Epidural analgesia is frequently used for the management of labor pain in parturients. The neurologic complications of epidural analgesia are rare, but they are catastrophic when they occur. We report here on a case of bilateral femoral neuropathy in a vaginal delivery patient with epidural analgesia. The patient complained of weakness of both thighs and numbness around both knees. Neurologic examination and electromyographic study revealed that they occurred due to the delivery itself. The patient had not fully recovered at eight weeks after delivery. The declining incidence of postpartum femoral neuropathy may reflect a reduced duration of labor in accordance with modern obstetric practice, and particularly the more frequent use of Caesarean delivery. The exact etiology of postpartum femoral neuropathy is unknown, and the possible factors are direct compression of nerves that are proximal within the pelvis by either the fetal head or birthing instruments, or this malady is the result of pressure induced ischemia at the level of the inguinal ligament when the pregnant woman is in the lithotomy position.
Analgesia, Epidural ; Female ; Femoral Neuropathy ; Head ; Humans ; Hypesthesia ; Incidence ; Ischemia ; Knee ; Labor Pain ; Ligaments ; Neurologic Examination ; Parturition ; Pelvis ; Postpartum Period ; Pregnancy ; Pregnant Women ; Thigh

BACKGROUND: Calcium plays a key role in vascular contraction and regulates receptor sensitivity to certain neurotransmitters. Calcium channel blockers are useful in the treatment of both clinical and experimental hypertension. The present study was designed to examine whether there is an alteration of the activity of calcium channels in association with the development of hypertension. METHODS: Deoxycorticosterone acetate(DOCA)-salt hypertension was made by subcutaneous implantation of DOCA(200mg/kg)strip plus saline drinking(1%) and 2-kidney, 1 clip(2KIC)hypertension by clipping the left renal artery with a silver clip(internal gap of 0.2mm). They were used 4 weeks later. Age-matched normal rats served as a control. Mean arterial pressure(MAP) and heart rate(HR) were continuously recorded from the right femoral artery. The drugs were administered intravenously. RESULTS: Vehicle alone was without effect on MAP or HR. In normotensive rats, nifedipine infusion(5 and 10ug/kg/min)caused a dose-dependent decrease in MAP without significant changes in HR, while Bay k 8644(Bay K, 5 and 10 ug/kg/min) increased MAP transiently. Both the depressor response to nifedipine and the pressor response to Bay k were more marked in DOCA-salt hypetensive rats than in normotensive rats. The maximal changes in MAP indced by nifedipine(5 and 50 ug/kg) or Bay K(5 and 50 ug/kg) were also enhanced in 2KIC hypertensive rats as compared with control rats. CONCLUSION: These results indicate that calcium channel inhibitors and activators can affect on the regulation of blood pressure in an opposite fashion. It is also suggested that the activity of calcium channels might be altered in the developement of experimental hypertension.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester* ; Animals ; Bays* ; Blood Pressure ; Calcium ; Calcium Channel Blockers ; Calcium Channels ; Desoxycorticosterone ; Femoral Artery ; Heart ; Hypertension ; Neurotransmitter Agents ; Nifedipine* ; Rats* ; Renal Artery ; Silver

No abstract available.
Humans

A crossed occlusion resulting from the presence of posterior teeth in one arch but no opposing teeth in the opposite arch results in collapse of the vertical dimension. In this case, the patient has a class III malocclusion with crossed occlusion and anterior crossbite. In order to evaluate the proper vertical dimension, provisional denture was used to stabilize the vertical occlusal dimension for 3 months. After, provisional fixed restoration was used for the stabilizing occlusal relationship and aesthetic improvement for lip support. Definitive prosthesis in implants in the mandible and abutments in the maxillary were using Porcelain-fused-to-metal crown (PFM) crown and the maxillary unilateral edentulous area was treated with removable partial dentures. Through this, proper support of the posterior region and normal anterior occlusal relationship were formed, and the patient was able to obtain aesthetically and functionally satisfactory treatment results.

Purulent pericarditis is a rare condition with a high mortality rate. We report a case of purulent pericarditis subsequently caused by Candida parapsilosis, Peptostreptococcus asaccharolyticus, Streptococcus anginosus, Staphylococcus aureus, Prevotella oralis, and Mycobacterium tuberculosis in a previously healthy 17-year-old boy with mediastinal tuberculous lymphadenitis. The probable route of infection was a bronchomediastinal lymph node-pericardial fistula. The patient improved with antibiotic, antifungal, and antituberculous medication in addition to pericardiectomy.
Adolescent ; Bronchial Fistula ; Candida ; Coinfection ; Fistula* ; Humans ; Male ; Mortality ; Mycobacterium tuberculosis ; Peptostreptococcus ; Pericardiectomy ; Pericarditis* ; Pericarditis, Tuberculous ; Prevotella ; Staphylococcus aureus ; Streptococcus anginosus ; Tuberculosis, Lymph Node*

A 47-year-old woman underwent orthotopic liver transplantation (OLT) for hepatitis B virus (HBV)-related end-stage liver cirrhosis. The patient received hepatitis B immunoglobulin prophylaxis after OLT. Despite the protective level of the serum anti-hepatitis-B surface antibody, HBV recurred at 22 months post-OLT and induced subacute hepatic failure. The pre-OLT HBV genome contained a complex mutation pattern in overlapping frame regions of the surface (S) and polymerase (P) genes, which is the same mutation pattern as seen in post-OLT HBV DNA. G145R and K141R mutations in the "a" determinant were detected only in the post-OLT sample. Clevudine (30 mg once daily) was administered for recurrent hepatitis B. Hepatitis B was reactivated with a flare-up, and a M204I mutation (YIDD mutant type) appeared with a higher viral load at 9 months after clevudine treatment. We report here a case of a YIDD mutation that developed in recurrent hepatitis B after OLT induced by an S-escape mutant.
Arabinofuranosyluracil ; DNA ; Female ; Genome ; Hepatitis ; Hepatitis B ; Hepatitis B virus ; Humans ; Immunoglobulins ; Liver ; Liver Cirrhosis ; Liver Failure ; Liver Transplantation ; Middle Aged ; Viral Load

PURPOSE: This study investigated the relationship between the laboratory results of patients diagnosed with lower limb arteriosclerosis obliterans (LASO) in an emergency department (ED), general characteristics, clinical manifestation, hematological conditions, and clinical views of severity. Another purpose of the study was to determine the factors that could contribute to clinical severity to facilitate the prediction and diagnosis of LASO in the ED. METHODS: From January 2005 to December 2012 we conducted a retrospective study on patients diagnosed with LASO in the ED. Included in the study were 52 patients diagnosed with LASO through CT. The patients were divided into two groups according to the Fontaine classification-for comparative analysis: "less severe" (for stage II and below) and "more severe" (for stage III and above). Vital signs, clinical findings, laboratory data, and CT findings were analyzed in each patient. The SPSS package with the Mann-Whitney U test, Fisher's exact test, and logistic regression were used for data analysis. A p-value <0.05 was considered statistically significant. RESULTS: The average age of patients diagnosed with LASO was 73.1+/-10.1 and male saccounted for 76.9% of the population (n=40). Based upon the levels of severity by the Fontaine classification, patients were divided into 28 "more severe" and 24 "less severe" cases. The "more severe" LASO patients showed a high pulse rate (p=0.017) and a higher current smoking rate (p=0.04). The laboratory data from "more severe" LASO patients showed significant differences in total white blood cell count (p=0.040), erythrocyte sedimentation rate (p=0.000), and the levels of lactate dehydrogenase (p=0.002), creatine kinase (p=0.000), creatine kinase-MB (p=0.002), myoglobin (p=0.000), and C-reactive protein (p=0.000). The significant factors that could affect clinical severity were erythrocyte sedimentation rate (OR 1.066, 95% CI 1.010-1.125, p=0.021), and the levels of lactate dehydrogenase (OR 1.015, 95% CI 1.002-1.029, p=0.027), creatine kinase-MB (OR 1.229, 95% CI 1.028-1.468, p=0.023), and C-reactive protein (OR 1.533, 95% CI 1.074-2.188, p=0.019). CONCLUSION: The patients diagnosed with more severe LASO showed a high pulse rate, a higher current smoking rate, high levels of inflammation (erythrocyte sedimentation rate and C-reactive protein), and high levels of muscle enzymes (lactate dehydrogenase, creatine kinase, myogolobin, creatine kinase-MB). The factors that could influence clinical severity were erythrocyte sedimentation rate, and the levels of lactate dehydrogenase, creatine kinase-MB, and C-reactive protein.
Arteriosclerosis Obliterans* ; Arteriosclerosis* ; Blood Sedimentation ; C-Reactive Protein ; Classification ; Creatine ; Creatine Kinase ; Diagnosis ; Emergencies* ; Heart Rate ; Humans ; Inflammation ; L-Lactate Dehydrogenase ; Leukocyte Count ; Logistic Models ; Lower Extremity* ; Male ; Muscles ; Myoglobin ; Oxidoreductases ; Peripheral Arterial Disease ; Retrospective Studies ; Smoke ; Smoking ; Statistics as Topic ; Vascular Diseases ; Vital Signs

PURPOSE: This study investigated the relationship between the laboratory results of patients diagnosed with lower limb arteriosclerosis obliterans (LASO) in an emergency department (ED), general characteristics, clinical manifestation, hematological conditions, and clinical views of severity. Another purpose of the study was to determine the factors that could contribute to clinical severity to facilitate the prediction and diagnosis of LASO in the ED. METHODS: From January 2005 to December 2012 we conducted a retrospective study on patients diagnosed with LASO in the ED. Included in the study were 52 patients diagnosed with LASO through CT. The patients were divided into two groups according to the Fontaine classification-for comparative analysis: "less severe" (for stage II and below) and "more severe" (for stage III and above). Vital signs, clinical findings, laboratory data, and CT findings were analyzed in each patient. The SPSS package with the Mann-Whitney U test, Fisher's exact test, and logistic regression were used for data analysis. A p-value <0.05 was considered statistically significant. RESULTS: The average age of patients diagnosed with LASO was 73.1+/-10.1 and male saccounted for 76.9% of the population (n=40). Based upon the levels of severity by the Fontaine classification, patients were divided into 28 "more severe" and 24 "less severe" cases. The "more severe" LASO patients showed a high pulse rate (p=0.017) and a higher current smoking rate (p=0.04). The laboratory data from "more severe" LASO patients showed significant differences in total white blood cell count (p=0.040), erythrocyte sedimentation rate (p=0.000), and the levels of lactate dehydrogenase (p=0.002), creatine kinase (p=0.000), creatine kinase-MB (p=0.002), myoglobin (p=0.000), and C-reactive protein (p=0.000). The significant factors that could affect clinical severity were erythrocyte sedimentation rate (OR 1.066, 95% CI 1.010-1.125, p=0.021), and the levels of lactate dehydrogenase (OR 1.015, 95% CI 1.002-1.029, p=0.027), creatine kinase-MB (OR 1.229, 95% CI 1.028-1.468, p=0.023), and C-reactive protein (OR 1.533, 95% CI 1.074-2.188, p=0.019). CONCLUSION: The patients diagnosed with more severe LASO showed a high pulse rate, a higher current smoking rate, high levels of inflammation (erythrocyte sedimentation rate and C-reactive protein), and high levels of muscle enzymes (lactate dehydrogenase, creatine kinase, myogolobin, creatine kinase-MB). The factors that could influence clinical severity were erythrocyte sedimentation rate, and the levels of lactate dehydrogenase, creatine kinase-MB, and C-reactive protein.
Arteriosclerosis Obliterans* ; Arteriosclerosis* ; Blood Sedimentation ; C-Reactive Protein ; Classification ; Creatine ; Creatine Kinase ; Diagnosis ; Emergencies* ; Heart Rate ; Humans ; Inflammation ; L-Lactate Dehydrogenase ; Leukocyte Count ; Logistic Models ; Lower Extremity* ; Male ; Muscles ; Myoglobin ; Oxidoreductases ; Peripheral Arterial Disease ; Retrospective Studies ; Smoke ; Smoking ; Statistics as Topic ; Vascular Diseases ; Vital Signs

No abstract available.
Heart ; Pulmonary Embolism ; Thrombosis

BACKGROUND AND OBJECTIVES: Heart rate variability(HRV) reflects the autonomic integration of heart. There were many reports that HRV in patients with myocardial infarction or heart failure is an independent prognostic factor to predict fatal arrhythmia and sudden cardiac death. But, the role of HRV is still controversial in stable angina patients without history of myocardial infarction. In this study, we tried to compare HRV indices between stable angina patients and normal subjects. MATERIALS AND METHODS: Twenty-one stable anginal patients without history of myocardial infarction (mean age : 57 +/- 2 years) and twenty-one relatively healthy persons without history of coronary heart disease (mean age : 53 +/- 2 years) were included in the study and underwent 24-hour ambulatory ECG monitoring. In patients group, all underwent coronary angiography after 24-hour ambulatory ECG monitoring. HRV was analyzed over the whole 24 hours, using time and frequency domain parameters, according to time phases and coronary angiographic severity. RESULTS: There were no significant differences in age, sex and cardiovascular risk factors, except hypertension (p=.001) between two groups. HRV indices such as rMSSD, pNN50, LF, HF, LFnorm and HFnorm were significantly decreased (p<0.05) in patients group. But the angiographic severity of coronary arteries did not show any significant effect on the HRV indices in patients group. CONCLUSIONS: We observed significantly reduced HRV indices in patients with stable angina without history of myocardial infarction.
Angina, Stable* ; Arrhythmias, Cardiac ; Coronary Angiography ; Coronary Disease ; Coronary Vessels ; Death, Sudden, Cardiac ; Electrocardiography ; Heart Failure ; Heart Rate* ; Heart* ; Humans ; Hypertension ; Myocardial Infarction* ; Risk Factors