Inducing Therapeutic Hypothermia in Cardiac Arrest Caused by Lightning Strike.

Only limited clinical scenarios are grounds for induction of therapeutic hypothermia. Its use in traumatic cardiac arrests, including those from lightning strikes, is not well studied. Nonshockable cardiac arrest rhythms have only recently been included in resuscitation guidelines. We report a case of full neurological recovery with therapeutic hypothermia after a lightning-induced pulseless electrical activity cardiac arrest in an 18-year-old woman. We also review the important pathophysiology of lightning-induced cardiac arrest and neurologic sequelae, elaborate upon the mechanism of therapeutic hypothermia, and add case-based evidence in favor of the use of targeted temperature management in lightning-induced cardiac arrest.

Prophylactic fibrinolysis through selective dissolution of nascent clots by tPA-carrying erythrocytes.

A fibrinolytic agent consisting of a tissue-type plasminogen activator (tPA) coupled to the surface of red blood cells (RBCs) can dissolve nascent clots from within the clot, in a Trojan horse-like strategy, while having minimal effects on preexisting hemostatic clots or extravascular tissue. After intravenous injection, the fibrinolytic activity of RBC-tPA persisted in the bloodstream at least tenfold longer than did that of free tPA. In a model of venous thrombosis induced by intravenously injected fibrin microemboli aggregating in pulmonary vasculature, soluble tPA lysed pulmonary clots lodged before but not after tPA injection, whereas the converse was true for RBC-tPA. Free tPA failed to lyse occlusive carotid thrombosis whether injected before or after vascular trauma, whereas RBC-tPA circulating before, but not injected after, thrombus formation restored blood flow. This RBC-based drug delivery strategy alters the fibrinolytic profile of tPA, permitting prophylactic fibrinolysis.

Sentinel Events Preceding Youth Firearm Violence: An Investigation of Administrative Data in Delaware.

INTRODUCTION: Accurately identifying youth at highest risk of firearm violence involvement could permit delivery of focused, comprehensive prevention services. This study explored whether readily available city and state administrative data covering life events before youth firearm violence could elucidate patterns preceding such violence. METHODS: Four hundred twenty-one individuals arrested for homicide, attempted homicide, aggravated assault, or robbery with a firearm committed in Wilmington, Delaware, from January 1, 2009 to May 21, 2014, were matched 1:3 to 1,259 Wilmington resident controls on birth year and sex. In 2015, descriptive statistics and a conditional logistic regression model using Delaware healthcare, child welfare, juvenile services, labor, and education administrative data examined associations between preceding life events and subsequent firearm violence. RESULTS: In a multivariable adjusted model, experiencing a prior gunshot wound injury (AOR=11.4, 95% CI=2.7, 48.1) and being subject to community probation (AOR=13.2, 95% CI=5.7, 30.3) were associated with the highest risk of subsequent firearm violence perpetration, though multiple other sentinel events were informative. The mean number of sentinel events experienced by youth committing firearm violence was 13.0 versus 1.9 among controls (p<0.0001). Within the sample, 84.1% of youth experiencing a sentinel event in all five studied domains ultimately committed firearm violence. CONCLUSIONS: Youth who commit firearm violence have preceding patterns of life events that markedly differ from youth not involved in firearm violence. This information is readily available from administrative data, demonstrating the potential of data sharing across city and state institutions to focus prevention strategies on those at greatest risk.

Fever in the postoperative patient.

Postprocedure fevers vary in the timing of their occurrence, duration, and severity. Such fevers do not all have an infectious cause, but they all require thorough investigation to rule out life-threatening conditions. This article summarizes the principles of diagnosis and management of postprocedure fevers for the emergency care provider.

Blood clearance and activity of erythrocyte-coupled fibrinolytics.

Conjugating tissue-type plasminogen activator (tPA) to red blood cells (RBCs) endows it with features useful for thromboprophylaxis. However, the optimal intensity and duration of thromboprophylaxis vary among clinical settings. To assess how the intrinsic properties of a plasminogen activator (PA) affect functions of the corresponding RBC/PA conjugate, we coupled equal amounts of tPA or Retavase (rPA; a variant with an extended circulation time, lower fibrin affinity, and greater susceptibility to PA inhibitors). Conjugation to RBC markedly prolonged the circulation of each PA in rats and mice, without detrimental effects on carrier RBC. The initial blood clearance of RBC/tPA was faster than RBC/rPA, yet it exerted greater fibrinolytic activity, in part due to greater resistance of tPA and RBC/tPA to plasma inhibitors versus rPA and RBC/rPA observed in vitro. Soluble and RBC-coupled tPA and rPA exerted the same amidolytic activity, yet RBC/tPA lysed fibrin clots more effectively than RBC/rPA, notwithstanding comparable fibrinolytic activity of their soluble counterparts. Conjugation to RBC suppressed rPA's ability to be activated by fibrin, whereas the fibrin activation of RBC-coupled tPA was not hindered. Therefore, the functional profile of RBC/PA is influenced by: pharmacokinetic features provided by carrier RBC (e.g., prolonged circulation), intrinsic PA features (e.g., clearance rate, resistance to inhibitors), and changes imposed by conjugation to RBC (e.g., loss of cofactor stimulation). These factors, different from those guiding the design of soluble PA for lysis of existing clots, can be exploited in the rational design of RBC/PA tailored for specific prophylactic indications.

Platelets inhibit the lysis of pulmonary microemboli.

Using tracings of (125)I-labeled fibrin(ogen) in rodents, we examined the hypothesis that platelets impede the lysis of pulmonary emboli. (125)I-Microemboli (ME, 3-10 micron diameter) lodged homogeneously throughout the lungs after intravenous injection in both rats and mice (60% of injected dose), caused no lethality, and underwent spontaneous dissolution (50 and 100% within 1 and 5 h, respectively). Although lung homogenates displayed the most intense fibrinolytic activity of all the major organs, dissolution of ME was much slower in isolated perfused lungs (IPL) than was observed in vivo. Addition of rat plasma to the perfusate facilitated ME dissolution in IPL to a greater extent than did addition of tissue-type plasminogen activator alone, suggesting that permeation of the clot by plasminogen is the rate-limited step in lysis. Platelet-containing ME injected in rats lysed much more slowly than did ME formed from fibrin alone. (125)I-Thrombi, formed in the pulmonary vasculature of mice in response to intravascular activation of platelets by injection of collagen and epinephrine, were essentially resistant to spontaneous dissolution. Moreover, injection of the antiplatelet glycoprotein IIb/IIIa antibody 7E3 F(ab')(2) facilitated spontaneous dissolution of pulmonary ME and augmented fibrinolysis by a marginally effective dose of Retavase (10 microg/kg) in rats. These studies show that platelets suppress pulmonary fibrinolysis. The mechanism(s) by which platelets stabilize ME and utility of platelet inhibitors to facilitate their dissolution deserves further study.