Delayed brain abscess as a complication of cerebral infarction: A rare case report and review of the literature

Abstract

Introduction

Systemic infections are a common complication of cerebral stroke, while the development of a cerebral abscess on the background of infarcted brain tissue is an extremely rare occurrence. Here, we present a new case alongside a literature review.

Case presentation

A previously healthy 37-year-old man presented with sudden right-sided weakness and speech difficulties, progressing to complete aphasia. Initial tests showed no abnormalities, but subsequent CT scans revealed left basal ganglia infarction. Despite treatment and improvement, three months later, his condition worsened, leading to surgical intervention to excision of a cerebral abscess caused by Staphylococcus aureus. Following successful surgery and treatment, the patient showed improvement and was discharged for regular follow-up care.

Discussion

The convergence of stroke and brain abscess poses serious clinical challenges, requiring prompt diagnosis and treatment to mitigate catastrophic consequences. Brain abscess, stemming from cerebral infection, may arise from various sources, including contiguous spread, hematogenous dissemination, or traumatic injury. Diagnosis is complicated by nonspecific radiological findings, which often lead to misdiagnosis. Risk factors include age, immunocompromised states, and certain medical conditions. Despite challenges, early detection and appropriate management, involving surgical drainage and antimicrobial therapy, are crucial for favorable outcomes.

Conclusion

Cerebral abscess following cerebral infarction is rare but should be suspected in patients with prior stroke or hemorrhage, experiencing worsening focal deficits and consciousness. Advanced age and comorbidities increase clinical suspicion.

Highlights

• •Cerebral abscess following cerebral infarction is exceptionally rare but crucial to consider in patients with progressive focal deficits and declining consciousness post-stroke or hemorrhage.
• •Distinguishing abscesses from strokes on imaging poses challenges; DWI and ADC maps aid diagnosis by detecting restricted diffusion common to both conditions.
• •Surgical drainage followed by antimicrobial therapy for 6-8 weeks remains the primary treatment.
• •Advanced age and comorbidities heighten suspicion for cerebral abscess.
• •Early detection and proper management are crucial for better patient outcomes.

1. Introduction

Cerebral stroke is a common neurological disorder, and is usually followed by systemic infections such as chest infection, urinary tract infection, and sepsis [1]. Cerebral abscess on top of the infarcted brain tissue is a very rare case [2]. It usually occurs a few weeks after an infectious insult, which typically follows the ischemic stroke [3]. In spite of that, those patients with cerebral stroke are considered to be at high risk of developing a cerebral abscess, and this condition is considered in their differential diagnosis if they experience neurological deterioration after a period of recovery [4]. Cerebral ischemia is considered a factor for the pathogenesis of brain abscess after stroke due to local decrease of tissue oxygenation and disruption of blood brain barrier in the infarcted area, which facilitates the formation of an abscess after bacteremia or sepsis [5].

According to our review of the medical literature, very few cases have been recorded. Here in our report we present a new case of a brain abscess that developed on the floor of an infarcted area with review of the literature.

This work is also reported in line with SCARE criteria which helped to improve the transparency and quality of this case report [16].

2. Case presentation

A previously healthy 37-year-old man presented to the emergency room with acute-onset right-sided weakness and motor dysphasia, which progressed to complete aphasia. Brain computed tomography (CT) revealed no abnormalities (Fig. 1). On admission, the patient was drowsy, with a blood pressure of 140/100 mmHg and a body temperature of 36.8 °C. He had motor aphasia and right hemiplegia. The patient was transferred to the intensive care unit (ICU) and treated with intravenous anticoagulants and other appropriate medications, but showed little improvement in his consciousness and weakness.

Fig. 1.

CT scan of the brain, axial plane, at the time of admission. It appears within the normal range without any abnormalities.

A brain computed tomography (CT) scan performed on the second day showed left basal ganglia infarction (Fig. 2). The patient's management continued with a proper medical regimen. Later on, the patient was transferred to a rehabilitation hospital and then discharged home with regular follow-up.

Fig. 2.

CT scan of the brain on the second day, axial plane. An infarct is seen in the left basal ganglia.

Three months later, after the patient's neurological recovery, there was an abrupt deterioration in his neurological status, mainly with respect to his speech and his right side weakness. He became aphasic and was unable to stand due to severe right hemiparesis and was transferred to our department.

On admission, the patient was drowsy with a blood pressure of 130/80 mmHg, a body temperature of 38.8 °C, and a pulse rate of 100/min. Physical examination revealed right hemiparesis and motor and sensory aphasia. Examination of the lungs, heart, abdomen, and ocular fundi was unremarkable. An extensive work-up was performed: chest X-ray, urinary and abdominal ultrasound, and abdominal and chest CT scans were all normal. Neuro-imaging was performed; MRI of the brain with contrast showed a left temporo-parietal thick-walled ring-enhanced lesion with marked perifocal edema and midline shift (Fig. 3), restricted diffusion (Fig. 4).

Fig. 3.

MRI on brain with contrast showed a left temporo-partial thick- walled ring of enhancement with marked peri-focal edema and midline shift.

Fig. 4.

MRI on brain, restricted diffusion of left temporo-parietal lesion (DWI).

Surgical intervention was decided for excision of the lesion. A left temporo-parietal craniotomy was done, exposing a partially vascular thick capsular abscess with complete excision (Fig. 6). The capsule was separated from the surrounding edematous brain tissue and purulent material was drained, and culture and sensitivity were requested, which revealed the growth of Staphylococcus aureus. Post-operative brain computed tomography (CT) was done and confirmed complete excision of the cerebral abscess (Fig. 5). During the next few weeks of appropriate treatment (Ceftriaxone 1 g BID for 2 weeks and levofloxacin 500 mg once daily for 6 weeks), the patient's neurological condition improved and he/she was discharged on routine follow-up.

Fig. 6.

The Abscess after total excision, where the entire capsule appears.

Fig. 5.

CT scan of the brain, post-operative, axial plane. Complete excision of the abscess is shown.

3. Discussion

Stroke and brain abscess are two serious conditions, and the convergence of these entities together can have catastrophic consequences, necessitating prompt diagnosis and treatment. Thereby compounding the clinical challenges posed by stroke [18].

Brain abscess is a form of cerebral infection that begins as a local area of cerebritis and ends in a collection of pus surrounded by a well vascularized capsule. There are many routes for an infection: (a) spread from a contiguous focus (i.e. middle ear infection and paranasal sinuses), (b) hematogenous spread to the brain from a distant focus, (c) traumatic head injury [7].

The acute onset of right side weakness, motor aphasia and alteration of consciousness on admission suggested an ischemic cerebral stroke that revealed no abnormalities on the initial basic CT scan. There are no specific radiological findings for brain abscess, so it is usually misdiagnosed as brain tumors or other intracranial lesions [6].

The risk factors for post-stroke brain abscesses remain largely unclear, though studies suggest they mainly affect older individuals. Immune-compromised conditions like diabetes, surgery, and aging may play a significant role, especially when combined. Additionally, Neurobrucellosis, congenital heart diseases, meningitis and endocarditis are implicated in increasing the occurrence of post-stroke brain abscesses [17], along with intravenous opiate use, which is associated with endocarditis, contributes to stroke incidence and subsequent abscess development [12]. Studies also indicate that the brain itself experiences immune compromise after a stroke, making it susceptible to infections and abscess formation [19]. Conversely, The patient in this report was young and had no notable medical history.

Brain abscesses may be bacterial, fungal, or parasitic. A special form of bacteria, fungi, and protozoa have been observed with increasing frequency as etiologic agents in immunocompromised patients [8].

Staphylococcus was the predominant pathogen isolated from post-stroke brain abscesses, with other factors such as Klebsiella and pneumococci being rarely isolated, along with negative cultures [14,21] The incidence of sterile abscesses in the brain reached 40 % of documented cases in the medical literature [20].

The presenting symptoms of brain abscess include headache, fever and altered consciousness. However, only one third of the patients experience the three symptoms together [9,10].

The age, immunologic state and type of etiologic agent are involved in the pathogenesis of the cerebral abscess. There is an overlap between the cerebral abscess and stroke along their clinical course, leading to a clinical scenario in which the development of a cerebral abscess over a previously infarcted brain region produces no additional deficit, thus delaying diagnosis [11].

Cerebral abscess on top of infarcted tissue occurs due to local tissue damage and a distant focus of infection. The vascular event, either ischemic or hemorrhagic, leads to local disruption of the blood brain barrier, which makes this infarcted region susceptible to microbial seeding in the event of bacteremia secondary to systemic infection, leading to the formation of a brain abscess [4].

Through our literature review, the latest review conducted on this issue was in 2020, which included 24 cases. Two cases were subsequently published, in addition to our current case, making the total number of cases 27 so far. Among these 27 cases, 4 cases developed brain abscess after decompressive craniectomy for stroke [12,14,17]. Table 1 is a comprehensive summary of all cases.

Table 1.

Summary of the published Brain Abscess Following Cerebral Infarction.

Authors	Age	Sex	Initial NIHSS	Last Known Well to Admission	Occlusion Territory	Treatment of Stroke	Past Medical History	Onset of Brain Abscess	Brain Abscess symptoms	Source of infection	Treatment of Brain Abscess	Pathogen found on culture	Outcome
Amonn	68	Male	-	-	Right Middle cerebral artery	-	Diabetes mellitus, Hypertension.	342 days	Fever	Hematogenous infection, Bronchiectasis	-	Staphylococcus aureus	Died
Ichimi	73	male	-	-	Left Middle cerebral arter	-	-	After 77 days	Fever	-	Aspirations + antibiotics	Proteus vulgaris	Favorable
Arentoft	59	Female	-	same day	Right Middle cerebral artery	-	Renal failure	After 12 days	Fever	Lung	-	Salmonella typhimurium	Died
Chen	70	Male	-	Same day	Right middle cerebral artery	-	-	After 5 weeks	Vomiting, fever	-	Stereotactic aspiration	Negative	Died
	56	Female	-	Same day	Left putaminal haemorrhagic infarction	-	Hypertension	After 9 weeks	Fever	Septicaemia	Surgical, antibiotics	Klebsiella pneumonia	Good
Davenport	16	Female	-	-	Left Anterior Cerebral Artery	-	-	After 4 weeks	Fever	Septicaemia	Surgery Antibiotics	Escherichia coli Enterococcus faecalis	Good
Shintani	40	Male	-	Before 5 days	Right posterior cerebral artery	-	No history	After 2 weeks	Fever	-	Surgical drainage	Streptococcus	Favorable
Beloosesky	68	Male	-	Same day	Left Middle cerebral arter	-	Hypertension, diabetes mellitus, stable ischemic heart disease, alcohol abuse	After 84 days	high fever	Urinary tract (Proteus mirabilis)	Craniotomy	Proteus Mirabilis	Died
Miyazaki	77	Male	-	Same day	Left Middle cerebral arter	-	Fibrillation and hypertension	After 385 days	High fever	Pneumoniae (S aureus)	Stereotactic aspiration	MRSA	Good
Kaplan	52	Female	-	-	Right Middle cerebral artery	-	-	After 56 days	Fever	Pneumoniae	Surgical drainage	Staphylococcus aureus	Favorable
	60	Male	-	-	Right thalamic	-	No history	After 7 weeks	Fever	Lung: interstitial fibrosis	Surgical antibiotics	-	Good
	40	Male	-	-	Lateral right insular lobe haemorrhagic infarction	-	No history	After 9 weeks	Fever	No	Surgical antibiotics	Staphylococcus aureus	Good
Emmez	64	Male	-	-	Left Middle cerebral arter	-	-	After 42 days	Fever	-	-	-	Favorable
Kraemer	33	Female	-	Same day	Left Middle cerebral arter	Intra-arterial thrombolytics, Angioplasty with stent deployment, intravenous anticoagulants	No history	After 7 weeks	High fever	Pneumonia	Surgical drainage	group C Streptococcus sp	Good
Jung	58	Male	-	-	Right Middle cerebral artery	-	Hypertension, Hyperlipidemia	After 6 weeks	Fever	-	Surgery Antibiotics	-	Good
Yamanaka	75	Male	-	Same day	Left Middle cerebral arter	Intra-arterial thrombolytic	-	After 13 months	High fever	-	-	Staphylococ-cus epidermis	Favorable
Albrech	35	Male	-	Same day	Left supplementary motor cortex	-	Intravenous heroin abuse	After 2 weeks	High fever	Septic-embolic	Surgical drainage	Fusobacterium nucleatum	Good
Garcia	52	Male	-	-	Right Middle cerebral artery	-	-	After 56 days	Fever	-	Surgical drainage	S. Methylo Resistant	Favorable
Wang	58	Male	-	-	Right Middle cerebral artery	-	Hypertension	After 6 weeks	Fever	-	Surgical drainage	-	Good
Noro F	56	Male	-	Same day	Bilateral occipital	Conservative treatment	Hypertension and dyslipidemia	After 116 days	episode of strong headache and visual deterioration without fever	-	Surgical drainage	Staphylococcus aureus	Good
Gueneg	66	Female	23	Same day (70 min)	Left middle cerebral artery	IV thrombolysis and thrombectomy	-	After 2 weeks	High fever	-	Surgical drainage	Staphylococcus Aureus	Good
Ramesh	67	Female	23	Same day	Left Middle Cerebral Artery	-	Hypertension, Depression, Diabetes mellitu	After 40 weeks	-	-	Surgical drainage	Staphylococcus warneri	Good
Raja K	35	Male	25	Before 2 days	Left middle cerebral artery	Intra-arterial thrombolytic	No history	After 6 months	Nil	Blood borne secondary to chest infection	Surgical excision + antibiotics	Negative	Good
	26	Male	-	Same day	Left middle cerebral artery	Left fronto-temporo-parietal decompressive craniectomy	Congenital heart disease	After 4 months	Nil	Brucella endocarditis	Surgical excision + antibiotics	Brucella melitensis	Good
Jonah	33	Male	15	-	Left posterior cerebral artery	-	opioid use disorder	After 3 weeks	High fever, headache	infective endocarditis	Craniotomy, Stereotactic aspiration	-	Good
Boukobza	72	Male	-	Same day	Right posterior cerebral artery	-	No history	After 30 days	High fever	Endocarditis vegetation	Conservative treatment	-	Good
Present case	37	Male	-	Same day	Left basal ganglia	Intravenous anticoagulants	No history	After 5 months	Deterioration of the neurological	-	Craniotomy	Staphylococcus aureus	Good

The proof of a causal link between the occurrence of brain abscess and cerebral infarction remains controversial and inconclusive. However, through our review of the literature and our summarization of similar recorded cases, there appears to be evidence supporting a connection between the two events. Most of the recorded cases had a history of high blood pressure, diabetes, or heart disease, and these are among the risk factors of strokes, in addition to a weak immune system, which increases the chance of infection So, the presence of the same reasons that increase the inevitability of the two diseases occurring successively denies the possibility of their occurrence by chance. Most of the cases carried a primary infection or a source of infection before it was transmitted to the brain whether this is due to what we mentioned in the first point or for other reasons, but this confirms that the occurrence of a brain abscess was not a coincidence with the occurrence of a stroke. The transmission of infection was limited to the infarcted place and no other surrounding places. This confirms the immunological weakness of the infarcted place as Chen et al. [4] (Table 1).

Most cases develop the abscess within a few weeks while the patient is still hospitalized, while a few develop it late after the patient's treatment, improvement, and discharge from the hospital. The period between the development of the abscess and the stroke varied depending on documented cases in the literature, ranging from weeks to months, and even up to a year [3,17,22,23]. as is the case with our current case, where the abscess developed 5 months after improvement and discharge.

Radiographically, it's difficult to differentiate between acute ischemic stroke and brain abscess on MRI as both may lead to restricted diffusion, edema, and enhancement with contrast [12].

Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps can help in diagnosis and localization of stroke. The restricted diffusion of water molecules, detected by these sequences, is not related to ischemic stroke only, and may occur in any pathology that results in cellular damage that disrupts the flow of water such as neuronal demyelination, brain tumor, or infection [12].

The treatment options of brain abscess involve surgical drainage, performed either by stereotactic puncture and aspiration or open surgical resection of the abscess and its capsule, followed by antimicrobial therapy for at least six to eight weeks [13].

Early diagnosis is related to better outcomes. The adequate management of associated pathology, early treatment of infectious complications, and a high index of suspicion will probably lead to a favorable prognosis and outcome [15].

4. Conclusion

Cerebral abscess as a complication of cerebral infarction, is a rare complication. A cerebral abscess should be suspected in patients with a previous history of cerebral stroke or intracerebral hemorrhage, suffering from progressive focal deficits and deteriorating level of consciousness. Advanced age and medical comorbidities affect the immunological potency and reinforce the clinical suspicion.

Consent of patient

Written informed consent was obtained from the patient for publication and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Ethical approval

Ethics clearance was not necessary since the University waives ethics approval for publication of case reports involving no patients' images, and the case report is not containing any personal information. The ethical approval is obligatory for research that involve human or animal experiments.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author contribution

Ahmad Alkheder: Validation, Writing – review & editing, Visualization, Methodology, Software, Writing – original draft, Formal analysis. Mohamed Kh. Elbadawy and Amr M.N.Azzam: Validation, Writing – review & editing, Visualization, Methodology, Software, Writing – original draft, Formal analysis. Mazen M.Taha: Validation, Formal analysis, Writing – review & editing. Khaled Alsayed Abualkhair: Validation, Formal analysis, Writing – review & editing. Mahmoud M. Taha: Supervision, Writing – review & editing, Project administration.

Guarantor

The corresponding author takes the full responsibility of the work.

Research registration number

This case report is not a first time of reporting, new device or surgical technique. So I would not need a Research Registry Unique identifying number (UIN).

Declaration of competing interest

The Authors disclose no conflicts.

Data availability

All data are available from the corresponding author on reasonable request. The case has not been presented at a conference or regional meeting.