We discuss the nuts and bolts of urinary infection with an obstructing stone with Ashley Winter (@AshleyGWinter), board certified urologist with a fellowship in male and female sexual medicine, and chief medical officer of Odela Health.
A patient with UTI (or even just undifferentiated sepsis) and a non-trivial ureteral stone generally needs decompression of the affected kidney, whether or not there is significant hydronephrosis on imaging. Hydro is sensitive to other factors, such as dehydration, but its absence does not rule out sepsis secondary to urinary obstruction. CT is more sensitive here than ultrasound, which is mostly useful for ruling in hydronephrosis. (Such patients will usually need a stent, not a nephrostomy, as the latter is difficult when there is little hydronephrosis.) From a urology perspective, the size and position of the stone is probably more important than the hydronephrosis.
That being said, be attuned to the possibility of a patient with another source of sepsis, and an incidental bacteriuria and kidney stone. Anesthesia and a urology procedure won’t help these people. A cleaner urinary sample (e.g. straight cath or Foley, if the initial sample was a “clean” catch) can sometimes help here.
Consider also that a completely obstructing stone may be hiding pyelonephritis because the bacteria and leukocytes cannot pass the stone. This is not a very common scenario, but can lead to a “clean” urinalysis, so consider it in a patient with an obstructing stone and septic picture.
Try to get a urine sample before giving antibiotics.
Intra-renal stones will usually not cause obstruction, but occasionally in the setting of abnormal anatomy they may, such as a stone in a caliceal diverticulum causing a local/segmental hydronephrosis.
Obstructing stone + UTI + unstable with sepsis = emergent decompression within hours. Overnight cases should generally be drained overnight. Stable patients can potentially wait longer.
Option #1 for decompression is a ureteral stent, which stretches from the intra-renal pelvis to the bladder, traversing the area of the stone, and is deployed via cystoscopy. Urine drains around the stent, not necessarily through it. Stents can usually only be left for a maximum of 3 months and should be removed when no longer needed (i.e. when serial imaging shows passage of the stone, or a procedure has been performed to remove the stone). Long-term stent requirements involve serial stent replacements. They are placed in the OR under some level of sedation. Very distorted anatomy, such as in oncology cases, may make it difficult to find the ureteral orifice or to traverse the ureter.
Option #2 is a percutaneous nephrostomy. These are placed by Interventional Radiology. The patient is proned (not possible in all patients), and imaging (usually ultrasound) is used to guide a needle to the renal pelvis, then a pigtail catheter using a Seldinger technique. This can often be done with local anesthesia only. Lack of significant pelvic dilation or large body habitus make these more difficult. The result is a nephrostomy tube and drainage bag, which can be aesthetically unappealing to many patients. Anticoagulation may be a contraindication since you’re puncturing the renal parenchyma. They are usually not intended to be permanent, but can be left long-term in some cases.
Stents tend to be more uncomfortable, sometimes creating flank pain or a sensation of the need to void even with an empty bladder. Urine can even reflux up the stent into the renal pelvis during voiding.
Urostomies can sometimes make the procedure to remove a massive intrarenal stone like a staghorn calculus, since percutaneous nephrolithotomy can use the pigtail for access. Smaller stones can be removed via ureteroscopy.
Some stones are impacted, which may be difficult to navigate across with a stent. Technical maneuvers can be attempted, but occasionally it can’t be done and nephrostomy needs to be done as a rescue.
Ultimately, stent vs nephrostomy often comes down to institutional and logistical considerations, such as availability of urology compared to IR. Many centers have policies on who to call first.
A common phenomenon is clinical deterioration after decompression. Some of this may be iatrogenic; both stenting and nephrostomy involve pressurizing the renal pelvis by injecting contrast, which can force out some bacteria into the circulation. Reducing the volume or rate of contrast injection may help with this.
Antibiotic coverage can be as routine for sepsis, but if there is complex urological history, remember to check prior cultures (including stone cultures, if available), which may reveal a history of resistant organisms.
Stented patients who fail to improve in the acute to subacute period may be experiencing stent migration. Check position with a plain x-ray (KUB); if the proximal portion is not curled, further imaging may be needed as it suggests it’s not in the kidney.
Stent removal can sometimes precipitate instability as well if there is some degree of infection present.
We explore the cutting edge practice of point-of-care ultrasound of the brain, including optic nerve sheath measurement, transcranial doppler, assessing midline shift, and more, with Aarti Sarwal, neurologist and neurointensivist, director of the neurocritical care unit at Wake Forest, and director of their neurovascular lab and ultrasound courses.
POCUS can potentially be used to identify elevated ICP by optic nerve sheath ultrasound or pupillary assessment (in patients with difficult-to-assess pupils due to edema or other factors). Midline shift can be seen and quantified via the temporal window, and hemorrhagic masses can potentially be visualized. Finally, spectral doppler of the cranial vessels can show changes in intracranial compliance, similar to that seen in formal TCDs during vasospasm.
Learning curve for these studies is probably around 50-100 studies until competence, but may be creeping closer to 30–50 and eventually lower due to improving education, and increasing awareness and skills with the general concepts being applied.
The linear probe can be used over a closed eyelid to visualize the iris, allowing assessment of pupil response when light in shined in the opposite eye; this can be useful when the lid cannot be opened, such as from edema or trauma. M-mode can even be used for quantitative pupillometry.
An increased diameter of the optic nerve sheath measured 3 mm from the globe (using the linear probe in a transverse, ear-to-ear axis) correlates with increased intracranial pressure, as the sheath is a continuation of the cranial space and tends to swell with higher ICP. Papilledema can also be seen here as bulging of the optic disc. Use the orbital or ocular preset, which reduces power (mechanical and thermal indexes) delivered to the eye.
A cutoff reflecting elevated ICP is usually somewhere in the 5-7 mm range. However, normal values vary a lot, and very acute ICP crisis can choke off the continuity and cause normal diameters, so simple measurement can imperfect (analogy: IVC measurement). Trending can be more useful if you can establish a baseline, and papilledema is somewhat more specific. In pediatrics, adjusting for head circumference can help.
Slower increases in ICP tend to be associated with larger optic nerve sheath diameters, whereas rapid increases may actually be associated with normal sheath diameter, due to edema at the basal cistern level choking off communication with the cranial vault.
Midline structures like the pineal gland, third ventricle, or septum pellucidum can be seen from the temporal ultrasound window; 85-95% of the population will have adequate windows here, at least on one side, with some decrease in old age. Males tend to have worse windows, windows worsen over time, and there is some ethnic variation.
Research is early, but distance of the midline structures from the probe can be compared with their distance from the opposite skull (i.e. in the deep field). Differences between the two can help diagnose and quantify midline shift. Caveats: it’s difficult to establish exactly the same angle when insonating opposing sides, and identical angles can be impossible due to limitations in the windows, so don’t compare that way. The region of edema may mean different structures are shifted while others are normal, or even that there is no shift (e.g. herniation is not lateral); ideally, pick a midline structure that makes sense for where their pathology is found. This is probably more useful for serial comparisons than absolute values, since your angle that penetrates the small temporal window will usually not be perfectly flat, but will be reproducible.
Global edema may not be seen in midline shift, but may be seen in the TCD waveforms. Spectral doppler of vessels like the MCAs should show low resistance waveforms in a normal brain (low systolic peaks, a long runoff and high diastolic), while in a tighter brain with higher ICP, resistance gets worse, with a higher systolic, quicker drop, and lower diastolic pressure, all the way up until diastolic pressures become less than zero and flow is oscillating (e.g. back-and-forth during the cardiac cycle, which reflects no overall flow and is consistent with brain death). TCD measurements can be directly extrapolated to ICP using a number of published formulas.
Research is early, but transtemporal B-mode seems to have good sensitivity (>95%) for detecting parenchymal hemorrhage in the brain, as long as it is large and fresh; new blood shows up as a hyperechoic lesion with shadowing.
We dive into when to initiate renal replacement therapy, the modalities, settings, and physics involved, troubleshooting problems, and more, with Dr. Paul Adams, a dual-trained nephrologist and intensivist at the University of Kentucky.
One of the better indications for early dialysis in the ICU patient is to control volume, which in an oliguric patient you know is likely to keep accumulating.
Help determine who is likely to eventually need dialysis (and hence deciding early vs late, not early vs maybe never) with a furosemide stress test: give 1-1.5 mg/kg of furosemide (160 mg is often about right), then if they don’t make about 1 ml/kg/hr of urine for a few hours, they’re likely to end up needing renal replacement therapy.
Realistically, most true indications for acute dialysis in the ICU are hyperkalemia, volume overload, or occasional toxicology.
CRRT is generally more effective at volume management, particularly preemptive volume management, because it continues throughout the day and can more easily keep up with inputs. It is also more hemodynamically stable.
CRRT can be done via CVVH (using convective flow to drag out fluid and solutes via pressure across a filter), CVVHD (using diffusion gradients to clear solute and fluid), or CVVHDF (using both). Which modality of CRRT is used tends to come down to institution and practitioner practice, although there are some clinical differences in amount of solute clearance and such.
Effluent is the balanced electrolyte fluid which is used for therapy, and can be run into the blood before reaching the filter (diluting it and improving filter life, but decreasing efficiency), after reaching the filter (purely to replace what was lost), and on the other side of the filter (creating a dialysis effect). Total effluent rate gets divided among these sites as you like.
UF (ultrafiltration) is essentially whatever fluid is lost that you’re not replacing.
About 25–30 ml/kg/hr is usually about the right effluent rate. A higher rate helps make up for interruptions during the day.
150–250 ml/hr bloodflow is about right; it generally has relatively little effect on clearance in CRRT (unlike in intermittent HD, where it directly impacts clearance).
Circuit life can be prolonged with anticoagulation. Heparin can be used either systemically or regionally (infused at the start of the circuit, then reversed at the end using protamine), or citrate can be used regionally (replaced with calcium at the end), although it requires close monitoring of ionized calcium levels (really the ratio between total and ionized calcium, since citrate-bound calcium still registers on total calcium assays; a total calcium more than 2-2.5x higher than ionized levels suggests citrate toxicity).
16–18 hours of CRRT is usually needed before you start to see an impact on serum solute levels. For critical levels like severe hyperkalemia, start with IHD instead to get a quick correction.
Pressure problems at the dialysis access are almost always due to anatomic issues like catheter placement. Try adjusting the line, such as placing it deeper. Reducing bloodflow may help, using a different site, or rarely pharmacologically paralyzing the patient.
Pressure problems at the filter (“transmembrane pressure” or TMP) are usually from clotting. Consider anticoagulation if not already being used, or pre-filter fluid. Inflammatory patients like in sepsis can have very dirty, clotty blood.
If a patient starts making 600-1000ml of urine daily, consider weaning of renal replacement. That is not common in the critically ill, even if they eventually have later renal recovery; transition to IHD is more common.
If volume inputs are still ample (many liters a day), it’ll be hard to keep up using IHD, since UF rates top out around a liter per hour. Stick with CRRT in that case.
Rhabdomyolysis “disproportionately” increases BUN and creatinine, since those are products of muscle breakdown; they may have adequate renal function (demonstrated by robust urine output) despite high numbers.
ECPR candidacy may account for age, comorbidities, and code duration. Physiologic age is probably more important than chronological age. No-flow time without CPR should be very brief (witnessed is best), but low-flow time (with CPR) can actually be very long and still have good outcomes with ECPR. New systems should probably have stricter inclusion criteria, as numerous poor outcomes can endanger a fledgling program.
The cause of arrest is usually not as important, partly because it’s often not known so early. ECPR can be a bridge to diagnosis and prognosis.
One team should run the ACLS arrest while another handles the ECMO cannulation; it’s not possible to effectively do both. The cannulator should have their own ultrasound machine, and can function alone, although at least one skilled assistant is helpful. Mechanical CPR devices help by reducing energy in the room and reducing movement of the lower body; if not present, assign someone to manually stabilize the pelvis.
Cannulation can be done by various services as long as they’re immediately available. Whoever it is should be comfortable using ultrasound. Cutdowns are probably not the preferred technique except in niche cases. A second service like CT surgery can arrive after a short delay to do the dilation and cannula placement if the in-department provider like EM or CCM can get initial access with smaller devices.
Get ready by setting up equipment, position the ultrasound, and get sterile. As the patient arrives, have someone strip the clothes, expose the femoral region, and prep it, then get started with venous and arterial access.
Vein vs artery cannot be distinguished without ultrasound, and can be difficult even with it. Don’t use anatomic location – use appearance. Arteries are thicker walled and small in cardiac arrest. TEE with a bicaval view to see your wire can be a huge help.
The femoral artery should be accessed between the ligament and the bifurcation. Too high means RP bleeding risk; too low means potential for vessel damage. Similar for the venous access, although it’s more forgiving.
Initially, place wires and then some kind of sheath, dilator, or line that will accept a larger, stiffer wire (Scott uses the Amplatz Superstiff). Going directly from needle to stiff wire is challenging and higher risk for vessel damage. This also means if you end up not proceeding to ECMO, you can just use the smaller sheaths for venous and arterial access.
Even when a pulse returns, it’s often safer to proceed to ECMO in good candidates with a long arrest time. Supporting them through the next few days when they’re high risk of re-arrest, reperfusion injury, and other complications is likely to be safer than letting their heart do the work.
Dilation for ECMO is similar to other dilation, just less forgiving. Follow the same consistent angle as the needlestick, constantly rack your wire, and consider dilating to a somewhat smaller cannula than in other VA ECMO situations, which is often tolerated post-arrest. Arterial cannulae of 17fr (women) to 19fr (men) or even smaller can achieve adequate flows, with venous cannulae of 19-23 Fr or even smaller.
Goal: 5 minutes from first needlestick to active bypass.
Ideally, one cannula per leg, but you can place both in the same side if needed. Certainly use the same side if using a cutdown.
Venous cannula for the arrest patient should have the tip in the SVC (i.e. traversing the RA, not stopping before it). Use TEE to visualize this, or measure externally from groin to right nipple.
Pumps can be pre-primed and sit waiting for 30-60 days in most cases; check manufacturer guidelines. Nurses can handle the pump with some extra training, at least for initial set-up, then transition care after 15 minutes or so to a perfusionist or ECMO-trained respiratory therapist.
Pan-CT everyone. In fact, pan-CT all your cardiac arrests, as traumatic bleeding is common. Maybe do a coronary artery CT as well.
Initial settings: 100% oxygen and titrate down quickly. Flow can be somewhat low compared to normal VA ECMO, allowing the native heart to keep some output and allowing smaller cannulas. Traditionally set sweep gas at roughly similar to bloodflow, but this tends to cause dramatic, rapid initial drops in PCO2, which may be harmful to a vulnerable brain; instead, start at a low sweep and gradually titrate it up.
Do NOT prognosticate cardiac function early; recovery may happen late, and early withdrawal falsely affects your outcome figures from ECPR cases. The best numbers can only be achieved when the ECPR team continues to “own” the patient during their initial ICU course and doesn’t allow early withdrawal of ECMO.
Neuroprognostication, conversely, tends to be easier; patients often stratify relatively early into clear good and bad outcomes. It should be established early on that families may want to pursue life support and that’s fine, but the team determines how long to continue ECMO, and it won’t be continued indefinitely.
Economics: ECPR pump runs are short (<1 week usually), and reimbursement is all up front, so it actually pays well compared to many ECMO types, like long VV courses.
The future: ideally, EMS would recognize good ECMO candidates and divert patients to ECPR centers. In rural areas, ED teams would be able to cannulate and start initially on ECMO, then transfer to larger referral centers.
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.
If considering ACS in any post-menopausal woman, you should also consider stress cardiomyopathy. Echo is the test of choice.
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.
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).
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.
The InterTAK score may give some guidance. Dr. Sorrell is working on echo criteria.
Cardiac CT may also be a helpful non-invasive tool.
Contraindications to stenting (e.g. bleeding) could also suggest utility in a non-invasive approach.
When addressing hemodynamics, always ask whether outflow tract obstruction is present or absent; this will be a critical decision-point.
Without obstruction, treat patients as usual. Vasopressors should not be viewed as potentially worsening the condition, and early beta blockers probably have no role.
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.
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.
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.
Hormone replacement may have a role.
RV involvement can occur atypically. It can help point to TCM, since this would be an unusual anatomic distribution for ACS.
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.
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.
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.
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.
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.
“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.
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.
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.
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.
Acute iron overdose can cause anion gap acidosis, GI symptoms including bleeding, and shock and an overal critically ill presentation.
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.
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.
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.
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.
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.
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.
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.
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!
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.
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.
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.
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.
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.
Dr. Albin’s handy pocket reference to work-up of encephalopathy and diagnosing autoimmune encephalitis.