An overview of interventional radiology with Dr. Bobby Chiong, board-certified interventional radiologist and chair of radiology at SBH Health System, with a focused look at what IR’s all about, coordination between care teams, vascular access, and troubleshooting.
Interventional radiologists can’t do everything, but they potentially can do almost anything, and you usually won’t know what’s possible unless you ask. They have the potential to play a role in many situations which we never realize. Even if just a consultation to discuss a case (particularly in complex, multi-disciplinary situations), a good IR will be happy to have a conversation.
Quote of the episode: “There’s all kind of procedures that I can do that you’ve never heard of… but I can’t tell you about them all, because there’s a lot of them.”
Bridging the gap between primary teams and IR is best accomplished by building relationships. Get to know your interventional radiologists, speak to them in person, and make an effort to reach out to them rather than just typing in an order and awaiting magic.
For nearly every vascular access attempt: ultrasound guidance, short-axis view, micropuncture needle.
Fluoroscopy helps vascular access by ensuring correct depth of the wire and catheter and the correct vessel each step of the way. You can live without it, but it’s a big help.
Can’t advance a wire? You’re not intravascular (dissecting the vessel, in the subcutaneous, or through the backwall), or you’re against a valve (try spinning the wire), or you’re hitting some stenosis or thrombosis.
One reason IR gets lines you can’t is by setting up their ultrasound properly. Spend some time with a radiologist or ultrasound tech to learn to really optimize your view. They also have a whole lot of options for needles and wires you probably don’t, and subtle differences in wire stiffness, needle bevels, etc may make the difference.
A detailed look at cirrhosis and acute-on-chronic liver failure as we typically see it in the ICU, with Dr. Elliott Tapper, gastroenterologist and transplant hepatologist, and director of the cirrhosis program at the University of Michigan in Ann Arbor.
When treating liver patients, think infection, infection, infection—and understand that with good care and reversal of the underlying cause, they can get better.
Lactulose is always the first line agent for hepatic encephalopathy. Rifaximin is a potential adjunct.
Ammonia levels are prone to sampling errors and correlate poorly with clinical encephalopathy. Although it may cause fights, there’s usually little value in monitoring it.
MELD is a useful tool for prognostication, but an admittedly blunt one that fluctuates in response to many factors.
AST tends to be higher than ALT in alcoholic hepatitis, partly because alcohol metabolism depletes B6, which is needed for ALT production. Cirrhosis also increases the halflife of AST. However, alcohol use is usually most easily detected from the history, not by comparing labs.
AST or ALT in the thousands is usually due to causes other than alcoholic hepatitis. In the hospital, rule out obstruction with an ultrasound, consider drug reaction, and consider clots (e.g. portal vein thrombosis), although this last isn’t the most common.
The most common cause of extrmely elevated liver enzymes in-hospital is probably cardiogenic shock, particularly some combination of system hypotension and venous congestion. Since portal vein pressures are intrinsically low, it doesn’t take much venous congestion to counter that flow gradient, leaving only the hepatic artery for perfusion. Unfortunately, the arterial circulation usually only provides about 20-30% of hepatic perfusion, which leaves the liver vulnerable to systemic hypotension.
Exacerbations of cirrhosis and liver failure most often present due to infection. Imbalances of fluid (i.e. hyper- or hypo-volemic) are common as well.
Diagnostic paracentesis is mandatory for these patients to rule out SBP. Every hour it’s delayed may increase mortality. Empiric treatment alone is not adequate (agents like ceftriaxone will often be the wrong choice). Overall, those who undergo paracentesis are less likely to die in the hospital.
The AGA (American Gastroenterology Association), AASLD (American Association for the Study of Liver Diseases), and SIR (Society of Interventional Radiology) all agree: not only is paracentesis generally safe in cirrhotic “coagulopathy,” providers should not even consider the INR when assessing risk. This number only reflects a portion of the clotting cascade, but does not show the “rebalancing” caused by other factors, such as increased platelet activity and increased factor VIII production. The net result is generally an increased tendency for clotting, not bleeding, unless other coagulopathic processes are present.
Bleeding from paracentesis is extremely rare, and generally due to mechanical reasons (usually puncturing a vessel), not coagulopathy. Just tap them!
When diagnosing new ascites, a SAAG >1.1 is usually due to portal hypertension, but can also be caused by heart failure (congestive hepatopathy). Total protein >2.5 in ascites is more suggestive of ascites.
>250 polys and positive culture in ascites is diagnostic of SBP. Innoculating culture bottles at the bedside increases the yield compared to just filling tubes.
Look outside the abdomen for infection too, with blood cultures, chest xrays, etc.
Alcoholic hepatitis per se may (maybe) be treated with steroids, but infection, renal injury, and other factors are relative contraindications. In any case, steroid treatment is not emergent and can be instituted after a day or two for the picture to settle. Consider the Lille score after 4 days to see if it’s worth continuing for a full 28 days.
In hepatic encephalopathy, a true induction dose of lactulose is needed. Consider 60ml q2h until they’re pooping or waking up. If they don’t wake up in 6 hours or so, this is more likely to be toxic encephalopathy from infection.
Since toxins are also cleared through the urine, address AKI as well. Consider fluids: 1.5g/kg of 25% albumin on day 1.
Hepatorenal syndrome is treated by norepinephrine (maybe terlipressin if you’re in the UK). Granted, many of these patients are already on it.
Liver transplant for alcoholic hepatitis can be tricky, but isn’t impossible at all, even in patients actively drinking up until their hospitalization. Attitudes toward this depend highly on the culture of the transplant center. The best candidates are those who have not yet had a full chance to engage with relapse prevention and substance use disorder care, and all of their medical processes should be either resolved or diagnosed (i.e. their primary problem should now be their liver failure, the causes of which should be clear, and there are no active infections or other processes that would threaten the transplant). Such patients certainly may be a risk for relapse, but will at least be alive to try. And ICU patients are likely to be sick enough to jump to the top of transplant lists. Don’t assume that transplant is impossible; discuss with the transplant team and let them decide.
MARS, or “liver dialysis” with hepatoblastoma cells in the filter, is interesting, but so far the evidence remains negative.
The conclusion of our scenario of severe intraparenchymal hemorrhage with resulting herniation, with a closer look at neurological exams, prognostication, and the flow of care after initial stabilization, as well as our mindset as caregivers in these psychologically challenging cases.
Early tracheostomy may not hold concrete benefits for neuro patients (i.e. improved mortality), but it often facilitates practical goals such as earlier liberation from the ventilator, early mobilization, and earlier discharge to rehab, which do have tangible utility.
Give frequent updates to family in cases of significant intracranial catastrophe. Avoid specific early prognostication unless the outcome is very obvious, but do emphasize poor prognostic signs, the importance of patience and endurance, and the likely quality of life given the available data.
Altered mental status is not always a contraindication to extubation in the persistently neuro-injured patient, although some such patients will indeed have difficulty protecting their airways.
These patients do improve, often after their ICU stay. Post-ICU follow-up is helpful to remind us of this, and when not possible, it’s good to simply remember that the ICU courses we perceive don’t always reflect eventual recovery.
A typical case of severe intraparenchymal hemorrhage with resulting herniation.
DOACs like apixaban (Eliquis), although not usually monitored using routine coagulation assays, tend to elevate the INR only slightly (e.g. 1.0–1.3 or so). A strikingly INR in warfarin-like ranges should raise suspicion for an additional occult cause of coagulopathy.
Manage elevated ICPs using the ENLS “tiered” approach. All neurosurgical patients should receive the tier 0 (basic management) therapies.
In the neuro-injured patient, seek “euboxia” to limit further brain injury: normal pH, normal PCO2, normal PaO2, normal BP, normal temperature etc.
Be wary relying solely upon the GCS to describe, or even to trend neurological function. A descriptive, granular survey of function (particularly motor function) is usually more useful, as well as easier to remember.
Part two of our interfacility transfer from Hell. Tyler Christifulli, FP-C, EMT-P (@christifulli88) and Sam Ireland FP-C, EMT-P (@ireland_sam1) show us how they handle GI bleeding, arrhythmias, shock, cardiac arrest, and more, all from the confines of a helicopter. Listen to Part 1 here.
Check out the great educational content from Tyler and Sam over at FOAMfrat, including blogs, podcasts, and online EMS continuing education.
When faced with an unstable patient in a wide complex tachycardia, stop thinking and just shock it.
As the nature of the transport (and the patient) changes, change your focus with it. The initial diagnosis is a starting point, not a headline.
Consider esmolol as an easily-titratable means of rate control in unstable patients.
Communicate ahead with the receiving hospital if urgent interventions will be needed upon your arrival.
Non-invasive positive pressure ventilation offers a preview of the hemodynamic response to intubation.
A grueling interfacility transfer gives Tyler Christifulli, FP-C, EMT-P (@christifulli88) and Sam Ireland FP-C, EMT-P (@ireland_sam1) the opportunity to show us how they handle airway management, GI bleeding, mechanical ventilation, cardiac arrest, and more, all from the confines of a helicopter.
Check out the great educational content from Tyler and Sam over at FOAMfrat, including blogs, podcasts, and online EMS continuing education.
Prepare the best you can before departing the sending facility, while acknowledging that that time may be a factor, and that some things can’t be predicted.
The close attention by 1:1 (or more) clinicians possible during critical care transport allows some issues, such as borderline airways, to be managed by close observation rather than early intervention.
Due to the limited medications and lab studies available, particular care should be used when managing DKA. Insulin therapy should target gentle glucose correction to avoid precipitous changes in pH, osmolarity, potassium, etc.
Transport medicine, whether from the back of an ambulance, helicopter, jet, or rickshaw, is an austere environment. Personnel, equipment, and time are all limited. A thoughtful approach to logistics, prioritization, workflow, timing, and detail is at least as important as a high-level understanding of pathology.
A restless patient experiences a series of dyssynchrony events during mechanical ventilation. Come see how Bryan wades through it all, and allow us to offer an academic, yet practical approach to this sometimes-confusing subject.
Start with ABCs and stabilizing the patient, then put on your thinking cap and try to optimize synchrony. It’ll reduce sedation requirements, lessen the risk of lung injury, and prevent mechanical ventilation from feeling like black magic.
Sedation is a last resort, but sometimes needed if the patient wants something (e.g. more volume) that we think is unwise.
Most dyssynchrony is the patient fighting the ventilator, so it can often be managed by allowing the patient to determine more variables within the breath. Go from volume control to pressure control, or pressure control to pressure support.
Sometimes, you won’t figure it out.
In the decompensating patient, use DOPES to remember the causes
D isplaced tube
O bstructed tube
E quipment failure
S tacking of breaths
Remember “peak pressure apnea,” a phenomenon of iatrogenic hypoventilation caused by the high pressure alarm setting.
The second piece of our in-depth look at the management of right heart failure, with a focus on preserving peri-intubation hemodynamics using the SAVIOR protocol—featuring its co-creator, anesthesiologist and intensivist from the University of Kentucky, Habib Srour. Check out part 1 here.
You don’t want to intubate patients with right heart failure, but if you do, you don’t want to do it in a hurry; a well-prepared approach will be far safer. That means doing it at the right time, not sooner and not later, and making what preparations you can before they’re needed.
Using awake intubation to gently transitioning from spontaneous breathing to mechanical ventilation via up-titration of pressure support (starting at zero) offers a gradual, reversible approach.
Sedation is often not needed for intubation. The KPET rule gives guidance if desired, but really only applies in isolation; combining drugs creates synergy in their effect and less is often needed.
An in-depth look at the management of right heart failure, with a focus on preserving peri-intubation hemodynamics using the SAVIOR protocol—featuring its co-creator, anesthesiologist and intensivist from the University of Kentucky, Habib Srour.
When facing undifferentiated shock and a complex picture, look for one point of data to help distinguish the etiology. Try touching the feet: cold is a good indicator of a significant cardiogenic component.
The flip side of hypoxic vasoconstriction is hyperoxic vasodilation of the pulmonary vasculature—i.e. an overly high FiO2 will tend to worsen V/Q matching.
To hemodynamically manage RV failure without worsening RV afterload, consider the Rule of 8s cocktail:
Epinephrine .08 mcg/kg/min
Dopamine 8 mcg/kg/min
Vasopressin .08 units/min
Inhaled epoprostenol (Veletri/Flolan) 8 ml/hr
The “lung pump” of negative pressure respiration provides a substantial amount of cardiac output, particularly in the setting of RV failure. Paralysis, sedation, and intubation removes this. The period of apnea also worsens acidosis which increases PVR.
The dead space to tidal volume ratio increases by at least 50% after intubation; it will be impossible to match an already-high spontaneous minute ventilation on the ventilator.