Background There is substantial variation in use of life sustaining technologies in patients near the end of life but little is known about variation in physicians’ initial ICU admission and intubation decision making processes. Objective To describe variation in hospital-based physicians’ communication behaviors and decision making roles for ICU admission and intubation decisions for an acutely unstable critically and terminally ill patient. Methods We conducted a secondary analysis of transcribed simulation encounters from a multi-center observational study of physician decision making. The simulation depicted a 78 year-old man with metastatic gastric cancer and life threatening hypoxia. He has stable underlying preferences against ICU admission and intubation that he or his wife will report if asked. We coded encounters for communication behaviors (providing medical information, eliciting preferences/values, engaging the patient/surrogate in deliberation, and providing treatment recommendations) and used a previously-developed framework to classify subject physicians into four mutually-exclusive decision-making roles: informative (providing medical information only), facilitative (information + eliciting preferences/values + guiding surrogate to apply preferences/values), collaborative (information + eliciting + guiding + making a recommendation) and directive (making an independent treatment decision). Subjects 24 emergency physicians, 37 hospitalists, and 37 intensivists from 3 US academic medical centers. Results Subject physicians average 12.4 (SD 9.0) years since graduation from medical school. 38/98(39%) physicians sent the patient to the ICU, and 9/98(9%) ultimately decided to intubate. Most (93/98 (95%)) provided at least some medical information, but few explained the short-term prognosis with (26/98 (27%)) or without intubation (37/98 (38%)). Many (80/98 (82%)) elicited the patient's intubation preferences, but few (35/98 (36%)) explored the patient's broader values. Based on coded behaviors, we categorized 1/98 (1%) as informative, 48/98 (49%) as facilitative, 36/98 (37%) as collaborative, and 12/98 (12%) as directive; 1/98 (1%) could not be placed into a category. No observed physician characteristics predicted decision making role. Conclusions The majority of the physicians played a facilitative or collaborative role, although a greater proportion assumed a directive role in this time-pressured scenario than has been documented in non-time pressured ICU family meetings, suggesting that physicians’ roles may be context-dependent.
This study in α-chloralose-anesthetized cats discovered an excitatory peroneal nerve-to-bladder reflex. A urethral catheter was used to infuse the bladder with saline and record bladder pressure changes. Electrical stimulation was applied to the superficial peroneal nerve to trigger reflex bladder activity. With the bladder distended at a volume ~90% of bladder capacity, superficial peroneal nerve stimulation (PNS) at 1-3 Hz and threshold (T) intensity for inducing muscle twitching on the posterior thigh induced large-amplitude (40-150 cmHO) bladder contractions. PNS (1-3 Hz, 1-2T) applied during cystometrograms (CMGs) when the bladder was slowly (1-3 ml/min) infused with saline significantly ( < 0.01) reduced bladder capacity to ~80% of the control capacity and significantly ( < 0.05) enhanced reflex bladder contractions. To determine the impact of PNS on tibial nerve stimulation (TNS)-induced changes in bladder function, PNS was delivered following TNS. TNS of 30-min duration produced long-lasting poststimulation inhibition and significantly ( < 0.01) increased bladder capacity to 140.5 ± 7.6% of the control capacity. During the post-TNS inhibition period, PNS (1-3 Hz, 1-4T) applied during CMGs completely restored bladder capacity to the control level and significantly ( < 0.05) increased the duration of reflex bladder contractions to ~200% of control. The excitatory peroneal nerve-to-bladder reflex could also be activated by transcutaneous PNS using skin surface electrodes attached to the dorsal surface of the foot. These results raise the possibility of developing novel neuromodulation therapies to treat underactive bladder and nonobstructive urinary retention.
Urologic surgery at the time of CRS-HIPEC is associated with longer operative times, length of stay and increased risk of major complications, but not with decreased overall survival. J. Surg. Oncol. 2016;113:218-222. © 2016 Wiley Periodicals, Inc.
This study tested the hypothesis that sacral neuromodulation, i.e., electrical stimulation of afferent axons in sacral spinal root, can block pudendal afferent inhibition of the micturition reflex. In α-chloralose-anesthetized cats, pudendal nerve stimulation (PNS) at 3-5 Hz was used to inhibit bladder reflex activity while the sacral S1 or S2 dorsal root was stimulated at 15-30 Hz to mimic sacral neuromodulation and to block the bladder inhibition induced by PNS. The intensity threshold (T) for PNS or S1/S2 dorsal root stimulation (DRS) to induce muscle twitch of anal sphincter or toe was determined. PNS at 1.5-2T intensity inhibited the micturition reflex by significantly ( P < 0.01) increasing bladder capacity to 150-170% of control capacity. S1 DRS alone at 1-1.5T intensity did not inhibit bladder activity but completely blocked PNS inhibition and restored bladder capacity to control level. At higher intensity (1.5-2T), S1 DRS alone inhibited the micturition reflex and significantly increased bladder capacity to 135.8 ± 6.6% of control capacity. However, the same higher intensity S1 DRS applied simultaneously with PNS, suppressed PNS inhibition and significantly ( P < 0.01) reduced bladder capacity to 126.8 ± 9.7% of control capacity. S2 DRS at both low (1T) and high (1.5-2T) intensity failed to significantly reduce PNS inhibition. PNS and S1 DRS did not change the amplitude and duration of micturition reflex contractions, but S2 DRS at 1.5-2T intensity doubled the duration of the contractions and increased bladder capacity. These results are important for understanding the mechanisms underlying sacral neuromodulation of nonobstructive urinary retention in Fowler's syndrome.
The involvement of ionotropic glutamate receptors in bladder overactivity and pudendal neuromodulation was determined in a-chloralose anesthetized cats by intravenously administering MK801 (a NMDA receptor antagonist) or CP465022 (an AMPA receptor antagonist). Infusion of 0.5% acetic acid (AA) into the bladder produced bladder overactivity. In the first group of 5 cats, bladder capacity was significantly (P , 0.05) reduced to 55.3610.0% of saline control by AA irritation. Pudendal nerve stimulation (PNS) significantly (P , 0.05) increased bladder capacity to 106.8 6 15.0% and 106.7 6 13.3% of saline control at 2T and 4T intensity, respectively. T is threshold intensity for inducing anal twitching. MK801 at 0.3 mg/kg prevented the increase in capacity by 2T or 4T PNS. In the second group of 5 cats, bladder capacity was significantly (P , 0.05) reduced to 49.0 6 7.5% of saline control by AA irritation. It was then significantly (P , 0.05) increased to 80.8613.5% and 79.06 14.0% of saline control by 2T and 4T PNS, respectively. CP465022 at 0.03-1 mg/kg prevented the increase in capacity by 2T PNS and at 0.3-1 mg/kg prevented the increase in capacity by 4T PNS. In both groups, MK801 at 0.3 mg/kg and CP465022 at 1 mg/kg significantly (P , 0.05) increased the prestimulation bladder capacity (about 80% and 20%, respectively) and reduced the amplitude of bladder contractions (about 30 and 20 cmH 2 O, respectively). These results indicate that NMDA and AMPA glutamate receptors are important for PNS to inhibit bladder overactivity and that tonic activation of these receptors also contributes to the bladder overactivity induced by AA irritation.
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