小儿胰腺实性假乳头状瘤肝转移一例

患儿：女，12岁。脐周腹痛，伴有恶心、呕吐反复发作2年余，加重10d，外院拟“急性胰腺炎”给予禁食、补液、对症支持治疗后症状不缓解，B超及CT示“胰腺占位”，为进一步诊治转入本院，门诊拟“胰腺占位”收入本科。体检：T36．8℃，P84次／min，R20次／min，BP105／70mmHg（1mmHg=0．133kPa），神清，精神可，全身皮肤黏膜无黄染，全身浅表淋巴结无肿大，心肺无异常，全腹平软，剑突下深压痛，无肌卫及反跳痛，     

发热 瘫痪 急性颅内高压

第一次查房 主治医师,入ICU后6h内。 住院医师 汇报病史。患儿,女,15岁。因发热8d、双下肢乏力进行性加重6d急诊入院。伴头痛、频繁呕吐,每日呕吐10余次。既往身体健康,无特殊病史,无急性传染病接触史。查体：T38．5℃,R50次／min,P95次／min,BP123／83mmHg（1mmHg=0．133kPa）,体质量35垤。精神萎靡。颅神经体征（-）,     

益萨林致急性肾功能衰竭1例报告

1病例资料 患儿,男,9岁,因右下腹痛3d在当地医院诊断为“阑尾炎”,给予静脉输注益萨林2．5g／d,共2d。当天即出现全程肉眼血尿,之后迅速无尿,即来我院就诊。入院查：T37．3℃,P90次／min,R24次／min．BP150／120mmHg。精神萎靡,皮肤无黄染。双眼睑无浮肿,双肺呼吸音清晰,未闻及哕音,心音有力。腹软,下腹压痛（＋）,无反跳痛,双肾区扣击痛（＋）。双下肢无浮肿,神经系统检查无异常。     

肝圆韧带巨大淋巴管瘤一例

患儿：女，4岁。因腹痛2d，肛门停止排便1d急诊入院。在外院诊断为肠梗阻，予以胃肠减压，通便补液，抗感染等对症处理，症状无改善，转我院。检查：体温37．3℃，脉搏108次／min，呼吸23次／min，血压85／65mm nHg（1mm Hg：0．133kPa）。急性痛苦面容，蜷曲体位，全腹膨隆，呈不规则形，上腹部较显著，腹肌紧，左下腹有压痛，无反跳痛，叩诊全腹实音，肠鸣音活跃，8次／min。肛门指检：无异常。实验室检查：血常规：白细胞计数17．61×10^9／L，中性粒细胞百分比84．8。急诊生化：正常。腹部平片：左上腹肠管充气扩张，可见短小液平面，未见明显膈下游离气体影，     

干扰素和羟基脲治疗原发性血小板增多症1例

患儿，男，14岁，因胸痛2个月，加剧3d入院。2个月前无明显诱因出现胸痛，为阵发性刺痛，可自行缓解，未治疗。近3d来诊。既往体健，家族中无类似疾病史。入院查体：体温37．2℃，脉搏78次／min，呼吸20次／min，血压120／80mmHg，体质量50kg。营养发育正常，前胸壁可见少许瘀斑，余皮肤未见出血点和发绀，胸骨无压痛，全身浅表淋巴结不大，心肺无异常，腹平软，肝肋下2cm，     

小儿非结石性急性坏疽性胆囊炎一例

患儿：男，7岁。阵发性上腹痛12h伴呕吐以急性胰腺炎诊断收住院。入院前12h无诱因出现上腹部阵发性疼痛，伴恶心呕吐，呕吐物为胃内容物，不含胆汁及血性物，腹痛缓解时尚有饥饿感。体检：患儿活动自如，检查时合作。T37．4℃，P104次／min，R26次／min，Bp100／65mmHg。巩膜无黄染，心肺听诊正常，腹部稍胀，无胃肠型，呼吸运动不受限，全腹未触及包块，胆囊及上腹均     

以阵发性腹痛为主要表现的肺吸虫病一例

患儿,女,8岁,于2003年10月12日入院。主诉反复腹痛1个月,表现为阵发性脐周疼痛,较剧烈,数分钟能自行缓解,无放射痛,与进食无关,无恶心、呕吐,无发热、畏寒,无腹泻、便血,每周腹痛发生3～4次。当地医院以“慢性胃炎”治疗多次,但疗效不明显,入院前2d于进食辛辣食物后再次腹痛,遂转诊本院。患儿既往体健,无类似疾患史。查体：体温37．0℃,心率98次／min,呼吸25次／min,血压88／59mmHg（1mmHg=0．133kPa）,精神可,神志清,面色略苍白,心肺听诊无特殊,全腹平软,肝脾肋下均未触及,未及包块,全腹无压痛,反跳痛,肠鸣音正常,全身皮肤无结节及包块。入院初步诊断：腹痛待查。     

急性间歇性卟啉病一例

患儿女 ,8岁 ,因腹痛 ,呕吐 1周入院。 1周来无诱因腹痛 ,呈发作性、程度不等的绞痛 ,剧烈时不能忍受 ,伴频繁呕吐胃内容物。家族中无类似疾病史。入院体检 :BP 1 0 3/ 71mmHg(1mmHg =0 .1 33kPa) ,R 30次 /min ,P 1 0 0次 /min ,T 37.2℃ ,精神萎糜 ,面苍白 ,对答切题 ,颈无抵抗 ,心肺未见异常。腹平坦 ,全腹均有压痛 ,无反跳痛及肌紧张 ,肝脾未触及肿大 ,肠鸣音活跃。腹部B超检查无异常发现 ,外周血、小便化验无异常。脑电图检查示 :轻～中度异常脑电图 (慢波增加 ,α波减少 )。初步诊断为腹型癫 ,开始予苯巴比妥钠片 50mg口服 3次 …     

腺病毒感染致儿童急性出血性膀胱炎1例

患儿,男,3岁,于入院前2d无明显诱因出现终末肉眼血尿,伴有血凝块,尿频、尿急、尿痛明显,无发热、咳嗽、流涕,无呕吐、腹泻。入院查体：发育正常,神志清楚,精神好,眼睑及全身无水肿,咽部无充血,双肺呼吸音清晰,未闻及干湿性啰音,心率80次／min,律齐,心音有力,各瓣膜听诊区未闻及杂音,腹平软,下腹部压痛明显,双肾区无叩击痛,尿道口无发红。尿常规：红细胞950个／HP,白细胞2个／HP,尿蛋白( )。两次尿相差镜检红     

小儿臀部骨化性肌炎一例

患儿：女，8岁。右侧臀部疼痛10余天，不敢行走来院。患儿自发病无发热，亦无明显外伤史。体检：T37℃、P85次／min、R20次／min、BP12／8kPa(1kPa=0．133mmHg)、体重19kg。发育营养正常，头颈心肺腹正常。右下肢活动受限，臀部肿胀、压痛明显，局部皮肤不红，触之无波动。髋关节功能受限，     

Acute glomerulonephritis

Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately severe poststreptococcal AGN (PSAGN) the above-mentioned features are present However, gross or microscopic hematuria may be the only abnormality. A similar picture may occasionally be produced by a variety of infections (when GN is referred to as post-infectious and the mechanism of glomerular damage and the renal histology are similar to that in PSAGN), primary renal glomerular disorders (eg. membranoproliferative GN, IgA nephropathy), collagen vascular diseases (systemic lupus erythematosus), systemic vasculitis (Henoch Schonlein purpura) and hereditary nephritis and some nonglomerular conditions. PSAGN may also present with one or more of its complications such as profound volume expansion with heart failure and hypertensive encephalopathy. PSAGN resolves rapidly and has an excellent prognosis. Patients with severe renal involvement and life threatening complications need expert supportive management. AGN with associated systemic features or very pronounced azotemia, nonstreptococcal AGN and unresolving GN need prompt, appropriate evaluation that often includes a renal biopsy. If extensive crescentic changes are found (crescentic GN), aggressive immunosuppression will be necessary.     

Acute myocarditis

Myocarditis is defined as inflammation of the myocardium accompanied by myocellular necrosis. Acute myocarditis must be considered in patients who present with recent onset of cardiac failure or arrhythmia. Often there is a history of an antecedent flu-like illness. Fulminant myocarditis is a distinct entity characterized by sudden onset of severe congestive heart failure or cardiogenic shock, usually following a flu-like illness. Giant cell myocarditis is a rare, frequently fatal disorder of unknown origin characterized by presence of giant cell inflammatory infiltrate in the myocardium. In recent years we have made good progress in understanding the causes, pathogenesis, natural history, diagnosis, and treatment of myocarditis. However, our knowledge is still far from complete. New information that extends our understanding of myocarditis is being reported constantly. This review summarizes recent advances in myocarditis, with an emphasis on the literature during the last year.