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Search Results: 1 - 10 of 1364 matches for " Bala Venkatesh "
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Stewart's Textbook of Acid-Base, 2nd edition
Bala Venkatesh
Critical Care , 2009, DOI: 10.1186/cc7906
Abstract: Retaining Stewart's original masterly work represents one of the highlights of the book. In the new section, the coverage is broad, and certain chapters such as those on intracellular [H], buffers, and the use of the Stewart model at the bedside are exceedingly well written. The chapters on the Stewart approach during pregnancy and a review of comparative animal physiology are useful additions.However, criticisms can be made. Important errors of fact have slipped through the proofreading process, along with some controversial assertions. To illustrate:Table 13.1: The normal plasma ionized calcium concentration is reported as 1 mEq/L, which is equivalent to 0.5 mmol/L. The normal plasma ionized calcium concentration ranges from 1.1 to 1.3 mmol/L. Similarly, the generic intracellular fluid (ICF) calcium concentration is reported as 35 mEq/L, which is equivalent to 17.5 mmol/L. This is exceedingly high. The intracellular [Ca] is of the order of nanomoles per litre.Table 21.1: The strong ion difference (SID) of gelofusine is reported as 30, whereas the correct value is 34 (manufacturer's data).Table 28.2: The SID of 5% albumin is reported as 0. The SID of 4% albumin is 12. The SID of 5% albumin is unlikely to be 0, which would result in a highly acidic solution.Section 27.4: It is suggested that elevated lactate from catecholamines results from increased Krebs cycle activity. It is actually due to accelerated glycolysis. In this section, it is also suggested that reliance on base excess as a resuscitation target in patients receiving catecholamines may lead to an inappropriate diagnosis of hypoperfusion, as base deficits can result purely from catecholamine-induced hyperlactatemia. Similar errors can result from the use of strong ion gap (SIG) (when lactate is not included in the calculation). Finally, it is asserted that standard base excess (SBE) is unstable as partial pressure of carbon dioxide (PCO2) changes. SBE, unlike actual base excess (ABE), is extremely stable
Topics in neuroanaesthesia and intensive care
Bala Venkatesh, Andrea Beindorf
Critical Care , 2003, DOI: 10.1186/cc2346
Abstract: The major attraction of the book is the summary of a large number of studies on various aspects of neurointensive care and anaesthesia, accompanied by a detailed bibliography at the end of each chapter. It thus provides a quick access to the medical literature on a specialized area of intensive care and anaesthesia, some of which may not be available on Medline or Pubmed. There are some good chapters, particularly those on measurement of cerebral blood flow and acute head injury. However, some drawbacks do exist.The main limitation of the book is the style of presentation. The layout of the headings and the subheadings makes it difficult for the reader to follow the sequence of presentation, and every now and then one has to go back a few pages to pick up on the theme. For example, the simple style of presentation found in chapter 1 is lost in chapter 2, where regulation of cerebral blood flow (arterial oxygen tension) and metabolic regulation of cerebral blood flow are discussed as separate subheadings. In the latter subsection, the coupling between oxygen consumption and cerebral blood flow is again reviewed.Important sections of neurointensive care such as status epilepticus, neuromuscular disorders and cerebrovascular diseases are not covered. The authors in the section on cerebral ischaemia mention that, as stroke patients do not come to the neurointensive care unit, these areas will not be discussed. However, with the advent of thrombolysis for ischaemic cerebrovascular accidents and more aggressive surgical drainage of intracerebral haematomata, these patients are increasingly being referred to the neurointensive care unit.Another notable limitation is the relative inequity in the apportioning of the discussion to experimental data versus current clinical practice. For example, the discussion on triple-H therapy for vasospasm occupies one page, while a discussion of experimental therapies spans more than three pages.A few factual errors and omissions have cre
Unmeasured anions: the unknown unknowns
Bala Venkatesh, Thomas J Morgan
Critical Care , 2008, DOI: 10.1186/cc6768
Abstract: Unmeasured ions have long captured the imagination of intensivists. Potential candidates include L-lactate, β-hydroxybutyrate, D-lactate, salicylate, formate and oxalate in toxicological situations, pyroglutamate, semisynthetic penicillins, sulphate and hippurate in renal failure, and occasionally urate and amino acids with catabolic states and total parenteral nutrition. Reports of increased tricyclic acid (TCA) cycle anions in shock are now emerging [1,2].Their presence is often inferred from the anion gap (AG), calculated as [Na+] + [K+] - ([Cl-] + [HCO3-]). When its reference range is exceeded, a search for unmeasured anions should commence, irrespective of the overall metabolic acid-base status, because a competing metabolic alkalosis can mask their presence. Likely culprits vary with the clinical scenario, but the search usually starts with L-lactate and β-hydroxybutyrate. During this process, stoichiometry is tracked between ΔAG (measured AG – normal AG) and the summed concentrations of suspect anions (always in mEq/l, because we are dealing in electrical neutrality). If ΔAG – [suspect anions] exceeds 2 to 3 mEq/l, then the involvement of other unmeasured anions is likely.Unfortunately, the AG is a flawed instrument. Both sensitivity and specificity are reduced by perturbations of albumin (remembering that albumin negative charge forms the bulk of the normal AG), pH, [Ca2+], [Mg2+] and [phosphate] [3]. The most promising alternative is the strong ion gap (SIG) [4,5] Like the AG, the SIG quantifies unmeasured anions minus unmeasured cations, but unlike its predecessor it is insulated from variations in [albumin], [phosphate], pH, [L-lactate], [Ca2+] and [Mg2+] [6].In the previous issue of Critical Care, Bruegger and colleagues [1] combine SIG calculations with capillary electrophoresis, and report that anions associated with the TCA cycle, specifically citrate and acetate, contribute to the metabolic acidosis of canine haemorrhagic shock. Their data originate
Clinical review: Adiponectin biology and its role in inflammation and critical illness
Katherine Robinson, John Prins, Bala Venkatesh
Critical Care , 2011, DOI: 10.1186/cc10021
Abstract: It is now known that adipose tissue is a dynamic endocrine organ in its own right, secreting a number of biologically active proteins, also known as adipokines [1]. One of these adipokines, adiponectin, has been recognised to play a major role in the pathogenesis of the metabolic syndrome. In recent years, its role in the modulation of inflammation has become increasingly apparent. There has therefore been a spate of research examining its role in critical illness and sepsis. In this review we will discuss the biology of adiponectin and its physiological role, with a predominant emphasis on its role in inflammation and critical illness.The source of adipokines is either the adipocytes themselves or the stromal vascular fraction within adipose tissue, comprising preadipocytes, endothelial cells, fibroblasts, leukocytes and macrophages [1]. Resident stromal macrophages are a source of IL-10 and arginase. However, 'classically activated' macrophages recruited from the circulation to obese adipose tissue secrete the pro-inflammatory cytokines TNF-α, inducible nitric oxide synthase, and IL-6. Adipocytes are responsible for the production of adiponectin, leptin, angiotensinogen and retinol-binding protein. Some adipokines, including monocyte chemoattractant protein-1 and apelin, are produced by both fractions [1,2].Adiponectin is a protein produced and secreted almost exclusively by adipocytes [3]. First described over a decade ago, the interest in the biology of adiponectin was spurred by the discovery of measurable concentrations in plasma, its structural resemblance to complement factor C1q and the consistent finding of decreased levels in obesity [4]. Adiponectin circulates in high concentrations in healthy adults and mice, accounting for 0.01% of total plasma protein and its plasma levels are a thousand times that of leptin [5]. Circulating levels of adiponectin range between 2 and 30 μg/ml in humans [4,6] and are generally higher in females than males [7]. This sexu
Changes in serum adiponectin concentrations in critical illness: a preliminary investigation
Bala Venkatesh, Ingrid Hickman, Janelle Nisbet, Jeremy Cohen, John Prins
Critical Care , 2009, DOI: 10.1186/cc7941
Abstract: Twenty three critically ill patients (9 severe sepsis, 7 burns, 7 trauma). Adiponectin assays on Days 3 (D3) and 7 (D7). Simultaneous, cortisol, cortisone and CRP measurements. Data from 16 historical controls were used for comparison.The mean plasma adiponectin concentration for the ICU cohort on D3 and D7 were not significantly different (4.1 ± 1.8 and 5.0 ± 3.3 mcg/ml respectively, P = 0.38). However, these were significantly lower than the mean plasma adiponectin in the control population (8.78 ± 3.81 mcg/ml) at D3 (P < 0.0001) and D7 (P = 0.002). Plasma adiponectin showed a strong correlation with plasma cortisol in the ICU group on both D3 (R2 = 0.32, P < 0.01) and D7 (R2 = 0.64, 0.001). There was an inverse correlation between plasma adiponectin and CRP on D7, R = -0.35.In this preliminary study, critical illness was associated with lower adiponectin concentrations as compared with controls. A significant relationship between plasma cortisol and adiponectin in critically ill patients was evident, both during the early and late phases. These data raise the possibility that adiponectin may play a part in the inflammatory response in patients with severe illness.Adiponectin, a hormone secreted exclusively by adipose tissue, plays an important role in the regulation of tissue inflammation and insulin sensitivity [1]. Perturbations in circulating adiponectin concentrations are associated with the metabolic syndrome, altered inflammatory response and insulin resistance [2]. Hypoadiponectaemia is also associated with impaired endothelium-dependent vasorelaxation [3]. Although several of the above features are also evident in human critical illness, the underlying mechanisms are not fully understood. Some of these manifestations have been attributed to changes in plasma cortisol profile.Data in patients with viral infections and human experimental endotoxaemia suggest altered release patterns of adiponectin in these states [4,5]. However, there are no published data
Acute fluid shifts influence the assessment of serum vitamin D status in critically ill patients
Anand Krishnan, Judith Ochola, Julie Mundy, Mark Jones, Peter Kruger, Emma Duncan, Bala Venkatesh
Critical Care , 2010, DOI: 10.1186/cc9341
Abstract: Nineteen patients undergoing cardiopulmonary bypass were studied. Serum 25(OH)D3, 1α,25(OH)2D3, parathyroid hormone, C-reactive protein (CRP), and ionised calcium were measured at five defined timepoints: T1 - baseline, T2 - 5 minutes after onset of cardiopulmonary bypass (CPB) (time of maximal fluid effect), T3 - on return to the intensive care unit, T4 - 24 hrs after surgery and T5 - 5 days after surgery. Linear mixed models were used to compare measures at T2-T5 with baseline measures.Acute fluid loading resulted in a 35% reduction in 25(OH)D3 (59 ± 16 to 38 ± 14 nmol/L, P < 0.0001) and a 45% reduction in 1α,25(OH)2D3 (99 ± 40 to 54 ± 22 pmol/L P < 0.0001) and i(Ca) (P < 0.01), with elevation in parathyroid hormone (P < 0.0001). Serum 25(OH)D3 returned to baseline only at T5 while 1α,25(OH)2D3 demonstrated an overshoot above baseline at T5 (P < 0.0001). There was a delayed rise in CRP at T4 and T5; this was not associated with a reduction in vitamin D levels at these time points.Hemodilution significantly lowers serum 25(OH)D3 and 1α,25(OH)2D3, which may take up to 24 hours to resolve. Moreover, delayed overshoot of 1α,25(OH)2D3 needs consideration. We urge caution in interpreting serum vitamin D in critically ill patients in the context of major resuscitation, and would advocate repeating the measurement once the effects of the resuscitation have abated.Vitamin D is synthesised in the skin through UV action on 7-dehydrocholesterol, to cholecalciferol. It is transported in the blood by the Vitamin D binding protein (VDBP) to the liver where it undergoes 25 hydroxylation to form 25(OH)D3, which in turn undergoes 1α hydroxylation (especially, but not exclusively in the kidneys) to form 1α,25(OH)2D3. Its traditionally recognised role is to maintain adequate serum calcium and phosphate levels, for bone mineralisation and optimal cardiac [1] and skeletal muscle function [2]. However, increasing data from biochemical, and molecular genetic studies indicate that vitamin
Tissue Doppler in critical illness: a retrospective cohort study
David J Sturgess, Thomas H Marwick, Christopher J Joyce, Mark Jones, Bala Venkatesh
Critical Care , 2007, DOI: 10.1186/cc6114
Abstract: This retrospective study was performed in a combined medical/surgical, tertiary referral intensive care unit. Over a 2-year period, 94 consecutive patients who underwent transthoracic echocardiography with E/E' measurement were studied.Mean Acute Physiology and Chronic Health Evaluation III score was 72 ± 25. Echocardiography was performed 5 ± 6 days after intensive care unit admission. TDI variables exhibited a wide range (E' 4.7–18.2 cm/s and E/E' 3.3 to 27.2). E' below 9.6 cm/s was observed in 63 patients (rate of myocardial relaxation below lower 95% confidence limit of normal individuals). Fourteen patients had E/E' above 15 (evidence of raised left ventricular filling pressure). E/E' correlated with left atrial area (r = 0.27, P = 0.01) but not inferior vena cava diameter (r = 0.16, P = 0.21) or left ventricular end-diastolic volume (r = 0.16, P = 0.14). In this cohort, increased left ventricular end-systolic volume, but not E/E', appeared to be an independent predictor (odds ratio 2.1, P = 0.007) of 28-day mortality (31%; n = 29).There was a wide range of TDI values. TDI evidence of diastolic dysfunction was common. E/E' did not correlate strongly with other echocardiographic indices of preload. Further evaluation of echocardiographic variables, particularly left ventricular end-systolic volume, for risk stratification in the critically ill appears warranted.Myocardial dysfunction is common in critically ill patients. Causes include ischaemia, trauma, surgery, sepsis, drugs and toxins. Transthoracic echocardiography is gaining acceptance as a powerful diagnostic tool in this setting [1]. In recent years, tissue Doppler imaging (TDI) has gained increasing acceptance as a means of noninvasively assessing myocardial properties [2] and estimating ventricular filling pressure [3,4], and as a prognostic tool in cardiac diseases [5,6]. However, there is a paucity of published data on TDI in critical illness.TDI is an echocardiographic technique that measures myocard
Measurement of tissue cortisol levels in patients with severe burns: a preliminary investigation
Jeremy Cohen, Renae Deans, Andrew Dalley, Jeff Lipman, Michael S Roberts, Bala Venkatesh
Critical Care , 2009, DOI: 10.1186/cc8184
Abstract: A prospective observational study carried out in a tertiary intensive care unit. Ten adult patients with a mean total burn surface area of 48% were studied. Interstitial cortisol was measured by microdialysis from patient-matched burnt and non-burnt tissue and compared with that of 3 healthy volunteers. Plasma sampling for estimations of total and free cortisol concentrations was performed concurrently.In the burn patients, mean total plasma and free plasma cortisol concentrations were 8.8 +/- 3.9, and 1.7 +/- 1.1 mcg/dL, (p < 0.001), respectively. Mean subcutaneous microdialysis cortisol concentrations in the burn and non-burn tissue were 0.80 +/- 0.31 vs 0.74 +/- 0.41 mcg/dL (p = 0.8), respectively, and were significantly elevated over the mean subcutaneous microdialysis cortisol concentrations in the healthy volunteers. There was no significant correlation between total plasma or free plasma and microdialysis cortisol concentrations. Plasma free cortisol was better correlated with total burn surface area than total cortisol.In this preliminary study, interstitial cortisol concentrations measured by microdialysis in burnt and non-burnt skin from patients with severe thermal injury are significantly elevated over those from healthy volunteers. Plasma estimations of cortisol do not correlate with the microdialysis levels, raising the possibility that plasma cortisol may be an unreliable guide to tissue cortisol activity.The severely burned patient suffers from a rapidly changing pathophysiology in the immediate post-burn period characterized by wound inflammation, cardiopulmonary instability, systemic inflammatory response syndrome and metabolic derangement. One of the integral components of this stress response is the activation of the adrenal axis resulting in an exaggerated output of cortisol. A number of studies have demonstrated increases in total plasma cortisol and adrenocorticotrophic hormone (ACTH) concentrations in the days following thermal injury [1-3].
Plasma protein C levels in immunocompromised septic patients are significantly lower than immunocompetent septic patients: a prospective cohort study
Rakshit Panwar, Bala Venkatesh, Peter Kruger, Robert Bird, Devinder Gill, Leo Nunnink, Goce Dimeski
Journal of Hematology & Oncology , 2009, DOI: 10.1186/1756-8722-2-43
Abstract: To assess serum Protein C concentrations in immunocompromised patients as compared to immunocompetent patients during sepsis, severe sepsis, septic shock and recovery.Prospective cohort study in a tertiary hospital. Patients satisfying inclusion criteria were enrolled after informed consent. Clinical variables were noted with sample collection when patients met criteria for sepsis, severe sepsis, septic shock and recovery. Protein C levels were measured using monoclonal antibody based fluorescence immunoassay.Thirty one patients participated in this study (22 immunocompromised, 9 immunocompetent). Protein C levels were found to be significantly lower in the immunocompromised group compared to the immunocompetent group, particularly observed in severe sepsis [2.27 (95% CI: 1.63-2.9) vs 4.19 (95% CI: 2.87-5.52) mcg/ml] (p = 0.01) and sepsis [2.59 (95% CI: 1.98-3.21) vs 3.64 (95% CI: 2.83-4.45) mcg/ml] (p = 0.03). SOFA scores were similar in both the groups across sepsis, severe sepsis and septic shock categories. Protein C levels improved significantly in recovery (p = 0.001) irrespective of immune status.Protein C levels were significantly lower in immunocompromised patients when compared to immunocompetent patients in severe sepsis and sepsis categories. Our study suggests a plausible role for APC in severely septic immunocompromised patients which need further elucidation.The role of Protein C pathway in regulating thrombosis, fibrinolysis and inflammatory cascade in a septic patient is well established. Both baseline serum protein C and early reduction in protein C concentrations have been found to be independent predictors of outcome in severe sepsis [1,2]. This in combination with blunted generation of activated Protein C (APC) act in concert with reduced expression of thrombomodulin to contribute to a procoagulant state during sepsis [3,4]. The resulting intravascular deposition of fibrin and microvascular thrombosis contributes to the organ dysfunction and mor
Prediction of hospital outcome in septic shock: a prospective comparison of tissue Doppler and cardiac biomarkers
David J Sturgess, Thomas H Marwick, Chris Joyce, Carly Jenkins, Mark Jones, Paul Masci, David Stewart, Bala Venkatesh
Critical Care , 2010, DOI: 10.1186/cc8931
Abstract: Twenty-one consecutive adult patients from a multidisciplinary intensive care unit underwent transthoracic echocardiography and blood collection within 72 hours of developing septic shock.Mean ± SD APACHE III score was 80.1 ± 23.8. Hospital mortality was 29%. E/e' was significantly higher in hospital non-survivors (15.32 ± 2.74, survivors 9.05 ± 2.75; P = 0.0002). Area under ROC curves were E/e' 0.94, TnT 0.86, BNP 0.78 and NTproBNP 0.67. An E/e' threshold of 14.5 offered 100% sensitivity and 83% specificity. Adjustment for APACHE III, cardiac disease, fluid balance and grade of diastolic function, demonstrated E/e' as an independent predictor of hospital mortality (P = 0.019). Multiple linear regression incorporating APACHE III, gender, cardiac disease, fluid balance, noradrenaline dose, C reactive protein, ejection fraction and diastolic dysfunction yielded APACHE III (P = 0.033), fluid balance (P = 0.001) and diastolic dysfunction (P = 0.009) as independent predictors of BNP concentration.E/e' is an independent predictor of hospital survival in septic shock. It offers better discrimination between survivors and non-survivors than cardiac biomarkers. Fluid balance and diastolic dysfunction were independent predictors of BNP concentration in septic shock.Septic shock in adults refers to a state of acute circulatory failure characterized by persistent arterial hypotension unexplained by other causes [1]. Although this clinical syndrome is heterogeneous with regard to factors such as causal micro-organism, patient predisposition, co-morbidity and response to therapy, a key element and unifying feature is the manifestation of cardiovascular dysfunction. Although the underlying cause of death in septic shock is often multifactorial, refractory hypotension and cardiovascular collapse are frequently observed in the terminal phases of the condition [2]. Whilst impaired systolic function has been identified as the major culprit, the contribution of diastolic dysfunction (a
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