Critical Care Scenarios

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We discuss invasive aspergillosis, with a focus on when to consider and how to make this difficult diagnosis in the general ICU population—with Dr. Shmuel Shoham (@ShohamTxID), Associate Professor of Medicine at Johns Hopkins, transplant infectious disease physician, and an extensively published expert in invasive fungal infections as well as host of the Transplant ID Cast.

Takeaway lessons

1. Invasive aspergillosis is among the most common diseases identified on autopsy studies of ICU patients that was not recognized prior to death. Not all of these deaths are attributable to the aspergillosis, but some likely were.
2. Infection in the ICU patient arises when there are abnormalities in the flow of fluid, anatomical barriers, and/or the immune defenses (particularly neutrophil function).
3. When infection occurs, what organism caused it? Generally, whatever the patient is colonized by. This is influenced by the local antibiogram, environmental exposures, and the hospital or ICU course to date.
4. In the majority of critically ill patients, it is reasonable to treat acute signs of infection with broad-spectrum antibiotics using a standard, protocolized approach. However, pick a metric or two to follow, and if not improving, consider further workup and/or modifications in coverage.
5. Tricky diagnoses like this are best made by multiple specialists in close discussion, such as ID, critical care, pulmonology, etc. The best clue is aberrancy—features of the presentation that do not seem to match the expected disease script of a “regular” infection—and this often requires the specific knowledge of specialists brought together through collaboration. This is particularly important when approaching a “normal” ICU patient without high pre-test probability for fungal infection; start by treating regular things and look for discordant notes.
6. Risk factors for invasive fungal infection include any immunosuppression that inhibits neutrophil or T-cell function, ranging from high-dose steroids, DMARDs (mycophenolate, methotrexate), neutropenia (e.g. transplant patients, leukemia), and bronchiectatic disease (cystic fibrosis, COPD, etc), but can include anything from low-dose steroids to general critical illness. HIV is not a common risk.
7. Recent serious bacterial or viral pneumonia is also an important risk for fungal superinfection (e.g. a week or two later), commonly seen after H1N1 and nowadays COVID.
8. Invasive candidiasis should be considered in patients with invasive devices.
9. Invasive filamentous fungal infections are not a common finding in routine ICU patients (generally ill, intubated, in the ICU for some time, etc.) with no specific risk factors… but it does occur.
10. When considering fungal infection, serum galactomannan and beta-D-glucan levels should be done. If looking at the lungs, bronchoscopy with BAL should be performed, and galactomannan tested on the BAL specimen as well along with both bacterial and fungal stains/cultures. An undifferentiated patient should also have BAL mycobacteria, modified AFB/nocardia, legionella, and possible PCR for pneumocystis sent.
11. Bronchoscopy is maybe… probably… better for this than blind suctioning via the ETT tube. Maybe.
12. Fungal infections that may occur in ICU patients are most often invasive candidiasis (anywhere), aspergillosis (usually lungs although potentially elsewhere), and rarely other filamentous fungi like histoplasmosis or cryptococcus.
13. B-d glucan is a nonspecific test with many confounders, although a reasonable screen for fungal infections, many of which can elevate it. Galactomannan, particularly in the airway, is quite specific for aspergillosis. However, galactomannan in the airway may still reflect colonization, not necessarily invasive infection.
14. Aspergillosis exposure can occur from smoking marijuana (it is often found in the crop), moldy buildings (e.g. basements), and gardening or mulching. Some fungi are particularly geographic, such as coccidiomycosis or histoplasmosis, so infection is unlikely in a patient with no exposure to those regions. However, aspergillus is found everywhere, and ultimately, no explanation is needed to explain colonization.
15. Aspergillemia proven on blood cultures is extremely rare; it is just not a high enough concentration to pop a positive blood culture and tends to localize in thrombi anyway. Many positive cultures are lab contaminants, with the possible exception of Aspergillus terreus. Fungal isolator bottles are not necessarily needed. Sputum cultures are much more useful, although still insensitive, and could still reflect airway colonization, not necessarily infection; its significance must be considered in the clinical context.
16. Candida in the sputum is similarly unhelpful when positive, but blood cultures are much more sensitive for candida and should always be considered true candidemia. However, they are still only around 50% sensitive. (B-d glucan can help here as well.)
17. Imaging, generally CT of the chest, can contribute to the diagnosis. Several classic findings for filamentous fungi can occur, such as a “halo” sign (edema around a nodule), or macronodules (>1 cm). However, most ICU patients have non-specific imaging findings.
18. Elevated galactomannan in both BAL and blood, in a patient with reasonable pre-test probability, and imaging consistent with the diagnosis, allows a presumptive diagnosis of probable invasive pulmonary aspergillosis. Most diagnoses are never more certain than this, which would require positive cultures from a sterile site (e.g. blood) or biopsy. Such patients should usually be treated.
19. Histoplasmosis can elevate galactomannan plus some other much less common fungi, but in most general ICU patients it should be considered specific to aspergillosis.
20. Treatment involves antifungals, usually a mold-active -azole or occasionally amphotericin B, and improving the patient’s immune substrate, such as removal of immunosuppression. Specific drug toxicities play an important role; infectious disease consultation should be pursued.
21. The undifferentiated septic shock patient usually does not have pulmonary aspergillosis (or other filamentous fungi), as it usually does not cause that presentation, but rather respiratory or other local organ failure. If aspergillosis coverage is desired in the initial antimicrobial regimen, caspofungin is most reasonable based on its side effect profile (and provides some coverage of invasive candidiasis, which does cause septic shock).
22. Overall, the key to diagnosis of aspergillosis in the ICU is a reasonable threshold to consider the diagnosis, recognizing the “skipping record” of a patient who doesn’t fit the normal stereotyped disease scripts (e.g. bacterial infections), intelligent workup particularly with biomarkers (b-d glucan, galactomannan), and multi-disciplinary collaboration.

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Brandon walks Bryan through a case of new, unexplained hypotension in the ICU, with a focus on approaching shock, the use of POCUS, and risk stratifying unexplained problems.

Takeaway lessons

1. Sudden changes in vital signs or other status are often due to precipitating factors, such as iatrogenic stimuli, whereas more gradual changes are often due to evolution of the underlying diseases. This is not always reliable.
2. Sudden changes can also be due to monitoring artifacts, such as inaccurate telemetry, problematic arterial lines, etc.
3. Failing arterial lines are usually damped (reduced amplitude), causing depressed systolic pressures and raised diastolics, but the MAP still tends to still be reliable.
4. Hypotension with a narrower pulse pressure is somewhat more suggestive of hypovolemia than vasodilation. This is not always reliable.
5. Point-of-care ultrasound is probably the single best tool for assessing unexplained hypotension, mainly because it can (within a few seconds) rule out most of the life-threatening, specifically treatable causes, such as cardiac tamponade, PE, cardiogenic shock, major hemorrhage, and tension pneumothorax. Distributive shock (e.g. from sepsis), while among the most common causes of hypotension in the ICU, is a diagnosis of exclusion.
6. A fluid bolus used diagnostically should be given fast, and all the faster if you’re not giving very much volume. Use a pressure bag and don’t leave the room.
7. One of the hardest acts of judgment in a clinician is to recognize whether a new finding is a “big deal” or not.

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Discussing ICU triage, risk stratification, and patient disposition with intensivist Eddy Joe Gutierrez (@eddyjoemd) of the Saving Lives Podcast.

For 20% off the upcoming Resuscitative TEE courses (through July 23, 2022), listen to the show for a promo code for CCS listeners!

Takeaway lessons

1. When a patient has borderline indications for requiring the ICU, generally, in the real world, they should go to the ICU. More often than not, “downtriage” results in a later, inevitable, yet delayed upgrade to the ICU.
2. Sometimes, borderline patients may need the ICU just to complete the workup and prove that they don’t need the ICU. This is annoying but inevitable; such patients can’t languish for a 12-hour evaluation in the ED no matter how much we might want them to. The ED needs to flow, and there’s no better diagnostic tool than time.
3. A good practical rule for which pulmonary emboli require the ICU are those that will, or may, require an intervention other than systemic anticoagulation. Examples include systemic thrombolysis, catheter-directed thrombolytics, thrombectomy, etc.
4. In theory, patients with a downward trajectory can remain outside the ICU until they reach the point where they require critical care, then can be upgraded. This can work as long as their deterioration is controlled and not precipitous, i.e. there’s time to safely recognize their status and move them to higher care when the time comes. But this is often not easy to know.
5. The location of care can influence care in non-obvious ways. For instance, a septic patient may receive excessive harmful IV fluid boluses as providers attempt to avoid an upgrade to the ICU to administer vasopressors.
6. Bed availability has no relation to patient disposition, other than the fact that patients forced to board outside the unit will probably, inevitably receive worse care.
7. The readiness to transfer a patient from the ICU is usually higher than the threshold for accepting them initially. This isn’t a fallacy. It’s due to the fact that the former has had a period of observation, whereas the latter has not yet demonstrated their trajectory.
8. When a sending provider (e.g. in the ED, floor, or an outside hospital) thinks a patient needs the ICU, and you don’t think so, they usually should win. A patient may not need the ICU, but if they can’t stay where they are, uptriage is the safety net.
9. Ultimately, safe triage is usually a process, not a snapshot, and patients may need to move more than once. Smooth and safe transfers of care usually comes down to details and knowledge of your specific institution, and navigating it well requires good communication. Teams that can’t talk to each other inevitably lead to deficiencies in care.
10. Making certain triage determinations by policy, committee, or guideline can help counteract the natural tendency (at least in the US) to always overtriage due to concern about personal provider risk.
11. Try to limit your second-guessing about other people’s triage decisions made in retrospect. It’s a lot easier after the fact.