Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock

OBJECTIVE: The objectives of this study were to determine myocardial injury in patients with septic shock by measuring serum cardiac troponin I (cTnI), to evaluate relationship between elevated cTnI and myocardial dysfunction and to determine if cTnI is a predictor of outcome in these patients. METHODS: Thirty-seven consecutive patients with septic shock were included in the study. Serum cTnI was measured at study entry and after 24 and 48 h. Transthoracic echocardiogram, electrocardiogram and regular biochemical and hemodynamic assessments were performed. RESULTS: Sixteen (43%) patients had elevated serum cTnI. These patients had higher need for inotropic/vasopressor support (94% vs. 53%, p=0.018), higher APACHE II score (28 vs. 20, p=0.004), higher incidence of regional wall motion abnormalities on echocardiography (56% vs. 6%, p=0.002), lower ejection fraction (46% vs. 62%, p=0.04) and higher mortality (56% vs. 24%, p=0.04) compared to normal cTnI patients. By multiple logistic regression analysis, serum cTnI and APACHE II score were independent predictor of death and length of stay in intensive care unit. Serum cTnI, APACHE II score, anion gap and serum lactate were independent predictor of need for inotropic/vasopressor support. Receiver-operating characteristics of serum cTnI as a predictor of death in septic shock were significant. The elevated serum level of cTnI correlated with the lower left ventricular ejection fraction (p<0.001). CONCLUSIONS: Myocardial injury can be determined in patients with septic shock by serum cTnI. Serum cTnI concentration correlates with myocardial dysfunction in septic shock. High serum cTnI predicts increased severity of sepsis and higher mortality. A close monitoring of patients with septic shock and elevated levels cTnI is warranted.     

Cardiac arrhythmia as initial presentation of aneurysmal subarachnoid hemorrhage

Cardiac arrhythmia and sudden death are most frequently caused by preexisting heart disease. Rarely, cardiac arrhythmia is a first symptom of an acute neurological event. We describe a patient with asystole and other cardiac arrhythmias, as initial symptoms of acute aneurysmal subarachnoid hemorrhage. Several aspects of cardiac arrhythmias and acute aneurysmal subarachnoid hemorrhage are discussed.     

雌激素与动脉瘤性蛛网膜下腔出血

近年来的研究表明,雌激素与动脉瘤性蛛网膜下腔出血关系密切.雌激素可通过多种途径影响颅内动脉瘤发生和发展过程,从而降低动脉瘤破裂发生率.雌激素还能缓解蛛网膜下腔出血后的脑血管痉挛.明确雌激素对动脉瘤性蛛网膜下腔出血的影响和机制,可能发现新的药物作用靶点,预防动脉瘤性蛛网膜下腔出血的发生及其导致的继发性损伤.     

Chronic cerebral paragonimiasis combined with aneurysmal subarachnoid hemorrhage

A 67-year-old Korean woman attended our hospital complaining of a severe headache. A brain computed tomography scan showed conglomerated, high-density, calcified nodules in the left temporo-occipito-parietal area and high-density subarachnoid hemorrhage in the basal cisterns. Magnetic resonance imaging of the brain shows multiple conglomerated iso- or low-signal intensity round nodules with peripheral rim enhancement. She underwent craniotomies to clip the aneurysm and remove the calcified masses. Paragonimus westermani eggs were identified in the calcified necrotic lesions. Results of parasitic examinations on the sputum and an enzyme-linked immunosorbent assay for P. westermani were all negative. The patient presented with headache and dizziness that had occurred for more than 30 years. She had not eaten freshwater crayfish or crabs. However, she had sometimes prepared raw crabs for several decades. Overall, this case was diagnosed as chronic cerebral paragonimiasis, in which she may have been infected through the contamination of utensils during the preparation of the second intermediate hosts, combined with a cerebral hemorrhage.     

动脉瘤性蛛网膜下腔出血的治疗指南（ASA 2009年版）（中）

5 aSAH的临床表现和诊断 aSAH的临床表现非常典型。约80％提供病史的患者描述症状为“有生以来最剧烈的头痛”，另20％的患者则有先兆性的头痛发作。而大多数颅内动脉瘤患者在动脉瘤破裂前无症状出现。     

动脉瘤性蛛网膜下腔出血的治疗指南（ASA2009年版）（下）

9医院特点及诊治体系 一些关于SAH预后的研究显示,患者预后与医院治疗的病例数相关。Cross等研究了1546家美国医院收治的16399例SAH患者,发现其中82％的医院每年收治SAH患者的例数〈19例,而64％的医院年均收治不足10例。研究显示,年均收治SAH患者〈10例的医院,其患者30d死亡率高于年均收治〉35例的医院（39％对27％,比值为1．4）。     

动脉瘤性蛛网膜下腔出血的治疗指南（ASA2009年版）（上）

蛛网膜下腔出血（SAH）是一种非常严重的常见疾病,在美国,每年约有3万人发病,约占所有卒中的5％。美国心脏协会（America Heart Association,AHA）曾于1994年发布了动脉瘤性SAH（aneurysmal SAH,aSAH）的治疗指南。在随后的十几年内,对aSAH的诊断方法、血管内和手术治疗技术和围手术期管理有了显著的进步,但这些并未改变aSAH预后较差的结果,其病死率仍高达45％,存活者亦有很高的残疾率。几项大规模的多中心前瞻性随机试验和前瞻性队列分析的结果,对aSAH的治疗方法产生了一定的影响,但同时快速发展的新治疗方法以及某些伦理和实践问题,提示我们有必要规范aSAH诊治相关的许多重要概念。     

非动脉瘤性与动脉瘤性蛛网膜下腔出血特点的分析

目的探讨非动脉瘤性与动脉瘤性蛛网膜下腔出血（aSAH）的临床特点。方法回顾性分析168例非aSAH和104例aSAH患者入院时的Hunt-Hess分级、CT检查（以德国Freiburg大学神经中心的标准,根据头部CT影像分型）、第1次全脑DSA检查、重复全脑DSA及短期和长期预后MRS（Modified Rankin Scale）评分等临床资料。结果①两组患者入院时的Hunt-Hess分级比较,差异有统计学意义,χ^2=74.023,P〈0.001。②两组CT分型比较差异有统计学意义,χ^2=117.486,P〈0.001。非aSAH和aSAH患者伴有脑室积血者分别为36.6%（41/112）和89.4%（93/104）,χ^2=72.254,P〈0.001;脑积水分别为34.8%（39/112）和74.0%（77/104）,χ^2=38.910,P〈0.001。③中脑周围型蛛网膜下腔出血和非中脑周围型蛛网膜下腔出血患者入院时,Hunt-Hess分级比较差异有统计学意义,χ^2=16.680,P〈0.01;经Spearman相关分析：入院时Hunt-Hess分级与CT分型之间无直线相关关系,r=-0.4,P〉0.05。④中脑周围型蛛网膜下腔出血患者脑积水和脑血管痉挛的发生率,分别为14.5%（8/55）和21.8%（12/55）,非中脑周围型蛛网膜下腔出血患者脑积水和脑血管痉挛的发生率,分别为54.4%（31/57）和42.1%（24/57）,两组比较,χ^2=19.575,P〈0.01和χ^2=5.283,P〈0.05。⑤168例非aSAH患者随访92例,MRS≤2分者占90.2%,中、重度残疾占3.3%;104例aSAH患者随访88例,MRS评分≤2分者占50.0%,中、重度残疾占34.1%,χ^2=8.42,P〈0.05。结论非aSAH比aSAH患者入院时Hunt-Hess分级低,并发症少、预后好,在中脑周围型蛛网膜下腔出血的患者中表现得更加明显。     

动脉瘤性蛛网膜下腔出血后慢性脑积水研究进展

慢性脑积水引起患者智能障碍、步态异常、尿失禁,给社会和家庭带来很大负担,该文对动脉瘤性蛛网膜下腔出血(aSAH)后慢性脑积水产生原因、诊断及治疗进展做一综述。     

动脉瘤性蛛网膜下腔出血后形成脑积水的相关因素

动脉瘤性蛛网膜下腔出血(SAH)后有6％~67％的患者将会发生脑积水。可发生于SAH后急性期(SAH后0~3 d)、亚急性期(SAH后4~13 d)或晚期(SAH后≥14 d)。有的脑积水必须进行永久性分流术,称为"分流术依赖性脑积水"。 Dorai等对718例动脉瘤性SAH患者进行了回顾性分     

Cardiac troponin I in perioperative myocardial infarction after coronary artery bypass surgery

BACKGROUND AND AIMS: Myocardial infarction after coronary artery bypass grafting is a serious complication and one of the most common causes of perioperative morbidity and mortality. The present study was designed to determine the relevance of serum cardiac troponin I as a specific diagnostic marker for perioperative myocardial infarction. METHODS: A cohort of 64 patients undergoing coronary artery bypass grafting was enrolled for prospective study. Postoperative blood samples were extracted and analyzed for total creatine kinase (CK), CKMB and cardiac troponin I activity. Perioperative infarction was defined as the development of new Q waves in the postoperative electrocardiogram together with congruent regional wall motion abnormalities in the echocardiogram and CK values greater than 400 IU/l with MB fraction greater than 40 IU/l. RESULTS: Perioperative infarction occurred in 12 patients. Higher cardiac troponin I values were observed in patients experiencing perioperative myocardial infarction than in those without infarction (p < 0.001). Cardiac troponin I values higher than 12 ng/ml 10 h after release of the aortic clamp best detected the presence of perioperative myocardial infarction, with an area under the characteristic receiver operating curve of 0.91 (95% CI, 0.82-0.97), a sensitivity of 90.9%, and a specificity of 88.5%.The mean stay in the intensive care unit was significantly longer for patients who suffered perioperative myocardial infarction (6.5 8.6 days) than for patients without perioperative infarction (4.7 7.5 days) (p < 0.005). CONCLUSIONS: Cardiac troponin I elevation appears to be an early, specific marker for the diagnosis of perioperative myocardial infarction after coronary artery bypass grafting.     

动脉瘤性蛛网膜下腔出血后延迟性脑缺血的研究进展

正Research progress in delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage LI Xue-feng,WANG Jian-cun,HU Guan-cheng. Jishou University School of Medicine,Hunan 416000,China     

Prevalence of pituitary deficiency in patients after aneurysmal subarachnoid hemorrhage

After aneurysmal subarachnoid hemorrhage (SAH), patients frequently present with persistent bodily, psychosocial, and cognitive impairments that resemble those of patients with untreated partial or complete pituitary insufficiency. Because of these similarities, the authors hypothesized that aneurysmal SAH may cause pituitary dysfunction. Pituitary function testing was performed in 40 aneurysmal SAH patients between 12 and 72 months after the SAH. A combined TRH-LHRH-arginine test and the insulin tolerance test were performed on two separate days. Only 18 of 40 (45%) of the tested patients had normal pituitary function. Five of 40 exhibited isolated severe GH deficiency (GHD), and an additional three of 40 had severe GHD plus corticotroph deficiency. Isolated corticotroph deficiency was seen in 13 of 40 patients, and one patient showed isolated thyrotroph deficiency. All but one patient with corticotroph insufficiency were female. Patients with severe GHD had gained significantly more weight since their SAH than patients without GHD and exhibited a significantly higher body mass index. None of the clinical parameters indicative of a poor neurological outcome in aneurysmal SAH were related to pituitary insufficiency. In summary, neuroendocrine dysfunction was identified in a substantial portion of patients with previous aneurysmal SAH and should be borne in mind as a potential long-term sequel of the illness.