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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We classified 41 patients in septic shock on the basis of cardiac index (CI) after volume expansion with plasma protein solution, in order to obtain adequate filling pressures. Five had decreased CI (less than 3.5 1/min per m2), 31 had moderately increased CI (3.5 - 7.0 1/min per m2) and 5 had extreme hyperdynamic shock with CI superior to 7.0 1/min per m2. Among the patients with increased CI, those with extreme hyperdynamic state (EHS) had lower total systemic and pulmonary arteriolar resistances (370 vs 658 and 52 vs 119 dynes X s X cm-5, respectively) and a higher stroke index (67 vs 46 ml/m2), in spite of similar right atrial pressures. In this latter group, blood lactate was higher (6.5 vs 2.1 mmol/l), acidosis was more severe and coagulation disorders more pronounced; all five patients maintained an extremely high CI until death, which supervened after a brief episode of sinus bradycardia. A similar clinical course was rarely observed in the remaining moderately hyperdynamic group, in which mortality rate was significantly lower (35%). Three of five patients with EHS (compared to 2 of 31 in the moderately hyperdynamic group) had liver cirrhosis, the fourth died of fulminant meningococcemia and the fifth had prolonged polymicrobial bacteremia before adequate treatment was begun. Thus, underlying liver disease or particularly severe and uncontrolled infection seems to predispose to EHS. It is concluded that septic shock with extremely high cardiac output and excessively low peripheral resistances represents a distinct subset with more severe metabolic and coagulation disorders, an unusual hemodynamic evolution and a particularly poor prognosis.
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PMID:An extreme form of the hyperdynamic syndrome in septic shock. 649 Oct 37

The purpose of the present investigation was to explore a possible relationship between cardiopulmonary function and small intestinal mucosal lesions in experimental septic shock. The filling pressure of the left ventricle of the heart (LVEDP) and the maximal pressure change during systole (max dP/dt) were monitored continuously by a tip-transducer catheter. The pulmonary and femoral arterial pressures and pressure changes in the trachea were recorded. The aortic blood flow was measured electromagnetically. Stroke volume, external cardiac work, and the pulmonary vascular resistance could be calculated. Twenty-two cats were made septic by i.v. infusion of live E. coli bacteria. Controls received saline i.v. After 2 hours of bacteremia, preload was increased by a rapid infusion of dextran to unmask cardiac dysfunction. Small intestinal specimens were taken for microscopical examination. The occurrence and the degree of mucosal damage was established. Thirteen cats had virtually normal mucosal appearances, whereas nine disclosed severe lesions. The loading procedure revealed a more pronounced cardiac dysfunction in cats with severe mucosal damage, compared to those without. Pulmonary vasoconstriction, bronchoconstriction, and impaired ventilation-perfusion ratio were also demonstrated, but these signs of pulmonary dysfunction did not differ when comparing animals with and without mucosal damage. A correlation between impaired cardiac function on one hand and hypotension--intestinal mucosal lesions on the other, suggests cardiotoxic material released from the damaged intestine as one contributing mechanism.
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PMID:Cardiopulmonary function as related to intestinal mucosal lesions in experimental septic shock. 674 24

Within the Cooperative Study of Sickle Cell Disease, 694 infants with confirmed sickle cell disease were enrolled at less than 6 months of age. Information about the nature and frequency of complications was collected prospectively over a 10-year period. Painful crises and acute chest syndrome were the most common sickle cell-related events in homozygous sickle cell anemia (SS), hemoglobin SC disease (SC), and S beta thalassemia patients (overall incidence in SS patients of 32.4 and 24.5 cases per 100 person-years, respectively). Bacteremia occurred most frequently in SS children under 4 years of age and in SC patients less than 2 years of age. The mortality rate was low in this cohort compared with that found in previous reports. Twenty children, all with Hb SS, died (1.1 deaths per 100 person-years among SS patients). Infection, most commonly with Streptococcus pneumoniae and Hemophilus influenzae, caused 11 deaths. Two children died of splenic sequestration, 1 of cerebrovascular accident, and 6 of unclear causes. Two patients underwent cholecystectomies, and 17 underwent splenectomies after one or more splenic sequestration crises. The experience of this cohort should reflect closely the true clinical course of those children with Hb SS and Hb SC disease who are observed in sickle cell centers in the United States.
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PMID:Clinical events in the first decade in a cohort of infants with sickle cell disease. Cooperative Study of Sickle Cell Disease. 749

To evaluate the clinical relevance of the experimental findings of a more severe cardiac depression in Pseudomonas (P.) than in non-P. sepsis, we retrospectively compared the hemodynamic data in 26 patients with P. sepsis (20 cases, single pathogen; six cases, more positive cultures with P. than with non-P. species), and 102 with non-P. sepsis. As in other studies, the left ventricular stroke work index (LVSWI) was used to assess cardiac performance. The two groups (all numbers are means) had a similar disease and sepsis severity profile (P. vs. non-P: septic shock, 81% vs. 87%; APACHE II scores, 29.1 vs. 29.2; Elebute sepsis scores, 18.1 vs. 18.1; mortality, 58% vs. 62%). Preload (pulmonary capillary wedge pressure 15.0 vs. 16.3 mm Hg) and systemic vascular resistance (588 vs 572 dyn.cm-5.sec) were comparable. Cardiac performance displayed no significant difference (LVSWI, 42.8 vs. 38.3 g.m/m2), a result reproduced in the subgroups with culture-proven bacteremia, with or without preexisting cardiovascular disease or septic shock. Thus, our data suggest that there is no difference in the degree of cardiovascular dysfunction in patients with Pseudomonas compared to non-Pseudomonas sepsis of otherwise equivalent disease severity.
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PMID:Pseudomonas sepsis does not cause more severe cardiovascular dysfunction in patients than non-Pseudomonas sepsis. 805 63

The purpose of this study was to compare the pathophysiology of bacteremia produced by intravenous infusion of either a Gram-positive (Staphylococcus aureus) or a Gram-negative (Escherichia coli) organism. Conscious, unrestrained, instrumented rats received S. aureus, E. coli, or sterile saline over 120 min, followed by a 240-min monitoring period. The infusates produced 90% (S. aureus,) 80% (E. coli), and 0% (saline) mortality at 24 hr. Neither bacterial group produced hypotension during the entire 360-min study period. E. coli produced early tachycardia and increased glucose, followed by decreased stroke volume and increased lactate and pO2. S. aureus caused early tachycardia followed by decreased pH, stroke volume, and cardiac output and increased lactate and systemic vascular resistance. Respiration rate and central venous pressure were not affected by either bacterial infusion. Compared to E. coli, S. aureus produced decreased pH, glucose, pO2, heart rate, and cardiac output and increased lactate, hematocrit, pCO2, and systemic vascular resistance. These data document quantitative differences in the acute response of the conscious rat to bacteremia caused by these isolates of E. coli and S. aureus.
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PMID:Comparison of Staphylococcus aureus and Escherichia coli infusion in conscious rats. 827 70

A previously healthy 40-year-old man experienced the sudden 'stroke-like' onset of homonymous hemianopsia due to a bacterial brain abscess. Clinical features and initial computed tomography (CT) suggested a stroke. Subsequent CT and magnetic resonance (MR) demonstrated a cerebral abscess, proven at surgery. It is extremely rare that a healthy individual without various risk factors, such as congenital heart disease, immunologic deficiency, diabetes mellitus, or pregnancy, presents with the above symptoms. The exact mechanism of this sudden 'stroke-like' onset in a patient with a bacterial brain abscess is unknown. One possibility is that paroxysmal septic emboli led to abscess formation within or near areas of embolic infarction. Another possibility is that a primary cerebral infarction was associated with secondary bacteremia. Surgical drainage revealed a bacterial (Streptococcus) abscess, but no identifiable source of infection.
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PMID:Sudden "stroke-like' onset of homonymous hemianopsia due to bacterial brain abscess. 898 24

In recent years substantial data accumulated in the literature supporting the direct detrimental effect of tobacco smoking on periodontal health. The significantly inferior periodontal condition of smokers cannot be solely attributed to poor oral hygiene, increased calculus formation and altered subgingival microflora. Smoking imposes a direct threat to the periodontal tissues. Smokers with excellent oral hygiene show significantly less periodontal bone height and attachment level than matches non-smokers. Smoking entails a 2.5 to 3.5 risk ratio for severe periodontal attachment loss. Smoking also interferes with the outcome of nonsurgical and surgical periodontal treatment and impairs periodontal regeneration. The pathomechanism of the tobacco smoking related periodontal destruction is just partly understood. Tobacco products can alter normal host responses to neutralize infections and can also stimulate pathologic mechanisms to destroy the surrounding tissues. Tobacco products can directly impair polymorphonuclear leukocyte functions. Smokers have less salivary IgA and decreased serum IgG concentration as well as depressed number of helper T lymphocytes. Consequently smoking today is considered as one of the major risk factors for destructive periodontitis. Periodontitis is also considered as a decisive risk factor for systemic diseases especially for cardiovascular disorders. A strong association has been shown between periodontal disease and coronary heart diseases, as well as between periodontal disease and cerebrovascular diseases (stroke). The subgingival microflora and the continuous latent bacteremia and endotoxemia originated from the periodontal pockets might be responsible for the damage of the vascular endothelial integrity, platelet functions and blood coagulation. Modern periodontal epidemiology rediscovered the old ide of "focal infections" and indicated that the general health has a crucial impact on the periodontal health and periodontal disease has also a major impact on the general health status of the patient.
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PMID:[The effect of smoking on the spread and frequency of periodontal disease]. 1033 78

The pathophysiologic events of sepsis mediated by interleukin-1 (IL-1) remain ill-defined. The purpose of this study was to identify the circulatory derangements of which IL-1 was a necessary mediator and evaluate its interactions with tumor necrosis factor (TNF) and the eicosanoids during graded bacteremia. Eleven adult female swine were anesthetized, mechanically ventilated, and monitored with pulmonary artery catheters and arterial lines; they received intravenously either saline vehicle (septic control, n = 6) or human recombinant IL-1 receptor antagonist (IL-1ra, n = 5). The animals were then infused with Aeromonas hydrophila (10(9)/mL) for 4 h at rates gradually increased from .2 mL/kg/h to 4 mL/kg/h over 3 h, then sacrificed after 4 h. Mean arterial pressure (MAP), left ventricular stroke work index (LVSWI), and systemic vascular resistance index (SVRI) were recorded at baseline and hourly thereafter, and plasma 6-keto-PGF1alpha (6-KETO), tumor necrosis factor-alpha (TNF) and leukotrienes B4(LTB4) and C4D4E4 (LTCDE), pg/mL, were measured by ELISA. MAP, LVSWI, arterial P(O2) all decreased in the septic control group to levels significantly below those of the IL-1 antagonist animals. Circulating 6-KETO, LTCDE, and TNF increased significantly in all septic animals. Plasma LTB, and TNF were reduced by IL-1 blockade, compared with septic controls. TxB2 was not affected by IL-1 inhibition. There were no intergroup differences in platelet aggregation, but the in vitro aggregation response decreased from baseline in septic controls to 54+/-27% (p < .05). IL-1 is necessary to the development of systemic hypotension impaired LVSWI, and increased intravascular platelet aggregation during graded bacteremia. Conversely, IL-1 helps to maintain stroke volume and low SVRI in graded bacteremia, possibly through increased prostacyclin release. It may contribute to impaired pulmonary gas exchange and increased tissue oxygen demands. TNF release is stimulated in the presence of unopposed IL-1 and may be synergistic with it in the adverse hemodynamic effects of endogenous IL-1. IL-1 is required for increased leukotriene and prostacyclin levels in this model, but it is not involved in thromboxane release. Whether the lack of survival benefit from IL-1ra in human sepsis is due to these mixed cardiopulmonary and mediator effects, to species differences, or to timing of IL-1ra administration is not clear from the data.
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PMID:Interleukin-1 mediates hemodynamic dysfunction and release of eicosanoids and tumor necrosis factor during graded bacteremia. 1045 32

Arteriovenous (AV) graft infection is a serious adverse event in hemodialysis patients; however, there is little published literature describing its consequences. We identified prospectively all AV graft infections occurring at our institution during a 4.5-year period. We analyzed immediate complications, as well as long-term consequences, including the need for subsequent vascular-access procedures and duration of catheter-dependent dialysis therapy. Ninety graft infections were identified in 78 patients, yielding a rate of 8.2 infections/100 graft-years. Patients with graft infection were much more likely to have a low serum albumin level (<3.5 g/dL) in the month preceding the infection compared with noninfected controls (73% versus 18%; P < 0.001). Infections occurred within 1 month of graft placement in 15%, at 1 to 12 months in 44%, and longer than 1 year from surgery in 41%. The pathogen was a gram-positive coccus in 97% of cases, particularly Staphylococcus aureus (60%) and Staphylococcus epidermidis (22%). The initial graft infection entailed hospitalization for a mean of 7.5 days. Eleven patients (12%) developed a total of 17 major complications, including death (5 patients), clinical sepsis requiring vasopressors (4 patients), septic arthritis (3 patients), epidural abscess (1 patient), endocarditis (1 patient), osteomyelitis (1 patient), myocardial infarction (1 patient), and cerebrovascular accident (1 patient). After removal of an infected graft, patients were catheter dependent for a median of 3.8 months. The duration of catheter dependence was less than 3 months in 36%, 3 to 6 months in 38%, 6 to 12 months in 14%, and greater than 1 year in 12%. During the period of catheter dependence, patients required a mean of 9.7 access procedures, including graft removal (1.0 procedure), nontunneled dialysis catheters (4.4 procedures), tunneled dialysis catheters (3.0 procedures), and new permanent accesses (1.4 procedures). In addition, patients averaged 0.85 episodes of bacteremia while they were catheter dependent. In conclusion, graft infection results in substantial morbidity, prolonged dependence on dialysis catheters, and multiple vascular-access procedures.
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PMID:Clinical consequences of infected arteriovenous grafts in hemodialysis patients. 1168 49

Neurologic complications, particularly brain infarction (ischemic stroke), are frequent and serious sequelae of total artificial heart (TAH) implantation. Most strokes that occur in TAH patients are due to embolism of thrombotic fragments originating on prosthetic surfaces. The emboli tend to lodge in the middle cerebral artery or its cortical branches and cause cortical syndromes. Cardioembolic strokes are characteristically heralded by the abrupt onset of a maximal neurologic deficit in an awake, often active patient. Cardioembolic strokes have a tendency to undergo hemorrhagic transformation. Anticoagulation is a major issue in stroke management: In anticoagulated patients, hemorrhagic transformation often results in major neurologic worsening; therefore, this risk must be weighed against the danger of recurrent embolism in the absence of anticoagulation. We recommend avoiding anticoagulation during the initial 24 to 48 hours after a stroke, especially in patients with large cardioembolic infarcts. Because of the many invasive procedures producing bacteremia in TAH patients, combined with the large area of prosthetic surfaces, infective endocarditis is a potential concern. Weighing the risks and benefits of anticoagulation in patients with infective endocarditis is likely to produce a controversial choice. Anticoagulation should probably be continued in such patients if they have total artificial hearts. The following article discusses the foregoing issues and presents recommendations for managing acute stroke in TAH patients.
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PMID:Stroke and the total artificial heart: neurologic considerations. 1522 32


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