Cases – Page 3 – Critical Care Scenarios

Episode 57: Hyponatremia with Paul Adams

We tackle the knotty dilemma of diagnosing and treating hyponatremia, with Dr. Paul Adams, a dual-trained nephrologist and intensivist at the University of Kentucky.

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Takeaway lessons

Start by asking whether the hyponatremia needs to be corrected emergently, as well as its cause. Instability means correct it emergently, and instability usually manifests as seizure.
While hyponatremia is often categorized by volume status, volume status is a tricky determination with ample gray area and room for overlap. It’s more useful to approach hyponatremia by asking whether ADH is active or not.
If urine osm is >300, ADH is definitely present to some extent.
The hypovolemic and/or low solute patient will be fixed with crystalloid, although they are at risk of overcorrection. Overcorrection almost always occurs due to autodiuresis, not from exogenously administered salt.
A high urine sodium implies lack of sodium reabsorption by the kidneys, more consistent with diuresis (thiazides) or ATN (failure of absorptive mechanisms). Low urine sodium is a broader differential, e.g. most of the appropriate-ADH hyponatremias.
While there is overlap between hypovolemia (often acute) and low solute intake (often more subacute/chronic), they are distinct syndromes. They can be differentiated by the urine osm: both urine sodiums will be low, but urine osm will be low only in the low solute patient (because they simply aren’t taking osms in). The hypovolemic is at greater risk of overcorrection as well.
It’s often impossible to determine how acute hyponatremia is, so generally assume chronic and correct slowly.
Overcorrection from acute hypovolemia will be mediated by dilute polyuria, so a good monitoring strategy may be to simply send serial urine osms, particularly if polyuria occurs. Have a low threshold to clamp them with DDAVP if it occurs.
When risk for osmotic demyelination is highest (risks: longer duration of hyponatremia, low solute intakes like malnourishment and alcoholism, and lower sodium), consider prophylactically clamping with DDAVP.
Use small boluses (100 ml) over about ten minutes to correct hyponatremia-induced seizures and repeat as needed until seizures stop. Trend labs but don’t stop until symptoms resolve, or you correct by 5 mEq. Most cases of true hyponatremia-induced seizure or severe encephalopathy will require around 500 ml total. Other concentrations could probably be used but are subject to logistical issues and are really just manipulating the amount of diluent volume.
Theoretically, inducing hyponatremia in neurologic patients could create the same risk as rapidly correcting hyponatremia, but data is limited and from a bedside perspective, this doesn’t generally seem to cause demyelination.
For SIADH, a loop diuretic can be useful, but the mainstay is fluid restriction. The right amount of restriction depends on free water clearance; a cirrhotic who only produces 500 ml of free water a day should theoretically be restricted below this intake (which is not easy).
Vaptans have a limited role outside specific use-cases like bridging to transplant (although not for liver – they may cause hepatotoxicity).
Confusing pictures (eg SIADH vs hypovolemia vs CSW) can be clarified by a sodium challenge – bolus a liter of normal saline and see what they do with the salt. Remember that if you give fluid with a lower osmolality than the urine osmolality – common in SIADH – you’ll actually dilute them and lower their sodium further.
Hypervolemic hyponatremia, e.g. from cirrhosis or heart failure, is generally correctable only by managing the underlying disease.
Truly chronic hyponatremia usually won’t cause acute symptoms like encephalopathy, but are associated with various more subtle medical complications like osteoporosis.
Oral salt like salt tablets are generally not a huge help for SIADH; salt handling is separate and inadequate sodium is not the issue. You can force some salt into them by simultaneously fluid restriction (although this is horrible for their thirst), but once they leave a controlled setting and can compensate with unmonitored water intake they’ll return to their set point.
Fludrocortisone takes a while to act (it’s a steroid) and probably has a limited role in hyponatremia. Remember it works on the kidneys and has no effect if urine is not made.

Resources

European-hyponatremia-guidelines Download

Episode 56: Resuscitation psychology with Dan Dworkis

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Discussing the psychology of emergency response, team dynamics, and debriefing with Dan Dworkis, MD, PhD, FACEP. He’s the Chief Medical Officer at the Mission Critical Team Institute, a board-certified emergency physician, and an assistant professor of emergency medicine at the Keck School of Medicine of USC where he works at LAC+USC. He performed his emergency medicine residency with Harvard Medical School at the Harvard Affiliated Emergency Medicine Residency at Massachusetts General Hospital / Brigham Health, and holds an MD and PhD in molecular medicine from the Boston University School of Medicine. He is the founder of The Emergency Mind Project, and the author of The Emergency Mind: Wiring Your Brain for Performance Under Pressure.

The Emergency Mind Project: www.emergencymind.com

The Emergency Mind Book: bit.ly/emindbook

The Emergency Mind Podcast: www.emergencymind.com/podcast

The Mission Critical Team Institute: www.missioncti.com

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Takeaway lessons

Intact teams train together, while swarm teams are ad hoc and must perform without prior preparation. Many healthcare teams are somewhere in between, a “jello” team. How to effectively swarm and run such a team is one of the common challenges in a hospital-based emergency.
Intentionally limit information input when needed. In the initial stages of resuscitation and stabilization, much of the medical history and other details may not be pertinent.
Identify your role when you walk into the code and ask who’s in charge. If there’s no response, identify that it’s you. Ask if there are pads on, if there’s IV access, the last rhythm, and who’s doing compressions next. These are step zero in your management. If someone is already in charge, ask how you can help.
Usually there’s no need to use names, which are tough to remember in the heat of the moment. Roles are adequate. In the long run you can seek to build those relationships further.
Nurse leaders can be a great way to offload the provider leading a code and tackle logistics like delegating tasks to the best person to handle them.
Cross-disciplinary simulation training builds relationships between staff, but also stress-tests procedures and even equipment setups.
If you’re not in a leadership position, lead change like a flock of starlings. When you change direction and nudge the handful of people nearest to you, you’ll create a wave of change that can propagate outwards. What can you do on this shift to make you and your team 1% better? Ask yourself and others, what did you learn from this case? What surprised you, what did you learn? What can we improve next time? Small, subtle changes like this build over time.
Seemingly complex decision pathways can often be simplified by considering what you can do and what it depends on. Bifurcations that don’t change what you do at this juncture can be eliminated.
Don’t waste suffering.
Initial steps in debriefing is to make sure the team is physically and psychologically okay, and ensure the team and equipment are prepared for the next patient.
Next, take two minutes with anyone who can spare the time to discuss what we learned from the patient. What went well, what went better? The room is always smarter than you individually; solicit opinions from everyone.
When numerous conflicting demands are present, optimize your performance by finding ways to streamline and protocolize decisions to reduce the number that need to be contemplated in the heat of the moment. Anything high yield, low risk, just make the decision ahead of time to do them without thought.

Episode 55: Undifferentiated encephalopathy and autoimmune encephalitis, with Casey Albin

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How to evaluate the patient with unexplained encephalopathy, and a practical approach to diagnosing autoimmune encephalitis with an emphasis on anti-NMDA receptor encephalitis—with Dr. Casey Albin (@CaseyAlbin), neurologist and neurointensivist, assistant professor of Neurology and Neurosurgery at Emory, and part of the NeuroEmcrit team.

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Takeaway lessons

Common causes of unexplained encephalopathy are:
- Metabolic/systemic problems (myxedema, hypercarbia, uremia, vitamin deficiency, etc), which are common, but often found on routine labs.
- Toxicologic exposures (drugs, heavy metals like Wilson’s, etc)
- Primary neurologic events. These differentiate into acute and subacute processes.
In the altered patient found down with normal CT head and grossly normal labs, consider seizure and tox causes.
Give thiamine indiscriminately and widely to patients with altered mental status; it is harmless and Wernicke-Korsakoff may fool you.
Start with the history and meds. Simple intoxications like baclofen overdose can cause incredibly dense coma.
Inquire as to recent history of behavioral changes, neurologic phenomena, illness, etc. Prolonged or subacute symptoms significantly narrow the differential of a neurologic cause.
Always consider basilar artery stroke in the obtunded patient with a non-focal exam! Get a CTA early to evaluate the posterior circulation, as they may be a candidate for thrombolysis or thrombectomy.
With an unexplained diagnosis suspected to be neurologic in nature, have a low threshold for obtaining MRI (generally with gadolinium), lumbar puncture, and EEG. The urgency and order of these may depend on clinical suspicion, other tests, and availability. A spot EEG to rule out status epilepticus, followed by either LP or MRI (whichever is available first) is often a good sequence.
Have a relatively high threshold to start anti-epileptics for “seizure risk” or for vaguely epileptiform activity on EEG in the absence of true seizure, particularly if continued EEG monitoring (either continuous or frequent spot studies) are readily available. These drugs tend to remain prescribed for a long time, are not often discontinued by downstream providers, and can lead to future polypharmacy and lifestyle impacts.
To unpack autoimmune causes, build a syndrome by considering the timeline and the affected areas (e.g. portions of the brain or spine involved on imaging).
Creutzfeldt-Jakob disease should be suspected from the clinical history, or classic MRI findings such as cortical ribboning and “hockey sticks” in the basal ganglia. Without some specific suspicion, testing is usually not indicated.
A normal brain MRI can occur in some autoimmune encephalitides. For instance, anti-NMDAR encephalitis can have absolutely normal MRIs, which can be a helpful differentiator from limbic encephalitis (the latter tending to have characteristic MRI findings).
The Mayo Clinic and ARUP laboratories have a broad autoimmune encephalitis panel that can be sent for undifferentiated encephalitis; it tests for multiple antibodies and is updated periodically in response to new research. It is not particularly cheap, but with the large number of overlapping syndromes, when autoimmune causes are suspected it is generally a better idea than targeted testing in all but the most classic clinical pictures.
Draw plenty of CSF for all these labs, at least 30 cc if possible. You don’t want to have to go back just because you thought of another test.
Normal CSF protein increases with age. A good rule of thumb for pathological elevation is CSF protein that is greater than the patient’s age.
With a sick patient and legitimate suspicion for an autoimmune cause responsive to immunomodulation, treat empirically. Your options are steroids (e.g. five days, 1000mg daily of methylprednisolone, then possible maintenance dosing depending on the diagnosis), plasma exchange (PLEX, usually 5 treatments, one every other day), or IV immunoglobulin (IVIG). Often you’ll combine pulse-dose steroids with one of the latter. Either PLEX or IVIG are a reasonable option, although some syndromes seem to respond better to PLEX. Either way , you’ll need to commit to doing this before autoimmune tests results (which takes around ten days), and generally continue treatment until you have your results, since clinical response in many syndromes may take weeks.
If test results are negative, consider repeating some studies (e.g. MRI the brain again), go over the history again, look for tests or diagnoses that weren’t considered, ask for help, and consult a reference or cheat sheet to look for what you missed.
With any possibility of any paraneoplastic syndrome, particularly anti-NMDAR encephalitis, perform a serious search for neoplasm: CT chest/abdomen/pelvis, testicular ultrasound, either MRI pelvis or transvaginal ultrasound of the ovaries, and sometimes PET scan, although this can be tough to perform due to poor inpatient reimbursement.
“Classic” NMDAR encephalitis is a younger woman with paranoia, progressing to catatonia and movement disorders, autonomic instability and storming, dyskinesias, hypersalivation, and in late stages, coma. With treatment they regress along the same pathway, and it generally does not recur, although full recovery is not guaranteed and may take many months; the intubated patient usually needs a trach and PEG, and can be difficult to manage due to their autonomic storming and vent dyssynchronies. Without treatment they often never recover.
With NMDAR and a negative malignancy workup, repeat surveillance imaging is usually warranted to keep searching for tumor.
Long-term immunosuppression is needed, so a steroid-sparing agent like rituximab is often used.

References

Dr. Albin’s handy pocket reference to work-up of encephalopathy and diagnosing autoimmune encephalitis.

New-22Mass22-or-22Encephalopathy22 Download

Episode 54: The critically ill patient with pulmonary hypertension, with Ray Foley

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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.

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Takeaway lessons

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).

References

IBCC on RV failure

Episode 53: Documentation and coding with Robert Oubre

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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.

Takeaway lessons

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.

References

Complex-PNA-CDI-Cheat-sheet Download

Episode 52: Pleural effusions in the ICU with Emily Fridenmaker

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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

CME credit provided courtesy of Academic CME. To claim your CME credit for this episode, click here to complete a short quiz.

Takeaway lessons

IMAGING
1. CXR – underestimate
  1. Lateral – 75mL (5-15 mL is normal)
  2. AP – 175mL
    iii. 500mL for 100% sensitivity
2. CT – overestimate
  1. Contrast can help delineate pleural surface
3. Ultrasound – goldilocks
  1. Can see 5-50mL fluid
  2. > 1cm generally safe to sample
INITIAL WORKUP
1. Thora – no absolute contraindications
  1. Should tap an effusion if you don’t know what’s causing it
    1. Diagnostic or therapeutic
    2. Does little to change hypoxia—can impact dyspnea though due to diaphragm length-tension relationships
    3. Complication rate = ??
  2. Differential
    1. Nucleated cells – greater than 50k usually paraPNA/empyema
    2. Lymphocytosis – TB, lymphoma, sarcoid, RA, yellow nail syndrome, chylothorax, cancer
    3. Eosinophilia – >10%; pneumo, hemo, infarction, asbestos, parasites, fungus, drugs, catamenial, malignancy, TB, CEP
    4. Mesothelial – normal in pleural fluid
  3. Light’s Criteria—protein and LDH (serum and pleural), albumin, cholesterol
    1. Aim was to have a high sensitivity, since shouldn’t miss an exudate
    2. The criteria—any one of them gives you an exudate
    3. Pleural protein/serum protein > 0.5—can be elevated by diuresis
    4. Serum albumin/pleural > 1.2
    5. Pleural LDH/serum LDH > 0.6
    6. Pleural fluid LDH > 2/3 ULN
    7. Cholesterol >45 can also help to indicate an exudate
    8. Glucose
      1. Low: complicated effusion/empyema, malignant, TB, lupus, rheumatoid pleurisy, esophageal rupture
    9. pH – normal is 7.6 due to bicarb gradient
      1. <7.3 – same conditions as low glucose ii. If low, higher yield on cytology for malignancy, less response to chemical pleurodesis
      2. Parapneumonic <7.15 – needs pleural space drainage
      3. Lidocaine will falsely drop the pH
    10. Amylase – pancreatic or esophageal etiologies
    11. ADA – TB; usually >40
    12. Cytology – malignant; sensitivity is 60%, 85% with second sample
TRANSUDATIVE VS EXUDATIVE
1. Transudative
  1. Atelectasis, CHF, hepatic hydrothorax, low albumin, iatrogenic, nephrotic syndrome, PD, urinothorax
2. Exudative
  1. Infectious, drug induced, trauma, malignancy (stage 4), CTD (RA, lupus, EGPA, GPA), hypothyroid/ovarian hyperstimulation syndrome, chylothorax, pancreatitis, sarcoid, post cardiac injury syndrome, radiation, PE, BAPE
PARAPNEUMONIC CLASSIFICATIONS
1. Simple – resolve with abx (1-2 weeks), don’t require drainage or special abx considerations
  1. Free flowing, sterile
  2. Exudative – neutrophilic predominance, normal pH and glucose level
2. Complicated – evidence of infection of the space
  1. Exudative, high white count, pH <7.2, glucose <40 (or 60?), LDH >1000, + gram stain
  2. Large, loculated, thickened pleura, air bubbles in effusion
3. Empyema (subset of complicated)
  1. Pus in the pleural space
  2. Longer clinical course, possibly subacute
    D. Complex
    i. Internal loculations
MANAGEMENT OF COMPLICATED PARAPNEUMONIC EFFUSIONS
1. Drainage usually required for source control—poorer prognosis without it
  1. Particularly if pH <7.15, low glucose, or LDH>1000
2. Empyema
  1. Loculated
  2. + gram stain or culture
  3. Thickened parietal pleura
3. Approach to drainage: Tube thoracostomy
  1. Small bore (10-14) similar efficacy to large
  2. MIST 1 – no difference in mortality or need for VATS between large, medium, or small bore tubes
    1. Retrospective—small bore noninferior
    2. Flush q6 to keep patent
  3. Suction is typical but not necessary
  4. Reimage after placement, when drainage slows
  5. Remove when less than 50-100mL for a couple of days, imaging is improved, clinically improving
  6. Reimage in about 2 weeks
4. Failure of drainage – Repeat imaging 24hrs after completion of chosen intervention
  1. Lytics, multiple tubes preferred before VATS
    1. Probably best for early, multiloculated effusions
    2. DNAse breaks down DNA, reducing viscosity. tPA is fibrinolytics, busts up loculations
    3. MIST 2 – less need for VATS (30-80%) with tpa (10)/dornase (5) BID x 3 days
    4. New data shows simultaneous admin may be as efficacious
  2. VATS if significant organization, trapped lung (can be elective)
    1. No mortality benefit shown
    2. Pleural hemorrhage – 1-7%, indication for VATS
    3. Indicated when abx, tube, lytics have failed
    4. Also indicated up front if there is significant organization, fibrothorax, trap
    5. May need to be converted to open thoracotomy
    6. Maybe reduced LOS? MIST 3 looking at early VATS vs early lytics
  3. Window thoracostomy/eloesser flap
ANTIMICROBIAL THERAPY
1. i. CAP – Rocephin + flagyl or unasyn
2. Lots of clinda resistance now
3. Atypicals rarely cause complicated effusions
4. MDRO risk factors – MRSA, pseudomonas, and anaerobes
5. Optimal duration unknown
  1. usually 2-3 weeks for complicated
  2. 4-6 weeks for empyema
  3. Can switch to PO when clinically improving
  4. Radiographic resolution can take weeks to months; this is not the goal
COMPLICATIONS OF PLEURAL SPACE INFECTIONS
1. Fibrothorax, pleural fibrosis
2. Restriction, unexpandable lung
3. Decortication not considered unless restriction/limitation present 6 months later

Episode 51: Resuscitating and deresuscitating with hypertonic saline, with Sean Barnett

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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.

Takeaway lessons

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.

References

Episode 50: Rib fractures and surgical plating with Ron Barbosa

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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.

Takeaway lessons

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.

Episode 49: Invasive pulmonary aspergillosis with Shmuel Shoham

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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.

Takeaway lessons

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.

Episode 48: Undifferentiated hypotension

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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.

Takeaway lessons

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.

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Continuing education for this episode

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Improved overall fluid balance / UOP / hemodynamics in diverse settings.

Diuresis

COVID

Anti-Inflammatory

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