Category: Cases

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We discuss the practicalities of using airway pressure release ventilation (APRV) with Dr. Rory Spiegel (@EMnerd_), emergency physician and intensivist at MedStar Washington Hospital Center (and EMNerd at Emcrit).

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Takeaway lessons

1. The most immediate benefit of APRV is to help restore lungs to FRC (functional residual capacity). While this can be achieved with PEEP, most people don’t use enough PEEP. APRV proves a higher mean airway pressure while also reducing sedation requirements, and provides a physiologically automatic titration of “PEEP” based on lung compliance.
2. Phigh can usually be set to equal the previous plateau pressure on a conventional mode (assuming reasonably appropriate settings there). This helps match higher Phigh to a more poorly compliant lung and vice versa. The release volume that results should be checked to give a sense of the effects; it should be more or less in the range of normal tidal volumes, although usually lower than your previous tidal volume on a conventional mode due to the intentional air trapping. (If it’s not lower, your Tlow may be set too long, allowing too much release.)
3. Thigh can range from 1.5 seconds to infinity. Longer T-high is better for recruitment, shorter is better for ventilation. When initially flipping to APRV, shorter Thigh is usually needed; try to match the patient’s minute ventilation (from the prior mode) fairly closely, although usually you’ll need to accept a small loss of ventilation. A too-long initial T-high is a common error; patients this sick usually cannot tolerate more acidosis. Usually an initial T-high of 2 seconds is about right.
4. Tlow should be set to terminate when the expiratory flow drops to 75% of the peak expiratory flow (so if the peak was 100 L/s, terminate Tlow when it drops to 75 L/s). This was about the point in pig models where alveolar derecruitment began to occur. Peak and end expiratory flow can be checked on most modern vents, although it may not be easy to find in the screens. Usually the right T-low is around 0.3–0.6 seconds.
5. Occasional patients may need a shorter T-low than this for optimal recruitment. But few need longer; Tlow should rarely be lengthened, even as patients recruit. Although the amount of air trapping will usually increase as the lung becomes more compliant (e.g. the same T-low duration will terminate expiration at 85% instead of 75% of peak expiratory flow), this is usually fine; this is when you’ll start weaning and stretching your Thigh.
6. Plow should be set to zero in almost all cases, allowing the fastest expiration (higher Plow reduces the driving pressure and substantially reduces expiratory flow). In a few vents (older Puritan Bennett, older Servos), the machine may attempt to synchronize with patient efforts by allowing the Tlow to “kick out” and extend, creating large release volumes and loss of desired air trapping. Increasing the Plow may provide some safety margin in this case, although switching from APRV altogether is probably the best solution.
7. As the patient recruits on APRV, release volume should gradually increase despite a fixed Phigh, as the lung recruits. The expiratory flow curve will flatten and the compliance will increase. Thus, release volumes are initially small—”lung protective” in conventional thinking—and later will increase. This increase should be allowed, as it’s still associated with a normal/low driving pressure, since the “PEEP” gradually increases as trapping increases. A large release volume + low driving pressure is felt to be lung protective in APRV thinking.
8. Driving pressure on ARPV can be checked on most vents by performing an expiratory (not inspiratory) hold to determine the effective “PEEP.”
9. Patients can breathe spontaneously on APRV and be comfortable, but this is mostly determined by lung recruitment and how close they are to FRC. When the lungs are still tightly closed, spontaneously breathing will not be either comfortable or safe, so when initially flipped to APRV, patients should NOT be breathing; they will look uncomfortable, require very high minute ventilation, and generate high pressures. (There is also great discomfort here due to the hypercarbia usually unavoidably present.) Use a shorter Thigh and ventilate using the vent releases in this period, while using deep sedation and/or paralysis to suppress breathing.
10. As patients stabilize and recruit, the minute ventilation needed to maintain pCO2 will drop as ventilation becomes more efficient. When MV and the CO2 approach normal physiologic ranges, sedation can be lightened and patients allowed to breathe. Ultimately, severe ARDS patients on APRV require less total sedation and need for paralysis than in other modes.
11. Weaning occurs as thus: CO2 will gradually fall and release volumes naturally increase as the lungs recruit. Eventually they become hypocapnic, so Thigh must be increased to reduce the minute ventilation. As MV reaches normal, stretching the Thigh further causes hypercapnia, so patients should now be allowed to start breathing spontaneously to make up the difference in MV. Breathing should look comfortable, with a benign clinical appearance and gentle inspiratory flows (not sharp peaks); if not, recruitment may not yet be optimal and it may not be time for spontaneous breathing.
12. Rory does not drop the Phigh during the weaning period, although many teach this; he finds it often causes derecruitment. He adjusts Phigh only in response to the perceived disease state; for example, it may need to be weaned as the disease improves and the initial Phigh may start to cause overdistention. He rarely touches it until the patient is ready for breathing. Once the patient is breathing spontaneously, this provides a good feedback tool to adjust Phigh; if you drop Phigh and spontaneous breathing looks worse (like a failed SBT – lower volumes, high rates), you derecruited them and Phigh should go back up. Spontaneous effort is a more sensitive and faster method of feedback than monitoring the release volumes alone.
13. Permissive hypercarbia is okay. But severe hypercarbia before starting APRV is a marker of advanced underlying disease and lung injury which may make it difficult to tolerate APRV, and persistent hypercarbia on APRV is a marker of failure—the lung is not recruiting, and the mode is probably not totally safe as a result (persistent acidosis + persistently high driving pressures and risk of overdistention of ventilated lung).
14. Hypotension is not necessarily a contraindication to APRV. Cardiac output is best when the lungs are at FRC, neither over- or under-distended. However, it’s true that the lungs “overdistend instantly, but recruit over time,” so until the lung recruits, intrathoracic pressure may be elevated, and delicate patients (eg hypovolemic) may not tolerate this well.
15. Pneumothorax should not be a contraindication to APRV. The more recruited the lungs, the less strain on each individual lung unit given the same overall driving pressure.
16. Using APRV is a skill that requires practice. However, it also helps create a general mindset of approaching the lung physiologically with the goal of restoring FRC, as well as appreciating the value of using minute ventilation as a marker of recruitment; these tools probably benefit patients even in other modes. With this approach, APRV can often be avoided, and used mainly as a rescue modality.

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We discuss the field of rehabilitation psychology, and how it can help patients with persistent critical illness, with Dr. Megan Hosey (@DrMeganHoseyPhD), clinical psychologist and assistant professor at Johns Hopkins School of Medicine, where she practices in the medical ICU.

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Takeaway lessons

1. Rehabilitation psychology is a specialty of clinical psychology that generally partners with patients who have acute illness or injury, and helps them adapt to life in these new circumstances. They discuss health behaviors, values and priorities, help patients find paths back to what they love, and assess cognitive and behavioral changes that accompany new illness. In the ICU, they can assist with the psychological aspects of care, particularly in patients with a prolonged stay where psychological factors play an important role in recovery, or for treatment-refractory delirium.
2. Delirium often dominates the patient experience of the ICU. This is primarily an experience of inattention, with relatively little awareness of their circumstances, the day, the context for events, and the presence of often-vivid hallucinations and delusions.
3. ICU care is highly anxiety provoking, with common questions of “when,” “why,” and many other (often unanswerable) questions. The more certainty and structure you can provide, the better.
4. Depression is common as well in longstanding inpatients, and is often better characterized as “hospital demoralization,” a fairly appropriate response to prolonged confinement and limited access to their regular life. This can lead to sensations of helplessness and hopelessness.
5. Motivation can be improved by strategies to reduce the emotional barriers to engagement, while also strengthening their sense of meaning—i.e. what matters to them, and how will their involvement help move towards that?
6. Effective psychological care relies on communication with the patient, and medical measures like tracheostomies and endotracheal tubes can be a barrier. Good care that minimizes sedation and delirium, close involvement from respiratory therapy and speech therapy (with tools like speaking valves), and non-verbal tools like speech boards, eye gaze, yes/nos, etc. are key.
7. Patients with persistent/chronic critical illness appreciate having their schedule set out for the day, to give them a clear sense for what to expect and reduce anxiety.
8. Try to build pleasurable activities into their day, aka “behavioral activation.” Doing things that are meaningful and pleasurable creates a positive feedback loop that enables more activity. Animal therapy, “sunshine therapy” (getting outside), music therapy (or just playing preferred music) are all valuable. Merely asking patients their preferred music and playing it can reduce anxiety and sedation requirement (see Linda Chlan’s work on this)
9. Relaxation strategies can be learned, and in the ICU setting, vital sign monitoring can even be used as a form of biofeedback to appreciate changes in heart rate or respiratory rate in response to stress.
10. Motivational interviewing emphasizes taking control over the aspects of their life that can be controlled.
11. Normalize and validate the difficulty of being in the hospital. (“It is very common for people to feel frustrated, scared, or down in the hospital. This makes sense as you’re away from the people and things that you love, all while not feeling well. We can work together to find ways to help you feel like yourself.”)
12. Create a schedule for the day to establish predictability and reduce anxiety. When possible, getting patient preferences (eg, morning rehab therapies, sitting up to chair for favorite tv show, evening wash up, recreate parts of bedtime routine from home, view church service remotely on Sundays via ipad, etc)
13. Give patients choice over some activities (what time of day rehab therapies? Preferred positions for peri care? pick a length of time to do trach collar trial vs. go as long as you can?)
14. Benzodiazepines as a treatment for anxiety in the hospitalized patient tend to be a short-term solution only, and may ultimately contribute to delirium. SSRIs or similar drugs might be a useful adjunct for patients who describe depressive symptoms like helplessness, hopelessness, worthlessness, guilt, etc.
15. Gentle attempts at reorientation are appropriate for the delirious patient. In more agitated patients, emphatic and repetitive attempts at reorientation are usually not helpful. “Join the journey” (or as the improv comics say, “Yes, and…”) by redirecting benign delusions toward productive ends rather than disputing them. Floridly delirious patients generally cannot comprehend, even if they are able to parrot back information to please the interrogator.
16. Consider implementing a “Get to Know Me” board; see Ognjen Gajic’s work

Resources

1. The Conversation Project: good questions about end of life care wishes
2. Vital Talk: quick guides on effective communication at end of life 
3. American Psychological Association, Division for Rehabilitation psychology: for anyone who has interest about what a rehab psychologist is and what they do
4. PADIS Guidelines
5. ABCDEF Bundle

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We discuss the principles and application of automatic tube compensation (ATC) on modern ventilators, with its creator Ben Fabry. Dr. Fabry is a professor and chair of biophysics at University of Erlangen-Nuremberg, originally trained as an electrical engineer, who originally developed ATC as part of his PhD program.

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Takeaway lessons

1. ATC, originally called “electronic extubation,” is meant to normalize or eliminate the resistance to flow created by the endotracheal tube. Since this resistance is always present, yet is dynamic and varies by flow (and tube size), it creates a continuous confounding variable, making the displayed pressure on the ventilator a measurement not of tracheal pressure, but of another, largely meaningless pressure (the pressure outside the patient).
2. ATC works by increasing airway pressure during spontaneous inspiration to eliminate the pressure gradient created by the tube at the current flow, and reducing it during expiration to reverse the effect.
3. While ATC can be used in any mode, it is mostly meant for pressure support or other spontaneous modes. It has no real role in volume control. In pressure control, it has little meaningful impact during inspiration, although it will reduce the airway pressure below the set PEEP during expiration, which may help facilitate expiration.
4. The original ATC test ventilator could drop pressure below atmospheric pressure during expiration, but this feature is not possible on modern ventilators, so the lowest possible pressure during ATC is zero (probably not quite even, that due to expiratory valve resistance). Some modern vents will not drop pressure during expiration at all.
5. In principal, actual tracheal pressure could be measured by a separate monitoring lumen. In practice, this is dangerous, as the lumen could be occluded by mucus, so the resistance constant is instead applied mathematically. The modifiers were derived empirically by testing a variety of tubes at different flow rates.
6. ATC will generally ask for the tube size. Length has some effect but a fairly trivial one, as resistance is mostly influenced by turbulence, which is mainly a product of diameter. Resistance is not a constant, but increases with (roughly) the square of the flow of gas.
7. A swivel connector on the ETT outlet adds about 1 cm H2O of resistance. An HME adds about 3 cm H2O.
8. Changes in gas composition at different FiO2 changes resistance trivially, although a mix like Heliox would change it significantly, and would make the internal calculations incorrect.
9. No fixed single pressure support value can accurately match tube resistance, due to its dynamic nature during and between breaths, even if you were willing to set the sort of pressure needed—which might be 50+ cm H2O in a strongly breathing patient.
10. The main downside of ATC is that modern ventilators don’t do it very well—they can only vary flow so quickly, so when there are brisk changes in pressure, they fail to match it. They usually can match only about 50% of tube resistance, with the worst at the start of a breath as they lag behind the initial drop in pressure. (You can appreciate this by seeing the airway pressure drop below the set PEEP.) Response is even less in some of the current generation of vents with radial blowers and slower valves
11. Quality check your ATC by watching the tracheal pressure—the vent will display this as a second pressure tracing. It should remain positive above the set PEEP for the whole breath. (The airway pressure should also remain positive, but the tracheal pressure will be a more sensitive marker.) If it becomes negative or drops to the PEEP at any point during inspiration, it implies a failure to fully support the patient. This problem can occur during vigorous spontaneous breathing in any mode, since it’s driven mostly by slow ventilator response; it is just compounded by ATC, because not only does flow have to vary to meet a set pressure, but the set pressure is varying during the breath too. The best way to solve this problem is probably better machines, with faster valves, and maybe situating them closer to the patient (shorter circuits) to speed up responsiveness.
12. When ATC fails to fully support, you can try adding PSV with a very fast rise time, but this is a bludgeon; the best mode is probably flow-proportional assist ventilation with ATC. PAV allows controlling not just tracheal pressure to a constant value, but alveolar pressure; it will further boost the pressure to try and maintain constant alveolar pressure during inspiration. Increase proportional assist until the tracheal pressure no longer drops below the PEEP. (You could achieve a similar effect by “lying” to your ATC and setting a smaller tube size, which will also increase the initial amount of support; but this is less precise and maybe less safe.) PAV plus ATC may be the ideal mode for patients spontaneously breathing without severe lung disease.
13. PAV could be used, by the way, in a patient with bronchospasm (or similar increase in airway resistance from physiologic factors), as it allows you to compensate for any amount of airway resistance you wish. However, it will only do this during inspiration, and will not drop pressure below the PEEP during expiration (i.e. to reduce autoPEEP and aid exhalation). This probably wouldn’t help them exhale anyway, since the resistance is in the lungs, not in the vent.
14. PSV in a weaker patient tends to mask some of their true spontaneous breathing patterns. ATC may unmask these, showing some odd patterns, such as very shallow or rapid breaths. This is not dyssynchrony; it is the true physiologic pattern that was merely being hidden in a less supportive mode. It is also not tiring, at least if the ATC is working correctly and you’re offering adequate support, because they are not experiencing resistance to breathing.
15. If present, a Cheyne Stokes pattern of breathing may also become amplified by the “signal boosting” properties of ATC, rather than being damped by inadequate support. If this results in phenomena like very long apneic pauses, it may (perhaps) be a problem.

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Our collaboration with Sarah Lorenzini of the Rapid Response RN podcast, discussing a case and general principles for diagnosing and managing obstructive shock. Check out the other episodes on shock in the Nurses’ Podcrawl 2024!

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We discuss the role of point-of-care ultrasound in evaluating the patient with kidney injury and assessing volume status, with Abhilash Koratala (@nephroP), nephrologist, Director of Clinical Imaging for Nephrology at the Medical College of Wisconsin, and champion of nephrology-focused ultrasound.

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Takeaway lessons

1. A quick kidney and bladder ultrasound to rule out urinary obstruction is appropriate for most significant AKIs, maybe even if it was done previously (as obstruction can develop at any time).
2. Ultrasound of the lungs and IVC help establish the presence of elevated filling pressures; if present, the VEXUS scan can be performed to establish the presence of venous congestion that might be contributing to kidney injury.
3. Pulmonary edema as evidenced by B-lines establishes that the patient is not fluid tolerant, and suggests that further volume loading may be harmful. It increases the chance that AKI is due to congestive nephropathy as well, although each can also occur in isolation (and of course AKI can be a cause, leading to volume retention and then pulmonary edema).
4. Abhilash does an 8-zone lung exam (2 anterior and 2 lateral zones on each side), which is plenty for cardiogenic pulmonary edema. He does not really count B-lines; if he sees B-lines in more than one dependent zone, he takes it as evidence the patient could be decongested.
5. IVC is a reasonable method of estimating RAP; it is not reliable to gauge fluid responsiveness or other questions. The internal jugular vein is a good fallback if the IVC is untenable or seems unreliable, such as if bandages limit access, or the presence of cirrhosis (which alters local vasculature in unpredictable ways). Look for the highest point of distention and measure roughly from the sternal angle, adding it to the right atrial depth to approximate the CVP (usually ~5 cm although this is not very reliable).
6. A non-plethoric IVC and absence of B-lines suggests a fluid tolerant patient. He uses the ACE guidelines of IVC >2.1 and <50% collapse with deep inspiration (sniff) to equate RAP ~15 mmHg.
7. In the presence of elevated RAP, VEXUS helps determine whether that change is likely to be affecting organ perfusion by altering flow characteristics. Higher VEXUS scores are well-associated with risk of AKI.
8. High RAP with a low VEXUS suggests that congestive nephropathy is not actively worsening renal function, whereas a higher VEXUS suggests the opposite. Serial VEXUS scans help track the progress of decongestion to dial in a patient to an optimal fluid balance.
9. VEXUS is a right-sided heart parameter, so the state of the left heart’s filling may differ somewhat (e.g. as evidenced by lung markers like pulmonary edema—so track your B-lines too!). It is probably more precise and reliable than other markers like peripheral edema.
10. Right and left heart filling should generally be well-linked. Venous congestion and elevated RAP usually indicate a well-filled LA as well, unless the lungs are acting as a significant resistor. If major PH is present, consider introducing measures like pulmonary vasodilators instead of further fluid loading; overdistending the RV will not help the LV.
11. Although portal vein pulsatility can usually move towards normal after optimal decongestion, hepatic vein waveforms may remain abnormal in some patients with TR, PH, etc. Flow chanegs in intrarenal vessels often lag behind other vessels, as renal edema takes time to resolve.
12. Hepatic vein waveform may be permanently blunted in cirrhotics, confounding it somewhat. Distinguishing the systolic and diastolic waves can also be hard to identify without ECG synching; ECG is highly recommended when available.
13. Portal vein is also probably unreliable in cirrhosis, due to portal hypertension and AVMs; it may be permanently pulsatile in some (although loss of pulsatility is still associated with decongestion). Since many cirrhotics have recurrent hospitalizations, you can compare against prior scans.
14. Intrarenal vessels are technically difficult, especially when patients cannot perform a breath hold; critically ill patients have a failure rate here >20%. It is easier in stable patients. However, CKD patients may have abnormal waveforms at baseline.
15. Overall, there should not be any disease state that falsely confounds ALL of the VEXUS vessels; while states like mechanical ventilation can increase flow changes and point to congestion, this is real congestion, not an artifact.
16. Invasive monitoring like a CVP or PA catheter replaces some of the function of the VEXUS scan, but VEXUS helps determine the degree of organ impact at the numbers reported by these devices. High filling pressures generally are associated with congestion and low pressures are associated with its absence, but VEXUS is often helpful in the gray area. Non-invasive measurements of filling using echo, such as RVSP or E/A and E/E’ may have a supplemental role as well; the latter may help distinguish cardiogenic from non-cardiogenic pulmonary edema, but do not tell much of a story about systemic congestion.
17. Femoral vein doppler could be a supplement to VEXUS, mainly when you cannot get or cannot trust one of the other vessels. It is farther from the heart, so may be less sensitive to changes in RAP. A normal femoral vein (continuous or mildly pulsatile) should probably not rule out venous congestion, but an abnormal femoral vein is very suggestive of it. This can sometimes be noted on routine DVT scans.
18. Abhilash runs a cardiorenal clinic where he finds outpatient VEXUS very useful to establish and monitor volume status. It is more difficult to use in a dialysis clinic due to lack of privacy and high patient volumes; quick lung ultrasound (8 or even 4 zone) might be more useful here.

References

Episode 4 with Philippe Rola on the VEXUS scan

NephroPOCUS

POCUS in AKI: Transcending boundaries: Unleashing the potential of multi-organ point-of-care ultrasound in acute kidney injury. Batool A, Chaudhry S, Koratala A. World J Nephrol 2023; 12(4): 93-103 [PMID: 37766842 DOI: 10.5527/wjn.v12.i4.93]

VEXUS for nephrologists: Koratala A, Reisinger N. Venous Excess Doppler Ultrasound for the Nephrologist: Pearls and Pitfalls. Kidney Med. 2022 May 19;4(7):100482. doi: 10.1016/j.xkme.2022.100482. PMID: 35707749; PMCID: PMC9190062.

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We discuss the phenomenon of CPR-induced consciousness (i.e. patients demonstrating awakeness during resuscitation) with Jack Howard, Intensive Care Paramedic at Ambulance Victoria in the northern suburbs of Melbourne, Australia, and first author on a recent literature review and Delphi-derived expert guideline on CPRIC management.

Takeaway lessons

1. Data is light, but perhaps 1% of cardiac arrests have some form of consciousness witnessed.
2. It is primarily a problem because of the potential to delay or interfere with care (either due to the emotional confrontation and surprise, or from actual physical interference with medical care). However, there are also ethical questions about patient suffering.
3. The first response in many people seeing CPRIC will be to stop CPR and assume they’ve made a mistake about loss of pulses.
4. CPRIC is associated with better outcomes, probably as a marker of better neurologic perfusion before and/or during arrest.
5. There was general agreement by the panel that ketamine should be used as first-line for CPRIC. If unavailable or if it fails, the group was unable to agree on a best second line; fentanyl, midazolam, or a paralytic are all options. In CPRIC that physically interferes with care, larger doses are appropriate.
6. Paralytics as a first line (without sedation) are never recommended.
7. There is minimal data on the effect on outcomes when CPRIC is treated. One small Ambulance Victoria study had a trend towards lower rates of ROSC when sedation was used.
8. Speak to patients as though they can hear and understand you.
9. It is not clear but very possible that a larger number of patients than those who demonstrate external awareness may have a degree of subclinical consciousness; interviews of survivors and EEG analysis has supported this.
10. Many CPRIC patients will have ROSC, but if they don’t, they are probably excellent candidates for ECPR/ECMO or other rescue interventions. A minimum of 45 minutes of resuscitation should be offered.

References

• The guideline: Howard J, Grusd E, Rice D, et al. Development of an international prehospital CPR-induced consciousness guideline: A Delphi study. Paramedicine. 2023;0(0). doi:10.1177/27536386231215608
• The preliminary scoping review: Howard J, Lipscombe C, Beovich B, Shepherd M, Grusd E, Nudell NG, Rice D, Olaussen A. Pre-hospital guidelines for CPR-Induced Consciousness (CPRIC): A scoping review. Resusc Plus. 2022 Nov 28;12:100335. doi: 10.1016/j.resplu.2022.100335. PMID: 36465817; PMCID: PMC9713363.
• The study mentioned about awareness during CPR: Parnia S, Keshavarz Shirazi T, Patel J, Tran L, Sinha N, O’Neill C, Roellke E, Mengotto A, Findlay S, McBrine M, Spiegel R, Tarpey T, Huppert E, Jaffe I, Gonzales AM, Xu J, Koopman E, Perkins GD, Vuylsteke A, Bloom BM, Jarman H, Nam Tong H, Chan L, Lyaker M, Thomas M, Velchev V, Cairns CB, Sharma R, Kulstad E, Scherer E, O’Keeffe T, Foroozesh M, Abe O, Ogedegbe C, Girgis A, Pradhan D, Deakin CD. AWAreness during REsuscitation – II: A multi-center study of consciousness and awareness in cardiac arrest. Resuscitation. 2023 Oct;191:109903. doi: 10.1016/j.resuscitation.2023.109903. Epub 2023 Jul 7. PMID: 37423492.

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We discuss the medications typically used after organ transplant, their impact on critical illness, and how to manage them when these patients show up sick—with Olivia Philippart, transplant clinical pharmacist specializing in liver and kidney transplant at University of Kentucky HealthCare.

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Takeaway lessons

1. Most kidney transplants will end up on a calcineurin inhibitor like tacrolimus (or the older cyclosporine), an anti-proliferative like mycophenolate mofetil (Cellcept) or the older azathioprine, and possibly corticosteroids (e.g. prednisone). Formulations for some of these may need to be adjusted based on your formulary, so consult your pharmacist to get the equipotent dose.
2. How these patients present, their degree of immunosuppression, and risk of rejection, are all heavily dependent on the time since transplant. A patient <6 weeks from transplant is high risk for nosocomial infections (e.g. post-op complications). A patient years out is mainly at risk of the same infections as anybody else, in addition to opportunistic infections related to their immunosuppression.
3. Latent viral infections unmasked by immunosuppression or acquired from the transplant are usually not a surprise, as these are tested for as part of the initial workup.
4. The highest risk of organ rejection and hence the highest degree of immunosuppression is in organs with substantial amounts of lymphoid tissue transplanted. The highest is small bowel, then lung, then heart/kidney/pancreas, then the least in liver (liver transplant can actually overall support immune function). Some livers can be maintained on monotherapy, while lungs usually need triple therapy, and often dual therapy is used in the middle category.
5. Durations of therapy for identified infections may be longer in the immunosuppressed than for routine ICU care.
6. Mycophenolate is the first agent to consider dose reducing or holding in the setting of active bacterial infection. How to handle this depends on the severity of infection and degree of concern for rejection.
7. Both our calcineurin inhibitors (tacrolimus and cyclosporine) are primarily cleared in the liver and gut, so when there is liver impairment or bowel problems, dose decreases are often needed. Dietary intake also reduces drug absorption whereas NPO status may increase it. These drugs are heavily protein bound so albumin fluctuations (e.g. from malnutrition) may impact free levels.
8. Drug interactions are common as well; CYP3A4 or PGP inhibitors like diltiazem or verapamil, azole antifungals, amiodarone, macrolides (although not azithromycin), and paxlovid will tend to increase levels, while inducers like phenytoin or phenobarbital will tend to decrease them.
9. Overall, the therapeutic index of the calcineurin inhibitors is small, so have a low threshold for checking trough levels early and often.
10. After holding a dose, the serum levels will normalize within 3-5 half-lifes, but full return of immune function may take several weeks. However, the baseline level of immunosuppression is usually not so profound that the difference between “off” and “on” is huge and binary.
11. Organ rejection is possible but rare when drugs are acutely held (for days, maybe a week or two) in setting of severe infection, as this is already a relatively immunosuppressed state. However, this depends heavily on the time from transplant, and the organ transplanted.
12. Mycophenolate levels (or mercaptopurine levels for the older azathioprine) tend not to fluctuate as much; the metabolism (via glucuronidation) is not as sensitive to hepatic function, so monitoring levels is rarely needed.
13. Most of our immunosuppressants are not significantly renally cleared, so renal injury (even dialysis) usually require no dose adjustment. However, they can be nephrotoxic, so high levels may CAUSE renal injury, not vice versa.
14. Tacrolimus is available in either immediate release capsule (taken twice daily) or a long-acting form (taken once daily). The latter helps to decrease peaks and some of the neurotoxicity (seizure, tremors), but cannot be opened. There is an 80% conversion between formulations (multiply the long-acting dose by 1.2, then divide by half to get the short-acting BID equivalent). Levels checked should always be troughs.
15. Short-acting tacrolimus capsules should not be opened and put down tubes, but can be opened and given sublingually (50% dose reduction)—just dribbled under the tongue—although nurses need to take special precautions like gowning and double gloving. There is also a liquid tacrolimus formulation available.
16. IV tacro exists, but has substantially higher nephrotoxicity, and the dose conversion is tricky; other routes are preferred.
17. Cyclosporine is available in suspension which can go down a feeding tube, or via IV form (dose reduction needed).
18. IV mycophenolate is available (1:1 conversion), as well as a liquid suspension.
19. Steroids can be used in the ICU as usual (e.g. stress dosing), and indeed temporarily converting transplant patients to a pure steroid regimen is a reasonable approach during critical illness (remember: 20 mg hydrocortisone is equivalent to 5 mg prednisone).
20. It’s generally sound to touch base with someone who knows a patient’s transplant history, even years out (often just their normal nephrologist, pulmonologist, etc in that case, not necessarily the original transplant team), when these patients are admitted for critical illness.
21. Calcineurin inhibitors can cause headaches, seizures, even PRES, hyperkalemia and hypomagnesemia, and hypertension, hypercholesterolemia, hyperglycemia/diabetes. Attributing these effects to the drug is usually a diagnosis of exclusion.

References

From: Fishman JA. Infection in Organ Transplantation. Am J Transplant. 2017 Apr;17(4):856-879. doi: 10.1111/ajt.14208. Epub 2017 Mar 10. PMID: 28117944.

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We discuss assessing patients prior to intubation or other airway management, including both elective and emergent circumstances, with Dr. Jed Wolpaw, anesthesiologist and intensivist from Johns Hopkins, anesthesiology residency program director, and host of the ACCRAC podcast.

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Takeaway lessons

1. Edentulous (toothless) patients are usually easier to intubate, but harder to mask ventilate. Heavy beards are harder to mask (can you trim it, or cover it with a Tegaderm?), larger neck circumferences, and larger tongues likewise.
2. Consider the history, particularly involving the head and neck anatomy. Is there surgical history here? Jaw or oral surgery? Prior trachs or oral/neck radiation? Rheumatoid arthritis or Down syndrome (which can cause atlanto-occipital instability and may warrant trying to limit any forced neck extension)?
3. Start by looking into the patient’s mouth (mouth open, sitting up, no “aah”):
   • Mallampati score (do you see the entire uvula, part of it, soft palate, or hard palate only?)
   • How is the dentition? Remove dentures if present. Are there loose teeth?
   • Is there an excess of soft tissue in the mouth (large tongue, etc)?
4. Evaluate the thyromental distance (thyroid bump to chin); <3 cm (or fingerwidths) suggests a more “anterior” airway.
5. Evaluate neck flexion and extension (passively if necessary) to appreciate limitations in neck mobility.
6. If the patient is able, evaluate how well the jaw can protrude/prognath: ability to bite more of the upper lip with the lower teeth is a good thing. This is probably the single most predictive test for airway difficult, although it usually requires patient cooperation.
7. Review the chart (or ask the patient) for prior documentation of intubation or anesthesia to determine if they have a history of a difficult airway. This can require some interpretation of the context and who was intubating previously. Good practice when documenting: write exactly what you did, and if it was difficult, write why! If you used a technique like awake intubation, a bougie, etc for elective or training reasons, document that reason so they don’t earn a label of a difficult airway forever.
8. The STOP-BANG score is used to predict post-anesthesia airway obstruction (i.e. OSA), and probably has some association with faster deoxygenation and difficult mask ventilation, but is generally not super relevant for intubation.
9. A patient with any concern for difficult intubation warrants consideration for factors also contributing to difficult LMA placement or cricothyrotomy. LMAs are difficult to place when the mouth opening is very small (about 2 inches) or the oral-laryngeal anatomy is unusual, and crics are difficult when the neck anatomy is impossible (eg a superimposed tumor, goiter, or heavily distorted anatomy). A patient who cannot have a cric may warrant an awake intubation to avoid the risk of inducing a patient who cannot be rescued.
10. Obesity is not a predictor of anatomically difficult intubation. Mask ventilation may be a little harder if there is increased oropharyngeal soft tissue. It is a predictor of physiologic difficulty (faster desat), though.
11. For emergent intubations: confirm code status, briefly evaluate the head/neck/mouth, use video laryngoscopy. Use hemodynamically stable agents for induction and reduce the dose, and ensure the team knows to subsequently sedate any patient who received a long-acting paralytic. Have a vasopressor drip ready, or better yet, running. Always set up everything and be prepared for every eventuality before you take away a patient’s ability to breathe.
12. Either RSI with paralytics, or perform awake intubation. Otherwise, never RSI the critically ill without neuromuscular blockade, which will reliably reduce your chances of success. Short-acting paralytics (succinylcholine) are brief—i.e. not much longer than the apneic period of a short-acting sedative—and long-acting paralytics (eg rocuronium) can be reversed with suggamedex, in the rare situations where letting the patient wake up and resume breathing is a smart move.
13. The one exception might be a ketamine-only intubation, which generally keeps the patient breathing, allowing you to either proceed to paralyzing or not depending on what you see, or maybe allow them to wake up.
14. While it’s nice if an emergent intubation has been NPO, it probably won’t change your technique; changes in gut motility in the critically ill mean almost anybody can have stomach contents. Treat most ICU patients as if they have a full stomach, i.e. RSI. The one exception: the PREVENT trial showed that mask ventilation during induction (usually a no-no for RSI) of critically ill patients does not increase aspiration risk and does reduce hypoxemia, so should probably usually be done.
15. In the highest aspiration risk patients like SBO or upper GI bleeding, keep the head of bed elevated, ensure ample/multiple suctions catheters, and be ready/willing to intubate the esophagus intentionally with your ETT and place it to suction to divert the stomach contents while you use a fresh ETT to intubate the glottis. Placing an NG beforehand to decompress the stomach is hit or miss as it can induce vomiting; it works better in a fully awake patient (who can manage any vomiting).
16. We should probably still learn and teach direct laryngoscopy, but do so using a video scope with regular-geometry blade.

References

1. PREVENT trial

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We discuss head and neck surgery with Dr. Alexandra Kejner, otolaryngologist at the Medical University of South Carolina specializing in transoral robotic surgery, reconstructive surgery including microvascular free tissue transfer, salivary neoplasms, and sialoendoscopic procedures.

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Takeaway lessons

1. Robotics has enabled much less invasive approaches to many head and neck procedures.
2. Major airway procedures create edema, and there is always risk for bleeding, so patients often remain intubated overnight.
3. The other common ICU indication is a free flap, a portion of tissue (potentially including skin, subcutaneous tissue, muscle, even bone) removed from a remote site and transplanted into the head and neck area, with vessels anastomosed. These are at risk of failure and require close monitoring.
4. Most of these procedures will involve placing a tracheostomy, and potentially a PEG (or NG). This facilitates both surgical access and early recovery.
5. Tumors are superficially resected with adequate margins, then reconstruction begins. Meanwhile, exposure of deeper structures and deeper resection occur, which may involve a jig to guide the removal (prepared in advance from imaging), and a matching cut to prepare the flap tissue. Lymph nodes are removed en bloc. Then the flap is transplanted and vessels anastomosed (at least one robust artery and vein), using microsurgery and teeny sutures (often 8-0 nylon).
6. As a supplement to the clinical exam, an implantable Doppler monitor is occasionally left in place to augment post-op monitoring of perfusion, as well as sometimes a Vioptix near-infrared spectroscopy device which performs real-time tissue oximetry.
7. On POD 0-1, hourly nursing monitoring of the flap is usually needed, with periodic provider checks. Changes in the exam (swelling, turgor, cap refill, color), signal, or bleeding may require return to the OR for revision. A single ICU night is the norm, although comorbidities are common and may require a longer stay if the stress of surgery unmasks other problems.
8. Laryngectomy may be performed, involving removal of the larynx (voice box), leaving a blind pouch; the lungs no longer connect to the upper airway in this case, and the entire team should be aware of this anatomy, as the patient cannot be intubated or their airway otherwise managed from above.
9. Most flaps will be on a baby aspirin and enoxaparin, but occasionally may use a heparin drip.
10. Most will receive three doses of dexamethasone, both to reduce edema and to treat any adrenal insufficiency.
11. Chlorhexadine or salt water oral rinses are performed to keep the operative site clean.
12. Multimodal pain management is needed for both the oral site and the donor flap site.
13. A drop in the Vioptix signal from the initial post-op reader, neck swelling, or difficulty breathing (dyspnea, hypoxia, etc) all warrant immediate involvement of the surgical team for danger to the airway or the flap. Flaps might also turn purple from venous congestion, sometimes a little later, also a surgical emergency.
14. A questioned flap might be scratched to see if it bleeds (which is good).
15. A patient in shock might need vasopressors, fluid, or to be hypotensive, none of which are great for a flap. A balanced approach is probably best. A low-dose phenylephrine drip may be the most appealing pressor, and vasopressin might be the riskiest. MAP >65 is a minimum, some prefer higher (>80).
16. Intro-operative feeding has been used in some centers due to the prolonged procedure times.
17. Flap failure historically was most often from a venous clot, but this has reduced over time; nowadays it’s often late failures due to a salivary fistula contaminating the area and creating a region of digestion, clot, and breakdown.
18. Surgeons will occasionally request deeper sedation (or even forcing the patient to maintain a specific neck position) to avoid dislodging monitors, disrupting a very delicate anastomosis, etc.
19. A swollen or firm anterior tongue, ooziness in the mouth, or a difficult airway on the initial intubation may lead a surgeon to request delaying extubation.
20. The immediate post-op appearance usually heals into a better eventual aesthetic result. Occasionally measures like prosthetics can be used.

References

1. Vasopressors improve outcomes in autologous free tissue transfer: A systematic review and meta-analysis
2. Postoperative Use of Vasopressors in Head and Neck Microvascular Reconstruction

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We learn about liver transplant with Dr. Meera Gupta, transplant surgeon at the University of Kentucky Healthcare Transplant Center, and surgical director of the Kidney and Pancreas Transplant Program. We discuss eligibility, triage, the peri-operative course, and important post-op complications.

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Takeaway lessons

1. Liver transplant eligibility is based on need, not time on the list. The MELD score (MELD 3 now, including albumin) is used for this, with MELD >9 (historically >15) considered the cutoff for transplant potentially exceeding the risk of not transplanting.
2. Livers can now be placed on warm perfusion pumps, allowing continued viability for much longer. This is mainly used in donors who died from cardiac death, those with high BMI or similar risks for primary non-function (i.e. the transplanted liver never starts working), and longer transport distances or expected operative times.
3. Incision is a large right subcostal incision, extended as needed. The liver hilum is dissected, preserving the feeding vessels. Caval clamping may be tested, then the liver is removed. This anhepatic phase in minimized to <60 minutes, preferably <45 minutes. The new liver is then anastomosed to the portal veins, vena cava, hepatic artery, and the bile duct. Some instability can occur during reperfusion, such as right heart strain, electrolyte abnormalities, or volume shifts.
4. Patients will usually remain intubated post-op, lines in place. Sedation ideally is limited so the patient can rouse and confirm the absence of encephalopathy. Systolic BP is closely watched (goal >90), as diastolic BP tends to be low in most liver failure patients. Hepatopulmonary patients can rest on the vent a little longer and are expected to remain on oxygen for the time being. Patients can be fed once extubated and stable.
5. High-dose steroids are loaded up front and then tapered, and oral immunosuppression initiated soon after.
6. Some AKI is common. Colloid like albumin is favored early.
7. Chronic thrombocytopenia is common and is monitored to determine when DVT prophylaxis can be started. Platelets >20k are targeted.
8. If INR >2, vitamin K is given empirically. FFP is usually not given prophylactically. Bleeding is usually considered a little preferable to clotting, in terms of ease of treatment.
9. A liver duplex is performed in the first 24 hours to ensure the new vascular supply is patent.