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Review Question - QID 104029

QID 104029 (Type "104029" in App Search)
A 45-year-old man arrives by ambulance to the emergency room after being involved in a very severe construction accident. The patient was found unconscious with a large metal spike protruding from his abdomen by a coworker who was unable to estimate the amount of time the patient went without medical aid. Upon arrival to the ER, the patient was unconscious and unresponsive. His vital signs are BP: 80/40, HR: 120 bpm, RR: 25 bpm, Temperature: 97.1 degrees, and SPO2: 99%.He is taken to the operating room to remove the foreign body and control the bleeding. Although both objectives were accomplished, the patient had an acute drop in his blood pressure during the surgery at which time ST elevations were noted in multiple leads. This resolved with adequate fluid resuscitation and numerous blood transfusions. The patient remained sedated after surgery and continued to have relatively stable vital signs until his third day in the intensive care unit, when he experiences an oxygen desaturation of 85% despite being on a respirator with 100% oxygen at 15 breaths/minute. On auscultation air entry is present bilaterally with the presence of crackles. A 2/6 systolic murmur is heard. Readings from a Swan-Ganz catheter display the following: central venous pressure (CVP): 4 mmHg, right ventricular pressure (RVP) 20/5 mmHg, pulmonary artery pressure (PAP): 20/5 mmHg. Pulmonary capillary wedge pressure (PCWP): 5 mm Hg. A chest x-ray is shown as Image A. The patient dies soon after this episode. What is the most likely direct cause of his death?
  • A

Diffuse alveolar damage

66%

115/174

Ventricular septal defect

3%

5/174

Myocardial free wall rupture

13%

22/174

Papillary muscle rupture

13%

23/174

Myocardial reinfarction

2%

4/174

  • A

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This individual is likely suffering from Acute Respiratory Distress Syndrome (ARDS) which is classified histologically as diffuse alveolar damage (DAD).

Acute respiratory distress syndrome is an acute onset bilateral patchy airspace disease which results in noncardiogenic pulmonary edema and severe hypoxemia. The criteria for diagnosis require an acute onset (generally less than 24 hours) of hypoxemia with bilateral infiltrates on chest radiographs. Additionally, there must be no evidence of increased left atrial pressure (PCWP <18), and severe hypoxemia (PaO2/FiO2 less than or equal to 200).

Mortelliti et al. review acute respiratory distress syndrome. They state that its pathophysiology involves an inciting local or systemic events that leads to pulmonary endothelial and epithelial damage that increases permeability. The first signs are tachypnea, hypoxia, and respiratory alkalosis. Experimental therapies for this disorder include nitric oxide and surfactant but have not been shown to improve mortality.

Frohlich et al. review future directions of ARDS therapy. They note that extracorporeal membrane oxygenation (ECMO) has provided some mortality benefit, but effective biological agents are thus far still unavailable.

Figure A: Bilateral patchy infiltrates on a chest radiograph as seen with ARDS.
Illustration A: Hematoxylin and Eosin staining of lung tissue showing hyaline membranes, a hallmark of DAD/ARDS.

Answers 2-5: The rest of the answer choices could result in similar signs and symptoms (pulmonary edema, hypoxemia) but would result in an increased PCWP (>18 mmHg) because they are the result of acute heart failure.

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