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Biomedical subjects

I S Grant

Publications and source records attributed to I S Grant.

At least 19 recordsLinked to original sources
PubMed2004

Propofol sedation using Diprifusor target-controlled infusion in adult intensive care unit patients.

This multicentre, non-comparative study investigated the range of target blood propofol concentrations required to sedate 122 adult intensive care patients when propofol was administered using Diprifusor target-controlled infusion systems together with opioid analgesia. Depth of sedation was assessed with a modified Ramsay score and the target blood propofol setting was adjusted to achieve the sedation desired for each patient. A desired level of sedation was achieved for 84% of the sedation period. In postcardiac surgery patients the median time-weighted average propofol target setting was 1.34 microg.ml(-1) (10th - 90th percentiles: 0.79-1.93 microg.ml(-1)). Values in brain injured and general ICU patients were 0.98 (10th - 90th percentiles: 0.60-2.55) microg.ml(-1) and 0.42 (10th - 90th percentiles: 0.16-1.19) microg.ml(-1), respectively. Measured propofol concentrations were generally close to values predicted by the Diprifusor system. Target settings in the range of 0.2-2.0 microg.ml(-1) are proposed for propofol sedation in this setting with titration as required in individual patients.

Adult↗
PubMed2003

Acute respiratory distress syndrome: an audit of incidence and outcome in Scottish intensive care units.

This prospective audit of incidence and outcome of the acute respiratory distress syndrome was conducted as part of the national audit of intensive care practice in Scotland. All patients with acute respiratory distress syndrome in 23 adult intensive care units were identified using the diagnostic criteria defined by the American-European Consensus Conference. Daily data collection was continued until death or intensive care unit discharge. Three hundred and sixty-nine patients were diagnosed with acute respiratory distress syndrome over the 8-month study period. The frequency of acute respiratory distress syndrome in the intensive care unit population was 8.1%; the incidence in the Scottish population was estimated at 16.0 cases.100,000(-1).year(-1). Intensive care unit mortality for acute respiratory distress syndrome was 53.1%, with a hospital mortality of 60.9%. In our national unselected population of critically ill patients, the overall outcome is comparable with published series (Acute Physiology and Chronic Health Evaluation II standardised mortality ratio = 0.99). However, mortality from acute respiratory distress syndrome in Scotland is substantially higher than in recent other series suggesting an improvement in outcome in this condition.

Adult↗
PubMed2002

Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management?

Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same. Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the long-term neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.

Animals↗
PubMed2002

Impact of early endovascular aneurysmal occlusion on outcome of patients in poor grade after subarachnoid haemorrhage: a prospective, consecutive study.

Patients in poor grade (WFNS IV and V) after aneurysmal subarachnoid hemorrhage (SAH) often have a bad outcome. To evaluate early GDC embolisation on such patients a prospective observational study, with comparison to a historical cohort was performed. From January 1996 to December 1998 113 patients were admitted to the Department of Clinical Neurosciences in poor grade after SAH (45 WFNS IV and 68 WFNS V). Eighty-one patients were managed actively with endovascular occlusion of the aneurysm (n = 42) where possible and delayed clipping (n = 16) where not. On an intention to treat basis, 46% had a favourable outcome (Glasgow Outcome Score IV or V) and 48% had died by 3 months. Compared to an historical cohort managed in the same unit between 1992 and 1995 (n = 62, 52% favourable outcome) these results suggest that early GDC aneurysmal occlusion has had a minimal impact on overall outcome.

Adult↗
PubMed2001

Outcome of long-stay intensive care patients.

OBJECTIVES: To assess the numbers, characteristics and outcome for patients requiring long-term intensive care. DESIGN AND SETTING: Observational cohort study in 23 Scottish intensive care units over a 3-year period. PATIENTS AND PARTICIPANTS: 323 patients with an ICU stay of 30 days or more. MEASUREMENTS AND RESULTS: Although representing only 1.6% of patients, those with long stays occupied 15.7% of bed-days. Hospital survival among these patients was 59.9%. With the available data it was not possible to discriminate survivors from non-survivors. CONCLUSIONS: Since these patients have a relatively high hospital survival, resources should not be withheld from them on the basis of prolonged ICU stay alone, even in countries with limited ICU provision.

APACHE↗
PubMed2001

Circulating tetrahydrobiopterin concentrations in patients with septic shock.

Nitric oxide synthase requires tetrahydrobiopterin for its activity. In animal models of sepsis, changes in circulating tetrahydrobiopterin concentrations precede increases in nitrate. We measured plasma tetrahydrobiopterin and nitrate concentrations on three consecutive days in 10 patients with septic shock and 10 critically ill control patients. Total nitrate concentration was measured after reduction of nitrite to nitrate. Tetrahydrobiopterin concentrations were measured using HPLC. The median (range) APACHE II score was 22 (13-27) in the patients with septic shock and 25 (7-28) in the control group. The nitrate concentration was significantly higher in patients with septic shock than in controls (P = 0.01) on all days but did not change with time. Tetrahydrobiopterin concentrations were highest in the patients with septic shock on day 1 only (P = 0.037). In the seven patients with renal failure, both nitrate and tetrahydrobiopterin concentrations tended to be higher than in the 13 patients without renal failure. The nitrate concentration correlated with tetrahydrobiopterin concentration on day 1 only (P = 0.05). In patients with septic shock, both tetrahydrobiopterin and total nitrate concentrations were higher than those in critically ill controls but were increased mainly in patients with renal failure. In summary, tetrahydrobiopterin concentration increases during septic shock, in line with increases in nitrate concentration. However, as for nitrate, concentrations

APACHE↗
PubMed2000

Pulmonary endothelial permeability and circulating neutrophil-endothelial markers in patients undergoing esophagogastrectomy.

OBJECTIVE: Esophagogastrectomy is an established surgical treatment for esophageal malignancy. The postoperative period may be complicated by the development of acute lung injury syndromes and thus, may provide a useful model in which to study the early pathogenic mechanisms of inflammatory lung injury. DESIGN: Open, prospective study. SETTING: High dependency and intensive therapy units. PATIENTS: Eight healthy male volunteers and 20 patients in the early postoperative period INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The lung protein accumulation index (PAI) of radiolabeled transferrin was determined by using a portable, double-isotope system. The following circulating inflammatory markers-thought to reflect neutrophil-endothelial activation and injury including circulating neutrophil elastase-soluble L-, E-, and P-selectins and thrombomodulin and von Willebrand factor antigen were assayed from venous blood samples The PAI for healthy volunteers was median -0.5 (range, -1.73 to 0.27) x 10(-3)/min and for patients undergoing esophagogastrectomy -0.005 (range, -1.53 to 2.28) x 10(-3)/min. There was no statistical difference between the two groups. In the postesophagogastrectomy group, a significant elevation in circulating levels of neutrophil elastase, soluble P- and E-selectin, thrombomodulin, and von Willebrand factor antigen were observed relative to the control group but only circulating plasma elastase demonstrated a significant correlation with the PAI (r2 = .23, p =.03). CONCLUSIONS: The data suggest patients undergoing esophagogastrectomy develop a inflammatory response but this is not a surrogate of permeability and other factors are likely to determine persistent injury to the alveolar-capillary barrier function in this patient group.

Aged↗
PubMed1999

Secretory leukocyte proteinase inhibitor is preferentially increased in patients with acute respiratory distress syndrome.

Inappropriate release of proteases from inflammatory and stromal cells can lead to destruction of the lung parenchyma. Antiproteinases such as alpha-1-proteinase inhibitor (alpha1-Pi), secretory leukocyte proteinase inhibitor (SLPI) and elastase-specific inhibitor (elafin) control excess production of human neutrophil elastase. In the present study, the concentrations of alpha1-Pi, SLPI and elafin found in bronchoalveolar lavage (BAL) fluid from control subjects, patients at risk of developing acute respiratory distress syndrome (ARDS) and patients with established ARDS were determined. Levels of all three inhibitors were raised in patients compared with normal subjects. SLPI was increased in the group of patients who were at risk of ARDS and went on to develop the condition, compared with the "at-risk" group who did not progress to ARDS (p=0.0083). Alpha1-Pi and elafin levels were similar in these two populations. In patients with established ARDS, both alpha1-Pi and SLPI levels were significantly increased, compared to patients at risk of ARDS who did (p=0.0089) or did not (p=0.0003) progress to ARDS. The finding of increased antiproteinases shortly before the development of acute respiratory distress syndrome provide further evidence for enhanced inflammation prior to clinical disease.

Bronchoalveolar Lavage Fluid↗
PubMed1999

Suxamethonium and critical illness polyneuropathy.

Administration of suxamethonium to patients with critical illness polyneuropathy may produce life-threatening hyperkalaemia. A questionnaire to assess the awareness of this problem was sent to all UK intensive care units. A clinical scenario suggestive of critical illness polyneuropathy was accompanied by a list of possible drugs used to facilitate endotracheal intubation. Most respondents (68.7%) chose suxamethonium while 20.4% avoided any muscle relaxant. This result suggests a worrying lack of appreciation of the dangers of suxamethonium use in critical illness polyneuropathy.

Adult↗
PubMed1998

Acute amiodarone-induced lung toxicity.

OBJECTIVE: To investigate any relationship between the pathological features of amiodarone-induced pulmonary toxicity (APT) and clinical use of amiodarone in patients dying from acute respiratory distress syndrome (ARDS). DESIGN: Retrospective study. Review of clinical and pathological findings of patients dying from ARDS. SETTING: Intensive Care Unit (ICU) and Pathology Department of University hospital. SUBJECTS: Ten patients with clinical diagnosis of ARDS, who died in ICU and underwent post mortem examination. INTERVENTIONS: Case note review of clinical details; independent review of histological specimens. MEASUREMENT AND RESULTS: Over a 3-year period, ten patients underwent post mortem examination, of whom seven had received amiodarone. Three patients who received longer than 48 h of amiodarone had histological changes of widespread lipoid pneumonia, a recognised pattern of APT. CONCLUSIONS: Acute amiodarone pulmonary toxicity is a definite pathological entity in ICU patients. High oxygen concentrations may be a risk factor, while pre-existing pathology, e. g. ARDS, may mask its development. Amiodarone should be used with caution in this group of patients.

Adult↗
PubMed1998

Proinflammatory mediator activity, endogenous antagonists and the systemic inflammatory response in intra-abdominal sepsis. Scottish Sepsis Intervention Group.

BACKGROUND: Severe intra-abdominal sepsis continues to carry a high mortality rate. The physiological response to sepsis in this condition and its relationship with proinflammatory mediators and their endogenous antagonists require further clarification. METHODS: Fifty-seven patients were stratified by Acute Physiology And Chronic Health Evaluation (APACHE) II score at the time of admission to an intensive care unit (group 1, score of less than 20; group 2, score of 20 or more). Serial measurements of clinical and immunological variables were made. RESULTS: Non-survivors from group 2 had a raised acute physiology score (P = 0.01), a higher peak serum interleukin (IL) 6 concentration (P = 0.03) and a depressed level of endogenous immunoglobulin (Ig) G class antiendotoxin core antibody (P = 0.005). In group 1, although organ failure score increased progressively in non-survivors, physiology score and peak IL-6 level were similar to those in survivors, and endogenous IgG class antiendotoxin core antibody titre rose (P = 0.02). In both groups IL-1 and tumour necrosis factor alpha were detected infrequently, but their natural antagonists were present in much higher concentrations in both survivors and non-survivors. Levels of C-reactive protein were raised in both but were not significantly different between survivors and non-survivors. CONCLUSION: During the development of organ failure and death, the pattern of proinflammatory mediators and their endogenous antagonists can vary markedly and may in part be determined by the extent of the initial physiological disturbance.

Acute-Phase Reaction↗