Episode 62: Running a cardiac arrest

Bryan puts Brandon through the paces, discussing the nuts and bolts of managing a code.

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Takeaway lessons

  1. Managing a room is less about asserting authority and more about leading by example. Cardiac arrest is a great microcosm and litmus test for your team dynamics for all resuscitation.
  2. Consider arterial lines early. IOs are usually fine for other access; central lines are rarely essential early.
  3. ACLS is fairly rote and can be easily delegated. The most important role of the team lead, other than assuring quality, is considering reversible causes of arrest.
  4. Consider calcium if hyperkalemia is possible and magnesium if there’s torsades.
  5. Use bedside ultrasound to rule out reversible causes like cardiac tamponade and tension pneumothorax, but don’t interrupt compressions.
  6. Once you have a pulse, expect to need continuous pressors, readdress your ABCs, ensure adequate monitoring, consider TTM, and consider reversible causes such as coronary ischemia.

Episode 61: ECPR with Scott Weingart

We chat with Scott Weingart of Emcrit about the use of crash VA ECMO for the cardiac arrest patient.

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Takeaway lessons

  1. ECPR candidacy may account for age, comorbidities, and code duration. Physiologic age is probably more important than chronological age. No-flow time without CPR should be very brief (witnessed is best), but low-flow time (with CPR) can actually be very long and still have good outcomes with ECPR. New systems should probably have stricter inclusion criteria, as numerous poor outcomes can endanger a fledgling program.
  2. The cause of arrest is usually not as important, partly because it’s often not known so early. ECPR can be a bridge to diagnosis and prognosis.
  3. One team should run the ACLS arrest while another handles the ECMO cannulation; it’s not possible to effectively do both. The cannulator should have their own ultrasound machine, and can function alone, although at least one skilled assistant is helpful. Mechanical CPR devices help by reducing energy in the room and reducing movement of the lower body; if not present, assign someone to manually stabilize the pelvis.
  4. Cannulation can be done by various services as long as they’re immediately available. Whoever it is should be comfortable using ultrasound. Cutdowns are probably not the preferred technique except in niche cases. A second service like CT surgery can arrive after a short delay to do the dilation and cannula placement if the in-department provider like EM or CCM can get initial access with smaller devices.
  5. Get ready by setting up equipment, position the ultrasound, and get sterile. As the patient arrives, have someone strip the clothes, expose the femoral region, and prep it, then get started with venous and arterial access.
  6. Vein vs artery cannot be distinguished without ultrasound, and can be difficult even with it. Don’t use anatomic location – use appearance. Arteries are thicker walled and small in cardiac arrest. TEE with a bicaval view to see your wire can be a huge help.
  7. The femoral artery should be accessed between the ligament and the bifurcation. Too high means RP bleeding risk; too low means potential for vessel damage. Similar for the venous access, although it’s more forgiving.
  8. Initially, place wires and then some kind of sheath, dilator, or line that will accept a larger, stiffer wire (Scott uses the Amplatz Superstiff). Going directly from needle to stiff wire is challenging and higher risk for vessel damage. This also means if you end up not proceeding to ECMO, you can just use the smaller sheaths for venous and arterial access.
  9. Even when a pulse returns, it’s often safer to proceed to ECMO in good candidates with a long arrest time. Supporting them through the next few days when they’re high risk of re-arrest, reperfusion injury, and other complications is likely to be safer than letting their heart do the work.
  10. Dilation for ECMO is similar to other dilation, just less forgiving. Follow the same consistent angle as the needlestick, constantly rack your wire, and consider dilating to a somewhat smaller cannula than in other VA ECMO situations, which is often tolerated post-arrest. Arterial cannulae of 17fr (women) to 19fr (men) or even smaller can achieve adequate flows, with venous cannulae of 19-23 Fr or even smaller.
  11. Goal: 5 minutes from first needlestick to active bypass.
  12. Ideally, one cannula per leg, but you can place both in the same side if needed. Certainly use the same side if using a cutdown.
  13. Venous cannula for the arrest patient should have the tip in the SVC (i.e. traversing the RA, not stopping before it). Use TEE to visualize this, or measure externally from groin to right nipple.
  14. Pumps can be pre-primed and sit waiting for 30-60 days in most cases; check manufacturer guidelines. Nurses can handle the pump with some extra training, at least for initial set-up, then transition care after 15 minutes or so to a perfusionist or ECMO-trained respiratory therapist.
  15. Pan-CT everyone. In fact, pan-CT all your cardiac arrests, as traumatic bleeding is common. Maybe do a coronary artery CT as well.
  16. Initial settings: 100% oxygen and titrate down quickly. Flow can be somewhat low compared to normal VA ECMO, allowing the native heart to keep some output and allowing smaller cannulas. Traditionally set sweep gas at roughly similar to bloodflow, but this tends to cause dramatic, rapid initial drops in PCO2, which may be harmful to a vulnerable brain; instead, start at a low sweep and gradually titrate it up.
  17. Do NOT prognosticate cardiac function early; recovery may happen late, and early withdrawal falsely affects your outcome figures from ECPR cases. The best numbers can only be achieved when the ECPR team continues to “own” the patient during their initial ICU course and doesn’t allow early withdrawal of ECMO.
  18. Neuroprognostication, conversely, tends to be easier; patients often stratify relatively early into clear good and bad outcomes. It should be established early on that families may want to pursue life support and that’s fine, but the team determines how long to continue ECMO, and it won’t be continued indefinitely.
  19. Economics: ECPR pump runs are short (<1 week usually), and reimbursement is all up front, so it actually pays well compared to many ECMO types, like long VV courses.
  20. The future: ideally, EMS would recognize good ECMO candidates and divert patients to ECPR centers. In rural areas, ED teams would be able to cannulate and start initially on ECMO, then transfer to larger referral centers.

Episode 59: Takotsubo cardiomyopathy with Vincent Sorrell

We look at stress (Takotsubo) cardiomyopathy in the setting of critical illness, with Dr. Vincent Sorrell. Dr. Sorrell is a cardiologist at the University of Kentucky, where he helped develop the Advanced Cardiovascular Imaging Program, and is current Acting Chief of both the Division of Cardiovascular Medicine and the Gill Heart and Vascular Institute.

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Takeaway lessons

  1. If considering ACS in any post-menopausal woman, you should also consider stress cardiomyopathy. Echo is the test of choice.
  2. While hypokinesis classically occurs at the apex in TCM, almost any distribution can occur; 10% or more will have atypical distributions, particular outside the traditional demographics (older women), such as the critically ill. Of course, atypical anatomical distributions can also occur in ACS due to distinct anatomy.
  3. Recurrence of TCM may occur with a different distribution. Recurrence occurs in up to 40% in the first four years. Withdrawal of beta blocker therapy may precipitate this, which may be a reason to select other therapies (e.g. ACE inhibition).
  4. In general, TCM is a diagnosis of exclusion after ruling out ACS. The ECG pattern is non-specific, but STE in V1 or lead I is unusual in TCM. ACS usually causes more troponin elevation than TCM, and matches the degree of EF reduction. Persistent troponin elevation in a patient without intervention may suggest a missed ACS instead of TCM, but you should generally not wait that long.
  5. The InterTAK score may give some guidance. Dr. Sorrell is working on echo criteria.
  6. Cardiac CT may also be a helpful non-invasive tool.
  7. Contraindications to stenting (e.g. bleeding) could also suggest utility in a non-invasive approach.
  8. When addressing hemodynamics, always ask whether outflow tract obstruction is present or absent; this will be a critical decision-point.
  9. Without obstruction, treat patients as usual. Vasopressors should not be viewed as potentially worsening the condition, and early beta blockers probably have no role.
  10. Anticoagulate as soon as it’s safe, when there are large wall motion abnormalities; this is similar to WMA from other causes. Apical ballooning is probably somewhat riskier than other distributions due to the flow patterns.
  11. The natural history of TCM involves recovery in most within 2 weeks, although the course during that period can vary widely. Almost all recover within a couple months.
  12. Outpatient care focuses on ACE inhibition, diuresis if needed, anticoagulation when appropriate, with a gradually decreasing emphasis on beta blockers. Aspirin and statins are not usually needed if there is no concomitant ACS.
  13. Hormone replacement may have a role.
  14. RV involvement can occur atypically. It can help point to TCM, since this would be an unusual anatomic distribution for ACS.

Episode 58: Toxic alcohols with Jerry Snow

We look at evaluating the patient with encephalopathy and unexplained anion gap, including the workup and treatment of toxic alcohol poisoning, with guest Dr. Jerry Snow (@ToxicSnowEM), medical toxicologist and director of the toxicology fellowship at Banner University Medical Center in Phoenix.

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Takeaway lessons

  1. A toxicologic exposure should be suspected, even without a clear story, based on the prehospital scene. EMS or family reports of chemicals, pill bottles, etc should be elicited. Prescribed medications should be questioned, as well as any other meds that could be available to the patient, such as older meds, current and older meds prescribed to family members, and supplements.
  2. Physical exam maneuvers high-yield for tox diagnosis include the pupillary exam, skin exam (diaphoretic vs dry), and examination of muscle tone and deep tendon reflexes.
  3. Laboratory clues of tox diagnoses include an elevated anion gap in the absence of common causes (lactate, ketones, uremia), as most of the remaining causes of a gap are toxins.
  4. Elevated osmolal gaps should also be investigated, although considered an insensitive test for most toxins. A serum chemistry, as well as salicylate and acetaminophen levels, should be sent routinely. An ECG should be checked for findings like interval prolongation and morphology changes.
  5. “Normal” osmolality varies too much for a low osm gap to be useful, but a clearly elevated gap is diagnostically helpful, particularly when its presence/absence is compared with the presence/absence of an anion gap.
  6. The most common source of methanol ingestion in the US is windshield wiper fluid; it’s also present in poorly-distilled homemade moonshine, hand sanitizer, model car fuel, food-warmer fuel, lacquer and paint thinner, and many others. For ethylene glycol, the most common US source is automotive antifreeze. In both cases, these are usually intentional ingestions.
  7. Toxic alcohol levels, namely methanol and ethylene glycol levels, are send-out tests in most centers and result too slowly to be useful in the early stages. You will need to treat empirically based on suspicion and perhaps based on osmolar gap.
  8. Urine tox screens rarely change management, and may lead to missed diagnoses due to anchoring. Many substances are not tested, and positive tests (e.g. for opioids or benzodiazepines)—even for substances that may explain the clinical picture—can be false positives. Even true positives do not rule out the presence of another medical or even a second toxicologic cause. Correlate cautiously with the clinical picture (e.g. opioid toxicity may not explain encephalopathy in a patient with normal pupils and hyperventilation), or simply don’t send it to begin with.
  9. Acute iron overdose can cause anion gap acidosis, GI symptoms including bleeding, and shock and an overal critically ill presentation.
  10. Ethanol has fallen out of favor for treatment of toxic alcohols, although it does work; it is logistically challenging, requiring frequent lab checks to ensure therapeutic levels, central venous access, and other fuss; complications are much higher than with fomepizole. It’s good for low-resource settings that may not have the more expensive fomepizole, however, and co-ingestion of ethanol with toxic alcohols provides some fortuitous initial protection until the ethanol level falls.
  11. Ethylene glycol and methanol are not themselves toxic, but as the parent alcohols are metabolized, they turn into toxic acids. The goal of fomepizole or ethanol is therefore to block this conversion (by alcohol dehydrogenase). This also means that if checked early after ingestion, osmolar gap will be high, but anion gap is low, as only the parent compounds are active osmoles. As metabolism continues, osmolar gap falls, but the anion gap increases. One upside of treatment with hemodialysis is that it clears both the parent alcohol and the toxic metabolites, so it’s helpful even in late presentations.
  12. Toxic alcohols may confuse testing for lactate. Some methods, mainly used on blood gas analyzers that report lactate, can be fooled by glycolate—a metabolite of ethylene glycol—and report a falsely elevated lactate. The same sample tested in the lab using another method may show a lower lactate. This “lactate gap” can be diagnostically useful if understood.
  13. A normal fomepizole course is two days, dosed every twelve hours, but monitoring should be done of either methanol/ethylene glycol levels (if lab turnaround is fast), or monitoring the pH, anion gap, and osm gap for response. If not resolved, a longer treatment course may be needed, and dose may need to be increased, as it induces its own metabolism.
  14. Hemodialysis may be used in the sickest patients, as a rescue, if pH is severely deranged, or if there is severe kidney injury, since renal clearance is needed to clear ethylene glycol. Fomepizole should usually still be given to temporize until treatment is completed, and may need to be dosed more frequently during dialysis as it is a dialyzable compound. A single prolonged HD session (eg 8 hours) is often adequate, and HD is superior to CRRT.
  15. Thiamine and pyridoxine (vitamin B6) can be given to help shunt toxic alcohols to benign metabolites, although evidence for this is fairly poor. Other supportive care is as routine.
  16. If acute toxicity is survived, ethylene glycol patients usually do well, although they occasionally have calcium crystal deposition in nerves and develop cranial nerve palsies or peripheral neuropathy. Methanol patients tend to do worse, sometimes developing permanent blindness and CNS pathology like delayed intracranial hemorrhage or Parkinsonism.
  17. Every hospital in the US has a poison control center available to them as a resource, which includes an on-call medical toxicologist who can discuss cases if needed. They are available even to review med lists and assist with diagnostic mysteries. The most common error in tox cases is the failure to consider a tox diagnosis!

Episode 57: Hyponatremia with Paul Adams

We tackle the knotty dilemma of diagnosing and treating hyponatremia, with Dr. Paul Adams, a dual-trained nephrologist and intensivist at the University of Kentucky.

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Takeaway lessons

  1. Start by asking whether the hyponatremia needs to be corrected emergently, as well as its cause. Instability means correct it emergently, and instability usually manifests as seizure.
  2. While hyponatremia is often categorized by volume status, volume status is a tricky determination with ample gray area and room for overlap. It’s more useful to approach hyponatremia by asking whether ADH is active or not.
  3. If urine osm is >300, ADH is definitely present to some extent.
  4. The hypovolemic and/or low solute patient will be fixed with crystalloid, although they are at risk of overcorrection. Overcorrection almost always occurs due to autodiuresis, not from exogenously administered salt.
  5. A high urine sodium implies lack of sodium reabsorption by the kidneys, more consistent with diuresis (thiazides) or ATN (failure of absorptive mechanisms). Low urine sodium is a broader differential, e.g. most of the appropriate-ADH hyponatremias.
  6. While there is overlap between hypovolemia (often acute) and low solute intake (often more subacute/chronic), they are distinct syndromes. They can be differentiated by the urine osm: both urine sodiums will be low, but urine osm will be low only in the low solute patient (because they simply aren’t taking osms in). The hypovolemic is at greater risk of overcorrection as well.
  7. It’s often impossible to determine how acute hyponatremia is, so generally assume chronic and correct slowly.
  8. Overcorrection from acute hypovolemia will be mediated by dilute polyuria, so a good monitoring strategy may be to simply send serial urine osms, particularly if polyuria occurs. Have a low threshold to clamp them with DDAVP if it occurs.
  9. When risk for osmotic demyelination is highest (risks: longer duration of hyponatremia, low solute intakes like malnourishment and alcoholism, and lower sodium), consider prophylactically clamping with DDAVP.
  10. Use small boluses (100 ml) over about ten minutes to correct hyponatremia-induced seizures and repeat as needed until seizures stop. Trend labs but don’t stop until symptoms resolve, or you correct by 5 mEq. Most cases of true hyponatremia-induced seizure or severe encephalopathy will require around 500 ml total. Other concentrations could probably be used but are subject to logistical issues and are really just manipulating the amount of diluent volume.
  11. Theoretically, inducing hyponatremia in neurologic patients could create the same risk as rapidly correcting hyponatremia, but data is limited and from a bedside perspective, this doesn’t generally seem to cause demyelination.
  12. For SIADH, a loop diuretic can be useful, but the mainstay is fluid restriction. The right amount of restriction depends on free water clearance; a cirrhotic who only produces 500 ml of free water a day should theoretically be restricted below this intake (which is not easy).
  13. Vaptans have a limited role outside specific use-cases like bridging to transplant (although not for liver – they may cause hepatotoxicity).
  14. Confusing pictures (eg SIADH vs hypovolemia vs CSW) can be clarified by a sodium challenge – bolus a liter of normal saline and see what they do with the salt. Remember that if you give fluid with a lower osmolality than the urine osmolality – common in SIADH – you’ll actually dilute them and lower their sodium further.
  15. Hypervolemic hyponatremia, e.g. from cirrhosis or heart failure, is generally correctable only by managing the underlying disease.
  16. Truly chronic hyponatremia usually won’t cause acute symptoms like encephalopathy, but are associated with various more subtle medical complications like osteoporosis.
  17. Oral salt like salt tablets are generally not a huge help for SIADH; salt handling is separate and inadequate sodium is not the issue. You can force some salt into them by simultaneously fluid restriction (although this is horrible for their thirst), but once they leave a controlled setting and can compensate with unmonitored water intake they’ll return to their set point.
  18. Fludrocortisone takes a while to act (it’s a steroid) and probably has a limited role in hyponatremia. Remember it works on the kidneys and has no effect if urine is not made.

Resources

Episode 56: Resuscitation psychology with Dan Dworkis

Discussing the psychology of emergency response, team dynamics, and debriefing with Dan Dworkis, MD, PhD, FACEP. He’s the Chief Medical Officer at the Mission Critical Team Institute, a board-certified emergency physician, and an assistant professor of emergency medicine at the Keck School of Medicine of USC where he works at LAC+USC. He performed his emergency medicine residency with Harvard Medical School at the Harvard Affiliated Emergency Medicine Residency at Massachusetts General Hospital / Brigham Health, and holds an MD and PhD in molecular medicine from the Boston University School of Medicine. He is the founder of The Emergency Mind Project, and the author of The Emergency Mind: Wiring Your Brain for Performance Under Pressure

The Emergency Mind Project: www.emergencymind.com

The Emergency Mind Book: bit.ly/emindbook

The Emergency Mind Podcast: www.emergencymind.com/podcast

The Mission Critical Team Institute: www.missioncti.com

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Takeaway lessons

  1. Intact teams train together, while swarm teams are ad hoc and must perform without prior preparation. Many healthcare teams are somewhere in between, a “jello” team. How to effectively swarm and run such a team is one of the common challenges in a hospital-based emergency.
  2. Intentionally limit information input when needed. In the initial stages of resuscitation and stabilization, much of the medical history and other details may not be pertinent.
  3. Identify your role when you walk into the code and ask who’s in charge. If there’s no response, identify that it’s you. Ask if there are pads on, if there’s IV access, the last rhythm, and who’s doing compressions next. These are step zero in your management. If someone is already in charge, ask how you can help.
  4. Usually there’s no need to use names, which are tough to remember in the heat of the moment. Roles are adequate. In the long run you can seek to build those relationships further.
  5. Nurse leaders can be a great way to offload the provider leading a code and tackle logistics like delegating tasks to the best person to handle them.
  6. Cross-disciplinary simulation training builds relationships between staff, but also stress-tests procedures and even equipment setups.
  7. If you’re not in a leadership position, lead change like a flock of starlings. When you change direction and nudge the handful of people nearest to you, you’ll create a wave of change that can propagate outwards. What can you do on this shift to make you and your team 1% better? Ask yourself and others, what did you learn from this case? What surprised you, what did you learn? What can we improve next time? Small, subtle changes like this build over time.
  8. Seemingly complex decision pathways can often be simplified by considering what you can do and what it depends on. Bifurcations that don’t change what you do at this juncture can be eliminated.
  9. Don’t waste suffering.
  10. Initial steps in debriefing is to make sure the team is physically and psychologically okay, and ensure the team and equipment are prepared for the next patient.
  11. Next, take two minutes with anyone who can spare the time to discuss what we learned from the patient. What went well, what went better? The room is always smarter than you individually; solicit opinions from everyone.
  12. When numerous conflicting demands are present, optimize your performance by finding ways to streamline and protocolize decisions to reduce the number that need to be contemplated in the heat of the moment. Anything high yield, low risk, just make the decision ahead of time to do them without thought.

Episode 55: Undifferentiated encephalopathy and autoimmune encephalitis, with Casey Albin

How to evaluate the patient with unexplained encephalopathy, and a practical approach to diagnosing autoimmune encephalitis with an emphasis on anti-NMDA receptor encephalitis—with Dr. Casey Albin (@CaseyAlbin), neurologist and neurointensivist, assistant professor of Neurology and Neurosurgery at Emory, and part of the NeuroEmcrit team.

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Takeaway lessons

  1. Common causes of unexplained encephalopathy are:
    • Metabolic/systemic problems (myxedema, hypercarbia, uremia, vitamin deficiency, etc), which are common, but often found on routine labs.
    • Toxicologic exposures (drugs, heavy metals like Wilson’s, etc)
    • Primary neurologic events. These differentiate into acute and subacute processes.
  2. In the altered patient found down with normal CT head and grossly normal labs, consider seizure and tox causes.
  3. Give thiamine indiscriminately and widely to patients with altered mental status; it is harmless and Wernicke-Korsakoff may fool you.
  4. Start with the history and meds. Simple intoxications like baclofen overdose can cause incredibly dense coma.
  5. Inquire as to recent history of behavioral changes, neurologic phenomena, illness, etc. Prolonged or subacute symptoms significantly narrow the differential of a neurologic cause.
  6. Always consider basilar artery stroke in the obtunded patient with a non-focal exam! Get a CTA early to evaluate the posterior circulation, as they may be a candidate for thrombolysis or thrombectomy.
  7. With an unexplained diagnosis suspected to be neurologic in nature, have a low threshold for obtaining MRI (generally with gadolinium), lumbar puncture, and EEG. The urgency and order of these may depend on clinical suspicion, other tests, and availability. A spot EEG to rule out status epilepticus, followed by either LP or MRI (whichever is available first) is often a good sequence.
  8. Have a relatively high threshold to start anti-epileptics for “seizure risk” or for vaguely epileptiform activity on EEG in the absence of true seizure, particularly if continued EEG monitoring (either continuous or frequent spot studies) are readily available. These drugs tend to remain prescribed for a long time, are not often discontinued by downstream providers, and can lead to future polypharmacy and lifestyle impacts.
  9. To unpack autoimmune causes, build a syndrome by considering the timeline and the affected areas (e.g. portions of the brain or spine involved on imaging).
  10. Creutzfeldt-Jakob disease should be suspected from the clinical history, or classic MRI findings such as cortical ribboning and “hockey sticks” in the basal ganglia. Without some specific suspicion, testing is usually not indicated.
  11. A normal brain MRI can occur in some autoimmune encephalitides. For instance, anti-NMDAR encephalitis can have absolutely normal MRIs, which can be a helpful differentiator from limbic encephalitis (the latter tending to have characteristic MRI findings).
  12. The Mayo Clinic and ARUP laboratories have a broad autoimmune encephalitis panel that can be sent for undifferentiated encephalitis; it tests for multiple antibodies and is updated periodically in response to new research. It is not particularly cheap, but with the large number of overlapping syndromes, when autoimmune causes are suspected it is generally a better idea than targeted testing in all but the most classic clinical pictures.
  13. Draw plenty of CSF for all these labs, at least 30 cc if possible. You don’t want to have to go back just because you thought of another test.
  14. Normal CSF protein increases with age. A good rule of thumb for pathological elevation is CSF protein that is greater than the patient’s age.
  15. With a sick patient and legitimate suspicion for an autoimmune cause responsive to immunomodulation, treat empirically. Your options are steroids (e.g. five days, 1000mg daily of methylprednisolone, then possible maintenance dosing depending on the diagnosis), plasma exchange (PLEX, usually 5 treatments, one every other day), or IV immunoglobulin (IVIG). Often you’ll combine pulse-dose steroids with one of the latter. Either PLEX or IVIG are a reasonable option, although some syndromes seem to respond better to PLEX. Either way , you’ll need to commit to doing this before autoimmune tests results (which takes around ten days), and generally continue treatment until you have your results, since clinical response in many syndromes may take weeks.
  16. If test results are negative, consider repeating some studies (e.g. MRI the brain again), go over the history again, look for tests or diagnoses that weren’t considered, ask for help, and consult a reference or cheat sheet to look for what you missed.
  17. With any possibility of any paraneoplastic syndrome, particularly anti-NMDAR encephalitis, perform a serious search for neoplasm: CT chest/abdomen/pelvis, testicular ultrasound, either MRI pelvis or transvaginal ultrasound of the ovaries, and sometimes PET scan, although this can be tough to perform due to poor inpatient reimbursement.
  18. “Classic” NMDAR encephalitis is a younger woman with paranoia, progressing to catatonia and movement disorders, autonomic instability and storming, dyskinesias, hypersalivation, and in late stages, coma. With treatment they regress along the same pathway, and it generally does not recur, although full recovery is not guaranteed and may take many months; the intubated patient usually needs a trach and PEG, and can be difficult to manage due to their autonomic storming and vent dyssynchronies. Without treatment they often never recover.
  19. With NMDAR and a negative malignancy workup, repeat surveillance imaging is usually warranted to keep searching for tumor.
  20. Long-term immunosuppression is needed, so a steroid-sparing agent like rituximab is often used.

References

Dr. Albin’s handy pocket reference to work-up of encephalopathy and diagnosing autoimmune encephalitis.

Episode 54: The critically ill patient with pulmonary hypertension, with Ray Foley

We look at the patient with known pulmonary hypertension admitted for new issues like sepsis and pneumonia, and how they differ from our usual bread and butter, with help from Dr. Raymond Foley, director of the medical ICU and the pulmonary/critical care fellowship at UConn Health, as well as director of their pulmonary vascular disease program.

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Takeaway lessons

  1. Evaluate for the risk of decompensation in a patient with known PH and acute illness by considering their most recent echocardiogram, and repeating it as soon as possible after admission. Signs of baseline and/or new RV strain, such as reduced TAPSE, septal bowing, etc, as well as pericardial effusion, suggest a poor reserve for the stresses of their new ICU course. Right heart cath or echo PA pressures are less relevant than their cardiac function; pulmonary pressures fluctuate and are much less relevant to the clinical picture.
  2. Common causes of decompensation of PH include sepsis, medication issues (such as interruption of continuous PH meds), and polypharmacy (such as introducing an alpha agonist to treat a URI).
  3. When admitting the acutely ill patient with known PH, strongly consider early transfer to a PH center, preferably the one that already knows the patient.
  4. Typically, continue to administer outpatient PH meds, unless forced to hold or convert them to another agent due to lack of enteral access, absorption issues, or other factors.
  5. Avoid intubation if at all possible, as this can easily provoke cardiovascular collapse. Avoid hypoxemia and hypercarbia as well, which can both lead to worsening pulmonary arterial pressures. Maintaining both of these goals may require a thoughtful decision on when a patient should transition from modalities like high-flow nasal cannula to intubation. Non-invasive positive pressure like CPAP/BiPAP may be a reasonable middle ground, but could still provoke some instability due to the positive pressure.
  6. Consider targeting a higher MAP than in other patients to maintain perfusion of the RV. A reasonable MAP goal is 65 plus the CVP.
  7. Norepinephrine is a reasonable first-line vasopressor, but vasopressin might be even smarter, as it has no effect of increasing on the PVR and at low doses may even reduce it (activating V1/V2 receptors in the pulmonary circulation). Epinephrine at lower doses is a good second line, providing inotropic support for the RV without much impact on PVR.
  8. Place an arterial line early. Consider a central one such as in the femoral artery if they’re sick. Place a central line; trending CVP can be helpful. If they’re really hemodynamically unstable, consider floating a PA catheter. Non-invasive cardiac output monitors are of questionable utility.
  9. If intubating, induce them thoughtfully, avoiding agents like propofol. Ketamine or etomidate may be wise. Consider pushing the BP higher to avoid episodes of hypotension.
  10. On the ventilator, be liberal with oxygen and don’t be in a rush to wean it. While hyperoxia is not needed, avoid hypoxia, even transiently. Oxygen is a potent pulmonary vasodilator, and is much better for these patients than giving them a higher PEEP.
  11. If shock and RV failure are progressing, consider a pulmonary vasodilator, such as inhaled nitric oxide (INO) or inhaled epoprostenol. These have similar effects, although INO is more expensive. Drugs like epo can also be given intravenously, but this has the downside of dilating the entire pulmonary circulation, which can worsen VQ matching; nebulizing it improves perfusion to ventilated alveoli while ignoring shunted lung units. A positive response is improved oxygenation, reduced PA and RA pressures, and improved cardiac output.
  12. Most patients in RV failure don’t need additional preload, and indeed may benefit from cautious diuresis. A CVP of around 8-12 is usually a good goal.
  13. Dobutamine and milrinone are all reasonable options for inotropes, depending on your comfort.
  14. Decompensated PH due to CTEPH can potentially be treated, even in the setting of critical illness, via surgical intervention (e.g. pulmonary endartarectomy).
  15. Consider mechanical support early, with the best choice probably being VA ECMO.
  16. Weaning of support, such as inhaled vasodilators, can be achieved by transitioning to other agents like IV or enteral vasodilators (e.g. sildenafil).

References

  1. IBCC on RV failure

Episode 53: Documentation and coding with Robert Oubre

An exploration of clinical documentation and billing/coding with Dr. Robert Oubre (@Dr_Oubre), full-time hospitalist and CDI Medical Director for a community hospital in southern Louisiana.

Takeaway lessons

  1. Acute respiratory failure is justified when there is altered gas exchange (SpO2 <90%, PaO2 <60, CO2 >60 with pH <7.35, or P/F <300), clinical signs of increased work of breathing (using accessory muscles, etc), and a patient requiring respiratory support more than 4L O2 by nasal cannula. Requiring additional monitoring is also contributory.
  2. Many diagnostic names for pneumonia, such as nosocomial pneumonia or HCAP, end up coding to the same thing. Higher reimbursement comes from billing for “Gram negative pneumonia,” which requires risk factors including being hospitalized and received IV antibiotics in the last 90 days, immunosuppressed (including diabetes, alcoholism, CHF, cirrhosis, chemotherapy, CKD, drug-induced neutropenia, chronic malnutrition), or have structural lung disease such as bronchiectasis. It also requires treating with an antibiotic that covers gram negatives, and treatment for 5 or more days. If you have all of this, you may be able to bill for “gram negative pneumonia.” Treatment can be presumptive and you may state this; actual culture data is not required for this, although it is supportive if available.
  3. Diagnoses that are suspected but never fully proven can still be billed, particularly if they end up on a discharge summary.
  4. When in doubt, more detail is always better in diagnostic labels.
  5. Spell out your findings and reasoning and you’ll get more grace on your diagnoses.
  6. Sepsis diagnoses are a mess. Reimbursers tend to like sepsis 3 definitions (qSOFA), core metrics may still use the older definitions. Many facilities may have their own policies on what definition to adopt. From a clinician’s perspective, at this point, you should probably just call it sepsis when you think it’s sepsis and let the billing will work itself out.
  7. Document every diagnosis that contributes in any way to their current stay, even if your active management is minimal – it generally contributes to their risks and complexity.
  8. In 2023, the whole billing paradigm is expected to change, with less emphasis on billing based on number of categories in the HPI, ROS, PE, etc, and complexity being instead based mainly on time and acuity.
  9. Various providers can document diagnoses and all will count, but if there is dispute it will usually fall to the attending of record to make a final call.
  10. The “case mix index” is an amalgamate of the overall complexity of your patient population, which is reviewed regularly and modifies overall reimbursement; this help capture complexities and costs of care beyond what’s shown by the specific DRGs. This is based on other diagnoses and factors; hence, document everything.
  11. At the end of the day, you may not like the requirements for documentation and how it’s linked to reimbursement, but it is the way it is, and doing a poor job doesn’t mean the system will change – it just means your employer will be under-reimbursed, which in the end does affect you and your patients.

References

Episode 52: Pleural effusions in the ICU with Emily Fridenmaker

Discussing pleural effusions in the critically ill, including how and when to drain them, methods of drainage, interpreting laboratory studies, and managing complications, with Dr. Emily Fridenmaker (@emily_fri), pulmonologist and intensivist at Charleston Area Medical Center in West Virginia.

Continuing education for this episode

CME credit provided courtesy of Academic CME. To claim your CME credit for this episode, click here to complete a short quiz.

Takeaway lessons

  1. IMAGING
    1. CXR – underestimate
      1. Lateral – 75mL (5-15 mL is normal)
      2. AP – 175mL
        iii. 500mL for 100% sensitivity
    2. CT – overestimate
      1. Contrast can help delineate pleural surface
    3. Ultrasound – goldilocks
      1. Can see 5-50mL fluid
      2. > 1cm generally safe to sample
  2. INITIAL WORKUP
    1. Thora – no absolute contraindications
      1. Should tap an effusion if you don’t know what’s causing it
        1. Diagnostic or therapeutic
        2. Does little to change hypoxia—can impact dyspnea though due to diaphragm length-tension relationships
        3. Complication rate = ??
      2. Differential
        1. Nucleated cells – greater than 50k usually paraPNA/empyema
        2. Lymphocytosis – TB, lymphoma, sarcoid, RA, yellow nail syndrome, chylothorax, cancer
        3. Eosinophilia – >10%; pneumo, hemo, infarction, asbestos, parasites, fungus, drugs, catamenial, malignancy, TB, CEP
        4. Mesothelial – normal in pleural fluid
      3. Light’s Criteria—protein and LDH (serum and pleural), albumin, cholesterol
        1. Aim was to have a high sensitivity, since shouldn’t miss an exudate
        2. The criteria—any one of them gives you an exudate
        3. Pleural protein/serum protein > 0.5—can be elevated by diuresis
        4. Serum albumin/pleural > 1.2
        5. Pleural LDH/serum LDH > 0.6
        6. Pleural fluid LDH > 2/3 ULN
        7. Cholesterol >45 can also help to indicate an exudate
        8. Glucose
          1. Low: complicated effusion/empyema, malignant, TB, lupus, rheumatoid pleurisy, esophageal rupture
        9. pH – normal is 7.6 due to bicarb gradient
          1. <7.3 – same conditions as low glucose ii. If low, higher yield on cytology for malignancy, less response to chemical pleurodesis
          2. Parapneumonic <7.15 – needs pleural space drainage
          3. Lidocaine will falsely drop the pH
        10. Amylase – pancreatic or esophageal etiologies
        11. ADA – TB; usually >40
        12. Cytology – malignant; sensitivity is 60%, 85% with second sample
  3. TRANSUDATIVE VS EXUDATIVE
    1. Transudative
      1. Atelectasis, CHF, hepatic hydrothorax, low albumin, iatrogenic, nephrotic syndrome, PD, urinothorax
    2. Exudative
      1. Infectious, drug induced, trauma, malignancy (stage 4), CTD (RA, lupus, EGPA, GPA), hypothyroid/ovarian hyperstimulation syndrome, chylothorax, pancreatitis, sarcoid, post cardiac injury syndrome, radiation, PE, BAPE
  4. PARAPNEUMONIC CLASSIFICATIONS
    1. Simple – resolve with abx (1-2 weeks), don’t require drainage or special abx considerations
      1. Free flowing, sterile
      2. Exudative – neutrophilic predominance, normal pH and glucose level
    2. Complicated – evidence of infection of the space
      1. Exudative, high white count, pH <7.2, glucose <40 (or 60?), LDH >1000, + gram stain
      2. Large, loculated, thickened pleura, air bubbles in effusion
    3. Empyema (subset of complicated)
      1. Pus in the pleural space
      2. Longer clinical course, possibly subacute
        D. Complex
        i. Internal loculations
  5. MANAGEMENT OF COMPLICATED PARAPNEUMONIC EFFUSIONS
    1. Drainage usually required for source control—poorer prognosis without it
      1. Particularly if pH <7.15, low glucose, or LDH>1000
    2. Empyema
      1. Loculated
      2. + gram stain or culture
      3. Thickened parietal pleura
    3. Approach to drainage: Tube thoracostomy
      1. Small bore (10-14) similar efficacy to large
      2. MIST 1 – no difference in mortality or need for VATS between large, medium, or small bore tubes
        1. Retrospective—small bore noninferior
        2. Flush q6 to keep patent
      3. Suction is typical but not necessary
      4. Reimage after placement, when drainage slows
      5. Remove when less than 50-100mL for a couple of days, imaging is improved, clinically improving
      6. Reimage in about 2 weeks
    4. Failure of drainage – Repeat imaging 24hrs after completion of chosen intervention
      1. Lytics, multiple tubes preferred before VATS
        1. Probably best for early, multiloculated effusions
        2. DNAse breaks down DNA, reducing viscosity. tPA is fibrinolytics, busts up loculations
        3. MIST 2 – less need for VATS (30-80%) with tpa (10)/dornase (5) BID x 3 days
        4. New data shows simultaneous admin may be as efficacious
      2. VATS if significant organization, trapped lung (can be elective)
        1. No mortality benefit shown
        2. Pleural hemorrhage – 1-7%, indication for VATS
        3. Indicated when abx, tube, lytics have failed
        4. Also indicated up front if there is significant organization, fibrothorax, trap
        5. May need to be converted to open thoracotomy
        6. Maybe reduced LOS? MIST 3 looking at early VATS vs early lytics
      3. Window thoracostomy/eloesser flap
  6. ANTIMICROBIAL THERAPY
    1. i. CAP – Rocephin + flagyl or unasyn
    2. Lots of clinda resistance now
    3. Atypicals rarely cause complicated effusions
    4. MDRO risk factors – MRSA, pseudomonas, and anaerobes
    5. Optimal duration unknown
      1. usually 2-3 weeks for complicated
      2. 4-6 weeks for empyema
      3. Can switch to PO when clinically improving
      4. Radiographic resolution can take weeks to months; this is not the goal
  7. COMPLICATIONS OF PLEURAL SPACE INFECTIONS
    1. Fibrothorax, pleural fibrosis
    2. Restriction, unexpandable lung
    3. Decortication not considered unless restriction/limitation present 6 months later