Apnea in preterm newborns: determinants, pathophysiology, effects on cardiovascular parameters and treatment

Apnea, especially in preterm newborns (AoP) is one of the common problems encountered at neonatal units. Numerous factors are likely to play a role in the etiology of apnea. Recent data sugest a role for genetic predisposition of AoP. It seems, that physiological rather than pathological immaturity of the respiratory, or cardiorespiratory control, play a major part in the pathophysiology of AoP. Immaturity of the brainstem, cerebral cortex, receptors of the lungs and the airways as well as of the chemoreceptors contribute to the development of apnea in preterm newborns. Several neurotransmitters (GABA, adenosin, endorphins) and their maturational changes are including in pathogenesis of apnea, too. The instability of the upper airway in preterm infants, asynchrony of musculature of the upper airway and diaphragm, pathological changes in the upper airway and malformations of the central nervous system might also contribute to the occurrence and severity of AoP. In newborns, apnea occurs more frequently in active sleep than in quiet sleep and the frequency of apnea in active sleep is higher in the warm conditions. Durations of apnea correlate with the body heat loss. Cardiovascular changes during apnea - bradycardia, peripheral vasoconstriction and various changes in peripheral blood flow and pressure occur together with changes in ECG. The standard clinical management of apnea includes non-pharmacological treatment (eliciting arousal reactions and reflex breathing by mechanical skin, or mucosa stimulations), pharmacological treatment (methylxanthines are preferred) and application of continuous positive airway pressure (CPAP) or in severe apnea - mechanical ventilation

Fluconazole Prophylaxis of Candida Infections in Preterm Neonates

Infections belong to the most serious health problems in neonates. Invasive candidiases are one of the leading causes of mortality and morbidity in Neonatal intensive care units (NICUs). A more cautious approach is adequate when dealing with fungal infections in premature neonates. Sometimes it is necessary to cure an infection at the very beginning just before manifestation of clinical symptoms. Neonatal colonization due to Candida albicans or non-albicans Candidae predisposes to invasive candidiasis. Pregnancies complicated by preterm delivery should be considered for screening and treatment of maternal Candida colonization to decrease the occurrence of neonatal fungal colonization and its consequences. It is important to prevent infection to spread among patients and avoid complications. Prophylaxis in neonates must be safe and effective. Most authors prefer selective prophylaxis. Fluconazole is the drug of choice for prophylaxis in extremely low birth weight (ELBW) neonates. The prophylaxis is beneficial especially in NICUs with high rates of invasive candidiases. The authors describe benefits and trends in prophylaxis. They also summarize evidence on timing, dosing, and effect of fluconazole prophylaxis

Effects of Conventional Mechanical Ventilation Performed by Two Neonatal Ventilators on the Lung Functions of Rabbits with Meconium-Induced Acute Lung Injury

Severe meconium aspiration syndrome (MAS) in the neonates often requires a ventilatory support. As a method of choice, a conventional mechanical ventilation with small tidal volumes (VT<6 ml/kg) and appropriate ventilatory pressures is used. The purpose of this study was to assess the short-term effects of the small-volume CMV performed by two neonatal ventilators: Aura V (Chirana Stara Tura a.s., Slovakia) and SLE5000 (SLE Ltd., UK) on the lung functions of rabbits with experimentally-induced MAS and to estimate whether the newly developed neonatal version of the ventilator Aura V is suitable for ventilation of the animals with MAS

Quick Diagnosis of Alkaptonuria by Homogentisic Acid Determination in Urine Paper Spots

Two methods are described for homogentisic acid (HGA) determination in dried urine spots (DUS) on paper from Alkaptonuria (AKU) patients, devised for quick early diagnosis. AKU is a rare autosomal recessive disorder caused by deficiency of homogentisate 1,2-dioxygenase, yielding in accumulation of HGA. Its massive excretion causes urine darkening by exposure to air or alkalinization, and is a diagnostic marker. The deposition of polymers produced after HGA oxidation within the connective tissues causes ochronotic arthritis, a degenerative joint disease manifesting in adulthood and only rarely in childhood. No early diagnosis is usually accomplished, awareness following symptom development