Biomedical subjects

Koshi Makita

Publications and source records attributed to Koshi Makita.

At least 19 recordsLinked to original sources

PubMed2006

Glutamate transporters GLAST and EAAT4 regulate postischemic Purkinje cell death: an in vivo study using a cardiac arrest model in mice lacking GLAST or EAAT4.

Cerebellar Purkinje cells represent a group of neurons highly vulnerable to ischemia. Excitotoxicity is thought to be an important pathophysiological mechanism in Purkinje cell death following ischemia. The glutamate transporter is the only mechanism for the removal of glutamate from the extracellular fluid in the brain. Therefore, glutamate transporters are believed to play a critical role in protecting Purkinje cells from ischemia-induced damage. Two distinct glutamate transporters, GLAST and EAAT4, are expressed most abundantly in the cerebellar cortex. GLAST is expressed in Bergmann glia, whereas EAAT4 is concentrated in the perisynaptic regions of Purkinje cell spines. However, the in vivo functional significance of these glial and neuronal glutamate transporters in postischemic Purkinje cell death is largely unknown. To clarify the role of these glutamate transporters in the protection of Purkinje cells after global brain ischemia, we evaluated Purkinje cell loss after cardiac arrest in mice lacking GLAST or EAAT4. We found that Purkinje cells with low EAAT4 expression were selectively lost after cardiac arrest in GLAST mutant mice. This result demonstrates that GLAST plays a role in preventing excitotoxic cerebellar damage after ischemia in concert with EAAT4.

Animals↗

PubMed2006

Antimigraine drug, zolmitriptan, inhibits high-voltage activated calcium currents in a population of acutely dissociated rat trigeminal sensory neurons.

BACKGROUND: Triptans, 5-HT(1B/ID) agonists, act on peripheral and/or central terminals of trigeminal ganglion neurons (TGNs) and inhibit the release of neurotransmitters to second-order neurons, which is considered as one of key mechanisms for pain relief by triptans as antimigraine drugs. Although high-voltage activated (HVA) Ca(2+) channels contribute to the release of neurotransmitters from TGNs, electrical actions of triptans on the HVA Ca(2+) channels are not yet documented. RESULTS: In the present study, actions of zolmitriptan, one of triptans, were examined on the HVA Ca(2+) channels in acutely dissociated rat TGNs, by using whole-cell patch recording of Ba(2+) currents I(Ba) passing through Ca(2+) channels. Zolmitriptan (0.1-100 microM) reduced the size of IBa in a concentration-dependent manner. This zolmitriptan-induced inhibitory action was blocked by GR127935, a 5-HT(1B/1D) antagonist, and by overnight pretreatment with pertussis toxin (PTX). P/Q-type Ca(2+) channel blockers inhibited the inhibitory action of zolmitriptan on I(Ba), compared to N- and L-type blockers, and R-type blocker did, compared to L-type blocker, respectively (p < 0.05). All of the present results indicated that zolmitriptan inhibited HVA P/Q- and possibly R-type channels by activating the 5-HT(1B/1D) receptor linked to G(i/o) pathway. CONCLUSION: It is concluded that this zolmitriptan inhibition of HVA Ca(2+) channels may explain the reduction in the release of neurotransmitters including CGRP, possibly leading to antimigraine effects of zolmitriptan.

Animals↗

PubMed2006

Receptor for advanced glycation end-products is a marker of type I cell injury in acute lung injury.

RATIONALE: Receptor for advanced glycation end-products (RAGE) is one of the alveolar type I cell-associated proteins in the lung. OBJECTIVES: To test the hypothesis that RAGE is a marker of alveolar epithelial type I cell injury. METHODS: Rats were instilled intratracheally with 10 mg/kg lipopolysaccharide or hydrochloric acid. RAGE levels were measured in the bronchoalveolar lavage (BAL) and serum in the rats and in the pulmonary edema fluid and plasma from patients with acute lung injury (ALI; n = 22) and hydrostatic pulmonary edema (n = 11). MAIN RESULTS: In the rat lung injury studies, RAGE was released into the BAL and serum as a single soluble isoform sized approximately 48 kD. The elevated levels of RAGE in the BAL correlated well with the severity of experimentally induced lung injury. In the human studies, the RAGE level in the pulmonary edema fluid was significantly higher than the plasma level (p < 0.0001). The median edema fluid/plasma ratio of RAGE levels was 105 (interquartile range, 55-243). The RAGE levels in the pulmonary edema fluid from patients with ALI were higher than the levels from patients with hydrostatic pulmonary edema (p < 0.05), and the plasma RAGE level in patients with ALI were significantly higher than the healthy volunteers (p < 0.001) or patients with hydrostatic pulmonary edema (p < 0.05). CONCLUSION: RAGE is a marker of type I alveolar epithelial cell injury based on experimental studies in rats and in patients with ALI.

Animals↗

PubMed2006

Subcutaneous emphysema and pneumomediastinum after translaryngeal intubation: tracheal perforation due to unsuccessful fiberoptic tracheal intubation.

A 77-year-old man was scheduled to undergo a cervical lymph node biopsy under general anesthesia. Although awake, nasotracheal fiberoptic intubation was initially planned because of an anticipated difficult airway, the attempt was unsuccessful. Orotracheal intubation was subsequently performed under direct laryngoscopy without difficulty. After initiating positive pressure mechanical ventilation, subcutaneous and mediastinal emphysema developed. The cause of this emphysema was considered to be tracheal perforation after an unsuccessful attempt at fiberoptic tracheal intubation.

Aged↗

PubMed2006

The evolution of cerebral ischemia in a rat model of complete unilateral carotid artery occlusion with severe hypotension as detected by diffusion-, T2-, and postcontrast T1-weighted magnetic resonance images.

Severe internal carotid artery stenosis or occlusion is considered to be one of the important causes of stroke. The authors created a complete unilateral carotid artery occlusion model in 15 Sprague-Dawley rats, induced severe hypotension for at least 36 minutes by exsanguination with the target mean arterial pressure being equal or less than 35 mmHg, and investigated the temporal and spatial evolution of cerebral ischemia by diffusion-, T2-, and postcontrast T1-weighted magnetic resonance images. Cerebral ischemia was detected in most regions of the right middle cerebral artery territory during exsanguination. There was no significant relationship between ischemic lesion volume detected on apparent diffusion coefficient (ADC) map (ADC lesion volume) and infarction volume found on histopathology. However, there was a linear relationship between the change in ADC lesion volume at blood reinfusion (after reinfusion minus before reinfusion) and the enlargement of the lesion volume during the postreinfusion period (Y = 0.4X + 161.7, P = 0.0066) and a significant logarithmic correlation between the volume of vasogenic edema found on postcontrast T1-weighted image at 1 hour of the postreinfusion period and the enlargement of the lesion volume during the postreinfusion period (Y = 62.1 x logX - 115.4, P = 0.022). In conclusion, although it may be difficult to predict the outcome of cerebral ischemia (infarction volume) from the lesion volume during exsanguination, the evolution of cerebral ischemia may be partly predicted by lesion volume changes seen on the ADC maps at the time of the blood reinfusion or by the severity of blood-brain barrier disruption at the early stage of the postreinfusion period.

Animals↗

PubMed2006

[Remifentanil].

Remifentanil is a potent mu-opioid receptor agonist and has some unique pharmacokinetic characteristics compared to other anilidopiperidine opioids (e.g. fentanyl, alfentanil, and sufentanil). As remifentanil is metabolised rapidly by nonspecific esterases that are widespread throughout the plasma and tissuses, its duration of action is very short. It is cleared very rapidly, and its clearance is not affected by renal and hepatic function. The context-sensitive half-time of remifentanil remains consistently short, even after administration for a long time. Consequently, emergence is quick even after anesthesia of long duration. As other piperidine opioids, remifentnil has some adverse effects such as respiratory depression, muscle rigidity, bradycardia, and nausea as well as vomiting. Because of the rapid dissipation of analgesic effect following remifentanil discontinuation, postoperative analgesia should be provided before or soon after anesthesia using longer-acting opioid analgesics, non-opioid analgesics, or local as well as regional anesthesia.

Analgesics, Opioid↗

PubMed2005

Blockade of nuclear factor-kappaB activation prevents hypodynamic shock and gastric hypoperfusion induced by endotoxin in anesthetized dogs.

OBJECTIVE: To investigate whether pyrrolidinone derivative (N2733), an inhibitor of nuclear factor (NF)-kappaB activation, improves altered metabolic and hemodynamic changes and organ dysfunctions caused by endotoxic shock. DESIGN AND SETTING: Prospective, randomized, animal study in a laboratory at a university hospital. SUBJECTS: Twenty-three anesthetized male beagle dogs (10-14 kg). INTERVENTIONS: Dogs were mechanically ventilated and monitored with a pulmonary arterial catheter and a gastric tonometer. A central venous catheter was inserted into the femoral vein, and lactated Ringer's solution (10 ml/kg per hour) was administered throughout the study period. Three groups of animals were studied: (a) the lipopolysaccharide (LPS) group (n=8), which received LPS (250 ng/kg per minute for 2 h); (b) the LPS plus N2733 group (n=8), which received N2733 (30 mg/kg intravenously and 10 mg/kg hour for 6 h) after the start of LPS; and (c) the N2733 group (n=7), which received N2733 (30 mg/kg intravenously and 10 mg/kg per hour for 6 h). MEASUREMENTS AND RESULTS: Changes in hemodynamics, blood gas, gastric intramural pH, and renal and hepatic function were measured for 6 h. Coadministration of N2733 increased oxygen delivery index and prevented the LPS-induced hypotension, metabolic acidosis, and gastric mucosal acidosis but did not affect renal or hepatic function. CONCLUSIONS: Administration of N2733 increased oxygen delivery index and prevented the LPS-induced hypotension and metabolic and gastric mucosal acidosis in an anesthetized canine endotoxic shock model, suggesting its beneficial effect on local blood flow against tissue hypoxia. These findings suggest that blockade of NF-kappaB activation prevents hypodynamic shock and gastric hypoperfusin in endotoxic shock.

Animals↗

PubMed2005

Delayed emergence from anesthesia resulting from cerebellar hemorrhage during cervical spine surgery.

Cerebellar hemorrhage is an unpredictable complication of spinal surgery. We encountered a case of cerebellar hemorrhage presenting with delayed emergence from anesthesia and hemiplegia after resection of an intradural extramedullar tumor from the cervical spine. Postoperative brain computed tomography revealed hematoma in the cerebellar vermis and right cerebellar hemisphere. The patient made a gradual recovery with conservative treatment. Although the mechanism of cerebellar hemorrhage remains speculative, loss of cerebrospinal fluid may play an important role. Cerebellar hemorrhage must therefore be considered in patients with unexplained neurological deterioration or disturbance on emergence from anesthesia after spinal surgery.

Aged↗

PubMed2005

[Anesthetic management of an infant with asplenia and single atrium single ventricle undergoing ear tube surgery for otitis media: a case report].

A 13-month-old girl with cyanotic congenital heart disease; single atrium, single ventricle, common atrioventricular (AV) valve, pulmonary atresia and total anomalous pulmonary venous drainage, suspected of asplenia underwent ear tube surgery for otitis media. She had undergone bilateral Blalock-Taussig shunts for her heart disease. She had congestive heart failure due to moderate to severe common AV valve regurgitation and often experienced respiratory tract infection with sputum. Oxyhemoglobin saturation measured by pulse oximetry was 75-80% and polycythemia was found in complete blood count. We chose tracheal intubation for her airway management because of a large amount of sputum. General anesthesia was maintained with sevoflurane, nitrous oxide and oxygen for ear tube surgery. During anesthesia she showed several episodes of desaturation which were well managed by frequent tracheal suctioning. Her circulation was stable with 50% N2O and sevoflurane 1.7-2.0%. The operation was performed uneventfully and the patient was discharged to the ward after tracheal extubation. Asplenia is frequently complicated with cyanotic congenital heart disease and increased susceptibility to bacterial infection. Anesthesia for these patients with upper respiratory infection should be managed with tracheal intubation even for a short surgery.

Abnormalities, Multiple↗

PubMed2005

[Critical incidents during regional anesthesia in Japanese Society of Anesthesiologists-Certified Training Hospitals: an analysis of responses to the annual survey conducted between 1999 and 2002 by the Japanese Society of Anesthesiologists].

BACKGROUND: Recently, a national survey in France including 35,439 patients who had received spinal anesthesia showed that the incidences of cardiac arrest and mortality associated with spinal anesthesia were 2.5 and 0.8 per 10,000 anesthetics, respectively. In this study, we investigated these values using data obtained from annual surveys conducted by the Japanese Society of Anesthesiologist (JSA). METHODS: Since 1994, JSA has conducted annual surveys concerning critical incidents in the operating theater by sending confidential questionnaires to JSA-certified training hospitals, then collecting and analyzing the responses. We investigated critical incidents associated with regional anesthesia using data from annual surveys between 1999 and 2002. The questionnaire was identical in each survey conducted during these years. The total number of anesthetics available for this analysis was 3,855,384, of which spinal anesthesia, combined spinal-epidural anesthesia and epidural anesthesia were performed in 409,338, 146,282, and 69,001 patients, respectively. In patients receiving regional anesthesia, 628 critical incidents including 108 cardiac arrests, and 45 subsequent deaths were reported. The causes of critical incidents were classified as follows: totally attributable to anesthetic management, due mainly to intraoperative pathological events, preoperative complications, and surgical management. IP consists of coronary ischemia including coronary vasospasm not suspected preoperatively, arrhythmias including severe bradycardia, pulmonary thromboembolism, and other conditions. Mortality was determined by postoperative day 7. Statistical analysis was performed by chi-square test and Mann-Whitney test. A p value less than 0.05 was considered significant. RESULTS: The incidences of cardiac arrest and mortality due to all etiologies were 1.69 and 0.76 with spinal anesthesia, 1.78 and 0.68 with combined spinal-epidural anesthesia, and 1.88 and 0.58/10,000 anesthetics with epidural anesthesia, respectively. The incidences of cardiac arrest and mortality due to anesthetic management were 0.54 and 0.02 with spinal anesthesia, 0.55 and 0.00 with combined spinal-epidural anesthesia, and 0.72 and 0.14/10,000 anesthetics with epidural anesthesia, respectively. These values did not significantly differ among regional anesthesia. Death attributable to anesthetic management was reported in 2 patients: both patients were classified as ASA-PS 3 E, and developed cardiac arrest; one due to inadvertent high spinal anesthesia with spinal anesthesia, and the other due to local anesthetic intoxication with epidural anesthesia. Anesthetic management and intraoperative pathological events comprised 33 and 43% of cardiac arrests, respectively. The distribution of causes of death was as follows: anesthetic management, 5%; intraoperative pathological events, 34%; preoperative complications, 35%; surgical management, 26%. Among the causes of anesthetic management-induced critical incidents, inadvertent high spinal anesthesia was the leading cause of cardiac arrest in spinal and combined spinalepidural anesthesia: 90% of arrests occurred in patients with ASA-PS 1+2; 88% in patients below 65 years of age; 45 and 25% in patients undergoing hip or lower extremities surgery, and cesarean section, respectively. Among the causes of intraoperative pathological event-induced critical incidents, pulmonary thromboembolism was the leading cause of cardiac arrest in spinal and combined spinal-epidural anesthesia: 59% of arrests occurred in patients with ASA-PS 1+2; 81% in patients above 66 years of age; 91% in patients undergoing hip or lower extremity surgery. CONCLUSIONS: The incidence of cardiac arrest and mortality associated with spinal anesthesia in Japan was shown to be in the same order as in France by analyzing a larger population. In patients with good ASA-PS, critical incidents occurred more often under regional anesthesia than under general anesthesia. Inadvertent high spinal anesthesia should be carefully avoided. We should also pay much attention to subclinical deep vein thrombosis in patients who were scheduled for hip or lower extremity surgery, and tourniquet- or bone cement-associated pulmonary embolism in these patients.

Anesthesia↗

PubMed2005

[Anesthetic management of a patient with paroxysmal nocturnal hemoglobinuria and suspected abdominal venous thrombosis].

A 59-year-old man with paroxysmal nocturnal hemoglobinuria (PNH) underwent an operation for lumbar disk herniation. He was given warfarin, aspirin, and steroid for PNH and suspected venous thrombosis. PNH is a hemolytic anemia due to an acquired red blood cell membrane defect at the stem cell level. The patient with PNH has a risk of massive hemolysis induced by stresses such as acidosis, fever, operation, trauma and overfatigue. Other main symptoms of PNH are venous thrombosis and deficient hematopoiesis. We prevented massive hemolysis by increasing the dose of steroid and avoiding acidosis, fever and dehydration during the perioperative period. Warfarin and aspirin were changed to dalteparin before operation for the prevention of venous thrombosis as well as for easy control of bleeding tendency. The perioperative course was uneventful without obvious hemolysis, venous thrombosis and unnecessary bleeding.

Anesthesia, General↗

PubMed2005

[Critical events in the operating room among 1,440,776 patients with ASA PS 1 for elective surgery].

BACKGROUND: The Japanese Society of Anesthesiologists (JSA) survey of critical incidents in the operating room has shown that preoperative complications are the leading causes of critical incidents, and affect the occurrence, severity and outcome of critical incidents which are due to causes other than preoperative complications. Causes of critical events in the operating room were examind in patients for elective surgery with American Society of Anesthesiologists physical status (ASA PS) 1. METHODS: JSA has conducted annual surveys of critical incidents in the operating room by sending and collecting confidential questionnaires to all JSA Certified Training Hospitals. From 1999 to 2002, 3,855,384 anesthesia patients were registered. Among these, 1,440,776 patients with ASA PS 1 for elective surgery were analyzed. The causes of critical incidents were classified as follows: totally attributable to anesthetic management (AM), mainly to intraoperative pathological events (IP), to preoperative complications (PC), and to surgical management (SM). IP consists of coronary ischemia mainly due to coronary vasospasm, arrhythmias, pulmonary embolism, and other conditions. RESULTS: The incidences of cardiac arrest, critical incidents other than cardiac arrest and subsequent death were 9.86, 59.41 and 3.12 per 100,000 anesthesia cases, respectively. IP and SM were responsible for 36.6% and 34.5% of cardiac arrest, respectively. AM and SM were responsible for 46.7% and 26.8% of critical incidents other than cardiac arrest, respectively. SM, IP and AM were responsible for 66.7%, 22.2% and 4.4% of subsequent deaths (within 7 postoperative days), respectively. Coronary ischemia and pulmonary embolism were the main causes of death due to IP. The incidences of cardiac arrest and death totally attributable to AM were 1.87 and 0.14 per 100,000 anesthesia cases, respectively. Medication problems were responsible for 48.1% of arrests, while airway/ventilation problems were for 57.2% of critical incidents other than arrest. Human factors (SM combined with AM) were responsible for 53.5%, 73.5%, and 71.1% of cardiac arrest, critical incidents other than arrest and death, respectively. CONCLUSIONS: Even in elective patients with good physical status, non-lethal incidents were not rare, and lethal incidents were also reported. We should pay significant attention to the following findings, and take some measures to overcome these problems especially related to human factors. Firstly, SM badly harmed some operative patients. Secondly, coronary vasospasm and pulmonary embolism were the main causes of death due to IP. Thirdly, drug administration and airway/ventilation management were the major causes of critical incidents totally attributable to AM. Human factors were responsible for 70.6% of critical incidents and 71.1% of deaths.

Anesthesia↗

PubMed2005

[A case of stagnation of a large amount of irrigation fluid in abdominal cavity during hysteroscopic myomectomy].

A 30-year-old woman was scheduled to undergo hysteroscopic myomectomy for uterine myoma. Spinal anesthesia was performed with 3 ml of 0.5% bupivacaine and she was sedated with intravenous propofol during the surgery. After the surgical procedure, propofol infusion was stopped. The patient soon awoke and vomited frequently and repeatedly. Her serum sodium concentration was as low as 129 mEq x l(-1) and fluid overload (water intoxication) was suspected. Because the abdominal X-P revealed that two parts of the surgical instrument remained in her uterine cavity at that time, hysteroscopic procedure was restarted. General anesthesia was induced with propofol and maintained with nitrous oxide and sevoflurane. During the procedure, uterus was accidentally perforated and one of the parts moved into the abdominal cavity. When the laparotomy started to fix uterine perforation, the abdomen of the patient became remarkably distended. During the laparotomy, it was revealed that 4800 ml of irrigation fluid had been accumulated in the abdominal cavity. Although hysteroscopic surgery is generally considered non-invasive, two major complications (fluid overload and uterine perforation) occurred in this case. This case suggests that anesthetists must remain alert for the signs of these complications during hysteroscopic surgery.

Abdominal Cavity↗

PubMed2004

Effects of partial liquid ventilation on lipopolysaccharide-induced inflammatory responses in rats.

To determine whether partial liquid ventilation (PLV) modified lung inflammatory response, we analyzed blood cytokine levels and cytokine mRNA expression in the lungs, using a rat model of endotoxemia. Thirty-six rats were allocated into one of four groups. The first group received conventional gas ventilation (CV group), the second group received 10 ml/kg perflubron intratracheally in combination with mechanical gas ventilation (PLV group), the third group received 20 mg/kg Escherichia coli lipopolyssacharide (LPS) intravenously in combination with mechanical gas ventilation (LPS group), and the fourth group received PLV and LPS (PLV + LPS group). Blood levels of TNF-alpha, IL-1beta, IL-6, IL-10, INF-gamma and IL-1 receptor antagonist were significantly increased in LPS and PLV + LPS groups. mRNA expression of pro- and anti-inflammatory cytokines in the lung tissue was also significantly increased in these groups. mRNA expression of IL-6 in PLV + LPS group was significantly increased in comparison with LPS group. Other cytokine mRNA expression including IL-10 and IL-1beta was also potentiated in PLV + LPS group, however this was not significant. Our results suggest that PLV does not protect the lungs against inflammation in systemic endotoxemia in rats.

Animals↗

PubMed2004

Receptor for advanced glycation end-products is a marker of type I lung alveolar cells.

Lung alveolar epithelial cells are comprised of type I (ATI) and type II (ATII) cells. ATI cells are polarized, although they have very flat morphology. The identification of marker proteins for apical and basolateral membranes of ATI cells is important to investigate into the differentiation of ATI cells. In this paper, we characterized receptor for advanced glycation end-products (RAGE) as a marker for ATI cells. RAGE was localized on basolateral membranes of ATI cells in the immunoelectron microscopy and its expression was enhanced in a parallel manner to the differentiation of ATI cells in vivo and in primary cultures of ATII cells. RAGE and T1 alpha, a well-known ATI marker protein, were targeted to basolateral and apical membranes, respectively, when expressed in polarized Madine Darby canine kidney cells. Moreover, RAGE was expressed in ATI cells after T1 alpha in vivo and in ex in vivo organ cultures. In conclusion, RAGE is a marker for basolateral membranes of well-differentiated ATI cells. ATI cells require some signal provided by the in vivo environment to express RAGE.

Animals↗

PubMed2004

Blocking the R-type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance.

Morphine is the drug of choice to treat intractable pain, although prolonged administration often causes undesirable side-effects including analgesic tolerance. It is speculated that voltage-dependent Ca(2+) channels (VDCCs) play a key role in morphine analgesia and tolerance. To examine the subtype specificity of VDCCs in these processes, we analysed mice lacking N-type (Ca(v)2.2) or R-type (Ca(v)2.3) VDCCs. Systemic morphine administration or exposure to warm water swim-stress, known to induce endogenous opioid release, resulted in greater analgesia in Ca(v)2.3(-/-) mice than in controls. Moreover, Ca(v)2.3(-/-) mice showed resistance to morphine tolerance. In contrast, Ca(v)2.2(-/-) mice showed similar levels of analgesia and tolerance to control mice. Intracerebroventricular (i.c.v.) but not intrathecal (i.t.) administration of morphine reproduced the result of systemic morphine in Ca(v)2.3(-/-) mice. Furthermore, i.c.v. administration of an R-type channel blocker potentiated morphine analgesia in wild-type mice. Thus, the inhibition of R-type Ca(2+) current could lead to high-efficiency opioid therapy without tolerance.

Analgesics, Opioid↗

PubMed2004

[Reexpansion pulmonary edema after removal of a giant thoracic tumor associated with long-time lung collapse and mediastinal shift].

A 64-year-old woman was admitted to our hospital for removal of a thoracic tumor. Chest X-ray and computed tomography demonstrated a giant thoracic tumor occupying the right thorax, with the right lung almost completely collapsed and the mediastinum shifted to the left. Her preoperative pulmonary function studies revealed %vital capacity of 30%, and her oxyhemoglobin saturation was 92% (room air). Anesthesia was maintained with sevoflurane and fentanyl. The trachea was intubated with an armored tube because of severe tracheal shift. Operation was performed in the supine position. A Swan-Ganz catheter was inserted from the right femoral vein under fluoroscopy with stand-by of percutaneous cardiopulmonary support. The tumor was removed segmentally, and her right lung was inflated gradually. Two hours after removal of the tumor, PaO2 decreased to 74.2 mmHg (FIO2 1.0), and a large amount of sputum was suctioned subsequently. We suspected re-expansion pulmonary edema (RPE) and administered steroid with frequent tracheal suctioning. The patient was transferred to ICU without extubation. Postoperative X-ray demonstrated diffuse alveolar infiltrates over the right lung field. The patient was followed by respiratory management and body fluid management with diuretic drugs. The trachea was extubated on the following day, and her postoperative recovery was uneventful thereafter. We should consider the occurrence of RPE at removal of the giant thoracic tumor.

Anesthesia, General↗

PubMed2004

[Surgical volume and mortality due to intraoperative critical incidents at Japanese Society of Anesthesiologists certified training hospitals: an analysis of the annual survey in 2002].

BACKGROUND: We have previously showed that surgical volume affects mortality due to intraoperative critical incidents among patients undergoing cardiac surgery, the surgery with the highest risk, using data obtained by the annual survey in 2001 conducted by the Japanese Society of Anesthesiologists (JSA). In this study, we investigated whether surgical volume affects mortality due to intraoperative critical incidents independent of the surgical site. METHODS: We investigated this relationship using data obtained from the 2002 annual survey conducted by the Subcommittee on Surveillance of Anesthesia-related Critical Incidents, JSA. Between January 1, 2002 and December 31, 2002, 1,987,988 patients were registered from 704 training hospitals certified by the JSA. Intraoperative critical incidents occurred in 2,844 patients. Of these, 804 patients died within 7 postoperative days. The overall mortality was 4.61 per 10,000 anesthetics. Hospitals were divided into 5 groups according to their annual surgical cases: Group A, fewer than 1,000 (62 hospitals); Group B, 1,000-1,999 (204 hospitals); Group C, 2,000-3,999 (288 hospitals); Group D, 4,000-5,999 (110 hospitals); Group E, more than 6,000 (40 hospitals). Hospitals were also divided into 2 groups according to mortality: Group 1, under 20.00 per 10,000 anesthetics (672 hospitals); Group 2, equal to or higher than 20.00 per 10,000 anesthetics (32 hospitals). Total number of deaths in Group 2 was 158. Mortality was expressed as the mean (95% confidence interval). Statistical analysis was performed using chi-square test and Fisher test. A p value of <0.05 was considered significant. RESULTS: The mortality rates in Groups A-E were 14.89 (8.48-21.3), 3.86 (3.05-4.67), 3.88 (3.19-4.57), 4.04 (3.20-4.88), and 3.12 (2.19-4.05) per 10,000 anesthetics, respectively. Average surgical cases and mortality in Group 1 were 2,789 (2,775-3,002) and 3.24 (2.90-3.58), respectively, while those in Group 2 were 1,672 (1,243-2,101) and 22.18 (30.58-45.94), respectively. If all patients in Group 2 (n=53,509) had been treated in the hospitals of Group 1, 139-143 deaths might have been avoided. CONCLUSIONS: Surgical volume was shown to affect mortality independent of the surgical site. Hospitals with low surgical volume should pay significant attention to improving surgical outcomes. These results also suggest that centralization or regionalization should be discussed from the perspective of socio-economical problems as well as patient safety.

Anesthesia↗