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2. Broad-spectrum intravenous antibiotics and fluid resuscitation should be started as soon as the diagnosis is suspected.
3. Nonoperative management may be an option for patients with well-contained perforations and minimal mediastinal or pleural contamination.
V. OUTCOME
In a retrospective review between 1990 and 2003, overall mortality was 18%. Mortality risk is influenced by the type of perforation, anatomic location, underlying disease, time to diagnosis, and choice of surgical or nonsurgical
treatment.[20] Early diagnosis and treatment are essential to outcome and reduce mortality by at least 50%. PEARLS AND PITFALLS
▪ Blood pressure should be measured in both arms during the evaluation of chest discomfort.
▪ Ischemic events related to occlusion of the left circumflex artery are electrocardiographically subtle.
▪ Relief of chest pain with nitroglycerin does not predict coronary artery disease in the acute setting and should not be used as a triage tool.[21]
▪ Troponin levels alone are unreliable in diagnosing recurrent MI. Always measure creatine kinase and creatine kinase myocardial band within the first 24 hours.
▪ Never forget to inquire about illicit drug use, especially in a young patient with chest pain.
▪ A history of chest discomfort suggesting an ACS and risk factors for atherosclerosis with persistently negative or normal electrocardiographic findings is highly suspicious for acute aortic dissection. ▪ Patients with intermediate or high clinical probability for PE should be given anticoagulation during the
diagnostic workup.
▪ Secondary spontaneous PTX often is associated with a greater degree of cardiopulmonary embarrassment than occurs with primary spontaneous PTX.
▪ Mackler's triad consists of vomiting, lower thoracic pain, and subcutaneous emphysema and refers to signs and symptoms seen in barogenic esophageal rupture.
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REFERENCES
1. Burt CW: Summary statistics for acute cardiac ischemia and chest pain visits to United States EDs, 1995-1996. Am J Emerg Med 1999; 17:552.
2. Weber JE, Hollander JE: Cocaine-associated chest pain: how common is myocardial infarction?. Acad Emerg Med 2000; 7:873.
3. Goldman L, Kirtane AJ: Triage of patients with acute chest pain and possible cardiac ischemia: the elusive search for diagnostic perfection. Ann Intern Med 2003; 139:987.
4. McCaig LF, Burt CW: National Hospital Ambulatory Medical Care Survey: 2002 emergency department summary. Adv Data 2004;1.
5. Wang K, et al: ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003; 349(22):2128.
6. De Lemos JA, Morrow DA: Combining natriuretic peptides and necrosis markers in the assessment of acute coronary syndromes. Rev Cardiovasc Med 2003; 4(Suppl 4):S37.
7. Graff LG, et al: Impact on the care of the emergency department chest pain patient from the Chest Pain Evaluation Registry (CHEPER) Study. Am J Cardiol 1997; 80:563.
8. Farkouh ME, et al: A clinical trial of a chest-pain observation unit for patients with unstable angina. Chest Pain Evaluation in the Emergency Room (CHEER) Investigators. N Engl J Med 1998; 339:1882.
9. Weber JE, et al: Validation of a brief observation period for patients with cocaine-associated chest pain. N Engl J Med 2003; 348:510.
10. Udelson JE, et al: Myocardial perfusion imaging for evaluation and triage of patients with suspected acute cardiac ischemia: a randomized controlled trial. JAMA 2002; 288(21):2693.
11. Klocke FJ, et al: ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation 2003; 108(11):1404.
12. Goldhaber SZ: Pulmonary embolism. N Engl J Med 1998; 339:93. 13. Dmowski AT, et al: Aortic dissection. Am J Emerg Med 1999; 17:372.
14. Hagan PG, et al: The International Registry of Acute Aortic Dissection (IRAD). JAMA 2000; 283(7):897. 15. von Kodolitsch , et al: Clinical prediction of acute aortic dissection. Arch Intern Med 2000; 160:2977. 16. Sahn SA, Heffner JE: Spontaneous pneumothorax. N Engl J Med 2000; 342(12):868.
17. Bense L, et al: Smoking and the increased risk of contracting spontaneous pneumothorax. Chest 1987; 92(6):1009.
18. Baumann MH, et al: Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi Consensus Statement. Chest 2001; 119:590.
19. Trachiotis GD, et al: Management of AIDS-related pneumothorax. Ann Thorac Surg 1996; 62:1608.
20. Brinster CJ, et al: Evolving options in the management of esophageal perforation. Ann Thorac Surg 2004; 77:1475. 21. Henrikson CA, et al: Chest pain relief by nitroglycerin does not predict active coronary artery disease. Ann Intern Med 2003; 139(12):979-986.
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Piccini & Nilsson: The Osler Medical Handbook, 2nd ed.
Copyright © 2006 Johns Hopkins UniversityChapter 8 – Acute Coronary Syndromes
Paul F. Frey, MD, MPH Richard Lange, MDFAST FACTS
▪
Acute coronary syndrome (ACS) consists of the signs and symptoms compatible with progressive or acute nonexertional myocardial ischemia and is divided into non–ST segment elevation ACS and ST segment elevation ACS.
▪ Risk stratification is important in guiding therapy for patients with non–ST segment elevation ACS.
▪
The electrocardiographic (ECG) diagnosis of ST segment elevation ACS is defined by more than 1 mm of ST segment elevation in two limb leads, more than 2 mm of ST segment elevation in two contiguous precordial leads, or a new or presumed new left bundle branch block.
▪ In the patient with ST segment elevation ACS, prompt reperfusion of the infarct-related artery (IRA) is essential.
▪ Aggressive risk factor modification and secondary prevention therapy should be applied to all patients with ACS.
1. Cardiovascular disease is the leading cause of death in the United States, accounting for more than 1 of