Exam and History
(LO 1) What is the earliest and most sensitive vital sign change in pediatric pneumonia, and what are the age-based tachypnea thresholds?
Tachypnea. It is above 60 breaths/min in infants under 2 months and above 50 at 2-12 months.
What are the harms of excess oxygen or prolonged dry oxygen flow?
Absorptive atelectasis (high FiO₂ washes out nitrogen, which splints alveoli open), hyperoxia-related oxidative injury, blunted hypoxic drive in chronic CO₂ retainers, and mucosal drying with thick secretions, impaired mucociliary clearance, and epistaxis.
(LO 6) Compare alveolar, interstitial, and airway-centered inflammation: what happens, and what do you see or hear?
Alveolar (typical bacteria): fluid and neutrophils fill air sacs, causing consolidation, focal crackles, dullness, increased fremitus, and low V/Q or shunt. Interstitial (some atypicals and viruses): wall inflammation and edema cause a thicker gas-exchange barrier, dry cough, diffuse crackles, and reduced compliance. Airway centered (viral, mycoplasma): epithelial damage, mucus, rhonchi, air trapping, wheeze.
(LO 10) What is the mechanism of action of beta-lactams, and which PD parameter predicts efficacy?
They bind penicillin-binding proteins, blocking peptidoglycan cross-linking and causing osmotic lysis (bactericidal). Efficacy is time-dependent: free drug concentration must stay above the MIC.
(LO 12) How do age-related changes in body water, protein binding, hepatic metabolism, and renal function affect antibiotic dosing
Neonates have more total body water and weaker protein binding, so hydrophilic drugs (beta-lactams) have a larger volume of distribution, lower peaks, and sometimes higher per-kg doses. Hepatic enzymes are immature at birth, rise over the first months, may exceed adult activity in early childhood, and reach adult levels by late puberty. GFR nears adult levels by 6-12 months and can exceed adult rates in preschoolers. Penicillin G half-life in infants can be as short as 30-40 minutes.
(LO 1) Which exam findings are red flags for impending respiratory failure, and what other findings call for urgent escalation?
Grunting and retractions. Others are severe retractions, nasal flaring, cyanosis, lethargy or altered mental status, apnea (especially in infants), inability to feed, dehydration, and low SpO₂ for age
What is the A-a gradient, and which causes of hypoxemia widen it or leave it normal?
A-a gradient = PAO₂ − PaO₂. V/Q mismatch, diffusion limitation, and shunt widen it. Hypoventilation leaves it normal (unless prolonged or with coexisting dead space) and is distinguished by hypercapnia.
(LO 6) What does a bacterial capsule do, and who is most at risk from encapsulated organisms?
It helps bacteria resist phagocytosis. Clearance needs opsonization (antibody and complement) and splenic clearance, so asplenia or functional asplenia (sickle cell disease) and antibody deficiency are highest risk.
(LO 10) How do H. influenzae, and M. catarrhalis resist beta-lactams, and how do you counterract this?
H. influenzae and M. catarrhalis produce beta-lactamase (use amoxicillin-clavulanate or 2nd/3rd-generation cephalosporins).
LO 12) How do obesity, renal or hepatic dysfunction, immunocompromise, change antibiotic selection or dosing?
Obesity: dosing is drug-specific (adjusted body weight for aminoglycosides, total body weight with TDM for vancomycin, extended infusions for time-dependent beta-lactams). Renal dysfunction: adjust dose or interval and monitor creatinine and levels. Hepatic dysfunction: adjust hepatically metabolized drugs (macrolides, clindamycin, metronidazole) and prefer renally cleared beta-lactams. Immunocompromise: broader coverage and higher or extended dosing.
(LO 1) What are the four mechanisms that can decrease urine output in a child with pneumonia?
Decreased intake, increased insensible losses (fever, tachypnea), SIADH, and prerenal hypoperfusion from sepsis.
Compare low-flow (variable FiO₂) and fixed FiO₂ oxygen devices, and describe when you would escalate
Low-flow: nasal cannula (1-6 L, ~24-40%), simple mask (6-10 L, ~24-40%), non-rebreather (10-15 L, ~80-95%). Fixed: Venturi mask and heated humidified high-flow (mild CPAP effect, avoids mucosal drying). Escalate to NIPPV or intubation for rising CO₂, fatigue, declining mental status, inability to protect the airway, or refractory hypoxemia.
LO 7) When is a chest radiograph indicated, and what are common findings in pneumonia?
Not routine for well-appearing outpatients. Obtain for hypoxemia or significant distress, suspected effusion or complication, admission, failure to improve after 48-72 hours, or an uncertain diagnosis. Focal opacity or air bronchograms suggest consolidation, a blunted costophrenic angle suggests effusion, multiple thin-walled cavities suggest necrotizing pneumonia, and a thick-walled cavity with an air-fluid level suggests abscess.
(LO 11) Why is azithromycin favored over erythromycin and clarithromycin in children, and what is the anesthesia-relevant concern with the other two?
Azithromycin has once-daily dosing, extensive tissue accumulation (half-life ~68 hours), better tolerability, and fewer CYP interactions. Erythromycin and clarithromycin inhibit CYP3A, which can raise midazolam levels and prolong sedation.
(LO 13) How does pneumonia progress into the pleural space, and how does it worsen oxygenation?
Three stages: exudative (sterile, free-flowing fluid), fibrinopurulent (bacteria, neutrophils, fibrin, loculations), and organizing (pleural rind and "trapped lung"). Effusions compress lung that remains perfused but poorly ventilated, causing V/Q mismatch and shunt, so SpO₂ falls, work of breathing rises, and the child may tire and retain CO₂
(LO 2) After a witnessed choking or vomiting episode, how do the likely organisms, lung location, and treatment change?
Anaerobic oral flora are likely. The dependent segments are involved (right lower lobe if upright; posterior upper or superior lower segments if supine). Coverage adds anaerobes (clindamycin or ampicillin-sulbactam).
(LO 5) Distinguish physiologic dead space from physiologic shunt.
Dead space is ventilated but not perfused (high V/Q). Shunt is perfused but not ventilated (low V/Q), as in pneumonia or atelectasis.
What can CBC, CRP/ESR, procalcitonin, and cultures tell you in pediatric pneumonia, and what can't they
Leukocytosis with neutrophilia and bands favors bacterial disease, but viral and atypical infections can have normal or mildly elevated WBCs. CRP, ESR, and procalcitonin help gauge severity and response but are nonspecific; low procalcitonin lowers but does not exclude typical bacterial disease. Blood cultures are for severe, hospitalized, complicated, or unresponsive cases; viral PCR is useful in hospitalized children; pleural fluid should get Gram stain and cultures.
(LO 14) Compare vancomycin's mechanism, lung and pleural penetration, adverse effects, and monitoring.
Vancomycin binds D-Ala-D-Ala to block cell wall cross-linking (time-dependent). It has moderate-to-poor lung and pleural penetration and is renally cleared. Adverse effects include the infusion reaction (pseudo-allergic mast cell activation), nephrotoxicity, and ototoxicity. Monitor with AUC/MIC of 400-600 or troughs of 10-20 mg/L drawn before the 4th dose.
(LO 13) Distinguish empyema, necrotizing pneumonia, and lung abscess.
Empyema is pus in the pleural space. Necrotizing pneumonia is destruction and liquefaction of lung tissue with multiple cavities. A lung abscess is a single localized, walled-off cavity with an air-fluid level
How do fever, respiratory distress, and respiratory failure differ in O₂ and CO₂ trends and in appearance?
Fever alone: normal SpO₂ and CO₂, and the child is interactive and well perfused. Compensated distress: tachypnea, retractions, flaring, mild-to-moderate hypoxemia, and normal or low CO₂. Respiratory failure: fatigue, decreased effort, altered mental status, bradycardia, apnea, significant hypoxemia despite oxygen, and rising CO₂.
(LO 3, 7) How does blood gas CO₂ change as pneumonia progresses, and what noninvasive tools track it?
PaCO₂ is low early (tachypnea, respiratory alkalosis), then falling PaO₂, then PaCO₂ normalizes and rises with muscle fatigue, ending in hypoxemia, hypercapnia, and respiratory acidosis. Tools are SpO₂, ETCO₂ (valuable on supplemental O₂ because ventilation can fall without SpO₂ falling), and transcutaneous CO₂ (mainly neonates and OR).
(LO 8) What is the evidence for viral-bacterial coinfection, and what should you do when a viral test is positive?
Influenza damages respiratory epithelium and impairs mucociliary clearance, allowing secondary S. pneumoniae, S. aureus, or MRSA pneumonia. Coinfection is reported in roughly 10-30% of hospitalized children with influenza. A positive viral PCR does not exclude bacterial infection, so integrate the whole picture.
(LO 14) Which anti-staph/MRSA drugs are bactericidal versus bacteriostatic, and why does it matter?
Vancomycin and ceftaroline are bactericidal. Linezolid is generally bacteriostatic (though it can be bactericidal against streptococci). Clindamycin is bacteriostatic or bactericidal depending on the situation, and it also suppresses toxin production.
(LO 13) When is an effusion observed, drained with a chest tube, treated with alteplase, or sent for surgery?
Observe a small, free-flowing effusion in a stable child on antibiotics. Drain moderate effusions with distress, large effusions, frank pus, instability, or significant loculation with an image-guided small-bore chest tube (12 Fr or smaller). Add intrapleural alteplase for loculated empyema (converts plasminogen to plasmin to break down fibrin); one studied regimen is 4 mg in 40 mL saline, clamped ~1 hour, every 24 hours for 3 doses. VATS is for extensive loculation, persistent sepsis despite correct drainage and fibrinolytics, trapped lung, or persistent bronchopleural fistula.