I just want to ask your opinions on the following case that came across our ICU.
A 35 year old woman gets admitted to our ICU following emergency C-section due to HELLP syndrome and possible DIC. Anesthesia reports difficult airway with severe desaturation on induction and possible aspiration of gastric content. Naturally we do a bronchoscopic check and find no evidence of gastric content aspiration. DIC turns out to be very benign and the patient is weaned and extubated in the night following on admission.
In the next 48 hours she develops typical radiographic and clinical signs of ARDS. When I start my night shift we find this woman very dyspneic and tachypneic. She is satting poorly around 85% - 90% at best under 40 L O2 flow via Optiflow (Upped the flow to 60 L/min which made a diff of about 2 - 4% on sats landing us at a steady 88 - 90%).
Decision is made to intubate. We try to pre-oxygenate by adding a NRM at 20 L/min O2 sats go up to 94%. Drugs of choice for this intubation were ketamine, fentanyl and rocuronium. Ketamine dosage was 1 mg/kg as by standard order in our institution. However it takes forever for this patient to get sedated we add another dose of ketamine at 1 mg/kg but she is desatting rapidly (decreased FRC is a ****). Patient is still fighting against BMV and sets are dropping to the 60's. We decide to push rocuronium anyway even though patient is still fighting the BMV to prevent ending up in a code situation.
As we pass the ETT (thankfully very easily) sats are in the 40's and the patient is naturally hemodynamically compromised. Once the ETT is in place sats come up quickly to around 90% and hemodynamics improve. We quickly start continuous sedation and analgesia.
Patient went on NO followed by HFOV and ECMO support once coagulation had improved. She survived without neurological impairment or any other form of impairment.
As we discussed this particular intubation we decided that it was unacceptable that it took so long for the patient to be sedated. Usually we see very rapid sedation under ketamine (e.g. within 1 minute), but this time it took two doses and we pushed paralytics as she was at or a little above being sedated enough. The delay in sedation cost us all our oxygenation reserve and had she not been this young etc. it could/would have been a code for sure.
We were wondering about what agents we could have used instead. We limited the choice to either propofol or etomidate. Anyone offering a rationale why using one over the other?
P.S. Patient had an elevated blood pressure at time of induction around 150/70 mmHg and sinustachy at 130/min (we attributed this to respiratory distress). Patient has increased WOB for at least 48 hours with resps peaking in their 40's that night. Clinically she could still speak complete sentences but that was accompanied by desats to high 70's and low 80's.
