Current anaesthesia and critical care最新文献

Acute Kidney injury (AKI) is a relatively common condition in the intensive care unit and is associated with an increase in mortality. Whilst it can be treated by the use of renal replacement therapies an independent increase in mortality still exists. It is therefore seems intuitive that the prevention of AKI should be associated with a reduction in both mortality and morbidity and an improvement in patient care for this reason there has been many attempts to develop strategies to reduce the incidence of AKI. These strategies involve the use of therapeutic agents to prevent renal failure, the avoidance of nephrotoxic agents and the maintenance of normal hydration and renal perfusion. More recently there has been focus on the early recognition of patients at risk of developing AKI and focussing care to avoid exacerbation of risk factors.

The stage at which acute kidney injury (AKI) is detected is dependent upon the definition used. More recently it has been demonstrated that even relatively small increments of serum creatinine portend a worse outcome. This has prompted the development of new definitions based on small rises in serum creatinine or decreases in urine output. Acute kidney injury on the intensive care unit (ICU) is usually multifactorial secondary to hypovolaemia and sepsis resulting in hypoperfusion of the kidneys. In patients with good baseline kidney function the condition is generally reversible if the patient regains health. However it has been recognised that kidney function does not always completely recover. An episode of AKI may represent an antecedent to the development of chronic kidney disease (CKD), and patients who already have CKD are at risk of AKI and further loss of function. Preventative measures should therefore be instituted as soon as possible in patients identified to be at risk of developing AKI. The cornerstone of treatment for patients who develop AKI remains renal replacement therapy (RRT). Ultimately it is hoped that the development of new biomarkers may enable earlier detection of patients at risk of developing AKI.

This is a case report of a patient with Crohn's disease admitted to hospital with a typical flare. The main symptoms were abdominal pain and haemorrhagic diarrhoea. During the current admission she was commenced on her first course of Infliximab.

The clinical benefits of monoclonal TNF-alpha inhibitors are described. The anxieties relating to infectious complications that may be, in part related to the TNF-alpha inhibition are also discussed. At present the impact of these agents on critical illness is unclear but as the use of these effective drugs increase it is inevitable there will be an increase in patients presenting with critical illness who are concurrently on this treatment. Some of the implications are outlined.

Local anaesthetic toxicity has been a known complication of local anaesthetics since use began in 1884 and it continues to be a problem in modern medical practice.

Local anaesthetic toxicity occurs due to raised plasma concentrations following high doses or inadvertent intravenous administration.

The clinical manifestations of toxicity are generally neurological, cardiac or both in origin.

Prevention is the best approach for toxicity, but in the event of its occurrence, lipid emulsion infusion has been recommended as part of the treatment algorithm.