The effect of the prone position on pulmonary mechanics is frame-dependent.

UNLABELLED: By compressing the abdomen and restricting chest wall movement, the prone position compromises pulmonary compliance. For spine surgery, placing the anesthetized patient into the prone position increases the risk of improper ventilation. In this study, we tested the hypothesis that the compromise in pulmonary compliance is related to the patient's body habitus and the surgical frame used to support the patient while in the prone position. Seventy-seven adult patients were divided into three groups according to body mass index: normal (n = 36) < or = 27 kg/m2, heavy (n = 21) 28-31 kg/m2, and obese (n = 20) > or = 32 kg/m2. Patients were placed in the prone position supported by chest rolls, a Wilson frame, or the Jackson spinal surgery table (Jackson table) according to the surgeon's preferences. Peak airway pressure (at the proximal endotracheal tube), pleural pressure (esophageal balloon), and mean arterial pressure were recorded in the supine position and prone position within 15 min of the turn. Dynamic mean (+/- SD) pulmonary compliance (mL/cm H2O) decreased when turning from the supine to the prone position in all three body mass groups when using chest rolls (normal 37+/-5 to 29+/-6; heavy 43+/-2 to 34+/-4; obese 42+/-8 to 32+/-6) or the Wilson frame (normal 39+/-6 to 32+/-7; heavy 43+/-16 to 34+/-10; obese 36+/-11 to 28+/-9). The dynamic pulmonary compliance was not altered in patients positioned on the Jackson table. Regardless of body habitus, using the Jackson table for prone positioning was not associated with a significant alteration in pulmonary or hemodynamic variables. We conclude that moving patients from the supine to the prone position during anesthesia results in a decrease in pulmonary compliance that is frame-dependent but that is not affected by body habitus. IMPLICATIONS: We hypothesized that compromise in pulmonary compliance in the prone position is related to the patient's body mass index and the surgical frame used. In this study, we demonstrated that prone positioning during anesthesia results in a decrease in pulmonary compliance that is frame-dependent but that is not affected by body mass index.

Estrogen increases cGMP in selected brain regions and in cerebral microvessels.

We have previously reported that exogenous and endogenous estrogen can amplify residual cerebral blood flow during experimental cerebral ischemia. Because estrogen has been linked to nitric oxide and cyclic guanosine monophosphate (cGMP) signaling in noncerebral tissue, we tested the hypothesis that long-term 17beta-estradiol treatment increases basal cGMP in brain homogenates and cerebral microvessels in female rabbits. We also determined whether there are important baseline gender-specific differences in regional cGMP. Adult female rabbits were implanted with 17beta-estradiol pellets, 10 mg (F10, n = 10) or 50 mg (F50, n = 13), and compared with untreated females (F, n = 19) and males with negligible estrogen (M, n = 19) (plasma 17beta-estradiol levels of 4+/-4 pg/mL in M, 7+/-5 pg/mL in F, 141+/-74 pg/mL in F10, and 289 +/-10 pg/mL in F50). Cyclic GMP was determined by radioimmunoassay in cerebellum, hypothalamus, caudate nucleus, hippocampus, and cortex. Cerebral microvessels were harvested from additional cohorts of untreated males and females or estradiol-implanted females (n = 6 per group). Basal cGMP was higher in F versus M only in cerebellum. Estrogen-induced increases in regional cGMP were prominent in hippocampus at all doses (M = 43+/-26, F = 43+/-21, F10 = 84+/-24, F50 = 117+/-55 fmol/mg protein) and in cortex at the high dose (M = 78+/-55, F = 88+/-51, F10 = 69+/-34, F50 = 143+/-52 fmol/mg protein). Similarly, microvascular cGMP increased only in females treated with the 50 mg dose (M = 77+/-13, F = 86+/-25, F10O = 106+/-35, F50 = 192+/-88 fmol/mg protein). Therefore, 17beta-estradiol increases cGMP content in parenchymal regions that are known physiologic targets for reproductive steroids but are also areas of selective vulnerability to ischemic insult. Further, high doses of estrogenic steroids could amplify cGMP signaling within the cerebral microvasculature.

The effect of needle gauge and lidocaine pH on pain during intradermal injection.

UNLABELLED: Local anesthetics can produce pain during skin infiltration. We designed a randomized, prospective trial to determine whether needle gauge and/or solution pH affect pain during the intradermal infiltration of lidocaine. After approval by our institution's human studies review board, 40 healthy adult volunteers gave their consent to participate in this study. All of the volunteers randomly received four intradermal injections. Each volunteer was blinded as to the content of the intradermal injections and to which needle size was used for each injection. Each volunteer randomly received a 0.25-mL intradermal injection of the following four solutions: 1) lidocaine 2% administered through a 25-gauge needle (lido-25); 2) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate, pH 7.26) administered through a 25-gauge needle (lido-bicarb-25); 3) lidocaine 2% administered through a 30-gauge needle (lido-30); and 4) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate) administered through a 30-gauge needle (lido-bicarb-30). In each patient, the injection site was in the same region for each of the four injections. The skin wheal was tested for appropriate anesthesia using a 19-gauge needle on the skin wheal. A visual analog pain score was recorded after each intradermal injection. The pain scores were significantly higher in the lido-25 (3.2 +/- 0.2) group than in the lido-30 (2.5 +/- 0.3), lido-bicarb-25 (1.9 +/- 0.2), and lido-bicarb-30 (1.3 +/- 0.2) groups. The lido-bicarb-30 injection was also rated as less painful than the lido-30 injection. We found no differences between the lidobicarb-25 and the lido-bicarb-30 injections. Complete analgesia for the 19-gauge needle pain stimulus was achieved in all patients for each injection. We conclude that, overall, the pain intensity of an intradermal injection of 2% lidocaine is low. The addition of sodium bicarbonate to 2% lidocaine decreases the pain associated with an intradermal skin wheal, and although the use of a 30-gauge needle decreases the pain of injection, the addition of sodium bicarbonate seems to have a greater overall effect than needle size. IMPLICATIONS: Forty volunteers randomly received four intradermal injections consisting of 2% lidocaine with or without sodium bicarbonate via a 25- or 30-gauge needle. The addition of bicarbonate had a greater overall effect than needle size in decreasing the pain associated with the intradermal injection of lidocaine.

Venous air embolism: a review.

Venous air embolism (VAE) can be a lethal complication of surgical procedures, during which (1) venous pressure at the site of surgery is subatmospheric or (2) gas is forced under pressure into a body cavity. Though classically associated with neurosurgery, VAE is also a potential complication of laparoscopic, pelvic, and orthopedic procedures. It is, therefore, essential for the practicing anesthesiologist to recognize and treat venous air entrainment. An in-depth review of the pathophysiology, clinical presentation, detection, prevention, and treatment of VAE is presented.

Diabetic chronic hyperglycemia and neurologic outcome following global ischemia in dogs.

We tested the hypothesis that the neuropathologic outcome following recovery from incomplete ischemia is similar in normoglycemia and diabetes. Incomplete global ischemia was induced for 20 min in two groups of dogs: (a) normoglycemic, nondiabetic controls (n = 11) and (b) chronic (3 months), diabetic hyperglycemic subjects (n = 12). Animals were allowed to recover from surgery for 7 days after which they were perfusion-fixed for neuropathology. On paraffin processed tissue stained with hematoxylin and eosin (H&E), ischemic neurons were counted and the per cent of cell damage determined. All control animals survived for 7 days postischemia. Four of 12 diabetic animals survived for 7 days, with the remaining eight diabetic dogs dying within the first 3 days. On day 7, the percentage of neurons showing ischemic cell change in the four diabetic survivors and the 11 nondiabetic controls was similar in the cerebellum, CA1, superior temporal gyrus, and caudate. However, diabetic dogs that did not survive the 7-day recovery period showed cerebellar swelling, reduced Purkinje cell densities, and herniation. During the 3 months prior to ischemia, morning (10.7 +/- 4.4 versus 11.2 +/- 5.2 mM) and afternoon (8.8 +/- 5.0 versus 9.4 +/- 5.3 mM) blood glucose levels in the four surviving and eight nonsurviving diabetic animals, respectively, were similar. However, preischemic blood glucose was significantly elevated in animals that did not survive (7.8 +/- 2.8 versus 15.8 +/- 7.3 mM in survivors and nonsurvivors, respectively). This study shows that diabetic animals surviving 7 days postischemia and nondiabetic controls have similar neuropathology. However, diabetic animals in which glucose control deteriorated during the 24-h prior to ischemia did not survive, possibly due to severe hindbrain edema. These results show that in diabetes, blood glucose control immediately prior to incomplete global brain ischemia is an important determinant of morbidity and neuropathology.

Capnography facilitates tight control of ventilation during transport.

OBJECTIVE: We tested the hypothesis that Paco2 would be more tightly controlled if end-tidal CO2 monitoring was used during hand ventilation for transport of intubated patients. DESIGN: Randomized, prospective analysis of the no-monitor and monitor-blind groups (the monitor was on the bed during transport but only the investigator was aware of the end-tidal CO2 values). Nonrandomized, prospective analysis of the monitor group (ventilation controlled using end-tidal CO2 value from monitor). SETTING: University hospital operating room and intensive care unit (ICU). PATIENTS: Fifty intubated patients who were transported from the operating room to the ICU or from the ICU to the neuroradiology suite were assigned randomly to one of two groups: a) no-monitor group (n = 25); and b) monitor-blind group (n = 25). An additional group (monitor group, n = 10) was subsequently added to the study. INTERVENTIONS: Capnography was instituted in all patients in a blocked fashion. MEASUREMENTS AND MAIN RESULTS: Arterial blood gases and end-tidal CO2 values were measured before and after transport. When comparing overall group data, pre- and post-Paco2 values were similar: monitor 39 +/- 2 vs. 41 +/- 2 torr (5.2 +/- 0.3 vs. 5.5 +/- 0.3 no-monitor 39 +/- 1 vs. 37 +/- torr (5.2 +/- 0.1 vs. 5.0 +/- 0.1 kPa). However, when comparing Paco2 values for individual patients, we found that there was significantly greater variability for Paco2 after transport when end-tidal CO2 was not used for control of ventilation during transport. CONCLUSIONS: These data do not support routine monitoring of end-tidal CO2 during short transport times in adult patients requiring mechanical ventilation. However, the monitor may prevent morbidity in patients requiring tight control of Paco2.

Global incomplete cerebral ischemia produces predominantly cortical neuronal injury.

BACKGROUND AND PURPOSE: We determined the neuropathologic damage in a canine model of global incomplete ischemia commonly used in a variety of physiological experiments. METHODS: We induced 20 minutes of incomplete ischemia in dogs (n = 9) by increasing intracranial pressure via intraventricular infusion of artificial cerebrospinal fluid to maintain a cerebral perfusion pressure of 10 mm Hg while keeping body temperature at 38 degrees C during and immediately after ischemia. After a 7-day recovery period, animals were perfusion-fixed for neuropathology. In hematoxylin and eosin preparations, ischemic neuronal injury was assessed, neurons were counted, and percentage of cell damage was determined. RESULTS: No focal neurological deficits or overt seizures were observed during the 7-day recovery period. In superior temporal gyrus, 49 +/- 11% and 70 +/- 10% damage (mean +/- SEM) was observed in layer III pyramidal cells in the crown and sulcus, respectively. All neocortical regions examined showed neuronal damage in layers III and/or V. In hippocampus, 59 +/- 11% damage of pyramidal neurons occurred in CA1, with dorsal (septal) hippocampus showing more injury than ventral (temporal) portions. The caudate nucleus (head) exhibited 27 +/- 7% neuronal injury. In cerebellar cortex (anterior lobule), 70 +/- 7% damage of Purkinje cells occurred, but different folia of cerebellum showed varying degrees of injury. Brain stem and thalamus were minimally affected despite reduced blood flow. Inflammatory changes (leukocytic infiltration and neuronal incrustations) were observed, but only when neuronal degeneration was severe. Pancellular necrosis and infarction did not occur. CONCLUSIONS: This animal model of ischemia causes reproducible neuronal injury primarily in cortical regions without pancellular necrosis and infarction. Damage to subcortical areas is less severe than to cortical areas, despite comparable reductions in regional cerebral blood flow. Therefore, in the presence of regionally uniform but incomplete cerebral ischemia, neocortical and hippocampal pyramidal neurons and cerebellar cortical Purkinje cells are more likely than subcortical neurons to degenerate; alternatively, pyramidal and Purkinje neurons degenerate before neostriatal neurons in this model. This neuronal degeneration may represent an intrinsic cellular mechanism without major contribution of cytotoxic pathways associated with inflammation.

Poor hemodynamic and metabolic recovery after global incomplete cerebral ischemia associated with short-term diabetes in dogs.

We determined the effect of 4-5 weeks of diabetes on ATP recovery following global incomplete cerebral ischemia. 31P magnetic resonance spectra of ATP, intracellular pH (pHi), and CBF (radiolabeled microspheres) were measured in three groups of anesthetized dogs (n = 8/group): chronic hyperglycemic diabetes (pancreatectomy followed by blood glucose of > 10 mM for 4-5 weeks); acute hyperglycemia (blood glucose of > 10 mM) during ischemia and reperfusion in nondiabetic dogs; and normoglycemic controls. Twenty minutes of incomplete ischemia was produced by ventricular fluid infusion to keep cerebral perfusion pressure (CPP) at 10 mm Hg during spontaneous variations in MABP. Intracranial pressure was increased initially to similar levels, resulting in a similar Cushing response among the groups. However, during the final 8 min of ischemia, MABP decreased to a greater extent in diabetic (86 +/- 42 mm Hg) than in hyperglycemic (162 +/- 30 mm Hg) and normoglycemic (135 +/- 54 mm Hg) groups and remained lower throughout 3 h of reperfusion. CPP was kept constant during ischemia, but was lower throughout reperfusion in diabetic dogs. During ischemia CBF was reduced similarly among groups: 5 +/- 3 ml.min-1 x 100 g-1 in hyperglycemic and normoglycemic and 4 +/- 3 ml.min-1 x 100 g-1 in diabetic dogs. During reperfusion early hyperemia was attenuated and delayed hypoperfusion was augmented (7 +/- 17 ml.min-1 x 100 g-1 by 180 min) as a result of low perfusion pressure in diabetics. However, medullary blood flow was similar among groups.(ABSTRACT TRUNCATED AT 250 WORDS)