Systemic illness

Systemic illnesses are associated with alterations in the hypothalamic–pituitary–peripheral hormone axes, which represent part of the adaptive response to stressful events and may be influenced by type and severity of illness and/or pharmacological therapy. The pituitary gland responds to an acute stressful event with two secretory patterns: adrenocorticotropin (ACTH), prolactin (PRL) and growth hormone (GH) levels increase, while luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyrotropin (TSH) levels may either decrease or remain unchanged, associated with a decreased activity of their target organ. In protracted critical illness, there is a uniformly reduced pulsatile secretion of ACTH, TSH, LH, PRL and GH, causing a reduction in serum levels of the respective target-hormones. These adaptations are initially protective; however, if inadequate or excessive they may be dangerous and may contribute to the high morbidity and mortality risk of these patients. There is no consensus regarding the type of approach, as well as the criteria to use to define pituitary axis function in critically ill patients. We here provide a critical approach to pituitary axis evaluation during systemic illness.     

High-altitude illness

High-altitude illness is the collective term for acute mountain sickness (AMS), high-altitude cerebral oedema (HACE), and high-altitude pulmonary oedema (HAPE). The pathophysiology of these syndromes is not completely understood, although studies have substantially contributed to the current understanding of several areas. These areas include the role and potential mechanisms of brain swelling in AMS and HACE, mechanisms accounting for exaggerated pulmonary hypertension in HAPE, and the role of inflammation and alveolar-fluid clearance in HAPE. Only limited information is available about the genetic basis of high-altitude illness, and no clear associations between gene polymorphisms and susceptibility have been discovered. Gradual ascent will always be the best strategy for preventing high-altitude illness, although chemoprophylaxis may be useful in some situations. Despite investigation of other agents, acetazolamide remains the preferred drug for preventing AMS. The next few years are likely to see many advances in the understanding of the causes and management of high-altitude illness.     

急性闭角型青光眼降压后的视网膜出血

目的观察急性闭角型青光眼降压治疗后的视网膜血管改变。方法对１２０例单眼急性闭角型青光眼经药物及滤过性减压手术治疗的老年病人于治疗后２～４０ｄ在直接检眼镜下进行观察。结果计有８名患者合并视网膜出血,占总人数的６．７％。结论青光眼降压治疗后,由于眼灌注压的改变,轴浆流的急性阻滞和视网膜血管的自主调节能力缺陷均可引起视网膜浅层出血。     

Parental childhood respiratory illness and respiratory illness in their infants

Parental histories of childhood respiratory trouble (CRT) were examined as risk factors for lower respiratory tract illnesses in healthy infants enrolled in the Children's Respiratory Study, Tucson, Arizona. A parental history of childhood respiratory trouble before age 16 was a risk factor for infantile lower respiratory tract illnesses (LRIs). Early age of onset of the parental CRT and those illnesses described as asthma or bronchiolitis showed the greatest risk: odds ratio = 2.8, P < 0.05. After controlling for known and suspected confounders, a parental history of CRT described as asthma or bronchiolitis with onset before age 3 was associated with wheezing LRls in their children, with an odds ratio of 2.6, P < 0.05. A parental history of CRT described as bronchitis/croup was associated with nonwheezing LRls in their children: odds ratio = 2.2, P < 0.05. These findings suggest a familial component to childhood respiratory trouble which may have a hereditary basis. Pediatr Pulmonol. 1993; 16:275–280. © 1993 Wiley-Liss, Inc.     

Critical illness myopathy

Acute myopathy is a common problem in intensive care units. Those at highest risk for developing critical illness myopathy are exposed to intravenous corticosteroids and paralytic agents during treatment of various illnesses. Diffuse weakness and failure to wean from mechanical ventilation are the most common clinical manifestations. Serum creatine kinase levels are variable. Electrodiagnostic studies reveal findings of a myopathic process, often with evidence of muscle membrane inexcitability. Based on animal model studies, the loss of muscle membrane excitability may be related to inactivation of sodium channels at the resting potential. In addition, human and animal pathologic studies reveal characteristic loss of myosin with relative preservation of other structural proteins. In some patients, there is also upregulation of proteolytic pathways, involving calpain and ubiquitin, in conjunction with increased apoptosis. Fortunately, the disorder is reversible, but there may be considerable morbidity.     

Patent Foramen Ovale Closure and Decompression Sickness Among Divers

BackgroundDecompression sickness is a diving-related disease that results in various clinical manifestations, ranging from joint pain to severe pulmonary and CNS affection. Complications of this disease may sometimes persist even after treatment with hyperbaric oxygen therapy. In addition, it may hamper the quality of life by forcing divers to restrict their recreational practice. The presence of a patent foramen ovale (PFO) increases the risk of decompression sickness by facilitating air embolization. Therefore, PFO closure may play a role in reducing such complications. However, PFO closure remains associated with its own set of risks and complications. We sought to assess the benefit and harm of PFO closure for the prevention of decompression sickness in divers.MethodsWe conducted a comprehensive search of MEDLINE, Embase, CENTRAL, and Web of Science. Two-armed studies comparing the incidence of decompression sickness with or without PFO closure were included. We used a random-effects model to compute risk ratios comparing groups undergoing PFO closure to those not undergoing PFO closure.ResultsFour observational studies with a total of 309 divers (PFO closure: 141 and no closure: 168) met inclusion criteria. PFO closure was associated with a significantly lower incidence of decompression sickness (PFO-closure: 2.84%; no closure: 11.3%; RR: 0.29; 95% CI: 0.10 to 0.89; NNTB = 11), with low heterogeneity (I² = 0%). The mean follow-up was 6.12 years (Standard deviation 0.70). Adverse events occurred in 7.63% of PFO closures, including tachyarrhythmias and bleeding.ConclusionPFO closure may potentially reduce the risk of decompression sickness among divers; however, it is not free of potential downsides, with nearly one in thirteen patients in our analysis experiencing an adverse event.     

Decompression of the small bowel by endoscopic long-tube placement

AIM: To investigate and compare the decompression effect on small bowel obstruction of a long tube inserted using either endoscopic or fluoroscopic placement.METHODS: Seventy-eight patients with small bowel obstruction requiring decompression were enrolled in the study and divided into two groups. Intubation of a long tube was guided by fluoroscopy in one group and by endoscopy in the other. The duration of the procedure and the success rate for each group were evaluated.RESULTS: A statistically significant difference in the mean duration of the procedure was found between the fluoroscopic group (32.6 ± 14.6 min) and the endoscopic group (16.5 ± 7.8 min) among the cases classified as successful (P < 0.05). The success rate was significantly different between the groups: 88.6% in the fluoroscopic group and 100% in the endoscopic group (P < 0.05).CONCLUSION: For patients with adhesive small bowel obstruction, long-tube decompression is recommended and long-tube insertion by endoscopy was superior to fluoroscopic placement.     

周围神经减压术治疗糖尿病周围神经病变

周围神经减压术是在20世纪80年代由美国周围神经外科协会原主席、霍普金斯大学医学院神经外科和整形外科Dellon教授发明的,是针对性解决下肢或上肢神经病变的一种手术。当糖尿病周围神经病变患者符合手术指征和手术时机时,对下肢周围神经病变者常采用腓总神经、腓深神经、胫神经松解三联手术,对上肢周围神经病变者常采用正中神经、尺神经和桡神经感觉支减压三联手术。同时作者结合文献阐述了腓总神经、腓深神经、胫神经松解三联手术和正中神经、尺神经(肌下转位)显微减压术的基本步骤,归纳总结了国内与周围神经减压术治疗糖尿病周围神经病变有关的基础研究和临床研究文献,以达到改善患者生活质量、预防糖尿病足和避免截肢的目的。