An established extracorporeal membrane oxygenation protocol promotes survival in extreme hypothermia.

BACKGROUND: Historical reports indicate that active rewarming with extracorporeal membrane oxygenation (ECMO) can salvage a patient after hypothermic cardiac arrest. We created a protocol that includes ECMO for extreme hypothermia to guide rewarming of the hypothermic patient. METHODS: A retrospective review of the ECMO rewarming protocol (2004-2006) was conducted. RESULTS: The active rewarming protocol is a flowchart that is available on our hospital intranet and can be accessed in the trauma bay. A severely hypothermic patient triggers the activation of a TRAUMA ONE-OP ECMO response. During the 2-year period, there were 5 activations of the system and 4 children were placed on ECMO. Two of the 4 were dramatically salvaged and eventually discharged neurologically intact. All 5 children were found pulseless at the scene before transport. The average time from the injury occurrence to arrival was 94 minutes (range, 41-181 minutes). Mean cardiopulmonary resuscitation time was 78.2 minutes (range, 37-152 minutes). The mean core temperature on arrival was 25.4 degrees C (range, 20.4 degrees C-28.6 degrees C). The average time from arrival to ECMO cannulation was 25.5 minutes (range, 16-37 minutes). CONCLUSION: A preemptive strategy for the severely hypothermic patient provides an organized approach and prompt response. Expeditious rewarming can make the difference in an opportunity for survival.

Meconium staining of amniotic fluid correlates with intestinal peel formation in gastroschisis.

Several studies in animal models demonstrate that peel formation in gastroschisis is due to the accumulation and activation of intestinal waste products (IWP) in the amniotic fluid. We reviewed our recent experience with gastroschisis and asked the following questions: First, does staining of the bowel and amniotic fluid with IWP correlate with intestinal peel formation? Second, what prenatal ultrasound findings indicate that peel formation is occurring in utero? Over two years, 16 neonates were treated for gastroschisis; twelve had been diagnosed by prenatal ultrasound and followed closely. Patients were grouped based on the presence of IWP in the amniotic fluid at the time of delivery (staining or no staining), and outcomes were reviewed. All neonates in the staining group (n=7) had a fibrinous peel present at the time of birth whereas a peel was absent in all neonates in the no-staining group (n=9). Matting of the bowel was seen by prenatal ultrasound in four patients in the staining group (0/8 in the no-staining group) and correlated with peel formation (Fisher's exact test p =0.007). Primary closure was done in 14 of the infants, and two required silo closure. In neonates with gastroschisis, staining of the amniotic fluid and bowel serosa with IWP correlated with intestinal peel formation. The ultrasound findings of matting correlated with both peel formation and staining with IWP. These results suggest that spillage of IWP into the amniotic fluid is one of the factors in peel formation in gastroschisis. Identification of matting of the bowel by prenatal ultrasound indicates formation of a peel.

Herpes simplex virus gene expression in neurons: viral DNA synthesis is a critical regulatory event in the branch point between the lytic and latent pathways.

Herpes simplex virus establishes a latent infection in peripheral neurons. We examined viral gene expression in rat peripheral neurons in vitro and determined that viral gene expression is attenuated and delayed in these neurons compared with that in Vero cells. In addition, using pharmacologic and genetic blocks to viral DNA synthesis, we found that viral alpha and beta gene expression was upregulated by viral DNA synthesis. Although maximal gene expression in neurons requires viral DNA synthetic activity, activation of viral gene expression was seen even in the presence of herpes simplex virus DNA polymerase inhibitors, but not in the absence of the origin-binding protein. Initiation of viral DNA synthesis is apparently a key regulatory event in the balance between the lytic and latent pathways in peripheral neurons.

Infection of sympathetic and sensory neurones with herpes simplex virus does not elicit a shut-off of cellular protein synthesis: implications for viral latency and herpes vectors.

Infection of non-neuronal cell types with herpes simplex virus type 1 (HSV-1) results in the degradation of host mRNA (Kwong & Frenkel 1987) and a shutoff in host protein synthesis (Roizman et al. 1965). This effect is mediated by a virion associated protein that is encoded by the viral vhs gene (Read & Frenkel 1983). This virion host shutoff (VHS) helps regulate viral gene expression and promotes efficient viral replication during the lytic cycle (Kwong & Frenkel 1987). Cultured sympathetic and sensory neurones, in contrast to primary rat fibroblasts, PC-12 cells, and Vero cells, showed no reduction in protein synthesis following infection with HSV-1. The resistance of neurones to VHS may be important in allowing establishment of a latent infection. In addition, this finding has a favourable impact on the idea of using HSV as a vector to deliver foreign genes into neurones.