Lightning rounds – Critical Care Scenarios

Lightning rounds 61: Credentialing and privileging, with Christopher Newman

We dive into the confusing rabbit hole of medical staffing, credentialing, and privileging, particularly for the critical care APP, with Chris Newman, pediatric critical care PA and Vice Chair for Clinical Performance at the University of Colorado.

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Takeaway pearls

The medical staff office regulates the medical staff, which includes physicians and APPs. The latter may actually be voiting “members” of the medical stuff, or have some kind of affiliate status; the relevance of this is their eligibility to vote and sit on its committees, which sets the policies and manages governance. Either way though, APPs are subject to the medical staff office’s regulation.
Credentialing is the process of ensuring medical staff have the right and competence to work in the hospital, mostly confirming basic job requirements like graduating training programs. Privileging is the process of determining what specific things you are allowed to do in the hospital.
Privileges are broken into core privileges, which are things any provider should know how to do (i.e. taught in school): perform H&Ps, order meds and tests, interpret them, etc. Special privileges are those that require additional training, usually procedures. Some of the latter may become core privileges over time.
Special privileges are needed for anything “infrequent and high risk,” which requires some judgment – i.e. if a procedure is not listed, does that mean you cannot do it, or that it does not even require special privileges? Which procedures are listed is determined by the judgment of the clinicians in medical staffing, and the list is not always perfect.
All of these processes are hospital based, usually not part of state law, and are also often subject to Joint Commission regulation. However your hospital handles them, it is expected to follow its own policies consistently.
Learners are managed under policies for proctoring, not privileges. A person with procedural privileges can generally supervise a learner without privileges to perform it; if that’s a student, it is considered to be “done” by the proctor, and if by a licensed provider without privileges, it is “done” by the learner under supervision. Such a learner may eventually obtain their own privileges (usually by meeting a requirement of either numbers or observed competence or both). The exact rules of how all this works is governed by a proctoring policy which can be looked up.
While many providers may feel it is accepted, or even an ethical obligation, to perform procedures they are trained but not privileged to perform in an emergency (i.e. to save a life when a privileged person is not immediately available), there is usually no explicit allowance for this in hospital policy, so buyer beware.
If you don’t like how your processes work, change them.

Lightning rounds 60: The nuances of insulin, with Melissa Nestor

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We chat with Melissa Nestor, clinical pharmacist in neurocritical care, about tho subtleties of glucose and insulin management in the ICU.

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Lightning rounds 59: The nuances of nebulizers, with Keith Lamb

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We explore the practical intricacies of nebulized medications, including timing, dosing, types of devices, and more, with Keith Lamb (@kdlamb1), RRT, RRT-ACCS, FAARC, FCCM.

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Lightning rounds 58: Steroids for septic shock with David Janz

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We dive into the common dilemma of when to give stress-dose corticosteroids in septic shock, with Dr. David Janz, pulm/crit intensivist with a Masters of Science in Clinical Investigation, former director of the Clinical Research Unit for the critical care section at LSU, founding member of the Pragmatic Critical Care Research Group, and associate Chief Medical Officer for LCMC.

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Takeaway lessons

The purported effect of corticosteroids in septic shock is to increase sensitivity of peripheral catecholamine receptors, either to endogenous or exogenous adrenergic hormones.
In the four large RCTs of this topic, two showed a beneficial outcome effect and two did not. The two positive trials also added fludrocortisone to the backbone steroid (usually hydrocortisone), though it seems dubious that this was the key difference (fludro has also been studied separately without effect). Those trials also generally enrolled sicker patients, i.e. on higher doses of pressor and more organ failure.
It is probably reasonable to add steroids when on escalating doses of your first-line pressor (e.g. norepinephrine), or when thinking of adding vasopressin, though the SCCM/Surviving Sepsis guidelines now suggest just giving steroids to everyone in septic shock, presumably to simplify decision-making, particularly for non-experts.
Most trials have used hydrocortisone 50 mg q6h or thereabouts, or an equivalent dose as a continuous infusion. The latter makes some physiologic sense but has not been shown to be beneficial head-to-head trials. Most likely, the exact dosing strategy is not too important. Alternate steroids are probably also reasonable, i.e. any moderate-dose parenteral corticosteroid probably gets you the desired effect.
Many trials continued steroids until the patient left the ICU, even if pressors have been weaned off. Most clinicians would probably stop them sooner than this, although we should acknowledge that their effect in raising blood pressure is reliable (sometimes helping to discontinue pressors as much as several days sooner), so continuing them longer could conceivably help with disposition (i.e. help them leave and stay out of the ICU), which is a good thing for hospitals and probably patients.
Dr. Janz stops steroids when the pressors are stopped, with no taper or wean. Some would do a short taper, but the more complex you make the process in a busy ICU, the more likely that someone will forget to discontinue them altogether, and that the patient will stay on steroids for their whole hospitalization (or forever). There is no physiologic suppression of the native steroid production with these durations of steroid therapy (usually 3-4 days, almost always <1 week), and an abrupt halt is what was done in the trials.
Etomidate has been repeatedly shown to cause a measurable decrease in cortisol levels, even after single doses (e.g. for intubation). However, this has not been shown to be associated with any negative outcome (most recently in the EVK trial).
There is very little data on whether steroids should be used in shock from other etiologies. It may make some sense in other inflammatory states, such as pancreatitis, post-CPB vasoplegia, etc. But we really don’t know. In a mixed shock state where sepsis is present along with something else like cardiogenic shock, Dr. Janz uses steroids; otherwise no.
Whether to always augment the home steroid dose in chronic steroid users, even without shock, has shifted—in the past, endocrinology guidelines were to always do this empirically (e.g. in steroid users undergoing surgery or some other stressor), now they still generally favor this but are moving towards increasing the home dose only if signs of adrenal crisis develop.

Lightning rounds 57: Burn critical care with Clint Leonard

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We explore the fascinating intricacies and unique features of the burned critically ill patient, with Clint Leonard, NP in the burn ICU at Vanderbilt and ABLS instructor.

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Want to work at the University of Kentucky? UK’s Anesthesia Critical Care department is hosting a hiring webinar on November 20, 2025 at 4:00PM EST.

Lightning rounds 56: The CHEST Critical Care APP cert, with Leeah Sloan

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We chat with Leeah Sloan, PA-C, co-chair of the Critical Care APP Steering Committee for the American College of CHEST Physicians (CHEST), about the newly available CHEST critical care certification for APPs.

The Vandalia CAMC Charleston APP critical care fellowship

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Lightning rounds 55: APP fellowships with Melissa Bridges

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Melissa Bridges, director of PA fellowships at Atrium Health and president of the Association of Post-graduate PA Programs (APPAP), chats with us (Bryan is president of APGAP, the Association of Post Graduate APRN programs) about PA/NP residencies/fellowships in critical care.

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Lightning rounds 54: Medical musicians with Andrew Schulman

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Andrew Schulman, medical musician, former ICU patient, and president of the Medical Musician Initiative, tells us how music can help the critically ill.

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Lightning rounds 53: GI Q&A with Elliot Tapper

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From constipation to hepatorenal syndrome. Fan favorite Elliot Tapper (@ebtapper, @ebtapper), gastroenterologist, transplant hepatologist, academic chief of hepatology, and director of the cirrhosis program at the University of Michigan, returns to answer a grab-bag of GI questions.

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Takeaway lessons

Constipation may be an “afterload” problem (outlet obstruction, usually identified by a stool ball), best treated by manual disimpaction or a lubricating suppository or enema; a “preload” problem (osmotic diuretics; often polyethylene glycol a good place to start); or a contractility problem (motility agents like senna or bisacodyl; these work where they touch, so give orally for proximal impaction, rectally for distal issues).
Ondansetron is a good first line anti-emetic. Olanzapine has good evidence for chemo-based nausea, prochlorperazine is also good. QTc should always be considered with these prolonging meds but torsades is really a rare effect from anti-emetics. Sniffing an isopropyl alcohol swab can also be effective in the short term, and has been equivalent to IV ondansetron (superior to oral) in studies.
Ultrasound is the most important tool to ensure a safe location for paracentesis, but the right lower quadrant is usually a good place to start (no spleen here).
A very acute CBD obstruction may lead to fulminant cholangitis, but maybe not much ductal dilation, because it hasn’t had time to dilate. (One out of five cases of ALT >1000 may be from hyperacute CBD obstruction.) Dilation should not be considered essential to diagnose cholangitis; empiric ERCP can be appropriate. (In the non-shocked patient, EUS to confirm obstruction before doing sphincterotomy may be useful intraprocedurally.)
In less obvious cases, MRCP can be useful, especially in a more stable patient, or when the diagnosis (or benefit of drainage) is less clear.
When stenting or drainage of the CBD directly is not possible, sometimes it can be accessed retrograde from the gallbladder – or sometimes draining the gallbladder may indirectly decompress the CBD. Most of the time this is not the first line approach.
Actually just doing a cholecystectomy first line may be the right option more often than not, if you can find an accepting surgeon.
Percutaneous chole tubes can sometimes cause downstream problems, particularly when patients
Cirrhotics get AKI for reasons other than hepatorenal syndrome… a lot. ATN is at least four times as common as HRS. Check the urine for casts, etc, but ultimately you can never be sure of the diagnosis up front, so time and response to treatment are always key diagnostic tools.
Blindly fluid challenging HRS up front is usually needed. But if you truly believe they’re euvolemic or even fluid overloaded, it’s appropriate to treat those is usual. Otherwise, challenge with fluid (albumin is not a magical choice, use anything).
Octreotide is not the treatment of choice for HRS in the ICU; use norepinephrine and titrate up until you see an increase in urine output (or it doesn’t work). Terlipressin works too but is pricey and more appropriate for outside the ICU.
Pumping lactulose into an ileus, or any gas- and volume-promoting agent, tends to worsen bloating without much help. You don’t want constipation to exacerbate the problem, but stimulating agents make the most sense, such as chewing gum, maybe senna/bisacodyl, etc. But it’s mostly wishful thinking. Methylnaltrexone makes some sense for those on opioids. Decompressing the colon via colonoscopy is a risk for perforation due to insufflation; decompressing from above (NG tube) makes more sense.
The best clearance of the stomach (for visualization during EGD) is from 250 mg IV given within <1 hr. But this can take time to obtain from the pharmacy, so metoclopramide is often used instead. Oral erythromycin does have data that it improves gastric emptying, but causes tachyphylaxis with prolonged use. Overall, oral and IV versions of these drugs are probably the same efficacy.
Nearly all diarrhea in the ICU is related to illness and critical care. Other than C diff and specific exposures, stop sending stool PCRs.
Loperamide or diphenoxylate/atropine (Lomotil) are almost always appropriate for diarrhea, and the most common error is underdosing; giving a dose or two every 1-2 hours may be needed (may be 8-16 pills in a day) until you get a response is wise. Even infectious diarrhea can usually be treated, with the goal of limiting output, not stopping it completely.
After 2-3 days of hepatic encephalopathy, with stool pouring out, continued altered mental status is probably not due to a deficiency of stooling.
Catharsis is the second thing to do in an encephalopathic cirrhotic patient; the first is to diagnose the cause, which is often a life threat such as infection. Paracentesis is part of the physical exam!

Lightning rounds 52: Echo tips with Michael Lanspa

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We chat with Dr. Michael Lanspa, intensivist and director of the Intermountain Critical Care Echocardiography Core Lab, about common pitfalls among bedside POCUS users and tricks for doing it better.

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Takeaway lessons

It’s a fallacy to think that any quantitative method of EF evaluation is truly objective; cardiologists eyeball the EF and adjust their calculation if it seems wrong.
EF is always loading sensitive, and will not reflect stroke volume accurately if the chamber is small or large. The eyeball/gestalt method is usually harder with non-symmetric contraction (i.e. RWMA).
LVOT VTI is often compromised by an off-axis angle of insonation (within 15 degrees will introduce negligible inaccuracy), and a poor signal (the VTI should ideally be hollowed out).
In general, tracking the VTI alone using a similar technique will yield more consistent results than attempting a full cardiac output calculation.
TAPSE fails when the free wall contracts more or less than the longitudinal contraction. This is common in PAH, where the free wall may be more impacted than the longitudinal function. The converse may occur in the LV in hypovolemia, where radial contraction may appear hyperdynamic but longitudinal shortening remains diminished.
s’ tends to “see” better with a poor view than TAPSE, as tissue doppler is more sensitive than M-mode.
With more severe TR, the doppler gradient tends to underestimate the RVSP, as the pressure equilibrates faster during systole.
A sniff test during IVC ultrasound is part of the standard echo method of estimating CVP. It is not well-proven to approximate volume responsiveness.
Remember that when dynamic LVOT obstruction occurs, LVOT VTI may be extremely high, but the stroke volume is not elevated — it’s balanced out by the reduction in effective orifice size (i.e. the LVOT diameter is not the diameter of the jet, which has been narrowed).
In general, eyeball assessment of regurgitation using color doppler and B-mode is probably all that’s needed for POCUS; attempting additional quantification is rarely high-yield.
Assessing aortic stenosis is generally an unreasonable ask for bedside POCUS users. The easiest tool is probably to get the best possible 2d view of the valve and eyeball its opening; a reasonable visualized valve excursion is probably not consistent with severe stenosis. Beyond that, obtain a full study.