Intraperitoneal instillation versus wound infiltration for postoperative pain relief after cesarean delivery: A prospective, randomized, double-blind, placebo-controlled trial.

AIM: To compare local anesthetic wound infiltration with intraperitoneal instillation of local anesthetic for analgesia after cesarean section under spinal anesthesia. METHODS: This study was conducted on 150 pregnant women undergoing elective cesarean section under spinal anesthesia. Spinal anesthesia was performed with 7 mg isobaric bupivacaine and 15 µcg fentanyl. The patients were randomized into three groups of 50 patients each: Group local anesthetic wound infiltration (LWI): 20 ml local anesthetic solution (10 ml 0.5% bupivacaine and 10 ml 2% lidocaine mixture) was administered subcutaneous wound infiltration at the end of surgery prior to skin closure and 20 ml saline was instilled into the uterine peritoneal area before fascia closure. Group intraperitoneal local anesthetic (IPLA): 20 ml local anesthetic solution (10 ml 0.5% bupivacaine and 10 ml 2% lidocaine mixture) was instilled into the uterine peritoneal area and 20 ml saline was administered subcutaneous wound infiltration. Group Placebo: 20 ml saline was instilled into the uterine peritoneal area and 20 ml saline was administered local subcutaneous wound infiltration. Pain scores at rest and on movement, total fentanyl consumption at 24 h, maternal satisfaction, and the time to first analgesic request were recorded. RESULTS: No statistically significant difference was observed in the postoperative pain scores at rest at 2, 12, and 24 h (p = 0.314, 0.343, and 0.735, respectively) and on movement at 12 and 24 h (p = 0.318 and 0.642, respectively) between the groups. The pain scores on movement at 2 h were significantly lower in Group IPLA compared with Group Placebo (p = 0.047). There were no significant differences between the groups in terms of total fentanyl consumption and the time to first analgesic request. CONCLUSION: The use of intraperitoneal instillation of bupivacaine and lidocaine reduces early the pain score on movement in women undergoing cesarean section under spinal anesthesia.

Predestinating Role of Cardiac Ganglia on Heart Life Expectancy in Rabbits After Brain Death Following Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: Cardiac ganglia are rechargeable batteries of the heart. The essential role of cardiac ganglia on cardiac life expectancy has not been examined following brain death. The aim of this study was to determine cardiac ganglia numbers and neuron density following subarachnoid hemorrhage (SAH). METHODS: Twenty-five hybrid rabbits were grouped as control (n = 5), sham (n = 5), and SAH (n = 15). The SAH groups' animals were subjected to injections of lethal dose of 2.00 cc autologous blood into their cisterna magna until linear EEG was obtained. The hearts of all animals were extracted following intracardiac formalin injection and examined. Cardiac ganglia and normal/degenerated neuron densities of cardiac neurons were recorded. RESULTS: The mean volume of normal neuron density of ganglia was 6.980 ± 830/mm3, and the degenerated neuron density of ganglia was 3 ± 1/mm3 in the control group, 6134 ± 712/mm3; 23 ± 9/mm3 in the sham group, 3456 ± 589; 1161 ± 72/mm3 in the surviving group; and 1734 ± 341/mm3, 4259 ± 865/mm3 in the dead animals in the SAH group. The algebraic results of heart work capacity (Wh) were estimated as 1375 ± 210 Wh in the control group, 1036 ± 225 in the sham group, 800 ± 110 Wh in the surviving group, and < 100 ± 20 in the dead animals in the SAH group. Degenerated cardiac neuron density/Wh correlation is statistically meaningful between the dead in the SAH group versus the SAH-surviving, sham, and control groups (P < .0005). CONCLUSIONS: Normal cardiac ganglia numbers and/or cardiac ganglia neuron density may be related to cardiac survival following brain death after subarachnoid hemorrhage.

Neurogenic Stress Cardiomyopathy Following Subarachnoid Hemorrhage Is Associated with Vagal Complex Degeneration: First Experimental Study.

BACKGROUND: Neurogenic stunned myocardium (NSM) is a devastating complication of subarachnoid hemorrhage (SAH). The most widely accepted mechanism in the pathogenesis of NSM and takotsubo cardiomyopathy is catecholamine-mediated direct myocardial injury. The aim of this study is to examine if there is any effect of sympathetic overactivity of the stellate ganglions on myocardial tissues, secondary to vagal complex degeneration in SAH-induced NSM. MATERIALS AND METHODS: This study was conducted on 25 New Zealand female rabbits. After the examination, all animals were assigned into 3 groups randomly: a control group (n = 5), a sham group (n = 5), and a study group (n = 15) that was subjected to experimental SAH with double injection of blood into the cisterna magna. After 7 animals exhibited NSM, all animals were killed. Their brains, vagal complexes, stellate ganglions, and hearts were extracted and examined by histopathologic methods. Degenerated nodose ganglion neurons and stellate ganglion neuron densities were compared with degenerated myocardial tissue/normal myocardial tissue ratios, and the results were analyzed with the Mann-Whitney U test. RESULTS: Three rabbits in the study group died immediately after the second injection of blood. NSM developed in 7 animals after 1 to 5 days, which was diagnosed with transthoracic echocardiography. Interestingly, the animals that developed NSM had more stellate ganglia neurons and more degenerated neuron densities of nodose ganglia (P < 0.001). CONCLUSIONS: NSM and takotsubo cardiomyopathy may be induced by vagal complex degeneration and sympathetic overactivity, which originated from more neurons, including stellate ganglia and more degenerated neuron densities of nodose ganglia.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study1.

PURPOSE: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. METHODS: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. RESULTS: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). CONCLUSION: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

The Effect of the Modified Thoracolumbar Interfacial Nerve Plane Block on Postoperative Analgesia and Healing Quality in Patients Undergoing Lumbar Disk Surgery: A Prospective, Randomized Study.

OBJECTIVE: The purpose of this study was to investigate the effect of the modified thoracolumbar interfascial plane block (TLIP) on postoperative analgesia and quality of recovery in patients undergoing lumbar disk surgery. METHOD: Ninety patients scheduled for lumbar disk surgery were divided into a control group (Group C) and a modified TLIP block group (Group T). Controlled analgesia was administered to both groups. Pain evaluation was performed at 30 min and at 1., 2., 4., 8.,12., and 24. hrs using a VAS scale, with patients at rest and duringand patients completed the QoR-40 quality of recovery inventory. RESULTS: Fentanyl used during postoperative 24 hours was 742.5±220.3 mcg in Group C and 446.0±241.98 in Group T. Postoperative fentanyl consumption was statistically significantly lower in Group T (p<0.001) with a statistically significant intergroup difference. The patient's pain, physical independence, physical comfort, psychological support, and emotional support were compared using the QoR-40 questionnaire survey. Significant differences in favor of Group T were observed (p<0.001, p=0.017, p=0.002, p=0.001 and p<0.001, respectively). Static and dynamic pain scores in Group C and Group T were recorded at 30 min and at 1, 2, 4, 8, 12, and 24h. Mean static scores were statistically significantly different in favor of Group T with the exception of 8th and 12h assessments (p<0.05). Dynamic scores were statistically significantly different in favor of Group T at all time points (p<0.05). CONCLUSION: Pain scores, opioid consumption and QoR-40 values after lumbar disk surgery were superior in the group undergoing TLIP. We think that the modified TLIP block may be an important method in terms of postoperative analgesia and patient recovery for lumbar spinal disk surgery.

Predictive Role of the Cervical Sympathetic Trunk Ischemia on Lower Heart Rates in an Experimentally Induced Stenoocclusive Carotid Artery Model by Bilateral Common Carotid Artery Ligation.

Bilateral common carotid artery ligation (BCCAL) leads to acute craniocervicocerebral ischemia, retrograde blood flow, increased blood pressure, and significant hemodynamic and histomorphological changes at the posterior cerebral vasculature. We examined the potential relationship between denervation injury following BCCAL-induced cervical sympathetic trunk (CST) ischemia and heart rate after permanent BCCAL. Rabbits (n = 25) were randomly divided into three groups: an unoperated control group (GI, n = 6); a sham-operated control group (GII, n = 6), and an experimental group subjected to BCCAL (GIII, n = 13); and then followed for one month. All animals were then sacrificed and the stellate ganglia (STGs) were examined histologically using stereological methods. The densities of degenerated neurons in the STGs were compared with heart rates and the results were analyzed with the Mann-Whitney U test. The mean normal neuron density in STGs was 10.340 ± 954/mm3 and the degenerated neuron density was 12 ± 3/mm3 in the GI group (p > 0.5). The mean heart rates and degenerated neuron densities of STGs were recorded as 267 ± 19/min and 237 ± 45/mm3 in GII (p < 0.005 for GII vs. GI); and 190 ± 11/min 1421 ± 230/mm3 in GIII (p < 0.0001 for GIII vs. GI and p < 0.005 for GIII vs. GII). An inverse and meaningful association was observed between the heart rate and degenerated neuronal density in the STGs. BCCAL may lead to hazardous histomorphological changes in the CST. A high density of degenerated neurons in the STG may provoke excessive sympathetic hypoactivity-related cardiac damage and bradyarrhythmias after stenoocclusive carotid artery diseases.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

Abstract Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

Coronary fat embolism following subarachnoid hemorrhage: an experimental study.

BACKGROUND: Subarachnoid hemorrhage (SAH) can lead to neurogenic pulmonary edema (NPE), and chylomicron metabolism may be altered unfavorably in acute lung injury. This study aimed to investigate the possible effect of NPE on the development of coronary fat embolism. METHODS: This study was conducted on 27 rabbits, 5 of which were used as the control (n=5). Experimental SAH was induced in 15 of the animals by injecting homologous blood into the cisterna magna, and the remaining 7 animals were administered only isotonic saline solution (Sham, n=7) in the same manner under general anesthesia. After 21 days, all the animals were euthanized, and their hearts, lungs, and brains underwent histopathological examination. RESULTS: Six animals died of SAH during the experiment, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. The histopathologic findings revealed minimal changes in the lungs, heart, and brains of the surviving animals; however, an abundant amount of fat globules was found in the coronary arteries of the six nonsurviving animals. There was a meaningful difference between the number of occluded coronary arteries with fatty globules in the surviving and nonsurviving animals (P<.001). However, the difference between the survivors and the isotonic-saline-injected group was not meaningful (P>.05). Coronary fat embolism was an important mortality factor following SAH (P<.005). CONCLUSIONS: In SAH-induced NPE, the leakage of chylomicrons into the systemic circulation may lead to coronary fat embolism, which has not yet been reported in the literature.

Vagal Ischemia Induced Lung Immune Component Infarct Following Subarachnoid Hemorrhage: An Experimental Study.

AIM: Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of NPE. We examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct in SAH. MATERIAL AND METHODS: Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH group (n=22). SAH was created by autologous blood injection into the cisterna magna and followed-up for 3 weeks. Vasospasm index (VSI) was defined as the ratio of the lung lymph node arteries (LLNA) wall section (wall ring) surface to the lumen surface. Degenerated axon numbers of vagal nerves, neuron densities of the nodose ganglion (NG) and VSIs of LLNA were compared for all groups. RESULTS: The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm < sup > 2 < /sup > , 30±5/mm < sup > 3 < /sup > , and 0.777±0.048 in the control group; 1300±100/mm2, 720±90/mm < sup > 3 < /sup > , and 1.148±0.090 in the animals with slight vasospasm (n=12); and 7300±530/mm < sup > 2 < /sup > , 5610±810/mm3, and 1.500±0.120 in the animals with severe vasospasm (n=10), respectively. CONCLUSION: Degenerated vagal axon and NG neuron density may be a causative factor in the development of LLNA vasospasm induced lymph node infarct in SAH. Lung lymph node infarct may be an important factor in the prognosis of NPE.

Preventive Role of Hilar Parasympathetic Ganglia on Pulmonary Artery Vasospasm in Subarachnoid Hemorrhage: An Experimental Study.

AIM: Pulmonary arteries are mainly innervated by sympathetic vasoconstrictor and parasympathetic vasodilatory fibers. We examined whether there is a relationship between the neuron densities of hilar parasympathetic ganglia and pulmonary vasospasm in subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: Twenty-four rabbits were divided into two groups: control (n=8) and SAH (n=16). The animals were observed for 20 days following experimental SAH. The number of hilar parasympathetic ganglia and their neuron densities were determined. Proportion of pulmonary artery ring surface to lumen surface values was accepted as vasospasm index (VSI). Neuron densities of the hilar ganglia and VSI values were compared statistically. RESULTS: Animals in the SAH group experienced either mild (n=6) or severe (n=10) pulmonary artery vasospasm. In the control group, the mean VSI of pulmonary arteries was 0.777±0.048 and the hilar ganglion neuron density was estimated as 12.100±2.010/mm < sup > 3 < /sup > . In SAH animals with mild vasospasm, VSI=1.148±0.090 and neuron density was estimated as 10.110±1.430/mm < sup > 3 < /sup > ; in animals with severe vasospasm, VSI=1.500±0.120 and neuron density was estimated as 7.340±990/mm < sup > 3 < /sup > . CONCLUSION: There was an inverse correlation between quantity and neuron density of hilar ganglia and vasospasm index value. The low numbers and low density of hilar parasympathetic ganglia may be responsible for the more severe artery vasospasm in SAH.

The role of vagal nerve root injury on respiration disturbances in subarachnoid hemorrhage.

AIM: We examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. RESULTS: Normal respiration rate, as measured in the control group, was 30 ± 6 bpm. In the SAH-induced group, respiration rates were initially 20 ± 4 bpm, increasing to 40 ± 9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28,500 ± 5,500 in both control and sham animals, whereas axon density was 22,250 ± 3,500 in survivors and 16,450 ± 2,750 in dead SAH animals. The severity of axonal degeneration of vagal nerves was greater in the six dead animals than in the survivors. CONCLUSION: If vagal nerves are lesioned, the muscles of respiration are paralyzed and respiratory reflexes are disrupted. That the ischemic and mechanical factors created by SAH cause vagal nerve root injury and respiration disorders may be inevitable and fatal.

Antihypertensive role of glossopharyngeal nerve stimulation by nifedipine using as calcium channel blocking agent in hypertension: an experimental study.

Nifedipine is a therapeutic drug in acute attacks of hypertension because of its rapid absorption from oral mucosa. Taste receptors are innervated by glossopharyngeal nerves (GPN) as well as by facial and vagal nerves. Sensory neurons of the GPNs are localised in the petrous ganglion (PG). Transection of the taste sensitive GPN fibres causes taste bud and PG degeneration and spontaneous hypertension. In this study, the role of chemical stimulation of the taste buds of the GPN by nifedipine and its role in treatment of hypertension were investigated in rabbits. Nifedipine was dropped sublingually (20 mg) for 4 days in the study group, followed by measuring blood pressures again. Then, the lingual branches of GPNs were cut. One month later, blood pressures were measured for 4 days. All animals were sacrificed humanely at the end of the experiment, and normal and degenerated neuron densities in the petrosal ganglions were enumerated stereologically. The antihypertensive effect of nifedipine decreased after GPNs denervation, in accordance with the increase of degenerated neurons in the PG. The chemical stimulation of taste buds of the GPNs by nifedipine may be an important effect of nifedipine application in addition to its calcium channel blocking effect. The rapid decrease in blood pressure following sublingual use of nifedipine may also result from the direct stimulation of taste buds innervated by the GPNs.

Destructive effect of monopolar electrocautery knife usage on femoral artery endothelium during spine surgery: experimental study.

OBJECTIVE: Circulatory disorders are observed in the lower extremities of some patients after spinal surgery when a monopolar electrocautery knife (MEK) is used. Despite known the knowledge that electric currents can be hazardous to living tissues, MEK has been widely used in spine surgery. In this study, we investigated if MEK can cause endothelial injury in femoral arteries (FA). MATERIALS AND METHODS: Eighteen rabbits were included in this study, two of which were used as the reference group. The remaining animals were subjected to paravertebral soft tissue dissection along levels L1-L4. Half of the animals were dissected with MEK, and the other half were dissected with scissors and bipolar cautery. One month after the surgery, endothelial changes of the FAs were examined stereologically. RESULTS: Endothelial desquamation, cytoplasmic and nuclear condensations, cellular shrinkage and cellular loss were developed in the FAs of the MEK group. The endothelial cell density was 270 cells/mm2 in normal animals, 240 cells/mm2 in the non- MEK group and 190 cells/mm2 in the MEK group. The difference between the non-MEK and normal groups was not meaningful (P>0.05). The difference between the MEK and non-MEK groups was statistically significant (P<0.05); differences between the MEK and normal animals were even more significant (P<0.001). CONCLUSION: Sharp dissection with MEK can have a detrimental effect on the endothelial cells of the FAs and cause postoperative circulatory disorders in the lower extremities. Therefore, long-term high-voltage electrocauterization should be avoided during spinal surgery unless absolutely necessary.

Tracheal Rupture due to Diffusion of Nitrous Oxide to Cuff of High-Volume, Low-Pressure Intubation Tube.

Tracheal rupture is a rare complication of endotracheal intubation. Risk factors include short neck, repeated attempts due to failed intubation, inappropriate stylus, over-inflation of the cuff, poor positioning of the tube, inappropriate tube size, weakened membrane structure due to steroid use, chronic obstructive pulmonary disease, tracheomalacia, kyphosis, and use of nitric oxide during the operation. In this article, we suggest that high-volume, low-pressure tubes may not always provide a low-pressure effect and could rupture due to reduced tracheal perfusion pressure and ischemic damage upon over-inflation.

Subhypnotic propofol infusion plus dexamethasone is more effective than dexamethasone alone for the prevention of vomiting in children after tonsillectomy.

BACKGROUND: Postoperative vomiting (POV) is a common complication after tonsillectomy. Dexamethasone is known to decrease postsurgical vomiting. In this study, we compared the effects of dexamethasone alone to dexamethasone plus propofol on postoperative vomiting in children undergoing tonsillectomy. METHODS: In a randomized double-blinded study, we evaluated 80 healthy children, aged 4-12 years, who underwent tonsillectomy with or without adenoidectomy. After anesthesia was induced by inhalation of sevoflurane, 0.15 mg x kg(-1) dexamethasone and 2 microg x kg(-1) fentanyl was administered i.v. to all patients. The patients in the dexamethasone plus propofol group received 1 mg x kg(-1) propofol before intubation and continuously after intubation at a rate of 20 microg x kg(-1) x min(-1) until the surgery was completed. Data for postoperative vomiting were grouped into the following time periods: 0-4 and 4-24 h. Data were analyzed using a Student's t-test and chi-squared analysis. RESULTS: The percentage of patients exhibiting a complete response (defined as no retching or vomiting for 24 h) increased from 37.5% in the dexamethasone-alone group to 75% in the dexamethasone plus propofol group (P = 0.001). Twenty-two patients (55%) in the dexamethasone-alone and nine patients (22.5%) in the dexamethasone plus propofol groups experienced vomited during 0-4 h (P = 0.003). Eight patients in the dexamethasone-alone group and three patients in the dexamethasone plus propofol group received ondansetron as a rescue antiemetic during the postoperative period. CONCLUSION: For children undergoing tonsillectomy, intraoperative subhypnotic propofol infusion combined with dexamethasone treatment provides a better prophylaxis against postoperative vomiting than does dexamethasone alone.

The role of adrenomedullin and brain natriuretic peptide levels in acute rheumatic fever in adults.

OBJECTIVE: Rheumatic fever, a multisystem disease following infection with group A beta-hemolytic streptococcus, is common among young (5-15 years) but can occur in adults as well. Recently, brain natriuretic peptide (BNP) has been validated as a marker of cardiac function and prognosis. Plasma adrenomedullin (ADM) levels are elevated in various pathological states including cardiovascular and inflammatory diseases. We aim to assess the relationship between ADM and BNP levels in adult patients with acute and convalescent rheumatic fever (ARF). METHODS: This case -controlled prospective study included 45 patients with ARF (mean age 21.04+/-1.91 years) and 30 age/gender-matched control subjects. Brain natriuretic peptide and adrenomedullin levels were studied in the acute and convalescent phase of ARF. Adrenomedullin was detected by enzyme immunoassay kit of peptides, while brain natriuretic peptide was measured by a commercially available instrument. The study was carried out between May 2006 and October 2006 in Atatürk University Medical Faculty Hospital. Statistical analysis was performed using Shapiro-Wilk, Mann Whitney U, Wilcoxon signed rank, Chi-square tests and Pearson correlation analysis. RESULTS: Plasma ADM and plasma BNP levels were significantly higher (p<0.05) in adults with ARF, regardless of whether they were in acute or convalescent phase of disease. Plasma ADM levels were 74.43+/-3.4 pmol/mL in acute phases, 59.35+/-1.45 pmol/mL in the convalescent phase, and 44.79+/-13.12 pmol/mL in control group. Plasma BNP levels were 197.51+/-47.41 pg/mL in the acute phase, 145.25+/-51.25 pg/mL in the convalescent phase, and 33.45+/-10.42 pg/mL in control group. The differences were statistically significant for all (p<0.05). Plasma ADM and BNP levels in the acute phase of disease showed significant negative correlation with the left ventricular ejection fraction (r=-0.56, p<0.05 and r=-0.61, p<0.05, respectively). CONCLUSION: In patients with acute and convalescent rheumatic fever, BNP and ADM levels were high compared to those of healthy subjects and this could be used as a complementary tool in the treatment and prognosis of ARF.

Anesthesia and airway management in two cases of apert syndrome: case reports.

Apert syndrome is a type of acrocephalosyndactilia that consists of craniofacial synostosis, midface hypoplasia and syndactyly, with an autosomal dominant inheritance pattern. During anesthesia, difficult intubation and ventilation may be observed because of abnormal airways. In one of our patients, visceral anomalies, such as esophageal stricture and post-strictural dilatation, may cause respiratory problems because of aspiration. The second case was a Mallampati grade 2 with craniofacial synostoses, midface hypoplasia and syndactyly. In the case of apert syndrome, anesthetists must be prepared for intubation difficulties, airway and ventilation problems and even visceral anomalies.

Histopathologic evaluation of neurogenic pulmonary edema after subarachnoid hemorrhage in rabbits.

OBJECTIVE: To investigate the effects of subarachnoid hemorrhage (SAH) on lung tissue. METHODS: We conducted this study on 20 rabbits in the Ataturk University Medical Faculty, Erzurum, Turkey in 2005. Experimental SAH was applied to all animals under general anesthesia. After 20 days, all animals were sacrificed. Their lungs were examined histopathologically. RESULTS: Foamy hemorrhagic parenchymal lesions, alveolar rupture, and subintimal fluid collection in the pulmonary vasculature were observed in the lungs of the non-surviving animals. However, minimal changes were found in the lungs of the surviving animals (p<0.01). CONCLUSION: Our results suggest that luminal narrowing of the lung vessels due to subintimal fluid collection plays an important role in the development of pulmonary hypertension and neurogenic pulmonary edema in SAH.