Canan Atalay

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.

Combining Intrathecal Bupivacaine and Meperidine during Caesarean Section to Prevent Spinal Anaesthesia-Induced Hypotension and other Side-Effects

This study compared intrathecal hyperbaric bupivacaine with low-dose intrathecal plain bupivacaine plus different doses of meperidine (pethidine), administered sequentially, with regard to blood pressure stability, post-operative analgesia and incidence of side-effects in 80 parturients undergoing caesarean section. Patients were randomly assigned to one of four groups (n = 20 each group): the HB group received 10 mg hyperbaric bupivacaine intrathecally; the BM35, BM30 and BM25 groups received 5 mg plain bupivacaine plus 35, 30 or 25 mg of meperidine intrathecally, respectively. The incidence of hypotension in the BM25 group was significantly lower than in the HB group. Nausea and vomiting were less prevalent in the BM25 group than in the HB and BM35 groups. In conclusion, sequential administration of 5 mg plain bupivacaine and 25 mg meperidine intrathecally provided better blood pressure stability and a lower incidence of side-effects than bupivacaine alone, without affecting quality of anaesthesia or surgical and patient satisfaction.

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.

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.

First Report of Vagal Ischemia Induced Lung Immune Componenet Infarct Following Subarachnoid Hemorrhage: 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.

A Suicide Attempt Using Zinc Phosphide (A Case Study)

DOI: 10.4328/JCAM.744 Received: 08.07.2011 Accepted: 09.08.2011 Printed: 01.01.2014 J Clin Anal Med 2014;5(1): 65-6 Corresponding Author: Ayşenur Sümer Coşkun, Department of Anesthesia and Reanimation, Medical Faculty, Atatürk University Erzurum, Turkey. T.: +90 4422341213 Fax: + 90 4422361301 GSM: +905356224482 E-Mail:anur.sumer@mynet.com Özet Çinko Fosfür, fare mücadelesinde zehirli buğday üretimi için kullanılır ve rodentisitin aktif maddesidir. İntihar amacıyla tarım ilacı [Zinc Phosphide (Zn3P2)] içen 17 yaşındaki erkek olgu acil serviste görüldüğünde: Genel durumu kötü, bilinci kapalı, kusmuğu ve cildinde sarımsak kokusu ve ileri derecece asidozu mevcuttu. Semptomatik tedavi uygulanan ve mekanik ventilatorde takip edilen olgu yatışının 5. günü psikiyatri kliniğine devir edildi.

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.

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.

The Effect of Preemptive Lornoxicam, Paracetamol and Paracetamol Lornoxicam Combinations on the Quality of Patient-Controlled Analgesia After Abdominal Surgery

1 Ayşenur Sümer Coşkun, Canan Atalay, Muhammed Emin Naldan, İlker İnce, Elif Oral, Nazım Doğan, Hüsnü Kürşad Atatürk Ünv. Tıp Fak. Anestezi ve Reanimasyon, Erzurum, Türkiye Preemptif Lornoksikam, Parasetamol ve Kombinasyonları / Preemptive Lornoxicam, Paracetamol and Combinations The Effect of Preemptive Lornoxicam, Paracetamol and Paracetamol Lornoxicam Combinations on the Quality of PatientControlled Analgesia After Abdominal Surgery Abdominal Cerrahi Geçiren Hastalarda Preemptif Lornoksikam, Parasetamol ve Parasetamol+Lornoksikam Kombinasyonunun Hasta Kontrollü Analjezi Kalitesine Etkisi