Critical care clinics
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Critical care clinics · Jan 2001
ReviewManagement of hypothyroidism and hyperthyroidism in the intensive care unit.
Thyroid storm and myxedema coma are uncommon problems in the ICU, but both usually present with typical findings, and when recognized early, are treatable. Thus, rapid recognition with early institution of therapy may be life saving. It is always important to search diligently to determine the underlying cause of the decompensation and to treat that aggressively.
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Stress hyperglycemia is common and likely to be associated with at least some of the same complications as hyperglycemia in true diabetes mellitus, such as poor wound healing and a higher infection rate. The predominant cause is the intense counterregulatory hormone and cytokine responses of critical illness, often compounded by excessive dextrose administration, usually as TPN. Although randomized data suggesting benefit of controlling hyperglycemia in hospitalized patients are paltry, prospective controlled trials are feasible and should be initiated. In the interim, the practice at the authors' institution is to use insulin to lower plasma glucose concentrations to a safe range of 150 mg/dL to 200 mg/dL in all patients.
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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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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
ReviewCytopathic hypoxia. Mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis.
Several lines of evidence support the notion that cellular energetics are deranged in sepsis, not on the basis of inadequate tissue perfusion, but rather on the basis of impaired mitochondrial respiration and/or coupling; that is, organ dysfunction in sepsis may occur on the basis of cytopathic hypoxia. If this concept is correct, then the therapeutic implications are enormous. Efforts to improve outcome in patients with sepsis by monitoring and manipulating cardiac output, systemic Do2, and regional blood flow are doomed to failure. Instead, the focus should be on developing pharmacologic strategies to restore normal mitochondrial function and cellular energetics.