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

  1. 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).
  2. 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.
  3. 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).
  4. 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.)
  5. 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.
  6. 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.
  7. Actually just doing a cholecystectomy first line may be the right option more often than not, if you can find an accepting surgeon.
  8. Percutaneous chole tubes can sometimes cause downstream problems, particularly when patients
  9. 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.
  10. 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).
  11. 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.
  12. 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.
  13. 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.
  14. Nearly all diarrhea in the ICU is related to illness and critical care. Other than C diff and specific exposures, stop sending stool PCRs.
  15. 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.
  16. After 2-3 days of hepatic encephalopathy, with stool pouring out, continued altered mental status is probably not due to a deficiency of stooling.
  17. 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

  1. 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.
  2. 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).
  3. 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).
  4. In general, tracking the VTI alone using a similar technique will yield more consistent results than attempting a full cardiac output calculation.
  5. 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.
  6. s’ tends to “see” better with a poor view than TAPSE, as tissue doppler is more sensitive than M-mode.
  7. With more severe TR, the doppler gradient tends to underestimate the RVSP, as the pressure equilibrates faster during systole.
  8. 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.
  9. 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).
  10. 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.
  11. 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.

Episode 89: Thrombectomy for stroke, with Justin Fraser

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We explore the world of thrombectomy for acute ischemic stroke with Justin F. Fraser (@doctorjfred), MD, FAANS, FAHA, Professor and Vice-Chair of Neurological Surgery and Director of Cerebrovascular Surgery and Neuro-interventional Radiology at University of Kentucky, where he specializes in cerebrovascular, endovascular, skull base, and endoscopic transsphenoidal surgery.

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Takeaway lessons

  1. In the opinion of Dr. Fraser, thrombectomy for qualifying patients with acute ischemic stroke is the current standard of care. Patients in non-thrombectomy centers should be transferred. Failure to do so is potentially negligent.
  2. Dr. Fraser feels there are few true contraindications to thrombectomy (as long as the patient’s goals are concordant), and the current indications should probably be most strokes <24 hours with a large vessel occlusion on CTA – i.e. ICA (including with a tandem extracranial carotid occlusion), MCA, ACA, or basilar. He no longer feels most cases need perfusion imaging as even large or older infarcts seem to benefit.
  3. The main current question is the utility of thrombectomy in “medium vessel occlusions,” such as M2 and more distal vessels.
  4. Radial artery access is growing in popularity, similar to its growth in cardiovascular interventions, now that devices have shrunk enough to fit. The right wrist is preferred.
  5. In general, qualifying patients should still receive systemic thrombolytics as soon as possible prior to performing thrombectomy, at least with the state of the evidence in 2025. This also helps manage any particles that embolize into more distal vessels during aspiration of a larger thrombus.
  6. Generally, thrombectomy is merely a process of aspirating an embolus. However, if thrombosis also involved an intracranial atherosclerotic narrowing, there may still be unstable stenosis afterwards, so about a third of cases also require stent placement. (Carotid occlusions are a different story and usually need stenting, just as with elective endarterectomies.) When stents are placed for this reason or for a carotid lesion, dual antiplatelet inhibition is usually needed; this may be started during the procedure with an intra-arterial agent if DAPT is not already on board.
  7. Thrombectomy can be performed under local anesthesia only, or under deeper sedation; the practice for Dr. Fraser’s group is to put everybody under general anesthesia. Anesthesia’s efforts are performed simultaneously to the interventional prep and should not delay it.
  8. Post-procedure blood pressure targets are controversial. Fraser targets SBP <160 for 24 hours to limit reperfusion hemorrhage.
  9. Post-procedure MRI is usually appropriate to delineate infarct size and to appreciate the degree of edema, potentially requiring decompressive craniectomy (large hemispheric or cerebellar stroke). If MRI is delayed, CT is appropriate, perhaps dual-energy CT to differentiate hemorrhage from contrast staining.
  10. Expanding thrombectomy to more patients in smaller hospitals requires more trained neurointerventionalists, but this is not a completely simple matter, as it must be balanced against adequate volume to maintain proficiency for the proceduralists and their teams. Smaller centers also need a link to a larger center that can support them for scheduling gaps and complications.

Resources

Society of Neurointerventional Surgery

Get Ahead of Stroke

Episode 87: Maternal-fetal monitoring with Stephanie Martin

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We learn about the basics of fetal monitoring in the critically ill pregnant woman and how to integrate them into our ICU workflows, with Stephanie Martin, MFM obstetrician and host of the Critical Care Obstetrics podcast and teacher at the Critical Care Obstretrics Academy.

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Takeaway lessons

  1. A fetus is considered potentially viable at 23-24 weeks gestational age, with 22-23 weeks being occasionally viable in specific circumstances and highly specialized centers. “Potentially viable” does not mean guaranteed survival, as fetal mortality is still quite high. In other words, at 23 weeks and above, intervention to promote fetal survival make sense. Every additional day of gestation improves outcomes.
  2. A conversation should occur preemptively between the mother, ICU, and obstetric teams to clarify what options will be considered—in some circumstances, early delivery (via C-section) is not desired due to the risk to the mother, and should not be assumed to be the contingency in all viable pregnancies. On the flip side, delivery of a non-viable fetus could still be appropriate for the mother’s health, such as in uterine infection or hemorrhage.
  3. If a fetus will not be delivered early, there may be no role for fetal monitoring.
  4. Fetal monitoring is therefore relevant at viable gestational ages. However, it is also more difficult for early pregnancies; the monitors can easily wander off a tiny fetus, and the strips are harder to interpret.
  5. Fetal monitors essentially monitor 1. Fetal heartrate (via Doppler), and 2. Uterine contraction. Heartrate is monitored primarily to determine variability, i.e. how much the rate changes from its average baseline in response to stimulus, particularly uterine contraction (which causes fetal stress of sorts). Poor variability with markers like late decelerations can be a sign of fetal acidosis and ischemia, particularly to the brain, which can increase the risk of fetal demise or birth defects such as cerebral palsy. Prematurity creates particular vulnerability to this.
  6. Maternal sedation leads to fetal sedation, which can make interpreting the heart rate more difficult.
  7. Uterine contractions rarely turn into labor, but they provide a natural stress test to the fetus.
  8. Much of the interpretation of “fetal distress” comes down to the context—for instance, maternal acidemia will always cause fetal acidemia, but in a rapidly reversible setting such as DKA, the best solution may simply be resuscitating the mother.
  9. Fetal distress is often an early marker of shock and other systemic stress, as uterine perfusion is sacrificed fairly early by the body in favor of other organs. This often manifests as uterine contractions.
  10. Any pregnant woman with a gravid uterus up to the umbilicus, or >20 weeks, who is critically ill, should not lie supine; the uterus will compress the great vessels and may cause shock. Elevate the head of the bed or tilt them laterally at all times. (During CPR, assign someone to manually displace the uterus to the left, as tilting the entire patient is challenging.)
  11. There is relatively little role for ultrasound or other tools for fetal monitoring; the gold standard is fetal heart rate monitoring.
  12. Paroxysms of vital sign changes (tachycardia, hypertension, etc) in a pregnant woman could be a subtle marker of contractions.
  13. With regards to ionizing radiation, generally, do whatever test you would do in a non-pregnant woman. Birth defects are generally established by the end of the first trimester, so in a viable pregnancy, it should not be a concern at all. While appropriate attention should be paid to avoiding needless radiation, if an important diagnosis needs to be made, do the x-ray or CT scan (or even fluoroscopy, likely the highest risk).
  14. In the post-partum patient, the longer it’s been since birth, the less likely a maternal illness is pregnancy-related. In the first week, assume it’s pregnancy related. In the first six weeks, consider it, especially hypertension complications. Cardiac problems (e.g. peripartum cardiomyopathy) can occur even later, especially as the diagnosis may be delayed. A common presentation is post-partum “asthma,” actually pulmonary edema, as the fluid bolus of delivery overloads a cardiomyopathic heart. The most hypercoagulable period in pregnancy is actually the first six weeks post-partum, so VTE is an important concern.