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Biomedical subjects

G Chéron

Publications and source records attributed to G Chéron.

58 records · Page 4Linked to original sources
PubMedDate not supplied

[Growth retardation and obstructive sleep apnea in infants].

BACKGROUND: Obstructive sleep apnea can induce growth retardation, with cardiac and/or neurologic manifestations. Tonsillectomy and adenoidectomy may improve failure to thrive. CASE REPORTS: Case n. 1: A 11 1/2-month-old boy was admitted because of feeding problems plus chronic nasopharyngeal secretions (eventually purulent) since the first months of life. He showed a low rate of weight gain since the age of 7 months and had been treated treated for gastroesophageal reflux for a few weeks. On admission, his weight was 6,220 g and his height was 70.5 cm. The tonsils were enlarged and the uvula was long. He displayed tachycardia (150/min). Polygraphic recordings during sleep showed numerous episodes of obstructive apnea. Arterial oxygen saturation (SaO2) during the night was low, frequently below 80%. Tonsillectomy and adenoidectomy immediately improved the quality of sleep. Nocturnal SaO2 and cardiac rythm improved one week later; there was a catch-up weight one month after surgery. Case n. 2: A 7-month-old boy, was admitted because chronic manifestations similar to those of case n. 1. His weight was 5,900 g and his height was 67.5 cm. He also had enlarged tonsils. He suffered from episodes of snoring and obstructive sleep apnea followed by waking and sweating. PaO2 was 70 mmHg and PaCO2 was 48 mmHg. Nocturnal SaO2 was frequently below 60%. Tonsillectomy and adenoidectomy resulted in a net improvement in sleep and weight, despite persistent episodes of nocturnal hypoxemia. CONCLUSIONS: Chronic hypertrophic tonsils and adenoids can interfere with weight gain. Growth retardation may dramatically improve after surgery, even if the tonsils and adenoids do not completely obstruct the nasopharynx.

Adenoidectomy↗
PubMedDate not supplied

[Acute renal insufficiency in Kawasaki disease].

BACKGROUND: Kawasaki disease is an acute inflammatory condition characterized by various combinations of features but renal involvement is rare. This report is of a case of Kawasaki disease complicated by acute kidney failure. CASE REPORT: A 10 year-old girl was admitted because of acute renal failure with fever. She developed a high fever, and her general condition was poor; she had developed a macular erythematous rash 10 days earlier for which she was given cefadroxil. At admission, she remained febrile and had strawberry tongue, pharyngitis, dry erythematous lips, bilateral conjunctivitis, cervical lymphadenopathy and desquamation of the skin on her hands. She was anemic (hemoglobin = 9.6 g%), leukocytotic (33,100/mm3), but with no burr, fragmented red blood cells or thrombocytopenia. Her plasma C-reactive protein level was 236 mg/l; her blood urea was 9.5 mmol/l, her creatininemia 288 mumol/l and proteinuria was 0.5 g/l without hematuria. Urine cultures did not grow. Her blood transaminase and gammaglutamyltransferase activities were elevated. Ultrasonography of kidneys and coronary arteries was normal. Kidney biopsy performed one day after admission showed no vascular or glomerular changes, but renal tubular necrosis, indicating urinary excretion of pigments. Tests for myoglobinemia, myoglobinuria and blood muscle enzyme activities were all positive. The renal failure disappeared within 10 days but the fever and inflammatory manifestations persisted for 1 1/2-2 months despite two treatments of intravenous gammaglobulins and continuous salicylate administration. The patient developed arthralgias at the end of the first month of disease, but recovered without renal or vascular complications. CONCLUSIONS: Several cases of renal involvement have been reported during the course of Kawasaki disease. They have been rarely documented by histological examination so that the vascular origin of changes has not been demonstrated. Myoglobinuria, as seen in muscular crush injury, and in our case possibly due to malignant hyperthermia, may be responsible for the transient acute renal failure.

Acute Kidney Injury↗