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An estimated 7% of pregnant women sustain trauma; a recent report claims 3.7 traumatic fetal deaths for every 100,000 live births. It seems likely that fetal mortality is increased even in cases of minor injury. The present survey of 112 emergency medicine residency programs at teaching hospitals yielded 87 responses (response rate, 78%). The 25-question survey asked about what routines are followed for assessing injured pregnant women and included a few hypothetical patients. A large majority of respondents (78%) reported routinely monitoring women with a viable fetus for 2 to 4 hours for anything more than minor extremity injury. One in five, however, instituted monitoring only for abdominal tenderness or pain. When fetal monitoring is carried out in the emergency department, an obstetric physician is involved more than half the time. Only 15% of programs have cardiotocographic equipment in the emergency department, and of the others, only one third have an established protocol for checking fetal heart tones (usually at 15-minute intervals). Nearly half of the programs would monitor the fetus routinely after a fall even if there were no abdominal pain or bleeding. Sonographic equipment is available in half the units. With a fetus of nonviable age, sonography usually is done only when there is lower abdominal pain. Without exception the programs have continual access to in-house emergency obstetrical consultation. When there is no obvious injury, the mechanism of injury is an important factor when deciding whether to carry out monitoring. For instance, ejection from a vehicular rollover and direct blunt abdominal trauma in an assault would prompt monitoring. This survey of emergency medicine residency programs indicate that the commonest approach to blunt trauma in pregnant women is to clear the mother in the emergency department and not monitor the fetus. Later patients are selectively sent to the obstetric area to check the fetus.

Cardiac memory is an uncommonly recognized entity in which T wave inversions on electrocardiogram (EKG) appear consistent with ischemia. Persistent deep T wave inversions are seen after return of normal depolarization in leads where the T waves were normal before pacing. These changes are generally recognized to occur in association with artificial pacemakers but may occur with other entities with intrinsic ventricular ectopic focus of depolarization, such as intermittent left bundle branch block. Although consideration of ischemia should be given priority, awareness of the benign nature of cardiac memory may allow some patients to avoid unnecessary work-up and admission. Sometimes the diagnosis cannot be confirmed definitively in the Emergency Department (ED) because many patients who have pacemakers also have coronary artery disease and only after a negative work-up for ischemia can one retrospectively presume cardiac memory as the likely etiology.

The possible role of interleukin 10 (IL-10) as an endogenous inhibitor of CD23-driven inducible nitric oxide synthase (iNOS) expression in human macrophages was investigated. Cross-linking of CD23 by a monoclonal antibody induced iNOS mRNA, as detected by RT-PCR, and the production of NO measured as the stable derivative, nitrite. A linear correlation was observed between CD23 expression and iNOS activity or NO2- production. The iNOS activity reached a maximum 48 h after ligation of CD23, then declined rapidly until 72 h. In parallel, nitrite production was detected after 24 h and reached a maximum after 48 h. In addition, ligation of the CD23 molecule induced, in a time-dependent manner, the production of IL-10. As this cytokine is known to regulate iNOS induction and activity, we evaluated the effect of a neutralizing mAb to IL-10 on CD23-induced iNOS activity and nitrite production by CD23-bearing macrophages and found that both were significantly enhanced. Furthermore, the addition of exogenous IL-10 suppressed CD23-driven iNOS mRNA expression, iNOS activity and production of nitrite. These data suggest that, after CD23-ligation at the cell surface of human phagocytes, the secretion of IL-10 downregulates the CD23-induced NO production at the transcriptional level, thus providing an efficient feed-back mechanism.

The capacity of human peripheral blood mononuclear cells and monocytes to generate nitrites, spontaneously or in response to Interleukin-4 was evaluated in vitro. Peripheral blood mononuclear cells and monocytes were found to release significant amounts of nitrites after 8 to 12 days in culture. This spontaneous production of nitrites was inhibited in the presence of 1 mM N G monomethyl- l -arginine, suggesting that this process was dependent upon the l -arginine metabolism. The present data also indicated that addition of Interleukin-4 generally resulted in an increased nitrite production, that was potentiated by IFN-γ, inactive alone. The response of human monocytes to Interleukin-4 was more heterogenous than that observed with unfractionated peripheral blood mononuclear cells. These results suggest that cell/cell interactions could play an important role in the activation of the nitric oxide synthase pathway in human.

Resting human blood monocytes from some donors were found to produce a small amount of 3'-5' guanine cyclic monophosphate (cGMP) in response to interleukin 4 (IL-4). A much higher response was observed when monocytes were preincubated with interferon (IFN-gamma), which alone was ineffective. Preincubation of monocytes with IL-4 led, in contrast, to their subsequent incapacity to generate cGMP in response to IL-4. The accumulation of cGMP induced by IL-4 in IFN-gamma preincubated monocytes was dose-dependent and peaked about 15 min after its addition. It was inhibited in the presence of NG-mono-methyl-L-arginine (L-NMMA), an inhibitor of the nitric oxide synthase pathway. This suppressive effect of L-NMMA was reverted by an excess of L- but not of D-arginine. Accumulation of cGMP was significantly reduced by addition of soluble guanylyl cyclase inhibitors, such as LY83583 [correction of LY83853] and methylene blue, but was not impaired in the presence of EGTA, suggesting that the pathway involved is calcium independent. In addition, IL-4 induced an increased secretion of nitrite by monocytes, that was potentiated by IFN-gamma and inhibited by L-NMMA. Taken together, these results suggest that the sequential exposure of monocytes to IFN-gamma and IL-4 elicits the release of NO from L-arginine, which in turn is capable to stimulate soluble guanylyl cyclase.

Normal human peripheral blood mononuclear cells (PBMC) produced IgE when stimulated with IL-4. In the present report it was shown that beta 2-adrenoceptor agonists, salbutamol and fenoterol, potentiated the IL-4-induced IgE production without significantly affecting the expression of the low affinity receptor for IgE at the cell surface of monocytes and B lymphocytes. However, beta 2-adrenoceptor agonists were shown to enhance at day 7 the IL-4-induced release of the soluble form of CD23 (sCD23) by PBMC. This effect was specific since a beta-adrenoceptor antagonist, D,L-propranolol, inhibited the IL-4-induced IgE production by these cells. Alternatively, the beta 2-adrenoceptor agonists inhibited the production by these cells of interferon-gamma (IFN-gamma) but did not affect the production of IL-4 when stimulated with phytohemagglutinin A + a phorbol ester. These data suggest that beta 2-adrenoceptor agonists influence the IL-4-induced IgE production in humans by enhancing the release of sCD23 and inhibiting the production of endogenous IFN-gamma. In addition to the effect on the IL-4-induced IgE production it was shown that beta 2-adrenoceptor agonists potentiated the effect of IL-4 on a human promonocytic cell line, U 937, by enhancing CD23 expression and release and by inducing the differentiation of these cells into monocyte-like cells. Taken together, these data indicate that beta 2-adrenoceptor agonists potentiated the effect of IL-4 and that this functional interaction is different considering the cell-lineage and the stage of differentiation of these cells.

Placement of a protective cervical collar is common in cases of acute head trauma. However, the effect of this collar on intracranial pressure is uncertain. This prospective study examined the change in measured cerebrospinal fluid pressure (CSFP) after the application of a rigid Philadelphia collar in 20 adult patients undergoing lumbar puncture. CSFP averaged 176.8 mm H2O initially and increased to an average of 201.5 mm H2O after collar placement (range 0 to 120). Although this difference of 24.8 mm H2O is statistically significant (P = .001), it is uncertain if this would be clinically important. Nonetheless, this small increment in pressure could be significant in patients who already have an elevated intracranial pressure.

A 24-year-old man was assaulted and sustained a stab wound to the left lower neck. When he arrived at the emergency department, he was hemodynamically stable. Although the wound had penetrated the platysma, on initial evaluation the patient did not appear to have sustained significant injury. Closer examination of the wound revealed chylous drainage, indicating injury to the cervical portion of the thoracic duct. The patient was taken to the operating room for exploration of the wound, during which an injury to the left internal jugular vein was identified and repaired. The thoracic duct, which had been severed, was ligated. The remainder of the patient's hospital course was unremarkable. The consistent association between penetrating injury to the cervical portion of the thoracic duct and injury to neighboring vascular structures is discussed.

A sexually transmitted disease is seldom considered in the differential diagnosis of patients with clinical gastritis. A patient with gastric syphilis is reported to alert emergency department physicians to this entity. History and physical findings of syphilis should be sought and rapid plasma reagin tests should be obtained in the patient with severe or refractory gastritis.

Study objectives: An unfortunate nationwide hospital patient flow epidemic exists. Emergency department (ED) outflow of admitted patients awaiting inpatient ward room placement contributes to this problem. One solution recognized in New York that was withdrawn from the Jointre Organizations (JCAHO) 2004 Hospital Accreditation Manual (draft version) was for admitted patients to wait outside the ED. We wish to learn what location patients prefer. Methods: A convenience sample of patients from the ED and inpatient ward in a tertiary urban center completed a survey differentiating boarding location preference, the degree they objected to boarding in each location, and rationale for their preference. None of the patients were actually in the hallway at the survey. The study was conducted from January to March 2004 after an institutional review board–expedited review. Results: Three hundred thirty-seven (96%) of 352 patients surveyed voiced a boarding location preference. Two hundred twenty-three (66.2%) patients preferred boarding in the inpatient ward hallway versus 114 (33.8%) in the ED. Two hundred sixty-four (75.9%) patients were surveyed on the ward and 88 (25%) in the ED. Boarding location preference was not affected by interview site. Less than a Commission on Accreditation of Healthca1.8% absolute difference existed across sites for ward and ED hallway preferences. A rationale for hallway preference was supplied by 146 (65.5%) who favored boarding in the ward and 80 (70.2%) who favored the ED. Of those preferring the ward, 74 (50.7%) patients desired to avoid the ED's high level of traffic, noise, commotion, or low level of privacy. Forty-three (29.5%) patients cited physical proximity to their room, to "get in faster," or "see your room." Seventeen (11.6%) pro-ward hallway patients' justification could be grouped under a common category characterized by feeling uncomfortable in the ED because it was "too dangerous" or "rough," made them nervous, had more germs or weird people, and had less cosmetic appeal. Of the patients opting for boarding in the ED, 46 (57.5%) patients justified their decision by reporting that health care and treatment would be quicker or better or involve physicians. Fourteen (17.5%) patients thought that the ED was more comfortable, safer, private, and spacious, with less traffic and fewer people to "look at me funny." The next most common justification was by 5 (6.3%) patients who believed they would reach their room in less time. When asked to choose their degree of objection, those desiring boarding in the ward and ED chose "no problem" (27.4 versus 21.9%), "minor inconvenience" (30.9% versus 31.6%), "dissatisfied" (23.4% versus 26.3%), "very dissatisfied but understand" (7.2% versus 7.9%), "very dissatisfied and angry" (10.8% versus 9.6%), or had no answer (0.4% versus 2.7%). Conclusion: Nearly twice as many patients would prefer to be boarded in an inpatient hallway in contrast to the ED hallway. In suboptimal situations when there is no other care location than the hallway, administrators and the JCAHO should also consider the admitted patient's preference. Patients in our hospital were surprisingly forgiving of the potential of being placed in the hallway.

The character of chest pain (CP) is a major factor determining triage and admission for patients presenting to the emergency department (ED). Previous studies have found atypical descriptions in as little as 10-15% of patients with true myocardial ischemic pain. Atypical descriptions may be more prevalent in the Deep South of the United States because of cultural differences in the semantic description of pain.A retrospective study of patients presenting to the ED of a southern U.S. urban hospital with enzyme-documented myocardial infarction was conducted to determine the prevalence of atypical CP descriptions. A multivariate analysis of those patients with atypical pain descriptions was conducted to determine the independent demographic factors associated with these descriptions.In a total of 77 subjects (56% black; 44% white) meeting the study criteria, 43% were found to have atypical elements in the character of their CP descriptions. Only the black race demographic was found to be significantly correlated with the atypical descriptions. The use of the descriptive term "sharp" accounted for nearly half of the atypical presentations.Regional differences in the description of the character of CP may result in misleading portrayals of ischemic heart disease in southern U.S. populations. These differences are associated with a higher prevalence of atypical CP because of semantic distinctions, such as the use of the term "sharp" as a descriptor of acuity rather than character or quality.

Interactions between CD23, the low-affinity receptor for IgE, and CD21, the C3d/EBV receptor, modulate several intracellular events in lymphocytes. A soluble form of CD21 (sCD21) corresponding to the extracellular domain of the receptor circulates in normal plasma. We now demonstrate that purified sCD21 acts as a functional ligand for CD23-expressing monocytes. Soluble CD21 induced an increase in intracellular cGMP levels and the production of IL-6 and TNF-alpha in IL-4-pretreated monocytes induced to express CD23 but not in unstimulated CD23- monocytes. The accumulation of cGMP and the production of TNF-alpha were inhibited by NG-monomethyl-L-arginine (L-NMMA), indicating that sCD21 activates the L-arginine pathway of NO production. We demonstrated that sCD21 activates NO synthase (NOS) since it was found to enhance the conversion of L-arginine into L-citrulline and induce the intracellular expression of inducible NOS in CD23+ monocytes. In addition, sCD21 was shown to up-regulate the expression of HLA-DR and CD40 and decrease that of CD14 on cultured CD23+ monocytes. Thus, in a fashion similar to IgE complexes, sCD21 is able to efficiently trigger CD23 signaling pathways, inducing the release of pro-inflammatory mediators by human monocytes. Soluble CD21 up-regulates the expression of molecules involved in antigen presentation, further suggesting a potential immunoregulatory function for the soluble molecule.