By William W. Hay, Myron J. Levin, Judith M. Sondheimer, Robin R Deterding
Present analysis & remedy in Pediatrics 18e deals concise, clinically-oriented insurance of the ambulatory and medical institution care of kids, from delivery via infancy and formative years. using the preferred present sequence layout, this convenient consultant solutions all of the questions that arise in day-by-day perform and offers the main points essential to make a legitimate analysis and therapy plan.
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Additional info for Current Pediatric Diagnosis & Treatment
Pediatrics 2000;106:358. [PMID: 10920168] Boyle RJ: Effects of certain prenatal drugs on the fetus and newborn. Pediatr Rev 2002;23:17. [PMID: 11773589] Chan O et al: New methods for neonatal drug screening. NeoReviews 2003;4:e236. Chasnoff IJ: Prenatal substance exposure: maternal screening and neonatal identification and management. NeoRevie Coyle MG et al: Diluted tincture of opium (DTO) and phenobarbital versus DTO alone for neonatal opiate withdrawa Pediatr 2002;140:561. [PMID: 12032522] Frank DA et al: Growth, development, and behavior in early childhood following prenatal cocaine exposure.
Respirations apnea) as heart rate and blood pressure begin to fall. This initial period of apnea lasts 30â 60 seconds. Gasping resp (3â 6/min) then begin, while heart rate and blood pressure gradually decline. Secondary or terminal apnea then ensu decline in heart rate and blood pressure. The longer the duration of secondary apnea, the greater the risk for hypoxic o cardinal feature of the defense against hypoxia is the underperfusion of certain tissue beds (eg, skin, muscle, kidneys, allows the perfusion of core organs (ie, heart, brain, and adrenals) to be maintained.
Table 1â 15. Signs and Symptoms Caused by Asphyxia. Hypoxic-ischemic encephalopathy, seizures Respiratory distress due to aspiration or secondary surfactant deficiency, pulmonary hemorrhage Persistent pulmonary hypertension Hypotension due to myocardial dysfunction Transient tricuspid valve insufficiency Anuria or oliguria due to acute tubular necrosis Feeding intolerance; necrotizing enterocolitis 41 42 Elevated aminotransferases due to liver injury Adrenal insufficiency due to hemorrhage Disseminated intravascular coagulation Hypocalcemia Hypoglycemia Persistent metabolic academia Hyperkalemia The clinical features of hypoxic-ischemic encephalopathy progress over time: birth to 12 hours, decreased level of consciousn tone, decreased spontaneous movement, periodic breathing or apnea, and possible seizures; 12â 24 hours, more seizures, ap jitteriness, and weakness; after 24 hours, decreased level of consciousness, further respiratory abnormalities (progressive apne brainstem signs (oculomotor and pupillary disturbances), poor feeding, and hypotonia.