Acute inferior ST-elevation myocardial infarction mimicked by direct lightning strike: a case report.

Background: Direct lightning strikes are rare, and multiple organ systems can be involved. Prognosis is dependent on the severity of the injury. Severe myocardial injury associated with transient electrocardiogram changes, which have been previously described, is a hazardous complication. Case summary: A 35-year-old man with no known past medical history presented unresponsive following a direct lightning strike while sitting in a portable toilet. High-quality cardiopulmonary resuscitation was started in the field, with return of spontaneous circulation (ROSC) after 1 h. Following ROSC, he received volume resuscitation and was maintained on multiple vasopressors. Electrocardiogram showed significant ST-elevations in inferior leads with elevated troponin I, consistent with inferior ST-elevation myocardial infarction. Labs revealed lactic acidosis, hyperkalaemia, acute kidney, and liver injury. Due to concern for plaque rupture, coronary angiography was performed and revealed no obstructive coronary artery disease. Vasopressor support and volume resuscitation were continued for extensive burns covering greater than 30% body surface area. The patient became progressively hypotensive, eventually precipitating pulseless electrical activity arrest. Emergent labs were notable for severe acidaemia. Despite aggressive interventions, he expired due to severe multi-organ failure. Discussion: Direct lightning injuries are rare with serious potential complications. Myocardial damage, either from direct electrical insult or from induced coronary vasospasm, can lead to multi-organ system failure.

Spontaneous splenic rupture from indeterminate dendritic cell proliferation: a case report.

Spontaneous splenic rupture is a rare and life-threatening phenomenon, usually associated with an underlying infectious, inflammatory, hematological, neoplastic or rheumatologic condition. Indeterminate cell tumor is a rare neoplastic dendritic cell disorder that is poorly understood but shares immunophenotypic markers for Langerhans cells without Birbeck granules. A 73-year-old man presented with upper abdominal pain after an unwitnessed fall. Computed tomography angiography showed splenomegaly and a large ruptured splenic subcapsular hematoma. Intraoperative findings from an emergency laparotomy revealed a large hemoperitoneum and a ruptured spleen. Microscopic sections identified numerous, mostly poorly formed, small nodules classified as a proliferation of indeterminate dendritic cell tumors.

Phosphodiesterase V inhibition reduces airway responsiveness, but does not improve the beneficial effect of deep inspiration.

BACKGROUND: Deep inspirations (DIs) can prevent (bronchoprotection; BP) and reverse (bronchodilation; BD) methacholine (Mch)-induced bronchoconstriction, but this effect is reduced or absent in people with asthma or airways hyperresponsiveness (AHR). The mechanisms of this defect are unknown. OBJECTIVE: To indirectly examine the role of guanosine 3',5'-cyclic monophosphate (cGMP) by testing the hypothesis that the phosphodiesterase (PDE) V inhibitor, sildenafil, would improve DI-induced BP in individuals with AHR. METHODS: Thirty-two individuals were screened and 15 met all the inclusion/exclusion criteria (7 subjects with AHR and 8 healthy subjects). A single-dose Mch challenge inducing a 20% reduction in FEV1 in the absence of DIs was first identified. Thereafter, every study participant had 4 pairs of visits, each pair testing DI-induced BP and BD against the single-dose Mch, with no drug, or pretreatment with 25, 50 and 100 mg of sildenafil, respectively, in consecutive order. RESULTS: Sildenafil did not influence baseline lung function. However, in the absence of DIs, the drug caused a dose-dependent attenuation of the Mch-induced decrease in FEV1 by 17% (median value; 25th percentile: 1, 75th percentile: 16), 35% (-3, 61) and 37% (13, 79) for the 25-, 50- and 100-mg doses, respectively (p = 0.0004). No differences between the two participant groups were found. There were no effects of sildenafil on DI-induced BP or BD. CONCLUSION: We infer from these results that the mechanism responsible for the defective ability of DIs to protect the airways from bronchoconstriction is unlikely to be due to dysregulation of cGMP. Of importance, a potential role for PDE V inhibition as a bronchoprotector treatment needs to be explored.

Bronchodilation response to deep inspirations in asthma is dependent on airway distensibility and air trapping.

In healthy individuals, deep inspirations (DIs) have a potent bronchodilatory ability against methacholine (MCh)-induced bronchoconstriction. This is variably attenuated in asthma. We hypothesized that inability to bronchodilate with DIs is related to reduced airway distensibility. We examined the relationship between DI-induced bronchodilation and airway distensibility in 15 asthmatic individuals with a wide range of baseline lung function [forced expired volume in 1 s (FEV(1)) = 60-99% predicted]. After abstaining from DIs for 20 min, subjects received a single-dose MCh challenge and then asked to perform DIs. The effectiveness of DIs was assessed by the ability of the subjects to improve FEV(1). The same subjects were studied by two sets of high-resolution CT scans, one at functional residual capacity (FRC) and one at total lung capacity (TLC). In each subject, the areas of 21-41 airways (0.8-6.8 mm diameter at FRC) were matched and measured, and airway distensibility (increase in airway diameter from FRC to TLC) was calculated. The bronchodilatory ability of DIs was significantly lower in individuals with FEV(1) <75% predicted than in those with FEV(1) ≥75% predicted (15 ± 11% vs. 46 ± 9%, P = 0.04) and strongly correlated with airway distensibility (r = 0.57, P = 0.03), but also with residual volume (RV)/TLC (r = -0.63, P = 0.01). In multiple regression, only RV/TLC was a significant determinant of DI-induced bronchodilation. These relationships were lost when the airways were examined after maximal bronchodilation with albuterol. Our data indicate that the loss of the bronchodilatory effect of DI in asthma is related to the ability to distend the airways with lung inflation, which is, in turn, related to the extent of air trapping and airway smooth muscle tone. These relationships only exist in the presence of airway tone, indicating that structural changes in the conducting airways visualized by high-resolution CT do not play a pivotal role.

The structural basis of airways hyperresponsiveness in asthma.

We hypothesized that structural airway remodeling contributes to airways hyperresponsiveness (AHR) in asthma. Small, medium, and large airways were analyzed by computed tomography in 21 asthmatic volunteers under baseline conditions (FEV1 = 64% predicted) and after maximum response to albuterol (FEV1 = 76% predicted). The difference in pulmonary function between baseline and albuterol was an estimate of AHR to the baseline smooth muscle tone (BSMT). BSMT caused an increase in residual volume (RV) that was threefold greater than the decrease in forced vital capacity (FVC) because of a simultaneous increase in total lung capacity (TLC). The decrease in FVC with BSMT was the major determinant of the baseline FEV1 (P < 0.0001). The increase in RV correlated inversely with the relaxed luminal diameter of the medium airways (P = 0.009) and directly with the wall thickness of the large airways (P = 0.001). The effect of BSMT on functional residual capacity (FRC) controlled the change in TLC relative to the change in RV. When the FRC increased with RV, TLC increased and FVC was preserved. When the relaxed large airways were critically narrowed, FRC and TLC did not increase and FVC fell. With critical large airways narrowing, the FRC was already elevated from dynamic hyperinflation before BSMT and did not increase further with BSMT. FEV1/FVC in the absence of BSMT correlated directly with large airway luminal diameter and inversely with the fall in FVC with BSMT. These findings suggest that dynamic hyperinflation caused by narrowing of large airways is a major determinant of AHR in asthma.

Absence of deep inspiration-induced bronchoprotection against inhaled allergen.

Deep inspiration-induced bronchoprotection appears to be a major mechanism through which airway obstruction by spasmogens is avoided. Loss of bronchoprotection is associated with airway hyper-responsiveness. Individuals with allergic rhinitis and no airway hyperresponsiveness develop obstruction after allergen inhalation. To test the hypothesis that deep inspiration-induced bronchoprotection is not active against allergic reactions, we performed four single-dose bronchial challenges, two with methacholine and two with allergen, on 10 subjects with allergic rhinitis. Without deep inspirations, the methacholine-induced reduction in FEV1 from baseline was 36.9 +/- 3.6% (mean +/- SEM); this was attenuated to 15.0 +/- 2.0 when five deep inspirations preceded methacholine inhalation (p = 0.0001). When allergen was inhaled, the reduction in FEV1 was 24.7 +/- 2.9% and 28.8 +/- 6.4% without and with deep inspirations, respectively. We conclude that bronchoprotection by deep inspirations is absent against allergic reactions. Understanding the cause of this phenomenon may shed light into the pathogenesis of airway hyperresponsiveness in allergic asthma.