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A 76-year-old male is brought to the ER with severe chest pain and diaphoresis. His past medical history is significant for diabetes mellitus type 2. hypertension and asymptomatic right carotid artery stenosis. His blood pressure is 120/70 mmHg and his heart rate is 75/min. EKG shows ST segment elevations greater than 'I mm in leads II, III and aVF. The patient is treated with streptokinase, morphine, IV fluids and a low-dose beta-blocker. Several hours later, the patient is comatose with asymmetric pupils and an irregular breathing pattern. This patient's current condition is most likely caused by:
0 A. Dissection of the ascending aorta
O B. Carotid artery thrombosis
O C. Interventricular septum perforation
O D. Pulmonary embolism
O E. Intracerebral hemorrhage
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E. Intracerebral hemorrhage?
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The patient described in this clinical vignette has chest pain, diaphoresis and a history of systemic atherosclerosis and diabetes is likely to be having a myocardial infarction. This clinical suspicion is substantiated by EKG findings consistent with an inferior ST elevation myocardial infarction (STEiv11). Treatment with thrombolytics such as streptokinase and tissue plasminogen activator has been shown to increase survival of patients with acute MI if administered within 6 hours of the onset of symptoms and in the absence of contraindications such as recent surgeries or gastrointestinal bleeding. Emergent cardiac catheterization is preferred to thrombolytic therapy if it is available at the institution where the patient presents.
Streptokinase is a protein synthesized by beta-hemolytic streptococci. It forms a complex with plasminogen that, in turn, cleaves plasminogen to form plasmin. Plasmin cleaves fibrin thereby dissolving thrombi. The streptokinase-plasminogen complex also destroys fibrinogen and clotting factors V and VII.
The most common side effect of streptokinase is hemorrhage. The patient described in this clinical vignette displays the signs of an intracerebral hemorrhage (Choice E), such as decreased level of consciousness, asymmetric pupils and irregular breathing. Hemorrhages may also occur in the GI tract or other organ systems.
(Choice A) Dissection of the ascending aorta manifests with excruciating tearing chest pain that radiates to the interscapular area. When dissection leads to rupture this process is nearly universally fatal. It occurs most commonly in patients With hypertension, Marfan and Ehlers-Danlos syndromes. CXR will show a widened mediastinum.
(Choice B) Carotid artery thrombosis can cause ischernic stroke and the symptoms described in this vignette, but in this case treatment with thrombolytics preceding onset of symptoms makes hemorrhagic stroke more likely.
(Choice C) Interventricular septum perforation results in a left-to-right shunt and symptoms of acute heart failure. It presents with chest pain, dyspnea, symptoms or cardiogenic shock and a harsh holosystolic murmur on the left sternal border.
(Choice ID) Pulmonary embolism manifests with acute onset of dyspnea, pleuritic chest pain and hemoptysis. Tachycardia, hypotension, cyanosis and loss of consciousness can occur when severe.
Educational Objective:
Streptokinase is a thrornbolytic agent that acts by converting plasminogen into plasmin, which subsequently degrades fibrin. Its most common side effect is hemorrhage. Streptokinase is a foreign protein derived from Streptococci and can induce hypersensitivity reactions.
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Streptokinase is a protein synthesized by beta-hemolytic streptococci. It forms a complex with plasminogen that, in turn, cleaves plasminogen to form plasmin. Plasmin cleaves fibrin thereby dissolving thrombi. The streptokinase-plasminogen complex also destroys fibrinogen and clotting factors V and VII.
The most common side effect of streptokinase is hemorrhage.
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Dissection of the ascending aorta manifests with excruciating tearing chest pain that radiates to the interscapular area
