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New Guidelines 2007 Edition
Karen Scruggs, MD Michael T. Johnson, MD
Copyright © 2007 by Current Clinical Strategies Publishing. All rights reserved. This book, or any parts thereof, may not be reproduced or stored in a retrieval network without the written permission of the publisher. The reader is advised to consult the drug package insert and other references before using any therapeutic agent. No warranty exists, expressed or implied, for errors and omissions in this text. Current Clinical Strategies Publishing 27071 Cabot Road Laguna Hills, California 92653 Phone: 800-331-8227 Fax: 800-965-9420 firstname.lastname@example.org Internet: www.ccspublishing.com/ccs Printed in USA ISBN 1-929622-74-0
Normal Newborn Care
I. Prenatal pediatric visit A. The prenatal pediatric visit usually takes place during the third trimester of the pregnancy. Maternal nutrition, the hazards of alcohol, cigarette smoking and other drugs, and the dangers of passive smoking should be discussed. Maternal illnesses and medications should be reviewed. Prenatal Pediatric Visit Discussion Issues Maternal History General health and nutrition Past and present obstetric history Maternal smoking, alcohol, or drug use Maternal medications Infectious diseases: Hepatitis, herpes, syphilis, Chlamydia rubella Maternal blood type and Rh blood groups Family History Newborn Issues Assessment of basic parenting skills Feeding plan: Breast feeding vs formula Car seats Circumcision of male infant II. Delivery A. Neonatal resuscitation 1. All equipment must be set up and checked before delivery. The infant who fails to breath spontaneously at birth should be placed under a radiant warmer, dried, and positioned to open the airway. The mouth and nares should be suctioned, and gentle stimulation provided. 2. The mouth should be suctioned first to prevent aspiration. Prolonged or overly vigorous suctioning may lead to bradycardia and should be avoided unless moderate-to-thick meconium is present in the airway. 3. The infant born with primary apnea is most likely to respond to the stimulation of drying and gentle tapping of the soles of the feet. The infant who fails to respond rapidly to these measures is experiencing secondary apnea and requires positive pressure bag ventilation with oxygen. 4. Adequate ventilation is assessed by looking for chest wall excursions and listening for air exchange. The heart rate should be assessed while positive pressure ventilation is being applied. If the heart rate does not increase rapidly after
ventilation, chest compressions must be started by an assistant. If the infant fails to respond to these measures, intubation and medications are necessary. Epinephrine can be administered via the endotracheal tube. Apgar scores are used to assess the status of the infant at 1 and 5 min following delivery.
Apgar Scoring System Sign Heart rate 0 Absent 1 Slow (<100 beats/min) 2 100 beats/min or more Strong cry
Weak cry; hypoventilation Some flexion Grimace
Muscle tone Reflex irritability Color
Active motion Cough or sneeze Completely pink
No response Blue or pale
Body pink; extremities blue
III. Early routine care of the newborn A. Vitamin K is given to the infant by intramuscular injection to prevent hemorrhagic disease of the newborn. B. Ocular prophylaxis against gonorrheal and chlamydial infection is administered after birth with erythromycin ophthalmic ointment. C. Umbilical cord blood syphilis serology is completed if there is no documented record of a negative third-trimester maternal test. Umbilical cord care consists of local application of triple dye or bacitracin ointment. D. Hepatitis B prophylaxis. If the mother is hepatitis B surface antigen-positive, or if she has active hepatitis B, the infant should be given an IM injection of hepatitis B immune globulin and a course of three injections of hepatitis B vaccine (before hospital discharge, and at 1 and 6 months of age). IV. Physical examination of the newborn A. General gestalt. The examiner should assess whether the infant appears to be sick or well. An unusual cry may indicate sepsis, hypothyroidism, a congenital anomaly of the larynx, or a chromosomal abnormality. B. Vital signs. The normal temperature of the newborn is 36.5 to 37.0 degrees C. The normal respiratory rate ranges from 40 to 60 breaths per minute, and the normal heart rate can range from 94 to 175 beats per minute. C. Assessment of the adequacy of fetal growth 1. Gestational age assessment. The gestational age of the newborn infant is assessed with the Ballard score of neuromuscular and physical maturity. 2. Premature infants a. A preterm infant is defined as an infant of less than 37 weeks' gestation, and a postterm infant is defined as being of greater than 42 weeks' gestation. b. Preterm infants may develop respiratory distress syndrome, apnea, bradycardia, and retinopathy of prematurity. Respiratory distress syndrome is recognized by tachypnea, grunting, retractions, an elevated oxygen requirement, and a roentgenographic picture of poor inflation and a fine homogeneous ground-glass appearance. D. Premature infants of less than 34-1/2 to 35 weeks' gestation are at increased risk for apnea and bradycardia. Apnea is defined as a respiratory pause of 20 sec or longer and frequently is accompanied by a drop in heart rate. E. Measurements and growth charts 1. Height, weight, and head circumference should be measured. A low-birth-weight infant is defined as any neonate with a birthweight <2,500 g.
Height, weight, and head circumference should be plotted as a function of gestational age on an intrauterine growth chart. 2. Factors that may result in an infant who is small for gestational age include chromosomal and other dysmorphic syndromes, congenital infections, maternal hypertension, smoking, uterine anomalies, and multiple gestations. 3. The small-for-gestational age infant is at greater risk for cold stress, hypoglycemia, hypocalcemia, and polycythemia. 4. The differential diagnosis for the large-for-gestational age infant includes maternal diabetes and maternal obesity. The large-for-gestational age infant is at risk for shoulder dystocia, birth trauma, and hypoglycemia. F. Examination of organ systems and regions 1. Head, face, and neck a. The head circumference is measured and plotted, and the scalp, fontanelles, and sutures are examined. Bruising and hematomas of the scalp should be noted. Cephalohematomas are subperiosteal and do not cross suture lines, whereas caputs are subcutaneous and do cross suture lines. b. Facial features that suggest a chromosomal anomaly include midfacial hypoplasia, small eyes, or low-set ears. Fetal alcohol syndrome is suggested by a small upper lip and a smooth philtrum. c. The eyes should be examined with an ophthalmoscope to document a red reflex. The absence of a clear red reflex is indicative of a retinoblastoma, cataract, or glaucoma. d. The lips, mouth, and palate are inspected and palpated for clefts. Nares patency can be documented by closing the mouth and occluding one nostril at a time while observing air flow through the opposite nostril. 2. Thorax and cardiovascular systems a. Chest wall excursions should be observed and the respiratory rate determined. The normal neonatal respiratory rate is 40 to 60 breaths per minute. b. Auscultation of breath and heart sounds. The normal heart rate during the first week of life may range from 94 to 175 beats per minute. 3. Abdomen and gastrointestinal system a. Visual inspection of the abdomen should assess symmetry and distension. b. Abdominal palpation for masses, hepatosplenomegaly, or renal masses is completed, and the anus should be visually inspected. 4. Genitourinary system. The genitalia are examined for ambiguous genitalia, which requires immediate endocrinologic and urologic consultation. 5. Musculoskeletal system a. Hip examination may detect developmental dysplasia. Risk factors for hip dysplasia include a family history, foot deformities, congenital torticollis, Down syndrome, and breech presentation. The female to male ratio is 7:1. Ultrasonography is used to evaluate suspected hip dysplasia. b. Fracture of the clavicle occurs in 0.2-3.5% of vaginal deliveries. Physical findings include local swelling and crepitations and an asymmetric Moro reflex. Treatment consists of making a sling by pinning the shirt sleeve of the involved side to the opposite side of the shirt. 6. Neurologic system a. The degree of alertness, activity, and muscle tone should be noted. The head circumference is plotted on the growth chart. b. The posterior midline area should be examined for evidence of neural tube defects. Pilonidal dimples with tufts of hair are evaluated with ultrasonography. V. Common neonatal problems A. Hypoglycemia 1. Hypoglycemia is common in premature infants, infants who are small for gestational age, infants
renal ultrasonography should be done and an intravenous fluid challenge may be given. D. High levels of bilirubin can cause an acute encephalopathy (ie. E. References. prolonged jaundice (>7 to 10 days in a full-term infant). and breast-fed infants have an increased incidence of jaundice. Hypoglycemic infants require early feedings or IV glucose.of diabetic mothers. Increased bilirubin load due to the high red blood cell volume in newborns and shortened blood cell survival. Bilious vomiting in the newborn is always abnormal and usually is caused by an intestinal obstruction. lethargy. Physical examination should seek bruising. 2. b. Bilirubin metabolism 1. Urinary problems. d. Deficient excretion of bilirubin. Causes of physiologic jaundice a. Deficient hepatic uptake and deficient conjugation of bilirubin. . pallor. 3. Vomiting in the newborn also may be caused by inborn errors of metabolism and congenital adrenal hyperplasia. Pathophysiology A. c. light colored stools. I. or an elevated direct bilirubin concentration (>2 mg/dL). Increased enterohepatic bilirubin reabsorption. meconium ileus (cystic fibrosis). or small or large size for gestational age. congenital anomalies. Clinical evaluation of jaundice in newborns A. dark urine. Anemia during the newborn period may be caused by hemolytic and congenital anemias. 2. Physiologic versus pathologic jaundice 1. petechiae. Differentiation between physiologic jaundice. weight loss. low Apgar scores. Asian newborns tend to have higher peak bilirubin concentrations and more prolonged jaundice. II. fetal-to-maternal hemorrhage. Neonatal Jaundice Jaundice is defined by a serum bilirubin concentration greater than 5 mg/dL. which is seen in many infants during the first week of life. Physiologic jaundice is characterized by unconjugated hyperbilirubinemia that peaks by the third or fourth day of life in full-term newborns and then steadily declines by 1 week of age. 2. Premature infants are more likely to develop jaundice than full-term babies. 2. see page 182. Ninety-nine percent of normal full-term infants will urinate by 24 hours. C. A delayed or absent passage of meconium may be caused by meconium plug syndrome. Coombs test. delayed passage of meconium. and infants who have experienced perinatal asphyxia. Hirschsprung disease. kernicterus). History may reveal abdominal distention. Conjugated hyperbilirubinemia never has a physiologic cause and must always be investigated. B. or vomiting. and testing of urine for reducing substances to exclude galactosemia. and occult hemorrhage. hematocrit. Clinical jaundice develops in 50% of newborns. Gastrointestinal problems 1. or imperforate anus. B. If urination has not occurred within 24 hours. Hypoglycemia is defined as a blood glucose of <40-45 mg/dL. cephalhematoma. Pathologic jaundice usually appears within the first 24 hours after birth and is characterized by a rapidly rising serum bilirubin concentration (>5 mg/dL per day). and pathologic jaundice is essential because pathologic jaundice is a sign of a more serious condition. poor feeding. placental abruption. Initial workup for neonatal hyperbilirubinemia includes measurements of total and direct bilirubin levels. Ninety-six percent of full-term newborns pass a meconium stool before 24 hours of age. Hyperbilirubinemia occurs frequently in the normal newborn because of increased production and decreased elimination of this breakdown product of heme. hepatosplenomegaly.
or exposure to drugs. D. Low-risk infants with minimal jaundice are observed for an increase in the jaundice intensity or a spread to the baby’s feet (jaundice advances from head-to-foot). Consequences of unconjugated hyperbilirubinemia. This type of hemolysis is relatively mild. Certain drugs given to the newborn may also induce hemolysis or decrease bilirubin excretion. Delay in intestinal transit time. Crigler-Najjar syndrome is a rare. upward-gaze paresis. a high-pitched cry. Subsequent Rh-positive fetuses may develop hemolysis. C. and late neurologic sequelae of choreoathetosis. Family history of jaundice. reticulocyte count. and central hearing loss. may cause hyperbilirubinemia. Type I is autosomal recessive. the danger of an elevated bilirubin concentration is minimal. Maternal history should assess history of chorioamnionitis. vacuum extraction. because bowel obstruction. B. In healthy newborns. 5. G6PD deficiency. Sepsis often causes increased breakdown of red blood cells and decreased hepatic excretion of bilirubin. such as spherocytosis and elliptocytosis. Increased bilirubin production 1. Failure to receive immune globulin in a previous pregnancy or abortion that involved risk of isoimmunization should be sought. intrauterine growth retardation. VI. Fetal-maternal blood group incompatibility is one cause of increased bilirubin production. is an important cause of hyperbilirubinemia and anemia in infants of Greek and Asian descent. 2. splenectomy. Patients present with extreme jaundice (bilirubin concentration >25 mg/dL) and have a very high risk of bilirubin encephalopathy. or maternal diabetes) may lead to hyperbilirubinemia. Increased bilirubin production and decreased excretion. 3. Hematoma. and measurement of serum bilirubin concentration. dystocia. Neonatal hypothyroidism is another cause of prolonged indirect hyperbilirubinemia. 3. diabetes. III. Breast feeding is associated with neonatal hyperbilirubinemia. or unexplained illness during pregnancy should be assessed. occult hemorrhage. and direct bilirubin level. V. or those with significant jaundice (serum bilirubin >15 mg/dL) require a complete blood cell count or hemoglobin. In infants of Asian or Greek descent. Diagnostic tests include blood group typing of both mother and infant. Rh sensitization occurs when an Rh-negative mother is exposed to Rh-positive blood cells. 4. Other minor blood group incompatibilities also can cause hemolysis and jaundice. spasticity. Ill or premature infants. a direct Coombs’ test.C. liver disease. Abnormalities of the red blood cell membrane. or polycythemia (fetomaternal or twin-to-twin transfusion. Decreased bilirubin excretion 1. Laboratory evaluation A. Bilirubin encephalopathy (kernicterus) is defined as the acute and often fatal syndrome characterized by opisthotonos. forceps delivery. a sex-linked disease. . and it can effectively be treated with phenobarbital. preeclampsia. blood smear. Greek or Asian race. lifelong deficiency of bilirubin excretion. It can occur when the mother’s blood group is O and the baby’s is A or B. and switching to formula feeding is unnecessary. Type II is autosomal dominant. Alpha thalassemia may occur in the neonatal period. B. Relief of the obstruction results in a decline in bilirubin concentration. Differential diagnosis of unconjugated hyperbilirubinemia A. increases the enterohepatic circulation. glucose6-phosphate dehydrogenase (G6PD) should be measured. IV. anemia. ABO incompatibility is the most common type of isoimmune hemolytic disease. inherited. Treatment A. 2. hypotonia. delayed cord clamping.
and expiratory grunting. grunting. C.Management of Hyperbilirubinemia in the Healthy Term Newborn Total serum bilirubin level. G. and treatment is discontinued when the bilirubin concentration drops below 12 mg/dL. I. mg/dL Age (H) Consider photothe rapy Photothe rapy Exchange transfusion if phototherapy fails . delivery and tends to worsen over time. cyanosis. Infants will have tachypnea. Phototherapy with blue light causes photoconversion of bilirubin to a water-soluble product that is excreted in urine and stool. without long-term pulmonary sequelae. intercostal and sternal retractions. or soon after.. Transient tachypnea of the newborn (TTN) usually presents as early respiratory distress in term or preterm infants. nasal flaring. RDS is diagnosed when a premature infant has respiratory distress and a characteristic chest radiograph. fluffy densities. Exchange transfusion therapy. Exchange transfusion is used for emergent treatment of markedly elevated bilirubin and for correction of anemia caused by isoimmune hemolytic disease. It is caused by delayed reabsorption of fetal lung fluid. . C. It occurs almost always in preterm infants who are born before the lungs are able to produce adequate amounts of surfactant. The chest radiograph appears normal in 2-3 days. D. sternal and intercostal retractions.. >15 >18 >20 . with homogeneous haziness or the “ground glass” appearance of lung fields. B. TTN is a very common. Respiratory distress may present with tachypnea. and cyanosis. and apnea. RDS is a lung disease caused by pulmonary surfactant deficiency. which appears as reduced lung volume. nasal flaring.. Symptoms of TTN include tachypnea. The symptoms rarely last more than 72 hours. >25 >30 >30 B.. Treatment of TTN consists of oxygen therapy. E.. F. >12 >15 >17 . Transient tachypnea of the newborn usually resolves within12-24 hours. Transient tachypnea of the newborn A. alveolar edema may appear as coarse.. Arterial blood gas reveals respiratory acidosis and mild-to-moderate hypoxemia. Respiratory distress usually begins at. Chest radiography shows diffuse atelectasis. Infants will usually recover fully. Hyperaeration of the lungs and mild cardiomegaly may be seen. The differential diagnosis includes pneumonia caused by group B streptococci.. D. Chest x-ray often reveals fluid in the interlobar fissures and perihilar streaking. and it is often seen following cesarean section because babies born by cesarean section have delayed reabsorption of fetal lung fluid. Respiratory distress syndrome A. II. C.. Respiratory Disorders of the Newborn Respiratory distress is a common problem during the first few days of life. retractions. and air bronchograms. >20 >25 >25 Exchange transfusion and phototherapy <24 25-48 49-72 >72 . Bilirubin concentrations are measured once or twice a day during phototherapy. B. nasal flaring. see page 182. References.
Oxygen saturation should be maintained at 92-95 percent. BPD is characterized by hypoxia. A slightly prolonged inspiratory duration of 0.E. and aspiration pneumonia. Respiratory support a. 3. c. increased HCO3 indicates metabolic compensation. The oxygen concentration (or flow rate by nasal cannula) may need to be increased . meconium aspiration syndrome. Management of bronchopulmonary dysplasia 1. hypoxemia or apnea. suggesting an important role for barotrauma and oxygen toxicity. Higher inspired oxygen concentration is required to maintain normal oxygenation. 2. Infants who remain ventilator-dependent for several weeks should be weaned gradually. Sepsis and pneumonia are part of the differential diagnosis of RDS. Oxygen. b. supplemental oxygen can be provided by hood or nasal cannula. Small tidal volumes are preferable to avoid additional mechanical injury. Surfactant therapy reduces mortality by 30-50% and pneumothorax by 50%. Survanta (every 6 hours for 4 doses) or Exosurf (every 12 hours for 2 doses) should be given. Ventilatory management 1. General supportive care. B. including immature lungs. and oxygen dependence that persists beyond 1 month of age. Surfactant replacement therapy should be initiated as soon as respiratory distress has been clinically diagnosed. The chest radiograph shows hyperexpansion and focal hyperlucency. also known as neonatal chronic lung disease (CLD). 2. hypercarbia. For infants exhibiting respiratory acidosis. neonatal pneumonia. Mechanical ventilation. Surfactant replacement therapy 1. E. Bronchopulmonary dysplasia (BPD. the arterial carbon dioxide tension should be allowed to rise to 55-60 mm Hg. congenital heart disease. Hypoxemia also may increase airway resistance in infants who have been weaned from assisted ventilation. Monitoring. Oxygenation should be monitored with pulse oximetry. is an important cause of respiratory illness in preterm newborns. Virtually all babies who develop BPD have had mechanical ventilation. G.5-0.6 sec sometimes is needed to promote uniform lung inflation. The incidence of BPD is inversely proportional to birthweight. An umbilical or radial arterial line is used to monitor blood gas levels and blood pressure. Infants who can maintain this PCO2 level with spontaneous breathing can be weaned to continuous positive airway pressure and then to supplemental oxygen alone. intermittent positive pressure ventilation will be required in addition to positive end-expiratory pressure (PEEP). III. Maintaining a positive end-expiratory pressure of 6 or 7 cm H2O may minimize atelectasis. alternating with strands of opacification. Most patients with BPD gradually improve as healing occurs and lung growth continues. D. To facilitate weaning. F. C. Bronchopulmonary dysplasia (BPD). chronic lung disease) A. Presumptive treatment with ampicillin plus gentamicin or cefotaxime usually is given until blood and CSF cultures are negative. Other neonatal diseases requiring oxygen and mechanical ventilation may also cause BPD. 2. after extubation. Signs of BPD include tachypnea and retractions. BPD is extremely common among infants who have severe RDS treated with mechanical ventilation. Blood gas measurements show respiratory acidosis with elevated PaVCO2. As long as the infant requires significant ventilatory support. Continuous positive airway pressure (CPAP) improves oxygenation and survival (5-7 cm H2O pressure). as long as pH is in the normal range. Supplemental oxygen should be provided to maintain arterial PO2 above 5055 mm Hg. Respiratory distress syndrome is the most common pulmonary disease causing BPD.
and irritabil- . the betaadrenergic agonist albuterol may improve pulmonary function. arrhythmias. Electrolyte supplements should be administered to compensate for increased urinary loss. Albuterol (1) In some ventilator-dependent preterm infants with evolving BPD who are two to three weeks of age. In infants who have pulmonary exacerbations attributed to pulmonary edema. Initial supplementation is 2 to 4 meq/kg per day of sodium chloride and 2 meq/kg per day of potassium chloride. and at least weekly with chronic use. chlorothiazide (10 to 20 mg/kg in two divided doses. hypokalemia. In ventilator-dependent infants. When infants reach term postmenstrual age. A premature formula or human milk with added fortifier is used in preterm infants. phosphorus. Serum electrolytes should be measured one to two days after initiating diuretic therapy. a longer course of furosemide (4 mg/kg in two divided doses PO on alternate days) may be given. Diuretics in infants with evolving or established BPD to achieve acute improvements in pulmonary function are useful. These adverse effects include tachycardia. albuterol. adequate nutrition must be provided in the reduced volume of feeding.1 mg) every four to six hours. In infants three to four weeks old who remain ventilator-dependent with evolving BPD.3. 6. c. and alkaline phosphatase are measured weekly or every other week. terbutaline) acutely decreases resistance and increases compliance. Human milk or premature formula must be supplemented to meet these needs. 4. Thiazide diuretics. Bronchodilators. PO) may be used as an alternative to furosemide. furosemide should be given (1 mg/kg per day IV or 2 mg/kg per day PO). 5. with an increase in dose. b. Additional calories and/or protein may be added. d. Diuretics. salbutamol. Protein and mineral intakes should be calculated each week to ensure that they are optimal. The metered dose inhaler (MDI) often is used in infants with BPD. Fluid intake should be restricted in infants with BPD to avoid pulmonary edema. supplemented human milk or a transitional formula is used. capillary blood gas (CBG) samples should be monitored to check PCO2 and pH. Albuterol is administered as one MDI actuation per dose (approximately 0. a. Fluid restriction a. Nutrition. d. Most infants can be managed with modest restriction of 140-150 mL/kg per day. (2) If the infant appears to improve with albuterol use of a long-acting betaadrenergic agonist such as salmeterol may be preferred to avoid adverse effects that have been associated with chronic use of albuterol. or to minimize the circulatory effect of a packed red blood cell transfusion. Infants with BPD have increased airway resistance and may have episodes of bronchoconstriction. and adjust as needed. Serum concentrations of calcium. b. In infants with severe BPD who appear to have short-term benefit from diuretic treatment. during feedings and sleep to maintain adequate oxygenation. Acute and chronic administration of diuretics (thiazide and/or spironolactone) improve lung mechanics in preterm infants with BPD. a. However. Pharmacologic therapy may include diuretics. Appropriate nutrition must be provided to ensure recovery and growth. Growth should be monitored. Inhaled or subcutaneous administration of beta-2 agonists (eg.
(2) Ipratropium can be used for its synergistic effect with albuterol in the treatment of acute episodes of reactive airway disease. which is administered by MDI and spacer (two to four puffs) or by nebulization (0. b. Infants with severe BPD may have acute episodes of bronchospasm leading to respiratory decompensation. These may be associated with viral infections. 7. b.5 mg/kg per hour may be given for one to two hours). A combination of inhaled ipratropium bromide and albuterol (Combivent) may be administered as one to two MDI actuations every four hours. the frequency is decreased as airflow improves. in ventilator-dependent infants with BPD. If bacterial infection is suspected. Corticosteroids. Infants with severe BPD who are dependent upon substantial support with mechanical ventilation and high concentrations of supplemental oxygen. A chest radiograph should be obtained to detect pulmonary parenchymal changes. Systemic corticosteroids. a short (five to seven days) tapering course of systemic dexamethasone (initial dose 0. Either regimen is followed by administration every one to four hours. Ipratropium bromide (1) Administration of the anticholinergic bronchodilator ipratropium bromide (inhaled doses of 25 micrograms/kg) to ventilator-dependent preterm infants improves respiratory system resistance and compliance. Management (1) Treatment should be initiated with albuterol. and give one to two puffs every 12 hours.25 mg/kg). although bacterial pneumonia is uncommon. systemic corticosteroid administration is associated with serious adverse effects and should be avoided if possible. b. Culture and Gram stain should be obtained of tracheal secretions that are purulent or have changed in volume or quality. treatment should be discontinued gradually as lung function stabilizes and before hospital discharge. If possible. If treatment with a beta-adrenergic agent and inhaled corticosteroids fails to reestablish stable pulmonary function. Alternatively. (2) If acute bronchospasm occurs in an infant receiving inhaled corticosteroids. or with tachycardia of >200 bpm. a. Systemic dexamethasone should be reserved for the exceptional infant with severe BPD who cannot be weaned from maximal ventilatory and oxygen support. However. may be considered. the dose is doubled for 7 to 14 days. may sometimes be treated with inhaled beclomethasone or fluticasone.15 mg/kg in 2 mL saline) every 20 minutes for three doses. Systemic corticosteroids improve lung mechanics and reduce the need for assisted ventilation in infants with established BPD. Salmeterol is given as one MDI actuation twice daily. Both systemic and inhaled administration have been used. c. antibiotic treatment should be initiated while awaiting culture results. Corticosteroids may reduce inflammation and improve lung function in infants with BPD. 8. Acute exacerbations a. Beclomethasone (42 µg per puff) or fluticasone (50µg per puff) may be used by MDI connected to the endotracheal tube. Another approach is continuous nebulization of albuterol (0. Ipratropium should be added if the response to albuterol is poor. a short course of prednisone (initial dose 1 mg/kg per day. tapered over five days) may be . Inhaled corticosteroids.ity. c.
3. and alkaline phosphatase concentrations. Patients should be weighed every one to three days while in the hospital. Growth. Immediate preparation 1. Medications should be prepared and an umbilical catheter and tray should be prepared. Appropriately sized ET tubes. Suction. (2) A target oxygen saturation of 92 to 94 percent is adequate to avoid hypoxemia and minimize the risk of additional lung injury caused by exposure to excessive oxygen concentrations. Monitoring a. The target saturation should be higher (94 to 96 percent) in infants with pulmonary hypertension.5. phosphorus. 0 (preterm) and No. Preparation A. 5 (or 6). 10 Fr Meconium aspirator Bag-and-Mask Equipment Oral airways.4 mg/mL. including periods while awake. and feeding.0 mm Medications Epinephrine 1:10. low-risk deliveries. Oxygenation (1) Oxygen saturation is monitored continuously with pulse oximetry during hospitalization.000. 30 cc Volume expanders-one or more of these: Albumin 5% solution Normal Saline Ringer’s Lactate solution Stylet Scissors Gloves Oxygen with flow meter and tubing Cushion rim face masks in newborn and premature sizes Mechanical Suction 8 Fr feeding tube and 20 cc syringe . Nutritional monitoring includes initial weekly measurement of blood urea nitrogen.0. Neonatal Resuscitation Equipment and Supplies Suction Equipment Bulb syringe Suction catheters.1(term newborn). I. Serum electrolyte concentrations should be measured every week in infants on diuretic therapy. 2. newborn and premature sizes Infant resuscitation bag with a pressure-release valve/pressure gauge to give 90-100% O2 Intubation Equipment Laryngoscope with straight blades. b. Advanced preparation requires acquisition and maintenance of proper equipment and supplies. albumin. oxygen. 250 cc Sterile water. After discharge. should be laid out. oxygen saturation should be measured for at least six to eight hours every one to two weeks. 8. proper-sized face mask and the resuscitation bag should be checked.5. cut to 13 cm. No. References.1 mL ampules Dextrose 10% in water. 3. and length and head circumference should be measured weekly.tried. 3 cc or 10 cc ampules Naloxone 0. 4. 9. Neonatal Resuscitation Neonatal resuscitation skills are important because of the potential for serious disability or death in high-risk infants and in a few unpredicted full-term. calcium. 3. sleeping. B. size 2. see page 182. Extra bulbs and batteries for laryngoscope Endotracheal tubes.
give PPV immediately by bag-mask. After 30 seconds. 1 cc. oxygen should be administered.0 mm Depth 7 cm 8 cm 9 cm 10 cm G. C. 3. and respiratory effort. Endotracheal intubation is initiated if the infant is nonresponsive to bag-mask PPV. 3 ½ and 5 Fr II. The upper airway is cleared by suctioning. 10 cc. 21. the mouth first. If cyanosis is present. the infant should be placed on a preheated radiant warmer. evaluate the response. 18 gauge Umbilical catheters. Suctioning should be limited to 5 seconds at a time. begin PPV with 100% O2. 1. E. If breathing is effective and pulse is >100 beats/min. or an oxygen mask may be used. Chest compressions are alternated with ventilations at a ratio of 3:1. Chest compressions should be started if the heart rate is <80 beats/min after 15-30 seconds of adequate ventilation. After delivery. Evaluation of heart rate 1. 80 compressions and 30 ventilations). . Neonatal resuscitation procedures A.0 mm 3.5 mm 3. If the heart rate is >100 beats/min. b. Bag-mask ventilation. 2. Positive pressure ventilation should be initiated if the infant is not breathing effectively after the initial steps. When the infant’s color is pink. The combined rate should be 120/min (ie. Ventilations should be given at a rate of 40-60/min. During delivery. a. and then the nose. The infant should be placed supine with its neck in a neutral position. If the infant is apneic or gasping. 3 cc. 50 cc Umbilical artery catheterization tray Cardiotachometer and ECG oscilloscope Alcohol sponges 3-way stopcocks 3 Fr feeding tube Umbilical tape Needles. infant evaluation includes assessment of muscle tone. A towel neck roll under the shoulders may help prevent neck flexion and airway occlusion. 25. 5 cc. If the pulse is >80 beats/min. color. If the heart rate is <100 beats/min. F. 2. using a bulb syringe. Tactile stimulation should be administered by gently slapping the soles of the feet or rubbing the back. Visible chest wall movement indicates adequate ventilation. the oxygen is gradually discontinued. B. PPV can be gradually discontinued after the infant is breathing effectively. The infant should be quickly dried with warm towels. positive pressure ventilation (PPV) is not needed. Epinephrine should be given if the heart rate remains below 80/minute after 30 seconds of PPV and chest compressions. 20 cc. Endotracheal Tube Size and Depth of Insertion From Upper Lip Weight <1000 g 1000-2000 g 2000-3000 g 3000 g or more Gestational Age <28 weeks 28-34 weeks 34-38 weeks 39->40 weeks Size 2. Free-flowing oxygen may be given at a rate of 5 L/min by holding the tubing 1/2 inch in front of the infant’s nose. ½ or 3/4 inch width Syringes.Miscellaneous Radiant warmer and towels or blankets Stethoscope Adhesive tape. chest compressions can be stopped and PPV continued until the heart rate is 100 beats/min and effective breathing is maintained. D.5 mm 4.
May dilute 1:1 with normal saline if given via ET Give over 5-10 min by syringe or IV drip Volume expanders Whole blood Albumin 5% Normal saline Ringer lactate 0. SQ acceptable Give slowly. Volume expanders.5 or 5.1 mg/kg (0. thin-walled and flat vein is used.25 mL/kg) IV. The large.0 mg/mL 1 mL IV. Sodium bicarbonate is recommended during prolonged resuscitation for infants refractory to other measures. Volume expansion is indicated for patients who have known or suspected blood loss and poor response to other resuscitative measures.0 Fr radiopaque catheter is inserted into the vein until a free flow of blood can be aspirated. c.1 mL/kg) IV. . SQ 2 mEq/kg IV Give rapidly Naloxon e 1. normal saline. IM.Neonatal Resuscitation Medications Medication Epinep hrine Concentr ation 1:10. 5. IM.5 mEq/mL 20 mL or two 10-mL prefilled syringes 4. see page 182.4 mg/mL 40 mL Naloxon e 1 mL 0.000 Prepar ation 1 mL Dosage 0. Albumin 5%. ET. SQ 1 mg/kg (0. Naloxone is contraindicated in infants of mothers who are addicted to narcotics. Naloxone hydrochloride is given to infants with prolonged respiratory depression following narcotic anesthesia given to the mother within 4 hrs before delivery. or Ringer’s lactate can be given in boluses of 10 mL/kg over 5 to 10 minutes.3 mL/kg IV or ET.5 mEq/mL (4. and a 3.1-0. IM. Umbilical vessel catheterization is recommended when vascular access is required. Other medications a. b. ET. May repeat in 35 min if HR is <80/min 10 mL/kg IV Rate/Prec autions Give rapidly. References. ET preferred. Sodium bicarbo nate 0.2% solution) diluted with sterile water to make 0. over at least 2 min. centrally located.
Symptoms include polyuria. Hyperosmolar dehydration and acid/base and electrolyte disturbances occur. weight loss. Management of diabetic ketoacidosis A. The sodium concentration of the fluid should provide 50% of the sodium deficit in the first 12 hours and the remainder in the next 36 hours (75 to 125 mEq/L sodium chloride). 10% of whom have type 1 diabetes. then at 2. polyuria. Classification of diabetes mellitus A. B. 2. Potassium replacement. acetone and cultures can be obtained at presentation. The peak age at diagnosis is 12 years. vomiting. DKA is associated with total body potassium depletion. C. D. B.to 6-h intervals At presentation. 60 mL/kg for moderate deficit. DKA can be seen at the time of diagnosis of type 1 diabetes or in the patient who has established disease if diabetes management is inadequate. Laboratory Monitoring During DKA Blood glucose: Serum sodium and potassium: Acid/base status: At presentation. repeated if hypovolemic shock persists.to 4-h intervals. then at 4. Immediate evaluation should assess the degree of dehydration by determining capillary refill. which leads to hyperglycemia and ketogenesis. Rehydration 1.9% saline over 30-60 minutes. or both. and postural heart rate and blood pressure. This deficit should be replaced by infusing potassium chloride at a rate . and 7580% of individuals develop type 1 diabetes before age 30. Diabetes mellitus is classified into two types: type 1 and type 2. Most cases among children and adolescents (95%) result from autoimmune destruction of the beta cells of the pancreas. 150 mL/kg for severe deficit). 2. Five percent of the population is affected by diabetes. 100 mL/kg for moderate deficit. Patients then should begin to receive maintenance fluid requirements added to the calculated fluid deficit (>2 y: 30 mL/kg for mild deficit. with glucose 200 mg/dL or higher at two hours Any abnormal test result must be repeated on a subsequent occasion to establish the diagnosis II. Type 1 diabetes 1. complete blood count. Criteria for Diagnosis of Diabetes Fasting plasma glucose 126 mg/dL or higher or Random plasma glucose 200 mg/dL or higher with symptoms of diabetes (fatigue. C. Initial fluid resuscitation consists of a 10-mL/kg bolus of 0. <2 y: 50 mL/kg for mild deficit. I. then hourly by fingerstick with glucose meter At presentation. Type 2 diabetes is caused by insulin resistance and relative insulin deficiency. skin temperature. polydipsia) or Abnormal two-hour 75-g oral glucose tolerance test result. impairment of insulin action. hyperpnea with shortness of breath. and abdominal pain. polyphagia. Type 1 diabetes is caused by absolute insulin deficiency. polydipsia. Venous pH and serum carbon dioxide Serum urea nitrogen. DKA is caused by insulin deficiency. Most type 2 diabetics do not require insulin injections and are obese. 90 mL/kg for severe deficit.General Pediatrics Diabetes Mellitus Diabetes mellitus consists of hyperglycemia caused by insulin deficiency.
like insulin lispro. F. Adolescents often need more. 2. Insulin aspart (Novolog) is another monomeric insulin. 2. The goal of therapy is to lower the glucose level by 50 to 100 mg/dL per hour. Insulin aspart.2 to 0. with a pH less than 7. and has a shorter duration of action than regular insulin. E. III.4 units of insulin per kg.1 U/kg per hour.1.to long-acting preparation and as pre-meal bolus doses of short-acting insulin (to cover the extra requirements after food is absorbed). Once the glucose level is in the range of 250 to 350 mg/dL. a 39% reduction in microalbuminuria. 5% glucose should be initiated. Insulin aspart has a slightly slower onset and longer duration of action than insulin lispro. Target Blood Glucose Range (Preprandial) Age Infants. If acidosis is severe. It is a rapid-acting insulin analog with an onset of action within 10 to 20 minutes. Most newly diagnosed patients with type 1 diabetes can be started on 0. Intensive management of diabetes results in a significant reduction in the development of diabetic complications: a 76% reduction in retinopathy. Long-term diabetes management A. 3. Dosing regimens. and a 60% reduction in neuropathy. b. and a duration of action of 2 to 4 hours. Regular insulin should be initiated as an intravenous infusion of 0. The dose can be adjusted upward every few days based upon symptoms and blood glucose measurements. Alkali therapy is usually not necessary to correct the acidosis associated with DKA. peak action at 30 to 90 minutes. toddlers Preschool children School-age children Glucose Levels (mg/dL) 120-220 100-200 70-150 B. Aspart reaches peak concentrations in 40-50 minutes and has a duration of action of 3-5 hours. Correcting acidosis. Insulin lispro is the preferred insulin preparation for pre-meal bolus doses. the infusate can be changed to 10% glucose. when the glucose level is between 180 to 240 mg/dL. .2. Starting dose of insulin. Insulin regimens 1. Lowering the glucose level 1. Monomeric insulins a. sodium bicarbonate can be infused slowly at a rate of 1 to 3 mEq/kg per 12 hours and discontinued when the pH exceeds 7. Insulin lispro (Humalog) has an onset of action within 5 to 15 minutes. can be injected immediately before meals. If the patient requires more than 4 mEq/kg of a potassium infusion. Insulin should be provided in two ways – as a basal supplement with an intermediate.of 3 mEq/kg per 24 hours after completion of the normal saline fluid resuscitation. 50% can be administered as potassium phosphate to help prevent hyperchloremic acidosis and hypophosphatemia.
5. with high-fat meals.5 Newly diagnosed patients and those who are in the remission phase may require less insulin. The most commonly used multiple-dose regimen consists of twicedaily injections of regular and intermediateacting insulin (NPH). . the morning dose of intermediate-acting insulin may not be sufficient to prevent a post-lunchtime rise in blood glucose concentrations. Loses its effect if it is left in the syringe for more than a few minutes. If the goal is relief from hyperglycemic symptoms with a regimen that is simple. Has a constant glucose-lowering profile without peaks and valleys. covering the morning. afternoon. In contrast to NPH insulin. 3. and overnight.or four-injection program. the dose should be adjusted downward. In many patients. the twice-daily regimen can be converted into a three. administration with the evening meal does not meet insulin needs on awakening.8-1. but the peaks tend to merge.8 5-11 Years (U/kg) 0. Injection of regular plus NPH insulin before breakfast and before dinner results in four peaks of insulin action. breakfast injection does not last until the evening meal. Although a twice-daily regimen improves glycemic control in most patients.6-0. Insulin glargine (Lantus). Regular insulin (Humulin R) Insulin glargine (Lantus) 5 to 8 hours The insulin should be given 20 to 30 minutes before the patient eats. which may make it the ideal basal insulin for intensive insulin therapy in type 1 diabetes. Twice-daily regimens.9 12-18 Years (U/kg) 0. While NPH insulin is the insulin most commonly given at bedtime. C. which increases the risk of hypoglycemia during the night. the time-action profile for insulin glargine has virtually no peak. evening.75-0. The intermediateacting insulin administered before the evening meal may not be sufficient to induce normoglycemia the next morning unless a larger dose is given. 4. Insulin regimens for intensive therapy of diabetes mellitus 1.Pharmacokinetics of Insulin Preparations Type of insulin Onset of action Peak of action Duration of action 2 to 4 hours Common pitfalls Insulin lispro (Humalog ) Insulin aspart (Novolog) 5 to 15 minutes 45 to 75 minutes 40 to 50 minutes 2 to 4 hours 10 to 20 minutes 30 minutes 3 to 5 hours Hypoglycemia occurs if the lag time is too long. allowing it to be administered once every 24 hours. 1 to 3 hours 5 to 7 hours 13 to 18 hours NPH insulin (Humulin N) 1 to 3 hours 6 to 12 hours 18 to 28 hours Lente insulin (Humulin L) 1 to 3 hours 4 to 8 hours 13 to 20 hours Total Daily Insulin Dosage <5 Years (U/kg) 0. Multiple daily injections. If necessary. insulin glargine may be equally effective for reducing HbA1c values and cause less hypoglycemia. then twice-daily NPH insulin will be effective in many patients. 2.
Monomeric insulins. I. Regular ovulatory menstrual cycles often do not develop until 1 to 1.0-10. Inhaled insulin may become an alternative to monomeric insulins in the future. Cycles are abnormal if they are longer than 8 to 10 days or if more than 80 mL of blood loss occurs. may be most useful in patients in whom high postprandial blood glucose concentrations and unexpected high blood-glucose values at other times are problems. Assessment of HbA1c Values HbA1c Values HbA1c >10% HbA1c 8.5 years of the onset of puberty should be evaluated. Amenorrhea A. II. . Primary amenorrhea is defined as the absence of menarche by age 16.5 units per kg taken five minutes before a meal. Absence of menses within 2 to 2.4. It causes a very rapid rise in serum insulin concentrations (similar to that achieved with subcutaneous insulin lispro). before meals and at bedtime. B. Adolescents frequently experience irregular menstrual bleeding patterns. and 5582% of cycles are anovulatory for the first 2 years after menarche. Quarterly measurement of hemoglobin A1c (HbA1c) assesses glycemic control and reflects the average blood glucose over the last 120 days. insulin lispro and insulin aspart. Anovulatory cycles typically cause heavier and longer bleeding.0% <8. D. which can include several consecutive months of amenorrhea. Blood glucose monitoring. B. Pathophysiology A. see page 182.0% Level of Glycemic Control Poor or minimal Average Excellent or intensive References.8 years. Puberty is considered delayed and warrants evaluation if breast development (the initial sign of puberty in girls) does not begin by the age of 13. Secondary amenorrhea is defined as the absence of 3 consecutive menstrual cycles or 6 months of amenorrhea in patients who have already established regular menstrual periods.5 years after menarche. The mean time between the onset of breast development and menarche is 2 years. 5. and the normal menstrual cycle is 21 to 35 days in length. Menstrual Disorders The median age of menarche is 12. Soaking more than 25 pads or 30 tampons during a menstrual period is abnormal. Children and adolescents should test their blood glucose levels at least four times a day. Typical premeal doses consists of 1. Bleeding normally lasts for 3 to 7 days and consists of 30 to 40 mL of blood.
and opiates. headache. Females with Turner syndrome have streak gonads. and decreased estradiol levels may be present.Differential Diagnosis of Amenorrhea Pregnancy Hormonal Contraception Hypothalamic-related Disorders Chronic or systemic illness Stress Athletics Eating disorders Obesity Drugs Tumor Pituitary-related Disorders Hypopituitarism Tumor Infiltration Infarction Ovarian-related Disorders Dysgenesis Agenesis Ovarian failure Resistant ovary Outflow Tract-related Disorders Imperforate hymen Transverse vaginal septum Agenesis of the vagina. Hypergonadotropic hypogonadism is caused by ovarian failure associated with elevated gonadotropin levels. b. and autoimmune disorders (thyroiditis. This syndrome is characterized by short stature. such as congenital hypopituitarism. and inadequate levels of estradiol. Turner syndrome (XO) may cause ovarian failure and a lack of pubertal development. Hypothalamic suppression is most commonly caused by stress. Amenorrhea with pubertal delay 1. and other endocrinopathies (thyroid disease and Cushing syndrome) may present with pubertal delay and low gonadotropin levels. and dieting (anorexia nervosa). when pubertal delay and amenorrhea occur together. uterus Uterine synechiae Androgen Excess Polycystic ovarian syndrome Adrenal tumor Adrenal hyperplasia (classic and nonclassic) Ovarian tumor Other Endocrine Disorders Thyroid disease Cushing syndrome C. a. shield chest. cervix. b. Addison disease). Hypogonadotropic hypogonadism is caused by hypothalamic dysfunction or pituitary failure. breast stimulation. stress associated with trauma or surgery. They do not initiate puberty or uterine development. congenital heart disease. An elevated FSH will establish this diagnosis. Prolactinomas present with galactorrhea. (4) Other disorders associated with galactorrhea and amenorrhea include hypothyroidism. and amenorrhea. It may not be diagnosed until adolescence. visual fields cuts. renal anomalies. tumor (pituitary adenoma). competitive athletics. or infiltration (hemochromatosis). absence of one of the X chromosomes. a. widely spaced nipples. 2. and Kallmann syndromes. (3) Craniopharyngioma is another tumor of the sella turcica that affects hypothalamicpituitary function. (1) Amenorrhea may be caused by problems at the level of the pituitary gland. c. Low or normal levels of LH and FSH will be present. (2) Prolactin-secreting pituitary adenoma (prolactinoma) is the most common pituitary tumor. Prader-Willi. . Hypothalamic abnormalities associated with pubertal delay include Laurence-MoonBiedl. phenothiazines. Kallmann syndrome is associated with anosmia. high arched palate. Ovarian failure resulting from autoimmune disorders or exposure to radiation or chemotherapy may also cause amenorrhea with p u b e r t a l d e l a y a s s o c i a t e d wi t h hypergonadotropic hypogonadism. webbed neck. Abnormalities of the pituitary and hypothalamus. Elevated prolactin levels are characteristic. presenting with pubertal delay and amenorrhea. Laurence-Moon-Biedl and Prader-Willi present with obesity.
Signs include hirsutism. or endometritis. Amenorrhea with normal pubertal development 1.D. Breast development and a growth spurt occur. Normal pubertal development of breast and pubic hair occurs. but an Xlinked inherited defect of the androgen receptor prevents response to testosterone. vagina. 2. which is usually associated with irregular bleeding. amenorrhea secondary to pregnancy always must be considered. and estradiol . 3. acne. 4. 4. A history of cyclic abdominal pain is common. Pregnancy should be excluded when amenorrhea occurs in a pubertally mature female. Contraceptive-related amenorrhea occurs with depot medroxyprogesterone (Depo-Provera). F. Ovulation occasionally can occur spontaneously. Agenesis of the vagina appears as a blindended pouch. but the uterus and vagina are absent. Transverse vaginal septum may cause obstruction. an ovarian and adrenal tumor or adrenal enzyme deficiency should be excluded. thyroid disease. Clinical evaluation of amenorrhea 1. which can determine if the karyotype is XX or XY. 2. and eating disorders may cause amenorrhea after normal pubertal development. including hormonal contraception. G. 3. Increased facial hair and midline hair over the sternum and lower abdomen are often present. Genital tract abnormalities 1. Insulin resistance. but menarche does not occur. PCO is the most common cause of persistent irregular menses. Polycystic ovarian disease. a. intervals of amenorrhea may also occur. and a midline abdominal mass may be palpable. 5. and possibly pelvic ultrasonography should be completed. 3. should be excluded. Androgen insensitivity (testicular feminization syndrome) is another common cause of vaginal agenesis. and it can help differentiate between müllerian agenesis and androgen insensitivity. Imperforate hymen will appear as a membrane covering the vaginal opening. breast development occurs because of conversion of androgens to estrogens. however. acquired abnormalities of the pituitary gland (prolactinoma). b. Tanner staging. If the anatomy is normal. Ovarian failure. eating disorders. Uterine synechiae (Asherman syndrome) should be suspected in amenorrheic females with a history of abortion. Polycystic ovary syndrome 1. 2. pelvic examination. Sheehan syndrome (pituitary infarction) is suggested by a history of intrapartum bleeding and hypotension. Absence of the uterus. Other disorders associated with amenorrhea and normal pubertal development. but little if any pubic or axillary hair is present. and drug use. Only 70% of patients have polycystic ovaries on ultrasound. athletics. PCO is probably an autosomal recessive disorder that affects ovarian steroidogenesis. a pregnancy test should be completed. Hormone replacement therapy is provided to initiate puberty. During puberty. Female-appearing external genitalia are present. The most common symptom is irregular periods beginning with menarche. The testes are at increased risk for developing tumors and must be removed. It is diagnosed by speculum examination. LH. or both requires a chromosomal analysis. can also present with amenorrhea. clitoromegaly. FSH. therefore. 3. glucose intolerance. and lipid abnormalities are common. and obesity (50%). 2. it does not require intervention. c. E. and stress. Chronic or systemic illness. These women have an XY chromosomal pattern with intra-abdominal or inguinal testes that produce testosterone. however. dilation and curettage. If hirsutism is severe.
4. Abnormal vaginal bleeding is characterized by excessive uterine bleeding or a prolonged number of days of bleeding. pregnancy-related complications. H. and prolactin levels are checked to exclude hypothyroidism and hyperprolactinemia. A testosterone level >200 ng/dL and DHEAS >700 μg/dL require further investigation to exclude a tumor. an ultrasonographic examination may detect polycystic ovaries. amount of bleeding. Electrolysis and spironolactone (50 mg tid) can decrease hirsutism. an MRI is necessary to exclude prolactinoma. Normal or low LH. infection. 6. C. An elevated LH-to-FSH ratio is common with PCO. Clinical evaluation of irregular vaginal bleeding 1. and symptoms of endocrine abnormalities or systemic illness should be evaluated. or strenuous athletics should modify their behavior and be prescribed calcium and hormonal replacement therapy (OCs) to reduce the risks of osteoporosis. 2. 4. A 17hydroxyprogesterone >2 ng/mL is followed by an ACTH stimulation test to diagnose 21-hydroxylase deficiency. central nervous system tumor. after which time they can be switched to an OC. Treatment of amenorrhea 1. symptoms of hypovolemia. hypothyroidism). pelvic inflammatory disease. High FSH and LH levels and a low estradiol level are indicators of gonadal dysgenesis (Turner syndrome) or autoimmune oophoritis. 2. 7. The most common cause of abnormal vaginal bleeding in adolescence is anovulation. stress. 8. III. Age of menarche. If the prolactin level is elevated. Or a l medroxyprogesterone or an oral contraceptive (OCs) should be prescribed to eliminate this risk. Hirsutism and acne are indicative of androgen excess and PCO. PCO is treated with OCs to regulate menses and to decrease androgen levels. history of sexual activity. 3. Postural vital signs may suggest hypovolemia. Turner syndrome or ovarian failure requires estrogen and progesterone at a dosage sufficient to induce pubertal development. Pelvic ultrasonography can be used to further assess pelvic anatomy. TSH. and estradiol levels indicate hypothalamic suppression. uterine or cervical carcinoma. Pregnancy must always be excluded if the individual is mature pubertally. Hormonal contraceptives are a common cause of breakthrough bleeding. Differential diagnosis of abnormal vaginal bleeding 1. menstrual pattern. foreign body. A morning 17-hydroxyprogesterone level will screen for nonclassic adrenal hyperplasia. A pelvic examination should assess pelvic anatomy and exclude trauma. FSH. 2. and retained tampons should be excluded. or an endocrinopathy (eg. Free-T4. 5. Total testosterone and dehydroepiandrosterone sulfate (DHEAS) levels are necessary to exclude ovarian and adrenal tumors. sexually transmitted diseases. B. or a pregnancy-related complication. genital trauma. Pregnancy. Hypoestrogenic and anovulatory patients with hypothalamic suppression caused by anorexia. 4. Blood dyscrasias or coagulation defects may occasionally be the initial presentation of abnormal vaginal bleeding. and uterine myomas are rare in adolescents. Abnormal vaginal bleeding A. Anovulation and the resulting lack of progesterone increases the risk of endometrial hyperplasia and endometrial cancer. Abnormal bleeding is common during the first 1 to 2 years after menarche because anovulatory cycles are frequent. 3.are indicated in order to distinguish ovarian failure from hypothalamic dysfunction. . Oral progestins can be given cyclically for 12 days every month or every third month. Vaginal tumors.
The patient should be continued on low-dose OCs for 3 to 4 months before allowing resumption of normal cycles. IV. athletics. foreign body. usually beginning 6 months to 1 year after menarche. craniopharyngioma Outflow tract-related. Blood transfusion is warranted only if the patient is severely symptomatic. uterine carcinoma. Thyroid disease. easily relieved by NSAIDs. intrauterine device Androgen excess. Secondary dysmenorrhea is defined as painful menses associated with pelvic pathology (bicornate uterus. A pregnancy test and complete blood count should be completed. stress. Gynecologic history should determine the relationship of the pain to the menstrual cycle. Stop all pills for 7 days and then begin cycling on a low dose OCP QD. 2. Intravenous conjugated estrogens (Premarin). Oral contraceptives. Mild bleeding or shortened cycles associated with a normal physical examination and normal vital signs requires only reassurance. cervicitis 3. obesity. cervical stenosis. One pill TID x 3 days. a bleeding time and von Willebrand screening panel will identify more specific coagulation disorders. They do not have the hormonal side effects of OCs. clotting abnormalities. 5. Ectopic pregnancy. eating disorder. anticoagulant medications Infectious causes. Trauma. One pill BID x 7 days. One pill QD x 7-14 days. Conjugated estrogen therapy is followed immediately by OCs and iron therapy. Fifty percent of adolescents experience dysmenorrhea B. abortion Hormonal contraception. Iron therapy should be included. Dilatation and curettage is used as a last resort. and they can be used alone in mild cases of abnormal vaginal bleeding. Mild anemia associated with stable vital signs is treated with a 35 to 50 mcg monophasic combination OC as follows: One pill QID x 4 days.Differential Diagnosis of Abnormal Vaginal Bleeding Pregnancy related. D. Thrombocytopenia. Treatment of irregular vaginal bleeding 1. and sexual activity. D. depomedroxyprogesterone Hypothalamic-related. 25 mg IV every 4-6 hours for 24 hours. Prolactinoma. If dysmenorrhea is severe. vaginal tumor. will stop the bleeding quickly. If the hematocrit is <7-8 mg/dL or if vital signs are unstable. 4. d. Laboratory evaluation a. It is the most common form of dysmenorrhea. Dysmenorrhea A. obstructing lesions of the genital tract should be excluded. b. Endometriosis is the most common cause (50%) of chronic pelvic pain in adolescents. adrenal hyperplasia Other endocrine causes. C. uterine fibroids and polyps. Chronic irregular vaginal bleeding mandates that prolactinoma and endocrine abnormalities (thyroid disease) be excluded. 3. severity. ovarian tumor. adrenal tumor. . Chronic or systemic illness. it is rarely necessary. PID. hospitalization is recommended. endometriosis. Polycystic ovarian syndrome. 2. however. ovarian neoplasms). A history of a very heavy period with menarche or repeated prolonged or heavy menses warrants a prothrombin time and partial thromboplastin time to screen for bleeding abnormalities. Pelvic inflammatory disease. polyp. Antiprostaglandin medications (NSAIDs) decrease menstrual blood loss significantly by promoting platelet aggregation and vasoconstriction. c. uterine myoma. Primary dysmenorrhea consists of crampy lower abdominal and pelvic pain during menses that is not associated with pelvic pathology. Signs of androgen excess indicate a need to exclude PCO. drugs Pituitary related. Evaluation of dysmenorrhea 1. adrenal disease Hematologic causes. If the pain is mild. cervical carcinoma. abnormalities of platelet function.
Nonpharmacologic therapy 1. Naproxen (Naprosyn) 500 mg load. or vascular birthmarks. Mefenamic acid (Ponstel) 500 mg loading dose. II. Urgency or a history of small. 2. and deep tendon reflexes that reflect spinal cord function all should be tested. Severe pain requires a pelvic examination to exclude genital tract obstruction. psychological components. Etiologic factors include genetics. Encopresis suggests constipation. Initial treatment consists of a prostaglandin synthesis inhibitor. History 1. daytime urinary symptoms. then 250 mg q6h. Bladder capacity can be measured in the office by having the child drink 12 oz of fluid on arrival. a. and maturational delay. Oral contraceptives are also very effective and can be added if the antiprostaglandin is not fully effective. C. or abnormal gait should be sought. anal. Cremasteric. see page 182. and psychosocial factors. sleep arousal dysfunction. Ultrasonography is useful for evaluating pelvic abnormalities or obstruction. 3. b. signs of sexual abuse. Laboratory/imaging studies. Mouth breathing may suggest sleep apnea with associated enuresis due to adenoidal hypertrophy. Most children who have nocturnal enuresis will have normal findings on physical examination. Naproxen sodium (Aleve) 550 mg load. Ibuprofen (Advil) 400-600 mg q4-6h. Clinical evaluation A. B. 3.and the physical examination (including the hymen) are normal. 4. Treatment of dysmenorrhea 1. Other pertinent details include the onset and pattern of wetting. parasomnias. bowel habits. Motivational therapy. E. weight. adnexal and/or uterosacral pain (endometriosis). frequent voids suggests bladder instability or small bladder capacity. References. and blood pressure should be recorded. 2. Height. then 275 mg q6h. then voiding into a calibrated cup. The ability to concentrate urine to 1. 2. Polyuria and polydipsia suggest diabetes insipidus or mellitus. Gastric irritation can be reduced by taking the drug with food. The child should be taken out of diapers or training pants and encouraged to . A urine culture should be obtained if the child has dysuria or an abnormal urinalysis. The skin of the lower back should be inspected for a sacral dimple. Nocturnal Enuresis Nocturnal enuresis affects approximately 5 to 7 million children in the United States. or a mass. voiding behavior. Physical examination 1. then 250 mg q6-8h. c. urodynamics. I. PID. Direct observation of the urinary stream is important if findings suggest an abnormality. d. All children should have urinalysis of a clean-catch midstream urine specimen. a speculum examination is not necessary. There is a slight male predominance of 60% for nocturnal enuresis. ectopic ureter. Nighttime snoring suggests adenoidal hypertrophy. Treatment A.015 or greater rules out diabetes insipidus and the absence of glucose rules out diabetes mellitus. nocturnal polyuria. abdominal. Parents may become concerned about nocturnal enuresis when their child reaches 5 to 6 years of age. sleep pattern. Dysuria suggest a urinary tract infection. which indicate spinal dysraphism. hair patches. medical conditions. A palpable bladder. initiated with the onset of bleeding and continued for as long as pain lasts. A detailed toilet training history and a family history of enuresis should be sought. palpable stool.
If there is no response within 1 week. Age-related treatments 1.8% of poisonings.empty the bladder completely prior to going to bed. I. b. 2. 2. 1. then should begin a slow decrease of the dose by 10 mcg/mo. Intermittent use of medication such as DDAVP can be useful for special events. DDAVP is a synthetic analog of arginine vasopressin (ADH). continuous use of medication is justified. Alarm systems can be used in combinat i o n wi t h b e h a v i o r a l t h e r a p y o r pharmacotherapy. Pharmacotherapy. The child should participate in morning cleanup. The cure rate may be as high as 70% long-term. The initial dose of DDAVP is 20 mcg PO or one 10-mcg puff in each nostril within 2 hours of bedtime. Side effects of DDAVP are rare and include abdominal discomfort. Fluids should be restricted for 2 hours prior to bedtime. and sleep disturbances. Imipramine (Tofranil) a. the dose can be titrated by 0. The eventual goal is to have the child self-awaken to void. hypertension. B. headaches. nausea. References. and epistaxis. Clinical evaluation of poisoning A. If use of an enuresis alarm does not stop wetting episodes. Behavioral therapy a. Ages 8 through 11 years. the starting dose is 0. Motivational and behavioral methods that assist the child in waking to void and that praise successful dryness are recommended. About 22% become dry with DDAVP. Patients may remain on medication for 3 to 6 months. Imipramine is inexpensive. The type of toxin involved should be determined. The high initial response rate of DDAVP is attractive for episodic use for summer camp and sleepovers.6 mg nightly. b. and having the child walk to the toilet when voiding is needed. Ages 12 years and older. with a slow tapering over 3 to 4 weeks. Children less than 6 years of age account for 60. Symptomatic hyponatremia with seizures is very rare. If oral medication is preferred. leading to injury or death. dry mouth. Dry-bed training involves waking the child over several nights. Mild side effects include irritability. Overdose can be lethal. Enuresis alarms have the highest overall cure rate. The starting dose is 25 mg taken 1 hour before bedtime for children ages 6 to 8 years and 50 to 75 mg for older children and adolescents. . 3. see page 182.2 mg up to a maximum of 0. The success rate is 15 to 50%. The dose may be increased in increments of 10 mcg every 1 or 2 weeks up to a maximum dose of 40 mcg. 2.2 mg (one tablet) 1 hour before bedtime. headache. b. DDAVP (Stimate) a. Medication for nocturnal enuresis seldom should be considered before 8 years of age. c. C. It decreases urine volume. Therapy may continue from 3 to 9 months. Imipramine increases bladder capacity and also may decrease detrusor muscle contractions. The enuresis alarm gives the best results in terms of response rate and low relapse rate. Hypnotherapy involves having the child practice imagery of awakening to urinate in the toilet or staying dry all night. Poisoning Poisoning is defined as exposure to an agent that can cause organ dysfunction. decreased appetite. Contraindications include habit polydipsia. Younger than age 8 years. c. The bioavailability is only 1% for the tablet and 10% for the nasal spray. and heart disease. The dose may be increased in 25-mg increments weekly up to 75 mg.
ergotism. solvents Amphetamines. gyromitra mushrooms. disulfiram. failure to thrive). iron. lead. organophosphates. nicotine. phencyclidine. phencyclidine. ephedrine. The syndrome is referred to as “Munchausen syndrome by proxy” when the abuse is perpetrated by a caretaker. salicylates. atropine. phenothiazines. iron.The time of the exposure and how much time has elapsed should be assessed. and vitamin A. factitious hypoglycemia. phencyclidine Amphetamine. ventilation. solvents. recurrent malabsorption syndrome. narcotics. The dose of the toxin should be assumed to be the maximum amount consistent with the circumstances of the poisoning. carbon monoxide. respiratory. isopropanol. phenylpropanolamine. gastrointestinal. Agents may include aspirin. acetone. cardiovascular. II. cocaine. laxatives. heavy metals Hypotensio n Tachypnea Hypoventila tion Coma Seizures Miosis Mydriasis Nystagmus Peripheral neuropathy . salicylates. cyanide. carbon monoxide. phenothiazines Hypothermia Breath odors: Mothballs Fruity Garlic Bitter almond Peanuts Hypertension Naphthalene. organophosphates Cyanide N-3-pyridylmethyl-N-4-nitrophenylurea (VACOR rat poison) Amphetamines. ethanol. carbon disulfide. C. anticonvulsants. phencyclidine. 2. nicotine. norepinephrine. benzodiazepines. tricyclic antidepressants (early) Antihypertensives. carbon monoxide. B. isoniazid. narcotics. cholinesterase-inhibiting pesticides. iron. The vital signs. chlorinated hydrocarbons. nicotine. codeine. skin. cocaine. phenylpropanolamine. insulin. carbamazepine. tricyclic antidepressants Barbiturates. tricyclic antidepressants (late) Amphetamine. cocaine. barbiturates. phenothiazines. aspirin. tricyclic antidepressants Narcotics. botulism. tricyclic antidepressants Phencyclidine. benzodiazepines. cocaine. cyanide. The first priority in a severely poisoned child is to maintain an airway. carbon monoxide. strychnine. camphor. cocaine. Physical Findings Associated with Specific Drugs and Chemicals Symptom or Sign Fever Agents Amphetamines. antihistamines. pesticides. paralytic shellfish poisoning. antihistamines. barbiturates. theophylline. narcotics. B. benzodiazepines. cyanide. table salt. thyroid. cyclic antidepressants. and neurologic systems should be assessed. ipecac. phenytoin Acrylamide. Physical examination A. phenothiazines. barbiturates. beta blockers. nail polish remover Arsenic. insulin. breath odors. anticholinergics. anticholinergics. Munchausen syndrome by proxy 1. cyclic antidepressants. recurrent acidosis. nitrites. strychnine Alcohols. anesthetics. chloral hydrate. hypoglycemics. arsenic. Chemical child abuse should be suspected when childhood poisonings are associated with an insidious and/or inexplicable presentation (eg. ethylene glycol. opiates. phenothiazines. and circulation. polymicrobial sepsis. lindane. salicylates Alcohols. phenothiazines. hydrocarbons. lithium. paradichlorobenzene Isopropanol. sedative-hypnotics. calcium channel blockers. fecal material.
The respiratory examination may reveal poisoning-associated wheezing (eg. ethanol. mescaline or amphetamines can cause visual or auditory hallucinations. grandiose delusions. cellular toxins. Sensorimotor examination may reveal peripheral anesthesia caused solvents. 2. Depressed consciousness. ethylene glycol. b. isopropyl alcohol. phenothiazines). amphetamine. iron poisonings). or paranoia. the osmolar gap will be elevated. The osmolar gap is derived from the measured serum osmolality minus the calculated serum osmolality (2 x Na + BUN/2. Neurologic examination 1. psychopharmaceutical agents. and rotatory nystagmus. Nervous system stimulants may be associated with tachypnea. cocaine). 2. A toxic screen of the blood and urine may include assays for acetone. irrational behavior. Central nervous system depressants may depress the respiratory drive. benzodiazepines. and shock associated with iron or arsenic. methanol. or phencyclidine. organophosphate pesticides) or sympathetic blockade (eg. anticonvulsants. B. Lysergic acid diethylamide (LSD). Tachypnea and hyperpnea may result from salicylate poisoning. D. Serum osmolarity 1. Occasionally. Cardiovascular effects 1. The history and physical examination will usually provide enough information to make a diagnosis and begin therapy. hydrocarbon) or asphyxia (eg. neuroleptics. or acrylamide. or ethylene glycol). Hypotension is caused by beta adrenergic blockade. or coma. confusion. 2. Urticaria suggests an allergic reaction. diabetes. When exogenous osmoles are present (eg. delirium. euphoria. III. antidepressants. Jaundice may signify hemolysis from naphthalene mothballs. disulfiram-ethanol. Cellular poisons will increase the respiratory rate. 2. The adolescent substance abuser may have needle tracks along veins or scars from subcutaneous injections. beta-blocker overdose or inhalants) or crackles (aspiration pneumonia. confusion. Toxic screens 1. Phencyclidine (PCP) causes agitation. methanol. b. ethanol. Skin examination 1. Laboratory assessment A. Central nervous system stimulants or neurotransmitter antagonists produce seizures. ethanol). such as ethanol. E. 3. Apnea may be associated with toxins causing weakness of respiratory muscles. Pupils. narcotics. isoniazid. or coma may result from toxins. Constricted pupils are caused by parasympathetic stimulation (eg.8 + glucose/18). or exogenous organic acids may cause a metabolic acidosis. Cyanosis suggests hypoxia secondary to aspiration (eg. acetaminophen. Respiratory effects 1. 2. in ethanol. Glue or gasoline sniffing can result in exhilaration. 3. sympatholytic agents. Dilated pupils can be caused by sympathetic stimulation (eg. Metabolic acidoses are classified as either . pesticides. rhabdomyolysis. antihistamines. Amphetamine or cocaine often cause agitation. and sudden death from cardiac dysrhythmias. slurred speech. pulmonary edema). 4. Ethanol. 2. ketoacids (eg. Sympathetic stimulation can cause hypertension with tachycardia.C. Benzodiazepines and narcotics (oxycodone) can cause drowsiness. Neurologic signs of substance abuse a. Lactic acid (eg. acetone. isopropanol. F. amphetamines. apnea due to central nervous system depressants). calcium channel blockade. isopropyl alcohol. dissociative delusional thinking. toxin screening of blood and/or urine can confirm the diagnosis. or methanol can cause an alcoholic state of intoxication. Anion gap acidosis a.
increased anion gap ([Na+ K] - [Cl + HCO3]) above 15 mEq/L (ethylene glycol, iron, isoniazid, methanol, or salicylate), or depressed anion gap (lithium), or normal anion gap (laxatives, colchicine). C. Other frequently ordered tests 1. Hepatic and renal function should be monitored because most toxins are detoxified in the liver and/or excreted in the urine. Many poisonings are accompanied by rhabdomyolysis (elevated creatinine phosphokinase levels) from seizures, hyperthermia, or muscle spasms. 2. Urine that fluoresces under Wood lamp examination is diagnostic of antifreeze poisoning. 3. Chest and abdominal radiographs may show radiopacities from calcium tablets, chloral hydrate, foreign bodies, iodine tablets, phenothiazine and antidepressant tablets, and enteric-coated capsules. 4. Serial electrocardiograms are essential with antiarrhythmic drugs, beta- blockers, calcium channel blockers, lithium, phenothiazines, theophylline, or tricyclic antidepressants. IV. Diagnostic trials A. For a few poisons, a “diagnostic trial” of an antidote can implicate an agent as the cause of a poisoning. Diagnostic Trials Toxin
Flumazenil 0.02 mg/kg Specific Fab antibodies
Consciousness improves Dysrhythmia resolves, hyperkalemia improves, consciousness improves Consciousness improves Pink “vin rose” urine Seizures abate Consciousness improves Dystonia and torticollis resolve
Insulin Iron Isoniazid Opiate Phenothiazine
Glucose 1 g/kg Deferoxamine 40 mg/kg Pyridoxine 5 g Naloxone 0.1 mg/kg Diphenhydra mine 1 mg/kg
IV IM IV IV IV
V. Management A. Poison centers can help with the diagnosis and management of poisonings, and assist in locating exotic antidotes. B. Initial management of poisoning involves maintaining an airway, providing ventilatory support, securing vascular access, and initiating resuscitation. C. Decontamination 1. Skin, mucous membrane, or eye exposures should be washed with a stream of lukewarm water for 15 to 20 minutes. Soap is used to decontaminate skin exposures. 2. Gastric lavage a. Decontamination by lavage is preferred over emesis in the emergency department because it is controllable. Contraindications include nontoxic ingestions, ingestions in which the substance is already past the stomach or absorbed, and caustic or hydrocarbon ingestions. It is most successful when performed within 90 minutes of the ingestion. For toxins associated with delayed gastric emptying (eg, aspirin, iron, antidepressants, antipsychotics) or for those that can form concretions (eg, iron, salicylates), lavage may be beneficial hours later. b. A large-bore (24-32F) orogastric tube is used, and 100- to 200-cc aliquots of warm, normal saline are infused/withdrawn until no more pill fragments are detectable in the lavage fluid or until about 2 liters have been exchanged. c. Activated charcoal is effective for absorbing
most drugs, but it is ineffective for alcohols, caustics, cyanide, heavy metals, lithium, and some pesticides. d. Overdoses of carbamazepine, tricyclic antidepressants, and procainamide are managed with multiple doses of charcoal. Contraindications to charcoal include a poisoning where esophageal endoscopy is contemplated, one in which the toxin is not adsorbed by charcoal, or a poisoning in which the patient has an ileus, gastrointestinal hemorrhage, or repeated retching. 3. Enhanced elimination a. Multiple doses of charcoal also can enhance elimination by “gastrointestinal dialysis.” Repetitive doses of charcoal are recommended for phenobarbital, salicylate, and theophylline poisoning. b. A cathartic, such as magnesium citrate, is recommended when charcoal is used because charcoal is constipating. Hemodialysis or hemoperfusion can be life-saving for severe intoxications. VI. Specific toxins A. Acetaminophen (APAP) 1. Single overdoses of greater than 150 mg/kg can cause liver failure. Nausea and abdominal pain are common. The patient may vomit repeatedly, be mildly lethargic, or remain asymptomatic. At 24 to 36 hours after the ingestion, abdominal tenderness and rising serum transaminase levels signify onset of hepatitis that peaks in severity by 96 hours. 2. The Rumack nomogram predicts the likelihood of hepatitis. The peak concentration is measured 4 hours after the ingestion; levels greater than 200 mcg/mL at 4 hours are associated with liver toxicity. 3. When acetaminophen has been taken in high dose, or when acetaminophen levels are in the range likely to cause hepatotoxicity, N-acetylcysteine (NAC) is given at a loading dose of 140 mg/kg, followed by 17 doses of 70 mg/kg separated by 4-hour intervals. 4. Once NAC has been started because of one toxic level, the full course should be given; there is no need to get repeated APAP concentrations. B. Alcohols 1. Alcohols include ethanol, ethylene glycol, methanol, and isopropyl alcohol. Antifreeze contains ethylene glycol, Sterno and windshield wiper fluid contain methanol, jewelry cleaners and rubbing alcohol contain isopropanol. 2. All of the alcohols cause inebriation, loss of motor control and coma. Ethylene glycol may cause acidosis, renal failure, and seizures. Methanol may cause metabolic acidosis, seizures, and blindness. Isopropyl alcohol can produce gastritis, ketosis, and hypotension. 3. Concentrations of ethylene glycol or methanol >20 mg/dL require the use of ethanol therapy to block alcohol dehydrogenase conversion to the toxic metabolites; hemodialysis is indicated for concentrations >50 mg/dL. Isopropanol or ethanol intoxications usually require only close monitoring with frequent measurements of serum glucose. Respiratory depression, seizures, and coma from ethanol poisoning and levels >300-400 mg/dL require hemodialysis. C. Caustics 1. Drain cleaners contain sodium hydroxide or sulfuric acid; toilet cleaners may contain hydrochloric or sulfuric acids. 2. Laundry or dishwasher detergents may contain sodium metasilicate or sodium triphosphate. 3. Signs of caustic ingestion include lip or tongue swelling; burning pain; dysphagia; drooling; and whitish or red plaques on the tongue, buccal or palatal mucosa, or in the perioral area. Caustics can cause severe burns to the esophagus or stomach even in the absence of symptoms. 4. Inhalations are managed with humidified oxygen. Skin exposures are washed carefully with soap and water and then treated like any other burn. 5. Strongly alkaline agents damage the upper esophagus. Hydrochloric, sulfuric (muriatic),
and other acids damage the lower esophagus and stomach. 6. Treatment of caustic ingestions. The child should be given nothing by mouth, and endoscopic evaluation should be performed 12 to 24 hours after the ingestion. Emesis, lavage and charcoal are contraindicated. Foreign body ingestion 1. Aspirated objects will cause symptoms of choking, gasping, coughing, cyanosis, wheezing, fever, and poor air entry. While chest radiography can confirm the diagnosis, a negative film does not rule out aspiration. A foreign body requires immediate removal by bronchoscopy. 2. Ingestion of disc batteries requires removal when lodged in the esophagus; those in the stomach or beyond should be followed with repeated abdominal films every 2 to 3 days to ensure passage. Disc batteries that have remained in one position for more than 7 days may require surgical removal. Coins or other foreign bodies past the esophagus can be managed with serial radiographs and parental vigilance for their passage. Hydrocarbons 1. Aliphatic hydrocarbons include kerosene, mineral oil, gasoline, and petrolatum. Kerosene and gasoline are capable of causing an aspiration pneumonia and CNS depression. Petrolatum, mineral oil and motor oil do not carry significant risk of injury. Aliphatic hydrocarbons in small doses are not harmful if left in the stomach. Emesis is contraindicated because of the risk of aspiration; decontamination should be attempted only if a very large dose was taken. 2. Aromatic hydrocarbons, such as xylene or toluene, are toxic. Aromatic hydrocarbon ingestions necessitate lavage. 3. Aspiration pneumonia is suggested by gasping, choking, coughing, chest pain, dyspnea, cyanosis, leukocytosis, and fever. A chest radiograph may not be diagnostic until hours after ingestion. Iron 1. Iron is present in many children’s multivitamins, although the worst cases of iron poisoning usually involve prenatal vitamins, which contain 60 mg of elemental iron per tablet. Iron is a metabolic poison and is corrosive to gastric mucosa, resulting in shock. 2. Ferrous sulfate is 20% elemental iron, ferrous fumarate 33%, and ferrous gluconate 11%. Little toxicity is seen at a dose of elemental iron less than 20 mg/kg. Mild symptoms of poisoning are seen at doses of 20-60 mg/kg; moderate-tosevere symptoms at doses of 60 to 100 mg/kg; life-threatening symptoms at doses greater than 100 mg/kg; and a lethal dose is 180 to 300 mg/kg. 3. Early symptoms include nausea, vomiting, fever, hemorrhagic diarrhea, tachycardia, hypotension, hyperglycemia, and acidosis. Intermediate symptoms (8 to 48 hours after ingestion) may include obtundation, coma, fulminant hepatitis, hypoglycemia, clotting abnormalities, pulmonary edema, and renal tubular dysfunction. 4. Laboratory findings include a metabolic acidosis with a high anion gap, an abdominal radiograph showing radiopaque pills in the stomach, an elevated white blood cell count greater than 15,000/mm3, and an elevated blood glucose >150 mg/dL. A serum iron concentration, obtained 4 hours after the ingestion, of less than 300 mcg/dL is not toxic; 300 to 500 mcg/dL is mildly toxic; 500 to 1000 mcg/dL is moderately to severely toxic; greater than 1000 mcg/dL is lifethreatening. 5. Treatment. Decontamination by lavage should be initiated; charcoal is not effective. Volume expansion with intravenous fluids, correction of electrolyte/acid-base disturbances, and intravenous deferoxamine are recommended. Salicylates 1. Aspirin overdoses greater than 150 mg/kg are toxic. Salicylates are locally corrosive, and tablets can form bezoars near the gastric outlet.
lethargy. Respirations often are rapid and deep. hypomagnesemia. Multiple-dose activated charcoal is effective. Hemodialysis is indicated for serum concentrations greater than 100 mg/dL. 2. Correction of acidemia. . and fever. 5. those greater than 70 mg/dL are associated with severe symptoms. which may be effective as long as 4 to 6 hours after the ingestion. and hyperglycemia (early) or hypoglycemia (late). confusion. and those greater than 100 mg/dL are life-threatening. see page 182. h yp okalemia. Laboratory findings include hypocalcemia.Salicylates stimulate the central respiratory center. Severe poisonings can be associated with seizures. hypokalemia. Early symptoms of toxicity include gastrointestinal pain. tinnitus. coma. vomiting. Serum aspirin concentration obtained 2 and 6 hours after the ingestion higher than 30 mg/dL are considered toxic. References. so that the metabolic acidosis is compensated by a respiratory alkalosis. and respiratory and cardiovascular failure. and hypocalcemia are important. nausea. 4. 3. Management includes lavage.
2 cm (30.0 cm (19. this rapid growth continues.0 cm (13.0 in) First molar s--14 mo Canines-19 mo Second molar s--24 mo 2 years 49. Advances occur in physical growth. Macrocephaly without hydrocephalus is associated with cognitive deficits caused by metabolic or anatomic abnormalities.0 kg (22 lb) Triples birthweight Central incisor s--6 mo Lateral incisor s--8 mo 1 year 47.7 lb) Regains birthw eight by 2 wk Doubles birthw eight by 5 mo 10. Macrocephaly may be caused by hydrocephalus. however. skin. Occipitofrontal circumference 1. Physical growth milestones A. 2. the presence of three or more indicative of developmental dysfunction. short stature in the family is reassuring. Many genetic syndromes are associated with short stature. Motor development milestones A. C.5 kg (6. Most isolated minor dysmorphic features are inconsequential. after which the growth rate decelerates.5 in) 76. and hands. Seventy-five percent of minor superficial dysmorphisms can be found by examining the face.5 lb) Quadruples birthwe ight B.8 cm (20. During the first few months of life. D. and psychosocial development.0 in) 12. which is associated with learning disabilities.or above-average size are otherwise normal. rolling and .0 to 12. there is an increased prevalence of developmental disabilities in these two groups. Microcephaly is associated with an increased incidence of mental retardation. large stature syndromes are less common.9 cm (35.6 to 7. motor development.0 cm (18. cognitive development. I. Microcephaly associated with genetic or acquired disorders usually has cognitive implications. Gross motor development begins with holding head up. When considering deviation from the norm. Birth weight is regained by 2 weeks of age and doubles by 5 months. Fifty percent of cases of macrocephaly are familial and have no effect on intellect. Dysmorphism. but there is no direct relationship between small head size and decreased intelligence. Average Physical Growth Parameters Age Head circumference 35. II. Motor milestones are ascertained from the developmental history and observation.4 to 27.5 kg (26.8 in) +2 cm/mo (0 to 3 mo) +1 cm/mo (3 to 6 mo) +0.0 in) 3.0 to 3. the finding of a large head size in one or both parents is reassuring.5 cm/mo (6 to 12 mo) Mean = 1 cm/mo Height Weight Dentition Birth 50. 2.3 in) 88. Height and weight 1.Developmental Pediatrics Infant Growth and Development Infancy consists of the period from birth to about two years of age. When evaluating the infant with macrocephaly. Although the majority of individuals who are of below.
problem-solving skills are the next best measure. 3. and ambulating. At 3 months. the infant learns to use objects as tools during play. the parent will show pleasure and joy. bunny hopping. III. c. pulling directly to a stand at 4 months (instead of to a sit). During the second year of life. the pincer grasp develops. such as a bell. The child will progress to finding an object that has been hidden under a cloth. and objects are initially brought to the mouth for oral exploration.” and its disappearance does not evoke a reaction. parents reinforce the repeated use of these sounds. Hand dominance prior to 18 months of age should prompt the clinician to examine the contralateral upper extremity for weakness associated with a hemiparesis.B. In the first year of life. 3. b. B. the infant will begin vocalizing after hearing an adult speak. most infants with mental retardation walk on time.” By 12 months of age. allowing the child to match objects that are the same and later to match an object to its picture. The 1-year-old child recognizes objects and associates them with their functions. The infant then learns that actions cause consistent effects. “dada”) is interpreted by the parents as a real word. 2. Early rolling (1 to 2 months). At this time. Initially. 3. 2. Expressive language skills reflect the ability to make thoughts. The infant begins to use the words “dada” and “mama” appropriately. Expressive language consists of cooing. Object permanence a. he begins to use them functionally as “tools” instead of mouthing. Prespeech period (0 to 10 months). the infant adds consonants to the vowel sounds in a repetitive fashion (babbling). Problem-solving skills 1. the child begins to label objects and actions and categorize them. precise manual exploration replaces oral exploration. They can follow a simple command as long as the speaker uses a gesture. Gross motor skills correlate least with cognitive potential. other than mama. In so doing. The infant will say at least one “real” word (ie. the infant accidentally discovers that his actions produce a certain effect. ideas. some infants understand as many as 100 words. Reaching becomes more accurate. C. Fine motor development 1. Spontaneous frog-legs posturing suggests hypotonia/weakness. C. progresses to sitting. banging. Red flags in motor development 1. The next skill in this sequence is the ability to locate an object under double layers (eg. dada) before his first birthday. 4. Infants next recognize and understand their own names and the meaning of “no. Early in the second year. As the pincer grasp and macular vision improve. 4. As expressive vocabulary in- . the infant also will begin to verbalize with sentence-like intonation and rhythm (immature jargoning). and throwing them. At 6 months of age. The infant’s realizes that people have names and objects have labels. 2. and then standing. Causality. W-sitting. Prior to the infant’s mastery of object permanence. When a random vocalization (eg. Receptive language skills reflect the ability to understand language. and persistent toe walking may indicate spasticity. and desires known to others. Thus. Persistent listing to one side at 3 months of age often is the earliest indication of neuromotor dysfunction. a cube is placed under a cup and then the cup is covered with a cloth). Naming period (10 to 18 months). 2. Midway through the second year. Language development 1. a person or object that is “out of sight” is “out of mind. Cognitive development milestones Language is the single best indicator of intellectual potential. Receptive language is characterized by an increasing ability to localize sounds. A. a gesture no longer is needed. and scissoring suggests spastic hypertonus.
but these vocalizations will gradually decline thereafter. After age 2. dressing. and by motor and cognitive skill attainment. Temperament represents the style of a child’s emotional and behavioral response to situations. B. 4. Emotional development. D. If deficiencies are global (ie. child neglect or abuse may be suspected. B. the child will have reached 50% of his adult height. Adaptive skills consist of the skills required for independence in feeding. In severe cases. Word combination period (18 to 24 months). Deaf infants will begin to babble on time at 6 months. Toddler Development Toddlerhood consists of the years from about 1 to 3 years of age. All children who have delayed language development should receive audiologic testing to rule out hearing loss. Colic may be an early indication of a “difficult” temperament. Growth rate and physical appearance A. there is a possibility of mental retardation. Adaptive skill development. Early word combinations are “telegraphic” (eg. Failure to develop social relationships suggests autism when it is accompanied by delayed or deviant language development and stereotypic behaviors.5 inches in height each year. Growth of the lower extremities often is accompa- . When recognition of and attachment to a caregiver develops. When a discrepancy exists between problemsolving and language abilities. A stranger should be able to understand at least 50% of the infant’s speech. and other activities of daily living. see page 182. which may be associated with maternal depression. I. Affective development is highlighted by the toddler’s striving for autonomy and independence. Growth often occurs in spurts. 2. Red flags in cognitive development 1. Delay in the appearance of a smile suggests an attachment problem. If either language or problem-solving skills is deficient. the possibility of a hearing impairment or a communication disorder should be excluded. “Go out”). 3. real words are added (mature jargoning). Red flags in psychosocial development 1. The infant learns to use smiling to manipulate the environment and satisfy personal needs. toddlers gain about 5 lb in weight and 2. the child is at high risk for a learning disability later. and it develops within a few months. skills are delayed in both domains). and the development of impulse control.5 years. Children begin to combine words 6 to 8 months after they say their first word. the infant will use about 25 words. Attachment represents the feeling of the infant for the caregiver. D. The infant becomes more discriminating in producing a smile as he begins to differentiate between familiar and unfamiliar faces. Language development provides an estimate of verbal intelligence. Delays in adaptive skills may indicate overprotective parents or an excessive emphasis on orderliness. 3. the rate of growth slows in the toddler years. 2. Social milestones begin with bonding. the simple sight of this person will elicit a smile. problem-solving provides an estimate of nonverbal intelligence. Cognitive development is characterized by the transition from sensorimotor to preoperational thought. Between the ages of 2 and 2. attachment to family. which reflects the feeling of the caregiver for the child. toileting. Psychosocial development A. 2. After the rapid growth of infancy. References. IV. 5. Development of adaptive skill is influenced by the infant’s social environment. Social development 1.creases. C. with only language being deficient. By 18 months. Emotions are present in infancy and motivate expression (pain elicits crying). 3.
Fine Motor Abilities 18 Months • • • • Making a tower of four cubes Releasing 10 cubes into a cup Scribbling spontaneously Imitating a vertically drawn line 24 Months • • • • • Building a seven cube tower Aligning two or more cubes to form a train Imitating a horizontally drawn line Beginning circular strokes Inserting a square block into a square hole 36 Months • • • • Copying a circle Copying bridges with cubes Building a tower of 9 to 10 blocks Drawing a person’s head IV. . Affective development A. Because of improved motor skills. II. B. Most children walk without assistance by 18 months. Most 3-year-olds have some degree of self-control. Fine motor skills A. steady walking pattern. Successful toileting usually occurs toward the end of the third year when the child becomes able to control his sphincter. seldom falling Running stiffly Walking up stairs with one hand held Seating self in a small chair Climbing into an adult chair Hurling a ball 24 Months • Running well without falling • Walking up and down stairs alone • Kicking a large ball 36 Months • • • • • Walking up stairs by alternating feet Walking well on toes Pedaling a tricycle Jumping from a step Hopping two or three times III. Autonomy and independence.5 to 3 years of age. Impulse control. At 2 years. The 18-month-old may have minimal impulse control and display several temper tantrums each day. which usually corrects by age 3 years. Success with consistent daytime dryness usually is not achieved until about 2. he can stack eight blocks. wide-leg gait of early toddlerhood becomes a flexible. The toddler may refuse to eat unless allowed to feed himself. and has the willingness to participate. The 18-month-old can make a tower of four blocks. Toddlers begin to develop impulse control. Gross Motor Abilities 18 Months • • • • • • Walking fast. get onto the potty. with heel-toe progression. One year later.nied by tibial torsion and physiologic bowing of the legs. Most 18-month-olds will hold the crayon in a fist and scribble spontaneously on paper. and the child may no longer may be willing to try new foods. Gross motor skills A. the transition from infancy to toddlerhood is marked increased autonomy and independence. undress. C. The percentage of body fat steadily decreases from 22% at age 1 year to about 15% at age 5 years. the stiff.
Complete object permanence has developed. E. Temperament determines how a child approaches a given situation. or emotional illness. favorite foods. After 18 months. and activities. toddlers use language to convey their thoughts and needs (eg. and the child can find an object under a blanket. C. Toddlerhood is characterized by a transition from sensorimotor to preoperational thinking. consisting primarily of the names of caregivers. he can draw primitive figures that represent people. spilling little food Verbalizing toileting needs Pulling on a simple garment Verbalizing immediate experiences Referring to self by name 36 Months • • • • Showing concern about the actions of others Playing cooperatively in small groups Developing the beginnings of true friendships Playing with imaginary friends D. Intellectual Abilities 18 Months • • • Pointing to named body parts Understanding of object permanence Beginning to understand cause and effect 24 Months • • • Forming mental images of objects Solving problems by trial and error Understanding simple time concepts 36 Months • • • • • Asking “why” questions Understanding daily routine Appreciating special events. and he develops elaborate play and imagination. Language A. By 3 years. the vocabulary increases to about 500 words. despite not seeing it hidden. Ten percent of children are less adaptable and tend to be emotionally negative and are considered “difficult. Attachment refers to the bond that forms between the infant and the caregiver. Cognitive development A. Preoperational thought is marked by the development of symbolic thinking. Progression from sensorimotor to symbolic thought occurs typically between 18 and 24 months of age. B. such as birthdays Remembering and reciting nursery rhymes Repeating three digits VI. By the age of 3 years. C. as the child becomes capable of forming mental images and begins to solve problems.” and about 50% of what the child says should be intelligible to strangers.” V. and 75% of speech is understandable to strangers. and frequently asks “why” questions. Beginning around age 2 years. drug use. Early two and three word sentences are referred to as “telegraphic speech. Language Skills . the toddler begins to put together phrases. hunger). Disorders of attachment may result from inconsistent caregiving and are more common in the presence of poverty.Social/Emotional Skills 18 Months • • • • Removing a garment Feeding self and spilling food Hugging a doll Pulling a toy 24 Months • • • • • Using a spoon. The 18-month-old has a vocabulary of at least 20 words. He begins to make complete sentences. B.
Temper tantrums are characteristic of 2-year-olds. Separation. difficult temperament.18 Months • • • • • Looking selectively at a book Using 10 to 20 words Naming and pointing to one picture card Naming an object (eg. Preschool children comply with adult requests about 50% of the time. Factors associated with greater sibling rivalry. but they should be infrequent by age 5. individual time with each parent. 2. Fantasy or pretend play gains prominence at about age 3. consequences for undesired behaviors. Preschool children often “regress” when a new baby is born. usually a soft object.” “you” Naming three picture cards Naming two objects Knowing four-directional commands 36 Months • • • • Using four to five word sentences Telling stories Using plurals Recognizing and naming most common objects References. The average 3-year-old child can separate easily from parents. thumb sucking. children frequently have frightening dreams that they can state are “not real. II. see page 182. Preschooler Development I. may be indistinguishable from reality. Fears and fantasies. include opposite gender. encouraging. At the age of 2 years. avoidance of forced interactions. A system of discipline should include positive reinforcement for desired behaviors. and interactions that promote the parentchild relationship. B. and corporal punishment. Pretend friends are very common in children up to the age of 4. and take turns. D. .” C. children should have mastered aggression and should be able to initiate play with a peer. have joint goals in their play together. By the age of 4. most play is parallel. and talking about the new baby are helpful. E. Family relationships A. and rational are more likely to have children who are self-reliant and self-controlled. Parents who are authoritative and firm but also warm. Oppositionality. Early fantasy. although there is another peak at 6 years in response to the stresses of schooling. Play 1. family discord. By the age of 3. Sibling classes. insecure pattern of attachment. Sibling interactions 1. a strong relationship between the older child and the father. exhibiting increased naughtiness. resulting in a tendency for fears. 2. ball) Following two-directional commands 24 Months • • • • • Using two to three word sentences Using “I. Some children cope by adopting a transitional object. good support for the mother. Mastery of aggressive impulses should improve after 2 1/2 years of age. Peer relationships A.” “me. which serves as a symbolic reminder of the parent. and altered toileting.
best friend <2 y difference. tells fanciful tales Common Makebelieve and dress up Imaginary friends May have one If present. follows rules in simple games. pours some Dresses with supervision. unfamiliar may be monsters Elaborate fantasy play. listens to stories Able to take turns. solitary play. “mine. may visit neighbor by self. turn. action figures. mimics domestic activities 20 min with peers Level of fantasy Simple fantasy play. self-talk. listens to stories Rule use Shares some Shares spontaneously. but with adult effort and motivation Independent . plays cooperatively with others Prefers peer play to solitary 5-year visit Group of friends Duration of interaction Briefly alone from adult. private Favorite toys/activi ties Things that move. pulls on simple garment Dresses all but tying Toileting Clean and dry. follows community rules Aggression Aggressive to get things Negotiates conflicts Development of Independence 2-year visit Eating Uses utensils 3-year visit Spills little. distinguishe s fantasy from reality. unbuttons some Clean and dry by selfmotivated approach 4-year visit Helps set table 5-year visit Helps cook Dressing Undresses. acts. prefers some friends over others. plays games 3-year visit Takes on a role. alternately demanding/coope rative Wants to please friends Follows rules of the game. books. beginning property rights. dresses and undresses dolls Sings a song. facility with rules. water. or fit together. copies others. offers toy.” “right places” Listens to stories. plays associatively with others 4-year visit Interactive games. sudden shifts in intensity of activity Symbolic doll.Peer Relationships 2-year visit Amount of interaction Parallel play with peers. music. dances.
high 4-year visit 5-year visit Standard Drawings Identifies Imitates Copies Vertical. Persistent and worsening stuttering beyond the age of 4 should be evaluated. By the age of 4. The typical 3-year-old can count three items. Sentence length increases by one or two words annually throughout the preschool period. Criterion for referral at 2 years of age is a less than a 50-word vocabulary or not putting two words together.” and “until”.5 years. “if. Communication A.5 and 4 years of age.” “sh.” and “th” sounds are not uncommon until age 7. The 5-year-old can count ten objects or more and should understand “before. They often mimic what others say (echolalia) up to age 2. Communication Skills in Preschoolers 2-year visit Vocabulary No jargon. B. Strangers should be able to understand 25% to 50% of what the 2-year-old child says. body. including head. The 3-year-old speaks in simple sentences of three or four words. prints letters III. Dysfluency (aberration of speech rate and rhythm) occurs transiently between about 2.” They can discuss emotions and tell jokes. then. strangers can understand the child 100% of the time. with at least the same number of words that the child is old.” “l. A 4-year-old who cannot converse with familiar people with sentences averaging three words should be evaluated. The 2-year-old has a vocabulary of approximately 150 to 500 words. Preschool children who have expressive language disorders tend to speak less often and convey less information than their peers.” “after. although errors in “r. E.Motor and Cognitive Play Skills 2-year visit Pencil grip Point down 3-year visit Awkward. C. scribble Shapes Horizontal. “My Mommy” or “More Milk”). 150 to 500 words 2 words 3 to 4 words 75% 4 to 5 words 100% 3-year visit 4-year visit 5-year visit Definitions Sentence length Intelligibility to stranger 25% . and a 4-year-old can count four items. cross Circle before cross 2 parts Longer line Directions Cross before square 6 parts Perso n-body parts Scissors One hand 6-9 Across paper Tower of 10 3 block bridge 5 block gate Cuts out square Square before triangle 10. The child should be speaking in two-word utterances (eg. arms. legs Block tower Block figure Aligns 4 for train Steps Other Turns pages 1 at a time Ties knot in string. A 5-year-old should use complete sentences containing five words. strangers should be able to understand the child 75% of the time. By 3 years of age.” “s. D.
2 opposites Motor development 2-year visit Walks forward Walks backward Runs Slightly bent 10 ft 3-year visit Swings arms 4-year visit Tandem walks Tandem 5-year visit Changing direction Alternating arms High equipment 26 to 30 in from both feet 16 in.2-year visit Grammat ic forms Verbs. under Which is longer. some adjectives and adverbs Talks about current action. gives first and last names. alternatin g 32 in. lands on both feet Stairs-up One step at a time . counts to 3 Describes recent experiences. knows number Relationships Which is bigger. recognizes letters of the alphabet. no jargon. counts to 4. knows telephone number and address Dysfluen cies not expected Fluency Dysfluenc y common Dysflue ncy common Some dysfluenc y Comprehension 2-year visit Number step command 100% for 1 without gesture 3-year visit 2 4-year visit 3 5-year visit Number of body parts Number of colors Gender Names 1.5 y) Jumps Both feet off floor Jumps down Step with both feet 18 in. can sing songs. names pictures 3-year visit Plurals. identifies 7 2 named Self 4 named Self and others Own names Refers to self by name Says “2" (not counted) First and last Numbers counted Counts to 3 10. one foot leads Over 10 in Climbs Out of crib (2. pronouns 4-year visit Past tense 5-year visit Future tense Typical examples Tells own age and sex. identifies gender Counts to 10 or more. lands on one foot first Without rail.
three to six times per year. C. II. Factors that determine classroom performance include eagerness to please adults. children increasingly enjoy strategy games and word play (puns and insults) that exercise growing cognitive and linguistic mastery. consider multiple points of view. Masturbation is common.5 kg (7 lb) and 6 cm (2. evaluate oneself and perceive the opinions of others. Cognitive and language development A. Muscular strength. and basic mathematics. Growth during the period averages 3-3. children use those fundamentals to learn increasingly complex materials. and interpret their perceptions in view of realistic principles. writing. . B. By third or fourth grade. Loss of deciduous (baby) teeth begins at about age 6 years of age. School-Age Child Development Middle childhood consists of years six through twelve. C. as does the ability to perform complex movements such as dancing. competitiveness. 1 or 2 arms Catches Bent arm Bounce pass Skips Skips Pedals 10 ft. willingness to work for a delayed reward. Growth occurs in irregular spurts lasting on average 8 wk. overhand Straight arms 10 ft.2-year visit Stairsdown One step at a time 3-year visit Alternating. D. no rail 1 sec on 1 foot 4-year visit Alternating 5-year visit Stands on one foot Kicks Tries 5 to 6 sec on each foot 10 sec kicks ball 6 ft 3 hops in place 5 forward 20 ft forward 10 times Hops Throws Throws 5 ft Bounce . I. or playing the piano. and ability to risk trying. children need to be able to sustain attention through a 45-min period. School-aged children increasingly apply rules. but interest in gender differences and sexual behavior remains of interest to many children. and stamina increase progressively. The head grows only 2-3 cm in circumference. This period is characterized by the ability to consider several factors. The sexual organs remain physically immature. By third grade. B. Healthy development requires increasing separation from parents and the ability to find acceptance in the peer group and to meet challenges outside the home. cooperativeness. coordination. Beginning in third or fourth grade. see page 182. Self-esteem is essential to the development of the school-aged child. Physical development A. self-confidence. The first 2 years of elementary school are devoted to acquiring the fundamentals of reading.5 in) per year. shooting basketballs. D. tricycle References.
Sibling relationships influence self-image. School-aged children display decreased emotional lability toward parents and an increasing involvement in relationships outside of the home. problems with reading comprehension. problems with peer relationships Expressive language Difficulty expressing feelings and using words for self-defense. completing assignments. ability to understand time Language Receptive language Ability to comprehend complex constructions. loyal supporters. attention and behavior problems caused by not understanding direction Cognitive Long-term memory Ability to acquire "automatic" skills Delayed mastery of the alphabet (reading and writing letters). only. planning. The beginning of school coincides with a child’s . approach to conflict resolution and interests. B. and role models. Regular chores provide an opportunity for children to contribute to the family. function words (eg. Milestones of a school child’s increasing independence include the first sleepover at a friend’s house and the first time at overnight camp. difficulty with basic reading and writing Description Associated Problems Proprioceptio n and motor control Poor handwriting. and long blocks of language (eg. and offer unconditional acceptance when failures occur. to control meanings by varying position and word endings. d. adopting them as role models. to construct meaningful paragraphs and stories Difficulty following directions. and behaving well Difficulty organizing assignments. with resulting frustration and physical acting out. requiring excessive effort Phonologic processing Delayed receptive language skills. struggling during "circle time" and with language skills. paragraphs) Ability to recall required words effortlessly (word finding). and telling time Selective attention Ability to listen and ignore distractions Sequencing Ability to remember things in order. School-aged children identify with same-sex parents. and the neighborhood. between b. celebrate successes. Social and emotional development proceeds in three contexts: the home. Siblings have critical roles as competitors. D. C. supporting selfesteem. and Language Processes Required for Elementary School Success Process Perceptual Visual analysis Ability to break a complex figure into components and understand their spatial relationships Ability to sense body position by feel and unconsciously program complex movements Ability to perceive differences between similar sounding words and to break down words into sounds Persistent letter confusion (eg. Cognitive. Social and emotional development A. nuances of speech. if. the school. and g). except). The parents’ moral judgments are internalized as the superego. spelling. The home is the most influential. when. slow handwriting. wandering attention. Parents should make demands for effort in school and extracurricular activities. III. inability to progress beyond basic mathematics Difficulty following multistep instructions.Perceptual.
disorganization. Impulsivity a. difficulty playing quietly. Attention-Deficit/Hyperactivity Disorder Attention-deficit/hyperactivity disorder (AD/HD) is a condition that appears in early childhood with symptoms of inattention. By the adolescent years. blurting out answers. poor concentration. I. Inattention typically is not apparent until the child is eight to nine years of age. Clinical features. Dangers such as busy streets. The impulsive symptoms typically are observed by the time the child is four years of age and increase during the next three to four years to peak in severity when the child is seven to eight years of age. Interactions with peers call on increasing conflict resolution or pugilistic skills. the hyperactive symptoms are barely discernible. References. They peak in severity when the child is seven to eight years of age. disruptive classroom behavior. Children may feel powerlessness in the world. Some children conform readily and enjoy easy social success. The symptoms affect cognitive.” b. The prevalence of AD/HD between 8 and 10% in school-aged children. impulsive symptoms usually remain a problem throughout the life of the individual. may be won through possessions (having the right toys) as well as through personal attractiveness. and poor attention to detail. symptoms of inattention usually are a lifelong problem. see page 182. Popularity. and strangers tax school-aged children’s common sense and resourcefulness. b. Similar to the pattern of impulsivity. poor follow-through with assignments or tasks. losing or misplacing things. after which they begin to steadily decline. Conformity is rewarded in school-aged children. an important part of self-esteem. AD/HD is comprised of three categories of symptoms: hyperactivity. and impulsivity. being easily distracted. Inattention a.further separation from the family and the increasing importance of teacher and peer relationships. 2. and social skills. accomplishments. and persist into adulthood in 70% of cases. In contrast to hyperactive symptoms. 3. impulsivity. F. academic underachievement. b. In addition to friendships that may persist for months or years. is manifested by difficulty waiting turns. and unintentional injury. and compensatory fantasies of being powerful may lead to a fascination with superheroes. experience with a large number of superficial friendships and antagonisms contributes to a child’s growing social competence. which almost always occurs in conjunction with hyperactivity in younger children. behavioral. hyperactivity. bullies. A. The hyperactive symptoms typically are observed by the time the child reaches four years of age and increase during the next three to four years. and social functioning. and frequent restlessness or seeming to be always “on the go. academic. those who adopt individualistic styles or have visible differences may be stigmatized. difficulty remaining seated. emotional. E. Inattention may include forgetfulness. Impulsive behavior. Hyperactive behavior is identified through excessive fidgetiness or talking. intruding or interrupting other’s activities. . AD/HD occurs two to four times more commonly among boys than girls. Core symptoms 1. and inattention. Hyperactivity a.
The symptoms must persist for at least six months. and impulsivity include mental retardation. The predominantly hyperactive-impulsive type. toys. school assignments. at school and at home). The symptoms do not occur exclusively during the course of a pervasive developmental disorder. as symptoms of hyperactivity and impulsivity peak. fetal alcohol syndrome. as symptoms of hyperactivity and impulsivity peak. 4. C. 5. The symptoms must be present in more than one setting (eg. diabetes mellitus. II. Children with the predominantly hyperactive-impulsive type of AD/HD (AD/HD-HI) usually are diagnosed at six to seven years of age. Other conditions to consider in children with symptoms of inattention. Children with the predominantly inattentive type of AD/HD (AD/HDI) usually are diagnosed at 9 to 10 years of age. The predominantly inattentive type. 3. Predominantly hyperactive-impulsive. and are not better accounted for by another mental disorder. Predominantly inattentive. The symptoms must be present before the age of seven years. stressful home environment. .B. sleep disorder. Differential diagnosis A. Classification. Combined type of AD/HD (AD/HD-C) usually is diagnosed at six to seven years of age. books) Distractions by extraneous stimuli Forgetfulness in daily activities Hyperactivity Fidgeting with hands or feet or squirming in seat Not remaining seated when expected Running about or climbing excessively Difficulty engaging in leisure activities quietly Often “on the go” or “driven by a motor” Excessive talking And/Or Impulsivity Tendency to blurt out answers before questions have been completed Difficulty awaiting turn Tendency to interrupt or intrude on others (eg. B. The combined type. Diagnostic criteria DSM-IV Diagnostic Criteria for Attention-Deficit/Hyperactivity Disorder At least six of the following symptoms of inattention or hyperactivity-impulsivity must be evident: Inattention Lack of attention to details or careless mistakes in schoolwork or other activities Difficulty sustaining attention in tasks or play activities Impression of not listening when spoken to directly Failure to follow through on instructions or finish schoolwork or duties Difficulty organizing tasks and activities Avoidance or dislike of tasks that require sustained mental effort (eg. 1. There must be clear evidence of clinically significant impairment in social. Three subtypes of AD/HD have been identified: 1. These disorders frequently coexist with AD/HD. school work or homework) Tendency to lose things necessary for tasks or activities (eg. The symptoms of AD/HD overlap with those of learning disabilities and behavioral and emotional problems. B. C. or other psychotic disorder. 3. fragile X syndrome. such as depression. schizophrenia. hyperactivity. anxiety. or post traumatic stress disorder. Some impairment from the symptoms must be present in two or more settings (eg. school and home). and seizure disorder. butting into conversations or games) Exclusionary Criteria A. inappropriate educational setting. pencils. hearing or visual impairment. asthma. 2. 6. the age at which symptoms of inattention become noticeable. Some hyperactive-impulsive or inattentive symptoms that caused impairment must have been present before age 7. 2. D. academic or occupational functioning.
As many as 90 percent of children will respond to at least one stimulant. school absences. Dysmorphic and neurocutaneous findings should be noted. The medical history should include prenatal exposures (eg.III. Family assessment should determine the age of onset of the symptoms. The immediate release prepara- . L. alcohol). Copies of report cards and samples of school work should be obtained. and functional impairment. K. A neurologic examination should be performed. Oppositional defiant disorder (ODD) coexists with AD/HD in 35% of cases. psychometric testing is valuable in narrowing the differential diagnosis because the core symptoms of AD/HD can be related to delayed processing skills. Similar to methylphenidate. 2. should be obtained. Dextroamphetamine (Dexedrine). Clinical evaluation A. 1. usually reversible adverse effects. including oppositional defiant disorder. The response rate for stimulant medication (ie. head trauma. and learning disabilities. depression. One-third of children with AD/HD have one or more comorbid conditions. Stimulant medications. Psychometric testing is not necessary for the routine diagnosis of AD/HD and does not distinguish children with and without AD/HD. language disorders. central nervous system infection. Developmental milestones. Methylphenidate (Ritalin). and at regular medication follow-up visits. causing the release of catecholamines in the central nervous system synapses. B. Nonetheless. and psychosocial stressors. Significant reduction in symptoms occurs at doses between 0. during medication titration. Depression coexists with AD/HD in 18% of cases and occurs more commonly in the inattentive and combined types.3 and 0. Anxiety disorder coexists with AD/HD in 26% of cases and is more common occurrence in children with the inattentive type of AD/HD. learning patterns. Family history of similar behaviors is important because the heritability of AD/HD is 80%. recurrent otitis media. perinatal complications or infections. both formulations are available in immediate and sustained release preparations. medical. Parent-child interactions should be observed. Rating scales should be completed by parents and teachers for diagnosis. Developmental history should include the onset and course of AD/HD symptoms and psychological. 4. with an AD/HD-specific behavior checklist and a narrative summary of classroom behavior and interventions. and developmental events. Stimulant drugs affect the dopaminergic and noradrenergic systems. M. E. head circumference. The child’s behavior in the office setting should be observed. anxiety disorder. Methylphenidate is available in immediate and sustained release preparations. IV.6 mg/kg. The examination should include height. 3. weight. C. I. G. and the degree of functional impairment. and medications. Conduct disorder coexists with AD/HD in 26% of cases. Comorbid disorders. School assessment should document the core symptoms. and learning disabilities. conduct disorder. Learning disability coexists with AD/HD range from 20 to 60%. reduction in hyperactivity or increase in attention is 70 percent. although symptoms of AD/HD may not be apparent in the clinic setting. the duration of symptoms. Methylphenidate and dextroamphetamine are the stimulants most commonly used to treat AD/HD in children. particularly language milestones. D. and vital signs. F. the settings in which the symptoms occur. These drugs have similar efficacy and have mild. DSM-IV criteria for conduct disorder include a repetitive and persistent pattern of behavior in which the basic rights of others or major ageappropriate societal norms or rules are violated. Treatment of attention-deficit/hyperactivity disorder in children A. H. drugs. J.
5 mg 2 times/da y >6 years 5 mg x 1 day 5 mg 2 times/da y 3 to 5 years 2.5 mg 2 times per day 3 to 5 years 2. Common side effects include anorexia or appetite disturbance (80 percent).5 mg/dose 10 mg 2 times/day 20 mg 40 mg Weekly increments of 5 mg/dose Amphetami neDextroamph etamine Adderall (5.5 to 5 mg Weekly increments of 2.5 mg/day x 1 day 2. most of which are transient. less common side effects include increased heart rate and blood pressure. and reversible with adjustments of dosing. and irritability. 10. Immediate-Release Stimulant Preparations for Children with Attention-Deficit/Hyperactivity Disorder Medication Initial dosing Dose advancement Maximum dose <25 kg 35 mg <25 kg 60 mg Methylpheni date* Methylpheni date Ritalin Methylin (5. 10 mg tablets) Dextroamph etamine Dexedrine (5 mg tablets) Dextrostat (5. 10.5. Deceleration of linear growth may occur. Approximately 15 to 30 percent of children who are treated with stimulant medications develop motor tics. 10. 30 mg tablets) Weekly increments of 2. 5.5 mg/day x 1 day. 20 mg tablets) Focalin• (2. 6. 5. half-life: 2 to 3 hours • For children >6 years of age Sustained-release Stimulant Preparations for Children with Attention-Deficit/Hyperactivity Disorder Medication How supplied Duration of action Maximum dose 60 mg Methylpheni date Methylpheni date SR one-pulse system Ritalin-SR one-pulse system 20 mg tablets 8 hours 20 mg tablets 8 hours 60 mg . social withdrawal. of short duration.5 mg/dose 40 mg Weekly increments of 5 mg/dose *Duration of action: 1 to 4 hours. 12.5 mg 2 times/da y >6 years 5 mg x 1 day 5 mg 2 times/da y Weekly increments of 2. Many of the side effects associated with methylphenidate and dextroamphetamine are mild. 20. 2. headache. sleep disturbances (3 to 85 percent). Adverse effects. 7.tion of dextroamphetamine-amphetamine has a duration of as long as six hours. and weight loss (10 to 15 percent). mg tablets) 5 mg/day x 1 day 5 mg 2 times/day x 1 day 5 mg 3 times/day Weekly increments of 5 mg per dose 2.5. but adult height is not affected. nervousness. 15.
a.2 mg/kg in either one or two daily doses. 40 mg capsules 8 hours 60 mg 10. constipation) and lowering of the seizure threshold.4 mg/kg or 100 mg. 54 mg tablets 12 hours 72 mg 5. Tricyclic antidepressants (TCAs [eg. Thus. have unacceptable side effects. It has not been compared directly to methylphenidate or dextroamphetamine. desipramine. adolescents.5 mg/kg for a minimum of three days and then titrated up to a daily dose of 1. Antidepressants a. 15. and 60 mg) and can be taken once or twice per day. dry mouth. dyspepsia. 30. methylphenidate and dextroamphetamine continue to be the treatments most widely recommended. abdominal pain. Atomoxetine (Strattera). an antidepressant that blocks the reuptake of norepinephrine and dopamine.Ritalin-SR two-pulse system Methylin ER one pulse system Metadate CD twopulse system Metadate ER onepulse system Concerta three-pulse system Dextroamph etamine Dexedrine spansule one-pulse system 20. 25. bupropion) have been reported to be beneficial in AD/HD. 20 mg tablets 8 hours 60 mg 18. Children weighing less than 70 kg should be started at a dose of 0. 36. Atomoxetine is the only AD/HD medication that is not a controlled substance. 20 mg tablets 8 hours 60 mg 20 mg capsules 8 hours 60 mg 10. the maximum daily dose should not exceed 1. 18. Electrocardiogram should be obtained at baseline and when the dose has been optimized because these agents can cause arrhythmia. Bupropion (Wellbutrin). has more stimulant properties than do the TCAs. and adults. b. 25. Adverse effects include weight loss. followed by an increase to 80 mg. 10. 20. Other medications. Nonstimulant medications usually are used when children respond poorly to a trial of stimulants. 40. Atomoxetine is an oral capsule (5. a selective norepinephrine reuptake inhibitor. decreased appetite. Atomoxetine has been demonstrated to be more effective compared to placebo. is approved for the treatment of children with AD/HD who are older than six years of age. 15 mg capsules 5 to 6 hours 45 mg Amphetamin eDextroamph etamine Adderall XR 5. particularly if the patient has comorbid anxiety. nausea. depression. and sleep disturbance. after two to four weeks. It is of modest efficacy in decreasing hyperactivity and aggressive behavior. or have significant comorbid conditions. the dose may be increased to a maximum of 100 mg. 30 mg capsules 8 hours 40 mg B. Side effects include anticholinergic effects (eg. nortriptyline]) and dopamine reuptake inhibitors (eg. imipramine. Tricyclic antidepressants are second-line therapy for AD/HD. or tic disorder. b. improvement in attention has not been documented objectively and the effects of these agents may be short-lived. 10. Adverse effects include motor tics . vomiting. 10. Patients who weigh more than 70 kg should be started at a dose of 40 mg for a minimum of three days. 2. c. 1.
2. 3.and a decreased seizure threshold. they can improve the behavior problems often seen in children with AD/HD. Although FTT occurs in all socioeconomic strata. Clinical evaluation of poor weight gain or weight loss A. A child younger than 2 years of age whose weight is less than 80% of the ideal weight for age. less developed reading skills. it is not a diagnosis. Clonidine may be useful in overaroused. whereas a child with the combined type of AD/HD who has difficulty with peer relationships may need medication every day. The underlying etiology must be determined. It has been used in children with AD/HD and comorbid tics or Tourette syndrome. During the titration stage. but not as effective as stimulants. lower social maturity. 2. FTT describes a sign. Small-for-gestational age infants. Many patients with FTT have either an organic or nonorganic cause. the child’s behavior rating scales should be assessed weekly and the medication adjusted as indicated. I. Feeding history should assess details of breast or formula feeding. depression. the comparable dose of the longacting agent can be tried. behavioral. Short-acting forms of medication usually are used to determine the optimal dose. it is more frequent in families living in poverty. 3. Infants who are normally lean. however. During the titration stage. 4. an alpha-2-adrenergic agonist. and environmental factors. a sizable number of patients have both psychosocial and organic causes for their condition. Preterm infants. 4. or aggressive individuals. A child younger than 2 years of age whose weight is below the 3rd or 5th percentile for age on more than one occasion. D. A child younger than 2 years of age whose weight crosses two major percentiles downward on a standardized growth grid. poorer language development. Children of genetically short stature. has been found to be effective in reducing symptoms in AD/HD. the optimal dosage and frequency of medication are determined. II. headache. Ten percent of children seen in the primary care setting show signs of growth failure. Titration. References. Exceptions to the previously noted criteria include the following: 1. easily frustrated. Pathophysiology A. Side effects of clonidine include sedation. 1. . C. 2. see page 182. The child should be seen at least every two to four weeks during this phase. 5. “Overweight” infants whose rate of height gain increases while the rate of weight gain decreases. Once the optimal dose is determined. B. Guanfacine (Tenex). Failure to Thrive Failure to thrive (FTT) is usually first considered when a child is found to weigh less than the third percentile for age and gender. Clonidine (Catapres). 3. Behavioral and psychological interventions have not been demonstrated to significantly reduce the core symptoms of AD/HD. Children with FTT attain lower verbal intelligence. The medication should be started on a weekend day so that parents can watch for adverse effects with the first doses. Diagnostic criteria for failure to thrive 1. and have a higher incidence of behavioral disturbances. a long-acting alpha-2noradrenergic agonist. A child with predominantly inattentive type of AD/HD may need medication only on school days. and hypotension. C. It has been used to treat AD/HD with Tourette syndrome when tics worsened with stimulants or when clonidine was poorly tolerated. However. FTT is a syndrome of malnutrition brought on by a combination of organic. has a longer half-life and fewer side effects than does clonidine. highly active. timing and introduction of solids.
urinary tract infection. If the bone age is normal. Smith-Lemli-Opitz-syndrome) ! Congenital syndrome (eg. and constitutional short stature. illnesses. maternal depression. tumor) ! Chronic infection (eg. infant temperament. acquired immunodeficiency syndrome) ! Gastrointestinal disorder (eg. Developmental history should cover gestational and perinatal history. and a tuberculin test. myopathies) ! Tracheoesophageal fistula ! Genetic syndrome (eg. Human immunodeficiency virus screening or a sweat test may be considered. . Psychosocial history should include family composition. If the child’s median age for weight is less than the median age for height. malrotation) ! Gastroesophageal reflux ! Drugs (eg. 4. Family history should include heights. Dysmorphic features and physical signs of central nervous system. Height. glossoptosis) ! Dyspnea (congenital heart disease. position and placement of the infant for feeding. cleft lip and palate micrognathia. isolation. and phosphorous to assess protein status and to look for biochemical rickets. iron deficiency) ! Psychosocial problems (eg. pulmonary. weight.who feeds the infant. developmental milestones. creatinine. hydrocephalus. child-rearing beliefs. apathy. pyloric stenosis. If all three measurements are consistently below the third percentile but show the same rate of increase over a period of time. employment status. and the infant’s daily routine. Laboratory testing. serum electrolyte levels. financial status. urine culture. fetal alcohol syndrome) Unavailability of Food ! Inappropriate feeding technique ! Inadequate volume of food ! Inappropriate food for age ! Withholding of food (abuse. alkaline phosphatase. While feeding and playing. hypotonia) ! Craniofacial anomalies (eg. C. B. unexplained bruises or scars. or signs of neglect or abuse (poor hygiene. stress. it is unlikely that the infant has a systemic chronic disease or a hormonal abnormality as the cause of poor weight gain. apathy) ! Central nervous system (CNS) pathology (eg. the infant probably had intrauterine growth retardation. Severe malnutrition requires measurement of albumin. Observation of the infant and caretaker. calcium. D. syrup of ipecac) III. urinalysis. Physical examination A. the child may be undernourished. psychosocial) Vomiting ! CNS pathology (increased intracranial pressure) ! Intestinal tract obstruction (eg. and head circumference should be plotted on a growth curve. cardiac. Diagnostic testing 1. or developmental delay. the infant may avoid eye contact or withdraw from physical attention and may show a poor suck or swallow. Three measurements that are below the 3rd percentile indicate an underlying organic disease. 2. and the caretaker’s own history of possible childhood abuse or neglect. and stooling or vomiting patterns. pulmonary disease) ! Feeding disorder ! Generalized muscle weakness/pathology (eg. hypertonia. or aversion to oral stimulation. neglect. B. 3. Causes of Inadequate Caloric Intake Lack of Appetite ! Anemia (eg. inherited diseases. blood urea nitrogen. pain from reflux esophagitis) Difficulty with Ingestion ! Psychosocial problems (eg. Ineffective feeding technique or inappropriate response to the infant’s physiologic or social cues may be displayed by the caretaker. rumination) ! Cerebral palsy/CNS disorder (eg. Radiologic determination of bone age. or inappropriate behavior) should be sought. Tests that will usually exclude an organic pathology include a complete blood count. D. or gastrointestinal disorders. weights. C. choanal atresia.
” or “ga. such as “mamama. see page 182. The number of calories per ounce of formula can be increased by adding less water (13 oz infant formula concentrate mixed with 10 oz water provides 24 kcal/oz high-calorie formula) or by adding more carbohydrate in the form of glucose polymers corn starch or fat in the form of medium-chain triglycerides or corn oil. In the first few months. consisting of blowing bubbles or the “raspberry. In the first 4 to 6 weeks. and visual communication (gestures). Language consists of auditory expressive ability (speech). inborn errors of carbohydrate metabolism) • Renal tubular acidosis • Chronic hypoxemia (eg. Treatment of failure to thrive A.” 3. ad libitum oral feedings are appropriate. Treatment of older children. infants sporadically say “mama” or “dada” without knowing the meaning of these . By 5 months.E. aminoacidopathies. the infant often demands and eats enough food to gain weight. B. Nutritional requirements in children with FTT usually are 150 kcal/kg per day. Treatment of infants 1. Between 6 and 8 months. 2. oil. margarine. 2. At this point. cyanotic heart disease) IV. References. A feeding evaluation by a nutritionist or an occupational therapist may detect a subtle feeding disorder. such as “da. Auditory expressive language development 1.” 5. Normal speech and language development A.” “ba. excess levothyroxine) • Endocrine disorders (eg.” “dadadada. The normal. Causes of Inadequate Calorie Absorption Malabsorption • Biliary atresia or cirrhosis • Celiac disease • Cystic fibrosis • Enzymatic deficiencies • Food (protein) sensitivity or intolerance • Immunologic deficiency • Inflammatory bowel disease Diarrhea • Bacterial gastroenteritis • Parasitic infection Hepatitis Hirschsprung Disease Refeeding diarrhea Causes of Increased Calorie Requirements Increased Metabolism/Increased Use of Calories • Chronic/recurrent infection (eg. Once nutritional recovery begins. hyperthyroidism. By 9 months. chronic lung disease) • Congenital heart disease/acquired heart disease • Malignancy • Chronic anemia • Toxins (lead) • Drugs (eg. and peanut butter. urinary tract infection. bilabial sounds begin. Speech and Language Development Language is defined as a symbolic system for the storage and exchange of information. receptive ability (listening comprehension). tuberculosis) • Chronic respiratory insufficiency (eg. hyperaldosteronism) Defective Use of Calories • Metabolic disorders (eg.” 4. the earliest sounds consist of cooing. Foods can be fortified with such items as milk products. C. consisting of the same syllable repeated. infants begin polysyllabic babbling. laughing and monosyllables appear. healthy infant requires an average of 100 kcal/kg of body weight per day. I.
The most common nongenetic cause of deafness is fetal CMV infection. By 2 years.” 6. By 9 months of age. II. 2. By 5 years. By 12 months. 4. infants comprehend the word “no. Between 9 and 12 months. 7. By 18 to 20 months. By 4 months of age the normal infant will turn his head to locate the source of a voice. infants appropriately wave bye-bye on command. pronouns appear (“me” and “you”). By 1 year of age. it should be three-fourths intelligible. Third year. These speech inflection patterns of are referred to as prosody.sounds. vocabulary growth velocity accelerates. By 9 months. By 6 to 7 months. Newborn infants respond to vocal stimuli by eye widening or changes in sucking rate. Between 8 and 9 months. Classification of speech and language disorders A. C. 9. B. 3. toddlers are producing two-word phrases. Visual language development 1. By 2 years of age. turning to inanimate stimuli. which consists of three. 7. 6. children will point to objects on command and name simple objects on command. a toddler should be using a minimum of 20 words. 2. A 30-month-old’s vocabulary should be too large for the parent to count (>150 words). Two children per thousand are deafened during the first 3 years of life. infants respond to one-step commands such as “Give it to me. (eg. an infant will attend selectively to his own name. By 24 months of age. One-third of congenital deafness is genetic in origin. Early during the second year of life toddlers produce jargon.” 7. children develop “telegraphic” speech. 4. 10. and it should be completely intelligible by age 4 years. expanding to 1500-2000 words by age 5. Vocabulary growth velocity reaches a rate of several new words per day. By 24 to 30 months. consisting of strings of different sounds. infants express their desire for an object by reaching and crying. 5. 8. By age 4 to 5 months. 10. During the first few weeks. infants use “mama” and “dada” consistently to label the appropriate parent. a social smile appears. the infant will display alert visual fixation.or 3-month-old infant watches and listens intently to adults and may vocalize back. 5. the 24-month-old should have a vocabulary of at least 50 words. infants indicate desired objects by pointing with the index finger. such as “want milk!” 12. children are able to follow threeand four-step commands. In the second year of life. speech-like inflection. by 3 years. By 4 to 6 weeks. 14. 15. and one-third is of unknown etiology. toddlers can follow novel two-step commands. such as patty cake and peek-a-boo. 6.” 8. starting at one new word per week at 12 months of age and increasing to one or more new words per day by 24 months of age. a child’s receptive vocabulary includes 800 words. infants acquire one or two words other than “mama. the child’s speech should be one-half intelligible.to five-word sentences. then go sit down”). By 7 to 9 months of age. with rising and falling. the infant will turn towards a voice. During the second year of life. The 2. infants reciprocate and eventually initiate gesture games. 9. One infant per thousand is born with bilateral. one-third is nongenetic. 2. By 2 years. 13. 11. By 10 months of age. “Put away your shoes. occurs 1 month later. such as a bell. 3. . 8. Hearing loss 1.” or “dada. infants play gesture games. By 36 months. By 12 months. Auditory receptive language development 1. severe-to-profound hearing loss.
Developmental language delay presents with expressive and receptive impairment. Stuttering involves repetition of shorter speech segments (“I wu . and below -5 SD is profound MR (IQ <25). . D. and an onset before 30 months of age. I want . C. Developmental language disorders (DLD) 1. Autistic children manifest delayed and deviant language. DLD are disorders characterized by selective impairment of speech and/or language development. 5. b. Moderate MR = -3 to -4 SD (IQ 54 to 40). and all children who are mentally retarded are language-delayed. vocal output gradually diminishes. DLD affects 5-10% of preschool children. Developmental testing by a speech/language pathologist should be undertaken once speech or language delay has been detected.” The prevalence peaks at 4% between 2 and 4 years of age and declines to 1% among older children and adults. Creatine kinase measurement to exclude Duchenne muscular dystrophy is indicated for boys who have speech delay plus gross motor delay but . Diagnostic evaluation of speech and language disorders A.B. D. Cooing and babbling may be reduced and delayed. severe MR = -4 to -5 SD (IQ 39 to 25). monotonously repetitious behaviors with an insistence on routines. Intelligence tests are standardized to a mean score of 100. wu . . 2. Physiologic disfluency involves repetition of whole words (“I want . C. Three percent of children are mentally retarded. Autism can be caused by most of the same etiologies that cause MR. C. autism. III. Physiologic dysfluency is characterized by a transient loss of normal rate and rhythm of speech. The prevalence is 0. . Clinical evaluation of speech and language disorders A. Deaf infants coo and babble normally until 6 months of age. Dysarthria in children usually is caused by cerebral palsy. B. Dysarthria is caused by a physical impairment of the muscles of speech production. 3. B. and mild MR is equivalent to an intelligence quotient (IQ) of 69 to 55. Human immunodeficiency virus (HIV) serology is recommended in higher risk speech-delayed children to exclude HIV encephalopathy. the etiology of DLD remains unknown. or developmental language disorder. In the majority of cases. DLD can be caused by sex chromosome aneuploidy. Autism manifests as delayed and deviant language development. Mental retardation 1. Infants with hearing-impairment. “Mild” MR is defined as -2 to -3 SD. wwwwant to go home”) or a complete inability to initiate a word. Mental retardation (MR) is defined as significantly subaverage general intellectual function plus delayed adaptive skills in the first 5 years of life. Stuttering a. . impaired affective development.2%. and it is normal in children between 2 and 4 years of age. 2. referred to as “blockage. Mentally retarded children manifest delay in all language areas. fragile X syndrome. Thereafter. and repetitious behaviors with an insistence on routines. Intelligence that is “significantly subaverage” is defined as more than 2 standard deviations (SD) below the mean. neonatal intracranial hemorrhage. or human immunodeficiency virus encephalopathy. Audiologic testing is indicated for all children with a sign of a speech or language disorder. Karyotype and DNA probe studies for fragile X are indicated in children who have mental retardation. however. 4. . impaired affective development. fetal alcohol effects. . . and affected boys outnumber affected girls by 3:1. E. I want to go home”). . Speech may be effortful and reduced in amount. IV. General intelligence is normal. Autistic type language disorder is marked by impaired pragmatics--failure to use language as a medium of social interaction. such as impaired intelligibility and delayed emergence of sentence structure. head trauma.
Cranial MRI is indicated in the presence of focal neurologic abnormalities or dysmorphic features suggestive of a structural brain abnormality (eg. F. . Stuttering requires referral to a speech pathologist. Hearing loss is treated with amplification. Management of speech and language disorders. Therapy for autism is directed at enhancing communication and social skills. hypertelorism. References. see page 182. midfacial hypoplasia.who do not have increased deep tendon reflexes. aberrant hair patterning). V. The child who has DLD should be referred for speech therapy.
C. carotid bruits. Normal murmurs include vibratory and pulmonary flow murmurs. diffuse diaphoresis. Auscultatory criteria signifying cardiac disease 1. dyspnea. E. and atypical chest pain also suggest the possibility of organic heart disease. Ejection or midsystolic clicks D. Ventricular septal defect (VSD) is a harsh pansystolic murmur of even amplitude that is audible at the lower left sternal border. C. Clinical evaluation of heart murmurs A. and the murmur of physiologic branch pulmonary artery stenosis. Failure to thrive. Ejection murmurs begin after the first heart sound. D.Family history of a congenital cardiovascular malformation increases the risk of a cardiac defect. an abnormally loud or single second heart sound 2. Patent ductus arteriosus (PDA) causes a murmur that is continuous.Cardiac Disorders Heart Murmurs Ninety percent of children will have an audible heart murmur at some point in time. or asymmetric pulses should be referred to a cardiologist. precordial bulging. tachypnea. such as with DiGeorge syndrome (type B interrupted aortic arch. tracheoesophageal fistula and esophageal atresia. Loud. The majority of children who have heart murmurs are asymptomatic. or imperforate anus are associated with congenital cardiac defects in 15-25% of infants. pansystolic. Ejection (crescendo-decrescendo) murmurs are caused by ventricular outflow obstruction. abnormal pulse volume) also should prompt referral to a cardiologist. B. Maternal collagen vascular disease may lead to fetal complete heart block. Physical examination A. B. however. Transient hypertrophic cardiomyopathy and tetralogy of Fallot are associated with maternal diabetes. truncus arteriosus). Gestational course should be reviewed for exposure to teratogens or maternal illnesses. hepatomegaly. late systolic. exercise intolerance. II. and located at the upper left sternal border. Noncardiac malformations. Cyanotic infants or children. louder in systole. a persistently hyperdynamic precordium. Less than 5% of heart murmurs in children are caused by cardiac pathology. Signs of congestive heart failure (inappropriate tachycardia. Characteristics of Organic Murmurs Lesion Shape Timing Location LLSB Other Findings Apical middiastolic murmur Higher pitched than VSD murmur Persistent S2 split Ventricular septal defect Mitral regurgitation Plateau Holosysto lic Plateau Holosysto lic Apex Atrial septal defect Ejection Systolic ULSB . or syncope signify potential cardiac dysfunction. Diaphragmatic hernia. F. Ventricular and atrial septal defects occur with fetal alcohol syndrome. I. feeding difficulties. In early infancy. unexplained persistent irritability or lethargy. Fourth heart sound or S4 gallop 3. abnormal rate or pattern of breathing. Fetal exposure to lithium may cause Ebstein anomaly of the tricuspid valve. cardiac malformations may manifest as persistent peaceful tachypnea (a respiratory rate greater than 60 breaths/min). diastolic. omphalocele. venous hums. or continuous murmurs. Twenty-five percent of children who have heart disease have extracardiac anomalies. Cyanosis.
S2 = second heart sound. One-third of neonates who have serious heart malformations may not have a detectable heart murmur during the first 2 weeks of life. Thirty percent of newborn infants subsequently determined to have heart disease are discharged from the newborn nursery as ostensibly healthy. ULSB = upper left sternal border. Heart murmurs in the newborn infant A. or syndromes. C. S2 = second heart sound. MLSB = mid-left sternal border. IV. A single second heart sound in a quiet neonate indicates: 1) the absence . No evidence of associated cardiac abnormalities. Normal Murmurs Type Shape Timing Pitch Location Other Findings Intensity <grade II Disappears in supine position Normal S2 split Vibratory Ejection Midsyst olic Low LLSBapex Venous hum Diamond Continuous Medium Subcla vicular Pulmonary flow Physiologic branch pulmonary artery stenosis Flow Systolic Medium ULSB Ejection Systolic Medium Entire chest Disappears by 4 to 6 months of age LLSB = lower left sternal border. Auscultation of the second heart sound. In healthy neonates. A persistently hyperdynamic precordium suggests organic heart disease. Criteria for diagnosis of a normal heart murmur 1. 90% of infants who have serious cardiac disease have persistent tachypnea after birth. 2.Lesion Shape Timing Location ULSB Other Findings Bounding pulses Patent ductus arteriosus Aortic valve stenosis Subvalvula r aortic stenosis Hypertrophic cardiomyopathy Coarctation Diamond Continuous Ejection Systolic URSB Ejection click No ejection click Ejection Systolic MLURSB Ejection Systolic LLSBapex Laterally displaced PMI Ejection Systolic ULSBLeft back ULSB Pulse disparity Pulmonary valve stenosis Tetralogy of Fallot Ejection Systolic Ejection click. the second heart sound is split audibly by 12 hours of age. extracardiac congenital malformations. wide S2 split Cyanosis Ejection Systolic MLSB LLSB = lower left sternal border. Differentiation of normal from pathologic murmurs A. B. URSB = upper right sternal border. PMI = point of maximal impulse. III. Asymptomatic patient. 3. Sixty percent of healthy term newborn infants have normal heart murmurs. ULSB = upper left sternal border. Persistent peaceful tachypnea should not be dismissed. Auscultatory features are characteristic of an innocent murmur. D.
wheezes. stabbing pain that improves when the patient sits up and leans forward. However. Hypertrophic obstructive cardiomyopathy is an autosomal dominant structural disorder. and pulsus paradoxus. adolescents are more likely to have pain associated with a psychogenic disturbance. and it is characterized by tenderness over the costochondral junctions. Cardiac infections are uncommon causes of pediatric chest pain. Musculoskeletal pain 1.of one outflow tract valve (aortic or pulmonary atresia). see page 182. decreased breath sounds on the affected side. there often is a family history of the condition. Supraventricular tachycardia is the most common arrhythmia. fever. vomiting and lightheadedness. 2. Crackles. Examination may reveal muffled heart sounds. References. Children with asthma. or tachycardia. c. An echocardiogram will confirm the diagnosis. tachypnea. asthma. The child usually is febrile. After a few days of fever. I. 3. 2. and has a friction rub. 2. . 2) an abnormal position of the great vessels (transposition of the great arteries or tetralogy of Fallot). a gallop rhythm. pneumonia. Young children are more likely to have a cardiorespiratory cause of their pain. Children may have a murmur that may be audible when standing or when performing a Valsalva maneuver. or decreased breath sounds are present. S p o n t a n e o u s pneumothorax or pneumomediastinum may occasionally cause chest pain with respiratory distress. and the electrocardiogram will be abnormal. Severe cough. A midsystolic click and a late systolic murmur may be detected. a. or pneumonia may cause chest pain because of overuse of chest wall muscles. persistent pulmonary hypertension). B. cystic fibrosis or Marfan syndrome are at high risk. Exercise-induced asthma may cause chest pain. Cardiac disease 1. therefore. 5. C. myocardial infarction can rarely result from anomalous coronary arteries.000 children who present to pediatric clinics. distant heart sounds. Respiratory conditions 1. Musculoskeletal pain is one of the most common diagnoses in children who have chest discomfort. the patient may develop pain or shortness of breath on exertion. or 3) pulmonary hypertension (ventricular defect. which can be confirmed with a treadmill test. Arrhythmias may cause palpitations or abnormalities on cardiac examination. or heart disease. The pain is sharp and exaggerated by physical activity or breathing. Costochondritis is common in children. Some children will have a pansystolic. 3. 3. b. Pericarditis presents with sharp. Mitral valve prolapse may cause chest pain secondary to papillary muscle or endocardial ischemia. Chest Pain in Children Chest pain is the presenting complaint in 6 per 1. neck vein distention. but premature ventricular beats or tachycardia also can cause episodes of brief sharp chest pain. is in respiratory distress. 4. Cardiac disease is a rare cause of chest pain in children. continuous or mitral regurgitation murmur or gallop rhythm that suggests myocardial dysfunction. such as cough. asthma. Myocarditis presents as mild pain that has been present for several days. Children frequently strain chest wall muscles while exercising. Trauma to the chest may result in a mild contusion or a rib fracture. Signs include respiratory distress. Chest radiography will show cardiomegaly in both of these infections. Differential diagnosis of chest pain in children A. The physical examination will reveal chest tenderness.
4. Exercise-induced chest pain may be caused by cardiac disease or exercise-induced asthma. rubs. E. Chronic pain is much more likely to have a idiopathic or psychogenic origin. Shingles may cause chest pain that precedes or occurs simultaneously with the rash. Physical examination 1. Pulmonary embolism is extremely rare in pediatric patients. Collagen vascular disorders may cause chest pain and pleural effusions. This condition is confirmed with a therapeutic trial of antacids. parental divorce. and worsened by reclining or eating spicy foods. 4. fever or palpitations associated with chest pain are signs of an organic etiology. Joint pain. 5. Oral contraceptives or recent abortion increase the risk. fever. Idiopathic chest pain. Mode of onset of pain. 7. Psychogenic chest pain may present with hyperventilation or an anxious appearance. Marfan syndrome may cause chest pain and fatal abdominal aortic aneurysm dissection. pleuritic pain. A radiograph confirms the diagnosis. Acute onset of pain is more likely to represent an organic etiology. Breast tenderness during puberty or early breast changes of pregnancy may present as chest pain. II. such as pneumothorax. Syncope. . A history and physical examination will reveal the etiology of chest pain in most cases. or Kawasaki disease. C. cough. muffled heart sounds or arrhythmias suggest a cardiopulmonary pathology. Abdominal tenderness may suggest abdominal pain that is referred to the chest. D.and palpable subcutaneous air. Burning pain in the sternal area suggests esophagitis. E. Coxsackievirus infection may lead to pleurodynia with paroxysms of sharp chest pain. 5. which is described as burning. substernal. 4. 3. 2. wheezes. Substance abuse (cocaine) or oral contraceptives should be sought in adolescents. but it should be considered in the adolescent girl who has dyspnea. and hemoptysis. Rales. muscle strain or choking on a foreign body should be sought. decreased breath sounds. 2. Reflux esophagitis often causes chest pain. Precipitating factors 1. Severe distress warrants immediate treatment for life-threatening conditions. Hyperventilation may be distinguished from respiratory distress by the absence of cyanosis or nasal flaring. Pallor or poor growth may suggest a malignancy or collagen vascular disease. murmurs. 2. Sickle cell disease may cause an acute chest syndrome. Miscellaneous causes of pediatric chest pain 1. D. The frequency and severity of the pain and whether the pain interrupts the child’s daily activity should be determined. 3. Stressful conditions at home or school should be sought. previous heart disease. F. A recent stressful event (separation from friends. Pain that wakes the child from sleep is more likely to be related to an organic etiology. 3. rash or fever may be suggested by the presence of collagen vascular disease. Family history may reveal familial hypertrophic obstructive cardiomyopathy. school failure) may often be related temporally to the onset of the chest pain. 6. 5. B. Trauma. 2. No diagnosis can be determined in 20-45% of cases of pediatric chest pain. Gastrointestinal disorders 1. Foreign body ingestion may cause chest pain when the object lodges in the esophagus. The history may reveal asthma. 4. 6. F. Clinical evaluation of chest pain A. Young males who have had recent leg trauma also are at risk. Sharp stabbing pain that is relieved by sitting up and leaning forward suggests pericarditis in a febrile child.
C. or subcutaneous air (pneumothorax or pneumomediastinum). and application of a heating pad. Children with chronic pain. Blood counts and sedimentation rates are of value if collagen vascular disease. analgesics. Musculoskeletal. Holter monitoring is warranted for syncope or palpitations. tenderness (musculoskeletal pain). Drug screening may be indicated in the older child who has acute pain associated with anxiety. respiratory distress. rest. a normal physical examination. III. A chest radiograph is warranted if the patient has fever. see page 182. F. arrhythmia. D.6. Referral to a cardiologist is recommended for children with known or suspected heart disease. Emergency department referral is necessary if the child is in severe distress or has a history of significant trauma. or click). References. Electrocardiography is recommended if the pain was acute in onset (began in the last 2-3 days) or if there is an abnormal cardiac examination (unexplained tachycardia. or abnormal breath sounds. syncope. or malignancy is suspected. murmur. Laboratory evaluation A. infection. or shortness of breath. tachycardia. Fever and cardiomegaly suggests pericarditis or myocarditis. or pain on exertion. B. G. a trial of antacids may be beneficial. C. The chest wall should be evaluated for bruises (trauma). Exercise stress testing or pulmonary function testing is appropriate for evaluation of cardiac disease or asthma. If esophagitis is suspected. palpitations. and no history suggestive of cardiac or pulmonary disease do not require laboratory studies. rub. B. Management of pediatric chest pain A. . psychogenic or idiopathic pain usually will respond to reassurance. hypertension. IV. E.
cystic fibrosis. shortness of breath. The FEV1 can be used for determining the degree of obstruction (mild. It declines in direct and linear proportion with clinical worsening of airways obstruction. including use of the accessory (eg. Wheezing may be heard in patients with mild. Postnasal drip syndrome can also lead to symptoms that include cough. Allergy skin testing involves prick skin tests. dyspnea. significant airway narrowing also may be present without wheezing. Albuterol) by metered-dose inhaler (MDI) is indicated during an initial work-up if baseline spirometry. Administration of a bronchodilator (eg. The classic triad of symptoms associated with asthma consists of cough. RAST involves blood measurement of the minute quantities of IgE antibody directed at particular antigens. I. moderate. and it increases with successful treatment of airways obstruction. which includes measurement of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC). Chest radiograph is almost always normal in patients with asthma. moderate. or severe airway narrowing. Differential diagnosis A. The presence or absence of wheezing on physical examination is a poor predictor of the severity of airflow obstruction in asthma. although they are not specific. and wheezing. and/or expectoration of phlegm. musical wheezes are characteristic of asthma. and viral bronchiolitis. There is a parental history of asthma in 50 percent of children with asthma. Its potential value is to detect rare complications and to exclude alternative diagnoses. B. sternocleidomastoid) muscles of breathing and a pulsus paradoxus. B. 2. high-pitched. Physical examination A. and cough. chest tightness. In children. The FEV1 reflects the average flow rate during the first second of forced vital capacity (FVC). IV. wheezing. Diagnosis of Asthma PEF (% personal best) or FEV2 (% predicted best) <60 Asthma diagnosis Step 4: severe persistent Step 3: moderate persistent Step 2: mild persistent Step 1: mild intermittent Days with symptoms* Continual Nights with symptoms Frequent Daily >5 times per month 3 to 4 times per month <2 per month >60 to <80 >2 times per week >2 times per week >80 >80 II. B. Physical findings that suggest severe airflow obstruction in asthma. Widespread. III. Drops of antigen-containing solution are placed in parallel rows on each forearm using a panel of up to 30 different allergens. 2. Laboratory testing A. Spirometry. Tests for allergy 1. is a useful pulmonary function test. breathlessness. History A. Various panels of antibodies can be ordered. considerations include foreign body aspiration. C. causing recurrent episodes of wheezing. . The FEV1 is the most important spirometric variable for assessment of airflow obstruction. 1.Allergic and Dermatologic Disorders Asthma Asthma is a chronic inflammatory disorder of the airways. or severe).
E. gastroesophageal reflux disease (GERD). V. Mast cell stabilizing agents such as cromolyn (Intal) and nedocromil (Tilade) are alternative medications for prevention of exercise-induced bronchoconstriction. and cough induced by angiotensin converting enzyme inhibitors. and beta-2 selectivity are recommended. Patients with mild intermittent asthma are best treated with an intermittent inhaled beta-2-selective adrenergic-agonist. D. Identifying and avoiding asthma "triggers" are essential in preventing asthma flare-ups. Two or fewer nocturnal awakenings per month. Common asthma triggers generally fall into the following six categories: allergens. C. Controlling trigger factors. pulmonary embolism. Symptoms of asthma occurring two or fewer times per week. including seasonal allergic rhinitis and conjunctivitis (“hay fever”). Patients for whom triggering of asthmatic symptoms can be predicted (eg. With the exception of aspiration. especially cigarette smokers. Mast cell stabilizing agents. post-viral tussive syndrome. PEFR measurement can be used to follow the impact of any relevant change in therapy upon lung function and to assess the severity of acute asthmatic exacerbations. irritants. Some illnesses are common comorbidities with asthma. respiratory infections. diffuse musical expiratory wheezing is not found in any of these other causes of persistent cough. perennial rhinitis. 4. considerations include COPD and heart failure. and post-nasal drip associated with rhinitis or sinusitis. the differential includes post-nasal drip. 2. recurrent or chronic sinusitis. In young and middle-aged adults considerations include bronchiectasis. Management of asthma A. Pharmacologic treatment of intermittent asthma. Monitoring. Short-acting inhaled beta-agonists. When persistent cough is the presenting complaint and the chest radiograph and lung function are normal. Cromolyn and nedocromil are effective when taken prior to an exposure but have no ability to relieve asthmatic symptoms once they have developed. In older patients. and emotional stress. PEFR >80 percent of predicted normal). . Regular monitoring of the peak expiratory flow rate (PEFR) should be encouraged in patients with moderate-to-severe asthma. Patients with mild intermittent asthma are defined as those who have: 1. and sarcoidosis. B. intermediate duration of effect (four to six hours). GERD. physical activity. 3. These medications provide additive protection when used in combination with a beta-agonist. C. Annual influenza vaccination is recommended for patients with asthma. 5. chemicals. exercise-induced bronchoconstriction) are encouraged to use their inhaled beta-agonist 10 minutes prior to exposure. Inhaled betaagonists with rapid onset of action. Peak-flow measurements when asymptomatic that are within the normal range (ie.B.
to mediumdose inhaled corticosteroid and long-acting bronchodilator (eg. 5-mg tab (Intensol). 5 mg per 5 mL. 1 inhalation q12h Albuterol SR (Volmax tablet.25 to 2 mg per kg per day) and reduce to lowest dosage. Serevent Diskus DPI) 2 puffs q12h. long-acting inhaled beta2 agonist or theophylline SR) Medication Short-acting bronchodilat or as needed: • Inhaled short-acting beta2 agonist or • Oral beta2 agonist Oral corticosteroids : Methylpredniso ne (Medrol). 5 mg/mL liquid Step 3: moderate.Stepwise Approach for Managing Asthma Asth ma Step 4: severe. persisten t Short-acting bronchodilat or as needed: • Inhaled short-acting beta2 agonist by nebulizer or spacer and face mask or • Oral beta2 agonist Short-acting beta2 agonist Albuterol (Airet nebulizer). 1-2 caps q4-6h PRN Long-acting beta2 agonist Salmeterol (Serevent MDI. once control is established • Low.5 mg in 3 mL q46h PRN (Proventil-HFA MDI) 2 puffs q46h PRN (Ventolin Rotacaps DPI). add systemic corticosteroids (0. 5 mg per 5 mL (Pediapred liquid). Daily anti-inflammatory medications. Proventil Repetabs) 4-8 mg bid Salmeterol/Fluti casone (Advair Diskus) 100 μg/50 μg 250 μg/50 μg 500 μg/50 μg 1 puff q12h . persis tent Quick relief Long-term control Daily anti-inflammatory medications: • High-dose inhaled corticosteroi d and • If needed. either: • High-dose inhaled corticosteroi d or. 2. 2-mg tablet Prednisolone (Prelone syrup). Prednisone 5-mg tablet (Deltasone).
450 mg (TR).5 mg q4-6h PRN . short-acting beta2 agonist or • Oral beta2 agonist No daily medication Drugs for Asthma Drug Formulation Dosage Inhaled beta2-adrenergic agonists. persis tent Quick relief Long-term control Daily anti-inflammatory medications Medication Short-acting bronchodilator as needed: • Inhaled short-acting beta2 agonist or • Oral beta2 agonist Inhaled corticosteroids • Beclomethaso ne (Beclovent MDI) 4-8 puffs bid (Vanceril DS MDI) 2-4 puffs bid • Budesonide (Pulmicort Turbuhaler DPI)1-2 inhalations bid. 2-4 puffs bid (Flovent Rotadisk) 1 bid. 10 mg qhs • Zileuton (Zyflo Flimtab). 4or 5-mg chewable tab.25 mg.5 mg. 1-2 bid. • Triamcinolone (Azmacort MDI) 4 puffs bid. 300 mg (SR). Pulmicort Respules. • Flunisolide (AeroBid MDI) 2-4 puffs bid • Fluticasone (Flovent). 20 mg bid • Montelukast (Singulair). 600-mg tab. 0. 24 puffs tid-qid • Nedocromil (Tilade) inhaler. short-acting Albuterol Proventil Proventil-HFA Ventolin Ventolin Rotacaps metered-dose inhaler (90 μg/puff) dry-powder inhaler (200 μg/inhalation) nebulized 2 puffs q4-6h PRN 1-2 capsules q46h PRN Albuterol Proventil multi-dose vials Ventolin Nebules Ventolin 2.5 mg in 3 mL q46h PRN (Proventil-HFA MDI) 2 puffs q46h PRN (Ventolin Rotacaps DPI). 600 mg qid • Cromolyn (Intal) inhaler. 2. 1-2 caps q4-6h PRN Step 1: mild.Stepwise Approach for Managing Asthma Asth ma Step 2: mild. interm ittent Short-acting bronchodilat or as needed <2 times per week: • Inhaled. 2-4 puffs bid-qid Short-acting beta2 agonist Albuterol (Airet nebulizer). Theophylline 200 mg. 10-mg tablet. 100300 mg bid Antileukotriene s • Zafirlukast (Accolate). 0.
2 puffs q12h 1 inhalation q12h Fluticasone/Sal meterol Advair Diskus 1 puff q12h Inhaled Corticosteroids Beclomethasone dipropionate Beclovent Vanceril Vanceril DoubleStrength Budesonide Pulmicort Turbuhaler Flunisolide AeroBid metered-dose inhaler (42 μg/puff) (84 μg/puff) dry-powder inhaler (200 μg/inhalation) metered-dose inhale r (250 μg/puff) metered-dose inhaler (44. 2. TheoDur.63-1.Drug Levalbuterol Xopenex Formulation nebulized Dosage 0. For adults.75 mg/puff) 2-4 puffs tid-qid tablets 10 mg qhs tablets 20 mg bid tablets 600 mg qid Nedocromil Tilade 2-4 puffs bid-qid Phosphodiesterase Inhibitor Theophylline Slo-Bid Gyrocaps. long-acting Formoterol Foradil Salmeterol Serevent Serevent Diskus dry-powder inhaler (12 μg/puff) metered-dose inhaler (21 μg/puff) dry-powder inhaler (50 μg/inhalation) dry-powder inhaler (100. Use of a spacer device (eg. Optichamber.25 mg q68h PRN Inhaled beta2-adrenergic agonist. Treatment of mild persistent asthma 1. or InspirEase) with the inhaled corticosteroids is recommended. Inhaled corticosteroids are administered twice daily. Unidur extended-release capsules or tablets 100-300 mg bid D. Asthmatic symptoms requiring relief with an inhaled bronchodilator more than once per week. 100 or 250 μg/inhalation) metered-dose inhaler (100 μg/puff) 4-8 puffs bid 2-4 puffs bid 1-2 inhalations bid 2-4 puffs bid Fluticasone Flovent Flovent Rotadisk 2-4 puffs bid (44 μg/puff) 1 inhalation bid (100 μg/inhalation) Triamcinolone acetonide Azmacort 2 puffs tid-qid or 4 puffs bid Leukotriene Modifiers Montelukast Singulair Zafirlukast Accolate Zileuton . a. the most frequently recommended choice of anti-inflammatory therapy is an inhaled corticosteroid. Observed fluctuations in PEFR of more than 20 percent. Inhaled corticosteroids. Aerochamber. 110 or 220 μg/puff) dry-powder inhaler (50. c. Ellipse. It is appropriate to begin regular treatment with anti-inflammatory medications when a patient has one of the following: a. Nocturnal awakenings as often as once every two weeks. 250 or 500 μg/puff) 1 puff bid.Zyflo Mast Cell Stabilizers Cromolyn Intal metered-dose inhaler (800 μg/puff) metered-dose inhaler (1. The triamcinolone acetonide MDI is manufactured . b.
4. Leukotrienes (leukotriene C4. The leukotriene-receptor antagonists inhibit the action of leukotrienes at their receptor. Hoarse voice and sore throat are less common side effects. Absorption is optimized by ingestion on an empty stomach. c. The budesonide Turbuhaler is not appropriate for use with a spacer. A second member of this drug category. Suppression of the hypothalamic-pituitary-adrenal axis can also occur. A small incidence (2 to 4 percent) of hepatic inflammation is associated with zileuton. b. 5lipoxygenase enzyme inhibitors block production of leukotrienes. Nocturnal awakenings more than once per week. Treatment with cromolyn and nedocromil requires compliance with a QID dosing schedule. a. Long-acting beta-agonists are not recommended as monotherapy for mild asthma. Fluticasone (Flonase) 110 or 220 µg/puff or budesonide (Rhinocort) 200 µg/inhalation provides potent topical corticosteroid therapy for moderate asthma with the convenience . d. Patients whose asthma is well controlled with nedocromil taken four times daily can gradually reduce the dosing schedule to twice daily. The development of asthmatic attacks that interfere with activity. D4 and E4) are potent chemical mediators of the allergic response in asthma. resulting in an increase in the prothrombin time. The only significant drug interaction is with warfarin. b. cromolyn and nedocromil. Zafirlukast (Accolate) is orally administered. Twice-daily dosing provides 24-hour bronchodilation. leading to the recommendation that liver function tests be checked before initiating therapy. monthly for the first three months of therapy. Treatment of moderate persistent asthma. Daily need for bronchodilator medications. The presence of any of the following is considered an indication of moderate disease: Daily symptoms of asthma. its relatively long half-life permits twice-daily dosing. 3. It is administered orally on a QID schedule. Salmeterol (Serevent) and formoterol (Foradil) are inhaled betaadrenergic agonists with a duration of action of at least 12 hours. are alternative choices when initiating regular preventive therapy in mild asthma. montelukast (Singulair) is suitable for once-daily dosing. Mast cell stabilizing agents a. This complication is infrequent when inhaled corticosteroids are administered with spacers and when patients rinse their mouths with water immediately after use. b. Leukotriene-modifying agents. and at three. Drug interactions include warfarin (increased prothrombin time) and theophylline (increased serum concentration). These drugs are particularly well suited to use in patients who refuse to use of any steroid preparation. E. Patients receiving regular anti-inflammatory therapy should continue to use their inhaled bronchodilator as needed for relief of symptoms and prior to exposure to known triggers of their symptoms. Long-acting inhaled beta-agonists. 1. The mast cell stabilizing agents. High-dose inhaled steroid.to sixmonth intervals thereafter. Adverse effects related to the eye and to skeletal metabolism are some of the more serious potential consequences of inhaled corticosteroid use. A short-acting beta-agonist should be used as needed. Zileuton (Zyflo) inhibits production of leukotrienes by interfering with metabolism of arachidonic acid by 5-lipoxygenase. Long-term use of inhaled corticosteroids in the doses recommended for mild asthma is generally well tolerated. PEFR 60 to 80 percent of normal. Cromolyn and nedocromil appear to be somewhat less effective than inhaled corticosteroids in controlling asthma. F. Oral candidiasis (thrush) is the most common side effect from the use of inhaled corticosteroids.with an attached spacer.
The major disadvantages of these drugs include the frequency of side effects. Atopic dermatitis affects 10 percent of children. References. B. Chronically involved areas become thick and fibrotic. Long-acting inhaled beta-agonists. The symptoms of atopic dermatitis resolve by adolescence in 50 percent of affected children. G. or 500 mcg per inhalation). a narrow therapeutic window. Atopic Dermatitis and Eczema Atopic dermatitis is a chronic inflammation of the skin that occurs in persons of all ages but is more common in children. (4) Possibly increased bone loss.of 2 to 4 puffs twice daily. Addition of a lipoxygenase inhibitor or leukotriene-receptor antagonist may improve asthma control (and permit reduction of the dose of inhaled corticosteroids) in moderate or severe asthma. or air pollutants. I. Long-acting oral bronchodilators. Attention to theophylline pharmacokinetics is essential in order to avoid toxicity. has an FEV1 below 60 percent of predicted. The patient with severe chronic asthma has frequent asthma exacerbations as a result of viral illnesses. Theophylline is a reasonable alternative for patients who are intolerant of long-acting betaagonists or who are unable to use a metered dose inhaler properly. including inhaled steroids at moderate-to-high dose or continuous. In patients requiring dual therapy. 3. 4. Lesions can develop secondary infections with crusting and weeping. Leukotriene-modifying agents. . Acute lesions are papules and vesicles on a background of erythema. Exposure to aeroallergens. see page 182. (2) Cataracts. The steroid dose is variable (100. Advair Diskus. and relative lack of bronchodilator potency b. combined dry powder formulations allow simultaneous delivery of both a corticosteroid and a long-acting beta-agonist (eg. Theophylline and sustained-release albuterol tablets are effective disease controllers when used in combination with regular anti-inflammatory therapy. Xerosis (dry skin) is characteristic. a. 2. Seretide. (3) Growth retardation. is usually awakened from sleep four to seven nights per week. Treatment of severe asthma. every-other-day or multiple-short courses of oral steroids. irritating chemicals. Diagnosis A. foods and emotional stress may worsen the rash. High doses of inhaled corticosteroids (greater than 1000 to 1500 µg/day) may cause several adverse systemic effects after long-term use: (1) Increased intraocular pressure. These individuals usually require multiplecontroller medications and bronchodilator medications used on a regular basis. Symbicort). allergens. 250. exercise. (5) Hypothalamic-pituitary-adrenal axis suppression. Subacute lesions may develop scales and lichenification. a. and is unable to achieve normal lung function despite chronic treatment with multiple medications.
D. ointment. Aquaphor. neck. 2. Tricyclic antidepressants such as doxepin (Sinequan) and amitriptyline (Elavil) also induce sleep and reduce pruritus. 0. and cotton gloves can be worn at night. cream.1% Betamethasone dipropionate cream (Diprosone).Diagnostic Features of Atopic Dermatitis Major features Pruritus Chronic or relapsing dermatitis Personal or family history of atopic disease Typical distribution and morphology of atopic dermatitis rash: Facial and extensor surfaces in infants and young children Flexure lichenification in older children and adults Minor features Eyes Cataracts (anterior subcapsular) Keratoconus Infraorbital folds affected Facial pallor Palmar hyperlinearity Xerosis Pityriasis alba White dermatographism Ichthyosis Keratosis pilaris Nonspecific dermatitis of the hands and feet Nipple eczema Positive type I hypersensitivity skin tests Propensity for cutaneous infections Elevated serum IgE level Food intolerance Impaired cell-mediated immunity Erythroderma Early age of onset C.1% (Valisone) Hydrocortisone valerate cream.1% (Elocon) Fluocinolone acetonide ointment. Older children and adults typically have involvement of the flexor surfaces (antecubital and popliteal fossa). 0. Basis. Dove. fingernails should be cut short. 0. 0. II. Exposure to pollens. 0. Lotions are least effective because of their alcohol content. molds. Vaseline. Eucerin. 0. A mild cleanser (eg. 1. Commonly Used Topical Corticosteroids Preparation Low-Potency Agents Hydrocortisone ointment. Ointments are superior to creams. a more potent steroid is needed.2% (Westcort) 60 g 45 g 45 g 60 g 45 g 60 g 60 g 60 g 60 g 30 g Size . ointment.01% (Synalar) Medium-Potency Agents Triamcinolone acetonide ointment (Aristocort A). face (cheeks and chin) and extensor surfaces of the extremities. pruritus commonly is present on the scalp. After bathing.05% Mometasone cream 0.05% (Aclovate) Triamcinolone acetonide cream.Treatment A. Pruritus that is refractory to moisturizers and conservative measures can be treated with sedating agents such as hydroxyzine (Atarax) and diphenhydramine (Benadryl). mites and animal dander may be important in some patients. mineral oil or baby oil). B. Soap should not be used unless it is needed for the removal of dirt.5% (Hytone) Mild-Potency Agents Alclometasone dipropionate cream. Systemic corticosteroids should be reserved for use in patients with severe treatment-resistant atopic dermatitis. Bathing and moisturizers. patients should apply a moisturizer liberally (eg. 0. In infants and young children.025% (Synalar) Betamethasone valerate cream. D. Kiss My Face or Cetaphil) may be used.1% (Aristocort) Fluocinolone acetonide cream. C. wrists and ankles. 0. Moisturel. To avoid injury to the skin from scratching. It is reasonable to use a mild topical steroid initially in infants and for intertriginous areas in patients of any age. If the dermatitis is severe. Bathing should occur once daily with warm water for five to 10 minutes.
Commonly Used Topical Corticosteroids . 3. Common causes of irritant contact dermatitis include overbathing. Contact with irritants 1. drooling. and lip licking is recommended. Eucerin. groin. Treatment of contact dermatitis A. Infants and children have rashes on the shoulders. II. Contact Dermatitis Contact dermatitis is an extremely common in the pediatric age group. The lower strength may be used in children >2 years old. A corticosteroid will usually bring improvement. Children older than 18 months old tend to have rashes on the neck and antecubital and popliteal fossae.E. but the potency should be tapered after the dermatitis is controlled. edematous papules and small vesicles. Tacrolimus is available in 0. Corticosteroid creams may sting when applied to acute lesions. Topical corticosteroids 1. with few adverse effects. There are two major forms of contact dermatitis: irritant and allergic. see page 182. Vaseline) to noninflamed skin. Contact dermatitis usually resolves by puberty. B. chest. The condition returns after the cessation of therapy. Showers or baths should be limited to no more than 5 minutes. abdomen. References. Pimecrolimus has anti-inflammatory activity. red. 2. The FDA has issued warnings about a possible link between the topical calcineurin inhibitors and cancer. High-potency steroids may be used for flare-ups. B. Cyclosporine (Sandimmune) has been effective in patients with refractory atopic dermatitis. Topical application is comparable to that of a potent topical steroid.03%. Clinical evaluation A. Avoidance of excessive bathing. Infants usually also have a rash on the face. prolonged contact with moisture and feces in the diaper. After bathing. C. Ivory. Tacrolimus (Protopic) is more potent than pimecrolimus in the treatment of severe or refractory atopic dermatitis. resulting from drooling. Corticosteroid ointments maintain skin hydration and maximize penetration. Infants often have bright red exudative contact dermatitis (slobber dermatitis) on the cheeks. 2. and susceptibility to bruising. It does not cause skin atrophy. rebound erythema. but it sometimes recurs at times of stress. 3. patients should apply a moisturizer (Aquaphor. Overuse of soap should be discouraged. 1% pimecrolimus cream is applied twice daily. Neutrogena) should be limited to the axilla. The FDA has issued warnings about a possible link between the topical calcineurin inhibitors and cancer. It also may be useful in patients who have atopic dermatitis and experience a flare or persistence of disease despite appropriate therapy. atopic dermatitis. although not always at the original level of severity. Chronic rubbing and scratching may cause lichenification and hyperpigmentation. Moisture. and feet. which may progress to weeping and crusting lesions. Use of high-potency agents on the face. C. It may be used in children >2 years old. Immunosuppressants and antineoplastics 1. genitalia and skinfolds may cause epidermal atrophy (“stretch marks”). localized reactions. and bubble baths. scalp and around the ears. hand washing. and back. 2. Use of nonirritating soaps (eg. Dove. Contact dermatitis usually first appears in infants 2-6 months of age. Acute lesions are itchy. Patch testing is useful for evaluation of persistent. I. Pimecrolimus (Elidel) is a non-steroid cream for the treatment of mild to moderate eczema. Mid. hands.1% and 0.and low-potency topical corticosteroids are used twice daily for chronic.
are somewhat useful for pruritus and are sedating. .5% (Hytone) Mild-Potency Agents Alclometasone dipropionate cream. 1-2 mg/kg. Nonsedating antihistamines. cream. such as diphenhydramine or hydroxyzine (Atarax).1% Betamethasone dipropionate cream (Diprosone). The peak incidence is between 9 and 12 months of age. 0. References. 0. Prednisone. 0.05% Mometasone cream 0. It varies in severity from mild erythema (with or without scales) to papules and macerated lesions. or ketoconazole III. such as cetirizine (Zyrtec). Allergic reactions to topical corticosteroids may occur. including the buttocks. 0. 0. 0. Management (1) Irritant diaper dermatitis can best be prevented by keeping the skin in the diaper area protected from urine and feces by increasing the frequency of diaper changes and by using superabsorbent disposable diapers.01% (Synalar) Medium-Potency Agents Triamcinolone acetonide ointment (Aristocort A). 0.1% (Cyclocort) Betamethasone dipropionate ointment (Diprosone) 0. Anticandidal agents such as nystatin (Mycostatin). D. see page 182. Diaper Dermatitis Diaper rash occurs in 50% of infants.05% (Aclovate) Triamcinolone acetonide cream. 0. ointment. 0. It is accentuated on the convex areas. or genitals.1% (Aristocort) Fluocinolone acetonide cream. 2. sparing the creases.025% (Synalar) Hydrocortisone butyrate 0. Antihistamines. and upper thigh. or for severe involvement of the hands. with 5% having severe rash. widespread reactions to poison ivy. 1. clotrimazole (Lotrimin). The frequency and severity of diaper dermatitis are significantly lower when the number of diaper changes per day is eight or more. E. Pathophysiology. is given PO and tapered over 10-18 days.1% cream. Superabsorbent disposable diapers significantly reduce the severity of diaper rash when compared to cloth diapers. ointment. a.Preparation Low-Potency Agents Hydrocortisone ointment. lower abdomen. 0. Breast fed infants have fewer diaper rashes than formula-fed infants. face. Systemic corticosteroids are reserved for severe. Classification of diaper dermatitis A.1% (Valisone) Hydrocortisone valerate cream. are helpful. Dermatoses related to diaper wearing 1. IV. Irritant diaper dermatitis is the most common form of diaper dermatitis.1% (Elocon) Fluocinolone acetonide ointment. ointment (Locoid) Betamethasone valerate cream.05% (Lidex) Size 30 g 60 g 60 g 60 g 60 g 45 g 45 g 60 g 45 g 45 g 60 g 60 g 45 g 60 g 4. genitalia. ointment.2% (Westcort) High-Potency Agents Amcinonide ointment. Mometasone (Elocon) is the least likely to cause an allergic reaction. loratadine (Claritin) and fexofenadine (Allegra). (2) A low-potency corticosteroid ointment (hydrocortisone 1%) should be applied four times daily with diaper changes.05% Fluocinonide cream.
called a dermatophytid or “id” reaction. clotrimazole (Lotrimin). Hydrocortisone 1% ointment may help decrease erythema and inflammation and can be applied at the same time. Oral nystatin (Mycostatin) suspension. Examination reveals red. which almost always involve the inguinal creases. Dermatophyte hand infection presents as dry scale on the palm. arcs. KOH scrapings may demonstrate pseudohyphae. (3) Thickly applied barrier creams. Griseofulvin is preferred for initial treatment at a starting dose of about 20 mg/kg per day. or annular patterns. and hair loss (kerion). miconazole (Monistat). or ketoconazole (Nizoral) applied 3-4 times daily. purulence. Dermatophyte infection often leads to secondary bacterial infection. 2. Clearing in previously affected areas produces the typical “ringworm” appearance. neck. Topical therapy is the initial treatment approach. Candidiasis is treated with topical nystatin (Mycostatin). The web spaces become red and scaly. zinc oxide pastes or Vaseline. C. Tinea capitis presents as inflammation with hair breakage and loss. Dermatophyte Infections Dermatophytes constitute a group of about 40 fungal species that cause superficial infections called dermatophytoses. It often develops after an episode of diarrhea. Topical therapy and keeping the involved areas as dry as possible is recommended for hand or foot tinea. B. oral fluconazole (Diflucan) 3 mg/kg per day as a pulse dose weekly x 2 or for a short course of 5 to 7 days may be of benefit. and proximal extremities. trunk. B. A hypersensitivity reaction to fungal antigen can develop. and scaling or with a “pityriasis rosealike” reaction that involves red. References. Tinea pedis and tinea manuum A. superficial edema involving the epidermis. edema. four times a day. The mother should be evaluated for candidal infection of the nipples or genital tract. In severe cases. Tinea capitis is contagious until after 2 weeks of systemic treatment. Candidal diaper dermatitis a. Tinea pedis infection is often interdigital and is induced by the warmth and moisture of wearing shoes. Fungal infection frequently spreads to involve the soles of the feet or the palms. Vesicle and blister formation and itching are common. b. may be helpful. Infection of just one hand in conjunction with infection of both feet is the most common pattern. . should be used if repeated episodes of candidal dermatitis occur. as described for tinea capitis. Tinea corporis (ring worm) and tinea cruris A. Topical antifungals are not effective for hair infection. Selenium sulfide shampoo (Selsun Blue) is used in conjunction with oral antifungals to reduce contagion. or tinea. C. such as A&D ointment. D.(Nizoral) should also be added. with dry scale and minimal redness. Dermatophytid reactions can be treated with topical corticosteroids. Scaling extends to the side of the foot or hand. Tinea cruris describes infection of the upper thigh and inguinal area. Dermatophyte infection of the body surface is termed tinea corporis. see page 182. A dermatophytid reaction may occur. scaly papules and small plaques. Oral therapy may be necessary for recalcitrant disease. III. B. These progressively enlarge to form expanding rings. scaly papules and ovoid plaques on the face. ringworm. Tinea capitis A. D. I. Candidal diaper dermatitis is characterized by beefy red plaques with white scales and satellite papules and pustules. Inflammatory changes can range from minimal scaling and redness that resembles mild seborrhea to tenderness. II. redness. Id reactions can present with either a dermatitis that includes redness.
or nail is the most rapid diagnostic method. Oral griseofulvin is effective and safe for treatment of tinea capitis in children. or nail from a possibly infected area is placed on a glass slide. Tab: 250 mg Topical Treatments for Tinea Pedis. Treatment should be continued for 8 to 12 weeks. hair. Microsize: Cap: 250 mg. Onychomycosis (tinea unguium) A. Fungal culture of scale and affected hair or nail can be accomplished by incubation at room temperature for 2 to 3 weeks. ridging. Dermatophyte infection of the nail plate is referred to as onychomycosis.IV. hair. A sample of scale. 330 mg Itraconazole (Sporanox) 4 to 6 mg/kg per day. Diagnosis A. B. Mycelex) Miconazole 2 percent (Micatin. thickening. Treatment A. its erratic oral absorption necessitates doses of about 20 mg/kg per day of the liquid preparation. VI. 250. However. MonistatDerm) Econazole 1 percent (Spectazol e) Ketoconaz ole 2 percent (Nizoral) Oxiconazol e 1 percent (Oxistat) X X X X Twice daily X X X X Twice daily X Once daily X X X Once daily X X X Once daily or twice daily Allylamines Naftifine 1 percent (Naftin) X X Once daily or twice daily . Systemic Antifungal Agents Griseofulvin 20 mg/kg per day of microsize liquid or 7 to 10 mg/kg per day of ultramicrosize tablets. V. B. and gently heated. Adverse effects associated with griseofulvin include headaches and gastrointestinal upset. Ultramicrosize griseofulvin can be administered at the lower dose of 8 to 10 mg/kg per day. susp: 125 mg/5 mL. 500 mg Ultramicrosize: Tab: 125. Potassium hydroxide (KOH) examination of scale. tab: 250. accumulation of debris beneath the distal aspect of the nail and little or no inflammation. characterized by dystrophy of the nail. breakage. but recurrence is very common. B. soln: 10 mg/mL Terbinafine (Lamisil) 3 to 5 mg/kg per day. 165. Oral treatment is required to clear infection. Tinea Cruris and Tinea Corporis Antifungal agent Pres cription Cre am Sol utio n or spra y Lot ion Pow der Freque ncy of application Imidazoles Clotrimazol e 1 percent (Lotrimin. discoloration. fragility. Liver function testing is not required when griseofulvin is used for 6 months or less. always administered with a fatty meal or beverage (such as milk). covered with a few drops of 30% KOH. The specimen is examined for spores and/or fungal hyphae. Cap: 100 mg.
Newer. Asymptomatic virus shedding may transmit the disease. nonoral or non-genital skin lesions. Virology and pathogenesis A. Two types of HSV exist: HSV-1 and HSV-2. I. HSV-1 may cause asymptomatic infection. nongenital skin lesions. irritability. and secretions. a substantial number of patients experience frequent painful recurrences or severe or lifethreatening illnesses. neonatal disease. Cap: 100 mg.5% can be added to antifungal therapy to reduce inflammation. which includes varicella zoster virus. Like all herpes viruses. mucous membranes. Both types can infect any anatomic site. Transmission A. 2. B. References. The illness is self-limited and usually of short duration. characterized by fever. encephalitis. Herpes Simplex Virus Infections HSV is a member of the herpes-virus family. oral lesions. Most HSV-infected patients have asymptomatic infections or the symptoms are only mildly uncomfortable. Primary infections cause more severe symptoms and signs. meningitis. Itraconazole (Sporanox) is effective and can be given orally at 3 to 5 mg/kg per day for 4 to 6 weeks or until clearing. B. vesicular. Oral/facial HSV infections 1. HSV-2 may cause asymptomatic infection. Many HSV infections are asymptomatic. and genital lesions C. 3. Hydrocortisone 1% or 2. Many individuals who have oral HSV lesions have no known history of prior gingivostomatitis. neonatal disease. However. F. Topical antifungals can be used once to twice daily to clear infections other than tinea capitis and onychomycosis. see page 182. Genital HSV infections 1. malaise. D. nonoral. and cervical adenopathy. pharyngitis. genital lesions. including extensive skin lesions. or ulcerative lesions with pain. Women who have had previous genital HSV-2 infection shed virus on 2% of days. but they can also cause papular. more potent topical agents with once-daily dosing can improve compliance.Topical Treatments for Tinea Pedis. and dysuria. and oral lesions II. myalgia. C. HSV-2 also may cause oral lesions and pharyngitis. particularly in sexually active individuals. The most common clinical manifestation of primary HSV-1 infection is gingivostomatitis. ten- . Tinea Cruris and Tinea Corporis Antifungal agent Pres cription Cre am Sol utio n or spra y X Lot ion Pow der Freque ncy of application Terbinafine 1 percent (Lamisil) X X Once daily or twice daily Once daily or twice daily Butenafine 1 percent (Mentax) X C. itching. HSV-1 and HSV-2 are transmitted from person to person through contact with infected skin lesions. urethral or vaginal discharge. Epstein-Barr virus. and both types may be transmitted in utero or perinatally. Tab: 250 mg E. followed by a 4-week period off of therapy. Affected areas should be kept as cool and as dry as possible. The incubation period is 1 to 26 days. Recurrent HSV-1 infections are most frequently characterized by oral and lip lesions. HSV-1 infection is extremely common in infants and children. soln: 10 mg/mL D. HSV tends to establish latent infection and eventually it reactivates and becomes infectious. 2. A liquid formulation is available. Terbinafine (Lamisil) orally at 3 to 6 mg/kg per day for 4 to 6 weeks is effective. and cytomegalovirus.
Polymerase chain reaction (PCR) can detect HSV DNA in CSF. Most patients who have genital HSV infection have few symptomatic recurrences. Seventy to 80% of infected infants are born to mothers who are unaware that they have genital HSV infection. Ninetyfive percent of cases are caused by HSV-1. a. headache. Disseminated HSV disease should be considered in any infant presenting with sepsis that is unresponsive to antibiotic therapy. 3. HSV is the most common cause of corneal blindness. HSV CNS disease has a 50% mortality if not treated. Infection in neonates results from vertical transmission during the peripartum period in 85%. HSV encephalitis 1. Disseminated disease is characterized by hepatitis. The diagnosis must be considered in any infant who presents with encephalitis. SEM disease most commonly presents in the first or second weeks of life with vesicular skin lesions which may occur anywhere on the body. 5. bradycardia. and it accounts for 35% of peripartum infections. or cranial nerve abnormalities. Neonatal HSV CNS disease most commonly presents in the second to third week of life. Topical steroids are contraindicated because they may facilitate spread of infection to the deep structures of the eyes. Only 60% will develop skin lesions during the illness. b. and extragenital lesions. Early initiation of therapy is critical when the diagnosis is suspected. with spike and slow wave activity localized to the temporal region. with treatment. a. substantial morbidity and mortality occurs. apnea. 2. abdominal pain. CT scan and MRI may reveal localized edema and hemorrhage suggestive of HSV infection. Eighty percent of persons who have a first episode of HSV-2 genital infection will experience a recurrence in the first year. Primary infections are often associated with fever. Routine CSF findings are not diagnostic. 4. Cerebrospinal fluid findings are nonspecific and include pleocytosis and increased protein. HSV disseminated disease presents in the first week of life. or who has both pneumonitis and hepatitis. although 30% of cases are caused by HSV-1. The incidence peaks at 5 to 30 years and at more than 50 years. The prognosis for HSV encephalitis without treatment is poor. and even with antiviral therapy. E. Most neonatal infections are caused by HSV-2. Seventy percent of untreated infants will progress to disseminated or CNS disease. and aseptic meningitis. Central nervous system disease is manifest as encephalitis. and disseminated intravascular coagulation. Skin lesions may not be present initially. 4. altered mental status. seizures. malaise. HSV encephalitis is characterized by acute fever. eye. Neonatal HSV infections 1. Skin. Eye infections a. Prompt institution of empiric therapy is essential when the clinical diagnosis is suspected. If the infection does not progress to involve the CNS or viscera. b. F. in utero or postpartum transmission rarely occurs. and it accounts for 20% of peripartum infections. pneumonitis. Bilateral patchy infiltrates are indicative of pneumonitis. Skin lesions have an erythematous base with clear or cloudy fluid. mortality is 18%. 2. 3. b. SEM disease has a low mortality. Electroencephalographic (EEG) findings can be diagnostic. HSV keratitis is characterized by conjunctivitis and dendritic lesions of the cornea. .der inguinal adenopathy. 5. mouth (SEM) disease accounts for 45% of peripartum infections. 3. HSV encephalitis is the most common viral infection of the CNS. HSV is rarely isolated by culture of the CSF. and focal neurologic symptoms and signs.
C. V. 3. Oral acyclovir has limited effect on the resolution of recurrent HSV disease. with a sensitivity of 75% and a specificity of 100%. Oral acyclovir decreases new lesion formation and improves symptoms in first episode genital HSV. Virus cultures of the infant’s conjunctivae. 2. U rticaria. Sexually active individuals known to have genital HSV infection should be advised to use latex condoms even during asymptomatic periods. E. In cases of recurrent disease. and genital lesions. The adult regimen is 400 mg three times a day. they should be placed in contact isolation. A thorough physical examination. and non-localized infections in immunocompromised patients. skin folds. Suppressive therapy is also used for infants who have HSV SEM disease. Angi o e d e m a Anaphylaxis and Urticaria. D. B. Dosage for first episodes of genital HSV infection is 250 mg q8h for 5 days. F. Immediate hypersensitivity is an antibody mediated reaction that occurs within minutes to hours of exposure to a particular antigen by an immune individual. such as neonatal HSV infection. at the onset of labor should exclude the presence of active genital lesions. staining for virus antigens with fluorescent antibodies detects HSV more rapidly. prompt cesarean section is recommended. Parenteral acyclovir is indicated for severe or potentially severe infections. PCR is a useful diagnostic procedure for HSV encephalitis. virus shedding may be too brief to be detected by virus culture. It has a more convenient dosage schedule than acyclovir and is approved for adolescents. S u p p r e s s i o n is indicated for immunocompromised patients or patients who have more than 6 genital recurrences a year. I. If HSV lesions are found during labor. especially urticaria. HSV encephalitis. References. 5 mg/kg q8h or 400 mg bid. pharynx. Acyclovir (Zovirax) 1. Famciclovir (Famvir) has a more convenient dosage schedule than acyclovir and is approved for adolescents. Circumcision is deferred. 5-10 mg/kg IV is given q8h for 10 to 21 days. C. and anaphylaxis are manifestations of the immediate hypersensitivity reaction. 1 gm orally twice a day for 5 days. Therapy for HSV infections A. Although less sensitive and specific than culture. including vaginal speculum exam. HSV-1 and HSV-2 can be isolated by virus culture from active skin. Valacyclovir (Valtrex) is an ester of acyclovir that has better oral absorption. Management of infants exposed to HSV at delivery 1. 2. see page 182. Pathophysiology . Herpes simplex is rarely is recovered from CSF by culture. CSF.III. Diagnosis of HSV infection A. Topical acyclovir is not effective for skin or oral lesions. Infants who are culture positive for HSV from any site after 24 hours of life are given acyclovir. Management of perinatal HSV infection A. IV. Oral acyclovir dosage is 20 mg/kg every 8 hours or 200 mg five times a day for 7-10 days. B. During the time when HSV-exposed infants are in the hospital. and for recurrent episodes it is 125 mg twice a day for 5 days. angioedema. The ophthalmic solution is useful for HSV keratitis. eye. Twenty percent of the population will have one of these manifestations. B. The most reliable predictor of the risk of perinatal transmission is whether a woman has active genital lesions at the time of delivery. C. in combination with IV acyclovir. Doses up to 20 mg/kg IV q8h are used for infants who have CNS or disseminated infection. at some time during life. and rectum at 24-48 hours can indicate whether HSV has been transmitted. For serious infections. such as neonatal disease and encephalitis.
chemicals and physical agents (detergents or ultraviolet light) can cause urticaria. should be given via nebulizer every 4-6 hours. Anaphylaxis is best prevented by avoidance of the cause.0 mg/mL) should be injected at 10-20 min intervals at 0. E. These usually cause hive formation for only a few hours to two days. Angioedema is similar to hives. and hypotension. 4.01 mL/kg SQ per dose. The lesions often develop after exercise. or drugs. exposure to heat.A. II. irregularly shaped wheals. bronchospasm. and drugs (opiates.3 mL per dose SQ. and it is treated with sun screens. 2. Symptoms of anaphylaxis include pruritus. anaphylaxis frequently is unanticipated. Mannitol. Urticaria A. Treatment of acute anaphylaxis 1. 1. vancomycin) may degranulate mast cells and cause a reaction that resembles anaphylaxis. Exercise urticaria is characterized by hives and bronchospasm after exercise. Angioedema A. Cold urticaria may be induced by exposure to cold. Oxygen should be administered (100%.5 mg/kg is the most effective treatment. Antigens. It may be caused by the same mechanisms that cause hives except that the immunologic events occur deeper in the cutis or in the submucosal tissue of the respiratory or gastrointestinal tract. insect venoms. particularly after exposure to cold or hot water or alcohol ingestion. Angioedema is often ac- . Treatment of urticaria. However. B. 3. eggs. Anaphylactoid reactions are not immunologically mediated. B. 5 frequently is found in patients with salicylate sensitivity. and products of animal origin. injection of the mucous membranes. Diphenhydramine 1. antitoxins to tetanus. 0. The wheals have a blanched center. IV. D. Individuals with a history of anaphylaxis should be provided with injectable epinephrine. Short-term desensitization may be needed in a patient requiring antibiotic treatment. These small papular urtications are pruritic and appear predominantly on the neck and upper thorax. 4 L/min) and the airway should be secured. Causes of anaphylaxis include penicillins.1-0. F.2 mL/kg in a 5 mg/mL solution. Cholinergic urticaria is characterized by the appearance of small punctate wheals. C. foods (peanuts. Genetic deficiencies of complement factor H or factor I may cause urticaria. Epinephrine in a 1:1000 dilution (1. Sensitivity to the food additive tartrazine yellow No. It causes diffuse circumscribed swelling. Urticaria generally is a selflimiting disorder and usually requires only antihistamines. or anxiety. Hydroxyzine 0. milk. Solar urticaria may be caused by various wavelengths of light (280-500 nm). Anaphylaxis is the acute reaction that occurs when an antigen is introduced systemically into an individual who has preexisting IgE antibodies. Anaphylaxis A. D. C. surrounded by a red flare. H. Angioedema is an area of circumscribed swelling of any part of the body.25 mg/kg every 6 hrs is also effective. Hives most commonly results from ingestion of foods. radiocontrast material. food additives. Prevention of anaphylaxis. Administration of diphenhydramine or chlorpheniramine and corticosteroids should be considered when a complete response to epinephrine does not occur. III. sweating. The patient has difficulty breathing from constriction of the major airways and shock due to hypotension caused by histamine release. with a maximum dose of 0. It is uncommon. Urticaria (or hives) is an intensely itchy rash that consists of raised. G. airborne allergens. B. C. and food dyes and flavors). Albuterol. 2. Patients who have these defects frequently develop severe hives. seafoods. but the reaction occurs deeper in the dermis. surrounded by a prominent erythematous flare. which may result in hypotension after immersion in cold water. Chronic urticaria is caused by ingestion of food substances that contain natural salicylates.
or steroids. about 10% of cases are caused by new spontaneous mutations. 50-300 mg/day. analgesics. Treatment consists of supportive therapy with IV fluids. at a dose of 2 mg/day.quired. Attacks of palatal and laryngeal edema may follow dental trauma or occur during upper respiratory infections. HANE is inherited as an autosomal dominant disease. Attacks of severe abdominal cramps and vomiting may be caused by edema of the bowel wall. antihistamines. can prevent attacks of angioedema. C. and death. 4. Stanozolol. Fresh frozen plasma is generally effective. HANE is characterized by episodes of localized subcutaneous edema of any part of the body. 2. or danazol. References. However. and airway management. which are passed to offspring. Hereditary Angioneurotic Edema (HANE) 1. B. pulmonary edema. Severe attacks of colic may occur during infancy. Prophylaxis against attacks of angioedema can be achieved with impeded androgens (ie. Acute angioedema does not generally respond to epinephrine. . 3. androgens that are only minimally virilizing). or it may be observed in an inherited disease known as hereditary angioneurotic edema (HANE). Laryngeal edema may sometimes progress to total upper airway obstruction. see page 182.
varicella. such as croup. Acute fever is defined as <7 days in duration. When the history and physical examination cannot identify a specific source of fever in an acutely ill. >39ºC. or roseola. >15. III. Children with pneumonia may have cough or tachypnea.2ºF). without clinical evidence of pneumonia. vomiting. In children 3 to 36 months of age presenting with a febrile illness. and 10 percent have focal soft tissue infections. The vast majority of young children with fever have an infectious cause. is identified in 4 percent. have pneumonia diagnosed on chest radiograph. A readily identifiable presumed bacterial illness is diagnosed in 56 percent of children. 3. Sepsis is suggested by a child who is ill-appearing. and cellulitis. septic arthritis. E. A child with a deep soft tissue or bone infection may be protecting the affected area. or cellulitis. pneumonia. B. and vomiting without diarrhea can occur in urinary tract infections. Risk factors or bacteremia 1. nontoxic-appearing child less than three years of age. an infectious syndrome. The threshold of fever that indicates the need for evaluation in a well-appearing child 3 to 36 months of age is 39ºC (102. D. or change in activity. . II. Causes of fever. febrile and without a source of infection. I. irritability or lethargy.000/microL. B. 30 percent have pneumonia. Age 3 to 36 months. usually tachypnea. Highly febrile young children (<5 years) may have occult pneumonia with fever and leukocytosis. Pneumonia. A. History must include information about oral intake. Serious bacterial infectious syndromes in children 3 to 36 months of age include meningitis. The source of infection may be a bacterial or viral illness. Most children with fever and pneumonia have an abnormality on physical exam. the illness is called fever without a source. suggesting respiratory tract disease. cough. Over 86 percent of these are otitis media.Infectious Diseases Fever Without a Source in Children 3 to 36 Months of Age Most children have a febrile illness before their third birthday. F. The majority of children have either a self-limited viral infection or a source of bacterial infection. Underlying medical conditions that increases the child’s risk for serious infection include sickle cell disease and urinary tract reflux. Assessment of fever is based upon core temperature. Urinary tract infection (UTI) may be the source of occult infection in infants and young children with fever. bronchiolitis. 2.000/microL. measured rectally. Twenty-six percent of 146 patients with fever >39ºC and WBC >20. The child who has not received three doses of the Hib and pneumococcal vaccines is at greater risk for occult bacteremia than the one who is fully immunized. Bacteremia sometimes occurs in a seriously ill patient with meningitis. Evaluation A. Less than one percent have meningitis. C. usually a virus.
Abdominal tenderness. The definitive diagnosis of a serious bacterial infection is often made with cultures. 6. Lesions in the oropharynx may identify herpes gingivostomatitis (anterior ulcers) or coxsackie virus (pharyngeal vesicles). 4. or WBC >20. D. such as petechiae. hydration and perfusion normal Social Situation Parents/caregiver mature and reliable Thermometer and telephone at child’s home Laboratory Criteria White blood cell count of 5. irregular or decreasing respiratory rate Head bobbing Stridor Paradoxic or abdominal breathing Chest retractions Central cyanosis Altered level of consciousness Fever with petechiae Tachypnea Grunting Prolonged expiration Nasal flaring Poor muscle tone Poor or delayed capillary refill Tachycardia C. fluid and antibiotic therapy initiated. Cultures. and cyanosis have the appearance of being toxic or septic. A clean catch is the preferred method of urine collection for culture in the child who is toilet-trained. e. They are considered to have a significant bacterial infection until proven otherwise. Urine. Chest radiograph may be appropriate in patients with tachypnea. Blood.500/mm3 Normal urinalysis (<5 white blood cells/highpower field) When diarrhea is present. tachypnea. f.000-15. Bag specimens should not be sent for culture because they are frequently contaminated. respiratory distress. CSF should be obtained from any patient with suspected meningitis. WBC and ANC counts.00025. not require lumbar puncture. rales or decreased breath sounds. Physical examination. although the inherent delay between the initial evaluation of the patient and the availability of culture results complicates management decisions.Clinical and Laboratory Findings in Toxic and Non-toxic Infants and Children Febrile Infants at Low Risk History No previous hospitalizations or chronic illness Term delivery without complications No previous antibiotic therapy Physical Examination Nontoxic clinical appearance No focal bacterial infection (except otitis media) Activity. Continuously monitored blood culture systems have decreased the length of time for a blood culture to turn positive. urine should be collected by catheterization or suprapubic aspiration. c.000/microL. CSF.000/mm3 Band cell count <1. Abnormal vital signs such as tachycardia. Increased work of breathing is indicated by nasal flaring. For the diapered child. d. oxygen saturation <97 percent.000/microL and absolute neutrophil count (ANC) >10. and admission to the hospital arranged.000/microL. Pain with bone palpation or passive joint range of motion. Laboratory testing 1. Skin findings. therefore.000/microL. Signs of infection a. Febrile children who are acutely ill with lethargy. or viral exanthem. poor perfusion. or pulse oximetry <95 percent. 20 percent of patients with occult bacteremia may have a WBC <15. Children who are being evaluated for fever without a source should be well-appearing and. cellulitis. and CSF should be obtained. 1. 5. less than 5 white blood cells/high-power field in stool Toxic Infant or Child Slow. hypoventilation or hyperventilation. b. urine. 2. Occult bacteremia is suggested by WBC >15. retractions or use of accessory muscle. Cultures of blood. . 3. However.
Bacterial Meningitis Therapy should be initiated immediately after the results of lumbar puncture (LP) are received or immediately after LP alone if the clinical suspicion is very high. urinalysis. urinalysis. 3. IV. CBC. Serum electrolytes. or signs of septic shock. have no underlying medical condition that would alter susceptibility to infection. urine and. For children 3 to 36 months of age. Blood tests. vomiting. Recent exposure to someone with meningitis. 7. E. urinalysis and urine culture should be obtained.000/microL or an abnormal urinalysis with parenteral ceftriaxone. Vaccines received. Symptoms consistent with a viral infection of the upper respiratory tract commonly precede the development of meningitis. the following testing and treatment strategies are recommended: CBC.Management A.000/microL are recommended. Children have a stiff neck. and two sets of blood cultures. Recent travel. Younger children are commonly irritable or lethargic. Recent head trauma or craniotomy. pending blood and/or urine culture results. with fever >39ºC. blood culture. Recommendations.000/microL. 2. References. B. History. blood urea nitrogen and serum creatinine . and antibiotic therapy with parenteral ceftriaxone when WBC >15. 6. For those children <6 months or those who are incompletely immunized. C.000-25. Presumptive antibiotic therapy should be initiated. CSF. 5. 2. A bulging or tense fontanelle in an infant or a sixth cranial nerve palsy suggests increased intracranial pressure (ICP). and no identifiable focus of infection should be evaluated as follows: A. blood cultures should be obtained and antibiotics should be administered empirically before the imaging study. I. 20 to 30 percent of children have a seizure prior to diagnosis. and for any child <36 months who has not been completely immunized. and the following historical information should be obtained before antibiotic treatment of presumed bacterial meningitis is instituted: 1. Seizure activity should be assessed. CXR when WBC >20. Pre-conjugate vaccine strategies 1.000/microL. Pretreatment evaluation A. B. see page 182. Alternatives for children who cannot receive ceftriaxone include clindamycin or a macrolide. For girls between 6 and 24 months of age and uncircumcised boys between 6 and 12 months who have received three doses each of Hib vaccine and PCV7. 4. Should this procedure be delayed by the need for cranial imaging. Initial blood tests should include a complete blood count with differential and platelet count. and chest radiograph if WBC >20. blood and urine cultures.000/microL should receive antibiotic therapy. Advanced illness is characterized by lethargy. Older children may complain of headache. The prevalence of occult bacteremia and the possibility of missing a case of meningitis were high enough to justify testing many children and using broad spectrum antibiotics. V. Children who are ill-appearing or have unstable vital signs should receive cultures of blood. dehydration. Patients with WBC >15. and nuchal rigidity. Serious drug allergies. 8. who are well-appearing. urine culture. Treatment is required for children with WBC >15. Recent use of antibiotics. Bacterial meningitis often presents with fever. D. Recent infections (especially respiratory and otic infections). The presence of a progressive petechial or ecchymotic rash. For children <6 months. or neck or back pain. photophobia. when meningitis is suspected. followed as soon as possible by the LP. and Kernig and Brudzinski signs may be present.
Cerebrospinal Fluid Findings in Normal and Infected Hosts Disorder Colo r WBC Count (/mm3) Glucose (mg/d L) >40 Protein (mg/d L) 90 Gram’ s Stain and culture negative negative Normal infant Normal child or adult Bacterial meningitis Viral meningitis clear <10 clear 0 >40 <40 cloud y 20010000 <40 100500 usually positive clear 25-1000 (<50% PMN) >40 50-100 negative Common Etiologic Agents of Meningitis by Age Group Organism 0-3 Mont hs 3-36 Month s 3-21 Years Immun ocompromise d Group B Streptococcus Escherichia coli Listeria monocytogen es Streptococcus pneumoniae Neisseria meningitidis Fungus Cryptococcus Tuberculosis Virus X X X X X X X X X X X X X X X X Note: Haemophilus influenzae no longer is a common pathogen in countries where the conjugate vaccines are used routinely. F. which may be less than 10 mg/dL. I. Polymerase chain reaction (PCR) of CSF and blood is most helpful for documenting meningococcal disease in the patient with negative cultures. usually composed primarily of neutrophils. H. Characteristic findings include an increased white blood cell (WBC) count. CSF examination should be obtained for cell count and differential. The CSF Gram stain is positive in 90 percent with pneumococcal meningitis and in 80 percent with meningococcal meningitis. A common complication of bacterial meningitis is hearing loss of varying severity. Gram stain. glucose and protein concentration. Bacterial antigen tests should be reserved for cases in which the initial CSF Gram stain is negative and culture is negative at 48 hours. Permanent neurologic sequelae occur in 16 to 36 percent of children who survive an episode of bacterial meningitis.concentrations are helpful in planning fluid administration. and a low glucose concentration. an elevated protein concentration. G. Neurologic sequelae and steroids. and culture. Children with focal neurologic findings or coma should receive a computer tomographic scan before LP. Cytocentrifugation of CSF enhances the likelihood of detection of bacteria on Gram-stained specimens. .
1. Corticosteroid therapy should be administered for H. influenzae type b meningitis. Dexamethasone for pneumococcal meningitis is recommended for infants and children 6 weeks of age and older. J. Repeat CSF analysis. Selected infants and children with bacterial meningitis have a repeat analysis of CSF between 24 and 36 hours after initiating therapy. Reexamination of CSF is recommended in the following situations: 1. To assure sterilization of the CSF in patients with resistant organisms, such as pneumococci resistant to cefotaxime or ceftriaxone. 2. When dexamethasone is administered for pneumococcal meningitis, which might interfere with the ability of the physician to assess clinical response such as resolution of fever. 3. When the clinical response to therapy for pneumococcal meningitis is poor despite treatment with appropriate agents. 4. Two to three days after the initiation of therapy for meningitis caused by a Gram negative rod. 5. Repeat CSF cultures should be sterile. II. Empiric therapy A. From age 1 to 24 months of age, S. pneumoniae followed by N. meningitidis are the two most common causes of bacterial meningitis. B. From age 2 through 18 years, N. meningitidis was the most common cause, accounting for more than one-half of cases, followed by S. pneumoniae. C. Infants and children with no known immune problem. Meningococcus and pneumococcus are the most likely organisms in immunocompetent infants and children who have been immunized with the conjugate H. influenzae vaccine. High doses of third-generation cephalosporins, such as cefotaxime (225 to 300 mg/kg per day in three or four divided doses; maximum dose 12 g per day) or ceftriaxone (100 mg/kg per day in one or two divided doses; maximum dose 4 g per day) plus vancomycin (60 mg/kg per day in four divided doses) should be started.
Dosages of Antibiotics Administered Intravenously to Newborn Infants and Children
Antibiotic Age (Days) Dosage Desired Serum Concentrations (Mcg/mL) Not critical to measure
0-7 7-30 >30
50 mg/kg/dose q8h 50-75 mg/kg/dose q6h 50-75 q6h 50 mg/kg/dose q8h 50-75 mg/kg/dose q6h 75 q6h 80-100 mg/kg/dose. At diagnosis, 12 h, 24 h, and every 24 h thereafter 2.5 mg/kg/dose q12h 2.5 mg/kg/dose q8h 2.5 mg/kg/dose q8h
0-7 7-30 >30
Not critical to measure
Not critical to measure
0-7 7-30 >30
Peak, 6-10 Trough,<2
Desired Serum Concentrations (Mcg/mL) Peak, 30-40 Trough, 5-10
0-7 7-30 >30
15 mg/kg/dose q12h 15 mg/kg/dose q8h 15 mg/kg/dose q6h
D. Children with known immune deficiency 1. S. pneumoniae and S. aureus were the two most common isolates causing meningitis among children with cancer and neutropenia. Cefotaxime or ceftriaxone plus vancomycin given are empiric coverage. If a Gram negative rod is observed on Gram stain of the CSF, the addition of an aminoglycoside is recommended. 2. S. pneumoniae and L. monocytogenes are the most likely causes of bacterial meningitis with defective cell-mediated immunity. In patients who are at risk for developing listerial infection, high doses of ampicillin (300 to 400 mg/kg per day in four or six divided doses) should be given along with cefotaxime or ceftriaxone plus vancomycin until results of cultures return. E. Patients with recent neurosurgery. In addition to the usual nosocomial pathogens, coagulase-negative staphylococci (S. epidermidis) and S. aureus are important causes of meningitis after neurosurgery. Empiric therapy in this setting consists of a combination of vancomycin and a third-generation cephalosporin. An aminoglycoside should be added if Gram-negative bacilli are noted on CSF Gram stain. III. Therapy for specific pathogens A. Haemophilus influenzae. Third-generation cephalosporins such as cefotaxime (200 mg/kg per day in three or four divided doses) and ceftriaxone (loading dose of 75 mg/kg followed by 100 mg/kg per day in one or two divided doses) are effective. Rifampin prophylaxis is indicated for the patient and selected close contacts. B. Neisseria meningitidis. Meningococcal meningitis is suggested by disease occurring in children and young adults, often accompanied by a diffuse, petechial rash. This infection is best treated with penicillin. A third-generation cephalosporin is an effective alternative to penicillin. The index patient may need to take rifampin or ceftriaxone to eradicate the organism from the nasopharynx, unless the meningitis was treated with ceftriaxone or cefotaxime. C. Streptococcus pneumoniae is the most common cause of meningitis in infants and children from 1 to 23 months of age. Treatment consists of penicillin for 10 to 14 days at a dose of 300,000 units/kg per day intravenously every four to six hours. Good results are also obtained with cefotaxime. Vancomycin would be administered until the pneumococcal isolate is determined to be susceptible to penicillin or cefotaxime. D. Listeria monocytogenes, a Gram positive rod, is an important cause of bacteremia and meningitis, particularly in patients with impaired cell-mediated immunity. Listeria is treated with ampicillin and gentamicin. References, see page 182.
Acute Otitis Media
Otitis media is the most frequent diagnosis in sick children visiting physicians’ offices. The disease is most prevalent in infancy. Fluid may persist for weeks to months after the onset of signs of acute otitis media despite treatment. I. Epidemiology A. The highest incidence of acute otitis media occurs between six and 24 months of age. The incidence then declines with age except for a limited reversal of the downward trend between five and six years of
age, the time of school entry. Acute otitis media is infrequent in school age children, adolescent, and adults. B. Risk factors 1. Age. The peak age-specific attack rate occurs between six and 18 months of age. Children who have had little or no experience with otitis media by the age of three years are unlikely to have subsequent severe or recurrent disease. 2. Sex. Males have a higher incidence of acute otitis media than females. II. Microbiology A. Bacteria. Most of the bacterial isolates from middle ear fluid are streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. The conjugate Haemophilus influenzae type b (Hib) vaccine has had little impact on Haemophilus acute otitis media because more than 90 percent of cases of Haemophilus acute otitis media are due to nontypable strains. B. Streptococcus pneumoniae is the most important bacterial cause of otitis media, associated with 25 to 40% of cases. C. Haemophilus influenzae. Nontypable strains of H. influenzae are second in importance in causing acute otitis media, responsible for 10 to 30% of cases. One-third to one-half of strains of H. influenzae recovered from middle ear fluids produce beta-lactamase. D. Moraxella catarrhalis has increased in frequency in middle ear aspirates of children with acute otitis media, responsible for 10%. More than 90% of strains produced beta-lactamase. E. Other bacteria. Group A streptococcus is only an occasional pathogen. Small numbers are identified for Staphylococcus aureus and anaerobic bacteria. Gram-negative bacilli are responsible for 20% of cases of acute otitis media in the first months of life, but these organisms are rarely present in the middle-ear effusions of older infants and children with acute otitis media. Pseudomonas aeruginosa is associated with chronic suppurative otitis media. F. Viruses. Viral infection is frequently associated with acute otitis media. Sixteen percent of middle-ear fluids of children with acute otitis media are associated with viruses, most frequently are respiratory syncytial virus, rhinoviruses, influenza viruses and adenoviruses. III. Clinical manifestations. Symptoms of acute otitis media include otalgia or ear pain, hearing loss, and vertigo. Otalgia is more common in adolescents and adults than in young children. A. Otorrhea or ear discharge or swelling about the ear (which may indicate disease of the mastoid) are specific physical findings, if present. Nonspecific symptoms and signs include fever, irritability, headache, apathy, anorexia, vomiting and diarrhea. IV. Diagnosis. The diagnosis of acute otitis media requires evidence of an acute history, signs and symptoms of middle ear inflammation, and the presence of middle ear effusion. A. The hallmark of establishing the diagnosis is the demonstration of fluid by pneumatic otoscopy; the finding of a red tympanic membrane alone is not sufficient to make a diagnosis. B. Otoscopic examination identifies a tympanic membrane that is often erythematous due to inflammation, bulges because of the expansion of fluid in the middle ear and is immobile because the middle ear is fluid rather than air filled. Cloudiness is also common. C. Aspiration of the middle ear fluid is warranted if the patient with acute otitis media is toxic, has immune deficits, or has failed prior courses of antibiotics.
Patients who fail amoxicillin-clavulanate should be treated with a three day course of parenteral ceftriaxone.V. or cefuroxime (30 mg/kg per day in 2 divided doses) can be used. A macrolide (erythromycin plus sulfisoxazole. including cefdinir. Lack of improvement by 48 to 72 hours suggests either another disease is present or the initial therapy was not adequate. and cefuroxime. Three consecutive doses is superior to a single dose. the signs of systemic and local illness usually resolve in 24 to 72 hours. Children should be given the first dose and then observed carefully for 48 hours. b.to seven-day course of antibiotics is appropriate for children ages 6 and older who have mild to moderate disease. cefpodoxime (10 mg/kg per day. pneumoniae and many of the resistant strains. 4. Only S. benzocaine. cefdinir (14 mg/kg per day in 1 or 2 doses). Five days of azithromycin (Zithromax) 10 mg/kg per day as a single dose on day 1 and 5 mg/kg per day for days 2 through 5) or clarithromycin ([Biaxin] 15 mg/kg per day divided into 2 doses) can be used. Ceftriaxone (50 mg/kg IM) is effective for the treatment of acute otitis media in children who fail amoxicillin. a. In patients who report penicillin allergy but who did not experience a Type 1 hypersensitivity reaction (urticaria or anaphylaxis). cefpodoxime. With antimicrobial therapy. However. and a single dose of azithromycin has been approved. pneumoniae that are highly resistant to penicillin will not respond to this regimen. . Duration of therapy a. Auralgan (combination of antipyrine. Erythromycin plus sulfisoxazole ([Pediazole] 50 to 150 mg/kg per day divided into 4 doses) may be the most effective. Alternatives include the drugs cited above for penicillin allergic patients. or clarithromycin) is preferred for children who have had a Type 1 reaction to amoxicillin or other beta-lactam antimicrobial agents. A 10-day course of an oral antimicrobial is recommended for the treatment of acute otitis media. Amoxicillin is the drug of choice for otitis media because it is effective. b. Ten-day therapy is more effective in patients under age 6. a second or even third dose should be given if clinical symptoms and signs do not respond to the first injection. Treatment and Prevention of Acute Otitis Media A. but is has an unpleasant taste. 2. 6.4 mg/kg per day of clavulanate in two divided doses) is recommended. and has a narrow microbiologic spectrum. azithromycin. Trimethoprim-sulfamethoxazole (Bactrim) may still be useful in regions where pneumococcal resistance to this combination is not a concern. a shorter course may be adequate. A five. The increased concentrations provide activity against most intermediate strains of S. Penicillin-allergic patients. is relatively inexpensive. Treatment failures. High-dose amoxicillin-clavulanate (90 mg/kg per day amoxicillin. The topical agent. and glycerin) improves ear pain scores at 30 minutes after treatment. 3. once daily). Symptomatic therapy 1. Doubling the dose to 80 to 90 mg/kg per day divided into two doses increases the concentration of amoxicillin in the middle ear. Ibuprofen and acetaminophen may improve pain. First-line antimicrobial therapy. with 6. 5. safe.
B. Children with severe and recurrent episodes of otitis media in the two. References. Influenza vaccine is now recommended for all infants 6 to 24 months of age and should be given in the fall to older children who have had recurrent episodes of acute otitis media in the preceding winter. Persistent middle-ear effusion is common after the resolution of acute symptoms and is not an indication of treatment failure. 10. their role in the prevention of recurrent acute otitis media is more controversial. 9. 15% develop croup. Pneumonia usually causes cough that persists day and night. 8.to five-year-old age groups are candidates for the conjugate vaccine. Vaccines a. D.Second-Line Antibiotic Therapy for Acute Otitis Media Drug Amoxicillinclavulanic acid (Augmentin) Dosage 40 mg/kg of amoxicillin component in 3 divided doses 500 mg in 2 divided doses 50 mg/kg IM Comments Diarrhea common Cefuroxime axetil (Ceftin) Ceftriaxone (Rocephin) 7. Grunting prevents collapse of narrowed airways and improves oxygenation. These surgical procedures do not appear to be an effective primary preventive measure for children with recurrent acute otitis media. Middle-ear effusion may persist after the onset of acute otitis media in 70 to 10% at three months. I. and 29% bronchiolitis. 34% tracheobronchitis. Amoxicillin or sulfisoxazole is used at one-half the therapeutic dose administered once a day during the fall. Conjugate pneumococcal vaccine is recommended for universal immunization of infants to age two years and selective immunization of children two to five years of age. Chest pain. Clinical evaluation of pneumonia A. Surgery a. b. Tachypnea. C. b. Older children may complain of diffuse chest or abdominal pain. Adenoidectomy with or without tonsillectomy has been documented to be of value in reducing the number of acute episodes for children who have recurrences after an initial placement of tympanostomy tubes. see page 182. Grunting occurs in 20% of infants who have bronchiolitis or pneumonia. Tympanostomy tubes have been accepted as a treatment for chronic otitis media or otitis media with effusion. Chemoprophylaxis should be considered for patients with three or more episodes of otitis media in six months and four or more episodes in 12 months. Pneumonia A lower respiratory tract infection (LRI) develops in one in three children in the first year of life. Pneumonia that involves the diaphragmatic pleura may present as abdominal pain. Increased respiratory rate is one of the earliest and most consistent signs of lower respiratory tract disease. . Cough. which is caused by persistent cough and repeated muscle contraction. Pneumonia causes chest pain when the infection develops near the pleura. Twenty-nine percent of these children develop pneumonia. winter and early spring. Patients who cough spontaneously throughout the office visit are likely to have lower respiratory tract disease.
Auscultation 1. who appear ill. early pulmonary edema.Abnormal Respiratory Rates by Age Age <2 months 2-12 months old >1 year old Abnormal >60 bpm >50 bpm >40 bpm E. or who are hospitalized. asthma. Wheezing is generated by narrowed airways. subglottic stenosis. They indicate pulmonary parenchymal disease. cyanosis will not manifest in the presence of anemia. or tracheal compression. Cyanosis occurs at an oxygen saturation of 67%. Laboratory tests 1. They should be obtained in infants and children with high fever. It is not a sensitive predictor of pneumonia because significant hypoxemia may be present before cyanosis is visible. Signs of consolidation include dullness to percussion and increased transmission of the voice on auscultation. Nasopharyngeal cultures for viruses and immunofluorescence studies for viral antigens are obtained when therapy with antiviral agents is being considered. F. . Bacterial antigen assays of urine by latex agglutination. 3. 2. 2. Chest radiograph. B. >39EC in children). however. 3. or upon hospitalization. Crackles are the fine popping sounds that occur when previously closed airways open suddenly. ill appearance. A chest radiograph should be obtained when the child with pneumonia appears acutely ill. G. It can be caused by bronchiolitis. 4. II. or antibody tests of blood are indicated when unusual infections are suspected or when pneumonia is unresponsive to therapy. Diagnostic evaluation of lower respiratory infections A. Retractions of the intercostal spaces may occur with pneumonia because of decreased compliance or increased airway resistance. WBC count should be obtained for children who have significant fever (>38EC in infants. Blood cultures are rarely positive in children with pneumonia.
35-42 weeks: 2.for those <26 weeks: 2. <2000 g and 8 to 28 days old: 150 mg/kg per day in 3 divided doses. OR Ceftriaxone (75 to 100 mg/kg once daily OR cefotaxime (100 to 200 mg/kg per day IV in 4 divided doses [MAX 10 to 12 g/day]) PLUS clindamycin (30 to 40 mg/kg per day IV in 3 or 4 divided doses [MAX 1 to 2 g/day]) if complicated by parapneumonic effusion Erythromycin (4o to 50 mg/kg per day in four divided doses). >43 weeks: 2.5r/kg per dose every 18 hours.Empiric Antibiotic Treatment of Pediatric Pneumonia Age group Empiric regimen Neonate Bacterial (not chlamydia) Ampicillin (for those <2000 g and 0 to 7 days old: 100 mg/kg per day in two divided doses. >2000 g and 8 to 28 days old: 200 mg/kg per day in four divided doses. OR Azithromycin (10 mg/kg on day 1 followed by 5 mg/kg daily for 4 more days [MAX 500 mg on day 1 and 250 mg thereafter]). 27-34 weeks: 2.5 mg/kg per dose every 24 hours.5 mg/kg per dose every 12 hours. >2000 g and 0 to 7 days old: 150o mg/kg per day in 3 divided doses.5 mg/kg per dose every 8 hours) Acyclovir (60 mg/kg per day IV in three divided doses Cefuroxime (150 mg/kg per day IV in three divided doses [MAX 4 g/day]). PLUS Gentamicin (gestational age plus weeks of life . OR Clarithromycin (15 mg/kg per day in two divided doses [MAX 1 g/day]) Oral regimens Amoxicillin (80 to 100 mg/kg per day PO in 3 divided doses [MAX 600 mg/day]) Parenteral regimens Ampicillin (150 to 200 mg/kg per day IV in 4 divided doses [MAX 10 to 12 g/day]) OR Cefuroxime (dosing as above) Viral (herpes simplex) One to four months Bacterial (not chlamydial) Chlamydial Four months to five years Bacterial (not Mycoplasmal or Chlamydia) .
pneumoniae isolates are now . Infants and older children 1.Age group Empiric regimen Older than five years Mycoplasmal/chlamydial Bacterial Eryth r o m ycin . The macrolides are generally recommended for the outpatient treatment of the older child and adolescent because of the greater likelihood of infection due to Mycoplasma pneumoniae and Chlamydia pneumoniae. Listeria monocytogenes. and Enterobacteriaceae spp. for patients three weeks to three months old or ampicillin (150 to 200 mg/kg per day in four divided doses) for those four months to four years old since disease caused by betalactamase-producing organisms (eg. higher doses (80 to 100 mg/kg per day PO in three divided doses up to a maximum of 2 to 3 g/d) are recommended. Since there are reports of antibiotic failures due to treatment of non-susceptible S. 2. Intravenous acyclovir (60 mg/kg in three divided doses for 21 days) should be considered for suspected patients. Approximately 50 percent of S. provides good coverage against the usual pathogens. pneumoniae with beta-lactams and concern for MRSA. B. OR cefuroxime (dosed as above) + coverage for Mycoplasma or Chlamydia III. Doxycycline (4 mg/kg PO per day in two divided doses up to a maximum of 200 mg/d) is an alternative. aureus (MRSA) infections. a z i t h r o m yc i n . Staphylococcus aureus and Haemophilus influenzae) is not likely in this older age group. especially if a macrolide hypersensitivity exists. Treatment of Community-Acquired Pneumonia in Children A. Other possible regimens include: a third-generation cephalosporin. 4. 5. Because of the increasing prevalence of pneumococcal penicillin-resistance. When bacterial disease is suspected. Ampicillin (dosed as for 4 months to 5 years). herpes simplex virus (HSV) is a possible cause of pneumonia. OR doxycycline. Pneumonia is treated with empiric intravenous ampicillin (150 mg/kg per day divided every 12 hours if meningitis is also suspected and 50 to 100 mg/kg every 12 hours if not) and gentamicin (dose based upon gestational age and renal function). During the first two weeks of life.. Neonates 1. cefuroxime (150 mg/kg per day in three divided doses up to a maximum of 4 to 6 g/d). especially Escherichia coli K1. 3. empiric treatment with Clindamycin (30 to 40 mg/kg per day in three to four divided doses up to a maximum of 1 to 2 g/d) is reasonable for complicated cases of community-acquired pneumonia. ceftriaxone (75 to 100 mg/kg once daily up to a maximum dose of 4 g/d) or cefotaxime (100 to 200 mg/kg per day in four divided doses up to a maximum of 10 to 12 g/d). clarithromycin (dosed as above). Amoxicillin is generally considered the drug of choice for the outpatient treatment of patients younger than five years of age with communityacquired pneumonia. a. 2. With the concern for increasing beta-lactam resistance among Streptococcus pneumoniae isolates and the increasing prevalence of community-acquired methicillin-resistant S. Bacterial pneumonia. group B streptococcus. the second-generation cephalosporin. This regimen will cover the most likely pathogens. severely ill patients requiring admission to the intensive care unit should be treated with vancomycin (40 mg/kg per day IV in four divided doses up to a maximum of 2 to 4 g/d) in addition to a third-generation cephalosporin and azithromycin.
Pathophysiology A.resistant to the macrolides. Bronchiolitis is most serious in infants who are less than one year old. pneumoniae or legionellosis is suspected. Bronchiolitis Bronchiolitis is an acute wheezing-associated illness. References. Therefore. Treatment should be continued for at least 10 days.2 kg and >7 days old). Chest radiographs of infants who have bacterial pneumonia may exhibit a diffuse reticular nodular appearance. hypoxemic. Streptococcus pneumoniae (pneumococcus). significantly tachycardic for age. Children who are toxic. Cultures of urine and cerebrospinal fluid should be obtained at the time of the blood culture. or have an underlying condition that may be worsened by the pneumonia require hospitalization. so a failure to respond may indicate the need to change therapy to high-dose amoxicillin or a cephalosporin for better pneumococcal coverage. C. Infants may have a single episode or may have multiple occurrences in the first year of life. who are passively exposed to tobacco smoke. blood cultures obtained before the initiation of antibiotics commonly grow the offending organism. Bacterial pneumonia in the first day of life may be impossible to distinguish from hyaline membrane disease or transient tachypnea of the newborn. accounting for 50% of cases of bronchiolitis requiring hospitalization. which occurs in early life. secondary to GBS. D.2 kg) and cefotaxime 100 mg/kg per day divided every 12 hours or 150 mg/kg per day divided every 8 hours (infants >1. Switch to oral therapy in patients who have received parenteral antibiotics when the patient has become afebrile for 24 to 48 hours and is able to keep down food. Hospitalization should be considered for most children less than four months of age. 6. IV. dyspneic. unless a viral etiology is suspected and they are relatively asymptomatic. Bronchiolitis occurs most frequently from early November and continues through April. Infants at risk include those who are raised in crowded living conditions. In the newborn who has bacterial pneumonia. For the older child admitted to the hospital. Epidemiology A. Listeria.2 kg) or every 8 hours (infants >1. see page 182. respiratory distress in newborns should be treated as bacterial pneumonia until proven otherwise. addition of a macrolide to the previously suggested antibacterial regimen may be necessary if M. Hospitalization. Gentamicin is an alternative. Empiric treatment should be initiated with ampicillin 100 mg/kg per day divided every 12 hours (infants <1. E. B. Infants also may develop bacterial pneumonia transnatally. However. II. Neonates A. especially those 1-3 months old. group D streptococci. The onset of symptoms tends to occur 12 to 24 hours after birth. unable to feed. pneumoniae. Seven to 10 days should be adequate for routine pathogens causing uncomplicated infection. and who are not breastfed. Infants born prematurely. B. or with chronic lung disease (CLD). preceded by signs and symptoms of an upper respiratory infection. dehydrated. Haemophilus influenzae. Duration of therapy. they tend to show normal or increased lung volumes with possible focal or coarse densities. I. Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis in infants and young children. in contrast to hyaline membrane disease. it is caused most commonly by Escherichia coli or by group B streptococci (GBS). B. C. . apneic. When associated with chorioamnionitis. but. and anaerobes also may be present in this setting. C. immunodeficiency or congenital heart disease are at especially high risk for severe RSV illness.
Infants with bronchiolitis present symptoms of an upper respiratory illness for several days and wheezing during the peak RSV season. The wheezing sound is harsh and low in pitch. Treatment of bronchiolitis in the hospital 1. Consolidation is noted in about 25% of children. V. Fever occurs in most young children. RSV is transmitted by contact with nasal secretions. diluted with 3. Symptoms of RSV may range from those of a mild cold to severe bronchiolitis or pneumonia. with a toxic. D. A few infants will respond to this therapy and avoid hospitalization. C. Symptoms usually last an average of 5 days. F. 3. the infant can be sent home. with temperatures ranging from 38E°C to 40E°C (100. Fine “crackles” are usually heard on inspiration. Arterial blood gases should be obtained to assess the severity of respiratory compromise. Ribavirin. 2. IV. It should be continued if an improvement in the respiratory status is noted.5 mL of saline (1:8) by nebulization. RSV infection frequently begins with nasal discharge. Hyperresonance of the chest wall may be present.C. Criteria for hospitalization 1. Respiratory failure is suggested by CO2 values of 45-55 mm Hg.4E°F to 104E°F).25% solution. 2. Dehydrated infant who is not feeding well. Outpatient management of bronchiolitis is appropriate for infants with mild disease. Carbon dioxide levels are commonly in the 30-35 mm Hg range. III. Enzyme-linked immunosorbent assays (ELISA) of nasal washings for RSV are highly sensitive and specific.5 mL of a 2. an antiviral agent. Oxygen tension below 66 mm Hg indicates severe disease. Congenital heart disease. Parainfluenza viruses are the second-most-frequent cause of bronchiolitis. Rhinovirus and mycoplasma pneumonia cause wheezing-associated respiratory illness in older children. Age <3 months. and oral albuterol continued. History of prematurity (especially less than 34 weeks). Shedding of virus occurs 1 to 2 days before symptoms occur. and cough. Before hospitalization. infants should receive an aerosolized beta-adrenergic agent. E. B. most commonly in the right upper or middle lobe. If the response is good. B. before and after outbreaks of RSV. D. produces modest . White blood cell count may be normal or elevated slightly. while parainfluenza virus and RSV can cause wheezing at any age. It is given every 20-30 minutes for severe croup. Influenza A virus. Other underlying lung disease 4. Hospitalized infants should receive hydration and ambient oxygen to maintain an oxygen saturation >92-93% by pulse oximetry. Diagnosis A. Unreliable parents. rhinovirus and Mycoplasma pneumonia can all cause bronchiolitis. pharyngitis. and the differential count may show neutrophilia. Racemic epinephrine is administered as 0. Management A. adenovirus. Restlessness and hyperinflation of the chest wall are signs of impending respiratory failure. distressed appearance). and wheezing can be heard in most infants without auscultation. Chest radiography typically shows hyperexpansion and diffuse interstitial pneumonitis. Substernal and intercostal retractions are often noted. and it is given every 4-6 hours for moderate croup. Clinical evaluation of bronchiolitis A. D. Oxygen saturation values of <95% suggest the need for hospitalization. C. 7. 6. Racemic epinephrine by inhalation may be administered as a therapeutic trial. 5. C. although severely affected infants may not have detectable wheezing. Low initial oxygen saturation suggestive of respiratory failure (O2 saturation <95%. Hoarseness or laryngitis is not common. B. Cyanosis of the oral mucosa and nail beds may occur in severely ill infants. and for 1 to 2 weeks afterwards. E. They cause illness during autumn and spring.
References. the use of palivizumab and RSV IGIV should be reserved for infants with additional risk factors. The dosage is 2 gm (diluted to 60 mg/mL) aerosolized over 2 hours tid for 3-5 days using an oxygen hood. especially those who require medical therapy. C Palivizumab does not interfere with the response to vaccines. Recommendations by the American Academy of Pediatrics for the use of palivizumab (Synagis) and RSV-IGIV: C Palivizumab (Synagis) or RSV-IGIV prophylaxis should be considered for infants and children younger than 2 years of age with chronic lung disease (CLD) who have required medical therapy for CLD within 6 months before the anticipated RSV season. Infants born at 29 to 32 weeks of gestation may benefit most from prophylaxis up to 6 months of age. and effectiveness. Palivizumab is administered intramuscularly in a dose of 15 mg/kg once a month during the RSV season. recent Age <6 weeks Neurologic diseases Heart failure of any cause RSV bronchiolitis and arterial O2 <65 mmHg Immunodeficiency due to chemotherapy Cystic fibrosis Severe combined immunodeficiency Multiple congenital anomalies Certain premature infants Metabolic diseases RSV bronchiolitis and a rising pCO2 VI. Decisions about duration of prophylaxis should be individualized according to the duration of the RSV season. Corticosteroid use in the treatment of bronchiolitis is not recommended. Infants born at 28 weeks of gestation or earlier may benefit from prophylaxis up to 12 months of age. safety. see page 182. and termination is March to May. Patients with more severe CLD may benefit from prophylaxis for 2 RSV seasons. the usual time for the beginning of RSV outbreaks is October to December. especially cyanotic Chronic lung disease Renal transplantation. Palivizumab is preferred for most highrisk children because of its ease of administration. Palivizumab (Synagis) is a humanized mouse monoclonal antibody that is given intramuscularly. Ribavirin is helpful in severely ill or high-risk patients. Indications for Ribavirin Use in Bronchiolitis Congenital heart disease.improvement in clinical illness and oxygenation. Treatment with ribavirin combined with RSV immune globulin administered either parenterally or by aerosol is more effective than therapy with either agent alone. C Infants born at 32 weeks of gestation or earlier without CLD or who do not meet the aforementioned criteria also may benefit from RSV prophylaxis. In most areas of the United States. but regional differences occur. C For patients born between 32 and 35 weeks of gestation. . C Prophylaxis for RSV should be initiated at the onset of the RSV season and terminated at the end of the RSV season. Prevention of RSV Infections A.
and anterior cervical adenopathy. Constitutional symptoms include fever and chills. Physical findings may include petechiae of the palate. I. B. A positive rapid antigen detection test may be considered definitive evidence for treatment of streptococcal pharyngitis. Only 5 to 10 percent of sore throats are caused by bacteria. B. Other bacteria that occasionally cause pharyngitis include groups C and G streptococci. vomiting. headaches and nausea. abdominal pain (especially in children) Marked inflammation of throat and tonsils Patchy discrete exudate Tender. Clinical presentation A.3EF). Throat culture is the gold standard for the diagnosis of streptococcal pharyngitis. C. Pharyngitis caused by group A beta-hemolytic streptococci has an incubation period of two to five days and is most common in children five to 12 years of age. Neisseria gonorrhoeae. This test has a specificity of greater than 95 percent but a sensitivity of only 76 to 87 percent. Patients with cough or coryza. pharyngeal and tonsillar erythema and exudates. myalgias. and 30 to 60 percent have a viral etiology (rhinovirus. Complications of Group A Beta-Hemolytic Streptococcal Pharyngitis Nonsuppurative complications Rheumatic fever Poststreptococcal glomerulonephritis Suppurative complications Cervical lymphadenitis Peritonsillar or retropharyngeal abscess Sinusitis Mastoiditis Otitis media Meningitis Bacteremia Endocarditis Pneumonia D. A rapid antigen detection test (rapid strep test) can be completed in five to 10 minutes. Features of Streptococcal Tonsillopharyngitis Sudden onset Sore throat (pain on swallowing) Fever Headache Nausea. A confirmatory throat culture should follow a negative rapid antigen detection test when the diagnosis of group A betahemolytic streptococcal infection is strongly suspected. which is sometimes linear on the groin and axilla (Pastia’s lines). The illness is diagnosed most often in the winter and spring. Chlamydia pneumoniae. C. Mycoplasma pneumoniae. enlarged anterior cervical nodes Scarlet fever Features rarely associated with streptococcal tonsillopharyngitis–suggestive of other etiologies Conjunctivitis Cough Laryngitis (stridor. Group A beta-hemolytic streptococcal pharyngitis usually is an acute illness with sore throat and a temperature higher than 38. The sensitivity of throat culture for group A beta-hemolytic streptococci is 90 percent. and Arcanobacterium haemolyticus. Suppurative complications of streptococcal pharyngitis occur as infection spreads from pharyngeal mucosa to . with group A betahemolytic streptococci being the most common. A sandpaperlike rash on the trunk. The specificity of throat culture is 99 percent. are less likely to have streptococcal pharyngitis. Diagnostic Testing A. is consistent with scarlet fever.5EC (101. croup) Diarrhea Nasal discharge (except in young children) Muscle aches/malaise II.Pharyngitis Approximately 30 to 65 percent of pharyngitis cases are idiopathic. adenovirus). The annual incidence of acute rheumatic fever is one case per 1 million population.
deeper tissues. III. Antibiotic Therapy Selected Antibiotic Regimens for Group A BetaHemolytic Streptococcal Pharyngitis
Dosing frequency Two or three times daily Two or three times daily Single injection Single injection Three divided doses Three times daily Two to four divided doses Four times daily Two to four divided doses --
Antibiotic Penicillin V (Veetids)
Dose/dosage Child: 250 mg
Duration 10 days
Adult: 500 mg
Penicillin G benzathine (Bicillin L-A)
Child: 600,000 units Adult: 1,200,000 units
Child: 40 mg per kg per day Adult: 500 mg
Erythromycin ethylsuccinat e (E.E.S. 400)
Child: 40 mg per kg per day
Adult: 400 mg
Child: 20 to 40 mg per kg per day Adult: not recommended
Child: 10 mg per kg on day 1; 5 mg per kg on days 2 through 5 Adult: 500 mg on day 1; 250 mg on days 2 through 5
Amoxicillinclavulanate potassium (Augmentin)
Child: 40 mg per kg per day
Two or three divided doses Two times daily Two divided doses Once daily Two to four divided doses Two times daily
Adult: 500 to 875 mg Cefadroxil (Duricef) Child: 30 mg per kg per day Adult: 1 g Cephalexin (Keflex) Child: 25 to 50 mg per kg per day Adult: 500 mg
10 days 10 days
A. Penicillin is the drug of choice for streptococcal pharyngitis. This antibiotic has efficacy and safety, a narrow spectrum of activity and low cost. About 10 percent of patients are allergic to penicillin. Cure rates are similar for 250 mg of penicillin V given two, three or four times daily. The use of intramuscularly administered penicillin may overcome compliance problems. B. Alternatives to penicillin 1. Amoxicillin a. In children, the cure rates for amoxicillin given once daily for 10 days are similar to those for penicillin V. The absorption of amoxicillin is unaffected by the ingestion of food. b. Amoxicillin is less expensive and has a narrower spectrum of antimicrobial activity than the once-daily antibiotics. Suspensions of this drug taste better than penicillin V suspensions, and chewable tablets are available. However, gastrointestinal side effects and skin rash may be more common with amoxicillin.
2. Macrolides a. Erythromycin is recommended in patients with penicillin allergy. Because erythromycin estolate is hepatotoxic in adults, erythromycin ethylsuccinate may be used. Erythromycin is absorbed better when it is given with food. About 15 to 20 percent of patients cannot tolerate the gastrointestinal side effects of erythromycin. b. Azithromycin (Zithromax) allows once-daily dosing and a shorter treatment course of five days. Azithromycin is associated with a low incidence of gastrointestinal side effects. 3. Cephalosporins a. A 10-day course of a cephalosporin has been shown to be superior to penicillin. The overall bacteriologic cure rate for cephalosporins is 92 percent, compared with 84 percent for penicillin. b. Cephalosporins have a broader spectrum of activity than penicillin V. Unlike penicillin, cephalosporins are resistant to degradation from beta-lactamase. First-generation agents such as Cefadroxil (Duricef) and cephalexin (Keflex, Keftab) are preferable to second- or third-generation agents. c. Cephalosporins are reserved for patients with relapse or recurrence of streptococcal pharyngitis. 4. Amoxicillin-clavulanate (Augmentin) is resistant to degradation from beta-lactamase produced by copathogens. Amoxicillin-clavulanate is often used to treat recurrent streptococcal pharyngitis. Its major adverse effect is diarrhea. IV. Management Issues A. Treatment Failure and Reinfection. Patients who do not comply with a 10-day course of penicillin should be offered intramuscular penicillin or a oncedaily oral macrolide or cephalosporin. Patients with clinical failure should be treated with amoxicillinclavulanate, a cephalosporin, or a macrolide. B. Contagion. Patients with streptococcal pharyngitis are considered contagious until they have been taking an antibiotic for 24 hours. Children should not go back to day care or school until their temperature returns to normal and they have had at least 24 hours of antibiotic therapy. References, see page 182.
Conjunctivitis is defined as inflammation of the conjunctiva; it is usually caused by infection or allergy. It is often referred to as “pink eye.” I. Etiology A. Neonatal conjunctivitis occurs in 1.6-12% of newborns. The most common cause is chemical irritation from antimicrobial prophylaxis against bacterial infection, followed by Chlamydia trachomatis infection. Haemophilus influenzae and Streptococcus pneumoniae may also cause infection in newborns. B. Rarely, gram-negative organisms, such as Escherichia coli, Klebsiella, or Pseudomonas sp can cause neonatal conjunctivitis. Neisseria gonorrhoeae is an unusual cause of neonatal conjunctivitis because of the use of ocular prophylaxis. C. Herpes simplex can cause neonatal keratoconjunctivitis; however, it is almost always associated with infection of the skin and mucous membranes, or with disseminated disease. D. In older infants and children, H influenzae is by far the most common identifiable cause of conjunctivitis, causing 40-50% of episodes. S pneumoniae accounts for 10% of cases, and Moraxella catarrhalis is the third most common cause. E. Adenovirus is the most important viral cause of acute conjunctivitis. This organism often causes epidemics of acute conjunctivitis. It causes 20% of childhood conjunctivitis (most occurring in the fall and winter months). II. Clinical presentation A. In the first day of life, conjunctivitis is usually caused by chemical conjunctivitis secondary to ocular prophylaxis.
B. Three to 5 days after birth, gonococcal conjunctivitis is the most common cause of conjunctivitis. C. After the first week of life and throughout the first month, chlamydia is the most frequent cause of conjunctivitis. Severe cases are associated with a thick mucopurulent discharge and pseudomembrane formation. D. Gonococcal conjunctivitis can present as typical bacterial conjunctivitis, or as a hyperacute conjunctivitis with profuse purulent discharge. There often is severe edema of both lids. E. In the older infant and child, both viral and bacterial conjunctivitis may present with an acutely inflamed eye. Typically, there is conjunctival erythema, with occasional lid edema. Exudate often accumulates during the night. F. Many patients who have both adenoviral conjunctivitis and pharyngitis also are febrile. The triad of pharyngitis, conjunctivitis, and fever has been termed pharyngoconjunctival fever. III. Diagnosis A. Neonates 1. In cases of neonatal conjunctivitis, a Gram stain and culture should be obtained to exclude N gonorrhoeae conjunctivitis. 2. Chlamydia trachomatis antigen detection assays have a sensitivity and specificity of 90%. B. Infants and older children. Outside the neonatal period, a Gram stain is usually not needed unless the conjunctivitis lasts longer than 7 days. The presence of vesicles or superficial corneal ulcerations suggests herpetic keratoconjunctivitis. IV. Differential diagnosis of conjunctivitis A. Systemic diseases. Most cases of red eye in children are caused by acute conjunctivitis, allergy, or trauma; however, Kawasaki disease, Lyme disease, leptospirosis, juvenile rheumatoid arthritis, and Stevens-Johnson syndrome may cause conjunctivitis. Glaucoma is a significant cause of a red eye in adults; however, it is rare in children. B. Allergic conjunctivitis 1. Allergic eye disease is characterized by pronounced ocular itching, redness, tearing, and photophobia. This recurrent disease has seasonal exacerbations in the spring, summer, and fall. Children who have allergic conjunctivitis often have other atopic diseases (rhinitis, eczema, asthma) and a positive family history. 2. Treatment a. Topical decongestants: Naphazoline 0.1% (Naphcon), phenylephrine (Neo-Synephrine), and oxymetazoline (OcuClear, Visine LR) may be used qid, alone or in combination with ophthalmic antihistamines, such as antazoline (Vasocon-A) or pheniramine maleate (NaphCon-A). b. Topical lodoxamide (Alomide) 0.1% ophthalmic solution, 1-2 drops qid, is helpful in more severe cases. c. Topical corticosteroids are helpful, but long-term use is not recommended; dexamethasone (Decadron) 1-2 drops tid-qid. V. Treatment of acute infectious conjunctivitis A. Gonococcal ophthalmia neonatorum is treated with ceftriaxone (50 mg/kg/day IV/IM q24h) or cefotaxime (100 mg/kg/day IV/IM q12h) for 7 days. B. Neonatal conjunctivitis caused by C trachomatis is treated with erythromycin, 50 mg/kg/day PO divided in 4 doses for 14 days. C. Bacterial conjunctivitis among older infants and children is treated with polymyxin-bacitracin (Polysporin) ointment, applied to affected eye tid. References, see page 182.
Cat and Dog Bites
Bite wounds account for approximately 1% of all emergency department visits: 10% of victims require suturing and 1-2% require hospitalization. I. Pathophysiology A. Dog bites account for 80-90% of animal bites. Infection develops in15-20% of dog bite wounds. B. Cat bites account for 15% of animal bites. Cat bites usually present as puncture wounds, of which 30-
wounds examined more than 24 hours after injury. A neurovascular examination and an assessment of wound depth should be completed. Bite wounds usually have a polymicrobial contamination. crush injury or avulsion. 2. Flavobacterium species. Microorganisms Isolated from Infected Dog and Cat Bite Wounds Aerobes. current medications and allergies. Eubacterium species. IV. Afipia felis. history of splenectomy. III. Enterobacter species. Actinomyces. Antimicrobial therapy 1. c. Staphylococcus aureus. do not require culture. Eikenella corrodens. history of chronic illness. Bacteroides species.The wound is measured and classified as a laceration. Devitalized. joint spaces. Blastomyces dermatitidis. Radiographs should be taken if there is considerable edema and tenderness around the wound or if bony penetration or foreign bodies are suspected. 2. malignancy. Fusobacterium species. B. B. Low-risk wounds seen within 24 hours after injury may be sutured. Laboratory and radiologic evaluation A. Haemophilus aphrophilus. High-risk bite wounds requiring prophylactic antibiotics a. Pasteurella Multocida is a gram-negative aerobe present in the oropharynx of dogs and cats. Prophylactic antibiotics are recommended for wounds that have a high risk of infection. puncture. b. C. Clinical evaluation of bite wounds A. that have no signs of infection. Prophylactic antibiotic treatment is given for 37 days. B. Capnocytophaga canimorsus. Leptotrichia buccalis. Wounds seen within 8 to 24 hours after injury. and bites of the hand should not be closed primarily. Bite wounds to the hand.to 50-mL syringe with an Angiocath. betahemolytic. Veillonella parvula Unusual Pathogens. Pseudomonas species. The circumstances of the injury should be documented. uninfected high-risk wounds seen 72 hours after initial injury may undergo delayed primary closure. Bites to the face and head have a good outcome and may be closed primarily. and irrigated with normal saline with a 20. or other immuno- . Cat bite wounds. acquired-immunodeficiency syndrome. Moraxella species. Neisseria species. aerobic and anaerobic cultures should be obtained. joint. foot or face. Photographs of the wound should be obtained if disfigurement has occurred or if litigation is anticipated. Pasteurella multocida. Streptococci: alpha-hemolytic. or wound adjacent to a prosthetic joint. The patient’s tetanus immunization status. bone. Deep puncture wounds. II. nerves.40% become infected. Wounds are evaluated for injuries to tendons. It is found in 20-30% of dog bite wounds and more than 50% of cat bite wounds. and the animal’s immunization status should be determined. Francisella tularensis V. or immunocompromising conditions should be assessed. The wound should be cleansed with 1% povidone iodine solution (Betadine). wounds requiring debridement. tendon or ligament. crushed tissue should be sharply débrided. If infection is present. clinically infected wounds. or bone. Staphylococcus epidermidis. d. blood vessels. Management of dog and cat bites A. liver or pulmonary disease. Full-thickness puncture wounds. Staphylococcus intermedius. Microbiology A. Wound care 1. Determine whether the animal was provoked and to record the time of the injury. 3. Underlying diabetes. B. gamma-hemolytic Anaerobes. severe crush injury and/or edema.
14. fungal infections. Human diploid cell vaccine (HDCV). Tetanus Immunization. Cellulitis is treated for 1014 days. in divided doses tid Adults: 1 g every 24 hours IM or IV Children: 50 mg/kg/d qd Adults: 500 mg qid Children: 50 mg/kg/day. If rabies infection is suspected.1 g q6h Adults: 1-2 g q24h Children: 50-100 mg/kg/day. in divided doses q6-8h Adults: 500 mg tid Children: 40 mg/kg/d.compromising condition. if rabies is contracted. 3. 7. skunks. Lymphadenopathy is caused by reactive hyperplasia of undetermined etiology in 50%. Rabies is transmitted when the saliva of an infected animal comes into contact with the broken skin or mucosa of another mammal.0 g q6h Adults: 3. Peripheral Children Lymphadenopathy in Palpable lymph nodes are often found in children because their immune systems are being activated by environmental antigens and the common organisms. see page 182. IM (separate from human diploid cell vaccine below). Treatment of infected wounds. Wild animals (raccoons. rabies prophylaxis is administered as follows: a. The incubation period ranges from 10 days to one year. in divided doses q6h Alternative Intravenous Antibiotics Ampicillin/sulbact am (Unasyn) Ticarcillinclavulanate (Timentin) Ceftriaxone (Rocephin) Adults: 1. Infected bite wounds are treated with amoxicillin/ clavulanate (Augmentin). 1 cc IM (not gluteal) given on days 1. in divided doses bid Adults: 500 mg tid Children: 40 mg amoxicillin/kg/day. 2.5-3. Animal bites should be regarded as tetanus prone. although tetanus infection resulting from cat and dog bites is rare. An untreated person has a less than 20% chance of contracting rabies from the bite of a rabid animal. such as Hodgkin disease. and 28. However. 3. Rabies immunoprophylaxis 1. including cat scratch disease. Thirteen percent have neoplastic diseases. the mortality rate is 100%. E. b. The incidence of rabies in persons who have been bitten by a dog is very low because most dogs have been vaccinated. in divided doses tid Amoxicillin/clavul anate (Augmentin) Ceftriaxone (Rocephin) Penicillin V Amoxicillin Intravenous Antibiotic of Choice Cefoxitin (Mefoxin) Adults: 1-2 g q4-8h Children: 25-50 mg/kg/day. or Langerhans cell histiocytosis (histiocytosis X). bats) are the most common source of rabies. Chronic dermatopathic or bacterial infections . D. Rabies immune globulin (RIG). Prophylactic Antibiotics for Dog and Cat Bites Outpatient Antibiotics Cephalexin (Keflex) Doxycycline (Vibramycin) Adults: 500 mg qid Children: 40 mg/kg/d PO qid Adults: 100 mg bid Children: 2-4 mg/kg/day. References. 20 IU/kg. Nearly one-third of children have granulomatous diseases. in divided doses q24h C. mycobacterial infections.
or because of a systemic infection. atypical mycobacteria. Infectious Etiologies of Cervical Adenitis Bacterial Viral Fungal/prot ozoal Other Localized Acute Staphylococcus aureus Streptococcus pyogenes Group B streptococcus Anaerobes Francisella tularensis Rubella Adenoviruses Herpes simplex virus Mumps Human herpesvirus 6 Toxoplasmos is Histoplasmos is Kawasaki syndrome Rickettsial pox Subacute or Chronic Tuberculosis Atypical mycobacteria Cat-scratch disease Generalized Syphilis Tuberculosis Scarlet fever Typhoid fever Leptospirosis Brucellosis virus HIV EpsteinBarr Cytomegal ovirus Measles Rubella Varicella Adenovirus Histoplasmos is Toxoplasmos is Rickettsial Scrub typhus Syphilis Actinomyc osis Nocardiosi s Brucellosi s Organism Associated with Infectious Cervical Lymphadenitis Neonates Staphylococcus aureus Group B streptococcal “cellulitis-adenitis” syndrome Infancy As above Kawasaki syndrome . b. such as toxoplasmosis and infectious mononucleosis caused by Epstein-Barr virus or cytomegalovirus. Only one-quarter of patients with enlarged cervical nodes have another serious disease. A. typically are caused by staphylococcal and streptococcal infection. I. Anatomy and definitions Normal lymph nodes usually are less than 1 cm in diameter. a. Cervical. II. Hard nodes. Differential diagnosis. Inflamed cervical nodes that develop over a few days and progress to fluctuation. or Bartonella henselae. Fluctuant cervical nodes that develop over weeks to months without significant inflammation or tenderness suggest infection with Mycobacterium tuberculosis. especially in children. Lymph nodes often are palpable in the inguinal region in healthy individuals. The nodes involved with Hodgkin disease are rubbery. Lymphadenopathy should be classified as localized (in only one region such as the neck or axilla) or generalized (more than one region). Lymphadenopathy can be caused by a vast array of diseases and drugs. often dicloxacillin. The anterior cervical lymph nodes often are enlarged because of a variety of infections of the head and neck. Localized 1. Upper posterior cervical lymphadenopathy rarely is associated with significant diseases in children. the agent of cat scratch disease. A.comprised the remaining 3 percent of patients. Treatment begins first with a course of antibiotics. are found infrequently in children. often associated with cancer in adults. which most often is mycobacterial. perhaps because chronic trauma and infection are common in the lower extremities. but incision and drainage may be indicated. Only 20 percent of biopsies will demonstrate a treatable disease. Nodes also may be palpable in the neck (particularly submandibular) because of previous head and neck infections.
coccidiodomycosis. inflammatory pseudotumor. drug reactions (phenyutoin) Hypothyroidism. plague. tularemia. Still’s disease. lymphogranuloma venereum. lipid storage diseases. cat scratch fever disease. cryptococcus Toxoplasmosis Secondary syphilis. rubella. chronic granulomatous diseases. rat bite fever Brucellosis. diphtheria. amyloidosis. dermatomysositis. chancroid. leukemia Angioimmunoblastic lymphadenopathy with dysproteinemia Autoimmune lymphoroliferative disease Rosai-Dorfmans’s disease H e m o p h a g o c y t i c lymphohistiocytosis Serum sickness. skin infections. Epstein-Barr virus. rheumatoid arthritis. measles. mumps. typhoid fever Human immunodeficiency virus. Castlemans’ disease.1 to 4 Years Staphylococcus aureus Streptococcus pyogenes Atypical mycobacteria 5 to 15 years Anaerobic bacteria Toxoplasmosis Cat-scratch disease Tuberculosis Causes of Peripheral Lymphadenopathy Cause Infections Bacterial Localized Streptococcal pharyngitis. herpes simplex virus. dengue fever Mycobacterium tuberculosis. ChurgStrauss syndrome Examples Generalized Viral Mycobacterial Fungal Protozoal Spirochetal Cancer Lymphoproliferat ive Immunologic Endocrine Miscellaneous . atypical mycobacteria H i s t o p l a s m o s i s . hepatitis B. Addison’s disease Sarcoidosis. Kikuchi’s disease. cytomegalovirus. h i s t i o c yt o s i s . leptospirosis. systemic lupus erythematosus. Lyme disease Metastatic. Kawasaki disease. lymphoma.
nontender. and many biopsied nodes show only hyperplasia. The nodes decrease in size after the acute presentation. account for most cases in children. 4.Drugs That Cause Lymphadenopathy Allopurinol Atenolol Captopril Carbamazepine Cephalosporins Gold Hydralazine Penicillin Phenytoin Primidone Pyrimethamine Quinidine Sulfonamides Sulindac Causes of Generalized Lymphadenopathy Mononucleosis syndromes HIV infection Secondary Syphilis Hepatitis B Tuberculosis Lyme Disease Measles Rubella Brucellosis Typhoid fever Systemic lupus erythematosus Rheumatoid arthritis Still’s disease Kawasaki disease Dermatomyositis Amyloidosis Serum sickness Leukemia Lymphoma 2. Palpable epitrochlear nodes are not always pathologic in children. 4. The nodes typically are soft. Diagnostic approach A. History 1. Mycobacterial infection can present with lymphadenopathy alone. Left supraclavicular adenopathy (“Virchow’s node”) suggests abdominal malignancy. Phenytoin can cause generalized lymphadenopathy. The axillary nodes receive drainage from the arm.5 to several centimeters. especially in the neck (scrofula). Mycobacterium avium complex and M. 5. and atypical mycobacterial infections. Right supraclavicular adenopathy is associated with cancer of the mediastinal lymph nodes. B. cat [cat scratch disease]. are common causes of axillary lymphadenopathy. scrofulaceum. varying in size from 0. and usually detected in the cervical. but a modest degree of adenopathy tends to persist. 5. Infections. 2. thoracic wall. Systemic lupus erythematosus. cervical. and occipital nodes develops in the majority of individuals during the second week of acute symptomatic HIV infection. Nodes are kidney-shaped. Generalized lymphadenopathy 1. Supraclavicular (or lower cervical) lymphadenopathy is associated with a high risk of malignancy (up to 75 percent). Nontender adenopathy primarily involving the axillary. Axillary. and inguinal areas. Inguinal lymphadenopathy in children usually is associated with no specific etiology unless the nodes are very large (>3 cm). and generalized lymphadenopathy. including cat scratch disease. and lymphadenopathy. also most often a lymphoma. Enlargement of lymph nodes occurs in 50 percent of patients with systemic lupus erythematosus (SLE). under- . Nodes typically are nontender. although hyperplastic nodes are found in over one-third. axillary. Medications may cause serum sickness that is characterized by fever. enlarge over weeks to months and can progress to matting and fluctuation. Epitrochlear. Exposures (eg. which helps to distinguish infectious mononucleosis from other causes of pharyngitis. Lymph node involvement is symmetric and involves the posterior cervical more than the anterior chain. discrete. and breast. Miliary tuberculosis may cause generalized lymphadenopathy. Other causes include infections of the forearm or hand. 2. arthralgias. Lymphadenopathy also may be present in the axillary and inguinal areas. 3. lymphoma. HIV. 3. rash. III. Localizing signs or symptoms suggestive of infection or malignancy. leukemia. pharyngitis. Mononucleosis is characterized by the triad of moderate to high fever.
Size. Firm. Fluctuant nodes may be necessary to relieve pain and treat obvious infection. C. This situation typically occurs with inflammatory processes. in addition to the liver and spleen. Tenderness suggests recent. Prescribe analgesics 3. Use of medications that can cause lymphadenopathy. deep fascia) by invading cancers or inflammation. Treatment of Acute Pyogenic Bacterial Lymphadenitis Symptomatic Therapy 1. high-risk behavior (eg. B. sexual behavior. Incise and drain nodes that have suppuration . Abnormal nodes generally are greater than 1 cm in diameter. night sweats. They also can become fixed to each other (“matted”). and malignancy. If these tests are normal. fever typically accompanies lymphadenopathy for the majority of the infectious etiologies. Biopsy is appropriate if an abnormal node has not resolved after four weeks. or weight loss suggestive of tuberculosis. immunologic stimulation. nodes in acute leukemia tend to be softer. lymphoma. Physical examination 1. 4. can determine whether it is truly local lymphadenopathy. ANA. injection drug use). PPD. Hard nodes are found in cancers that induce fibrosis (scirrhous changes) and when previous inflammation has left fibrosis. Constitutional symptoms such as fever. Patients with generalized lymphadenopathy should have a CBC and chest radiograph. travel.or second-generation cephalosporin or dicloxacillin) if nothing else in the history and physical examination suggests malignancy. RPR. Malignancy is more likely to be found in nodes larger than 2 cm. moist dressings 2. cervical. rapid enlargement that has put pain receptors in the capsule under tension. Location. Fixation. 2. tick bite [Lyme disease]). Diagnostic tests 1. Palpation of inguinal. 4. but it also can occur because of hemorrhage into a node. Consistency. or other malignancy.cooked meat [toxoplasmosis]. HIV antibody determination. Abnormal nodes can become fixed to adjacent tissues (eg. serologic test for acute EBV and CMV infections. rubbery nodes are found in lymphomas and chronic leukemia. and heterophile test. 3. 5. other considerations include an erythrocyte sedimentation rate. 3. Apply warm. or immediately in patients with other findings suggestive of malignancy. Incision and drainage. and axillary nodes. Patients with localized (especially cervical) lymphadenopathy can be observed for three to four weeks and treated empirically with antibiotics (first. Normal lymph nodes are freely movable in the subcutaneous space. 2. 3.
bedding. worms migrate through the anus. one 100-mg tablet orally. Fresh stool may also be obtained by rectal examination. II. or in infants 1 mo of age: IV Nafcillin (Nafcil) 150 mg/kg day OR IV Cefazolin (Ancef) 150 mg/kg/day after aspiration of node Suppuration: IV antibiotics as above and incision and drainage No prominent systemic symptoms. vulvovaginitis. but serious infections may cause symptoms ranging from abdominal discomfort to severe pain. see page 182. and the homeless. A. Ascariasis A. At night. The infection is fairly common in the rural southeastern United States and is frequent among immigrants. The pinworm (Enterobius vermicularis) is the most common helminth. migrant laborers. D. The stool is usually negative for ova and worms. Stool examination. loss of appetite.Antimicrobial Therapy Suspected staphylococcal/group A and B streptococcal disease Cellulitis or marked enlargement. I. Intestinal Helminths Intestinal helminth infestations most commonly affect travelers. or suppuration: Dicloxacillin (Dynapen) 25 mg/kg/day OR Cephalexin (Keflex) 50 mg/kg/day OR Clindamycin (Cleocin) 30 mg/kg/day Suspected anaerobic infection with dental or periodontal disease. Anorexia. rectal prolapse. The disorder tends to occur in temperate climates. A second dose is given 10 days later. pruritus. B. Microscopic eggs infest clothing. Examination of the stool for ova and parasites is the most important test for helminthic infection. Treatment 1. include: Penicillin V 50 mg/kg/day or Clindamycin (Cleocin) 30 mg/kg/day OR Group A streptococcal infection Aqueous penicillin G 50 000 IU/kg/day IV OR Penicillin V 50 mg/kg/day PO OR Cephalexin 50 mg/kg/day PO OR Erythromycin ethylsuccinate 40 mg/kg/day PO Group B streptococcal disease in infants Aqueous penicillin G 200 000 IU/kg/day IV. Intestinal helminth infections are usually asymptomatic. Specimens are collected on three separate mornings. To obtain the eggs. Pinworms are about 10 mm in length. The female worm has a pin-shaped tail. restlessness. The entire family is treated. then deposit their eggs and die on the perianal skin. is safe and effective. Clinical evaluation A. children of foreign adoptions. and intractable anal itching. colorless eggs measure 50 to 60 µm and are flattened on one side. The elongate. nausea. Stools are collected using plastic wrap under the toilet seat. Enterobiasis A. moderate-to-severe systemic symptoms. if sensitive. Many patients are asymptomatic. B. then taped to glass slides and taken to a laboratory for examination. diarrhea. These parasitic infections are associated with day-care centers and overseas travel. Dogs and cats do not spread this infection. Pinworms are diagnosed by examining the perianal skin. C. a tongue blade covered with clear tape is placed sticky-side down over the perianal skin in the morning. E. III. and death may occur. often spreading to the entire family. Roundworms (Ascaris lumbricoides) measure up to 18 inches in length. Hives and eosinophilia may develop. Worms may also be visualized if the anus is examined late at night or early in the morning. cellulitis. and the perianal area kept clean. References. refugees. Mebendazole (Vermox). Pinworms present as anal pruritus in irritable children. Heavier infections may cause insomnia. Infested clothing and bedding are washed and fingernails should be kept trimmed. and other surfaces. 2. bowel obstruction. lumbricoides only . Relapses are common. and the worms may sometimes spontaneously exit the body through the anus.
However. 2. B. 2. Trichuriasis A. which they use to consume 0. Treatment of trichuriasis is the same as for ascariasis. Mebendazole (Vermox). saginata since its eggs can cause cysticercosis. causing neurocysticercosis. Hookworms 1. Treatment 1. C. Treatment consists of mebendazole as described above and iron supplementation. 2. with a thread-like anterior portion. abdominal cramping. Whipworm eggs incubate in the soil. the larvae may invade the central nervous system. Filariform larvae are capable of penetrating intact skin.03-0. B. . diarrhea. Dwarf tapeworm is the most common tapeworm in the U. b. A follow-up examination of stool for ova and parasites should be performed in two months. Ingestion of food contaminated with mouse droppings may spread the infection. Fish tapeworm is occasionally transmitted by undercooked fish. causing mild blood loss and symptoms similar to proctitis and inflammatory bowel disease. 3. especially from the Great Lakes region. chronic fatigue. Whipworm (Trichuris trichiura) infestation is less common than Ascaris infestation. 4. 3.infests humans. Symptoms are usually absent but may include pruritus. IV. C. and they may persist in the soil for more than a decade until they are accidentally consumed. Beef tapeworm is transmitted by inadequately cooked beef. This tapeworm is 1 inch in length. It can occasionally causes megaloblastic anemia. Patients with neurocysticercosis frequently present with seizures.15 mL of blood per day for 10 to 15 years. Hookworms develop in the soil from eggs in feces. Persistent unexplained eosinophilia in a patient from a region where Strongyloides infection is endemic should prompt serologic testing because stool specimens are often negative. persisting for 40 years or more in the small intestine. The larvae are capable of penetrating the bare feet and causing a pruritic rash. Diagnosis is made by passage of ribbon-like tapeworm segments or by finding the eggs in a stool. reaching up to 10 to 15 feet in length in the gut. Manifestations include iron deficiency anemia.S. Adult hookworms are about 10 µm in length. failure to thrive. loss of appetite. Adult whipworms are 30-50 µm in length. D. they travel to the colon. 5. Ascaris eggs reach the soil in feces. and hives may occur. Tapeworms 1. Pork tapeworm is found in immigrants from Central and South America. When swallowed. and colitis. Treatment consists of thiabendazole (Mintezol). 2. most patients experience only vague abdominal discomfort or nausea. 100 mg bid for three days. Pork tapeworm is far more dangerous than T. Strongyloidiasis 1. see page 182. Family screening is recommended. Treatment of all tapeworms consists of praziquantel (Biltricide) or niclosamide (Niclocide). and depression. geophagia. Less common parasites A. a. They can live in the intestine and produce eggs for several years. It can also be spread in feces or as a sexually transmitted disease. This diagnosis should be considered in the evaluation of a patient from Central or South America with a new-onset seizure disorder. pneumonia. References. with a hooked anterior end. nana infection may cycle in immigrant children for years. In severe cases. Rectal prolapse. H. In the gut. The larvae eventually reach the small intestine. worms may cause intestinal obstruction. B. occurring in the southeastern states and in foreign immigrants. V. the invasion of human tissue by larval forms. C.
Clinical evaluation A. plus clindamycin (10 mg/kg/dose q8h IV). the cause is much more likely to be conjunctivitis. The organisms that most frequently cause periorbital cellulitis following trauma are Staphylococcus aureus and Streptococcus pyogenes (group A beta-hemolytic streptococci). and visual acuity should be tested. Periorbital and orbital cellulitis cause eyelid swelling. Pathogenesis of periorbital cellulitis A. rather than periorbital or orbital cellulitis. anaerobic bacteria. and the remaining 15%. Clinical findings include a temperature of 39°C or more and a peripheral white blood cell count of greater than 15. About one-fourth of isolates are S aureus. Ceftriaxone (50 mg/kg. one-tenth.to 10-day course of therapy. and the pathogen is isolated from the blood in about two thirds of these cases.Orbital and Periorbital Cellulitis Periorbital cellulitis is a bacterial infection of the skin and structures superficial to the orbit. C. Virtually all involved eyelids will be erythematous or violaceous. II. Blood culture for bacterial pathogens should be obtained. and bilateral lid involvement are present. 2. such as ceftriaxone (50 mg/kg qd IM or IV) or cefotaxime (50 mg/kg/dose q6h IV). Globe displacement (proptosis). Periorbital cellulitis usually occurs in children younger than 2 years of age. an insect bite. orbital abscess. Hib disease accounts for fewer than 15% of periorbital cellulitis. Signs of trauma or local infection are observed in one-third of patients. I. Since the introduction of H influenzae type b conjugate vaccines (HbCV). one-fifth. Orbital cellulitis.000/mm³ suggests bacteremic disease. or infection with herpes simplex or varicella zoster viruses. The most common causes of eyelid redness and swelling are allergy. one-fifth. see page 182. S pneumoniae. and antimicrobial therapy should consist of a third-generation cephalosporin. B. IV. orbital cellulitis is a bacterial infection of the orbit. the child may be started on a broad-spectrum oral agent such as ampicillin/clavulanate (Augmentin) or Trimethoprim/sulfamethoxazole (Bactrim) to complete a 7. abnormal movement (ophthalmoplegia). C. B. White blood cell count greater than 15.000/mm³. Children who have signs of orbital cellulitis should be hospitalized. Periorbital cellulitis usually occurs after the skin near the eye has been broken by trauma. other bacteria. 2. If the blood culture remains negative. Treatment A. not to exceed 1 g) is given IM or IV. trauma. Laboratory evaluation 1. Periorbital cellulitis can be managed on an outpatient basis if there is no orbital involvement and the child does not appear toxic. or pain on movement should be sought. Lumbar puncture should be performed on all children younger than 1 year of age who have not had at least two doses of H influenzae B vaccine. a purulent discharge. S pyogenes. A child who has received a second dose of HbCV more than 1 week before the onset of eyelid swelling is very unlikely to have HIB disease. References. When conjunctival inflammation. D. A bacterial pathogen is identified in only 30% of cases of periorbital cellulitis. III. Periorbital cellulitis 1. B. Pathogenesis of orbital cellulitis A. and cavernous sinus thrombosis. 3. and insect stings or bites. one-tenth. HiB. Orbital cellulitis may progress to subperiosteal abscess. with the swelling being unilateral in 95-98% of cases. B. . E.
B.Tuberculosis The number of cases of tuberculosis in children younger than five years of age in cities has increased 94. If the repeat PPD test is positive. Natural history of tuberculosis A. the child should be treated for 9 months. or 6 weeks after the MMR vaccine dose. If the repeat PPD test remains negative. 25% of tuberculosis disease is extrapulmonary. Thirty to 50% of all household contacts of infectious adults will have a positive PPD. The size of the PPD reaction determined to be positive varies with the risk of tuberculous infection. 2. because of transient immunosuppression from the live MMR vaccine. Extrapulmonary disease is more common in children than in adults. Children at risk for infection 1. Tuberculosis infection is initiated by the inhalation of organisms into the lung. the purified protein derivative (PPD) test usually becomes positive. I. A PPD test is recommended for children in highrisk groups. 3. D. A false-negative PPD test may occur within 6 weeks of an MMR vaccination. tuberculosis strain is considered in selecting a prophylactic or treatment regimen. The diameter of the induration is measured 48 to 72 hours after PPD placement. and/or small parenchymal infiltrates. and the chest radiograph may be only minimally abnormal. II. In children. and prophylactic therapy can be discontinued. Children who do not have clinical disease. Reactivation. miliary tuberculosis. Healed primary tuberculosis may leave calcified deposits in the lung parenchyma and/or hilum. Contact with the person with contagious tuberculosis who infected the child must be prevented until the source case is no longer infectious. A positive PPD test requires an evaluation for tuberculous disease. Diagnosis of tuberculosis in children A. adenitis. or in the elderly. Any child with a positive PPD test should be evaluated for active pulmonary and extrapulmonary tuberculosis with a history and physical examination and posteroanterior and lateral chest radiographs. and bone and joint infections. Reactivation is most likely to occur during adolescence. C. Children and young adolescents are more likely than adults to have tuberculous meningitis. the organisms spread to the hilar lymph nodes. but who harbor a reservoir of quiescent organisms may develop tuberculous disease later in life. during an episode of immunosuppression. simultaneously with the MMR vaccine dose. the child is assumed not to be infected. B. During the incubation period. A screening PPD test of 5 tuberculin units can be placed before a dose of measlesmumps-rubella (MMR) vaccine. During an incubation period. 10 mg/kg/day. in the presence of chronic disease. usually isoniazid (Laniazid). All household contacts of adults with active disease should be tested by PPD. Children who are known contacts and who are PPD negative. The susceptibility of the source case’s M. Primary tuberculosis is often completely asymptomatic. This condition is considered primary tuberculosis. The PPD is repeated in 3 months to check for conversion to a positive PPD test.3% in the last four years. with hilar adenopathy. Children exposed to tuberculosis 1. The source of the child’s infection should be determined. . 2. should receive prophylactic therapy. that lasts 2 to 10 weeks. which would indicate infection.
and South and Central America. positive respiratory system findings. hilar or cervical adenopathy. B. Gastric aspirates in children who are too young to produce a deep sputum sample c. Adenopathy. and children who are exposed to adults at high risk for tuberculosis. or whose parents were born in. Previous vaccination with bacille CalmetteGuerin (BCG) vaccine does not change the interpretation of the PPD test. Africa and Latin America. III. children who are homeless. symptoms of tuberculosis. d. Mexico.Criteria for a Positive PPD Test in Children Reaction of 5 mm or more Children suspected of having tuberculosis (chest x-ray consistent with active or previously active tuberculosis. High tuberculous infection rates occur in Southeast Asia. meningitis. C. b. the Caribbean. children who have previously been treated for tuberculosis. The work-up for a child with a positive PPD test or suspected tuberculosis includes the following: 1. regions where tuberculosis is highly prevalent Children frequently exposed to adults who are HIV infected. incarcerated or institutionalized persons. and migrant farm workers Children with other medical risk factors (Hodgkin’s disease. Clinical evidence suggestive of tuberculosis. History. Diagnostic tests a. 2. lymphoma. “aseptic” meningitis. Chest x-ray (posteroanterior and lateral). If the organism may be resistant to one of the standard medications. If possible. Cultures and smears of appropriate body fluids in children with suspected extrapulmonary tuberculosis. diabetes mellitus. Eastern Mediterranean countries. . joint or bone infection. Sputum collection or induction in children who are able to produce a deep sputum sample. residents of nursing homes. ethambutol (Myambutol [or streptomycin in children too young for visual acuity testing]) should be included. IV. children who live in large cities. chronic renal failure) Reaction of 15 mm or more Children older than 4 years without any risk factors 3. Risk factors for exposure to tuberculosis. Drug-resistant tuberculosis should be suspected in children who are exposed to immigrants from Asia. homeless persons. Africa. 4. adult source case. Physical examination. corticosteroid therapy) Reaction of 10 mm or more Children younger than 4 years of age Children born in. 3. poor and medically indigent city dwellers. or pleural effusion. clinical signs of tuberculosis) Children in close contact with persons who have known or suspected infectious tuberculosis Children with immunosuppressive conditions (HIV infection. Tuberculosis must be considered when a child presents with pneumonia that is unresponsive to antibiotic treatment. Treatments should be directly observed to ensure compliance. Evaluation of tuberculosis in children A. the susceptibility results of the adult source case should guide the medication choice. Treatment of active tuberculosis A. IV and other street drug users. Western Pacific countries. bone or joint disease. or who are from areas in which isoniazid resistance occurs in more than 4% of cases.
rifampin (Rifadin). antibiotics administered. Occasionally. acute otitis media. miliary disease and bone/joint disease Meningitis. B. The following past . Treatment of latent tuberculosis infection A. rifampin. a n d pyrazinamide. recent illnesses. I. 10-15 mg/kg/day. older children may present with failure to thrive. History. and abdominal pain. followed by 4 months of daily or twice-weekly isoniazid and rifampin Same as for pulmonary disease Comments Medications can be given 2 o r 3 times/week under direct observation in the initial phase Extrapulmonary disease. The presence of another potential source for fever (upper respiratory tract infection. or hypertension secondary to prior unrecognized UTIs. urinary symptoms. 10-20 mg/kg/day. Urinary Tract Infections in Children Urinary tract infections (UTI) are a common problem in childhood. Clinical features A. hypertension. frequency. UTI includes both cystitis and pyelonephritis. max 2. HIV testing should be completed for any older child or adult with tuberculosis. followed by 10 months of daily or twice-weekly isoniazid and rifampin V. Signs and Symptoms of UTI In Children Newborns Infants and Preschoolers Diarrhea Failure to thrive Vomiting Fever Strong-smelling urine School-Age Children Vomiting Fever Strong-smelling urine Abdominal pain Frequency Dysuria Urgency Enuresis Jaundice Hypothermia Sepsis Failure to thrive Vomiting Fever C. Older children with UTI may have fever. see page 182. References. The child with tuberculous infection or disease may return to school or child care after drug therapy has been initiated and clinical symptoms have resolved. B. Suprapubic tenderness and costovertebral angle tenderness may be present. Infants and young children with UTI can present only with fever. Other less common symptoms of UTI in infants include conjugated hyperbilirubinemia and failure to thrive. 20-40 mg/kg/day. but no signs of active disease. incontinence. which may lead to renal scarring. Exposure to drug-resistant tuberculosis requires more specific therapy. The height and duration of fever.Treatment Regimens for Active Tuberculosis Type of Disease Pulmonary ease disPrimary Regimen Two months of isoniazid. urinary symptoms (dysuria. miliary disease. and use of barrier contraceptive method should be assessed. Children with a positive PPD test. should receive isoniazid for 9 months if they are younger than 18 years and for at least 6 months if they are 18 years of age or older. pyrazinamide and streptomycin. max 600 m g/ d a y. nephropathy. acute gastroenteritis) does not rule out the possibility of UTI.0 g/day. macroscopic hematuria). max 300 mg/day. vomiting. and bone/joint disease Two months of daily isoniazid. and end stage renal dysfunction. urgency. except meningitis.
frequency. sexually transmitted diseases (STDs). A child with a positive nitrite test is very likely to have a UTI. 2. II. abdominal pain. Incontinence. III. White race. Previous UTIs. Examination of urine using these three techniques has been termed an “enhanced urinalysis. Clean catch specimen is the preferred method of urine collection in a toilet-trained child. penile and labial adhesions). The presence of two or more of the following five variables predicts UTI accurately: a. Previous undiagnosed febrile illnesses. An uncentrifuged specimen. All older girls with urinary symptoms suggestive of UTI should have a urine specimen obtained for urinalysis and culture. Vesicoureteral reflux (VUR). the odds of UTI are much higher than the odds of occult bacteremia. c. A hemocytometer (results reported as WBC/mm3). a urine culture should still be obtained in children with suspected UTI who have a negative dipstick test. Physical examination.” In young children. The differential diagnosis of an older child presenting with urinary symptoms and bacteriuria includes nonspecific vulvovaginitis. lack of proper stream. 1. e. and Kawasaki disease may present with fever. A catheterized specimen is preferred in the diapered child. D. Chronic constipation. In children vaccinated against Haemophilus influenzae and Streptococcus pneumoniae. 2. 6. urgency. Temperature >39ºC. E. Decision to obtain urine 1. absence of upper respiratory infection. Absence of another source of fever on history or examination (ie. temperature. 2. and pyuria. C. 4. withholding maneuvers. acute otitis media. Blood pressure. Chronic urinary symptoms. b. Family history of frequent UTIs. urethritis secondary to an STD (particularly Chlamydia). 2. and other sources of fever should be evaluated. Differential diagnosis of a well-appearing infant with fever without a definite source includes UTI and occult bacteremia. A Gram stained specimen. Therefore. repeated contaminated specimen or repeated low colony counts). and anatomic abnormalities. Definition of a UTI . Catheterization is not feasible (eg. b. 3. Results from catheterized specimen are inconclusive (eg. 2. and a vaginal foreign body. Age under one year. vaginal foreign body. A suprapubic aspirate is recommended when: 1. c. appendicitis. Microscopic examination 1. d. Dipstick tests are convenient but may miss some children with UTI (sensitivity 88%). gastroenteritis). Suprapubic aspiration also may be used to collect a specimen in young children. 5. Fever for more than two days. the enhanced urinalysis offers the best combination of sensitivity and specificity for predicting a UTI in children. suprapubic and costovertebral tenderness. External genitalia should be examined for vulvovaginitis. Urine culture should be performed in most patients. The accuracy of microscopic analysis is improved by using: a.history should be obtained: 1. urinary calculi. B. VUR and other genitourinary abnormalities. Patients with group A streptococcal infection. Diagnosis A. D.
A. . Children with recurrent UTI 5. Children who are not responding to outpatient therapy. and prevention of urinary tract infections in children A. Choice of antibiotics. A three-day course of antibiotics is recommended in older children with their first episode of cystitis (low risk of recurrence or complications). The radionuclide VCUG is more sensitive than contrast VCUG has a sensitivity of 78 to 91%). the presence of duplication and dilatation of the ureters. Renal ultrasonography can demonstrate the size and shape of the kidneys. A blood culture is not necessary in children over two months with UTI. E. Children under five years of age with a febrile UTI. Quinolones are effective and resistance is rare. and children with recurrent UTI. girls under the age of three years with a first UTI.000 cfu/mL A. Males of any age with a first UTI. 2. Management.Culture Criteria for Significant Bacteruria Method Suprapubic aspiration Urethral catheterization Best catch Colony Count Any bacteria >10. Imaging. Voiding cystourethrogram is an excellent test to establish the presence and degree of VUR. B. 2.to 14-day course of an antimicrobial is recommended for young children and for those with recurrent or febrile UTIs.and third-generation cephalosporins and gentamicin although these drugs are not effective in treating enterococcal infections. D.000 cfu/mL >50. which makes it more suited for grading VUR. 2. coli is the most common pathogen causing UTI. and trimethoprim-sulfamethoxazole (TMP-SMX) should be used with caution because increasing resistance to these antibiotics. Gram staining of the urine can aid in the choice of initial antimicrobial therapy. C. prognosis. and 50 percent of E. B. An ultrasound in children with a UTI who do not respond promptly to therapy is recommended. amoxicillinclavulanate or ampicillin-sulbactam. First-generation cephalosporins. Children less than one month of age with high fever and a positive urinalysis should have a lumbar puncture performed. Children with UTI who do not respond promptly to therapy. Routine VCUG for children is recommended under the age of five years with a febrile UTI. Hospitalization. 3. Radionuclide VCUG involves catheterization to fill the bladder with a radioactive liquid and recording of VUR during voiding. Cefixime has been shown to be effective in the treatment of outpatients with UTI. 4. Girls under three years of age with a first UTI. Recommendations for imaging 1. C. who are vomiting and therefore cannot tolerate oral medication. Alternatives include second. Routine performance of renal ultrasonography is not recommended following diagnosis of a first UTI in children in whom prenatal ultrasonography has been performed in a reputable center at >30 to 32 weeks of pregnancy. The contrast VCUG provides a better anatomic resolution. Routine imaging is recommended for: 1. 1. and the existence of gross anatomic abnormalities. or who are not able to be adequately followed should be managed as inpatients. I. since approximately 1 percent with UTI may also have bacterial meningitis IV. males of any age with a first UTI. coli are resistant to amoxicillin or ampicillin. A 10. Duration of therapy 1. but safety in children is still unknown.
Low-dose long-term antimicrobial therapy. 500 mg] 40 mg of amoxicillin kg/day PO q8h [susp: amoxicillin 125 mg/clavulanate/5 mL. Treatment of dysfunctional elimination decreases UTI recurrence and is associated with faster resolution of VUR. tab: amoxicillin 250 mg/clavulanate. Children with grades IV and V VUR and older children are less likely to experience spontaneous resolution. tabs: 250. Prompt diagnosis and treatment of UTI reduces renal scarring. Breakthrough UTIs are most common in girls. Prophylaxis should be discontinued after age five to seven years. amoxicillin 500 mg/clavulanate] 6-12 mg/kg/day (trimethoprim) q12h [susp: trimethoprim 40 mg/sulfamethoxazole 200 mg/5 mL] Cefprozil (Cefzil) Cefixime (Suprax) Cefuroxime (Ceftin) Amoxicillin/clavulan ate (Augmentin) Trimethoprim/sulfa methoxazole (Bactrim) D. Prophylaxis consists of TMP-SMX or nitrofurantoin in half the usual therapeutic doses given at bedtime. 250 mg/5 mL. 100 mg/5 mL. Amoxicillin and cephalosporins are not recommended for prophylaxis since infection with resistant strains is likely to emerge. however. Older children with persistent severe VUR (grades IV and V). 5. Children with VUR. and those with lesser degrees of VUR but with progressive scarring while on prophylaxis.5 mg /kg/day(IV. IV) q24h 7. 4. Treatment of dysfunctional . 200 mg] 30 mg/kg/day PO q12h [susp: 125 mg/5 mL. 3. 6. Eight to 30 percent of children with UTI experience reinfections.5 mg/kg/day IV/IM q8h 100 mg/kg/day IV/IM q6h Dosage (mg/kg/day) 100 mg /kg/day (IV) q6-8h 100-200 mg of ampicillin/kg/day q6h 3-7. should be prescribed for recurrent febrile UTIs and scarring. even if low-grade VUR persists. IM) q8h Antibiotic Therapy for Urinary Tract Infections with Mild Symptoms Agent Cefpodoxime (Vantin) Dosage 10 mg/kg/day PO q12h [susp: 50 mg/5 mL. may experience GI adverse events. which will resolve spontaneously. The goal of treating vesicoureteral reflux (VUR) is to prevent progressive renal damage. 500 mg] 8 mg/kg/d PO qd-bid [susp: 100 mg/5 mL. The majority of young children with VUR have low-grade (grade I to III) VUR. 250. Children with recurrent UTI symptoms. One out of every five patients on prophylactic nitrofurantoin doses. Children with dysfunctional elimination. tab: 200.400 mg] 125-500 mg PO q12h [125. Mild-to-moderate VUR is treated with low-dose long-term antimicrobials until resolution of VUR. 2. Long-term management and follow-up 1. should undergo ureteral reimplantation. tabs: 100 mg. such as six to 12 months of TMP-SMX or nitrofurantoin.Antibiotic Therapy for Urinary Tract Infections with Severe Symptoms Agent Neonate Ampicillin and Gentamicin Older Child Ceftriaxone (Rocephin) Cefotaxime (Claforan) Ampicillin/sulbactam (Unasyn) Gentamicin 50 mg /kg/day (IM.
2. Viral croup affects 3-5% of all children each year. Upper airway obstruction in school age and older children tends to be caused by severe tonsillitis or peritonsillar abscesses. cause loud stridor accompanied by a hoarse voice and barky cough. References. D.elimination includes the use of laxatives and timed voiding (scheduled voids every two to three hours). Clinical evaluation of upper airway obstruction and stridor A. causing 90% of cases. 4. viral croup and retropharyngeal abscess are the most common causes of upper airway obstruction. The disease is usually self-limited. severe tonsillitis or retropharyngeal abscess. Patients with suspected epiglottitis. Children in the 1. Gradual onset of symptoms. B. Viral Laryngotracheitis (Croup) Acute laryngotracheitis (viral croup) is the most common infectious cause of acute upper airway obstruction in pediatrics. I. a person skilled at intubation must accompany the child at all times. 2. If a supraglottic disorder is suspected. Very acute onset of symptoms suggests epiglottitis. dysphagia and a preference for sitting upright. Stridor is the most common presenting feature of all causes of acute upper airway obstruction. 2. such as croup. severe respiratory distress from an obstruction. It is a harsh sound that results from air movement through a partially obstructed upper airway. usually preceded by upper respiratory infection symptoms. 3. Croup is most common from the late fall to early spring. such as epiglottitis. or suspected foreign body inhalation should be taken to the operating room for direct laryngoscopic visualization and possible intubation. C. although cases may occur throughout the year. Maintaining an adequate airway takes precedence over other diagnostic interventions. Supraglottic disorders. Patient age 1. Causes of Upper Airway Obstruction in Children Supraglottic Infectious Disorders Epiglottitis Peritonsillar abscess Retropharyngeal abscess Severe tonsillitis Subglottic Infectious Disorders Croup (viral laryngotracheitis) Spasmodic croup Bacterial tracheitis Non-Infectious Causes Angioedema Foreign body aspiration Congenital obstruction Neoplasms External trauma to neck . Subglottic lesions. 2. cause quiet. suggests viral croup. wet stridor. Facial edema and urticaria suggests angioedema. From infancy to 2 years of age. Emergency management of upper airway obstruction 1. see page 182. 1.to 2-year-old age group are most commonly affected. Mode of onset 1. A history of a choking episode or intermittent respiratory distress suggests a foreign body inhalation. a muffled voice.
“air hungry.Characteristics of selected causes of Upper Airway Obstruction Epiglott itis Laryngotr acheobronchitis (Croup) Bacterial Tracheit is Foreign Body Aspiration History Incidence in children presenting with stridor Onset 8% 88% 2% 2% Rapid. 3 days. anxious. 1-7 days Prodrom e.” supine position exacerbates Increased early Normal Variable Moderate Proportional to fever No effect Variable Yes Normal Normal Position No effect on airway obstruction No effect Respiratory rate Increased late Normal Increased if bronchial obstruction present . 412 hours Prodrome . then 10 hours 3 mo-2 years None Acute or chronic Age 1-6 years 3 mo-3 years OctoberMay Parainflue nza viruses Edema and inflammation of trachea and bronchial tree Any Season None None Etiology Haemop hilus influenza Inflammatory edema of epiglottis and supraglottitis Staphylo coccus Many Pathology Trachea l-bronchial edema. necrotic debris Localized tracheitis Signs and Symptoms Dysph agia Difficulty swallo wing Drooling Stridor Yes No No Rare Yes No Rare No Yes No Rare No Inspirator y Inspiratory and expiratory Hoarse Barking Minimally elevated Increased late Inspirato ry Variable Voice Cough Temper ature Heart rate Muffled No Markedly elevated Increased early Erect.
6 mg/kg IM) given one time early in the course of croup results in a shorter hospital stay and reduces cough and dyspnea. anxiety. When the diagnosis is uncertain or the patient requires hospitalization. As airway obstruction increases retractions. C. B. F. IV. B. 4. Dexamethasone (0. trachea. and 3% of those children need airway support. The prognosis for croup is good. Hypoxic or cyanotic patients require oxygen via mask and may require intubation. Ten percent of croup patients have severe respiratory compromise requiring hospital admission. Influenza viruses A and B and mycoplasma have been implicated in patients older than 5 years. The majority of patients who have croup do not require hospitalization. Severe stridor. and rhinovirus may also cause croup. x-rays can be helpful. Racemic epinephrine has alpha-adrenergic properties. Stridor becomes less apparent as muscle fatigue worsens. parainfluenza type 2. Decreased air entry on auscultation. Patients who do not require hospitalization should not receive steroids. carbon dioxide accumulation. oral fluids. and antipyretics are the mainstays of home therapy. and tachypnea may occur. Laboratory evaluation. Inpatient treatment of laryngotracheitis A. Cyanosis is a late sign. B. Acetaminophen decreases fever and oxygen consumption in the febrile patient with croup. 2.25% solution. restlessness. E. It is given every 20-30 minutes for severe croup. C. Parainfluenza type 3. and bronchi eventually develop. Subglottic edema and inflammation of the larynx. Parainfluenza virus type 1 causes 40% of all cases of laryngotracheitis.Differentiation of Epiglottitis from Viral Laryngotracheitis Clinical Feature Retractions Wheezing Cyanosis “Toxicity” Preference for sitting Epiglottitis present absent present present yes Viral Croup present occasionally present present in severe cases absent no II.5 mL of a 2. respiratory syncytial virus (RSV). Viral croup begins gradually with a 1-2 day prodrome. or obtundation. however. Corticosteroids reduce subglottic edema and inflammation. The posteroanterior neck radiograph of a patient with viral croup shows symmetrical narrowing of the subglottic space (“steeple sign”). and it is given every 4-6 hours for moderate croup. tachycardia. diluted with 3. Patients with mild viral croup usually are not admitted to the hospital and can be treated safely at home. V. develop. Signs that indicate the need for an artificial airway include decreased respiratory effort and decreased level of consciousness. The diagnosis of viral croup is based primarily on the history and clinical findings. which decrease subglottic inflammation and edema. 3. D. Indications for hospitalization 1. Racemic epinephrine is administered as 0. hypoxemia. resembling an upper respiratory infection. D.5 mL of saline (1:8) by nebulization. Pulse oximetry may aid in assessing the severity of respiratory compromise. Significant retractions. causing wheezing and stridor. a subset of children who . intravenous hydration may become necessary in the very ill child. H. Low-grade fever and nocturnal exacerbation of cough are common. Vaporizers. 5. Oral hydration is essential to help loosen secretions. however. Agitation. Clinical manifestations A. Dusky or cyanotic skin color. restlessness. Epidemiology and etiology of viral laryngotracheitis (Croup) A. III. and respiratory acidosis. RSV commonly affects infants younger than 12 months of age. Severe obstruction leads to respiratory muscle exhaustion. G. All patients suspected of having viral croup should be given humidified air.
2. 6. 4. The abdominal pain is usually bilateral and rarely of more than two weeks’ duration. Documented STD. 3. multiple.have croup will later be identified as having asthma. Pregnancy test is negative. These major determinants include lower abdominal tenderness. Tenderness in the right upper quadrant does not exclude PID. References. 5. C. 2. Erythrocyte sedimentation rate (ESR). Laboratory Evaluation for Pelvic Inflammatory Disease • • • • • • • Pregnancy test Microscopic exam of vaginal discharge in saline Complete blood counts Tests for chlamydia and gonococcus Urinalysis Fecal occult blood test C-reactive protein(optional) . Clinical evaluation A. Only one-half of patients with PID have fever. signs that may increase the suspicion of PID) include: 1. C. Purulent endocervical discharge and/or acute cervical motion and adnexal tenderness by bimanual examination is strongly suggestive of PID. Diagnostic criteria and guidelines.3EC). Dyspareunia. >38. I. 3. The CDC has recommended minimum criteria required for empiric treatment of PID. Lower abdominal pain is the cardinal presenting symptom in women with PID. fever. which may or may not be symmetrical. Vaginal discharge. African-American ethnicity. Rectovaginal examination should reveal the uterine adnexal tenderness. The examination suggests PID. Nonbarrier contraception. or symptomatic sexual partners. Empiric treatment for pelvic inflammatory disease is recommended when: 1. 4. New vaginal discharge. The index of suspicion for the clinical diagnosis of PID should be high. although the character of the pain may be quite subtle. urethritis. 5. B. Pelvic inflammatory disease accounts for approximately 2. and cervical motion tenderness. B. B. 3. and chills can be associated signs. 7. because approximately 10 percent of these patients have perihepatitis (Fitz-Hugh Curtis syndrome). C-reactive protein. oviducts. Abdominal examination reveals diffuse tenderness greatest in the lower quadrants. Previous episode of PID. especially in adolescent women. Fever (oral temperature >101EF. PID is a community-acquired infection initiated by a sexually transmitted agent. Abnormal uterine bleeding occurs in one-third or more of patients with PID. and ovaries. Risk factors for PID: 1. Oral contraception. The onset of pain during or shortly after menses is particularly suggestive. Physical examination A. adnexal tenderness. Age less than 35 years. proctitis. Minor determinants (ie.5 million outpatient visits and 200. Rebound tenderness and decreased bowel sounds are common. 6. Demographics (risk factors) are consistent with PID. Diagnosis A. 2. III. see page 182. Systemic signs. New. Pelvic Inflammatory Disease Pelvic inflammatory disease (PID) is an acute infection of the upper genital tract in women.000 hospitalizations annually. involving any or all of the uterus. II.
Diagnostic testing A. B. Health-care providers should maintain a low threshold for the diagnosis of PID. If a cervical Gram stain is positive for Gram-negative intracellular diplococci. Neisseria gonorrhoeae and Chlamydia trachomatis. C-reactive protein(optional). and the demonstration of cervical gonorrhea or chlamydia infection. 2. C. B. Fewer than onehalf of PID patients exhibit leukocytosis. Fecal occult blood test. and sexually active young women with lower abdominal. Urinalysis. cefoxitin (Mefoxin. C. if negative. Gram stain and microscopic examination of vaginal discharge may provide useful information. An alternative is an initial single dose of ceftriaxone (Rocephin. 6. Outpatient therapy 1. Tests for chlamydia and gonococcus. Microscopic exam of vaginal discharge in saline. D. 2 g IM plus probenecid 1 g orally). abnormal cervical/vaginal discharge. However. and cervical motion tenderness should receive empiric treatment. Recommendations A. 875 mg PO BID) for 7 to 10 days. and Proteus spp. 2. 5. and physical examination) suggest PID empiric treatment should be initiated. E. 400 mg twice daily) or levofloxacin (Levaquin. Laboratory testing for patients suspected of having PID always begins with a pregnancy test to rule out ectopic pregnancy and complications of an intrauterine pregnancy. cefixime or ceftriaxone should be used. A urinalysis and a stool for occult blood should be obtained because abnormalities in either reduce the probability of PID. The specificity of these clinical criteria can be enhanced by the presence of fever. adnexal. it is of little use. but coverage should also be provided for groups A and B streptococci. Klebsiella spp.IV. and anaerobes. V. must be treated. followed by amoxicillin-clavulanate (Amoxicillin. the CDC suggests either . the CDC recommends either oral ofloxacin (Floxin. For outpatient therapy. 875 mg PO) once by directly observed therapy. or another parenteral third-generation cephalosporin. 1 g PO for Chlamydia coverage) and Amoxicillin-clavulanate (Amoxicillin. Quinolones are not recommended to treat gonorrhea acquired in California or Hawaii.). Complete blood counts. 500 mg once daily) with or without metronidazole (Flagyl. or California. The two most important initiators of PID. For inpatient treatment. 3. B. symptomatic. Ultrasound imaging is reserved for acutely ill patients with PID in whom a pelvic abscess is a consideration. the specificity is only 39 percent. If the patient may have acquired the disease in Asia. 4. followed by doxycycline (100 mg orally twice daily) with or without metronidazole for 14 days. Hawaii. Recommended laboratory tests: 1. Inpatient therapy 1. 500 mg twice daily) for 14 days. Blood counts have limited value. If clinical findings (epidemiologic.. the probability of PID greatly increases. elevated ESR and/or serum C-reactive protein. Differential Diagnosis of Pelvic Inflammatory Disease Appendicitis Ectopic pregnancy Hemorrhagic ovarian cyst Ovarian torsion Endometriosis Urinary tract Infection Irritable bowel syndrome Somatization Gastroenteritis Cholecystitis Nephrolithiasis VI. Treatment of pelvic inflammatory disease A. Pregnancy test. Increased white blood cells (WBC) in vaginal fluid may be the most sensitive single laboratory test for PID (78 percent for >3 WBC per high power field. Another alternative is azithromycin (Zithromax. Gram negative enteric bacilli (Escherichia coli. 7. 250 mg IM).
2. Ampicillin-sulbactam (Unasyn). 900 mg IV Q8h. E. 500 mg IV Q8h). Gastrointestinal Disorders Acute Abdominal Pain The evaluation of abdominal pain in children is problematic because the pain is often difficult to localize. I. Annual screening is recommended for all sexually active women under age 25 and for women over 25 if they have new or multiple sexual partners. 7. 450 mg PO QID) for a total of 14 days. B. or California. Serologic tests for syphilis. D. liver abscess. Referred abdominal pain occurs when poorly localized visceral pain is felt at a distant location. caused by inflammation. cefixime or ceftriaxone should be used. 500 mg IV Q24h. D. . References. which is referred to the ipsilateral neck and shoulders. see page 182. 4. Clinical evaluation A. or cefoxitin (Mefoxin. Gallbladder pain may be felt in the lower back or infrascapular area. Cefotetan (Cefotan).of the following regimens: a. Pancreatitis. Papanicolaou smear. 400 mg IV Q12h or levofloxacin (Levaquin. plus metronidazole (Flagyl. 2. Hepatitis B surface antigen determination and initiation of the vaccine series for patients who are antigen negative and unvaccinated. Intraabdominal fluid may cause shoulder pain on reclining. 3 g IV Q6h plus doxycycline (100 mg IV or PO Q12h) 3. 1 g PO once) should be given as soon as the patient is tolerating oral intake. Generalized pain in the epigastrium usually comes from the stomach. 6. 500 mg IV QD) with or without metronidazole (Flagyl. Hawaii. History should include the quality. Parenteral administration of antibiotics should be continued for 24 hours after clinical response. b. azithromycin (Zithromax. Pancreatic pain often is referred to the posterior flank. 2 g IV Q6h) plus doxycycline (100 mg IV or PO Q12h) b. Serology for the human immunodeficiency virus (HIV). and the history in children is often nonspecific. duodenum. is usually well localized. Hepatitis C virus serology. timing. Periumbilical pain usually originates in small bowel and colon or spleen. and type of abdominal pain. Clindamycin (Cleocin). Parietal pain. 3. If the patient may have acquired the disease in Asia. Alternative regimens: a. The following regimen may also be used: Levofloxacin (Levaquin). Ureterolithiasis often presents as pain radiating toward the ipsilateral groin. Right lower lobe pneumonia may be perceived as right upper quadrant abdominal pain. Quinolones are not recommended to treat gonorrhea acquired in California or Hawaii. 1. 500 mg IV Q8h). or the pancreas. With this regimen. II. A retest for chlamydia should be completed in 3 to 4 months after chlamydia treatment because of high rates of reinfection. Rectal or gynecological pain often is perceived as sacral pain. followed by doxycycline (100 mg PO BID) or clindamycin (Cleocin. C. or a splenic hemorrhage cause diaphragmatic irritation. cholecystitis. Pain of sudden onset often denotes colic. 5. 2 g IV Q12h. Ofloxacin (Floxin). plus gentamicin (1-1. Localization of abdominal pain A.5 mg/kg IV q8h) 2. 5. 4. 4. Parenteral therapy is continued until the pelvic tenderness on bimanual examination is mild or absent. Additional evaluation: 1. 3. 1.
000 supports the diagnosis. When the plain abdominal x-ray is normal. Usually abdominal pain will precede vomiting. 2. F. gastrointestinal tract. which will establish the diagnosis. It is characterized by severe. Rectal examination a. Colic pain usually originates from the biliary tree. with the inflamed mass causing irritation of the sigmoid colon. Intussusception is characterized by vomiting. Melena suggests upper gastrointestinal bleeding. C. adnexa. c. Slower onset of pain suggests inflammatory conditions. intermittent cramping. 4. and palpated for distention. B. The most vulnerable age group is 4-10 months old. vomiting. A. The interval between abdominal pain and vomiting is shorter when associated with colic. D. IV. Tests for occult blood in the stool should be performed. but children up to 7 years old may be at risk. such as appendicitis. Vomiting. followed by intervals when the pain is less intense. Diarrhea. and pelvic masses. C. Fever a. Colic results from spasms of a hollow viscus organ secondary to an obstruction. Pelvic examinations are mandatory for postmenarchal and/or sexually active female patients. and currant jelly stools (60%). III. The abdomen may be soft and nontender between episodes of colicky pain. 3. Gross blood in the stool suggests ectopic gastric mucosa. Treatment consists of radiologic reduction. Mild diarrhea with the onset of abdominal pain suggests acute gastroenteritis or early appendicitis. A. urinary system. intussusception cannot be excluded without a barium enema. E. Thoracic disease (eg. or uterus and tubes. and peritonitis. Physical examination 1. pancreatitis. Abdominal x-ray. A mass may be felt on rectal exam in 2-7% of younger patients with appendicitis. Intussusception Intussusception is the most common cause of bowel obstruction between 2 months and 5 years of age. or polyps. pneumonia) may be the cause of abdominal pain associated with fever. necessitating gastric aspiration for blood. Meckel’s diverticula. The abdomen should be observed. irritability. which is . pancreatic duct. D. b. E. A sausage-shaped mass in the right upper quadrant (RUQ) may be palpable. perforation or acute ischemia caused by torsion or volvulus. b. or cholecystitis. and the patient presents quietly without much motion and appears ill. uterus. The rectal examination may also be used to evaluate the cervix. lethargy with right lower quadrant (RLQ) tenderness and guarding are diagnostic of appendicitis in the very young patient until proven otherwise. Delayed vomiting for many hours is often associated with distal bowel obstruction or ileus secondary to peritonitis. Often there are radiographic signs of bowel obstruction. Appendicitis Fever. B. 2. auscultated. C. Inflammatory pain is caused by peritoneal irritation. Blood and mucus (currant jelly stool) suggests inflammatory bowel disease or intussusception. masses. Costovertebral angle tenderness with fever suggests pyelonephritis or a high retrocecal appendicitis. Children older than 2 years old present with a perforated appendix about 30-60% of the time. A WBC >15. The groin must be examined to exclude an incarcerated hernia or ovary. This incidence declines as the age of the child increases. The leading edge of the intussusception is usually outlined with air. or torsion of an ovary or testicle. Fever is common. but eventually it becomes distended. An ultrasound of the appendix may be useful. Delayed onset of diarrhea may indicate a perforated appendicitis. d. localized tenderness. The pain is initially less severe and is exacerbated by movement.B. colicky abdominal pain (85%) with drawing up of the legs.
the scrotum and its contents must be examined. Ultrasound may show pelvic fluid and the cyst. C. usually in association with hemolytic disease. The leading causes of gonadal pain in females are ovarian cysts and torsion of uterine adnexal structures. Midgut volvulus A. Jaundice is present in 25-55%. it usually occurs in adolescent males at puberty or shortly afterwards. back pain. D. Torsion is associated with unilateral. Abdominal. VIII. Infants with rapid deterioration and obstructed loops of bowel require immediate surgery. vaginal bleeding. It is uncommon and usually seen in late adolescence.effective in 80-90%. Testicular torsion may present as lower abdominal pain. an UGI series with water-soluble. which usually subsides within 12-24 hours. hypovolemia.53% of all pregnancies. Obstruction of the superior mesenteric artery may cause ischemic necrosis of the gut. most commonly in adolescents. VII. Symptoms usually begin about 5 days before diagnosis. The patient may also have subacute or chronic symptoms. Nausea and vomiting. VI. and shock may follow. but occasionally abdominal tenderness is absent. which may be associated with recent trauma or cold. sudden. with a transverse orientation. and/or amenorrhea. B. B. severe pain with nausea and vomiting. Although testicular torsion may occur at any age. and/or cervical tenderness are often found on pelvic examination. The cervix may be soft (Godell’s sign) and bluish in color (Chadwick’s sign). Gallbladder disease A. other symptoms of pregnancy. IX. Gonadal pain in males A. with intermittent pain for days. Cholecystitis is suggested by RUQ pain. Testicular torsion is a surgical emergency and must be treated within 6 hours of the onset of the pain to save the testicle. Ectopic pregnancy A. but it may affect infants who are only a few weeks of age. Midgut volvulus results from the improper rotation and fixation of the duodenum and colon (malrotation). Radioisotopic scanning evaluates biliary and gallbladder function. C. Cholecystitis in children occurs most commonly in the adolescent female. Ultrasonography delineates gallstones and is the study of choice to screen for gallbladder disease. and lightheadedness may also be present. B. V. Abdominal x-ray reveals a classic double bubble caused by duodenal obstruction. D. The examination may reveal adnexal fullness and uterine enlargement. B. In males with lower abdominal pain. radiating to the right subscapular area. The gonad is tender and elevated in the scrotum. non-ionic. Ectopic pregnancy occurs in 0. B. followed by abdominal distention and GI bleeding. adnexal. C. spiral or corkscrew sign) is found. Signs of ectopic pregnancy include abdominal pain in any location. Torsion of uterine adnexal structures 1. or epigastric pain. fever. RUQ tenderness. Bleeding into the cyst or cystic rupture causes pain. The first sign of volvulus is bilious vomiting. C. and a RUQ mass. Radiographic reduction is contraindicated if there is peritoneal irritation or toxicity. Gonadal pain in females A. Ovarian cysts are responsible for 25% of childhood ovarian tumors. Treatment consists of removal of the ectopic pregnancy by laparoscopy or exploratory laparotomy. Ectopic pregnancy must be considered in any postmenarchal. an immediate laparotomy is necessary. which may be fatal. Infants in the first month constitute the majority of the cases. sexually active adolescent with abdominal pain. Evaluation includes a pregnancy test and ultrasound. bilious vomiting. isoosmolar contrast will confirm midgut volvulus. Pneumatosis intestinalis or distal bowel obstruction may also be apparent. The pain is usually diffuse and periumbilical in younger . If malrotation or volvulus (beak. Peritonitis. If the infant is not critically ill.
Malignant neoplasms may cause torsion in 35% of cases. I. About 13-17% of adolescents experience weekly pain. Surgical exploration may sometimes salvage the ovary. associated with blood in the stool. Irritable bowel syndrome. unrelated to meals or activities.Discitis • Vascular disorders . It presents as a tender left lower quadrant mass.Postsurgical adhesions .Crohn disease . The criteria for making this diagnosis are: 1) abdominal pain relieved by defecation.Adhesions from pelvic inflammatory disease • Cystic teratoma of ovary • Musculoskeletal disorders .Linea alba hernia . and an organic etiology cannot be found. sedimentation rate.Small bowel lymphoma . RAP occurs in 10-15% of children between the ages of 4 and 16 years. The degree of interference with normal activities and school attendance are out of proportion to the frequency and severity of the episodes. and rarely if ever sufficient to awaken the child from sleep.patients. Fever and leucocytosis are usually present. the pain may radiate initially to the anterior thigh or ipsilateral groin. stool ova and parasites) II. age of onset Characteristic features of abdominal pain Evidence of physical or psychological stressful stimuli Environmental reinforcement of pain behavior Normal physical examination (including rectal examination and stool guaiac) • Normal laboratory evaluation (CBC. Functional abdominal pain. Some children who have RAP manifest characteristics of irritable bowel syndrome (IBS). urine culture.Malrotation with or without volvulus . The growth pattern and findings on the physical examination are normal. but in older children and adolescents. 2) . The pain occurs in episodes that are periumbilical. A technetium nuclear scan may confirm the diagnosis.Intussusception . Clinical Aspects A. B. RAP is rare among children younger than 5 years of age. B. Recurrent Abdominal Pain Recurrent abdominal pain (RAP) includes any child or adolescent who has recurrent abdominal pain for which the family seeks medical attention and explanation.Angioneurotic edema • Ureteropelvic junction obstruction • Appendiceal colic • Dysmenorrhea .Infection (tuberculosis. Yersinia) . The majority of children who have RAP are considered to have a functional etiology. The overall incidence appears to peak at 10 to 12 years. see page 182. More than 90% of the time a “disease” will not be defined and the family will be left with a “functional” explanation. Bleeding is seen in 35-40% of childhood cases. Vague abdominal pain with hemoccult positive stools suggests a Meckel diverticulum. 2. self-limited.Mesenteric thrombosis .Ectopic pregnancy .Eosinophilic gastroenteritis . 3. urinalysis. References. Epidemiology A.Endometriosis .Polyarteritis nodosa • Abdominal migraine • Acute intermittent porphyria • Psychiatric disorders Diagnostic Criteria for Functional Abdominal Pain • • • • • • Chronicity Compatible age range. Meckel diverticulum are present in 2% of the population. X.Muscle pain . Differential Diagnosis of Recurrent Abdominal Pain • • • • Functional abdominal pain Fecal impaction Parasitic infection Partial small bowel obstruction . Meckel diverticulum A. Ultrasound will identify the mass accurately. Physical exam may reveal muscle rigidity and fixation of the mass on pelvic examination.
A strong family history of migraine is usually present. diarrhea. H. and when it is associated with anorexia. “Red Flags” on History of Recurrent Abdominal Pain • Localization of the pain away from the umbilicus • Pain associated with change in bowel habits. 3) altered stool form (hard or loose or watery). The child goes days between bowel movements and the stool is bulky and hard. I. The abdomen should be examined gently and thoroughly while observing the child’s response to palpation. These causes can be diagnosed by ultrasonographic examination. endometriosis. K. and perirectal involvement. or nocturnal bowel movements • Pain associated with night wakening • Repetitive emesis. hematochezia and tenesmus. particularly diarrhea. and context in which the pain occurs. J. Asian. loose stools. Findings on abdominal and rectal examinations may confirm the diagnosis. bowel habits. Jewish. E. and cramping abdominal pain. Clinical assessment The history should assess the location. Constipation. Height and weight should be recorded and compared to previous growth data. skin tags. more frequent stools at the onset of the pain. such as recurrent fever. vegetables and higher-fiber foods. Crohn disease may cause abdominal pain. Physical and sexual abuse may cause RAP. constipation. and African-American persons are predisposed to lactase deficiency. sometimes with associated headache. The diagnosis is made by breath hydrogen testing or a therapeutic trial of restriction of milk products. Endoscopy will confirm the diagnosis. but diarrhea usually is the predominant complaint. school performance. Infestation/infection. a plain abdominal radiograph may be needed. Infection with Yersinia enterocolitica and giardia can cause diarrhea associated with abdominal cramps and pain. A. nature. Lactose intolerance. and oral. Peptic ulcer disease is very uncommon is children. Abdominal migraine usually is recognized when episodes of paroxysmal abdominal pain occur in association with nausea and vomiting. depression. Gynecologic conditions. sleep patterns. The perianal area should be examined for fissures. recurrent vomiting. The relationship of the pain to school and social/family stressors is important. when it awakens the child from sleep. and discomfort accompanied by negative endoscopic and biopsy findings. bloating. or social maladjustment should be assessed. Inflammatory bowel disease. pelvic inflammatory disease. D. Review of systems should cover the child’s diet. III. G. anxiety. and associated symptoms. therefore. . Medication use should be assessed. B. Ulcerative colitis may present with abdominal pain. and ovarian cyst may cause RAP. Early menarche.C. loss of appetite or energy • RAP occurring in a child younger than 4 years of age C. frequency of the pain. Mediterranean. anemia. The most common causes of constipation in children are inadequate intake of fruits. Nonulcer dyspepsia is a symptom complex of epigastric pain. nausea. joint. growth and pubertal delay. or signs of sexual abuse. A rectal examination is not routinely performed. F. and 5) associated bloating or abdominal distension. or gastrointestinal bleeding. Physical Examination. Lactose ingestion will cause bloating. and sensitive history taking is required to elucidate its possible role. The degree to which the pain interferes with the child’s activities should be defined. lethargy. especially if bilious • Constitutional symptoms. 4) passage of mucus. Helicobacter pylori-associated peptic ulcer disease should be suspected when abdominal pain is primarily epigastric. and an unwillingness to evacuate the bowels. Family function. testing for H pylori should not be part of the preliminary evaluation of a child who has RAP.
see page 182. In the presence of diarrhea. CNSD occurs when fluid intake exceeds the absorptive capacity of the intestinal tract. I. a stool for enteric culture and ova and parasite examination is indicated. Children have 3 to 6 large. References. Radiography. with frequent. serum protein and albumin levels. Abdominal ultrasonography can be valuable when obstructive uropathy hydronephrosis. B.“Red Flags” on Physical Examination for Recurrent Abdominal Pain • • • • • • Loss of weight or decline in height velocity Organomegaly Localized abdominal tenderness. or when the pain localizes to the lower quadrants in a female. particularly removed from the umbilicus Perirectal abnormalities (eg. sorbitol) in fruit juices contributes to CNSD. Enteric infections or infestations require treatment with appropriate medications. Disordered intestinal motility 4. watery bowel movements daily. Factors causing CNSD 1. and examination of a stool specimen for occult blood. Abdominal migraine may warrant a trial of migraine prophylaxis. redness. D. . Enteric duplication also may be revealed by ultrasonography. B. Upper gastrointestinal endoscopy with biopsies will confirm the diagnosis when the pattern of pain strongly suggests peptic ulcer disease. Excess fluid intake 2. Carbohydrate malabsorption from excessive juice ingestion 3. Prophylactic pizotifen. A single view of the abdomen can be useful to confirm constipation. V. Lactose malabsorption. Constipation requires treatment with regular stool softeners. C. Functional recurrent abdominal pain will be the diagnosis in the majority of cases. Ultrasound is appropriate when the pain is lateralized. Laboratory investigations should usually be limited to a complete blood count. with 3-6 large. Malabsorption of carbohydrates (sucrose. E. Chronic nonspecific diarrhea (CNSD) presents in toddlers between 18 months and 3 years of age. Endoscopy and biopsy will confirm the diagnosis. A lactose-free diet for several weeks with lactase-treated milk should be tried. or skin tags) Joint swelling. fructose. large. Ice cream and cheese should be avoided. urinalysis. or amitriptyline could be considered. Excessive fecal bile acids 5. Chronic Nonspecific Diarrhea Diarrhea is considered chronic when it persists for longer than 3 weeks. The parents should maintain a sympathetic attitude that acknowledges the pain but encourages continued activities and school attendance. watery stools in the absence of physical or laboratory signs of malabsorption or infection and without effect on growth or development. CNSD presents between 18 months and 3 years. If IBD is a possible diagnosis. Management A. propranolol. Erythrocyte sedimentation rate. The diarrhea spontaneously resolves in 90% of children by 40 months of age. loose. C. D. when there are abnormalities on urinalysis. cyproheptadine. or gall bladder disorders are suspected. watery stools per day for more than 3 weeks. Low fat intake B. ovarian cysts. Psychogenic pain may respond to the intervention of a psychologist or psychiatrist. and stool for occult blood should be obtained. or heat Ventral hernias of the abdominal wall IV. Investigations A. C. ulceration. Parents should refrain from questioning the child about the pain if the child is not complaining. A trial of increasing fiber by dietary modification may be useful. preceded by an enema. fissures. Pathogenesis A.
E. anorexia. producing symptoms when sucrose-containing formula or foods are introduced. less than 3 months of age.D. A family history of irritable bowel syndrome. blood. protein intolerance. C. 2. eczematoid rash (from essential fatty acid deficiency). Infants who have milk-induced enterocolitis are younger. D. infectious diarrhea. Signs of malnutrition or malabsorption include lack of subcutaneous fat. B. Lactase deficiency may cause diarrhea associated with milk ingestion. C. Giardia and Cryptosporidium are common and should be excluded with 3 stool samples for ova and parasites. and head circumference are essential. fat. and medications should be sought. D. and malabsorption. Stool Evaluation Test pH Reducing substances Neutral fat Result <5. inflammatory bowel disease. Congenital lactase deficiency is extremely rare and symptoms are present from birth if an infant is fed human milk or a lactose-containing formula. There is an absence of nausea. A diet history should determine the total calories. fever. Disaccharidase deficiency can be confirmed by eliminating the specific carbohydrate or by breath hydrogen analysis. Growth chart plotting of weight. Congenital sucrase-isomaltase deficiency is rare. flatulence. abdominal pain. celiac disease. Usage of antibiotics. Differential diagnosis A. deviation from the growth chart or a downward trend suggests inadequate caloric intake or a disease other than CNSD. iron. The differential diagnosis of chronic diarrhea in the 6. Milk-induced colitis occurs in infants younger than 1 year of age who typically appear healthy but lose blood in their stool after ingesting milk protein. A fresh stool specimen is tested for neutral fat. Children who have CNSD should continue to grow normally. 4. 3. weight loss. . milk and juice consumed daily. Clinical evaluation of chronic nonspecific diarrhea A. Fecal pH and reducing substances will reveal carbohydrate malabsorption if the pH is less than 5. The current number and type of stools should be determined. and it should assess prior trials of food elimination. Genetically acquired lactase deficiency is common. or poor growth. The timing of introduction of foods into the diet relative to the onset of diarrhea. Laboratory tests 1. 2. Physical examination 1. occult blood. These infants may be severely ill with bloody diarrhea. easy bruising. glossitis. E. height. pH and reducing substances. 2. Lactase deficiency 1. and a 3-day diet history should be assessed. cryptosporidiosis Occult blood Giardia antigen Ova and parasites III. vitamins. B. vomiting. II. or hyporeflexia. 3. Neutral fat suggest pancreatic insufficiency. or food allergies should be sought. Stooling is most frequent in the morning and does not occur during sleep. and Giardia antigen.5 or if reducing substances are greater than 1+.5 >1+ Disease Carbohydrate malabsorption >40 globules/high power field Positive Positive Positive Pancreatic insufficiency Enteritis or colitis Giardiasis Giardiasis. but it usually is not symptomatic before 5 years of age. Occult fecal blood is inconsistent with CNSD unless there is a perianal rash.to 36-month-old child includes disaccharidase deficiency. enteric infection.
or vegetable oil are liberally added to foods for children less than 2 years of age. asthma. Anal stenosis accounts for 20% of these abnormalities. G. Persistent difficulty with the passage of stool may lead to impaction. and fecal soiling. The anus appears very small with a central black dot of meconium. C. Children who have protein allergies tend to come from families that have allergic histories. Constipation Constipation is common in infants and children. and growth failure. Celiac disease must be confirmed by intestinal biopsy. and excessive cow milk intake should be excluded during the history. I. and affected children may have eczema. Screening for celiac disease consists of a D-xylose absorption test and a serum celiac disease panel (antigliadin. 2. and the infant . Switching from the bottle to the cup also decreases fluid intake. margarine. bloating and flatulence. abdominal pain. Anal inspection at the time of birth reveals anorectal anomalies in one in every 2. Evaluation of constipation in neonates and infants 1. low-lactose milk can be used or lactase drops can be added to milk. The most common causes are cystic fibrosis and celiac disease. Inadequate fluid intake. allergic rhinitis. Conditions Associated With Constipation Condition Lack of Fecal Bulk Common Causes High-carbohydrate or high-protein diet Undernutrition Excessive cow milk intake Dehydration Infantile renal acidosis Diabetes insipidus Idiopathic hypercalcemia Spinal cord lesions Anorectal stenotic lesions Intrinsic and extrinsic masses Strictures Aganglionosis (Hirschsprung disease) Amyotonia congenita Cerebral palsy Hypertonia Hypothyroidism Abnormally Hard Stools Abnormally Dry Stools Nervous System Lesion Mechanical Obstruction Diseases That Complicate Defecation II. antiendomysial. Dietary fiber can be increased by consumption of fresh fruits and vegetables or by the addition of bran. and antireticulin antibodies). B. stool withholding. undernutrition. weakness and decreased activity. and chronic vomiting. F. The problem usually resolves after modification of the child’s fluid and dietary regimen. Butter. weight loss. Fluid intake should be reduced to less than 100 mL/kg/day.500 live births. see page 182. Giardia or Cryptosporidium enteric infections are commonly transmitted by asymptomatic carriers at child care centers.hypoproteinemia. Water is substituted for juice to reduce the child’s interest in drinking. Pathophysiology A. If lactose intolerance is present. IV. Fat intake is increased to 4 g/kg/day by adding whole milk to the diet. poor appetite. Management of CNSD A. References. Malabsorption presents with chronic diarrhea. Diagnosis is confirmed by Giardia antigen in stool or three stools for ova and parasites. Foul-smelling diarrhea usually is associated with abdominal distension and flatus. Neonates and infants younger than 1 year of age A. Chronic diarrhea and failure to thrive warrants a sweat test.
must make an intense effort to pass a ribbon-like stool. The abdomen may be distended and stool can often be palpated on abdominal examination. 3. Hirschsprung disease a. Hirschsprung disease accounts for 20-25% of cases of neonatal obstruction, and it is more common in males. Symptoms develop during the first month of life in 80%. The majority of infants are unable to pass stool normally during the first week. b. Infants with Hirschsprung disease usually fail to pass meconium during the first 48 hours of life. The abdomen is usually distended and tympanitic. Abdominal peristaltic activity may be visible, and fecal masses may be palpable. The anal canal and rectum are empty of feces. c. Plain abdominal radiographs reveal gas and stool in the colon above the rectum. A rectosigmoid index (the diameter of the rectum divided by the diameter of the sigmoid) of less than one is consistent with Hirschsprung disease. d. When findings from the history, physical, and plain abdominal radiographs suggest Hirschsprung disease, contrast examination of the unprepared colon should be obtained. The diagnosis is confirmed by endoscopic biopsy. B. Management of simple constipation in infants 1. Dietary corrective measures are the initial therapy for infants with simple constipation. Increasing fluid intake and adding carbohydrate sugar to the formula often corrects the problem. 2. Infants that do not respond to dietary measures are treated with a mineral oil preparation. Routine suppository administration, enemas, and stimulant laxatives should be avoided. III. Older infants and children A. Evaluation 1. Fluid and dietary fiber intake should be assessed. Older children with chronic constipation and stool withholding usually also have fecal incontinence. 2. Moveable fecal masses are often appreciated in the left colon and sigmoid. 3. The lower back should be examined for a deep pilonidal dimple with hair tuft and/or sacral agenesis, suggestive of myelodysplasia. Anal inspection may reveal primary anal disease. Normal anal tone found on rectal examination indicates normal anal innervation. The rectal vault may be filled with inspissated stool. 4. Anteroposterior and lateral x-rays of the abdomen usually reveal a large rectal/rectosigmoid impaction with variable amounts of stool throughout the remainder of the colon. B. Management of chronic constipation 1. Distal impaction should be removed with hypertonic phosphate enemas (Fleet enema). Usually three enemas are administered during a 36- to 48-hour period. 2. Mineral oil should be prescribed. The initial dose of mineral oil is 30-75 mL twice daily. Mineral oil is tasteless, and it can be taken with fruit juice, Kool-Aid, or a soft drink. After one month, the oil is tapered by 15 mL (0.5 oz) per dose. Haley’s MO is a mineral oil solution of 1.4 gm/5 mL. 3. The child should sit on the toilet, with proper foot support, for five minutes after the evening meal to take advantage of the gastrocolic reflex. A bulk-type stool softener (eg, Metamucil) should be initiated when the mineral oil dosage has been tapered to 15 mL twice daily. References, see page 182.
Acute gastroenteritis consists of diarrheal disease of rapid onset, often with nausea, vomiting, fever, or abdominal pain. It occurs an average of 1.3-2.3 times per year between the ages of 0 and 5 years. Most episodes of acute gastroenteritis will resolve within 3 to 7 days. I. Pathophysiology. Gastroenteritis in children is caused by viral, bacterial, and parasitic organisms, although the vast majority of cases are viral or bacterial in origin.
II. Viral gastroenteritis A. All of the viruses produce watery diarrhea often accompanied by vomiting and fever, but usually not associated with blood or leukocytes in the stool or with prominent cramping. B. Rotavirus is the predominant viral cause of dehydrating diarrhea. Rotaviral infections tend to produce severe diarrhea, causing up to 70% of episodes in children under 2 years of age who require hospitalization. Rotavirus infection tends to occur in the fall in the southwest of the US, then sweeping progressively eastward, reaching the northeast by late winter and spring. C. Norwalk viruses are the major cause of large epidemics of acute nonbacterial gastroenteritis, occurring in schools, camps, nursing homes, cruise ships, and restaurants. D. Enteric adenovirus is the third most common organism isolated in infantile diarrhea. III. Bacterial gastroenteritis A. The bacterial diarrheas are caused by elaboration of toxin (enterotoxigenic pathogens) or by invasion and inflammation of the mucosa (invasive pathogens). B. Secretory diarrheas are modulated through an enterotoxin, and the patient does not have fever or myalgias or tenesmus, or white or red blood cells in the stool. The diarrhea is watery, often is large in volume, and often associated with nausea and vomiting. C. Invasive diarrhea is caused by bacterial enteropathogens, and is accompanied by systemic signs, such as fever, myalgias, arthralgias, irritability, and loss of appetite. Cramps and abdominal pain are prominent. The diarrhea consists of frequent passing of small amounts of stool within the mucus. Stool examination reveals leukocytes, red blood cells, and often gross blood.
Acute Diarrhea Patterns and Associated Pathogens
Secretory/enterotoxigenic Characterized by watery diarrhea and absence of fecal leukocytes Inflammatory Characterized by dysentery (ie, fever and bloody stools), fecal leukocytes, and erythrocytes
Food poisoning (toxigenic) Staphylococcus aureus Bacillus cereus Clostridium perfringens Shigella Invasive E coli Salmonella Campylobacter
Enterotoxigenic Escherichia coli Vibrio cholera Giardia lamblia Cryptosporidium Rotavirus Norwalk-like virus C difficile Entameba histolytica
IV. General approach to the patient with gastroenteritis A. Determining and managing the fluid losses, dehydration and electrolyte abnormalities is more important than ascertaining the specific microbiologic cause. B. History should assess recent antibiotic use, underlying diseases, other illnesses in the family, travel, untreated water, raw shellfish, attendance at a child care center, and foods eaten recently.
Clinical Evaluation and Treatment of Acute Diarrhea
Step One--Assess child for degree of dehydration No dehydration Mild/severe dehydration--------> Continue oral hydration and feeding Initiate rehydration by oral route (intravenous for severely dehydrated patients)
Step Two--Assess Clinical History for Etiologic Clues Etiologic Clue Fever, crampy abdominal pain, tenesmus History of bloody stool Fever and abdominal pain Current or previous antibiotic use Multiple cases and common food source Etiology Suggested Inflammatory colitis or ileitis Shigella, enteroinvasive E coli, amebiasis, other bacterial causes Yersinia enterocolitis Antibiotic-associated enteritis or pseudomembranous colitis Incubation <6 hours: Staphylococcus aureus, Bacillus cereus Incubation >6 hours: Clostridium perfringens Vibrio parahaemolyticus Bacterial (Salmonella), viral (rotavirus), or parasitic (isosporiasis, Cryptosporidium)
Ingestion of inadequately cooked seafood Recent measles, severe malnutrition, AIDS, other causes of immunosuppression
Step Three--Examine Stool: Indicated for: Visual examination Microscopic examination for white/red blood cells All patients Finding: Gross blood Etiology Suggested: Dysentery, colitis, invasive organism Shigella, enterohemorrh agic EC, enteroinvasive EC, Campylobacter , Clostridium, E histolytica Giardia, Amoeba, Cryptosporidiu m, Isospora, Strongyloides
Patients who have had diarrhea >3 days, fever, blood in stool, weight loss Diarrhea >10 days
Red cells and leukocytes Red cells without leukocytes Positive
Parasitic examination (wet mount, acid-fast staining, or concentration) Clostridium difficile toxin
Patients taking antibiotics
C difficile colitis
Assessment of Diarrheal Dehydration
Clinical Finding Affect/se nsorium Eyes Mucous membrane Tears when crying Thirst Mild (10-40 mL/ kg) Normal Normal Normal Moderate (50-90 mL/kg) Severe (100-130 mL/ kg) Stupor Deeply sunken Very dry
Irrita bility Sunk en Dry
++++ or unresponsive Very reduced (2-3 sec) Severely depressed
Skin turgor (capillary refill) Fontanelle Pulse Pulse rate Blood pressure
Reduce d (<1 sec) Depr essed Full Eleva ted Normal Weak
Full Normal Normal
Feeble or absent Very rapid Low or absent
C. Fluid therapy 1. Mild-to-moderate dehydration a. Mildly or moderately dehydrated children. Oral rehydration solution (ORS) is the preferred method of rehydrating a child with
correction should be slower. Oral fluids should be initiated as soon as the patient can drink. and fresh fruits and vegetables. Severe dehydration clinically is associated with a loss of 10-12% of body weight in fluids and electrolytes (100 to 120 mL/kg). fruits. d. applesauce. Antidiarrheal compounds (eg. are generally well tolerated. it should begin with an isotonic solution (normal saline. with the remainder of the deficit (70 mL/kg) over the next 2. particularly in the setting of fever. breastfeeding should be continued. Intravenous rehydration a. should be avoided. Prevention of dehydration a. hydration may be continued orally. Well-tolerated foods include complex carbohydrates (rice. whereas sports drinks. such as Gatorade. Shigella is the cause of bacterial dysentery and is the second most commonly identified bacterial pathogen in diarrhea between the ages of 6 months and 10 years. For infants. this amount plus additional losses should be infused. 2. may be given glucose-electrolyte solution in addition to their regular diets to replace stool losses. 3. wheat. rice. They should be given simultaneously with intravenous fluids until the total fluids administered have replenished the calculated deficit. The BRAT diet (bananas. Fatty foods and foods high in simple sugars. Pedialyte. Children who have diarrhea. The diet should emphasize complex carbohydrates. Ceralyte. Shigella) . fever. Introducing the child’s regular form of milk early in the course of therapy is recommended. D. Microscopic stool examination. or persistence of the diarrhea for more than 3 days may trigger a laboratory pursuit of an etiologic agent. The effectiveness of antimicrobial therapy is well established in shigellosis. Laboratory examinations A. b. In most western countries. diphenoxylate. toast) does not supply optimal nutrition. until the calculated fluid loss has been replenished. therefore. but not dehydrated. ORS should be given at 50 mL/kg (mild dehydration) or 100 mL/kg (moderate dehydration) over a 4-hour period. with no sugary or fatty foods. rotavirus is the most common cause of childhood diarrhea. E. Yersinia. bread. The well-hydrated child should continue to consume an age-appropriate diet and drink more than the usual amounts of the normal fluids. Naturalyte or Pediatric Electrolyte is appropriate. In such patients. 4.dehydration. with infusion rates no more than 30 mL/kg over the first hour and the remaining 70 mL/kg over 5 hours. F. b. Infusion rates of 40 mL/kg are given over the first 30 minutes.5 hours. Infusion rates of up to 100 mL/min are appropriate in older children. c. such as starches. cereals). When the patient is stable. Replacement of stool losses (at 10 mL/kg for each stool) and of emesis (estimated volume) will require adding appropriate amounts of solution to the total. If the child is breast fed. lactated Ringer). V. Apple juice and soft drinks. and vegetables. Subsequent maintenance fluids should be given orally. Children who have diarrhea and are not dehydrated should continue to be fed age-appropriate diets. Infalyte. cereal. Refeeding 1. Treatment consists of ceftriaxone or cefixime. B. potatoes. The presence of blood in the stool. If erythrocytes and white blood cells are present. such as juices and soft drinks should be avoided. When intravenous rehydration is required. yogurt. lean meats. Antibiotic therapy. loperamide. It causes watery diarrhea with mucus and gross blood. 2. Severely dehydrated children who are in a state of shock must receive immediate and aggressive intravenous (IV) therapy. bismuth compounds. Salmonella. a bacterial pathogen (Campylobacter. such as cola. Kaopectate) should not be used to treat acute diarrhea.
and gynecomastia. Cimetidine (Tagamet). C. B. diarrhea. Infants with GER are thriving and represent the majority of infants who present with this condition. or respiratory disease. Infants with GER regurgitate without inadequate growth. no diagnostic study is required. Although scintigraphy may best quantify gastric emptying or aspiration. Soft bedding materials should be avoided in this setting.should be suspected. it is not as commonly used as the upper GI examination (barium fluoroscopy). D. dizziness. The prevalence of GER peaks between one to four months of age. Potential side effects include headaches. esophagitis. If the diagnosis is unclear. Clinical manifestations A. Prone positioning is not routinely recommended as first-line management of simple regurgitation without evidence of GERD. In most cases of GER. III. Pharmacologic management 1. The recommended starting dosage is 10 mg per kg per dose four times daily before meals and at bedtime for eight weeks. see page 182. Patients with GERD may manifest persistent regurgitation with secondary poor weight gain and failure to thrive. and iron deficiency anemia. Potential side effects include headaches and malaise. but ranitidine has fewer central nervous system and anti-androgenic side effects. persistent respiratory symptoms. H2-receptor antagonists a. Laboratory evaluation in this setting is generally not indicated. Conservative treatment of GER involves thickened feedings and positional changes in infants. References. stool for viral particles or rotavirus antigen (Rotazyme [R]) may be helpful. C. Completely upright and prone positioning is beneficial in infants with GERD. feeding problems. GERD occurs in approximately one in 300 infants. Ranitidine (Zantac) 1-2 mg per kg per dose two to three times daily (2-6 mg per kg per day) is the starting dosage. Management A. Gastroesophageal Reflux Gastroesophageal reflux (GER) is a common condition involving regurgitation. b. Smaller. signs of esophagitis. Regurgitation occurs in 40 to 65 percent of healthy infants. more frequent feedings are recommended in older infants and children. Many red blood cells in the absence of white blood cells suggests the presence of Entamoeba. B. and dietary modification in children. Rotavirus should be suspected in a one-year-old presenting in the winter months with a three-day history of vomiting and watery diarrhea with mild dehydration. Healthy infants who regurgitate may be managed by thickening feedings with up to one tablespoon of dry rice cereal per 1 oz of formula. GER implies a functional or physiologic process in a healthy infant with no underlying systemic abnormalities. pain. including persistent irritability. I. and changes in neurobehavior. . Gastroesophageal reflux disease (GERD) is a pathologic process in infants manifested by poor weight gain. Diagnostic evaluation. and usually resolves by six to 12 months of age. Other infants may manifest signs of esophagitis. Stool culture should be reserved for individuals whose diarrhea has not responded to fluid and feeding and for those who have fever and the presence of leukocytes or red blood cells in the stool. II.
and fecal leukocytes. The most common symptoms are abdominal pain. fever. B. crypt abscesses. four times daily 1 to 2 mg per kg per dose. and serologic titers for Entamoeba histolytica may also be necessary. dizziness. retinol-binding protein). and levels of serum proteins (eg. prealbumin. with superficial erosions and ulcerations. which correlates with severity of disease. It is migratory. Initial evaluation of chronic diarrhea A. Colonoscopy or flexible sigmoidoscopy with biopsy is valuable in characterizing mucosal injury. D. Ashkenazi Jews are afflicted more often than non-Jewish populations. Histologic features of ulcerative colitis include diffuse shallow ulceration of the mucosa. often involving the hip. Prokinetic agent: Cisapride (Propulsid) is the prokinetic of choice for GERD. Inflammation characteristically begins in the rectum. thickening of the muscularis mucosa. Ulcerative colitis A. two to three times daily 0. The incidence ranges from 4 to 15 cases per 100. transferrin. Ankylosing spondylitis and sacroiliitis. Abdominal plain films with the patient in upright and supine positions should be obtained in patients with severe disease to detect perforation. and its course parallels that of the colitis. three to four times daily Side effects Headaches. II. Laboratory studies include levels of C-reactive protein. tests for ova and parasites. Inflammatory Bowel Disease I. ankle. Diagnostic evaluation 1. It is usually monoarticular and asymmetric. Cisapride is available through a limited access program if other therapies are not effective. wrist. Among family members. typically present as low back pain with morn- .000. Arthritis is the most common extraintestinal manifestation of ulcerative colitis. Reports of fatal arrhythmias have emerged. with a higher risk of the disease in young females than males. 2. Musculoskeletal. diarrhea. Clostridium difficile toxin. D. and 30% have total colonic involvement. friable. Specific cultures for Yersinia enterocolitica. Ulcerative colitis (UC) is the most common cause of chronic colitis. this drug is only available via a limited access program. Thirty percent of UC patients present with disease limited to the rectum. see page 182. B. References. or thumbprinting. the risk is tenfold higher. Disease may present at any time but does so most often during adolescence and young adulthood. The mucosa is erythematous. or elbow. and pronounced inflammatory cell infiltration. The initial diagnostic evaluation of chronic diarrhea includes stool cultures for enteric pathogens. 2. gynecomastia Headaches and malaise Ranitidine (Zantac) Cisapride (Propulsid)* Cardiac arrhythmia. 40% have more extensive disease but not extending beyond the hepatic flexure. toxic megacolon. C. albumin. or axial arthritis.Dosages and Side Effects of H2-Receptor Agonists and Prokinetic Agents Agents Cimetidine (Tagamet) Dosage 10 mg per kg per dose. and edematous. and malaise. The degree of anemia indicates the severity of mucosal injury and duration of illness.2 mg per kg per dose. Inflammation is localized primarily in the mucosa. diarrhea *Because of the small potential risk of serious arrhythmias. Extraintestinal manifestations a. rectal bleeding. C. isolation of toxigenic strains of Escherichia coli. It increases lower esophageal sphincter pressure and esophageal contractile amplitude. which assess nutritional status. diarrhea.
and capsule olsalazine (Dipentum) 1 g/day. These patients may require rehydration or blood transfusion. Fever. anal skin tags. B. abdominal pain. e. Rectal preparations of mesalamine (Rowasa enema and suppository) can deliver higher concentrations to the distal colon for proctitis. Manifestations may include hepatic steatosis. 2. Balsalazide. Corticosteroids. such as perirectal fistulas. A. About 20% of patients have evidence of perianal disease. ing stiffness. c. Patients treated with balsalazide are more likely to achieve a symptomatic remission (88% vs 57%) or a complete remission (62% vs 37%). C. Inflammation is characterized by transmural extension and irregular involvement of the intestinal tract. and iritis may occur. the patient is weaned off the steroids to alternate-day therapy over 4 to 8 weeks. Rowasa (4 g) is the only enema preparation of 5ASA. 4. and became asymptomatic in 10 days compared to 25 days with delayed-release mesalamine. Crohn disease Crohn disease (CD) is a chronic inflammatory process. which may involve any portion of the gastrointestinal tract from the mouth to the anus. 2. The overall risk is two to four times higher in first-degree relatives. anal ulcerations or fissures. Management of ulcerative colitis Mild-to-moderate cases of ulcerative colitis 1. B. mesalamine (Asacol) is usually started. It is more common in females. Intravenous corticosteroids (methylprednisolone). Episcleritis. and aphthous ulcers. Abnormalities may include erythema nodosum. or perirectal abscesses. Crohn disease causes extra-intestinal manifestations like those of ulcerative colitis. The target dosage for the tablet Asacol (in divided doses) is 2. and local therapy should be initiated. caused by chronic blood loss and a mildly elevated white blood cell count are common. C. suppositories) with corticosteroids and mesalamine. Limited left-sided colonic disease or rectosigmoid disease may respond to local therapy (enemas. Balsalazide (Colazal). Moderately severe cases of ulcerative colitis 1. only the colon is affected. strictures. Diagnostic evaluation 1. Once the patient has stabilized. and fatigue are common.4 g/day. uveitis. diarrhea. with intervening normal tissue (“skip areas”). primary sclerosing cholangitis (4%). D. IV. Mesalamine (Asacol) is an oral 5-ASA compound used for active ulcerative colitis. Other complications include nephrolithiasis and a hypercoagulable state. Hydrocortisone retention enema (Cortenema). and olsalazine sodium (Dipentum) is used for maintenance therapy. Other features of Crohn disease include rectal sparing. 3. a prodrug of mesalamine (5-aminosalicylic acid) for oral treatment of mildly to moderately active ulcerative colitis. lichen planus. and ileal involvement. Fluid and electrolyte status must be stabilized and blood transfusions given as needed. Prednisone usually is started at a dose of 1 to 2 mg/kg per day for 1 to 2 weeks. Most often.III. 1. Miscellaneous. cobblestone appearance. pyoderma gangrenosum. cholelithiasis. d. weight loss. in about 25% of cases. Hepatobiliary. Crohn disease often has its onset during adolescence and young adulthood. Dermatologic. Ocular. Anemia. Rectal bleeding is not as prominent a feature in Crohn disease as it is in ulcerative colitis. and pericholangitis. Fulminant ulcerative colitis requires immediate hospitalization. b. a low-residue diet. . the capsule (Pentasa) 4 g/day. is effective for distal ulcerative colitis. Endoscopic findings include focal ulcerations and inflammation is interrupted by skip areas. 2. the distal ileum and proximal colon are involved. A.
hirsutism. diarrhea Rout e Side Effects Local irritation Nephrotoxicity Watery diarrhea Methylprednis olone Hydrocortisone Enema Foam 0. Treatment is similar to that of ulcerative colitis. bone marrow suppression 1. hypertension. see page 182. References. B. . If the patient has not improved for 2 to 4 weeks after maximal medical therapy. If the patient deteriorates clinically or develops complications (hemorrhage. cataracts. Immunosuppressive agents. Surgery for Crohn disease is not curative. C. massive weight loss. Treatment of Inflammatory Bowel Disease Dose/da y 5-Aminosalicylic Acid Mesalamine (Asacol) Mesalamine (Rowasa) Enema Suppository Mesalamine (Pentasa) Olsalazine (Dipentum) Basalazine (Colazal) 30-50 mg/kg 2-4 g qd 500 mg bid 50-60 mg/kg 20-30 mg/kg 2. hypertension Cyclosporine IV PO Antibiotics Metronidazole 10-20 mg/kg PO/I V Peripheral neuropathy. A.broad-spectrum antibiotics (metronidazole. Indications include obstruction or intractable symptoms. and bowel rest are initiated. Disease almost always recurs after surgery. Surgery is curative for UC. parenteral nutrition. an aminoglycoside. Cyclosporine may be beneficial in refractory patients. Antibiotics (metronidazole and ciprofloxacin) are useful in mild-to-moderate CD and perianal disease. and ampicillin). poor growth. Prednisone can induce a remission in 70% of patients who have small bowel disease. and significant systemic symptoms may need to be hospitalized. metallic taste Miscellaneous Folic acid 1 mg PO V. Patients with severe colitis. Management of Crohn disease. obesity. Corticosteroids and mesalamine (Asacol) are the mainstays of therapy.6 mg/kg PO 100 mg QD-BID 80 mg QD-BID PR PR Local irritation Same as enema Immunosuppressants 6mercaptopurin e Azathioprine 1-1.5-2 mg/kg 2-4 mg/kg 4-6 mg/kg PO Same as for 6mercaptopurine Nephrotoxicity Hirsutism.8-1. toxic megacolon). 2. emergency surgery is performed.25 g tid Steroids Prednisone 1-2 mg/kg PO Osteoporosis. adrenal suppression Same as for prednisone PR PR PO PO PO PO Nephrotoxicity Chills. a colectomy should be considered. Mercaptopurine and azathioprine are reserved for patients with continuous disease activity despite corticosteroid therapy.5 mg/kg PO Pancreatitis.
which is characterized by passive movement of gastric contents into the esophagus.Persistent Vomiting Vomiting is defined as the forceful expulsion of gastric contents through the mouth. Clinical evaluation of vomiting Etiology of Vomiting by Age Newborn Obstruction Malrotation of bowel Volvulus Intestinal atresia Intestinal stenosis Meconium ileus Meconium plug Hirschsprun g disease Imperforate anus Incarcerated hernia Necrotizing enterocolitis Gastroesoph ageal reflux Paralytic ileus Peritonitis Milk allergy Infant Pyloric stenosis Foreign bodies Malrotation (volvulus) Duplication of alimentary tract Intussuscept ion Meckel diverticulum Hirschsprun g disease Incarcerated hernia Gastroenterit is Gastroesoph ageal reflux Pancreatitis Appendicitis Celiac disease Paralytic ileus Peritonitis Sepsis Meningitis Otitis media Pneumonia Pertussis Hepatitis Urinary tract infection Hydrocephalus Subdural hematoma Intracranial hemorrhage Mass lesion (abscess. usually secondary to gastric outlet obstruction caused by hypertrophic pyloric stenosis or pylorospasm. Vomiting can be caused by a benign. Vomiting is usually preceded by nausea. increased salivation. Projectile vomiting results from intense gastric peristaltic waves. II. disorders of organic acid metabolism Congenital adrenal hyperplasia Neonatal tetany Obstructive uropathy Renal insufficiency Inborn errors of metabolism Fructose intolerance Adrenal insufficiency Metabolic acidosis Renal disorders Obstructive uropathy Renal insufficiency Obstructive uropathy Renal insufficiency . I. Pathophysiology of vomiting A. self-limited process or it may be indicative of a serious underlying disorder. and retching. Retching often precedes vomiting and is characterized by spasmodic contraction of the expiratory muscles with simultaneous abdominal contraction. C. galactosemia. It is distinct from regurgitation. B. tumor) Older Child Intussuscepti on Foreign bodies Malrotation (volvulus) Meckel diverticulum Hirschsprun g disease Incarcerated hernia Adhesions Gastrointestinal disorders (infectious/inflammatory) Gastroenterit is Peptic ulcer disease Infectious disorders (nongastrointestinal) Sepsis Meningitis Meningitis Otitis media Pharyngitis Pneumonia Hepatitis Urinary tract infection Subdural hematoma Intracranial hemorrhage Brain tumor Other massoccupying lesion Migraine Motion sickness Hypertensive encephalopa thy Adrenal insufficiency Diabetic ketoacidosis Neurologic disorders Hydrocephalus Kernicterus Subdural hematoma Cerebral edema Metabolic and endocrine disorders Inborn errors of metabolism: Urea cycle defects.
or history of consanguinity. Clinical evaluation of vomiting in the neonate 1. Inborn errors of metabolism should be considered in any acute neonatal illness. Abdominal pain typically wakes the patient from sleep. Necrotizing enterocolitis a. III. Peptic ulcer disease should be suspected if there is a family history of ulcer disease. but may occur at birth or present as late as 5 months. hypotonia. volvulus. and blood in the stool. 3. a rapid increase in head circumference. b. Gastroesophageal reflux a. such as lethargy. 2. such as failure to thrive. Five percent of infants whose parents had pyloric stenosis develop this disorder. GER occurs in 65% of infants and is caused by inappropriate relaxation of the lower esophageal sphincter. Symptoms of NEC include abdominal distention. meconium ileus. An olive-size mass may be palpable in the right upper quadrant. b. Metabolic disorders a. or reflux esophagitis. or if there is hematemesis or unexplained iron deficiency anemia. and shock. hydrocephalus and cerebral edema. diarrhea. and convulsions. 2. b. bowel atresia. or an unexplained fall in hematocrit. suggests intestinal obstruction or systemic infection. GER is considered “pathologic” if symptoms persist beyond 18 to 24 months and/or if significant complications develop. NEC is the most common inflammatory condition of the intestinal tract in the neonate. apnea. . Clinical evaluation of vomiting in childhood A. Males are affected more often than females. meconium plug. Central nervous system abnormalities. B. although 10% of affected newborns present at term. including persistent vomiting. Associated features may include lethargy. Gastroesophageal reflux (GER) is defined as retrograde movement of gastric contents into the esophagus. Factors that suggest a metabolic disorder include early or unexplained death of a sibling. Symptoms of pyloric stenosis usually begin at age 2 to 3 weeks. The infant who has NEC also may present with nonspecific signs of systemic infection. Peptic ulcer in early childhood is often associated with vomiting. Clinical evaluation of vomiting in infancy 1. Bilious vomiting. duplications of the bowel. incarcerated hernia. Anatomic abnormalities of the gastrointestinal tract that may present in the first week of life with bilious vomiting and abdominal distention include malrotation. bilious vomiting. at any age. such as intracranial hemorrhage. multiple spontaneous maternal abortions. and aganglionosis (Hirschsprung disease). Neurologic disorders. recurrent episodes of bronchospasm and pneumonia. NEC occurs mainly in preterm infants. Gastrointestinal allergy. 4. 3. Hypertrophy of the pylorus causes gastric outlet obstruction at the pyloric canal. Vomiting. apnea. colic and gastrointestinal loss of blood may occur. should be suspected in the neonate who has neurologic deficits. Cow milk allergy is rare in infancy and early childhood and generally resolves by 2 to 3 years of age. Pyloric stenosis is a major consideration in infants. Pyloric stenosis a. b. temperature instability.Newborn Toxins Infant Digoxin Iron Older Child Digoxin Iron Lead Food poisoning Pregnancy Anorexia nervosa Bulimia Psychogenic etiology Other A.
and an empty rectal ampulla suggests Hirschsprung disease. Other factors predisposing to pancreatitis include viral illnesses (mumps). however. E. Decreased anal sphincter tone and large amounts of hard fecal material in the ampulla suggests fecal impaction. Volume depletion often results from vomiting. Abnormal masses. 2. Constipation. cholelithiasis. Laboratory evaluation A. C. C. dry mouth. and a family history of pancreatitis. VI. Supine and upright or left lateral decubitus radiographic views are necessary for detecting congenital anatomic malformations or obstructive lesions. D. Initial therapy should correct hypovolemia and . Plasma amino acids and urine organic acids should be measured if metabolic disease is suspected because of recurrent. water-soluble contrast is indicated when anatomic abnormalities and/or conditions that cause gastric outlet obstruction are suspected. B. Persistent vomiting without other gastrointestinal or systemic complaints suggests an intracranial tumor or increased intracranial pressure. which may radiate to the mid-back. D. Upright plain films may demonstrate free air under the diaphragm. Barium enema should be performed to detect lower intestinal obstruction. Urinalysis may detect a urinary tract infection or suggest the presence of a metabolic disorder. Plain radiographs of the abdomen 1. and it may also be therapeutic in intussusception. Liver chemistries and serum ammonia and glucose levels should be obtained if liver disease is suspected. enlarged organs. V. F. Central nervous system disorders. Subtle neurologic findings (eg. manifesting as sunken fontanelles. Pancreatitis 1. Ultrasonography of the abdomen is the initial imaging test for suspected pyloric stenosis. C. Upper gastrointestinal series with nonionic. and increased bowel sounds suggests intestinal obstruction.B. visible peristalsis. azathioprine). B. VII. hypertriglyceridemia. absence of tears. sausage-shaped mass in the right upper quadrant and an empty right lower quadrant (Dance sign). 3. 2. Serum electrolytes should be obtained when dehydration is suspected. and decreased urine output. Patients usually complain of epigastric pain. Air-fluid levels suggest obstruction. Serum lipase levels may be more helpful because it remains elevated for a number of days following an acute episode. drugs (steroids. Digital rectal exam. ataxia. Serum amylase is frequently elevated in patients who have acute pancreatitis. Free air in the abdominal cavity indicates a perforated viscus. Pancreatitis is a relatively rare cause of vomiting. congenital anomalies of the biliary or pancreatic ducts. but should be considered in the child who has sustained abdominal trauma. Physical examination of the child with persistent vomiting A. head tilt) should be assessed and a detailed neurologic examination should be performed. increased rectal sphincter tone. IV. iso-osmolar. decreased skin turgor. B. Treatment A. unexplained episodes of metabolic acidosis. A hypertrophic pylorus may manifest as a palpable “olive” in the right upper quadrant. guarding or tenderness should be sought. Abdominal distension. C. Imaging studies A. Serum ammonia should be obtained in cases of cyclic vomiting to exclude a urea cycle defect. E. two-thirds of vomiting infants will have a negative sonogram and will subsequently require an upper gastrointestinal series. Intussusception is often associated with a tender. Peritoneal irritation should be suspected when the child keeps his knees drawn up or bends over. D. although this finding is nonspecific and may be seen with gastroenteritis.
infectious gastrointestinal illnesses.electrolyte abnormalities. Prochlorperazine and chlorpromazine have anticholinergic and antihistaminic properties and are used to treat vomiting caused by drugs. Antiemetic drugs may be indicated for postoperative emesis. 3. cytotoxic drug-evoked emesis. Diphenhydramine and dimenhydrinate are useful in treating the symptoms of motion sickness or vestibulitis. Bilious vomiting requires surgical consultation. motion sickness. see page 182. Pharmacologic therapy 1. oral rehydration therapy is usually adequate for treatment of dehydration. and by placing a nasogastric tube connected to intermittent suction. Bilious vomiting and suspected intestinal obstruction is managing by giving nothing by mouth. 2. and gastroesophageal reflux disease. . Antiemetic agents usually are not required because most instances of acute vomiting are caused by self-limited. radiation. and gastroenteritis. References. In acute diarrheal illnesses with vomiting. C. B.
Most febrile illnesses associated with febrile seizures are caused by common infections (tonsillitis. B. The problem almost always resolves without sequelae. and 9% of children who have febrile seizures will have 3 or more. Management of febrile seizures A. The tonic phase is followed by the clonic phase of repetitive. B. A lumbar puncture (LP) is indicated if there is any suspicion of meningitis. II. IV. The most common age of onset is in the second year of life. CT or MRI are seldom helpful and are not performed routinely. Fewer than 5% of children who have febrile seizures develop epilepsy. III. Laboratory studies should evaluate the source of fever. There is no risk of brain damage. After the first febrile seizure. C. Risk factors for the development of epilepsy following febrile seizures include suspicious or abnormal development before the first seizure. followed by loss of consciousness and muscular rigidity. Physical examination 1. During this tonic phase. Febrile seizures occur in 2-4% of young children. Hospital admission is necessary if the child is unstable or if meningitis remains a possibility. 2. presence of meningismus. which is then followed by postictal lethargy or sleep. Febrile seizures usually occur early in the course of a febrile illness. An underlying illness that may require treatment should be sought. D. Only a small minority will develop non-febrile seizures later. I. family history of afebrile seizures. a tense or bulging fontanelle. The younger the child’s age when the first febrile seizure occurs. The child should be kept in the emergency department or physician’s office for at least several hours and re-evaluated. 8% last longer than 15 minutes. A. often as the first sign. or trauma should be assessed. The seizure may be of any type. Most children will have improved and be alert. Short duration of fever before the initial seizure and relatively lower fever at the time of the initial seizure are risk factors. The electroencephalogram (EEG) is not helpful in the evaluation of febrile seizures because it is not predictive of recurrence risk of later epilepsy. Family history of febrile or afebrile seizures should be evaluated. and complex first febrile seizure.Neurologic and Rheumatic Disorders Febrile Seizures Febrile seizures are the most common convulsive disorder of childhood. Recurrence 1. but the most common is tonicclonic. Parental counseling . Clinical evaluation A. apnea and incontinence may occur. Kernig or Brudzinski sign. Pathophysiology. 2. Epilepsy. upper respiratory infections. Epidemiology. Symptoms of infection. Family history of febrile seizures is a risk factor for recurrence. Higher temperature and a history of febrile seizures in a close relative are risk factors for the development of a febrile seizure. medication exposure. Other seizure types may be characterized by staring with stiffness or limpness or only focal stiffness or jerking. otitis media). and any focal abnormalities in muscle strength or tone should be sought. A febrile seizure is defined as a seizure associated with fever in infancy or early childhood (usually between 3 months and 5 years of age) without evidence of intracranial infection or other cause. Initially there may be a cry. E. The level of consciousness. 33% of children will experience one or more febrile seizures. the greater the likelihood of recurrence. rhythmic jerking movements. Children of preschool age are subject to frequent infections and high fevers. B. Encephalitis or meningitis must be excluded. Most seizures last less than 6 minutes. A complete description of the seizure should be obtained from a witness. and the child may be sent home if the cause of the fever has been diagnosed and treated.
Behavior immediately prior to the event. The recurrence risk increases to 37 percent in children in whom the seizure is related to a prior neurological insult (remote symptomatic). There is a risk of further febrile seizures during the current or subsequent febrile illnesses. The advantages of vaccines must be weighed against the risk of pertussis if immunization is postponed. may be idiopathic and nonrecurrent. visual distortions. no obvious precipitating circumstances are present. If the seizure does not stop after 10 minutes. References. the child should be brought to the hospital. The physician should obtain . E. The child who is neurologically normal. H. however. On rare occasions.1. such as cerebral palsy. the parent should place the child on his side or abdomen with the face downward. Physical description. C. obtaining a history of the events leading up to the seizure is important because they may be more suggestive of a nonseizure diagnosis. and has an unprovoked seizure with no evident cause (idiopathic seizure) has a 24 percent risk of having another seizure in the next year." which is actually the first clinical manifestation of the seizure. Control of fever with antipyretics (acetaminophen) and sponging is recommended. this information is valuable for localizing. Did the seizures occur only with illness and fever? D. etc) or manifest an alteration in behavior or mood? F. Setting in which episodes occur. but this practice has not been proven to lower the risk of recurrent febrile seizures. More commonly. Thus. B. auditory or visual hallucinations or illusions. and the likelihood of developing epilepsy or recurrent non-febrile seizures is very small. Febrile seizures occur most commonly following a DPT immunization because pertussis provokes fever. Prognosis after a first seizure. Thus. such as a metabolic or infectious disorder. I. nausea or unusual feelings in the abdomen or chest. Most seizures are random events. Nothing should be forced between the teeth. Long-term management A. but is reserved for very young children who have sustained multiple seizures associated with focal postictal paralysis. an unusual smell or taste. V. Parents are advised that febrile seizures do not cause brain damage. Childhood immunizations. or may represent the beginning of epilepsy. Are the seizures precipitated by a particular stimulus? Seizures rarely are precipitated by mild trauma. If another seizure occurs. present? These symptoms are considered an "aura. see page 182. has no history of a prior neurological illness. D. B. A child’s first seizure may be caused by an acute illness. Prophylaxis with diazepam or phenobarbital is not routinely necessary. Diazepam may be administered orally and rectally during febrile illnesses to prevent recurrences of seizures. Oral diazepam is given in three divided doses to a total of 1 mg/kg per day when the child is ill or feverish. 2. the neurological examination and neuroimaging studies are normal. such as facial or extremity twitching. What activity was the patient engaged in immediately prior to the seizure? Does the patient mention any sensory or autonomic symptoms (numbness. such as sound or an unexpected touch. C. determining the time of day and the activity in which the child was engaged prior to the seizure is important. G. The first seizure. Seizures The majority of children with epilepsy have an idiopathic disorder. Was focal motor activity. seizures may be precipitated by environmental stimuli. Clinical evaluation of seizures A. and increases to 70 percent in the next year in patients who have had two seizures (excluding sequential seizures in 24 hours). many nonepileptic syndromes have characteristic precipitating circumstances or occur in specific locations.
Are limb movements unilateral. What was the patient’s behavior post-event? Did the child recover immediately. relatively symmetric. usually are associated with an alteration of consciousness. which suggests an inherited disorder. the retinal changes of a neurocutaneous disorder. and low self-esteem because of depression. A developmental history should be obtained.a description of the patient’s color. particularly a recessively metabolic disorder. What was the duration of the event? Most seizures are short-lived. or more irregular and thrashing? Bilateral motor seizures. meningitis. with particular attention given to any plateau or loss of developmental milestones. true clonic (rhythmic flexion movements or rhythmically interrupted tonus). The child may be having increasing difficulty at school because of peer ridicule. J. if passive opening is actively resisted. 3. hypoxic-ischemic encephalopathy). A family history of seizures is suggestive of a dominantly inherited epileptic disorder. A. K. . 2. or signs of an earlier infection should be sought. a low academic performance as a result of limited cognitive function. he/she usually will become cyanotic. In contrast. What was the patient’s response to verbal commands. tonic or clonic movements. Other elements of the history 1. International Classification of Epileptic Seizures Partial Seizures –Simple partial (consciousness retained) –Complex partial (consciousness impaired) –Partial seizure with secondary generalization Generalized Seizures –Absence seizures –Myoclonic seizures –Clonic seizures –Tonic seizures –Tonic-clonic seizures –Atonic seizures Unclassified Seizures I. Family history should assess the possibility of consanguinity. a patient with a pseudoseizure may suddenly return to normal after a painful stimulus or shouting of his or her name. or more painful stimulation? Generalized motor seizures cannot be interrupted by vocal or tactile/painful stimulation. 3. Behavior during the event 1. Patients with true generalized motor seizures tend to keep their mouths open during the tonic phase of the seizure. an episode of confusion or loss of contact with the environment that lasts more than five minutes should raise the suspicion of a nonepileptic event. A cardiac cause for the event should be considered if the child is described as pale. or was there postictal confusion or somnolence? Was the child able to communicate verbally immediately after the event? 2. II. L. 4. A nonepileptic seizure should be suspected if the patient has minimal to no movement during the seizure and is unresponsive for more than two minutes. synchronous. Are the eyes and mouth closed? A pseudoseizure should be considered if the patient keeps the eyes tightly closed during the seizure and. particularly. particularly those involving all the extremities and the trunk with generalized. involving a limb or the face only? Psychosocial assessment. Stimulus-provoked clonic/tonic activity during a generalized motor seizure is more consistent with a pseudoseizure. If a child has a color change during a seizure. Physical examination Congenital ocular defects. pinching. bilateral. The examiner should search for a history of previous illnesses that often are followed by seizures (eg. Behavior after the event 1. Was postictal weakness present? Was it global or focal. particularly a generalized motor seizure. 2. Seizures often are accompanied by cognitive and developmental delay.
In the benign partial epilepsies. The cutaneous features of tuberous sclerosis. the risk of seizure recurrence is higher. Children with absence seizures. carnitine. Treatment of Seizures and Epileptic Syndromes in Children A. and infantile spasms are virtually always treated. Cardiac examination. Laboratory testing and neuroimaging A.B. the caféau-lait spots of neurofibromatosis. urine for quantitative organic acids. the EEG is the most valuable predictor of recurrence. C. Benign focal epilepsy syndromes may manifest generalized EEG discharges as well as a photoparoxysmal response (epileptiform activity provoked by repetitive light flashes). and unusual skull shapes noted. may be needed to diagnose those syndromes missed on routine karyotype analysis. focal or multifocal spike and slow wave discharges typically appear during drowsiness and light sleep. In children with an idiopathic seizure. is necessary if concern exists about a cardiogenic cause. Many parents elect to avoid therapy if the seizures are infrequent and/or mild. B. . Epileptiform activity may appear in only one state (usually sleep). particularly in boys and occasionally in girls with maternal family histories of mental retardation. body asymmetries. D. IV. lactate and pyruvate. Episodes of disturbed neurological function caused by decreased cardiac output (eg. C. the nevi of the linear nevus syndrome. More sophisticated genetic analyses. the facial angioma of Sturge-Weber syndrome. The abdominal examination may reveal organomegaly. including an ECG. An awake and asleep EEG should be obtained. Most children with recurrent seizures should have an MRI scan. usually without the use of contrast. prolonged QT syndrome or pulmonary hypertension) may closely mimic complex partial seizures. Laboratory screening in undiagnosed epilepsy. Electroencephalogram (EEG). Virtually every child with recurrent seizures should have an EEG awake and while sleeping. Obtaining an awake and a sleep EEG and optimizing the timing of the EEGs should maximize the chances of finding epileptiform activity. and DNA analysis for fragile X syndrome. B. Sleep. Routine assessment consists of a serum (and often CSF) amino acid analysis. III. glucose. In children with seizures that result from a past injury or insult. ammonia. routine chromosomal karyotype (virtually all chromosomal syndromes can manifest seizures). such as FISH studies. E. is the sleep-activated focal spikes. Neuroimaging. however. Predictors of recurrence. The most striking and diagnostic pattern. and the swirling hypopigmentation of Ito syndrome all are characteristic physical findings. which more typically are seen in the idiopathic generalized epilepsies. Many patients with benign partial epilepsy are not treated if seizures are relatively infrequent. Treating a child with an idiopathic first seizure is usually not recommended. V. the recurrence risk was 41 percent in the first 12 months after the initial seizure if the EEG was abnormal compared with 15 percent in children with a normal EEG. suggesting a storage disease. drop attacks. serum calcium. A. An idiopathic first seizure. Dysmorphic features should be sought and other congenital anomalies.
The AED dose should be increased until seizures stop (regardless of the serum level). usually at every return visit. PHT. TPM: topiramate.CBZ. TGB: tiagabine.CNZ 1 . diplopia.ESM. LTG 2 . PRM. PB: phenobarbital. focal) Antiepileptic drug 1 . VPA. ESM 2 . prednisone 2 . TPM 1 . The therapeutic range is different for each patient. PB.ESM (drop attacks).PRM. VPA: valproic acid (divalproex sodium) D. the dose should be increased at intervals not exceeding five half-lives to allow the serum level to plateau between each dosage increment. 3.VPA. FBM 1: First-line drugs 2: Second-line drugs CBZ: carbamazepine.VPA. Most AEDs should be started at about 10 to 25 percent of the planned maintenance dose. CRZ: clorazepate. CRZ. LTG: lamotrigine. dysfunction. CNZ.LTG 1 . TPM 1 . PRM: primidone. anemia. Serum levels should be used only as guides to therapy. whereas others require levels above the range. Increase by 5 mg/kg/d every wk to 20-30 mg/kg/d in 2 or 3 divided doses Dizziness. TPM.LTG. carbamazepine XR (Tegretol XR) Partial epilepsy Tonicclonic Begin 10 mg/kg/d.ACTH. liver. CNZ. GBP: gabapentin. VPA. Antiepileptic drug therapy 1. many achieve seizure control at levels below the recommended range. PHT: pheytoin. LEV: levetiracetam. drowsiness.Epileptic Syndromes and Recommended Antiepileptic Syndrome Localization-related (partial. If seizures are frequent. CNZ (?). PHT. ESM: ethosuximide.GBP. AEDs with a long half-life can be started at close to the maintenance dose. Laboratory monitoring is done in all children receiving AEDs. Common Anticonvulsant Drugs Drug Seizure Type Oral Dose Serum Level mcg/ mL 102 Side Effects and Toxicities Carbama zepine (Tegretol) . OXC: oxcarebazepine. or levels reach a high or supratherapeutic range without a significant impact upon seizure frequency. VPA. FBM: felbamate. 2. unremitting side effects occur. OXC 2 . CNZ: clonazepam.CBZ. b. Drug dose a. LEV 1 . LTG. TPM (?) Generalized epilepsies Absence seizures Generalized tonic-clonic Juvenile myoclonic epilepsy Myoclonic absence Infantile spasms Lennox-Gastaut syndrome 2 . LMG 2 . PB TPM 2 .VPA (?). leucopoenia .
0. blurred vision Topirama te (Topama x) Partial epilepsy Tonicclonic Nephrolithia sis. rarely blood dyscrasias Felbamat e (Felbatol) Partial epilepsy Tonicclonic Headache. fatigue.400 to 3. Maximum. hepatitis <2 Somnolence. Increase to maintenance dose of 5 to 15 mg/kg/d. Begin 25 to 50 mg Increase to 200 to 400 mg/day in 2 doses Begin 4 mg Increase to 32 to 64 mg in 2-4 doses Begin 300 to 600 mg Increase to 600 to 2.200 mg/ 2. ataxia.05 mg/kg per wk. Increase by 0.600 mg two to three times daily Begin 300 mg/d.356. nausea. vomiting.Drug Seizure Type Oral Dose Serum Level mcg/ mL 6.05 mg/kg/d. dizziness.000 mg Increase to 1. headache.2 mg/kg/d in 2 or 3 divided doses Begin 10 to 20 mg/kg/d in 2 divided doses. short attention span. irritability.400 mg in 2 doses Begin 1. paresthesia s. drooling. drowsiness. tremor. Increase by 300 mg/d every 3 to 5 days. may be increased to 50 mg/kg/d 600 to 1. StevensJohnson syndrome. insomnia. depression Ethosuxi mide (Zarontin) Absence Myoclon ic 40160 Drowsiness. temper tantrums. behavioral abnormalities. weight loss Tiagabin e (Gabitril) Partial epilepsy Narrow spectrum of activity Oxcarbaz epine (Trileptal) Partial epilepsy Hyponatre mia Levetirac etam (Keppra) Focal epilepsy Zonisami de (Zonegra n) Focal epilepsy Nephrolithia sis. aplastic anemia. Maximum 900 to 1200 mg/d in 3 equally divided doses Begin 2 mg/kg/d in 2 equal doses. headache. weight gain Gabapen tin (Neuronti n) Partial epilepsy Tonicclonic Lamotrigi ne (Lamictal) Partial epilepsy Tonicclonic LennoxGastaut 3543 3 Severe rashes.000 mg in 2 doses Begin 100 to 200 mg Increase to 400 to 600 mg every day in 2 doses 3 to 5 mg/kg/d in 1 or 2 divided doses Drowsiness. weight loss Phenobarbital Tonicclonic Partial epilepsy 15-40 Hyperactivity. depression of cognitive function . altered sleep pattern.8 Side Effects and Toxicities Clonazep am (Klonopin ) Myoclon ic Absence Begin 0.000 to 3. nystagmus. irritability.
Valproic acid (divalproex) is associated with a high incidence of minor elevations of liver enzymes and serum ammonia. Usual dose. the medication should be stopped.000. ataxia. Topiramate causes a mild to moderate chronic metabolic acidosis in two-thirds of children and can cause nephrolithiasis. intermittently. Begin 30 to 40 mg/kg/d. occurring in two per 575. F. If the ANC falls below 800 to 1000. Begin 10 mg/kg/d.414 Agitation. b. The level of ketosis can be monitored daily in the urine and. The serum gamma glutamyl transpeptidase (GGT) elevated in 75 percent and alanine aminotransferase (ALT) in 25 percent. Epilepsy surgery. E. if the white blood count (WBC) or absolute neutrophil count (ANC) is significantly decreased. 20 to 60 mg/kg/d in 2 or 3 divided doses. . dizziness. drowsiness. gum hypertrophy. Stevens Johnson syndrome Aggressive behavior and personality changes similar to those for phenobarbital Primidon e (Mysoline ) Tonicclonic Partial epilepsy Myoclon ic Begin 50 mg/d in two divided doses. tremor. a repeat study is done in three to four weeks and may be repeated again until the counts stabilize. weight gain. The serum bicarbonate should be measured at baseline and monitored periodically thereafter. Severe aplastic anemia or agranulocytosis is rare. Gradually increase to 150 to 500 mg/d divided into 3 equal doses. alopecia. Obtain a CBC after the first month of carbamazepine therapy. Increase by 10 mg/kg per wk. The diet suppresses seizure frequency by at least 50 percent in 40 percent of patients. Dose reduction or drug discontinuation should be considered in patients with persistent or severe metabolic acidosis. Complications of chronic metabolic acidosis include impaired growth and rickets or osteomalacia. skin rash. which appears to have an anticonvulsant effect. Some are refractory despite numerous medications and are not candidates for or fail the ketogenic diet. The high-fat content and relative absence of carbohydrate produces a persistent ketosis. often appearing in the first two to three months of therapy. Carbamazepine. 5. Maximum. Leukopenia is not uncommon with carbamazepine. headache. a. Hepatic enzyme elevations greater than three times normal should be repeated in several weeks and the medications stopped if levels are increasing rapidly or the child is symptomatic. in the serum. hepatotoxicity Vigabatri n (Sabril) Partial epilepsy 1. ataxia 4. Increase by 5 to 10 mg/kg per wk.Drug Seizure Type Oral Dose Serum Level mcg/ mL 293 Side Effects and Toxicities Phenytoi n (Dilantin) Partial epilepsy Tonicclonic 5m6 mg/kg/d in 2 divided doses Hirsutism. G. 1. Ketogenic diet consists of three to four parts fat to one part protein and carbohydrate. 80 to 100 mg/kg/d in 2 equal doses 132 Sodium valproate (Depakot e) Tonicclonic Absence Myoclon ic Partial epilepsy Unclassified 50100 Weight gain. Most children achieve reasonably good seizure control with anticonvulsant medication.
H. head circumference. E. Analgesic use should be determined. recurrent acute. It is characterized by periodic episodes of paroxysmal headache accompanied by nausea. A social and educational history may identify significant stresses. Many children who fail AED therapy and the ketogenic diet are not candidates for standard epilepsy surgery. If increased intracranial pressure or an intracranial lesion is suspected. The presence of retinal venous pulsation on funduscopy provides evidence of normal intracranial pressure. Surgical approaches can be divided into relatively noninvasive (vagal nerve stimulator) and invasive (local resection. Physical and Neurological Examination of the Child with Headaches Feature Growth parameters Significance Chronic illness may affect linear growth Hypothalamopituitary dysfunction may disturb growth Increased intracranial pressure prior to fusion of the sutures may accelerate head growth Evidence of trauma or a neurocutaneous disorder Hypertension Signs of increased intracranial pressure Neurologic abnormality May reflect an intracranial arteriovenous malformation Head circumference Skin Blood pressure Neurologic examination Cranial bruits . and a detailed neurologic examination is essential. Neuroimaging should be performed prior to the lumbar puncture. a computed tomographic (CT) head scan should be performed. and relief with sleep. Approximately 30 percent of adults treated in a randomized (highcurrent stimulation) have a 50 percent or better seizure reduction. Clinical evaluation A. or cerebral edema. D.Surgical interventions should be considered in children who have persistent. I. lobar or multilobar resection. an intracranial mass lesion. Headache Chronic or recurrent headaches occur 75% of children by 15 years. References. Headaches are characterized as isolated acute. However. Lumbar puncture may be helpful if pseudotumor cerebri is suspected. Papilledema. lumbar puncture may result in herniation of the brain in patients who have obstructive hydrocephalus. C. Physical examination should include measurement of growth parameters. Others may undergo resective surgery and still have excessive numbers of seizures. corpus callosotomy. Magnetic resonance imaging (MRI) may be required to diagnose subtle vascular abnormalities or hypothalamopituitary lesions. Investigations. These patients may be candidates for vagal nerve stimulation. or chronic progressive. abdominal pain. hemispherectomy. B. and blood pressure. Vagal nerve stimulation. Visual acuity should be measured. Migraine is the most common headache syndrome in children. machinery-like cranial bruit. chronic nonprogressive. see page 182. The teeth should be examined and sinusitis should be sought. vomiting. An arteriovenous malformation may cause an asymmetric. frequent seizures. and multiple subpial transection) procedures.
This dose may be repeated in two to four hours.to 12-hour intervals. Migraines may be associated with a preceding aura. Its use is reserved for the emergency department prior to the administration of dihydroergotamine (DHE). Midrin consists of isometheptene mucate (a sympathomimetic agent). 2.to sixhour intervals. In adolescents. although their use is not approved. Management of migraine headache in children A. a dose of up to 20 mg can be given. Ibuprofen should not be given to patients with abdominal pain. dichloralphenazonel (a mild sedative). b. lack of sleep. If nausea and vomiting are prominent. Nasal sumatriptan is given to younger children in an initial dose of 5 mg. A family history of motion sickness is common. 3. or certain foods.25 mg/kg orally or intramuscularly every four to six hours.25 to 0. Sumatriptan given by the subcutaneous or intranasal route reduces headache severity in 70 percent. Naproxen should not be given to patients with epigastric pain or nausea. Phenothiazines may have additional antimigraine properties. d. if needed. headache is relieved within one or two hours . Acute dystonic reactions may occur. with a maximum dose of 1000 mg. A combination analgesic can be tried if single analgesics fail to relieve pain in children older than eight years of age. Rectal administration may be preferable.5 mg/kg per dose orally. Naproxen (250 mg tablet) can be given to children older than 12 years of age.5 mg/kg IV. and a fourth capsule 90 minutes later. Additional doses may be given at four. and acetaminophen. throbbing. The dose is 1. Ibuprofen may provide faster relief than acetaminophen. oral. no more than three doses should be given in 24 hours. b. b. Other analgesics. c. Ibuprofen is given in a dose of 5 to 10 mg/kg at 4 to 8-hour intervals (maximum 50 mg/kg in 24 hours). which usually involves visual phenomena. or tinnitus. d. 10 mg can be tried. and have a low incidence of acute extrapyramidal reactions. Triptans are contraindicated in basilar artery and hemiplegic migraine because of vasospasm. The headache is usually unilateral or bilateral. a. 2. dizziness. up to a maximum of 1 mg/kg per day. intramuscularly. II. Dimenhydrinate also is an effective antiemetic. If this dose is ineffective. The triptans are highly effective. and associated with nausea or vomiting.F. Antiemetics. Intravenous ketorolac successfully treats migraine in 55 percent.25 mg/kg PO every six hours. NSAIDs and acetaminophen. Metoclopramide administered intravenously appears to reduce nausea and vomiting associated with migraine. Nasal sumatriptan spray is effective and should be considered for the acute treatment of migraine in adolescents 12 to 17 years old. Doses are 0. or rectally. a. Acetaminophen is administered in an initial dose of 10 to 20 mg/kg (one or two 325 mg tablets). recurrent. a third dose one hour later. Photophobia or phonophobia is common. excitement. The dose for adolescents is two capsules at the onset of the headache. 4. Triptans are widely used in children. After a 6 mg dose. early use of an antiemetic may relieve symptoms and facilitate sleep. The dose can be repeated up to three times per day at 8. oral administration is effective in 50 percent. menstruation. a. but should not exceed three doses in 24 hours. c. it should not be given intravenously. and nasal preparations are available. Ketorolac can be administered intravenously or orally. The dose is 0. followed by 1 mg/kg every six hours or 0. A family history of migraine is obtained in up to 80% of children who have migraine. A second dose of 10 to 20 mg/kg may be given in two to four hours if symptoms persist. c. Early administration of acetaminophen or ibuprofen is helpful. Abortive treatment 1. Triptans are serotonin agonists with an affinity for the 5-HT 1b/1d receptor. Subcutaneous sumatriptan is an effective therapy for migraine. Migraine episodes may be triggered by stress. Parenteral. Migraine 1.
Similar doses of nasal spray are used in older children. Oral sumatriptan is effective and useful in children.5 or 5 mg). Thrombocytopenia may occur at higher doses. which is used for migraine prophylaxis. This dose may be repeated in two to four hours if needed. e. The initial dose is 25 mg. Prophylactic treatment is used when headaches are frequent (more than four times per month) or if severe and prolonged headache . with at least two weeks between changes. it may be repeated once in four to six hours if the headache returns. c.25 to 0. Prophylactic treatment is used when headaches occur more than four times per month. Side effects include appetite stimulation with weight gain. with a maximum of 50 mg. 5. a. Valproate has teratogenic effects. a. The initial dose in adolescents is 25 mg. This may be repeated in 20 minutes if the symptoms persist. diabetes. A reasonable therapeutic range is 50 to 100 mg/dL. if analgesics do not provide relief a trial of sumatriptan nasal spray should be initiated. If frequent headaches persist. Other triptans may be tried in patients older than 10 years of age who do not respond to sumatriptan: rizatriptan ([Maxalt] 5 mg wafer) or zolmitriptan ([Zomig] 2. Cyproheptadine (4 to 12 mg at bedtime) is used for prophylaxis in the younger child. Appetite stimulation with weight gain limits use.in 46%. Additional reported adverse events include transient hair loss and polycystic ovary syndrome. If there is no benefit. b. gastrointestinal upset. dizziness. folic acid also should be given. given at night. somnolence. b. Children with nausea and vomiting should receive promethazine (Phenergan) 0. Flunarizine is a calcium channel blocker. C. Thus. Somnolence occurs. with a maximum dose of 4 mg/kg per day. Valproate is started in a dose of 10 to 15 mg/kg in two divided doses. 2. The dose can be increased in increments of 15 mg/kg to a maximum dose of 60 mg/kg per day. the dose is advanced slowly by 5 mg increments. In children at least five years of age. If no improvement occurs. Propranolol is the prophylactic treatment most commonly used in children. A single daily 5 mg oral dose of amitriptyline. which is unavailable in the United States. Nonspecific electrocardiographic changes and changes in atrioventricular conduction may occur. 3. Abortive treatment begins with either acetaminophen or ibuprofen. They should be used with caution in depression. Valproate should be used cautiously in children younger than age five years of age because of potential hepatotoxicity. The heart rate should be >60 bpm after one minute of exercise. and tremor. an electrocardiogram should be obtained. In adolescent females at risk for pregnancy. Chronic therapy with propranolol reduces the frequency of migraine in 60 to 80 percent. often is effective.5 mg/kg rectally and repeat as needed at intervals of four to six hours. two 5 mg units of nasal spray may be given together. Valproate decreases headache frequency by 50 percent. b. In children older than 10 years without vomiting. Cyproheptadine (Periactin) is a histamine and serotonin antagonist. B. Serum anticonvulsant concentration should be monitored every three to six months. Begin with 5 mg. 2. Amitriptyline is used commonly for migraine prophylaxis in children. c. Recommendations 1. oral sumatriptan is an option. Beta-blockers are contraindicated in children with asthma. no more than three doses should be given in 24 hours. or orthostatic hypotension. 1. The dose rarely should exceed 60 mg. Liver function tests and complete blood count should be monitored every two to three months. Treatment with flunarizine 5 mg/day is associated with a significant reduction in headache frequency. Ibuprofen is given in an initial dose of 10 mg/kg (maximum dose 50 mg/kg). Propranolol is initiated in a dose of 1 mg/kg in three divided doses. a. 4. with a maximum of 20 mg. doses up to 50 mg can be used. Heart rate and orthostatic blood pressure should be monitored every three months.
a.1/100. arrhythmias.5/100. unexplained fever. Valproate is given primarily to boys older than five years of age. myocardial infarction.000 children <5 years). complications such as coronary artery aneurysm. Diagnosis requires the presence of fever lasting five days or more without any other explanation. however. valproate (Depakote) should be used for prophylaxis. maximum dose 1. 25 mg). Used with metoclopramide. with a maximum dose of 4 mg/kg per day.results in frequent school absences or prevents important daily activities. . Valproate is started in a dose of 10 to 15 mg/kg in two to three divided doses orally. Kawasaki Disease Kawasaki disease (KD) is one of the most common vasculitides of childhood. may repeat in 1-2 hours. In older children. start at low dose and increase slowly 10 to 15 mg/kg in two divided doses. Bilateral conjunctival injection. or 20 mg in one nostril. Can be repeated q8h. can be repeated at doses of 0. This drug should bed avoided in adolescent females because of weight gain and polycystic ovary syndrome. see page 182. Initial dose of 1 mg/kg PO (maximum. The annual incidence is highest among Asians and Pacific Islanders (32. intermediate among African Americans (16. followed by 10 to 15 mg/kg q 4 h up to a maximum dose of 65 mg/kg per day (maximum.25 to 1 mg/kg q 4 to 6 h 1 mg/kg IM for severe attacks Dihydroergotamine (DHE) Prophylactic Agents for Migraine Amitriptyline (Elavil) Propranolol (Inderal) Valproate (Depakote) 5-10 mg qhs 1 to 4 mg/kg per day. c.000 mg/day) 1 to 12 years: 10 mg/kg PO q 4 to 6 h More than 12 years: 200 to 400 mg PO q 4 h.1/100.000 children <5 years of age).000 children <5 years of age). and lowest among Caucasians (9. increased by 15 mg/kg to a max 60 mg/kg per day References. If propranolol is not well tolerated. cyproheptadine (Periactin) is used in a dose of 4 to 12 mg per day. combined with at least four of the five following physical findings: 1. KD should be considered in any infant with prolonged. I. depressed myocardial contractility and heart failure. Treatment of Acute Migraine Episodes Simple analgesics Acetaminophen Initial dose of 20 mg/kg PO.9/100. 10. and peripheral arterial occlusion may develop.5 to 1 mg IV over 3 min in children >10 y. It is typically a self-limited disorder.200 mg/day 5 mg/kg PO q 12 h. The dose can be increased in increments of 15 mg/kg to a maximum dose of 60 mg/kg per day. 3. b. maximum dose 750 mg/day Ibuprofen (Advil) Naproxen (Aleve) Antiemetics Promethazine (Phenergan) Chlorpromazine (Compazine) Other Drugs Sumatriptan (Imitrex) 6 mg SC. may repeat after 2 hours 0. max 12 mg/day Oral: 25-50 mg PO once.000 children <5 years) and Hispanics (11. given orally once at bedtime. In children younger than six years of age. Diagnosis A. propranolol is the first choice in a starting dose of 1 mg/kg in three divided doses. may repeat in 2 hours Intranasal: 5.
and a left-shift in the white blood cell count. Atypical Kawasaki disease. Inflamed oral mucosae (fissured lips. Elevated transaminase levels or mild hyperbilirubinemia often occur. erythrocyte sedimentation rate. and periungual desquamation (convalescent phase). C-reactive protein [CRP]. including injected or fissured lips. Cervical adenitis (unilateral >1. A. polymorphous but nonvesicular) D.5 cm in diameter).2. 5. at least 85 percent of those with typical KD develop palmar erythema. lack the ocular and articular involvement typical of KD. including erythema of palms or soles or edema of hands or feet (acute phase). have fewer than four signs of mucocutaneous inflammation) may have incomplete or atypical KD. Oral mucous membrane changes. Mucous membrane changes are most characteristic of KD and are generally present in more than 90 percent of children with any form of the disease. 3. Bilateral conjunctival injection B. 4. Differential diagnosis. By the second week of illness. dorsal edema. Rash may not be manifest in 7 to 10 percent of children with KD. Adenopathy is missing in up to 90 percent of children with atypical disease.000. Renal involvement may occur in KD but is uncommon. such as Stevens-Johnson syndrome or serum sickness. Drug reactions. injected pharynx. and alpha-1 antitrypsin). some patients who manifest five or six signs may have other conditions. Hand and feet inflammation (periungual peeling around 14-21 days) III. No alternate diagnosis IV. In addition.000/mm3 (reactive thrombocytosis). D. Children who do not meet the criteria may have an incomplete or atypical form of KD. IV. KD is most commonly confused with other infectious exanthems of childhood. The urinalysis commonly reveals white blood cells on microscopic examination. The cardinal manifestation most likely to be absent in all cases of atypical KD is cervical lymphadenopathy. Toxin-mediated illnesses. IVIG should be administered as . B. or strawberry tongue. Intravenous immunoglobulin should be administered at a dose of IVIG 2g/kg. V. Systemic inflammation is manifest by elevation of acute phase reactants (eg. C. Initial management. D. Peripheral extremity changes. Outcomes appear to be comparable to children with complete disease. Polymorphous rash. Measles. C. A. Children suspected of having KD who do not fulfill diagnostic criteria (ie. perineal accentuation. Cervical lymphadenopathy (at least one lymph node >1. normochromic anemia. Rash (truncal. In comparison. especially betahemolytic streptococcal infection and toxic shock syndrome.5 cm diameter. KD often presents with a normocytic. echovirus. Kawasaki Syndrome: Diagnostic Criteria I. non-fluctuant) C. B. B. Those patients suspected of having atypical disease may require further testing such as slit lamp examination and echocardiography to confirm the diagnosis. a minority of children develop obstructive jaundice from hydrops of the gallbladder. Fever plus 3/5 criteria are diagnostic when coronary abnormalities are present II. as a single dose over 8 to 12 hours. Children with incomplete KD fail to demonstrate peripheral extremity changes in 40 percent of cases. At least four of five features A. Laboratory studies A. In addition. strawberry tongue) E. platelet counts generally rise and may reach 1. A. Fever for >5 days (usually >102EF) II. leukocytosis. III. and adenovirus cause mucocutaneous inflammation but typically have less evidence of systemic inflammation and lack the extremity changes seen in KD. C. B. Patients who fulfill the criteria for Kawasaki disease are hospitalized and treated with intravenous immune globulin (IVIG) and aspirin. may mimic KD but with subtle differences in the ocular and mucosal manifestations. or periungual desquamation.
Vaccinations. Diagnosis. Subsequently. Repeated examinations should be performed during the first two months to detect arrhythmias. should be postponed in children who have been treated with IVIG. I. Passively acquired antibodies persist for up to 11 months following IVIG administration.Other rheumatic diseases . fever. or other constitutional symptoms suggest a different diagnosis. The knee is often swollen. Pauciarticular JIA affects the large joints (knees. such as ibuprofen. Systemic manifestations (other than uveitis) are characteristically absent. If a single joint is involved. 2. A. Pauciarticular JIA affects females more often than males. and rarely Reye syndrome. and they may interfere with vaccine immunogenicity. If two or more joints are involved. D. B. It is less common over five years of age and rarely begins after age 10. Aspirin is continued until laboratory studies (eg. platelet count and sedimentation rate) return to normal. The risks of aspirin include transaminitis.Nonrheumatic conditions of bones and joints . Aspirin is given as 30 mg/kg/day to >100 mg/kg/day in four divided doses during the acute phase of illness. They may be warm. unless coronary artery abnormalities are detected by echocardiography. Juvenile Rheumatoid Arthritis Pauciarticular onset juvenile idiopathic arthritis (JIA) is defined as involvement of fewer than five joints. wrists.Childhood malignancies . The administration of live virus vaccines. transient hearing loss. ankles. C. The diagnosis of pauciarticular onset JIA is based upon the presence of arthritis in four or fewer joints during the first six months of disease.soon as a diagnosis of KD is established. The involved joints are typically swollen and tender to compression. this phase of therapy typically is complete within two months of the onset of disease. but virtually never begins in the hips. Long-term complications of pauciarticular JIA. Children with coronary artery abnormalities receive long-term antithrombotic therapy with aspirin. The typical child with pauciarticular JIA is a girl who is noticed to be limping without complaint. Limitation of motion may not be present. include uveitis and leg length discrepancy. American College of Rheumatology Criteria for Diagnosis of JRA Diagnostic Requirements For JRA • Documented arthritis of one or more joints for 6 weeks or longer • Exclusion of other conditions associated with childhood arthritis . Follow-up. arthritis must be present for at least three months and multiple alternative causes of arthritis must be excluded. including measles and varicella. An echocardiogram should be obtained early in the acute phase of illness and six to eight weeks after onset to confirm the efficacy of treatment. Patients older than six months of age who require long-term aspirin therapy should receive yearly influenza immunization because of the possible increased risk of Reye syndrome.Infectious diseases . see page 182. It is the most common subgroup of JIA. The peak incidence of pauciarticular JIA is in the second and third years. aspirin is administered in low doses (3 to 5 mg/kg/day) for its antiplatelet action. D. Often the family notices that the child “walks funny” in the morning. C. They should receive the inactivated vaccine. 1. valvular insufficiency. may be used for prolonged episodes of arthritis. References.Miscellaneous conditions II. A child with large joint involvement beginning in the early teenage years most commonly has a spondyloarthropathy. B. or myocarditis. Thus. heart failure. constituting about 50 percent of cases of JIA. elbows). but after a little while seems fine. rash. Alternative anti-inflammatory agents. chemical hepatitis. and regular cardiac evaluation. but they should not be erythematous. arthritis must be present for at least . Clinical presentation A.
These conditions are usually associated with elevated acute phase reactants. proper gait should be maintained by placing an appropriate lift in the opposite shoe. with the elimination of exclusions. and a normal platelet count. the opposite of pauciarticular JIA. Uveitis 1. Fifty-four percent remit completely. there is a normal white blood cell count without a left shift. if ever. Children with plant thorn synovitis.On motion . Leg length discrepancies of less than 1 cm are probably not important.At rest Loss of Joint Motion . The subgroup of children with pauciarticular JIA who have detectable ANAs are at greatest risk of developing iridocyclitis. Methotrexate and other immunosuppressive drugs are rarely. The most serious complication of pauciarticular JIA. Screening must be performed by an ophthalmologist and includes a complete slit lamp examination.six weeks. it is likely that permanent and irreversible damage has already occurred. Leg length discrepancy. resolving within six months. The erythrocyte sedimentation rate is close to normal. A. occurring in approximately 20 percent of children. required. La. these are manifestations of a spondyloarthropathy. There may be significant asymmetric overgrowth when a single knee joint is involved. IV. Objective Signs of Arthritis Joint Swelling . Differential diagnosis 1. However. A few children with typical pauciarticular disease evolve into chronic destructive arthritis. and RNP. Joint injection with glucocorticoids early in the course of pauciarticular JIA may prevent leg length discrepancies. Medical therapy. 2.Stiffness of joints Joint Warmth Joint Erythema B. Children over the age of 9 years with arthritis involving the hips or knees and enthesiopathic symptoms also do not have pauciarticular JIA. by the time the child complains of pain in the eye or difficulty seeing. There should not be any systemic complications of pauciarticular JIA other than uveitis.Synovial hypertrophy . or even Lyme disease are mistakenly diagnosed with pauciarticular JIA. Antibodies to dsDNA. 3. but is more typical of psoriaform arthritis. Ro. is the development of uveitis or iridocyclitis (inflammation of the anterior uveal tract and the adjacent ciliary body). Treatment of juvenile rheumatoid arthritis A. some children will have disease activity in one or two joints for a prolonged period that does not respond to NSAIDs. osteomyelitis.Swelling of periarticular tissues Joint Pain .On palpation (tenderness) . Uveitis is often initially silent. These conditions are often acutely painful with sudden and dramatic onset. 2. Most cases of pauciarticular JIA are benign. III.Increased amounts of synovial fluid . Sm. . B. 2. Course and prognosis. Laboratory findings 1. septic arthritis. Thus. Recurrences occur in 20 percent of children. Pauciarticular onset JIA is usually responsive to nonsteroidal antiinflammatory drugs (NSAIDs) or selective COX-2 inhibitors. resulting in a leg length discrepancy over time. and rheumatoid factor should be absent. routine screening is necessary. When they become greater. Dactylitis (a swollen finger or toe) may be pauciarticular. Antinuclear antibodies (ANAs) are frequently present in pauciarticular JIA and are associated with an increased risk of iridocyclitis. ANAs are typically present in low or moderate titers in a homogeneous pattern. however. C. The major morbidity is typically related to the development of uveitis.
maximum dose 1. lupus nephritis. skin rash. urinary frequency. 24-hour urinary calcium excretion Serum creatinine. C. or immunoglobulin (Ig) A nephropathy. B. Dysuria.5% and 1% of all children. or Henoch-Schönlein purpura. Each urine sample that tests positive for blood by dipstick must be examined microscopically to confirm the presence of intact RBCs. Aspirin. brown. streptozyme titer Renal ultrasonography Plain abdominal film if nephrolithiasis is suspected . References. and suprapubic pain or tenderness suggests a urinary tract infection or hypercalciuria. The urine may be yellow. Etanercept is best reserved for children with a significant elevation of the erythrocyte sedimentation rate. Clinical evaluation A. Abdominal.NSAID Treatment of Juvenile Rheumatoid Arthritis Ibuprofen (Motrin) 1 to 12 years: 10 mg/kg PO q 4 to 6 h More than 12 years: 200 to 400 mg PO q 4 h. Renal and Urologic Disorders Hematuria Hematuria occurs in about 0. Each of these forms of glomerulonephritis usually is associated with proteinuria and RBC casts. Henoch-Schönlein purpura. If microscopic hematuria has been present for 1 month or more. C3. Vigorous exercise such as jogging or bike riding may cause hematuria. Intraarticular injection of glucocorticoids may be helpful if only a single joint is involved and there has been an inadequate response to NSAIDs after three or more months of therapy. hemolytic uremic syndrome. back or flank pain. Hematuria with a concurrent upper respiratory infection strongly suggests IgA nephropathy. thereby reducing its activity. It is defined as more than 5 to 10 RBCs per high-power microscopic field from a centrifuged midstream voided urine sample. Evaluation of Hematuria Patient history. non-steroidal anti-inflammatory agents. pallor. antibiotics. D. hypertension. nephrolithiasis.200 mg/day 5 mg/kg PO q 12 h. joint swelling or tenderness. or smoky. or bloody diarrhea suggests postinfectious glomerulonephritis. suggests child abuse. red. A history of edema. family history. see page 182. methyldopa. further investigation for the cause is indicated. poststreptococcal acute glomerulonephritis must be ruled out. If sore throat or pyoderma precedes the hematuria by 7 to 30 days. abdominal pain. C. Hemoglobin and myoglobin will produce the same color changes on the dipstick as intact RBCs. physical examination Examination of urine for red blood cell casts and crystals Screening for proteinuria with a dipstick Examination of urine of first-degree relatives for hematuria Urine culture Urinary calcium/urinary creatinine. maximum dose 750 mg/day Naproxen (Aleve) B. pink. Etanercept (Enbrel) is a soluble tumor necrosis factor alpha (TNFa) receptor fusion protein that binds TNFa. and other drugs can cause hematuria. Abdominal pain may be associated with an abdominal mass. I. especially when associated with bruising.
blebs. ureteropelvic junction obstruction. serum albumin. and streptozyme titer.Differential Diagnosis of Persistent Hematuria Without Proteinuria Urinary tract infection Hypercalciuria With Proteinuria Urinary tract infection Poststreptococcal acute glomerulonephritis IgA nephropathy Thin basement membrane disease Sickle cell disease or trait Renal cystic disease Henoch-Schönlein purpura Membranoproliferative glomerulonephritis Lupus nephritis Alport syndrome Hemolytic-uremic syndrome Other forms of glomerulonephritis Nephrolithiasis Renal anatomic abnormalities E. G. A family history of autosomal dominant polycystic kidney disease requires that this disease be ruled out by ultrasound. A complete blood count. a renal biopsy usually is indicated. Ultrasonography of the kidneys and urinary bladder is recommended to rule out polycystic kidney disease. C3. blood sickle cell preparation in African-American children. C4.or 24-hour urine collection or a urine protein:urine creatinine ratio on a single voided sample. serum creatinine. Urinalysis. dialysis or renal transplantation with bilateral deafness and ocular abnormalities suggests Alport syndrome. When confirmatory serologic tests are nondiagnostic. urinary calcium. A family history of nephrolithiasis raises the diagnostic possibility of nephrolithiasis or hypercalciuria. A family history of hematuria without renal failure may be seen with thin basement membrane disease. The presence of proteinuria (>1+ on dipstick) strongly suggests glomerulonephritis. I. chronic renal failure. serum electrolytes. Proteinuria 1. F. A family history of hematuria. RBCs from areas of the urinary tract other than glomeruli will be normal in size with smooth edges (eumorphic). Familial Causes of Hematuria Polycystic kidney disease Thin basement membrane disease Sickle cell disease or trait Alport syndrome (hereditary nephritis with deafness) Hypercalciuria with family history of nephrolithiasis H. An audiogram is indicated for children suspected of having Alport syndrome. Preliminary tests should include a urine culture. or burrs (dysmorphic RBCs) correlate with a glomerular origin of the RBC. urinary creatinine ratio. serum creatinine. If proteinuria is present on urinalysis. blood urea nitrogen. tumor. urinary protein excretion should be measured by a timed 12. A screening urinalysis on first-degree family members is also important. antistreptolysinO titer. and stones. Renal Structural Abnormalities Associated with Hematuria Polycystic kidney disease Ureteropelvic junction obstruction Vesicoureteral reflux Renal or bladder stones. The diagnosis of glomerulonephritis demands microscopic inspection of the urinary sediment for RBC casts. J. test for lupus erythematosus. streptozyme titer. Sickle cell disease or sickle cell trait in the patient’s family may suggest this diagnosis. diverticula or tumors Renal arteriovenous fistula Foreign bodies . C3. RBCs that have bizarre shapes. and antinuclear cytoplasmic antibody titer are indicated to clarify the type of glomerulonephritis. hepatitis B screen. 2. Nonglomerular bleeding usually is associated with normal urinary protein excretion and an absence of RBC casts.
vomiting. sunken eyes Sunken Not visible even with supraclavi cular pressure Very delayed capillary refill (>4 sec). including type and volume of food and drink. and hypermetabolic states. Estimation of deficit 1. Maintenance fluid and electrolytes 1. Fluids and Electrolytes Disorders affecting the body fluids and electrolytes are treated by supplying maintenance requirements.020 >1. Estimation of volume depletion should assess fever. Sensible losses. 2. and weight change should be determined. oliguria . account for 50% of daily fluid requirements. hyperventilation. I. diarrhea. B. Maintenance Requirements for Fluid and Electrolytes Body Weight Water Volume 0 to 10 kg 100 mL/kg 10 to 20 kg 1000 mL + 50 mL/kg for each kg >10 kg 3 mEq/kg 2 mEq/kg 5 mEq/kg >20 kg 1500 mL + 20 mL/kg for each kg >20 kg 3 mEq/kg 2 mEq/kg 5 mEq/kg Sodium Potassium Chloride 3 mEq/kg 2 mEq/kg 5 mEq/kg 3. should be measured. and urine output. correcting volume and electrolyte deficits. ongoing gastrointestinal losses. and replaced on a volume for volume basis. Abnormal losses. acrocyanotic or mottled skin Oliguria or anuria Thirst Mucous Membranes Tears Slight Normal Present Moderate Dry Decreased Anterior Fontanelle External Jugular Vein Normal Visible when supine Normal to sunken Not visible except with supraclavicul ar pressure Delayed capillary refill. Caloric requirements for growth can be estimated as equivalent on a kcal-for-mL basis to water requirements. Estimation of Dehydration Degree of Dehydration Weight Loss-Infants Weight Loss-Children Pulse Blood Pressure Mild 5% 3-4% Normal Normal Moderate 10% 6-8% Slightly increased Normal to orthostatic.020. prolonged diarrhea or burns.References. tenting. Factors that increase the requirements for calories and water are fever (10% for each degree). primarily urinary. Recent feeding. such as those arising from nasogastric aspiration. Dehydration A. 2-4 sec (decreased turgor) Skin Capillary refill <2 sec Urine Specific Gravity (SG) >1. see page 182. physical activity. and by replacing ongoing abnormal losses. >10 mm Hg change Irritable Severe 15% 10% Very increased Orthostatic to shock Behavior Normal Hyperirritable to lethargic Intense Parched Absent tears. cool.
2. Euvolemic hyponatremia may also occur in infants fed excessively diluted infant formula. cramps. The percent dehydration is used to calculate the milliliters of body water deficit per kilogram of body weight. congestive heart failure. pulmonary disorders. associated with edema. Isonatremic dehydration 1. proximal renal tubular acidosis. plasma Na+ concentration should be corrected at no more than 10-12 mEq/L/day. Other causes of hypovolemic hyponatremia include percutaneous losses or third space sequestration of fluid (ascites. c. The majority of patients who have gastroenteritis can be treated with oral rehydration therapy. altered states of consciousness. Pedialyte. C. Symptoms include apathy. Hypervolemic hyponatremia. CNS infection. Hypovolemic patients who have hyponatremia first require volume repletion with normal saline. 3. and coma. maintenance needs are provided. Five percent glucose should be used as the stock solution and NaCl is added according to the estimated need. Rehydralyte) are given as tolerated to provide 50 mL/kg over 4 hours in mild dehydration. If the correction of fluid and electrolyte losses is excessively rapid. Children who have isonatremic dehydration require 8 to 10 mEq of Na+ per kg of body weight for repletion of deficit and 3 mEq/kg per day for maintenance. Moderate volume depletion should be treated with oral fluids. may result from water retention and excess Na+. b. Once rehydration is accomplished. d. (2) Renal sodium loss (urinary Na+ >20 mEq/L) may be caused by diuretics. nausea.2. providing maintenance. The first phase of treatment rapidly expands the vascular volume. saltwasting nephropathy. headache. Intravenous normal saline or Ringers lactate (10-20 mL/kg) should be given over 1 hour. and certain drugs. seizures. Hyponatremia and hyponatremic dehydration 1. This Na+ is given in a volume consisting of the calculated maintenance for water and the estimated water deficit. which is caused by water retention (urinary Na+ is usually >20 mEq/L). b. Parenteral fluids should be given for severe volume depletion. weakness. D. The most common cause of dehydration in infants is diarrhea. and replacing ongoing abnormal losses. KCl is added at a concentration of 20 mEq/L. vomiting. The signs and symptoms of hyponatremia correlate with the rapidity and extent of the fall in serum Na+ concentration. the brain may sustain injury. Small aliquots of oral hydration solution (Ricelyte. In severe depletion. The most common cause of euvolemic hyponatremia is the syndrome of inappropriate antidiuretic hormone secretion. and abdominal distention or ileus. Children who have a brief illness and anorexia usually present with isotonic dehydration. Management of hyponatremia a. maintenance fluid is given at 100 mL/kg per day. intractable vomiting. peritonitis). Hypervolemia. cirrhosis. Parenteral rehydration a. and up to 100 mL/kg over 6 hours in moderate dehydration. c. 3. Euvolemia. burns. 4. In severe hyponatremia. Differential diagnosis of hyponatremia a. and lack of or resistance to mineralocorticoid. b. Once urine flow occurs. Oral rehydration a. as in nephrosis. 2. then a solution containing salt is given to correct the Na+ deficit (10 to 12 mEq/kg of body weight or 15 mEq/kg in severe hyponatremia) and to provide the Na+ maintenance needs (3 mEq/kg per day) . Causes include tumors. or renal failure. The next phase of treatment is aimed at correcting the deficit. Resol. Hypovolemia (1) The most frequent cause of hypovolemic hyponatremia is viral gastroenteritis with vomiting and diarrhea. half of the calculated deficit is given over the first 8 hours and the second half over the next 16 hours.
Potassium disorders A. Total body Na+ most commonly is decreased. protracted vomiting. Children may display hyperkalemia in metabolic acidosis. Affected patients frequently exhibit lethargy or confusion. For a serum Na+ concentration >160 mEq/L. b. diuretics. this amount should be given over a 24-hour period. Hypernatremia and hypernatremic dehydration 1. in renal tubular acidosis.observed [Na+]) x body weight in kg x 0. or respiratory distress. Intracellular K+ concentration can be estimated from the electrocardiogram. extreme muscle weakness. E. which may reveal flattened T waves. renal tubular disease).6 II. Hypovolemic patients who have hypernatremia require a hypotonic solution containing salt to restore the Na+ deficit (2-5 mEq/kg of body weight) and to provide the Na+ maintenance (3 mEq/kg of Na+) in a solution containing 2040 mmol/L of KCl and 5% glucose. 3. ileus). If the patient is likely to be hypophosphatemic. decreased peristalsis. Manifestations of h yp o k a l e m i a i n c l u d e a r r h y t h m i a s . lethargy. This cause should be excluded by repeating the measurement on a free-flowing venous sample. B. b. In the presence of cardiac arrhythmias.5 mEq/L) is “pseudohyperkalemia” from hemolysis of the blood sample. patients should receive KCl intravenously with cardiac monitoring. 2. An elevated serum Na+ concentration should be corrected by no more than 10 mEq/L per day. vomiting. Hypokalemia (serum K+ concentration <3 mEq/L) is most frequently caused by gastrointestinal K+ losses or renal losses (nasogastric suction. may cause hypernatremia in the presence of persistent fever. disorientation) requires urgent therapy to prevent seizures or coma.in a 5% dextrose solution. Once the serum K+ is stabilized. or hypoaldosteronism. renal failure. (2) A correction using 3% saline over 4 hours can be calculated according to the following formula: Sodium deficit in mEq = (125 . shortened P-R interval and QRS complex. muscle twitching. KCl should be used. and rhabdomyolysis. oral administration is preferable. . For a serum Na+ concentration of 120 to 130 mEq/L. tissue catabolism. hyperreflexia. Symptomatic hyponatremia (headache. The most common cause of hyperkalemia (K+ >5. the rehydration should be spread out over several days to lower the Na+ concentration to 150 mEq/L by 10 mEq/day. b. Management a. Hyperkalemia 1. the rehydration should be spread out over several days at a rate of 10 mEq/day. For a serum Na+ concentration <120 mEq/L. In metabolic alkalosis. a phosphate salt should be used. Initial therapy requires administration of normal saline or Ringers lactate to restore circulating plasma volume. The hypernatremic patient is usually also dehydrated. 2. Fever is common. this volume should be given over 24hours. or convulsions. For a serum Na+ concentration of 150-160 mEq/L. a citrate salt should be used. neuromuscular excitability (hyporeflexia or paralysis. cyclophosphamide). Differential diagnosis a. Other causes of hypernatremia include water and Na+ deficit from skin losses or renal losses. and water losses from central or nephrogenic diabetes insipidus (DI) or drugs (lithium. and eventually U waves. and the skin may feel thickened or doughy. Diarrhea. and decreased fluid intake. (1) Hypertonic saline (3% saline solution) should be used to raise the serum Na+ by 1 to 2 mEq/L per hour or halfway toward normal during the first 8 hours. 3. Hypokalemia 1. c. which usually results in isonatremic or hyponatremic dehydration. b. Management a. volume depletion. c. anorexia.
volume replacement is the primary mode of therapy. The amount to infuse is calculated with the following formula: Amount to infuse in mEq = weight in kg (15 -observed [HCO3-]) x 0. peaked T waves and shortened QT intervals at K+ concentrations >6 mEq/L and depressed ST segment and widened QRS complex at K+ concentrations >8 mEq/L. Bicarbonate should be given when plasma HCO3. Thus. Increased anion gap acidosis may be caused by diabetic ketoacidosis. Glucose. resulting in moderate-to-severe metabolic acidosis. neuromuscular irritability. paresthesias. the duration is less than 30 minutes. These unmeasured anions are referred to as the anion gap. Management a. Normal anion gap (hyperchloremic) acidosis (1) This disorder occurs when HCO3. and seizures.is <5 mmol/L. arrhythmias. lactic acidosis. Differential diagnosis a. Emergent therapy to reverse potentially lifethreatening hyperkalemia consists of intravenous calcium. The pH of the body fluids normally is between 7. In patients with GI loss of acid from vomiting. hypotension.5 gm/kg. III. The onset of action is rapid. B. and low in Cl . confusion. and it causes a compensatory increase in ventilation (respiratory alkalosis) and a fall in pCO2.35 and 7. and nasogastric aspiration.(Cl +HCO3-) = 10-12 mEq/L 3. Addition of a fixed acid to the extracellular fluid causes the formation of unmeasured anions. and renal failure. 5. 0. Alkalosis results from a gain of base or a loss of acid. 2. high in K+. 4. b. Severe hyperkalemia is treated with hemodialysis. b. however. Acid-base disorders A. Treatment of acidosis a. and pulmonary edema. arrhythmias. With severe watery diarrhea. urinary Cl. The common clinical manifestations are lethargy. The electrocardiogram demonstrates narrow. the symptoms in affected male infants appear in the first weeks of life and include dehydration and failure to thrive together with low serum Na+ and high K+ concentrations. can be given over 30-60 minutes when EKG changes are present.45..5 b.is lost from the body. Manifestations of hyperkalemia include cardiac arrhythmias. (2) Failure to excrete acid occurs in mild chronic renal insufficiency and RTA. muscle weakness. Manifestations of acidosis include depressed myocardial contractility. Bicarbonate should be added to a hypotonic solution and given as a continuous infusion over 1 hour. Differential diagnosis a. c. Diarrheal fluid is high in HCO3-. b. 3. Sodium polystyrene sulfonate (Kayexalate) (1 gm/kg) can be given by high-rectal enema or orally.concentration is usually below 20 mEq/L. Causes of metabolic alkalosis include alkali administration.2. diarrhea causes hypokalemia and hyperchloremic acidosis. ethylene glycol). Metabolic acidosis 1. Diagnosis a. In salt-losing congenital adrenal hyperplasia. ingestion of toxins (aspirin. Metabolic alkalosis 1. Cushing syndrome. due to complete deficiency of the enzyme 21hydroxylase. and paralysis. Acidosis results from the addition of acid or the removal of alkali from body fluids. vomiting. Affected female infants usually are diagnosed at birth because of ambiguous genitalia. 2. which can be estimated as: Anion gap = Na+ . Emergent administration of glucose will cause K+ to redistribute to the intracellular space. C. 4. Bartter syndrome or . either through the gastrointestinal tract or the kidneys.
and seizures. Rebreathing into a bag may decrease the severity of symptoms. confusion. The maximal grade of reflux Is significantly lower in African-American children. 5. decreased renal function. and course A. Children with three urinary tract infections with unusual organisms. Respiratory alkalosis 1. secondary to hyperventilation. Caucasian children were three times more likely to have VUR than African-American children. . proteinuria. Children who have a positive RNC on screening. b. II. Children with recurrent UTI. Young children and infants (0 to less than 2 years of age) are more likely to have VUR than older children. Causes of respiratory alkalosis include hyperventilation caused by CNS disorders and panic disorder. Grade II . Causes of respiratory acidosis include airway obstruction. 3. Respiratory acidosis is induced by an increase in pCO2. 6. Vesicoureteral reflux occurs in 1 percent of newborns and 30 to 45% in young children with urinary tract infection. Grade I . Grading of VUR based on findings from a contrast voiding cystourethogram (VCUG). Girls under the age of three years with a first UTI. grade III as moderate. References. Postnatal diagnosis of VUR is usually made after a UTI. VUR is present in 10 to 40% of all fetuses with prenatally diagnosed hydronephrosis. Age. which lowers plasma pH. Children with other prenatal renal anomaly. Respiratory acidosis 1. Treatment involves correcting the underlying disorder. Treatment consists of mechanical ventilation and correction of the underlying disorder. and sometimes end stage renal disease (ESRD). diagnosis. renal injury with subsequent hypertension. I. There is significant ureteral dilation and tortuosity. Therapy consists of identifying and treating the underlying pathology. Gender. VUR is present in one percent of newborns. Girls are twice as likely to have VUR after an initial febrile UTI. Screening of is recommended because of the increased familial incidence of VUR. see page 182. III. Any male child with a first UTI. and pulmonary disorders. Grades I and II are classified as mild reflux. 2. C. Postnatal presentation. All the calyces are blunted with a loss of papillary impression and intrarenal reflux may be present. VUR predisposes to acute pyelonephritis by allowing bacteria to migrate from the bladder to the kidney.primary aldosteronism may cause metabolic alkalosis. Grade V . Prenatal presentation. Grade IV . resulting in dizziness. Any child under five years of age with a febrile UTI. and grades IV and V as severe.Reflux only fills the ureter without dilation. Epidemiology. One-half of the calyces are blunted. A. 3. The presence of VUR is suggested prenatally by the finding of hydronephrosis via ultrasonography. 4. A. Presentation. D. provision of Clwill allow the kidney to excrete the excess base.Reflux fills and mildly dilates the ureter and the collecting system with mild blunting of the calyces. Girls were twice as likely to have reflux than boys.Reflux fills and grossly dilates the ureter and the collecting system. B.Reflux fills the ureter and the collecting system without dilation. E. Screening of siblings and parents of children with VUR. In mild-to-moderate alkalosis. Grade III . renal failure. 2. Vesicoureteral Reflux Vesicoureteral reflux (VUR) is defined as the retrograde passage of urine from the bladder into the upper urinary tract. The risk of VUR is increased in young children with urinary tract infection. 2. Respiratory alkalosis is caused by a decrease in pCO2. Pyelonephritis may lead to renal scarring. C. Treatment a. with an incidence that ranges from 30 to 45%. 7. Routine VCUG should be therefore performed among the following groups: 1.Massive reflux grossly dilates the collecting system. B.
surgery is optional 1 to 5 V Antibiotic prophylaxis 6 or greater I and II Antibiotic prophylaxis 6 or greater III and IV Antibiotic prophylaxis If renal scarring or bilateral reflux. By five years of age. spontaneous resolution occurrs in 80% of patients. 2. B. a renal ultrasound is recommended at three months of age. IV. either with . C. V. should be treated medically because they have a high likelihood of spontaneous resolution. There is a 60% resolution rate for unilateral disease and less than 10% resolution rate for bilateral reflux over five years regardless of age at presentation. The oldest group of children 5 to 10 years of age with bilateral reflux have less than 20% resolution over five years. Siblings with a history of febrile illnesses or recurrent urinary tract infections. Children below one year of age. Children (one to two years) with unilateral disease have a 70% resolution rate. regardless of grade of reflux. and a radionuclide cystogram (RNC) is recommended at six months or at the time of diagnosis of the index patient. a RNC is recommended. In siblings below two years of age without a history of unexplained febrile illnesses or urinary tract infections. Renal scarring has been associated with VUR with 30 to 60% of patients having evidence of renal scarring at initial diagnosis of VUR. Grade IV. B. a renal ultrasound is recommended. In siblings between two and four years of age without a history of unexplained illnesses or urinary tract infections. Grade III. E. Grade V. surgery is optional If renal scarring or bilateral reflux. a VCUG is recommended. years Less than 1 1 to 5 1 to 5 Grade of reflux Treatment Comments All grades I and II III and IV Antibiotic prophylaxis Antibiotic prophylaxis Antibiotic prophylaxis If renal scarring or bilateral reflux. Spontaneous resolution is rare. surgery is optional If renal scarring or bilateral reflux. surgery is optional 6 or greater V Surgical repair A. In siblings above six years of age or parents without a history of unexplained febrile illnesses or urinary tract tract infections. 3. abnormal ultrasound.1. Management of vesicoureteral reflux Treatment of Children with Vesicoureteral Reflux Clinical presentation Age of patient. Clinical course A. Surgery is a reasonable option if they have grade V reflux and renal scarring. 4. Grades I and II. or RNC. D. All patients with grade I or II reflux.
Patients who have undergone surgical correction require a post-operative VCUG or RNC to document whether the surgery was successful. either unilateral or bilateral disease. or significant antibiotic side effects. C. grade of reflux. 3. and a normal ultrasound. Postnatal. Medical treatment consists of prophylactic antibiotic therapy with trimethoprim-sulfamethoxazole. Children between one and five years of age with grade III or IV reflux. Mandatory urine cultures are required whenever there are urinary symptoms suggestive of UTI or unexplained fever. DMSA scans are recommended in patients with reflux who have an abnormal ultrasound and in infants who have a febrile urinary infection. Renal ultrasound is not as sensitive in detecting renal scars as DMSA scan and has not been as useful in follow-up. surgery is recommended. Yearly evaluation is currently recommended. RNC is the preferred modality as there is less radiation. Surveillance cultures are obtained every three to four months. VI. Follow-up A. E. Children between one and five years of age with grade V without renal scarring can be treated medically. trimethoprim alone. should be treated medically. Urine cultures are required whenever there are urinary symptoms suggestive of UTI or unexplained fever. One daily dose is administered at bedtime at one-half the usual dose for treating an acute infect E. Screening for VUR on a yearly basis with RNC. This group of patients are predominantly female and present after an initial febrile illness. Surveillance cultures are obtained every three to four months. Surgery is a reasonable option if there is bilateral reflux and renal scarring. and whether the reflux is unilateral or bilateral. .unilateral or bilateral disease. D. Surgery should also be considered if medical therapy fails either due to poor compliance. Monitoring of reflux is done by either VCUG or RNC. F. C. surgical treatment is recommended. or nitrofurantoin. demonstrated reflux. B. Children six years or older with grade V reflux should be treated surgically. If the reflux is bilateral and/or there is renal scarring. Patients who are treated medically need to be monitored in the following manner: 1. If there is renal scarring. The rate of spontaneous resolution is dependent upon age. 2. G. breakthrough infections due to antibiotic resistance. D. Children six years or older with unilateral grade IIIIV reflux without renal scarring can be treated medically. should be treated medically as they have high likelihood of spontaneous resolution.
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