Emergent Conditions Flashcards
Prep
best next step in someone p/w markedly decreased responsiveness
endotracheal intubation (management of airway)
first step in tx any child who has had toxic ingestion
Airway stabilization
GI decontamination agent of choice in pediatric patients
activated charcoal
When can flumazenil be used in overdose situation?
- 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
use of gastric lavage in acute poisoning management
gastric lavage is not indicated!
- esp. C/I in hydrocarbon or caustic substance ingestion
Information available from poison control centers
- 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.
SIADH
- features seen on labs
- 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
Tx. SIADH
- 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_
findings assoc. with adrenal insufficiency 2/2 traumatic brain injury
- hyponatremia
- hyperkalemia
- non-anion gap, metabolic acidosis
- hemodynamic instability
- hypoglycemia
Evaluation of suspected magnet ingestion
- 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
- Urgent surgical evaluation
Management of Magnet Ingestion
-
single magnet ingestion
- conservative
- serial radiographic follow-up to ensure progression
- magnet precautions
-
multiple magnet ingestion
- asx –> serial exam and XR Q4-6 hrs
- sx or multiple magnets w/o progression on XR –> surgical removal
Potential complications of magnet ingestion
- 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
5 day old neonate p/w sx and lab findings of meningitis; CT scan of the head shows multiple brain abscesses
- **most likely organism? **
-
Citrobacter Koseri
- enteric gram neg. organism
- other gram-negative organisms:
- Cronobacter, Serratia marcescens
- **Salmonella **species have also been associated with brain abscesses in neonates.
Tx. brain abscess in a neonate (likely caused by Citrobacter)
- Surgical drainage
-
Empiric abc therapy:
- 3rd-gen cephalosporin i.e cefotaxime or a
- carbapenem, i.e meropenem
a 7 yo boy p/w inappropriate sexual behavior (touching genitals), vesicular lesions on glans and dysuria - what should you suspect?
sexual abuse
Balanitis
- definition
- association
- inflammation of the glans penis
- associated with diaper dermatitis in young children.
causes of small vesicular lesions in anogenital region
- STIs - HSV, syphilis
- other viruses (Epstein-Barr virus)
- other systemic conditions (Behçet disease, Crohn disease)
next best step in possible ingestion of tablets containing iron
- 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.
-
serum iron level, approx 4 hours after ingestion
Pathophysiology of Iron toxicity
- 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.
Stages of Iron Toxicity: Stage 1
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.
Stages of Iron Toxicity: Stage 2
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. *
Iron Toxicity: Stage 3
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.
Iron Toxicity: Stage 4
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.
Iron Toxicity: Stage 5
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
Management of Acute Iron Toxicity 2/2 ingestion
- 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.
S/E: Deferoxamine
- hypotension
- renal failure
- acute respiratory distress syndrome (ARDS),
- Yersinia sepsis
Clinical Findings in elevated ICP
- 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)
First step in management of patient with elevated ICP
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
Management: pseudotumor cerebri
- LP: opening and closing pressures can aid dx
- acetazolamide
which meds should be avoided at all costs when a patient has elevated ICP?
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.
Neonate p/w direct hyperbilirubinemia, hepatomegaly with dysfunction (INR 1.95) w/in 24 hours of commencing feeding; urine positive for reducing substances
- 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.
Neonate p/w of liver involvement, marked by elevated transaminases, hypocholesterolemia, and hyperbilirubinemia. No reducing substances in urine. Dx?
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)
Evaluation of jaundice persisting > 2 weeks
- 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
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?
-
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
CF in anterior mediastinal mass with 2ndary superior vena cava syndrome
- 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
Causes of Cardiogenic Shock
- impaired contractility
- myocarditis, primary neuromusc dz, metabolic dz
- arrhythmias
- outflow tract obstruction
- impaired filling
- diastolic dysfunction, restrictive CM, lesions of reduced cavity size, tamponade
acute bilirubin encephalopathy
- 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.
Management/Treatment:
moderate-severe acute bilirubin encephalopathy
- 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.
benign neonatal clonus
- jerking movements of extremities seen in neonate during sleep
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?
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.
Treatment:
Necrotizing Fasciitis
- prompt surgical debridement
- removes necrotic tissue and decreased toxin production
- IV antibiotic therapy
- Clindamycin + Penicillin agent
acquired cholesteatoma
- pathophysiology
- location
- 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
Warning signs for a cholesteatoma
- 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
Complications of a cholesteatoma
- sensorineural hearing loss
- cranial nerve palsies (CN 6, 7)
- vertigo
- venous thrombosis
- CNS infections (brain abscess, meningitis).
- invasive local destruction - temporal bone, ossicles
Management of suspected cholesteatoma
- prompt ENT consultation
- Treatment:
- surgical excision (recurrence risk is high)
Next step for any patient with swelling in a single joint associated with fever?
immediate referral for orthopedic evaluation
- rule out septic arthritis which is a medical emergency
Characteristics of inflammatory joint pain
- 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
Orthopedic cause of joint pain - characteristics
- constant pain
Overuse joint pain
- 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.
causes of night-time joint pain
- benign nocturnal limb pain of childhood (“growing pains”)
- benign joint hypermobility
- severe nighttime pain - consider leukemia and lymphoma
Benign joint hypermobility
joint pain that:
- occurring at the end of the day
- worsened with activity, and improved with rest
- in a child with joint hyperextension.
Benign nocturnal limb pain of childhood (“growing pains”)
is characterized by nighttime chronic intermittent bilateral shin pain without daytime symptoms or limitation.
Clinical findings in a newborn that would make you suspect esophageal atresia?
- next step in assessment?
- diagnosis?
- 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)
PE findings of erythema, swelling, and pain over the mastoid bone with displacement of the pinna outwardly
- Diagnosis?
- next step?
- diagnostic steps?
- 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
Risk Factors and complications in mastoiditis
-
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
MC pathogens in mastoiditis
- 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
