Graded carbon dioxide laser-induced subglottic injury in the rabbit model.

OBJECTIVE: To conduct an endoscopic and histologic analysis of the subglottic effects of various carbon dioxide laser-induced injuries in the rabbit model. DESIGN: Animals were assigned to either a control (cricothyroidotomy only) group or 4 (cricothyroidotomy and posterior subglottic laser) groups that were injured using varying systematically controlled carbon dioxide laser power exposures (5 W, 8 W, and 12 W), with durations of 2 or 4 seconds, and surface area exposures (25% or 40%). SUBJECTS: Twenty-seven New Zealand white rabbits. INTERVENTIONS: The subglottis was approached via cricothyroidotomy. Control airways were immediately closed, while injured airways were subjected to graded carbon dioxide laser exposures prior to closure. Airways were endoscopically monitored preoperatively, immediately postoperatively, and on postoperative days 1, 7, 14, and 21, after which the animals were humanely killed and subglottic tissue harvested for histological evaluation. RESULTS: Clinical observation revealed no significantly obstructive (acute) stenosis during the duration of the study. Endoscopic visualization revealed the formation of posterior subglottic scarring. Histological analysis of the mucosa revealed that use of carbon dioxide laser resulted in a statistically significant (unpaired, 2-tailed t test, P<.05) proportional thickening of the lamina propria layer, without significant changes in the epithelial and cartilaginous layers. In addition, mucosal blood vessel size increased proportional to the power of the laser delivered to the area (P<.05). CONCLUSIONS: Carbon dioxide laser-induced injury to the subglottis caused localized scarring, lamina propria thickening, and increased vascularity, which resolved with time and was not associated with significant airway obstruction. This model describes a systematic, controlled, and reproducible method of investigating subglottic injury.

Vital Signs and Physiologic Derangement in Patients With Thoracic Trauma in Iraq and Afghanistan.

BACKGROUND: Triage is the act of stratifying the need for medical attention. Effective triage must account for injury patterns and severity. Personnel making triage decisions must also consider the patients' physiologic states. Vital signs can possibly be used to assess for the presence of physiological derangements such as coagulopathy, acidosis, or a significant base deficit. Providers could use this knowledge to assist with triage at casualty collection points where laboratory studies or point of care testing may not be available. METHODS: With institutional approval, data were extracted from the Joint Theater Trauma Registry for all patients with thoracic trauma between 2002 and 2012. Patients were identified by International Statistical Classification of Diseases and Related Health Problems, 9th Revision (ICD-9) codes. Heart rate (HR), systolic blood pressure (SBP), and pulse pressure were correlated with coagulopathy (international normalization ratio ≥ 1.5), acidosis (pH < 7.2) or an elevated base deficit (>6) on admission. Sensitivity, specificity, positive predictive values, negative predictive values, and odds ratios were calculated. FINDINGS: HR > 100, SBP < 90, or pulse pressure <30 were associated with an increased risk for acidosis (odds ratio 3.06 [95% confidence interval 2.48-3.78], 4.72 [3.85-5.78], and 2.73 [2.15-3.48], respectively), coagulopathy (2.21 [1.72-2.83], 4.55 [3.57-5.80], and 2.73 [2.15-3.48], respectively), and base deficit >6 (2.17 [1.88-2.50], 3.48 [2.87-4.22], and 2.22 [1.78-2.77], respectively). HR was a moderately sensitive marker (0.74), whereas SBP was a specific marker (0.93). DISCUSSION: SBP < 90 is an effective marker for ruling in physiologic derangement after thoracic trauma. HR > 100 was associated with over twice the odds for physiologic derangement. Vital signs can be used to assess for physiologic derangement in the population studied and may help in triage.

The most altruistic living organ donor: a best friend.

Living organ donors are growing in number and account for a substantial proportion of organs transplanted. Types of living organ donors include family members, anonymous donors, and friends. Although familial donation is the most common form of living organ donation, anonymous donation and donation among friends are gaining popularity. Society has placed living organ donors at the top of the altruistic ladder. However, one's altruistic motives for living organ donation may be affected by the type of relationship he or she has with the organ recipient. Although family relationships are close, pressure and coercion from family members may make informed consent difficult. Anonymous donors do not have the pressure associated with a familial donation, but psychological and self-worth issues may influence their choice to donate. Friendship incorporates the close relationships associated with familial donation and the freedom associated with anonymous donation. Using Aristotle's definition of true friendship, the author argues that best friends are the only true altruistic living organ donors and therefore may be preferable to family donors or anonymous donors.

Modest maternal caffeine exposure affects developing embryonic cardiovascular function and growth.

Caffeine consumption during pregnancy is reported to increase the risk of in utero growth restriction and spontaneous abortion. In the present study, we tested the hypothesis that modest maternal caffeine exposure affects in utero developing embryonic cardiovascular (CV) function and growth without altering maternal hemodynamics. Caffeine (10 mg.kg(-1).day(-1) subcutaneous) was administered daily to pregnant CD-1 mice from embryonic days (EDs) 9.5 to 18.5 of a 21-day gestation. We assessed maternal and embryonic CV function at baseline and at peak maternal serum caffeine concentration using high-resolution echocardiography on EDs 9.5, 11.5, 13.5, and 18.5. Maternal caffeine exposure did not influence maternal body weight gain, maternal CV function, or embryo resorption. However, crown-rump length and body weight were reduced in maternal caffeine treated embryos by ED 18.5 (P < 0.05). At peak maternal serum caffeine concentration, embryonic carotid artery, dorsal aorta, and umbilical artery flows transiently decreased from baseline at ED 11.5 (P < 0.05). By ED 13.5, embryonic aortic and umbilical artery flows were insensitive to the peak maternal caffeine concentration; however, the carotid artery flow remained affected. By ED 18.5, baseline embryonic carotid artery flow increased and descending aortic flow decreased versus non-caffeine-exposed embryos. Maternal treatment with the adenosine A(2A) receptor inhibitor reproduced the embryonic hemodynamic effects of maternal caffeine exposure. Adenosine A(2A) receptor gene expression levels of ED 11.5 embryo and ED 18.5 uterus were decreased. Results suggest that modest maternal caffeine exposure has adverse effects on developing embryonic CV function and growth, possibly mediated via adenosine A(2A) receptor blockade.