Background
Left ventricular (LV) tamponade is rare. LV tamponade can occur in cases of a loculated pericardial effusion overlying the LV and in cases of circumferential pericardial effusions in patients with severe pulmonary arterial hypertension (PAH). Both causes of LV tamponade share the common feature of not presenting with the classical features of cardiac tamponade. However, the therapeutic approach of the two is different.
Case summary
Here, we report two cases of LV tamponade. The first patient was a case of post-mitral valve replacement who presented with loculated posterior pericardial effusion with LV tamponade. Due to the loculated and posterior nature of the effusion, his pericardial fluid was drained from the axilla by echocardiographic and fluoroscopic guidance. The second patient presented with features of severe PAH with a circumferential pericardial effusion and LV tamponade. Due to the circumferential nature of the effusion, the pericardiocentesis was performed from the subxiphoid route.
Discussion
The pathophysiology of LV tamponade must be determined accurately before performing pericardiocentesis. Left ventricular tamponade in patients with severe PAH and non-loculated circumferential effusion can be drained from the subxiphoid route, while LV tamponade due to loculated effusion overlying LV must be drained by echocardiographic and fluoroscopic guidance from the axilla.
Context:Dysplastic pulmonary valve stenosis is a less common variety of valvular pulmonary stenosis. It is known to be part of Noonan syndrome. Bony hand anomalies in patients of pulmonary stenosis are very rare.Case report:A 50-year-old lady, with no significant past history, presented with slowly progressive breathlessness and fatigue, and had progressed from NYHA class 1 to 2 over 2 years. She had unilateral absent first metacarpal and diagnosed on workup to have dysplastic pulmonary valve stenosis and was treated with balloon valvuloplasty.Conclusion:Dysplastic pulmonary valve stenosis can rarely be associated with bony hand anomalies like absent first metacarpal.
The differential diagnosis of shock following percutaneous coronary intervention (PCI) is vast. Access site complications and bleeding can cause hypovolemic shock. Peri-procedural myocardial infarction, abrupt closure, stent thrombosis, coronary dissection and coronary perforation have a stormy presentation. Vasovagal shock is manifested by bradycardia and hypotension and quickly responds to atropine. Anaphylactic shock secondary to contrast administration can be stormy but usually responds to steroids or adrenaline. Septicemia due to unsterile techniques can cause a less dramatic shock. Acute adrenal insufficiency causing shock following PCI has not been described to the best of our knowledge. We report the case of a 54-year-old woman who underwent successful multivessel PCI. She had refractory unexplained shock following the PCI with no much response from inotropic or intra-aortic balloon pump. After ruling out all possible causes of shock and clinical suspicion of adrenal insufficiency, she was treated with steroids resulting in dramatic improvement in her hemodynamics.
Stevens–Johnson syndrome (SJS) is an acute life-threatening mucocutaneous reaction caused by excessive necrosis and detachment of the epidermis. It is commonly drug induced and phenytoin is a common precipitant. Phenytoin, an antiepileptic drug, is also known to cause myocarditis. Phenytoin causing both myocarditis and SJS in the same patient is very rare and can lead to increased morbidity and mortality. Here, we describe the case of a 43-year-old male who developed SJS and myocarditis secondary to phenytoin. In spite of aggressive resuscitative efforts, the patient could not be revived. Thus, a combination of myocarditis with SJS increases the mortality and should be considered in patients with SJS secondary to phenytoin and associated shock.
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