Acute Respiratory Distress Syndrome (ARDS)

Patient presentation:
T.T., a 53 year old male, presented to the ER after several days of fever, cough, sore throat, runny nose, body aches, headache, chills, fatigue, shortness of breath, and progressive difficulty breathing. His PMH included: hypertension, GERD, chronic back pain, hyponatremia, bilateral inguinal hernia, vasectomy, lumbar disc surgery, and genital herpes. Upon examination T.T’s had labored breathing with accessory muscles, crackled lung sounds, and vital signs were: HR: 104, BP: 78/48, SaO2: 80% on 100% non-rebreather, temp: 37.9°C. As he progressively became more lethargic, produced incomprehensible words, and went into an unresponsive state, he was intubated and transferred to the MICU.

Differential list:
Flu, ARDS

Diagnosis:

 The symptoms and the results of the tests were consistent with ARDS secondary to H1N1 flu.

Treatment:
The patient was placed on the ventilator, had a femoral arterial line inserted, and a subclavian triple lumen catheter placed.  T.T. was started on Levophed®, which was titrated according to the hospital protocol to treat hypotension for a target MAP of 60. In addition, the patient was placed on the ARDS protocol. According to the protocol, the ventilator’s FiO2 and PEEP were adjusted according to the patient’s oxygenation status. As the PaO2 and SaO2 decreases, oxygenation is supported by raising the FiO2 and PEEP in the vent settings. The increased FiO2 provides more oxygen to treat the hypoxia while the PEEP helps to recruit the alveoli. Despite attempts to maintain the patient’s PaO2 and SaO2 above 88%, the patient minimally responded to the vent setting adjustments. The patient was sedated on a continuous infusion of fentanyl and Versed® for a RASS (Richmond Agitation-Sedation Scale) goal of -4. This allows the ventilator to do the work and while preventing the patient from bucking, overbreathing, and fighting the vent. Despite all efforts, the patient continued to decompensate to the point that the patient’s vent settings had an FIO2 100% and PEEP: 18.  The physicians decided to add nitric oxide to the vent, which causes pulmonary vasodilation and bronchodilation. By this point, the patient continued to be hypoxemic, hypotensive, and ABG showed that he was in respiratory acidosis (pH: 7.17, PaCO2: 65, PaO2: 65, HCO3: 22). At this point, he continued to deteriorate, was septic, and had multisystem failure (renal, GI, pulmonary, cardiac, etc.).

Outcome:
After 3weeks of attempting to treat the underlying problem of H1N1 flu and ARDS, the patient continued to be hypotensive (despite being on multiple vasopressors) and hypoxemic. Due to the patient’s poor prognosis of having multiple organ failure, H1N1, and ARDS, the physician decided to consult the family about his condition, patient’s wishes, and code status. As a result, the family understood what was going on, decided to not escalate care, and made him a DNR. Two days after the family’s decision, the patient passed away.

Case created by Tina Thieu, 2011.