pearls 1
a urine sodium greater than 40 meq/L suggests acute tubular necrosis
urine sediment that shows renal tubular epithelial cells and muddy brown casts is diagnostic for acute tubular necrosis [see my renal failure lecture under renal physiology ] .
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Transient tachypnea of the newborn [ Wet Lung Disease (Transient Tachypnea of the Newborn) (TTN) (Retained Fetal Lung Liquid)
Transient tachypnea of the newborn (TTN) is a disease common in infants throughout the world and has been encountered by all physicians who care for newborn infants
 . Infants with TNN present within the first few hours of birth with
 tachypnea,
 increased oxygen requirement,
 and occasional hypoxia noted on arterial blood gases without concomitant carbon dioxide retention.
 When managing an infant with TTN, it is important to observe for signs of clinical deterioration that may suggest other diagnoses and to observe closely for the development of fatigue
 occurs due to latent fluid remaining in the lungs post-partum.
 it usually follows normal delivery.
 Look for tachypnea, retractions of the chest expiratory grunting and cyanosis.
 It is do to slow absorption of fetal lung fluid with
 decreased pulmonary compliance,
 increased dead space and low tidal volume.
 A newborn with transient tachypnea (TTN) has extra fluid in his lungs which causes him to:
 This rapid breathing begins shortly after birth and the baby's breathing rate usually becomes normal within 24 to 48 hours
 Transient tachypnea is fast breathing that gradually gets better.
 It is thought to be due to slow reabsorption of fetal lung fluid.
 Before birth the lungs continuously make fluid.
 Some of this fluid is squeezed out as the baby comes down the birth canal.
 The rest must be absorbed by the baby during the first minutes to hours of life.
 In babies with TTNB this process may last hours to days.
 TTNB is more common in babies delivered by cesarean section because they did not have fluid squeezed out with delivery.
The baby will have some difficulty with breathing. S/he may
 breathe rapidly [TACHYPNEA]
 make the "ugh" sound with each breath, called grunting.
 have a widening of the nostrils with each breath, called flaring.
 need extra oxygen. Room air is 21% oxygen.
 The baby needs higher oxygen to stay pink.
 The roentgenographic findings are mild to moderate overaeration, symmetric parahilar patches or streaks, and occasionally mild cardiomegaly or pleural effusions .
 The right lung may be more opacified than the left.
 The chest film returns to normal by 48-72 hours of age.
..
Pathophysiology:
 Noninfectious acute respiratory disease develops in approximately 1% of all newborn infants and results in admission to a critical care unit.
 TTN is the result of a delay in clearance of fetal lung liquid.
 Respiratory distress typically was thought to be a problem of relative surfactant deficiency, but it is now characterized by an airspace-fluid burden secondary to the inability to absorb fetal lung liquid.
 In vivo experiments have demonstrated that lung epithelium secretes Cl - and fluid throughout gestation but only develops the ability to actively reabsorb Na + during late gestation.
 A t birth, the mature lung switches from active Cl- (fluid) secretion to active Na+ (fluid) absorption in response to circulating catecholamines.
 Changes in oxygen tension augment the Na +-transporting capacity of the epithelium and increase gene expression for the epithelial Na + channel (ENaC).
 The inability of the immature fetal lung to switch from fluid secretion to fluid absorption results, at least in large part, from an immaturity in the expression of ENaC, which can be upregulated by glucocorticoids.
 Both pharmacologic blockade of the lung's EnaC channel and genetic knockout experiments using mice deficient in the ENaC pore-forming subunit have demonstrated the critical physiologic importance of lung Na + transport at birth.
 When Na + transport is ineffective, newborn animals develop respiratory distress; hypoxemia; fetal lung liquid retention; and, in the case of the ENaC knockout mice, death.
 Bioelectrical studies of human infants' nasal epithelia demonstrate that both TTN and respiratory distress syndrome (RDS) have defective amiloride-sensitive Na + transport.
 These results suggest that infants with neonatal RDS have, in addition to a relative deficiency of surfactant, defective Na + transport, which plays a mechanistic role in the development of the disease.
 An infant born by cesarean delivery is at risk of having excessive pulmonary fluid as a result of having not experienced all of the stages of labor and subsequent low release of counter-regulatory hormones at the time of delivery.
Frequency:
In the US: Frequency is equivalent universally. Approximately 1% of infants have some form of respiratory distress that is not associated with infection. Respiratory distress includes both RDS (ie, hyaline membrane disease) and TTN. Of this 1%, approximately 33-50% is TTN.
Mortality/Morbidity: TTN is generally a self-limited disorder without significant morbidity. TNN resolves over a 24- to 72-hour period.
Race: No racial predilection exists.
Sex: Risk is equal in both males and females.
Age: Clinically, TTN presents as respiratory distress in full-term or near-term infants
 Signs of respiratory distress (eg, tachypnea, nasal flaring, grunting, retractions, cyanosis in extreme cases) become evident shortly after birth.
 The disorder is indeed transient, with resolution occurring usually by age 72 hours.
Physical: Physical findings include tachypnea, with variable grunting, flaring, and retracting. Extreme cases also may exhibit cyanosis.
Causes:
 The disorder results from delayed absorption of fetal lung fluid following delivery.
 TNN commonly is observed following birth by cesarean delivery because infants do not receive the thoracic compression that accompanies vaginal delivery.
 Cesarean delivery
 Studies utilizing lung mechanic measurements were performed on infants born by either cesarean or vaginal delivery. Milner et al noted that the mean thoracic gas volume was 32.7 mL/kg for infants born vaginally and 19.7 mL/kg for infants born via cesarean delivery. Importantly, chest circumferences were the same. Milner et al noted that the infants born via cesarean delivery had higher volumes of interstitial and alveolar fluid compared to those born vaginally, even though the overall thoracic volumes were within the normal range.
 Epinephrine release during labor has an effect on fetal lung fluid. In the face of elevated epinephrine levels, the chloride pump responsible for lung liquid secretion is inhibited, and the sodium channels that absorb liquid are stimulated. As a result, net movement of fluid from the lung into the interstitium occurs. Therefore, in the lack of this normal surge in counter-regulatory hormones in the infant, excursion of pulmonary fluid is limited.
 Maternal asthma and smoking
 In a recent study, Demissie et al performed a historical cohort analysis on singleton live deliveries in New Jersey hospitals during 1989-1992. After controlling for confounding effects of important variables, infants of mothers with asthma were more likely to exhibit TTN than infants of mothers in the control group.
 Schatz et al studied a group of 294 pregnant women with asthma and a group of 294 pregnant women without asthma with normal pulmonary function test results. The groups of women were matched for age and smoking status. TTN was found in 11 infants (3.7%) of the women with asthma and in 1 infant (0.3%) of the women from the control group. No significant differences between asthmatic and matched control subjects in other TTN risk factors were observed.
 Prolonged labor
 Other recent studies have found that obstetric histories of mothers of newborns with TTN were characterized by longer labor intervals and a higher incidence of failure to progress in labor leading to cesarean delivery.
 Excessive maternal sedation, perinatal asphyxia, and elective cesarean delivery without preceding labor are not frequently associated with TTN.
DIFFERENTIALS DIAG:
Pneumomediastinum
Pneumonia
Pneumothorax
Respiratory Distress Syndrome
Respiratory Failure
Other Problems to be Considered:
 Cerebral hyperventilation
 Metabolic acidosis
Lab Studies:
 Arterial blood gas
 An ABG is important to ascertain the degree of gas exchange and acid-base balance.
 Consider an intraarterial catheter if the infant's inspired fraction of oxygen exceeds 40%.
 Hypoventilation is very uncommon, and partial carbon dioxide tensions are usually low because of the tachypnea. However, a rising carbon dioxide tension in an infant with tachypnea may be a sign of fatigue and impending respiratory failure.
 Pulse oximetry
 Continuously monitor infants by pulse oximetry for assessment of oxygenation.
 Pulse oximetry allows the clinician to adjust the level of oxygen support needed to maintain appropriate saturation.
Imaging Studies:
 Chest x-ray
 The chest x-ray (CXR) is the diagnostic standard for TTN.
 The characteristic findings are prominent perihilar streaking, which correlates with the engorgement of the lymphatic system with retained lung fluid, and fluid in the fissures. Patchy infiltrates also have been described.
 A follow-up CXR may be necessary if the clinical history suggests meconium aspiration syndrome or neonatal pneumonia. In these cases, the CXR shows persistent infiltrates. Abnormalities resolve by 72 hours of life in cases of TTN.
How is transient tachypnea treated?
 have his/ her respirations, heart rate, and blood oxygenation monitored.
 In addition your baby may need one of the following:
 Oxygen. This can be given through a plastic hood placed over the baby's head or by oxgen into the isolette.
 CPAP (Continuous Positive Airway Pressure).
 This is oxygen delivered under a small amount of pressure usually through little tubes that fit into the nostrils of the nose.
 Delivering oxygen under pressure helps keep the fluid out of the air sacs and speeds up its reabsorption.
 Medical care is supportive. As the retained lung fluid is absorbed by the infant's lymphatic system, the pulmonary status improves.
 Supportive care includes intravenous fluids and gavage feedings (until the respiratory rate has decreased enough to allow oral feedings). Supplemental oxygen to maintain adequate arterial oxygen saturation, maintenance of thermoneutrality, and an environment of minimal stimulation are the therapies necessary for these infants.
 As TTN resolves, the infant's tachypnea improves, oxygen requirement decreases, and the CXR shows resolution of the perihilar streaking.
 Infants with TTN may have signs that last from a few hours to several days. Rarely, an infant may develop a worsening picture of respiratory distress after several days. This may require more aggressive support including the use of continuous positive airway pressure (CPAP) by nasal prongs or endotracheal tube, or mechanical ventilation.
Consultations: Infants with TTN occasionally may require consultation by a neonatologist. Consider this consultation if the fraction of inspired oxygen exceeds 40%, if metabolic or respiratory acidosis is present, if CPAP or mechanical ventilation is required, if the infant begins to display fatigue (periodic breathing or apnea), or if the infant fails to improve by age 48-72 hours.
Diet: Infants with TTN generally are supported by intravenous fluids or gavage feedings. Oral feedings are withheld until the respiratory rate is consistently normal (<60 bpm).
The use of medications for TTN is minimal. Aside from the use of antibiotics for a period of 36-48 hours after birth until sepsis has been ruled out, no further pharmacotherapy generally is prescribed. Diuretics have not been shown to be beneficial.
Drug Category: Antibiotics - Used when sepsis is clinically suggested. Antibiotics generally consist of a penicillin (usually ampicillin) and an aminoglycoside (usually gentamicin) or a cephalosporin (usually cefotaxime). Choices are based on local flora and antibiotic sensitivities.
Drug Name
|
Ampicillin- A penicillin antibiotic with activity against gram-positive and some gram-negative bacteria. Ampicillin binds to penicillin-binding proteins (PBPs), inhibiting bacterial cell wall growth.
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Pediatric Dose
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<2000 g: 50 mg/kg/d IV/IM divided q12h
>2000 g: 75 mg/kg/d IV/IM divided q8h
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Contraindications
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Documented hypersensitivity
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Interactions
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Probenecid increases the serum concentration of ampicillin
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Pregnancy
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B - Usually safe but benefits must outweigh the risks.
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Precautions
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Dose adjustments may be necessary in patients diagnosed with renal failure
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Drug Name
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Gentamicin- Provides gram-negative aerobic coverage. Gentamicin also provides synergistic activity with penicillins against gram-positive bacteria including enterococcus. Gentamicin inhibits protein synthesis by irreversibly binding to bacterial 30S and 50S ribosomes.
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Pediatric Dose
|
<29 weeks GA: 2.5 mg/kg/dose IV/IM q24h
30-36 weeks GA: 3 mg/kg/dose IV/IM q24h
>37 weeks GA: 2.5 mg/kg/dose IV/IM q12h
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Contraindications
|
Documented hypersensitivity to gentamicin or any other aminoglycosides
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Interactions
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Amphotericin B, cyclosporine, cephalosporins, and furosemide may increase the risk of renal toxicity
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Pregnancy
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D - Unsafe in pregnancy
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Precautions
|
Nephrotoxicity and ototoxicity may be associated with prolonged elevated trough concentrations; monitor levels to minimize the risk of toxicity and to optimize therapy
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 The time course is variable. It may last hours or days.
 Gradually the baby's need for oxygen will decrease.
 Then, his/her respiratory rate will slowly come down to normal.
 Some babies have fast respirations for several days.
 , once it resolves, it does not come back.
Further Inpatient Care:
 After resolution of TNN, focus further inpatient care on routine newborn management.
 No further medical therapy concerning the infant's pulmonary function is required.
Transfer:
 When managing an infant with TTN, it is important to have appropriately trained support staff. Infants with TTN and pneumonia or meconium aspiration may have similar clinical presentations. Therefore, staff members must be competent in recognizing worsening respiratory distress or impending failure and must be able to appropriately resuscitate the infant.
 Transfer generally is indicated by the need for a higher level of observation and/or care.
Complications:
 Few potential complications exist.
 Gross et al noted a population of 55 pregnancies after which newborns developed TTN compared to 355 pregnancies after which respiratory distress did not occur. Neonatal complications and procedures often associated with prematurity were found to be significantly increased in the infants who developed TTN. Therefore, potential complications can occur in these patients. Carefully monitor infants for signs of worsening respiratory distress.
Prognosis:
 Prognosis is excellent.
 Asthma: Schaubel et al looked at neonatal characteristics as risk factors for preschool asthma. The study demonstrated that infants with TTN are at an increased risk for hospitalization from asthma during the preschool years.
Patient Education:
 Inform parents that TTN is usually a self-limited disorder and is not life threatening
Note streak densities in the parahilar regions and patchy
infiltrates in the right lung
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Epiglottitis is an infection of the epiglottis and supraglottic structures.
MEDICAL EMERGENCY
It more precisely should be called acute supraglottitis, because inflammation of the supraglottic structures can cause this constellation of symptoms without actually involving the epiglottis itself
It characteristically occurs in children ages 2-7 years old and is caused by Haemophilus influenzae type b also known as H. influenzae
Haemophilus influenza a gram negative pleomorphic rod appears pink of gram stain.
 Epiglottitis has an abrupt onset of high fever, sore throat and dysphagia, moderate to severe respiratory distress, stridor, and lethargy .
 These children appear very toxic with flushed skin and often sits leaning forward with mouth open and chin extended in an effort to maintain their airways.
 The dysphagia does not allow them to clear their oral secretions, and they are often drooling on presentation.
 The voice is also muffled, called a "hot potato" voice, because it sounds as if the child is talking with a hot potato in his or her mouth.
 The child may also show intercostal retractions and perioral cyanosis and sounds stridorous
 These children may be so tired from their work of breathing that they may present with lethargy, fatigue, or even frank respiratory failure
 Diagnosis is often presumptively based on history and observation of the child at a distance!
 Physical examination should be done expediently and with careful attention so as not to increase the child's anxiety.
 This is imperative!!! Increased anxiety in the child may lead to reflex laryngospasm, acute airway obstruction, and respiratory arrest.
 Even minor annoyances to the child such as placement of electrocardiogram or ECG leads, or placement of mist by his or her face may cause the child to cry and possibly obstruct the airway.
 The child should remain with a trusted caretaker at all times, often in their arms.
 Close monitoring should be done by observation with emergency equipment readily available
 . Do not attempt direct visualization of the epiglottis in the emergency room or office by depressing the tongue as this may also cause reflex laryngospasm and obstruction, which may lead to respiratory arrest
 Toxic Appearance
 Hot Potato Voice
 Dysphagia
 and Sore Throat
 Fever
 Stridor
 Lethargy
Endolateral neck x-rays show classic swelling of the epiglottis on the lateral film.
This is also known as the "thumb" sign as it resembles the size and shape of the human thumb .
The anteroposterior film is usually unremarkable.
 If the child shows classic signs and symptoms, direct visualization of the supralaryngeal area is carried out promptly using a laryngoscope or bronchoscope.
 The patient is anesthetized with an inhalation anesthetic, an intravenous line is started with blood sent to the laboratory for culture and CBC, and the larynx and supraglottic tissues are inspected.
 The diagnosis is based on the finding of swollen cherry-red supraglottic structures usually including the epiglottis .
 There is thickening of the aryepiglottic folds and arytenoid cartilages, which form the lateral and posterior aspects of the laryngeal vestibule and actually cause the marked upper airway obstruction in acute epiglottitis
 . These thickened aryepiglottic folds and arytenoid cartilages cause the "thumb sign" on the x-ray - the swollen epiglottis itself does not.
 An appropriately sized, uncuffed endotracheal tube is inserted with direct visualization and mechanical ventilation initiated
 Cultures of the epiglottis and throat should also be taken in the operating room.
 The child is taken to the intensive care unit where mechanical ventilation is continued .
Systemic antibiotics directed against H. influenzae such as ampicillin and chloramphenicol combined or single agents such as ceftriaxone or cefotaxime, should be started as soon as possible.
 Ventilation is continued and direct visualization of the epiglottis is done on a daily basis until the edema resolves, generally within 24-48 hours. Systemic antibiotics are administered for approximately 2 weeks.
 Note that respiratory isolation of the patient for the first 24 hours of antibiotic treatment is necessary.
 The CBC is remarkable for a leukocytosis with a marked left shift but this is not specific.
 Rapid latex particle agglutination of urine or serum for H. influenzae may confirm the diagnosis before blood or direct epiglottis cultures grow.
 The physician should also consider doing a lumbar puncture for possible meningitis as this organism is highly invasive.
Racemic epinephrine and corticosteroids are not helpful in the treatment of epiglottitis.
 Control measures for invasive H. influenzae type b are very important since asymptomatic carriage in the nasopharynx of household contacts and possibly day care centers is quite high.
Chemoprophylaxis with rifampin given once daily for 4 days eradicates H. influenzae in approximately 95% of carriers.
Rifampin prophylaxis should be given to all household contacts regardless of age where at least one household contact is less than 48 months of age.
 A nasopharyngeal culture should be done before treatment.
 Chemoprophylaxis should be instituted as soon as possible after diagnosis of H. influenzae type b is made.
 Guidelines for the treatment of day care contacts but not definitive recommendations have been set forth by the American Academy of Pediatrics.
 Vaccination to prevent H. influenzae disease was originally begun in 1985 in the United States for children 24 months or older, but in October 1990 H. influenzae type b conjugate vaccines were approved for children 2 months of age and older.
 Any children less than 24 months experiencing invasive H. influenzae disease such as epiglottitis should be vaccinated with the standard regimen for age as they might not acquire natural immunity from the infection. If the child is older than 24 months, then the disease itself most likely will cause natural immunity, and immunization is not needed
 In the future, physicians should expect to see less invasive H. influenzae disease as more children receive adequate immunization.
 Complications associated with epiglottitis include
 otitis media,
 adenitis,
 meningitis,
 pericarditis,
 and pneumonia.
 Mortality may be as high as 5-10% owing to difficulties in maintaining the airway early in the illness
 The differential diagnosis includes the various members of the croup syndromes especially viral croup and also foreign bodies
 . Note that the epiglottis may be enlarged for other reasons, but these causes do not show the life-threatening clinical syndrome of acute epiglottitis
Characteristic
|
Viral Croup
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Acute Epiglottis
|
Age
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3 mo.-5 years
|
2-7 years
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Organism
|
Viral
|
H. Influenza: type b
|
Incidence
|
Common
|
Rare
|
Clinical Presentation
|
Gradual onset
Mild URI symptoms
Barky cough
Low fever
|
Sudden onset
Drooling
Sitting forward
High fever
|
Physical Exam
|
Respiratory distress
Inspiratory stridor
|
Toxic appearance
"Hot potato voice"
|
X-ray and Projection
|
Steeple sign
A/P view
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Thumb sign
Lateral view
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Treatment
|
Humidification
Racemic epinephrine
|
Epiglottitis protocol
|
Causes of an Enlarged Epiglottis on X-ray
 Prominent Normal Epiglottis
 Omega-Shaped Epiglottis
 Angioneurotic Edema
 Stevens-Johnson Syndrome
 Hemophilia
 Aryepiglottic Cyst
 Epiglottic Cyst
 Foreign Body
 Trauma including Caustic, Thermal, Irradiation, or Chemical
 Chronic Epiglottitis
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High risk pregnancies
Maternal status:
 Teenage (< 16)
 Elderly (> 40)
 Low socioeconomic status
 Maternal illness:
 Diabetes
 Hypertension
 Rh sensitization
 Severe anaemia
 Previous pregnancies:
 Previous abortions
 Previous stillbirths
 Previous early neonatal deaths
 Previous preterm infants
 Present pregnancy:
 No antenatal care
 Hypertension
 Multiple pregnancy
 Polyhydramnios
 Abnormal presentation or position
 Certain drugs - alcohol, smoking
 Preterm labour
 Severe fetal growth retardation
 High risk pregnancies should be delivered in hospitals where appropriate facilities are available.
Fetal distress
If the fetus becomes hypoxaemic it develops bradycardia with shunting of blood away from less vital organs to the brain. This is an appropriate physiological response to stress. Meconium may also be passed and the fetus may make gasping respiratory movements, aspirating amniotic fluid and meconium into the upper airways.
Fetal hypoxaemia is usually transient, intermittent and occurs towards the end of a uterine contraction (a late deceleration). If the placental blood flow from the mother is able to recover between contractions a metabolic acidosis does not develop and the fetus is said to be stressed. When this ability to compensate fails, tissue hypoxia results in a metabolic acidosis. Only now can the fetus be regarded as distressed.
Fetal heart rate monitoring and the assessment of scalp pH (normally above pH 7,25) are used to detect fetal distress. Unfortunately these methods cannot always differentiate the stressed from the distressed fetus
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