Critical Care - Latest articles

Efficacy of oral chlorhexidine in critical care

Matt P Wise, Jade M Cole, David W Williams, Mike A Lewis and Paul J Frost — 2008-05-14

No abstract as submission is letter

Clinical review: The role of the intensive care physician in mass casualty incidents: planning, organisation, and leadership

Peter J Shirley and Gerlinde Mandersloot — 2008-05-14

There is a long-standing, broad assumption that hospitals will ably receive and efficiently provide comprehensive care to victims following a mass casualty event. Unfortunately, the majority of medical major incident plans are insufficiently focused on strategies and procedures that extend beyond the pre-hospital and early-hospital phases of care. Recent events underscore two important lessons: (a) the role of intensive care specialists extends well beyond the intensive care unit during such events, and (b) non-intensive care hospital personnel must have the ability to provide basic critical care. The bombing of the London transport network, while highlighting some good practices in our major incident planning, also exposed weaknesses already described by others. Whilst this paper uses the events of the 7 July 2005 as its point of reference, the lessons learned and the changes incorporated in our planning have generic applications to mass casualty events. In the UK, the Department of Health convened an expert symposium in June 2007 to identify lessons learned from 7 July 2005 and disseminate them for the benefit of the wider medical community. The experiences of clinicians from critical care units in London made a large contribution to this process and are discussed in this paper.

Causes of a high physiological dead space in critically ill patients

Peter D Wagner — 2008-05-14

Since around 1950, physiological deadspace - the ratio of (arterial - mixed expired) PCO2 to arterial PCO2 - has been a useful clinical parameter of pulmonary gas exchange. In this issue, Niklason (1) reminds us that physiological deadspace, while easily measured, consolidates potentially very complex physiological derangements into a single number. Niklason shows how shunts raise arterial PCO2, thereby increasing deadspace, and how changes in other variables such as cardiac output and acid/base state further modify it. It requires a solid understanding of respiratory physiology to properly interpret physiological deadspace in the critically ill.

The promise of next generation colloids

Ben C Creagh-Brown and Timothy W Evans — 2008-05-14

The aim of perioperative haemodilution is to reduce loss of red blood cells during elective surgery. The oncotic and molecular characteristics of the various plasma substitutes employed determine how effectively normovolaemia is maintained, and their non-oncotic effects include alterations in microvascular perfusion. In the previous issue of Critical Care, Martini and colleagues assessed the effects of haemodilution with either polyethylene glycol (PEG)ylated albumin or a commercially available hydroxyethyl starch-based colloid in a hamster haemorrhage model. PEGylated albumin was superior to hydroxyethyl starch, as reflected by survival, haemodynamic parameters and assessment of the microcirculation using intravital microscopy.

Optic nerve sonography in the diagnostic evaluation of adult brain injury

2008-05-13

IntroductionThe optic nerve sheath diameter (ONSD) may be increased in brain-injured patients, especially children, with intracranial hypertension. We investigated whether measurements of the ONSD were correlated with simultaneous non-invasive and invasive measurements of the intracranial pressure (ICP) in brain-injured adults. Methods: Seventy-six critical care patients (58 males, 47 +/- 18 years old) were included in the study. Fifty patients suffered from brain injury, while 26 had no intracranial pathology and served as controls. Initially, brain-injured patients were evaluated clinically (Glasgow Coma Scale, GCS) and by a semi-quantitative (I to VI) neuroimaging scale (Marshall Scale, MS). Thereafter, all cases were divided into patients with moderate (MS= I and GCS>8, n= 18) and severe (MS= II to VI and GCS[less than or equal to]8, n= 32) brain injury. All patients underwent non-invasive measurements of the ICP (eICP) by transcranial Doppler sonography, and synchronous ONSD measurements by optic nerve sonography. Finally, invasive measurements of the ICP by an intraparenchymal catheter were performed in patients with severe brain injury. Results: ONSD and eICP were both significantly increased (6.1 +/- 0.7 mm and 26.2 +/- 8.7 mmHg, respectively, P<0.0001) in patients with severe brain injury as compared to patients with moderate one (4.2 +/- 1.2 mm and 12.0 +/- 3.6 mmHg, respectively) and to controls (3.6 +/- 0.6 mm and 10.3 +/- 3.1 mmHg, respectively). Furthermore, in patients with severe brain injury the ONSD measurements were strongly correlated to the eICP values (r = 0.80, P<0.0001), as well as to the neuroimaging scale results (r = 0.82, P< 0.001). In the patients with severe brain injury the ONSD measurements correlated to the invasive ICP values (r = 0.68, P= 0.002). The best cut-off value of ONSD for the prediction of elevated ICP was 5.7 mm (sensitivity 74.1%, specificity 100%). Conclusion: ONSD measurements correlate with non-invasive and invasive measurements of the ICP, as well as with head CT scan findings in brain-injured adults. Hence, optic nerve sonography may serve as an additional diagnostic tool, which could alert clinicians for the presence of elevated ICP, whenever invasive ICP evaluation is contraindicated and/or is not available. This trial is ISRCTN registered (ISRCTN 91941687)

Good night, sleep tight: the time is ripe for critical care providers to wake up and focus on sleep

Randall S Friese — 2008-05-12

The role of sleep during recovery from acute illness has been overlooked for decades. Advances in the support of critically ill patients have been made in mechanical ventilation, specialized nutrition support, highly specific antibiotic therapy, and early rehabilitation. However, the promotion of sleep – a basic tenet for survival – has been actively ignored by critical care providers. Bourne and coworkers recently conducted a small clinical trial that describes improved sleep efficiency with oral melatonin use in critically ill patients.

Severe hyperlactatemia with normal base excess: a quantitative analysis using conventional and Stewart approaches

2008-05-08

Background: Critically ill patients might present complex acid-base disorders, even when pH, PCO2, [HCO3-], and base excess ([BE]) are normal. Our hypothesis was that the acidifying effect of severe hyperlactatemia is frequently masked by alkalinizing processes that normalize the [BE]. Therefore, our goal was to quantify these disorders using both Stewart and conventional approaches. Methods: 1,592 consecutive patients were prospectively evaluated on intensive care unit admission. Patients with severe hyperlactatemia (lactate level greater than or equal to 4.0 mmol/l) were grouped according to low or normal [BE] (< or > -3 mmol/l). Results: Severe hyperlactatemia was present in 168 of the patients (11%). One hundred and thirty-four patients had low [BE] (80%) while 34 (20%) did not. Shock was more frequently present in low-[BE] group (46 vs. 24%, p = 0.02) and chronic obstructive pulmonary disease in the normal-[BE] group (38 vs. 4%, p < 0.0001). Levels of lactate were slightly higher in patients with low [BE] (6.4 +/- 2.4 vs. 5.6 +/- 2.1 mmol/l, p = 0.08). According to our study design, pH, [HCO3-], and strong ion difference were lower in patients with low [BE]. Patients with normal [BE] had lower plasma [Cl-] (100 +/- 6 vs. 107 +/- 5 mmol/l, p < 0.0001) and higher differences between the changes in anion gap and [HCO3-] (5 +/- 6 vs. -1 +/- 4 mmol/l, p < 0.0001). Conclusions: Critically ill patients may present severe hyperlactatemia with normal values of pH, [HCO3-], and [BE] as a result of associated hypochloremic alkalosis.

Adrenal insufficiency in prolonged critical illness

2008-05-08

IntroductionAdrenal insufficiency is frequently found in critically ill patients and affects their prognosis. But little is known about how the adrenal function changes during prolonged critical illness. This study was conducted to investigate the dynamic changes of cortisol levels in patients with critical illness who do not improve after treatment. Methods: This observational cohort study was performed in the intensive care units of a university hospital. Acutely ill patients with initial cortisol level above 34mug/dL but without improvement after treatment, and who had follow-up cortisol levels during their critical illness, were studied. All clinical information and outcomes were recorded. Results: Fifty-three patients were included. Ten patients had follow-up cortisol levels > 34mug/dL, 32 patients between 34 and 15mug/dL, and 15 patients < 15mug/dL. Outcomes did not differ significantly among the three groups with different second cortisol levels. In Cox regression analysis, patients who survived to hospital discharge with second cortisol levels < 15mug/dL had a longer hospital length of stay (p = 0.004, odds ratio 14.8, 95% confidence ratio 2.4 to 90.0). Conclusion: The majority of acutely ill patients who remained in critical condition had decreased serum cortisol levels. Lower follow-up cortisol levels might lead to worse clinical outcomes. Repeated testing for adrenal function is suggested for patients with prolonged critical illness.

A phase 1 trial of nebulised heparin in acute lung injury

Barry Dixon, John D Santamaria and Duncan J Campbell — 2008-05-06

IntroductionAnimal studies of acute lung injury (ALI) suggest nebulised heparin may limit damage from fibrin deposition in the alveolar space and microcirculation. To date no human studies have been undertaken. We assessed the feasibility, safety and potential anti-coagulant effects of administration of nebulised heparin to patients with ALI. Methods: An open label phase 1 trial of 4 escalating doses of nebulised heparin. A total of 16 ventilated patients with ALI were studied. The first group was administered a total of 50,000 U/day, the second 100,000 U/day, the third 200,000 U/day and the fourth 400,000 U/day. Assessments of lung function included the arterial to inspired oxygen ratio (PaO2/FiO2), lung compliance and the alveolar dead space fraction. Monitoring of anti-coagulation included the activated partial thromboplastin time (APTT) and the thrombin clotting time (TCT). Bronchoalveolar lavage (BAL) fluid was collected and prothrombin fragment (PTF) and tissue plasminogen activator (t-PA) levels were assessed. Analysis of variance was used to compare the effects of dose. Results: No serious adverse events occurred for any dose. The changes over time for the PaO2/FiO2, lung compliance and the alveolar dead space fraction levels were similar for all doses. A trend to increased APTT and TCT levels was present with higher doses (p = 0.09 and 0.1, respectively). For the highest dose the APTT reached 64 seconds and following cessation of nebulised heparin fell to 39 seconds (p = 0.06). In BAL samples a trend to reduced PTF levels was present with higher doses (p = 0.1), while t-PA levels were similar for all doses. Conclusions: Administration of nebulised heparin to mechanically ventilated patients with ALI is feasible. It was not associated with any serious adverse events and at higher doses increased APTT levels. Larger trials are required to further investigate the safety and efficacy of nebulised heparin. In these trials due consideration must be given to systemic anti-coagulant effects. Trial registration: Australian Clinical trials registry ACTRN12606000388516

Bench-to-bedside review: Sepsis, severe sepsis and septic shock – does the nature of the infecting organism matter?

Hongmei Gao, Timothy W Evans and Simon J Finney — 2008-05-06

International guidelines concerning the management of patients with sepsis, septic shock and multiple organ failure make no reference to the nature of the infecting organism. Indeed, most clinical signs of sepsis are nonspecific. In contrast, in vitro data suggest that there are mechanistic differences between bacterial, viral and fungal sepsis, and imply that pathogenetic differences may exist between subclasses such as Gram-negative and Gram-positive bacteria. These differences are reflected in different cytokine profiles and mortality rates associated with Gram-positive and Gram-negative sepsis in humans. They also suggest that putative anti-mediator therapies may act differently according to the nature of an infecting organism. Data from some clinical trials conducted in severe sepsis support this hypothesis. It is likely that potential new therapies targeting, for example, Toll-like receptor pathways will require knowledge of the infecting organism. The advent of new technologies that accelerate the identification of infectious agents and their antimicrobial sensitivities may allow better tailored anti-mediator therapies and administration of antibiotics with narrow spectra and known efficacy.

Diagnosing sepsis: does the microbiology matter?

Jonathan Cohen — 2008-05-06

Sepsis is caused by infection, and knowing what type of organism is causing the infection certainly matters in terms of both epidemiology and selecting antibiotic therapy. Although there is considerable laboratory evidence that micro-organisms initiate sepsis in different ways, the clinical consequences are usually indistinguishable. New drugs that target specific points in the activation pathway are starting to emerge, and these will require us to be much more accurate in how we diagnose sepsis.

Cerebral perfusion in sepsis-associated delirium

2008-05-05

IntroductionThe pathophysiology of sepsis-associated delirium is not completely understood and the data on cerebral perfusion in sepsis are conflicting. We tested the hypotheses that cerebral perfusion and selected serum markers of inflammation and delirium differ in septic patients with and without sepsis-associated delirium. Methods: We investigated 23 adult patients with sepsis, severe sepsis, or septic shock with an extracranial focus of infection and no history of an intracranial pathology. Patients were investigated after stabilisation within 48 h after admission to the intensive care unit. Sepsis-associated delirium was diagnosed using the confusion assessment method for the intensive care unit (CAM-ICU). Mean arterial pressure (MAP), blood flow velocity in the middle cerebral artery using transcranial Doppler, and cerebral tissue oxygenation using near-infrared spectroscopy were monitored for one hour. An index of cerebrovascular autoregulation was calculated from MAP and FV data. CRP, IL-6, S-100b and cortisol were measured during each data acquisition. Results: Data from 16 patients, of which 12 had sepsis-associated delirium, were analysed. There were no significant correlations or associations between MAP, cerebral blood flow velocity or tissue oxygenation and sepsis-associated delirium. However, we found a significant association between sepsis-associated delirium and disturbed autoregulation (p = 0.015). IL-6 did not differ between patients with and without sepsis-associated delirium but we found a significant association between elevated CRP (p = 0.008), S-100b (p = 0.029), and cortisol (p = 0.011) and sepsis-associated delirium. Elevated CRP was significantly correlated with disturbed autoregulation (Spearman Rho = 0.62, p = 0.010). Conclusions: In this small group of patients, cerebral perfusion assessed with transcranial Doppler and near-infrared spectroscopy did not differ between patients with and without sepsis-associated delirium. However, the state of autoregulation differed between the two groups. This may be due to inflammation impeding cerebrovascular endothelial function. Further investigations defining the role of S-100b and cortisol in the diagnosis of sepsis-associated delirium are warranted. Trial registration: ClinicalTrials.gov NCT00410111