Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.
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PMID:Rational treatment of acid-base disorders. 219 65

Hypokalemia has been previously reported as a cause for respiratory impairment complicating therapy for diabetic ketoacidosis. A case is presented with a short interval of hypoventilation documented by hypercapnia. A reversal from hypercapnia to hypocapnia occurred when the serum potassium level became normal after potassium replacement. Causes of muscular weakness other than hypokalemia were considered unlikely on the basis of clinical and laboratory data. The present report records the occurrence of hypoventilation associated with hypokalemia in diabetic ketoacidosis and serves to underscore the need for adequate potassium replacement during the treatment of this disorder.
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PMID:Hypokalemic hypoventilation complicating severe diabetic ketoacidosis. 676 71

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
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PMID:Hyperglycemic crises and their complications in children. 1731 23

* Based on some research evidence, DKA is a significant contributor to morbidity and mortality in children who have type 1 diabetes, and cerebral edema is responsible for most of the deaths during DKA in children. (Dunger, 2004). * Based on strong research evidence, treatment of DKA requires replacement of water and electrolytes and correction of the insulin deficiency. (Dunger, 2004). * Based on some research data and consensus opinion, after providing initial volume expansion (if needed), fluid resuscitation of children who have DKA should be calculated to rehydrate evenly over at least 48 hours. Initial fluid resuscitation should be with an isotonic solution; subsequent fluid management should be with a solution that has a tonicity of at least 0.45% saline. (Dunger, 2004). * Based on strong research evidence, insulin treatment for DKA should begin at a dose of 0.1 units/kg per hour and generally should remain at or above this level until the ketoacidosis is resolved. (Dunger, 2004). * Based on some research evidence, risk factors for the development of cerebral edema during treatment of DKA include the severity of acidosis, greater hypocapnia (after adjusting for the degree of acidosis), higher blood urea nitrogen concentration at presentation, and treatment with bicarbonate. (Dunger, 2004; Glaser, 2002).
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PMID:Management of diabetic ketoacidosis in children and adolescents. 1904 33