Brain Abscess in Emergency Medicine

Updated: May 18, 2017
  • Author: Naomi George, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Brain abscess is a focal intracranial infection that may present as a life-threatening emergency. It begins with an area of unencapsulated inflammation, known as cerebritis, and develops into a collection of necrotic pus surrounded by a vascular capsule. Brain abscess occurs as the result of a complication of variety of infections, trauma, or surgery and carries significant morbidity and mortality. [1, 2]

For centuries, brain abscess was thought of as almost certainly fatal. In 460 BCE, Hippocrates cautioned his readers of the condition, "For there is danger that the man may become delirious and die" and recommended intracranial drainage as the only cure. [3] However, over the last half century, the epidemiology of this condition has shifted dramatically [4] ; improvements in the detection and treatment of ear, sinus, and orofacial infections has decreased the incidence of brain abscess as a consequence of direct spread of infection. Meanwhile, the population prevalence of chronic immune suppression and immunocompromise has grown, and with it there has been a rise in opportunistic and fungal brain abscess. Indeed, case fatality rates have decreased from 40% to 10% over the past 50 years. [5]  Management of these complex patients may require close cooperation of specialists in infectious disease, radiology, and neurosurgery.



Animal and human modeling of brain abscess has demonstrated a 4-stage process of disease progression. [6, 7] The process begins with direct inoculation of microorganisms into the brain parenchyma, resulting in focal inflammation in the 1-3 days following, which is referred to as early cerebritis. [8]

Polymorphic neutrophils are then recruited, leading to edema. Glial cells are activated, and the area of inflammation continues to grow as the central zone develops coagulation necrosis; this is a hallmark of the second stage, called late cerebritis, which occurs at approximately 3-6 days. [9, 10]

A well-vascularized, ring-enhancing capsule forms after approximately 2 weeks and may be seen on CT. As the host defenses mount, the capsule is walled off, thus completing the development of the abscess.

The fourth stage is often marked by considerable gliosis on the cortical surface of the abscess. Tissue destruction is likely dependent on the virulence of the organism and the exuberance of the host response. [11]

The pathogenesis of an invading organism that has inoculated the brain parenchyma is variable and dependent on the initial site of infection, host factors, and geographic location. Infection can be due to bacteria, fungi, or protozoa. Brain abscess has traditionally been classified by the primary source of the pathogen, [2, 12] with the most common etiologies being direct extension, metastatic spread, and intracranial penetrating trauma.

Direct extension

Brain abscess may be caused by the contiguous spread of pathogens from a primary focus of infection outside of the CNS that extends into the brain. Pathogens may originate from adjacent bone, teeth, sinus mucosa, internal auditory canal, or cochlear structures and travel into the intracranial vault via venous drainage or valveless emissary veins, thus inoculating the brain parenchyma. [12] Abscess caused by direct extension usually leads to a solitary lesion.

Although less common, brain abscess has been described as a complication of frontal, ethmoidal, or sphenoidal sinusitis. [13] Dental infections can lead to brain abscess via either contiguous or hematogenous routes. Meningitis rarely results in brain abscess by direct extension, particularly in adults, and therefore in most cases the finding of brain abscess should not prompt a search for meningeal infection via lumbar puncture. [14]

In the past, chronic otitis media and mastoiditis were the most common underlying etiologies; however, complications of these infections have decreased in incidence with improvements in diagnostic modalities and antibiotic therapy. Overall, abscess caused by direct extension now comprises 12-25% of all brain abscesses [2] ; however, where adequate healthcare infrastructure is lacking, direct extension continues to comprise approximately 50% of brain abscess collectively. [15, 16]

Metastatic spread

Hematogenous seeding of the brain from an extracranial source is the second most common etiology of brain abscess, accounting for approximately 25% of cases. While most bacteremias do not cause brain abscess, when they do, abscesses are frequently multiple and are often found in the distribution of the middle cerebral artery or watershed zones. [12, 17] When hematogenous spread is the underlying cause, there is often an additional predisposing factor; patients with comorbid conditions such as congenital heart disease with right-to-left shunt, pulmonary venous malformations, or hereditary hemorrhagic telangiectasia are at relatively high risk for brain abscess. [18]

Among extracranial sources, chronic pulmonary infections such as lung abscess, bronchiectasis, and empyema have been frequently associated with hematogenous brain abscess. Bacteremias associated with endocardial, abdominal, pelvic, or skin infections can lead to brain abscess. Approximately 15% of cases have no identifiable source. [1]

Intracranial trauma

The formation of brain abscess after intracranial trauma or neurosurgical intervention is well described. In the case of penetrating trauma, brain abscess may form as an immediate or delayed complication; direct inoculation of pathogens can quickly lead to abscess formation, whereas a retained foreign body or focus of necrotic tissue can serve as a nidus of infection months or years after the initial insult. [19, 20] Compared with earlier series, there has been an increase in the proportion of brain abscess caused by direct trauma or neurosurgical intervention; the incidence in recent studies has ranged from 2-37%. [2, 21, 22] One factor accounting for this trend is the relative decline in otogenic brain abscess. Variability in outcome depends greatly on the age and underlying condition of the patient.




United States

The etiology, incidence, and outcome of brain abscess vary greatly across populations. In developed countries, brain abscess is now a rare entity in the general population, with approximately 1,500-2,500 cases reported annually in the United States and an estimated incidence rate of 0.3-1.3 cases per 100,000 per year. [23] Immunocompromised patients form a special subpopulation that sustains a higher incidence of brain abscess. [24]


Populations in low-resource settings have a higher burden of brain abscess. [25] It accounts for less than 1% of intracranial lesions in the developed world, as opposed to roughly 8% in developing countries. [26, 27] Without access to advancements in diagnostic imaging and antibiotic regimens, the development of brain abscess from otogenic and odontogenic infections continues unabated. Additionally, populations with increasing prevalence of HIV infection have witnessed a concomitant increase in incidence of brain abscess. [28]

Underlying pathophysiology of brain abscess varies across locales, with mycobacterial infection (tuberculoma) being more common in parts of Asia, whereas neurocysticercosis is more prevalent in parts of Latin America and is also becoming more prevalent in the United States, particularly among immigrant communities. [29]


In the preantibiotic era, mortality from brain abscess was nearly 100%. [25] Despite the introduction of antibiotics and improvements in neurosurgical drainage techniques, the mortality rate remained around 30-50% through the 1970s. The introduction of enhanced neuroimaging techniques, such as CT and MRI, allowed for rapid, accurate diagnosis and localization of brain abscess. [30] In most modern series, the mortality rate is typically less than 15%. [22, 31, 16] Rupture of a brain abscess infrequently occurs and is associated with a high mortality rate (up to 80%). [2]

Significant morbidity, including seizures, persistent weakness, aphasia, or cognitive impairment, affects an estimated at 20-30% of survivors. [22] In pediatric populations, outcomes have been shown to vary according to how rapidly antibiotics are initiated. [32] Favorable outcomes have been associated with a number of factors, including initial Glasgow Coma Scale score of higher than 12, absence of underlying disease, or sepsis. [22]


No compelling evidence exists for racial differences in the incidence of brain abscess.


Although brain abscess can affect both sexes, in multiple series of both pediatric and adult patients, the male-to-female ratio of brain abscess has been demonstrated to range from 2:1 to as great as 4:1. [16, 33, 15]


Throughout the first half of the 20th century, the age distribution of brain abscess was bimodal, with the highest rates being among children and adults older than 60 years. However, advancement in vaccination trends and antibiotic strategies, as well as a growing population of chronically immunosuppressed patients, has led to a shift in the demographics towards the middle decades. [34] Overall, about 25% of cases of brain abscesses still occur in children, typically among those aged 4-7 years. [35] In pediatric series, congenital heart disease remains the most common predisposing factor. [36]