Baroreflex function in females: changes with the reproductive cycle and pregnancy.

This review briefly describes the changes in baroreflex function that occur during female reproductive life, specifically during the reproductive cycle and pregnancy. The sensitivity or gain of baroreflex control of heart rate and sympathetic activity fluctuates during the reproductive cycle, reaching a peak when gonadal hormone levels increase, during the follicular phase in women and proestrus in rats. The increase in baroreflex sensitivity (BRS) is likely mediated by estrogen because ovariectomy in rats eliminates the BRS increase, the cyclic profile of changes in BRS mirror the changes in estrogen, and estrogen acts in the brainstem to increase BRS. In contrast, pregnancy depresses both BRS and the maximal level of sympathetic activity and heart rate evoked by severe hypotension. The decrease in BRS may be mediated by a reduction in the actions of insulin in the arcuate nucleus to support the baroreflex. In addition, increased levels of the neurosteroid progesterone metabolite 3α-OH-DHP act downstream in the rostral ventrolateral medulla to suppress maximal baroreflex increases in sympathetic activity. Consequently, these changes in baroreflex function impair blood pressure regulation in the presence of hypotensive challenges such as orthostasis and hemorrhage, a common event during delivery. As a result, peripartum hemorrhage is a major cause of human maternal death.

Pregnancy impairs baroreflex control of heart rate in rats: role of insulin sensitivity.

Recent studies in rabbits suggest that insulin resistance and reduced brain insulin contribute to impaired baroreflex control of heart rate (HR) during pregnancy; however, the mechanisms are unknown. The rat model is ideal to investigate these mechanisms because much is known about rat brain baroreflex neurocircuitry and insulin receptor locations. However, it is unclear in rats whether pregnancy impairs the HR baroreflex or whether insulin resistance is involved. Therefore, this study tested the hypothesis that in rats pregnancy decreases HR baroreflex sensitivity (BRS) and that this decrease is related to concurrent decreases in insulin sensitivity (IS). BRS was quantified before, during, and after pregnancy using complementary methods: 1) spontaneous BRS (sBRS) derived from sequence method analysis of telemetric, continuous arterial pressure recordings; and 2) maximal BRS of complete sigmoidal baroreflex relationships. IS was measured (hyperinsulinemic euglycemic clamp) to determine whether BRS and IS change in parallel. sBRS was reduced at midgestation [pregnancy day 10 (P10)], returned to nonpregnant (NP) levels on P18, and fell again at late gestation (P20) (sBRS in ms/mmHg: NP, 1.66 + or - 0.04; P10, 1.17 + or - 0.11; P18, 1.55 + or - 0.12; P20, 1.31 + or - 0.05; n = 5; P < 0.05). Similar triphasic patterns were observed for both maximal BRS [in beats x min(-1) x mmHg(-1): NP, 4.45 + or - 0.52 (n = 10); P11-12, 2.76 + or - 0.11 (n = 7); P17-18, 3.79 + or - 0.14 (n = 5); P19-20, 2.32 + or - 0.40 (n = 8); P < 0.0001] and previous and current measurements of IS (in mg glucose x kg(-1) x min(-1): NP, 32 + or - 2; P19-20, 15 + or - 1; P < 0.0005). Furthermore, during pregnancy, the standard deviation (SD) of MAP increased, and the SD of HR decreased, indirectly suggesting baroreflex impairment. sBRS increased transiently during parturition, and sBRS, maximal BRS, and IS normalized 3-4 days postpartum. In conclusion, pregnancy decreases HR BRS in rats. The parallel temporal changes in BRS and IS suggest a mechanistic link.

Baroreflex sensitivity varies during the rat estrous cycle: role of gonadal steroids.

Baroreflex sensitivity (BRS) increases in women during the luteal phase of the menstrual cycle, when gonadal hormones are elevated, but whether a similar cycle-dependent variation in BRS occurs in rats is unknown. In addition, whether cyclic BRS changes depend on gonadal steroids has not been previously investigated. To test these hypotheses, BRS was determined in cycling female rats using two approaches: 1) baroreflex control of renal sympathetic nerve activity (RSNA) in anesthetized rats; 2) cardiovagal spontaneous BRS (sBRS) in conscious rats instrumented for continuous telemetric measurements of mean arterial pressure (MAP) and heart rate (HR). MAP, HR, and sBRS were also measured in rats 2-3 and 5-6 wk following ovariectomy (OVX), to eliminate gonadal steroids. In anesthetized rats, RSNA BRS gain was increased (P < 0.01) during proestrus (-4.8+/-0.5% control/mmHg) compared with diestrus/estrus (-2.8 +/- 0.3% control/mmHg). Similarly, a proestrous peak in sBRS was observed in conscious rats (1.66 +/- 0.07 ms/mmHg, proestrus; 1.48 +/- 0.06 ms/mmHg, diestrus/estrus; P < 0.001). OVX eliminated estrous cycle-induced variation in sBRS. In addition, OVX reduced (P < 0.05) diurnal variations in MAP (5.9 +/- 0.3 vs. 3.9 +/- 0.5 mmHg) and HR [54 +/- 4 vs. 39 +/- 3 beats per minute (bpm)], and abolished diurnal variations in sBRS. Finally, while MAP, HR, and sBRS were decreased 2-3 wk following OVX, approximately 3 wk later, MAP and sBRS increased, and HR decreased further. No changes in MAP, HR, or sBRS were seen with time in sham OVX controls. In summary, RSNA and cardiovagal sBRS vary during the rat estrous cycle, and this variation is abolished by OVX. We conclude that sex steroid hormones are required for both cyclic and diurnal changes in BRS in rats.

Tracheostomy after anterior cervical spine fixation.

BACKGROUND: Patients with cervical spine injury may require both anterior cervical spine fusion and tracheostomy, particularly in the setting of associated cervical spinal cord injury (SCI). Despite the close proximity of the two surgical incisions, we postulated that tracheostomy could be safely performed after anterior spine fixation. In addition, we postulated that the severity of motor deficits in patients with cervical spine injury would correlate with the need for tracheostomy. METHODS: A retrospective review was undertaken of all adult trauma patients diagnosed with cervical spine fractures or cervical SCI admitted between June 1996 and June 2001 at our university Level I trauma center. Demographic data, severity of neurologic injury based on the classification of the American Spinal Injury Association (ASIA), complications, and use and type of tracheostomy were collected. In the subgroup of patients with unstable cervical spine injury that underwent anterior stabilization and tracheostomy, data regarding timing and technique of these procedures and wound outcomes were also collected. Categorical data were analyzed using chi analysis using Yates correction when appropriate, with p <0.05 considered significant. RESULTS: During this time period, 275 adult survivors were diagnosed with cervical spinal cord or bony injury. Forty-five percent of patients with SCI (27 of 60) and 14% of patients without SCI (30 of 215) underwent tracheostomy (p <0.001). Moreover, on the basis of the ASIA classification system, 76% of ASIA A and B patients, 38% of ASIA C patients, 23% of ASIA D patients, and 14% of ASIA E patients were treated with tracheostomy (p <0.001). In the subgroup that underwent both anterior spine fixation and tracheostomy (n=17), the median time interval from spine fixation to airway placement was 7 days (interquartile range, 6-10 days), with 71% of these tracheostomies performed percutaneously. No patient developed a wound infection or nonunion as a consequence of tracheostomy placement, and there were no deaths because of complications of either procedure. CONCLUSION: These data support the safety of tracheostomy insertion 6 to 10 days after anterior cervical spine fixation, particularly in the presence of cervical SCI. The presence of severe motor neurologic deficits was strongly associated with the use of tracheostomy in patients with cervical spine injury. Percutaneous tracheostomy, which is our technique of choice, may be advantageous in this setting by virtue of creating only a small wound. The optimal timing and use of tracheostomy in patients with cervical spine injury requires further study.

Enterocutaneous fistula and ventral hernia after absorbable mesh prosthesis closure for trauma: the plain truth.

HYPOTHESIS: The severity of abdominal injury is the determining factor for the development of enterocutaneous fistula and ventral hernia after absorbable mesh prosthesis closure (AMPC) for trauma. METHODS: We conducted a retrospective analysis of case series that included 140 consecutive trauma patients with AMPC surviving more than 48 hours from October 1, 1989, to March 31, 2000, at a Level I trauma center. The days until abdominal wall reconstruction was used as a measure of exposure of the viscera to the mesh. The abdominal trauma index (ATI) was used as the measure of injury severity. Statistical analysis included t test comparisons, logistic regression analysis, and life-table analysis for hernia development. RESULTS: Enterocutaneous fistula occurred in 10 patients (7.1%). The ATI (mean, 32.5 +/- 23.1) was the only variable independently associated with fistula formation (p = 0.01). The risk of fistula increased by 4% for each 1 unit increase in ATI (95% confidence interval [CI], 1-7%). One hundred seventeen patients (84%) survived to completion of abdominal wall reconstruction over a mean of 18.9 +/- 22.5 days and 3.6 +/- 1.9 operations. The number of days until abdominal wall reconstruction was the only variable independently associated with ventral hernia development (p < 0.001). The likelihood of fascial closure decreased by 26% (95% CI, 16-44%) per day and the risk of ventral hernia increased by 16% (95% CI, 9-23%) per day. The hernia development rate at 4 years (per life table) was 67% for the total, 13% for patients with delayed fascial closure, and 80% for patients requiring other closure techniques. CONCLUSION: Although the severity of abdominal injury is the most important factor for fistula formation, the most important factor for ventral hernia development is the duration of AMPC. Daily interventions, such as mesh tightening, may be necessary to limit ventral hernia in these high-risk patients.

Mechanism of acute ascites formation after trauma resuscitation.

BACKGROUND: Severely injured patients have been observed to acutely develop ascites; however, the pathogenesis of this rare phenomenon is poorly understood. OBJECTIVES: To report the factors common among severely injured patients developing ascites and to formulate a hypothesis regarding its origin. METHODS: Retrospective review of case series. RESULTS: We identified 9 injured patients between January 1, 1993, and December 31, 1998, who acutely developed significant amounts of ascites. The mean +/- SD estimated ascites volume was 2.0 +/- 0.8 L. All 9 patients had severe shock and were mechanically ventilated before abdominal decompression for the abdominal compartment syndrome. The mean +/- SD peak inspiratory pressure was 39.0 +/- 5.8 cm H2O. The mean +/- SD volumes of crystalloid and blood product infusion before decompression were 16.1 +/- 10.2 L and 5.2 +/- 4.8 L, respectively, in a mean +/- SD of 17 +/- 15 hours. In comparison, the mean +/- SD volumes of crystalloid and blood product transfusion among 100 contemporary, randomly selected patients undergoing trauma laparotomy were 5.1 +/- 5.5 L and 1.1 +/- 2.5 L, respectively (P<.001). Eight patients had only extra-abdominal injuries, while 1 patient had a combination of extra- and intra-abdominal injuries. Two patients were found to be cirrhotic by liver biopsy, but the other 7 patients had no known preexisting hepatic disease. Eight patients had absorbable mesh temporary abdominal closure, and 1 patient had primary fascial closure. There was persistent ascitic drainage in 5 patients; however, in all but 1 patient with cirrhosis, the drainage did not persist beyond 3 days. Two patients died, 1 of sepsis and the other of a closed head injury. CONCLUSIONS: Common denominators of posttraumatic ascites include shock, massive fluid resuscitation, and elevated intrathoracic pressure. The rapid onset of ascites in the setting of elevated intrathoracic pressure suggests that the patient's ability to clear ascitic fluid is overwhelmed.

Medical management of abdominal compartment syndrome: case report and a caution.

We report the case of a 55 year old woman who developed abdominal compartment syndrome [ACS] following total gastrectomy for caustic ingestion. Contributing factors for the development of ACS included peritonitis and massive fluid resuscitation for cardiovascular support of septic shock. The adverse cardiovascular and pulmonary effects of intra-abdominal hypertension [IAH] were reversed with pharmacological neuromuscular blockade [NMB]. Surgical decompression of ACS was, therefore, postponed, but the patient required re-operation for intra-abdominal sepsis several days later and subsequently died. Although medical management of ACS with NMB may lower IAH and reverse its negative cardiopulmonary effects, surgical decompression may still be required for definitive treatment.

Tracheal stenosis after percutaneous dilational tracheotomy.

OBJECTIVE: In many critical care units percutaneous dilational tracheotomy (PDT) has become an alternative to open tracheotomy. Although significant tracheal stenosis after PDT has been reported, the exact incidence is unknown. We report our findings on endoscopic laryngotracheoscopy for a group of patients who had undergone PDT more than 6 months before their examination. STUDY DESIGN AND SETTING: We did a retrospective review of 108 trauma patients who underwent PDT at least 6 months before enrollment in the study. Twenty-eight patients were either deceased or ineligible. Participation requests were mailed to the last recorded address of 80 patients. Thirty-four of those patients were contacted by phone, and 14 indicated their willingness to participate. Only 10 patients were able to make it to the clinic for examination. After transorally anesthetizing the hypopharynx and larynx with 4% lidocaine, each patient underwent flexible laryngotracheoscopy. Findings were categorized as normal or tracheal stenosis (<25%, 25% to 50%, or >50%). RESULTS: The tracheotomy site was virtually undetectable in 5 patients. In 4 patients, a scar was visible at the tracheotomy site, but there was no decrease in cross-sectional area. In 1 patient there was a 25% to 50% stenosis. All patients were completely asymptomatic with regard to airway and voice quality. CONCLUSION: One out of 10 patients in our series had a significant but asymptomatic stenosis after PDT. The risk of tracheal stenosis in PDT appears to be the same as that of open tracheotomy.