Critical Care Scenarios

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A few rapid-fire cases from the emergency department, with Dr. Seth Trueger (@mdaware), emergency physician at Northwestern University and digital media editor for JAMA Network Open.

[Sorry for the shotty audio quality in this one!–eds.]

Takeaway lessons

1. Many decisions in the ED are less about what to do, and more about when to do it. Time and location are key considerations for efficient care.
2. Goals of care starts in the ED, and not with lip service. Yes, temporize with supportive care while you go through the process, but do the work—find a legitimate representative or documentation of the patient’s wishes to determine what they’d want before you commit them to lengthy, aggressive life support. Aggressive but non-invasive medical care may also strike a good balance, keep everyone happy, and often avoid the need for invasive measures.
3. Over 1/3 of patients 65+ in the ED (excluding trauma and cardiac arrest) will die during that admission within 3 days.
4. The best ED provider intubates the “right” number of patients, while bad ones may intubate either too few or too many.
5. While ethically, extubating and withholding intubation should be equivalent, in practice the former feels more difficult.
6. Emergency staff have limited bandwidth. Evaluate the opportunity cost of everything you do. It’s not about whether it’s valuable or indicated; is it more valuable than whatever you or the nurses could be doing instead?
7. “Where is this patient going?” is always, ultimately, the main question of the EM provider. This differs from the main questions of many of their consulting and admitting specialties.
8. ICU time and ED time are different. In the ED, the ability to limit the amount of work is itself limited, so the judicious provider needs to jealously protect that time. In the ICU, we have a useful (albeit sometimes flexible) cap: our total number of beds.
9. Remember that nobody sees anyone else’s denominator. How many patients the ED sends home, how many consults don’t get called, how many floor patients are managed there instead of coming to the unit; these blind spots tend to promote small-mindedness and inter-disciplinary judgment.

References

Patel KK, Young L, Howell EH, et al. Characteristics and Outcomes of Patients Presenting With Hypertensive Urgency in the Office Setting. JAMA Intern Med. 2016;176(7):981–988. doi:10.1001/jamainternmed.2016.1509

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A look at oncology-related emergencies in the ICU, with Leon Chen (@CCMNP), NYC nurse practitioner specializing in oncology critical care.

Takeaway lessons

1. Extremely elevated leukocyte count should always raise suspicion for a “liquid tumor” such as leukemia.
2. The principal acute complication is leukostasis from poor flow, potentially causing hyperviscosity issues such as stroke, MI, pulmonary embolism, and mesenteric ischemia. Such patients are (despite their white count) also functionally immunosuppressed and at risk for infectious complications.
3. Fungal infection is not uncommon, but does not necessarily need empiric coverage up front.
4. Don’t hesitate to be broad with your investigations. Feel free to CT widely, cover broadly with antimicrobials, etc. Consider bronchoscopy for BAL.
5. Tumor lysis syndrome is always a possibility and can occur spontaneously in patients with such extreme leukocyte elevations. Check labs such as BMP, magnesium, calcium, phosphate, LDH, and uric acid every ~4 hours at first; however, the risk is probably highest for lysis when the white count begins to fall (e.g. due to initiating treatment).
6. Tumor lysis is much more common with liquid than solid tumors, and much more with certain chemotherapy regimens.
7. Extreme leukocytosis can cause “leukocyte larceny,” where blood gasses demonstrate false hypoxemia due to leukocytes consuming oxygen in the sample before it can be processed. Pulse oximetry is more reliable.
8. Spurious “pseuohyperkalemia” can also occur due to lysis of delicate immature leukocytes. This can be resolved with whole blood samples or point-of-care assays, which decrease transport time and sample agitation.
9. Uric acid is associated with renal injury and may need medical treatment. Allopurinol prophylaxis is generally safe, but rasburicase is the treatment of choice if uric acid is very high. LDH elevation is benign but are a good marker of response to treatment, as it should drop with appropriate chemotherapy.
10. Pulmonary hyperviscosity usually results in clear lungs on imaging. If infiltrates are present, consider infection. Also consider PCP pneumonia and fungal studies.
11. Leukapheresis, a dialysis-like process, involves selective removal of leukocytes to reduce viscosity.
12. Prophylaxis: Bactrim is a good choice for PCP, but beware of hyperkalemia. Atovaquone, pentamidine are next line options. Acyclovir for viral prophylaxis and posaconazole for fungal (galactomannan and beta-d glucan are helpful)
13. The blast count is suggestive of leukemia, but definite diagnosis will require bone marrow biopsy.
14. Initial stabilization of this sort of oncologic emergency is within the bailiwick of most hospitals, but it’s reasonable to then consider transfer to a specialty oncology center for the focused treatments like leukapheresis and chemotherapy.

References

A good, free review: Klemencic S, Perkins J. Diagnosis and Management of Oncologic Emergencies. West J Emerg Med. 2019 Mar;20(2):316-322. doi: 10.5811/westjem.2018.12.37335. Epub 2019 Feb 14. PMID: 30881552; PMCID: PMC6404710.

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The second part of our overview of interventional radiology with Dr. Bobby Chiong, board-certified interventional radiologist and chair of radiology at SBH Health System, with a focused look at some common IR procedures, namely abscess drainage and GI bleeding. Listen to part 1 here.

Takeaway lessons

1. Common goals would be INR <2.0, platelets >50k. If leaving an indwelling line or device, less may be okay, as it will tamponade the spot. Ignore the INR completely for purely cirrhotic patients. Although guidelines are fairly clear, many clinicians use their own rules.
2. Fluid collections are abscesses if they have rim enhancement on contrast CT. Without contrast you’re left guessing. (No oral contrast please!)
3. If necessary, most collections can be drained, somehow. Relevant considerations such as anatomy are subtle and often operator-dependent. Move the bladder out of the way by draining it, move bowel by hydrodissection, go in transvaginally or transrectally… options are numerous but not universal. Talk to your proceduralist.
4. When hoping to find and embolize bleeding, you’re usually best to start with a CTA. You need two phases, so non-contrast and arterial, or arterial and delayed, or… whatever. (No oral contrast please!) But find the bleeding. CTA is more sensitive than catheter angiography, and gives a general idea as to the region of bleeding. Going straight to IR without the CTA and without even a general idea of the region means a looong process of searching by catheterizing numerous vessels. Skipping the CTA isn’t even necessarily contrast-sparing, as it may take several hundred cc’s of contrast just to find the source.
5. With gastric bleeding, usually start with femoral artery access, access the celiac trunk, find the left gastric artery, then either just empirically start placing some gelfoam to reduce arterial pressure, or localize the specifically bleeding vessel if possible.

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An overview of interventional radiology with Dr. Bobby Chiong, board-certified interventional radiologist and chair of radiology at SBH Health System, with a focused look at what IR’s all about, coordination between care teams, vascular access, and troubleshooting.

Takeaway lessons

1. Interventional radiologists can’t do everything, but they potentially can do almost anything, and you usually won’t know what’s possible unless you ask. They have the potential to play a role in many situations which we never realize. Even if just a consultation to discuss a case (particularly in complex, multi-disciplinary situations), a good IR will be happy to have a conversation.
2. Quote of the episode: “There’s all kind of procedures that I can do that you’ve never heard of… but I can’t tell you about them all, because there’s a lot of them.”
3. Bridging the gap between primary teams and IR is best accomplished by building relationships. Get to know your interventional radiologists, speak to them in person, and make an effort to reach out to them rather than just typing in an order and awaiting magic.
4. For nearly every vascular access attempt: ultrasound guidance, short-axis view, micropuncture needle.
5. Fluoroscopy helps vascular access by ensuring correct depth of the wire and catheter and the correct vessel each step of the way. You can live without it, but it’s a big help.
6. Can’t advance a wire? You’re not intravascular (dissecting the vessel, in the subcutaneous, or through the backwall), or you’re against a valve (try spinning the wire), or you’re hitting some stenosis or thrombosis.
7. One reason IR gets lines you can’t is by setting up their ultrasound properly. Spend some time with a radiologist or ultrasound tech to learn to really optimize your view. They also have a whole lot of options for needles and wires you probably don’t, and subtle differences in wire stiffness, needle bevels, etc may make the difference.

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A detailed look at cirrhosis and acute-on-chronic liver failure as we typically see it in the ICU, with Dr. Elliott Tapper, gastroenterologist and transplant hepatologist, and director of the cirrhosis program at the University of Michigan in Ann Arbor.

Takeaway lessons

1. When treating liver patients, think infection, infection, infection—and understand that with good care and reversal of the underlying cause, they can get better.
2. Lactulose is always the first line agent for hepatic encephalopathy. Rifaximin is a potential adjunct.
3. Ammonia levels are prone to sampling errors and correlate poorly with clinical encephalopathy. Although it may cause fights, there’s usually little value in monitoring it.
4. MELD is a useful tool for prognostication, but an admittedly blunt one that fluctuates in response to many factors.
5. AST tends to be higher than ALT in alcoholic hepatitis, partly because alcohol metabolism depletes B6, which is needed for ALT production. Cirrhosis also increases the halflife of AST. However, alcohol use is usually most easily detected from the history, not by comparing labs.
6. AST or ALT in the thousands is usually due to causes other than alcoholic hepatitis. In the hospital, rule out obstruction with an ultrasound, consider drug reaction, and consider clots (e.g. portal vein thrombosis), although this last isn’t the most common.
7. The most common cause of extrmely elevated liver enzymes in-hospital is probably cardiogenic shock, particularly some combination of system hypotension and venous congestion. Since portal vein pressures are intrinsically low, it doesn’t take much venous congestion to counter that flow gradient, leaving only the hepatic artery for perfusion. Unfortunately, the arterial circulation usually only provides about 20-30% of hepatic perfusion, which leaves the liver vulnerable to systemic hypotension.
8. Exacerbations of cirrhosis and liver failure most often present due to infection. Imbalances of fluid (i.e. hyper- or hypo-volemic) are common as well.
9. Diagnostic paracentesis is mandatory for these patients to rule out SBP. Every hour it’s delayed may increase mortality. Empiric treatment alone is not adequate (agents like ceftriaxone will often be the wrong choice). Overall, those who undergo paracentesis are less likely to die in the hospital.
10. The AGA (American Gastroenterology Association), AASLD (American Association for the Study of Liver Diseases), and SIR (Society of Interventional Radiology) all agree: not only is paracentesis generally safe in cirrhotic “coagulopathy,” providers should not even consider the INR when assessing risk. This number only reflects a portion of the clotting cascade, but does not show the “rebalancing” caused by other factors, such as increased platelet activity and increased factor VIII production. The net result is generally an increased tendency for clotting, not bleeding, unless other coagulopathic processes are present.
11. Bleeding from paracentesis is extremely rare, and generally due to mechanical reasons (usually puncturing a vessel), not coagulopathy. Just tap them!
12. When diagnosing new ascites, a SAAG >1.1 is usually due to portal hypertension, but can also be caused by heart failure (congestive hepatopathy). Total protein >2.5 in ascites is more suggestive of ascites.
13. >250 polys and positive culture in ascites is diagnostic of SBP. Innoculating culture bottles at the bedside increases the yield compared to just filling tubes.
14. Look outside the abdomen for infection too, with blood cultures, chest xrays, etc.
15. Alcoholic hepatitis per se may (maybe) be treated with steroids, but infection, renal injury, and other factors are relative contraindications. In any case, steroid treatment is not emergent and can be instituted after a day or two for the picture to settle. Consider the Lille score after 4 days to see if it’s worth continuing for a full 28 days.
16. In hepatic encephalopathy, a true induction dose of lactulose is needed. Consider 60ml q2h until they’re pooping or waking up. If they don’t wake up in 6 hours or so, this is more likely to be toxic encephalopathy from infection.
17. Since toxins are also cleared through the urine, address AKI as well. Consider fluids: 1.5g/kg of 25% albumin on day 1.
18. Hepatorenal syndrome is treated by norepinephrine (maybe terlipressin if you’re in the UK). Granted, many of these patients are already on it.
19. Liver transplant for alcoholic hepatitis can be tricky, but isn’t impossible at all, even in patients actively drinking up until their hospitalization. Attitudes toward this depend highly on the culture of the transplant center. The best candidates are those who have not yet had a full chance to engage with relapse prevention and substance use disorder care, and all of their medical processes should be either resolved or diagnosed (i.e. their primary problem should now be their liver failure, the causes of which should be clear, and there are no active infections or other processes that would threaten the transplant). Such patients certainly may be a risk for relapse, but will at least be alive to try. And ICU patients are likely to be sick enough to jump to the top of transplant lists. Don’t assume that transplant is impossible; discuss with the transplant team and let them decide.
20. MARS, or “liver dialysis” with hepatoblastoma cells in the filter, is interesting, but so far the evidence remains negative.

References

SIR Guidelines on paracentesis in coagulopathy: Patel IJ, Rahim S, Davidson JC, et al. Society of Interventional Radiology Consensus Guidelines for the Periprocedural Management of Thrombotic and Bleeding Risk in Patients Undergoing Percutaneous Image-Guided Interventions-Part II: Recommendations: Endorsed by the Canadian Association for Interventional Radiology and the Cardiovascular and Interventional Radiological Society of Europe. J Vasc Interv Radiol. 2019;30(8):1168-1184.e1. doi:10.1016/j.jvir.2019.04.017

Importance of early paracentesis: Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol. 2014;109(9):1436-1442. doi:10.1038/ajg.2014.212

Failure to perform paracentesis is associated with increased mortality: Orman ES, Hayashi PH, Bataller R, Barritt AS 4th. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol. 2014;12(3):496-503.e1. doi:10.1016/j.cgh.2013.08.025

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The conclusion of our scenario of severe intraparenchymal hemorrhage with resulting herniation, with a closer look at neurological exams, prognostication, and the flow of care after initial stabilization, as well as our mindset as caregivers in these psychologically challenging cases.

Takeaway lessons

1. Early tracheostomy may not hold concrete benefits for neuro patients (i.e. improved mortality), but it often facilitates practical goals such as earlier liberation from the ventilator, early mobilization, and earlier discharge to rehab, which do have tangible utility.
2. Give frequent updates to family in cases of significant intracranial catastrophe. Avoid specific early prognostication unless the outcome is very obvious, but do emphasize poor prognostic signs, the importance of patience and endurance, and the likely quality of life given the available data.
3. Altered mental status is not always a contraindication to extubation in the persistently neuro-injured patient, although some such patients will indeed have difficulty protecting their airways.
4. These patients do improve, often after their ICU stay. Post-ICU follow-up is helpful to remind us of this, and when not possible, it’s good to simply remember that the ICU courses we perceive don’t always reflect eventual recovery.

References

Nestor MA, Boling B. Reversing Direct Oral Anticoagulants in Acute Intracranial Hemorrhage. Crit Care Nurse. 2019 39 (3): e1–e8.

ENLS Intracranial Hypertension and Herniation Protocol

ICH score

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A typical case of severe intraparenchymal hemorrhage with resulting herniation.

Takeaway lessons

1. DOACs like apixaban (Eliquis), although not usually monitored using routine coagulation assays, tend to elevate the INR only slightly (e.g. 1.0–1.3 or so). A strikingly INR in warfarin-like ranges should raise suspicion for an additional occult cause of coagulopathy.
2. Manage elevated ICPs using the ENLS “tiered” approach. All neurosurgical patients should receive the tier 0 (basic management) therapies.
3. In the neuro-injured patient, seek “euboxia” to limit further brain injury: normal pH, normal PCO2, normal PaO2, normal BP, normal temperature etc.
4. Be wary relying solely upon the GCS to describe, or even to trend neurological function. A descriptive, granular survey of function (particularly motor function) is usually more useful, as well as easier to remember.

References

Nestor MA, Boling B. Reversing Direct Oral Anticoagulants in Acute Intracranial Hemorrhage. Crit Care Nurse. 2019 39 (3): e1–e8.

ICH score

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Part two of our interfacility transfer from Hell. Tyler Christifulli, FP-C, EMT-P (@christifulli88) and Sam Ireland FP-C, EMT-P (@ireland_sam1) show us how they handle GI bleeding, arrhythmias, shock, cardiac arrest, and more, all from the confines of a helicopter. Listen to Part 1 here.

Check out the great educational content from Tyler and Sam over at FOAMfrat, including blogs, podcasts, and online EMS continuing education.

Takeaway lessons

1. When faced with an unstable patient in a wide complex tachycardia, stop thinking and just shock it.
2. As the nature of the transport (and the patient) changes, change your focus with it. The initial diagnosis is a starting point, not a headline.
3. Consider esmolol as an easily-titratable means of rate control in unstable patients.
4. Communicate ahead with the receiving hospital if urgent interventions will be needed upon your arrival.
5. Non-invasive positive pressure ventilation offers a preview of the hemodynamic response to intubation.

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A grueling interfacility transfer gives Tyler Christifulli, FP-C, EMT-P (@christifulli88) and Sam Ireland FP-C, EMT-P (@ireland_sam1) the opportunity to show us how they handle airway management, GI bleeding, mechanical ventilation, cardiac arrest, and more, all from the confines of a helicopter.

Check out the great educational content from Tyler and Sam over at FOAMfrat, including blogs, podcasts, and online EMS continuing education.

Takeaway lessons

1. Prepare the best you can before departing the sending facility, while acknowledging that that time may be a factor, and that some things can’t be predicted.
2. The close attention by 1:1 (or more) clinicians possible during critical care transport allows some issues, such as borderline airways, to be managed by close observation rather than early intervention.
3. Due to the limited medications and lab studies available, particular care should be used when managing DKA. Insulin therapy should target gentle glucose correction to avoid precipitous changes in pH, osmolarity, potassium, etc.
4. Transport medicine, whether from the back of an ambulance, helicopter, jet, or rickshaw, is an austere environment. Personnel, equipment, and time are all limited. A thoughtful approach to logistics, prioritization, workflow, timing, and detail is at least as important as a high-level understanding of pathology.