Critical care clinics
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N-6 and n-3 PUFAs from the diet are absorbed and reach the cell where they interact with fatty acid binding proteins within cell membranes and cytoplasm. They are processed in the endoplasmic reticulum (desaturation-elongation reactions, lipid synthesis, eicosanoid and epoxide production) and in peroxisomes (beta-oxidation, synthesis, oxidation products). They interact with receptors, ion channels, and nuclear elements; the result is modulation of gene expression. PUFA-induced alterations result in modulation of local and systemic inflammation and inflammatory disease activity.
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Critical care clinics · Jan 2001
ReviewManagement of decompensated diabetes. Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome.
DKA and HHS represent two extremes in the spectrum of decompensated diabetes mellitus. Their pathogenesis is related to absolute or relative deficiency in insulin levels and elevations in insulin counterregulatory hormones that lead to altered metabolism of carbohydrate, protein, and fat and varying degrees of osmotic diuresis and dehydration, ketosis, and acidosis. In DKA, insulin deficiency and ketoacidosis are the prominent features of the clinical presentation, and insulin therapy is the cornerstone of therapy. ⋯ In younger patients with mixed features, rapid correction of metabolic abnormalities and, consequently, of hyperosmolarity by administration of hypotonic fluids and insulin should be avoided to decrease the risk for precipitating cerebral edema. In addition, if ketoacidosis has been a prominent feature in a mixed case, the patient may have type 1 diabetes with no residual pancreatic islet beta cell secretion and may subsequently need ongoing, life-long insulin therapy after resolution of the acute episode of decompensated diabetes. ICU admission is indicated in the management of DKA, HHS, and mixed cases in the presence of cardiovascular instability, inability to protect the airway, obtundation, the presence of acute abdominal signs or symptoms suggestive of acute gastric dilatation, or if there is not adequate capacity on the floor unit to administer the intravenous insulin infusion and to provide the frequent and necessary monitoring that must accompany its use.
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Hypocalcemia is common in the ICU and is a marker of poor prognosis. The mechanisms behind the low calcium levels include extravasation, increased chelation, intracellular overload of calcium, and an altered parathyroid hormone (PTH) secretion. Hypocalcemia and an altered PTH secretion seem to be related to systemic inflammation, but it is not known today if this response is appropriate or not. Therefore, a general supplementation with calcium in these patients cannot be recommended at this stage.
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There is significant evidence to show that many patients with hyponatremia and intracranial disease who were previously diagnosed with SIADH actually have CSW. The critical difference between SIADH and CSW is that CSW involves renal salt loss leading to hyponatremia and volume loss, whereas SIADH is a euvolemic or hypervolemic condition. ⋯ The mechanisms underlying CSW are not understood but may involve ANP or other natriuretic factors and direct neural influence on renal function. Future investigation is needed to better define the incidence of CSW in patients with intracranial disease, identify other disorders that can lead to CSW, and elucidate the mechanisms underlying this syndrome.
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The nature of organ injury during critical illness would suggest that antioxidant therapy might be effective as prophylaxis and therapy. To date, the results of human trials with these agents have yielded somewhat disappointing results. Future trials using better-defined primary endpoints for outcome and newly developed agents and modes of administration may result in successes in this field.