Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of laryngoscopy and intubation with or without topical lidocaine anesthesia on the endocrine stress response was investigated in six groups of 40 orthopedic surgery patients differing in premedication and technique of lidocaine application (one- or two-step method). Controls were included without lidocaine application. Plasma levels of catecholamines (by HPLC) were measured before induction and 1, 5, and 10 min after intubation, ADH-levels (by RIA) before induction and 5 and 10 min after intubation. In addition, mean arterial pressure (MAP, MAP), HR, and the incidence of coughing and cardiac arrhythmias were observed. The statistical evaluation (analysis of variance with repeated measures on one factor) considered P values of less than 0.05 significant. There was no influence of laryngoscopy and intubation on plasma catecholamine levels during the observation period. A continuous decrease in both levels of epinephrine and norepinephrine was significant. ADH levels showed no significant changes. Lidocaine had no influence on these endocrine parameters. MAP and HR increased after intubation in all groups studied. The increase in HR was less pronounced after lidocaine treatment. Coughing (4 patients) and ventricular dysrhythmia (2 patients) were observed only in patients without lidocaine treatment. In conclusion, no influence of different modes of treatment on the endocrine stress response during intubation became obvious. There was no indication that the cardiovascular symptoms during laryngoscopy and intubation are caused by systemic stress. An explanation may be a direct neural impulse via sympathetic efferents to the heart. On the other hand, topical application of lidocaine did prevent coughing and cardiac irritation, and the increase in HR was attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The endocrine stress-reaction to orotracheal intubation and topical anesthesia with lidocaine]. 368 17

A 64-year-old Japanese male was admitted to Kotoh General Hospital because of fever and cough on July, 14, 1997. Laboratory data showed hypereosinophilia (11,500/microliter) and high titer of anti-myeloperoxidase antineutrophil cytoplasmic antibody (319 EU). A physical examination revealed progressive peripheral neuropathy. He had been diagnosed as having bronchial asthma since November, 1996. Therefore, he was diagnosed as having Churg-Strauss syndrome (CSS). He was treated with methylprednisolone pulse therapy (500 mg/day for 3 days) and oral prednisolone (PSL, 60 mg/day). However, peripheral neuropathy was rapidly progressive, and echocardiogram revealed cardiac hypofunction (ejection fraction (EF); 39%). He was refereed to Akita University Hospital for further examination. On admission, laboratory data showed hyponatremia (125 mEq/l) with inappropriate secretion of antidiuretic hormone (ADH, 13.0 pg/ml). Atrial natriuretic peptide was normal (26 pg/ml). Urinary osmorality was 488 mOsm/l, and urinary sodium excretion was 86 mEq/l. Renal, adrenal, and thyroid functions were normal. From these data, his hyponatremia was caused by syndrome of inappropriate secretion of ADH (SIADH). After cyclophosphamide-pulse therapy (500 mg) and oral administration of cyclophosphamide (50 mg/day) and PSL (50 mg/day), peripheral neuropathy improved gradually, and his serum sodium returned to normal, but cardiac hypofunction continued. A possible relationship between SIADH and CSS is discussed.
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PMID:[Severe peripheral neuropathy, cardiac hypofunction, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Churg-Strauss syndrome]. 1061 73