九华痔疮栓治疗肛裂致过敏性休克

1例17岁女性,因肛裂使用九华痔疮拴治疗.在首次用药后2～3 min,患者突然出现全身瘙痒、嘴唇肿胀,皮肤出现大小不等的风团.立即就诊,给予地塞米松10 mg肌内注射,50%的葡萄糖注射液20 ml+10%葡萄糖酸钙10 ml静脉推注,并给予开塞露20 ml将痔疮栓排出.之后患者出现全身无力,意识模糊.查体:P 108次/min,R 30次./min,BP 70/48 mm Hg.立即肌内注射0.1%肾上腺素0.3 ml和静脉补液.4 h后症状完全消失,P 70次/min,R 18次/min,BP 120/80 mm Hg.患者痊愈出院.     

静脉注射氟比洛芬酯致过敏反应2例

1病历摘要例1:男,70岁,体重40kg。因胃癌术后肝转移收住入院,患者入院时BP100/60mm Hg,HR72次/min,消瘦,恶病质状态,腹部疼痛难忍,口服曲马多效果欠佳。应用氟比洛芬酯注射液50mg静脉注射,静脉注射过程中,患者出现胸闷、憋气、呼吸困难,HR120次/min,BP80/40mm Hg,立即通知医生,停用氟比洛芬酯,换输生理盐水,遵医嘱给予氧气吸入,静脉注射地塞米松10mg,肌内注射盐酸异丙嗪50mg,5min后患者症状缓解,BP90/60mm Hg,HR80次/min,呼吸平稳。例2:女,65岁,体重70kg。乳腺癌术后行第六次巩固化疗,患者入院时BP110/70mm Hg,HR76次/min,WBC1.6×109/L,应用瑞白300μg皮下注射,1次/d,2d后出现全身疼痛,遵医嘱给予氟比洛芬酯注射液50mg静脉注射,5min后,患者出现皮肤瘙痒,恶心呕吐,呼吸急促,BP150/100mm Hg,HR110次/min,立即通知医生,遵医嘱给予吸氧,静脉注射地塞米松5mg,肌内注射盐酸异丙嗪25mg,肌内注射甲氧氯普胺20mg。患者10min后症状缓解,BP120/80mm Hg,HR...     

抢救蜂蜇伤致过敏性休克1例

患者,男,26岁。左颈部被蜂蜇伤3min 后感头晕、胸闷、心悸、恶心,20min 后送至我院。查体：T 36℃,R 26次/ min,P 124次/ min,HR 124次/ min,BP 66/40mm Hg,意识尚清,呈昏睡状,面色苍白,四肢湿冷,眼睑及口唇明显肿胀,呼吸急促,双肺闻及散在哮鸣音,心音低钝。左颈部可见一个淤点,其周围潮红肿胀,全身密布红色风团,尤以面部、颈部、胸部为重。诊断：蜂蜇伤致过敏性休克。立即给予吸氧,肾上腺素1mg 皮下注射,地塞米松注射液10mg,维生素 C 注射液2.0g 加入10%葡萄糖50ml 中静脉推注,异丙嗪注射液50mg 肌内注射,35min后患者逐渐恢复意识,症状消失,生命体征平稳。4h 后再次出现过敏性休克症状,查体：R 26次/ min,P 128次/ min,BP 60/30mm Hg,诊断：迟缓相 I 型变态反应致过敏性休克。立即给予地塞米松10mg 静脉推注,肾上腺素1mg 皮下注射,异丙嗪50mg 肌内注射,同时给予氢化可的松300mg 静脉滴注及吸氧等治疗,并做好气管插管准备。40min 后上述症状明显缓解,生命体征平稳,住院巩固治疗2d 后痊愈出院。     

头孢美唑钠停用1个月后再次使用出现过敏反应

1例57岁肝炎后肝硬化男性患者因腹腔感染给予头孢美唑钠2 g溶于5%葡萄糖100 ml中静脉滴注.滴注结束后约5 min,患者突然出现寒颤、胸闷.查体:P 130次/min,R 24次/min,BP 130/70 mm Hg,血氧饱和度0.95,双肺呼吸音粗.立即给予吸氧,静脉给予地塞米松2 mg和10%葡萄糖酸钙.40 min后患者症状缓解.2.5 h后,患者P 96次/min,R 22次/min,BP 110/70 mm Hg.追踪病史示患者在1个月前曾静脉滴注头孢美唑钠2 g,2次/d,共15 d,未见不良反应.     

荧光素钠注射液过敏性休克致醒状昏迷

1例68岁女性糖尿病性视网膜病变患者,为行眼底血管造影检查使用1%荧光素钠注射液5 ml静脉注射行过敏试验.静脉注射后3 min,患者出现呼吸困难,意识不清,BP 40/20 mm Hg,心跳停止1 min.立即给予肌内注射异丙嗪50 mg,地塞米松10 mg,肾上腺素1 mg治疗.后来查体:P 124次/min,BP 147/81 mm Hg,患者处于醒状昏迷.住院175 d后,患者以醒状昏迷出院.     

昂丹司琼引起过敏性休克

1例50岁肺腺癌男性患者化疗前为预防呕吐给予奥美拉唑40 mg静脉滴注,以及昂丹司琼8 mg静脉滴注.昂丹司琼滴注约15 min时,患者前胸和双臂出现皮疹.停用昂丹司琼,给予地塞米松和异丙嗪治疗.40 min后皮疹遍及全身,继之出现视物模糊、出冷汗、胸闷、乏力、脉搏弱及心音低.查体:HR 75次/min,BP 50/40 mm Hg.给予吸氧、皮下注射肾上腺素、静脉推注地塞米松及静脉滴注多巴胺治疗.患者症状缓解,5 h后生命体征平稳.     

甲氧氯普胺致锥体外系反应

1例42岁女性患者,因患急性胃肠炎给予口服甲氧氯普胺10 mg,3次/d;阿莫西林1.0 g,3次/d.首次服药30 min后,患者出现四肢不自主运动,行走困难,头颈向左扭转,下颌偏斜,吐舌,语言含糊.查体:T 36.5℃,P 96次/min,R 24次/min,BP 100/70 mm Hg,神志清楚,反应迟钝,面具脸,头颈向左侧扭转,双侧腱反射亢进,病理反射阴性.考虑为甲氧氯普胺所致锥体外系反应,立即给予阿托品1 mg肌内注射,地西泮5 mg肌内注射.30 min后上述症状逐渐消失.停服甲氧氯普胺,继续服用阿莫西林,上述症状未再出现.     

破伤风抗毒素脱敏注射致过敏性休克

1例22岁的男性患者,因右额部外伤行清创缝合术,术后由于破伤风皮试结果为阳性,给予破伤风抗毒素(TAT)常规脱敏注射.第1次肌内注射TAT 150 U,15 min后患者躯干出现微痒感,无皮疹.第2次肌内注射TAT 300 U,后约2 min,患者出现头昏、视力模糊、胸闷.立即给予平卧.查体:T 37.5℃,P 74:K/min,R 20;K/min,BP 40/20 mmHg;神志清楚,面色苍白,四肢发冷;心音低钝,HR 74;K/min.诊断为过敏性休克.立即吸氧,并给予肾上腺素、异丙嗪、山莨菪碱、地塞米松、葡萄糖酸钙、低分子右旋糖酐和碳酸氢钠.5 h后患者恢复正常.     

复方丹参注射液致过敏性休克1例分析

对复方丹参注射液致过敏性休克1例分析如下。1病历摘要男,72岁。因阵发性胸骨后疼痛17a,加重1d,门诊以冠心病、心绞痛、陈旧性心梗收入院。既往无药物过敏史。入院时T36℃,P76次/min,R20次/min,BP120/75mm Hg,神志清醒,痛苦面容,心音低钝,偶发早搏。入院后,予以输氧、扩血管、改善微循环等治疗,并每日静脉滴注复方丹参注射液8ml+5%葡萄糖注射液500ml,患者自觉症状明显改善。患者住院第8天的第1项治疗为静脉滴注复方丹参注射液一组液体,在输液20min后患者突然出现腰部酸痛、头痛、寒颤、脉细弱。查体:T39.2℃,P121次/min,BP150/75mm Hg。考虑为输液反应,立即停止补液,予以复方氨基比林2ml、654-210mg、非那根25mg、地塞米松10mg肌内注射,吸氧,但病情未被控制,患者出现神志恍惚,呼吸急促,血压下降,面色苍白,手足厥冷,查体示BP75/45mm Hg,P135次/min,R30次/min,立即按过敏性休克抢救,予以抗组胺药、糖皮质激素及升压药抢救2d后,症状得以控制,但低血压仍持续数日后方恢复正常。2讨论复方丹参注射液是由丹参、降香2味中药经提取加...     

注射用阿奇霉素致过敏性休克1例

1 病例患者,女,25岁,体质量:48 kg.因咳嗽、咯黄脓痰持续3 d来院就诊,初步诊断为急性支气管炎.查体T:36.2℃,R:20次/min,P:70次/min,BP:110/75 mm Hg.给予注射用阿奇霉素0.25 g加入5%GS 250 mL中,40滴/min,静脉滴注.滴入约30 mL时,患者出现眩晕、耳鸣,伴恶心、呕吐,诉心悸.测T:36℃,R:17次/min,P:88次/min,BP:90/60 mm Hg,诊断为过敏性休克.立即停止输液,给氧气3 L/min,进行心电监护,同时给予甲强龙40 mg静脉注射,肾上腺素0.5 mg静脉注射,症状缓解不明显,又给予甲强龙80 mg加入0.9%氯化钠注射液250 mL中静脉滴注,维生素B6 0.2 g加入5%GNS 500 mL中静脉滴注.15 min后,T:36℃,R:19次/min,P:75次/min,BP:100/65 mm Hg,患者生命体征趋于平稳.     

Study of a microencapsulation process of a virucide agent by a solvent evaporation technique

Abstract

A highly water-soluble virucide agent was microencapsulated by a water/oil/water emulsification-solvent evaporation method. An aqueous drug solution was emulsified into a solution of polymer in methylene chloride, followed by emulsification of the primary emulsion in an external aqueous phase. Microcapsules were formed after solvent evaporation, the solidification of the microcapsule walls was followed by an optical method. The influence of stirring speed was analysed to find the optimal hydrodynamic conditions with respect to the process yield, corresponding to the weight of obtained microcapsules per litre of water/oil/water emulsion, the initial virucide agent content and the drug release kinetics. The optimal conditions were obtained for the complete suspension speed. The improvement of the microencapsulation process was attempted by increasing the concentration of the primary emulsion and by the reuse of the external aqueous phase after removal of the microcapsules.     

Community pharmacy as a performance: a participant observer's account of a day in the life of a locum

Objective — To understand, from a dramaturgical viewpoint, the performance of “community pharmacy.” Method — Participant observation supported by focus groups and semistructured interviews; the study adopted a grounded theory approach. Setting — Fieldwork was conducted within 21 community pharmacies in East Anglia, England. Key findings — Pharmacists identify with their setting and stage props. On the stage of community pharmacy, the pharmacist crucially converts the drug into medicine, during a complex and well‐rehearsed performance. There are sometimes distractions, which make the performance sub‐optimal. Other insights included what counts as error, how to manage stress, and the fact that the trust on which professional practice rests is at stake when expressive performance fails. Conclusion — It is possible to conduct ethnography of community pharmacy and this is among the first such studies of British community pharmacy. Were the pharmacist to leave the stage and its props (the drugs), only to advise patients on medicines, the performance of community pharmacy, as we know it, might disappear.     

Amelioration of sulfur mustard skin injury following a topical treatment with a mixture of a steroid and a NSAID

The ability to ameliorate sulfur mustard (HD)-induced oedema by treatment with anti-inflammatory drugs was reported previously after screening four steroids and four non-steroidal anti-inflammatory drugs (NSAIDs) using the mouse ear vesicant model. Following the screening study, one steroid and one NSAID (Adexone and Voltaren) were selected as the most effective, and a mixture of the two was chosen for the present more extensive research. The effect of the combined treatment on clinical, biochemical and histopathological parameters following HD insult was studied. Mice ears were exposed to 0.2 micro l of HD for 10 min to produce a moderate skin injury. Oedema development peaked ca. 48 h following exposure, as determined by weighing ear biopsies. Histological observations at that time exhibited damage to the epidermis and dermis. An increase in prostaglandin E (PGE) was measured in skin homogenates, starting 8 h following exposure and lasting at least up to 48 h post-exposure. A topical treatment using the above anti-inflammatory mixture significantly reduced inflammatory parameters when applied up to 4 h following exposure. These parameters included extent of oedema, levels of PGE, area of clinical damage and extent of cytotoxic injury (vesications and damaged epithelial cells). Thus, a combination of a steroid and NSAID was found to be effective in reducing the intensity of HD skin injury and possibly shortening the time to full recovery. The treatment, however, did not prevent completely the ensuing cytotoxic processes in the epithelial layer.     

Occurrence of a new cephalosporoate in a culture broth of a Cephalosporium acremonium mutant.

A new metabolite was isolated from the culture filtrate of a deacetylcephalosporin C-producing mutant, derived from Cephalosporium acremonium ATCC 14553, by means of adsorption on activated carbon, column chromatography on DEAE-Sephadex A-25 and gel filtration through a Sephadex G-10 column. The compound was identified as D-5-amino-5-carboxyvaleramido-(5-formyl-4-carboxy-2H, 3H, 6H-tetrahydro-1, 3-thiazinyl) glycine by spectral analyses, elucidation of hydrolysis products of the compound, and comparison of characteristics of the compound with those of a synthetic authentic compound.     

Role of a pharmacist in a seizure clinic

The involvement of a clinical pharmacist in a Department of Veterans Affairs seizure clinic is described. A pharmacist who had served a residency in ambulatory care began working in a seizure clinic in 1988 after obtaining the cooperation of a neurologist interested in a multidisciplinary approach to patient care. A clinical protocol was developed to guide the pharmacist's participation. The seizure clinic is staffed by the clinical pharmacist, a pharmacy resident, and a neurologist and is currently treating 162 adult male veterans. Of the 162 patients, 159 are receiving anti-convulsant therapy. The role of the pharmacist is to assist the neurologist in providing patient-care services. The pharmacist interviews each patient, performs a neurological assessment and mental status evaluation, and orders laboratory tests. Information is recorded by the pharmacist on a history form and a subjective and objective assessment and planning form. The pharmacist presents the findings to the neurologist, and the patient is then interviewed jointly by the pharmacist and the neurologist. Between appointments, the pharmacist follows up on abnormal laboratory test values and informs patients of any necessary dosage adjustments. More time is available for patient care, there has been an increase in the detection of adverse drug reactions and disease states, and record keeping has improved. A pharmacist assumed a primary-care role in a seizure clinic by interviewing and assessing patients, ordering laboratory tests, and participating in the selection and adjustment of anticonvulsant therapy.