider, Melissa A.; Pomidor, Michelle A.
Publication:Journal of Neuroscience Nursing
Article Type:Case study
Date:Apr 1, 2016
Words:3522
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