Minoxidil in severe hypertension

Summary Minoxidil is a potent anti-hypertensive drug which acts on the peripheral arteriolar smooth muscle. It was administered to 14 patients with severe hypertension where standard therapy failed to control the blood pressure. The mean initial blood pressure was 209/129 when receiving treatment. Minoxidil was given in doses varying from 7.5 to 40 mg (mean = 24 mg) and was associated with propranolol (mean dose = 170 mg) and furosemide (mean dose = 120 mg). Twelve patients had an adequate therapeutic response. The systolic blood pressure was reduced by 44 mm Hg which represents a 23±3% reduction and the diastolic blood pressure was reduced by 33 mm Hg which represents a 26±3% reduction. Two patients were considered treatment failures and two patients died during Minoxidil treatment. Three patients showed electrocardiographic changes caracterized by T wave inversion at the onset of Minoxidil treatment and these changes were reversible in two. All patients except two had hirsutism and two women developped polymenorrhea. Other side effects consisted of tachycardia and weight gains. One patient with lupus erythematodes had an exacerbation of her disease while on Minoxidil. Minoxidil represents a useful and effective adjuvant to the treatment of resistant hypertension. It can delay bilateral nephrectomy in patients with terminal renal failure and high blood pressure.     

Neutrophil function in severe sepsis

Sepsis and septic shock continue to be a major cause of morbidity and mortality in critically ill patients. During the onset of sepsis, several inflammatory mediators, including cytokines, chemokines and nitric oxide are released systemically and mediate most of the pathophysiological events present in sepsis and septic shock, such as cardiovascular dysfunction and target-organ lesions. Polymorphonuclear leukocytes are critical effector cells during the inflammatory process and their migration to the infection focus is extremely important for the local control of bacterial growth and consequently for the prevention of bacterial dissemination. In experimental models and in human sepsis a profound failure of neutrophil migration to the infection focus is observed. It seems that the failure of neutrophil migration is dependent on toll-like receptor 4 (TLR4) and mediated by cytokines and chemokines, which induce the production of nitric oxide that inhibits neutrophil adhesion to venular endothelium and also the neutrophil chemotactic ability.     

Antibiotics in severe acute pancreatitis

Acute pancreatitis (AP) is a local inflammatory response with systemic effects and an adverse evolution in 20% of cases. Its mortality rate is 5–10% in sterile and 15–40% in infected pancreatic necrosis. Infection is widely accepted as the main reason of death in AP. The evidence to enable a recommendation about antibiotic prophylaxis against infection of pancreatic necrosis is conflicting and difficult to interpret. Up to date, there is no evidence that supports the routine use of antibiotic prophylaxis in patients with severe AP. Treatment on demand seems to be the better option, avoiding excessive treatment and selection of bacterial. In infected acute pancreatitis, antibiotics of choice are imipenem, meronem or tigecycline in patients allergic to beta-lactams. Also fluconazole must be given in determinate clinical situations.     

Adrenal function in acute severe asthma

Adrenocortical function was assessed by the intravenous short synacthen test in 22 control subjects and 68 patients admitted to hospital with acute severe asthma. The cortisol increment was subnormal in 19 of the 68 asthmatics. This included 11 of the 14 patients on continuous oral steroids, seven of the 29 patients who had had occasional courses of oral steroids, one of the seven on inhaled steroids only, and none of the 18 who had had no steroids. Adrenal suppression was greatest in those patients taking oral steroids in divided daily doses. Nineteen of 43 patients were on or had taken oral steroids in this fashion. Of those 19 patients with low cortisol increments only one half had received supplementary steroids in the 24 hours preceding admission. Based on the synacthen test, serum DHEA-SO4 values were not a good discriminant of adrenocortical function. Adrenal insufficiency may be an important cause of death in acute severe asthma in New Zealand.     

Ticarcillin-clavulanic acid therapy in severe infections

Twenty patients with severe infections were treated with a fixed combination of ticarcillin + clavulanic acid. Nineteen of them had severe underlying diseases. Fifteen were bacteraemic; four of these were in shock. Eleven were infected with microorganisms resistant in vitro to ticarcillin. Eleven were clinically cured, 6 improved and 3 failed to respond, the latter being infected with ticarcillin-resistant microorganisms (2 E. coli, 1 P. mirabilis). Six patients experienced side-effects, which were usually mild and reversible, consisting mainly of moderate elevation of serum transaminases. In one patient ticarcillin-clavulanic acid was stopped due to worsening of a pre-existing drug hepatitis.     

经内镜手术治疗急性重症胰腺炎140例临床分析

目的 探讨经内镜治疗急性重症胰腺炎的价值.方法 采用内镜乳头括约肌切开术+鼻胆管引流术或鼻胰管引流术治疗急性重症胰腺炎140例(内镜组),按血淀粉酶恢复正常时间、腹痛消失时间、外科手术率、病死率、并发症等指标评估疗效,并与常规治疗的124例急性重症胰腺炎(对照组)相比较.结果 内镜组和对照组血淀粉酶恢复正常时间分别为(3.2±1.5)d和(6.6±1.2)d,腹痛消失时间分别为(3.1±1.6)d和(7.5±1.8)d,外科手术率分别为0.7%(1/140)和6.5%(8/124),病死率分别为0.7%(1/140)和7.3%(9/124),并发症发生率分别为3.6%(5/140)和41.9%(52/124),两组比较差异有统计学意义(P<0.01、P<0.01、P<0.05、P<0.01、P<0.01).结论 内镜乳头括约肌切开术+鼻胆管引流术(或鼻胰管引流术)对急性重症胰腺炎疗效确切,可作为急性重症胰腺炎的常规治疗手段.     

Assisted ventilation in severe childhood asthma

Our experience of assisted ventilation in severe childhood asthma over a three year period is reviewed. One per cent of children with an acute attack of asthma required ventilatory support during this time. There were no deaths and no long term sequelae resulting from assisted ventilation. The number of children requiring this type of management however, provides further evidence to support the thesis that asthma is not only common but severe in New Zealand.     

重度溃疡性结肠炎的治疗进展

重度溃疡性结肠炎治疗的基本原则为激素冲击疗法。随着对其发病机制理解的深入,涌现出不同的治疗方法和新型制剂,本文就其治疗进展进行综述。     

重度产后出血的介入治疗

目的 评价重度产后出血经导管动脉栓塞（TAE）治疗的可行性及安全性.方法 29例重度产后出血患者,采用Seldinger穿刺技术,选择双侧子宫动脉插管,DSA明确出血位置后以明胶海绵颗粒栓塞.结果 插管成功率100％,术后止血有效率100％,手术时间30～50min.结论 TAE创伤小、疗效好、恢复快、无严重并发症,应作为严重产后出血首选的治疗方法.     

Exchange transfusion in severe infant salicylism

We used exchange transfusion as an alternative to hemodialysis in an infant with severe salicylism. A 4-mo old, 5 kg male was presented to a local hospital with acute vomiting, tachypnea, hyperpnea and intermittent agitation and lethargy. Shortly after a generalized tonic-clonic seizure he passed several tablets in his stool. Salicylate (ASA) level was 85 mg/dL. He was transferred to our institution for further management: i.v. fluids, activated charcoal, whole bowel irrigation and supplementation with sodium bicarbonate, potassium and calcium. The patient's mental status and gas exchange deteriorated and he was intubated. Despite large amounts of sodium bicarbonate and potassium, severe hypokalemia, anion gap metabolic acidosis and aciduria persisted for 10 h. The small size of the infant precluded use of hemodialysis. An exchange transfusion using 180 mL/kg packed red blood cells reconstituted in fresh frozen plasma was performed. The pre-exchange transfusion ASA level was 70.1 mg/dL; the post-exchange transfusion ASA level was 34.4 mg/dL. There was rebound elevation of ASA to 35.2 mg/dL at 6 h post-exchange transfusion. The 18, 36 and 48 h post-exchange transfusion ASA levels were 20.2, 6.8 and < 2 mg/dL respectively. The ASA level dropped 17.6% before, 41.9% in 8.5 h during, and 40.5% by 48 h after the exchange transfusion. There were no complications. The patient recovered completely to his pre-morbid state. Double volume exchange transfusion was used safely as an effective alternative to hemodialysis in this case of severe infant salicylate poisoning.     

Role of chemokines in severe asthma

The severe asthma phenotype is exhibited by a subset of asthma patients whose asthma symptom is poorly controlled by current therapies. Severe asthma represents a high unmet medical need and warrants research into the mechanisms driving the underlying pathophysiology. It is hypothesized that the underlying pathology associated with severe asthma is driving the symptoms experienced by these patients, which may share common features with mild to moderate asthma or may represent a unique pathological phenotype. For the purpose of this review, the pathophysiology associated with asthma in general are described and extended to incorporate severe asthma. Chemokines may contribute towards multiple features of asthma pathophysiology and this current review focuses on the biology of chemokines pertaining to asthma pathophysiology. Chemokines are important recruiters and activators of inflammatory cells and these infiltrating cells interact with resident cells, such as fibroblasts and it is through these pathways that chemokines appear to exert multiple biological actions. Clinical trials are underway with therapeutics targeting chemokine pathways for other inflammatory diseases. It is hoped that the information generated from these studies will contribute towards furthering our understanding of chemokine biology and be applied towards targeting severe asthma.