Ketamine during an emergent intubation

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Specializes in GICU, PICU, CSICU, SICU.

Hi all,

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.

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Sounds like the dosage was the problem, not necessarily the choice of meds. For RSI, start with 2mg/kg; this will produce sedation in 30 seconds. Even so, I wonder why they chose ketamine over etomidate? Etomidate is FAST, and the dosage is kind of hard to mess up on. Just one 20mg dose for the average adult does the job nicely.

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I did some work in the ED prior to nursing school, and our doctors favored etomidate over propofol for RSI. The general consensus was that propofol poses a higher risk for hypotension and bradycardia while etomidate is much safer, and generally free from those negative side effects. I saw propofol used a few times, and we sometimes used it as a maintenance infusion, but we usually used etomidate for our initial sedation during RSI.

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Specializes in Nurse Anesthesia, ICU, ED.

It easy to "arm-chair QB" this situation, but these are my thoughts:

Based on the info presented, I think that propofol (PPF) would be the best agent to use for RSI, post-partum pts are a little hyperdynamic and given the pts BP and HR listed could tolerate the transient drop. Further, the respiratory depressive effect of PPF could allow for easier positive pressure ventilation with a BMV, it is cerebral protective, and has a similar onset to ketamine.

Etomidate, while it does not affect hemodynamics like PPF, can suppress hypothalamic-pituitary-adrenal (HPA) axis, even with a single induction dose. this would be bad in a critically ill patient.

Ketamine, in the doses listed and as a previous posted stated was too low to be effective. the termination of action by induction drugs is related to re-distribution, ketamine has a large Vd and thus would move from the central circulation to peripheral tissues. although ketamine can prevent BP and HR lability in healthy pts, it can be a myocardial depressant when pts are catecholamine depleted. finally, ketamine can inhibit platelet aggregation, another consideration in a pt with HELLP/DIC.

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Etomidate, while it does not affect hemodynamics like PPF, can suppress hypothalamic-pituitary-adrenal (HPA) axis, even with a single induction dose. this would be bad in a critically ill patient.

My understanding is that there is no evidence of any adverse effects of this, that there is no effect on mortality or adverse outcomes, and further, there are no contraindications for use of etomidate for RSI. We only intubate critically ill patients in the ED, and we always use etomidate.

Propofol, on the other hand, reduces oxygen delivery to the tissues r/t its adverse cardiovascular effects, and in someone in respiratory failure, this would be concerning to me.

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People used to think the etomidate did not increase m+m, but that is not the consensus now. Even a single dose has been shown to cause prolonged adrenal supression that increases m+m, especially in septic shock. Use of etomidate during mechanical ventilation increased mortality from 28% (morphine + benzos) to 77% (morphine + etomidate).

I prefer fentanyl/midazolam + micro propofol doses to facilitate intubation in critically ill patients.

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Specializes in CCT.

Couple of thoughts. First, when and how much fent was given? This is as likely your reason for desaturation as the ketamine.Ketamine was an appropriate choice of induction agent in this case as one of the vaunted properties of ketamine is it's ability to sedate while leaving respiratory drive intact. The dose, as has already been noted, was inappropriate. Were you actively ventilating with the BVM or simply allowing the patient to breathe through it? Instead of trying to ventilate a fighting, ****** off patient, try NIPPV, or seal a BVM (better yet a Jackson Rees circuit) with PEEP attached and allow them to breathe through it with the O2 on "sssshhhhh" as an EM doc described to me one day. What you get is better O2 delivery to the distal end of the pulmonary tree without the discomfort and gastric insulation of positive pressure ventilaton. Do this while your preparing the patient for intubation.It sounds like this lady is very lucky she didn't end up dead or with a hole in the trachea. Airway disasters like this have a way of "gut checking" everyone involved to never make the same mistakes again.

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None of those links provide any conclusive evidence that using a single bolus dose of etomidate to facilitate RSI increases morbidity and mortality; rather, it is all speculation. Clearly, more research is needed.

In the meantime, as it is with almost every single medication in existence, we must weigh the benefits vs. the risks. Etomidate is an induction agent of choice for RSI for a reason, and I suspect it will remain so for some time, until something new and better comes along.

At any rate, it would appear that ketamine was chosen because that is the practice at the OP's facility, and that the dose was inadequate.

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Controversies surrounding the use o... [Ann Pharmacother. 2010 Jul-Aug] - PubMed - NCBI

Etomidate versus ketamine for rapid sequence intubati... [Lancet. 2009] - PubMed - NCBI

Acute adrenal insufficiency aft... [J Intensive Care Med. 2007 Mar-Apr] - PubMed - NCBI

http://www.ncbi.nlm.nih.gov/pubmed/20403156

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[TD]Anaesthesia. 1984 Oct;39(10):973-81.[h=1]Mortality amongst multiple trauma patients admitted to an intensive therapy unit.[/h]Watt I, Ledingham IM.[h=3]Abstract[/h]A retrospective review of 428 severely injured patients admitted to an intensive therapy unit between 1969 and 1982 was performed. The patients' primary injuries were assessed using the injury severity score (ISS), and subsequent complications using the complications impact index and sepsis score. Between 1969 and 1980 mortality fluctuated between 19% and 29% but rose to 47% (p less than 0.05) during 1981-82 in spite of an unchanged ISS. The increased mortality was confined to ventilated patients surviving more than 5 days from injury and was associated with multiple organ failure and severe infection. The rapid and sustained increase in mortality could not be explained by any obvious change in severity of injury or referral pattern. The only deliberate change in management related to the combination of analgesic/sedative drugs used in ventilated patients. During 1979 to 1982 mortality was 28% in patients given morphine with or without benzodiazepines and 77% in those given morphine and etomidate (p less than 0.0005). After discontinuation of the latter regimen (May 1983) and resumption of the former analgesic/sedative combination, mortality fell to 25% (p less than 0.005). Possible mechanisms leading to increased mortality include adrenocortical insufficiency or depth of anaesthesia.[/TD]

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I try not to use it if I don't have to. Not worth the risk IMO.

But I agree a large RCT would be nice.

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I'm guessing that stat refers to using etomidate for continuous sedation, not a single bolus for RSI. You're right, it is pretty much consensus that using etomidate for continuous sedation does increase M&M. The jury is still out on the use of the single bolus dose, though.

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I think we can all agree that it increases morbidity and hemodynamic sequalae as it increases the likelihood of vasopressor dependence in the PO period. Yes jury is still out on if it increases mortality.

And yes the ventilator study is when used as a maintenance agent (this study is probably why this is not practiced anymore today).

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