B r a i n Ab s c e s s

Tess Slazinski,
KEYWORDS  Brain abscess  Intracerebral abscess  Central nervous system infections  Computed tomography  Magnetic resonance imaging  Aspiration  Excision KEY POINTS 
Brain abscess is an area of infection within the parenchyma of the brain.  Formation and maturation of brain abscess typically takes 2 weeks.  Early recognition of symptoms and modern diagnostic testing have improved the outcomes for brain abscess.
MN, RN, CCRN, CNRN, CCNS

INTRODUCTION

Brain abscess is a focal, intraparenchymal, or meningeal infection that develops into a collection of pus surrounded by a well-circumscribed capsule.1,2 Brain abscess has been a known complication of otitis media, mastoiditis, frontal or ethmoid sinusitis, dental infections, bacterial endocarditis, and congenital heart defect.3 This article addresses the pathophysiology, pathogenesis, clinical manifestations, diagnostic criteria, and nursing considerations for patients with a brain abscess.
BACKGROUND

Brain abscess has been traditionally recognized as a central nervous system infection with a poor outcome.4,5 Patients frequently present with rapid neurologic deterioration, which has contributed to fear of this disease.5 Modern techniques for brain biopsy, neuroimaging, and laboratory culture analysis have improved the prognosis.6 In addition, early diagnosis and treatment have improved the outcome of this condition.6–8 The prognosis is related to the initial presentation, response to antibiotic therapy, and any systemic conditions or risk factors that may impede immunologic attempts to clear the infection.5 The mortality rates reported in recent large case series range from 8% to 25%.6,8–11 According to one author’s 10-year data collection on treatment of brain abscess, excision is associated with a better prognosis than aspiration.6 Poor

Disclosures: None. Critical Care Nursing Services, Cedars- Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA E-mail address: tslazin@aol.com Crit Care Nurs Clin N Am 25 (2013) 381–388 http://dx.doi.org/10.1016/j.ccell.2013.04.001 ccnursing.theclinics.com 0899-5885/13/$ – see front matter Ó 2013 Elsevier Inc. All rights reserved.

26 Cerebral abscesses usually form at the gray–white matter junction where microinfarction damages the blood-brain barrier. immunocompromise. ventriculitis. and peripheral gliosis.23–25 The common organisms from direct sources are listed in Table 1. Prevotella spp. Haemophilus spp Enterobacteriaceae. Haemophilus spp. neurosurgical procedures can be a direct source of development of brain abscess. multilobular process. The edema may lead to life-threatening complications such as uncal or brainstem herniation.12–14 The developed abscess consists of 3 layers: a center polymorphonuclear leukocytes and necrosis. ventricular rupture. and older age. Developed countries have seen decreased rates of brain abscess as the result of ear infections. by the frontoparietal. Pseudomonas aeruginosa. Clostridium spp Staphylococcus spp.16 The direct spread from a contiguous site usually causes a single brain abscess. hyperemia.17. Bacteroides spp Staphylococcus aureus. Enterobacter spp . in descending order of frequency. and occipital lobes. The microorganism enters the brain and produces an initial area of focal cerebritis. Pseudomonas aeruginosa. Streptococcus spp.5 PATHOPHYSIOLOGY A brain abscess may occur as a single focus involving contiguous lobes. or as a contiguous. which accounts for 20% to 60% of cases. which leads to a softening. and petechial hemorrhage.14 PATHOGENESIS Bacteria may invade the brain either by direct spread.2. Table 1 Common organisms from direct sources of brain abscess Direct Source of Infection Paranasal sinuses Odontogenic Otogenic Penetrating head trauma Neurosurgical procedures Microorganism Streptococcus spp. This type of trauma may be the result of any invading foreign body or retained fragments that can result in necrotic tissue and serve as a nidus for infection. frontal or ethmoid sinuses (frontal lobe).19–22 Penetrating trauma to the brain is another direct method of infection.18 Brain abscess arising from a sinus infection remains an important consideration in both adults and children. fibroblasts from the capillaries adjacent to the focal cerebritis deposit collagen fibers to contain and encapsulate the purulent focus. edema. cerebellar.3 The most common sites of brain abscesses are the frontal and temporal lobes followed. a collagenous capsule surrounding the central areas. Enterobacter spp. Bacteroides spp.382 Slazinski prognostic factors include worse functional status at presentation.2 After 2 to 3 weeks. and dental infection (frontal lobe). parietal. or through hematogenous seeding.15 A brain abscess acts as an expanding mass lesion and causes edema in the surrounding tissue. or meningitis. Primary infections that can directly spread to the cerebral cortex include subacute and chronic otitis media and mastoiditis (inferior temporal lobe and cerebellum). Fusobacterium spp. Hematogenous spread via bacteremia is associated with multiple abscesses in the distribution of the middle cerebral artery.2 In addition. Bacteroides spp. Streptococcus spp.12 The early lesion (first 1–2 weeks) is poorly demarcated with no evidence of tissue necrosis. Fusobacterium spp Streptococcus spp.

DIAGNOSIS Computed tomography (CT) is performed for emergency cases. endoscopic sclerosis of esophageal varices. Headache onset may be sudden or gradual. impaired judgment. As the abscess increases in size. and/or contralateral hemiparesis. intra-abdominal infections. Fusobacterium spp. Patients with frontal-lobe lesions may have drowsiness. esophageal dilation.2 Unfortunately. Staphylococcus aureus Streptococcus spp . and intrapulmonary right-to-left shunting in patients with arteriovenous malformations. Enterobacter spp Viridans streptococci. Table 2 Common organisms from hematogenous seeding Hematogenous Infection Source Lungs Urinary tract Endocarditis Congenital cardiac malformations (especially right-to-left shunts) Microorganism Streptococcus spp. Parietal-lobe lesions may lead to patients presenting with homonymous hemianopsia. cyanotic congenital heart diseases. Clinical manifestations for patients may include decreased level of consciousness. the study must be performed with a contrast agent. and/or papilledema. which results in a delay in establishing the diagnosis. which is often localized to the side of the abscess. Focal neurologic deficits occur in 50% of patients and occur days to weeks after the onset of headache. The diagnosis is made at an average of 13 to 14 days after the onset of symptoms. The lesion has different appearances based on the age of the abscess.12 If the abscess ruptures into the subarachnoid space.Brain Abscess 383 Conditions that lead to hematogenous seeding of the brain include chronic pulmonary infections. patients may display signs of increased intracranial pressure. These manifestations can lead to catastrophic complications such as uncal or brainstem herniation. which is usually a reliable indicator of infection. CLINICAL MANIFESTATIONS The clinical manifestations of brain abscess may be nonspecific. the headache is sudden and severe. fever. Neurologic deficits from temporal-lobe involvement may include Wernicke aphasia.32 The most common symptom is headache. Actinomyces spp Pseudomonas aeruginosa. vomiting.32 The deficit depends on location of the brain abscess. and homonymous superior quandranopsia.27–31 The common organisms from hematogenous seeding are listed in Table 2. occurs in only 50% of patients with a brain abscess. When a brain abscess is suspected. Cerebellar abscess may manifest as ataxia and nystagmus. contralateral facial droop.12. Nuchal rigidity occurs in 15% of patients with brain abscess and is most commonly associated with occipital-lobe abscess or an abscess that has ruptured into the subarachnoid space. The pain tends to be severe and usually not relieved with over-the-counter remedies. seizures. palsies of cranial nerves III and VI. skin infections.13 Early cerebritis appears as an irregular area of low density that does not enhance following contrast injection. bacterial endocarditis. pelvic infections. Patients with abscesses that involve the brainstem may present with multiple cranial nerve findings and contralateral hemiparesis. and impaired proprioception and stereoagnosis.

the lesion enlarges with thick and diffuse ring enhancement following contrast injection.8. encapsulated fungal brain abscesses.40 Surgical excision is not performed as often as needle aspiration. Nurses play a significant role in decreasing the complications associated . glucocorticoids (dexamethasone). which increases the T1 intensity and causes more prominent enhancement of lesions than a CT scan.39 NURSING CONSIDERATIONS Critical care nurses.39 Brain abscesses should be reaspirated if they fail to change in size or expand in diameter. and Mycobacterium tuberculosis. Needle aspiration is performed by placing a burr hole. and indications are summarized in Table 3.38 The usual course of antibiotic therapy is 4 to 8 weeks. MRI should be performed with gadolinium. and provides better visualization of the brainstem. In addition. and surgical drainage. The treatment usually requires a combination of antibiotics. and multiloculated abscesses. Amplification of 16S ribosomal DNA by polymerase chain reaction increased the number of bacterial species isolated from brain abscesses in comparison with standard culture. and is preferred for lesions that involve the speech areas and motor and sensory cortices. The ring contrast enhancement represents breakdown of the blood-brain barrier and development of an inflammatory capsule.2 Serology specimens may aid in the diagnosis of Toxoplasma gondii or neurocysticercosis infections.40 It is also the preferred method for comatose patients. Diffusion-weighted MRI is capable of differentiating ring-enhancing lesions caused by a brain abscess from neoplastic lesions. dosage. The neurosurgery service needs to be consulted at the time of initial diagnosis of brain abscess. who care for critically ill patients. more accurately estimates the extent of central necrosis. MRI is preferred over CT because it is more sensitive for early cerebritis and in detecting satellite lesions.2 Current literature has demonstrated promising results from 16S ribosomal sequencing studies.39 Stereotactic guidance has improved the precision of needle aspiration. because of a greater risk for neurologic complications. Excision may be the treatment of choice for the following situations: traumatic brain abscess (to remove bone chips and foreign material). and fungal culture. and fungal stains should be performed to aid in the identification of the etiologic agent. Medications. then inserting the needle under CT guidance. modified acid-fast stain for Nocardia. There must be an index of suspicion for central nervous system infection. signs of increased intracranial pressure. and aerobic. According to the investigators. In addition. are vital members of the health care team.33. and cerebral edema. The aspirate needs to be cultured for aerobes and anaerobes. and increased abscess ring diameter. anaerobic. Needle aspiration and surgical excision have both been used to treat brain abscess.384 Slazinski As cerebritis evolves. mycobacterial.35–37 TREATMENT The clinical manifestations of brain abscess can be subtle.39 Surgical excision may be necessary after aspiration when the following occur: no clinical improvement within 1 week. Magnetic resonance imaging (MRI) is the preferred study. ring enhancement.34 Laboratory specimens obtained from stereotactic CT-guided aspiration or surgery should be sent for Gram stain. several new species were identified. and anticysticercal antibodies on cerebrospinal fluid specimens. Anti-Toxoplasma immunoglobulin G antibody may be present in blood. which may lead to a delay in treatment. fungi. special stains including an acid-fast stain for mycobacteria.

where the site of abscess is usually the frontal lobe) Penicillin G 20 to 24 million units per day IV in Administered in combination with six equally divided doses Metronidazole. especially for oral Ceftriaxone 2 g IV every twelve hours focus Cefotaxime 2 g IV every four to six hours OR Ceftriaxone and Metronidazole OR Cefotaxime and Metronidazole Vancomycin 30 mg/kg IV daily in two equally divided doses adjusted for renal function 2 g IV every four hours 2 g IV every four hours 30 mg/kg IV daily in two equally divided doses adjusted for renal function 2 g IV every eight hours 2 g IV every eight hours 1 g IV every eight hours 2 g IV every four hours 2 g IV every four hours Brain abscess from hematogenous spread Nafcillin or oxacillin would replace Vancomycin when susceptibility testing reveals methicillin-sensitive S Aureus Postoperative neurosurgical patients Vancomycin and ceftazidime OR Vancomycin and cefepime OR Vancomycin and meropenem Nafcillin or oxacillin would replace Vancomycin when susceptibility testing reveals methicillin-sensitive S Aureus Brain abscess following penetrating trauma Vancomycin and ceftriaxone OR Vancomycin and cefotaxime Nafcillin or oxacillin would replace Vancomycin when susceptibility testing reveals methicillin-sensitive S Aureus Nafcillin Oxacillin Vancomycin Ceftazidime Cefepime Meropenem Nafcillin Oxacillin Vancomycin Ceftriaxone Cefotaxime Nafcillin Oxacillin 30 mg/kg IV daily in two equally divided doses adjusted for renal function 2 g IV every twelve hours 2 g IV every four to six hours 2 g IV every four hours 2 g IV every four hours Abbreviation: IV.Brain Abscess 385 Table 3 Summary of antibiotic therapy for brain abscess Drug name Dosage Indication Metronidazole 15 mg/kg IV loading dose.3 The frequency of the neurologic assessment depends on the severity of the patient’s condition. examination of meningeal irritation may indicate abscess rupture or subarachnoid hemorrhage. or sinus source (ie. and Brudzinski and Kernig signs are . Nuchal rigidity. with this group of patients. by 7. or abscess rupture. A baseline neurologic examination and serial neurologic assessment assist in early recognition of findings that indicate increased intracranial pressure from an expanding lesion. and cranial nerves. where the site of abscess is usually the temporal lobe or cerebellum. Components of the neurologic examination that may demonstrate neurologic decline are level of consciousness. or frontal or ethmoid sinusitis. otogenic. cerebral edema.5 mg/kg IV every eight hours. In addition. motor examination. intravenous. followed Brain abscesses arising from oral. not to exceed 4 g/day chronic otitis or mastoiditis.

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