35 episodes

Join us as we talk through clinical cases in the ICU setting, illustrating important points of diagnosis, treatment, and management of the critically ill patient, all in a casual, "talk through" verbal scenario format.

Critical Care Scenarios Critical Care Scenarios

    • Health & Fitness

Join us as we talk through clinical cases in the ICU setting, illustrating important points of diagnosis, treatment, and management of the critically ill patient, all in a casual, "talk through" verbal scenario format.

    Episode 30: Diabetic ketoacidosis

    Episode 30: Diabetic ketoacidosis

    Diagnosing and treating DKA, including fluid management, lab studies, insulin management, managing acid-base abnormalities, transitioning off your drips, and all the rest.







    Takeaway lessons







    * Calculate your anion gap and perhaps your strong ion difference (or bicarb gap). In most cases, consider checking a b-hydroxybutyrate and a lactate to confirm the diagnosis, but hyperglycemia + anion gap generally equals DKA.* Ask what triggered DKA. The most common causes are medication non-compliance (or an inadequate regimen), and a stressor like infection.* Bolus fluid until euvolemic, just like any patient. These people are often severely hypovolemic, particularly from polyuria, but they vary; you’ll need to assess them and decide their needs. Ultrasound and clinical examination are helpful.* Start an insulin drip, with or without a bolus. A common regimen is 1 unit per 10 kg of bodyweight as both a bolus and a starting drip rate. Check hourly fingersticks and adjust as you go to reduce the glucose at a modest rate.* Check q4h basic chemistries to follow electrolytes and the anion gap. If potassium gets down into the normal range, give more. If it gets low, stop the drip; it’s going to get lower. You can check a blood gas up front (a VBG is fine) but it usually doesn’t need to be trended.* Once the glucose drops below 200-250, start some IV fluid containing dextrose. This prevents “overshoot” and allows you to continue the insulin drip at a low rate until the ketosis has cleared.* Once the gap has been closed for two consecutive checks, you can transition to a subcutaneous regimen. Give long-acting insulin, wait two hours, then turn off the drip. Calculate the dose by either restarting their home regimen (if it was previously effective) or by estimating their 24-hour insulin requirement, splitting it into 50% basal and 50% short acting, then cutting that basal dose to about 50-80% to create a safety margin. Give short-acting as either fixed prandial doses or sliding scale, either qACHS (with meals and at night), or q4-q6h.* Once the drip comes off, they should eat some kind of meal.* Check one more chemistry, then they can usually leave the unit.* Alcoholic, starvation, or medication-related ketacidosis presents like DKA, but without severe hyperglycemia. If severe, treat them similarly, but since it won’t take long to drop their glucose, start supplemental dextrose early. Mild to moderate cases don’t need insulin at all, only nutrition.* In general, disable insulin pumps upon admission; they can potentially be restarted once DKA has resolved. Endocrinology is helpful for this.

    • 45 min
    Episode 29: Lightning rounds #2

    Episode 29: Lightning rounds #2

    A vascular access roundtable, discussing our practices surrounding arterial lines, central lines, PICC lines and midlines, and PA catheters. When do we place them? When can they come out? What sites do we like? When (and how) do we use ultrasound? What’s up with the axillary site, why does Brandon hate PICCs, the age-old debate on ultrasound probe orientation… all this and more.

    • 38 min
    Episode 28: Diuresis, deescalation, and liberation with Matt Siuba

    Episode 28: Diuresis, deescalation, and liberation with Matt Siuba

    How to take the well-resuscitated critically ill patient, get fluid out of them, deescalate their antibiotics, wean their sedation, reduce vent support, extubate, and get them out of the ICU—with Dr. Matt Siuba (Twitter: @msiuba), an intensivist at the Cleveland Clinic with an abiding interest in “zentensivism,” the art of doing less.







    Takeaway lessons







    * Portal vein pulsatility is a quick and useful addition to IVC assessment when evaluating volume status, particularly in ventilated patients where quick “eyeball” assessments of IVC variability is difficult (and measuring it is a pain). Consider pulse pressure variation too, in patients with a regular cardiac rhythm and on the vent.* Start a journey of diuresis with furosemide, dose 40 times the serum creatinine. If you have a lot of work to do, or you expect resistance, add a thiazide (e.g. metolazone), and if more than a couple days of diuresis is expected, add spironoloctone as well to limit potassium wasting. Aim for >1–3 liters negative fluid balance per day, and generally schedule diuretics instead of manually spot dosing. Even if scheduled, however, follow up on urine output so you can increase the next dose if the last wasn’t adequate.* Alternately if kidney function is quite poor, consider a furosemide stress test of 1 mg per kg of bodyweight (or 1.5 mg per kg for those with prior loop diuretic exposure). If output is poor, e.g. 65) or those with chronic cardiopulmonary diseases to HFNC. The latter is reasonable in most patients whose acute hypoxic disease has not yet fully resolved.* When to downgrade patients from the ICU is less dependent on how long it’s been since extubation or getting off pressors,

    • 1 hr 6 min
    Episode 27: Wilderness medicine with Ross Hofmeyr

    Episode 27: Wilderness medicine with Ross Hofmeyr

    Management of an alpine medicine scene including discussion of HAPE (High Altitude Pulmonary Edema), HACE (High Altitude Cerebral Edema), and suspension syndrome, with Dr. Ross Hofmeyr (@rosshofmeyr), anesthesiologist in the Department of Anaesthesia and Perioperative Medicine at the University of Cape Town, as well as cofounder and medical director of WildMedix, the oldest wilderness medicine support group in South Africa.







    Takeaway lessons







    * Scene safety comes first, which in a high-altitude setting includes consideration for the acclimatization of your team.* Other than ABCs, think WMX:* W= Factors of the Wilderness environment, such as altitude and exposure.* M= Materials and Manpower; what’s needed for the rescue and what’s available?* X= Exit strategy; from the start, think about how (and how rapidly) you’re getting out.* Spinal stabilization is not feasible until a suspended patient can reach a stable location.* Suspension syndrome (aka harness suspension syndrome, harness hang syndrome, suspension trauma) is a phenomenon of reduced venous return due to immobility while suspended in a vertical position (exacerbated by, although not requiring, a restrictive harness). Similar orthostasis can occur in healthy individuals forced to stand upright and immobile (at parade rest) without active muscle pumps, except they will then fall and self-reperfuse. In suspended patients, cardiac arrest can occur during suspension due to loss of preload, and further instability can occur after flow is restored due to a crush-syndrome-like reperfusion phenomenon with cold, acidotic blood. A hanging patient may be temporized by lifting their legs to a more horizontal position.* Lowering a suspended patient is always easier than lifting them.* If possible, consider deferring intubation in very austere settings, unless you realistically have the equipment, manpower, and space to transport a sedated, apneic patient while continuously ventilating them.* Optic nerve sheath ultrasound can be a big diagnostic aid for ruling in cerebral edema in the setting of HACE or head trauma. A diameter >9–10 mm is suspicious for elevated ICP, >15 mm is a reliable rule-in, 6–9 mm is unclear. Differences between the two sides are concerning.* The first treatment for any altitude sickness is oxygen; the second is descent. Everything else is temporizing or supportive.* HACE is part of the spectrum of acute mountain sickness, and is caused by increased hydrostatic pressure and capillary permeability, leading to vasogenic edema. It tends to be caused by hypobaric hypoxemia, causing an afferent–efferent imbalance in cerebral vasculature.* HAPE is caused by hypoxic pulmonary vasoconstriction and perhaps increased vascular permeability. It can cause severe hemorrhagic pulmonary edema.* Give dexamethasone 8 mg IV (IM is okay too) for suspected HACE. No mannitol. Hypertonic saline can be considered but is poorly studied, and probably not smart while still far from help.* Portable hyperbaric chambers can provide a substantial relative decrease in a patient’s altitude (the difference is more dramatic at higher altitudes), useful for temporization when immediate descent is impossible. However, they are bulky and completely envelope the patient, limiting further access for care. Provide other measures first, pressurize them therapeutically, then generally remove them from the bulky device for transport.* Acetazolamide may help accelerate the acclimatization process, but can only do so much, and has no role in treating acute mountain sickness.* >5,000 ft (1,500 m) or so is considered “high altitude” (some purists call 1,500–2,500 m/5,000–8,200 ft “intermediate altitude”). However, true altitude illness usually occurs above 3,500 m (11,500 ft),

    • 1 hr 8 min
    Episode 26: ICU sedation, mobility, and delirium with Dale Needham

    Episode 26: ICU sedation, mobility, and delirium with Dale Needham

    How to manage the intubated critically ill patient while keeping them awake, non-delirious, and mobile, with Dr. Dale Needham, FCPA, MD, PhD.







    Dr. Needham is a Professor of Pulmonary and Critical Care Medicine as well as Physical Medicine and Rehabilitation at the Johns Hopkins University. He is also director of their Outcomes After Critical Illness and Surgery (OACIS) group, an attending intensivist in the medical intensive care unit, and the medical director of the Critical Care Physical Medicine and Rehabilitation program.







    Takeaway lessons







    * Start vent sedation with as-needed boluses of fentanyl alone. This is primarily for tube-related discomfort, with the assumption that patients may not need sedation per se unless they demonstrate the need. More fentanyl is often needed early on. If a long-acting paralytic was used for intubation, do consider a one-time benzo push or a larger opioid bolus for the initial period of paralysis.* 25 mcg of fentanyl PRN every hour is a good starting point unless the patient is larger or opioid-tolerant. However, you can rapidly escalate the dose as needed. Even large bolus doses in a patient who has proven the need is preferable to routinely using a drip. Reserve the opioid drips for patients who require frequent boluses, and reserve sedatives for those who remain agitated after analgesia is in place.* Soft restraints will often be used initially as patients emerge, but then may come off if patients prove to be well-oriented and cooperative. Very loose restraints are also an option over tightly restrictive restraints, serving only as a reminder.* Mobility can start as soon as the day of intubation if the clinical picture and logistics are amenable.* Well-trained nurses may be the best people to determine the need for additional sedation, restraints, sitters, etc. Restraints may sometimes worsen delirium and agitation; assess for their effects.* Even in delirious patients, start with analgosedation (e.g. fentanyl)—these patients can’t tell you when they have pain, and pain is itself deliriogenic. After that, consider escalating to either dexmedetomidine, or PRN antipsychotics like haloperidol (which you can convert to oral quetiapine if it works).* Remember that antipsychotics will neither prevent or treat delirium, and are only acting as a sedative for safety’s sake. If electing that approach, monitor QTc, start low (e.g. 1 mg haloperidol IV) and double it as needed until good effect is seen.* Benzos are a last line, except in special circumstances (seizure, alcohol withdrawal) as they may worsen delirium, even if they temporarily hide it by extinguishing signs of agitation. Mostly, they defer the delirium to someone else’s shift. Hardly any patient goes from deep sedation to wakefulness without passing through a period of frank delirium.* Mobilize early, even in patients modestly delirious and confused; it helps engage them, manages the pain of immobility, and tires them out to enable better sleep. It does require some attention towards safety by nursing and therapists; safety events related to mobility are minimal in good systems.* It’s always hard to “escape” the vicious cycle of sedation and delirium once severe agitation is requiring multiple drips and deep sedation. Skilled nursing is key, with the shared understanding that sedation is harmful and needs to be (safely) weaned ASAP. Start with weaning the most deliriogenic medications, like benzos, then perhaps propofol. Expect a period of agitation and treat it with dexmedetomidine or PRN antipsychotics; use the approach of escalating antipsychotic as above, and if it works consider an oral antipsychotic for more steady state effect. * “Chronic” ICU patients (stuck there for weeks or months,

    • 45 min
    Episode 25: Rhabdomyolysis

    Episode 25: Rhabdomyolysis

    Initial workup, fluid management, renal replacement, and other subtleties of caring for the critically ill patient with rhabdomyolysis.







    Takeaway lessons







    * Rhabdomyolysis is defined by elevated levels of creatinine kinase and/or myoglobin in the serum secondary to skeletal muscle breakdown with release of cellular contents. Common causes are crush or compartment syndrome, prolonged downtime on hard ground in patients who fell and cannot stand back up, and a variety of less common phenomena.* Monitor with serum CK and/or myoglobin every 4–12 hours. Urine myoglobin is usually elevated, and AST/ALT, troponin, LDH, and potassium are all commonly high as well.* The mainstay of treatment is vigorous hydration to flush the kidneys and prevent nephrotoxicity from myoglobin precipitation in the tubules. Historically this was via sodium bicarbonate (as myoglobin is less likely to precipitate in an alkaline environment) and forced diuresis with mannitol. These can be considered, but isotonic crystalloid may be as good in most cases.* Do consider bicarb in the most severe cases, particularly if renal failure seems incipient. Maybe consider diuresis if the urine output is poor and fluid balance is increasingly positive. If oliguric due to AKI, consider reducing fluids, as the goal is urine output, not hypervolemia.* Consider trending CK until it peaks, which may require dilution by the lab if it exceeds the upper limit of their assay. A CK that continues to rise may indicate an ongoing source of muscle injury. Consider trending urine pH as well if alkalinizing the urine with bicarb, targeting a pH >6.5.* The lion’s share of rhabdo is mild or moderate, and often an incidental finding in the setting of other illness or injury. Occasional cases are severe and high risk for renal failure. The McMahon score can be used to try and predict these cases.* In general, the role of hemodialysis or CVVH is the same as for anyone: renal replacement if kidney injury progresses to the point where it’s indicated. Some experimental work is underway with super high-flux CVVH filters which may help clear myoglobin, but in general CRRT has no disease-specific effects on rhabdo.

    • 33 min

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