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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Percutaneous suprapubic cystostomy is generally considered to be a safe procedure provided the bladder is distended adequately, as palpable bladder is the landmark for insertion of a trocar. This report describes fatality due to septicemia and hemorrhage following suprapubic catheter insertion in a tetraplegic male patient with long-term indwelling urethral catheter drainage and urine infection with Escherichia coli, Pseudomonas species, and Enterococcus faecalis. Before the surgical procedure was begun, the urinary bladder was distended by repeated injection of 50 mL of sterile, 0.9% sodium chloride through the urethral catheter with a catheter-tip syringe until the bladder became palpable in the suprapubic region; by this time, the bladder had been filled forcibly with 500 mL of saline. Percutaneous cystostomy was performed with the use of an Add-a-Cath trocar and cannula (Femcare Limited, Nottingham, Nottinghamshire, UK). Immediately after a 16 French Foley catheter had been inserted, the drainage fluid appeared heavily stained with blood. The patient developed septicemia, and a blood culture report, received posthumously, showed growth of E. coli. Despite resuscitative measures, the patient expired 13 hours after suprapubic catheter insertion. Postmortem examination revealed bilateral hydronephrosis with fluid and clotted blood in the renal pelves and ureters; the urinary bladder showed a thick wall and hemorrhagic mucosa. This fatal incident raises the question of whether forcible distention of the urinary bladder for percutaneous cystostomy is safe in patients with spinal cord injury who have a small-capacity bladder, infected urine, and ischemic heart disease. In such patients, it may be prudent to avoid forcible distention of the urinary bladder and instead perform ultrasound-guided or fluoroscopically guided suprapubic cystostomy.
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PMID:Fatality due to septicemia and hemorrhage in a patient with spinal cord injury and ischemic heart disease with the need for long-term catheter drainage. 1675 Nov 67

We analyzed survival rates of 144 prevalent patients on maintenance hemodialysis from 1998 to 2003 at the Department of Nephrology and Dialysis, Rijeka University Hospital, Rijeka, Croatia, and evaluated risk factors predicting their survival. Included were only end-stage renal disease (ESRD) patients on maintenance hemodialysis treatment dialysed more than 6 months before entering the study and who were clinically stable. The patients were randomised in two groups according to the presence or absence of diabetic nephropathy as the cause of ESRD and followed-up. The patient's death as outcome measure was recorded. The survival rates were estimated by the Kaplan-Meier method. The major causes of death were cardiovascular disease in 40 (60.6%) patients. An acute myocardial infarction in 15 (22.7%) patients was the major single cause of death. We found a significantly lower survival of diabetic patients than non-diabetic patients (P=0.0013). The most important predictors of death among diabetic patients on maintenance hemodialysis were hyperglycaemia (P<0.001), ischemic heart disease (P=0.004), hypercholesterolemia (P=0.013), and low delivered dialysis dose (P=0.013). The survival of diabetic patients undergoing hemodialysis was much worse than survival of non-diabetic patients. The cardiovascular disease remained the major cause of death in both groups. Early detection of pre-existing cardiovascular risk factors and diseases, and treatment of infections leading to sepsis, are of great importance, as they may influence the survival rates. Intensive management of diabetic patients is essential.
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PMID:Comparison of survival between diabetic and non-diabetic patients on maintenance hemodialysis: a single-centre experience. 1682 39

Because of changing demographics, increasing numbers of patients with IHD are presenting for noncardiac surgery, and the risks of perioperative morbidity and mortality are significant. The Lee Cardiac Risk Index is applicable in defining perioperative cardiac risk: however, ACC/AHA guidelines may not be applicable comprehensively. The role of biomarkers in risk stratification still needs to be defined. Structured management protocols that help assess, diagnose, and treat patients with IHD preoperatively are likely to help decrease postoperative morbidity and mortality, but clearly are not applicable to all patients. Augmented hemodynamic control with beta-blockers or alpha-2 agonists and modulating inflammation by statins can play an important role in improving outcomes in many patients with IHD; preoperative coronary revascularization may be of limited value. Intraoperative anesthetic management that minimizes hemodynamic perturbations is important; however, the choice of a particular technique typically is not critical. Of critical importance is the postoperative management of the patient. Postoperative myocardial injury should be identified, evaluated, and managed aggressively. Secondary stresses such as sepsis, extubation, and anemia, which can increase demand on the heart, should be treated or minimized. Clearly, optimal care of the patient with IHD entails closely coordinated assessment and management throughout the preoperative, intraoperative, and postoperative phases, if one is to optimize short- and long-term outcomes.
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PMID:Ischemic heart disease. 1724 Jun 2

Emergency cholecystectomy for acute cholecystitis in critically ill patients with organ failure and sepsis carries a high risk of morbidity and mortality. Temporizing interventions such as laparoscopic cholecystostomy can help the patient to recover from the critical illness by deferring the definitive procedure to a later, safer period. We describe our experience of laparoscopic cholecystostomy performed in two critically ill patients. In the first case, a 56-year-old man with hypertension, diabetes, and ischemic heart disease, was admitted for evaluation of malena. During the course of his stay, he developed acute calculous cholecystitis, acute renal failure, and right pleural effusion. In the second case, a 68-year-old man presented with diabetes, hypertension, diabetic nephropathy, acute chronic renal failure, and acute calculous cholecystitis. Both patients failed to improve with conservative measures and underwent laparoscopic cholecystostomy under local anesthesia and sedation in view of severe comorbidities and sepsis. Both patients recovered from sepsis. Laparoscopic cholecystectomy was performed uneventfully after six and eight weeks, respectively, and both patients were doing well at one-year follow-up.
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PMID:Laparoscopic cholecystostomy is a safe and effective alternative in critically ill patients with acute cholecystitis: two cases. 1736 78

Gastric perforation in association with incarceration of a hiatus hernia rarely features on a list of differential diagnoses of acute chest pain. A patient presented to the emergency department with acute chest pain characteristic of myocardial ischaemia. Several risk factors for ischaemic heart disease (IHD) were present. Investigations revealed normal cardiac enzymes and normal electrocardiography both initially and at 90 mins. A chest radiograph demonstrated the presence of a hiatus hernia. The patient was diagnosed with, and treated for, unstable angina. A troponin T test at 12 h post-admission was normal. The patient's clinical condition continued to deteriorate. The source of her pain was found to be gastric perforations in association with an incarcerated hiatus hernia. Her postoperative course was complicated by pulmonary and intra-abdominal sepsis necessitating admission to the intensive care unit where she remained for 23 days. This case highlights the challenge that non-cardiac chest pain presents to the acute care physician. Patients who present with risk factors for and symptoms consistent with a diagnosis of IHD may have non-cardiogenic pathology which can be life-threatening.
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PMID:Gastric perforation secondary to incarcerated hiatus hernia: an important differential in the diagnosis of central crushing chest pain. 1765 2

Sepsis is generally viewed as a disease aggravated by an inappropriate immune response encountered in the afflicted individual. As an important organ system frequently compromised by sepsis and always affected by septic shock, the cardiovascular system and its dysfunction during sepsis have been studied in clinical and basic research for more than 5 decades. Although a number of mediators and pathways have been shown to be associated with myocardial depression in sepsis, the precise cause remains unclear to date. There is currently no evidence supporting global ischemia as an underlying cause of myocardial dysfunction in sepsis; however, in septic patients with coexistent and possibly undiagnosed coronary artery disease, regional myocardial ischemia or infarction secondary to coronary artery disease may certainly occur. A circulating myocardial depressant factor in septic shock has long been proposed, and potential candidates for a myocardial depressant factor include cytokines, prostanoids, and nitric oxide, among others. Endothelial activation and induction of the coagulatory system also contribute to the pathophysiology in sepsis. Prompt and adequate antibiotic therapy accompanied by surgical removal of the infectious focus, if indicated and feasible, is the mainstay and also the only strictly causal line of therapy. In the presence of severe sepsis and septic shock, supportive treatment in addition to causal therapy is mandatory. The purpose of this review is to delineate some characteristics of septic myocardial dysfunction, to assess the most commonly cited and reported underlying mechanisms of cardiac dysfunction in sepsis, and to briefly outline current therapeutic strategies and possible future approaches.
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PMID:Sepsis and the heart. 1769 45

The clinical course of cryoglobulinemic syndrome (CS) is usually slow; however, fast aggravations have been frequently reported in recent years. In these cases vasculitic ischemic tissue damage accounts for glomerular involvement, neuropathy, cutaneous ulcers, ischemic heart disease, lung or jejunal impairment and stroke. Other critical events in CS may be represented by sepsis, liver insufficiency, hepatocellular carcinoma and non-Hodgkin's lymphomas. Sometimes emergency can not be controlled and the evolution is fatal. Long-term follow up, emergency outcome and cause of death have not been considered in controlled studies, in large series. Here we report a 53-year old woman affected by IgG-IgMk type II HCV-related mixed cryoglobulinemia, who presented several critical events over the course of the disease, which required therapeutical emergency interventions. The latter consisted of plasma exchange, cytotoxic agents, corticosteroids, intravenous immunoglobulin, antihypertensive drugs, antibiotics, and rituximab. Eventually no therapy was effective and the patient died from a catastrophic-like syndrome. This case is relevant because it enables us to consider some important steps in the treatment of emergency in CS.
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PMID:Emergency in cryoglobulinemic syndrome: what to do? 1793 11

The echocardiography can provide important and relevant information and the critically ill patient presents a challenge for the echocardiographer: from limitations in image acquisition to interpretation in the context of rapid physiological and intervention changes. The most frequent reason for requesting an echocardiogram in the ICU is probably to assess left ventricular function. In any case, information of direct relevance for clinical management can in relationship to abnormalities of structure and function can be obtained and used to estimate pulmonary arterial and venous pressures. It can help to investigate the consequences of myocardial ischemia, valvular dysfunction and pericardial disease and detect changes characteristic of specific conditions (e.g. sepsis, pulmonary thromboembolism), although this must be interpreted in the context of each individual patient. The echocardiography also can be used to monitor the therapeutic interventions. The applications of echocardiography in the critical care setting are reviewed, with special emphasis on the assessment of cardiac physiology.
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PMID:[Echocardiography in the Intensive Care Unit]. 1857 Aug 34

Procalcitonin (PCT) is known to be a biological diagnostic marker for severe sepsis, or septic shock in critically ill patients. There are still contrasting data about a role of procalcitonin in patients with acute myocardial infarction or cardiogenic shock, and in those with acute coronary syndromes, that is, non-ST-elevation myocardial infarction or unstable angina. We evaluated plasma levels of procalcitonin and C-reactive protein (CRP) in 52 patients admitted to our intensive cardiac care unit (ICCU): 14 patients with cardiogenic shock (CS) following ST-elevation myocardial infarction (STEMI), 15 patients with uncomplicated ST-elevation myocardial infarction (STEMI), and 24 with non-ST-elevation myocardial infarction or unstable angina (NSTEMI/UA). In all patients, infective processes were excluded. Procalcitonin values were significantly higher in CS patients with respect to the other two subgroups (P < 0.001, P < 0.001) while CRP levels were higher than NSTEMI/UA patients (P < 0.001) but not with respect to STEMI patients (P = 0.063). No correlations were found in cardiogenic shock patients between CRP and PCT values (R = 0.02; P = 0.762, ns). Procalcitonin levels measured on ICCU admission are significantly higher in patients with cardiogenic shock following the acute myocardial infarction, and they are not correlated with those of CRP. The degree of myocardial ischemia (clinically indicated by the whole spectrum of ACS, from unstable angina to cardiogenic shock ST-elevation following myocardial infarction) and the related inflammatory-induced response are better reflected by CRP (which was positive in most acute cardiac care patients of all our subgroups), than by PCT which seems more reflective of a higher degree of inflammatory activation, being positive only in all CS patients.
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PMID:Procalcitonin in patients with acute coronary syndromes and cardiogenic shock submitted to percutaneous coronary intervention. 1963 70

Natriuretic peptides play a central role in cardiovascular, endocrine, and renal homeostasis and can be considered physiologic antagonists to the renin-angiotensin-aldosterone system. ANP and BNP in the circulation are derived primarily from the myocardium, whereas CNP is mainly derived from endothelial cells and the central nervous system. Increased ventricular and atrial diastolic wall stretch augment synthesis and release of BNP and NT-proBNP from cardiomyocytes, and is the principal stimulus controlling BNP production. Circulating BNP and NT-proBNP levels are increased in heart failure in proportion to disease severity, but elevated levels may also be observed in other cardiac and noncardiac disease states, including cardiac arrhythmias, ventricular hypertrophy, myocardial ischemia, pulmonary embolism, acute and chronic cor pulmonale, renal failure, anemia, hyperthyroidism, and sepsis. Fully automated analyses of both BNP and NT-proBNP can be rapidly performed on large hospital-based platforms as well as on small point-of-care devices.
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PMID:Natriuretic peptides: physiologic and analytic considerations. 1963 Nov 73


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