BACKGROUND: The apnea test is an essential component in the clinical determination of brain death, however it may incur a significant risk of complications such as hypotension, hypoxia and even cardiac arrest. We analyzed the risk factors associated with a failed apnea test during brain death assessment in order to predict and avoid these adverse events. METHODS: Medical records on apnea tests performed for brain-dead donors at our institution between January 2009 and January 2016 were retrospectively reviewed. Age, gender, etiology of brain death, use of catecholamines and results of arterial blood gas analysis (ABGA), systolic/diastolic blood pressure (SBP/DBP), mean arterial pressure and central venous pressure prior to apnea test initiation were collected as variables. A-a gradient and P(aO2)/F(iO2) were calculated for more precise assessment of the respiratory system. In total, 267 cases were divided into two groups based on those who completed the apnea test and those who failed the test. RESULTS: 13 cases failed the apnea test. Among them, seven cases failed due to severe hypotension (SBP < 60 mmHg) and the others failed due to refractory hypoxia. In terms of hemodynamic state, SBP was significantly higher in the completed test group than the failed group (126.5 ± 23.9 vs. 103 ± 15.2, respectively; p = 0.001). In ABGA, the completed test group showed significantly higher P(aO2)/F(iO2) (313.6 ± 229.8 vs. 141.5 ± 131.0, respectively; p = 0.008) and a lower A-a gradient (278.2 ± 209.5 vs. 506.2 ± 173.1, respectively; p = 0.000). In multivariable analysis, low SBP (p = 0.003) and high A-a gradient (p = 0.044) were independent risk factors associated with a failed apnea test. CONCLUSIONS: Although the unexpected adverse events during the apnea test for brain death determination do not occur frequently, they can be fatal. If a brain-dead patient has low SBP and a high A-a gradient, clinicians should pay more attention and prepare for potential complications prior to the apnea test.
Anoxia ; Apnea* ; Arterial Pressure ; Blood Gas Analysis ; Blood Pressure ; Brain Death* ; Brain* ; Catecholamines ; Causality ; Central Venous Pressure ; Heart Arrest ; Hemodynamics* ; Humans ; Hypotension ; Medical Records ; Respiratory System ; Retrospective Studies ; Risk Factors ; Tissue Donors

The funding acknowledgment in this article was omitted.

No abstract available.
Calcinosis* ; Heel* ; Humans ; Infant*

PURPOSE: The incidence of clinical nephritis is much higher especially in younger ages and in about one half of the cases, it also shows nephrotic syndrome. Thus, we examine the clinical and pathologic consideration of children with lupus nephritis and their treatment modality to improve the prognosis. MATERIAL AND METHOD: Among 67 cases of children under eighteen who were diagnosed SLE, 50 patients with hematuria and proteinuria from Jan. 1980 to Dec. 1996 were selected for the review. RESULTS: The ratio of the male to female patient was 1:3.5 and the average age at the diagnosis was 11.85+/-3.2 years old. Most common clinical manifestations at the time of the diagnosis were fever and skin rashes and the common laboratory results were proteinuria, hematuria, Out of 50 cases, 33 cases had renal biopsy. The results were 17 cases of Class IV, 7 cases of Class lll, 5 cases of Class lll, 3 cases of Class V and 1 case of Class l. Different treatment modalities were carried out; Corticosteroid only 21 cases, Corticosteroid+Azathioprine 25 cases, Corticosteroid+Cyclophosphamide 3 cases, and Corticosteroid+Cyclosporine A 1 case. However, there were no significant difference in the recurrence and complete remission rate of lupus nephritis in between each treatment groups. Average follow-up period was 37+/-23 months. Of all the follow-ups, 7 patients were dead. CONCLUSION: Early diagnosis should be carried out with renal biopsy, and should be considered for vigorous therapy, which currently includes high doses of corticosteroids and immunosuppressive drugs. Among these immunosuppressive agents, azathioprine has a lower incidence of long-term complications and low costs might be recommended. In addition, regular check-up for anti-DNA antibody, serum complement concentration and appropriate moniroting and management for the adverse effects of the treatment should enable to reach the continuous remission.
Adrenal Cortex Hormones ; Azathioprine* ; Biopsy ; Child* ; Complement System Proteins ; Diagnosis ; Early Diagnosis ; Exanthema ; Female ; Fever ; Follow-Up Studies ; Hematuria ; Humans ; Immunosuppressive Agents ; Incidence ; Lupus Nephritis* ; Male ; Nephritis ; Nephrotic Syndrome ; Prognosis ; Proteinuria ; Recurrence

No abstract available.
Dermoscopy* ; Diagnosis

BACKGROUND: A majority of patients undergoing chemical peeling complain of pain severe enough to disturb the process of the peeling. However, there has been few controlled studies on pain control during chemical peeling. OBJECTIVES: We evaluated the efficacy and safety of pretreatment with intramuscular ketorolac (Tarasyn, 30 mg) and oral diazepam(Valium, 5 mg) in comparison with control and diazepam groups, and compared the sensitivity of pain between two sexes. METHODS: The patients were randomly assigned to one of three groups; control, diazepam, and ketorolac plus diazepam groups. Pain intensity was assessed 5 times at every ten minutes from the beginning of the peeling using visual analog scale(VAS). RESULTS: At every 10 minutes of pain assessment, ketorolac plus diazepam group recorded the lowest VAS among the three groups. Except at the first 10 minutes, nificant. There was no significant difference in the pain intensity between the sexes at all five times. After application of Jessner`s solution, there was significant increase of VAS in all groups. CONCLUSION: The ketorolac pretreatment is a safe and effective modality of pain relief prior to chemical peeling without the adverse reactions.
Diazepam ; Humans ; Ketorolac* ; Pain Measurement ; Premedication*

Even though the nonketotic hyperglycemia is a metabolic disorder, it complicates hemic- horea-hemiballism rarely. Moreover, generalized chorea-ballism associated with nonketotic hyperglycemia in diabetes mellitus is very rare, so it has not been reported in Korean literature. Although the precise pathophysiologic mechanisms of these disorders are still poorly understood, deficiency of gamma aminobutyric acid (GABA) in nonketotic hyperglycemia or reduced GABAnergic inhibition by striatal lesion may increase inhibitory output to subthalamic nucleus. These result loss of pallidal inhibition and produce contralateral hemichorea-hemiballism. The striatal lesions, such as transient ischemia with reactive astrocytosis or small amount of petechial hemorrhage, are related with changes of magnetic resonance image (MRI) findings presumably. We report a diabetic old woman who developed generalized chorea-ballismus as a very rare complication of nonketotic hyperglycemia. Her brain MRI showed high signal intensity in left lentiform nucleus and right pallidum on T1 weighted images and low signal intensity in bilateral putamen on T2 weighted images with highly enhanced corresponding lesions on T1 weighted enhancement images.
Brain ; Corpus Striatum ; Diabetes Mellitus* ; Female ; gamma-Aminobutyric Acid ; Gliosis ; Hemorrhage ; Humans ; Hyperglycemia* ; Ischemia ; Magnetic Resonance Imaging ; Putamen ; Subthalamic Nucleus

The complement system is known to be involved in the pathogenesis of the skin lesions in pernphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis, epidermolysis bullosa acquisita, and systemic lupus erythematosus. Authors examined the skin specimens of each disease cases, who did not show any evidence of complement deficiency, to determine the deposition of complement components(C4, C3, Chb-9) and their inhibitors(C4bp, Factor H, S-protein) by modified direct immunofluorescence. We also looked at the staining pattern and localization, for further insights of their pathobiologic contributions in each disease. The findings of deposits of complement components up to C9, as well as inhibitor proteins at the primary histopathologic sites, in the majority of those cases, may indicate that the complement system, to certain extent, involves the inflamrnatory reactions in these diseases. The co-localization of C5b-9 and S-protein could be regarded as the consequence of in situ formation of SC5b-9 complexs or as the result of non-lytic adsorbed complexes of fluid phase SC5b-9. The pathologic role of the complement seems to depend mostly on the complement-fixing biologic property and the amount of the tissue bound immune complexes, which are often heterogeneous to different diseases and among different patients.
Antigen-Antibody Complex ; Complement Factor H ; Complement Membrane Attack Complex ; Complement System Proteins* ; Dermatitis Herpetiformis ; Epidermolysis Bullosa Acquisita ; Fluorescent Antibody Technique, Direct ; Humans ; Lupus Erythematosus, Systemic ; Pemphigoid, Bullous ; Skin ; Skin Diseases*

Pathological laughing and crying(PLC) is a condition that is characterized by episodic, brief, contextually inappropriate, uncontrollable outbursts of laughing and/or crying. It can be observed in patients with various neurological disorders. PLC often causes distress in interpersonal functioning and activities for patients and their families. PLC can be recognized easily with proper understanding of the condition and its nature. Also it generally shows good response to various pharmacological treatments. This review aims to encourage the diagnosis and treatment of PLC by providing definition and clinical presentation of PLC, analysis of its pathophysiology and various current treatment options.
Crying* ; Diagnosis ; Humans ; Nervous System Diseases