First Case of Necrotizing Fasciitis and Septicemia Caused by Pigmentibacter ruber.

We report the first case of necrotizing fasciitis caused by Pigmentibacter ruber. The isolated strain could not be identified by biochemical characterization or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry but was identified as P. ruber by 16S ribosomal RNA and whole-genome sequencing. Although much remains unknown about the pathogenicity of this bacterial species in humans, it has been shown to cause life-threatening infections such as septicemia and necrotizing fasciitis. Because the isolate was highly resistant to ß-lactams, it was difficult to treat with antimicrobial therapy. Thus, further documentation of cases and analyses are required.

A case of severe paraquat poisoning treated by continuous hemodiafiltration without sequelae.

Background: In a suicide attempt, a 49-year-old male ingested pesticides. He arrived at the hospital restless and vomiting blue liquid. Case Presentation: The patient was diagnosed with paraquat poisoning at a lethal dose and experienced renal dysfunction during treatment. He underwent continuous hemodiafiltration (CHDF). Hemodialysis was temporarily initiated and found to improve renal function. He was discharged on day 36 in good condition. He remains well with only mild renal impairment and no pulmonary fibrosis, 240 days after the incident. The fatality rate of paraquat poisoning is approximately 80%, regardless of the treatment. Early hemodialysis combined with CHDF within 4 h has been reported to be effective. In this case, CHDF was initiated approximately 3 h after paraquat administration and showed a successful outcome. Conclusion: CHDF should be performed as soon as possible to treat paraquat poisoning.

A Case of Heatstroke Encephalopathy With Abnormal Signals on Brain Magnetic Resonance Imaging.

Herein, we present a case of heatstroke encephalopathy with abnormal brain magnetic resonance imaging (MRI) signals. A 19-year-old man lost consciousness while working outdoors when the temperature was 35°C. His Glasgow Coma Scale score at presentation was E1V1M1, and his body temperature was 39°C. Chest computed tomography revealed bilateral infiltrates, and tests for urinary pneumococcal antigens were positive. He was diagnosed with heatstroke preceded by pneumococcal pneumonia. He was subsequently treated with antibiotics, and body surface cooling was performed. A diffusion-weighted brain MRI performed on day eight revealed abnormal bilateral hyperintensities from the cortex at the frontal lobe apex of the subcortex. Moreover, he had reduced spontaneity, dysarthria, nystagmus, tremor, and ataxia of both the upper limbs. He was diagnosed with heatstroke encephalopathy. On day 28 since admission, the abnormal MRI signals disappeared. Subsequently, the patient's spontaneity improved, but his other neurological dysfunctions persisted. This case study demonstrates that MRI may not be a sensitive indicator of the prognosis of heatstroke encephalopathy.

Caffeine poisoning successfully treated by venoarterial extracorporeal membrane oxygenation and emergency hemodialysis.

BACKGROUND: Caffeine overdose can cause life-threatening circulatory failure, neurological abnormalities, and ventricular fibrillation. We report the case of a patient with caffeine poisoning who was successfully treated with early hemodialysis and venoarterial extracorporeal membrane oxygenation. CASE PRESENTATION: A 43-year-old man who had ingested pills containing 20 g caffeine was transported to the hospital 100 min after ingestion. Hemodynamic collapse and refractory arrhythmia were most likely the potential complications. The patient developed ventricular fibrillation when placed in the left lateral decubitus position. Return of spontaneous circulation with defibrillation and introduction of venoarterial extracorporeal membrane oxygenation were followed by emergency dialysis, which led to rapid improvement in the clinical findings. CONCLUSION: Acute caffeine poisoning in a patient who developed an arrhythmia was successfully treated using an indwelling arterial and venous sheath followed by venoarterial extracorporeal membrane oxygenation.

First report in Japan of a delivery of a woman with the 2019 novel coronavirus disease.

On April 2, 2020, we received a maternal transport from a local city hospital of a pregnant woman (38 weeks and 0 days of gestation) in her 20s, who had the 2019 novel coronavirus disease (COVID-19). We performed an emergency cesarean section with spinal anesthesia because of an abnormal fetal heart rate pattern. A healthy 3106-g male baby was delivered. All the severe acute respiratory syndrome coronavirus 2 polymerase chain reaction tests of nasal and oral discharges, anal swabs and blood samples of the neonate at 9 h, 30 h and 4 days after birth were negative. Because the mother was diagnosed as having COVID-19 pneumonia, the neonate was given formula milk. The mother's nasal discharge samples at 20 and 21 days were negative. The mother first held her baby in her arms on the 22nd day after birth, and they were discharged on the following day. To the best of our knowledge, this is the first report in Japan of a delivery of a baby from a woman infected with COVID-19.

Splenic mass of uncertain etiology in a 15-year-old male patient: a case report.

BACKGROUND: There are few reports on spleen masses, and solitary splenic abscesses with abdominal pain have not been reported in younger age groups. We report a case of a splenic mass of uncertain etiology in a 15-year-old boy. CASE PRESENTATION: A 15-year-old boy visited the emergency department with abdominal pain. Abdominal ultrasonography revealed a thin-walled multilobular splenic cyst. Computed tomography revealed a cystic shadow and a septate structure in the spleen. Magnetic resonance imaging examination revealed a high-signal region on the T2-weighted image. The neutrophil ratio in the white blood cell count of 8,330/µL was high (80%), and splenic abscess could not be ruled out. Thus, therapy with 2 g/day fosfomycin was initiated. Abdominal pain disappeared on day 3 of hospital stay, and the patient was discharged on day 8. CONCLUSION: Antibiotic therapy can be effective against very acute onset splenic abscesses, although surgical treatment is usually carried out.

Autophagy in the Central Nervous System and Effects of Chloroquine in Mucopolysaccharidosis Type II Mice.

Mucopolysaccharidosis type II (MPS II) is a rare lysosomal storage disease (LSD) involving a genetic error in iduronic acid-2-sulfatase (IDS) metabolism that leads to accumulation of glycosaminoglycans within intracellular lysosomes. The primary treatment for MPS II, enzyme replacement therapy, is not effective for central nervous system (CNS) symptoms, such as intellectual disability, because the drugs do not cross the blood-brain barrier. Recently, autophagy has been associated with LSDs. In this study, we examined the morphologic relationship between neuronal damage and autophagy in IDS knockout mice using antibodies against subunit c of mitochondrial adenosine triphosphate (ATP) synthetase and p62. Immunohistological changes suggesting autophagy, such as vacuolation, were observed in neurons, microglia, and pericytes throughout the CNS, and the numbers increased over postnatal development. Oral administration of chloroquine, which inhibits autophagy, did not suppress damage to microglia and pericytes, but greatly reduced neuronal vacuolation and eliminated neuronal cells with abnormal inclusions. Thus, decreasing autophagy appears to prevent neuronal degeneration. These results suggest that an autophagy modulator could be used in addition to conventional enzyme replacement therapy to preserve the CNS in patients with MPS II.

Membranous tracheal stenosis in a patient with anorexia nervosa and self-induced vomiting- challenges in securing the airway.

We report a rare case of acquired membranous tracheal stenosis in a patient with anorexia nervosa and a history of self-induced vomiting, but without a history of tracheal intubation or tracheostomy. A 50-year-old woman presented with difficulty in breathing and swallowing, self-expectoration, and impaired consciousness due to acute benzodiazepine intoxication. Bronchoscopic examination was performed after tracheotomy and placement of a tracheostomy tube failed to secure her respiratory tract and ventilation continued to deteriorate. A flap-like membranous structure was identified on the posterior tracheal wall, obstructing the tracheostomy tube. Physical compression of the membranous structure improved ventilation. Bronchoscopic examination is generally recommended prior to performing tracheostomy in patients suspected to have post-intubation tracheal obstruction. Based on our findings, we suggest that these examinations should also be performed in patients with conditions associated with chronic irritation of the respiratory tract, including those with a prolonged history of self-induced vomiting.

[Change in Serum Levels of New Hepatic Fibrosis Marker "Mac-2 Binding Protein Glycosylation isomer (M2BPGi)" in Patients with Chronic Hepatitis C during the Treatment of Pegylated Interferon and Ribavirin].

The sustained virological response (SVR) rate in the patients with HCV has currently reached to 90% by the progression of anti-viral therapy. However, several reports demonstrated that hepatocellular carcinoma develops even in the patients with SVR. It is widely accepted that liver fibrosis plays a pivotal role in hepatocellular carcinogenesis. Thus, an accurate staging for liver fibrosis is necessary to improve long-term prognosis of hepatitis C patients. Recently, Mac-2 binding protein glycosylation isomer (M2BPGi) was identified as a novel hepatic fibrosis marker. In the present study, we compared the value of M2BPGi in serum before and after the anti-viral therapy in hepatitis C patients. The value of M2BPGi in patients with F2, F3, or F4 stagings was significantly higher than that in F1 staging. Moreover, the value of M2BPGi significantly decreased after the treatment with pegylated interferon plus ribavirin similarly to other liver fibrosis-related markers. In addition, the value of M2BPGi in patients with SVR was significantly decreased after the anti-viral therapy (P < 0.0001). The reduction of M2BPGi in SVR patients was thought to reflect the improvement of liver fibrosis, in conjunction with the reduction of viral load, after the treatment. In conclusion, the measurement of M2BPGi in serum might be useful in monitoring the improvement of liver fibrosis by anti-viral therapy.

Effects of intrathecal and intracerebroventricular administration of luteolin in a rat neuropathic pain model.

Luteolin, a major component of flavones, is known to have various physiological properties. Although luteolin reportedly has an antinociceptive effect on acute and inflammatory pain, little is known about its effect on neuropathic pain. The aim of the present study was to determine whether luteolin could ameliorate hyperalgesia in the central nervous system using a neuropathic pain model. Chronic constriction injury to the sciatic nerve was induced in male Sprague-Dawley rats. Luteolin (0.1-1.5 mg) was administered intrathecally or intracerebroventricularly to examine the central effects on mechanical, thermal, and cold hyperalgesia using the electronic von Frey test, plantar test, and cold plate test, respectively. A rotarod test was also performed to assess motor function in normal rats. Spinally applied luteolin dose-dependently attenuated mechanical and cold hyperalgesia, but it had no effect on thermal hyperalgesia. At the highest dose, luteolin affected motor performance. The spinal action of luteolin on mechanical hyperalgesia was inhibited by intrathecal pretreatment with the γ-aminobutyric acidA (GABAA) receptor antagonist bicuculline and µ-opioid receptor antagonist naloxone, but not by intrathecal pretreatment with either the benzodiazepine receptor antagonist flumazenil or glycine receptor antagonist strychnine. Supraspinal application of luteolin had no antihyperalgesic effects in any test. These findings suggest that luteolin ameliorates mechanical and cold hyperalgesia at least in part by activating GABAA receptors in a flumazenil-insensitive manner and µ-opioid receptors in the spinal cord, but that the supraspinal regions are unlikely to contribute to the antihyperalgesic action of luteolin. Luteolin could be a candidate therapeutic agent for neuropathic pain.

[Examination of relationship between lactate clearance and neurologic outcome in cardiac arrest induced by ventricular fibrillation].

A significant relationship between lactate clearance and mortality rates in cardiac arrest cases has been reported. However, the relationship between lactate clearance and neurologic outcomes in cardiac arrest cases is not clear. We examined lactate clearance in cardiac arrest cases induced by ventricular fibrillation. We investigated 13 patients with cardiac arrest induced by ventricular fibrillation from April, 2006 to March, 2012 in which therapeutic hypothermia was performed. Patients were classified into two groups: those with a favorable neurologic outcome (n=7) and those with a poor outcome (n=6). We compared lactate clearance levels between the two groups. There was no significant difference in lactate concentrations at admission and 8 or 24 hours lactate clearance between the two groups 8 or 24 hours after admission. This result suggests we may not predict the neurologic outcome of cardiac arrest cases induced by ventricular fibrillation using lactate clearance.

Chlorogenic acid administered intrathecally alleviates mechanical and cold hyperalgesia in a rat neuropathic pain model.

Chlorogenic acid (CGA), one of the most abundant dietary polyphenols, is known to have various physiological properties. Although CGA is reported to have an antinociceptive effect on acute and inflammatory pain, little is known about its effect on neuropathic pain or its action site. The aim of the present study was to determine whether intrathecally administered CGA can ameliorate hyperalgesia in a neuropathic pain model. Chronic constriction injury to the sciatic nerve was induced in male Sprague-Dawley rats. CGA (0.5, 1, or 2mg) was administered intrathecally to examine the effects on mechanical, thermal, and cold hyperalgesia using the electronic von Frey test, plantar test, and cold plate test, respectively. A rotarod test was also performed to assess motor function. To identify the neurotransmitter pathway involved in the spinal action of CGA, the present study examined the effect of intrathecal pretreatment with several antagonists of spinal pain processing receptors on the action of CGA in the electronic von Frey test and cold plate test. Spinally applied CGA dose-dependently alleviated mechanical and cold hyperalgesia. Conversely, CGA had no effect on thermal hyperalgesia. At the highest dose, CGA affected motor performance. The antihyperalgesic action of CGA was partially reversed by bicuculline, an γ-aminobutyric acidA (GABAA) receptor antagonist, at a dose that did not affect baseline behavioral responses. These findings suggest that CGA ameliorates mechanical and cold hyperalgesia partly by activating GABAergic transmission in the spinal cord, and that CGA may be useful for novel treatments for neuropathic pain.

Antinociceptive effect of intrathecal administration of hypotaurine in rat models of inflammatory and neuropathic pain.

Hypotaurine is an intermediate in taurine biosynthesis from cysteine in astrocytes. Although hypotaurine functions as an antioxidant and organic osmolyte, its physiological role in the central nervous system remains unclear. This study used behavioral assessments to determine whether hypotaurine influenced nociceptive transmission in acute, inflammatory, and neuropathic pain. The tail flick, paw pressure, and formalin tests were performed in male Sprague-Dawley rats to examine the effects of the intrathecal administration of hypotaurine (100, 200, 400, 600 µg) on thermal, mechanical, and chemical nociception. Chronic constriction injury (CCI) to the sciatic nerve was induced in the rats, and the electronic von Frey test and plantar test were performed to assess the effects on neuropathic pain. To determine which neurotransmitter pathway(s) was involved in the action of hypotaurine, in this study, we examined how the antagonists of spinal pain processing receptors altered the effect of 600 µg hypotaurine. To explore whether hypotaurine affected motor performance, the Rotarod test was conducted. Hypotaurine had antinociceptive effects on thermal, mechanical, and chemical nociception in the spinal cord. In CCI rats, hypotaurine alleviated mechanical allodynia and thermal hyperalgesia. These effects were reversed completely by pretreatment with an intrathecal injection of strychnine, a glycine receptor antagonist. Conversely, hypotaurine did not affect motor performance. This study demonstrated that intrathecal hypotaurine suppressed acute, inflammatory, and neuropathic pain. Hypotaurine may regulate nociceptive transmission physiologically by activating glycinergic neurons in the spinal cord, and it is a promising candidate for treating various pain states.

Celecoxib potently inhibits TNFalpha-induced nuclear translocation and activation of NF-kappaB.

Celecoxib is a specific inhibitor of cyclooxygenase 2 (COX2). While it has been used for the treatment of chronic inflammatory conditions, including rheumatoid arthritis, its detailed anti-inflammatory mechanism has not been clarified. Here, we found that Celecoxib potently inhibited TNFalpha-induced transcriptional activity and DNA binding activity of NF-kappaB; however, Celecoxib had no effect on TNFalpha-induced IKK activation and degradation of IkappaBalpha and IkappaBbeta, suggesting that it inhibited NF-kappaB activation via suppressing downstream of IKK activation and IkappaBs degradation. Interestingly, it was also found that Celecoxib abrogated TNFalpha-induced nuclear accumulation of the NF-kappaB p65 subunit. As a result, TNFalpha-induced expression of inflammatory cytokines, CXCL1/KC and CCL2/MCP-1, was clearly inhibited by Celecoxib. On the other hand, Celecoxib had no effect on the TNFalpha-induced nuclear translocation of c-jun and activation of ERK, JNK, p38 and Akt. Taken together, these data indicate that Celecoxib specifically inhibits TNFalpha-induced NF-kappaB activation at the level of its nuclear translocation. This negative regulation of NF-kappaB activation by Celecoxib might be an important mechanism leading to its anti-inflammatory activity.

Anesthetic management of a patient with Gerstmann-Sträussler-Scheinker syndrome (mutation of prion protein).

Gerstmann-Sträussler-Scheinker Syndrome (GSS) is a rare, infectious syndrome related to a mutation in the prion protein. A 60-yr-old, 152-cm, 31-kg woman with GSS was scheduled for open gastrostomy. This is the first report about an anesthetic experience in a patient with GSS. We describe our experience and precautions in the anesthetic management of a GSS patient.

[Complications related to anesthesia in the University of Occupational and Environmental Health Hospital].

BACKGROUND: Complications related to anesthesia remain a problem. We studied the incidence of complications during anesthesia in 2688 patients who had undergone anesthesia in the University of Occupational and Environmental Health Hospital. METHODS: We checked the anesthesia records retrospectively and analyzed the collected data for the incidence of complications during anesthesia. RESULTS: The total incidence of complications during anesthesia was 8.7%:5.5% related to circulation and 1.9% to respiration. CONCLUSIONS: Complications related to anesthesia should be prevented as much as possible through anesthesiologists' efforts in protocol development and skilled assistance.

The effects of the tramadol metabolite O-desmethyl tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M1 or M3 receptors.

O-desmethyl tramadol is one of the main metabolites of tramadol. It has been widely used clinically and has analgesic activity. Muscarinic receptors are involved in neuronal functions in the brain and autonomic nervous system, and much attention has been paid to these receptors as targets for analgesic drugs in the central nervous system. We have reported that tramadol inhibits the function of type-1 muscarinic (M(1)) receptors and type-3 muscarinic (M(3)) receptors, suggesting that muscarinic receptors are sites of action of tramadol. However, the effects of O-desmethyl tramadol on muscarinic receptor functions have not been studied in detail. In this study, we investigated the effects of O-desmethyl tramadol on M(1) and M(3) receptors, using the Xenopus oocyte expression system. O-desmethyl tramadol (0.1-100 microM) inhibited acetylcholine (ACh)-induced currents in oocytes expressing the M(1) receptors (half-maximal inhibitory concentration [IC(50)] = 2 +/- 0.6 microM), whereas it did not suppress ACh-induced currents in oocytes expressing the M(3) receptor. Although GF109203X, a protein kinase C inhibitor, increased the ACh-induced current, it had little effect on the inhibition of ACh-induced currents by O-desmethyl tramadol in oocytes expressing M(1) receptors. The inhibitory effect of O-desmethyl tramadol on M(1) receptor was overcome when the concentration of ACh was increased (K(D) with O-desmethyl tramadol = 0.3 microM). O-desmethyl tramadol inhibited the specific binding of [(3)H]quinuclidinyl benzilate ([(3)H]QNB) to the oocytes expressed M(1) receptors (IC(50) = 10.1 +/- 0.1 microM), whereas it did not suppress the specific binding of [(3)H]QNB to the oocytes expressed M(3) receptors. Based on these results, O-desmethyl tramadol inhibits functions of M(1) receptors but has little effect on those of M(3) receptors. This study demonstrates the molecular action of O-desmethyl tramadol on the receptors and may help to explain its neural function.

[The management of extirpation of chronic expanding hematoma after thoracoplasty in the chest].

A 71-year-old man was scheduled for an extirpation of chronic expanding hematoma (CEH) of his right thorax. He had a history of right thoracoplasty for tuberculosis 37 years previously. He complained of dyspnea that had deteriorated over three months. His inflammatory responses including general fatigue and fever due to chronic empyema remained to be resolved. The chest computed tomography revealed that the CEH remarkably compressed the trachea and the heart resulting in the cause of left mediastinal deviation. General anesthesia was induced with fentanyl and propofol, and maintained with sevoflurane. During general anesthesia, mean central venous pressure (CVP) via the right femoral vein and arterial blood pressure (ABP) via the left radial artery were monitored. Bilateral peripheral vein catheters with 16 G could effectively provide huge amount of transfusion. Although his blood loss was 10,000 ml because of superior vena caval rupture and oozing from pleura, prompt and adequate management of hemodynamics could be maintained using CVP and ABP monitoring. The CEH is known as a specific type of chronic empyema and its extraction would require ingenuity since there are number of factors associated with diagnosis, indication and prevention. Each case is to be evaluated individually and managed carefully.

[Management of sevoflurane anesthesia for a patient with multiple drug allergies].

There have been several reports on anesthesia for a patient with a history of multiple drug allergies. We present here anesthesia for a 33-year-old woman with histories of multiple drug allergies. She was scheduled to undergo total abdominal hysterectomy. We could not perform preoperative screening of the drugs using a dermal test because of a high risk of anaphylactic shock. Anesthesia was induced and maintained with sevoflurane and nitric oxide. The operation was finished without complications and her postoperative course was uneventful. It is important preoperatively to obtain histories of allergies adequately for recognition of allergens.

The reliability of the Bellhouse test for evaluating extension capacity of the occipitoatlantoaxial complex.

UNLABELLED: We examined the reliability of an airway evaluation test to assess the occipitoatlantoaxial (OAA) extension capacity described by Bellhouse et al. (Bellhouse test) in 20 adult volunteers with normal cervical spines. Each subject sat upright with the head in the neutral position and was then asked to extend the head maximally while attempting to move the neck as little as possible. The angle from the neutral position to the extreme extension was measured using the goggle-goniometer. Lateral cervical radiographs were taken in these positions, and the OAA extension angle was radiographically measured. Median values for OAA extension measured radiographically and extension of the head measured with the Bellhouse test were 21.5 degrees and 30 degrees, respectively. Extension of 9.5 degrees occurred at the subaxial regions, which could not be detected by inspecting surface contours of the neck. The extent of the subaxial extension was almost consistent with the degree of overestimation of the OAA extension capacity by the Bellhouse test. Because the subaxial extension occurred independent of the degree of the OAA extension, a strong relationship between the angle measured with the goggle-goniometer and the OAA extension angle measured radiographically was not established (P < 0.01, r(2) = 0.44). These findings mean that the test is not always accurate to evaluate the OAA extension capacity and will fail to detect a reduction of the OAA extension capacity if the subaxial regions are normal. Therefore, these problems derived from the Bellhouse test offer a potential for missing a prediction of difficult tracheal intubations because reduced OAA extension is one of the important factors that make intubation difficult. IMPLICATIONS: The Bellhouse test was not always accurate to evaluate the actual occipitoatlantoaxial extension capacity because of the inevitable occurrence of the subaxial extension. This may mean that some difficult endotracheal intubations will be unpredictable.