Intra-Cardiac Arrest Use of Stellate Ganglion Block for Refractory Ventricular Tachycardia.

BACKGROUND: Refractory ventricular dysrhythmia, or electrical storm, is a cardiac condition consisting of three or more episodes of ventricular dysrhythmia resistant to treatment within a 24-hour period. These dysrhythmias carry high morbidity and mortality if not diagnosed and abated promptly. When traditional resuscitative algorithms fail to return a patient to a perfusing rhythm, providers need to consider other, more novel techniques to terminate these dangerous dysrhythmias. One approach is the use of a stellate ganglion block, which has been documented in the literature only a handful of times for its resuscitative use in cardiac arrest. CASE SERIES: This case series details two cases from an urban emergency department (ED) in a large metropolitan city, where the use of ultrasound-guided stellate ganglion blocks during cardiac arrest provided successful ablation of the tachydysrhythmia. The first case involves a patient who went into cardiac arrest while in the ED and was found to be in refractory pulseless ventricular tachycardiawhile. The second case describes a patient who went into a witnessed out-of-hospital cardiac arrest while with emergency medical services. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The stellate ganglion block is a procedure currently being used as a treatment modality for a variety of neurologic, psychological, and cardiac conditions. This intervention may provide a viable and lifesaving option for emergency physicians to adopt when traditional resuscitative algorithms fail to break resistant ventricular tachydysrhythmias.

Interplay of Trypanosome Lytic Factor and innate immune cells in the resolution of cutaneous Leishmania infection.

Trypanosome Lytic Factor (TLF) is a primate-specific high-density lipoprotein (HDL) complex that, through the cation channel-forming protein apolipoprotein L-1 (APOL1), provides innate immunity to select kinetoplastid parasites. The immunoprotective effects of TLF have been extensively investigated in the context of its interaction with the extracellular protozoan Trypanosoma brucei brucei, to which it confers sterile immunity. We previously showed that TLF could act against an intracellular pathogen Leishmania, and here we dissected the role of TLF and its synergy with host-immune cells. Leishmania major is transmitted by Phlebotomine sand flies, which deposit the parasite intradermally into mammalian hosts, where neutrophils are the predominant phagocytes recruited to the site of infection. Once in the host, the parasites are phagocytosed and shed their surface glycoconjugates during differentiation to the mammalian-resident amastigote stage. Our data show that mice producing TLF have reduced parasite burdens when infected intradermally with metacyclic promastigotes of L. major, the infective, fly-transmitted stage. This TLF-mediated reduction in parasite burden was lost in neutrophil-depleted mice, suggesting that early recruitment of neutrophils is required for TLF-mediated killing of L. major. In vitro we find that only metacyclic promastigotes co-incubated with TLF in an acidic milieu were lysed. However, amastigotes were not killed by TLF at any pH. These findings correlated with binding experiments, revealing that labeled TLF binds specifically to the surface of metacyclic promastigotes, but not to amastigotes. Metacyclic promastigotes of L. major deficient in the synthesis of surface glycoconjugates LPG and/or PPG (lpg1- and lpg5A-/lpg5B- respectively) whose absence mimics the amastigote surface, were resistant to TLF-mediated lysis. We propose that TLF binds to the outer surface glycoconjugates of metacyclic promastigotes, whereupon it kills the parasite in the acidic phagosome of phagocytes. We hypothesize that resistance to TLF requires shedding of the surface glycoconjugates, which occurs several hours after phagocytosis by immune cells, creating a relatively short-lived but effective window for TLF to act against Leishmania.