THE ORIGINAL ON CALL PROBLEM CONCEPT STARTED WITH NEONATOLOGY
In 1988 the first edition of NEONATOLOGY Dr. Tricia Gomella presented the concept of the "ON CALL PROBLEM". The goal was to provide practical approach to common problems in the NICU and to serve as an effective teaching tool. This pioneering "ON CALL" problem solving concept approach has been replicated across numerous specialties and many other publications. Here are two current examples from the 7th Edition of NEONATOLOGY Edited by Dr. Tricia Gomella: Eye Discharge and Conjunctivitis and Pneumothorax
SAMPLE ON CALL PROBLEM FROM
NEONATOLOGY 7th Edition, Tricia Lacy MD Editor
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53 Eye Discharge and Conjunctivitis
I. Problem. A purulent eye discharge is noted in a 3-day-old infant. Eye discharge in a neonate is usually caused by conjunctivitis or congenital lacrimal duct obstruction. Neonatal conjunctivitis (ophthalmia neonatorum) is an inflammation of the surface or covering of the eye that presents with eye discharge and hyperemia in the first 4 weeks of life. It is the most common ocular disease in neonates. Most infections are acquired during vaginal delivery. In the United States the incidence of infectious conjunctivitis is 1–2%; in the world it is 0.9–21%. Congenital lacrimal duct obstruction (CLDO) (dacryostenosis) is a condition where there is a blockage of the lacrimal drainage system. It occurs in ~5–6% of infants. The symptoms are persistent tearing and a mucoid discharge in the inner corner of the eye.
II. Immediate questions
A. How old is the infant? Age may be helpful in determining the cause of eye discharge. For conjunctivitis: in the first 6–24 hours of life, conjunctivitis is often due to ocular prophylaxis (usually silver nitrate drops; it may also be from tetracycline, erythromycin, or gentamicin). After 24–48 hours, a bacterial infection is most likely; the most common neonatal organisms areNeisseria gonorrhoeae(2–7 days but can present later) andStaphylococcus aureus(5–14 days).Chlamydia trachomatisconjunctivitis is usually seen after the first week of life (5–14 days) and often presents as late as the second or third week. Herpes conjunctivitis is seen 6–14 days after birth.Pseudomonas aeruginosainfections are typically seen between 5 and 18 days. Note: Bacterial infections can occur anytime. Lacrimal duct obstruction usually manifests at 2 weeks of age, but can be seen in the first few days to the first few weeks after birth.
B. Is the discharge unilateral or bilateral? Unilateral conjunctivitis is most often seen with S.aureus,P. aeruginosa, and herpes simplex (HSV) and adenovirus. Bilateral conjunctivitis is seen with infection caused byN. gonorrhoeaeor by the use of ocular prophylaxis. Chlamydia usually develops in one eye but affects the other after 2–7 days. Lacrimal duct obstruction usually causes unilateral discharge, but up to 20 % of infants have bilateral obstruction.
C. What are the characteristics of the discharge (purulent vs watery)? Purulent discharge is more common with bacterial infection.A serous discharge is more common with a viral infection. Gonorrhea has a profuse purulent discharge. Greenish discharge is more characteristic ofP. aeruginosa. Chlamydial infection can be wateryearly and purulent later, but a blood-stained discharge is typical. Herpes conjunctivitis usually has a nonpurulent and serosanguineous discharge. Lacrimal duct obstruction can cause watery tears in the corner of the eye or tears draining from the eyelid down the cheek. It can also cause a mucus or yellowish discharge in the eye.
D. Did the infant receive eye prophylaxis? Prophylaxis is used to decrease the risk of developing ocular gonorrheal infection (prevent blindness) and it also decreases the risk of nongonococcal and nonchlamydial conjunctivitis in the first 2 weeks of life.Remember, infants can still get gonococcal conjunctivitis with prophylaxis (risk drops from 50 to 2%). Prophylaxis is mandatory in the United States but may not be in other countries. Failure rates of eye prophylaxis and better screening and maternal therapy is causing a reevaluation of this process, especially in areas where maternal infection is low. Proper technique is as follows: give within 1 hour of birth; wipe each eyelid with sterile cotton; 2 drops of 1% silver nitrate solution or a 1-cm ribbon of either 1% tetracycline or 0.5% erythromycin are introduced into each lower conjunctival sac and not rinsed out. Ointment may be wiped away after 1 minute. Massage the eyelids to spread the ointment. Single-dose containers are recommended. For the very premature infant with fused eyes, apply the prophylactic agent without separating the eyelids. Prophylaxis can be with 1% tetracycline ophthalmic ointment or solution (evidence suggests better outcomes and more effectiveness), 2.5% povidone-iodine solution (not approved in United States but is used elsewhere), 1% silver nitrate solution (recommended over erythromycin if the patient population has a high number of penicillinase-producing N. gonorrhoeae), and 0.5% erythromycin ointment. Other alternatives are neomycin, chloramphenicol and azithromycin (used when there was a shortage of erythromycin), and gentamicin (used during a shortage but caused severe ocular reactions, so not recommended). A newer therapy is fusidic acid.
E. Does the mother have a history of sexually transmitted infections? Infants who pass through the birth canal of an infected mother with gonorrhea or chlamydia have an increased conjunctivitis risk.Neonatal conjunctivitis is frequently diagnosed in infants born to human immunodeficiency virus (HIV)-infected mothers.
F. Is the infant at high risk? Neonates are at increased risk for conjunctivitis and a more serious case of it because of decreased tear production, lack of immunoglobulin IgA in tears, decreased immune function, absence of lymphoid tissue of the conjunctiva, and decreased lysozyme activity.Risk factors may include mode of delivery, exposure of the infant to infectious organisms, no or inadequate prophylaxis after birth, ocular trauma/local eye injury during delivery, poor hygienic conditions, premature rupture of membranes (PROM), prolonged delivery, prematurity, mechanical ventilation, increased birthweight, history of midwife interference, HIV-infected mother, poor prenatal care, documented or suspected sexually transmitted infection, infection after delivery from direct contact from health care worker, or aerosolization. Neonates are at an increased risk for congenital lacrimal duct obstruction with Down syndrome, Goldenhar sequence, clefting syndromes, any midline facial anomaly, hemifacial microsomia, and craniosynostosis.
G. Is the infant low birthweight and low gestational age? An infant with conjunctivitis who has a low birthweight and low gestational age has a higher risk of having a conjunctivitis caused by a gram-negative organism (Klebsiella spp., Escherichia coli, Serratia marcescens, P.aeruginosa, and Enterobacter spp.). Premature infants have an increased risk of congenital lacrimal duct obstruction.
III. Differential diagnosis. Eye discharge can be conjunctivitis (ophthalmia neonatorum due to infectious, chemical/inflammatory cause) or due to an obstruction (congenital lacrimal duct obstruction). Other diagnoses that may cause an eye discharge in an infant are foreign body, orbital or preseptal cellulitis, entropion, trichiasis, eye trauma (corneal abrasion following delivery), dacryocystitis, keratitis, subconjunctival hemorrhage (breakage of vessels during delivery), congenital anomalies of the nasolacrimal system, corneal epithelial disease, neonatal abstinence (lacrimation), and congenital glaucoma.
A. Chemical/inflammatory conjunctivitis. Usually secondary to silver nitrate ocular drops and is the most common cause of conjunctivitis in underdeveloped countries. Chemical conjunctivitis can occur from other prophylactic ocular antibiotics used after birth, but it occurs less often. It is a nonpurulent inflammation of the eye that causes a watery discharge, conjunctival injection, and swelling within several hours of instilling the medication. The conjunctivitis shows a maximum inflammatory response around 48 hours and usually clears by the fourth day.
B. Infectious conjunctivitis. Bacterial, viral, or chlamydial infectious conjunctivitis in the newborn is caused by C. trachomatis (2–40%), N. gonorrhoeae (<1%), herpes simplex (<1%), and other bacterial microbes (30–50%). Other microbes include Staphylococcus spp., Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus mitis, group A and B streptococci, Enterobacter, Acinetobacter, Neisseria cinerea, Corynebacterium spp., Moraxella catarrhalis, S. marcescens, Stenotrophomonas maltophilia, E. coli, viridans streptococci, Klebsiella pneumoniae, Eikenella corrodens, and P. aeruginosa. Epidemiology of gram-negative conjunctivitis: Klebsiella spp. (23%), E. coli (17%), S. marcescens (17%), P. aeruginosa (3%), and Enterobacter spp. (2%).
1. Mechanisms of infection
a. Infections acquired through vaginal birth. Typically N. gonorrhoeae, C. trachomatis, group B streptococci, or HSV. They tend to reflect sexually transmitted infections in the community. Any bacteria that are normally present in the vagina (not sexually transmitted) can also cause neonatal conjunctivitis.
b. Cesarean section delivery can be associated with ascending infections. Risk factors include amniotic fluid leak, vaginal examinations, and use of internal monitors.
c. Postnatally acquired infections. Infection from organisms which are present in the environment (normal skin flora or nasopharyngeal flora). Examples are S. aureus (coagulase negative most common in one study), Staphylococcus epidermidis, Streptococcus spp., Pseudomonas spp., Serratia spp., Klebsiella spp., and Enterococcus spp. Pseudomonas infections are more typical in hospitalized preemies beyond 5 days of birth.
2. Gonococcal conjunctivitis. Most commonly transmitted from the mother during vaginal birth. The transmission rate from an infected mother to her newborn is 30–50%. It tends to occur 3–5 days after birth with abrupt onset. Usually bilateral, the eyes are very red (hyperacute conjunctivitis) with a thick, purulent drainage and swelling. The lid has chemosis (edema) and a conjunctival membrane may be present. This is an emergency because, left untreated, it can cause a corneal ulcer and perforation within hours. The incidence is low because of prophylactic ocular treatment immediately after birth. Infants can have systemic manifestations: sepsis, meningitis, rhinitis, stomatitis, arthritis, and anorectal infection.
3. Chlamydial conjunctivitis. Transmitted from the mother and develops in 30–40% of infants delivered vaginally to infected untreated mothers. Topical prophylaxis with erythromycin does not prevent but reduces the incidence of chlamydial ophthalmia neonatorum. Prophylaxis does not eradicate nasopharyngeal colonization or pneumonia. The eyes have a moderate drainage, redness, and conjunctival and eyelid swelling. It can be unilateral or bilateral and usually starts out as a watery discharge that becomes purulent and copious later. Corneal opacification, chemosis, and pseudomembranes may be present. Pneumonia is present in 10–20% of infants with chlamydial conjunctivitis. Otitis, pharyngeal, and rectal colonization can occur. Repeated and chronic infections of C. trachomatis can cause trachoma (rare in the United States), which is a chronic follicular keratoconjunctivitis that causes scarring and neovascularization of the cornea that can result in blindness.
4. Pseudomonas conjunctivitis. Usually a nosocomial infection and is becoming more common in nurseries. It can lead to a devastating corneal ulceration, perforation, endophthalmitis, and death. The organism thrives in moisture-filled environments such as respiratory equipment and occurs most often in hospitalized premature infants or those with depressed immunity. It can be responsible for epidemic conjunctivitis in premature infants. Infants with pseudomonas conjunctivitis can have systemic complications.
5. Herpes simplex keratoconjunctivitis. Herpes simplex type 2 (HSV-2) can cause unilateral or bilateral conjunctivitis, optic neuritis, chorioretinitis, and encephalitis, and it is the most frequent viral cause of conjunctivitis. The conjunctivitis can be superficial or may involve the deeper layers of the cornea; vesicles may appear on the nearby skin. The infants can have lid edema, conjunctival injection, and a watery nonpurulent discharge. A conjunctival membrane may be present. Most of these infections are secondary to HSV-2 sexually transmitted infection (maternal genital tract ascending infection) or through the birth canal or by transplacental mechanisms; 15–20% are caused by HSV-1. Suspect herpes if the conjunctivitis is not responding to antibiotic therapy. Most neonatal HSV-1 infections are related to contact with someone with an active infection (fever blister or cold sore) in the perinatal period.
6. Viral causes (other than herpes). These are usually associated with other symptoms of respiratory tract disease due to adenovirus, enterovirus, and parechovirus. There is usually redness, and it is more commonly unilateral. The discharge is usually mild and watery and is rarely purulent. Preauricular adenopathy can be seen.
7. Other bacterial infections. (See Section III.B.) The conjunctivitis from other microbial agents usually presents as a milder form of conjunctivitis. It can cause conjunctival injection, chemosis, and a discharge. Infections caused by Haemophilus spp. and S. pneumoniae are associated with dacryocystitis (inflammation of the nasolacrimal sac). Staphylococcal conjunctivitis is usually a nosocomial infection. It is the most frequent isolate, but may not cause conjunctivitis in infants who are colonized. It can cause conjunctival hyperemia. Methicillin-resistant S. aureus (MRSA) conjunctivitis can also occur and has been associated with nurseries and neonatal intensive care units (NICUs).
C. Congenital lacrimal duct obstruction (dacryostenosis) occurs in ~5–6% of infants. The nasolacrimal duct may fail to canalize completely at birth. The obstruction is usually at the nasal end of the duct and is usually unilateral. The symptoms are persistent tearing and a mucoid discharge in the inner corner of the eye. One in 5 infants may have transient discharge (watery and sticky, particularly after sleep) due to a delay in the normal development and opening of the tear duct that resolves spontaneously. Dacryocystitis is a secondary infection in the lacrimal sac.
A. Physical examination
1. Ophthalmic examination. Examine both eyes/eyelids for swelling and edema and check the conjunctiva for injection (congestion of blood vessels) and chemosis (conjunctival swelling). A purulent discharge, edema, and erythema of the lids as well as injection of the conjunctiva are suggestive of bacterial conjunctivitis. Check for ulcerations and the presence of a red reflex.
2. Perform a physical examination. To rule out signs of respiratory or systemic infection. Evaluate for periorbital edema and adenopathy.
B. Laboratory studies
1. Gram-stained smear of the discharge to check for white blood cells (a sign of infection) and bacteria (to identify the organism). A sample of the discharge should also be submitted for culture and sensitivity testing (chocolate agar and/or Thayer martin media for N. gonorrhoeae and blood agar for other bacteria). Findings on Gram stain:
a. N. gonorrhoeae conjunctivitis. Gram-negative intracellular diplococci and white blood cells (WBCs).
b. S. aureus conjunctivitis. Gram-positive cocci in clusters and WBCs.
c. P. aeruginosaconjunctivitis. Gram-negative bacilli and WBCs.
d. Conjunctivitis caused by Haemophilus spp. Gram-negative coccoid rods.
e. Streptococcal or enterococci. Streptococci are gram-positive spherical cocci, and enterococci are gram-positive lancet-shaped encapsulated diplococci.
f. Other gram-positive organisms. S. pneumoniae, S. viridans, S. epidermidis, group A and B streptococci, and Corynebacterium species.
g. Other gram-negative organisms. E. coli, K. pneumoniae, S. marcescens, Proteus, Enterobacter, H. influenzae, Acinetobacter, P. aeruginosa, N. cinerea, M. catarrhalis, E. corrodens, and S. maltophilia.
h. Herpes simplex. See lymphocytes, plasma cells, and multinucleated giant cells.
i. C. trachomatis. Neutrophils, lymphocytes, and plasma cells.
j. Chemical conjunctivitis. See neutrophils and lymphocytes (occasionally).
k. Lacrimal duct obstruction. The Gram stain is negative or there is normal conjunctival flora unless there is an overlying infection.
2. If a chlamydial infection is suspected, material is gathered for Giemsa staining by scraping (not swabbing) the lower palpebral conjunctiva with a wire loop or blunt spatula to obtain epithelial cells.The testing must include conjunctival epithelial cells because C. trachomatis is an obligate intracellular organism and exudates are not adequate for testing. This is a specific (but not sensitive) method for detecting conjunctivitis. Cotton or Calgonite swabs have not proved to be adequate. If chlamydial infection is present, typical cytoplasmic inclusion bodies (basophilic intracytoplasmic) are seen within the epithelial cells. Culture of the organism is the gold standard. Nucleic acid amplification tests (NAATs) can be used. Most commonly used is the polymerase chain reaction (PCR), since it has a higher sensitivity and specificity. Other NAATs include transcription-mediated amplification (TMA) and strand displacement amplification (SDA). Other tests available include antigen detection tests (direct immune fluorescent assay [DFA] and enzyme immunoassay tests [EIA]) and DNA probes. Check local lab availability.
3. If herpes is suspected, a conjunctival scraping shows multinucleated giant cells with intracytoplasmic inclusions. Eosinophilic intranuclear inclusions in epithelial cells are seen on Papanicolaou smear. Also, the conjunctiva should be swabbed and transported on special viral transport media for culture.
4. In gonococcal infection, blood and cerebrospinal cultures must be obtained. Other sites should be cultured if appropriate. Appropriate cultures from the mother and partner should be obtained.
C. Imaging and other studies. None are usually needed.
1. Fluorescein dye disappearance test. Best test to rule out lacrimal duct obstruction. Instill one drop of fluorescein into the lower conjunctiva of each eye. After 5 minutes, evaluate if any dye is still present. If there is significant dye present in the eye then an obstruction may exist. If the dye disappears, then there is no obstruction. Alternatively, a cobalt blue light can be used to see if the dye is still present.
V. Plan. Complications (perforation of the cornea, blindness, Chlamydia pneumonia) can be severe, so it is important to treat as soon as possible. Do not wait for the culture results to treat the infant. Send the culture, and based on the Gram, Giemsa, and Pap stains, start empirical treatment. See Appendix F for specific isolation guidelines.
A. Important facts in the management of conjunctivitis
1. Infection can spread easily from one eye to another or to other people by touching the eye or drainage.Proper and frequent hand washing and wearing gloves is essential.
2. Drainage is contagious for 24–48 hoursafter beginning treatment.
3. Irrigate eye with sterile isotonic saline to remove accumulated purulent drainage.
4. Systemic treatment is required for gonococcal, staphylococcal, Chlamydia, pseudomonas, and herpetic conjunctivitis.Some recommend systemic treatment for H. influenzae conjunctivitis since it is often associated with otitis media or other severe infections such as sepsis and meningitis.
5. Avoid eye patching.
6. Consultation with an ophthalmologist or pediatric infectious disease specialist should be considered.
7. Evaluate all for signs of systemic disease. Infants with conjunctivitis are at risk for secondary infections such as sepsis, meningitis, and pneumonia.
8. Some institutions will treat all neonatal conjunctivitisfor gonococcal conjunctivitis until culture results are available because of the rapid and severe progression of the disease.
9. Some institutions will treat all gonococcal conjunctivitisfor chlamydia also.
10. Follow daily for signs of improvementor worsening.
11. Breast milk/colostrum to treat conjunctivitis. Colostrum and breast milk contain antimicrobial and anti-inflammatory properties and have been used to treat conjunctivitis or mucopurulent discharge from nasolacrimal duct obstruction. Colostrum is more effective than mature breast milk because it has higher concentrations of antibodies, especially IgA. Because evidence is limited and studies are conflicting, this treatment is not recommended.
B. Chemical conjunctivitis. Observation only is needed as this usually resolves within 48–72 hours. Lubrication with artificial tears may be helpful QID.
C. Gonococcal conjunctivitis. This is considered an emergency. Because of the high prevalence of penicillin (PCN)-resistant N. gonorrhoeae, the treatment is not PCN but a third-generation cephalosporin (eg, ceftriaxone). Note:Gonococcal conjunctivitis can occur even with appropriate eye prophylaxis in infants delivered to mothers with positive maternal gonococcal infection.
1. Isolate the infant during the first 24 hours of parenteral antibiotic therapy. Both mother and partner need full medical examinations and treatment. Mother cannot visit the baby until she receives 24 hours of antibiotics.
2. Evaluate for disseminated disease (arthritis, meningitis, sepsis, anorectal infection).Cultures to include blood, eye discharge, cerebrospinal fluid (CSF), and other sites as noted above.
3. Tests for concomitant infection with C.trachomatis, congenital syphilis, and HIV. The mother and sexual partner should also be evaluated and treated. Check maternal hepatitis B surface antigen.
4. Because of the high rate of coinfection, it is usually recommended to treat for chlamydia. Mother and sexual partner should also be treated.
5. For gonococcal conjunctivitis without dissemination, administer a single dose of ceftriaxone, 25–50 mg/kg IV or IM; in low birthweight infants, use 25–50 mg/kg/d IM or IV (up to a maximum of 125 mg).An alternative therapy is cefotaxime in a single dose (100 mg/kg, given IV or IM).
6. For gonococcal conjunctivitis with dissemination, ceftriaxone, 25–50 mg/kg IV or IM, may be given once every day for 7 days.If meningitis is present, it should be given for a total of 10–14 days. An alternative therapy is cefotaxime (recommended for hyperbilirubinemic infants) at 50–100 mg/kg/d, given IV or IM in 2 divided doses for 7 days or 10–14 days if meningitis is present.
7. In healthy infants (no conjunctivitis) born to mothers with gonococcal infection, topical antimicrobial therapy is inadequate.A single dose of ceftriaxone (25–50 mg/kg IV or IM) not to exceed 125 mg is given. Cefotaxime is an alternative (100 mg/kg IV or IM as a single dose). Topical antimicrobial therapy is not necessary if systemic therapy has been given.
8. Irrigate the eyes with sterile isotonic saline (normal saline) solution immediately and at frequent intervals (every 1–2 hours) to remove mucopurulent discharge until clear. Topical antibiotics are not necessary when systemic antibiotics are used and are only recommended when a corneal ulcer is present.
9. Ophthalmologic consultationis usually requested because gonococcal ophthalmia can lead to corneal perforation and blindness.
D. Chlamydial conjunctivitis. Evaluate for systemic disease (pneumonia, otitis, pharyngeal and rectal colonization). Pneumonia has been reported in 20% of infants with chlamydial conjunctivitis.
1. Recommended neonatal prophylaxisdoes not prevent neonatal chlamydial conjunctivitis.
2. Topical treatment with antibioticsis ineffective and unnecessary.
3. Oral erythromycin base or ethylsuccinate, 50 mg/kg/d, in 4 divided doses for 14 days by mouth is recommended.Azithromycin therapy (20 mg/kg qd for 3 days) may be effective but data are limited. Oral sulfonamides may be used after the immediate neonatal period for infants who do not tolerate erythromycin. A second course of antibiotics is sometimes required because ~20% of cases recur after antibiotic therapy. Infantile hypertrophic pyloric stenosis (IHPS) has been seen in infants <6 weeks treated with erythromycin. Counsel patients about the risk and signs of IHPS. The American Academy of Pediatrics (AAP) still recommends erythromycin because other treatments have not been well studied.
4. Macrolide antibioticssuch as azithromycin, clarithromycin, and roxithromycin may be more effective against chlamydia but have not been well studied in this group.
5. Infants born to mothers with untreated chlamydia are at a high risk for infection.Prophylactic antibiotic treatment is not indicated. Monitor for infection. If adequate follow-up is not possible, some clinicians advocate treatment. Mothers and sexual partners of infected infants should be treated for C. trachomatis.
E. Pseudomonas conjunctivitis
1. Isolate the patientand implement standard precautions unless infection is resistant where contact precautions are indicated.
2. Evaluate for systemic disease if indicated (sepsis, meningitis, pneumonia, brain abscess, and others).Infants with low birthweight and lower gestational age have an increased risk for systemic disease.
3. Parenteral therapy is recommended because Pseudomonas is a virulent organism.Use a b-lactam antibiotic or an appropriate cephalosporin plus an amino-glycoside (gentamicin) for a minimum of 10–14 days. For infections that include meningitis, ampicillin or cephalosporin plus an aminoglycoside is recommended for 21 days. Remember there is increasing antibiotic resistance; therefore, some are recommending third- and fourth-generation antibiotics.
4. Treat with gentamicin ophthalmic ointment 4 times per day for 2 weeks.Treat with fortified topical antibiotics.
5. Ophthalmology consultation is critical because the infection may be devastating. Infectious disease consult may also be helpful, especially with Pseudomonas meningitis.
F. Herpes simplex conjunctivitis
1. Isolate the patient;implement contact precautions.
2. Obtain a complete set of viral cultures (blood, cerebrospinal fluid, eyes, stool or rectum, urine, mouth or nasopharynx, and any lesions).Obtain a CSF PCR.
3. Administer topical ophthalmic therapywith 3% vidarabine ointment or 1% trifluridine ointment or 0.1% iododeoxyuridine (all are proven to be effective) 5 times per day for 10 days (every 2 hours for 14 days).
4. Systemic acyclovir therapy for a minimum of 14 days if SEM (skin, eye, mouth) disease.If central nervous system disease or disseminated disease is present, treat for a minimum of 21 days. (For dosage, see Chapter 148.) The dose is 60 mg/kg/d IV divided tid.
5. Ophthalmologic evaluation and follow-up are necessary because chorioretinitis, cataracts, and retinopathy may develop.
G. Other bacterial infections
1. Local saline irrigation.
2. Topical antibiotics only are usually required.For gram-positive organisms: erythromycin or bacitracin. For gram-negative organisms: gentamicin or tobramycin or ciprofloxacin. Some authors recommend Neosporin ophthalmic for most bacterial infections. Ophthalmic ointment: 0.5- to 1-cm ribbon in each eye every 6 hours for 7 days. Ophthalmic solution: 1–2 drops into each eye every 4 hours for 7 days. Ointment preferred over eye drops for neonates because they have reduced washout effect.
3. Haemophilus influenzae infection may require further evaluation of the infant (rule out sepsis, meningitis, and other infections if indicated), and systemic antibiotics may be necessary.
4. MRSA conjunctivitis. Treatment depends on the clinical situation; some do not need to be treated. Topical chloramphenicol eye drops have been used but are not recommended. Tobramycin/Polytrim ophthalmic solutions are recommended. See Chapter 110.
5. For gram-negative conjunctivitis in premature low birthweight infants remember there is increasing antibiotic resistance, especially among the b-lactam antibiotics.Third- and fourth-generation antibiotics are recommended.
H. Lacrimal duct obstruction
1. Most clear spontaneously without treatment. Massaging the inside corner of the eye over the lacrimal sac, with expression toward the nose, may help to establish patency.
2. If the problem does not resolve and symptoms persist (usually after 6–7 months), the infant should be evaluated by an ophthalmologist. Probing of the duct is indicated with a success rate of >90%.
3. Dacryocystitis. Treated with probing of the duct and either topical or systemic antibiotics depending on the severity of the infection.
Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2012 Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2012.
SAMPLE ON CALL PROBLEM FROM
NEONATOLOGY 7th Edition, Tricia Lacy MD Editor
Downloaded from WWW.NEONATOLOGYBOOK.COM
I. Problem. An infant may have a pneumothorax (an abnormal accumulation of air or gas in the pleural space, between the visceral and parietal pleura). It can develop spontaneous or be secondary to trauma. A pneumothorax occurs more often in the neonatal period than any other time in life.
A. Spontaneous pneumothorax
1. Primary spontaneous pneumothorax (PSP). Occurs when there is no obvious precipitating factor, no clear cause, it is idiopathic, without lung disease. Familial spontaneous pneumothorax is a rare cause in neonates.
2. Secondary spontaneous pneumothorax (SSP). Occurs from underlying lung disease (respiratory distress syndrome [RDS], meconium aspiration syndrome [MAS], and others).
B. Traumatic pneumothorax
1. Iatrogenic occurs from an accidental insult during a procedure such as central line placement or thoracentesis.
2. Positive pressure ventilation (mechanical or noninvasive ventilation) can cause barotrauma.
3. Chest trauma can occur when blunt or penetrating trauma occurs to the chest (rare in neonate).
C. Tension pneumothorax. A life-threatening condition that occurs when air is trapped in the pleural cavity under positive pressure. Air goes into the pleural cavity during inspiration, but no air is allowed to escape during expiration. It acts as a 1-way valve. Because air is trapped, intrathoracic positive pressure rises, lung volume decreases, and pressure compresses the mediastinum and causes a shift, with increased pulmonary vascular resistance. This results in an increase in central venous pressure, decrease in venous return to the heart, and a decrease in cardiac output. This causes displacement of mediastinal structures and cardiopulmonary compromise.
D. Persistent pneumothorax. A pneumothorax that persists >7 days in the absence of mechanical problems.
II. Immediate questions
A. Are symptoms of tension pneumothorax present? A tension pneumothorax occurs when air is trapped in the pleural cavity under positive pressure. A tension pneumothorax presents as a medical emergency, and the patient’s status will deteriorate acutely. The following signs may be seen with tension pneumothorax: cyanosis, hypoxia, tachypnea, a sudden decrease in heart rate with bradycardia, a sudden increase in systolic blood pressure followed by narrowing pulse pressure and hypotension, an asymmetric chest (bulging on the affected side), distention of the abdomen (secondary to downward displacement of the diaphragm), decreased breath sounds on the affected side, and shift of the cardiac apical impulse (most consistent finding) away from the affected side. A cyanotic upper half of the body with a pale lower half can be seen.
B. Is the patient asymptomatic? An asymptomatic pneumothorax is present in 1–2% of neonates. It occurs more frequently in males and term and post-term infants. It is usually unilateral. Most of these cases are discovered on chest radiograph at admission. Up to 15% of these infants were meconium stained at birth.
C. Is mechanical ventilation being used? The incidence of pneumothorax in patients receiving positive-pressure ventilation is 15–30%. A life-threatening tension pneumothorax may result from mechanical ventilation.
D. Are there risk factors for a pneumothorax? Neonates delivered between 30 and 36 weeks, moderately preterm, or term by caesarean section have a higher incidence of pneumothorax. The following are associated with an increased risk: male infant, low birthweight, premature, meconium-stained amniotic fluid, vacuum extraction, a low 1-minute Apgar score, ventilator treatment, perinatal asphyxia, cardiopulmonary resuscitation, transient tachypnea, RDS, MAS, pneumonia, pulmonary hypoplasia, urinary tract anomalies, infants who were resuscitated at birth, continuous positive airway pressure, and positive pressure ventilation. a1-Antitrypsin deficiency may play a role in some cases of spontaneous pneumothorax of the newborn.
III. Differential diagnosis. Radiologically, the differential diagnosis can include pneumomediastinum, congenital lobar emphysema, atelectasis with compensatory hyperinflation, congenital diaphragmatic hernia, congenital cystic adenomatoid malformation, and a large pulmonary cyst. Clinically, it can present as any process that causes respiratory distress, and it is important to exclude other causes of respiratory distress in a neonate: RDS, endotracheal tube obstruction/displacement, aspiration, congenital heart disease, asphyxia, congenital diaphragmatic hernia (CDH), congenital cystic adenomatoid malformation (CCAM), or pleural effusions. Suddenrapid deterioration in a neonate can be from a tension pneumothorax, pneumopericardium, or a massive pericardial effusion/cardiac tamponade (umbilical venous catheter).
1. Symptomatic pneumothorax (includes tension vs nontension pneumothorax). Nontension symptoms: irritability, grunting, pallor cyanosis, restlessness, apnea, mild tachypnea, respiratory distress. Tension symptoms are noted in Section II.A previously.
2. Asymptomatic pneumothorax.
3. Persistent pneumothorax.
B. Pneumomediastinum. Air in the mediastinal space that may be confused with a true pneumothorax. On the radiograph, mediastinal air can elevate the lobes of the thymus (called “angel wing” or “spinnaker sail” sign), and the air can also track within the extrapleural space and outline the inferior aspect of the heart (“continuous diaphragm sign”). See Figure 11–19.
C. Congenital lobar emphysema. A rare anomaly of lung development that presents with respiratory distress and pulmonary lobar hyperinflation. Overdistention of one lobe secondary to air trapping occurs most commonly (47–50%) in the left upper lobe. Other lobe involvement is right upper lobe (20%), right middle lobe (28%), and lower lobes (rare). The causes of congenital lobar emphysema are multifactorial.
D. Atelectasis with compensatory hyperinflation. Compensatory hyperinflation may appear as a pneumothorax on a chest radiograph.
E. Pneumopericardium. In neonates, pneumopericardium and tension pneumothorax can both present as sudden and rapid clinical deterioration. In pneumopericardium, the blood pressure drops, heart sounds are distant or absent, and pulses are muffled or absent. Massive abdominal distention can also be seen. In tension pneumothorax, the blood pressure may initially increase, but then hypotension follows. The chest radiograph easily differentiates the two. A pneumopericardium has a halo of air around the heart (see Figure 11–18). The more common event is a tension pneumothorax. If one is unsure and time does not permit radiographic verification, quick transillumination can be done. If not available or unsure of results, it is better to insert a needle in the chest on the suspected side. If no response, then a needle should be inserted on the other side. If there is still no response, then the diagnosis of pneumopericardium should be considered.
F. Congenital diaphragmatic hernia (CDH). A developmental defect in the diaphragm allows the abdominal viscera to protrude into the chest, which causes pulmonary hypoplasia and decreased pulmonary vasculature and dysfunction of the surfactant system. Ninety percent are on the left side. CDH is often mistaken as a left tension pneumothorax. Presents with respiratory distress, cyanosis, and circulatory insufficiency. It can be hard to differentiate a left-sided pneumothorax from a typically left-sided CDH. With CDH, the abdomen is scaphoid, and the spleen cannot be palpated. There can be a mediastinal shift on radiograph. If chest tubes are placed, there is a risk of perforating the herniated viscus.
G. Congenital cystic adenomatoid malformation (CCAM). This rare congenital abnormality of the lung results from abnormal embryogenesis and reduced alveolar growth. The infants present with respiratory distress. Tachypnea and cyanosis can be presenting signs that are similar to a pneumothorax. Many of these are detected on ultrasound prenatally. A chest radiograph usually identifies the mass containing air-filled cysts. (See Chapter 135.)
H. Congenital pulmonary cysts. These are space occupying, involve one or more lobes, have atelectasis of the adjacent lobe, and have symptoms similar to pneumothorax.
IV. Clinical findings
A. Physical examination. Specific findings are discussed in Section II.A. Transillumination is a useful rapid bedside technique in neonates (see Section IV.C and Chapter 40).
B. Laboratory studies. Blood gas levels may show decreased Pao2 and increased Pco2, with resultant respiratory acidosis.
C. Imaging and other studies
1. Transillumination of the chest is a rapid bedside method to identify a pneumothorax. Always verify the diagnosis of pneumothorax by a chest radiograph if time permits. The room lights are lowered, and a fiber optic transilluminator is placed along the posterior axillary line on the side on which pneumothorax is suspected. If a pneumothorax is present, the chest “lights up” on that side. The transilluminator may be moved up and down along the posterior axillary line and may also be placed above the nipple. Transilluminate both sides of the chest and then compare the results. If severe subcutaneous edema is present, transillumination may be falsely positive. Premature infants with pulmonary interstitial emphysema may also have a false-positive transillumination. Large infants with thick chest walls do not transilluminate well.
2. Chest radiographs are the method of choice for diagnosing pneumothorax. Early pneumothoraces are difficult to diagnose. Early on, there is separation of lung from the chest wall with no lung markings in that space. In infants there is a tendency of pleural air to cloak diaphragmatic and mediastinal surfaces. A pleural line is often not seen, but a well-defined costophrenic sulcus (deep sulcus sign) can be observed. The following films will aid the diagnosis:
a. Anteroposterior (AP) view of the chest (see Figure 11–20) will show the following:
i. A shift of the mediastinum away from the side of pneumothorax (with tension pneumothorax).
ii. Depression of the diaphragm on the side of the pneumothorax (with tension pneumothorax).
iii. Displacement of the lung on the affected side away from the chest wall by a radiolucent band of air.
b. Cross-table lateral view will show a rim of air around the lung (“pancaking”).It will not help to identify the affected side. You must have an AP film to identify the side of the pneumothorax. This film must be considered together with the AP view to identify the involved side. Pleural air tends to collect anteriorly and may require the CT or lateral decubitus view.
c. Lateral decubitus view (shot through the AP position) will detect even a small pneumothorax not seen on a routine chest radiograph. The infant should be positioned so the side of the suspected pneumothorax is up (eg, if pneumothorax is suspected on the left side, the film is taken with the left side up).
3. Ultrasound examination of the lungs. The absence of lung sliding (grainy appearance) and comet tails (normal pleura reflecting sound waves) confirms the ultrasound diagnosis of a pneumothorax. The sensitivity and specificity of ultrasound is 100% and 93% for a complete pneumothorax, and 79% and 100% for a radio-occult pneumothorax. As a bedside tool, this is useful to diagnose a pneumothorax.
4. Transcutaneous carbon dioxide (tcpCO2) reference percentiles with changes over time can indicate a pneumothorax or a blocked or misplaced endotracheal tube.
5. Echocardiography and renal ultrasound may be indicated in spontaneous pneumothorax in term infants, as some of these infants can have renal and cardiac anomalies.
A. Symptomatic pneumothorax
1. Tension pneumothorax. Symptomatic (tension) pneumothorax is an emergency! A 1- to 2-minute delay could be fatal. If a tension pneumothorax is suspected, act immediately. It is better to treat in this setting, even if it turns out that there is no pneumothorax. There is no time for x-ray confirmation. If the patient’s status is deteriorating rapidly, a needle or catheter over needle can be placed for aspiration, followed by formal chest tube placement. There is no specific sign that distinguishes a tension from a nontension pneumothorax. Signs of a tension pneumothorax from above can also occur in a nontension pneumothorax, except the signs and symptoms are more severe in a tension pneumothorax.
a. Needle aspiration (see Figure 70–1) can be done as an emergency. Often times this is all that is necessary if the infant is not on a ventilator. If on a ventilator, a chest tube placement may need to be followed by needle aspiration.
See Emergency Pneumothorax Needle Image Below
i. The site of puncture should be at the second intercostal space along the midclavicular line on the suspected side of pneumothorax. Cleanse this area with antibacterial solution. The fourth intercostal space at the anterior axillary line can also be used (needle would be inserted above the fifth rib).
ii. Connect a 23- or 25-gauge butterfly needle or a 22- or 24-gauge catheter over needle (Angiocath) to a 10–20-mL syringe with a stopcock attached.
iii. Palpate the third rib at the midclavicular line. Insert the needle (perpendicular to the chest surface) over the top of the third rib at the second intercostal space, and advance it until air is withdrawn from the syringe. Have an assistant hold the syringe to withdraw the air. The needle may be removed before the chest tube is placed if the infant is relatively stable, or it may be left in place for continuous aspiration while the chest tube is being placed. If an Angiocath is used, the needle can be removed and the catheter left in place.
b. Chest tube placement is discussed in Chapter 27. This is necessary in most infants on mechanical ventilation with a tension pneumothorax.
c. If the infant does not improve with a chest tube. Suspect extrapleural air leaks such as a pneumoretroperitoneum, which has been reported in infants with pneumothorax. If air is still present on the radiograph, consider these causes: obstruction of the tube with blood or pleural fluid, disconnected drainage tube, ineffective water seal, new air leak, or a lung perforation.
2. Nontension pneumothorax. Depending on the infant, oxygen supplementation, needle aspiration, chest tube placement, or conservative management (oxygen, close observation) is done.
a. Mild symptoms. Some require observation only.
b. Symptomatic spontaneous pneumothorax (not on ventilator). Needle aspiration and possible chest tube placement. In one study the majority of infants did not require a needle aspiration or chest tube and could be managed with supplemental oxygen or close observation.
c. Symptomatic spontaneous pneumothorax (on the ventilator). Needle aspiration and chest tube placement. Some infants on a ventilator who have a pneumothorax could be treated conservatively without a chest tube, but they usually are more mature, on lower ventilator settings, and had better gases at the time of the pneumothorax as compared with the infants who required a chest tube.
B. Asymptomatic pneumothorax
1. If positive-pressure mechanical ventilation is being used:
a. Needle aspiration/chest tube. A chest tube will probably need to be inserted because the ventilator pressure will prevent resolution of the pneumothorax, and tension pneumothorax may develop. Sometimes needle aspiration is allthat is needed. If a pneumothorax develops in a patient who is ready to be extubated, clinical judgment must be used in deciding whether a chest tube should be placed.
b. Expectant management. Recent studies are showing that some select infants on a ventilator can be managed without a chest tube.
2. If positive-pressure mechanical ventilation is not being administered and there is no underlying lung pathology,these may be considered.
a. Close observation with follow-up chest radiographs every 8–12 hours or sooner if the infant becomes symptomatic. The pneumothorax will likely resolve within 24–48 hours.
b. Nitrogen washout therapy (controversial). Allows a more rapid resolution of the asymptomatic pneumothorax but is infrequently used due to the toxicity of 100% oxygen. The infant receives 100% oxygen for 8–12 hours; less nitrogen is able to enter the lungs, and at the same time absorption of nitrogen from the extrapleural space is increased and then exhaled. The total gas tension is decreased, which also facilitates absorption of nitrogen by the blood. The method should be used only in full-term infants in whom retinopathy of prematurity will not be a problem. Some NICUS give only enough oxygen to maintain a pulse oximetry reading >90% and have found resolution to be similar to the hyperoxic group.
C. Persistent pneumothorax. Generally defined as a pneumothorax that persists >7 days in the absence of mechanical problems. Sometimes infants who have chest tubes still have air leaks that persist for more than a week. These infants have episodes of instability when air reaccumulates; some require a new or replacement chest tube and an increase in their ventilator settings. These are treated to decrease the complications associated with air leaks (air embolus, hypotension, intracranial hemorrhage). The following have been used:
1. High-frequency oscillatory ventilation (HFOV) or high-frequency jet ventilation (HFJV) can be used due to lower mean airway pressures.
2. Unilateral lung intubation has been reported as an efficient and relatively safe therapy for pneumothorax. Duration of therapy should be a minimum of 48 hours.
3. Fibrin glue, such as CryoSeal C (ThermoGenesis Corp., Rancho Cordova, CA), has been injected in the chest tube with a marked reduction in the air leak. Risks include hypercalcemia, localized tissue necrosis, bradycardia, diaphragmatic paralysis, and pneumothorax on the contralateral side. More studies are needed before this treatment can be routinely recommended.
D. Pneumomediastinum. May progress to a pneumothorax or pneumopericardium. Close observation is required.
E. Congenital lobar emphysema. If asymptomatic, conservative management with observation. If symptomatic or respiratory failure is occurring, the treatment is usually surgical excision of the affected lobe.
F. Atelectasis with compensatory hyperinflation
1. Chest physiotherapy and postural drainage should be initiated. Chest physiotherapy should be used with caution in premature infants. A study showed an association with intraventricular hemorrhage and porencephaly in extreme premature infants.
2. Treatment with bronchodilators is indicated.
3. Positioning the infant with the affected (hyperinflated) side down may speed resolution.
4. Bronchoscopy. May be necessary with mucous plug.
G. Pneumopericardium. This should be treated emergently by pericardiocentesis (see Chapter 38).
H. Cystic adenomatoid malformation or congenital cyst. Surgery is the treatment of choice.
FIGURE 70–1. Site of emergency needle aspiration for tension pneumothorax is puncture at the second intercostal space (ICS) along the midclavicular line.
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