72 year old male presents to the ER with lethargy, fatigue, exertional dyspnea, fever of 102 and hypotension. He is mildly hypoxic per ed reports. He’s placed on 3L, diagnosed with pna based on a chest film demonstrating bilateral multi focal opacities with superimposed edema, started on abx and given a 30ml/kg fluid challenge. He is noted to have a creatinine of 5.2 which is new, a potassium of 5.9 and a bicarbonate of 15. First lactate is 6. After fluids lactate is 3 and His map is around 75 and he is admitted to SDU. Around 2 am you are called by the night nurse that his saturation’s have worsened greatly and he is more tachypneic. He is now on bipap, presumably started by the floor intern. Nurse said he has crackles. No fever. He is awake and answers questions but does appear labored pausing to speak partial sentences. His stat chest xry looks wet but with persistent infiltrated that appear worsened. You pull up old records and note his EF last month was 55%. There is also a mention of history of adrenal insufficiency but he is not on glucocorticoids. He has no peripheral edema. Current bipap settings are 18/10 @100%. Abg 7.21/38/51/14 with sat of 82%.
Questions for Tuesday
1) what are you going to do with regards to his current respiratory status?
2)if you are going to intubate him, what are you going to use for induction agents and why?
Questions for Tuesday
1) what are you going to do with regards to his current respiratory status?
2)if you are going to intubate him, what are you going to use for induction agents and why?
This is a patient that has sepsis from pneumonia that is now having increased work of breathing and worsening hypoxia. We have concerns about this patient about having severe ARDS. His PaO2 to FiO2 ratio is 51. He has new worsening opacities, it has been less than 1 week since he was diagnosed with pneumonia and there is no reported history of heart failure. We cannot completely rule out flash pulmonary edema from cardiac causes at this time though. He has therefore failed non-invasive ventilation and we would need to intubate this patient using RSI in order to better ventilate this patient.
ReplyDeleteAll patients getting RSI need both neuromuscular blockade and sedation. For a patient in respiratory distress the first choice options for sedation are etomidate and ketamine. There is controversy regarding use of etomidate in the setting of adrenal insufficiency. It has been shown to suppress the adrenals, however there is no clear evidence that a single dose given for induction has worse outcomes. I would avoid using propofol in the patient due to concern for hypotension. Ketamine would be a good choice for this patient.
First choice for neuromuscular blockade would usually be succinylcholine due to its shorter duration and half life. Unfortunately we cannot use succinylcholine in this patient due to the hyperkalemia of 5.9. I would therefore choose rocuronium.
https://lifeinthefastlane.com/ccc/ardsnet-ventilation-strategy/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635268/pdf/jtd-07-10-1699.pdf
Uptodate
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resident360.nejm.org
1. Not much room to improve his O2 saturation/ requirement therefore I would check his Code status and if appropriate, intubate. His P/F ratio is 51% which indicates possible severe ARDS vs severe pulmonary edema. would obtain a BNP and echo. Subsequently, would place a central line if indicated and an arterial line to monitor CVP. After ruling out heart failure, would treat as ARDS and limit fluid, use low TV on the vent per ideal body weight and check plateau pressure to ensure that it remains below 30.
ReplyDelete2. To intubate I would avoid etomidate due to contraindication in adrenal insufficiency and avoid succinylcholine to prevent worsening of his hyperkalemia.
I would cycle his BP to make sure that he is no longer hypotensive and if appropriate would give him propofol. If BP still low would give him ketamine and watch his BP.
1. Patient should have been started on CPAP for cardiogenic edema. Given the patient’s low CO2 the patient doesn’t need a rate of 18, which is what he is on now with the BiPAP. At the least I would switch him to CPAP 12/6 with a repeat ABG in an hour. However given the patient’s distress and hypoxia they may not do well on the CPAP so I would ask the patient if they would allow an elective intubation. Also given the patient’s lactate of 3 the patient is still not perfusing well and needs additional fluid support. Given the acute renal function, low EF and already volume overloaded status it would be expected that the patient’s respiratory status would decline even on CPAP.
ReplyDelete2. For intubation the patient would need a paralytic and an induction agent. Given the patient’s recent hypotension the patient would need etomidate for induction but this would be contraindicated with his renal function and adrenal insufficiency,A. Ketamine would be a good option because it is useful in septic shock and does not cause adrenal insufficiency. Propofol is another option but is not useful in hypotension, B. Succinylcholine is contraindicated in hyperkalemia so I would use rocurionium as a paralytic, B.
1. He would need to be immediately intubated at this point as he is acidotic with a pH of 7.21 and a Pao2 of 51 with o2 sats in the low 80’s even with a peep of 10 and 100% Fio2, especially with signs of labored breathing like tachypnea and only speaking partial sentences. He does meet the inclusion criteria for ARDS since we do have an EF and no signs of left atrial hypertension, persistent infiltrates on CXR, and a Pao2/Fio2 ratio of 51.
ReplyDelete2. For induction, we should avoid etomidate due to history of adrenal insufficiency as etomidate can decrease the secretion of cortisol and lead to worsening adrenal insufficiency. We should also avoid propofol due to recent hypotension. In this case, we could use ketamine for sedation. As for paralytic agents, we should avoid succinylcholine with his hyperkalemia, so rocuronium would need to be used. Assuming he has ARDS, this is the initial ventilation strategy:
1. calculate predicted body weight
2. select any ventilator mode
3. achieve a TV of 6mL/kg
4. set RR to maintain optimal MV (not > 35/min)
5. aim for SpO2 88-95% or PaO2 55-80mmHg
6. increase PEEP with increasing FiO2 (5-24cmH2O)
aim for plateau pressure <30cmH2O
– pH goal = 7.30-7.45 (if < 7.15 increase TV, give NaHCO3)
7. I<E
https://lifeinthefastlane.com/ccc/ardsnet-ventilation-strategy/
https://www.openanesthesia.org/etomidate_adrenal_suppression/
Nejm360
Patient is in severe sepsis secondary to pneumonia and is managed according to the sepsis protocol with fluids and antibiotics.In addition , adrenal insufficiency is also contributing to hypotension and hyperkalemia. CXR shows bilateral pulmonary opacities with noncardiogenic pulmonary edema that is the most important characteristic of ARDS while sepsis is the most common cause of ARDS. Patient is desaturating at 100 % Fio2 on bipap so the next step is intubation and mechanical ventilation. In this case we will prefer ketamine over etomidate for induction because of adrenal insufficiency while we will prefer rocuronium over succinylcholine for NM blockage because of hyperkalemia.
ReplyDeleteGood responses by everyone. There are several topics that I wanted to address in this question stem. The 1st is rather straightforward although it may not always seem that way. It is recognizing a patient that is failing noninvasive mechanical ventilation. Airway protection was mentioned by several of you which is a good point, but in general we refer to the concept of protecting ones airway in relation to their mental status, ability to comprehend what is going on in this situation, having a gag reflex and having the ability to clear secretions. I mentioned that this patient is awake and alert and is speaking to you during the rapid response. The patient by definition is protecting the airway. If the patient can articulate appropriately, there airway is not compromised. However, what I was trying to demonstrate was the fact that the patient's level of hypoxemia, a PaO2 to FiO2 ratio of 51 (saturation of 82 percent and PO2 of 51 on 100 percent BiPAP) is quite severe. In addition he has to pause when speaking to you and is unable to complete sentences without taking a breath. This demonstrates he has very severe hypoxemia and is working to breathe despite maximal settings (20/6) on noninvasive mechanical ventilation. This patient by definition is failing the BiPAP for hypoxia and work of breathing (patients can also fail BiPAP for hypercapnia which is a different process) and thus this patient needs to be intubated and placed on invasive mechanical ventilation to alleviate their work of breathing. It is important to know when assessing a patient who is hypoxic, what their saturations are both by SpO2 and PO2, and then coupling this as to what their oxygen source is. If the saturation is 82 percent and the patient is on room air as opposed to 100 percent BiPAP, those are 2 very different PaO2 to FiO2 ratios. In addition, recognizing what is the underlying drive of the respiratory failure is important. This patient has bilateral, multifocal opacities, a PaO2 to FiO2 ratio of under 200 and interstitial cephalization and superimposed edema with normal left ventricular systolic function (noncardiogenic pulmonary edema). This is the definition of ARDS. Coupling that diagnosis with his current assessment and oxygen requirements mandates mechanical ventilation. So good job in recognizing he needs to be intubated.
ReplyDeleteQuestion 2 is a broad topic about rapid sequence intubation choices. There are several options for induction and paralysis. There were several tid bits in the question stem which were designed to either direct you in a particular way for a paralytic (rocuronium) or meant to mislead/trick you into not using a particular induction agent (etomidate). Everyone should familiarize themselves with the airway assessment prior to intubating someone. There will be a references at the bottom, 1 of which will be to the airway assessment that is taught during the difficult airway course, a course I highly recommend to everyone practicing inpatient Medicine as an attending with ventilated patients. This is a lesson unto itself in terms of examining someone's airway and trying to find things which would lead to inability to ventilate and/or inability to intubate (yes these are 2 different concepts) when approaching elective intubation. You should all familiarize yourself with these pneumonics, they are very quick assessments done right at bedside. As for the drug choices themselves. Induction agents include etomidate, ketamine, propofol, fentanyl and Versed. Paralytic agents include the depolarizing succinylcholine and the non-depolarizing rocuronium and vecuronium. It is important to note that rapid sequence intubation requires an induction agent and a paralytic. Extensive studies have been done demonstrating that withholding a paralytic does nothing but decrease success chance in obtaining the airway in the setting of a rapid sequence intubation. The exceptions are awake intubation and fiber optic intubation in the setting of angioedema when the induction agent is used to allow visual inspection of the airway because of high concern that the airway may be compromised and thus the paralytic is initially withheld. In 95+ percent of patients however, once the induction agent is given, the airway is just as compromised as if the paralytic is given, provided you are able to ventilate the patient. This concept is of vital importance. The ability to ventilate the patient. This is part of the aforementioned initial airway assessment. If you have established that you can ventilate the patient effectively with bag-mask ventilation, then in appropriate rapid sequence fashion, an induction agent and paralytic should be given together to best optimize your chance at obtaining the airway. As for the paralytics, the only question that you need to ask herself is whether not the patient has hyperkalemia as this is a contraindication to using succinylcholine. Succinylcholine can cause rapid elevations in serum potassium level which can lead to significant arrhythmias. This patient had a potassium of 5.9 in the setting of acute renal failure. This patient should not receive succinylcholine but rather rocuronium at a dose of 1.2 milligram/kilogram. Is important to note that the non-depolarizing paralytics have substantially longer half lives then succinylcholine which is why succinylcholine is the 1st line choice for rapid sequence intubation. Paralysis following succinylcholine is somewhere in the range of 2-3 minutes with rapid onset of 30 seconds. Rocuronium and vecuronium take somewhere in the neighborhood of 45 seconds and 2 minutes respectively for onset but last closer to 30 minutes. Thus in patients where there is concern for ventilation a more rapid onset and offset paralytic is the ideal choice, that being succinylcholine. However it is important to remember that there are patients were it needs to be avoided and this is 1 of those patients.
ReplyDeleteThe 3rd major teaching point for this case is the ongoing controversy regarding the use of etomidate and whether or not it produces significant adrenal insufficiency and more importantly whether or not that is clinically relevant. At this point there have been multiple studies that demonstrated that a single dose of etomidate for rapid sequence intubation does in fact cause acute adrenal suppression. However, there are multiple individual trials and a large meta-analysis comprimising 8 trials as well as a direct, blinded, randomized control, head to head trial between etomidate and ketamine which demonstrates that although there is definite acute, transient, reversible adrenal suppression with etomidate, there is no statistically significant difference in any major outcome. This included no statistically significant difference in SOFAmax score, 28 day mortality, catecholamine’s/ vasopressor requirements, median ventilator free days, median hospital free days, mortality or morbidity. There are other similar trials which were done in a retrospective cohort review method that have also demonstrated the same point in that etomidate has been shown to cause transient adrenal suppression often times with hypotension however there has not been shown any statistically significant differences in primary clinical end points with regards to this adrenal suppression. The bottom line/take away point is, while it is fine to use ketamine or other induction agents such as propofol or versed in patients who may have adrenal insufficiency and/or are septic and hypotensive, the data demonstrates it is completely reasonable to use etomidate for RSI in this same patient population and it is just one of the factors regarding the patient's overall clinical picture that should also be taken into consideration when making the decision on choice of induction agent.
ReplyDeletehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220037/
http://www.cochrane.org/CD010225/ANAESTH_etomidate-for-sedating-critically-ill-people-during-emergency-endotracheal-intubation
http://europepmc.org/articles/PMC3940683
http://www.theairwaysite.com/pages/page_content/Airway_home.aspx
http://documents.theairwaysite.com/documents/Walls_8093_CH_03.pdf