Author: Brandon O

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Looking at trauma from the perspective of a surgeon, with a focus on the perennial dilemma of when a patient needs surgery. Our guest is trauma surgeon Dr. Dennis Kim (@traumaicurounds), associate professor of Clinical Surgery at UCLA and medical director of the Harbor-UCLA Medical Center SICU, as well as host of the Trauma ICU Rounds podcast.

Takeaway lessons

1. Trauma patients who are hypotensive or otherwise unstable should be assumed to be bleeding, bleeding, bleeding until proven otherwise, and should have a very low threshold to proceed directly to the operating room for exploration.
2. Airway is not the first priority in most trauma patients and can often wait until a patient is resuscitated—in many hemorrhaging patients, it can wait until the OR. Likewise, many penetrating injury patients with palpable pulses can wait for further resuscitation (whether blood or anything else) until surgery. The treatment for bleeding is hemostasis.
3. The exception is patients with concomitant brain injury, in whom permissive hypotension should not be allowed. However, don’t delay the unstable patient from the OR by getting a CT of the head.
4. Don’t forget examination of the back, and hair-bearing areas like the axillae and groin, which can easily hide penetrating wounds.
5. Consider using the shock index, the heart rate/SBP, to detect underlying shock. Over .8 or 1 is highly suspicious.
6. Operative prep for exploratory laparotomy is usually from the chin to the knees. Although a midline laparotomy incision is the typical starting point, injuries can track more widely than you expect, and there should be the ability to open the chest or access the groin (for femoral exploration, conduits, etc) without repositioning or re-prepping.
7. Damage control surgery involves evacuating hematoma, packing to provide initial hemostasis, then securing bleeding (by coagulation, suturing, packing, etc), resecting or reperfusing ischemic tissue, and securing injured bowel. In patients with continued metabolic or coagulopathic instability, surgery typically stops there with the abdomen left open and a wound vac (e.g. Abthera) placed. More stable patients may tolerate more extensive initial repairs.
8. The most expeditious repair for open bowel injury is simply stapling the bowel shut in discontinuity. However, there are some arguments for repairing it early (by anastamosis/stoma creation), as discontinuous bowel becomes edematous, becomes an obstacle to later closure, and may be difficult to eventually reconnect.
9. Orthopedic injuries should be manually reduced and perfusion ensured, splinted (e.g. pneumatically), then definitively addressed by Orthopedics at their convenience. Traction splinting is usually not done in the ED. In patients planned to receive a contrast CT, perfusion to a threatened limb can often be easily evaluated by simply adding an arterial study (extremity run-off) to your pan-scan.
10. Ultrasound (eFAST) and plain x-rays (chest and pelvis) are useful tools for rapid evaluation in the ED. Although not as definitive as CT, they are safer and quicker, and can rapidly rule-in many problems needing immediate intervention.
11. Instead of giving TXA as the CRASH dose of 1 g up front plus a 1 g drip, give 2 g upfront. The drip tends to get forgotten.
12. Bowel edema noted on CT should raise suspicion for occult bowel perforation, which is very difficult to primarily visualize on CT.
13. Serial abdominal exams are a valid way to follow a questionable abdomen. These should ideally be repeatedly done by the same person, looking for worsening tenderness, pain, or rigidity, and combined with lab trends (e.g. trending a CBC every 4–8 hours to follow the leukocytosis).
14. The lungs mirror the abdomen! Worsening respiratory status should raise suspicion for a worsening abdominal process, such as evolving infection. Evaluate such things with a contrast CT; non-contrast scans are very difficult to interpret in a complex abdomen.
15. When assessing for possible infection in a post-surgical abdomen, antibiotics, patience, and possible IR-guided drainage (after enough time has passed for abscesses to organize) are usually the mainstays. Surgical exploration is helpful only when a specifically surgical process exists, such as a leaking dowel, and becomes increasingly risky as time passes and adhesions develop. Diagnostic laparoscopy or enteral contrast can occasionally be helpful in picking up a surgical leak.

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Evaluation of ischemic stroke, decisions for tPA and thrombectomy, supportive critical care, and monitoring for cerebral edema—with returning guest Thomas Lawson (@TomLawsonNP), nurse practitioner in the neurocritical care unit at OSU Wexner Medical Center and James Cancer Hospital. Thomas is now also a PhD student at the OSU College of Nursing where he studies the epidemiology of delirium in critically ill stroke patients, and recently cofounded the Board Review Associates AG-ACNP board review course.

Takeaway lessons

1. The first priorities after suspected ischemic stroke is head CT to rule out hemorrhage, screening for tPA rule-outs, and establishing a “last known normal” time. The window for systemic tPA is 3-4.5 hours from known onset of symptoms, although the sooner the better.
2. Patients who are not candidates for tPA should receive some form of perfusion imaging (such as a CT perfusion scan) to characterize the size of the infarct and at-risk penumbra, as well as angiography (e.g. CTA) to assess for the presence of large-vessel occlusions (e.g. ICA, M1), which may mean there is an opportunity for endovascular interventions such as thrombectomy. Smaller vessel occlusions are a less evidence-supported zone and are more dependent on the interventionalist’s judgment.
3. If there is an opportunity for thrombectomy in a patient who is not a tPA candidate (and these days, potentially even one who is), yet your center cannot perform it, consider stat transfer to somewhere that can.
4. The preferred initial (and follow-up) neurologic exam is the NIH stroke scale. Check a blood glucose and blood pressure as well.
5. Post-tPA and/or thrombectomy patients should go to a neuro-capable ICU for hourly neurologic checks and blood pressure control.
6. BP should be maintained under 180/105 after tPA, or usually somewhat lower (e.g. <160) after thrombectomy alone. Use labetalol and/or hydralazine but have a low threshold for using a drip, usually nicardipine. The newer, quicker-titrating drip clevidipine can be useful too. Later, blood pressure targets can be down-titrated and eventually brought towards “normal” — but watch out for pressure-dependent neurologic function from imperfectly-reperfused stenoses.
7. Sodium should ideally be normal-ish early. If edema occurs later in the setting of large strokes, you may need to drive sodium up to provide an osmolar gradient, either by a hypertonic infusion or intermittent boluses.
8. Chemical DVT prophylaxis should be held 24 hours after tPA (along with aspirin and pretty much anything else that could make you bleed), after which you’ll repeat a CT to screen for bleeding. If still none, you can and should start heparin or LMWH. When to start or resume full anticoagulation is a more nuanced question, as large strokes always portend a risk of hemorrhagic conversion.
9. A non-urgent MRI is usually nice to evaluate the degree of infarction, although it infrequently changes care.
10. Medium- and long-term recovery is variable and depends heavily on the patient and various other factors including luck. Early, high-quality rehab is key.

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The art of taking a critically ill, heavily sedated, floridly delirious patient on aggressive vent support and pulling them out of the loop of sedation, immobility, and delirium. With Kali Dayton, ACNP-BC (@HomeIcu), critical care nurse practitioner and host of the Walking Home from the ICU podcast, where she looks closely at these issues, including interviews with survivors describing their ICU experiences.

A spiritual successor to our talk with Dale Needham, this time focusing more on details and practical approaches.

Takeaway lessons

1. Good care to optimize long-term function is also good care to optimize short-term survival and morbidity.
2. Benzodiazepines are normally a poor choice for sedation given their deliriogenic properties. However, using benzos in patients with alcohol dependence is more appropriate. It can also be rationally used in more subacute patients in whom benzos aren’t being used as sedation but only as anxiolytics—i.e. low doses of an agent like clonazepam to preserve level of arousal but treat anxiety, much like it’s used in the outpatient setting.
3. The combative behavior of delirious patients isn’t inexplicable; it’s a rational response to their perceived situation, which often involves vivid hallucinations of sexual abuse, torture, fractured realities, threats to loved ones, and similar horrors.
4. Favor dexmedetomidine in patients who do need a sedative drip, but aim only for calm, not a depressed level of consciousness.
5. Delirious (non-combative) patients can often still be mobilized to the extent tolerated, and it tends to actually improve their mental status. Limited activity is better than none. Concerns for self-extubation are usually easily managed by gentle restraint or redirection, as these patients are usually physically weak. A dexmedetomidine drip is not necessarily a contraindication to mobility.
6. Ventilator settings are rarely a contraindication to mobility. Increased FiO2 may be necessary and is acceptable. Modes can be adjusted as needed. While exertion may increase respiratory needs, this change is rarely precipitous or “dangerous”; adjustments can simply be made as needed.
7. Fatigue induced by exercise is a good thing and may facilitate further reduction in sedation. Allow patients to nap, but not too long (to preserve a normal sleep-wake cycle). In an ideal world, aim for three mobility sessions daily: two on the day shift and one before bed.
8. Proning does not necessarily mandate deep sedation and/or paralysis. It can be a “therapy, not a lifestyle,” with patients proned for a period of time (but awake and interactive) and then turned back up to perform mobility and other activities.
9. Awake, non-delirious patients can require more “work” to mobilize etc, but in many other ways require less work. They understand their situation, can assist with their own care, protect their own tube, etc. They are part of their care, not working against it.
10. With good care, tracheostomies are rarely needed for the most common reason of oversedation and weakness. Mobility and light sedation can be practiced without them. However, they may still occasionally be needed for truly refractory lung disease or anatomic issues like airway abnormalities.
11. Sedated patients appear to be resting and comfortable, but they are not, and follow-up interviews reveal they are actually internally suffering from their delusions. On balance, most would much rather be awake but experiencing their true reality (even if bored or uncomfortable) rather than sedated and experiencing the horrific false realities of delirium.

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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

1. 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.
2. Ask what triggered DKA. The most common causes are medication non-compliance (or an inadequate regimen), and a stressor like infection.
3. 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.
4. 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.
5. 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.
6. 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.
7. 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.
8. Once the drip comes off, they should eat some kind of meal.
9. Check one more chemistry, then they can usually leave the unit.
10. 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.
11. In general, disable insulin pumps upon admission; they can potentially be restarted once DKA has resolved. Endocrinology is helpful for this.

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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

1. 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.
2. 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.
3. 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. <200 ml in 2 hours, consider moving towards dialysis early.
4. Tolerate a modest pressor increase induced by diuresis, such as norepinephrine within the 0.2 micrograms/kg range. However, volume overloaded patients usually tolerate volume removal fine, even if on pressors.
5. Furosemide has a threshold and a ceiling, and there’s not much space between them, so feel free to give go fairly big in dosing without fear of complications.
6. An elevated creatinine due to intrinsic renal injury is no contraindication to diuresis. In fact, it may improve with volume removal, if secondary to congestive nephropathy.
7. Labs twice a day is fine for almost everyone, if labs are needed at all.
8. Generally, don’t tap transudative pleural effusions solely for the purpose of fluid removal, except in non-intubated patients with very large effusions and respiratory distress.
9. In general, wean FiO2 using pulse oximetry, not the blood gas.
10. Even more than absolute finalization of cultures, deescalation of antibiotics should be informed by identification of the source and patient risk factors. A “surprise” resistant organism not predictable using these facts is a fairly uncommon event.
11. Have a low threshold to switch stable, intubated patients to a pressure support mode. If fatiguing, consider giving more support instead of going to a control mode. PS of up to 8–15 cmH2O is very reasonable, and usually more comfortable (and less sedation-demanding) than forcing patients to accept a low tidal volumes on VCV. If a rate is needed, consider pressure control. A very variable tidal volume on PS may also be a good reason to give a set inspiratory time or volume.
12. Night-time or late extubations are mostly dependent on staffing. If experienced providers are on hand, the clock should be no deterrent. If staffing is limited, it might give more pause. On the other hand, if your extubation practices are aggressive, most of these candidates were probably already extubated in the morning.
13. Consider routinely extubating very obese patients to BiPap, and elderly patients (>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.
14. When to downgrade patients from the ICU is less dependent on how long it’s been since extubation or getting off pressors, and more dependent on whether any disease process with the potential to worsen is still present (such as an uncontrolled source of sepsis).
15. The most common cause of error in deescalation is doing it too slowly. Being “conservative” exposes patients to iatrogenic harm from prolonged intubation, antibiotics, lines, and ICU stays; that harm of omission isn’t better or safer than the alternate harms of commission. A patient who is admitted to the ICU, aggressively resuscitated, then rapidly improves and gets turned around isn’t moving “too fast”—that’s exactly the goal. Step up fast, step down fast.

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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

1. Scene safety comes first, which in a high-altitude setting includes consideration for the acclimatization of your team.
2. Other than ABCs, think WMX:
   1. W= Factors of the Wilderness environment, such as altitude and exposure.
   2. M= Materials and Manpower; what’s needed for the rescue and what’s available?
   3. X= Exit strategy; from the start, think about how (and how rapidly) you’re getting out.
3. Spinal stabilization is not feasible until a suspended patient can reach a stable location.
4. 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.
5. Lowering a suspended patient is always easier than lifting them.
6. 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.
7. 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.
8. The first treatment for any altitude sickness is oxygen; the second is descent. Everything else is temporizing or supportive.
9. 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.
10. HAPE is caused by hypoxic pulmonary vasoconstriction and perhaps increased vascular permeability. It can cause severe hemorrhagic pulmonary edema.
11. 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.
    1. 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.
12. Acetazolamide may help accelerate the acclimatization process, but can only do so much, and has no role in treating acute mountain sickness.
13. >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), aka “very high altitude,” as above this level, it becomes impossible to hyperventilate enough to normalize alveolar oxygen concentration (PAO2).
14. Above this level (~10,000 ft), gradual acclimatization is recommended. Sleeping altitude should only increase by about 500 m (1500–2000 ft) per day, and every second day should be a rest day.