5.2 Pulmonary Embolus & Acute Respiratory Infection

Pulmonary Embolus & Acute Respiratory Infection

Pulmonary Embolus in the PICU

Pulmonary embolism (PE) is less common in children than in adults, but critically ill pediatric patients carry elevated risk. Classic risk amplifiers include indwelling central venous catheters, malignancy and chemotherapy, cyanotic or complex congenital heart disease, recent surgery or major trauma, prolonged immobilization, nephrotic syndrome, obesity, oral contraceptives in adolescents, and inherited thrombophilias. Hospital-acquired venous thromboembolism often begins in the upper extremities related to lines—so unexplained ipsilateral facial or arm swelling plus new hypoxemia should raise suspicion.

Pathophysiologically, emboli increase alveolar dead space: ventilation continues to lung units that are under-perfused. SpO2 may fall, EtCO2 can drop relative to PaCO2 (widened gradient), and the right ventricle faces acute afterload. Severe PE presents with hypotension, syncope, profound hypoxemia, or PEA arrest. Nursing priorities are airway and oxygenation support, hemodynamic monitoring, avoidance of unnecessary PEEP increases that further load the RV until the team directs settings, rapid notification, anticoagulation or thrombolysis per intensivist/hematology plan, and preparation for advanced therapies in massive PE. Imaging (CT pulmonary angiography when safe, or other modalities based on stability and kidney function) confirms the diagnosis; do not delay resuscitation for a scan in an unstable child.

Pneumonia, Bronchiolitis, and Viral Respiratory Disease

Bronchiolitis (often RSV, also rhinovirus, hMPV, and others) is a leading cause of infant respiratory failure in season. Inflammation and mucus plug small airways, producing wheeze, crackles, hyperinflation, and V/Q mismatch. Support is largely supportive: oxygen or HFNC/NIV as needed, hydration, nasal suction, and monitoring for apnea in young infants. Pneumonia—viral, bacterial, or mixed—causes alveolar consolidation, fever, and hypoxemia; bacterial disease may progress to parapneumonic effusion or empyema. Aspiration pneumonia follows impaired swallow, seizures, or GERD-related events. Immunocompromised children may harbor opportunistic pathogens and deteriorate faster.

Nursing care integrates work-of-breathing scores, secretion management, antibiotic timing when bacterial disease is suspected, and recognition of complications (pneumothorax after coughing/positive pressure, SIADH in some pneumonias, septic shock). For viral illness, avoid unnecessary bronchodilator “trials” that do not change the disease course in typical bronchiolitis; follow evidence-based pathways.

Isolation and Infection Prevention

Match isolation to the organism and policy. Many respiratory viruses and bacterial pathogens such as influenza and pertussis call for droplet precautions; RSV and some pathogens also need contact precautions because of prolonged environmental survival on surfaces. Suspected measles, varicella, or tuberculosis require airborne precautions with appropriate room and respirator use. Cohorting during surges is common; still perform hand hygiene between every patient. Teach families that masks and gowns protect other children on the unit, not only staff.

ABG Interpretation Scenarios

Read ABGs as a story. Step 1: look at pH (acidemia <7.35, alkalemia >7.45). Step 2: identify the primary process—PaCO2 for respiratory, HCO3−/base excess for metabolic. Step 3: assess oxygenation (PaO2 and the FiO2 context). Step 4: decide if compensation is present and whether the picture matches the bedside exam.

Example patterns you will defend on the exam: (1) Infant with bronchiolitis—pH 7.28, PaCO2 62, PaO2 55 on FiO2 0.40 → acute respiratory acidosis with hypoxemia; escalate ventilatory support and treat fatigue. (2) Adolescent after PE—pH 7.48, PaCO2 30, PaO2 58 on FiO2 0.50 → acute respiratory alkalosis from tachypnea plus hypoxemia from dead space/shunt physiology; support oxygen and hemodynamics. (3) Child with pneumonia and diarrhea—pH 7.20, PaCO2 38, HCO3− low → metabolic acidosis with inadequate respiratory compensation if CO2 is not falling; treat shock and perfusion. (4) Neuromuscular child tiring—pH 7.30, PaCO2 58, PaO2 near normal on modest FiO2 → pure hypercapnic failure; noninvasive or invasive ventilatory support is the fix, not more oxygen alone.

Oxygen without ventilation is a common trap: climbing FiO2 while PaCO2 rises and the child grows quieter is failure, not success. Pair every ABG with work of breathing, mentation, and EtCO2 trends so interventions match physiology.

When infection and PE compete on the differential, use the timeline and risk profile. Gradual fever, focal crackles, and consolidative infiltrates favor pneumonia; abrupt dead-space hypoxemia after line placement or immobility favors embolus. Either pathway can end in intubation, but anticoagulation, thrombolysis, or embolectomy decisions are PE-specific and require rapid team activation. For infectious respiratory failure, timely cultures (when indicated), isolation compliance, and source control (including drainage of empyema when present) are the nursing-linked levers that shorten PICU stay. Reassess ABGs after each major change in support so you can prove the intervention worked—or escalate again without delay.