Episode 50: Rib fractures and surgical plating with Ron Barbosa

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.

Lightning rounds #18: How to give a conference presentation

Brandon and Bryan chat about academic presentations… how to prepare and submit them, selecting the right venue, giving a good talk, and the elephant in the room: why to do it at all.

TIRBO #14: Trajectories of illness and critical care

How the arc of disease peaks and falls, and how the curve of our care should match it to avoid under- or over-treatment.

Episode 49: Invasive pulmonary aspergillosis with Shmuel Shoham

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.

Lightning rounds #17: Reading chest x-rays

Brandon and Bryan share their approaches to the chest x-ray in the ICU. Plus: Bryan’s an FCCM!

Here’s the Radiology Masterclass.

Episode 48: Undifferentiated hypotension

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.