Anna Finley Caulfield, MD

All Publications

• The State of Neurocritical Care Fellowship Training and Attitudes toward Accreditation and Certification: A Survey of Neurocritical Care Fellowship Program Directors FRONTIERS IN NEUROLOGY Dhar, R., Rajajee, V., Caulfield, A., Maas, M. B., James, M. L., Kumar, A., Figueroa, S. A., McDonagh, D., Ardelt, A. 2017; 8: 548

  Abstract

  Neurocritical care as a recognized and distinct subspecialty of critical care has grown remarkably since its inception in the 1980s. As of 2016, there were 61 fellowship training programs accredited by the United Council for Neurologic Subspecialties (UCNS) in the United States and more than 1,000 UCNS-certified neurointensivists from diverse medical backgrounds. In late 2015, the Program Accreditation, Physician Certification, and Fellowship Training (PACT) Committee of the Neurocritical Care Society (NCS) was convened to promote and support excellence in the training and certification of neurointensivists. One of the first tasks of the committee was to survey neurocritical care fellowship training program directors to ascertain the current state of fellowship training and attitudes regarding transition to Accreditation Council for Graduate Medical Education (ACGME) accreditation of training programs and American Board of Medical Specialties (ABMS) certification of physicians. First, the survey revealed significant heterogeneities in the manner of neurocritical care training and a lack of consistency in requirements for fellow procedural competency. Second, although a majority of the 33 respondents indicated that a move toward ACGME accreditation/ABMS certification would facilitate further growth and mainstreaming of training in neurocritical care, many programs do not currently meet administrative requirements and do not receive the level of institutional support that would be needed for such a transition. In summary, the results revealed that there is an opportunity for future harmonization of training standards and that a transition to ACGME accreditation/ABMS certification is preferred. While the results reflect the opinions of more than half of the survey respondents, they represent only a small sample of neurointensivists.

  View details for PubMedID 29163327

• Metronidazole-Induced Encephalopathy: Not Always a Reversible Situation NEUROCRITICAL CARE Hobbs, K., Stern-Nezer, S., Buckwalter, M. S., Fischbein, N., Caulfield, A. F. 2015; 22 (3): 429-436

  Abstract

  Metronidazole is a nitroimidazole antimicrobial drug prescribed to treat infections caused by anaerobic bacteria and protozoa. Uncommonly, it causes central nervous system (CNS) toxicity manifesting as metronidazole-induced encephalopathy (MIE).Case report.A 65-year-old woman with hepatitis B cirrhosis (Child-Pugh class C, MELD 21) developed progressive encephalopathy to GCS 4 during a 3-week course of metronidazole for cholecystitis. Initial MRI was consistent with CNS metronidazole toxicity, with symmetrical T2 hyperintensity and generally restricted diffusion in bilateral dentate nuclei, corpus callosum, midbrain, superior cerebellar peduncles, internal capsules, and cerebral white matter. Laboratory values did not demonstrate significant electrolyte shifts, and continuous EEG was without seizure. High-dose thiamine was empirically administered. Lumbar puncture was not performed due to coagulopathy and thrombocytopenia. Despite discontinuation of metronidazole and keeping ammonia levels near normal, the patient did not improve. MRI was repeated 1 week after discontinuation of metronidazole. Although there was decreased DWI hyperintensity in the dentate nuclei, diffuse T2 hyperintensity persisted and even progressed in the brainstem, basal ganglia, and subcortical white matter. Petechial hemorrhages developed in bilateral corticospinal tracts and subcortical white matter. T1 hypointensity appeared in the corpus callosum. She was transitioned to comfort measures only and died 12 days later.MIE is an uncommon adverse effect of treatment with metronidazole that characteristically affects the dentate nuclei but may also involve the brainstem, corpus callosum, subcortical white matter, and basal ganglia. While the clinical symptoms and neuroimaging changes are usually reversible, persistent encephalopathy with poor outcome may occur.

  View details for DOI 10.1007/s12028-014-0102-9

  View details for PubMedID 25561434

• Christine Anne Cunegonde Wijman, MD, PhD (1965-2013). Neurocritical care Finley Caulfield, A., Venkatasubramanian, C. 2013; 19 (1): 135-136

  View details for DOI 10.1007/s12028-013-9855-9

  View details for PubMedID 23690248

• Natural History of Perihematomal Edema After Intracerebral Hemorrhage Measured by Serial Magnetic Resonance Imaging STROKE Venkatasubramanian, C., Mlynash, M., Finley-Caulfield, A., Eyngorn, I., Kalimuthu, R., Snider, R. W., Wijman, C. A. 2011; 42 (1): 73-80

  Abstract

  knowledge on the natural history and clinical impact of perihematomal edema (PHE) associated with intracerebral hemorrhage is limited. We aimed to define the time course, predictors, and clinical significance of PHE measured by serial magnetic resonance imaging.patients with primary supratentorial intracerebral hemorrhage ? 5 cm(3) underwent serial MRIs at prespecified intervals during the first month. Hematoma (H(v)) and PHE (E(v)) volumes were measured on fluid-attenuated inversion recovery images. Relative PHE was defined as E(v)/H(v). Neurologic assessments were performed at admission and with each MRI. Barthel Index, modified Rankin scale, and extended Glasgow Outcome scale scores were assigned at 3 months.twenty-seven patients with 88 MRIs were prospectively included. Median H(v) and E(v) on the first MRI were 39 and 46 cm(3), respectively. Median peak absolute E(v) was 88 cm(3). Larger hematomas produced a larger absolute E(v) (r(2)=0.6) and a smaller relative PHE (r(2)=0.7). Edema volume growth was fastest in the first 2 days but continued until 12 ± 3 days. In multivariate analysis, a higher admission hematocrit was associated with a greater delay in peak PHE (P=0.06). Higher admission partial thromboplastin time was associated with higher peak rPHE (P=0.02). Edema volume growth was correlated with a decline in neurologic status at 48 hours (81 vs 43 cm(3), P=0.03) but not with 3-month functional outcome.PHE volume measured by MRI increases most rapidly in the first 2 days after symptom onset and peaks toward the end of the second week. The timing and magnitude of PHE volume are associated with hematologic factors. Its clinical significance deserves further study.

  View details for DOI 10.1161/STROKEAHA.110.590646

  View details for PubMedID 21164136

• A comparison of cooling techniques to treat cardiac arrest patients with hypothermia. Stroke research and treatment Finley Caulfield, A., Rachabattula, S., Eyngorn, I., Hamilton, S. A., Kalimuthu, R., Hsia, A. W., Lansberg, M. G., Venkatasubramanian, C., BAUMANN, J. J., Buckwalter, M. S., Kumar, M. A., Castle, J. S., Wijman, C. A. 2011; 2011: 690506-?

  Abstract

  Introduction. We sought to compare the performance of endovascular cooling to conventional surface cooling after cardiac arrest. Methods. Patients in coma following cardiopulmonary resuscitation were cooled with an endovascular cooling catheter or with ice bags and cold-water-circulating cooling blankets to a target temperature of 32.0-34.0°C for 24 hours. Performance of cooling techniques was compared by (1) number of hourly recordings in target temperature range, (2) time elapsed from the written order to initiate cooling and target temperature, and (3) adverse events during the first week. Results. Median time in target temperature range was 19 hours (interquartile range (IQR), 16-20) in the endovascular group versus. 10 hours (IQR, 7-15) in the surface group (P = .001). Median time to target temperature was 4 (IQR, 2.8-6.2) and 4.5 (IQR, 3-6.5) hours, respectively (P = .67). Adverse events were similar. Conclusion. Endovascular cooling maintains target temperatures better than conventional surface cooling.

  View details for DOI 10.4061/2011/690506

  View details for PubMedID 21822470

• Management of acute ischemic stroke NEUROLOGIC CLINICS Caulfield, A. F., Wijman, C. A. 2008; 26 (2): 345-?

  Abstract

  Stroke is the third leading cause of death and the leading cause of disability in the United States. This article summarizes the management of acute ischemic stroke, including conventional and novel therapies. The article provides an overview of the initial management, diagnostic work-up, treatment options, and supportive measures that need to be considered in the acute phase of ischemic stroke.

  View details for DOI 10.1016/j.ncl.2008.03.016

  View details for PubMedID 18514817

• Critical care of acute ischemic stroke CRITICAL CARE CLINICS Caulfield, A. F., Wijman, C. A. 2006; 22 (4): 581-?

  Abstract

  Stroke is the third leading cause of death and the leading cause of disability in the United States. This article summarizes the critical care of acute ischemic stroke, including conventional and novel therapies. The article provided an overview of the initial management, diagnostic workup, treatment options, and supportive measures that need to be considered in the acute phase of ischemic stroke.

  View details for DOI 10.1016/j.ccc.2006.09.001

  View details for PubMedID 17239745