Pediatric Neurogenic Pulmonary Edema After Brain Tumor Removal Complicated with Severe Myocardial Injury: A Case Report.

BACKGROUND Neurogenic pulmonary edema (NPE) is a rare complication of neurological insults, such as traumatic brain injury and intracranial hemorrhage, in children. NPE frequently accompanies left ventricular (LV) dysfunction mediated via central catecholamine surge and inflammation. A high serum natriuretic (BNP) level was prolonged even after the LV contraction was improved in this case with severe myocardial injury. The overloading stress to the LV wall can last several days over the acute phase of NPE. CASE REPORT A 6-year-old boy developed NPE after the removal of a brain tumor in the cerebellar vermis, which was complicated by hydrocephalus. Simultaneously, he experienced LV dysfunction involving reduced global contraction with severe myocardial injury diagnosed by abnormally elevated cardiac troponin I level (1611.6 pg/ml) combined with a high serum BNP level (2106 pg/ml). He received mechanical ventilation for 4 days until the improvement of his pulmonary edema in the Intensive Care Unit (ICU). On the next day, after the withdrawal of mechanical ventilation, he was discharged from the ICU to the pediatric unit. Although the LV contraction was restored to an almost normal range in the early period, it took a total of 16 days for the serum BNP level to reach an approximate standard range (36.9 pg/ml). CONCLUSIONS Even in a pediatric patient with NPE, we recommend careful monitoring of the variation of cardiac biomarkers such as BNP until confirmation of return to an approximate normal value because of the possible sustained overloading stress to the LV wall.

Efficacy of high-frequency spinal cord stimulation for fibromyalgia syndrome in two cases: case reports.

BACKGROUND: Reports on the effectiveness of spinal cord stimulation (SCS) for the alleviation of fibromyalgia syndrome (FMS) pain are scarce. We report two cases of effective high-frequency SCS at 1000 Hz against upper- and lower-limb pain in patients with FMS. CASE PRESENTATION: Two women with widespread pain were diagnosed with FMS and the pain gradually worsened. A 1-week SCS trial was conducted in each patient. In both cases, the patients complained of unpleasant sensations during 10-Hz SCS. However, the pain was alleviated after 1000-Hz stimulation without irritation. Therefore, leads and a generator were implanted, after which they felt almost no pain. Moreover, the dose of the oral medication could be reduced and the patients returned to their daily lives. CONCLUSION: SCS at 1000 Hz may effectively treat pain associated with FMS. Therefore, performing an SCS trial for patients with FMS with intractable pain might be worthwhile.

Incidence and characteristics of early elevation of cardiac troponin I after intrathoracic surgery: A single-center retrospective observational study.

The early elevation of cardiac troponins within 24 hours after noncardiac surgery is reportedly associated with increased postoperative morbidities. Several predisposing factors, including the frequent occurrence of hypoxia and increased pulmonary arterial pressure, may likely contribute to this elevation, especially after intrathoracic surgery. Therefore, this retrospective study aimed to elucidate the incidence and characteristics of the early elevation of cardiac troponin I after intrathoracic surgery. This study included 320 patients who underwent intrathoracic surgery between January 1, 2018, and June 30, 2021. Specific perioperative variables were retrospectively collected from their electrical clinical records. The serum concentration of high-sensitivity cardiac troponin I (hs cTnI) was measured twice immediately after the intensive care unit arrival and on the following day. We grouped these patients into two: the early elevation of hs cTnI (EECT) group (hs cTnI value > 26.2 ng/L by at least 1 measurement) and the non-early elevation (non-EECT) group. Patient characteristics were then compared between these groups. The hs cTnI level elevated within 24 hours postoperatively in 103 patients (32.2%). In univariate analysis, intraoperative variables, including the duration of unilateral ventilation (199.2 minutes, P = .0025) and surgery (210.6 minutes, P = .0012), estimated blood loss volume (406.7 mL, P = .0022), percentage of stored red blood cell (RBC) transfusion (10.7%, P = .0059), and percentage of lobectomy or combination of other lung resection types (88.3%, P = .00188), were significantly higher in the EECT group than in the non-EECT group. In the log-rank test, prolonged hospitalization was more prevalent in the EECT group (P = .0485). Furthermore, multivariate analysis revealed 3 independent risk factors for the early elevation of hs cTnI: coexisting chronic renal failure (odds ratio [OR], 3.25), lobectomy or combined resections (OR, 2.65), and stored RBC transfusion (OR, 3.41). The early elevation of hs cTnI commonly occurs after intrathoracic surgery, with an incidence of 32.2%. Its 3 independent risk factors are coexisting chronic renal failure, lung resection type, and stored RBC transfusion.

Anti-inflammatory effects of dopamine on microglia and a D1 receptor agonist ameliorates neuroinflammation of the brain in a rat delirium model.

Microglia play a central role in neuroinflammatory processes by releasing proinflammatory mediators. This process is tightly regulated along with neuronal activities, and neurotransmitters may link neuronal activities to the microglia. In this study, we showed that primary cultured rat microglia express the dopamine (DA) D1 receptor (D1R) and D4R, but not D2R, D3R, or D5R. In response to a D1R-specific agonist SKF-81297 (SKF), the cultured microglia exhibited increased intracellular cAMP levels. DA and SKF suppressed lipopolysaccharide (LPS)-induced expression of interleukin-1ß (IL-1ß) and tumor necrosis α (TNFα) in cultured microglia. Microglia in the normal mature rat prefrontal cortex (PFC) were sorted and significant expression of D1R, D2R, and D4R was observed. A delirium model was established by administering LPS intraperitoneally to mature male Wistar rats. The model also displayed sleep-wake disturbances as revealed by electroencephalogram and electromyogram recordings as well as increased expression of IL-1ß and TNFα in the PFC. DA levels were increased in the PFC 21 h after LPS administration. Increased cytokine expression was observed in sorted microglia from the PFC of the delirium model; however, TNFα, but not IL-1ß expression, was abruptly decreased 21 h after LPS administration in the delirium model, whereas DA levels were increased. A D1R antagonist SCH23390 partially abolished the TNFα expression change. This suggests that endogenous DA may play a role in suppressing neuroinflammation. Administration of the DA precursor L-DOPA or SKF to the delirium model rats inhibited the expression of IL-1ß and TNFα. The simultaneous administration of clozapine, a D4R antagonist, strengthened the suppressive effects of L-DOPA. These results suggest that D1R mediates the suppressive effects of LPS-induced neuroinflammation, in which microglia may play an important role. Agonists for D1R may be effective for treating delirium.

Hemodynamic deterioration due to increased anterior and posterior cardiac compression during posterior spinal fusion for scoliosis with pectus excavatum.

Hemodynamics may deteriorate during the perioperative period when performing posterior spinal fusion in patients with pectus excavatum and scoliosis. A 13-year-old teenager diagnosed with Marfan syndrome had thoracic scoliosis and pectus excavatum. Thoracic scoliosis was convex to the right, and a right ventricular inflow tract stenosis was observed due to compression induced by the depressed sternum. The patient underwent T3-L4 posterior spinal fusion surgery for scoliosis. Deterioration of hemodynamics was observed when the patient was placed in the prone position or when the thoracic spine was corrected to the left front. Postoperative computed tomography examination showed that the mediastinal space was narrowed due to the corrected thoracic spine. Special attention should be paid in the following cases: (1) severe pectus excavatum, (2) right ventricular inflow tract compression due to depressed sternum on the left side, (3) correction of the thoracic spine on the left front, (4) long-term surgery, and (5) risk of massive bleeding. In some cases, pectus excavatum surgery should be prioritized.

Enhanced recovery from fulminant myocarditis by treatment with the combined use of the Impella left ventricular assist device with extracorporeal membrane oxygenation: a case series.

BACKGROUND: We experienced two adult cases of fulminant myocarditis with severe cardiogenic shock where Impella left ventricular assist device [left ventricle (LV)-Impella] was concomitantly used with venoarterial extracorporeal membrane oxygenation (V-A ECMO). CASE PRESENTATION: A 67-year-old man and a 49-year-old man with fulminant myocarditis were transferred to our hospital with mechanical support of V-A ECMO and IABP. Impella 5.0 and Impella CP were implanted 21 h and 17 h after establishing V-A ECMO for each case. Within 1 week, the patients' LV function progressively improved. Then the Impellas were withdrawn after discontinuing V-A ECMO. They were discharged from the intensive care unit within the following 8 days. CONCLUSIONS: The optimal introducing timing of LV-Impella is not currently precise. However, this case report suggests that the initiation of LV-Impella within at least 24 h after establishing V-A ECMO may be acceptable for the recovery of cardiac function.

Perioperative management of emergent cesarean section in a patient with peripartum cardiomyopathy and orthopnea: a case report.

Perioperative management of pregnant women with heart failure is difficult. Management of anesthesia in pregnant women is especially difficult because all of the currently available choices present challenges. We report a patient with peripartum cardiomyopathy (PPCM) who required an emergent cesarean section and discuss the possible tactics for managing anesthesia. A 40-year-old primipara with severe cardiac and respiratory failure required an emergent cesarean section at 39+1 gestational weeks. Her left ventricular ejection fraction was between 10% and 15%, and she had orthopnea. General anesthesia was planned after inserting sheaths for percutaneous cardiopulmonary support from the femoral artery and vein. However, when the patient was asked to lie down on the operation bed, she panicked and resisted because of labor pain and dyspnea. Therefore, anesthesia was induced instead of the initial plan. Finally, we successfully managed the anesthesia and delivered the newborn. There are no alternatives to general anesthesia in patients with PPCM presenting with orthopnea. Anesthesia induction in the supine position is impossible in such patients owing to dyspnea. Anesthesia should be started with light sedation in the sitting position, and ketamine or low-dose remifentanil may be an option to maintain maternal hemodynamics and prevent neonatal asphyxia.

Independent Predicting Factors for Subcutaneous Emphysema Associated with Robotic-Assisted Laparoscopic Radical Prostatectomy: A Retrospective Single-Center Study.

OBJECTIVES: Subcutaneous emphysema (SCE) is a complication associated with laparoscopic surgery. Severe SCE complicated by excessive hypercarbia may afford detrimental effects in surgical patients with cardiac dysfunction. Robotic-assisted laparoscopic radical prostatectomy (RALP) has several predisposing factors that contribute to SCE. The main purpose of our single-center retrospective study was to determine the preoperative and intraoperative predicting factors for SCE associated with RALP and to determine the actual incidence of SCE. METHODS: In total, 229 adult male patients underwent standardized RALP for prostate cancer over the period of 1 May 2016 to 31 October 2018 at the Ehime University Hospital. We reviewed electronic clinical records for individual characteristics including age, body weight, height, coexisting disorders, preoperative ASA physical status, and the length of postoperative hospital stay. We also reviewed surgical and anesthetic records for the operation time, anesthetic method, and the partial pressure of end-tidal CO2 (PetCO2) during RALP. To determine the presence of SCE, we examined supine chest X-rays obtained after the completion of surgery. RESULTS: We found 55 cases (24.0%) of SCE. Multiple logistic regression analysis showed that a BMI < 25 kg/m2 (OR: 3.0, 95% CI: 1.25-7.26) and a maximum value of PetCO2 of 46 mmHg or greater (OR: 23.3, 95% CI: 8.22-66.1) were independent predicting factors for SCE. CONCLUSION: These two predicting factors may be helpful to recognize the occurrence of SCE. Anesthesiologists should protect against SCE progression with the earlier detection of SCE for safe anesthetic management in patients undergoing RALP.

Takotsubo Cardiomyopathy Induced by Very Low-Dose Epinephrine Contained in Local Anesthetics: A Case Report.

BACKGROUND Takotsubo cardiomyopathy is a reversible left ventricular dysfunction triggered by emotional or physical stress. Perioperatively, takotsubo cardiomyopathy is sometimes induced by various psychological factors, such as stress from surgery, and non-psychological factors, such as epinephrine misinjection. This report describes a case of takotsubo cardiomyopathy induced by the administration of very low-dose epinephrine contained in a local anesthetic. CASE REPORT A 78-year-old woman with mycosis in the maxillary sinus was scheduled to undergo endoscopic sinus surgery. After the submucosal injection of 3 mL of local anesthetic (lidocaine, 0.5%; epinephrine, 1: 200 000) immediately before the incision, her heart rate and blood pressure reached 135 beats per min and 254/185 mmHg, respectively, inducing ventricular tachycardia. After receiving 50 mg of lidocaine, her cardiac rhythm resumed a normal sinus rhythm, without cardioversion. As her hemodynamics stabilized, the surgical procedure began as planned. Postoperative electrocardiography, echocardiography, and coronary arteriography demonstrated takotsubo cardiomyopathy. Subsequently, her cardiac movement gradually improved, and she was discharged from the hospital on postoperative day 9. CONCLUSIONS To the best of our knowledge, this is the first reported case in which a very small amount of epinephrine (0.015 mg) induced takotsubo cardiomyopathy. Therefore, epinephrine should be used cautiously, especially in the nasal mucosa, vaginal mucosa, and uterus, where blood flow is relatively high. If unexpected hemodynamic alterations and ST-segment abnormalities occur after epinephrine administration, asymptomatic takotsubo cardiomyopathy should be considered.

Disseminated intravascular coagulation as a complication of bursitis: angiogenesis and repetitive bleeding as potential factors for disseminated intravascular coagulation: a case report.

BACKGROUND: Malignant tumors, such as acute leukemia and solid cancers, frequently cause disseminated intravascular coagulation. However, cases of disseminated intravascular coagulation as a complication of bursitis were not reported previously. CASE PRESENTATION: A 72-year-old Japanese woman was scheduled to undergo resection of a rapidly growing subcutaneous tumor-like lesion on her left back. Preoperative blood tests suggested disseminated intravascular coagulation. The resected lesion was cystic tumor containing a hematoma. After the operation, the patient completely recovered from disseminated intravascular coagulation, indicating that disseminated intravascular coagulation in this case was caused by the tumor. Pathological examination of the resected tumor revealed considerable fibrin deposition and angiogenesis on the cyst wall, which was presumably a response to inflammation and indicated presence of repetitive intratumoral bleeding, subsequently leading to a diagnosis of chronic hemorrhagic bursitis. CONCLUSIONS: Clinicians should note that, despite being benign, soft-tissue tumors accompanied by inflammation with angiogenesis and repetitive intratumoral bleeding can cause disseminated intravascular coagulation, albeit rarely.

Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model.

The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP- cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2-/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.

Microglia and Macrophages in the Pathological Central and Peripheral Nervous Systems.

Microglia, the immunocompetent cells in the central nervous system (CNS), have long been studied as pathologically deteriorating players in various CNS diseases. However, microglia exert ameliorating neuroprotective effects, which prompted us to reconsider their roles in CNS and peripheral nervous system (PNS) pathophysiology. Moreover, recent findings showed that microglia play critical roles even in the healthy CNS. The microglial functions that normally contribute to the maintenance of homeostasis in the CNS are modified by other cells, such as astrocytes and infiltrated myeloid cells; thus, the microglial actions on neurons are extremely complex. For a deeper understanding of the pathophysiology of various diseases, including those of the PNS, it is important to understand microglial functioning. In this review, we discuss both the favorable and unfavorable roles of microglia in neuronal survival in various CNS and PNS disorders. We also discuss the roles of blood-borne macrophages in the pathogenesis of CNS and PNS injuries because they cooperatively modify the pathological processes of resident microglia. Finally, metabolic changes in glycolysis and oxidative phosphorylation, with special reference to the pro-/anti-inflammatory activation of microglia, are intensively addressed, because they are profoundly correlated with the generation of reactive oxygen species and changes in pro-/anti-inflammatory phenotypes.

A case report of thrombotic complete obstruction of the ascending aorta as a complication of Venoarterial extracorporeal membrane oxygenation support: steps to prevent thrombosis.

BACKGROUND: Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is an essential device in the field of emergency and intensive-care medicine. However, long-term use of VA-ECMO has various severe complications, including thrombosis. CASE PRESENTATION: A 60-year-old man underwent his third aortic root replacement using a homograft because of infectious endocarditis. Although the operation was difficult because of severe adhesion caused by the two previous interventions, aortic root replacement using a homograft was performed. At the time of withdrawal from cardiopulmonary bypass, the maintenance of hemodynamics was difficult because of bleeding from the surgical site, leading to hypovolemic shock. Cardiac function subsequently deteriorated; therefore, VA-ECMO was established and the operation was finished. Three days later, thrombus was formed inside the homograft and completely occluded ascending aorta. Evacuation of hematoma was performed, however, cardiac function was not ameliorated. Eventually, the patient had brain infarction and died. To prevent thrombus formation in very severe low cardiac output cases under VA-ECMO management after surgery, to prevent the stagnation of the blood flow from VA-ECMO will be necessary because anticoagulant therapy will be difficult. Impella ventricular assist device which is recently used widely generates anterograde blood flow and effectively prevents stagnation. CONCLUSIONS: To prevent thrombus formation in cases of very severe low cardiac output, Impella® should be combinatorially introduced from the beginning of VA-ECMO establishment to prevent thrombosis.

Chronic constriction injury of the sciatic nerve in rats causes different activation modes of microglia between the anterior and posterior horns of the spinal cord.

Chronic constriction injury of the sciatic nerve is frequently considered as a cause of chronic neuropathic pain. Marked activation of microglia in the posterior horn (PH) has been well established with regard to this pain. However, microglial activation in the anterior horn (AH) is also strongly induced in this process. Therefore, in this study, we compared the differential activation modes of microglia in the AH and PH of the lumbar cord 7 days after chronic constriction injury of the left sciatic nerve in Wistar rats. Microglia in both the ipsilateral AH and PH demonstrated increased immunoreactivity of the microglial markers Iba1 and CD11b. Moreover, abundant CD68+ phagosomes were observed in the cytoplasm. Microglia in the AH displayed elongated somata with tightly surrounding motoneurons, whereas cells in the PH displayed a rather ameboid morphology and were attached to myelin sheaths rather than to neurons. Microglia in the AH strongly expressed NG2 chondroitin sulfate proteoglycan. Despite the tight attachment to neurons in the AH, a reduction in synaptic proteins was not evident, suggesting engagement of the activated microglia in synaptic stripping. Myelin basic protein immunoreactivity was observed in the phagosomes of activated microglia in the PH, suggesting the phagocytic removal of myelin. CCI caused both motor deficit and hyperalgesia that were evaluated by applying BBB locomotor rating scale and von Frey test, respectively. Motor defict was the most evident at postoperative day1, and that became less significant thereafter. By contrast, hyperalgesia was not severe at day 1 but it became worse at least by day 7. Collectively, the activation modes of microglia were different between the AH and PH, which may be associated with the difference in the course of motor and sensory symptoms.

Hemolytic reaction in the washed salvaged blood of a patient with paroxysmal nocturnal hemoglobinuria.

BACKGROUND: In patients with paroxysmal nocturnal hemoglobinuria (PNH), the membrane-attack complex (MAC) formed on red blood cells (RBCs) causes hemolysis due to the patient's own activated complement system by an infection, inflammation, or surgical stress. The efficacy of transfusion therapy for patients with PNH has been documented, but no studies have focused on the perioperative use of salvaged autologous blood in patients with PNH. CASE PRESENTATION: A 71-year-old man underwent total hip replacement surgery. An autologous blood salvage device was put in place due to the large bleeding volume and the existence of an irregular antibody. The potassium concentration in the transfer bag of salvaged RBCs after the wash process was high at 6.2 mmol/L, although the washing generally removes > 90% of the potassium from the blood. This may have been caused by continued hemolysis even after the wash process. Once activated, the complement in patients with PNH forms the MAC on the RBCs, and the hemolytic reaction may not be stopped even with RBC washing. CONCLUSIONS: Packed RBCs, instead of salvaged autologous RBCs, should be used for transfusions in patients with PNH. The use of salvaged autologous RBCs in patients with PNH should be limited to critical situations, such as massive bleeding. Physicians should note that the hemolytic reaction may be present inside the transfer bag even after the wash process.

Carbon monoxide poisoning-induced delayed encephalopathy accompanies decreased microglial cell numbers: Distinctive pathophysiological features from hypoxemia-induced brain damage.

Carbon monoxide (CO) causes not only acute fatal poisoning but also may cause a delayed neurologic syndrome called delayed encephalopathy (DE), which occasionally occurs after an interval of several days to several weeks post-exposure. However, the mechanisms of DE have not been fully elucidated. This study aimed to clarify the pathophysiology of CO-induced DE and its distinctive features compared with hypoxemic hypoxia. Rats were randomly assigned to three groups; the air group, the CO group (exposed to CO), and the low O2 group (exposed to low concentration of O2). Impairment of memory function was observed only in the CO group. The hippocampus tissues were collected and analyzed for assessment of CO-induced changes and microglial reaction. Demyelination was observed only in the CO group and it was more severe and persisted longer than that observed in the low O2 group. Moreover, in the CO group, decreased in microglial cell numbers were observed using flow cytometry, and microglia with detached branches were observed were observed using immunohistochemistry. Conversely, microglial cells with shortened branches and enlarged somata were observed in the low O2 group. Furthermore, mRNAs encoding several neurotrophic factors expressed by microglia were decreased in the CO group but were increased in the low O2 group. Thus, CO-induced DE displayed distinctive pathological features from those of simple hypoxic insults: prolonged demyelination accompanying a significant decrease in microglial cells. Decreased neurotrophic factor expression by microglial cells may be one of the causes of CO-induced DE.

Comparison of the detrimental features of microglia and infiltrated macrophages in traumatic brain injury: A study using a hypnotic bromovalerylurea.

Microglia and blood-borne macrophages in injured or diseased brains are difficult to distinguish because they share many common characteristics. However, the identification of microglia-specific markers and the use of flow cytometry have recently made it easy to discriminate these types of cells. In this study, we analyzed the features of blood-borne macrophages, and activated and resting microglia in a rat traumatic brain injury (TBI) model. Oxidative injury was indicated in macrophages and neurons in TBI lesions by the presence of 8-hydroxy-2'-deoxyguanosine (8-OHdG). Generation of mitochondrial reactive oxygen species (ROS) was markedly observed in granulocytes and macrophages, but not in activated or resting microglia. Dihydroethidium staining supported microglia not being the major source of ROS in TBI lesions. Furthermore, macrophages expressed NADPH oxidase 2, interleukin-1ß (IL-1ß), and CD68 at higher levels than microglia. In contrast, microglia expressed transforming growth factor ß1 (TGFß1), interleukin-6 (IL-6), and tumor necrosis factor α at higher levels than macrophages. A hypnotic, bromovalerylurea (BU), which has anti-inflammatory effects, reduced both glycolysis and mitochondrial oxygen consumption. BU administration inhibited chemokine CCL2 expression, accumulation of monocytes/macrophages, 8-OHdG generation, mitochondrial ROS generation, and proinflammatory cytokine expression, and markedly ameliorated the outcome of the TBI model. Yet, BU did not inhibit microglial activation or expression of TGFß1 and insulin-like growth factor 1 (IGF-1). These results indicate that macrophages are the major aggravating cell type in TBI lesions, in particular during the acute phase. Activated microglia may even play favorable roles. Reduction of cellular energy metabolism in macrophages and suppression of CCL2 expression in injured tissue may lead to amelioration of TBI.

Effect of dexmedetomidine on intraocular pressure in patients undergoing robot-assisted laparoscopic radical prostatectomy under total intravenous anesthesia: A randomized, double blinded placebo controlled clinical trial.

STUDY OBJECTIVE: To study the effects of intraoperative dexmedetomidine on the intraocular pressure (IOP) in patients undergoing robot-assisted laparoscopic radical prostatectomy (RALRP) under propofol-remifentanil anesthesia. DESIGN: Double-blind, randomized controlled trial. SETTING: Operating room. PATIENTS: Forty consenting male patients aged ≥20 to <80 years with American Society of Anesthesiologists physical status classes I and II. INTERVENTIONS: The patients were randomly assigned to either dexmedetomidine (DEX) (n = 20) or control (n = 20) group. Anesthesia was induced and maintained using propofol, remifentanil, and rocuronium. In the dexmedetomidine group, dexmedetomidine was administered at 0.4 µg/kg/h immediately after anesthesia induction until the end of the surgery, whereas normal saline was administered as placebo in the control group. MEASUREMENTS: IOP was measured using a rebound tonometer. Time points of measuring IOP were as follows: T1: before anesthesia induction, T2: 5 min after intubation, T3: 60 min after placing patient in the Trendelenburg position, T4: 120 min after placing patient in the Trendelenburg position, T5: 180 min after placing patient in the Trendelenburg position, T6: 5 min after placing patient in a horizontal position, T7: 5 min after extubation, and T8: 30 min after extubation. MAIN RESULTS: A linear mixed model analysis demonstrated a significant intergroup difference in IOP over time and during pneumoperitoneum in the steep Trendelenburg position. IOP at T5 was significantly lower in the dexmedetomidine group than in the control group even after post-hoc analysis in the steep Trendelenburg position periods with Bonferroni correction. CONCLUSIONS: Dexmedetomidine combined with propofol decreases IOP in the steep Trendelenburg position during RALRP.

Development of a postoperative occlusive thrombus at the site of an implanted inferior vena cava filter: A case report.

RATIONALE: Although an inferior vena cave (IVC) filter is placed to prevent fatal pulmonary embolism (PE), several complications associated with an IVC filter have been reported. We describe a case with symptomatic PE, of which the origin was an occlusive IVC thrombus that developed from the placement of an IVC filer after a laparoscopy-assisted total gastrectomy (LATG). PATIENT CONCERNS: A 71-year-old man underwent LATG under general anesthesia alone. He had an IVC filter implanted 13 years ago. An intravenous infusion of unfractionated heparin was substituted for the discontinuation of oral warfarin four days before the surgery. The proposed operation was performed and took a total of 404 minutes including the total duration of pneumoperitoneum that took 374 minutes. After the surgery, he experienced severe shivering reactions that required frequent bolus infusions of antihypertensive drugs. On the third postoperative day, he complained of dyspnea after taking a short walk, and subsequently lost consciousness. While he spontaneously recovered without requiring any resuscitation efforts, we performed computed tomography (CT) examination for suspected PE. DIAGNOSES: The CT showed that a massive thrombus was occupying the intravenous space from the IVC filter to the left common iliac vein with several embolic defects in the peripheral pulmonary arteries present. INTERVENTIONS: An anticoagulant therapy was established with 10 mg of oral apixaban given twice a day for the first four days, followed by a reduction to 5 mg. OUTCOMES: On the 17th postoperative day, an ultrasound vascular examination confirmed the complete disappearance of deep venous thrombus (DVT). LESSONS: As an IVC filter itself may be a potential source of DVT, we should carefully manage patients with a previously implanted IVC filter throughout the perioperative period.