Category: Cases

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Best practices in care of the critically ill patient with COVID-19 pneumonia are not known at this time. However, practical lessons from the ground are filtering in from those who have seen many of these patients, and Dr. Nicole King—critical care anesthesiologist, ECMO-ologist at the University of Cincinnati, and alumnus of the New York City COVID surge—is here to walk us through her experiences.

Takeaway lessons

1. Do your swabs, cultures, and antigens to check for other viral and atypical pneumonias; other diseases still exist.
2. Check a D-dimer to stratify hypercoagulability.
3. Worsening tachypnea, distress, and ventilatory (not hypoxic) failure are a marker to upgrade care and/or intubate a borderline COVID patient.
4. Treat initially with steroids per the RECOVERY trial (dexamethasone 6 mg daily for 10 days); then, if needing ICU or especially if needing intubation, consider the DEXA-ARDS protocol (20 mg daily for 5 days, then 10 mg daily for another 5 days). You may consider remdesevir or convalescent plasma at this point in the science, but don’t expect too much effect.
5. Very prolonged courses on non-invasive positive pressure ventilation (CPAP/BiPAP) may be more acceptable here than in other diseases; although not very appealing it may be preferable to intubation. Try cycling on and off to improve tolerability. Consider an NG tube for nutrition.
6. However, beware of profoundly large tidal volumes in spontaneously breathing patients due to their remarkable air hunger, which may predispose to lung injury—spontaneous pneumothorax can occur even in these non-invasive patients.
7. When air hunger is profound, you may need to decide whether to sedate them to control tidal volumes, or allow (potentially harmful) large volumes, or try to limit them with the vent with the possible result of a dyssynchronous and air hungry patient.
8. It’s not clear whether intubation worsens outcomes, but it’s clear that the patients who require intubation seem to do very poorly; part of the reason may be selection for high-risk patients as we try to avoid intubating when possible, but part may be iatrogenesis from things like sedation and paralysis.
9. PEEP is not very high-yield on many of these patients—either they need little recruitment (good compliance) or their compliance is so poor they are minimally recruitable—but since they are frequently so borderline, they still often end up on high PEEPs because they need whatever little margin of recruitment it does provide.
10. APRV makes sense and may have a role, but you will generally need to avoid paralysis and lighten sedation, as CO2 can become very hard to manage without significant spontaneous breathing.
11. Prone early, when the lungs are still recruitable and salvageable. It’s unclear whether it’s beneficial for lung protection even when the benefit on oxygenation is not impressive. It can be logistically challenging due to obesity and hemodynamic instability.
12. If considering ECMO, do it early. A prolonged course (intubated >10–14 days or on high vent settings for >7 days) is a contraindication, as permanent lung injury has already set in and recovery is less likely. To achieve this, aggressively manage early with usual methods, then if they seem to be refractory, consider ECMO as soon as the trajectory is clear—don’t give them a “waiting period” of days/weeks of vent failure first.
13. VV ECMO is usually adequate, particularly if you cannulate early enough that cardiovascular collapse has not set in, and may limit the iatrogenic harms. Whether VA ECMO may have a role for those with PE and RV strain is unclear.
14. Early tracheostomy is reasonable, but it’s not a panacea—most patients still end up needing significant vent support, sedation, etc.
15. 20 days after their initial symptom onset, patients are likely no longer infectious and isolation precautions can be withdrawn, regardless of testing.
16. During and perhaps for a prolonged period after their peak illness, some of these patients will have a persistently elevated respiratory drive—tachypnea, high minute ventilations and work of breathing—that may not portend anything acutely untoward, or at least may not be preventable.
17. When patients start looking worse, look at the right heart, which will often be strained from high PEEP and/or the presence of PEs. Treat the latter, and consider inhaled pulmonary vasodilators.

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Initial approach, supportive care, risk stratification, and management of the troublesome complications for ruptured subarachnoid aneurysm, with Thomas Lawson (@TomLawsonNP), nurse practitioner in the neurocritical care unit at OSU Wexner Medical Center.

Takeaway lessons

1. SAH + shock or hypoxemia = suspect neurogenic pulmonary edema and/or Takotsubo cardiomyopathy.
2. Aneurysmal SAH is much different from traumatic and other etiologies of SAH. Not only does it require securing the aneurysm (early rebleeding is associated with substantially increased mortality), it conveys generally greater morbidity.
3. The “hanging chicken sign” at the base of the skull (across the basilar cisterns) is the most distinctive SAH finding on head CT. Look also for associated IPH or IVH, as well as signs of hydrocephalus, such as third ventricle enlargement or presence of a temporal horn in the lateral ventricles (normally just a faint C-shaped slit).
4. Use either the Hunt and Hess or WFNS scores to prognosticate mortality, while considering the Modified Fischer score to assess risk of vasospasm, a complication usually occurring between 3–14 days (sometimes up to 21) days after onset of symptoms.
5. With any acute neuro changes in the SAH patient, strongly consider the “stat stat” head CT to assess for rebleeding or worsening hydrocephalus. Also assess for functioning of an EVD, as an obstructed tube may indicate hydrocephalus as well.
6. For deterioration in later timeframes, go with a CTA (or transcranial dopplers) to assess for vasospasm. If present, talk to your neurointerventionalists about offering catheter-directed vasodilators, such as verapamil or nicardipine; also, augment the BP to perfuse past the spasm.
7. Many patients who spasm will continue to spasm. Watch diligently as some may need repeated neuro-intervention. IV milrinone and intra-thecal nicardipine (into an EVD) are available as last-ditch efforts.
8. CTA will not show thrombosed aneurysms; such patients need a catheter angiogram and/or repeat imaging.
9. “Triple H therapy” for SAH—hypertension, hypervolemia, and hypernatremia (or hemodilution) is dead. Just shoot for reasonable hypertension, plus euvolemia. Target a normal MAP and SBP <220.
10. Polyuria should prompt concern for cerebral salt wasting, which is often followed by vasospasm. It can be distinguished from SIADH by the presence of hypovolemia.
11. If a patient has no seizures noted, a 3–7 day course of anti-epileptics (e.g. levetiracetam) is reasonable. If they do seize, continue for longer.
12. EVDs can come out when the daily drainage is dwindling. Then wean by raising the pop-off by about 5 cm H2o per day, monitoring the neuro exam and perhaps CT scans. Once at 20 cm H2O, clamp it, then consider removal. Occasionally patients may have permanent dysfunction of their arachnoid granulations and need a VP shunt, although this must usually be placed in a delayed fashion to avoid blockage by proteinaceous CSF early on.

References

Consensus guidelines: Grasso G, Alafaci C, Macdonald RL. Management of aneurysmal subarachnoid hemorrhage: State of the art and future perspectives. Surg Neurol Int. 2017 Jan 19;8:11. doi: 10.4103/2152-7806.198738. Erratum in: Surg Neurol Int. 2017 Apr 26;8:71. PMID: 28217390; PMCID: PMC5288992.

IV milrinone: Lannes M, Teitelbaum J, del Pilar Cortés M, Cardoso M, Angle M. Milrinone and homeostasis to treat cerebral vasospasm associated with subarachnoid hemorrhage: the Montreal Neurological Hospital protocol. Neurocrit Care. 2012 Jun;16(3):354-62. doi: 10.1007/s12028-012-9701-5. PMID: 22528278.

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A patient with multiple abdominal gunshot wounds, resuscitated before and after damage control surgery by the legendary Scott Weingart (@emcrit): emergency physician, surgical intensivist by way of Shock Trauma in Baltimore, director of an emergency critical care program, and longtime innovator in medical education and FOAM via the EMCrit podcast and blog.

Our 1st anniversary episode!

Takeaway lessons

1. In an ideal world, penetrating abdominal trauma in an unstable patient would proceed directly to the OR with no delay by the ED. Resuscitation, obtaining access, and so forth can occur in the OR perioperatively.
2. Have a low threshold for activating the massive transfusion protocol. (A positive FAST would reinforce that decision.)
3. Venous access: an introducer sheath (Cordis) or dialysis catheter in the femoral or subclavian veins. Blind subclavian lines may be ideal but are a dying skill (ultrasound-guided subclavians are too slow). Femoral lines are somewhat less desirable with abdominal trauma as the IVC may be violated. Always use ultrasound for the fem. Ultrasound-guided IJ is okay if that’s all your people are comfortable with. Peripherals are okay, a RICC is better, but central access is most reliable.
4. Arterial access: consider an 18g femoral arterial line in the common femoral artery, allowing BP monitoring but also wire insertion in case endovascular procedures are needed, such as REBOA or IR embolization. A 16g arterial is a bit over-large but okay. 20g is okay but needs upsizing later.
5. Give TXA if within 1 hour (not 3 hours) of injury: 1 gram with the first unit of blood. (2 grams is an option too.) The need for the subsequent maintenance drip can be determined by TEG later.
6. Not too much role for TEG in the initial ED presentation. Takes too long for the “clot stability” portion to develop anyway. But it’s useful after surgery, during the post-acute phase.
7. A secondary CT scan, even performed after initial damage control surgery, can be very useful to localize non-obvious lesions which may require a secondary repair. If not performed, a careful clinical tertiary survey is mandatory to evaluate for extremity perfusion (i.e. a missed vascular injury) and other injuries not noted during surgical exploration.
8. Labs are slow. Point of care labs are a little better. During the most acute period, mostly transfuse to target vitals (MAP >65 or so). As they begin to achieve hemostasis, things slow down, and it start to become possible to follow labs. Continue to use a balanced ratio unless you can use TEG to guide FFP and platelets.
9. Check body temperature and use forced-air rewarming if needed.
10. Some degree of distributive shock can result from the post-traumatic inflammatory (SIRS) response, especially downstream of the first hour or two. Vasopressin may be the first line agent for this, as many trauma patients are vasopressin-depleted. Still, assume all shock is hemorrhagic until proven otherwise. Skin temperature helps some, as vasodilation = warm but hypovolemia = cold. As volume is replaced, vasopressors come off, and perfusion overall improves; a “good” BP with ice-cold extremities is still in shock and still organ-injurious.
11. Most importantly, shock is a vicious cycle, so the sooner you can correct hypoperfusion, the less secondary distributive shock and organ failure you’re likely to see down the road.
12. Push calcium chloride to maintain a normal ionized calcium, which may have a nice BP effect as well.
13. Use ultrasound (as windows allow), particularly to rule out the need for inotropes.
14. Empiric cryo not a bad idea early. Later, use either TEG or labs, in which case target a fibrinogen level of >150 or even >200.
15. Consider PCCs (KCentra) if: 1. FFP is delayed or unavailable; 2. Very behind in resuscitation (i.e. unbalanced resuscitation or lots of crystalloid so far); 3. Patient is on warfarin; 4. Cirrhotics.
16. Activated Factor VII (NovoSeven) probably has no role at this point. It makes transient clots, but not durable ones, and causes pathologic thrombi; outcomes are poor. PCCs including activated VII is probably better, if you must.
17. Autotransfusion (i.e. from chest tube drainage) is a logistical pain, clotty, and really only a substitute for PRBCs, since after hitting the container it contains almost no clotting factors or platelets. Usually not worth the bother. Banked whole blood would be much better, but is also a logistical challenge from a systems perspective.
18. Serious ongoing bleeding in excess what can be matched with a properly-executed MTP is probably a soft indication to surgically reexplore, or at least consider imaging for missed injuries, since purely “medical” bleeding will infrequently be so brisk. Particularly when the initial exploration was in the setting of serious multi-trauma, missing an injury is common, particularly when they’re under-resuscitated (and hence “permissively” hypotensive) at the time of exploration.
19. If you must give crystalloid instead of blood, consider hypertonic saline, preferably buffered.
20. Tolerating a lower MAP (maybe down to 50–55) may be better than giving high doses of vasopressors or crystalloid while waiting for blood. If bleeding seems to have stopped, however, you might start treating hypotension as purely distributive shock and allow higher vasopressor doses.
21. In a young trauma patient with good baseline condition, aggressive curative care is probably ethical almost ad infinitum. It’s often reasonable to continue efforts until they arrest and die or resources are exhausted.
22. The truly sick trauma patient does not “take a joke,” and absolutely requires your undivided attention and the most astute, timely, on-the-ball care you can provide. Your normal “max effort” is not enough; like a lazy runner, you need to push and find your true limits in order to save these people.

References

1. The ICU trauma resuscitation: More reading on the post-op resuscitation process.

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Looking at the workflow of a fresh post-op open heart surgery patient, as well as what to do when it devolves into cardiac tamponade, with (returning) guest Brendan Riordan, cardiothoracic ICU PA (@concernecus) at the University of Washington, and his NP colleague Kris Ramilo (@krsrml0).

[Audio quality was a bit dodgy in this one; sorry all!–eds.]

Takeaway lessons

1. Handoff from the OR to ICU team is a tricky time, and should ideally be somewhat formalized, involve both surgical and anesthesia teams at the bedside, and including talk about what happened, what they expect, and things to look out for.
2. The ERAS (Early Recovery After Surgery) protocol has entered the CT surgery world as ERACS, including post-op measures for typical cases such as reversal of neuromuscular blockade and a 4-hour target for extubation (versus the usual 6 hours). Most routine cases will aim to be “bloodless,” i.e. only transfusing autologous (“Cell Saver” blood), as transfusion of banked blood is considered an STS measure.
3. Milking or stripping chest tubes during the immediate post-op period to maintain patency may or may not be necessary as a routine practice, but should certainly be attempted if output drops or tamponade is suspected.
4. Point-of-care TTE is always difficult in these patients, due to their windows being obscured by dressings; the apical 4-chamber will often be the most useful view. When seriously considering graft failure, TEE may be valuable to diagnose graft failure (by noting regional wall motion abnormality), as well as appreciating cardiac tamponade.
5. As in all cases, tamponade in this setting is diagnosed by echocardiographic pericardial effusion plus signs of tamponade physiology (chamber collapse, etc), with the caveat that effusions may be loculated or unusual-appearing due to the recent violation of the pericardium.
6. With a PA catheter, remember that narrowing of the PA pulse pressure and convergence of the CVP and PA pressures (particularly via a falling PA pressure) is classic for tamponade physiology.
7. Resternotomy is not something to be undertaken lightly, but still must be performed immediately and aggressively when indicated. Close involvement with the surgical team is usually essential to make this decision.
8. Adding an inotrope can be somewhat diagnostic, as patients with mere myocardial stunning will improve, whereas patients with tamponade will generally have little response.
9. Give calcium chloride freely to the unstable post-cardiac surgery patient.
10. Be aggressive with fluid resuscitation and consider epinephrine up to 0.06–0.08 mcg/kg/min or dopamine (if you must) up to 3–5 mcg/kg/minute.
11. The purpose of reopening the chest is to avoid external chest compressions, which tend to abuse RCA grafts (which sit just below the sternotomy wires), and are generally ineffective anyway compared to internal cardiac massage, since the pressure chamber of the chest is not intact.
12. The role of the ICU team while the surgical team reopens the chest is typically to assist with sedation, ventilator management, and hemodynamics. Anesthesia may or may not be present but is often performing TEE.
13. Patients reopened at the bedside will often be left with open chests, and planned to return back to the OR for washout and closure the next day. Plan on prophylactic antibiotics (e.g. vancomycin).

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A few rapid-fire cases from the emergency department, with Dr. Seth Trueger (@mdaware), emergency physician at Northwestern University and digital media editor for JAMA Network Open.

[Sorry for the shotty audio quality in this one!–eds.]

Takeaway lessons

1. Many decisions in the ED are less about what to do, and more about when to do it. Time and location are key considerations for efficient care.
2. Goals of care starts in the ED, and not with lip service. Yes, temporize with supportive care while you go through the process, but do the work—find a legitimate representative or documentation of the patient’s wishes to determine what they’d want before you commit them to lengthy, aggressive life support. Aggressive but non-invasive medical care may also strike a good balance, keep everyone happy, and often avoid the need for invasive measures.
3. Over 1/3 of patients 65+ in the ED (excluding trauma and cardiac arrest) will die during that admission within 3 days.
4. The best ED provider intubates the “right” number of patients, while bad ones may intubate either too few or too many.
5. While ethically, extubating and withholding intubation should be equivalent, in practice the former feels more difficult.
6. Emergency staff have limited bandwidth. Evaluate the opportunity cost of everything you do. It’s not about whether it’s valuable or indicated; is it more valuable than whatever you or the nurses could be doing instead?
7. “Where is this patient going?” is always, ultimately, the main question of the EM provider. This differs from the main questions of many of their consulting and admitting specialties.
8. ICU time and ED time are different. In the ED, the ability to limit the amount of work is itself limited, so the judicious provider needs to jealously protect that time. In the ICU, we have a useful (albeit sometimes flexible) cap: our total number of beds.
9. Remember that nobody sees anyone else’s denominator. How many patients the ED sends home, how many consults don’t get called, how many floor patients are managed there instead of coming to the unit; these blind spots tend to promote small-mindedness and inter-disciplinary judgment.

References

Patel KK, Young L, Howell EH, et al. Characteristics and Outcomes of Patients Presenting With Hypertensive Urgency in the Office Setting. JAMA Intern Med. 2016;176(7):981–988. doi:10.1001/jamainternmed.2016.1509

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A look at oncology-related emergencies in the ICU, with Leon Chen (@CCMNP), NYC nurse practitioner specializing in oncology critical care.

Takeaway lessons

1. Extremely elevated leukocyte count should always raise suspicion for a “liquid tumor” such as leukemia.
2. The principal acute complication is leukostasis from poor flow, potentially causing hyperviscosity issues such as stroke, MI, pulmonary embolism, and mesenteric ischemia. Such patients are (despite their white count) also functionally immunosuppressed and at risk for infectious complications.
3. Fungal infection is not uncommon, but does not necessarily need empiric coverage up front.
4. Don’t hesitate to be broad with your investigations. Feel free to CT widely, cover broadly with antimicrobials, etc. Consider bronchoscopy for BAL.
5. Tumor lysis syndrome is always a possibility and can occur spontaneously in patients with such extreme leukocyte elevations. Check labs such as BMP, magnesium, calcium, phosphate, LDH, and uric acid every ~4 hours at first; however, the risk is probably highest for lysis when the white count begins to fall (e.g. due to initiating treatment).
6. Tumor lysis is much more common with liquid than solid tumors, and much more with certain chemotherapy regimens.
7. Extreme leukocytosis can cause “leukocyte larceny,” where blood gasses demonstrate false hypoxemia due to leukocytes consuming oxygen in the sample before it can be processed. Pulse oximetry is more reliable.
8. Spurious “pseuohyperkalemia” can also occur due to lysis of delicate immature leukocytes. This can be resolved with whole blood samples or point-of-care assays, which decrease transport time and sample agitation.
9. Uric acid is associated with renal injury and may need medical treatment. Allopurinol prophylaxis is generally safe, but rasburicase is the treatment of choice if uric acid is very high. LDH elevation is benign but are a good marker of response to treatment, as it should drop with appropriate chemotherapy.
10. Pulmonary hyperviscosity usually results in clear lungs on imaging. If infiltrates are present, consider infection. Also consider PCP pneumonia and fungal studies.
11. Leukapheresis, a dialysis-like process, involves selective removal of leukocytes to reduce viscosity.
12. Prophylaxis: Bactrim is a good choice for PCP, but beware of hyperkalemia. Atovaquone, pentamidine are next line options. Acyclovir for viral prophylaxis and posaconazole for fungal (galactomannan and beta-d glucan are helpful)
13. The blast count is suggestive of leukemia, but definite diagnosis will require bone marrow biopsy.
14. Initial stabilization of this sort of oncologic emergency is within the bailiwick of most hospitals, but it’s reasonable to then consider transfer to a specialty oncology center for the focused treatments like leukapheresis and chemotherapy.

References

A good, free review: Klemencic S, Perkins J. Diagnosis and Management of Oncologic Emergencies. West J Emerg Med. 2019 Mar;20(2):316-322. doi: 10.5811/westjem.2018.12.37335. Epub 2019 Feb 14. PMID: 30881552; PMCID: PMC6404710.

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The second part of our 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 some common IR procedures, namely abscess drainage and GI bleeding. Listen to part 1 here.

Takeaway lessons

1. Common goals would be INR <2.0, platelets >50k. If leaving an indwelling line or device, less may be okay, as it will tamponade the spot. Ignore the INR completely for purely cirrhotic patients. Although guidelines are fairly clear, many clinicians use their own rules.
2. Fluid collections are abscesses if they have rim enhancement on contrast CT. Without contrast you’re left guessing. (No oral contrast please!)
3. If necessary, most collections can be drained, somehow. Relevant considerations such as anatomy are subtle and often operator-dependent. Move the bladder out of the way by draining it, move bowel by hydrodissection, go in transvaginally or transrectally… options are numerous but not universal. Talk to your proceduralist.
4. When hoping to find and embolize bleeding, you’re usually best to start with a CTA. You need two phases, so non-contrast and arterial, or arterial and delayed, or… whatever. (No oral contrast please!) But find the bleeding. CTA is more sensitive than catheter angiography, and gives a general idea as to the region of bleeding. Going straight to IR without the CTA and without even a general idea of the region means a looong process of searching by catheterizing numerous vessels. Skipping the CTA isn’t even necessarily contrast-sparing, as it may take several hundred cc’s of contrast just to find the source.
5. With gastric bleeding, usually start with femoral artery access, access the celiac trunk, find the left gastric artery, then either just empirically start placing some gelfoam to reduce arterial pressure, or localize the specifically bleeding vessel if possible.

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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.

Takeaway lessons

1. 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.
2. 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.”
3. 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.
4. For nearly every vascular access attempt: ultrasound guidance, short-axis view, micropuncture needle.
5. 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.
6. 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.
7. 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.

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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.

Takeaway lessons

1. When treating liver patients, think infection, infection, infection—and understand that with good care and reversal of the underlying cause, they can get better.
2. Lactulose is always the first line agent for hepatic encephalopathy. Rifaximin is a potential adjunct.
3. 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.
4. MELD is a useful tool for prognostication, but an admittedly blunt one that fluctuates in response to many factors.
5. 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. Bleeding from paracentesis is extremely rare, and generally due to mechanical reasons (usually puncturing a vessel), not coagulopathy. Just tap them!
12. 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.
13. >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.
14. Look outside the abdomen for infection too, with blood cultures, chest xrays, etc.
15. 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.
16. 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.
17. Since toxins are also cleared through the urine, address AKI as well. Consider fluids: 1.5g/kg of 25% albumin on day 1.
18. Hepatorenal syndrome is treated by norepinephrine (maybe terlipressin if you’re in the UK). Granted, many of these patients are already on it.
19. 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.
20. MARS, or “liver dialysis” with hepatoblastoma cells in the filter, is interesting, but so far the evidence remains negative.

References

SIR Guidelines on paracentesis in coagulopathy: Patel IJ, Rahim S, Davidson JC, et al. Society of Interventional Radiology Consensus Guidelines for the Periprocedural Management of Thrombotic and Bleeding Risk in Patients Undergoing Percutaneous Image-Guided Interventions-Part II: Recommendations: Endorsed by the Canadian Association for Interventional Radiology and the Cardiovascular and Interventional Radiological Society of Europe. J Vasc Interv Radiol. 2019;30(8):1168-1184.e1. doi:10.1016/j.jvir.2019.04.017

Importance of early paracentesis: Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol. 2014;109(9):1436-1442. doi:10.1038/ajg.2014.212

Failure to perform paracentesis is associated with increased mortality: Orman ES, Hayashi PH, Bataller R, Barritt AS 4th. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol. 2014;12(3):496-503.e1. doi:10.1016/j.cgh.2013.08.025

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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.

Takeaway lessons

1. 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.
2. 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.
3. 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.
4. 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.

References

Nestor MA, Boling B. Reversing Direct Oral Anticoagulants in Acute Intracranial Hemorrhage. Crit Care Nurse. 2019 39 (3): e1–e8.

ENLS Intracranial Hypertension and Herniation Protocol

ICH score