Critical Care Scenarios

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We talk about diagnosis, treatment, and subsequent care of the patient with bacterial meningitis, with Emory neurointensivist Casey Albin, MD (@caseyalbin).

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Takeaway lessons

1. Many septic patients have altered mental status, but suspicion should be raised for CNS infection when there is also: headache, photophobia, vomiting, or any possibility of seizure activity.
2. Meningitis and encephalitis are separate entities usually involving different organisms, different imaging findings, and with different prognostic implications and downstream complications. However, at the early diagnostic stage, they can be largely lumped together.
3. Empiric antimicrobials must consider CNS penetration. Piperacillin/tazobactam (ie Zosyn) has very little. Ceftriaxone is better. Cefepime is fine, although the prospect of cefepime neurotoxicity may make neurologists leery; ceftazidime is fine too. Add vancomycin (not necessarily for MRSA but for resistant Strep pneumo), acyclovir (for HSV), and a liberal approach to adding ampicillin for Listenia for anybody older, immunocompromised, or in the midst of an outbreak.
4. Dexamethasone has been shown to reduce hearing loss after Strep pneumo meningitis. If suspicion for meningitis is strong early, it’s reasonable to give early (before or concurrent with antibiotics). It’s probably not worth giving >24 hours later.
5. The main benefit of lumbar puncture is to allow stopping or narrowing antimicrobials without treating with the entire empiric cocktail for a full two weeks. (There is also the chance of identifying a resistance organism.)
6. Ideally, LP is done before antimicrobials. However, if non-culture-based diagnostics are available such as PCR panels, successful diagnosis can often occur even after antibiotic administration. It’s worth doing the LP even if late and no PCR is available, as the signature of protein, glucose, etc will often still be useful. (At least, up front in a patient who might have CNS infection, avoid creating new obstacles like loading them with anticoagulation, antiplatelets, low molecular weight heparin, etc.)
7. Most patients will already have a CT head performed before LP is considered, making the question of whether this is necessary (to assess risk of downward herniation) fairly moot. However, if not, it should probably be done prior to LP in anyone with an altered level of consciousness.
8. Order from all CSF: Gram stain and culture, cell counts (first and last tubes), glucose, protein, and HSV PCR. (VZV generally does not cause clinical meningitis per se, usually causing a meningitis vasculitis, e.g. in someone with small-vessel strokes.) If available, order PCR arrays too, although some centers may not run it unless the CSF WBC count is elevated (e.g. >5). In a patient with any immunocompromise, test for cryptococcus as well. Other immunosuppressed testing is case-specific.
9. Always measure opening pressure. This is not accurate in a patient sitting up. While technically possible to puncture a patient sitting up, then rotate them with assistance to lay flat, it’s not easy or elegant. In a sick patient, just do the LP laying down.
10. Remember that opening pressure is measured at the bedside in centimeters of water, but should be converted to millimeters of mercury to be clinically applicable.
11. Draw at least 20 cc of CSF in all cases. If opening pressure is high (and CT not concerning), fill the four tubes (~36 cc) and measure the closing pressure. Few patients are harmed by draining <40 cc. Draining >40-50 can create some risk for herniation or hemorrhage (eg small subdural hemorrhage) and should not be done thoughtlessly.
12. Meaningfully elevated CSF protein should not just be “high,” but should exceed the patient’s age.
13. Any meningitis patient with an altered mental status should at least have a spot EEG, and possibly long-term EEG depending on the findings.
14. Any meningitis patient with a high opening pressure on LP, who is sufficiently obtunded to be intubated, should be considered for invasive ICP monitoring (e.g. EVD), if available. Otherwise, close monitoring for ICP crisis with neuro and pupil checks and serial CT scans.
15. Treating high ICP in meningitis with EVD or lumbar drain is often appropriate.
16. Any neurologic deterioration after antibiotics and other initial care is very likely either seizure or ICP crisis. These are fixable patients; diagnose and treat these complications aggressively.
17. Transcranial doppler may be a useful non-invasive screen for elevated ICP, by revealing a high-resistance waveform (high pulsatility index) as ICP increases.

Resources

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We discuss the practical barriers to implementing the A-F ICU liberation bundle, with Kali Dayton, ACNP-BC (@daytonicu), host of the Walking Home from the ICU podcast, and consultant to ICUs working on these issues.

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We discuss transfusion reactions, risks, and management, including infection, consent, TRALI, TACO, and hemolytic reactions—with Dr. Joe Chaffin (@bloodbankguy), the “Blood Bank Guy” and transfusion medicine specialist.

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Takeaway lessons

1. The risk of transfusion-related infection (HIV, hepatitis B, and hepatitis C) is around 1 in 3 million.
2. Acute hemolytic transfusion reactions (usually due to clerical errors or unit mix-ups) occur about 1 in every 75 or 76 thousand transfusions. Mortality is only one per million or so, however.
3. Simple febrile transfusion reactions occur about 1/100-300 transfusions.
4. Transfusion is always slightly immunosuppressing, perhaps increasing risk of post-op infection, cancer recurrence, etc. This effect is real, but small and not easily quantified.
5. Urticarial reactions (hives) seem trivial to clinicians, but can be very frightening to patients, even causing them to refuse future transfusions.
6. 80% of hemolytic reactions initially present with only fever, perhaps some chills. There is no way to differentiate from non-hemolytic febrile reaction at this stage. While the odds favor a non-hemolytic reaction, if you presume this and continue your transfusions, you are relying on luck, and you will eventually be wrong, which would be an indefensible medical error.
7. Once a hemolytic reaction is obvious, you waited too long. The main determinant of mortality after hemolytic transfusion reaction is the volume of blood transfused.
8. Typical workup for a febrile, possible hemolytic reaction is to confirm the labels and clerical match, then return the blood to the blood bank, where they will check patient blood for hemolysis, direct Coomb’s, and usually repeating the ABO/Rh testing. This can cause a delay in transfusion and maybe loss of the unit of blood; by typical regulations, once blood is removed from the blood bank or portable cooler, it must be transfused within 4 hours or wasted.
9. The hallmark of ABO mismatch is severe intravascular hemolysis. Most other hemolytic reactions yield extravascular hemolysis, e.g. in the spleen. Cytokine storm will be be seen. Compared to the myoglobin released in rhabdomyolysis, the free hemoglobin released in intravascular hemolysis is not quite as nephrotoxic (the resulting AKI may be more related to shock than from direct toxicity).
10. Hemolysis is only destructive to the transfused blood, so anemia per se generally does not develop. One exception can occur in sickle cell patients, where transfusion can induce a “hyperhemolysis” phenomenon where native red cells are also hemolyzed.
11. Mortality from acute hemolytic reactions is fairly low in previously healthy patients. Patients already critically ill may not do as well.
12. TRALI is mostly diagnosed by consensus criteria. “Definitive” TRALI (there is no longer a less definite category) is defined as:
    • No evidence of lung injury prior to transfusion
    • Onset within 6 hours after end of transfusion
    • P/F ratio <300 or SaO2 <92% on room air
    • Radiographic evidence of bilateral infiltrates with no evidence of left atrial dysfunction
13. The challenge when hypoxia occurs after transfusion is usually to distinguish TRALI from TACO. The latter is mere volume overload; the former occurs when pre-existing inflammation primes neutrophils for activation in the lungs, whereupon factors in the transfused blood causes neutrophil activation as a second hit. The most common of these triggers is incompatible anti-HLA antibodies in the transfused blood.
14. TRALI is largely a clinical diagnosis. However, if a case of possible TRALI is reported, the donor will be investigated and potentially screened for anti-HLA antibodies (something usually not done without a suspicious case). Other products from that donor will also be recalled from the bank. Report your possible TRALI cases!
15. Now that female donors with previous pregnancies are excluded from donating plasma (without HLA screening), the old truism that plasma-rich products (e.g. FFP or platelets) are the highest risk for inducing TRALI is no longer true; the most common precipitant is PRBCs. Any product can induce TRALI, however, including HLA antibody-negative products.

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We talk the nitty-gritty of assessing the right heart using echocardiography, with our friend Matt Siuba (@msiuba), intensivist at the Cleveland Clinic and master of zentensivism.

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Takeaway lessons

1. RV echo starts with evaluating three things: size, squeeze, and septal kinetics.
   • Size should be <2/3 the LV
   • Squeeze can be assessed in a variety of ways
   • The septum should not be bowing into the LV.
2. Dilation is an early and somewhat compensatory finding, and can be used as a screening test (the “D-dimer of RV dysfunction”). Septal changes are probably later and more of a sign of dysfunction (i.e. not compensatory).
3. Evaluating the RV’s ejection fraction is impractical due to its complex shape (without 3D echo or cardiac MRI or other advanced tools). So methods like TAPSE that reduce it to its longitudinal function become a more practical surrogate.
4. TAPSE is not an isolated marker of RV contractility, but a marker of the overall RV-PA unit. However, this is probably a feature, not a failure. You don’t really want to know how the RV is contracting in the abstract, but how it’s contracting in its current loading conditions. So TAPSE will vary by afterload and preload, but not artifactually—i.e. if the loading conditions change and TAPSE improves, then contractility is better in the current conditions.
5. s’ is similar to TAPSE, and similarly limited (mainly evaluating longitudinal function). It assesses velocity, not movement, which theoretically may represent something different (maybe a better marker of function?), although that difference is not very well studied; some studies do suggest that s’ may be more sensitive to changes after adding an inotrope, but who knows if that means anything. The most common cause for a big discrepancy between TAPSE and s’ is probably technical error, not a clinical distinction.
6. RVSP can be useful as a marker of afterload, but says nothing about the cause of RVSP—high left sided pressures vs high PVR—and also incorporates the RV function, so separating all this out can be difficult.
7. TAPSE/PASP (or TAPSE/RVSP) ratio might be a somewhat more accurate marker of RV/PA coupling, but not really clear if it’s clinically better than using the TAPSE alone, which is already a fair marker of RV/PA coupling. By measuring more things, it also introduces more room for technical error (usually underestimating RVSP), such as the need to estimate the TV gradient and the CVP. More tricuspid regurgitation will also tend to reduce the ratio, without necessarily indicating better RV function.
8. CVP estimates derived from the IVC are very unreliable in the critically ill. Many chronic PH patients have chronically distended IVCs regardless of their RAP. Using a transduced CVP is probably better. You can also just trend the TV gradient as a marker of its own and ignore the CVP component.
9. Shortening of the PA acceleration time (PAAT or PVAT) is a useful marker of pulmonary afterload. Notching of the waveform usually indicates a very high afterload, much more likely to be caused by pulmonary factors than high left heart pressures.
10. Fractional area change of the RV is another tool for approximating the LV “EF” which may work better in chronic dysfunction, where TAPSE may be misleadingly preserved. However, it requires a good view of the RV free wall, which is not always achievable.
11. Strain measurement has not yet penetrated point-of-care ultrasound machines reliably, but use is increasing. While still load-dependent, strain measurement is not angle dependent, which may make it helpful for right heart assessment.
12. In the less common clinical scenario of RV infarction/ischemia, most of the above still applies, yet the pulmonary afterload will not necessarily be elevated. In almost every other case, the problem driving RV failure is usually the afterload, hence reducing the afterload is usually the easiest treatment.
13. A proposed algorithm:
    1. Look for RV dilation
    2. Assess contractility using TAPSE and/or s’ (or other methods like eyeball gestalt, fractional area change, etc)
    3. Assess afterload using PA acceleration time and notching
    4. Compare contractility and afterload in context with the clinical scenario to understand the right heart’s function and conditions, with the understanding that your marker of contractility also incorporates the afterload to some extent.
14. Don’t forget that invasive monitoring, from CVP to a PA catheter, is always an option as well. CVP is “for free” and rarely wrong if you know how to interpret it, including the waveform, and in the sickest patients, a Swan can be quite helpful, particularly for monitoring; multiple advanced echo studies are not always possible or reliable, particularly with rotating shift staff.
15. If you have a Swan, wedge it. Otherwise it’s just a cardiac output monitor. Some fancy newer devices also allow measuring PA and RV pressures separately, which is an evolving science.