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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
Invasive candidiasis should be considered in patients with invasive devices.
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.
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.
Bronchoscopy is maybe… probably… better for this than blind suctioning via the ETT tube. Maybe.
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.
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.
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.
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.
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.)
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.
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.
Histoplasmosis can elevate galactomannan plus some other much less common fungi, but in most general ICU patients it should be considered specific to aspergillosis.
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.
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).
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.
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.
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.
Sudden changes can also be due to monitoring artifacts, such as inaccurate telemetry, problematic arterial lines, etc.
Failing arterial lines are usually damped (reduced amplitude), causing depressed systolic pressures and raised diastolics, but the MAP still tends to still be reliable.
Hypotension with a narrower pulse pressure is somewhat more suggestive of hypovolemia than vasodilation. This is not always reliable.
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.
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.
One of the hardest acts of judgment in a clinician is to recognize whether a new finding is a “big deal” or not.
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!
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Try to limit your second-guessing about other people’s triage decisions made in retrospect. It’s a lot easier after the fact.
We review a case of massive intraparenchymal hemorrhage progressing to brain death, including the process of brain death testing and declaration, with Dr. Casey Albin (@CaseyAlbin), neurologist and neurointensivist, assistant professor of Neurology and Neurosurgery at Emory and part of the NeuroEmcrit team.
For 20% off the upcoming Resuscitative TEE courses (through July 23, 2022), listen to the show for a promo code for CCS listeners!
In general, in patients with good baseline function, it’s reasonable to be fairly aggressive with initial care, such as placement of intracranial pressure monitors, even if long-term goals of care are unclear—it can always be escalated.
Although ICH score is associated with mortality, the original study allowed withdrawal of care at discretion of the clinicians, so the data may be tainted by self-fulfilling prophecy—withdrawal of care may lead to poor prognosis in some cases, not always the reverse.
Sodium goals are ideally titrated to ICP (with invasive monitoring). In its absence it’s best to target clinical findings, unless you have tools like TCDs or optic nerve sheath ultrasound, or just frequent CT scans. Arbitrary sodium goals are rarely helpful.
There is good evidence for decompressive hemicraniectomy for large MCA infarct IF the patient is young; it is less clear in the elderly. If it’s going to be done, do it early.
If herniation is clear via ICP or imaging, don’t spare sedation for the sake of a neuro exam, unless you’re at the point of stepping back and assessing for long-term futility and possible brain death.
4-5 days into admission is often when families begin to understand the nature of a devastating neurologic injury. In some cases, discussion of futility and brain death may be initiated by families after doing their own research.
The first step is holding sedation and waiting ~5 half-lives for confounding drugs to clear; impaired renal or hepatic clearance should be taken into account here. (Pharmacy may be helpful.) Paralysis should be held and train-of-four can be used to confirm. Drug levels can be used to confirm clearance of opioids, etc if needed.
The law (Uniform Declaration of Death Act) doesn’t always agree with guidelines (while hospital policies may differ even further). The UDDA requires complete brain death, whereas the AAN’s guidelines don’t necessarily require pituitary death (patient need not be in DI), but all do require more than just brainstem death—for example, a locked-in patient would not qualify.
Expect and manage DI, as hypovolemia and hypernatremia may make the patient too unstable to tolerate brain death testing. Consider a vasopressin drip, replace volume, etc.
As the chest wall becomes denervated, it loses elastic recoil, while hypovolemia may cause very hyperdynamic cardiac function. The combination can cause strong chest wall vibrations which may autotrigger the ventilator, often confusing staff and family who believe the patient is breathing spontaneously.
Perform brain death testing in a systematic, scrupulous manner. Print your hospital policy and use it as a formal checklist. You’ll need a bright penlight, a tongue depressor or Yankhauer catheter, a Q-tip or gaue for corneal reflexes, 50 ml x2 of ice-cold water and a syringe with an IV catheter on the tip for cold calorics, and some kind of insufflation catheter or a T-piece for apnea testing.
Pitfalls: remember to test corneals by touching the actual cornea, not the sclera. Cold calorics are performed by irrigating the ear canal and watching for gaze deviation (any deviation shows brainstem activity). Gag reflex must be checked all the way in the back of the oropharynx with vigorous stimulation. Cough and pain responses must also be checked with substantial stimulation. Warn family ahead of time about the possibility of purely reflexive triple flexion.
Consider bringing the family to watch, which helps encourage transparency. Warn them ahead of time that if the test is confirmatory, it will indicate the patient is dead by brain criteria.
You generally want an arterial line for the apnea test, and have vasopressors running and ready to maintain the SBP >100. Put the patient on 100% FiO2 and get a baseline ABG showing normocapnia and a PAO2 >200. (If the patient has a baseline elevated PACO2, follow your local policy.) Oxygenate the patient passively, such as by inserting an insufflation catheter hooked up to oxygen down the ET tube after disconnecting the ventilator. Uncover the patient’s chest and watch for chest rise.
A confirmatory apnea test is one where the PACO2 rises by 20 points, without any clinical signs of breathing; hence the team needs to be in the room, physically observing the patient. An equivocal test is one where the test cannot be completed or the PCO2 fails to adequately rise to confirm adequate levels. Most tests are completed by 10 minutes, but start sending blood gasses earlier than that (e.g. at 6, 8, 10 minutes), as you may need to terminate the test due to instability while waiting for the most recent gas and you’ll want to know if the patient had finished.
Confirmatory/ancillary tests can be done if the clinical and apnea tests cannot be done, or are not completely definitive due to confounding factors. They can include TCDs, nuclear flow studies, or EEG if specialized equipment and readers are available. Catheter-directed 4-vessel cerebral angiography is another option, but CTA/MRA are not. Most of these tests are looking for intracranial circulatory arrest, i.e. lack of blood flow to the brain—dead cells have no metabolic demand and shunt blood away.
Perform brain death testing as soon as clinically appropriate; they only become more unstable.
We discuss the clinical presentation and management of AFE with guests Dr. Stephanie Martin (Twitter: @OBCriticalCare, Instagram: @criticalcareob), medical director for Clinical Concepts in Obstetrics and a Maternal Fetal Medicine specialist in Scottsdale, Arizona with expertise in critical care obstetrics. She is also co-host of the Critical Care Obstetrics podcast. We’re also joined for a patient perspective by Miranda Klassen (@afefoundation), Executive Director of the AFE Foundation, and her husband Bryce Klassen, CCRN, ICU Supervisor at Scripps Memorial Hospital Encinitas.
AFE is poorly understood but is probably caused by exposure of amniotic fluid (skin cells, hair, vernix, etc) to maternal blood, causing a severe inflammatory reaction. Although it may contribute, it is probably not mainly due to obstructive shock, as seen in pulmonary embolism.
AFE is rare. Some clinicians will go an entire career without seeing it. However, it certainly happens and has tremendous consequences when it does.
As a rule, ACLS care is the same for pregnant women. The main exception is that if ROSC is not obtained immediately, you must perform a resuscitative Caesarean section within the first 4 minutes, aiming to have the baby delivered within 5. Without this, the chances of recovering the mother are slim: the gravid uterus interferes with compressions, compresses the IVC, and causes other problems. Achieving this in non-obstetric areas requires a carefully thought-out process. Time must not be wasted transporting the patient elsewhere. The only equipment absolutely required is a scalpel, although this too can be hard to find if you haven’t optimized your process. In short, if you have a pregnant woman in your ICU, figure out now what you’re going to do now if she codes.
Due to the logistical challenges, most of these resuscitative C-sections are actually done in 6-15 minutes. This is not the goal.
During CPR, the gravid uterus should be manually displaced to one side, preferably the left. (It is no longer recommended to tilt the patient laterally, since this interferes with compressions.)
AFE is rare, but with excellent care it is survivable.
Bleeding post C-section is usually not significant. The abdomen can be left open, and can even be used for aortic access to check for the pulse, or occlude the aorta (either manually or by cross-clamp).
A normal fibrinogen level in a pregnant or immediately post-partum female is elevated (often in the ~600s), so a “normal” level should be considered low. Use this to follow DIC. Bleeding and clotting may both occur.
Although pregnant women have a subtle physiologic hemodilution, their normal hemoglobin should not drop below 11, so for our purposes, anemia still denotes anemia.
Resuscitating the immediately post-partum woman should not mean great confusion about safe medications. Use whatever is necessary to save her life. Any impacts on breastmilk can be managed by pumping and either saving or dumping it as appropriate.
A compensated respiratory alkalosis via hyperventilation should be expected during pregnancy (the mother must have a lower PCO2 than the fetus to create a gradient for fetal ventilation). This persists post-partum, so it’s probably appropriate to aim to maintain this by increasing minute ventilation, even although it’s likely not as critical since there’s no longer a fetus to support.
The most important post-partum care after an emergency like this remains supportive critical care. Eventually the mother can be transferred to a post-partum obstetric unit, but these are not high acuity floors (with nurse:patient ratios as high as 8:1) and this needs not be rushed. OB staff can come to the ICU to assist and educate as needed.
If you have a suspected AFE, call the AFE Foundation 24/7 (307-363-2337) for advice and to coordinate collection of specimens, which must be done promptly and is badly needed to improve our understanding of this disease.
Amniotic fluid embolism: principles of early clinical management. Pacheco, Luis D, Klassen, M., et. al. American Journal of Obstetrics & Gynecology.
Society for Maternal-Fetal Medicine (SMFM). Pacheco LD, Saade G, et al. Amniotic fluid embolism: diagnosis and management. Am J Obstet Gynecol 2016; 215:B16.
Stafford, IA, Moaddab, A, Dildy, GA (2019) Evaluation of proposed criteria for research reporting of amniotic fluid embolism. AJOG, 220, 285-287.
Combs CA, Montgomery DM, Toner LE, Dildy GA, Patient Safety and Quality Committee, Society for Maternal-Fetal Medicine, Society for Maternal-Fetal Medicine Special Statement: Checklist for initial management of amniotic fluid embolism, American Journal of Obstetrics
Amniotic fluid embolism: Pathophysiology from the perspective of pathology. Tamura N, Farhana M, Oda T, Itoh H, Kanayama N. J Obstet Gynaecol Res. 2017;43(4):627. Epub 2017 Feb 11.
Kiranpreet, K., Bhardwaj, M, Kumar, P., Singhai, S., Singh, T., & Hooda, S. (2016). Amniotic fluid embolism. J Anesthesiol Clin Pharmacol, 32(2), 153-159.
Zelop CM, Einav S, Mhyre JM, Lipman SS, Arafeh J, Shaw RE, Edelson DP, Jeejeebhoy FM; American Heart Association’s Get With the Guidelines-Resuscitation Investigators. Characteristics and outcomes of maternal cardiac arrest: A descriptive analysis of Get with the guidelines data. Resuscitation. 2018 Nov;132:17-20. doi: 10.1016/j.resuscitation.2018.08.029. Epub 2018 Aug 28. PMID: 30170022.
A look at rehabilitation and mobility in the critically ill, from the perspective of our skilled therapists—with Heidi Engel, PT, DPT of UC San Francisco, long-term provider of acute care therapy, researcher in ICU rehabilitation, and founding member of the SCCM’s ICU Liberation program.
Tolerance of pressure support ventilation is often a good marker that a patient is ready to start meaningful PT. Before that, the harm may exceed the benefit, unless there’s a specific reason why activity may help move them along, such as attenuating delirium and agitation and improving tolerance of the ET tube.
The most common complaints and stressors of ICU patients are: feeling thirsty, feeling traumatized and afraid, the inability to communicate, and feeling “air hungry” due to the strange mechanics of mechanical ventilation and other respiratory modalities.
In many cases, rehab will require convincing patients to get over an initial hump. Breathing, strength, and discomfort may initially be a challenge but will improve with activity.
You may need to choose priorities: do you want to push vent liberation or mobility today?
Bring the light during daytime hours to improve the circadian rhythm, but direct fluorescent lights are harsh and can encourage closed eyes. Natural, indirect light is better.
Although PT and OT have complementary roles, they will sometimes try to see patients together, which can have downsides by underemphasizing the unique aspects of each role, reducing total rehab time, and relegating one skilled therapist to acting as merely a set of hands.
The presence of any sedation, even “gentle” agents like precedex, creates an obstacle to effective PT.
Getting patients up to a chair helps with agorophobia by changing their perspective from their tiny bed-shaped home.
Heidi’s rehab process
Check the RASS and CAM-ICU scores
Explain to patient the importance of the endotracheal tube and not touching it. Bring all equipment to the side of the bed with the ventilator.
Perform some gastroc/hamstring stretching to initiate mobility and help wake the patient up
Ask them to follow commands, such as: push! Can they follow? Do the vent and vitals remain okay?
Sit them up at edge of bed, arrange equipment. Observe head control, trunk control, breathing, vitals, orthostasis, etc.
bring a big mobility device, see if they can stand.
While they’re up, use the opportunity to clean the linen, wash their face, comb their hair, clean their posterior.
COVID is making it harder, often just for practical reasons: PPE limiting mobility, noise from filters and masks, families not present, weird autonomic and orthostatic issues… all far more time consuming. However, they do get better and many times do very well, sometimes even recovering faster than similar non-COVID patients. Omicron has not been as bad.
Dedicated therapy teams for the ICU add cost, but cost analyses have shown the benefit (in terms of reducing length of stay and other expenses) to actually result in net cost savings.
In-bed, non-weight-bearing activities such as passive range of movement exercise is perhaps better than nothing, but is nowhere near as useful as weightbearing activity out of bed, and has not shown the same clinical benefits in the literature. Every day of out-of-bed activity may pay back several fewer days of rehab down the road.
The hows, whys, logistics, and applications of focused, bedside transesophageal echocardiography performed by critical care and EM providers, with Felipe Teran, assistant professor of emergency medicine at Weill Cornell and director of the Resuscitative TEE Project.
As a rule, resuscitative TEE is performed in patients with a secured airway.
TEE views are not unlike TTE views, just at a different angle (often backwards/upside down down). The technical skills are very similar, and skilled TTE users will find the learning curve short. There are actually fewer probe manipulations (in and out, left and right, and Omniplane rotation, along with some less-used ones like flexion/extension).
The same questions you’d typically ask with TTE can be asked with TEE: is there tamponade? is there cardiogenic shock? is there RV failure? is there hypovolemia? These can be answered even in patients with technically-difficult surface windows.
Some questions hard to answer with TTE can be answered with TEE, such as obtaining reliable RV inflow-outflow views and reliable valve assessments.
Some new questions can be answered with TEE alone: is there aortic dissection? are catheters and wires (ECMO, Impella, pacing wires, etc) optimally placed?
TEE has specific applications in cardiac arrest: are chest compressions optimally positioned on the chest? What is the rhythm? It provides monitoring much more continuous than intermittent TTEs, since it can be left in place.
In an ideal world, resuscitative TEE would be handled very much like TTE, and performed in a similar way—not restricted to some small group of “superusers” or for very rare cases.
When implemented by trained users in appropriately-selected cases (e.g. in shock with inadequate transthoracic windows), it impacts care virtually 100% of the time.
An overview of the role and contributions of a clinical pharmacist in the ICU, with Laura Means Ebbitt of the University of Kentucky, a clinical pharmacist specializing in colorectal/ENT surgery and critical care.
A clinical pharmacist is a “knowledge pharmacist,” dispensing advice rather than medications. They round with the team to review meds and answer questions about routes, interactions, etc, follow up on patient education and post-discharge coordination, assist with medications during cardiac arrests and other emergencies, and provide other clinically-oriented guidance and oversight. Most have completed post-graduate residency programs.
Clinical pharmacists generally have an important role for antibiotic regimen selection, monitoring, and stewardship.
They consider cost in a way that providers rarely do.
They provide patient education that we typically defer or omit.
They’re great at catching deviations in good ICU practices, such as missing DVT or stress ulcer prophylaxis, managing and reconciling home medications, and coordinating nutrition needs (particularly with TPN).
Part two of our discussion with fan favorite Matt Siuba (@msiuba), Cleveland Clinic intensivist, on complications in critical care and how to prevent and manage them. Today we focus on respiratory failure after extubation, and unintentional self-extubation.
When considering extubation of borderline patients, extubating to high flow nasal cannula or CPAP/BiPAP is often a good compromise. This is probably at least a little better than waiting for them to struggle before applying the support, plus it’s easier to assess their course. They can always come off if they look stellar.
Set up for extubation success by first optimizing volume status, sedation strategies, mobility, and other good liberation practices.
If concerned about pulmonary edema, a trial of a “tube compensation” mode alone (versus pressure support with PEEP) may be a good “strict” trial, as compared to more primitive ZEEP or T-piece trials.
Post-extubation stridor is not always predictable, although known airway trauma should raise suspicions. If severe, or even borderline, patients should be promptly reintubated. If more mild, a trial of a couple hours on medical therapies and NIPPV is reasonable. Try steroids (dexamethasone 10 mg IV or so).
Cuff leak tests are not very predictive and as likely to mislead as help. Visual inspection of high-risk airways for laryngeal edema may be helpful, although remember that a large tube in a small airway may never have a leak (and always visually look tight), yet may not be at risk for narrowing after tube removal.
Self-extubation should prompt emergent preparation to oxygenate and reintubate, although you can assess their stability before actually doing it. Remove the tube if still stuck in the mouth. Stop sedative drips that suppress breathing.
If agitation precludes oxygenation, consider antipsychotics. Dexmedetomidine may be useful in this situation, but takes a good 30-60 minutes to get loaded, so you may need another agent as a bridge. Don’t use a loading dose of dex, but starting at a higher rate (>0.6) is smart.
A patient intubated primarily because of agitation will usually do fine after extubation, whether intentional or accidental. The main problem is that agitation precludes a clear, easily-interpretable SBT.
“Extubation hesitancy” is a common error in the ICU. Clinicians are overly hesitant about failed extubations but not worried enough about prolonged intubation courses from the failure to try. Accept that a 0% chance of reintubation means leaving people on the vent for too long; acknowledge risks, plan for fallbacks, and don’t take failure personally; optimize the circumstances; but in the end, try. Risk need not be zero, it should just be lower than the risk of continued mechanical ventilation. “Not everybody is going to be ready every day, but you should treat every day like it’s extubation day.”
The immediacy of the psychological feedback when a patient self extubates gives it primacy and power in our minds. It’s easy to see its harms, while it’s harder to see the harms of the oversedation that prevents it. “Overcautious” is really “overmedicalizing” and is not a safer flavor of risk.