Good morning and welcome to today's session on Neurology, Toxicology, ID, and the ever-popular Miscellaneous. My name is John Savransky and I'd like to welcome you to this session. This webcast is being recorded. The recording will be available in 24 to 48 hours in the content section of the course. Please note the disclaimer stating that the content to follow is for informational or educational purposes only. This session is intended to be interactive with polling questions and the ability to ask questions of the faculty. When a polling question pops up, simply select your answer and click submit. If you do have a question for the faculty, please use the Q&A section in your toolbar and if you'd like to chat with other attendees, please use the chat function. We are privileged to have three renowned faculty today. Today's faculty consists of Drs. Greg Martin, Janice Zimmerman, and Javier Preventia. None of the faculty today have anything to disclose. Without further ado, Dr. Preventia, please feel free to get started with our first question. Thank you. So first, we have a 52-year-old woman who was admitted to the ICU immediately after a middle cerebral artery aneurysm clipping. She has no previous medical or surgical history. She has smoked one pack per day for 30 years and is a current smoker. Hunt and Hess score is 2, Glasgow Coma score is 15, the World Federation of Neurological score grade is 1, and the Modified Fisher scale score is 3. To optimize cerebral perfusion pressure, in addition to prescribing nimodipine, which of the following actions should be taken to prevent vasospasm and delayed cerebral ischemia? A, initiate hypervolemia and maintain immunoterol pressure greater than 90. B, maintain uvolemia and maintain immunoterol pressure greater than 90. Initiate hypervolemia and maintain a systolic pressure greater than 180, and maintain uvolemia and maintain a systolic pressure of less than 120 are your options. So it looks as though everybody has chosen choice B, which is maintain uvolemia, and that is actually the correct answer. So it turns out that there's a lot in this question, and I just want to go over a couple of main things. One is the term hypervolemia, I'm not sure what that means. I suspect that it means over distending the left ventricle, which to me sounds like you develop pulmonary edema and put less oxygen in your blood and you decrease your cardiac output, which decreases blood flow to the brain. So I don't believe in hypervolemia ever. I think the term uvolemia, this optimized volume and make sure patients aren't volume depleted, is actually important. Whether the patient is in the period of what we call vasospasm or not, maintaining immunoterol pressure that's adequate for brain perfusion makes sense, especially if there's spasm of the arteries, which could restrict blood flow. If patients are in the period of vasospasm, sometimes we increase or augment blood pressure. The evidence for that's pretty dubious, but we continue to do it. So it turns out that answer B, maintain uvolemia, that was not the correct answer that people got. Maintain uvolemia and immunoterol pressure of 90 is the safest thing to do in the period before the patient has vasospasm. And then hypervolemia possibly or increasing blood pressure and augmenting blood flow in patients who are in the period of vasospasm. So the correct answer is B. So the second question is a 27-year-old woman who's gravida 1, para 0 with a 10-week viable gestation develops generalized tonic-clonic seizure disorder. Emerging control of the seizures is achieved with lorazepam. Which of the following maintenance anti-epileptic medications is most suitable during her pregnancy? And the answers are valproate, phenytoin, phenobarbital, or levatoracetam. You can make your selection. Okay, and it looks like everybody chose levotiracetam, which is the correct answer. It turns out that there's not a lot of evidence about the newer antiepileptic agents, but there is a lot of evidence about the older ones. Particularly valproate has been shown when administered early in pregnancy to cause neural tube disorders. Phenytoin has been known to cause the hydantoin fetal syndrome. And phenobarbital, although it's less well described, has been shown to decrease cognitive achievement in children by third grade. And all that data is very, very old. So it's unclear where all of it stands up. Levotiracetam, on the other side, has never really been evaluated that carefully, although a recent analysis showed that the newer antiepileptic agents seem to have fewer birth defects and seem to also have fewer cognitive effects. So levotiracetam is the one that most of us are most comfortable with, and it's probably the best choice, not because it seems to be the best choice, but it seems to be the least of the bad choices. And the other issue is that stopping antiepileptics during pregnancy does have a risk of fetal loss due to seizures. So it's not recommended to abruptly stop antiepileptics in people who need them. The next question is a 73-year-old man who presents to the emergency department after being assaulted. He struck innumerable times in the head and torso. And on arrival, his Glasgow Coma Scale score is 7. He's otherwise hemodynamically stable. He's orotracheally intubated for airway protection. A CT reveals an open skull fracture and a small frontal contusion, diffused subarachnoid hemorrhage, and a nonoperative liver laceration. In addition to a GCS score of 7, which of the following is an indication for the placement of an intracranial pressure monitor? And your answers are CT findings of diffused subarachnoid hemorrhage, age older than 65, open skull fracture, need for mechanical ventilation, or nonoperative liver laceration. And I see that there's two answers. So most of the audience said CT findings of diffused subarachnoid hemorrhage, and someone said need for mechanical ventilation. So the Glasgow Coma Score of 7, almost all patients will need mechanical ventilation just because they're so obtunded that they can't protect their airway. This question I find a bit tricky in the sense that there are two different sets of guidelines for the need for intracranial pressure monitoring in patients with traumatic brain injury. All of them include a Glasgow Coma Scale of less than 8. But in the Glasgow Coma Scale of less than 8, the patients segregate into two different types. Patients that have evidence of intracranial abnormalities, subarachnoid hemorrhage and brain contusion, in this man's case, would lead to the need for monitoring. If this patient did not have the frontal contusion or the subarachnoid hemorrhage, then age greater than 40 is actually a reason to put in a bolt. So in this case, B would also be correct if it wasn't for the fact that the patient had a subarachnoid hemorrhage. So I think in this case, the abnormality in the brain plus the low GCS would have necessitated a bolt. If the patient didn't have intracranial abnormality but was still obtunded and still had a Glasgow Coma Scale of less than 8, then they probably would have needed a bolt as well because they were greater than age 40. And so age older than 65 would have been incorrect either way, but it's age older than 40. And then there are a few other criteria for patients who don't have intracranial abnormalities who need it, but being on mechanical ventilation is not one of them. Okay, so, sorry about this. So a 41-year-old man is admitted to the ICU with a severe traumatic brain injury, Glasgow Coma Scale of four, very low. Sustained in a motor vehicle accident eight hours ago when he was ejected through the windshield into a tree. Vital signs are that his temperature rectally is 37.8 degrees Celsius. His heart rate is 56 beats per minute. His respiratory rate is 14 beats per minute. His blood pressure is 114 over 68 and his adrenal pressure is 16 millimeters of mercury. Which of the following should be instituted prophylactically? A, decompressive craniectomy. B, methylprednisolone. C, systemic cooling with a target temperature of 35 degrees. Or D, sequential compression stockings. And the answers here vary between sequential compression stockings and decompressive craniectomy. And the correct answer is actually sequential compression devices. And the reason for that answer is that the patient at the initiation of their injury probably doesn't need a decompressive hemicraniectomy unless there's evidence on CT of diffuse edema or herniation. And none of that is in this demonstration. The same thing, methylprednisolone is the one medication that's contraindicated in the setting of traumatic brain injury and should never be given to patients because the mortality is higher. Systemic cooling was tested in a large trial called the Urotherm trial where it was tested against normal therapy or conventional therapies for management of severe traumatic brain injury with high ICPs as a mechanism of improving outcome. And it failed to reach the end point there. It does turn out that lowering target temperature does lower ICP. So if your goal is that patient has uncontrolled ICP, lowering temperature actually is a good way of doing that. It's not necessarily the first line choice for doing that or even the second line choice. But what they've shown is it is a therapy compared to conventional therapies. It doesn't improve outcome. And then finally, sequential compression devices, patients with any kind of traumatic injury, but more importantly, brain injury and spinal cord injury because of the paralysis in their arms and legs have a very high risk of developing DVTs and sequential compression devices have been shown to improve outcomes by basically decreasing the risk of pulmonary embolism. So the next question, a 53-year-old man presents to the emergency department with a self-inflicted gunshot wound to the head, in which he has a devastating bi-hemispheric brain injury. He is in an irreversible coma without any confounding variables. He's currently normal-tensive on vasopressors, on mechanical ventilation with an FiO2 of 0.50 and a positive end-desperatory pressure of 5 millimeters of mercury, and with absent brain stem reflexes. In addition, the patient is nomothermic and not anonatremic. Given these findings, which of the following situations would mandate that an ancillary test be performed to determine whether the patient is dead by neurologic criteria? And your answers are A, hemodynamic instability requiring vasopressors, absent corneal and pharyngeal gag reflexes, pharyngeal reflexes, instability preventing completion of an apnea test, or mechanical ventilation with FiO2 of 0.50 and a PEEP of 5 millimeters of mercury. And it looks like everybody answered this question correctly. So the answer is instability preventing completion of the apnea test. We are very, we've taken a very strong attempt to educate people about the diagnosis of death by neurologic criteria or brain death as having three components. The one component, the first component to this is that you have to have a reasonable story for why the patient would be in an irreversible coma with brain damage. And this person's obviously bi-hemispheric brain injury from his gunshot wound qualifies. The second one is that they have to have a physical exam that makes sense. And in this case, the patient has absence of all of the appropriate reflexes that would make it appropriate to declare him dead. And then finally, they have to have an apnea test that's well-conducted and that shows that the patient has no initiation of respiration with a CO2 challenge. The reasons you do ancillary testing is if you can't meet any of the second two criteria, if you can't meet the first criteria, you need to go back and meet those first criteria. The second and third criteria is the physical exam and the apnea testing. If they can't be completed either because the patient has trauma to their face or because they are missing an eye because of his previous surgery, or if they can't complete the apnea test due to hemodynamic instability. Now, that doesn't necessarily mean that the instability that occurs can't be treated during the apnea test with increasing pressors because it can. But if they still can't complete the apnea test, then ancillary testing can help confirm the diagnosis. So, the answer to that is C. Greg Martin. Yeah, thanks, Javier. So the next question is about a 54-year-old man who's diagnosed with infection-related ventilator-associated complications on day 10 of his ICU stay. He gets empiric initial antibiotic treatment with piperacillin, tazobactam, levofloxacin, and vancomycin. And four days later, the cultured aspirates return with E. coli that's sensitive to piperacillin and tazobactam. The team discontinues the vancomycin and the levofloxacin. The patient's afebrile, the white blood cell count, has decreased to 8,000 from 18,000 since starting antibiotics. And the question is, for what total antibiotic duration should this patient be treated for his ventilator-associated complication? And the options are eight days, 10 days, 14 days, or 21 days. So we have a smattering of responses of votes today, eight, 10, and 14, all three. And the key to this question is that we recognize the prolonged antibiotic exposure, particularly for people with ventilator-associated pneumonia, leads to a variety of adverse consequences. So we're trying to get the time of the treatment exactly aligned with what's needed for treating the infection. And there's both the consequences from the medication itself, as well as potential infectious complications of things like colonization with multi-resistant organisms, as well as secondary infections. There is a well-done study published in JAMA many years ago now that shows comparing an eight- and a 15-day duration of treatment that eight days was superior for most infections, including E. coli, not necessarily for all infections, including some of the non-fermenting gram-negatives like pseudomonas, but in this case, eight days would be the appropriate treatment. Let's move on to the next questions. The next question, a 60-year-old, six-foot-tall man who went and had emergent surgery for a perforated diverticulum that had septic shock with multiple organ dysfunction. He weighs 80 kilos, and despite correction of the perforated bowel, he's been unable to be liberated from mechanical ventilation for the past eight days. His FiO2 is increased to 60%. He has positive index respiratory pressure, a peep of 10 centimeters of water. He's developed a new fever and has increasing generalized edema. His medications at this time include piperacillin-tazobactam, fluconazole, famotidine, and heparin. His abdominal TT reveals no fluid collection or abscess formation, and his chest radiograph reveals persistent bilateral infiltrates with increasing oral tracheal secretions. His laboratory reveals a white blood cell count of 18,000, platelets of 20,000, a blood urea nitrogen of 28, creatinine of 1.5. So which of the following treatments should be eliminated from consideration for this patient? Daptomycin, lenazolid, televansin, or vancomycin? So let's go ahead and vote. And here we have a mixture of responses as well. So everyone recognizes that vancomycin is not appropriate in this person, but there were several responses about the other three. So the key to this one is recognizing that this is a late-onset ventilator-associated pneumonia, which is very likely to be MRSA as the pathogen, and then thinking of the options for treating that. So lenazolid and vancomycin can be recommended by the Infectious Disease Society of America and others. And if the MRSA is susceptible, you can use things like clindamycin. You may remember that televansin is a black box warning against its use in patients with moderate renal insufficiency, particularly if they have a low creatinine clearance less than 50. This patient does not, so televansin would be an option. The key to this question, though, is that daptomycin is not an option because not only is it inhibited by pulmonary surfactant, but it doesn't really get adequate concentrations in the pulmonary space, and therefore it's not recommended for use for treating VAP and other MRSA pneumonias. So the answer to this one was daptomycin should be eliminated from consideration of treating this patient. The next question, a 60-year-old woman with methicillin-resistant staph aureus, MRSA bacteremia, who does not have endocarditis and continues to work in clinically despite seven days of vancomycin therapy. So she's allergic to sulfa, and follow-up cultures on day six of her infection reveal that her cultures remain positive and have the following susceptibility profile. It's MRSA that's growing. It's resistant to penicillin, resistant to oxacillin, and resistant to vancomycin, intermediate to lenazolid, and intermediate to daptomycin. So the question is, which of the following is the most appropriate antimicrobial for this patient at this time? A, vancomycin for four to six weeks, to quinipristin-dolphopristin at an appropriate dose every eight hours. C, sulfamethoxazole trimethoprim every 12 hours. Or D, colistamethate every 12 hours. All right, so everyone got this one correct. The correct answer is B, quinopristin-dalphopristin. And the keys here are that in treating an infection that's not responding to therapy, continuing vancomycin is not an appropriate choice. We also recognize that she's allergic to sulfa. Therefore, sulfamethoxazole is not appropriate. Callistamethate is effective against gram-negative bacteria, but would not be expected to be effective against MRSA bacteremia. So quinopristin-dalphopristin is the synergistic antibiotic combination that is approved for use in treating MRSA infections, and in this case would be the most logical choice. And the next question, a 65-year-old man admitted to the ICU with four days of productive cough, fever, pleuritic right-sided chest pain, and progressive dyspnea. On physical exam, he has a temperature of 39.1, a heart rate of 125, respiratory rate of 22, blood pressure of 95 over 40, and an oxygen saturation of 94% on four liters of oxygen binasal cannula. Examination reveals crackles and agaphony on the right lung base. His white blood cell count is 26,000 with 20% band forms. A CT scan of the chest demonstrates a right lower lobe consolidation and a moderate-sized loculated pleural effusion with pleural thickening. IV purposylantase or Bactam and a bolus of IV crystalloid fluid are administered. A chest tube is placed, and 750 mLs of purulent fluid is drained. The question is, which of the following would be expected after the administration of intrapleural deoxyribonuclease, DNase, and tissue plasminogen activator, TPA, twice per day for three days? First, a markedly elevated risk of hemorrhage. Second, an increased risk for surgical referral. Third, reduction in mortality. Or fourth, improved drainage of the infected pleural fluid. Let's go ahead and vote. Good, so we've got, the majority of people got the correct answer, which was improved drainage of infected pleural fluid. There were also some other votes for other options. So there was a very nice study, the MIS-2 trial. It was a large trial published that showed using this drug combination in patients with infected pleural fluid, that using those two together resulted in better drainage. You can expect improved drainage of the infected fluid, potentially also a lower rate of surgical referral. So you wouldn't expect an increased need for surgical referral. There was no change in mortality in the groups, and actually it was found to be safe. So there was no increased risk of hemorrhage as well. So the outcome expected for that intervention would be D, improved drainage of infected pleural fluid. So with that, I will hand over the next question to Janice Zimmerman. Thank you. So we're gonna have a few toxicology questions. So this one is straightforward here. Propofol infusion syndrome is characterized by metabolic acidosis plus hypoglycemia, coagulopathy, and hepatic encephalopathy, or rhabdomyolysis, myocardial dysfunction, and renal insufficiency, or C, hypotension, cardiac dysrhythmias, and status epilepticus, or D, rhabdomyolysis, elevated temperature and muscle rigidity. Okay, you'll see the boats show. Okay, the correct answer is B. I will acknowledge that there's quite a bit of overlap. I think everyone understands A is hepatic encephalopathy, and D is malignant hyperthermia, or neuroleptic malignant syndrome, probably. There's an overlap between B and C. So propofol infusion syndrome, the most common characteristics are rhabdomyolysis and acidosis, primarily lactate, and also an abnormal EKG or arrhythmias and renal dysfunction. You can also see fever. You can see hypotension. Now, C is meant to suggest tricyclic antidepressants, but you can also see hypotension and cardiac dysrhythmias in propofol infusion syndrome, and you may see seizures, but usually not status epilepticus. So it's not quite as straightforward. There is a little overlap, but propofol infusion syndrome should be kept in your mind when you see increasing acidosis in someone, increasing need for vasopressors in someone who is on higher doses or even lower doses over a longer period of time. We can go to the next question. Okay, a 24-year-old is evaluated on New Year's Eve for mental status change. Laboratory results reveal elevated creatinine, a normal BUN, a normal pH, a normal anion gap, no blood alcohol concentration, an increased osmolal gap, and an increased acetone level. Ingestion of which of the following types of alcohol is most likely to produce this patient's presentation? Isopropyl alcohol, methanol, ethylene glycol, or ethanol? So board exams tend to like questions about toxic alcohols, perhaps not necessarily about this type of simple, straightforward question, but it's helpful to know the metabolism and clinical manifestations. Okay, those who voted about two-thirds got the right answer, which is A, in this case, isopropyl alcohol. And the key here is a normal anion gap. So all alcohols will give you an osmolal gap, and you will not see metabolic acidosis with either ethanol or isopropyl alcohol, but they already gave you a negative blood alcohol concentration. And they also gave the other clue, which is an increase in acetone level. I'm not sure what an acetone level is, but basically you can see urine ketones or blood ketones because isopropyl is metabolized through acetone. So the correct answer is isopropyl alcohol. Next question. Okay, you have a 56-year-old. He's brought to the emergency department after being found confused and agitated and has a seizure. Witnessed by his sister following 24 hours of nausea, vomiting. He's unable to provide a history in the ED, but his sister reports he has a long history of bipolar disorder and has been doing well since being on lithium for about two years. She thinks he recently started taking ibuprofen for aches and pains in his back. His lithium level is 5.3 millimoles per liter. Based on his clinical manifestations and drug level, treatment with IV fluid and which of the following acute therapies should be initiated? This is a great question and also hopefully it's pretty straightforward. Okay, all of you got the correct answer, which is hemodialysis. So the key here, I always like to think they have a severe, severe elevation of their lithium level and they're symptomatic. So you can get lithium toxicity, first of all, with overdose but also in the setting of anything that impairs renal function. So he's had 24 hours of nausea and vomiting. So he has dehydration and he may have renal dysfunction and perhaps the ibuprofen that was started may have played a role as well in some renal compromise. So the key here is to dialyze this patient. Now, the level is not so much as critical and remember that the chronic ingester will have toxicity at lower levels. So in the chronic ingester, it's often suggested to dialyze if the level is greater than 2.5. If someone just that's never taken lithium has taken it, you may see levels as high as six and that may actually be asymptomatic. So go with the symptoms as well as the clinical presentation and the lithium level. Next. Next. Okay. A 20-year-old with a significant past medical history of depression and anxiety is being evaluated in the emergency department after being found unconscious by a family member. On presentation, the patient is abdundant with a Glasgow Coma Scale score of eight and is intubated for airway protection. So here we have the significant laboratory data, pH 7.19, PCO2 17, sodium is okay, bicarb is low at 10 and you have elevation of both the AST, ALT and the alkaline phosphatase. So serum ethanol concentration is low at 56 milligrams per deciliter and you have an osmolar gap of 42. Your analysis reveals microscopic hematuria and calcium oxalate crystals. So which of the following treatments is most appropriate? Anacetyl cysteine, omepazole activated charcoal or methylene blue. Okay. Oh, that's interesting. Got methylene blue here. Well, this is actually a classic toxic alcohol. So they're giving you at altered mental status the CNS effects of any alcohol. They give you a severe metabolic acid doses with a huge anion gap and you also have that osmolar gap. So that's the key that you have an alcohol on board. You have a low serum ethanol, so it's not due to that and plus ethanol doesn't give you an anion gap acid doses. The other clue they gave you are the calcium oxalate crystals, which can be seen in about a third of patients with ethylene glycol poisoning. So here the treatment of choice would be from epazole. If they didn't give you from epazole, they would probably given you maybe IV ethanol or they may have even just put in dialysis. But in this patient where there's both alcohol and acids present, you need both from epazole to prevent further metabolism of the alcohol and dialysis to remove the acid metabolites. So I think we go back to Dr. Provencio for the next questions. Sorry about that. Thank you. Okay, so the next question, a 49 year old woman is admitted to the ICU after a Whipple procedure for pancreatic cancer. She's extubated in the operating room and currently has severe pain and moderate level of anxiety after awaking from anesthesia. Which of the following medication combinations is the most appropriate initial treatment and your choices are diazepam, is the most appropriate initial treatment. And your choices are dexmedetomidine and haloperidol, fentanyl and midazolam, morphine and etomidate, Ketorolac and propofol, fentanyl and dexmedetomidine. And I can see everybody chose fentanyl and dexmedetomidine, which is appropriate. The couple of things about these choices, it's important to understand that choice A does not have a component for pain. The dexmedetomidine can potentiate the effects of opiates but doesn't have primary pain as far as most of the studies have shown. And haloperidol also is not a pain medicine. Fentanyl and midazolam was an old go-to, especially in the medical intensive care unit for pain. Midazolam has a relatively short half-life, so does fentanyl. So if you discontinue the medications, you can get an acute pain syndrome. More importantly, midazolam has a very high risk of delirium and therefore we're trying to avoid using benzodiazepines whenever possible. Choice C, etomidate, shouldn't be used as a recurring medication because of the risk of adrenal insufficiency. And Ketorolac as well is not a good substitute for opiates in the setting of most types of pain, the exception being oral surgery where Ketorolac has been shown to be somewhat helpful. But ultimately, fentanyl and dexmedetomidine for abdominal surgery would make the most sense. And now we'll go back to Greg Martin. Thanks, Javier. Our next case is a 75-year-old man who has a history of stage four lung cancer and advanced emphysema. He's on mechanical ventilation after developing a post-viral multilobar staph pneumonia. His ICU course has been complicated by ARDS and multi-organ failure. And on hospital day 10, he remains in critical condition. He's been in intensive care for over a year and is currently in the intensive care unit and on hospital day 10, he remains on maximal ventilatory support, deeply sedated with neuromuscular blockade. His mean arterial pressure is 58 despite norepinephrine and vasopressin. A family meeting is held to discuss goals of care. His wife and children are in agreement that the patient would not have wanted to be sustained on life support indefinitely given his poor prognosis. And they asked that advanced life support be removed and that the remainder of his care be focused on measures that maximize comfort. The question is, which of the following is the best approach in this end of life scenario? A, to discontinue neuromuscular blocking agents and promptly remove the endotracheal tube while he remains sedated. B, titrate down rather than abruptly discontinue vasopressors as sudden withdrawal of hemodynamic support may lead to discomfort. C, administer opioids using a combination of bolus doses and infusion to treat pain and dyspnea as life support measures are withdrawn. Or D, use judicious doses of benzodiazepines and opioids as pharmacologic agents used to treat discomfort frequently hasten death. Let's give everyone the chance to vote now. We're jumping into the ethics section of questions. So we have a variety of responses here, but the majority of people got the answer correct. And the correct answer is C, to administer opioids using a combination of bolus doses with infusion. And the key here is to remember that opioids are the mainstay of treatment for managing pain and dyspnea. And particularly regarding dyspnea, opioids are very effective at eliminating or improving the work of breathing, reducing oxygen consumption, but also reducing the anxiety associated with breathlessness and the central perception of dyspnea. And the other important component here is that bolus doses need to be used concurrently with the infusion because when infusion doses escalate, you need to use bolus doses in order to address signs of suffering or even just to remain on the right dose in the pharmacokinetic curve. The other elements that may be options here, for instance, the use of the immediate withdrawal of neuromuscular blocking agents and then extubation while remaining sedated is not acceptable largely because you have no ability to assess comfort in those patients because they may remain neuromuscularly blocked and therefore you don't have a way of administering or knowing when to administer the right dose of opioids. So discontinuing neuromuscular blocking agents and removing the tube is not appropriate. It is important to remember clinically that some patients who have received prolonged neuromuscular blockers that may take some time for those to wear off and you can monitor that and still at the same time try and make decisions about appropriate comfort management. Similarly, the discontinuation of vasopressors does not lead to any undue burden or discomfort. And in fact, rapid discontinuation is more timely and more humane in many cases than titrating them down slowly. And finally, benzodiazepines have several important properties including being hypnotics and anxiolytics and in fact can be synergistic when used with opioids but the question about whether they should be used to frequently because they frequently hasten death rests on an ethical principle which is a little bit different and we'll have another ethics question in a minute but the most recent sort of interpretation of this is that the focus should be on comfort of the patient and to relieve symptoms and suffering. And if there's an unintended consequence of hastening death but that still is achieving the appropriate goal in the best way. So the goal is not to hasten death but you would not use it because of that concern. Let's go to the next question. The next question, a patient who resides in an extended care facility due to advanced dementia has COPD and dysarthria from a remote stroke is now three weeks status post a sigmoid colectomy and a Hartman procedure for perforated diverticulitis. His course has been complicated by pneumonia and ventilator dependent respiratory failure. He's developed multi-system organ failure and his sole surviving relative is a widowed daughter. The daughter relates that her father would not want to continue receiving medical care given the poor prognosis with multi-system organ failure and instead would want to receive comfort care. As a result, the daughter expects her father to die but believes that he would find a comfortable death to be an acceptable outcome. The question is, which of the following ethical principles best describes the daughter's interaction with the staff? A, paternalism, B, substituted judgment, C, non-maleficence, D, power of attorney or E, legal moralism. Good, so most people got this correct. The principle here is substituted judgment. And remember that in this case, the daughter is making decisions for the patient, in this case, her father, and she's identified a goal that she believes her father would have set for himself if he was able to do so. And therefore, we're using substituted judgment, which is the principle that you can supply, you can make a decision supplied for someone else when they're unable to do it, but you're doing it in, you're substituting your judgment for theirs, but you're using their principles to make that decision. And implicit in that is the principle of beneficence, meaning that the judgment is being made in the patient's best interest, and also non-maleficence, which is obviously the action in ensuring that what you're doing is not creating or causing harm. So the key here is to recognize that a family member or another care provider making a decision for the person who's unable to do it for themselves, if they're doing it as in this case, using the decision that the father would have made that he'd been able to do it himself is using substituted judgment. I will now hand it back to Dr. Janice Zimmerman for the next question. Okay. A member of the rapid response team is called to evaluate a patient in respiratory distress. The patient has tachycardia and a saturation of 85% on 100% non-rebreathing face mask. On physical examination, the patient's spiromental distance is two finger breaths, and he has prognathic upper incisors. There is no previous intubation note available, but his history is pertinent for previous cervical fixation after a trauma. The question is, what is the first choice of technique for intubating this patient? A, direct laryngoscopy following administration of succinylcholine. B, direct laryngoscopy after administration of rocuronium. C, video laryngoscopy after the administration of rocuronium. D, awake fiberoptic-assisted intubation, or E, fiberoptic-assisted intubation after the administration of rocuronium. Okay. Majority here got the correct answer, which is D, awake fiberoptic-assisted intubation. This is a difficult airway scenario, and that's important that when you're given information, you evaluate if this is a difficult airway. The clues here, the spiromental distance is two finger breaths. You usually want at least three finger breaths or six centimeters. The prognathic upper incisors, so the overbite, is another potential risk factor. Also, he's had previous surgery on his neck, which comes into play with neck mobility. He will have limited neck mobility. Another scenario they could give you is a patient with arthritis, cervical arthritis, or ankylosing spondylitis. Other risk factors that you can look at for a difficult airway would be tongue size, mouth opening, you want at least six centimeters, or again, that three finger breath, obesity, and also a short, thick neck, although there's no one criteria that really is going to say this is a difficult airway. The reason D is correct, if you look at all the other four, they all paralyze the patient, and that would be the wrong answer. If possible, you're always going to want an awake intubation in a patient who may have a difficult airway. The one awake intubation you're given is E, which is fiberoptic-assisted. Now, they could also have given you a video laryngoscopic intubation as long as the patient was awake. They could have given you an LMA, although with this degree of hypoxia, that's not likely to be effective, but the key here is an awake intubation. Let's go to the next question. Okay. A 72-year-old man has undergone a partial lung resection for squamous cell carcinoma. Four hours after admission to the ICU from the post-anesthesia care unit, he becomes abtunded with partial airway obstruction, a respiratory rate of four, and falling arterial oxygen saturation by pulse oximetry. He received six milligrams of epidural morphine and 150 micrograms of epidural fentanyl via lumbar epidural catheter approximately eight hours before ICU admission. Underlying conditions include chronic obstructive pulmonary disease and coronary artery disease with stable angina. Which of the following interventions is most appropriate? A, immediate nasotracheal intubation to protect airway patency and provide ventilatory assistance. B, immediate oral tracheal intubation to protect airway patency and provide ventilatory assistance. C, immediate effective ventilatory support via a bag mask while 80 micrograms of naloxone is administered via the epidural catheter. Or D, immediate naloxone, 0.4 milligrams IV push. Okay. Well, this is a difficult question and probably goes into the anesthesia realm with the epidural anesthesia. The correct answer is D, give IV naloxone immediately. And that is based on the fact that first of all, C is incorrect because naloxone has unpredictable effects when given via epidural catheter. So you don't want to give naloxone via epidural catheter. Now you could say that you want to intubate the patient, but you'd like to avoid that complication or that procedure with potential complications if you can. So this is a classic narcotics toxicity. So the correct answer would be to give naloxone first. And if they respond, you can always set up a naloxone drip and titrate to the patient's comfort such that you have an adequate respiratory rate, but you're still maintaining some degree of anesthesia for the patient. Okay. Go on to the next. Hello again. So our next question is about a 55 year old man who's admitted to the ICU with community acquired pneumonia and hypoxia. He's placed on high flow nasal cannula with an FIO2 of one and 60 liters of flow. Broad spectrum antibiotics are administered, but his condition continues to deteriorate and he develops worsening tachypnea, hypoxia, and severe respiratory distress. The decision is made to proceed with tracheal intubation. On examination of the airway, his mouth opening is greater than three centimeters. Neck mobility is normal. Thyromental distance is greater than six centimeters and the malampoti score is one. Which of the following would be expected of video laryngoscopy rather than direct laryngoscopy is used to facilitate tracheal intubation? A, an increased likelihood of successful intubation on the first attempt. B, improved glottic view. C, a reduced rate of post-intubation complications. Or D, a reduced time to successful intubation. Go ahead and vote now. Good. So most people got the question correct. And the correct answer is B, improved glottic view. Some other people looked at some of the other options. And remember that there's a couple of really elegant studies that have compared direct laryngoscopy and video laryngoscopy in this setting. And the key element in all of those studies is that you get an improved glottic view. So consistently you're going to see that and therefore B is definitely correct. The question then becomes which of the other options may also be correct or are they distracting you? And the studies have shown that there is no change or benefit in terms of the likelihood of successful intubation or the time to intubation. And it also does not appear to improve or reduce the rate of post-intubation complications. So in this case with this kind of patient who has a normal airway, does not have a difficult airway, the answer is B, an improved glottic view. And now back to Javier for the next question. So a 24-year-old woman who has asthma came to the emergency department because of cough, wheezing, and dyspnea. Aggressive treatment with inhaled albuterol and IV aminophilin and corticosteroids is ineffective. The patient is transferred to the ICU and an intracranial tube is placed and mechanical ventilation and sedation are begun. Because of continued dyssynchrony with mechanical ventilation, Vecuronium 7 mg bolus is given followed by a 2 mg per hour IV infusion. Prior to the administration of the neuromuscular blocking agent, percutaneous electrodes are placed over the ulnar nerve at the level of the wrist and a four of four twitches of equal strength are felt with the train of four stimulation. Because the patient continues to be dyssynchronous with the ventilator and because of the train of four findings, the Vecuronium infusion is increased over the next four to six hours, at which time the patient's no longer over breathing the ventilator and the train of four twitches stimulation of the ulnar nerve elicits no contractions of the abductor pollicis muscle. Which of the following recommendations is most appropriate to evaluate the degree of paralysis? And your choices are changing the nerve stimulator electrode placement, B increasing the train of four stimulation current from 60 to 80, C checking post-tetanic count, D replacing the nerve stimulator or E changing electrode polarity. And I see we have a smattering of answers, which is actually good because this is actually a quite difficult question because we don't do a lot of train of four stimulation anymore and oftentimes it's done in nursing protocols and not really thought of too much. So the train of four is a way of assessing how much paralytic is on board by basically looking at how many mechanical stimulations or electrical stimulations of a nerve lead to muscle contraction. Because eventually what happens is that with each stimulation of the electrical nerve, the amount of acetylcholine released into the cleft is lower on subsequent because it just takes a while for the nerve terminal to actually accumulate acetylcholine. And because of that, with each stimulation, there's a less strong stimulus because there's less acetylcholine in the cleft to actually cause muscle contraction. So we use this as a way of, of judging the amount of paralytic. What happens though, when you get to the point where you have no stimulation at all, at that point, there's a couple of different possibilities. It takes about 70% of the receptors to be blocked in order for, for you to lose the tetanic stimulation, but the difference between 70 and a hundred percent is actually pretty big. All of them have the same finding on train of four, on train of four. So there are some things that you can do if you don't think your train of four is working, changing the nerve stimulator, electrode placement, checking the post, uh, checking, increasing, um, replacing the nerve stimulator or changing the electrode polarity are all things you can do. But in this patient, because they already had a train of four that was in place and was working prior to the stimulation of the, of the, uh, uh, prior to the initiation of the increased doses of Vecuronium, it seems unlikely that it wouldn't be working now. Now it does turn out that if you've given the patient seven or eight liters of fluid at the same time, that there may be some issues with the location, but in this case, it doesn't seem to be the case. So those aren't, um, those aren't appropriate. The other one is increasing the train of four stimulation current from 60 amps to 80 milliamps. Most times we do the train of four at 30 milliamps and 60 milliamps is already a relatively large dose. Increasing to 80 milliamps doesn't usually stimulate anything because it's way above the threshold at which sodium and potassium channels will actually stimulate to, to start a nerve conduction. So that doesn't use that is not usually helpful. So what you're left with is checking the post-tetanic count. And the post-tetanic count is a trick you play. And what it basically does is by stimulating a nerve over and over again, you allow leak of calcium into the nerve terminal, particularly into the, into the terminal at the, uh, at the snap at the synapse. And because of that, what happens eventually is, is you get so much calcium in the, in the system that you actually lead to release of large, large amounts of, um, of acetylcholine. And therefore you get, you get nerve conduction on the post-tetanic side, on the post stimulation side, the release of calcium also stimulates the nerve directly. So ultimately what this tells you is, is how much in excess of the train of four being zero you are. So if you get more than five, um, contractions with post-tetanic stimulation, that usually means that the paralytic is a little bit over edge, but it's going to turn. But if you turn it off, we'll come back to something normal. If it's less than that, then it may take a really long time to actually get, um, to get things back. So in this case, you can use this as a trick to say, have I way overshot or have I kind of overshot? And, uh, and if you've kind of overshot, then you can cut down on the dose and wait for it to come back. If you weigh overshot, then you probably need to stop the paralytic altogether and wait for it to come back. But knowing full well that it may take a long time to come back. And I have the next one as well. So an 86 year old woman with ventilator associated pneumonia necessitated mechanical ventilation has consistently received a score of four on the intensive care and intensive care delirium screening checklist. Um, meaning that she has delirium. Currently she's receiving lorazepam for sedation at two milligrams per hour, which is the following is the best course of action. Given the above information and your answers are a continual raise a pam at two milligrams an hour and titrate the dose down as possible. B at a fentanyl continuous infusion to decrease the lorazepam C transition from lorazepam to dexmedetomidine beginning at 0.2 micrograms per kilogram per hour. And, or D can discontinue lorazepam infusion initiate midazolam infusion at two milligrams per hour. And most of you got this correct, which is a transition from lorazepam to dexmedetomidine. But I think all of you got correct. The idea that decreasing the lorazepam or getting rid of the lorazepam is probably the most effective thing you can do to get rid of delirium. So benzodiazepines are a little bit controversial, but most people's eyes are the most like is the most important cause of delirium in patients who were in the ICU and removing benzodiazepines from the equation is most likely to to resolve delirium. So in, in this case, adding fentanyl continuous infusion to, and to decrease lorazepam, if you can remove the lorazepam would be great. Having said that, dexmedetomidine does much of the same things that lorazepam does. Whereas fentanyl is a pain medicine, lorazepam is an anxiolytic and or sedative. Dexmedetomidine is also an anxiolytic and sedative. So therefore the transition from lorazepam to dexmedetomidine seems like it's the most reasonable and has been shown in studies to be effective. And now we go back to Dr. Martin. Thank you again, Javier. So the last question of the day, a 35 year old man recovering from ARDS, and on day seven, he's alert and cooperative, but remains ventilator dependent. He's on pressure support of 14, a PEEP of five, FIO2 of 35%. His spontaneous tidal line on those settings is 400 mLs. And his spontaneous respiratory rate is 22 breaths per minute. He's tolerating full internal nutrition and his laboratory values include a hemoglobin of nine, a white blood cell count of 9,000. So the question is which of the following is the best next intervention to improve outcome in this patient? A, to transfuse red blood cells, to a desired hemoglobin level of 10, B, to institute mobilization and physical therapy, C, to supplement internal feeding with glutamine, or D, to infuse dexmedetomidine nightly for sleep. Go ahead and vote. Good. So everyone got this correct. So the correct answer is to institute mobilization and physical therapy as a form of ICU rehabilitation. And the key element to recognize here is you have a patient who has awake, his laboratory studies are quite normal, he's not delirious, but he remains on mechanical ventilation without the clear ability to wean and liberate himself. So recognizing that ICU acquired weakness is present in somewhere between 25 and 60% of mechanically ventilated patients. And although the ideology of it is multifactorial, we recognize that muscle injury from systemic inflammation, along with the critical illness, as well as the deconditioning from immobilization is responsible. So it's been suggested that early physical therapy and mobilization as forms of ICU rehabilitation may prevent or even reverse the physical impairments and improve clinical outcomes. You may have seen, and many of you may be using this intervention in your ICUs, and the proposed benefits of early PT and critical illness include decreasing the inflammatory load, promotion of the microcirculation, and counteracting the protein catabolism in skeletal muscles. And in fact, a recent systematic review and meta-analysis on physical therapy in the ICU concluded that PT appears to confer significant benefits in improving quality of life, physical functioning, and peripheral and respiratory muscle strength, and in increasing ventilator-free days and decreasing hospital and ICU length of stay. So in this patient, in this case, you would expect that with this implementation or with this initiative, you may be able to get him off the ventilator more quickly and get him out of the hospital, therefore, faster. The hemoglobin value in this case is adequate, and liberal transfusion has other consequences that would be adverse and would not suggest transfusing him to a hemoglobin level of 10. The patient doesn't have delirium, therefore the use of dexmedetomidine is not necessarily helpful or warranted. And finally, the use of glutamine in critically ill patients has been studied, but it does not improve clinical outcomes and does have adverse consequences and may actually make things worse. So with that, I will hand it back to our leadership to take over from here. So I'd like to thank the audience for attending and especially to thank our expert faculty for providing such useful information. This recording will be available in 24 to 48 hours in the content section of the course. This concludes our presentation today and actually is the third of the sessions, and we want to thank you very much for participating. Have a fine day.

neurology

toxicology

ID

miscellaneous topics

neurologic emergencies

toxic alcohol ingestions

difficult airways management

ICU rehabilitation

ethical principles