Wednesday, May 14, 2014
How do steroids help in epilepsy treatment?
The mechanism of action of ACTH and steroids in epilepsies is not known. It is likely independent of adrenal corticosteroid release. Check uptodate http://www.uptodate.com/contents/management-and-prognosis-of-infantile-spasms?source=outline_link&view=text&anchor=H6#H6
Tuesday, May 13, 2014
Friday, May 9, 2014
POPE
http://www.jccjournal.org/article/S0883-9441%2810%2900062-6/fulltext#section6
Postobstructive pulmonary edema (POPE) also referred to as negative pressure pulmonary edema is a potentially life-threatening clinical scenario in which immediate-onset pulmonary edema develops after upper airway obstruction. Two distinct subclasses of POPE have been described in the literature: type I is associated with forceful inspiratory effort in the context of an acute airway obstruction, whereas type II occurs after relief of a chronic partial airway obstruction. Common etiologies for type I POPE include laryngospasm, epiglottitis, croup, choking/foreign body, strangulation, hanging, endotracheal tube obstruction, laryngeal tumor, goiter, mononucleosis, postoperative vocal cord paralysis, and near drowning. Type II is more common after relief of a chronic partial upper airway obstruction, as may be expected after adenoidectomy/tonsillectomy, laryngeal mass resection, correction of choanal stenosis, or reduction of a hypertrophic redundant uvula. In the adult population, POPE is most commonly caused by laryngospasm and upper airway tumors, whereas in the pediatric age group, epiglottitis, croup, and laryngotracheobronchitis are more common etiologies.
The pathophysiology of postobstructive pulmonary edema is multifactorial, involving components of negative pressure pulmonary edema, hypoxia, and an hyperadrenergic state. The major component is the negative pressure pulmonary edema that develops in patients with POPE type I. The event is triggered when an attempted inspiration occurs against an occluded airway. It has been reported that a forceful inspiration against such glottic obstruction could result in a maximum intrathoracic pressure of −140 cm H2O from a baseline of −4 cm H2O. This event then leads to an increase in venous return and blood flow to the right side of the heart as well as a decrease in the flow from the left side as a result of increased afterload. This combination causes increased pulmonary blood volume and elevated pulmonary venous pressures, which lead to an increase in hydrostatic pressures and edema formation. In addition, as a result of the elevated negative intrapleural pressure due to obstruction, the pressure is transmitted to the interstitium and alveoli and causes an increase in the hydrostatic gradient favoring transudation of fluid from the pulmonary capillary to the pulmonary interstitial space, resulting in pulmonary edema. The increased negative pressure is the possible component that explains why healthy young men who generate greater negative intrapleural pressures have an increased incidence of POPE.
Although POPE is an important etiologic factor to consider in the setting of acute postoperative respiratory distress, the differential diagnosis must also include other causes including aspiration pneumonitis, pulmonary embolism, anaphylaxis, iatrogenic volume overload, and cardiogenic or neurogenic pulmonary edema. When evaluating these patients, a chest x-ray is essential in differentiating between aspiration pneumonitis and POPE. In POPE, there is rapid onset and resolution of radiologic changes and concomitant clinical changes, with most resolving within 24 hours. In the setting of aspiration pneumonitis, studies suggest that radiologic changes lag behind the clinical signs and only half had cleared after 3 days. It is important to differentiate cardiogenic and iatrogenic volume overload from POPE, due to their different management strategies. A review of the patient's history looking for preexisting myocardial dysfunction or a physical examination identifying a gallop or murmur can help establish the correct diagnosis. In addition, an electrocardiogram (to identify arrhythmias, ischemia, or infraction) or an echocardiogram (to assess myocardial performance) may also be included to help determine if the pulmonary edema is due to a cardiogenic etiology.
Postobstructive pulmonary edema (POPE) also referred to as negative pressure pulmonary edema is a potentially life-threatening clinical scenario in which immediate-onset pulmonary edema develops after upper airway obstruction. Two distinct subclasses of POPE have been described in the literature: type I is associated with forceful inspiratory effort in the context of an acute airway obstruction, whereas type II occurs after relief of a chronic partial airway obstruction. Common etiologies for type I POPE include laryngospasm, epiglottitis, croup, choking/foreign body, strangulation, hanging, endotracheal tube obstruction, laryngeal tumor, goiter, mononucleosis, postoperative vocal cord paralysis, and near drowning. Type II is more common after relief of a chronic partial upper airway obstruction, as may be expected after adenoidectomy/tonsillectomy, laryngeal mass resection, correction of choanal stenosis, or reduction of a hypertrophic redundant uvula. In the adult population, POPE is most commonly caused by laryngospasm and upper airway tumors, whereas in the pediatric age group, epiglottitis, croup, and laryngotracheobronchitis are more common etiologies.
The pathophysiology of postobstructive pulmonary edema is multifactorial, involving components of negative pressure pulmonary edema, hypoxia, and an hyperadrenergic state. The major component is the negative pressure pulmonary edema that develops in patients with POPE type I. The event is triggered when an attempted inspiration occurs against an occluded airway. It has been reported that a forceful inspiration against such glottic obstruction could result in a maximum intrathoracic pressure of −140 cm H2O from a baseline of −4 cm H2O. This event then leads to an increase in venous return and blood flow to the right side of the heart as well as a decrease in the flow from the left side as a result of increased afterload. This combination causes increased pulmonary blood volume and elevated pulmonary venous pressures, which lead to an increase in hydrostatic pressures and edema formation. In addition, as a result of the elevated negative intrapleural pressure due to obstruction, the pressure is transmitted to the interstitium and alveoli and causes an increase in the hydrostatic gradient favoring transudation of fluid from the pulmonary capillary to the pulmonary interstitial space, resulting in pulmonary edema. The increased negative pressure is the possible component that explains why healthy young men who generate greater negative intrapleural pressures have an increased incidence of POPE.
Although POPE is an important etiologic factor to consider in the setting of acute postoperative respiratory distress, the differential diagnosis must also include other causes including aspiration pneumonitis, pulmonary embolism, anaphylaxis, iatrogenic volume overload, and cardiogenic or neurogenic pulmonary edema. When evaluating these patients, a chest x-ray is essential in differentiating between aspiration pneumonitis and POPE. In POPE, there is rapid onset and resolution of radiologic changes and concomitant clinical changes, with most resolving within 24 hours. In the setting of aspiration pneumonitis, studies suggest that radiologic changes lag behind the clinical signs and only half had cleared after 3 days. It is important to differentiate cardiogenic and iatrogenic volume overload from POPE, due to their different management strategies. A review of the patient's history looking for preexisting myocardial dysfunction or a physical examination identifying a gallop or murmur can help establish the correct diagnosis. In addition, an electrocardiogram (to identify arrhythmias, ischemia, or infraction) or an echocardiogram (to assess myocardial performance) may also be included to help determine if the pulmonary edema is due to a cardiogenic etiology.
Subscribe to:
Posts (Atom)