Pediatrics Flashcards
APGAR scoring is a method of assessing newborn infants at ——— and ——— minutes of life with a scale of ————
1
5
0–10
(Further assessments are recorded at 5-minute intervals until a score of at least 7 is achieved)
Apgar scores do not predict the
overall infant outcome, nor are they diagnostic
Apgar scoring scale:
Apgar score is based on appearance, pulse, grimace, activity, and respiration
Pulse of 130, acrocyanotic, grimaces to stimulation, moving all extremities and crying. Apgar Score?
8
Note: 2pts for pulse, 1 for color, 1 for irritability (to get full points for withdraw, they have to withdraw from stimulus), 2 for tone, and 2 for respiration)
What does the APGAR tell you at each time point?
General info about how the newborn tolerated labor (1min) and the newborn’s response to resuscitation (5min)
What does the APGAR not tell you?
What to do next (does not guide therapy) OR
How the baby will turn out (does NOT predict neurologic outcome)
When assessing Moro on an LGA newborn, the right arm remains extended and medially rotated: Dx and Next step?
Dx: Erb-Duchenne C5-C6 (upper trunk).
(Klumpke is C8-T1 (lower trunk))
Next step: Refer if not better by 3- 6mo for neuroplasty
Erb-Duchenne Palsy: Cause? Appearance?
Cause: Most common brachial plexus injury, caused by lateral traction (on neck during delivery) of the C5 and C6 nerve roots (upper trunk)
Apperence: The arm is adducted and internally rotated, but the grasp reflex is intact (If C7 is involved, the wrist is held in a flexed position (waiter’s tip))
Brachial plexus injuries can occur during birth when traction is used with
shoulder dystocia
Klumpke Palsy: Cause? Appearance?
Cause: Traction or tear of lower trunk C8-T1 roots (upward force on arm during delivery; Least frequent brachial plexus injury)
Appearance: The wrist and hand are weak (claw-hand) and lack a grasp reflex. If sympathetic nerves are involved, unilateral miosis (Horner syndrome) may result.
When palpating the clavicles on a LGA newborn, you feel crepitus and discontinuity on the left: Dx?
Dx: Clavicular Fracture.
Tx: Will form a callus in 1wk. No tx needed. Can use figure of 8 splint.
(Different from adult med; newborns bones more apt for remodeling)
Complete clavicular fracture may diminish the ——— reflex.
ipsilateral Moro
All macrosomic infants should be examined for signs of —(2)—
birth trauma and hypoglycemia
A medical student rotating in the nursery notices severe scalp swelling in a newborn male. The edema from the lesion crosses suture lines. What is the Dx and NBSIM?
Caput Succedaneum. Is simply a swelling of the scalp secondary to “barotrauma” from going through the birth canal. Completely benign and resolves within days.
A medical student rotating in the nursery notices severe scalp swelling in a newborn female. The edema from the lesion does not cross suture lines. What is the Dx and NBSIM?
Cephalohematoma. Is a subperiosteal bleed. Resolves in weeks-months. Increased risk for anemia/jaundice as the blood resorbs.
A medical student rotating in the nursery notices streaks of blood emanating from the vagina of a 3 day old newborn female. What is the Dx and NBSIM?
Normal/reassure the parents. Arises secondary to withdrawal of maternal hormones (uterus shedding).
Caput succedaneum vs cephalohematoma: Presentation and location?
Caput succedaneum is external to the periosteum. Caput crosses the midline of the skull and suture lines, unlike a cephalohematoma, which is below the periosteum and does not cross suture line
Caput succedaneum: Cause? Presentation? Prognosis?
Cephalohematoma: Cause? Presentation? Prognosis?
See pic: Edema. Crosses suture lines.
Note: pitting edema
See pic: “Fluctuance. Doesn’t cross suture lines.”
Maternal diabetes can lead to what in newborn after placental supply of glucose is removed?
Elevation of maternal glucose
causes elevated fetal glucose, leading to fetal hyperinsulinism, which can result in hypoglycemia in the newborn after placental supply of glucose is removed.
Mothers with pre-existing diabetes (esp type 1): important management steps
Control glc in the 1st trimester & take 4mg folate/day
Mothers with pre-existing diabetes (esp type 1): important associated birth defects
Placental insufficiency/IUGR, Congenital heart dz, NTD, Caudal regression syndrome, Small left colon syndrome
Umbilical vein vs artery: oxygenation of blood
Umbilical vein = oxygenated blood
Umbilical artery = deoxygenated blood
2 y/o M w/ multiple ear infxns, diarrheal episodes & pneumonias. No tonsils seen on exam. Dx? Time course? Labs?
Dx: Bruton agammaglobulinemia -x-linked
(No tonsils=b cell problem)
Time course: infx start @ 6-9mo (why?)
Labs: Absence of B cells on flow cytometry, low levels of all Igs
Define X-linked (Bruton) agammaglobulinemia
Defect in BTK, a tyrosine kinase gene, no B-cell maturation; X-linked recessive (increased in Boys)
Key findings X-linked (Bruton) agammaglobulinemia
■ Male
■ No palpable lymph nodes
■ No tonsil
■ Respiratory and gastrointestinal infections (Recurrent/chronic sinopulmonary infections with encapsulated organisms
(Haemophilus influenzae, Streptococcus pneumoniae); Severe/chronic gastrointestinal infections due to lack of IgA (Giardia))
B cell, IgG, IgM, IgA, IgE for X-linked (Bruton) agammaglobulinemia:
All decreased
Diagnosing X-linked (Bruton) agammaglobulinemia:
Look for very low or absent mature B lymphocytes and all immunoglobulin classes. No production of protective antibodies occurs.
Infants with Bruton’s agammaglobulinemia remain well for the first ——— due to ———
6 months
the presence of maternal IgG antibodies
Treating X-linked (Bruton) agammaglobulinemia:
Monthly IV immunoglobulin. (Immunoglobulin infusions confer passive immunity.) Prophylactic antibiotics if immunoglobulin treatment alone fails. Live vaccines are contraindicated; other vaccines lack an appreciable antibody response
X-linked (Bruton) agammaglobulinemia: Defecit, B cells, T cells, Ig, Clinical, Infections, TX
Deficit: X-linked arrest of B-cell
maturation
B cells: no
T cells: normal
Ig: no/low titer
Clinical: no palpable lymph nodes, no tonsils
Infections: Pneumococcal, Rotaviral, Giardia
Tx: IVIG
17 y/o F with decreased levels of IgG, IgM, IgE, and IgA but normal numbers of B cells. Dx? Complications?
Dx: CVID (acquired) (note: adolescent or young adult, b cells normal, but immunoglobulins are low) (less severe and comes on later than Bruton agammaglobulinemia)
Complications: Increased lymphoid tissue —> increased risk for lymphoma
Define Common Variable Immunodeficiency (CVID)
Group of B cell disorders with Defect in B-cell differentiation
CVID most commonly presents when?
in second decade of life
Key features CVID
■ Lymphadenopathy, splenomegaly.
■ Association with autoimmune diseases: RA, lupus, idiopathic thrombocytopenia.
■ Lymphoid interstitial pneumonitis, granulomas on various organs.
■ Increased risk of malignancies: lymphoma.
■ Sinopulmonary infections: encapsulated organisms.
■ Gastrointestinal (GI) infections: Giardia.
B cell, IgG, IgM, IgA, IgE for CVID:
All decreased except B cells normal
CVID: Defecit, B cells, T cells, Ig, Clinical, Infections, TX
Deficit: Dysfunctional B-cells
Can be familial
B cells: normal
T cells: normal
Ig: Low IgA, IgG, and/or IgM. Low titers
Clinical: Lymphadenopathy, autoimmune lymphomas
Infections: Pneumococcal,
Giardia, sinusitis
Tx: IVIG
Most common B-cell defect. Recurrent URIs, diarrhea.
Dx? Complication?
Dx: Selective IgA deficiency
Complication: Anaphylaxis reaction if given blood containing IgA
Selective IgA deficiency: Define
Deficiency of IgA-predominant immunoglobulin on mucosal surfaces due to failure of B cells to differentiate into IgA-secreting plasma cells
(This is the most common of the primary antibody deficiencies, occurring in 1 in 600 persons)
Selective IgA deficiency: signs and syptoms
Usually asymptomatic, but may have recurrent respiratory or GI infections; Allergies; Associated with autoimmune diseases: celiac disease
IgA is the major immunoglobulin within the
upper airway
Patients with selective IgA deficiency can develop ——— with blood product exposure that may lead to ———
anti-IgA antibodies
fatal anaphylaxis with blood or IVIG infusion (IVIG should be used with caution in patients with IgA deficiency)
B cell, IgG, IgM, IgA, IgE for selective IgA deficiency:
All normal except IgA low
Selective IgA deficiency: Defecit, B cells, T cells, Ig, Clinical, Infections, TX
Deficit: No switch to IgA
B cells: normal
T cells: normal
Ig: No IgA; Normal IgM, IgG, and titers
Clinical: Allergies, celiac disease
Infections: Mostly respiratory or gastrointestinal
Tx: IVIG is contraindicated
A 2-month-old infant with a heart defect and cleft palate has cough and tachypnea. He has a history of seizures. Chest x-ray shows diffuse infiltrates and no thymic shadow. Serum calcium is 6.5 mg/dL. Think?
DiGeorge syndrome
DiGeorge syndrome is a ———deficiency that results from failure of development of the ———, which are responsible for ——— development. These result in what presentation clinically? ———
T-cell
third and fourth pharyngeal pouches (due to deletion on chromosome 22)
thymus and parathyroid gland
lack of T-cell-mediated immunity, tetany, and congenital defects of the heart and great vessels (Without treatment, the condition is fatal)
Signs and sxs of DiGeorge syndrome:
■ Dysmorphic features: hypertelorism, cleft palate.
■ Congenital heart disease: truncus arteriosus, interrupted aortic arch.
■ Hypoparathyroidism presents as hypocalcemic seizures (“tetany”).
■ Recurrent infections: opportunistic infections when T-lymphocyte counts
are low.
DiGeorge Syndrome = Catch 22
Cardiac abnormality
Abnormal facies
Thymic hypoplasia
Cleft palate
Hypocalcemia
22 (abnormality on chromosome 22)
——— is the diagnostic test of choice for all microdeletion/ duplication syndromes. ——— does not have a high enough resolution to detect all of them. ——— is a screening test and should only be used to test family members after the breakpoints of the deletion have already been determined.
Chromosomal microarray
Karyotype
FISH
3wk old M with seizure, truncus arteriosus, micrognathia. Dx?
DiGeorge Syndrome
(“And no thymus - I couldn’t give u no thymus, that would give it away”; truncus arteriosus tightly linked with DiGeorge)
Genetic defect DiGeorge Syndrome
Microdeletion on Chr22
What types of infxns in childhood in DiGeorge Syndrome?
Candida, viruses, PCP pneumonia
(“Funguses, viruses- things T cells usually take care of”)
Truncus arteriosus definition:
A single arterial trunk that emerges from the ventricles, supplying the coronary, pulmonary, and systemic circulations (truncus overrides a VSD)
Truncus arteriosus association:
DiGeorge syndrome
Sign and sxs of Truncus arteriosus:
CXR shows cardiomegaly and increased pulmonary vascular markings.
CHF and cyanosis in the first week
Initial left-to-right shunt symptoms include: Dyspnea, Frequent respiratory infections, FTT
The second heart sound is prominent and single due to the single semilunar valve.
Peripheral pulses are strong, often bounding.
Often, a systolic ejection click can be appreciated.
——— account for most cases of failure to thrive (FTT) in the United States.
Psychosocial reasons
(FTT is caused by inadequate nutrition. It is defined as a weight below the third percentile with a decreased rate of weight gain, or a fall off the growth chart by two percentiles.)
Heart defect associated with DiGeorge syndrome. CXR shows ↑pulm blood flow and bi-ventricular hypertrophy. Dx? Tx?
Dx: Truncus arteriosis. Eisenmenger develops early.
Tx: Do surg in 1st few weeks of life
Define Eisenmenger syndrome
This syndrome can occur in unrepaired left-to-right shunts (i.e., VSD) that cause an increased pressure load on the pulmonary vasculature; Pulmonary vasculature pressure overload can result in irreversible arteri- ole changes; Pulmonary vascular obstructive disease may develop over several years; The pulmonary HTN reverses the left-to-right shunt; Persistent HTN maintains an enlarged right ventricle and can dilate the main pulmonary segment (evident on CXR)
Infant w/ severe infxns, no thymus or tonsils. Severe lymphopenia. Dx?
SCID. (“This kids is really screwed. No thymus=problem with T cells; no tonsils=problem with B cells; put them together- that’s SCID”)
See infxns w/ bacterial, viral and opportunistic bugs.
A 4-month-old female with FTT presents with respiratory distress. She has a temperature of 101°F (38.3°C), RR 70 breaths/min, and oxygen saturation of 91% (on room air). Thrush and bilateral rhonchi are present but no lymphadenopathy. Her white blood cell count is 16.2/mm3, 83% neutrophils, 11% monocytes. Chest x-ray shows diffuse bilateral interstitial infiltrates. Think:
Pneumocystis jirovecii pneumonia (PCP)
Infection with opportunistic organisms such as PCP is common in infants with SCID. Absence of lymph nodes in an infant with FTT is suggestive of SCID. Thrush, extensive diaper rash, and FTT are the prominent features.
Define SCID
Abnormalities of both humoral and cellular immunity
Onset of SCID at ——— months of age, with key sxs of:
3
No palpable lymph nodes, Opportunistic infections, Failure to thrive
Causes of SCID:
X-linked SCID most common form
Adenosine deaminase deficiency: about 15% of all SCID cases
Signs and sxs SCID
■ Presents within first 3 months with diarrhea, pneumonia, otitis, sepsis, FTT, and skin rashes
■ Increased frequency and/or severity of infections
■ Persistent infection with opportunistic organisms (Candida, mycobacteria,
herpes viruses, CMV, PCP)
■ Absent lymph nodes, hypoplastic thymus
Lab findings SCID:
■ Lymphopenia
■ Decreased serum IgG, IgA, and IgM.
■ Low or no T and B cells.
Inheritance of SCID
MC is XLR.
AR is an ADA deficiency
Tx SCID
Pediatric emergency! Need bone marrow transplant by age 1 or death.
Protective Measures to be taken in SCID:
■ Protective isolation
■ Irradiation of all blood products
■ Avoidance of live vaccines
Tx SCID
■ Aggressive antimicrobial treatment of even mild infections.
■ Recombinant adenosine deaminase replacement
■ Stem cell transplantation or gene therapy.
(Death within first year if untreated.)
A 10-month-old male presents with a temperature of 101.6°F (38.7°C) and a 3 × 4-cm abscess of the left buttock. His WBC count is 19.9/mm3, 77% neutrophils. At the age of 5 months, he had staphylococcal cervical lymphadenitis that required drainage. His uncle also had recurrent abscesses. Think:
CGD.
3 y/o M child w/ recurrent swollen, infected lymph nodes in groin and staph aureus skin abscesses
Dx: Chronic granulomatous disease
Cause: XLR. PMNs can ingest but not kill catalase + bugs. (Why they get recurrent Staph abscesses)
CGD Definition
Most common inherited phagocyte disorder; 70% X-linked, 30% autosomal recessive; NADPH oxidase complex defect leads to defective production of reactive oxygen species in neutrophils and macrophages; Susceptibility to catalase-positive microorganisms; Granulomatous inflammatory responses occur due to macrophage functional impairment.
CGD sxs:
■ Recurrent bacterial and fungal infections that begin in the first year of life: pneumonia, abscesses of the skin, soft tissue, organs (perianal/perirectal, liver, lung), lymphadenitis, osteomyelitis, bacteremia/fungemia, superficial skin infections (cellulitis/impetigo).
■ Growth failure, abnormal wound healing, diarrhea.
■ Hepatomegaly, splenomegaly, lymphadenopathy (enlarged by granulomas).
Catalase-positive infections in CGD include:
Aspergillus, S. aureus, Burkholderia, Serratia, Nocardia, Candida, Salmonella.
(SPACE- Staphylococcus aureus, Pseudomonas, Aspergillus, Candida, Enterobacter)
Dx of CGD with?
Nitrotetrazolium blue (yellow means they have the dz)
New test is Flow cytometry w/ DHR-123 (Dihydrorhodamine oxidation test (preferred))
A 10-month-old boy presents with thrush despite 10 days of nystatin. He had four episodes of otitis media. Physical examination shows thrush and multiple eczema patches. Both tympanic membranes are dull. His WBC is 7.6/mm3, Hb 11.3 g/dL, platelet count 97/mm3. His uncle died in infancy of infection. Think:
Wiskott-Aldrich syndrome.
Wiskott-Aldrich syndrome is an X-linked recessive syndrome characterized by the classic presentation of eczema, thrombocytopenia, and otitis media (immunodeficiency). The initial manifestation usually is petechiae or bleeding in the first few months of life.
18mo M baby w/ severe ezcema, petechiae, and recurrent ear infxns.
Wisckott-Aldrich Syndrome.
Definition Wiskott-Aldrich syndrome
X-linked-recessive disorder of cell cytoskeleton, presents as eczema, thrombocytopenia, and increased susceptibility to infection.
Oral candidiasis at greater than ——— of age should arouse suspicion for the presence of an immunodeficiency.
6 months
3 key features of Wiskott-Aldrich syndrome:
■ Eczema
■ Thrombocytopenia
■ ↑ IgA/IgE
Wiskott-Aldrich syndrome: Deficit, B cells, T cells, Ig, Clinical, Infections, Tx
Deficit: X-linked, defective cytoskeleton of the cells
B cells: normal
T cells: normal
Ig: High IgA, IgE and
Low IgM, titers
Clinical: Eczema, TCP
Infections: OIs (PCP), severe HSV and VZV
Tx: BMT, IVIG
Wiskott-Aldrich syndrome often present w/ (caught because of this specific event)
prolonged bleeding after circumcision (because thrombocytopenia is a characteristic)
Ig makeup in Wiskott-Aldrich syndrome
Low IgM, high IgA and IgE, slightly low IgG.
An 18 mo male is brought to the ED with shortness of breath. A CXR on admission is notable for a well defined consolidation in the left upper lung lobe. This is the child’s 6th episode of pneumonia in the past 9 mo. He was recently placed on a course of high dose amoxicillin and clavulanate for a severe ear infection. His vital signs include a temperature of 102.9, HR 170 bpm, RR 30 bpm (so severely tachycardic and tachypneic). There is no cervical lymphadenopathy or evidence of reactive hyperplasia in the back of his throat. His mom’s brother died last year from a severe Strep Pneumo infection. What is the most likely cause of this patient’s presentation?
a. Failed development of the 3rd and 4th pharyngeal pouches.
b. Failed differentiation of CD19 and 20+ cells.
c. Deficiency of a dimeric immunoglobulin.
d. Deficiency of an enzyme that deaminates adenosine.
e. X linked mutation in the WASP gene.
The best answer here is B. This child has Bruton’s agammaglobulinemia.
(From btk gene mutation; recurrent bacterial infections)
Note: B cells are CD19 and CD20 positive.
(Hypoplasia of lymphoid tissue classic clue; no tonsils seen)
For Bruton’s agammaglobulinemia, why is sex of the child relevant?
-Consider this diagnosis if you get a history of a boy (it should 100% not be a girl on the NBME)
with recurrent sinopulmonary infections.
-Since the disorder is X linked, you should have a family history of men having this disorder.
For Bruton’s agammaglobulinemia, diagnosis is with?
a simple CBC
For Bruton’s agammaglobulinemia, tx?
Consider giving regular IVIG injections.
For Bruton’s agammaglobulinemia, when do sxs begin developing?
Most of problems crop up at > 6 mo age since maternal IgG disappears from the infant’s serum around that time.
For immunodeficiencies, pay attention to the “bug pattern” on your exam: ——— = B cell problem vs ——— = T cell problem.
Encapsulated bacterial infections = B cell problem
Viruses/fungi = T cell problem
DiGeorge Syndrome: 4 key characteristics
The combo of a:
- T cell deficiency (no thymus) (recurrent viral and fungal infections; for ex pcp pneumonia caused by the fungus Pneumocystis jirovecii)
- hypocalcemia (no parathyroids, seizures)
- truncus arteriosus
- low set ears
Kids w/SCID often present with:
FTT, recurrent opportunistic infections (e.g Candida), and a chronic diarrhea (exams almost always mention diarrhea)
In SCID, you should not find a ——— on a CXR
thymic shadow (just like DiGeorge Syndrome)
In SCID, need to avoid
live attenuated vaccines
Ataxia-telangiectasia - 3 key features:
■ Telangiectasias of conjunctivae
and exposed areas
■ Ataxia
■ Lymphoma
Definition Ataxia-telangiectasia
This autosomal-recessive disorder of DNA repair presents as telangiectasias, ataxia, and variable extent of T-cell deficiency, with progressive loss of T helpers. Both humoral and cellular immunodeficiency occur.
Patients with ataxia telangiectasia have ——— deficiencies.
IgA and T Cell
Ataxia telangiectasia: Deficit, lymphocytes, Ig, Clinical, Infections, Tx
Deficit: AR, defect in DNA repair
Lymphocytes: Progressive loss of T4
Ig: Low IgA, IgE, and titers
Clinical: Wobbly gait, red sclerae, lymphomas; Increased serum α-fetoprotein
Infections: OIs, sinopulmonary
Tx: Antibiotics
Thymic hypo- or aplasia results in a
deficiency of functional T cells
In a kid with partial albinism, recurrent respiratory infections, and neuro problems (+ exam Q telling you of giant granules in the cytosol), think of
Chediak Higashi dz as your dx (LYST gene mutation- AR disease is caused by a lysosomal-trafficking regulator gene mutation, resulting in fusion of intracellular granules and dysfunctional neutrophil degranulation.)
Sxs and labs in Chediak Higashi Dz:
Sxs:
■ Recurrent skin infections and pneumonias, esp. Staphylococcus aureus
■ Partial oculocutaneous albinism
■ Mild bleeding diathesis;
■ Progressive peripheral neuropathy
Labs:
■ Giant gray granules in the cytoplasm of nucleated cells.
■Leukopenia, neutropenia.
■ Chemotaxis test.
Key features of selective IgA deficiency:
Note: Older kids
Key features of Wiskott-Aldrich syndrome:
Thrombocytopenia, eczema, X linked (so expect to see on test in boys)
Key features of ataxia telangiectasia:
Ataxia before telangiectasia (a before t)
Key features of SCID:
B cell problems (so recurrent bacterial infections) and T cell problems (so recurrent viral and fungal infx)
Multiple causes but big one for exams is adenosine delaminate deficiency; il2 receptor defect can also cause (Remember, IL-2 receptor you find it on essentially every T cell; il2 secreted by T cells: Stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells)
Sxs tend to show up very early in life before 6mo (compared to Bruton’s agammaglobulinemia showing up after 6 mo)
A 2-month-old male has a temperature of 103°F, HR 200 beats/min, RR 50 breaths/
min, and appears lethargic. His umbilical cord has not separated; the surrounding skin is erythematous and indurated. He is admitted for sepsis. His white blood cell count is 22,000/mm3 with 90% neutrophils. Think:
defective neutrophil migration (leukocyte adhesion deficiency)
Sxs leukocyte adhesion deficiency
■ Neutrophilia without inflection
■ Failure of separation of umbilical cord, with secondary omphalitis and sepsis.
■ Poor wound healing.
■ Bacterial infections without pus.
■ Severe gingivitis.
Key points leukocyte adhesion deficiency:
Kid has all these Dz where they form abcesses but there is no pus; or delayed separation of umbilical cord; integrin defect (cd18)
Key points CVID:
See bruton like presentation but in older kid (like teenager); have low levels of most immunoglobulins (give away vs bruton is age range: teenager=cvid; vs <1yo but>6mo=bruton)
Consider CGD as the dx (NADPH oxidase deficiency) in a kid with:
recurrent infections with catalase +ve bugs (especially Aspergillus/S. Aureus)
(Don’t have NADP oxidase cannot make superoxide radicals; catalase positive organisms can break down hydrogen peroxide to water and oxygen - can thrive and cause recurrent infections)
How to Dx CGD?
Remember the Nitroblue Tetrazolium/Dihydrorhodamine tests which are used for dx. (Exams used to focus on Nitroblue Tetrazolium, but now beginning to focus on Dihydrorhodamine)
Txt CGD
IFN-Gamma may help.
Describe Stertor
Low-pitched sound like nasal congestion experienced with a cold or the sound made with snoring
(Noisy breathing, snoring sounds, Lots of mucous, congestion mainly nasal upper throat)
Describe Stridor
higher-pitched noise that occurs with obstruction in the extra- thoracic airway
(Concerned about issue in Upper respiratory)
Describe Wheezing
high-pitched noise that occurs during expiration due to narrowing, spasm, or obstruction of the smaller airways in the lungs (whistley, usuallly hear with stethoscope)
Inspiratory stridor suggests
laryngeal obstruction
Expiratory stridor suggests
tracheo-bronchial obstruction
Biphasic stridor suggests
subglottic or glottic anomaly
Common cold (upper respiratory infection): definition and common causes
Definition: multi-etiology illness has symptoms including cough, congestion, and rhinorrhea
Causes: >200 viruses—especially rhinoviruses (30–50%), coronavirus (10–15%), influenza (5–15%), parainfluenza, respiratory syncytial virus (RSV), adenovirus, metapneumovirus.
The best treatment for the common cold is
to increase oral fluids, not pharmacologic treatment
Avoid aspirin in young children due to the theoretical risk of
Reye syndrome
Mucopurulent rhinitis may accompany a common cold: what does it indicate?
does NOT necessarily indicate sinusitis; it is not by itself an indication for antibiotics
Infants typically breathe through their nose; thus, the common cold can trigger
respiratory distress in the young infant due to mucous obstruction of the nares
(Judicious use of nasal saline drops and suctioning is important to relieve the obstruction)
A 7-year-old girl is well when she leaves for school but arrives home afterward with
a sore throat and runny nose. She is also coughing and sneezing. Think:
Rhinovirus. Rhinovirus colds frequently start as a sore or “scratchy” throat with a runny nose.
A 17-year-old male has acute onset of fever, cough, conjunctivitis, and pharyngitis.
Think:
Adenovirus. Characteristic presentation: pharyngitis, rhinitis, and conjunctivitis (also known as pharyngoconjunctival fever)
Symptomatic treatment for influenza in healthy children
fluids, rest, acetaminophen, or ibuprofen
Treatment for influenza in children at risk
Initial treatment should begin as soon as possible (ideally within 48 hours of illness onset) with a single neuraminidase inhibitor such as oral oseltamivir or inhaled zanamivir; intravenous peramivir
and oral baloxavir are alternatives (some indication age group differences in which to use)
Influenza can be severe in children with congenital heart disease, bronchopulmonary dysplasia (BPD), asthma, cystic fibrosis, and neuromuscular disease; if influenza vaccination is contraindicated, these high-risk patients would be candidates for influenza postexposure prophylaxis.
Tx pregnant patients with H1N1
5-day course of antiviral
treatment (oseltamivir is preferred during pregnancy)
During influenza, there is an increased risk for
bacterial superinfection; most common organisms are Staphylococcus aureus and Streptococcus pneumoniae
Recommendations for influenza- vaccine in children (23-24)
annual influenza vaccination for all children without medical contraindications starting at 6 months of age. Any licensed influenza vaccine (injection and intranasal) appropriate by age and health status can be used for vaccination.
Croup: most common pathogen and key sxs/signs
most common pathogen: Parainfluenza virus
key sxs/signs: Barking cough, steeple sign
Epiglottitis: most common pathogen and key sxs/signs
most common pathogen: H. influenzae type B
key sxs/signs: Tripod position, thumb sign
Tracheitis: most common pathogen and key sxs/signs
most common pathogen: S. aureus, H. influenzae type B
key sxs/signs: Rapidly progressive, biphasic stridor
Bronchiolitis: most common pathogen and key sxs/signs
most common pathogen: Respiratory syncytial virus
key sxs/signs: Paroxysmal wheezing
Bronchitis: most common pathogen and key sxs/signs
most common pathogen: Viral
key sxs/signs: Productive cough
Pharyngitis: most common pathogen and key sxs/signs
most common pathogen: Viral, group A strep
key sxs/signs: Sore throat, tonsillar involvement
Bacterial pneumonia: most common pathogen and key sxs/signs
most common pathogen: S. pneumoniae
key sxs/signs: Productive cough, lobar consolidation
Pulmonary abscess: most common pathogen and key sxs/signs
most common pathogen: S. aureus, group A strep, anaerobes
key sxs/signs: Cavity with air-fluid level
——— is the most common cause of stridor in a febrile child.
Croup
Croup is the most common infectious cause of acute ———obstruction.
upper airway
——— at home but ——— in ED: Think croup.
Stridor and distress
calm and free of stridor
Define croup
Viral upper respiratory tract infection with inflammation and narrowing in the subglottic airway; most commonly Parainfluenza virus; occurs in children 3 months to 3 years of age in fall and winter months
Key sxs croup
■ Inspiratory stridor.
■ Seal-like, barking cough
■ Symptoms are worse at night, with sudden onset of symptoms.
Key diagnostic sign for croup
Steeple sign—narrowing of tracheal air column just below the vocal cords
In croup, ——— that is unresponsive to racemic epinephrine suggests that hospital admission is needed.
Stridor at rest
Epiglottitis: Sequence of treatment and confirmatory radiographs
acute airway emergency: treatment should not be delayed to obtain confirmatory radiographs
Epiglottitis is a true medical emergency. If suspected, DO NOT:
■ Examine the throat
■ Use narcotics or sedatives, including antihistamines
■ Attempt venipuncture or other tests
■ Place patient supine
Definition Epiglottitis
This condition is an acute, life-threatening bacterial infection of epiglottic and supraglottic tissues; most commonly Haemophilus influenzae type B; Usually occurs between 2–6 years of age, but it can occur at any age; Suspect in unvaccinated children and immunodeficient children (H. influenzae immunization has nearly eliminated epiglottitis in young children)
Sxs Epiglottitis
■ Sudden onset of inspiratory stridor and respiratory distress.
■ Three Ds: dysphagia, drooling, and distress.
■ Tripod position—hyperextended neck, leaning forward, mouth open.
■ Muffled voice (“hot potato” voice).
■ High fever (usually the first symptom).
■ Tachycardia is a constant feature.
■ The child will appear toxic.
■ Severe respiratory distress develops within minutes to hours.
Dx Epiglottitis
■ Laryngoscopy—swollen, cherry-red epiglottis.
■ Lateral neck x-ray to confirm (obtain portable x-ray): Swollen epiglottis (thumbprint sign)
Tx Epiglottitis
■ Secure the airway (endotracheal intubation in OR).
■ Administer ceftriaxone for 7–10 days.
■ Use rifampin prophylaxis for close family contacts with incompletely immunized or immunocompromised children.
(Treat epiglottitis with third-generation cephalosporin and anti-staphylococcal agents (clindamycin, vancomycin) against MRSA. Ideally, a blood or epiglottic culture will clarify the causative organism and allow monotherapy.)
Cephalosporins coverage by generation:
1st Generation: Good Gram-Positive; Poor Gram-Negative
2nd Generation: OK Gram-Positive; OK Gram-Negative
3rd Generation: Poor Gram-Positive; Good Gram-Negative
4th Generation: Pseudomonas + Good gram-positive and negative
5th Generation: MRSA + Good gram-positive and negative
Cephalosporins moa:
Cephalosporins work by disrupting bacterial cell wall synthesis. Similar to penicillin, cephalosporins are beta-lactam antibiotics. This means cephalosporins contain a beta-lactam ring in their molecular structure. The beta-lactam ring binds to penicillin-binding proteins, which would normally cross-link and strengthen bacterial cell walls. This disrupts bacterial cell wall synthesis and results in bacterial death (bactericidal).
Cephalosporins drugs in each generation:
First Generation = “FA/PHA”
Second Generation = “Everything Else”
Third Generation = “ONE/TEN/IME”
Fourth Generation = “PI”
Fifth Generation = “ROL”
An 18-month-old boy awakens at night with sudden onset of inspiratory stridor and a barking cough with difficulty breathing that subsides on route to the emergency department. He has had a runny nose and cough for 2 days. On examination, he has a barky cough and inspiratory stridor only with agitation. Think:
Croup
A 4-year-old unvaccinated boy brought to the ED is flushed, making high-pitched noises on forced inspiration, leaning forward in his mother’s lap, and drooling. His illness started with a fever and sore throat, rapidly progressing to difficulty swallowing, drooling, restlessness, and stridor. He appeared toxic and anxious. A lateral neck x-ray shows a thumbprint sign. Think:
Epiglottitis. Get him to an OR to intubate and treat!
The classic presentation is the “three Ds” (drooling, dysphagia, and distress).
1 y/o w/ fever to 100.5 & “barking” cough and loud noises on inspiration. Dx?
Croup
Croup: Most common bug?
Parainfluenza virus
Croup: X-ray buzzword?
“steeple sign”
Croup: Treatment?
Mist, epinephrine neb, steroids
(Tx: “racemic epi” “steroids are 2nd line”)
2 y/o w/ fever to 104 & drooling w/ intercostal retractions and tripod position.
Epiglottitis
Epiglottitis: Most common bug?
H. Flu B (only in unimmunized), Strep pyo, strep pneumo, staph
Epiglottitis: X-raybuzzword?
“thumbprint sign”
Epiglottitis: Next best step?
Go to OR and intubate (want to intubate in OR- because any manipulation of epiglottis can cause spasm, loss of airway, and death - don’t try to intubate in ER or office- go to OR)
Epiglottitis: Treatment?
Anti-staph abx + 3rd generation cephalosporin
(Racemic Epi won’t cut it here need to treat bug with abx)
The term “wheeze” should get you thinking about a:
lower respiratory tract infection (LRTI)
Lower respiratory tract infection (LRTI) for a kid < 2 yo, consider:
(Alternatively, when would you consider PNA?)
RSV as the offending organism (bronchiolitis, usually there’s cough/runny nose some days before).
To go with PNA, you need other evidence in the Q like an XR revealing consolidation, or mention of terms like dull to percussion and increased tactile fremitus.
(If kid less than 2, probably do not have group A strep pharyngitis)
For RSV bronchiolitis, TOC?
supportive care/humidified O2
Ribavirin use is controversial. For high risk kids (e.g. pulmonary problems), consider palivizumab (RSV-specific monoclonal antibody) as prophylaxis. Bronchodilators DO NOT help.
(Re bronchodilators from book: Trial of nebulized albuterol although no long-term benefit is shown (only 20–50% are responders; discontinue if no objective benefit).)
Bronchiolitis is the most common serious respiratory infection in children ——— years.
<2
——— causes more than 50% of cases of bronchiolitis.
RSV
——— are the only source of RSV infection
Humans
RSV bronchiolitis symptoms tend to peak on days ———
3–5
Define bronchiolitis
This is a viral infection of the lower respiratory tract, which occurs after upper respiratory symptoms; RSV—most common cause.
A previously healthy 4-month-old has rhinorrhea, cough, and a low-grade fever. The child then develops tachypnea, mild hypoxemia, and hyperinflation of lungs. Think:
Bronchiolitis.
Classic presentation: acute onset of cough, wheezing, and increased respiratory effort after an upper respiratory tract prodrome (fever and runny nose), during winter months
Prevention RSV in high-risk infants?
From divine intervention: Palivizumab (RSV-specific monoclonal antibody) is given monthly before and during RSV season in high-risk infants (typically premature infants, infants with chronic lung disease, and patients with congenital heart disease and cardiac compromise).
Current update on vaccines:
RSV preventive antibody products
There are two RSV antibody products that can help prevent severe RSV disease in infants and young children: Nirsevimab (Beyfortus), and Palivizumab (Synagis).
Nirsevimab is recommended for:
All infants younger than 8 months of age born during RSV season or entering their first RSV season. Except in rare circumstances, most infants younger than 8 months of age do not need nirsevimab if they were born 14 or more days after their mother got RSV vaccine.
Some children aged 8 through 19 months who are at increased risk for severe RSV disease and entering their second RSV season.
Palivizumab (Synagis) use is limited to:
Some children younger than age 24 months of age with certain conditions that place them at increased risk for severe RSV disease. It must be given once a month during RSV season.
RSV vaccine
An RSV vaccine (Abrysvo, Pfizer) is recommended during weeks 32 through 36 of pregnancy to prevent severe RSV disease in infants. This vaccine should typically be given September through January.
Symptoms of asthma can be identical to bronchiolitis. Suspect asthma instead with:
■ Family history of asthma or atopy
■ Prior episodes of wheezing
■ Response to bronchodilator
9mo infant w/ runny nose, wheezy cough, T = 101.5, and RR = 60. Retractions are visible and pulse ox is 91%. Dx? Most common bug?
Dx: Bronchiolitis
Most common bug? RSV. Confirm w/ swab
(This kid would meet criteria for hospitalization; not every kid with bronchiolitis needs to be hospitalized- but this. Kid in respiratory distress)
Bronchiolitis: CXR findings?
Hyperinflation w/ patchy atelectasis
Bronchiolitis: Treatment?
Hospitalize if respiratory distress. Albuterol nebs. NO steroids
(Re bronchodilators from book: Trial of nebulized albuterol although no long-term benefit is shown (only 20–50% are responders; discontinue if no objective benefit).)
Bronchiolitis: Who needs vaccine?
From Emma holiday: There is a RSV vaccine but very few kids quality. Palivizumab for premies, CHD, lung dz (like CF), immune dz
Current update:
RSV preventive antibody products
There are two RSV antibody products that can help prevent severe RSV disease in infants and young children: Nirsevimab (Beyfortus), and Palivizumab (Synagis).
Nirsevimab is recommended for:
All infants younger than 8 months of age born during RSV season or entering their first RSV season. Except in rare circumstances, most infants younger than 8 months of age do not need nirsevimab if they were born 14 or more days after their mother got RSV vaccine.
Some children aged 8 through 19 months who are at increased risk for severe RSV disease and entering their second RSV season.
Palivizumab (Synagis) use is limited to:
Some children younger than age 24 months of age with certain conditions that place them at increased risk for severe RSV disease. It must be given once a month during RSV season.
RSV vaccine
An RSV vaccine (Abrysvo, Pfizer) is recommended during weeks 32 through 36 of pregnancy to prevent severe RSV disease in infants. This vaccine should typically be given September through January.
Contrast normal vs consolidated vs atelectatic lung:
Question 1:
Question 2:
The term “stridor” should get you thinking about ——— like ———
URTI
epiglottitis (usually the Q will mention something about super high fevers and acute onset respiratory distress/drooling/difficulty swallowing; also tripoding) OR laryngotracheobronchitis (croup)
Croup is typically caused by
parainfluenza virus
Croup is a ——— obstruction
subglottic
(In contrast to epiglottitis which is also a URTI but is supraglottic)
Consider croup dx in an infant with sxs of
fever/cough/runny nose (“viral prodrome”) who then develops inspiratory stridor and a barky/seal like cough
(The Q may be nice and mention the sxs being worse at night)
Croup: Tx
racemic epinephrine (“opens up the airway”)
(Bronchodilators help for croup)
Croup: CXR
“steeple sign”
Epiglottitis arises from ——— obstruction
supraglottic
Epiglottitis CXR
thumbprint sign
Epiglottitis Next Step?
Do not perturb the child. Prepare for emergent intubation (call your friendly anesthesiologist).
The ——— vaccine has strongly reduced the incidence of epiglottitis
Hemophilus Influenza B
For a kid that was perfectly normal (no fever nothing) who develops sudden respiratory distress, think of
foreign body ingestion (use a flexible laryngo/bronchoscope
