Fatal injury: characteristics and prevention of deaths at the scene

BACKGROUND: Almost half of all trauma deaths occur at the scene. It is important to determine if these deaths can be prevented. METHODS: Penetrating or blunt force trauma deaths were identified through the Office of the Medical Examiner during a 2-year period. Data were also obtained through review of these records. RESULTS: There were 312 deaths at the scene that received no medical care. Almost 60% were firearm-related. About 80% of the victims were men, and 55% of these deaths occurred in people between 20 and 49 years old. Suicide accounted for nearly half of these deaths. Eighty percent of these injured people had Abbreviated Injury Scale scores of 5 or 6. CONCLUSION: Almost 60% of deaths at the scene occurred at the same time as injury and reflect severe injury to vital regions of the body. These findings suggest that primary prevention of the initial event causing injury may be more important than definitive prehospital emergency medical care to prevent these deaths.     

Long-term results of silicone expander for moderate and severe Brown syndrome (Brown syndrome “plus”)

Background: The treatment of Brown syndrome has been undergoing an evolution toward more effective procedures with fewer operative interventions. Dr Kenneth Wright has introduced a procedure of superior oblique muscle tenotomy with a silicone expander to reduce the incidence of overcorrection. Methods: There was a retrospective study of 20 eyes of 19 consecutive patients with moderate or severe Brown syndrome (Brown syndrome “plus”). Follow-up ranged from 12 to 72 months. The expander, which varies 6 to 10 mm in length, was placed in all patients in the tenotomized superior oblique muscle tendon 5 mm nasal to the nasal border of the superior rectus muscle using 7-0 or 8-0 Prolene suture without violating the inner layer of the intermuscular septum. The intermuscular septum was closed over the silicone expander. Results: One hundred percent of patients had resolution of the down shoot in adduction and some or full ability to elevate the eye in adduction. Twenty percent of patients required reoperation (12.5% using 5-8 mm expanders) for overcorrection. Restriction of downgaze was not seen postoperatively. Patients often show an undercorrection 1 to 6 months postoperatively and improve or occasionally overcorrect at 1 to 2 years postoperatively. One patient with a 10-mm expander extruded the implant. Discussion: Placement of a 5- to 8-mm silicone expander in the tenotomized superior oblique muscle tendon is an effective means of correcting Brown syndrome with a low rate of reoperation. Initial undercorrection should not discourage the surgeon because improvement may continue for up to 3 years. The goal of treatment should be to convert a moderate or severe Brown syndrome (Brown syndrome plus) to a mild Brown syndrome (“true” Brown syndrome). Conclusion: This technique reduces the need for either simultaneous or subsequent inferior oblique muscle weakening and represents an advance in the treatment of Brown syndrome. (J AAPOS 1999;3:328-32)     

H1 and H2 receptor antagonists and hepatic oxygen supply-demand relationship in pigs

The hypothesis that histamine receptor (H1 and H2) blockade beneficially affects the hepatic oxygen supply-demand relationship was tested during experiments performed on 13 miniature pigs. Hepatic arterial and portal blood flows were measured with electromagnetic flowmeters. Cardiac output was determined by thermodilution. H1 and H2 receptor blockade was achieved with promethazine, 5 mg.kg-1 and cimetidine 30 mg.kg-1 IV, respectively. The study demonstrated no significant effect of H1 and H2 receptor blockade on hepatic oxygen uptake and no noticeable effects of cimetidine on hepatic circulation. However, promethazine decreased total hepatic blood flow, primarily by decreasing portal blood flow; this resulted in an increase in oxygen extraction as reflected in a decreased oxygen content in hepatic venous blood. The results reject the posed hypothesis: H1 receptor antagonist promethazine decreased, while H2 receptor antagonist cimetidine did not affect hepatic blood flow and oxygen supply; hepatic oxygen demand remained unaffected during H1 and H2 receptor blockade.     

Glutamatergic drugs exacerbate symptomatic behavior in a transgenic model of comorbid Tourette's syndrome and obsessive-compulsive disorder

We previously created a transgenic mouse model of comorbid Tourette's syndrome and obsessive-compulsive disorder (TS+OCD), by expressing a neuropotentiating cholera toxin (CT) transgene in a subset of dopamine D1 receptor-expressing (D1+) neurons thought to induce cortical and amygdalar glutamate output. To test glutamate's role in the TS+OCD-like disorder of these transgenic mice (D1CT-7 line), the effects of glutamate receptor-binding drugs on their behavior were examined. MK-801, a non-competitive NMDA receptor antagonist that indirectly stimulates cortical-limbic glutamate output, aggravated a transgene-dependent abnormal behavior (repetitive climbing and leaping) in the D1CT-7 mice at doses insufficient to induce stereotypies, and more readily induced stereotypies and limbic seizure behaviors at high doses. NBQX, a seizure-inhibiting AMPA receptor antagonist, reduced only the MK-801-dependent stereotypic and limbic seizure behavior of D1CT-7 mice, but not their transgene-dependent behaviors. These data imply that TS+OCD-like behavior is mediated by cortical-limbic glutamate, but that AMPA glutamate receptors are not an essential part of this behavioral circuit. Our findings lead to the prediction that the symptoms of human Tourette's syndrome and obsessive-compulsive disorder are elicited by excessive forebrain glutamate output.     

Evaluation of low-dose endotoxin administration during pregnancy as a model of preeclampsia

BACKGROUND: Recent evidence implicates nitric oxide (*NO) in the pathogenesis of preeclampsia. The authors tested the hypothesis that administration of low-dose endotoxin to pregnant rats mimics the signs of preeclampsia in humans and that *NO and *NO-derived species play a role in that animal model. METHODS: Endotoxin was infused at doses of 1, 2 and 10 microg/kg over 1 h to rats on day 14 of pregnancy. Mean arterial pressure, urinary protein, urinary and plasma nitrite plus nitrate (NO2- + NO3-) concentrations, and platelet count were measured before and after the endotoxin infusion. In another group of pregnant rats, the nitric oxide synthase inhibitor L-nitroarginine methyl ester (L-NAME) was administered in drinking water at a dose of 3 mg x kg(-1) x d(-1) starting on day 7 of pregnancy. Endotoxin was then infused at 10 microg/kg on day 14 of pregnancy. Kidneys and uteroplacental units were examined histologically and analyzed immunohistochemically for 3-nitrotyrosine. RESULTS: Endotoxin administration at doses of 2 and 10 microg/kg caused proteinuria and thrombocytopenia in pregnant rats, but did not result in hypertension. Urinary NO2- + NO3- concentration, reflective of tissue *NO production rates, was significantly elevated in pregnant rats that received endotoxin at 10 microg/kg. Ingestion of L-NAME caused hypertension. Tissues from pregnant rats treated with L-NAME, endotoxin at 10 microg/kg, and a combination of L-NAME and endotoxin had increased 3-nitrotyrosine immunoreactivity. CONCLUSION: Nitric oxide either directly or through secondary species plays a significant role in the biochemical and physiologic changes that occur in a rodent model of endotoxin-induced injury.