Critical Care Scenarios

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We explore the controversial area of using hypertonic saline to support hemodynamics, protect the kidneys, and facilitate diuresis in the critically ill patient. Our guest is Dr. Sean Barnett, hypertonic aficionado and nephrologist with a focus in critical care.

Takeaway lessons

1. The furosemide stress test in the shocked patient is a useful means to assess renal prognosis and determine whether oliguria is due to a prerenal state or ATN. 1mg/kg for the diuretic-naive or 1.5mg/kg for those with previous loop diuretic exposure, then monitor urine for the first 2 hours. If they make 200ml of urine, chances are good that the kidneys are still working to some extent, and the patient is less likely to proceed to needing dialysis.
2. In the case of prerenal azotemia, massive ongoing fluid overload via crystalloids can be mitigated by instead giving small boluses of hypertonic saline. A 100ml 3% saline bolus has a third of the sodium and a ninth of the volume of a 1000ml normal saline bolus, but because of the concentrated sodium load, still increases flow to the kidneys and effectively shuts off the patient’s RAAS axis that’s been activated by the shock. There are few tools that can suppress renin as potently as a hypertonic saline bolus, even a small one.
3. Angiotensin II is a key driver of capillary permeability: high RAAS = high capillary leak states. Downregulating this feedback loop with hypertonic helps to escape the shock-fluid cycle.
4. Combine the 3% bolus with furosemide and you’ve increased renal perfusion at the same time as you’ve stimulated diuresis. It’s a great approach for diuresing the patient who’s still in shock.
5. Albumin is less effective on its own, although albumin combined with hypertonic saline seems to have excellent synergy, outperforming each alone, allowing the preservation of intravascular volume that many believe they’re getting from albumin alone. Concentrated (e.g. 25%) albumin is not as good, does not reduce capillary permeability, and may be nephrotoxic.
6. Anything you can do to increase renal perfusion will help protect the kidneys during shock, and this is exactly what concentrated hypertonic saline can do.
7. With the small hypertonic boluses used here (rarely more than ~300ml in a day), the serum sodium usually does not rise by much. Just monitor it and ensure you’re giving adequate free water, especially if diuresis occurs.
8. Scheduled 3% boluses of ~100 ml every 8 hours or so, combined with scheduled furosemide boluses, is an effective diuretic strategy in the shocked, overloaded patient with heart failure.
9. Hypertonic saline stimulates ANP and nitric oxide by both stretching and creating hypertonicity in the right atrium; this helps decrease PVR and supports both sides of the heart.
10. A 3% saline infusion can work brilliantly to facilitate ultrafiltration during CRRT. Overloaded patients may be intolerant of volume removal because it’s being pulled straight out of the RV, which can be a tough stimulus in an unstable heart; hypotension and arrhythmias can occur. Hypertonic saline can support preload without adding much volume; it pulls volume into the vascular space for CRRT to filter out. Trending ScvO2 from the tip of the dialysis catheter can be a good guide as to whether UF is helping or hurting the heart as well.
11. The best evidence for hypertonic saline is to support diuresis. The next best evidence base is for cirrhosis with volume overload. As an IV fluid, the best data is in the surgical literature, generally showing it as equal or better to other fluids. Using it during CRRT has weaker evidence, although many nephrologists will use it during regular dialysis.
12. 3% saline is certainly safe and causes no issues with increases blood viscosity. It is safe through peripheral IVs as well.
13. The effect can be proven by checking the urine sodium and urine osmolality. The former is generally low and the latter high in the patient whose kidneys are conserving due to shock. Give them 3%, and the urine sodium shoots up while the urine osms decrease, as the RAAS axis and ADH become attenuated.

References

Improved overall fluid balance / UOP / hemodynamics in diverse settings. 

https://link.springer.com/article/10.1007/s00134-020-06132-0

https://journals.lww.com/annalsofsurgery/fulltext/2014/09000/the_hyslar_trial__a_prospective_randomized.5.aspx?casa_token=B1zfybqWhEYAAAAA:2QEHFpXKGY8dUDSqJpN4hrI8jz1K6_A75t5pSpbAUn5YLmZXFBisetKuRO50q6HGAXfTaL_KA0PAlo6lXM58I2xl6wXF-

https://journals.lww.com/shockjournal/FullText/2015/03000/Comparison_of_3__and_7_5__Hypertonic_Saline_in.7.aspx?casa_token=yGinfDHpavQAAAAA:ynzZ5fHTZkSRlkBiFoz_DHl0EhmdO7HG0gbonrlOJljz1l8kxW-Ur6xqGwiC5A8dew3IiwhAi8la22puhq3aAPrfi0-E

https://www.ahajournals.org/doi/abs/10.1161/01.CIR.41.1.97

Diuresis

https://www.ingentaconnect.com/content/wk/ccm/2021/00000049/00000011/art00005

https://link.springer.com/article/10.1007/s00059-013-4041-6

https://www.sciencedirect.com/science/article/abs/pii/S0270929511001355

https://link.springer.com/article/10.1007/s00059-010-3394-3

https://journals.physiology.org/doi/full/10.1152/ajprenal.00686.2020

COVID

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9253300/

https://link.springer.com/article/10.1186/s13063-020-04634-2

https://www.researchgate.net/profile/Paola-Rosati/publication/345765160_Hypertonic_saline_nasal_irrigation_and_gargling_as_an_inexpensive_practical_adjunctive_weapon_to_combat_asymptomatic_SARS-CoV-2_infections_A_case_report/links/5fad195a299bf18c5b6a1aa6/Hypertonic-saline-nasal-irrigation-and-gargling-as-an-inexpensive-practical-adjunctive-weapon-to-combat-asymptomatic-SARS-CoV-2-infections-A-case-report.pdf

Anti-Inflammatory

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1449974/

https://journals.lww.com/jtrauma/Fulltext/2000/10000/Hypertonicity_Prevents.2.aspx?casa_token=usB9uYwpcS0AAAAA:4IwYxvh4E2Tm5NjcbkEwr3C-r0FwkKyVOVhLlSewPABY85zrx5gedIHmoDcw2MA1sDx5_6T5Qb-6XPe0blmHBIwe2Nya

https://journals.lww.com/jtrauma/Fulltext/1997/04000/Hypertonic_Saline_Resuscitation_Decreases.4.aspx?casa_token=c_TsE2LFt_kAAAAA:LiaOb-JeONa3wo26fO1_-M3Ayx3rc7kpXOzWXDkDrOIxuV_2Wwwm-HhbddHOp22io7H7AvPIXMcqVNm0_dxKaO1uLVTW

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We look at the rib fracture patient requiring ICU admission, including a discussion of surgical repair, with Dr. Ron Barbosa (@rbarbosa91), Portland trauma surgeon and SICU director at Legacy Emmanual Medical Center.

Takeaway lessons

1. Algorithms and protocols for admitting disposition exist but are generally poorly predictive. ICU admission in rib fracture patients is still most often a matter of clinician judgment and bed availability.
2. Pain management should include multi-modal therapies including acetaminophen, lidocaine patches, a muscle relaxer such as methocarbamol, and perhaps NSAIDs, as well as a reasonable opioid regimen (oral and/or IV). An opioid IV PCA is a good next step, followed by regional/neuraxial anesthesia, most often a thoracic epidural, although other options such as On-Q pumps also exist. Pain consultation services (i.e. via anesthesia) are a good resource.
3. LMWH (e.g. enoxaparin) is a potential contraindication to an epidural. Consider holding DVT chemoprophylaxis if it’s potentially on the table, or going to daily instead of twice-daily dosing.
4. The primary risk to rib fracture patients is respiratory deterioration. Unfortunately, there is no clear timeline when this risk has passed; judgment needs to be used with an eye to their overall trajectory and how much support they’re requiring.
5. Surgical rib fixation is determined by anatomic accessibility, radiographic appearance, concern for injury to other structures, and other factors. The main indications are usually prevention of respiratory decline and stabilizing bony displacement at risk of injuring the lung and vessels.
6. The most obvious ribs to repair are severe chest wall deformity and flail segments. Patients on the ventilator are good candidates as well, as fixation may allow them to be liberated.
7. Ribs 1-2 are generally not accessible, and 3 usually not as well. Ribs 11-12 are accessible but (since they’re floating) fixation is usually not considered helpful to stabilizing the chest. Thus, most repairs are limited to ribs 4-10.
8. Imaging is helpful but not definitive. Some of the worst-looking scans will do well clinically without repair, and vice versa. However, note that some imaging will worsen over time, and occasionally are worth repeating after the admitting scans; displacement may worsen or effusions may grow.
9. Pleural effusions (usually hemothorax) are relevant insofar as a growing effusions may need VATS to evacuate it, and if VATS is being performed it’s sensible to perform plating at the same time, so trying to align the timing is helpful, although not always possible. Guidelines suggest plating ribs within the first three days when possible—not always enough time to determine the need for thoracoscopy.
10. Trauma surgery, thoracic surgery, and orthopedics all might do this procedure depending on the local environment, but often it comes down to trauma. This may be influenced by psychological secondary factors, as it’s a long, laborious, poorly-reimbursed procedure, and hence may tend to fall to the primary team.
11. CT reconstruction is invaluable for surgical planning, including the surgical approach (potentially lateral thoracotomy, vertical or hockey-stick incisions near the spine, etc). Some are specialized to this procedure and hence require specific experience with them, and not all fractures may be reachable with one incision. Try to avoid cutting muscles of respiration.
12. Imaging will also guide the decision of which ribs seem to warrant repair, and which are amenable to repair given anatomic considerations. Not all fractures in a flail segment need to be repaired to successfully stabilize the chest.
13. Repair consists of a series of specialized plates that require customized bending and fixation. These techniques are well-known to orthopedists but less so for trauma surgeons.
14. Other than the usual complications of surgery (bleeding, anesthesia, etc), complications are relatively few. Plates may occasionally need to be removed for pain or infection, but rarely.

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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.