Clinical practice. Evaluation and management of chronic mitral regurgitation.
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Biomedical subjects
Publications and source records attributed to C M Otto.
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OBJECTIVE: To determine whether hyperglycemia is associated with head trauma in dogs and cats and whether the degree of hyperglycemia corresponds to severity of neurologic injury or outcome. DESIGN: Retrospective study. ANIMALS: 52 dogs and 70 cats with head trauma and 122 age- and species-matched control dogs and cats. PROCEDURE: Severity of head trauma was classified as mild, moderate, or severe. Blood glucose concentrations recorded within 1 hour after admission were compared between case and control animals and among groups when case animals were grouped on the basis of severity of head trauma or outcome. RESULTS: Blood glucose concentration was significantly associated with severity of head trauma in dogs and cats and was significantly higher in dogs and cats with head trauma than in the control animals. However, blood glucose concentration was not associated with outcome. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that dogs and cats with head trauma may have hyperglycemia and that degree of hyperglycemia was associated with severity of head trauma. However, degree of hyperglycemia was not associated with outcome for dogs and cats with head trauma. Because hyperglycemia can potentiate neurologic injury, iatrogenic hyperglycemia should be avoided in patients with head trauma.
Companion animals with sepsis and multiple organ dysfunction can be the most challenging of all patients to treat. Current research in humans and laboratory models offers some exciting insights into the pathophysiology behind some of our most frustrating clinical challenges. This article applies several current concepts to a clinical case of pancreatitis and secondary sepsis to illustrate some of the cardiovascular, immune, and coagulation abnormalities commonly seen.
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Macrophages are commonly cultured at a PO2 of 149 Torr, but tissue macrophages in vivo live in an environment of much lower oxygen tension. Despite the many potential mechanisms for changes in oxygen tension to influence nitric oxide (NO) synthesis, there have been few reports investigating the effect of PO2 on macrophage NO production. With the use of a culture chamber designed to rigorously control oxygen tension, we investigated the effects of culture PO2 on macrophage NO production, inducible nitric oxide synthase (iNOS) activity, iNOS protein, and tumor necrosis factor production. NO production and iNOS activity were linearly related in the range of 39.4 to 677 Torr, but not in the range of 1.03 to 39.4 Torr. Therefore, results obtained in vitro for the high oxygen tensions commonly used in cell culture were quantitatively and qualitatively different from results obtained in cells cultured at the lower oxygen tensions that more accurately reflect the in vivo environment. The influence of oxygen tension on NO production has implications for cell culture methodology and for the relationship between microcirculatory dysfunction and inflammatory responses in rodent models of sepsis.
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OBJECTIVE: To determine whether dogs with naturally occurring canine parvoviral (CPV) enteritis have laboratory evidence of hypercoagulability. DESIGN: Case-control study. Animals-9 dogs with naturally occurring CPV enteritis and 9 age-matched control dogs. PROCEDURE: Blood was collected from all dogs within 24 hours of admission for thromboelastography (TEG) and determination of activated partial thromboplastin time (aP-TT), prothrombin time (PT), antithrombin III (AT) activity, and fibrinogen concentration. Fibrin-fibrinogen degradation product (FDP) concentration, D-dimer concentration, and platelet count were obtained in dogs with CPV enteritis only. Records were reviewed for evidence of thrombosis or phlebitis. RESULTS: All 9 dogs with CPV enteritis had evidence of hypercoagulability, determined on the basis of significantly increased TEG maximum amplitude and decreased AT activity. Fibrinogen concentration was significantly higher in dogs with CPV enteritis than in control dogs. The aPTT was moderately prolonged in dogs with CPV enteritis, and FDP concentration was < 5 mg/ml in 7 of 9 dogs. No dogs had a measurable D-dimer concentration. Platelet counts were within reference range. Four of 9 dogs had clinical evidence of venous thrombosis or phlebitis associated with catheters. One dog had multifocal splenic thrombosis identified at necropsy. CONCLUSIONS AND CLINICAL RELEVANCE: Dogs with CPV enteritis have a high prevalence of clinical thrombosis or phlebitis and laboratory evidence of hypercoagulability without disseminated intravascular coagulopathy. Thromboelastography may help identify hypercoagulable states in dogs.
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OBJECTIVE: To document the clinical, clinicopathologic, and pathologic findings in cats with severe sepsis, identify abnormalities unique to this species, and identify criteria that could be used antemortem to diagnose the systemic inflammatory response syndrome in cats. DESIGN: Retrospective study. ANIMALS: 29 cats confirmed to have severe sepsis at necropsy. PROCEDURE: Pertinent history, physical examination findings, and results of hematologic and biochemical testing were extracted from medical records. RESULTS: Clinical diagnoses included pyothorax, septic peritonitis, bacteremia secondary to gastrointestinal tract disease, pneumonia, endocarditis, pyelonephritis, osteomyelitis, pyometra, and bite wounds. Physical examination findings included lethargy, pale mucous membranes, poor pulse quality, tachypnea, hypo- or hyperthermia, signs of diffuse pain on abdominal palpation, bradycardia, and icterus. Clinicopathologic abnormalities included anemia, thrombocytopenia, band neutrophilia, hypoalbuminemia, low serum alkaline phosphatase activity, and hyperbilirubinemia. Necropsy findings included multi-organ necrosis or inflammation with intralesional bacteria. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that severe sepsis in cats is characterized by lethargy, pale mucous membranes, signs of diffuse abdominal pain, tachypnea, bradycardia, weak pulses, anemia, hypoalbuminemia, hypothermia, and icterus. Recognition of this combination of clinical findings should facilitate the diagnosis of severe sepsis in cats.
BACKGROUND: The ability to predict the rate of hemodynamic progression in an individual patient with valvular aortic stenosis has been elusive. The purpose of the present study was to evaluate whether the rate of change in aortic valve area (AVA) measured during the ejection phase of a cardiac cycle predicts the rate of hemodynamic progression in patients with asymptomatic aortic stenosis. METHODS AND RESULTS: In 84 adults with initially asymptomatic aortic stenosis and a baseline AVA of > or =0.9 cm(2), annual echocardiographic data were obtained prospectively (mean follow-up 2.8+/-1.3 years). With the initial echocardiogram, the ratio of AVA measured at mid-acceleration and mid-deceleration to the AVA at peak velocity was calculated. The primary outcome variable was the annual rate of change in AVA (rate of progression), with rate of progression classified as rapid (a reduction in AVA of > or =0.2 cm(2)/y) or slow (<0.2 cm(2)/y). Rapid progression was significantly associated with an AVA ratio of > or =1.25 (P=0.004, risk ratio 3.1, 95% CI 1.2 to 7.9). The sensitivity, specificity, and positive predictive value of AVA ratio of > or =1.25 for the prediction o rapid progression of valvar aortic stenosis was 64%, 72%, and 80% respectively. The decrease in ejection fraction measured from the initial to final echocardiogram was small but greater for patients with an AVA ratio of > or =1.25 (-4+/-7% versus +2+/-7%, P<0.001). CONCLUSIONS: A flow-dependent change in AVA can be measured during a routine transthoracic echocardiographic study. The rate of change in AVA is an additional measure of disease severity and may be used to predict an individual's risk for subsequent rapid disease progression.
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BACKGROUND: Although aortic-valve stenosis is clearly associated with adverse cardiovascular outcomes, it is unclear whether valve sclerosis increases the risk of cardiovascular events. METHODS: We assessed echocardiograms obtained at base line from 5621 men and women 65 years of age or older who were enrolled in a population-based prospective study. On echocardiography, the aortic valve was normal in 70 percent (3919 subjects), sclerotic without outflow obstruction in 29 percent (1610), and stenotic in 2 percent (92). The subjects were followed for a mean of 5.0 years to assess the risk of death from any cause and of death from cardiovascular causes. Cardiovascular morbidity was defined as new episodes of myocardial infarction, angina pectoris, congestive heart failure, or stroke. RESULTS: There was a stepwise increase in deaths from any cause (P for trend, <0.001) and deaths from cardiovascular causes (P for trend, <0.001) with increasing aortic-valve abnormality; the respective rates were 14.9 and 6.1 percent in the group with normal aortic valves, 21.9 and 10.1 percent in the group with aortic sclerosis, and 41.3 and 19.6 percent in the group with aortic stenosis. The relative risk of death from cardiovascular causes among subjects without coronary heart disease at base line was 1.66 (95 percent confidence interval, 1.23 to 2.23) for those with sclerotic valves as compared with those with normal valves, after adjustment for age and sex. The relative risk remained elevated after further adjustment for clinical factors associated with sclerosis (relative risk, 1.52; 95 percent confidence interval, 1.12 to 2.05). The relative risk of myocardial infarction was 1.40 (95 percent confidence interval, 1.07 to 1.83) among subjects with aortic sclerosis, as compared with those with normal aortic valves. CONCLUSIONS: Aortic sclerosis is common in the elderly and is associated with an increase of approximately 50 percent in the risk of death from cardiovascular causes and the risk of myocardial infarction, even in the absence of hemodynamically significant obstruction of left ventricular outflow.
As the incidence of valvular disease in the elderly is increasing, understanding of its pathogenesis and natural progression as well as surgical approaches and device technologies are improving. Future studies are needed to develop medical interventions that slow or halt the degenerative valvular processes associated with aging. In addition, mechanical approaches with lower operative risks should be explored and the search should continue for a valve substitute that is durable, hemodynamically efficient, easy to implant, and does not require anticoagulation. Hopefully, future intervention trials will include quality of life assessments such as symptoms, functional capacity and perceptions of well being. At present, the degenerative valvular processes must be followed closely by the clinician, and individual management decisions for the elderly based on the type and severity of valve disease, comorbid medical conditions, and the risks and benefits of intervention, along with patient preferences, rather than on the chronologic age of the patient. It is becoming clear that both survival and quality of life outcomes can improve by consideration of surgery at the onset of indications, before further deterioration eliminates the opportunity to provide benefit for the elderly patient with valvular disease.
BACKGROUND AND METHODS: The goal of this study was to examine the ability of physical examination to predict valvular aortic stenosis severity and clinical outcome in 123 initially asymptomatic subjects (mean age 63 +/- 16 years, 70% men) followed up for a mean of 2.5 +/- 1.4 years. RESULTS: Doppler aortic jet velocity correlated with systolic murmur intensity (P =.003) and timing (P =.0002), a single second heart sound (P =.01), and carotid upstroke delay (P <.0001) and amplitude (P <.0001). However, no physical examination findings had both a high sensitivity and a high specificity for the diagnosis of severe valvular obstruction. Clinical end points were reached in 56 subjects (46%), including 8 deaths and 48 valve replacements for symptom onset. Univariate predictors of outcome included carotid upstroke delay (P =.0008) and amplitude (P =.0006), systolic murmur grade (P <.0001) and peak (P =.0003), and a single second heart sound (P =.003). On multivariate Cox regression analysis, the only physical examination predictor of outcome was carotid upstroke amplitude (P =.0001). CONCLUSIONS: Although physical examination findings correlate with stenosis severity, echocardiography still is needed to exclude severe obstruction reliably when this diagnosis is suspected.
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