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Another method is to apply the cream and then place plastic wrap around the penis in a tubelike fashion to direct the urine stream out and away from the cream acne 7 weeks pregnant cheap elimite master card. Acetaminophen is ineffective for the management of severe pain associated with the circumcision procedure skin care heaven coupon 30 gm elimite purchase with visa, but it provides some analgesia in the postoperative period. Acetaminophen has been found to decrease pain 6 hours after circumcision (Howard et al, 1994). In addition, a parenteral opioid, such as morphine or fentanyl, is typically required. The pain of a lumbar puncture is compounded by both the needle puncture and the distress caused by the body position required for the procedure. Chest tube insertion requires an intravenous opioid, adequate local analgesia (lidocaine), or both. Once medication administration has begun, careful monitoring for side effects can decrease potential adverse events related to administration of pain medications to infants. A key component of effective pain management is reassessment after a painful intervention, although this is difficult to do with limited pain assessment tools. Cyclooxygenase enzymes are responsible for the breakdown of arachidonic acid to prostaglandins. Moreover, development of the central nervous, cardiovascular, and renal systems is dependent on prostaglandins. Administering 10 mg/kg may be inadequate for pain control, because this dose is based on antipyretic doseresponse studies. The maximum recommended daily dose is 75 to 90 mg/kg for infants, 45 to 60 mg/kg for term and preterm neonates more than 32 to 34 weeks of postconceptual age, and 25 to 40 mg/kg/day for preterm neonates 28 to 32 weeks of postconceptual age (Berde and Sethna, 2002; Morris et al, 2003). Rectally administered acetaminophen has a longer halflife, but absorption is highly variable because it depends on the individual infant and placement of the suppository. It should also be noted that the suppository may contain all of the drug in its tip and should be divided lengthwise if a partial dose is desired. The analgesic effect of acetaminophen may be additive when the agent is administered with opioids. This coadministration may enable a decrease in the opioid dose and therefore in corresponding opioid side effects; however, demonstration of this potential benefit awaits further study (van der Marel et al, 2007). Opioid dosing depends on the severity of the pain as well as the age and clinical condition of the infant. Opioids should be used in infants younger than 2 months only in a monitored setting such as an intensive or intermediate care unit (Yaster et al, 2003). Some clinicians propose a more conservative recommendation, restricting the use of opioids to monitored settings for any infant younger than 6 months. Morphine Morphine remains the standard for pain management in neonates, although not necessarily because it has been shown to be the most effective analgesic. Morphine is metabolized in the liver by uridine diphosphate glucuronyltransferase into two active metabolites: (1) morphine6-glucuronide (M6G), a potent opiate receptor agonist, and (2) morphine-3-glucuronide (M3G), a potent opiate receptor antagonist. Because of slow renal excretion, the metabolites can accumulate substantially over time (Bouwmeester et al, 2003a, 2003b; Saarenmaa et al, 2000). There is a potential for late respiratory depression because of a delayed release of morphine from less well-perfused tissues and the sedating properties of the M6G metabolite (Anand et al, 2000). Because the predominant metabolite of morphine in infants is M3G, a potent opiate receptor antagonist, using the lowest dose possible to achieve the needed analgesia should be considered. Escalating morphine doses will also increase the levels of M3G in the infant, interfering with the goal of adequate analgesia. Doses as low as 1 to 5 g/kg/h can provide adequate analgesia, minimizing the risk of accumulation of high M3G levels with Acetaminophen Acetaminophen is the most widely administered analgesic in patients of all ages. Acetaminophen inhibits the activity of cyclooxygenase in the central nervous system, decreasing the production of prostaglandins, and peripherally blocks pain impulse generation (Arana et al, 2001). Neonates are able to form the metabolite that results in hepatocellular damage (Arana et al, 2001); however, it is inappropriate to withhold acetaminophen in newborns because of concerns of liver toxicity. Current recommendations are for less frequent oral dosing (every 8 to 12 hours in preterm and term neonates), because of slower clearance times, and higher rectal dosing because of decreased absorption (Arana et al, 2001; van Lingen et al, 1999). Typical oral doses for acetaminophen are 10 to 15 mg/kg every 6 to 8 hours for term neonates and 10 to 15 mg/kg every 4 to 6 hours for infants. Clearance or elimination of morphine and other opioids is prolonged in infants, because of the immaturity of the cytochrome P-450 system at birth. The rate of elimination and clearance of morphine in infants 6 months and older approaches that in adults. Chronologic age seems a better indicator than gestational age of how an infant metabolizes opioids (Scott et al, 1999; Yaster et al, 2003). Infants are at greater risk for opioid-associated respiratory depression because of their immature responses to hypoxia and hypercarbia. There is an increase in unbound or free morphine and M6G available to reach the brain as a result of the reduced concentration of albumin and alpha1 acid glycoproteins (Houck, 1998). Hypotension, bradycardia, and flushing constitute the response to the histamine release and rapid intravenous administration of morphine. Histamine release may cause bronchospasm in infants with chronic lung disease, although this is not commonly seen (Anand et al, 2000). Morphine sedation may result in extended need for ventilatory support in neonates (Anand et al, 1999; Bhandari et al, 2005).

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In addition to the expense of the initial hospitalization skin care untuk kulit berjerawat order elimite master card, the cost of caring for a late preterm baby can also be compounded by the increased incidence of hospital readmissions and the long-term care issues related to persistent problems skin care routine for dry skin purchase cheap elimite online. The effects of the increasing number of late preterm births create a societal burden in lost productivity, as parents take extended leave from work to be with their fragile newborns. More importantly, there may be lasting effects with neurodevelopmental delays extending into early school age. Because a significant proportion of brain growth occurs during the last 6 weeks of gestation (Adams-Chapman, 2006), late preterm infants are vulnerable to neuronal injury and disruption of normal brain development. Whereas more longitudinal studies are needed, preliminary studies show that late preterm infants are more likely to have a diagnosis of developmental delay within the first 3 years of life, require special needs preschool resources, and have more problems with school readiness (Morse et al, 2009). Given their large numbers, the overall socioeconomic effects of the late preterm births can be significant. Strategies are required that can reduce the preventable fraction of late preterm births and work toward reducing the morbidity in others, when continuation of the pregnancy is deemed harmful to the fetus or the mother. This chapter explores the pathophysiology of the major morbidities that affect late preterm infants and discusses the unique challenges faced by clinicians in the management of these conditions. Many late preterm infants develop respiratory distress soon after birth (sustained distress for more than 2 hours after birth accompanied by grunting, flaring, tachypnea, retractions, or supplemental oxygen requirement), which studies show occurs more often in late preterm infants than in term newborns (28. Not surprisingly, of the affected babies, the incidence of respiratory maturity has prompted the name change to late preterm (Box 33-1). The term late preterm and the gestational age limits were established by a panel of experts convened by the National Institutes of Health and the National Institute of Child Health and Human Development in 2005. While developing these criteria, the group considered many factors, including the obstetric guidelines that consider 34 weeks to be a maturational milestone. Such predisposition is attributed to a developmental increase in smooth muscle in the walls of pulmonary blood vessels. Management of neonates who develop significant pulmonary hypertension can be challenging, given the self propagated nature of hypoxia-induced pulmonary vasoconstriction. A review of the Extracorporeal Life Support Organization Neonatal Registry from 1989 to 2006 by Dudell and Jain (2006) found that 14. If the net ion movement is from the apical surface to the interstitium, an osmotic gradient would be created, which would in turn direct water transport in the same direction, either through aquaporins or by diffusion. Overall survival rate was significantly lower (74%) for late preterm infants compared with term infants (87%) (Dudell and Jain, 2006). Why is it that, even in situations in which amniotic fluid testing shows a mature surfactant profile, late preterm infants are at risk for developing respiratory distress Throughout much of gestation, fetal lungs actively secrete fluid into alveolar spaces via a chloride secretory mechanism. The fluid that accumulates in the developing lung plays a critical role by providing a structural template that prevents the collapse of the developing lung and promotes its growth. At the time of delivery, the lung epithelium becomes integral in the process of switching from placental to pulmonary gas exchange (Bland, 2001; Jain, 1999). For effective gas exchange to occur in the lungs, alveolar spaces must be cleared of excess fluid, and pulmonary blood flow must be increased to match ventilation with the perfusion that is taking place. If either the ventilation or perfusion is inadequate, the infant will have a difficult time transitioning and will develop respiratory distress. In addition, during fetal development, many abnormalities can occur and interfere with the normal production of this lung fluid. Some problems during development include pulmonary artery occlusion, diaphragmatic hernia, and uterine compression of the fetal thorax from chronic leak of amniotic fluid. All these conditions inhibit normal lung development and growth (Jain and Eaton, 2006). In the alveolar epithelia, glucocorticoids were found to induce lung sodium reabsorption in the late gestation fetal lung (Tomashek et al, 2007). In addition to increasing transcription of sodium channel subunits, steroids increase the number of available channels, by decreasing the rate at which membrane-associated channels are degraded, and increase the activity of existing channels. Glucocorticoids have also been shown to enhance the responsiveness of lungs to -adrenergic agents and thyroid hormones (Venkatesh and Katzberg, 1997). In addition to problems with lung fluid clearance, several other factors may contribute to the overall burden of respiratory morbidity (Hansen et al, 2008; Kolas et al, 2006; Levine et al, 2001; Morrison et al, 1995; Roth-Kleiner et al, 2003; Villar et al, 2007). Because of the risks and complications associated with amniocentesis, this testing is done infrequently (Dudell and Jain, 2006), especially in light of recent studies showing that even late preterm infants and some early term infants born by cesarean section before the onset of labor have respiratory distress despite having mature surfactant profiles. This finding prompted the American College of Obstetrics and Gynecologists (2002) to recommend scheduling elective cesarean section at 39 weeks or later or waiting for the onset of spontaneous labor, but unfortunately factors related to the convenience of scheduled elective cesarean section deliveries for both families and providers will continue to influence the timing of elective cesarean section (Dudell and Jain, 2006). Late preterm infants often have poor coordination of sucking and swallowing because of neuronal immaturity, decreased oromotor tone, and inability to generate adequate intraoral pressures during sucking (Engle et al, 2007; Kinney, 2006; Polin et al, 2003; Raju et al, 2006). Breastfeeding has also been shown to be more difficult for early term or late preterm infants compared with term infants (Raju, 2006). These problems are compounded by the variations in practice and nutritional management of these infants, given the paucity of published studies in this regard. Recent studies have shown that issues such as hypoglycemia and poor feeding contributed to 27% of all late preterm babies requiring intravenous fluids, compared with only 5% of their term counterparts (Wang et al, 2004). The challenge then becomes providing adequate nutrition to support growth and equate the energy expenditure that can occur when the infant faces issues such as hypothermia, sepsis, and respiratory distress, which are often seen in late preterm infants. Studies show that the energy expenditure of nongrowing low-birthweight infants (birthweight less than 2500 g) is 45 to 55 cal/ kg/day (Adamkin, 2006). The concern over the use of lipids in the late preterm infant with lung disease stems from adult studies showing that failure to clear infused lipids has an adverse effect on gas exchange in the lungs (Greene et al, 1976). Contrary to those findings, preterm neonates randomized to different lipid infusion rates did not demonstrate any effect on alveolar-arterial oxygen gradient, arterial blood pH, or oxygenation when randomly assigned to modest doses of lipids (0. The concern is that the high polyunsaturated fatty acid content of lipid emulsions (with excess omega 6-linoleic acid) feeds into the arachidonic acid pathways, leading to synthesis of prostaglandins and leukotrienes, which can increase vasomotor tone and result in hypoxemia (Adamkin, 2006). In general, nutritional experts recommend that 34- and 35-week late preterm infants receive nutrient-enriched (22 kcal/oz) milk, whereas older 36- and 37-week late preterm infants with an uncomplicated neonatal course be fed unfortified milk after discharge (Adamkin, 2006).

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Just as careful temperature monitoring during hypothermia is necessary for the safe transport of these patients acne inversa images elimite 30 gm sale, observational studies suggest that the avoidance of hyperthermia is critically important skin care 999 discount elimite 30 gm free shipping. In an observational study, Laptook et al (2008) noted an increase in mortality or disability in asphyxiated neonates who had elevated skin or esophageal temperatures. As additional studies are completed, therapeutic hypothermia may enter common clinical and transport practices. When combined with other therapeutic interventions, hopefully therapeutic hypothermia will have a greater effect on the consequences of perinatal asphyxia. Attention to the basics of airway, breathing, and circulation should continue throughout the transport, because the major anticonvulsants used to treat neonatal seizure all have potential side effects, most commonly respiratory depression and hypotension. Controversy remains as to whether to treat all forms of neonatal seizures, although treatment seems prudent in the transport environment (Bartha et al, 2007). In animal models, seizures create neural, biochemical, and structural changes that have long-term cognitive and behavioral consequences (Thibeault-Eybalin et al, 2009). Both of the large-scale clinical hypothermia trials for hypoxic ischemic encephalopathy noted poorer prognosis for children with hypoxic ischemic encephalopathy with seizures (Gluckman et al, 2005; Shankaran et al, 2005). Glass et al (2009) compared magnetic resonance imaging findings and the presence of seizures in a group of newborns with suggested hypoxic ischemic encephalopathy. Adjusting for the magnetic resonance imaging results, patients with seizures were more likely to have long-term neurologic issues than those without seizures (Glass et al, 2009). The ideal anticonvulsant agent would reliably stop clinical and electrographic seizures with minimal adverse effects (Thibeault-Eybalin et al, 2009). Topirmante, levetiracetam, bumetanide, and zonisamide have all been used to treat neonatal seizures, but there have been no randomized trial to demonstrate their effectiveness compared with current therapies. Further work is necessary to develop more effective and safer antiepileptic drugs so that, along with potentially neuroprotective strategies, the vulnerable and immature brain can be protected. Several trials and studies have been proposed to hopefully elucidate a better treatment strategy (Clancy, 2006). Neonatal Seizures the highest rate for seizures in pediatrics occurs during the neonatal period, with an incidence of 2 to 3. Phenobarbital, phenytoin, or midazolam have not been shown to significantly improve seizure management or reduce morbidity and mortality (Booth and Evanse, 2004; Carmo and Barr, 2005; Painter et al, 1999). Despite the evidence of limited efficacy, phenobarbital remains the first line of therapy to treat neonatal seizures (Painter et al, 1999; Sankar and Painter, 2005). Before initiating therapy, the transport team needs to consider the diverse causes for neonatal seizures. The preoperative care of the patient affects postoperative outcomes and mortality (Mahle and Wernovsky, 2000; Mahle et al, 2000; Robertson et al, 2004; Simsic et al, 2007; Wernovsky et al, 1995, 2000). The most common nursery findings prompting diagnosis of heart disease in the nursery were an isolated murmur, cyanosis, or both (Berkley et al, 2009; Table 29-1). In a single emergency department review of patients younger than 5 months with undiagnosed cardiac disease, the most common presentation was congestive heart failure, shock, and cyanosis; if restricting the findings to a neonatal population, shock and profound cyanosis were the presenting symptoms (Savitsky et al, 2003). This finding is consistent with other centers showing a preponderance of left-sided obstructive lesions (excluding hypoplastic left heart syndrome) in those diagnosed postnatally (Friedberg et al, 2009). Although debate is ongoing as to the appropriateness of routine pulse oximetry as a screening tool (Sendelbach et al, 2008), the detection of saturations of less than 95% has a sensitivity of 72% to 77%, specificity rates over 99%, and false-positive rates of 0. These neonates are likely to have heart lesions that depend on blood flow through a patent ductus arteriosus to contribute to either systemic or pulmonary blood flow, or improvement of intercirculatory mixing. In babies with ductal-dependent pulmonary blood flow, hypoxemia is lessened as the ductus opens, and the resultant metabolic acidosis will resolve. Babies with systemic flow that is dependent on the ductal connection to provide flow to the descending aorta will have congestive heart failure, low cardiac output, or shock, which is unlikely to be treatable by standard measures without reopening the ductus arteriosus. Patients with transposition of the great arteries will have improved intercirculatory mixing with a patent ductus arteriosus (Wernovsky, 2008; Wernovsky and Jonas, 1998). In presentations with hypoxemia that is unresponsive to supplemental oxygen, congestive heart failure, or shock, simultaneous attention is devoted to the basics of neonatal advanced life support and to assurance of a patent ductus arteriosus. A stable airway must be maintained, allowing for adequate alveolar oxygenation and ventilation. Reliable venous access is important, and arterial monitoring is helpful for ongoing assessment of blood pressure, acid-base status, and gas exchange. Volume resuscitation, inotropic support, and correction of metabolic acidosis may be required to maximize cardiac output and tissue perfusion. Blood glucose and ionized calcium should be checked and treated to achieve normal range for age. An evaluation for sepsis is typically performed simultaneously, and empiric antibiotic therapy is initiated while evaluation continues. Supplemental Oxygen Supplemental oxygen is a potent pulmonary vasodilator and systemic vasoconstrictor, and it can adversely affect the physiology in neonates with a single ventricle, as well as those with two ventricles with an unrestrictive ventricular septal defect or great vessel communication (see Chapter 55, Congenital Heart Disease). In these babies, the ratio of pulmonary vascular resistance to systemic vascular resistance will determine the proportion of blood flow to each vascular bed. The oxygen-induced pulmonary vasodilation can decrease pulmonary vascular resistance and increase pulmonary blood flow at the expense of systemic blood flow, thus reducing systemic output. Titrating oxygen via nasal cannula or face mask to a target peripheral saturation of 75% to 85% usually corresponds to adequate blood flow in both the pulmonary and systemic systems. In the setting of normal hemoglobin, cardiac output, and oxygen consumption, these oximetry values will provide adequate oxygen delivery.

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Free T4 levels reach concentrations of biologic significance in the adult by midgestation acne under the skin generic 30 gm elimite with amex. Studies using rat models have demonstrated that this thyroid hormone is important for corticogenesis early in the pregnancy (Morreale de Escobar et al skin care 4men wendy buy elimite online, 2004). Therefore if thyroxinebinding globulin is increased, then T3 resin uptake may be in the euthyroid to slightly increased range in a patient who has true hyperthyroidism. Hollingsworth (1989) has reviewed the assessment of thyroid function tests in nonpregnant and pregnant women, along with the differential diagnosis of hyperthyroidism during pregnancy. Some affected infants have widespread evidence of autoimmune disease, including thrombocytopenic purpura and generalized hypertrophy of the lymphatic tissues. Thyroid storm can occur shortly after birth, or the infant may have disease that is transient in nature, lasting from 1 to 5 months. Infants born to mothers who have been treated with thioamides may appear normal at birth, but demonstrate signs of thyrotoxicosis at 7 to 10 days of age, when the effect of thioamide suppression of thyroxine synthesis is no longer present. The measurement of thyroid-stimulating antibodies is useful in predicting whether the fetus will be affected. The therapeutic goal is to achieve a euthyroid, or perhaps slightly hyperthyroid, state in the mother while preventing hypothyroidism and hyperthyroidism in the fetus. Once the disorder is under control, however, it is important to keep the dose as low as possible, preferably less than 100 mg daily, because this drug crosses the placenta and blocks fetal thyroid function, possibly producing hypothyroidism in the fetus. In women with cardiovascular effects, the use of betablockers may be appropriate to achieve rapid control of thyrotoxicosis. Because administration of propranolol to pregnant women has been associated with intrauterine growth restriction and impaired responses of the fetus to anoxic stress as well as postnatal bradycardia and hypoglycemia, the doses must be closely controlled. Iodides have also been used, particularly in combination with betablocking agents, to control thyrotoxicosis. Because of the inhibition of the incorporation of iodide into thyroglobulin, a large, obstructive goiter can develop in the fetus. Surgery during pregnancy is best reserved for cases in which the mother is hypersensitive to antithyroid drugs, compliance with medication is poor, or drugs are ineffective in controlling the disease. Daneman and Howard (1980) reported on the outcome of nine infants with neonatal thyrotoxicosis and noted normal growth, but a high incidence of craniosynostosis and intellectual impairment. It may be necessary to treat the asymptomatic mother with thioamides and propranolol (and thyroid replacement) during pregnancy to treat the infant and prevent serious neonatal morbidity and long-term problems. Mothers with thyrotoxicosis who are taking normal doses of thioamide can safely breastfeed their infants, although thioamide appears in breast milk in low amounts. Neonatal Neurologic Development In humans, early epidemiologic data from iodine-deficient areas of Switzerland suggested a link between mental retardation in the children of women with abnormal thyroid function (Gyamfi et al, 2009). It has been demonstrated that early transplacental passage of thyroid hormone is important for normal neurodeveloment of the fetus. If maternal T4 levels are low, fetal T3 in the brain will be low even if the maternal and fetal serum T3 are normal (Morreale de Escobar et al, 2004). Studies involving rats-which, like humans, are dependent on maternal thyroid hormone early in development-have demonstrated that thyroid hormone receptor is present in the brain before neural tube closure, suggesting a biologic role (Morreale de Escobar et al, 2004). Lavado-Autric et al (2003) have demonstrated that in iodine-deficient rat pups, there is aberrant neuronal migration, blurring of the cytoarchitecture, and abnormal morphology in the somatosensory cortex and hippocampus. Early in human development there is expression of nuclear thyroid receptors, which are already occupied by T3, suggesting that normal maternal T4 levels are necessary for normal cortical development (Morreale de Escobar et al, 2004). Given the increased risk of adverse perinatal and neurodevelopmental outcomes, all women with overt hypothyroidism should be treated in pregnancy. A follow-up study on these same infants, tested in both motor and mental scores at 1 and 2 years of age, found significantly lower scores in infants born to mothers with low free T4 levels (Pop et al, 2003). Other causes of primary hypothyroidism include iodine deficiency, thyroidectomy, or ablative radioiodine therapy for hyperthyroidism. Women with over hypothyroidism are at increased risk of pregnancy complications, such as a higher rate of miscarriage, preeclampsia, placental abruption, growth restriction, and stillbirth (Casey and Leveno, 2006). The signs and symptoms of hypothyroidism are usually insidious and easily confused with those of normal pregnancy including fatigue, cold intolerance, cramping, constipation, weight gain, hair loss, insomnia, and mental slowness. Based on the available animal and clinical data, the American Association of Clinical Endocrinologists, the American Thyroid Association, and the Endocrine Society recommend universal screening for all pregnant women. However, the American College of Obstetricians and Gynecologist (2001) recommend that screening should be performed only in women who have risk factors, such as pregestational diabetes, or who are symptomatic. Universal screening is not recommended by the American College of Obstetricians and Gynecologist, given that decision and cost effectiveness studies on the effects of such a strategy are currently lacking. Furthermore, data are lacking regarding therapy dosing, efficacy, or whether medication should be stopped after pregnancy in otherwise asymptomatic women with subclinical hypothyroidism and hypothyroxinemia. A multicenter randomized trial is currently underway to examine whether screening and treatment of hypothyroxinemia or subclinical hypothyroidism have a long-term effect on neurodeveloment of offspring clinicaltrials. Clinical management guidelines for obstetrician-gynecologists: gestational diabetes, ObstetGynecol 98:525-538, 2001. American Diabetes Association: Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, Diabetes Care 25(Suppl 1): S5-S20, 2002. Moore A significant spectrum of maternal medical disorders may complicate pregnancy. Some of these disorders, although readily manageable in nonpregnant patients, can be lethal to pregnant women. As a result, two questions arise for the specialist caring for a pregnant woman with a medical complication. During pregnancy, any potential medical therapy should be considered carefully to minimize fetal risk. For example, thalidomide and diethylstilbestrol were prescribed in the past for morning sickness and recurrent miscarriages, respectively, on the basis of the reasonable hypotheses that maternal sedation would decrease nausea and increased estrogens would support the placenta and reduce the likelihood of first-trimester loss. Unfortunately, the use of both of these agents led to significant and tragic congenital anomalies in the offspring.

Usage: t.i.d.

However acne that itches cheap 30 gm elimite mastercard, there is concern for harm associated with the administration of base acne gel prescription 30 gm elimite order with visa, including increased mortality and intraventricular hemorrhage (Papile et al, 1978; Simmons et al, 1974; Usher, 1967), increased cerebral blood volume regardless of rate of administration (van Alfen-van der Velden et al, 2006), and decreased intracellular pH with cellular injury (Lipshultz et al, 2003). If therapy with base is warranted, the clinician has three options: sodium bicarbonate, sodium (or potassium) acetate, and tromethamine. Sodium bicarbonate is the most widely used buffer in the treatment of metabolic acidosis in the neonatal period. Bicarbonate should not be given if ventilation is inadequate, because its administration results in an increase in Paco2 with no improvement in pH and an increase in intracellular acidosis. Therefore sodium bicarbonate should be administered slowly and in diluted form only to newborns with documented metabolic acidosis and adequate alveolar ventilation. Subsequent doses of sodium bicarbonate are then based on the results of additional blood gas measurements. When clinicians are faced with a chronic metabolic acidosis caused by a prematurity-related proximal renal tubular acidosis with bicarbonate wasting, many choose to replace these losses over time. In this instance, either sodium or potassium acetate can be used as an alternative to sodium bicarbonate. It has been shown in one study to be an effective alternative to sodium bicarbonate in correcting this type of acid-base abnormality when added to parenteral nutrition (Peters et al, 1997). Infants randomized to acetate had an increased base excess and pH and increased Pco2, and they received less bicarbonate boluses compared with control infants. In certain clinical situations, tromethamine can be used as an alternative buffer to sodium bicarbonate. The theoretical advantages of tromethamine over sodium bicarbonate in the treatment of metabolic acidosis of the newborn include its more rapid intracellular buffering capability, its ability to lower Paco2 levels directly, and the lack of an increase in the sodium load (Schneiderman et al, 1993). Although there are controversies regarding the actual bicarbonate space in humans, the 30% of total body weight in the formula represents its estimated volume of distribution in the neonate. Because the end-product (chelated tromethamine) is a cation that is excreted by the kidneys, oliguria is a relative contraindication to the repeated use of this buffer. Tromethamine administration also has been associated with the development of acute respiratory depression, most likely secondary to an abrupt decrease in Paco2 levels as well as from rapid intracellular correction of acidosis in the cells of the respiratory center (Robertson, 1970). Furthermore, because hypocapnia is associated with decreases in brain blood flow and a higher incidence of white matter damage, especially in the immature preterm neonate, close monitoring of Paco2 is of paramount importance when tromethamine is being used. Finally, when large doses of tromethamine are administered, hyponatremia (Seri et al, 1998b), hypoglycemia, hyperkalemia, an increase in hemoglobin oxygen affinity, and diuresis followed by oliguria can occur. Because the tromethamine solution is hyperosmolar, and because rapid infusion of tromethamine can also lower blood pressure and intracranial pressure (Duthie et al, 1994), slow infusion is recommended. Because potassium moves from the intracellular to the extracellular space in exchange for H+ when acidosis occurs, the presence of a total body potassium deficit might not be appreciated during metabolic acidosis. Hypokalemia may become evident only as the pH increases and potassium returns to the intracellular space. Furthermore, intracellular acidosis cannot be completely corrected until the potassium stores are restored. Therefore close monitoring of serum electrolytes and potassium supplementation are important during the correction of metabolic acidosis in the sick newborn. Respiratory Acidosis Respiratory acidosis occurs when a primary increase in Paco2 develops secondary to impairments in alveolar ventilation that result in an arterial pH of less than 7. Primary respiratory acidosis is a common problem in newborns, and causes include hyaline membrane disease, pneumonia owing to infection or aspiration, patent ductus arteriosus with pulmonary edema, chronic lung disease, pleural effusion, pneumothorax, and pulmonary hypoplasia. Management of respiratory acidosis is directed toward improving alveolar ventilation and treating the underlying disorder. For sick newborns, adequate ventilation must often be provided by mechanical ventilation. Therefore tromethamine should be used only as a temporizing measure in severe respiratory acidosis until alveolar ventilation can be improved. The most common causes of this type of metabolic alkalosis in the newborn period are continuous nasogastric aspiration, persistent vomiting, and diuretic treatment. Less common causes of H+ losses are congenital chloride-wasting diarrhea, certain forms of congenital adrenal hyperplasia, hyperaldosteronism, posthypercapnia, and Bartter syndrome. In the past, a metabolic alkalosis was intentionally created when sodium bicarbonate or tromethamine was used to maintain an alkaline pH to decrease pulmonary vasoreactivity in infants with persistent pulmonary hypertension, a practice not recommended anymore. The obvious clinical benefits of allowing this physiologic extracellular volume contraction to occur, especially in the critically ill newborn, clearly outweigh the clinical importance of a mild contraction alkalosis that develops after recovery. No specific treatment is needed in such cases, because with the stabilization of the extracellular volume and renal function after recovery, acid-base balance rapidly returns to normal. In the last condition, there is a direct stimulation of Na+ reabsorption coupled with H+ loss in the proximal tubule, and an indirect stimulation of H+ loss in the distal nephron by the increased activity of the renin-angiotensin-aldosterone system. Contraction alkalosis responds to administration of saline to replace the intravascular volume in conjunction with additional potassium supplementation to account for renal potassium wasting. In the other disorders, however, the primary problem of reduced glomerular filtration rate or elevated aldosterone must be treated for the alkalosis to resolve. One of the most commonly encountered clinical scenarios of chronic metabolic alkalosis actually occurs in the form of a mixed acid-base disorder in a preterm infant with chronic lung disease on long-term diuretic treatment. By stimulating proximal tubular Na+ reabsorption and thus H+ loss, distal tubular H+ secretion, and renal ammonium production, the diuretic-induced hypokalemia contributes to the severity and maintenance of the metabolic alkalosis. Furthermore, metabolic alkalosis per se worsens hypokalemia, because potassium moves intracellularly to replace hydrogen as the latter shifts into the extracellular space. Although the serum potassium concentration may be decreased, the serum levels in the newborn do not accurately reflect the extent of total-body potassium deficit because potassium is primarily an intracellular ion, with approximately 98% of the total body potassium being in the intracellular compartment.

References

  • Winchester DE, Wen X, Xie L, Bavry AA. Evidence of pre-procedural statin therapy a metaanalysis of randomized trials. J Am Coll Cardiol 2010;56(14):1099-1109.
  • Schenarts PJ, Phade SV, Agle SC, et al. Field hypotension in patients who arrive at the hospital normotensive: a marker of severe injury or crying wolf? NC Med J. 2008;69:265-269.
  • Lokhandwalla, M., Sturtevant, B. Mechanical haemolysis in shock wave lithotripsy (SWL). I. Analysis of cell deformation due to SWL flow-fields. Phys Med Biol 2001;46:413-437.
  • Belin P, Van Eeckhout P, Zilbovicius M, et al. Recovery from nonfluent aphasia after melodic intonation therapy: A PET study. Neurology 1504;47:1996.
  • Heaton, N. D., Hogan, B., Michell, M., Thompson, P., & Yates- Bell, A. J. (1989). Tuberculous epididymo-orchitis: Clinical and ultrasound observations. British Journal of Urology, 64(3), 305n309.
  • Philippou Y, Parker RA, Volanis D, et al: Comparative oncologic and toxicity outcomes of salvage radical prostatectomy versus nonsurgical therapies for radiorecurrent prostate cancer: a meta-regression analysis, Eur Urol Focus 2(2):158n171, 2016.
  • Dutsch M, Marthol H, Stemper B, Brys M, Haendl T, Hilz MJ. Small iber dysfunction predominates in Fabry neuropathy. J Clin Neurophysiol 2002;19:575- 586.
  • Das A, Boggaram V. Proteasome dysfunction inhibits surfactant protein gene expression in lung epithelial cells: mechanism of inhibition of SP-B gene expression. Am J Physiol Lung Cell Mol Physiol 2007;292(1):L74-84.