We look at the patient with known pulmonary hypertension admitted for new issues like sepsis and pneumonia, and how they differ from our usual bread and butter, with help from Dr. Raymond Foley, director of the medical ICU and the pulmonary/critical care fellowship at UConn Health, as well as director of their pulmonary vascular disease program.
Evaluate for the risk of decompensation in a patient with known PH and acute illness by considering their most recent echocardiogram, and repeating it as soon as possible after admission. Signs of baseline and/or new RV strain, such as reduced TAPSE, septal bowing, etc, as well as pericardial effusion, suggest a poor reserve for the stresses of their new ICU course. Right heart cath or echo PA pressures are less relevant than their cardiac function; pulmonary pressures fluctuate and are much less relevant to the clinical picture.
Common causes of decompensation of PH include sepsis, medication issues (such as interruption of continuous PH meds), and polypharmacy (such as introducing an alpha agonist to treat a URI).
When admitting the acutely ill patient with known PH, strongly consider early transfer to a PH center, preferably the one that already knows the patient.
Typically, continue to administer outpatient PH meds, unless forced to hold or convert them to another agent due to lack of enteral access, absorption issues, or other factors.
Avoid intubation if at all possible, as this can easily provoke cardiovascular collapse. Avoid hypoxemia and hypercarbia as well, which can both lead to worsening pulmonary arterial pressures. Maintaining both of these goals may require a thoughtful decision on when a patient should transition from modalities like high-flow nasal cannula to intubation. Non-invasive positive pressure like CPAP/BiPAP may be a reasonable middle ground, but could still provoke some instability due to the positive pressure.
Consider targeting a higher MAP than in other patients to maintain perfusion of the RV. A reasonable MAP goal is 65 plus the CVP.
Norepinephrine is a reasonable first-line vasopressor, but vasopressin might be even smarter, as it has no effect of increasing on the PVR and at low doses may even reduce it (activating V1/V2 receptors in the pulmonary circulation). Epinephrine at lower doses is a good second line, providing inotropic support for the RV without much impact on PVR.
Place an arterial line early. Consider a central one such as in the femoral artery if they’re sick. Place a central line; trending CVP can be helpful. If they’re really hemodynamically unstable, consider floating a PA catheter. Non-invasive cardiac output monitors are of questionable utility.
If intubating, induce them thoughtfully, avoiding agents like propofol. Ketamine or etomidate may be wise. Consider pushing the BP higher to avoid episodes of hypotension.
On the ventilator, be liberal with oxygen and don’t be in a rush to wean it. While hyperoxia is not needed, avoid hypoxia, even transiently. Oxygen is a potent pulmonary vasodilator, and is much better for these patients than giving them a higher PEEP.
If shock and RV failure are progressing, consider a pulmonary vasodilator, such as inhaled nitric oxide (INO) or inhaled epoprostenol. These have similar effects, although INO is more expensive. Drugs like epo can also be given intravenously, but this has the downside of dilating the entire pulmonary circulation, which can worsen VQ matching; nebulizing it improves perfusion to ventilated alveoli while ignoring shunted lung units. A positive response is improved oxygenation, reduced PA and RA pressures, and improved cardiac output.
Most patients in RV failure don’t need additional preload, and indeed may benefit from cautious diuresis. A CVP of around 8-12 is usually a good goal.
Dobutamine and milrinone are all reasonable options for inotropes, depending on your comfort.
Decompensated PH due to CTEPH can potentially be treated, even in the setting of critical illness, via surgical intervention (e.g. pulmonary endartarectomy).
Consider mechanical support early, with the best choice probably being VA ECMO.
Weaning of support, such as inhaled vasodilators, can be achieved by transitioning to other agents like IV or enteral vasodilators (e.g. sildenafil).
An exploration of clinical documentation and billing/coding with Dr. Robert Oubre (@Dr_Oubre), full-time hospitalist and CDI Medical Director for a community hospital in southern Louisiana.
Acute respiratory failure is justified when there is altered gas exchange (SpO2 <90%, PaO2 <60, CO2 >60 with pH <7.35, or P/F <300), clinical signs of increased work of breathing (using accessory muscles, etc), and a patient requiring respiratory support more than 4L O2 by nasal cannula. Requiring additional monitoring is also contributory.
Many diagnostic names for pneumonia, such as nosocomial pneumonia or HCAP, end up coding to the same thing. Higher reimbursement comes from billing for “Gram negative pneumonia,” which requires risk factors including being hospitalized and received IV antibiotics in the last 90 days, immunosuppressed (including diabetes, alcoholism, CHF, cirrhosis, chemotherapy, CKD, drug-induced neutropenia, chronic malnutrition), or have structural lung disease such as bronchiectasis. It also requires treating with an antibiotic that covers gram negatives, and treatment for 5 or more days. If you have all of this, you may be able to bill for “gram negative pneumonia.” Treatment can be presumptive and you may state this; actual culture data is not required for this, although it is supportive if available.
Diagnoses that are suspected but never fully proven can still be billed, particularly if they end up on a discharge summary.
When in doubt, more detail is always better in diagnostic labels.
Spell out your findings and reasoning and you’ll get more grace on your diagnoses.
Sepsis diagnoses are a mess. Reimbursers tend to like sepsis 3 definitions (qSOFA), core metrics may still use the older definitions. Many facilities may have their own policies on what definition to adopt. From a clinician’s perspective, at this point, you should probably just call it sepsis when you think it’s sepsis and let the billing will work itself out.
Document every diagnosis that contributes in any way to their current stay, even if your active management is minimal – it generally contributes to their risks and complexity.
In 2023, the whole billing paradigm is expected to change, with less emphasis on billing based on number of categories in the HPI, ROS, PE, etc, and complexity being instead based mainly on time and acuity.
Various providers can document diagnoses and all will count, but if there is dispute it will usually fall to the attending of record to make a final call.
The “case mix index” is an amalgamate of the overall complexity of your patient population, which is reviewed regularly and modifies overall reimbursement; this help capture complexities and costs of care beyond what’s shown by the specific DRGs. This is based on other diagnoses and factors; hence, document everything.
At the end of the day, you may not like the requirements for documentation and how it’s linked to reimbursement, but it is the way it is, and doing a poor job doesn’t mean the system will change – it just means your employer will be under-reimbursed, which in the end does affect you and your patients.
Discussing pleural effusions in the critically ill, including how and when to drain them, methods of drainage, interpreting laboratory studies, and managing complications, with Dr. Emily Fridenmaker (@emily_fri), pulmonologist and intensivist at Charleston Area Medical Center in West Virginia.
Continuing education for this episode
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CXR – underestimate
Lateral – 75mL (5-15 mL is normal)
AP – 175mL iii. 500mL for 100% sensitivity
CT – overestimate
Contrast can help delineate pleural surface
Ultrasound – goldilocks
Can see 5-50mL fluid
> 1cm generally safe to sample
Thora – no absolute contraindications
Should tap an effusion if you don’t know what’s causing it
Diagnostic or therapeutic
Does little to change hypoxia—can impact dyspnea though due to diaphragm length-tension relationships
Complication rate = ??
Nucleated cells – greater than 50k usually paraPNA/empyema
Lymphocytosis – TB, lymphoma, sarcoid, RA, yellow nail syndrome, chylothorax, cancer
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
3% saline is certainly safe and causes no issues with increases blood viscosity. It is safe through peripheral IVs as well.
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.
Improved overall fluid balance / UOP / hemodynamics in diverse settings.
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.
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