Digamber Behera

Delayed presentation of amniotic fluid embolism: lessons from a case diagnosed at autopsy.

Abstract:  Amniotic fluid embolism (AFE) syndrome, a catastrophic cause of respiratory failure typically occurs during labour, or soon after delivery. Systemic hypotension is the most prominent haemodynamic alteration documented in patients with AFE, a consequence principally of severe left‐sided heart failure. A 22‐year‐old female was admitted to the respiratory intensive care unit with severe eclampsia and acute respiratory failure 4 h following delivery. Her blood pressure was elevated (systolic 150–180 mm Hg, diastolic 90–110 mm Hg) throughout the admission. She succumbed in spite of therapy for eclampsia and mechanical ventilation. Autopsy revealed large numbers of polygonal, anucleate foetal squames and mucin in the pulmonary vasculature typical of AFE while changes of eclampsia were found in the liver and kidneys. It appears that AFE syndrome can have a delayed presentation, as late as 4 h after delivery and haemodynamic collapse may not be mandatory if the patient has coexisting systemic hypertension secondary to severe eclampsia.

Analysis of static pulmonary mechanics helps to identify functional defects in survivors of acute respiratory distress syndrome.

ObjectiveTo assess the utility of static lung pressure-volume measurements in identifying and categorizing pulmonary function test defects in survivors of acute respiratory distress syndrome (ARDS). DesignCross-sectional. SettingPulmonary function laboratory at a tertiary referral hospital in northern India. PatientsSix survivors of ARDS reporting for their first follow-up visit after discharge. Measurements and Main ResultsSpirometry and whole body plethysmography were performed to evaluate lung volumes and to collect static lung pressure-volume data; the latter were subjected to monoexponential analysis. Three patients had a restrictive ventilatory defect as evidenced by diminished vital capacity and total lung capacity, but only one had reduced static lung compliance. The other two patients had reduced recoil pressure at total lung capacity, suggestive of respiratory muscle weakness. Two other patients with normal lung volumes had reduced static lung compliance. Exponential analysis of pressure-volume data in the three patients with reduced static lung compliance was consistent with reduced distensibility and loss of lung units in one patient each. Additionally, two patients had high values for shape constant of the exponential curve, indicative of air space distention. ConclusionsDetailed analysis of static pressure-volume data can identify pulmonary function abnormality and categorize the dominant mechanism responsible for restrictive ventilatory defects in survivors of ARDS, even in patients with normal lung volumes. In addition to lung fibrosis, neuromuscular weakness also contributes to decline in pulmonary function.

Interferon-γ 1b: impact of new indications (idiopathic pulmonary fibrosis)

Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive disease with inadequate response to conventional treatment with corticosteroids and/or immunosuppressive agents in most patients. Interferon-γ (IFN-γ), an antifibrotic agent, has been proposed as a novel therapeutic approach. Several investigators have shown a relative decrease in systemic and pulmonary IFN-γ activity in patients with IPF. Experimental evidence from animal and human studies also suggests that IFN-γ administration may ameliorate lung fibrosis. Clinical experience is, however, limited to a single clinical trial that showed objective functional improvement in a small number of patients treated with IFN-γ and low-dose corticosteroids. Further research is needed to characterise the efficacy, safety and optimum route of administration of this agent before it can be recommended for use in routine clinical practice.