Critical care : the official journal of the Critical Care Forum
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Constipation is the most common gastrointestinal complication associated with opioid therapy in chronic pain patients, and also frequently occurs in sedated intensive care unit patients. Conventional therapy may not provide sufficient relief from constipation, which can be severe enough to limit opioid use or the dose. In a recent study on terminally ill patients suffering from laxative-resistant opioid-induced constipation, Thomas and colleagues demonstrated subcutaneous methylnaltrexone to rapidly induce defecation. This appealing result might also have favourable prospects for intensive care patients, as their outcome is often codetermined by recovery of bowel functioning.
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Comment
Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm.
Common medical conditions that require mechanical ventilation include chronic obstructive lung disease, acute lung injury, sepsis, heart failure, drug overdose, neuromuscular disorders, and surgery. Although mechanical ventilation can be a life saving measure, prolonged mechanical ventilation can also present clinical problems. ⋯ This mechanical ventilation-induced diaphragmatic weakness is important because the most frequent cause of weaning difficulty is respiratory muscle failure due to inspiratory muscle weakness and/or a decline in inspiratory muscle endurance. Therefore, developing methods to protect against mechanical ventilation-induced diaphragmatic weakness is important.
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Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction. ⋯ Low dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.
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Comment
The inflammation-coagulation axis as an important intermediate pathway in acute lung injury.
Markers of inflammation, coagulation, and fibrinolysis predict an adverse outcome in patients with sepsis. These markers also seem predictive of an adverse outcome in patients with localized infection and inflammation, such as in acute lung injury. ⋯ In the present issue of Critical Care, McClintock and colleagues demonstrate that these biomarkers retain their predictive effect even if lung-protective ventilation strategies are applied. Besides being biomarkers that predict outcome in patients with acute lung injury, their activation of inflammation and coagulation seems also to play a pivotal role in the pathogenesis of acute lung injury, and may thereby represent an interesting novel target for therapeutic intervention.
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Acute lung injury (ALI) may arise both after sepsis and non-septic inflammatory conditions and is often associated with the release of fatty acids, including oleic acid (OA). Infusion of OA has been used extensively to mimic ALI. Recent research has revealed that intravenously administered recombinant human activated protein C (rhAPC) is able to counteract ALI. Our aim was to find out whether rhAPC dampens OA-induced ALI in sheep. ⋯ In ovine OA-induced lung injury, rhAPC dampens the increase in pulmonary artery pressure and counteracts the development of lung edema and the derangement of arterial oxygenation.