Critical care involves the care of the sickest patients in the hospital. Critically ill patients have usually been through a significant insult to their body (such as trauma, infection, burn) and have developed organ failure and require life-support. Critical Care is the largest theme bringing together clinicians and scientists from diverse backgrounds and includes collaborative research from hospitals throughout north-west London. Investigations range from evaluating biological mechanisms of organ failure through to the development of innovative technologies which allow the short-term and long-term support and recovery of organs.
Many people are exposed to the environment of an Intensive care unit (ICU) either personally or through a family member. It is often a life-changing event and our work aims to reduce this impact facilitating post-ICU recovery.
Research themes:
- Acute Respiratory Distress Syndrome (ARDS)
- Burn injury
- Extracorporeal life support
- Functional outcomes and health service research
- Sepsis
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Conference paperAntcliffe D, Wolfer A, O'Dea KP, et al., 2015,
Profiling Of Eicosanoids And Cytokines As An Aid To Diagnosing Pneumonia On Intensive Care
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Conference paperNguyen RT, Thippeswamy G, Ravishankar S, et al., 2015,
Impact Of Arterial Oxygen Levels On Cerebral Oxygen Delivery And Return Of Spontaneous Circulation In Cardiac Arrest
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Journal articleGrover V, Pantelidis P, Soni N, et al., 2014,
A biomarker panel (Bioscore) incorporating monocytic surface and soluble TREM-1 has high discriminative value for ventilator-associated pneumonia: a prospective observational study
, PLOS One, Vol: 9, ISSN: 1932-6203 -
Journal articlePatel A, Laffan MA, Waheed U, et al., 2014,
Randomised trials of human albumin for adults with sepsis: systematic review and meta-analysis with trial sequential analysis of all-cause mortality
, British Medical Journal, Vol: 349, ISSN: 0959-8138Objective To assess the efficacy and safety of pooled human albumin solutions as part of fluid volume expansion and resuscitation (with or without improvement of baseline hypoalbuminaemia) in critically unwell adults with sepsis of any severity.Design Systematic review and meta-analysis of randomised clinical trials, with trial sequential analysis, subgroup, and meta-regression analyses.Data sources PubMed, PubMed Central, Web of Science (includes Medline, Conference Proceedings Citation Index, Data Citation Index, Chinese Science Citation Database, CAB abstracts, Derwent Innovations Index), OvidSP (includes Embase, Ovid Medline, HMIC, PsycINFO, Maternity and Infant Care, Transport Database), Cochrane Library, clinicaltrials.gov, controlled-trials.com, online material, relevant conference proceedings, hand searching of reference lists, and contact with authors as necessary.Eligibility criteria Prospective randomised clinical trials of adults with sepsis of any severity (with or without baseline hypoalbuminaemia) in critical or intensive care who received pooled human albumin solutions as part of fluid volume expansion and resuscitation (with or without improvement of hypoalbuminaemia) compared with those who received control fluids (crystalloid or colloid), were included if all-cause mortality outcome data were available. No restriction of language, date, publication status, or primary study endpoint was applied.Data extraction Two reviewers independently assessed articles for inclusion, extracted data to assess risk of bias, trial methods, patients, interventions, comparisons, and outcome. The relative risk of all-cause mortality was calculated using a random effects model accounting for clinical heterogeneity.Primary outcome measure All-cause mortality at final follow-up.Results Eighteen articles reporting on 16 primary clinical trials that included 4190 adults in critical or intensive care with sepsis, severe sepsis, or septic shock. A median of 70.0 g daily of p
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Journal articleVizcaychipi MP, Watts HR, O'Dea KP, et al., 2014,
The Therapeutic Potential of Atorvastatin in a Mouse Model of Postoperative Cognitive Decline
, ANNALS OF SURGERY, Vol: 259, Pages: 1235-1244, ISSN: 0003-4932- Author Web Link
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- Citations: 38
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Journal articleOrme RMLE, Perkins GD, McAuley DF, et al., 2014,
An efficacy and mechanism evaluation study of Levosimendan for the Prevention of Acute oRgan Dysfunction in Sepsis (LeoPARDS): protocol for a randomized controlled trial
, Trials, Vol: 15, Pages: 1-10 -
Journal articleRoberts JA, Paul SK, Akova M, et al., 2014,
DALI: Defining Antibiotic Levels in Intensive Care Unit Patients: Are Current β-Lactam Antibiotic Doses Sufficient for Critically Ill Patients?
, CLINICAL INFECTIOUS DISEASES, Vol: 58, Pages: 1072-1083, ISSN: 1058-4838- Author Web Link
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- Citations: 691
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Journal articlePatel A, Brett SJ, 2014,
Identifying Future Risk From Routine Tests?
, Critical Care Medicine, Vol: 42, Pages: 999-1000, ISSN: 0090-3493 -
Journal articleWalden AP, Clarke GM, McKechnie S, et al., 2014,
Patients with community acquired pneumonia admitted to European Intensive Care Units: an epidemiological survey of the GenOSept cohort
, Critical Care, Vol: 18IntroductionCommunity acquired pneumonia (CAP) is the most common infectious reason for admission to the Intensive Care Unit (ICU). The GenOSept study was designed to determine genetic influences on sepsis outcome. Phenotypic data was recorded using a robust clinical database allowing a contemporary analysis of the clinical characteristics, microbiology, outcomes and independent risk factors in patients with severe CAP admitted to ICUs across Europe.MethodsKaplan-Meier analysis was used to determine mortality rates. A Cox Proportional Hazards (PH) model was used to identify variables independently associated with 28-day and six-month mortality.ResultsData from 1166 patients admitted to 102 centres across 17 countries was extracted. Median age was 64 years, 62% were male. Mortality rate at 28 days was 17%, rising to 27% at six months. Streptococcus pneumoniae was the commonest organism isolated (28% of cases) with no organism identified in 36%. Independent risk factors associated with an increased risk of death at six months included APACHE II score (hazard ratio, HR, 1.03; confidence interval, CI, 1.01-1.05), bilateral pulmonary infiltrates (HR1.44; CI 1.11-1.87) and ventilator support (HR 3.04; CI 1.64-5.62). Haematocrit, pH and urine volume on day one were all associated with a worse outcome.ConclusionsThe mortality rate in patients with severe CAP admitted to European ICUs was 27% at six months. Streptococcus pneumoniae was the commonest organism isolated. In many cases the infecting organism was not identified. Ventilator support, the presence of diffuse pulmonary infiltrates, lower haematocrit, urine volume and pH on admission were independent predictors of a worse outcome.
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Journal articleGordon AC, Mason AJ, Perkins GD, et al., 2014,
The interaction of vasopressin and corticosteroids in septic shock: A pilot randomized controlled trial
, Critical Care Medicine, Vol: 42, Pages: 1325-1333, ISSN: 0090-3493OBJECTIVES: Vasopressin and corticosteroids are both commonly used adjunctive therapies in septic shock. Retrospective analyses have suggested that there may be an interaction between these drugs, with higher circulating vasopressin levels and improved outcomes in patients treated with both vasopressin and corticosteroids. We aimed to test for an interaction between vasopressin and corticosteroids in septic shock. DESIGN: Prospective open-label randomized controlled pilot trial. SETTING: Four adult ICUs in London teaching hospitals. PATIENTS: Sixty-one adult patients who had septic shock. INTERVENTIONS: Initial vasopressin IV infusion titrated up to 0.06 U/min and then IV hydrocortisone (50 mg 6 hourly) or placebo. Plasma vasopressin levels were measured at 6-12 and 24-36 hours after hydrocortisone/placebo administration. MEASUREMENTS AND MAIN RESULTS: Thirty-one patients were allocated to vasopressin + hydrocortisone and 30 patients to vasopressin + placebo. The hydrocortisone group required a shorter duration of vasopressin therapy (3.1 d; 95% CI, 1.1-5.1; shorter in hydrocortisone group) and required a lower total dose of vasopressin (ratio, 0.47; 95% CI, 0.32-0.71) compared with the placebo group. Plasma vasopressin levels were not higher in the hydrocortisone group compared with the placebo group (64 pmol/L difference at 6- to 12-hour time point; 95% CI, -32 to 160 pmol/L). Early vasopressin use was well tolerated with only one serious adverse event possibly related to study drug administration reported. There were no differences in mortality rates (23% 28-day mortality in both groups) or organ failure assessments between the two treatment groups. CONCLUSIONS: Hydrocortisone spared vasopressin requirements, reduced duration, and reduced dose, when used together in the treatment of septic shock, but it did not alter plasma vasopressin levels. Further trials are needed to assess the clinical effectiveness of vasopressin as the initial vasopressor therapy with or
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