Ruptured posterior communicating artery aneurysm presenting as acute subdural hematoma

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Estimate v Kahn’s Scoring system: Complete data was available on 41 subjects. Agreement between estimated and calculated P(DVT) was 34%, yielding a kappa of ⫺0.23 (95% confidence interval [CI] ⫽ ⫺0.47, 0.02). In 16 (39%) of the subjects, the EPs underestimated P(DVT), whereas in 11 (27%) subjects the physician overestimated the P(DVT) (P ⫽ .06 test for symmetry). Estimate v Wells Scoring system: Complete data was available on all 48 subjects. Agreement between estimated and calculated P(DVT) was 52% yielding a kappa of 0.25 (95% CI ⫽ 0.05, 0.44). In 18 (38%) of the subjects, the EPs underestimated P(DVT), whereas in 5 (10%) subjects the physician overestimated the P(DVT) (P ⫽ .03 test for symmetry). Eleven of the 12 patients calculated to have a high P(DVT) by the Wells’ score were estimated by the physicians to have a lower P(DVT). Two scoring systems have been suggested to be able to decrease the need for emergent compression ultrasonography and serial ultrasonography.3,9,13,14 Of the 2 systems, the one by Wells has been incorporated into clinical practice guidelines. The poor level of agreement between the estimated and calculated P(DVT) suggests that physician intuition should not replace the calculated P(DVT) in these clinical guidelines. Doing so could lead to both inappropriate use of d-dimer assay and ultrasonography as well as inappropriate use of their results. Failure to accurately determine the P(DVT) could lead to overreliance on a single ultrasonography or d-dimer to rule out DVT. Our study has several criticisms. The sample size was small leading to wide confidence intervals for the kappa scores, and we used a convenience sample that could have biased our results. However, Miron et al, also found poor agreement between Wells score and physician estimate of P(DVT).15 Unlike our results, however, they showed that physicians were more likely to overestimate rather than underestimate P(DVT). Lack of agreement does not have to mean the physician intuition was worse than the calculated P(DVT). Indeed, studies in other areas have suggested that similarly constructed systems do not perform well when used by an independent group of investigators.16-21 Unfortunately, our sample size was too small to validate the scoring system. However, the scoring system by Wells has already been independently validated.15 In conclusion, clinical intuition of pretest probability should not replace a validated scoring system for determining pretest probability in the context of a clinical practice guideline to evaluate patients with suspected first-time DVT. HOWARD A. SMITHLINE, MD TIMOTHY J. MADER, MD FAHAD M.N. ALI, MD MICHAEL N. COCCHI, BS Department of Emergency Medicine Baystate Medical Center, Springfield Tufts University School of Medicine Boston, MA

References 1. Haeger K: Problems of acute deep venous thrombosis: The interpretation of signs and symptoms. Angiology 1969;20:219-223 2. Anand S, Wells P, Hunt D, Brill-Edwards P, Cook D, Ginsberg J: Does this patient have deep vein thrombosis? JAMA 1998;279: 1094-1099 3. Anderson D, Wells P, Stiell I, et al: Management of patients with suspected deep vein thrombosis in the emergency department: Combining use of a clinical diagnosis model with D-dimer testing. J Emerg Med 2000;19:225-230 4. Hayden S, Brown M: Likelihood ratio: A powerful tool for incorporating the results of a diagnostic test into clinical decisionmaking. Ann Emerg Med 1999;33:575-580 5. McAlister F, Straus S, Guyatt G, Haynes R: Users’ guides to the medical literature: XX. Integrating research evidence with the care of the individual patient. Evidence-Based Medicine Working Group. JAMA 2000;283:2829-2836

6. Wells P, Hirsh J, Anderson D, et al: Accuracy of clinical assessment of deep-vein thrombosis. Lancet 1995;345:1326-1330 7. Kahn S: The clinical diagnosis of deep venous thrombosis: Integrating incidence, risk factors, and symptoms and signs. Arch Intern Med 1999;158:2315-2323 8. Cabana M, Rand C, Powe N, et al: Why don’t physicians follow clinical practice guidelines? A framework for improvement. JAMA 1999;282:1458-1465 9. Kahn S, Joseph L, Abenhaim L, Leclerc J: Clinical prediction of deep vein thrombosis in patients with leg symptoms. Thromb Haemost 1999;81:353-357 10. Wells P, Hirsh J, Anderson D, et al: A simple clinical model for the diagnosis of deep-vein thrombosis combined with impedance plethysmography: Potential for an improvement in the diagnostic process. J Intern Med 1998;243:15-23 11. StataCorp: Stata Statistical Software. College Station, TX: Stata Corporation, 1999 12. Bowker A: A test for symmetry in contingency tables. Journal of the American Statistical Society 1948;43:572-574 13. Anderson D, Wells P, Stiell I, et al: Thrombosis in the emergency department: Use of a clinical diagnosis model to safely avoid the need for urgent radiological investigation. Arch Intern Med 1999; 159:477-482 14. Wells P, Anderson D, Bormanis J, et al: Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet 1997;350:1795-1798 15. Miron M, Perrier A, Bounameaux H: Clinical assessment of a suspected deep vein thrombosis: Comparison between a score and empirical assessment. J Intern Med 2000;247:249-254 16. Sanson B, Lijmer J, Mac Gillavry M, Turkstra F, Prins M, Buller H: Comparison of a clinical probability estimate and two clinical models in patients with suspected pulmonary embolism. ANTELOPE-Study Group. Thromb Haemost 2000;83:199-203 17. Wells P, Anderson D, Ginsberg J: Assessment of deep vein thrombosis or pulmonary embolism by the combined use of clinical model and noninvasive diagnostic tests. Semin Thromb Hemost 2000;26:643-656 18. Charlson M, Ales K, Simon R, MacKenzie C: Why predictive indexes perform less well in validation studies. Is it magic or methods? Arch Intern Med 1987;147:2155-2161 19. Harrell F, Lee K, Califf R, Pryor D, Rosati R: Regression modelling strategies for improved prognostic prediction. Stat Med 1984;3:143-152 20. Harrell F, Lee K, Matchar D, Reichert T: Regression models for prognostic prediction: Advantages, problems, and suggested solutions. Cancer Treat Rep 1985;69:1071-1077 21. Poses R, Cebul R, Collins M, Fager S: The importance of disease prevalence in transporting clinical prediction rules. The case of streptococcal pharyngitis. Ann Intern Med 1986;105:586-591

RUPTURED POSTERIOR COMMUNICATING ARTERY ANEURYSM PRESENTING AS ACUTE SUBDURAL HEMATOMA To the Editor:—Subdural hematoma (SDH) is a frequent occurrence in the elderly population. Patients often present after the development of a dull headache over hours to days accompanied by mental status changes. Typically, SDH is caused by traumatic disruption of the superficial cerebral veins or the cortical veins that bridge the temporal lobe to the sphenoparietal and petrosal sinuses. Most are located over the cerebral convexity, especially in the parietal region, or just above the tentorium cerebelli.1 Expansion of the SDH ceases once the intracranial pressure rises to equal the venous pressure. SDH can be divided into two types—simple and complicated. Simple SDHs account for approximately 45% of all acute SDH and are distinguished from complicated SDHs by the absence of parenchymal damage. Complicated SDH has been associated with a 53% mortality rate, compared with 21% for simple SDH.2 Copyright 2003, Elsevier Science (USA). All rights reserved. 0735-6757/03/2102-0020$30.00/0 doi:10.1053/ajem.2003.50067

CORRESPONDENCE

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FIGURE 1. Noncontrast head CT and intracranial angiography images. (A) Large left-sided holohemispheric subdural hematoma heterogenous in appearance. (B) Left temporal parenchymal hematoma, measuring approximately 6 ⫻ 3 cm, with surrounding vasogenic edema and sulcal effacement. The hematoma has a swirling, heterogeneous appearance which is suspicious for active bleeding, acute bleeding superimposed on chronic bleeding, or blood mixed with cerebrospinal fluid. There is a left to right midline shift of 2.5 cm, and the contralateral ventricle is entrapped. (C) Injection of the left common carotid artery demonstrates anterograde but decreased flow within the left internal carotid artery, anterior cerebral, and middle cerebral arteries. There is a 4-mm left posterior communicating artery aneurysm pointing laterally and posteriorly near the origin of the left posterior communicating artery (arrow). There is tremendous left temporal lobe mass effect with elevation of the left middle cerebral artery candelabra branches cephalad and medially as well as deviation of the left anterior cerebral artery across the midline. An 81-year-old woman with hypertension suddenly developed a severe headache followed by loss of consciousness. Her Glasgow Coma Scale (GCS) score was 15 at the time of presentation and quickly declined to 5. On physical examination, she was comatose. Her blood pressure was 153/67 mm Hg, pulse was 82 beats/min, and she was breathing spontaneously at a rate of 28 breaths/min with an oxygen saturation of 99% on room air. Both pupils were 5 mm, irregular, and nonreactive to light. Both corneal reflexes and the gag reflex were intact. She had increased tone throughout and both upper limbs were in extension. Both lower limbs exhibited triple flexion on exposure to painful stimulus. Her reflexes were hyperactive bilaterally, the right side being greater than the left side, and plantar responses were extensor bilaterally. A noncontrast head CT revealed a large, left-sided SDH with associated intraparenchymal temporal lobe hematoma and midline shift (Fig 1A, B). Mannitol and hyperventilation therapies were instituted immediately. Given the history and the appearance of the hematoma, aneurysm was suspected, and the patient immediately underwent an intracranial angiogram, which revealed a 4-mm saccular, left posterior communicating artery aneurysm, thought to be the etiology of the hematoma (Fig 1C). The patient was transferred directly to the operating room from the angiography suite, pentobarbital coma was induced, and emergent clipping of the aneurysm was performed with drainage of the SDH. After surgery, however, the patient failed to improve over several days and support was withdrawn. SDHs are frequently seen in the elderly after head trauma or falls. They have rarely been described as being secondary to a ruptured cerebral artery aneurysm. Arteries implicated include the middle cerebral, anterior cerebral, internal carotid, vertebral, and posterior communicating.3 Only a few cases of posterior communicating artery aneurysm rupture leading to acute SDH have been reported.3-6 Subarachnoid hemorrhage is the most common result of a ruptured cerebral artery aneurysm, although acute subdural blood has been estimated to occur in up to 3% of cases.7 The mechanisms for SDH development secondary to aneurysmal rupture are not entirely clear. Two theories have been proposed. The

first theory proposes a tear of the arachnoid leads to direct bleeding changes into the subdural space. Such a tear would be possible in an aneurysm adherent to the arachnoid. The second theory proposes that a hemorrhage in the setting of hypertension can result in pia-arachnoid rupture and extravasation of blood into an intracerebral or subdural location.3 Most cases of aneurysmal rupture leading to SDH occur in the distribution of the middle and anterior cerebral arteries.3 This patient illustrates a rare cause of SDH, namely that of a ruptured posterior communicating artery aneurysm. Atypical features of the presentation include the acute onset of severe headache, rapid deterioration of mental status, absence of known trauma, and a CT scan demonstrating a larger than expected hematoma with the suggestion of on-going bleeding. A high index of suspicion for a vascular anomaly must always be maintained with the development of an acute SDH in the absence of a history of trauma. Further radiologic investigation (searching for an aneurysm, cortical arteriovenous malformation, or dural-based tumor) is warranted before any surgical intervention is performed. JACK W. TSAO, MD, DPHIL Department of Neurology JUSTINE L. WALDMAN, MD Department of Emergency Medicine GEOFF T. MANLEY, MD, PHD Department of Neurosurgery University of California–San Francisco San Francisco, CA

References 1. Gean AD: Imaging of head trauma. New York: Raven Press; 1994, pp 78-89 2. Jamieson KG, Yelland JDN: Surgically treated traumatic subdural hematomas. J Neurosurg 1972;37:137-149 3. Kondziolka D, Bernstein M, ter Brugge K, Schutz H: Acute subdural hematoma from ruptured posterior communicating artery aneurysm. Neurosurgery 1988;22:151-154

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4. Ranganadham P, Dinakar I, Mohandas S, Singh AK: A rare presentation of posterior communicating artery aneurysm. Clin Neurol Neurosurg 1992;94:225-227 5. Rusyniak WG, Peterson PC, Okawara SH, Pilcher WH, George ED: Acute subdural hematoma after aneurysmal rupture; Evacuation with aneurysmal clipping after emergent infusion computed tomography: Case report. Neurosurgery 1992;31:129-132 6. Smith JK, Castillo M: Ruptured aneurysm presenting with a subdural hematoma. Am J Roent 1995;165:491-492 7. O’Leary PM, Sweeny PJ: Ruptured intracerebral aneurysm resulting in a subdural hematoma. Ann Emerg Med 1986;15:944-946

TIME TO BODY SURFACE MAP ACQUISITION COMPARED WITH ED 12-LEAD AND RIGHT-SIDED ECG To the Editor:—Diagnosing the etiology of chest pain in patients in the ED can be a challenging process. There is currently a 2% to 10% missed acute myocardial infarction (AMI) rate among patients presenting to the ED with chest pain with a 25% mortality rate in this group.1,2 The imperfect sensitivity of the standard 12-lead electrocardiogram (ECG) accounts for a significant percentage of missed AMI cases.3 Many investigators have attempted to increase the diagnostic yield of the ECG by analyzing leads additional to the standard 12.4-6 The 80-lead body surface map (BSM) has been developed in an attempt to address this interest and potentially increase the sensitivity for detecting ischemia in patients experiencing chest pain.7-11 We sought to evaluate the time required for ED BSM acquisition and to compare BSM acquisition time with standard 12-lead times. We also compared BSM acquisition time with national benchmark ECG findings provided by the National Registry of Myocardial Infarction database (NRMI) as well as the American College of Cardiology (ACC) recommendations. This trial enrolled patients presenting to the ED with chest pain during a 1-month study period at our 600-bed, tertiary-care hospital (Maine Medical Center, Portland, ME) with an annual ED census of 50,000 patients. The Institutional Review Board approved the study protocol. Study-eligible patients included those presenting with the chief complaint of nontraumatic chest pain who received a standard 12-lead ECG. An ECG technician performed the initial ED ECG (PageWriter XLi Cardiograph, Hewlett Packard Co., Palo Alto, CA). An independent observer recorded the technician ECG acquisition time in seconds. The acquisition time was defined as the time interval from the technician’s first contact with the patient to printing of an acceptable ECG. During the patient’s ED visit, a research nurse obtained a second 12-lead ECG plus a right-sided ECG and BSM. The research nurse completed the second 12-lead ECG and right-sided ECG using the standard ECG equipment. The BSM was acquired through use of a portable device (Prime ECG System, Meridian Medical Technologies, Inc., Columbia, MD) with acquisition time defined as the interval from initial contact to monitor display of a complete BSM. Benchmark comparison data from NRMI have demonstrated mean door-to-ECG times of approximately 8 minutes.12 Similarly, the ACC recommends the initial ECG be completed in less than 10 minutes from the time of a patient’s arrival in the ED.13 Twenty-four patients presenting to the ED with chest pain were enrolled in the study group, yielding 23 completed BSMs. The study group consisted of 13 men and 10 women with a mean age of 57 years (range, 26-91 y). Eighty-three percent (19 of 23) of patients weighed less than 100 kg. There were no diaphoretic patients.

Copyright 2003, Elsevier Science (USA). All rights reserved. 0735-6757/03/2102-0021$30.00/0 doi:10.1053/ajem.2003.50062

FIGURE 1. Time for 12-lead and body surface map acquisition } (BSM), } 95% CI. Three men required shaving for the technician-applied 12-lead ECG with an additional 2 men requiring shaving for BSM lead placement. The time required to shave patients was included in the ECG and BSM acquisition times. The mean time for the ECG technician to produce a 12-lead ECG was 183 seconds (95% confidence interval [CI]: 157-208; Fig 1). This time was compared with a mean BSM acquisition time of 398 seconds (95% CI: 366-430). The longest BSM acquisition time was 585 seconds with 87% of the BSMs obtained in less than 8 minutes. The mean acquisition time for a research nurse to perform a 12-lead ECG was 145 seconds (95% CI: 126-163). The mean research nurse time to obtain a 12-lead plus a right-sided ECG was 236 seconds (95% CI: 214-259). Eighty-seven percent of BSMs were obtained in less than 8 minutes. No patient required a BSM or ECG acquisition time exceeding 10 minutes. Body surface mapping in patients presenting to the ED with chest pain appears to add a small, clinically insignificant time interval when compared with traditional 12-lead ECG. When available on patient arrival, the time required to obtain an ED BSM appears to be within acceptable standards for ECG acquisition. The Prime ECG System is designed to generate a BSM from an 80-lead “vest” (64 anterior and 16 posterior electrodes). After BSM data collection, the Prime ECG System analyzes a representative QRST complex from the 80 leads. A color-coded “map” is then created based on area-under-the-curve analysis of selected complex segments. The BSM is displayed on the system’s monitor with an immediate printing option available. Although this investigation used a research nurse for BSM acquisition, the application of the Prime ECG System requires little additional training beyond that required for standard 12-lead ECG. A limitation of this investigation is the research nurse awareness of the investigation objective at the time of ECG and BSM acquisition. The investigators attempted to account for this limitation by comparing research nurse times for standard 12-lead ECG acquisition with the ECG technician’s 12-lead times. This report is not submitted as a substitute or attempt at a comprehensive assessment of ED BSM technology. Reports with larger patient numbers in the setting of routine clinical BSM application will more completely assess this new technology. TIMOTHY R. FOX, MD JOHN H. BURTON, MD TANIA D. STROUT, RN, BSN DAVID T. BACHMAN, MD GEORGE L. HIGGINS, MD Department of Emergency Medicine Maine Medical Center Portland, ME