ABSTRACT
A 23-year-old man presented with abdominal pain after suffering blunt trauma caused by a seatbelt injury. His low platelet count of 137 × 10(9)/L was initially attributed to trauma and his underlying hypersplenism due to glucose-6-phosphate dehydrogenase (G6PD) deficiency. Despite conservative management, his platelet count remained persistently reduced even after his haemoglobin and clotting abnormalities were stabilised. After a week, follow-up imaging revealed an incidental finding of a pseudoaneurysm (measuring 9 mm × 8 mm × 10 mm) adjacent to a splenic laceration. The pseudoaneurysm was successfully closed via transcatheter glue embolisation; 20% of the spleen was also embolised. A week later, the platelet count normalised, and the patient was subsequently discharged. This case highlights the pitfalls in the detection of a delayed occurrence of splenic artery pseudoaneurysm after blunt injury via routine delayed phase computed tomography. While splenomegaly in G6PD may be a predisposing factor for injury, a low platelet count should arouse suspicion of internal haemorrhage rather than hypersplenism.
Subject(s)
Humans , Male , Young Adult , Abdominal Pain , Diagnosis , Accidents, Traffic , Aneurysm, False , Diagnostic Imaging , Therapeutics , Embolization, Therapeutic , Methods , Follow-Up Studies , Glucosephosphate Dehydrogenase Deficiency , Diagnosis , Injury Severity Score , Rare Diseases , Risk Assessment , Seat Belts , Splenic Artery , Wounds and Injuries , Tomography, X-Ray Computed , Methods , Treatment Outcome , Wounds, Nonpenetrating , DiagnosisABSTRACT
<p><b>INTRODUCTION</b>The angiographic findings and prognosis of patients with complete atrioventricular block (AVB) complicating acute inferior myocardial infarction (MI) remain unclear.</p><p><b>MATERIALS AND METHODS</b>The clinical and angiographic findings of 70 consecutive patients with complete AVB were compared with those of 319 patients with inferior MI without AVB (control group) admitted within the same study period.</p><p><b>RESULTS</b>Patients with complete AVB were older (68 +/- 12 vs 63 +/- 13 years; P = 0.004) and clustered with clinical features indicative of larger infarct size, such as right ventricular infarction, cardiogenic shock, or low left ventricular ejection fraction (LVEF). The onset of the complete AVB was observed within 24 hours in 62 (88.6%), preceded by second-degree AVB in 26 (37.1%) and the escape QRS complex was wide in 8 (11.4%) patients. In patients with complete AVB, a dominant right coronary artery occlusion was found in >95% of cases and in-hospital mortality was increased (27.1% vs 10.7%; P = 0.000), especially in those with widen QRS escape rhythm (75.0%). Reperfusion therapy had a positive impact on the natural course of complete AVB.</p><p><b>CONCLUSIONS</b>Complete AVB in acute inferior MI was associated with advanced age and larger infarct size. Complete AVB was virtually always caused by dominant right coronary artery occlusion. The in-hospital mortality was significantly higher, but improved by reperfusion therapy. No permanent pacemaker is performed at a mean follow-up of 47 months.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Age Factors , Atrioventricular Block , Diagnostic Imaging , Mortality , Coronary Angiography , Electrocardiography , Hong Kong , Epidemiology , Hospital Mortality , Inferior Wall Myocardial Infarction , Diagnostic Imaging , Mortality , Kaplan-Meier EstimateABSTRACT
Thrombin is a pivotal molecule in acute myocardial infarction (MI) because of its extensive procoagulant and prothrombotic actions. Antithrombin therapy is an important component of the pharmacotherapy for acute MI. The standard agent used in clinical practice, unfractionated heparin (UFH), is associated with the disadvantages of variable anticoagulant effect, inability to inhibit clot-bound thrombin, neutralization by platelet factor 4, and the propensity to cause thrombocytopenic complications. Novel thrombin inhibitors have been developed to overcome these disadvantages. Although possessing the property of inhibiting both fluid-phase and clot-bound thrombin, the direct thrombin inhibitor hirudin has been shown to give marginal benefits over UFH as adjunct to fibrinolysis in ST-elevation MI. Bivalirudin, another direct thrombin inhibitor, is able to reduce reinfarction in patients treated with streptokinase and is a new anticoagulant treatment option in this setting. The pharmacokinetic characteristics of better availability, longer half-life, and dose-independent clearance together with the ability of inhibiting both thrombin generation and activity make the low-molecular-weight heparins (LMWHs) an attractive alternative to UFH. The favorable benefit/risk profile of the LMWHs as adjunct to different generations of fibrinolytic agents is setting the stage for larger clinical trials to confirm their role as the antithrombin agent of choice for STEMI.