Abstract
Mycotic aneurysms (MAs) are a rare but life-threatening complication of infective endocarditis (IE), resulting from septic emboli lodging in cerebral vessels and leading to aneurysm formation. This case report describes a 17-year-old female who developed multiple MAs during treatment for IE, resulting in catastrophic neurological decline and eventual death. After undergoing open-heart surgery for vegetation excision, our patient then developed intracranial bleeding due to mycotic aneurysms rupture, which led to her death after an unsuccessful decompressive craniotomy. This case highlights the importance of early recognition and timely intervention in the management of MAs in the context of IE, as well as the need for protocols to improve outcomes in these high-risk patients. The high mortality rate associated with ruptured MAs highlights the critical nature of these complications and the challenges in their management.
Keywords: Mycotic, aneurysm, infective endocarditis, septic embolism, intracranial, case report
Introduction
Mycotic aneurysms (MAs) are rare but serious complications of infective endocarditis (IE), resulting from infected emboli—often from heart valve vegetations—lodging in cerebral vessels, especially the middle cerebral artery. Though their incidence is low (~2%) [1], ruptured MAs carry high mortality.
We report a 17-year-old female with IE complicated by multiple MAs. This case highlights the critical need for early recognition and timely intervention. We also review the clinical course, diagnostic tools, and management strategies for MAs, underscoring the importance of clear protocols to improve outcomes.
Case presentation
A 17-year-old female presented with fever, fatigue, and recurrent vomiting for 4 days. Her history included arthralgia, palpitations, diarrhea, and a skin rash on the dorsum of her hands and soles of her feet. There was no history of chest pain, shortness of breath, cough, or weight loss. She also reported decreased urine output. The patient had no pertinent past medical or surgical history. On assessment, she was febrile (38.6°C), normotensive (108/60 mmHg), and tachycardic (heart rate 136 bpm). She appeared pale and had hemorrhagic spots on the sclera bilaterally. On cardiac auscultation, she had normal heart sounds with a holosystolic murmur best heard at the fifth left intercostal space radiating to the left axilla. Pulmonary examination revealed decreased breath sounds in the lower lung zones bilaterally. A petechial blanching skin rash was noted on the dorsum of the hands and the soles of the feet. Physical examination of the lower limbs showed no edema or calf tenderness. She was conscious, oriented, and alert, but agitated. Her Glasgow Coma Scale (GCS) was 15/15.
On admission, electrocardiogram showed sinus tachycardia with T-wave inversion in leads I and aVL and poor R-wave progression. Troponin I was elevated at 5.47 ng/ml. Arterial blood gas revealed mixed respiratory alkalosis and metabolic acidosis. Complete blood count showed leukocytosis (28 000/μl, 95% neutrophils), normocytic anemia, and thrombocytopenia (21 000/μl), prompting platelet transfusion. Hemoglobin dropped from 9.5 to 7.8 g/dl. Serum potassium was 3.4 mEq/l, calcium 6.9 mg/dl, with normal sodium (145 mmol/L) and magnesium (2.13 mg/dl). Urinalysis revealed +2 hematuria with 70 RBC/HPF, no proteinuria. BUN was elevated at 42 mg/dl; creatinine was normal (0.8 mg/dl). PT and aPTT were prolonged (16.9 and 39 s). C-reactive protein was elevated at 54 mg/l; erythrocyte sedimentation rate was normal (5 mm/h).
The patient's condition deteriorated with a decreased level of consciousness, prompting immediate intubation, nasogastric tube and central line insertion, and correction of hemoglobin drop and hypokalemia. She was admitted to the ICU. Lumbar puncture revealed WBC 3/μl, glucose 50 mg/dl, protein 60 mg/dl, and RBC 297/μl. A full septic workup, including three sets of blood cultures, urinalysis, and urine culture, was done. Blood cultures grew aerobic Staphylococcus aureus and anaerobic Klebsiella pneumoniae, both sensitive to meropenem and cefazolin. Empirical antibiotics (gentamicin, vancomycin, meropenem) were started. Other cultures were negative. Urine output was 0.5 ml/kg/h. TEE showed mild global LV hypokinesis (EF 45%), moderate diastolic dysfunction, mild–moderate TR and MR, and large multi-lobed mobile masses (4 × 2 × 2 cm) in the left atrium attached to the mitral annulus. Abdominal ultrasound showed mild ascites, bilateral pleural effusion (left-predominant), and increased renal parenchymal echogenicity suggestive of acute kidney injury; otherwise unremarkable.
On the second day of admission, the patient underwent open-heart surgery with vegetation excision. Postoperative TEE showed normal LV systolic function (EF 60%), moderate eccentric TR, and a hole in the anterior mitral leaflet with moderate MR. A follow-up TEE on postoperative day 2 revealed severe MR, mild to moderate TR, and EF of 52%. Mitral valve replacement was planned. CT angiography of the chest and contrast-enhanced CT of the abdomen and pelvis (Fig. 1) showed no pulmonary embolism but revealed other findings.
Figure 1.
CT scan of the abdomen and pelvis with IV contrast showed non-enhancing areas in the spleen and kidneys which were suggestive of infarction. Also, periportal and pericholecystic fluid was noted, which indicates liver congestion and mild ascites.
On the same day, the patient developed acute kidney injury (AKI) and continued to severely deteriorate, until she was connected to Continuous Renal Replacement Therapy (CRRT) on the second postoperative week. During the CRRT session, she developed hypotension and became unconscious with fixed dilated pupils. So, An urgent CT scan of the head was done and showed intraventricular haemorrhage, intraparenchymal haemorrhage and midline shifting. CT angiography of the brain was done urgently and showed several mycotic aneurysms (Fig. 2). So the patient underwent an emergency decompressive craniotomy. Unfortunately, she developed intraoperative cardiac arrest, the resuscitation failed and the patient passed away.
Figure 2.
Brain CT scan without IV contrast. Axial (A) and coronal (B) view images showed a large acute temporo-parietal intraparenchymal hemorrhage extending to the ventricular system, measured about 40 × 44 × 41 mm in size, with a resultant midline shifting to the left side of about 13 mm, associated with subarachnoid hemorrhage.
Figure 3.
Brain CT angiography. Coronal (A) and axial (B) view images showed a right MCA saccular focal lesion representing aneurysm seen at M3 portion measuring 10 × 9 mm.
Discussion
Clinical significance and learning points
Infective Endocarditis (IE) is a serious infection of the heart valves, often leading to the formation of septic emboli. These emboli can lodge in various organs, including the cerebral vessels, causing mycotic aneurysms (MAs). The middle cerebral artery and its branches are the most commonly affected sites [2]. Although rare, MAs are life-threatening complications of IE [2]. MAs associated with IE predominantly occur in middle-aged patients, typically around 40 years of age [3]. Unlike our case which highlights a 17-year-old patient with IE who developed multiple MAs, ultimately leading to neurological deterioration and death.
The key learning point here is the poor prognosis of ruptured MAs and the urgent need for early detection and prompt treatment. In patients diagnosed with IE, the incidence of associated MAs is approximately 2% [1]. often resulting in devastating neurological outcomes. Early detection through routine screening and timely intervention can significantly improve the chances of survival and reduce the risk of neurological deficits.
Mortality and neurological impact of ruptured MAs
When MAs rupture, the mortality rate can reach 80% [1]. Rupture often results in hemorrhagic strokes, brain damage, and high intracranial pressure, leading to rapid neurological decline [4]. In this case, our patient’s aneurysm rupture resulted in intracerebral hemorrhage, and despite immediate intervention, the patient succumbed to the complications of the rupture. Prompt identification of MAs, ideally before rupture, is crucial for improving outcomes.
Outcomes and importance of early diagnosis
Delayed diagnosis of MAs in this case likely worsened the outcome. Although the patient showed signs of IE and neurological decline, MAs were not promptly identified, allowing rupture. This highlights a gap in clinical practice—early screening for MAs in IE patients with neurological symptoms is crucial due to the high mortality of ruptured MAs.
CT angiography (CTA) and digital subtraction angiography (DSA) are the best tools for diagnosing MAs [4]. Early imaging in high-risk IE patients could prevent rupture and enable timely treatment, improving survival [4, 5]. In this case, brain CT and CTA revealed multiple cerebral vessel dilatations, confirming several mycotic aneurysms.
Comparison of treatment approaches
The treatment options for MAs in the context of IE involve antibiotics, surgical intervention, and, in some cases, endovascular procedures [4]. Antibiotic therapy is fundamental to controlling the infection and preventing further embolic events. However, once an aneurysm ruptures, urgent surgical intervention is required [6].
The decision to operate on the brain versus the heart first is a difficult one. Heart surgery before brain surgery poses the risk of increasing intracranial pressure or causing brain hemorrhage, while brain surgery is typically prioritized once rupture occurs. In this case, the patient underwent heart surgery prior to the deterioration, and the craniotomy performed after the rupture did not prevent death [6].
Endovascular treatment, specifically embolization has shown promise in some cases, particularly for aneurysms that are difficult to access surgically. However, the effectiveness of these procedures is still being debated [7–9]. Surgical treatment, including clipping or trapping, can be effective but carries the risk of ischemic complications [5].
In our patient, the cardiovascular department team decided to do open heart surgery with vegetation excision 3 weeks before sudden deterioration. Urgent brain CT showed intraventricular hemorrhage and intraparenchymal hemorrhage with midline shifting. Immediately, she was taken to the theater room for decompressive craniotomy. Unfortunately, she developed cardiopulmonary arrest with no resuscitation response.
Routine screening for mycotic aneurysms
The most critical recommendation from this case is the need for routine screening for mycotic aneurysms in patients with infective endocarditis, especially when neurological symptoms are present. Screening techniques such as CT angiography (CTA) should be employed early in the diagnostic workup of IE patients, especially those with complicated infections or persistent neurological symptoms [4]. Routine screening could lead to earlier detection, allowing for preventive interventions before rupture occurs [4, 5].
Recent studies have emphasized that screening for MAs in high-risk patients with IE could reduce the incidence of aneurysm rupture and improve patient outcomes. Early detection through imaging, combined with appropriate treatment, could significantly impact survival rates, especially in young patients who might otherwise be overlooked [4, 5].
Conclusion
This case highlights the devastating consequences of ruptured mycotic aneurysms in the setting of infective endocarditis and underscores the importance of early detection. Routine screening for MAs should be considered for all patients with IE, particularly those presenting with neurological symptoms. Early imaging can guide treatment decisions and help prevent the progression of MAs to rupture. Clinicians must remain vigilant in screening for this rare but life-threatening complication to improve patient outcomes.
Acknowledgements
The completion of this case could not have been possible without the participation and assistance of many people whose names may not be enumerated like our patient’s family, their contributions are sincerely appreciated and gratefully acknowledged.
Contributor Information
Hind Neiroukh, Alquds University, Abu Dis P144, Palestine.
Hanin Shatrit, Alquds University, Abu Dis P144, Palestine.
Sarmad Sultan, Alquds University, Abu Dis P144, Palestine.
Sarah Warasna, Alquds University, Abu Dis P144, Palestine.
Maher Aljodi, Cardiovascular surgery Dep, Al-Mezan Hospital, Hebron P7060796, Palestine.
Tharwat Aljodi, Neurosurgery Dep, Al-Mezan Hospital, Hebron P7060796, Palestine.
Conflict of interest
No conflicts of interest.
Funding
No sources of funding.
Ethical approval
no approval is required.
Consent
Verbal consent taken from patient family.
Guarantor
Dr. Maher Aljodi.
Dr. Hind Neiroukh.
References
- 1. Oohara K, Yamazaki T, Kanou H. et al. Infective endocarditis complicated by mycotic cerebral aneurysm: two case reports of women in the peripartum period. Eur J Cardiothorac Surg 1998;14:533–5. 10.1016/S1010-7940(98)00221-8 [DOI] [PubMed] [Google Scholar]
- 2. Chambers HF, Bayer AS. Native-valve infective endocarditis. N Engl J Med 2020;383:567–76. 10.1056/NEJMcp2000400 [DOI] [PubMed] [Google Scholar]
- 3. Fowler VG, Scheld WM, Bayer AS. Endocarditis and intravascular infections. Mand Douglas Bennett’s Princ Pract Infect Dis 2015;1:990–1028.e11. 10.1016/B978-1-4557-4801-3.00082-5 [DOI] [Google Scholar]
- 4. Kuo I, Long T, Nguyen N. et al. Ruptured intracranial mycotic aneurysm in infective endocarditis: a natural history. Case Rep Med 2010;2010:1–7. 10.1155/2010/168408 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5. Chun JY, Smith W, Halbach VV. et al. Current multimodality management of infectious intracranial aneurysms. Neurosurgery. 2001;48:1203–14. [DOI] [PubMed] [Google Scholar]
- 6. Dokponou YCH, Hakkou M, Ouambi O. et al. A rare cause of hemiparesis: intracranial Mycotic aneurysm—a case report, and review of the literature. Open J Mod Neurosurg 2021;11:171–9. 10.4236/ojmn.2021.113021 [DOI] [Google Scholar]
- 7. Nakahara I, Taha MM, Higashi T. et al. Different modalities of treatment of intracranial mycotic aneurysms: report of 4 cases. Surg Neurol 2006;66:405–9. 10.1016/j.surneu.2006.01.021 [DOI] [PubMed] [Google Scholar]
- 8. Frizzell RT, Vitek JJ, Hill DL. et al. Treatment of a bacterial (mycotic) intracranial aneurysm using an endovascular approach. Neurosurgery. 1993;32:852–4. 10.1227/00006123-199305000-00023 [DOI] [PubMed] [Google Scholar]
- 9. Endovascular treatment of ruptured, peripheral cerebral aneurysms: parent artery occlusion with short Guglielmi detachable coils - PubMed [Internet]. H J Cloft, [cited 2024 Nov 30]. Available from: https://pubmed.ncbi.nlm.nih.gov/10094361/ [PMC free article] [PubMed]