Kluyvera intermedia bacteremia with septic shock: A case report.

Background: Kluyvera intermedia is a bacterium indigenous to humans. But Kluyvera intermedia bacteremia has been not reported thus far. We report a case of Kluyvera intermedia bacteremia with septic shock due to left obstructive pyelonephritis as a result of urolithiasis. Case presentation: A 66-year-old woman with septic shock due to left obstructive pyelonephritis was transferred to our hospital. Tazobactam/Piperacillin 4.5 g was administered every 8 h for 5 days. The patient's condition improved, and she was transferred back to the previous hospital. Kluyvera intermedia was obtained by blood cultures. The patient was successfully treated with a two-week course of antibiotics. Conclusions: We describe the first case of bacteremia with septic shock caused by Kluyvera intermedia. Kluyvera intermedia can be a causative pathogen of septic shock. Since this bacterium has not been reported in the past, we expect further reports and the accumulation of cases in the future.

Acute myeloid leukaemia presenting with ecthyma gangrenosum as the first manifestation: A case report.

RATIONALE: Ecthyma gangrenosum (EG) is an uncommon cutaneous infection usually associated with Pseudomonas aeruginosa bacteremia in immunocompromised patients, particularly those with underlying malignant diseases. Despite its rarity, especially in immunocompetent or nondiagnosed immunodeficiency patients, EG can present as the first manifestation of an underlying immunosuppression. PATIENT CONCERNS: A 42-year-old Japanese man was admitted to our hospital with a 3-day history of a painless red macule on his right forearm and fever. DIAGNOSES: Blood culture on admission revealed the presence of Pseudomonas aeruginosa, whereas pus culture of the skin lesion showed Pseudomonas aeruginosa and methicillin-susceptible Staphylococcus aureus positivity. INTERVENTIONS: Additional bone marrow aspirate examination and immunophenotyping were performed to confirm the diagnosis of acute promyelocytic leukaemia with PML-retinoic acid alpha receptor. OUTCOMES: The patient was successfully treated with a 14-day course of antibiotics, and no evidence of relapse was noted. The patient achieved complete remission after treatment for acute promyelocytic leukaemia. LESSONS: It should be kept in mind that EG is an important cutaneous infection that is typically associated with P aeruginosa bacteremia and the presence of underlying immunodeficiency, such as acute leukaemia.

Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

BACKGROUND: Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient's prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient's prognosis after carbon monoxide poisoning. METHODS: Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. RESULTS: The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). CONCLUSIONS: Patients' prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

Burning Mouth Syndrome Induced by Angiotensin-Converting Enzyme Inhibitors.

Burning mouth syndrome (BMS) is characterized as the sensation of burning in the tongue or any other area of the oral mucosa without a medical or dental cause. BMS's pathophysiology is poorly understood and may be caused by its association with various factors, particularly with antihypertensive or psychotropic medicines. Although BMS is a relatively common intraoral disorder in the dental field, emergency physicians rarely recognize it. We report a 53-year-old Japanese woman who presented to our ED with a three-week history of a strange taste and burning tongue. The patient had poor control of hypertension, captopril, an angiotensin-converting enzyme (ACE) inhibitor, was added three weeks before presentation. We discontinued her ACE inhibitor and changed her medication to a beta-blocker. After two weeks, her symptoms improved. Emergency physicians must be aware that ACE inhibitors play some roles in the pathogenesis of BMS. The correct diagnosis of the condition depends on recognizing the disease and improving the quality of life.

Glycogenic hepatopathy following attempted suicide by long-acting insulin overdose in patient with type 1 diabetes.

Patients with poorly controlled insulin-dependent type 1 or type 2 diabetes rarely present with glycogenic hepatopathy, which is characterized by hepatomegaly and liver enzyme abnormalities. Glycogenic hepatopathy occurs as a consequence of excessive accumulation of glycogen in hepatocytes caused by insulin. We report a young male patient with type 1 diabetes mellitus who developed glycogenic hepatopathy following a suicide attempt by insulin overdose via subcutaneous injection. The patient's medication/nutrition compliance and adherence to insulin were poorly controlled due to comorbid schizophrenia. Our patient required a large amount of continuous glucose to maintain euglycemia for persistent intractable hypoglycemia induced by overdose of long-acting insulin. On admission day 4, the patient presented elevated transaminases, hepatomegaly, and lactic acidosis. Computed tomography revealed swollen liver parenchyma with a diffusely high absorption. The patient gradually recovered without any medical intervention except for adequate control of blood sugar and was moved to a psychiatric ward on day 8 for schizophrenia management. This report may help emergency physicians be aware of the common symptoms, clinical course, and pathophysiology of glycogenic hepatopathy. Doctors should include glycogenic hepatopathy in the differential diagnosis of abnormal liver enzymes and hepatomegaly for those with poorly controlled insulin-dependent diabetes mellitus or unstable blood sugar levels due to insulin overdose like our patient.

Transient Global Amnesia in a Patient Presenting with Hypertensive Emergency; a Case Report.

Transient global amnesia (TGA) is characterized by the abrupt onset of global amnesia, particularly anterograde amnesia. The pathophysiology of TGA is poorly understood and it could be caused by various factors and be associated with various diseases. We report a 58-year-old man who presented to the local emergency room with TGA lasting for several hours. The patient had complete anterograde amnesia without a past medical history of migraine or neurological findings. His systolic blood pressure on presentation was 220 mmHg, which was immediately treated with intravenous calcium ion influx inhibitor. Other than global amnesia, there was no evidence of neurological disturbance. Computed tomography and magnetic resonance imaging results were unremarkable. After treatment of his hypertension, his amnesia resolved within 12 hours. Emergency department physicians may encounter TGA. Correct diagnosis of the condition depends on recognizing the disease.

Invasive Aspergillosis After Non-Fatal Drowning.

BACKGROUND: Pneumonitis and pneumonia after non-fatal drowning are common and the pathogens involved are numerous. However, invasive aspergillosis after non-fatal drowning in immunocompetent individuals is relatively rare. Here, we report a case of invasive aspergillosis complicated by pulmonary embolism after non-fatal drowning that proved fatal. CASE PRESENTATION: A 75-year-old Japanese man accidentally fell into a creek and was brought to a local hospital. His oxygenation steadily deteriorated to the point that he required intubation and mechanical ventilation. He was then transferred to the emergency department at our hospital. On arrival, he had severe respiratory dysfunction with diminished breath sounds. Radiography of the chest and computed tomography of the lungs showed diffuse bilateral infiltrates. The diagnosis was acute respiratory distress syndrome caused by aspiration pneumonitis as a result of non-fatal drowning and septic shock. Despite intensive care, the patient's hypoxia continued to worsen and he died on day 7. Computed tomography scans obtained at autopsy showed that both lungs were extensively infiltrated with effusion. An embolus was also detected in the right pulmonary artery. Microscopic analysis revealed diffuse filamentous fungi throughout the lungs, heart, stomach, thyroid gland, and the pulmonary embolus, which were identified as Aspergillus fumigatus by culture. CONCLUSION: Invasive aspergillosis should also be considered in immunocompetent patients with severe respiratory failure after non-fatal drowning who do not respond to broad-spectrum antibiotics. Angioinvasive aspergillosis can even result in fatal pulmonary embolism; hence, early targeted testing for Aspergillus species and empiric intravenous voriconazole should be considered in such cases.

A case of spontaneous mesenteric hematoma successfully diagnosed and treated with aggressive imaging.

INTRODUCTION: Spontaneous mesenteric hematoma is an uncommon syndrome triggered by bleeding localized in the mesenteric vascular tree of a bowel segment for no apparent underlying reason. We herein report a surgical patient with an extremely rapidly growing spontaneous mesenteric hematoma that we successfully diagnosed using careful radiologic examination. PRESENTATION OF CASE: A 56-year-old old male presenting sudden onset lower abdominal pain was referred to our emergency department. At the time of admission, his physical examination revealed stable vital signs without radiological abnormality. On the following day, the patient suddenly presented hypotension, tachycardia, and increased abdominal pain. Contrast-enhanced computed tomography examination showed a mass with both high- and low-density areas with a 130 mm maximum diameter bordering the transverse colon. Since interventional radiologists were not available, we decided to perform emergency exploratory laparotomy. On laparotomy, a 13 × 8 cm hematoma was found in the mesentery of the transverse colon. As bleeding was noted from the branches of the middle colic artery and gastrocolic artery, these responsible vessels were ligated. The patient was finally given the diagnosis of spontaneous mesenteric hematoma. DISCUSSION AND CONCLUSION: The present case, initially diagnosed as enterocolitis, suddenly manifested hypovolemic shock. Close monitoring for any signs of further deterioration, as well as aggressive imaging diagnosis, enabled us to avoid delays in treatment. Early diagnosis and treatment of mesenteric hematomas are essential to prevent them from rupturing and triggering life-threatening adverse events.

Novel role of neuronal Ca2+ sensor-1 as a survival factor up-regulated in injured neurons.

A molecular basis of survival from neuronal injury is essential for the development of therapeutic strategy to remedy neurodegenerative disorders. In this study, we demonstrate that an EF-hand Ca2+-binding protein neuronal Ca2+ sensor-1 (NCS-1), one of the key proteins for various neuronal functions, also acts as an important survival factor. Overexpression of NCS-1 rendered cultured neurons more tolerant to cell death caused by several kinds of stressors, whereas the dominant-negative mutant (E120Q) accelerated it. In addition, NCS-1 proteins increased upon treatment with glial cell line-derived neurotrophic factor (GDNF) and mediated GDNF survival signal in an Akt (but not MAPK)-dependent manner. Furthermore, NCS-1 is significantly up-regulated in response to axotomy-induced injury in the dorsal motor nucleus of the vagus neurons of adult rats in vivo, and adenoviral overexpression of E120Q resulted in a significant loss of surviving neurons, suggesting that NCS-1 is involved in an antiapoptotic mechanism in adult motor neurons. We propose that NCS-1 is a novel survival-promoting factor up-regulated in injured neurons that mediates the GDNF survival signal via the phosphatidylinositol 3-kinase-Akt pathway.

Activation of presynaptic GABAA receptors increases spontaneous glutamate release onto noradrenergic neurons of the rat locus coeruleus.

In order to further explore how GABA can modulate the excitability of noradrenergic neurons of the locus coeruleus (LC), we investigated the presence of GABA(A) receptors on glutamatergic nerve terminals and the functional consequences of their activation. We used mechanically dissociated immature rat LC neurons with adherent nerve terminals and patch-clamp recordings of spontaneous excitatory postsynaptic currents. Activation of presynaptic GABA(A) receptors by muscimol facilitated spontaneous glutamate release by activating tetrodotoxin-sensitive Na(+) channels and high-threshold Ca(2+) channels. Bumetanide (10 microM), a potent blocker of Na(+)-K(+)-Cl(-) cotransporter, diminished the muscimol-induced facilitatory action of glutamate release. Our results indicate that the Na(+)-K(+)-Cl(-) cotransporter accumulates Cl(-) inside the nerve terminals so that activation of presynaptic GABA(A) receptors causes depolarization. This GABA(A)-receptor-mediated modulation of spontaneous glutamatergic transmission is another mechanism by which GABA and its analogues can regulate the excitability and activity of noradrenergic neurons in the LC.

GABAB receptor transduction mechanisms, and cross-talk between protein kinases A and C, in GABAergic terminals synapsing onto neurons of the rat nucleus basalis of Meynert.

The transduction mechanisms underlying presynaptic GABAB receptor-mediated inhibition of transmitter release have been characterized for a variety of synapses in the central nervous system (CNS). These studies have suggested a range of transduction mechanisms, including a role for second messengers such as protein kinases A (PKA) and C (PKC). In the present study, we have examined the intracellular signalling pathways underlying baclofen-induced inhibition of GABA release from terminals synapsing onto rat basalis of Meynert neurons using patch-clamp recordings. Baclofen, a selective GABAB receptor agonist, reversibly decreased both evoked and spontaneous, miniature, GABAergic inhibitory postsynaptic currents (eIPSCs and mIPSCs, respectively). Such baclofen actions were completely abolished by CGP55845A, a selective GABAB receptor antagonist, and by staurosporine, a non-selective PKA and PKC inhibitor. The mIPSC frequency was still decreased by baclofen even in the presence of 4 AP, a K+ channel blocker, and Cd2+, a voltage-dependent calcium channel blocker. Pharmacological activation or inhibition of PKC activity affected basal GABA release and mildly affected the response to baclofen. Inhibition of the cAMP/PKA cascade also affected basal GABA release and, in a subset of neurons, occluded the effects of baclofen, suggesting that the GABAB receptor-mediated inhibitory action on GABA release was mediated via decreases in PKA activity. In addition, PKA inhibition occluded the effects of PKC modulation on both basal GABA release and on the response to baclofen. Our results characterize the transduction pathway of baclofen at these nucleus basalis of Maynert (nBM) synapses and show, for the first time, some cross-talk between the cAMP/PKA and PKC pathways in mammalian presynaptic nerve terminals.

Subarachnoid hemorrhage caused by dural arteriovenous fistula of the sphenobasal sinus--case report.

A 59-year-old woman presented with a rare middle fossa dural arteriovenous fistula (AVF) unrelated to the cavernous sinus manifesting only as subarachnoid hemorrhage. Angiography revealed shunts between the meningeal branches of both the internal and external carotid arteries and the sphenobasal sinus. The AVF drained into the superficial middle cerebral vein (SMCV) which had a varix and an anastomosis to a superior cerebral vein. The arterial supply vessels were eliminated surgically and the sinus was excised. Bleeding did not recur and there was no venous infarction. Dural AVF of the sphenoparietal sinus is associated with pulsatile exophthalmos and dural AVF of the sphenopetrosal sinus with tinnitus, but dural AVF of the sphenobasal sinus has no obvious symptom. Simple interruption of the SMCV at the penetration of the arachnoid membrane was possible because of the absence of a draining vessel to preserve AVF patency, but the arteries were eliminated in this patient to prevent formation of another AVF.