Rifat Tokyay

Mass-Casualty Terrorist Bombings In Istanbul, Turkey, November 2003: Report of the Events and the Prehospital Emergency Response

BACKGROUND This paper describes the two mass-casualty, terrorist attacks that occurred in Istanbul, Turkey in November 2003, and the resulting pre-hospital emergency response. METHODS A complex, retrospective, descriptive study was performed, using open source reports, interviews, direct measurements of street distances, and hospital records from the American Hospital (AH) and Taksim Education and Research State Hospital (TERSH) in Istanbul. RESULTS On 15 November, improvised explosive devices (IEDs) in trucks were detonated outside the Neve Shalom and Beth Israel Synagogues, killing 30 persons and injuring an estimated additional 300. Victims were maldistributed to 16 medical facilities. For example, AH, a private hospital located six km from both synagogues, received 69 injured survivors, of which 86% had secondary blast injuries and 13% were admitted to the hospital. The TERSH, a government hospital located 1 km from both synagogues, received 48 injured survivors. On 20 November, IEDs in trucks were detonated outside the Hong Kong Shanghai Banking Corporation (HSBC) headquarters and the British Consulate (BC), killing 33 and injuring an estimated additional 450. Victims were maldistributed to 16 medical facilities. For example, TERSH, located 18 km from the HSBC site and 2 km from the the BC received 184 injured survivors, of which 93% had secondary blast injuries and 15% were hospitalized. The AH, located 9 km from the HSBC site and 6 km from the BC, received 16 victims. CONCLUSION The twin suicide truck bombings on 15 and 20 November 2003 were the two largest terrorist attacks in modern Turkish history, collectively killing 63 persons and injuring an estimated 750 others. The vast majority of victims had secondary blast injuries, which did not require hospitalization. Factors associated with the maldistribution of casualties to medical facilities appeared to include the distance from each bombing site, the type of medical facility, and the personal preference of injured survivors.

Effects of hypertonic saline dextran resuscitation on oxygen delivery, oxygen consumption, and lipid peroxidation after burn injury

We compared the effects of lactated Ringers (LR) and hypertonic saline dextran (HSD) on postburn cardiovascular function, O2 consumption, lipid peroxidation, and bacterial translocation. Miniature pigs with 40% total body surface area (TBSA), third-degree burns received, 30 minutes postburn, either Parkland resuscitation (LR group, n = 8) or HSD, 10 mL/kg/30 minutes, followed by LR, 4 mL/kg/%burn over the next 23 hours (HSD group, n = 8). The HSD prevented the early decrease in cardiac index (CI); the early increase in the resistance of the systemic, mesenteric, celiac, and renal vascular beds; and the decrease in mesenteric O2 consumption seen after burns when LR alone is used for resuscitation. The HSD also moderated the systemic and mesenteric lipid peroxidation. Bacterial translocation was less in the HSD group (3 of 8 animals) compared with the LR group (5 of 8 animals), but was not statistically different. Hypertonic saline dextran may be beneficial in improving the postburn microcirculation and attenuating postburn oxidant-induced lipid peroxidation in the systemic tissues and the gut.

Effects of anesthesia, surgery, fluid resuscitation, and endotoxin administration on postburn bacterial translocation

The aim of the study reported here was to assess the effects of some clinically relevant factors on the incidence and outcome of postburn bacterial translocation. Miniature pigs in 8 groups (n = 6 in each) underwent: (1) general anesthesia (GA); (2) operation (insertion of Swan-Ganz, arterial, and portal catheters) under GA; (3) burn (40% total body surface area, third degree, under GA); (4) burn and operation; (5) burn, operation, and resuscitation (Parkland); (6) burn, operation, and resuscitation plus endotoxin (100 micrograms/kg IV bolus, 2nd day). Groups 1-6 were killed at 48 hours and tissue samples were harvested for bacteriologic culture. Groups 7 and 8 were the same as 2 and 5, respectively, but were killed at 96 hours. Resuscitation and endotoxin increased postburn bacterial translocation but only endotoxin promoted systemic sepsis. In the absence of additional trauma, translocated bacteria were cleared by 96 hours postburn.

Halof hane markedly reduces mesenteric blood flow but does not impair gut mucosal oxygenation in pigs

We investigated the effect of halothane on in mesenteric blood flow and gut mucosal oxygenation. Pittman-Moore mini-pigs (n = 6) were chronically instrumented with aortic, pulmonary arterial (Swan-Ganz), and mesenteric venous catheters and an intestinal tonometer. Blood flow in the superior mesenteric artery was measured with an ultrasonic flow probe. On the day of the experiment, data were obtained before and during halothane administration (1.5% end-tidal). Halothane caused a marked decrease in mesenteric blood flow, associated with an increase in mesenteric vascular resistance. Likewise mesenteric oxygen delivery and consumption were significantly decreased under halothane, while the oxygen extraction rate of the intestine was not significantly changed. There was no significant change in intramucosal gut pH after halothane administration, which indicates that an adequate mucosal tissue oxygenation was maintained. We conclude that the marked halothane-induced reduction in mesenteric blood flow did not seem to impair the oxygenation of the gut mucosa in our experimental model.

Thromboxane receptor blockade with BM 13,177 following toxic airway damage by smoke inhalation in sheep

Thromboxane may play an important role in the pathogenesis of smoked mediated injury. We studied this possibility in 13 chronically instrumented sheep, which had the left lung exposed to smoke. BM 13,177, a thromboxane receptor antagonist, was given intravenously to six animals prior to smoke inhalation and during the experimental period. Seven animals received the vehicle. All animals were studied for 24 h under ventilatory support, then killed prior to harvesting lung tissue. Airway peak and plateau pressures in the vehicle-treated animals were elevated by 27% and 25% from baseline at 24 h post smoke inhalation. Concomitantly, the left pulmonary vascular resistance index rose continuously throughout the study period (baseline = 822 +/- 58; 24 h = 1819 +/- 84 dyn.s.cm-5.m2).BM 13,177 treatment completely prevented the rise in airway pressure, while the left pulmonary vascular resistance index was significantly attenuated (baseline = 726 +/- 79; 24 h = 1470 +/- 158 dyn.s.cm-5.m2) resulting in a significantly higher percentage of cardiac output being delivered to the smoked lung, compared to vehicle-treated animals. Thromboxane receptor blockade did not prevent smoke induced pulmonary edema formation. There was likewise no effect of BM 13,177 on the systemic hemodynamic changes seen following smoke inhalation. There was a decrease in cardiac index and an increase in systemic vascular resistance index in both groups. We conclude that smoke induced changes in airway and pulmonary vascular resistances may be mediated by thromboxanes. However, thromboxanes appear to play no role in the development of pulmonary edema and elevation of systemic vascular resistance following smoke inhalation injury.

The effect of dopamine on pulmonary hemodynamics and tissue damage after inhalation injury in an ovine model.

Hypoxic pulmonary vasoconstriction and reduced blood flow occur as a result of smoke inhalation. The aim of this study was to investigate how the amelioration of blood flow reduction by the vasodilator dopamine affects histopathologic outcome. We exposed the left lungs of chronically instrumented sheep (n = 12) to smoke, awakened them, and studied them for 24 hours. Six hours after inhalation injury, the sheep received randomized infusions of dopamine (9 micrograms/kg/min) or equal volumes of 0.9% saline solution. Pulmonary resistance in the left lungs of animals in the group that received saline solution rose continuously throughout the study period (624 +/- 48 dyne.sec.cm-5/m2 to 1747 +/- 140 dyne.sec.cm-5/m2, baseline to 24 hours after injury). Dopamine treatment caused a significantly lower vascular resistance in the injured lung than did saline solution between 8 and 24 hours after injury. The histologic evaluation of the injured lungs showed epithelial necrosis and cast formation in both groups in addition to an increased wet/dry ratio. No difference in lung injury between the groups could be distinguished. We conclude that the amelioration of blood flow reduction by treatment with dopamine in the lungs that were exposed to smoke did not affect pulmonary damage after inhalation injury.