Critical Care Scenarios

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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

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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.

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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.