Case reports of atrial and pericardial rupture from blunt cardiac trauma.

BACKGROUND: Blunt cardiac trauma is diagnosed in less than 10% of trauma patients and covers the range of severity from clinically insignificant myocardial contusions to lethal multi-chamber cardiac rupture. The most common mechanisms of injury include: motor vehicle collisions (MVC), pedestrians struck by motor vehicles and falls from significant heights. A severe complication from blunt cardiac trauma is cardiac chamber rupture with pericardial tear. It is an exceedingly rare diagnosis. A retrospective review identified only 0.002% of all trauma patients presented with this condition. Most patients with atrial rupture do not survive transport to the hospital and upon arrival diagnosis remains difficult. CASE PRESENTATION: We present two cases of atrial and pericardial rupture. The first case is a 33-year-old female involved in a MVC, who presented unresponsive, hypotensive and tachycardic. A left sided hemothorax was diagnosed and a chest tube placed with 1200 mL of bloody output. The patient was taken to the OR emergently. Intraoperatively, a laceration in the right pericardium and a 3 cm defect in the anterior, right atrium were identified. Despite measures to control hemorrhage and resuscitate the patient, the patient did not survive. The second case is a 58-year-old male involved in a high-speed MVC. Similar to the first case, the patient presented unresponsive, hypotensive and tachycardic with a left sided hemothorax. A chest tube was placed with 900 mL of bloody output. Based on the output and ongoing resuscitation requirements, the patient was taken to the OR. Intraoperatively, a 15 cm anterior pericardial laceration was identified. Through the defect, there was brisk bleeding from a 1 cm laceration on the left atrial appendage. The injury was debrided and repaired using a running 3-0 polypropylene suture over a Satinsky clamp. The patient eventually recovered and was discharged home. CONCLUSIONS: We present two cases of uncontained atrial and pericardial rupture from blunt cardiac trauma. Contained ruptures with an intact pericardium present as a cardiac tamponade while uncontained ruptures present with hemomediastinum or hemothorax. A high degree of suspicion is required to rapidly diagnose and perform the cardiorrhaphy to offer the best chance at survival.

Small vestibular schwannomas can cause gait instability.

PURPOSE: To confirm whether detailed gait analysis can detect gait instability in patients with small vestibular schwannoma (VS) with an apparently normal gait. METHODS: Twenty-two patients (7 males, 15 females; 40-64 years old) with small VS and nine healthy age- and weight-matched controls were enrolled. Small VS was defined as the longest diameter less than 20mm from the porus acusticus internus on MRI with no brainstem compression. Each subject was asked to walk straight for a distance of 8m with tactile sensors attached to both feet, and repeat two trials with eyes open and closed. Gait variables of stance, swing, double support, stability, and average length of the trajectories of the center of force (TCOF) during stance were recorded and analyzed. RESULTS: No significant differences in the stability of the TCOF were found during gaits with eyes open and closed between the two groups. No obvious changes in gait variables were recognized with eyes open between the two groups. However, under gait with eyes closed, the values of the coefficient of variation (CV) of the gait phase were significantly greater in stance and swing in the VS group than in the normal group. In addition, patients with canal paresis (CP) showed greater CV values in gait phase related parameters than those who without CP during gait with eyes closed. CONCLUSIONS: Patients with small VS may have an apparently normal gait, but their vestibular deficit could be detected by proper use of gait analysis, especially with visual deprivation.

Janus kinase 2 (JAK2) regulates prolactin-mediated chloride transport in mouse mammary epithelial cells through tyrosine phosphorylation of Na+-K+-2Cl- cotransporter.

Epithelial chloride (Cl-) transport is achieved by the coordinated action of symporters such as the Na+-K+-2Cl- cotransporter (NKCC1) and chloride channels such as the cystic fibrosis transmembrane conductance regulator (CFTR). As a secretory tissue, mammary epithelial cells are obvious candidates for such mechanisms, but Cl- transport and its hormonal regulation have been poorly delineated in mammary epithelial cells. We determined whether the mammary epithelial cell line, HC11, transports chloride and whether this was regulated by PRL, a hormone known to stimulate ion transport. HC11 cells express both CFTR and NKCC1. Exposure to PRL or PGE1 increased Cl- transport in HC11 cells. This was inhibited by the NKCC1 blocker, furosemide, and by the Cl- channel inhibitor, diphenylamine 2-carboxylate. Dose and time course of PRL action indicate that PRL had maximal effect on Cl- transport at 1 microg/ml and at 10 min of stimulation. Examination of the signaling pathways suggests that the PRL effect on Cl- transport does not involve an increase in [Ca2+]i or MAP kinase activity. RT-PCR analyses indicate that HC11 cells express mRNA for Janus kinase 1 (JAK1), JAK2, and signal transducer and activator of transcription 5 (STAT5) but not for JAK3. PRL treatment of HC11 cells increased phosphorylation of STAT5. The JAK2 inhibitor AG490 blocked phosphorylation of STAT5 and PRL-induced, but not PGE1-induced, Cl- transport. NKCC1, but not CFTR, is tyrosine phosphorylated in HC11 cells. PRL enhanced tyrosine phosphorylation of NKCC1, and this effect was attenuated by the JAK2 inhibitor AG490. These results are the first demonstrations of a role for tyrosine phosphorylation of NKCC1 and of the PRL-JAK2 cascade in the regulation of Cl- transport.

Evidence that systemic relaxin promotes moderate water consumption during late pregnancy in rats.

The protein hormone relaxin is secreted by the ovaries throughtout the second half of the 23 day pregnancy in the rat. We recently reported that neutralization of endogenous relaxin with monoclonal antibodies for rat relaxin decreases water consumption during the daily light period during the second half of pregnancy in rats. The apparent effects of relaxin on water consumption, however, were extremely modest. One explanation for the failure to observe a greater relaxin-dependent effect on water consumption is failure of the monoclonal antibody for rat relaxin to neutralize all circulating relaxin. A second explanation is that circulating relaxin has only slight effects on water consumption. This investigation was conducted with an experimental model in which circulating relaxin was removed in order to re-examine the effects of relaxin on water consumption during the daily light period in late pregnancy in rats. On day 9 (D9) of pregnancy, before the presence of relaxin (R) in the circulation, primiparious pregnant rats were ovariectomized (O) or sham ovariectomized (C). Throughout the remainder of pregnancy, rats were treated with combinations of either progesterone (P) and estrogen (E, group OPE) or progesterone, estrogen and porcine relaxin (group OPER) in doses that restore physiological parameters to values similar to those that occur during the second half of pregnancy in intact rats. Progesterone and estrogen were administered by Silastic tubing implants and porcine relaxin was administered via miniature osmotic pump. Sham-ovariectomized animals received either the hormone vehicles (group SC) or no implants (group IC). Water consumption was measured daily from D4 to D20 at both 0700 and 2100 h which was when the lights went on and off respectively. Water consumption increased as pregnancy continued from D10 to D20 during the daily 10 h dark periods (P < 0.01), but not during the 14 h light periods for all four groups. Daily water consumed by rats in group OPE was significantly lower (P < 0.05) than that consumed by shamovariectomized rats from D17 to D20 and lower than that consumed by rats in group OPER on D20. During the dark period there was no difference in water consumption among groups. During the light period, however, group OPE consumed significantly less water (P < 0.05) than group C from D18 to D22. Moreover, there was a consistent tendency (P < 0.13) for the water consumption to be greater in rats in group OPER than in those in the relaxin-deficient group OPE during the daily light period from D11 to D20 of pregnancy. We conclude that the increase in water consumption that occurs during the daily dark periods during the second half of pregnancy is not attributable to circulating relaxin. Circulating relaxin promotes only modest increases in water consumption during the daily light periods during late pregnancy in the rat.