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Other less common causes of late-onset thrombocytopenia include inborn errors of metabolism and Fanconi anemia (rare). Novel tools to evaluate platelet production and aid in the evaluation of thrombocytopenia have been recently developed and are likely to become widely available to clinicians in the near future. Guidelines for the evaluation of neonates with late-onset thrombocytopenia (72 hours of life). Immune thrombocytopenia occurs due to the passive transfer of antibodies from the maternal to the fetal circulation. The maternal autoantibody also crosses the placenta, resulting in destruction of fetal platelets and thrombocytopenia. If blood cannot be collected from the parents in a timely fashion, neonatal serum may be screened for the presence of anti-platelet antibodies. However, to confirm the diagnosis, it is important to follow the platelet count frequently until a normal count is achieved. If the patient is clinically stable and does not have evidence of an intracranial hemorrhage, platelets are usually given when the platelet count is less than 30 103/mcL, although this is arbitrary. If the patient has evidence of an intracranial hemorrhage, the goal is to maintain a platelet count greater than 100 103/mcL. Platelets can also be washed to eliminate the plasma, but this induces more damage to the platelets than concentrating them (19). Other large studies confirmed an incidence of severe neonatal thrombocytopenia in this population ranging from 8. If the infant has mild thrombocytopenia, however, the platelet count should be repeated in 2 to 3 days, since it usually reaches the nadir between days 2 and 5 after birth. Cranial imaging should be obtained in all infants with platelet counts 50 103/mcL to evaluate for intracranial hemorrhage. There is in general little correlation between fetal platelet counts and either maternal platelet counts, platelet antibody levels, or history of maternal splenectomy. However, attempts to measure the fetal platelet count before delivery are not recommended due to the risk associated with such attempts. In regard to the mode of delivery, there is no evidence that cesarean section is safer for the fetus with thrombocytopenia than uncomplicated vaginal delivery. Recent studies have shown that there is great variability in neonatal transfusion practices in the United States and worldwide (28,29). To a large extent, this is attributable to the paucity of scientific evidence in the field. A more recent retrospective study evaluated whether platelet counts 50 103/mcL could be safely tolerated in neonates. This study concluded that using a platelet count of 30 103/mcL as a transfusion threshold was a safe practice for stable neonates with no prior hemorrhages (31). Based on this limited evidence, we currently propose administering platelet transfusions to neonates according to the criteria shown in Table 47. There is more consensus in regard to the platelet product that should be transfused. Most experts agree that neonates should receive 10 to 15 mL/kg of a standard platelet suspension, either a platelet concentrate ("random-donor platelets") or apheresis platelets. Each random-donor platelet unit has approximately 50 mL of volume and contains approximately 10 109 platelets per 10 ml (32). When making platelet transfusion decisions, it is important for neonatologists to be aware of the risks associated with these transfusions. In the case of platelet suspensions, the risk of bacterial contamination is higher than the combined risk of all viral infections for which platelets are routinely tested. It is unclear from these studies whether this association simply reflects sicker patients receiving more platelets or whether platelet transfusions adversely affect outcomes. Nevertheless, while we await for data from well-designed randomized controlled studies, platelet transfusion decisions in neonates should be made thoughtfully, carefully balancing the risks and benefits in each individual patient. Thrombocytopenia among extremely low birth weight neonates: data from a multihospital healthcare system. Circulating megakaryocytes and their progenitors in early thrombocytopenia in preterm neonates. Endogenous thrombopoietin levels and effect of recombinant human thrombopoietin on megakaryocyte precursors in term and preterm babies. Inherited thrombocytopenia: congenital amegakaryocytic thrombocytopenia and thrombocytopenia with absent radii.

Clinical considerations: Topical 2% nitroglycerin ointment may be used for significantly swollen extremity. May cause local irritation, inflammation, necrosis, and sloughing with or without signs of infiltration. Therapeutic serum concentration: 8 to 15 mcg/mL for first 3 weeks of life, then 10 to 20 mcg/mL secondary to changes in protein binding. Indications: Duodenal and gastric ulcers, gastroesophageal reflux disease, and hypersecretory conditions. Clinical considerations: Because of the absence of possible endocrine toxicity and drug interactions, ranitidine is preferred over cimetidine. Increased gastric pH may promote the development of gastric colonization with pathogenic bacteria or yeast. Drug interactions: May increase serum levels of theophylline, warfarin, and procainamide. Indications: Treatment of documented or assumed metabolic acidosis during prolonged resuscitation after establishment of effective ventilation. Adverse effects: Pulmonary edema, respiratory acidosis, local tissue necrosis, hypocalcemia, hypernatremia, metabolic alkalosis, hypokalemia. Solution may be made by crushing eight 25 mg tablets and suspending powder in 50 mL of simple syrup (stable for 28 days, refrigerated). Drug interactions: May potentiate ganglionic blocking agents and other antihypertensive agents. Adverse reactions: Hyperkalemia, vomiting, diarrhea, hyperchloremic metabolic acidosis, dehydration, hyponatremia, decrease in renal function. Treatment: Full-term infants with respiratory failure that is due to meconium aspiration, pneumonia, or persistent pulmonary hypertension. Aliquots should be administered with infant in different positions to facilitate spreading of surfactant. Repeat doses are usually determined by evidence of continuing respiratory distress or if patient requires 30% inspired oxygen. Monitor oxygen saturation and heart rate continuously during administration of doses. Rapid improvement in lung oxygenation and compliance may occur and require a decrease in support. After administration of each dose, monitor arterial blood gases frequently to detect and correct postdose abnormalities of ventilation and oxygenation. Precautions: A videotape demonstrating surfactant administration procedure is available from Ross Laboratories and Forest Laboratories and should be viewed before use of their products. Improves hepatic metabolism of essential fatty acids in infants with cystic fibrosis. Adverse reactions: Hepatotoxicity, nausea, vomiting, abdominal pain, and constipation. Indications: Drug of choice for serious infections caused by methicillin-resistant staphylococci, penicillin-resistant pneumococci, and coagulase-negative staphylococcus. The oral route is used for the treatment of Clostridium difficile, if metronidazole has failed. Precautions: Use with caution in patients with renal impairment or those receiving other nephrotoxic or ototoxic drugs; dosage modification required in patients with impaired renal function. Cardiac arrest, fever, chills, eosinophilia, and neutropenia reported after prolonged administration (3 weeks); phlebitis may be minimized by slow infusion and more dilution of the drug. If extravasation occurs, consider using hyaluronidase around periphery of an affected area. Also reported are ototoxicity and nephrotoxicity, especially if administered concurrently with other nephrotoxic or ototoxic medications.

If the child is at risk for congenital syphilis, evaluation should include the following: a. Other tests as clinically indicated, including long-bone radiographs, chest radiograph, liver function tests, cranial ultrasonography, ophthalmologic examination, and auditory brainstem responses. All seroreactive infants should have a physical examination and nontreponemal titer every 2 to 3 months until the test becomes nonreactive or the titer decreases fourfold. If the titer is found to increase or remain reactive at 6 to 12 months, the infant should undergo reevaluation for signs of active syphilis and re-treatment should be seriously considered. Health care personnel as well as family members and other visitors should wear gloves when handling infants with congenital syphilis until therapy has been administered for at least 24 hours. Those who have had close contact with an infected infant or mother before precautions were taken should be examined and tested for infection, and treatment should be considered. Indeed, there were only 11,540 cases reported in the United States in 2009, the lowest recorded since reporting was initiated in 1953 (3). In contrast, the chest radiograph in adult type reactivation disease often shows pulmonary cavities in the upper lung zones. In other cases, there may be significant fever or cough, the latter often related to impingement of bronchi by enlarged lymph nodes. After being inspired by a new host, the respiratory droplets may travel to the alveoli, where they are ingested by alveolar macrophages. For the first several days, there is relatively unrestricted bacterial replication, and the organisms can spread to the regional lymph nodes and the bloodstream (6). Acquired immunity typically develops within 2 to 8 weeks, at which point the individual will react to the tuberculin skin test. Sensitivity to tuberculin may take longer to evolve in neonates and young children (9). In the majority of infected individuals, the infection is controlled and remains asymptomatic (latent). The reactivation of latent infection is more likely in individuals with specific underlying illnesses such as pneumosilicosis, diabetes, end-stage renal disease, and cancer of the head and neck or any form of immune suppression. The disease can take decades to emerge, presumably after intercurrent declines in immunity (6). Pregnancy does not alter the response to a tuberculin skin test, and there have been no adverse effects on women or their infants from tuberculin testing (10). Although there is no evidence for teratogenic concerns, some experts recommend waiting until the second trimester to initiate treatment. Radiographic findings consistent with active disease include adenopathy, focal or multinodular infiltrates, cavitation, and decreased expansion of the upper lobes of the lung. Although many women may be asymptomatic, possible symptoms include fever, cough, weight loss, malaise and fatigue, or hemoptysis (8,15). Malaise, fatigue, and vomiting can often be mistaken for other pregnancy-associated conditions. The length of therapy of each drug is dependent upon the sensitivity results of the organism. Additional drugs contraindicated in pregnant women include kanamycin, amikacin, capreomycin, and fluoroquinolones. Hematogenous spread through the umbilical vein from an infected placenta to the fetal liver and lungs (can also involve the gastrointestinal tract, bone marrow, skin, or mesenteric nodes). Inhalation or ingestion of infected amniotic fluid, in utero or at the time of birth, leading to primary infection in the lungs or gastrointestinal tract. If these criteria are not met, the infection was probably acquired postnatally in the following ways: a. However, it is important to identify the source of infection such that proper precautions are taken and the source can be appropriately treated (6,20). Although symptoms may be present at birth, they are more commonly observed between 2 and 4 weeks of life. Infection is more likely to disseminate in neonates compared with children older than 2 years of age and adults due to a more vulnerable immune system (20). Tissue from lymph nodes, liver, lung, bone marrow, skin lesions, and the placenta may reveal organisms on pathologic examination and culture. Drug sensitivities should be performed on any organism grown from these cultures as well as organisms grown from maternal isolates. Asymptomatic neonate, active infection in the mother (or household contact) (4,7,12).

Poorly functioning placentas with extensive vasospasm or infarction have an increased resistance to flow that is particularly noticeable in fetal diastole. Umbilical artery Doppler flow velocimetry may be used as part of fetal surveillance based on characteristics of the peak systolic frequency shift (S) and the end-diastolic frequency shift (D). The two commonly used indices of flow are the systolic:diastolic ratio (S/D) and the resistance index (S-D/S). Intrapartum assessment of fetal well-being is important in the management of labor. Continuous electronic fetal monitoring is widely used despite the fact that it has not been shown to reduce perinatal mortality or asphyxia relative to auscultation by trained personnel but has increased the incidence of operative delivery. The noninvasive methods are ultrasonic monitoring and surface-electrode monitoring from the maternal abdomen. The most accurate but invasive method is to place a small electrode into the skin of the fetal presenting part to record the fetal electrocardiogram directly. When the electrode is properly placed, it is associated with a very low risk of fetal injury. Approximately 4% of monitored babies develop a mild infection at the electrode site, and most respond to local cleansing. A tocodynamometer can be strapped to the maternal abdomen to record the timing and duration of contractions as well as crude relative intensity. When a more Prenatal Assessment and Conditions 9 precise evaluation is needed, an intrauterine pressure catheter can be inserted following rupture of the fetal membranes to directly and quantitatively record contraction pressure. Invasive monitoring is associated with an increased incidence of chorioamnionitis and postpartum maternal infection. Parameters of the fetal monitoring record that are evaluated include the following: i. In isolation, tachycardia is poorly predictive of fetal hypoxemia or acidosis unless accompanied by reduced beat-to-beat variability or recurrent decelerations. The autonomic nervous system of a healthy, awake term fetus constantly varies the heart rate from beat to beat by approximately 5 to 25 bpm. Reduced beat-to-beat variability may result from depression of the fetal central nervous system due to fetal immaturity, hypoxia, fetal sleep, or specific maternal medications such as narcotics, sedatives, -blockers, and intravenous magnesium sulfate. These decelerations are more commonly seen in active labor when the fetal head is compressed in the pelvis, resulting in a parasympathetic effect. The onset, nadir, and recovery of the deceleration occur after the beginning, peak, and end of the contraction, respectively. Late decelerations are the result of uteroplacental insufficiency and possible fetal hypoxia. As the uteroplacental insufficiency/hypoxia worsens, (i) beat-to-beat variability will be reduced and then lost, (ii) decelerations will last longer, (iii) they will begin sooner following the onset of a contraction, (iv) they will take longer to return to baseline, and (v) the rate to which the fetal heart slows will be lower. Umbilical cord compression secondary to a low amniotic fluid volume (oligohydramnios) may be alleviated by amnioinfusion of saline into the uterine cavity during labor. A fetal scalp blood sample for blood gas analysis may be obtained to confirm or dismiss suspicion of fetal hypoxia. Many obstetric units have replaced fetal scalp blood sampling with noninvasive techniques to assess fetal status. Fetal nuchal translucency: ultrasound screening for fetal trisomy in the first trimester of pregnancy. With appropriate management, women with good glycemic control and minimal microvascular disease can expect pregnancy outcomes comparable to the general population. Women with advanced microvascular disease, such as hypertension, nephropathy, and retinopathy, have a 25% risk of preterm delivery because of worsening maternal condition or preeclampsia. In women who begin pregnancy with microvascular disease, diabetes often worsens, but in most, the disease return to baseline. Preconception glucose control may reduce the rate of complications to as low as that seen in the general population. Diabetes that antedates the pregnancy can be associated with adverse fetal and maternal outcomes. The most important complication is diabetic embryopathy resulting in congenital anomalies.