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Diagnosis Deconstructed

Diagnosis Deconstructed

Mind Your Vs and Qs

Morchi, Ravi MD

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doi: 10.1097/01.EEM.0000464086.51238.12

    A full-term boy born by elective C-section presented to our pediatric ED five weeks after birth in respiratory distress. He had nasal congestion and trouble breathing one day prior, and an older brother had similar symptoms. Two hours before arrival, his level of alertness deteriorated with his eyes “rolling back.”

    Inspection. He was 4.8 kg, lethargic, tachypneic to 80, and had intercostal and subcostal retractions. The initiation of a breath starts with outward movement of the chest wall and descent of the diaphragm, generating negative intrathoracic pressure. But if the underlying pulmonary parenchyma is not compliant enough to fill with air passively, the visceral pleura lags as the parietal pleura moves outward. The result is exaggerated negative intrapleural pressure and dimpling of skin between ribs.

    Auscultation. Rales and early expiratory wheezing diffusely. Collapsed or fluid-filled alveoli become audible as they pop open during the inspiratory cycle, and bronchioles are already critically narrowed at the start of expiration.

    Monitor. Heart rate of 100 rose to 160 with BVM ventilation and high-flow oxygen. He remained hypoxic to 90 percent, however, working excessively, and occasionally bradycardic from apneic episodes. Brainstem vasomotor and respiratory center depression caused by poor oxygenation and perfusion.

    Bedside testing. Glucose of 202, pH 7.16, pCO2 79, and lactate of 4. Respiratory acidosis and muscle hypoperfusion. He was intubated with midazolam, fentanyl, and rocuronium, and placed on RR of 45 with PEEP of 6 and PIP of 24. Pressure support was provided for additional breaths above 45.

    CV. Practitioners noted an early systolic III/VI crescendo-decrescendo murmur across the lower sternal border but without radiation to the axilla or associated thrill. Hepatic edge palpated 3 cm below the costal margin. Possibly a ventricular septal defect with left to right flow and increased RV preload and forward pulmonary vascular congestion. No diastolic component or radiation to the back to suggest a patent ductus arteriosus. Pre- and post-ductal limb saturations and blood pressures were not initially obtained, but the likelihood of ductal dependent systemic blood flow was deemed low.

    A 10 cc/kg bolus was initiated. Right lower extremity blood pressure ranged from 73-100/36-60 mm Hg. Midazolam sedation resulted in transient hypotension corrected by serial 10 cc/kg boluses. Judicious use of fluid and close blood pressure monitoring for the tendency toward pulmonary vascular congestion with an increased pulmonary to systemic flow ratio (qP/qS).

    RSV antigen positive. The virus infects respiratory epithelial cells resulting in their fusion into multinucleated conglomerates (syncytia). Sloughed bronchiolar syncytia cause air trapping from a partial obstruction to expiratory flow or collapse when a complete blockage halts both inspiratory and expiratory air movement. Both decrease ventilation (v). An overcirculated RV and pulmonary arterial system in the setting of left to right flow across a VSD compounds the problem with increased pulmonary perfusion (Q). The v/Q mismatch worsens hypoxemia.

    End-tidal CO2 was 40, but the blood pCO2 post-intubation was more than 100 with auscultatory findings of expiratory obstruction. So the RR was decreased to 30 and inspiratory time down to 0.5 while the trachea was aggressively suctioned. End-tidal CO2 would rise to 60, an encouraging result because serial blood gases showed a pCO2 in the same range. A rise in ETCO2 indicative of improved expiratory flow in this case, as blood (alveolar) CO2 could make its way up to the tracheal lumen.

    Data. RUL, RML, LUL infiltrates and a normal heart size on chest x-ray. Thirty-four percent bands on CBC. Ampicillin and cefotaxime initiated for possible concomitant bacterial pneumonia.

    Hypovolemic hyponatremia to 123 with lethargy and upward eye deviation upon presentation, initially concerning for a tonic infantile seizure. The CNS disturbance, however, was probably caused by hypoperfusion, hypoxia, hypercarbia, and a component of direct neuronal dysfunction in sepsis, rather than being attributed primarily to sodium.

    ECG displayed sinus tachycardia, right axis deviation from RVH, and LVH with secondary repolarization abnormalities. Normal right dominance of a neonatal circuit? Or manifestations of a left to right shunt demanding more from the right ventricle?

    He was admitted to the pediatric ICU where he continued to advance on pressure-regulated ventilation with attention to expiratory flow. An echocardiogram demonstrated a 5 mm diameter membranous ventricular septal defect with a peak interventricular gradient of 59 mm Hg, but otherwise normal four-chamber function.

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