EMS defibrillation-first policy may not improve outcome in out-of-hospital cardiac arrest

OBJECTIVE: Early defibrillation using automated external defibrillators (AEDs) has been advocated to improve survival in witnessed out-of-hospital cardiac arrest (OHCA) due to pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF). However, when VT/VF is untreated and prolonged for more than a few minutes, defibrillation using AEDs may fail. METHODS: This retrospective study reviewed the charts from local emergency medical service (EMS) between the years 1993 to 2001 to evaluate the value of the AED after its introduction into our EMS. All witnessed OHCA due to VT/VF were analysed; cases of collapse witnessed by EMS were excluded. The primary endpoint was defined as survival to hospital discharge and at 1-year follow-up, and the secondary endpoint as survival without major neurological deficit. A total of 76 patients were treated for witnessed VT/VF before the implementation of the AED and 92 patients after its implementation. RESULTS: Before the introduction of paramedic AED defibrillation, physician defibrillation was performed at 15.6 min (+/-5.5, S.D.). After the introduction of AED defibrillation, paramedic defibrillation was performed at 5.7 min (+/-2.4, S.D.); the mean response interval from the call to defibrillation was shortened significantly (P<0.001). At the same time, survival to hospital discharge decreased from 23.7% (18/76 patients) to 14.1% (13/92) (P=0.112) and at 1-year follow-up from 17.1% (13/76) to 9.8% (9/92) (P=0.161). Favourable neurological outcome at 1-year follow-up also decreased from 14.5% (11/76) to 8.7% (8/92) (P=0.239). CONCLUSION: Implementation of the AED did not improve survival or a favourable neurological outcome in patients with OHCA due to VF/VT. However, with 5.7 min time to defibrillation, our EMS did not meet the criteria for early defibrillation. For prolonged periods of VT/VF, initial basic life support (BLS) may be superior to immediate AED. If response times of <4 min cannot be attained by the emergency systems, reconsidering of resuscitation algorithms seems to be advisable.     

Fracture healing following high energy tibial trauma: Ilizarov versus Taylor Spatial Frame

Introduction

The optimal treatment of high energy tibial fractures remains controversial and a challenging orthopaedic problem. The role of external fixators for all these tibial fractures has been shown to be crucial.

Methods

A five-year consecutive series was reviewed retrospectively, identifying two treatment groups: Ilizarov and Taylor Spatial Frame (TSF; Smith & Nephew, Memphis, TN, US). Fracture healing time was the primary outcome measure.

Results

A total of 112 patients (85 Ilizarov, 37 TSF) were identified for the review with a mean age of 45 years. This was higher in women (57 years) than in men (41 years). There was no significant difference between frame types (p=0.83). The median healing time was 163 days in both groups. There was no significant difference in healing time between smokers and non-smokers (180 vs 165 days respectively, p=0.07), open or closed fractures (p=0.13) or age and healing time (Spearman''s r=0.12, p=0.18). There was no incidence of non-union or re-fracture following frame removal in either group.

Conclusions

Despite the assumption of the rigid construct of the TSF, the median time to union was similar to that of the Ilizarov frame and the TSF therefore can play a significant role in complex tibial fractures.     

Chediak-Higashi gene in humans. I. Impairment of natural - killer function

Natural-killer (NK)-cell function was profoundly depressed in donors homozygous for the Chediak-Steinbrinck-Higashi syndrome (C-HS) gene when compared with age- and sex-matched normals. This apparent defect was not simply a result of a delayed response because little cytolysis was evident in kinetics experiments even after 24 h of incubation. NK cells from C-HS donors failed to lyse adherent (MDA, CEM, and Alab) or nonadherent (K562 and Molt-4) tumor cell lines or nontransformed human fetal fibroblasts. Therefore, the apparent C-HS defect was not a result of a shift in target selectivities. In addition, the depressed reactivity did not appear to be a result of suppressor cells or factors because: (a) enriched NK populations (nonadherent lymphocytes bearing receptors for the Fc portion of IgG) from C-HS donors were low in NK-cell function, (b) C-HS mononuclear cells did not inhibit the cytotoxicity of normal cells in coculture experiments, and (c) cells from the C-HS donors remained poorly reactive even after culture for up to 7 d. The nature of the defective NK activity in C-HS patients is not clear but may lie within the lytic mechanism rather than at the level of the recognition structure or population size because the frequency of target-binding cells was normal. In vitro NK activity could be partially restored by interferon treatment. Combined with the results presented in the following paper (4), these observations suggest that the C-HS gene causes a selective immunodeficiency disorder, mainly involving NK cells. This finding, in conjunction with the high incidence of spontaneous possibly malignant, lymphoproliferative disorders in these patients, may have important implications regarding the theory of immune surveillance mediated by NK cells.