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?
Fever and lactate indicating septic picture. Although, patient may have diastolic CHF with preserved EF. Regardless, appropriate fluid administration for sepsis. Patient then acutely decompensates following fluid bolus. Possible shock? Fluid resuscitation should continue despite PE demonstrating crackles and apparent respiratory decompensation. However, Patient will need to be intubated to protect airway.
ReplyDeleteFor induction agents, Etomidate is customarily used for hemodynamically unstable patients because it does not affect BP or heart rate, however it transiently inhibits cortisol biosynthesis and would not be DOC in patient with adrenal insufficiency. Propofol is not appropriate due to dose-dependent hypotension and propensity to decrease cardiac contractility. Methohexital; similar to propofol with dose-dependent hypotension and decreased cardiac contractility. Ketamine may be the preferred drug to induce patient.
The patient gives cause for concern given that he is at 100% Fio2 with poor oxygenation and apparent increased work of breathing. His renal function is questionable and he was given a sepsis protocol fluid challenge which appears to have complicated his respiratory status. By current intubation criteria, he meets the thresholds of 1) inadequate oxygenation 2)failing to protect his airway by increased work of breathing and /or 3) anticipated need for intubation because of same. As for induction agents, normally etomidate would be forst choice in this scenario due to its hemodynamic stability, but its record of adrenal suppression makes it less favorable for this patient. other choices may be ketamine which has fast onset and analgesia; is hemodynamic profile offers stablity and may actually benefit this patient through broncodilation.
ReplyDeleteDue to increased work of breathing and hypoxia on his abg, I would ask him if he would like to be intubated. As for agents, his map is 75, and being septic shock his map should stay >65, I would use ketamine for induction agent and rocuronium for paralysis due to his high K. Succinylcholine has been associated with increasing the K. Due to the adrenal insufficiency, etomidate has been shown to cause adrenal suppression. Adrenal suppression can lead to post tubation hypotension, which increases in hospital mortality.
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 mention 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 failed 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. 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 sources. 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 with 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 and 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 tick bit in the question stem which were designed to either direct in a particular way for a paralytic (good job picking this up Stephanie) or med to mislead/trick you into not using a particular induction agent (etomidate). Everyone should familiar eyes them self 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 on to 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 familiar eyes 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 induction agent to allow visual inspection of the airway is done 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 inappropriate rapid sequence fashion, and 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 like stent 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 some with the neighborhood of 45 seconds and 2 minutes respectively were onset but last closer to 30 minutes. Thus in patients with 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 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 and compressing 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 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 and points with regards to this adrenal suppression. The bottom line/take away point is, while it is completely 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 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