Massive fetomaternal hemorrhage resulting in profound anemia and shock is associated with high perinatal morbidity and mortality. Although diagnosis before delivery is difficult, the clinical index of suspicion rises when a woman presents with history of decreased or absent fetal movements and antenatal monitoring shows a sinusoidal rhythm strip. The diagnosis can be made quickly by demonstration of fetal red blood cells in the maternal circulation and there is consistent recommendation in the literature to immediately order a Kleihauer-Betke test. Clinical manifestations of a fetomaternal hemorrhage depend on the volume of blood lost and the rate with which it occurred. The severely compromised anemic infant indicative of acute hemorrhage will be pale with gasping respirations and signs of circulatory shock. Immediate intervention with volume resuscitation is crucial for optimal outcome. This article describes a patient with massive fetomaternal hemorrhage and subsequent devastating neonatal complications. The focus of this article is to provide clinical guidance for the management and care of the infant affected by profound anemia.
A case of neonatal thyrotoxicosis secondary to maternal autoimmune hyperthyroidism is reported in an infant born at 34 weeks gestation who presented with tachycardia, jitteriness, diarrhea, and a small goiter. Propranolol and oxygen were used to treat high-output cardiac failure and transient persistent pulmonary hypertension. The infant's response to propylthiouracil therapy, gradual resolution of cardiac and systemic symptoms, and normaliziation of thyroid studies are described. Thyroid physiology and function and the special considerations in a premature infant are reviewed. An overview of maternal autoimmune hyperthyroidism and the implications for the developing fetus and neonate are presented. The risk factors for, and clinical presentation of, hyperthyroidism are outlined and treatment strategies highlighted. The nursing care of infants with hyperthyroidism is carefully described with an emphasis on the surveillance for and management of multisystem manifestations.
Total colonic aganglionosis (TCA) is a rare, hybrid form of Hirschsprung's disease. It is a functional rather than mechanical obstruction, characterized by the absence of intrinsic ganglion cells in the myenteric and submucosal plexuses of the bowel wall. Ganglion cells regulate normal colonic peristaltic activity. Paucity of ganglion cells results in an aganglionic segment of bowel that is functionally abnormal and does not propagate the normal peristaltic wave that moves to it from the proximal ganglionic bowel. The lesion originates in the rectum and extends proximally over a variable distance of the bowel. The further the lesion extends, the more difficult the management becomes. Clinical and radiologic findings can be useful in diagnosis, but they are not pathognomonic. The definitive diagnosis is made following suction biopsy of the rectum, colon, and ileum. Ultimate treatment for TCA is surgical, although no single surgical procedure has been proven superior. Total parenteral nutrition during the postoperative period is essential to ensure appropriate fluid and electrolyte status. Improvements in supportive care and earlier recognition and diagnosis of TCA in infants have led to a significantly increased rate of survival since the lesion was first recognized. The embryology, pathogenesis, clinical presentation, diagnosis, management prognosis, and outcome of TCA are discussed. A case study is presented.
Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is the most common cause of recurrent hypoglycemia in neonates and infants. It is a disorder of glucose homeostasis characterized by unregulated hyperinsulinemia and profound hypoglycemia. PHHI may be differentiated from other causes of hypoglycemia by demonstrating the persistence of inappropriately high insulin levels regardless of blood glucose concentration. Prompt recognition and treatment of PHHI is critical because uncorrected hypoglycemia in the newborn period is associated with permanent damage to the central nervous system and subsequent mental retardation. The aim of therapy is to maintain euglycemia to protect the developing brain from possible damage. Despite recent advances in medical treatment, subtotal pancreatectomy is often necessary. This article will review the function of insulin, glucagon, and somatostatin, pathophysiology of hyperinsulinism, clinical manifestations, differential diagnosis, management, and reported neurologic outcomes of newborns and infants with PHHI.
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