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PEDS Board Review > Emergent Conditions > Flashcards

Emergent Conditions Flashcards

Prep

1
Q

best next step in someone p/w markedly decreased responsiveness

A

endotracheal intubation (management of airway)

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2
Q

first step in tx any child who has had toxic ingestion

A

Airway stabilization

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3
Q

GI decontamination agent of choice in pediatric patients

A

activated charcoal

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4
Q

When can flumazenil be used in overdose situation?

A
  • clear cases of single agent, BDZ overdose in first-time user
  • do NOT give in cases of:
    • chronic BDZ use
    • unknown overdoses
    • TCA overdoses
  • lowers seizure threshold and may precipitate seizures
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5
Q

use of gastric lavage in acute poisoning management

A

gastric lavage is not indicated!

  • esp. C/I in hydrocarbon or caustic substance ingestion
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6
Q

Information available from poison control centers

A
  • providing recommendations for the management of human exposures
  • supply information on
    • _​_poisons
    • poison prevention
    • drugs and drug identification
    • teratogenicity of various agents
    • occupational, medical, and environmental concerns
  • manage cases involving both human and animal exposures.
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7
Q

SIADH

  • features seen on labs
A
  • hyponatremia
  • decreased urine output
  • state of hypervolemia or euvolemia
  • elevated FeNa (>2%) [Urinary Na > 40]
  • causes increased water absorption in the renal collecting duct, and therefore, decreased renal water excretion
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8
Q

Tx. SIADH

A
  • fluid restriction, to atleast 1/2 of maintenance fluid requirements
  • if severe, furosemide
  • if mental status deterioration, signs of impending herniation, or seizures occur 2/2 hyponatremia –> tx with 3% hypertonic saline
    • ​do NOT exceed correction of _ > 10-12 meQ/L in 24 hour period_
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9
Q

findings assoc. with adrenal insufficiency 2/2 traumatic brain injury

A
  • hyponatremia
  • hyperkalemia
  • non-anion gap, metabolic acidosis
  • hemodynamic instability
  • hypoglycemia
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10
Q

Evaluation of suspected magnet ingestion

A
  1. Plain film XR, lateral & AP, of neck and abdomen
    • single view will not be able to specific if one or two have been ingested as can be overlapping
  2. Urgent surgical evaluation
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11
Q

Management of Magnet Ingestion

A
  1. single magnet ingestion
    • conservative
    • serial radiographic follow-up to ensure progression
    • magnet precautions
  2. multiple magnet ingestion
    • ​​asx –> serial exam and XR Q4-6 hrs
    • sx or multiple magnets w/o progression on XR –> surgical removal
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12
Q

Potential complications of magnet ingestion

A
  • may attract across layers of bowel and lead to:
    • pressure necrosis, fistula, perforation, infection, or obstruction requiring intestinal resection
  • intraperitoneal hemorrhage
    • mesenteric vessels become trapped between attracted bowel loops
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13
Q

5 day old neonate p/w sx and lab findings of meningitis; CT scan of the head shows multiple brain abscesses

  • **most likely organism? **
A
  • Citrobacter Koseri
    • enteric gram neg. organism
  • other gram-negative organisms:
    • Cronobacter, Serratia marcescens
  • **Salmonella **species have also been associated with brain abscesses in neonates.
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14
Q

Tx. brain abscess in a neonate (likely caused by Citrobacter)

A
  • Surgical drainage
  • Empiric abc therapy:
    • 3rd-gen cephalosporin i.e cefotaxime or a
    • carbapenem, i.e meropenem
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15
Q

a 7 yo boy p/w inappropriate sexual behavior (touching genitals), vesicular lesions on glans and dysuria - what should you suspect?

A

sexual abuse

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16
Q

Balanitis

  • definition
  • association
A
  • inflammation of the glans penis
  • associated with diaper dermatitis in young children.
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17
Q

causes of small vesicular lesions in anogenital region

A
  • STIs - HSV, syphilis
  • other viruses (Epstein-Barr virus)
  • other systemic conditions (Behçet disease, Crohn disease)
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18
Q

next best step in possible ingestion of tablets containing iron

A
  • abdominal XR
  • lab studies
    • serum iron level, approx 4 hours after ingestion
      • <350 μg/dL (62.6 μmol/L): asx or mild course
      • _350 to 500 μg/dL (_62.6-89.5 μmol/L): mild to moderate GI sx, but rarely serious
      • > 500 μg/dL (89.5 μmol/L) are at risk of developing serious systemic toxicity.
    • ​ABG: metabolic acidosis in a well-appearing child is a warning sign for the development of shock.
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19
Q

Pathophysiology of Iron toxicity

A
  • toxic to numerous cellular processes in its ferric form.
  • free radical production and lipid peroxidation, which results in damage to the body’s tissues.
  • Local toxicity (manifested as abdominal pain, vomiting, diarrhea, and gastrointestinal [GI] bleeding) results from damage to the GI mucosa
  • systemic toxicity results from injury to the cardiovascular system and liver.
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20
Q

Stages of Iron Toxicity: Stage 1

A

Stage 1 (0-6 hours after ingestion):

  • Direct injury to the GI mucosa--> vomiting, diarrhea, abdominal pain, hematemesis, hematochezia.
  • In severe cases, hypovolemic shock, metabolic acidosis, death 2/ 2 loss of GI fluid and blood.

Many patients with mild to moderate toxicity do not progress beyond this stage.

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21
Q

Stages of Iron Toxicity: Stage 2

A

Stage 2 (6-12 hours after ingestion)

  • aka “relative stability” or “quiescent” stage
  • patients appear to be improving clinically during this period.
    • Symptoms may fully resolve
    • redistribution into the reticuloendothelial system
  • may have mild metabolic acidosis
  • It is crucial to differentiate children in this phase from those with mild toxicity in whom symptoms have truly resolved. *
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22
Q

Iron Toxicity: Stage 3

A

Stage 3 (12-24 hours after ingestion)

  • Severe systemic toxicity
  • Signs may include:
    • gastrointestinal hemorrhage, altered mental status, seizures, cardiovascular collapse, renal failure, hepatic failure, coagulopathy, and profound metabolic acidosis.
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23
Q

Iron Toxicity: Stage 4

A

Stage 4 (within 48 hours after ingestion):

  • Dose-dependent hepatotoxicity
    • elevated LFTs

Following shock, hepatic failure is the second most common cause of death from iron poisoning.

24
Q

Iron Toxicity: Stage 5

A

Stage 5 (2-8 weeks after ingestion):

  • Gastrointestinal obstruction
    • strictures develop from iron-induced damage to the GI tract.
    • location: gastric outlet
  • CF –> abdominal pain and vomiting
25
Q

Management of Acute Iron Toxicity 2/2 ingestion

A
  • ABCs; aggressive supportive care with fluid resuscitation
  • if XR neg and pt asx
    • no immediate interventions indicated
  • if XR shows iron tablets (radio-opaque)
    • GI decontamination via whole bowel irrigation
  • ​​Chelation therapy with deferoxamine
    • significant clinical manifestations of iron poisoning
    • serum iron level > 500 μg/dL (89.5 μmol/L)
    • metabolic acidosis.
26
Q

S/E: Deferoxamine

A
  • hypotension
  • renal failure
  • acute respiratory distress syndrome (ARDS),
  • Yersinia sepsis
27
Q

Clinical Findings in elevated ICP

A
  • headache w/ photophobia
  • vomiting: worse when supine, nighttime or early morning
  • hypertension, bradycardia
  • papilledema
  • full or bulging fontanelle in infants
  • abducens palsy
  • dilated, poorly reactive, or asymmetric pupils
  • Late findings = obtundation, decerebrate posturing, apnea, and dilated and unreactive pupils (uncal or tonsillar herniation)
28
Q

First step in management of patient with elevated ICP

A

Head CT

  • to evaluate for the presence or absence of hydrocephalus, and if present, whether it is obstructive or nonobstructive.
    • obstructive hydrocephalus can result in herniation of brain contents if LP is performed
29
Q

Management: pseudotumor cerebri

A
  • LP: opening and closing pressures can aid dx
  • acetazolamide
30
Q

which meds should be avoided at all costs when a patient has elevated ICP?

A

Narcotics and sedatives

  • In elevated ICP, hyperventilation is a natural compensatory mechanism to decrease the blood component of the cranial vault because hypocapnia decreases cerebral blood flow. Even a slight increase in Pco2 from slowed respirations because of narcotics can lead to herniation and death.
31
Q

Neonate p/w direct hyperbilirubinemia, hepatomegaly with dysfunction (INR 1.95) w/in 24 hours of commencing feeding; urine positive for reducing substances

A
  • should be considering inborn error of metabolism, spec. carbohydrate metabolism
  • MC = galactosemia
  • **dx. **erythrocyte galactose-1-phosphate uridyltransferase (GALT) activity, erythrocyte galactose-1-phosphate concentration, and GALT molecular genetic testing (<5% of control)
  • tx. early dietary management (lactose or galactose restricted diet initiated w/in 10 days after birth)
  • children with galactosemia are at ncreased risk for developmental, cognitive, and motor delay.
32
Q

Neonate p/w of liver involvement, marked by elevated transaminases, hypocholesterolemia, and hyperbilirubinemia. No reducing substances in urine. Dx?

A

Tyrosinemia Type 1

  • deficiency in fumarylacetoacetate hydrolase (FAH)
    • maleylacetoacetate and fumarylacetoacetate are converted to toxic metabolites succinylacetone and succinylacetoacetate
  • hepatorenal toxicity
  • Dx. elevated urine succinylacetone
    • inhibits porphyrin synthesis –> accum. 5 aminolevulinate (potent neurotoxin)
33
Q

Evaluation of jaundice persisting > 2 weeks

A
  • measure bili levels, if direct bili elevated:
  • evaluate for extrahepatic biliary obstruction (EBA vs. choledochal cyst)
    • liver usg - looking for choledochal cyst
    • percutaneous liver biopsy at 1 mo age
  • ​evaluation for intrahepatic bile duct paucity (α-1-antitrypsin deficiency and Alagille syndrome)
    • ​obtain a1 anti-trypsin level
34
Q

Onset of generalized facial swelling combined with facial plethora in a child with respiratory findings should prompt clinicians to consider what diagnosis?

How would you evaluate this further?

A
  • Superior vena cava syndrome
    • very rare in children
    • MC 2/2 mediastinal malignancies (non Hodgkin lymphoma, ALL)
  • eval. Plain radiography of the chest
    • get in any child w/ suspected mediastinal mass
35
Q

CF in anterior mediastinal mass with 2ndary superior vena cava syndrome

A
  • swelling of face, neck or upper chest
  • facial plethora or cyanosis
  • prominent neck or chest veins
  • cough –> dyspnea, orthopnea
  • hoarse voice/stridor
  • chest pain
  • wheezing
  • pleural or pericardial effusion
36
Q

Causes of Cardiogenic Shock

A
  • impaired contractility
    • ​myocarditis, primary neuromusc dz, metabolic dz
  • arrhythmias
  • outflow tract obstruction
  • impaired filling
    • ​diastolic dysfunction, restrictive CM, lesions of reduced cavity size, tamponade
37
Q

acute bilirubin encephalopathy

A
  • early findings: nonspecific
  • moderate ABE: arching of the neck and trunk, increasing lethargy, decreased feeding, and irritability with a shrill cry
    • intervention at this point may prevent sequelae of kernicterus
  • severe ABE: bicycling movements of the arms and legs, inconsolable crying, inability to eat, fever, seizures, and coma.
38
Q

Management/Treatment:

moderate-severe acute bilirubin encephalopathy

A
  • immediate exchange transfusion - even if serum bili levels are falling
  • evaluation of cause:
    • total and direct bilirubin
    • blood type/ Coomb’s
    • complete blood cell count
    • G6PD deficiency testing.
39
Q

benign neonatal clonus

A
  • jerking movements of extremities seen in neonate during sleep
40
Q

an adolescent patient p/w a scratch wound that developed severe pain, exquisite sensitivity, and bluish discoloration at the site of skin injury; on exam, he appears ill - most likely dx?

A

Necrotizing fasciitis​

  • group A B-hemolytic streptococcus
  • mixed infection with anaerobic cpt (C. perfringens)
    • persons with underlying medical conditions such as diabetes, recent surgery, immune compromise, or peripheral vascular disease.
41
Q

Treatment:

Necrotizing Fasciitis

A
  • prompt surgical debridement
    • removes necrotic tissue and decreased toxin production
  • ​IV antibiotic therapy
    • ​Clindamycin + Penicillin agent
42
Q

acquired cholesteatoma

  • pathophysiology
  • location
A
  • MC than congenital (95% vs 5%)
  • usually result of chronic middle ear disease
  • persistent inflammatory mediators + chronic eustachian tube dysfxn –> atrophy of TM, formation of retraction pockets which deepen w/ time –> pouch forms that traps desquamating cells
  • MC locations:
    • Old tympanostomy tube sites,
    • the posterosuperior portion of the TM,
    • pars flaccida
43
Q

Warning signs for a cholesteatoma

A
  • white round mass behind an intact TM
  • deep retraction pocket with or without granulation tissue
  • focal granulation on the surface of the TM
  • persistently draining ear for more than 2 weeks despite treatment
  • new-onset hearing loss in a previously operated ear
44
Q

Complications of a cholesteatoma

A
  • sensorineural hearing loss
  • cranial nerve palsies (CN 6, 7)
  • vertigo
  • venous thrombosis
  • CNS infections (brain abscess, meningitis).
  • invasive local destruction - temporal bone, ossicles
45
Q

Management of suspected cholesteatoma

A
  • prompt ENT consultation
  • Treatment:
    • surgical excision (recurrence risk is high)
46
Q

Next step for any patient with swelling in a single joint associated with fever?

A

immediate referral for orthopedic evaluation

  • rule out septic arthritis which is a medical emergency
47
Q

Characteristics of inflammatory joint pain

A
  • Morning pain that lasts 1 hour or more
  • improving throughout the day
  • persistent swelling
  • Limping more pronounced in the morning and improves with activity
  • decreased ROM
48
Q

Orthopedic cause of joint pain - characteristics

A
  • constant pain
49
Q

Overuse joint pain

A
  • Pain that is worsened by a specific activity
  • worse on more active days
  • transient swelling that comes and goes, lasting a few hours to a day
  • limping usually worsened with activity.
50
Q

causes of night-time joint pain

A
  • benign nocturnal limb pain of childhood (“growing pains”)
  • benign joint hypermobility
  • severe nighttime pain - consider leukemia and lymphoma
51
Q

Benign joint hypermobility

A

joint pain that:

  • occurring at the end of the day
  • worsened with activity, and improved with rest
  • in a child with joint hyperextension.
52
Q

Benign nocturnal limb pain of childhood (“growing pains”)

A

is characterized by nighttime chronic intermittent bilateral shin pain without daytime symptoms or limitation.

53
Q

Clinical findings in a newborn that would make you suspect esophageal atresia?

  • next step in assessment?
  • diagnosis?
A
  • CF – spitting, drooling, choking, and respiratory distress bc of cont’d inability to handle secretions or feedings.
  • next step?
    • failed insertion of orogastric tube
  • diagnosis?
    • CXR - will show coiling of orogastric tube in esophagus
  • prompt identification leads to > 95% survival
  • >50% of infants with other assoc abnormalities (VACTERL)
54
Q

PE findings of erythema, swelling, and pain over the mastoid bone with displacement of the pinna outwardly

  • Diagnosis?
  • next step?
  • diagnostic steps?
A
  • mastoiditis +/- acute/chronic otitis media
  • next step?
    • consult ENT
    • tympanocentesis for culture
    • broad spec abx
  • diagnosis:
    • based on clinical findings
    • if imaging warranted –> CT is first choice for det. extent of disease; if intracranial extension suspected –> MRI
55
Q

Risk Factors and complications in mastoiditis

A
  • Risk Factors
    • recurrent otitis media
    • age < 2 yo

​Complications of mastoiditis:

  • extracranial: cholesteatoma, subperiosteal abscess, facial nerve palsy, hearing loss, labrynthitis, osteomyelitis, Bezold abscess of SCN
  • intracranial: meningitis, brain abscess, epidural/subdural empyema, carotid artery or venous sinus thrombosis

​

56
Q

MC pathogens in mastoiditis

A
  • Strep. pneumo
  • strep pyogenes
  • staph aureus
  • Chronic mastoiditis
    • polymicrobial - anaerobes and gram neg bacilli (E.coli, pseudomonas, Klebsiella)
  • ​pseudomonas –> consider as cause in child w/ hx of recurrent OM and recent abx use
57
Q
A

PEDS Board Review (10 decks)

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