Critical Care Scenarios

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Claim your CME credit here!

Find us on Patreon here!

Buy your merch here!

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.

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Click here to claim your CME credit!

Find us on Patreon here!

Buy your merch here!

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

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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