Platypnea-Orthodeoxia syndrome (POS) is a rare clinical entity characterized by dyspnea and arterial desaturation while in the upright position. The various pathophysiologic mechanisms leading to POS has puzzled clinicians for years. The hypoxia in POS has been attributed to the mixing of the deoxygenated venous blood with the oxygenated arterial blood via a shunt. The primary mechanisms of POS in these patients can be broadly classified based on intracardiac abnormalities, extracardiac abnormalities and miscellaneous etiologies. A Patent Foramen Ovale (PFO) was the most common reported site of an intracardiac shunt. In addition to PFO, intracardiac shunt leading to POS has been reported from either an Atrial Septal Defect (ASD) or an Atrial Septal Aneurysm (ASA). Most patients with an intracardiac shunt also demonstrated a secondary anatomic or a functional defect. Extracardiac causes of POS included intra-pulmonary arteriovenous malformations and lung parenchymal diseases. A systematic evaluation is necessary to identify the underlying cause and institute an appropriate intervention. We conducted a review of literature and reviewed 239 cases of POS. In this article, we review the etiology and pathophysiology of POS and also summarize the diagnostic algorithms and treatment modalities available for early diagnosis and prompt treatment of patients presenting with symptoms of platypnea and/or orthodeoxia.

Diaphragm excursion measured during SBT is an imperfect predictor of the outcome of extubation. Maintenance of diaphragm excursion between A/C and SBT has good performance characteristics by AUC analysis. Diaphragm contraction velocity has poor ability to predict outcome of extubation.

Splenectomy predisposes patients to a slew of infectious and non-infectious complications including pulmonary vascular disease. Patients are at increased risk for venous thromboembolic events due to various mechanisms that may lead to chronic thromboembolic pulmonary hypertension (CTEPH). The development of CTEPH and pulmonary vasculopathy after splenectomy involves complex pathophysiologic mechanisms, some of which remain unclear. This review attempts congregate the current evidence behind our understanding about the etio-pathogenesis of pulmonary vascular disease related to splenectomy and highlight the controversies that surround its management.

No abstract

BACKGROUNDHydrocarbon pneumonitis, resulting from aspiration of diesel/petrol or other hydrocarbons can present as acute onset breathlessness. Most of the cases involve siphoning of the fuel tank in our country, which is a common practice. If not recognised early, the condition may be fatal. 1 CASE PRESENTATIONA 24-year-old, heavy duty crane operator presented in the emergency department with acute onset breathlessness at rest, present since 8 h. He denied having had fever, trauma, intoxications, lower limb swelling/tenderness and smoking and left-sided chest pain. There was no history of heart disease. On enquiry, he revealed to have siphoned the diesel tank of his heavy duty crane which he operated, suspecting it to have air trapped in the tank. Dyspnoea followed after that. On examination, the patient was afebrile, pulse rate was 108/min, regular, blood pressure was 100/70 and respiratory rate of 32/min with nasal fl aring. Jugular venous pressure was not raised. Air entry was reduced with occasional crepitations in bilateral lung bases. INVESTIGATIONSArterial blood gases (ABG) showed hypoxemia with pH -7.34, partial pressure of carbon dioxide -45, partial pressure of oxygen -51 and saturation of oxygen -84% on room air. ECG showed sinus tachycardia; complete haemogram did not reveal any abnormality. Liver/renal function tests were normal. Chest x-ray revealed bilateral lower zone pneumonitis ( fi gure 1 ).