Common symptom-based neonatal problems that may result in ED visits include irritability, colic, upper airway complaints, apnea and periodic breathing, GI symptoms, eye complaints, and abnormal movements.
Normal crying was discussed earlier (see "Normal Neonatal Vegetative Functions"), and Table 114-2 lists the important causes of irritability in the neonate. Obtain a thorough history focusing on symptoms other than crying, such as changes in feeding, temperature instability, and vomiting, and perform a systematic head-to-toe examination. Palpate the fontanelles for signs of dehydration (sunken) or infection or intracranial hemorrhage (bulging). If corneal abrasion is possible, examine the eyes with fluorescein staining.7 Inspect the mouth for oral thrush and check diaper area and groin for rashes, hair tourniquets (also check fingers and toes), and hernias or testicular torsion. Auscultate the heart to appreciate dysrhythmias or murmurs, and observe respiratory effort that may point to a pulmonary or metabolic cause of irritability. Obtain a bedside glucose in all neonates with altered mental status, vomiting, or a history of poor oral intake. Examine the abdomen for tenderness, distension, or discoloration suggestive of intra-abdominal pathology and the extremities for signs of trauma.
If a careful history and complete physical examination reveal no source for the crying and the infant quiets during the ED visit, further testing is unnecessary and parents can be reassured and advised to follow up with their primary care physician.
Colic is a symptom complex consisting of the sudden onset of paroxysmal crying, a flushed face, circumoral pallor, tense abdomen, drawn up legs, cold feet, and clenched fists. The cause is not known. Colic is defined as a paroxysm of crying for ≥3 hours per day for ≥3 days per week over a 3-week period. It may begin as early as the first week of life but seldom lasts beyond 3 to 4 months of age. Infant colic is a diagnosis of exclusion. Physical examination is normal, and laboratory tests are not required. However, when the diagnosis is unclear, a careful history, physical examination, and appropriate laboratory investigations are necessary to rule out conditions listed in Table 114-2.
There is no specific treatment for colic. Overfeeding without adequate burping during feedings may result in an irritable, crying infant. Improved feeding practices may decrease symptoms.
Administration of drugs or sedatives is contraindicated. A 1-week trial of hypoallergenic formula (non–cow's milk protein) may help. Infant colic can create significant caregiver stress and fatigue and is a risk factor for nonaccidental neonatal trauma. Carefully assess the caretaker's mental health and explore strategies to provide respite if needed.
Cough and Nasal Congestion
Cough associated with sneezing and nasal congestion is usually due to viral upper respiratory infection. Neonates with underlying pulmonary or heart disease such as bronchopulmonary dysplasia or hypoplastic left heart may develop respiratory failure with even mild upper respiratory infections. Inquire about sick siblings and perinatal infectious risk factors. Pay attention to the relation between respiratory symptoms and feeding that might suggest reflux and aspiration, or even congenital tracheoesophageal fistula, as a cause. Respiratory difficulty when quiet and improvement during crying suggest choanal atresia. Treat the underlying condition: cough is the infant's primary protective reflex; do not give cough suppressants to neonates. Over-the-counter cold medications are not effective, may be dangerous in infants, and are contraindicated for children <24 months old. Treat nasal congestion with instillation of saline drops and bulb suctioning.
Noisy Breathing and Stridor
Noisy breathing is a common presenting complaint in neonates and is usually benign, but consider serious underlying pathology. Distinguish between inspiratory and expiratory sounds through careful listening in order to distinguish stertor, stridor, and wheezing. Stertor is an inspiratory sound like snoring or snorting that localizes to the nose or nasopharynx and is usually benign, but can be a symptom of choanal stenosis. Inability to pass a small nasogastric tube through the affected nostril is diagnostic of this condition. Stridor is a sign of upper airway obstruction and may be evident on both inspiration and expiration. The most common cause of stridor in neonates is laryngomalacia, which is characterized by noisy, crowing, inspiratory sounds, usually present from birth, that usually decrease during the first year of life. Nasal pharyngoscopy by an otolaryngologist confirms the diagnosis.
Stridor may also be a symptom of congenital anomalies causing a fixed obstruction anywhere from the nose to the trachea and bronchi, such as webs, cysts, atresia, stenosis, clefts, and hemangiomas. Stridor from fixed lesions is often biphasic, although it may be predominant in either inspiration or expiration. Stridor worsening with cry or increased activity suggests laryngomalacia, tracheomalacia, or subglottic hemangioma (which often become symptomatic after the first few weeks of life). Stridor accompanied by feeding difficulties suggests a vascular ring, laryngeal cleft, or tracheoesophageal fistula. Occasionally an H-type tracheoesophageal fistula may present in the first month of life or later with recurrent pneumonia, respiratory distress after feedings, and problems clearing mucus. Tracheal stenosis may present initially with noisy breathing or a high-pitched cry and disproportionate respiratory distress with mild upper respiratory infections. Stridor with hoarseness or weak cry suggests vocal cord paralysis, which is typically present at birth. Infants who were intubated in the neonatal period may develop subglottic stenosis causing stridor. Infection (e.g., croup, epiglottitis, and abscess) as a cause of stridor in neonates is rare and is associated with fever. When the diagnosis is in doubt, admit the neonate for further evaluation, which may include pharyngoscopy, bronchoscopy, radiographs, or even ultrasonography.
APNEA AND PERIODIC BREATHING
Periodic breathing, which occurs in normal neonates, must be differentiated from apnea; however, periodic breathing may precede apnea, and both may occur in the same patient. Periodic breathing is alternating periods of a normal or fast respiratory rate with periods of a slow rate of respiration, with pauses of 3 to 10 seconds between breaths. Apnea is cessation of breathing for ≥20 seconds, or cessation of breathing for a period <20 seconds accompanied by bradycardia, cyanosis, or a change in muscle tone. It signifies critical illness and warrants investigation and admission for monitoring and therapy. Apnea may be precipitated by any of the disease conditions listed in Table 114-4 and usually indicates respiratory muscle fatigue and impending respiratory arrest. Provide airway and ventilatory support, and search for the cause. If no obvious cause is found, presume sepsis, obtain cultures, and initiate broad-spectrum antibiotics and acyclovir if there is concern for herpes simplex virus. Chapter 115, Sudden Infant Death Syndrome and Apparent Life-Threatening Event, covers conditions associated with apnea in detail.
Common GI symptoms that bring neonates to the ED include feeding difficulties, gastroesophageal reflux, vomiting, blood in the diaper, diarrhea and dehydration, abdominal distension, and constipation.
Most visits for feeding difficulties occur because parents perceive that the infant's food intake is inadequate; normal feeding and benign feeding problems are discussed earlier (see "Normal Neonatal Vegetative Functions"). Rarely, anatomic abnormalities may cause difficulty in feeding and swallowing. A careful history usually pinpoints such difficulties as having started at birth, and these infants appear malnourished and dehydrated. Potential causes include upper GI abnormalities (e.g., stenoses, strictures, laryngeal clefts, or cleft palate) and compression of the esophagus or trachea by a double aortic arch. Infants with a recent decrease in intake usually have acute illness, most often infectious, and should be evaluated urgently.
Regurgitation and Gastroesophageal Reflux
Regurgitation of small amounts of milk or formula is common in neonates due to reduced lower esophageal sphincter pressure and relatively increased intragastric pressure. Regurgitation is independent of effort or muscular contraction and likely represents the ultimate degree of GI reflux. Parents may confuse regurgitation with vomiting. As long as the neonate is gaining weight, parents can be reassured that regurgitation is of no clinical significance and will decrease as the infant grows. Strategies to reduce reflux include thickening of feeds and upright feeding positioning. Infants who are not thriving or have respiratory symptoms related to feeding should be investigated for anatomic causes of regurgitation or chronic aspiration.
Regurgitation rarely results from pathologic processes, such as intrinsic compression of the esophagus or, occasionally, compression of the trachea, in which case it is usually accompanied by stridor and cough. Dysphagia, irritability, feeding aversion, anemia, and malnutrition are sequelae of chronic regurgitation with esophagitis, but this condition is rare. Investigations such as pH monitoring, endoscopy, and biopsy confirm the diagnosis of reflux esophagitis.
Vomiting results from forceful contraction of the diaphragm and abdominal muscles. A detailed discussion of vomiting in childhood is provided in chapter 128, Vomiting, Diarrhea, and Dehydration in Children, while surgical conditions that present with vomiting are discussed in chapter 130, Acute Abdominal Pain in Children; those specific to the neonatal period are briefly discussed here.
Vomiting beginning at birth is most likely due to an anatomic abnormality, such as tracheoesophageal fistula (with esophageal atresia), upper GI obstruction (e.g., duodenal atresia, which has a higher incidence among Down's infants), or midgut malrotation. Vomiting may be a symptom unrelated to the GI tract, such as increased intracranial pressure, metabolic disorders, or infections (e.g., sepsis, urinary tract infections, and gastroenteritis).
Projectile vomiting is usually seen in infants with pyloric stenosis and may assume its characteristic pattern, projectile vomiting at the end of feeding or shortly thereafter, after the second and third weeks of life. Pyloric stenosis classically presents between 6 weeks and 6 months of age and is the most common surgically correctible cause of vomiting in newborns. The vomitus does not contain bile or blood, and typically the infant appears well with an increased appetite. Perform an abdominal examination with the infant relaxed and the stomach empty. Observe for prominent gastric waves progressing from left to right. Palpate for a firm olive-shaped mass under the liver edge. Observe the neonate feeding to confirm projectile vomiting and distinguish this from regurgitation. Definitive diagnosis is most commonly made with ultrasound examination of the pyloric length and diameter, although barium studies may also make the diagnosis.8
The well-appearing infant without dehydration, malnutrition, or electrolyte abnormalities can be discharged with a plan for outpatient surgical correction. Admit ill-appearing or dehydrated infants.
Other Surgical Causes of GI Complaints
Emergent surgical causes of vomiting in the neonate include malrotation with volvulus, intussusception, necrotizing enterocolitis, and incarcerated hernia, all of which are discussed in chapter 130.8
Parents may come to the ED complaining of blood in the neonate's diaper. Several important distinctions must be made: first, confirm that the discoloration is blood by testing with a guaiac card if possible; it is not uncommon in the neonatal period to find urinary crystals that may cause an orange or red discoloration in the diaper that can be mistaken for blood. If blood is confirmed, the next important distinction is whether the origin is the GI tract or, in girls, the vagina. Bloody or mucous discharge is common and normal in female neonates due to withdrawal from placental estrogen. Physical examination may reveal a small anal fissure as the source of bleeding. In the first 2 to 3 days of life, blood in the diaper is most commonly due to maternal blood that is swallowed during delivery. This possibility may be confirmed by the Kleihauer-Betke or Apt-Downey test, performed on a stool sample or scraped from the diaper if possible, which differentiates fetal from maternal hemoglobin in the stool. After the first few days of life, most causes of blood in the diaper are idiopathic, but consider coagulopathies, necrotizing enterocolitis, allergic or infectious colitis, and congenital defects. Cow's milk allergy is an immunoglobulin E–mediated disorder, but most infants have cow's milk protein intolerance rather than true allergy. Both conditions cause changes in the bowel mucosa that result in gassy, bloody, and mucous bowel movements; painful feeds; and worsened reflux. Eosinophils may be present in the stool, and the diagnosis may be confirmed by resolution of the problem after cow's milk is removed from the diet. For unresponsive or severe cases, endoscopy and biopsy may be needed for diagnosis. A newborn with a single event of hematochezia and no concerning findings may be observed as an outpatient. Persistent symptoms or concerning exam findings should be further evaluated, and depending on the infant's condition (hydration status and weight gain), admission with appropriate subspecialty care may be necessary (see chapter 131, Gastrointestinal Bleeding in Infants and Children).
Diarrhea and dehydration are discussed in detail in chapter 128, and fluid and electrolyte therapy in chapter 129, Fluid and Electrolyte Therapy in Infants and Children. Diarrhea is abnormally frequent and liquid stools (Table 114-1). The modifier abnormal is critical because stools can normally be frequent and liquid in young children. Consider infection in addition to feeding-related causes, although infectious diarrhea is predominantly seen in older infants in the United States. Neonates are particularly susceptible to dehydration and electrolyte abnormalities associated with severe diarrhea. In an infant, the normal extracellular fluid volume is 25% of body weight; therefore, a loss of 8% of body weight as extracellular fluid results in severe dehydration.
Weigh all neonates with diarrhea unclothed to allow comparison with previous weights and to provide a baseline for monitoring subsequent weights during the course of the disease. Start the physical examination with a general assessment of mental status and hydration (see Table 129-2).9 Document rectal temperature, pulse, and blood pressure, which provide additional information concerning the degree of illness. Consider rectal examination to look for anal fissures as a potential source of blood, and obtain a stool sample for detection of occult blood, culture, examination for leukocytes, measurement of pH, and detection of reducing substances.
Obtain serum electrolytes, particularly sodium and glucose, in all neonates with diarrhea and dehydration. Markedly elevated serum urea nitrogen with a relatively normal creatinine may indicate recent or rapid dehydration. Serum creatinine values tend to be low in infants and young children, and a creatinine value of 1 milligram/dL may represent a doubling in the normal value. In addition to stool testing as above, obtain a urine sample in the setting of fever to evaluate for urinary tract infection.
Admit most newborns with ongoing GI losses to the hospital for rehydration, since the loss of even seemingly small volumes of stool may cause severe dehydration in the neonate. Diarrhea, particularly when bloody or containing mucus, may be a symptom of a more severe surgical abdominal process, such as volvulus, intussusception, or necrotizing enterocolitis, although all three of these conditions typically present with vomiting as well.
Abdominal distention may be normal in neonates and is usually due to lax abdominal musculature, relatively large intra-abdominal organs, and distension from swallowed air. If the infant is comforTable and feeding well and the abdomen is soft, there is no need for concern. Abdominal distention may also occur in association with bowel obstruction, constipation, necrotizing enterocolitis, or ileus due to sepsis or gastroenteritis. Congenital organomegaly (e.g., hepatomegaly, splenomegaly, or renal enlargement) undetected in the perinatal period also may cause abdominal distention.
Infrequent bowel movements in neonates do not necessarily mean that the infant is constipated. Infants occasionally may go without a bowel movement for 5 to 7 days and then pass a normal stool. However, if the neonate has never passed stools, especially if there has not been a stool in the first 48 hours of life, consider intestinal stenosis, Hirschsprung's disease, or meconium ileus associated with cystic fibrosis. Constipation occurring after birth but within the first month of life suggests Hirschsprung's disease, hypothyroidism, anal stenosis, or an anteriorly displaced anus. Correct anatomic positioning of the anus is determined by measuring the distance between the gluteal cleft and the posterior fourchette in girls or the median raphe in boys. The anus should be no more anterior than two thirds of this distance. Neonates with constipation should have a careful evaluation of the lumbosacral spine for evidence of occult dysraphism, which may be associated with neurogenic bowel or bladder. The diagnosis of Hirschsprung's disease is supported by absence of feces on rectal examination, a tonic or tight sphincter tone, and an abrupt change in bowel luminal size on barium enema, and is confirmed by a rectal biopsy demonstrating absence of ganglion cells. Infants with hypothyroidism present with constipation, feeding problems, a weak or hoarse cry, a large anterior fontanelle, hypothermia, hypotonia, and peripheral edema. Thyroid testing as part of the routine newborn metabolic screen varies from state to state in the United States.
Jaundice signifies hyperbilirubinemia and can represent normal newborn physiology or a pathologic process. Bilirubin is a breakdown product of hemoglobin that is conjugated in the liver by glucuronyl transferase before it is excreted with bile into the GI tract. Once bilirubin reaches the intestinal lumen, brush border enzymes deconjugate some of the bilirubin, which is then reabsorbed through enterohepatic circulation. The remainder of the bilirubin is either oxidized by intestinal bacteria to urobilinogen (which is excreted in the urine) or passed in the feces, creating the normal yellow color of neonatal stool. Physiologic jaundice is characterized by a slow rise in bilirubin (<5 milligrams/dL per 24 hours), with a peak of 5 to 6 milligrams/dL during the second to the fourth days of life and a decrease to <2 milligrams/dL by 5 to 7 days. Decreased neonatal hepatic glucuronyl transferase activity, a shortened life span of neonatal red blood cells and relative polycythemia, and decreased intestinal bacterial colonization all lead to an increase in enterohepatic circulation that produces the normal rise in bilirubin seen in physiologic jaundice. Other processes, both benign and pathologic, often cause bilirubin levels that are significantly higher than 6 milligrams/dL, and excessive hyperbilirubinemia can lead to permanent brain injury—kernicterus. Practice parameters for the evaluation and treatment of neonatal jaundice are summarized in Table 114-6.10
TABLE 114-6Neonatal Risk and Bilirubin Treatment Threshold for Hyperbilirubinemia ||Download (.pdf) TABLE 114-6 Neonatal Risk and Bilirubin Treatment Threshold for Hyperbilirubinemia
|Age of Neonate |
|Bilirubin Treatment Threshold (milligrams/dL) ||24 h ||48 h ||72 h ||96 h ||5 d ||6 d ||7 d |
|Low-risk neonates* ||12 ||16 ||19 ||21 ||22 ||23 ||23 |
|Intermediate-risk neonates† ||9 ||13 ||15 ||16 ||17 ||17 ||17 |
|High-risk neonates‡ ||8 ||11 ||13 ||14.5 ||15 ||15 ||15 |
Distinguishing between physiologic and pathologic neonatal jaundice is important, and the timing of the onset of jaundice in the newborn provides useful clues. Table 114-7 lists various causes of hyperbilirubinemia in the neonate and their timing.
TABLE 114-7Causes of Jaundice in Neonates ||Download (.pdf) TABLE 114-7 Causes of Jaundice in Neonates
|<24 h ||Hemolysis due to ABO, Rh incompatibility |
|Congenital infection (rubella, toxoplasmosis, cytomegalovirus infection) |
|Excessive bruising from birth trauma (cephalohematoma or intramuscular hematoma) |
|Acquired infection (e.g., sepsis, pneumonia) |
|2–3 d ||Physiologic |
|3 d–1 wk ||Acquired infection (e.g., sepsis, urinary tract infection, pneumonia) |
|Congenital decrease in glucuronyl transferase (e.g., Crigler-Najjar syndrome, Gilbert's syndrome) |
|Congenital infections (syphilis, toxoplasmosis, cytomegalovirus infection) |
|>1 wk ||Breast milk jaundice |
|Acquired infection (e.g., sepsis, urinary tract infection, pneumonia) |
|Biliary atresia |
|Congenital and acquired hepatitis |
|Red cell membrane defects (e.g., sickle cell anemia, spherocytosis, elliptocytosis) |
|Red cell enzyme defects (e.g., glucose-6-phosphate dehydrogenase deficiency) |
|Hemolysis due to drugs |
|Endocrine disorders (hypothyroidism) |
|Metabolic disorders (galactosemia, fructosemia) |
|Pyloric stenosis |
The evaluation of the jaundiced neonate begins with a thorough history, including maternal infections during pregnancy; maternal blood type and RhoGAM® administration; estimated gestational age (i.e., term or preterm); feeding patterns, including formula or breast milk, frequency, duration, and whether maternal milk supply is adequate and latching successful; stool history, including timing of first stool and transitional stools, color (yellow, acholic), and frequency; regurgitation or vomiting; urine output; and documented fever. A family history of hemolytic anemia or prior neonatal jaundice might indicate an inherited disorder. Review maternal and fetal medications. When possible, obtain results of the infant's blood type and maternal antibody screen.
On physical examination, note the degree of jaundice, which progresses in a cephalocaudal direction, although the level of jaundice does not reproducibly correlate with serum bilirubin levels. Scleral icterus is typically noted with serum bilirubin >5 milligrams/dL. Examine the head for cephalohematoma and assess the fontanelles for signs of dehydration or possible infection. Palpate the abdomen for organomegaly that might signify congenital infection or liver disease.
It is important to distinguish unconjugated hyperbilirubinemia from conjugated hyperbilirubinemia. Unconjugated hyperbilirubinemia is much more common, presents earlier in the neonatal period, and is related to the normal or abnormal breakdown of hemoglobin, although inherited enzyme deficiencies or infection may be pathologic causes. Conjugated hyperbilirubinemia results from the inability to excrete bilirubin into the bile and intestines and is usually the result of primary hepatic or biliary disease such as biliary atresia or hepatitis. Conjugated hyperbilirubinemia is always pathologic and often presents later in the neonatal period with jaundice, acholic stools, and dark urine.
At a minimum, laboratory studies for the jaundiced neonate should include a direct and indirect bilirubin. Transcutaneous bilirubin measurement correlates fairly well with total serum levels but does not distinguish conjugated and unconjugated bilirubin. Transcutaneous measurement is thus limited to very low-risk neonates with a normal physical examination.11,12 When other pathologic conditions are suspected, the evaluation should be determined by the differential diagnosis and may include a CBC for anemia and red cell indices, a blood smear for hemolysis, reticulocyte count, and liver function tests. When infection is a concern, obtain appropriate cultures and Gram stains (urine, cerebrospinal fluid).
Septic infants with hyperbilirubinemia may have an increase in bilirubin by greater than the accepTable 5 milligrams/dL per 24-hour period and have other features of sepsis, such as vomiting, abdominal distention, respiratory distress, and poor feeding. Breast milk jaundice is thought to be due to the presence of substances that inhibit glucuronyl transferase in the breast milk; it may start as early as the third to fourth day and reaches a peak of 10 to 27 milligrams/dL by the third week of life. Although cessation of breastfeeding will result in a rapid decline of bilirubin over 2 to 3 days, it is not routinely recommended. Breast milk jaundice is unlikely to cause kernicterus and usually can be treated with phototherapy, when necessary. This should be distinguished from breastfeeding jaundice, or starvation jaundice, which can occur when a newborn is exclusively breastfed and the mother's milk supply is still inadequate. Poor oral intake resulting in reduced bowel movement and bilirubin excretion through the GI tract, coupled with relative dehydration, may accentuate physiologic jaundice. Optimizing the neonate's feeding pattern with controlled supplementation, whether with expressed breast milk, donated breast milk, or formula, usually resolves the problem, but severe hyperbilirubinemia may require treatment.
The treatment of hyperbilirubinemia depends on the cause, but for most cases of unconjugated hyperbilirubinemia, phototherapy is sufficient. Phototherapy causes a configurational change in the bilirubin structure that allows it to be excreted in the urine. There is no additional benefit to IV fluids coupled with phototherapy, so enteral feeding should always be encouraged, although the dehydrated infant may require fluid resuscitation. Extreme levels of hyperbilirubinemia are treated emergently with exchange transfusion and require admission to hospital.
Risk factors include hemolysis risks (e.g., isoimmune hemolytic disease, glucose-6-phosphate dehydrogenase deficiency, ABO incompatibility), sepsis (lethargy, temperature instability, irritability), asphyxia, hypoalbuminemia, and acidosis. In the first 24 hours of life, response to phototherapy is less predictable, and specific exchange transfusion indications are less certain during this period.
Clear eye discharge, and occasionally crusting over of the eyelashes without associated conjunctival redness or irritation, is commonly seen in neonates and infants and results from narrow or obstructed nasolacrimal ducts. This condition usually resolves spontaneously and requires antibiotics only when complicated by conjunctival erythema and inflammation (conjunctivitis or dacryocystitis). Ophthalmologic consultation for nasolacrimal duct probing is appropriate if this problem persists past 12 months of age or earlier if complicated by recurrent infection.
Corneal irritation or abrasion can result from an eyelash or scratch from a fingernail. Perform fluorescein staining and evaluate with a Wood's lamp or a hand-held slit lamp to identify corneal abrasions. Acute glaucoma, although rare, also presents as a red, teary eye. The cornea is cloudy, the anterior chamber is shallow, and the intraocular pressure may be increased. Promptly consult pediatric ophthalmology for all suspected cases of glaucoma.
Conjunctivitis is described in detail in chapter 119, Eye Emergencies in Infants and Children. The most common causes of neonatal conjunctivitis are chemical irritation, bacterial or chlamydial infection, and herpes simplex infection. Chemical conjunctivitis due to ocular prophylaxis usually occurs on the first day of life and requires no treatment.
Gonococcal conjunctivitis generally has its peak time of onset between 3 and 5 days after birth. Despite antibiotic prophylaxis at delivery, the failure rate of prophylaxis is about 1%. Neisseria gonorrhoeae invades superficial layers of the conjunctiva and, if untreated, causes corneal ulceration and can result in permanent loss of vision. For diagnosis, obtain a Gram stain and culture for N. gonorrhoeae. Treat gonococcal conjunctivitis with cefotaxime (50 milligrams/kg IV or IM). Cefotaxime is recommended for neonates, as ceftriaxone can displace bound bilirubin and precipitate kernicterus. Perform septic workup including lumbar puncture. Disseminated disease should be suspected until CSF cultures are negative. Supportive care includes ocular irrigation with normal saline as soon as diagnosis is suspected, with frequent irrigation until the discharge is eliminated. Admit the neonate and obtain ophthalmology consultation. Topical antibiotic treatment alone is inadequate and unnecessary when systemic antibiotic treatment is given.
Chlamydial conjunctivitis becomes evident by the end of the first week throughout the first month after birth. The disorder varies in severity, from mild to severe hyperemia with a thick, profuse mucopurulent discharge and pseudomembrane formation. There often is severe edema of both lids. Because isolation of Chlamydia trachomatis requires specialized tissue cultures, assure proper technique in collecting culture specimens (e.g., Dacron swabs) and specimens for antigen detection.
Treat chlamydial conjunctivitis and pneumonia in neonates with oral erythromycin (50 milligrams/kg PO per day in four divided doses, for 14 days). Oral sulfonamides may be used after the immediate neonatal period for infants who do not tolerate erythromycin. Topical treatment is unnecessary. Because the efficacy of erythromycin therapy is approximately 80%, a second course is sometimes required. A specific diagnosis of C. trachomatis infection in an infant should prompt the treatment of the mother and her sexual partners.
The finding of vesicles anywhere on the skin or mucous membranes in association with neonatal conjunctivitis suggests herpes simplex infection and warrants a full sepsis evaluation with cerebrospinal fluid evaluation for herpes simplex virus and treatment with acyclovir, 20 milligrams/kg/dose three times a day.
ABNORMAL MOVEMENTS AND SEIZURES
Seizures are covered in detail in chapter 135, Seizures in Infants and Children. It is important to distinguish benign sleep myoclonus in infancy and the normal startle reflex from actual seizures. Sleep myoclonus consists of rhythmic myoclonic jerks observed when the infant is drowsy or in quiet sleep and can be suppressed upon touching and/or waking the infant; the startle reflex is a single myoclonic jerk with extension of the arms and legs triggered by noise or tactile stimulation. Tetany due to hypocalcemia is associated with congenital syndromes, such as DiGeorge's syndrome, and must also be distinguished from seizure activity. Recognition of seizures in the newborn period is important, because seizure management and outcome are different than at any other age. Neonatal seizures are likely to present with subtle manifestations, such as eye deviation, tongue thrusting, eyelid fluttering, apnea, pedaling movements, or arching, rather than generalized activity. Neonatal seizures usually indicate a severe underlying structural or metabolic problem and are rarely idiopathic.
Acknowledgment: The authors gratefully acknowledge the contributions of Tonia J. Brousseau, the lead author of this chapter in the previous edition.