Peds ER Flashcards

1
Q

CPS criteria for AOM?

A

To properly diagnose AOM, there must be fluid behind the tympanic membrane (a middle ear effusion) and specific signs and symptoms of middle ear inflammation (indicating that this fluid is pus

Signs of a middle ear effusion:

An immobile tympanic membrane (as demonstrated by pneumatic insufflation, tympanogram or acoustic reflectometry) or presence of liquid in the external ear canal as a result of tympanic membrane rupture (acute otorrhea)
+/- Opacification of the tympanic membrane (not secondary to scarring)
+/- Loss of the bony landmarks behind the tympanic membrane (specifically loss of the short or lateral process of the malleus)
+/- A visible air fluid level behind the tympanic membrane

Signs of middle ear inflammation:

Bulging tympanic membrane with marked discoloration (hemorrhagic, red, gray or yellow)

Acute onset of symptoms:

Rapid onset of ear pain (otalgia), or unexplained irritability in a preverbal child

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2
Q

Organisms for AOM?

A

The most common pathogens in the post-pneumococcal vaccine era are Streptococcus pneumoniae (31%) and nontypeable Haemophilus influenzae (56%) and Moraxella catarrlis (16%)

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3
Q

Management of AOM?

A

Treatment of pain is essential for all children diagnosed with AOM. Topical analgesics such as benzocaine-antipyrene are recommended for routine use, unless there is a known perforation of the TM. Acetaminophen 15 milligrams/kilogram or ibuprofen 10 milligrams/kilogram can be used.

Consider the use of a wait-and-see prescription for the treatment of uncomplicated AOM. Parents are given a prescription and told to wait and see for 48 to 72 hours, and if the child is not better or becomes worse, to fill the prescription. Contraindications to the use of a wait-and-see prescription are: age < 6 months, an immunocompromised state, ill-appearance, recent use of antibiotics or the diagnosis of another bacterial infection. If any of these conditions are met, the child should be prescribed an immediate antibiotic.

Amoxicillin 40-50 milligrams/kilogram/dose PO given twice daily (or 30 milligrams/kilogram/dose three times daily) times daily remains the first drug of choice for uncomplicated AOM.

Second line antibiotics include amoxicillin/clavulanate 40–50 milligrams/ kilogram/dose given twice daily. Cefpodoxime 5 milligrams/kilogram/dose PO twice daily, cefuroxime axetil 15 milligrams/kilogram/dose twice daily, cefdinir 7 milligrams/kilogram/dose PO once or twice daily, and ceftriaxone 50 milligrams/kilogram/dose IM for 3 daily doses are alternatives. For patients allergic to the previously mentioned antibiotics, azithromycin 10 milligrams/kilogram/dose PO on the first day followed by 5 milligrams/kilogram/dose PO for 4 more days can be used.

Infants younger than 60 days with AOM are at risk for infection with group B Streptococcus, Staphylococcus aureus, and gram-negative bacilli and should undergo evaluation and treatment for presumed sepsis.

In uncomplicated AOM, symptoms resolve within 48 to 72 hours; however, the middle ear effusion may persist as long as 8 to 12 weeks. Routine follow-up is not necessary unless the symptoms persist or worsen.

If mastoiditis is suspected, obtain a CT scan of the mastoid. If the diagnosis is confirmed, obtain consultation with an otolaryngologist and start parenteral antibiotics.

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4
Q

Common organisms for otitis externa?

A

It is commonly caused by Pseudomonas aeruginosa, Staphylococcus epidermidis, and Staphylococcus aureus, which often coexist.

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5
Q

Clinical features of otitis externa?

A

Peak seasons for OE are spring and summer, and the peak age is 9 to 19 years. Symptoms include earache, itching, and, less commonly, fever. Signs include erythema, edema of EAC, white exudate on EAC and TM, pain with motion of the tragus or auricle, and periauricular or cervical adenopathy.

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6
Q

Treatment of otitis externa?

A

Cleaning the ear canal with a small tuft of cotton attached to a wire applicator is the first step. Place a wick in the canal if significant edema obstructs the EAC.

Treat mild OE with acidifying agents alone, such as 2% acetic acid (VoSol).

Consider oral analgesics, such as ibuprofen at 10 milligrams/kilogram/dose every 6 hours.

Fluoroquinolone otic drops are now considered the preferred agents over neomycin containing drops. Ciprofloxacin with hydrocortisone, 0.2% and 1% suspension (Cipro HC), 3 drops twice daily or ofloxacin 0.3% solution 10 drops twice daily can be used. Ofloxacin is used when TM rupture is found or suspected.

Oral antibiotics are indicated if auricular cellulitis is present.

Follow-up should be advised if improvement does not occur within 48 hours; otherwise routine follow-up is not recommended. Malignant OE is characterized by systemic symptoms and auricular cellulitis. This condition can result in serious complications and requires hospitalization with parenteral antibiotics.

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7
Q

Major pathogens of acute bacterial sinusitis?

A

The major pathogens in childhood are Streptococcus pneumoniae, Moraxella catarrhalis, and nontypeable Haemophilus influenzae.

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8
Q

Clinical features of acute bacterial sinusitis?

A

Two major types of sinusitis may be differentiated on clinical grounds: acute severe sinusitis and mild subacute sinusitis. Acute severe sinusitis is associated with elevated temperature, headaches, and localized swelling and tenderness or erythema in the facial area corresponding to the sinuses. Such localized findings are seen most often in older adolescents. Mild subacute sinusitis is manifest in childhood as a protracted upper respiratory infection associated with purulent nasal discharge persisting in excess of 2 weeks. Fever is infrequent. Chronic sinusitis may be confused with allergies or upper respiratory infections.

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9
Q

Management of acute bacterial sinusitis?

A

Patients with mild symptoms suggestive of a viral infection can be observed for 7 to 10 days, with no antibiotics prescribed. Suspect acute bacterial sinusitis if symptoms persist or are severe: fever > 39°C, purulent nasal drainage for > 3 days and ill-appearance.

For children with mild to moderate sinusitis, treat with amoxicillin (40–50 milligrams/kilogram/dose PO twice daily) for 10 to 14 days.

For children who present with severe symptoms, are in day care or have recently been treated with antibiotics, prescribe oral second- and third-generation cephalosporins such as cefprozil (7.5 to 15 milligrams/kilogram PO twice a day), cefuroxime (15 milligrams/kilogram PO twice a day), and cefpodoxime (5 milligrams/kilogram PO twice a day).

Intranasal steroids have shown modest benefits and are recommended if antibiotics do not result in improvement in the first 3 to 4 days of treatment.
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10
Q

Modified Centor Criteria?

A
The patients are judged on four criteria, with one point added for each positive criterion:
    History of fever
    Tonsillar exudates
    Tender anterior cervical adenopathy
    Absence of cough

The Modified Centor Criteria add the patient’s age to the criteria:
Age 44 subtract 1 point

The point system is important in that it dictates management. Guidelines for management state:

0 or 1 points - No antibiotic or throat culture necessary (Risk of strep. infection <10%)
2 or 3 points - Should receive a throat culture and treat with an antibiotic if culture is positive (Risk of strep. infection 32% if 3 criteria, 15% if 2)
4 or 5 points - Treat empirically with an antibiotic (Risk of strep. infection 56%)

The presence of all four variables indicates a 40 - 60% positive predictive value for a culture of the throat to test positive for Group A Streptococcus bacteria. The absence of all four variables indicates a negative predictive value of greater than 80%.The high negative predictive value suggests that the Centor Criteria can be more effectively used for ruling out strep throat than for diagnosing strep throat.

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11
Q

Clinical features of Herpangina, hand, foot, and mouth disease (HFM)?

A

Herpangina causes a vesicular enanthem of the tonsils and soft palate, affecting children 6 months to 10 years of age during late summer and early fall. The vesicles are painful and can be associated with fever and dysphagia. HFM disease usually begins as macules which progress to vesicles of the palate, buccal mucosa, gingiva, and tongue. Similar lesions may present on the palms of hands, soles of feet, and buttocks. Herpes simplex gingivostomatitis often presents with abrupt onset of fever, irritability, and decreased oral intake with edematous and friable gingiva. Vesicular lesions often with ulcerations are seen in the anterior oral cavity.

Treatment is supportive. Parental fluids PRN if child cannot tolerate orally.

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12
Q

Clinical features of GAS pharyngitis?

A

Peak seasons for GABHS are late winter or early spring, the peak age is 5 to 15 years, and it is rare before the age of 2. Symptoms (sudden onset) include sore throat, fever, headache, abdominal pain, enlarged anterior cervical nodes, palatal petechiae, and hypertrophy of the tonsils. With GABHS there is usually the absence of cough, coryza, laryngitis, stridor, conjunctivitis, and diarrhea. A scarlatinaform rash associated with pharyngitis almost always indicates GABHS and is commonly referred to as scarlet fever.

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13
Q

Clinical features of EBV?

A

Ebstein Barr Virus (EBV) is a herpes virus and often presents much like streptococcal pharyngitis. Common symptoms are fever, sore throat, and malaise. Cervical adenopathy may be prominent and often is posterior and anterior. Hepatosplenomegaly may be present. EBV should be suspected in the child with pharyngitis nonresponsive to antibiotics in the presence of a negative throat culture.

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14
Q

Clinical features of gonococcal pharyngitis?

A

Gonococcal pharyngitis in children and nonsexually active adolescents should alert one to the possibility of sexual abuse. Gonococcal pharyngitis may be associated with infection elsewhere including proctitis, vaginitis, urethritis, or arthritis.

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15
Q

Diagnosis of EBV pharyngitis?

A

Diagnosis of EBV is often clinical. A heterophile antibody (monospot) can aid in the diagnosis. The monospot may be insensitive in children < 2 years of age and is often negative in the first week of illness. If obtained, the white blood cell count may show a lymphocytosis with a preponderance of atypical lymphocytes.

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16
Q

Diagnosis of gonococcal pharyngitis?

A

Diagnosis of gonococcal pharyngitis is made by culture on Thayer-Martin medium. Vaginal, cervical, urethral, and rectal cultures also should be obtained if gonococcal pharyngitis is suspected.

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17
Q

Diagnosis of GAS pharyngitis?

A

Centor criteria –> rapid. If rapid negative then send to culture.

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18
Q

Treatment of GAS pharyngitis?

A

Antibiotics for the treatment of GABHS pharyngitis should be reserved for patients with a positive rapid antigen test or culture. Antibiotic choices for GABHS include penicillin V (children 250 milligrams PO twice daily, adolescent/adult 500 milligrams PO twice daily); benzathine penicillin G 1.2 million units IM (600,000 units IM for patients weighing less than 27 kg); and erythromycin ethylsuccinate 10 to 20 milligrams/kilogram/dose PO given twice daily for 10 days. Antipyretics and analgesics should be routinely prescribed until symptoms resolve.

Reality: amox

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19
Q

Treatment of gonococcal pharyngitis?

A

Treat gonococcal pharyngitis with ceftriaxone 250 milligrams IM. When gonococcal pharyngitis is suspected, empiric treatment of chlamydia is recommended with azithromycin 1 gram PO given in the emergency department. Appropriate follow-up should be encouraged for treatment failure and symptomatic contacts. Follow-up for suspected gonococcal pharyngitis should include local reporting agencies and social service investigations.

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20
Q

Treatment of EBV pharyngitis?

A

EBV is usually self-limited and requires only supportive treatment including antipyretics, fluids, and rest. A dose of dexamethasone 0.5 milligrams/kilogram PO to a maximum of 10 milligrams once may be given for more severe disease presentations

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21
Q

Clinical features, DDx and Dx of cervical lymphadenitis?

A

Cervical Lymphadenitis

Acute, unilateral cervical lymphadenitis is commonly caused by Staphylococcus aureus or Streptococcus pyogenes. Bilateral cervical lymphadenitis is often caused by viral entities such as EBV and adenovirus. Chronic cervical lymphadenitis is less common but may be caused by Bartonella henselae (also called occuloglandular fever) or Mycobacterium species.

Clinical Features

Acute cervical lymphadenitis presents with tender, 2 to 6 cm nodes often with overlying erythema. Bilateral cervical lymphadenitis presents with small, rubbery lymph nodes and usually self-resolves. Bartonella results from the scratch of a kitten with ipsilateral cervical lymphadenitis and often concurrent conjunctivitis.

Diagnosis and Differential

Most cases are diagnosed clinically, although culture may guide effective antimicrobial treatment. Differential may also include sialoadenitis (infection of the salivary glands), which is usually caused by Staphyloccocus aureus or Streptococcus pyogenes, as well as gram-negative and anaerobic bacteria.

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22
Q

Treatment of cervical lymphadenitis?

A

Either amoxicillin plus clavulanic acid, 30 to 40 milligrams/kilogram/dose given twice daily or clindamycin 10 to 15 milligrams/kilogram/dose given three times daily are recommended first line antibiotics for the treatment of acute cervical lymphadenitis.

The presence of a fluctuant mass may require incision and drainage in addition to antimicrobial therapy.

Most cases of acute bilateral cervical lymphadenitis resolve without antibiotics, as they often represent viral infection or reactive enlargement. Chronic cases of lymphadenitis are often treated surgically, with directed antimicrobial therapy in some cases depending on clinical diagnosis.

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23
Q

Normal vegetative functions in a neonate?

A

Bottle-fed infants generally take 6 to 9 feedings (2 to 4 oz) in a 24-hours period, with a relatively stable pattern developing by the end of the first month of life. Breast-fed infants generally prefer feedings every 1 to 3 hours. Infants typically lose up to 12% of their birth weight during the first 3 to 7 days of life. After this time, infants are expected to gain about 1 oz/d (20 to 30 grams) during the first 3 months of life. The number, color, and consistency of stool in the same infant changes from day to day and differs among infants. Normal breast-fed infants may go 5 to 7 days without stooling or have 6 to 7 stools per day. Color has no significance unless blood is present or the stool is acholic (ie, white).

A normal respiratory rate for a neonate is from 30 to 60 breaths/min. Periodic breathing (alternating episodes of rapid breathing with brief (< 5 to 10 seconds) pauses in respiration) is usually normal. Normal newborns awaken at variable intervals that can range from about 20 minutes to 6 hours. Neonates and young infants tend to have no differentiation between day and night until approximately 3 months of age.

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24
Q

DDx inconsolability

A
Corneal abrasion
Hair tourniquet (finger, toe, penis)
Stomatitis
Intracranial hemorrhage
Fracture (nonaccidental trauma)
Nasal obstruction/congestion
Inborn error of metabolism
Acute infection (sepsis, urinary tract infection, meningitis)
Congenital heart disease (including supraventricular tachycardia)
Abdominal emergency (incarcerated hernia, volvulus, intussusception)
Testicular torsion
Encephalitis (herpes)
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25
Q

Colic

A

Intestinal colic is the most common cause of excessive (but not inconsolable) crying. The cause is unknown. The incidence is about 13% of all neonates. The formal definition includes crying for at least 3 hours per day for at least 3 days per week over a 3-week period. Intestinal colic seldom lasts beyond age 3 months. No effective treatment has been identified. In general, the initial diagnosis of colic is not made in the emergency department and it is a diagnosis of exclusion.

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26
Q

Fever in a neonate - management

A

Fever in the neonate (age 28 days or younger) is defined as the history of documented fever by a parent or presence of a rectal temperature of 38°C (100.4°F) or higher in the ED. Fever in the neonate must be taken seriously, and at this point in time the proper management includes a complete septic work-up, administration of parenteral antibiotics, and admission.

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27
Q

Blood in stool - neonate

A

Although bacterial infection may cause bloody diarrhea, this is rare in neonates. The most common causes of blood in the stool in infants younger than 6 months are cow’s milk intolerance and anal fissures. Breast-fed infants may have heme-positive stool from swallowed maternal blood due to bleeding nipples. Necrotizing enterocolitis may present as bloody diarrhea and usually presents with other signs of sepsis (eg, jaundice, lethargy, fever, poor feeding, or abdominal distention). Abdominal radiography may demonstrate pneumatosis intestinalis or free air.

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28
Q

Constipation in neonate - when is it

  • DDx
  • management
A

Infrequent bowel movements in neonates do not necessarily mean that the infant is constipated. Stool patterns can be quite variable and breast-fed infants may go 1 week without passing stool and then pass a normal stool. Inquire about the passage of meconium in the first 24 to 48 hours of life; infants without normal stooling in the first 2 days of life may have anatomic anomalies (eg, intestinal stenosis or atresias), cystic fibrosis, Hirschsprung disease, or meconium ileus or plug. Constipation that develops later in the first month of life suggests Hirschsprung disease, hypothyroidism, anal stenosis, or anterior anus. Rarely, botulism can present with constipation that precedes neurologic symptoms (cranial nerve deficits, hypotonia, weak cry). Laxatives and enemas are contraindicated in neonates.

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29
Q

Clinical signs of sepsis in infant?

A

Clinical signs may be vague and subtle in the young infant, including lethargy, poor feeding, irritability, or hypotonia. Fever is common; however, very young infants may be hypothermic. Tachypnea and tachycardia are usually present as a result of fever but also may be secondary to hypoxia and metabolic acidosis. Sepsis can rapidly progress to shock, manifest as prolonged capillary refill, decreased peripheral pulses, altered mental status, and decreased urinary output. Hypotension is usually a very late sign of septic shock in children and, in conjunction with respiratory failure and bradycardia, indicates a grave prognosis

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30
Q

Clinical features and diagnosis of meningitis in children

A

Meningitis may present with the subtle signs that accompany less serious infections, such as otitis media or sinusitis. Irritability, inconsolability, hypotonia, and lethargy are most common in infants. Older children may complain of headache, photophobia, nausea, and vomiting and exhibit the classic signs of meningismus with complaints of neck pain. Occasionally, meningitis presents as a rapidly progressive, fulminant disease characterized by shock, seizures, or coma, or with febrile status epilepticus

Diagnosis is made by lumbar puncture and analysis of the cerebrospinal fluid (CSF). The CSF should be examined for white blood cells, glucose, and protein and undergo Gram stain and culture. Herpes encephalitis should be considered in the seizing neonate and any child with CSF pleocytosis. In the presence of immunocompromise, infections with opportunistic or unusual organisms should be considered. Cranial computed tomography should be performed before lumbar puncture in the presence of focal neurologic signs or increased intracranial pressure..

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31
Q

Initial antibiotics for neonate with sepsis/meningitis?

A

Ampicillin, 100 milligrams/kilogram

plus

Cefotaxime, 50 milligrams/kilogram

HSc uses amp and gent

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32
Q

DDx stridor in child

A

Laryngomalacia, due to a developmentally weak larynx, accounts for 60% of stridor in the neonatal period, but is self-limited and rarely requires treatment. Common causes of stridor in children > 6 months of age discussed here include viral croup, epiglottitis, bacterial tracheitis, airway foreign body, retropharyngeal abscess, and peritonsillar abscess. Other etiologies include Ludwig’s angina and oropharyngeal trauma

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33
Q

Clinical features of croup (laryngotracheobronchitis)

A

Viral croup is responsible for most cases of stridor after the neonatal period. It is usually a benign, self-limited disease caused by edema and inflammation of the subglottic area. Children ages 6 months to 3 years are most commonly affected, with a peak at an age of 12 to 24 months.

Croup occurs mainly in late fall and early winter, typically, beginning with a 1- to 5-day prodrome of cough and coryza, followed by a 3- to 4-day period of classic barking cough, though cough and stridor may be abrupt in onset. Symptoms peak on days 3 to 4 and are often perceived as more severe at night. Physical examination classically shows a biphasic stridor, although the inspiratory component usually is much greater.

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34
Q

Diagnosis and DDx of croup

A

The diagnosis of croup is clinical: a barking, seal-like cough and history or finding of stridor in the appropriate setting is diagnostic. The differential diagnosis includes epiglottitis, bacterial tracheitis, or foreign body aspiration. Radiographs are not necessary, unless other causes are being considered. Lateral neck and chest radiographs may demonstrate the normally squared shoulders of the subglottic tracheal air shadow as a pencil tip, hourglass, or “steeple sign” though this sign is neither sensitive nor specific for croup.

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35
Q

Management of croup?

A

Patients with significant stridor should be kept in a position of comfort with minimal disturbance; monitor pulse oximetry and provide oxygen as needed.

Administer dexamethasone 0.15 to 0.6 milligrams/kilogram (10 milligrams max) PO or IM (may use the IV formulation orally). Nebulized budesonide (2 milligrams) may be clinically useful in moderate to severe cases. Even patients with very mild croup symptoms benefit from steroids, therefore most ED patients diagnosed with croup should be treated with corticosteroids.

Nebulized racemic epinephrine, 0.05 mL/kg/dose up to 0.5 mL of a 2.25% solution, should be used to treat moderate to severe cases (significant stridor at rest). Alternatively L-epineprhine (1:1000), 0.5 mL/kg (to a maximum of 5 mL) can be used. Children with stridor associated only with agitation do not need epinephrine.

Although intubation should be performed when clinically indicated, aggressive treatment with epinephrine results in less than a 1% intubation rate. When necessary, consider a smaller endotracheal tube than estimated by age to avoid trauma to the inflamed mucosa.

Helium plus oxygen (Heliox), typically in a 70:30 mixture, may prevent the need for intubation in the most severe cases. Heliox can be effectively given with a maximum oxygen concentration of 40%, therefore, patients requiring higher FiO2 are not candidates for Heliox.

Children with persistent stridor at rest, tachypnea, retractions, and hypoxia or those who require more than two treatments of epinephrine should be admitted to the hospital.

Discharge criteria include the following: at least 3 hours since the last dose of epinephrine, nontoxic appearance, no clinical signs of dehydration, room air oxygen saturation greater than 90%, parents able to recognize changes in the patient’s condition, and no social concerns with access to telephone and relatively short transit time to the hospital.

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36
Q

Clinical features, dx and ddx of epiglottitis

A

Epiglottitis is life threatening and can occur at any age. Historically caused by Haemophilus influenza, vaccination has decreased the occurrence of epiglottitis and shifted the median age of presentation toward older children and adults. In immunized children, most cases are caused by strep and staph species.

Clinical Features

Classically, there is abrupt onset of high fever, sore throat, and drooling. Symptoms may progress rapidly to stridor and respiratory distress. Cough may be absent and the voice muffled. The patient is toxic in appearance and may assume a tripod or sniffing position to maintain the airway. The presentation in older children and adults can be subtler. The only complaint may be severe sore throat, with or without stridor. The diagnosis is suggested by severe sore throat, normal-appearing oropharynx, and a striking tenderness with gentle movement of the hyoid.

Diagnosis and Differential

Radiographs are usually unnecessary to make the diagnosis in patients with a classic presentation. If the diagnosis is uncertain, then lateral neck films should be taken at the bedside in extension and during inspiration with a minimum of disturbance. If it is necessary for the patient to be moved to the radiology suite, a physician trained in airway management should be present at all times. The epiglottis is normally tall and thin, but in epiglottitis, it is very swollen and appears squat and fat like a thumbprint (called the “thumb sign”) at the base of the hypopharynx. False negative radiographic evaluations do occur, and, if suspicion remains, gentle direct visualization of the epiglottis is necessary to exclude the diagnosis. Blood cultures are positive in up to 90% of patients, whereas cultures from the epiglottis are less sensitive.

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37
Q

Management of epiglottitis?

A

Keep the patient seated and upright. Provide oxygen and administer nebulized racemic or L-epinephrine . Heliox also can be attempted.

In the event of total airway loss, attempt bag-valve-mask ventilation.

Alert a referral center or pediatric otolaryngologist to coordinate decisions regarding definitive management.

The most experienced individual should perform intubation as soon as the diagnosis is made. Use sedation, paralytics, and vagolytics as indicated. Multiple endotracheal tube sizes must be immediately available. For the patient who is able to maintain their airway, use of paralytics must be accompanied by the certainty that intubation will be successful or that a surgical airway can immediately be performed if unsuccessful.

Steroids may be employed to decrease mucosal edema of the epiglottis. Use methylprednisolone 1 milligram/kilogram IV every 6 hours or dexamethasone 0.15 to 0.6 milligrams/kilogram IV.

Administer antibiotics only after airway management: cefuroxime 50 milligrams/kilogram IV per dose, cefotaxime 50 milligrams/kilogram IV per dose, or ceftriaxone 50 milligrams/kilogram IV per dose are appropriate empiric options. In regions with increased cephalosporin resistance, vancomycin 10 milligrams/kilogram/dose should be added.

38
Q

Bacterial tracheitis - presentation, ddx, management

A

Bacterial tracheitis (membranous laryngotracheobronchitis or “bacterial croup”) is uncommon and can present as either a primary or secondary infection. The mean age of presentation is between 4 and 8 years of age, compared with younger ages as had been previously described. It is usually caused by S aureus, S pneumoniae, or -lactamase–producing gram-negative organisms (Haemophilus influenza and Moraxella catarrhalis).

Clinical Features

Patients with bacterial tracheobronchitis have more respiratory distress than do patients with croup. Children appear septic and present similarly to those with epiglottitis, with the following exceptions: severe inspiratory and expiratory stridor, occasionally with thick sputum production, and a raspy hoarse voice but no dysphagia.

Diagnosis and Differential

Radiographs of the lateral neck and chest usually demonstrate subglottic narrowing of the trachea with irregular densities and ragged and indistinct borders.

Emergency Department Care and Disposition

Manage patients as above for epiglottitis; more than 85% require intubation. Ideally, perform intubation and bronchoscopy in the operating room where cultures and Gram stain may be obtained to guide antibiotic therapy.

Administer empiric parenteral antibiotics: ampicillin/sulbactam 50 milligrams/kilogram/dose or ceftriaxone 50 milligrams/kilogram IV per dose plus clindamycin 10 milligrams/kilogram/dose. In areas with increasing S. aureus resistance, consider the addition of vancomycin 10 milligrams/kilogram IV every 6 hours.

39
Q

FB aspiration - clinical features, ddx and management

A

At presentation many patients are asymptomatic. There may or may not be a witnessed aspiration. The primary symptom is cough, which is classically abrupt in onset, and may be associated with gagging, choking, stridor, or cyanosis. Signs depend on the location of the FB and the degree of obstruction: stridor with a FB in the laryngotracheal area; wheezing with a bronchial FB. Symptoms are unreliable in localizing the level of FB, however: wheeze is present in 30% of laryngotracheal FB aspirations and stridor is found in up to 10% of bronchial aspirations. Eighty percent to 90% of FBs are located in the bronchus. Patients with immediate onset of severe stridor and cardiac arrest usually have laryngotracheal aspirations.

Diagnosis and Differential

FB aspiration is easily confused with more common causes of upper respiratory diseases because 36% of patients have fever, 35% have wheezes, and 38% have rales. Plain chest radiographs can be normal in > 50% of tracheal FB and 25% of bronchial FB; more than 75% of FB in children < 3 years of age are radiolucent. In cases of complete obstruction, atelectasis may be found. In partial obstructions, a ball valve effect occurs, with air trapping caused by the FB leading to hyperinflation of the obstructed lung. Thus, in a stable cooperative child, inspiratory and expiratory posteroanterior chest radiographs may be helpful. In a stable but noncooperative child, decubitus films may be used but are less sensitive than fluoroscopy. FB aspiration is definitively diagnosed preoperatively in only one-third of cases; thus, if clinically suspected, laryngoscopy is indicated.

Upper esophageal FB are usually radiopaque and can impinge on the posterior aspect of the trachea. Patients may present with stridor, and typically have dysphagia. Radiographically, flat FBs such as coins are usually oriented in the sagittal plane when located in the trachea (which appear as a thick line in an anterioposterior chest radiograph) and in the coronal plane when in the esophagus (which appear round on an anterioposterior chest radiograph).

Emergency Department Care and Disposition

If FB aspiration or airway obstruction is clearly present, perform BLS procedures to relieve airway obstruction (see Chapter 3).

If BLS maneuvers fail, undertake direct laryngoscopy with Magill forceps to remove the FB. If the FB cannot be seen, orotracheal intubation with dislodgement of the FB distally may be lifesaving.

Consider racemic epinephrine or Heliox as symptomatic palliatives.

Definitive treatment usually requires rigid bronchoscopy in the operating room under general anesthesia.

40
Q

Retropharyngeal abscess - clinical features, dx and management

A

Retropharyngeal abscess is the second most commonly seen deep neck infection, and usually occurs in children between 6 months and 4 years of age. Patients classically appear toxic and present with fever, drooling, dysphagia, and inspiratory stridor. Patients may hold their neck in an unusual position with torticollis, hyperextension, or stiffness. Dysphagia and refusal to feed occur before significant respiratory distress. Patients may develop rapidly fatal airway obstruction from sudden rupture of the abscess pocket. Aspiration pneumonia, empyema, mediastinitis, and erosion into the jugular vein and carotid artery are reported complications.

Diagnosis and Differential

Physical examination of the pharynx may show a retropharyngeal mass. Although palpation commonly will demonstrate fluctuance, this could lead to rupture of the abscess. Lateral neck radiograph performed during inspiration may show a widened retropharyngeal space. The diagnosis is suggested when the retropharyngeal space at C2 is twice the diameter of the vertebral body or greater than one half the width of C4. CT of the neck with IV contrast is thought to be almost 100% sensitive and very helpful in differentiation between cellulitis and abscess.

Emergency Department Care and Disposition

Immediate airway stabilization is the first priority. Intubate unstable patients before performing CT.

Antibiotic choice is controversial because most retropharyngeal abscesses contain mixed flora. Consider ampicillin/sulbactam 50 milligrams/kilogram/dose IV hours and/or clindamycin 10 milligrams/ kilogram IV hours. Substitute ceftriaxone 50 milligrams/kilogram/dose for ampicillin/sulbactam in the penicillin-allergic patient.

Consider adjunctive treatment with parenteral steroids (eg, dexamethasone 0.15 to 0.6 milligrams/kilogram IV to a maximum of 10 milligrams).

Consult otolaryngology for operative incision and drainage as indicated. Although cellulitis and some very small abscesses may do well with antibiotics alone, most require surgery.

41
Q

Peritonsillor abscess - clinical features, dx and management

A

Peritonsillar abscess in children most commonly presents in adolescents with an antecedent sore throat. Patients usually appear acutely ill with fevers, chills, dysphagia/odynophagia, trismus, drooling, and a muffled “hot potato” voice.

The uvula is displaced away from the affected side. As a rule, the affected tonsil is anteriorly and medially displaced.

Diagnosis and Differential

The diagnosis can typically be made through careful visualization of the oral cavity. Classic findings include uvular deviation away from the abscess, soft palate displacement, trismus, and localized fluctuance; airway compromise may occur. In typical cases, imaging studies are unnecessary, though in patients with toxic appearance or atypical exam findings, computed tomography (CT) with contrast or ultrasound is indicated.

Emergency Department Care and Disposition

Treat most cases with needle aspiration, antibiotics, and pain control. Administer topical (eg, benzocaine or endocaine spray), oral (eg, oxycodone or vicodin), or parenteral (eg, fentanyl, morphine) analgesics, then aspirate the abscess using a large gauge needle. Avoid deep penetration which could injure adjacent vascular structures and result in significant bleeding. The last centimeter of the tip of a needle guard can be cut off, and carefully reattached to the aspirating syringe, covering all but the end of the needle, to limit the depth of penetration.

Consider clindamycin 10 milligrams/kilogram IV hours or ampicillin/sulbactam 50 milligrams/kilogram/dose IV hours. Definitive follow-up is essential in all cases. Oral antibiotics for outpatient treatment include amoxicillin/clavulanate 22.5 milligrams/kilogram/dose given twice daily.

Formal incision and drainage in the operating room is sometimes necessary, especially in young or uncooperative patients. Most patients can be discharged safely on oral antibiotics following drainage

42
Q

ED care of Asthma?

A

An inhaled 2-agonist, most often albuterol, is the mainstay of acute asthma therapy.

Administer oxygen for saturations below 95%.

Give albuterol by metered-dose inhaler with spacer (4 to 8 puffs every 20 min x 3 doses then Q 1 to 4 hours); or by intermittent nebulization (0.15 milligram/kilogram, minimum 2.5 milligrams, every 20 min x 3 doses, then 0.15-0.3 milligram/kilogram up to 10 milligrams every 1 to 4 hours); or continuously (0.5 milligram/kilogram/h).

Administer systemic corticosteroids in all but the mildest cases that respond immediately to albuterol. Early administration, even at the time of triage, decreases hospital admission rates. Prednisone or prednisolone (2 milligrams/kilogram/d, maximum 60 milligrams/d) are the preferred agents. A 3 to 5 day course is usually sufficient and does not require tapering. These medications are generally contraindicated in varicella-susceptible patients who have or might have exposure to varicella. Dexamethasone (0.6 milligram/kilogram to a maximum of 10 milligrams) may be used as a single dose in lieu of a short burst of shorter acting steroid. The IV formulation may be given orally and may be associated with less vomiting than prednisolone.

Give ipratropium with nebulized or meter-dosed albuterol (0.25 to 0.5 milligram Q 20 min x 3 doses).

Systemic -agonists have no advantage over inhaled albuterol except in the patient with minimal ventilation. Terbutaline has selective 2 activity and can be administered SQ (0.01 milligram/kilogram, maximum 0.4 milligram, Q 20 min x 3 doses) or IV (0.01 milligram/ilogram load over 5 to 10 min then 0.001 to 0.01 milligram/kilogram/min). Epinephrine continues to be used by some clinicians for its -agonist activity that may shrink edematous mucosa (SQ: 0.01 milligram/kilogram, maximum 0.5 milligram, Q 15 min).

Consider magnesium sulfate (50 to 75 milligram/kilogram, maximum 2 grams, IV over 10 to 20 min) in the patient with poor ventilation.

Consider ketamine (2 milligrams/kilogram IV followed by 2 to 3 milligrams/kilogram/h) in severe disease to delay or prevent respiratory failure and the need for assisted ventilation.

Helium-oxygen (Heliox) as a 60:40 or 70:30 (helium:oxygen) mix may restore laminar airflow and improve alveolar ventilation. Nebulized albuterol may be administered with this treatment. A maximum FiO2 of 40% can be administered with helium so patients requiring high concentrations of oxygen are not candidates for this therapy.

Administer IV fluids (normal saline) to patients in status asthmaticus who have decreased oral intake or are NPO due to the severity of the episode.

Admit children to the hospital who do not respond adequately to treatment (eg, persistent hypoxemia or failure to normalize aeration over 2 to 4 hours) or whose caretaker may not be able to provide necessary ongoing care.

Respiratory failure may be avoided by rapid escalation of the above treatments. However, patient fatigue or persistent bronchospasm may nonetheless occur, and for this reason the need for endotracheal intubation and mechanical ventilation should be anticipated and planned for. Because laryngoscopy may precipitate severe laryngo- or bronchospasm, the decision to intubate should be carefully considered. The most experienced operator available should perform the procedure, and a carefully considered sequence of rapid-sequence intubation medications chosen. These often include premedication with atropine (0.02 milligram/kilogram, minimum 0.5 milligram; maximum 1 milligram) and lidocaine (1.5 milligrams/kilogram) and sedation with ketamine (2 milligrams/kilogram), followed by paralysis using succinylcholine (2 milligrams/kilogram) or rocuronium (1 milligram/kilogram) to provide optimal intubating conditions.

Discharge planning should include an “action plan” (available at http://www.nhlbi.nih.gov.proxy2.lib.umanitoba.ca/health/public/lung/asthma/actionplan_text.htm), albuterol as MDI or nebulizer, oral steroids, and follow-up with the primary care provider.

43
Q

Asthma - clinical features and dx

A

The patient with an acute exacerbation may present with cough, wheezing, shortness of breath, chest tightness and/or chest pain. Cough is as frequent a manifestation as wheezing, and wheezing may be absent if airway obstruction is severe. Rales or rhonchi may be present but are usually due to atelectasis and thus are localized and clear with bronchodilator treatment. Tachypnea is a sensitive sign, and together with accessory muscle use is an accurate measure of severity. Elevation of pulsus paradoxus, decreased aeration on chest auscultation, and patient fatigue are potential signs of impending respiratory failure.

Hypoxemia is usually mild (SpO2 > 92%) and due to V/Q mismatch, which may worsen during initial treatment with bronchodilators for a period of 1 to 2 hours requiring oxygen therapy. If available, end-tidal CO2 (ETCO2) by capnometry should be monitored during severe exacerbations. Hypocapnia is expected early in the course of an asthma exacerbation, thus a normal or minimally elevated ETCO2 may be a sign of impending ventilatory failure.

Diagnosis and Differential

The diagnosis of bronchospasm is made clinically. The chronic diagnosis of asthma is rarely made in the ED, as spirometry, the criterion standard, is not routinely available in the ED. Although peak expiratory flow is often recommended for children > 5 years, it frequently underestimates the severity of airway obstruction. If available, FEV1 is the preferred measure of severity, with percent predicted level defining severity: 40% correlates with mild-moderate airway obstruction, and < 40% correlates to a severe exacerbation.

Because viral infections are the most common precipitant of asthma exacerbations in children, and because fever is a common associated sign, fever alone does not indicate the need for a chest radiograph. It may be considered for infants and young children with a first episode of wheezing to exclude anatomic abnormalities or foreign body. For others, a radiograph is indicated when localized findings (rales or decreased breath sounds) do not resolve with bronchodilator treatment or when there is concern for possible pneumothorax (pain or significant hypoxia) or foreign body. The pediatric respiratory assessment measure (PRAM) is one of the few severity scores that has been validated, and each ED should have a preferred score to facilitate severity assessment and communication amongst providers.

The differential diagnosis of wheezing in infants and children is extensive and should consider patient age, presenting signs and symptoms, overall clinical course, and results of ancillary testing, if indicated.

44
Q

Clinical features and dx of bronichiolitis?

A

Bronchiolitis is the most frequent lower respiratory infection in the first 2 years of life and is most commonly caused by respiratory syncytial virus (RSV). Infection causes acute airway inflammation and edema, small airway epithelial cell necrosis and sloughing, increased mucus production and mucus plugs, and bronchospasm, all of which can vary considerably between patients and during the course of the illness.

Clinical Features

Most patients have rhinorrhea typical of an upper respiratory infection (URI) in addition to variable signs and symptoms of lower respiratory infection, including fever, wheezing, tachypnea, cough, rales, use of accessory muscles and nasal flaring. Apnea is of great concern in young infants (see below), as is dehydration. Hypoxemia, cyanosis or altered mental status or fatigue are ominous signs and may portend respiratory failure. Management decisions should consider signs of severity as well as the typical time course for illness: severity increases over the first 3 to 5 days with total duration of illness 7 to 14 days. Sustained immunity does reliably occur, and reinfection with recurrence of illness is not uncommon.

Diagnosis and Differential

Diagnosis is clinical and does not require laboratory or radiologic studies. The above signs and symptoms occurring from November to March are sufficient for diagnosis. Serial observations (including pulse oximetry) and reassessment is key to determining disposition, and patients with risk factors for apnea and/or severe disease with possible respiratory failure should be identified early, including: (a) young developmental age (< 6–12 weeks) or: prematurity (< 37 weeks); (b) witnessed apnea, (c) hemodynamically significant congenital heart disease (on medication for CHF; moderate to severe pulmonary hypertension; cyanotic CHD), (d) chronic lung disease (bronchopulmonary dysplasia; congenital malformations; cystic fibrosis), and (e) immunocompromise.

Routine testing for RSV or other pathogens is indicated only if the information is necessary for placement decisions for hospitalized patients. Routine performance of radiographs increases inappropriate antibiotic use and does not change time to recovery. Radiographs are indicated only if other diseases or foreign body are suspected, or if the patient does not improve or whose disease is more severe than expected.

45
Q

Management of bronchiolitis

A

Nasal suctioning and saline drops: suctioning of the nasal passages after saline instillation may substantially decrease work of breathing, correct hypoxemia, and enable the patient to feed normally. Nasal vasoconstrictors are not indicated and have resulted in tachydysrrythmia.

Provide oxygen to maintain saturations > 90% to 92%.

Nebulized - and -agonists should not be routinely used. However, use of a 2-agonist (albuterol) might be considered, particularly if there is a personal or family history of asthma. Epinephrine (0.5 mL of 1:1000 in 2.5 mL saline) may be beneficial due to -agonist mediated mucosal vasoconstriction with reduction of edema. If these medications are used, an objective measure (eg, respiratory rate or bronchiolitis score) should be used to assess response.

Consider nebulized hypertonic saline (3% or 5%, 3 to 5 mL by nebulizer) to decrease mucus production and viscidity.

Provide isotonic IV fluids (NS) if necessary. Patients with bronchiolitis may not be able to feed normally, and when respiratory rates exceed 60 to 70 breaths/min there is increased risk of aspiration of feedings.

Helium-oxygen (Heliox, see above) may delay or avoid respiratory failure and need for invasive ventilation in severe cases.

Corticosteroids should not be used routinely for patients with bronchiolitis. A trial of dexamethasone and epinephrine published in 2009 concluded that this combination was beneficial, however, the benefit was marginal and the doses of dexamethasone were large. Potential adverse effects of these medications and lack of sufficient evidence for benefit preclude their routine use.

Ventilatory support: noninvasive measures (CPAP or BiPAP) may improve oxygenation and ventilation, decrease work of breathing, and delay or obviate the need for endotracheal intubation. Additionally, application of CPAP may prevent further apnea in affected infants.

Decision for hospitalization: consider whether risk factors for apnea and/or severe disease are present (see Diagnosis above). Additional indications for hospitalization are persistent hypoxia, tachypnea, or abnormal work of breathing, and inability to feed or maintain hydration. Decision-making must also consider the time-point of disease progression (severity increases over the first 3 to 5 days of illness), the ability of caretakers to manage the illness, and the availability of follow-up.

46
Q

Pathogens common in neonates. What Abx do you use empirically?

A

Group B strept, E. coli, Listeria monocytogenes

Amp and gent or amp and cefotax

47
Q

Pathogens in the 1-3 month old. What Abx do you use empirically?

A

Group B strept, Strept pnumoniae, Hemophilus influenzae

Amp and cefotax or amp and ceftriaxone

48
Q

Pathogens in the 3-24 month old. What Abx do you use empirically?

A

S. pneumoniae, H. influenzae, S. aurus, N. meningitidis

Cefotax or ceftriaxone

49
Q

Pathogens to worry about in immunocomprimised pediatric patient. What Abx do you use empirically?

A

S. aureus, Proteus, Pseudomonas, Enterobacteriaceae

Vanco and ceftaz and ticarcillin or tobramycin or gentamicin

50
Q

“Classic” signs of meningitis?

A

Headache, photophobia, stiff neck, change in mental status, bulging fontanelle, nausea and vomiting.

51
Q

What is Brudzinski’s sign?

A

The irratated meninges are stretched, with neck flexion causing the knees and hips to flex involuntarily

52
Q

What is Kernig’s sign?

A

Nerve root irritation when hip is flexed to 90 degrees and the examiner is unable to passively extend the leg fully.

53
Q

How do you treat ICP?

A

Elevate head of bed to 30 degrees, controlled ventilation to keep PaCO2 between 30 and 35mmHg.

54
Q

Symptoms of toxic shock syndrome?

A

High fever, diffuse desquamating erythroderma, vomiting, abdominal pain, diarrhea, myalgaia and nonspecific neurological abnormalities. Hypotension can follow and be profound.

55
Q

Pathogen for TSS?

A

S. aureus of which 67% are phage type 1

56
Q

What is the other name for Kawasaki syndrome?

A

Mucocutaneous lymph node syndrome

57
Q

Age range for Kawasaki?

A

18 to 24 months with 80-85% cases occur before 5 years of age

58
Q

Diagnostic criteria for Kawasaki syndrome?

A

Fever persisting at least 5 days† and the presence of at least 4 of the following 5 principal features:

  1. Changes in extremities: Acute: Erythema and edema of hands and feet Convalescent: Membranous desquamation of fingertips
  2. Polymorphous exanthema
  3. Bilateral, painless bulbar conjunctival injection without exudate
  4. Changes in lips and oral cavity: Erythema and cracking of lips, strawberry tongue, diffuse injection of oral and pharyngeal mucosae
  5. Cervical lymphadenopathy (≥1.5 cm in diameter), usually unilateral
    * Patients with fever and fewer than 4 principal symptoms can be diagnosed as having Kawasaki disease when coronary artery disease is detected by 2-dimensional echocardiography or coronary angiography. Other diagnoses should be excluded. The physician should be aware that some children with illness not fulfilling these criteria have developed coronary artery aneurysms.

†Many experts believe that in the presence of classic features, the diagnosis of Kawasaki disease can be made by experienced observers before day 5 of fever.

59
Q

Phases of Kawasaki disease?

A

Acute (febrile) phase lasts 7 to 15 days and is the period where you see symptoms. Fever is high and sustained.

Subacute phase lasts 2 to 4 weeks and begins with resolution of fever and elevation of platelets. Desquamation occurs - first noted in periungual region with peeling underneath the finger and toenails. Complicaations such as coronary artery aneurysms and hydops of the gallbladder will develop. May have mild hemolytic anemia.

Recovery or covalescent phase - may last months or years. Coronary artery disease may be recognized here.

60
Q

Complications of Kawasaki?

A

Most serious are cardiac - coronary artery aneurysms, valvular insufficiency, CHF, myocardial infarction, dysrhythmia, rupture of aneurysms, and pericardial effusions.

Most common cause of early death in KS is MI in subacute phase.

Hydrops of gallbladder - self limited condition that occurs in 3% of patients and is functional rather than obstructive distention. Its an acalculous cholecystitis.

Other - complication include iridocyclitis or anterior uveitis ( ~80% of patients), mastoiditis, necrotic pharyngitis, renal infarcts, gangrene of the fingers and toes, encephalopathy and subarrachnoid hemorrhage.

61
Q

Management of KS?

A

Admit for IV gammaglobulin, aspirin therapy, and cardiac evaluation (echo). Will also need optho exam (anterior uveitis in up to 85% of patients)

Aspirin therapy in tiers - high (100mg/kg/day in 4 doses) until day 14 then low dose (3 to 5 mg/kg/day as single dose)

62
Q

Name three subclasses of helminths that cause parasitic infections.

A
  1. Nematodes - roundworms
  2. Cestodes - flatworms
  3. Trematodes - flukes
63
Q

Treatment for Ascaris lumbricoides?

A

Albendazole (400mg po) or pyrantly pamoate (11 mg/kg orally as a single dose; max 1g). If intenstinal obstruction, piperazine salts to facilitate rapid expulsion.

64
Q

Treatment for Enterobius vermicularis (pinworm)?

A

Mebendazole 100mg po as a single dose and then repeat at 2 weeks.

65
Q

Presentation of Giardia lamblia?

A

Flatulence, nonbloody diarrhea or constipation, abdominal distension, pain, fever, weight loss, and fat, carb and vitamin malabsorption.

66
Q

Treatment for scabies?

A

Single application of 5% permethrin cream for children over 2 months. Treat entire family (6 week incubation period)

67
Q

DDx of abdominal pain in 0-3 months?

A
Emergent:
Necrotizing enterocolitis
Volvulus
Testicular torsion
Incarcerated hernia
Trauma
Toxic megacolon
Tumor

Nonemergent:
Colic
Acute gastroenteritis
Constipation

68
Q

Ddx of abdominal pain 3 month to 3 years?

A
Emergent:
Intussusception
Testicular torsion
Trauma
Volvulus
Appendicitis
Toxic megacolon
Vaso-occlusive crisis
Nonemergent:
Acute gastroenteritis
Constipation
Urinary tract infections
Henoch-Schonlein purpura (HSP
69
Q

DDx of abdominal pain 3 years to adolescence?

A
Emergent:
Appendicitis
Diabetic ketoacidosis
Vaso-occlusive crisis
Toxic ingestion
Testicular torsion
Ovarian torsion
Ectopic pregnancy
Trauma
Toxic megacolon
Tumor
Nonemergent:
Constipation
Acute gastroenteritis
Nonspecific viral syndromes
Streptococcal pharyngitis
Urinary tract infections
Pneumonia
Pancreatitis
Cholecystitis
Renal stones
HSP
Inflammatory bowel disease
Gastric ulcer disease/gastritis
Ovarian cyst
Pregnancy
Pelvic inflammatory disease
70
Q

How does a volvulus present?

A

Malrotation of the intestine can present with life-threatening volvulus. Symptoms include bilious vomiting, abdominal distention, and obstipation, or, occasionally, streaks of blood in the stool. The vast majority of cases presents within the first month of life. Patients are ill appearing and may present in compensated or decompensated shock. Distended loops of bowel overriding the liver on abdominal radiographs, and a “bird’s beak” appearance on an upper GI series are suggestive of this diagnosis. Immediate surgical consultation and aggressive fluid resuscitation are critical to maximize outcomes.

71
Q

How does pyloric stenosis present?

A

Pyloric stenosis usually presents with progressive nonbilious, projectile vomiting occurring just after feeding. Infants with pyloric stenosis are often described by parents as ravenous. Pyloric stenosis occurs most commonly in the third or fourth week of life, is familial and more common in first-born males. A left upper quadrant pyloric mass, or “olive,” may be present, and peristaltic waves may be noted following a feeding trial in the ED. Ultrasound is the imaging modality of choice. Electrolytes may demonstrate a characteristic hypochloremic metabolic alkalosis, which must be corrected prior to definitive surgical care. While pyloric stenosis is not a surgical emergency, the resultant dehydration from persistent vomiting requires immediate medical treatment.

72
Q

How does intussusecption present?

A

Intussusception occurs when one portion of the bowel telescopes into another, which can result in a partial or complete obstruction, bowel-wall edema, and eventually ischemia. The greatest incidence occurs between 6 to 18 months of age. The classic presentation of intermittent paroxysms of abdominal pain with pain-free intervals (or lethargy), vomiting (may be bilious) and “currant jelly stool” are not present in all patients. Stool guaiac testing may reveal occult blood. Providers must have a high index of suspicion for intussusception in patients presenting with nonspecific changes in mental status or who are ill appearing without any apparent etiology. In equivocal cases, ultrasound is a sensitive test with a high negative predictive value and may demonstrate the classic “target sign”. In more classic cases, air or barium enema can be both diagnostic and therapeutic. Radiologic reduction requires the presence of a pediatric surgeon for irreducible cases or perforation during the procedure.

73
Q

How does constipation present? What do you need to think of in regards to serious pathologies?

A

Constipation, defined as infrequent, hard stools, is a common cause of abdominal pain in children and may be a sign of either a pathologic (eg, Hirschsprung disease, cystic fibrosis, spinal cord abnormality) or functional process. History is key to the diagnosis. For neonates, verify passage of meconium in the first 24 hours of life. A rectal examination is recommended to assess presence of stool, rectal tone, sensation, and size of the anal vault. A careful lower extremity neurologic examination should be completed to assess for neuromuscular causes. A single upright abdominal radiograph may be helpful to visualize fecal retention or impaction, and to help rule out the concern for obstruction. Treatment in the ED with suppositories or enemas may be necessary, and outpatient maintenance therapy is essential to prevent recurrence. Admission is indicated for patients with impaction associated with vomiting, dehydration, and failure of outpatient treatment.

74
Q

How does HSP present?

A

Henoch-Schönlein purpura is an idiopathic vasculitis of children between 2 and 11 years of age. HSP classically presents with acute abdominal pain, lower extremity purpura, and arthritis. Routine laboratory testing is not needed for classic cases, but can help rule out other conditions. A urinalysis should be obtained to identify hematuria, with subsequent renal function tests when blood is present. Abdominal pain in HSP is caused by bowel wall edema and GI vasculitis. Microscopic and even gross GI bleeding is not uncommon, though rarely life threatening. HSP is a known risk factor for intussusception in older children and this must be considered in patients with significant abdominal pain. Treatment of HSP is primarily supportive: joint pain responds well to non-steroidal antiinflammatory medications; severe abdominal pain may improve with corticosteroids. Consultation and follow-up with a pediatric rheumatologist or nephrologist may be necessary for more severe symptoms or renal involvement with hypertension.

75
Q

Upper GI bleeding DDx based on age?

A
Less than 2 months:
Swallowed maternal blood
Stress ulcer
Vascular malformation
Hemorrhagic disease of newborn (vitamin K deficiency)
Coagulopathy/bleeding diathesis
2 months to 2 years:
Gastroenteritis
Toxic ingestion
Mallory-Weiss tear
Vascular malformation
Esophagitis
Stress ulcer
Bleeding diathesis
GI duplication
Foreign body
>2 years:
Gastroenteritis
Mallory-Weiss tear
Peptic ulcer disease
Toxic ingestion
Vascular malformation
Gastritis
Varices
Hematobilia
Foreign body
76
Q

Lower GI bleeding DDx based on age?

A
0 to 2 months:
Swallowed maternal blood
Milk allergy
Infectious colitis
Intussusception
Volvulus
Meckel diverticulum
Necrotizing enterocolitis
Vascular malformation
Hemorrhagic disease of newborn
Hirschsprung disease
Congenital duplications
2 months to 2 years:
Anal fissure
Gastroenteritis
Milk allergy
Intussusception
Volvulus
Meckel diverticulum
Hemolytic uremic syndrome
Henoch-Schönlein purpura
Polyps: benign, familial
Inflammatory bowel disease
GI duplication
Dieulafoy lesion
>2 Years:
Anal fissure
Gastroenteritis
Hemorrhoids
Polyps
Colitis (infectious, ischemic)
Meckel diverticulum
Intussusception
Hemolytic uremic syndrome
Henoch-Schönlein purpura
Inflamatory bowel disease
Angiodysplasia
Celiac disease
Dieulafoy lesion
Rectal ulcer syndrome
Peptic ulcer disease
77
Q

What are the clinical features of UTI in pediatrics?

A

There are 3 age-based clinical presentations for pediatric UTIs. Neonates present with a clinical presentation indistinguishable from that of sepsis, and they may have symptoms that include fever, jaundice, poor feeding, irritability, and lethargy. Older infants and young children typically present with gastrointestinal complaints that may include fever, abdominal pain, vomiting, and a change in appetite. School-age children and adolescents typically present with adult-type complaints such as dysuria, urinary frequency, urgency, and hesitancy. Although the majority of infants and young children with fever and UTI have upper-track disease and require long-course antibiotic treatment, older children and adolescents without fever, flank pain, and flank tenderness are likely to have simple cystitis and can be treated with shorter course therapy similar to adults.

78
Q

Role of urinanalysis in identifying UTI in peds?

A

Because younger children void frequently and do not store urine in the bladder long enough to accumulate leukocytes or nitrites, urinalysis is insensitive in this age group and culture should be sent regardless of dipstick results. Microscopic urinalysis is more specific and is typically considered positive for infection if more than 5 white blood cells per high power field and bacteria are seen. A positive microscopic urinalysis has a sensitivity of 65% for identifying culture-proven UTI. Neither urinary test strips nor microscopic urinalysis can be used to definitively rule out pediatric UTI, though evidence is mounting that delaying treatment until culture results return does not alter the long-term outcome and antibiotics can be safely withheld in the setting of a negative urinalysis and microscopy.

79
Q

How to treat UTI in peds?

A

The treatment and disposition of infants and children with UTI depend on age and are based on the severity of concurrent symptoms. In general, antibiotics should not be given until after urine culture has been obtained.

  1. Treat neonates for sepsis and obtain cultures of blood and CSF in addition to urine. Administer parenteral antibiotics and admit to the hospital: ampicillin (50 milligrams/kilogram/dose) plus gentamicin (3-5 milligrams/kilogram/dose) or ampicillin (50 milligrams/kilogram/dose) plus cefotaxime (50 milligrams/kilogram/dose) are appropriate empiric choices.
  2. Treat infants from 1 month to 2 years of age who are dehydrated, have persistent vomiting, appear ill or septic, or are medically complicated typically with intravenous antibiotics such as ceftriaxone, cefotaxime, or cefepime (all are dosed at 50 milligrams/kilogram/dose).

Well appearing infants in this age group may be treated with oral antibiotics, which are as effective as parenteral treatment. A third generation cephalosporin such as cefpodoxime (5 milligrams/kilogram/dose given twice daily) or cefdinir (7 milligrams/kilogram/dose given twice daily), is recommended. Treat for 10 to 14 days, as short-course therapy is less effective in young children. High rates of resistance to cephalexin, amoxicillin, and trimethoprim-sulfamethoxasole are now widespread, though these may be appropriate based on local sensitivities.

  1. Children older than 2 years who are otherwise doing well and tolerating oral fluids are treated as outpatients with oral antibiotics for at least 7 days with close follow-up with their primary doctors. Emergency physicians should be familiar with the antibiotic-resistance patterns in their geographic area. Appropriate oral antibiotic choices to treat pediatric UTIs include cefixime (8 milligrams/kilogram/d, divided twice daily), cefpodoxime (5 milligrams/kilogram/day divided twice daily) or cefdinir (7 milligrams/kilogram/dose given twice daily). Depending on local sensitivities, trimethoprim/sulfamethoxazole (3 to 6 milligrams/kilogram/dose TMP, 15 to 30 milligrams/kilogram/dose SMX, given twice daily), or cephalexin (10 to 25 milligrams/kilogram/dose, given 4 times a day), may be used.
  2. Adolescent females with cystitis or acute pyelonephritis are treated similarly to adults
80
Q

List 6 of the most common presentations of pediatric heart disease and common causes of each.

A

There are 6 common clinical presentations of pediatric heart disease: cyanosis, shock, congestive heart failure (CHF), pathologic murmur, hypertension, and syncope.

Cyanosis: TGA, TOF, TA, Tat, TAVR
Shock: Coarctation, HPLHS
Congestive heart failure: Coarctation, PDA, ASD, VSD
Murmur: Shunts: VSD, PDA, ASD, Obstructions (eg, valvular stenosis), Valvular incompetence
Hypertension: Coarctation

Syncope
Cyanotic: TOF
Acyanotic: Critical AS

81
Q

How to distinguish between respiratory and cardiac causes of cyanosis?

A

For the neonate presenting with cyanosis, the hyperoxia test helps to differentiate respiratory disease from cyanotic congenital heart disease (although imperfectly). When placed on 100% oxygen, the infant with cyanotic congenital heart disease will fail to demonstrate an increase in Pao2, while those with respiratory causes will often respond with an improvement in pulse oximetry.

82
Q

Name ther common cyanotic and acyantotic lesions of the heart.

A

The differential diagnosis for cyanosis or shock due to congenital heart disease typically includes cyanotic lesions: transposition of the great vessels, tetralogy of Fallot, and other forms of right ventricular outflow tract obstruction or abnormalities of right heart formation. Acyanotic lesions that can present with shock include severe coarctation of the aorta, critical aortic stenosis, and hypoplastic left ventricle. It should be noted that cyanosis may accompany shock of any cause.

83
Q

What is the most common cyanotic heart lesion in the first week of life and its presentation?

A

Transposition of the great vessels represents the most common cyanotic defect presenting in the first week of life. This entity is easily missed due to the absence of cardiomegaly or murmur (unless there is a coexistent ventricular septal defect [VSD]). Symptoms (before shock) include central cyanosis, increase respiratory rate, and/or feeding difficulty. There is usually a loud and single S2. Chest radiographs may show an “egg on a string” shaped heart with a narrow mediastinum and increased pulmonary vascular markings. ECG may show right-axis deviation and right ventricular hypertrophy.

84
Q

What is the most common cyanotic heart lesion and its presentation?

A

Tetralogy of Fallot is the most common cyanotic congenital heart disease overall, and can present with cyanosis later in infancy or childhood. Physical examination reveals a holosystolic murmur of ventricular septal defect, a diamond-shape murmur of pulmonary stenosis, and cyanosis. Cyanotic spells in the toddler may be relieved by squatting. Chest radiograph may show a boot-shape heart with decreased pulmonary vascular markings or a right-sided aortic arch. The ECG often demonstrates right ventricular hypertrophy and right axis deviation.

Hypercyanotic episodes, or “tet spells,” may bring children with tetralogy of Fallot to the ED in dramatic fashion. Symptoms include paroxysmal dyspnea, labored respirations, increased cyanosis, and syncope. Episodes frequently follow exertion due to feeding, crying, or straining with stools and last from minutes to hours.

85
Q

How do you manage a cyanotic child in the ER?

A

Emergency Department Care and Disposition

  1. Cyanosis and respiratory distress are first managed with high-flow oxygen, cardiac and oxygen monitoring, and a stable intravenous or intraosseous line. Caveat: Neonates tolerate low oxygen saturations well due to oxygen-avid fetal hemoglobin; oxygen is a potent pulmonary vasodilator and may lead to “pulmonary steal” of systemic blood flow, worsening systemic shock in ductal-dependent systemic blood flow such as coarctation of the aorta. Treatment with prostaglandins (see below) is critical in these instances.
  2. For severe shock in infants suspected of having shunt-dependent lesions, prostaglandin E1 should be given in an attempt to reopen the ductus. Treatment begins with 0.05 to 0.1 microgram/kilogram/min; this may be increased to 0.2 microgram/kilogram/min if there is no improvement. Side effects include fever, skin flushing, diarrhea, and periodic apnea.
  3. Immediate consultation should be obtained with a pediatric cardiologist and, if the patient is in shock, a pediatric intensivist.
  4. Management of hypercyanotic spells consists of positioning the patient in the knee-to-chest position and administration of morphine sulfate 0.2 milligram/kilogram SC, IM, or IO. Resistant cases should prompt immediate consultation with a pediatric cardiologist for consideration of phenylephrine for hypotension or propranolol for tachycardia.
  5. Noncardiac causes of symptoms should be considered and treated appropriately, including a fluid challenge of 10 to 20 mL/kg of normal saline solution, and empiric administration of antibiotics as indicated. Fluids should be administered more judiciously to neonates with congenital heart disease, typically in 10 mL/kg boluses.
  6. Epinephrine is the initial drug of choice for hypotension. An infusion is started at 0.05 to 0.5 microgram/kilogram/min and titrated to the desired blood pressure.

By definition, these children are critically ill and require admission, usually to the neonatal or pediatric intensive care unit.

86
Q

How does CHF present in the pediatric population?

A

Congestive heart failure from congenital or acquired heart disease typically presents after the neonatal period, typically in the second or third month of life (congenital) or later in childhood (acquired causes). The distinction between pneumonia and CHF in infants requires a high index of clinical suspicion and is often difficult. Pneumonia can cause a previously stable cardiac condition to decompensate; thus, both problems can present simultaneously. Presenting symptoms include poor feeding, diaphoresis, irritability or lethargy with feeding, weak cry, and, in severe cases, grunting, nasal flaring, and respiratory distress. Note that the early tachypnea of CHF in infants is typically “effortless” and the first manifestation of decompensation, followed by increased work of breathing and rales on examination.

87
Q

DDx of CHF based on age?

A

Early-onset CHF is associated with ductal-dependent lesions such as coarctation of the aorta and may be abrupt in onset; persistent patent ductus arteriosis (PDA) may also present in the neonatal period with CHF. Rarely, sustained tachyarrhythmias may present with CHF in the neonatal period. By contrast, lesions that result in pulmonary over-circulation such as VSD or atrial septal defect (ASD) present with gradual development of failure in the second or third month of life. Onset of CHF after age 3 months usually signifies acquired heart disease such as cardiomyopathy or myocarditis. The exception is when pneumonia, endocarditis, or another complication causes a congenital lesion to decompensate.

88
Q

How does cardiomyopathy present?

A

Cardiomyopathy presents with respiratory distress and feeding difficulties. A pathologic gallop (S3 and or S4) is key to recognition. Rales and organomegally are often present and cardiomegaly and pulmonary vascular congestion are noted on chest radiography.

89
Q

How does myocarditis present?

A

Myocarditis is often preceded by a viral respiratory illness and needs to be differentiated from pneumonia. As with pneumonia, the infant usually presents in distress with fever, tachypnea, and tachycardia. ECG may show diffuse ST changes, dysrhythmias, or ectopy, which is associated with an increased risk of sudden death. Chest radiograph shows cloudy lung fields from inflammation or pulmonary edema. Cardiomegaly with poor distal pulses and prolonged capillary refill, however, distinguish it from common pneumonia. Once cardiomegaly is discovered, hospital admission and an echocardiogram are indicated.

90
Q

How does pericarditis present?

A

Usually pericarditis presents with pleuritic and positional chest pain. Muffled heart sounds and a friction rub may be present on physical examination. Cardiomegaly is seen on a chest radiograph. An echocardiogram is performed urgently to distinguish a pericardial effusion from dilated or hypertrophic cardiomyopathy and to determine the need for pericardiocentesis.

91
Q

What does pure right-sided CHF likely represent?

A

If an infant presents in pure right-side CHF, the primary problem is most likely to be pulmonary, such as cor pulmonale. In early stages, periorbital edema is often the first noticeable sign. This may progress to hepatomegaly, jugular venous distention, peripheral edema, and anasarca

92
Q

How to manage CHF in peds ER?

A

Emergency Department Care and Disposition

  1. The infant who presents with mild tachypnea, hepatomegaly, and cardiomegaly should be seated upright in a comfortable position, oxygen should be given, and the child should be kept in a neutral thermal environment to avoid metabolic stresses imposed by hypothermia or hyperthermia.
  2. If the work of breathing is increased or CHF is apparent on chest radiograph, 1 to 2 milligrams/kilogram furosemide should be administered parenterally.
  3. Hypoxemia is usually corrected by administration of oxygen, fluid restriction, and diuresis, although continuous positive airway pressure is sometimes necessary.
  4. Stabilization and improvement of left ventricular function is often first accomplished with inotropic agents. Digoxin is used in milder forms of CHF. The appropriate first digitalizing dose to be given in the ED is 0.02 to 0.03 milligram/kilogram.
  5. When CHF progresses to cardiogenic shock (absent distal pulses and decreased end-organ perfusion), continuous infusions of inotropic agents, such as dopamine or dobutamine, are indicated instead of digoxin. The initial starting range is 2 to 10 micrograms/kilogram/min.
  6. Aggressive management of secondary derangements, including respiratory insufficiency, acute renal failure, lactic acidosis, disseminated intravascular coagulation, hypoglycemia, and hypocalcaemia should be implemented.
  7. Definitive diagnosis and treatment of congenital defects presenting with CHF often requires cardiac catheterization followed by surgical repair. Consider prostaglandin E1 in ductal dependent cases.