There are numerous tickborne diseases that can infect humans and cause disease. Several different tick species are responsible for transmitting these diseases and can be found throughout different geographic regions of the United States. In addition, some tick species can transmit more than one disease. Symptoms can be similar among the tickborne diseases and […]
Author: Kristen Kann, MD (EM Staff Physician, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)
Brain abscesses are relatively rare compared to other CNS infections encountered by the emergency physician, such as meningitis, but are extremely important to consider and recognize due to the differences in diagnosis, treatment, and outcomes for the patient. There are approximately 2,000 cases of brain abscess in the United States annually.1 Some important risk factors include immunocompromised state (HIV/AIDS, transplant recipients, chronic alcoholism), injection drug use, and violation of the cranial or spinal spaces due to trauma or surgery.1
The most likely causative agent of a brain abscess depends on the patient and the likely source of the infection. Most CNS abscesses are bacterial, with 60% being polymicrobial.4 Immunocompromised patients will have a higher risk for fungal (Candida and Aspergillus most commonly)5 and parasitic infections. Patients in, or recently returned from, endemic areas may also be at risk for CNS tuberculosis or neurocysticercosis. In general, Streptococci are involved in approximately 70% of CNS abscesses, and Staphylococci in approximately 20%.4
Abscesses can be primary, but are most often either from direct spread (1/3 of cases) or distant sources (1/3 of cases).2 Contiguous spread can occur from the sinuses, the middle ear, or dental infections, while the most common distant source of infection is the pulmonary system.1 Hematogenous spread appears to be increased in systemic hypoxic states such as chronic pulmonary disease or congenital heart disease.2 The remaining cases are either iatrogenic, related to trauma, or of an unknown source.
One of the biggest challenges for emergency physicians in the diagnosis of brain abscess is the lack of a reliable, sensitive, and specific clinical picture. Many patients presenting with brain abscess have a clinical picture consistent with meningitis, sepsis, or other infectious process, and the classic triad of fever, headache, and focal neurologic signs is present in less than one third of patients.2 Headache is the most common symptom of brain abscess, occurring in about 70% of cases, but characteristics of the headache (such as generalized vs one-sided, gradual or sudden onset) are not reliable indicators of an underlying abscess. Focal neurologic signs such as aphasia, hemiparesis, or a visual field deficit are important findings, as they are less common in other, more diffuse CNS infections such as meningitis and are contraindications to lumbar puncture. Nuchal rigidity, in the case of a CNS abscess, should increase concern for rupture of the abscess into the CSF spaces and possible impending decompensation. Fever is present in less than 50% of patients at presentation and should NOT be used to rule out CNS abscess. Seizures are the most common complication of brain abscesses but are rarely the first presenting sign.1, 2
The work up for brain abscesses has two key features: IMAGING WITH CONTRAST, and AVOIDANCE OF LUMBAR PUNCTURE.
CT scan, while not as sensitive for MRI in the diagnosis of brain abscess, is much more widely available to the EP, and it is the most likely first imaging modality that will be obtained. IV contrast should be ordered in any patient in whom a brain abscess is suspected, including those with high risk historical features, focal neurologic signs, or a history of CNS trauma or surgery. An abscess may appear only as an area of lower density (also known as cerebritis) early in the course of illness, but as the abscess matures, encapsulation causes the characteristic “ring enhancement” on CT with contrast.
LP is contraindicated in patients with possible increased ICP caused by a space-occupying lesion such as a brain abscess.3 Clinical findings that should trigger the EP to consider deferring an LP, at least until after imaging, include focal neurologic deficit, papilledema, seizures, head trauma, or a rapid change in level of consciousness. Exam findings consistent with elevated intracranial pressure include decreased mental status, vomiting, seizures, and possibly Cushing’s Triad of increased blood pressure, decreased heart rate, and erratic respirations. Exam findings concerning for uncal herniation include unilateral third-nerve palsy (pupillary dilation and loss of light reflex) and altered mental status.
It is important to note that LP plays no role in the diagnosis of brain abscess- culturing the causative organism is unlikely, and there are no specific findings in CSF that will diagnose brain abscess. Due to the overlapping presentations of meningitis and brain abscess, however, there is some data about LP results. One study of 65 patients showed a mean protein level of 250 mg/dL (range 90 to 425 mg/dL); mean glucose level 39 mg/dL (range 11 to 58 mg/dL); and mean white cell count 4407 per microL (range 80 to 5006 per microL).6
Other laboratory tests that may be obtained include a CBC with differential, a chemistry panel (to assist with dosing of empiric antibiotics and evaluate for other causes of altered mental status), and blood cultures. Though blood cultures are only positive about 10% of the time, they may be useful to the inpatient team, especially if no specific source is suspected (in which case, direct culture of the source infection is likely to be more useful than blood cultures).
ED management of brain abscess centers on diagnosis, empiric antibiotics, and consultation with neurosurgery. Almost all abscesses will need to be drained, unless there are only very small abscesses in deep brain structures that may not be amenable to drainage. If the patient is very stable and neurosurgical consultation is available with a plan for aspiration within 24 hours, an argument could be made for delay in administration of antibiotics until the abscess can be sampled for cultures. This will allow for guidance of therapy and, possibly, avoidance of some side effects of broad, long term antibiotic coverage. However, in the patient with altered mental status or unstable clinical status, empiric treatment should be started as soon as feasible in the Emergency Department.
Empiric therapy for bacterial brain abscess includes a third generation cephalosporin such as ceftriaxone plus metronidazole. Patients with recent trauma or surgery on the CNS should receive additional coverage for MRSA (usually vancomycin), and patients at risk for tuberculosis, fungal infection, or parasitic infection should receive specific treatments for those organisms in addition to empiric antibiotics. Empiric steroids are not indicated in all patients, but may be useful in patients with concern for cerebral edema. Treatment is usually continued for 6-8 weeks, with follow-up imaging to evaluate for response to treatment.5
– Brain abscesses, though rare, are important for emergency physicians to consider due to important differences in management.
– At risk patients include those with immunocompromise, violation of the CNS spaces through trauma or surgery, and those with a history of possible source infections such as dental, sinus, or middle ear infections.
– The presentation is vague, but headache and focal neurologic findings or altered mental status, with or without a fever and nuchal rigidity, should alert the EP to the possibility of a brain abscess.
– These findings necessitate imaging with IV contrast, and an LP should be avoided due to the possibility of herniation.
– Empiric antibiotics such as Ceftriaxone + Metronidazole, possibly Vancomycin, and targeted treatment for patients at risk for fungal or parasitic infections, should be started as quickly as possible in ill-appearing patients.
– Neurosurgery should be consulted early to assist in source control and long term treatment.
References / Further Reading:
- Meurer, W. J. (2014). Central Nervous System Infections in Rosen’s Emergency Medicine, 8th
- Ma O. Chapter 148. Central Nervous System and Spinal Infections in Tintinalli’s Emergency Medicine Manual, 7th
- Euerle, B.D. (2014). Spinal Puncture and Cerebrospinal Examination in Roberts and Hedges’ Clinical Procedures in Emergency Medicine, 6th
- Moorman, J. P. (2013) Acute Infections of the Central Nervous System: Meningitis and Brain Abscess in Gantz’s Manual of Clinical Problems in Infectious Disease
- Anderson, N.C., Koshy A.A., and Roos, K.L. (2016) Bacterial, Fungal and Parasitic Diseases of the Nervous System in Bradley’s Neurology in Clinical Practice
- Tattevin P et al., Bacterial Brain Abscesses: A Retrospective Study of 94 Patients Admitted to an Intensive Care Unit, Am J Med. 2003; 115(2):143
This is a retrospective, single-center report regarding the incidence of adverse events in patients found to have “hypertensive urgency” in the outpatient setting. This was defined formally as any systolic blood pressure measurement ≥180 mmHg or diastolic measurement ≥110 mmHg. Their question of interest was, specifically, whether patients referred to the ED received clinically-important diagnosis ("major adverse cardiovascular events"), with a secondary interest in whether their blood pressure was under better control at future outpatient visits.
Over their five-year study period, there were 59,535 patient encounters meeting their criteria for “hypertensive urgency”. Astoundingly, only 426 were referred to the Emergency Department. Of those referred to the ED, 2 (0.5%) received a MACE diagnosis within 7 days, compared with 61 (0.1%) of the remaining 58,109. By 6 months, MACE had equalized between the two populations – now 4 (0.9%) in the ED referral cohort compared with 492 (0.8%) in those sent home. Hospital admission, obviously, was higher in those referred to the ED, but apparently conferred a small difference in blood pressure control in follow-up.
The authors go on to perform a propensity-matched comparison of the ED referrals to the sent home cohort, but this is largely uninsightful. The more interesting observation is simply that these patients largely do quite well – and any adverse events probably happen at actuarial levels rather than having any specific relationship to the index event.
I appreciate how few patients were ultimately referred to the Emergency Department in this study; fewer than 1% is an inoffensive number. That said, zero percent would be better.
“Characteristics and Outcomes of Patients Presenting With Hypertensive Urgency in the Office Setting”
The post entitled “CIWA Demystified” is one of the most popular on this blog. This type of symptom triggered therapy for alcohol withdrawal applies some degree of objectivity to a somewhat subjective problem. However, it is possible to take it too far.
A retrospective review of registry patients who received CIWA guided therapy was performed. A total of 124 records were reviewed for appropriateness of CIWA useand adverse events. They found that only about half of patients (48%) met both usage criteria (able to communicate verbally, recent alcohol use). And 31% did not meet either criterion! There were 55 nondrinkers in this study, and even though 64% of them could communicate that fact, they were placed on the protocol anyway! Eleven patients suffered adverse events (delirium tremens, seizures, death). Four of them did not meet criteria for use of the protocol.
Bottom line: In order to be placed on the CIWA protocol, a patient must have a recent history of alcohol use, and must be able to communicate verbally. Some physicians assume that patients with autonomic hyperactivity or psychological distress are withdrawing and order the CIWA protocol. This can cover up other causes of delirium, or may make it worse by administering benzodiazepines. This represents inappropriate use of the protocol!
Reference: Inappropriate use of symptom-triggered therapy for alcohol withdrawal in the general hospital. Mayo Clin Proc 83(3):274-279, 2008.