Critical Care Scenarios

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

We look at stress (Takotsubo) cardiomyopathy in the setting of critical illness, with Dr. Vincent Sorrell. Dr. Sorrell is a cardiologist at the University of Kentucky, where he helped develop the Advanced Cardiovascular Imaging Program, and is current Acting Chief of both the Division of Cardiovascular Medicine and the Gill Heart and Vascular Institute.

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

1. If considering ACS in any post-menopausal woman, you should also consider stress cardiomyopathy. Echo is the test of choice.
2. While hypokinesis classically occurs at the apex in TCM, almost any distribution can occur; 10% or more will have atypical distributions, particular outside the traditional demographics (older women), such as the critically ill. Of course, atypical anatomical distributions can also occur in ACS due to distinct anatomy.
3. Recurrence of TCM may occur with a different distribution. Recurrence occurs in up to 40% in the first four years. Withdrawal of beta blocker therapy may precipitate this, which may be a reason to select other therapies (e.g. ACE inhibition).
4. In general, TCM is a diagnosis of exclusion after ruling out ACS. The ECG pattern is non-specific, but STE in V1 or lead I is unusual in TCM. ACS usually causes more troponin elevation than TCM, and matches the degree of EF reduction. Persistent troponin elevation in a patient without intervention may suggest a missed ACS instead of TCM, but you should generally not wait that long.
5. The InterTAK score may give some guidance. Dr. Sorrell is working on echo criteria.
6. Cardiac CT may also be a helpful non-invasive tool.
7. Contraindications to stenting (e.g. bleeding) could also suggest utility in a non-invasive approach.
8. When addressing hemodynamics, always ask whether outflow tract obstruction is present or absent; this will be a critical decision-point.
9. Without obstruction, treat patients as usual. Vasopressors should not be viewed as potentially worsening the condition, and early beta blockers probably have no role.
10. Anticoagulate as soon as it’s safe, when there are large wall motion abnormalities; this is similar to WMA from other causes. Apical ballooning is probably somewhat riskier than other distributions due to the flow patterns.
11. The natural history of TCM involves recovery in most within 2 weeks, although the course during that period can vary widely. Almost all recover within a couple months.
12. Outpatient care focuses on ACE inhibition, diuresis if needed, anticoagulation when appropriate, with a gradually decreasing emphasis on beta blockers. Aspirin and statins are not usually needed if there is no concomitant ACS.
13. Hormone replacement may have a role.
14. RV involvement can occur atypically. It can help point to TCM, since this would be an unusual anatomic distribution for ACS.

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

We look at evaluating the patient with encephalopathy and unexplained anion gap, including the workup and treatment of toxic alcohol poisoning, with guest Dr. Jerry Snow (@ToxicSnowEM), medical toxicologist and director of the toxicology fellowship at Banner University Medical Center in Phoenix.

Find us on Patreon here!

Buy your merch here!

Click here to claim your free CME credit!

Takeaway lessons

1. A toxicologic exposure should be suspected, even without a clear story, based on the prehospital scene. EMS or family reports of chemicals, pill bottles, etc should be elicited. Prescribed medications should be questioned, as well as any other meds that could be available to the patient, such as older meds, current and older meds prescribed to family members, and supplements.
2. Physical exam maneuvers high-yield for tox diagnosis include the pupillary exam, skin exam (diaphoretic vs dry), and examination of muscle tone and deep tendon reflexes.
3. Laboratory clues of tox diagnoses include an elevated anion gap in the absence of common causes (lactate, ketones, uremia), as most of the remaining causes of a gap are toxins.
4. Elevated osmolal gaps should also be investigated, although considered an insensitive test for most toxins. A serum chemistry, as well as salicylate and acetaminophen levels, should be sent routinely. An ECG should be checked for findings like interval prolongation and morphology changes.
5. “Normal” osmolality varies too much for a low osm gap to be useful, but a clearly elevated gap is diagnostically helpful, particularly when its presence/absence is compared with the presence/absence of an anion gap.
6. The most common source of methanol ingestion in the US is windshield wiper fluid; it’s also present in poorly-distilled homemade moonshine, hand sanitizer, model car fuel, food-warmer fuel, lacquer and paint thinner, and many others. For ethylene glycol, the most common US source is automotive antifreeze. In both cases, these are usually intentional ingestions.
7. Toxic alcohol levels, namely methanol and ethylene glycol levels, are send-out tests in most centers and result too slowly to be useful in the early stages. You will need to treat empirically based on suspicion and perhaps based on osmolar gap.
8. Urine tox screens rarely change management, and may lead to missed diagnoses due to anchoring. Many substances are not tested, and positive tests (e.g. for opioids or benzodiazepines)—even for substances that may explain the clinical picture—can be false positives. Even true positives do not rule out the presence of another medical or even a second toxicologic cause. Correlate cautiously with the clinical picture (e.g. opioid toxicity may not explain encephalopathy in a patient with normal pupils and hyperventilation), or simply don’t send it to begin with.
9. Acute iron overdose can cause anion gap acidosis, GI symptoms including bleeding, and shock and an overal critically ill presentation.
10. Ethanol has fallen out of favor for treatment of toxic alcohols, although it does work; it is logistically challenging, requiring frequent lab checks to ensure therapeutic levels, central venous access, and other fuss; complications are much higher than with fomepizole. It’s good for low-resource settings that may not have the more expensive fomepizole, however, and co-ingestion of ethanol with toxic alcohols provides some fortuitous initial protection until the ethanol level falls.
11. Ethylene glycol and methanol are not themselves toxic, but as the parent alcohols are metabolized, they turn into toxic acids. The goal of fomepizole or ethanol is therefore to block this conversion (by alcohol dehydrogenase). This also means that if checked early after ingestion, osmolar gap will be high, but anion gap is low, as only the parent compounds are active osmoles. As metabolism continues, osmolar gap falls, but the anion gap increases. One upside of treatment with hemodialysis is that it clears both the parent alcohol and the toxic metabolites, so it’s helpful even in late presentations.
12. Toxic alcohols may confuse testing for lactate. Some methods, mainly used on blood gas analyzers that report lactate, can be fooled by glycolate—a metabolite of ethylene glycol—and report a falsely elevated lactate. The same sample tested in the lab using another method may show a lower lactate. This “lactate gap” can be diagnostically useful if understood.
13. A normal fomepizole course is two days, dosed every twelve hours, but monitoring should be done of either methanol/ethylene glycol levels (if lab turnaround is fast), or monitoring the pH, anion gap, and osm gap for response. If not resolved, a longer treatment course may be needed, and dose may need to be increased, as it induces its own metabolism.
14. Hemodialysis may be used in the sickest patients, as a rescue, if pH is severely deranged, or if there is severe kidney injury, since renal clearance is needed to clear ethylene glycol. Fomepizole should usually still be given to temporize until treatment is completed, and may need to be dosed more frequently during dialysis as it is a dialyzable compound. A single prolonged HD session (eg 8 hours) is often adequate, and HD is superior to CRRT.
15. Thiamine and pyridoxine (vitamin B6) can be given to help shunt toxic alcohols to benign metabolites, although evidence for this is fairly poor. Other supportive care is as routine.
16. If acute toxicity is survived, ethylene glycol patients usually do well, although they occasionally have calcium crystal deposition in nerves and develop cranial nerve palsies or peripheral neuropathy. Methanol patients tend to do worse, sometimes developing permanent blindness and CNS pathology like delayed intracranial hemorrhage or Parkinsonism.
17. Every hospital in the US has a poison control center available to them as a resource, which includes an on-call medical toxicologist who can discuss cases if needed. They are available even to review med lists and assist with diagnostic mysteries. The most common error in tox cases is the failure to consider a tox diagnosis!

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

1. 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.
2. 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.
3. If urine osm is >300, ADH is definitely present to some extent.
4. 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.
5. 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.
6. 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.
7. It’s often impossible to determine how acute hyponatremia is, so generally assume chronic and correct slowly.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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).
13. Vaptans have a limited role outside specific use-cases like bridging to transplant (although not for liver – they may cause hepatotoxicity).
14. 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.
15. Hypervolemic hyponatremia, e.g. from cirrhosis or heart failure, is generally correctable only by managing the underlying disease.
16. Truly chronic hyponatremia usually won’t cause acute symptoms like encephalopathy, but are associated with various more subtle medical complications like osteoporosis.
17. 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.
18. 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