In preterm neonates delayed cord clamping along with lowering the infant below perineum or incision site and administration of ergometrine to mother has significant benefits in terms of increase in hematocrit, higher temperature on admission, and higher blood pressure and urinary output during perinatal transition.
Ventricular outpouching is a rare finding in prenatal sonography and the main differential diagnoses are diverticulum, aneurysm, and pseudoaneurysm in addition to congenital cysts and clefts. The various modes of fetal presentation of congenital ventricular outpouching include an abnormal four-chamber view on fetal two-dimensional echocardiogram, fetal arrhythmia, fetal hydrops, and pericardial effusion. Left ventricular aneurysm (LVA)/nonapical diverticula are usually isolated defects. Apical diverticula are always associated with midline thoracoabdominal defects (epigastric pulsating diverticulum or large omphalocele) and other structural malformations of the heart. Most patients with LVA/congenital ventricular diverticulum remain clinically asymptomatic but they can potentially give rise to complications such as ventricular tachyarrhythmias, systemic embolism, sudden death, spontaneous rupture, and severe valvular regurgitation. The treatment of asymptomatic LVA and isolated congenital ventricular diverticulum is still undefined. In this review, our aim is to outline a systematic approach to a fetus detected with ventricular outpouching. Starting with prevalence and its types, issues in fetal management, natural course and evolution postbirth, and finally the perpetual dilemma of serial observation or surgical correction is discussed.
Aluminum, the most abundant metal on the planet, though inert can lead to toxicity when repeatedly exposed. Infants mainly get exposed to aluminum via formula milk whereas NICU babies are exposed to it through parenteral nutrition. Moreover, in pre-term babies with feed intolerance, when added with aluminum containing antacids develop abnormal accumulation of aluminum. Aluminum toxicity inadvertently leads to hypophosphatemia, metabolic bone diseases with occasional hypercalcemia as well as many other systemic involvements in the form of encephalopathy, dementia and microcytic anaemia. With stoppage of oral antacid, transition from parenteral nutrition to enteral feeds and supplementation of phosphate, causes gradual resolution of toxicity over a period of time.
Candida species are currently one of the most common causes of nosocomial infection in neonatal intensive care units with Candida tropicalis emerging as a frequent offending agent. Colonization precedes systemic invasive fungal infections in neonates. It generally manifests with lethargy, increased apneic episodes, feeding intolerance, late-onset thrombocytopenia, hypoglycemia, unexplained hyperglycemia, poor perfusion, and need for increased ventilator requirement. We report a 10-day-old neonate, with late-onset sepsis by C. tropicalis, presenting as generalized erythroderma. We present this case to highlight that nosocomial candidemia with C. tropicalis can present as generalized erythroderma in neonates. Maintaining adequate oral or parenteral fluidintake with monitoring of serum electrolytes is mandatory.
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