Category: Cases

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Our collaboration with Sarah Lorenzini of the Rapid Response RN podcast, discussing a case and general principles for diagnosing and managing obstructive shock. Check out the other episodes on shock in the Nurses’ Podcrawl 2024!

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We discuss the role of point-of-care ultrasound in evaluating the patient with kidney injury and assessing volume status, with Abhilash Koratala (@nephroP), nephrologist, Director of Clinical Imaging for Nephrology at the Medical College of Wisconsin, and champion of nephrology-focused ultrasound.

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Takeaway lessons

1. A quick kidney and bladder ultrasound to rule out urinary obstruction is appropriate for most significant AKIs, maybe even if it was done previously (as obstruction can develop at any time).
2. Ultrasound of the lungs and IVC help establish the presence of elevated filling pressures; if present, the VEXUS scan can be performed to establish the presence of venous congestion that might be contributing to kidney injury.
3. Pulmonary edema as evidenced by B-lines establishes that the patient is not fluid tolerant, and suggests that further volume loading may be harmful. It increases the chance that AKI is due to congestive nephropathy as well, although each can also occur in isolation (and of course AKI can be a cause, leading to volume retention and then pulmonary edema).
4. Abhilash does an 8-zone lung exam (2 anterior and 2 lateral zones on each side), which is plenty for cardiogenic pulmonary edema. He does not really count B-lines; if he sees B-lines in more than one dependent zone, he takes it as evidence the patient could be decongested.
5. IVC is a reasonable method of estimating RAP; it is not reliable to gauge fluid responsiveness or other questions. The internal jugular vein is a good fallback if the IVC is untenable or seems unreliable, such as if bandages limit access, or the presence of cirrhosis (which alters local vasculature in unpredictable ways). Look for the highest point of distention and measure roughly from the sternal angle, adding it to the right atrial depth to approximate the CVP (usually ~5 cm although this is not very reliable).
6. A non-plethoric IVC and absence of B-lines suggests a fluid tolerant patient. He uses the ACE guidelines of IVC >2.1 and <50% collapse with deep inspiration (sniff) to equate RAP ~15 mmHg.
7. In the presence of elevated RAP, VEXUS helps determine whether that change is likely to be affecting organ perfusion by altering flow characteristics. Higher VEXUS scores are well-associated with risk of AKI.
8. High RAP with a low VEXUS suggests that congestive nephropathy is not actively worsening renal function, whereas a higher VEXUS suggests the opposite. Serial VEXUS scans help track the progress of decongestion to dial in a patient to an optimal fluid balance.
9. VEXUS is a right-sided heart parameter, so the state of the left heart’s filling may differ somewhat (e.g. as evidenced by lung markers like pulmonary edema—so track your B-lines too!). It is probably more precise and reliable than other markers like peripheral edema.
10. Right and left heart filling should generally be well-linked. Venous congestion and elevated RAP usually indicate a well-filled LA as well, unless the lungs are acting as a significant resistor. If major PH is present, consider introducing measures like pulmonary vasodilators instead of further fluid loading; overdistending the RV will not help the LV.
11. Although portal vein pulsatility can usually move towards normal after optimal decongestion, hepatic vein waveforms may remain abnormal in some patients with TR, PH, etc. Flow chanegs in intrarenal vessels often lag behind other vessels, as renal edema takes time to resolve.
12. Hepatic vein waveform may be permanently blunted in cirrhotics, confounding it somewhat. Distinguishing the systolic and diastolic waves can also be hard to identify without ECG synching; ECG is highly recommended when available.
13. Portal vein is also probably unreliable in cirrhosis, due to portal hypertension and AVMs; it may be permanently pulsatile in some (although loss of pulsatility is still associated with decongestion). Since many cirrhotics have recurrent hospitalizations, you can compare against prior scans.
14. Intrarenal vessels are technically difficult, especially when patients cannot perform a breath hold; critically ill patients have a failure rate here >20%. It is easier in stable patients. However, CKD patients may have abnormal waveforms at baseline.
15. Overall, there should not be any disease state that falsely confounds ALL of the VEXUS vessels; while states like mechanical ventilation can increase flow changes and point to congestion, this is real congestion, not an artifact.
16. Invasive monitoring like a CVP or PA catheter replaces some of the function of the VEXUS scan, but VEXUS helps determine the degree of organ impact at the numbers reported by these devices. High filling pressures generally are associated with congestion and low pressures are associated with its absence, but VEXUS is often helpful in the gray area. Non-invasive measurements of filling using echo, such as RVSP or E/A and E/E’ may have a supplemental role as well; the latter may help distinguish cardiogenic from non-cardiogenic pulmonary edema, but do not tell much of a story about systemic congestion.
17. Femoral vein doppler could be a supplement to VEXUS, mainly when you cannot get or cannot trust one of the other vessels. It is farther from the heart, so may be less sensitive to changes in RAP. A normal femoral vein (continuous or mildly pulsatile) should probably not rule out venous congestion, but an abnormal femoral vein is very suggestive of it. This can sometimes be noted on routine DVT scans.
18. Abhilash runs a cardiorenal clinic where he finds outpatient VEXUS very useful to establish and monitor volume status. It is more difficult to use in a dialysis clinic due to lack of privacy and high patient volumes; quick lung ultrasound (8 or even 4 zone) might be more useful here.

References

Episode 4 with Philippe Rola on the VEXUS scan

NephroPOCUS

POCUS in AKI: Transcending boundaries: Unleashing the potential of multi-organ point-of-care ultrasound in acute kidney injury. Batool A, Chaudhry S, Koratala A. World J Nephrol 2023; 12(4): 93-103 [PMID: 37766842 DOI: 10.5527/wjn.v12.i4.93]

VEXUS for nephrologists: Koratala A, Reisinger N. Venous Excess Doppler Ultrasound for the Nephrologist: Pearls and Pitfalls. Kidney Med. 2022 May 19;4(7):100482. doi: 10.1016/j.xkme.2022.100482. PMID: 35707749; PMCID: PMC9190062.

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We discuss the phenomenon of CPR-induced consciousness (i.e. patients demonstrating awakeness during resuscitation) with Jack Howard, Intensive Care Paramedic at Ambulance Victoria in the northern suburbs of Melbourne, Australia, and first author on a recent literature review and Delphi-derived expert guideline on CPRIC management.

Takeaway lessons

1. Data is light, but perhaps 1% of cardiac arrests have some form of consciousness witnessed.
2. It is primarily a problem because of the potential to delay or interfere with care (either due to the emotional confrontation and surprise, or from actual physical interference with medical care). However, there are also ethical questions about patient suffering.
3. The first response in many people seeing CPRIC will be to stop CPR and assume they’ve made a mistake about loss of pulses.
4. CPRIC is associated with better outcomes, probably as a marker of better neurologic perfusion before and/or during arrest.
5. There was general agreement by the panel that ketamine should be used as first-line for CPRIC. If unavailable or if it fails, the group was unable to agree on a best second line; fentanyl, midazolam, or a paralytic are all options. In CPRIC that physically interferes with care, larger doses are appropriate.
6. Paralytics as a first line (without sedation) are never recommended.
7. There is minimal data on the effect on outcomes when CPRIC is treated. One small Ambulance Victoria study had a trend towards lower rates of ROSC when sedation was used.
8. Speak to patients as though they can hear and understand you.
9. It is not clear but very possible that a larger number of patients than those who demonstrate external awareness may have a degree of subclinical consciousness; interviews of survivors and EEG analysis has supported this.
10. Many CPRIC patients will have ROSC, but if they don’t, they are probably excellent candidates for ECPR/ECMO or other rescue interventions. A minimum of 45 minutes of resuscitation should be offered.

References

• The guideline: Howard J, Grusd E, Rice D, et al. Development of an international prehospital CPR-induced consciousness guideline: A Delphi study. Paramedicine. 2023;0(0). doi:10.1177/27536386231215608
• The preliminary scoping review: Howard J, Lipscombe C, Beovich B, Shepherd M, Grusd E, Nudell NG, Rice D, Olaussen A. Pre-hospital guidelines for CPR-Induced Consciousness (CPRIC): A scoping review. Resusc Plus. 2022 Nov 28;12:100335. doi: 10.1016/j.resplu.2022.100335. PMID: 36465817; PMCID: PMC9713363.
• The study mentioned about awareness during CPR: Parnia S, Keshavarz Shirazi T, Patel J, Tran L, Sinha N, O’Neill C, Roellke E, Mengotto A, Findlay S, McBrine M, Spiegel R, Tarpey T, Huppert E, Jaffe I, Gonzales AM, Xu J, Koopman E, Perkins GD, Vuylsteke A, Bloom BM, Jarman H, Nam Tong H, Chan L, Lyaker M, Thomas M, Velchev V, Cairns CB, Sharma R, Kulstad E, Scherer E, O’Keeffe T, Foroozesh M, Abe O, Ogedegbe C, Girgis A, Pradhan D, Deakin CD. AWAreness during REsuscitation – II: A multi-center study of consciousness and awareness in cardiac arrest. Resuscitation. 2023 Oct;191:109903. doi: 10.1016/j.resuscitation.2023.109903. Epub 2023 Jul 7. PMID: 37423492.

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We discuss the medications typically used after organ transplant, their impact on critical illness, and how to manage them when these patients show up sick—with Olivia Philippart, transplant clinical pharmacist specializing in liver and kidney transplant at University of Kentucky HealthCare.

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Takeaway lessons

1. Most kidney transplants will end up on a calcineurin inhibitor like tacrolimus (or the older cyclosporine), an anti-proliferative like mycophenolate mofetil (Cellcept) or the older azathioprine, and possibly corticosteroids (e.g. prednisone). Formulations for some of these may need to be adjusted based on your formulary, so consult your pharmacist to get the equipotent dose.
2. How these patients present, their degree of immunosuppression, and risk of rejection, are all heavily dependent on the time since transplant. A patient <6 weeks from transplant is high risk for nosocomial infections (e.g. post-op complications). A patient years out is mainly at risk of the same infections as anybody else, in addition to opportunistic infections related to their immunosuppression.
3. Latent viral infections unmasked by immunosuppression or acquired from the transplant are usually not a surprise, as these are tested for as part of the initial workup.
4. The highest risk of organ rejection and hence the highest degree of immunosuppression is in organs with substantial amounts of lymphoid tissue transplanted. The highest is small bowel, then lung, then heart/kidney/pancreas, then the least in liver (liver transplant can actually overall support immune function). Some livers can be maintained on monotherapy, while lungs usually need triple therapy, and often dual therapy is used in the middle category.
5. Durations of therapy for identified infections may be longer in the immunosuppressed than for routine ICU care.
6. Mycophenolate is the first agent to consider dose reducing or holding in the setting of active bacterial infection. How to handle this depends on the severity of infection and degree of concern for rejection.
7. Both our calcineurin inhibitors (tacrolimus and cyclosporine) are primarily cleared in the liver and gut, so when there is liver impairment or bowel problems, dose decreases are often needed. Dietary intake also reduces drug absorption whereas NPO status may increase it. These drugs are heavily protein bound so albumin fluctuations (e.g. from malnutrition) may impact free levels.
8. Drug interactions are common as well; CYP3A4 or PGP inhibitors like diltiazem or verapamil, azole antifungals, amiodarone, macrolides (although not azithromycin), and paxlovid will tend to increase levels, while inducers like phenytoin or phenobarbital will tend to decrease them.
9. Overall, the therapeutic index of the calcineurin inhibitors is small, so have a low threshold for checking trough levels early and often.
10. After holding a dose, the serum levels will normalize within 3-5 half-lifes, but full return of immune function may take several weeks. However, the baseline level of immunosuppression is usually not so profound that the difference between “off” and “on” is huge and binary.
11. Organ rejection is possible but rare when drugs are acutely held (for days, maybe a week or two) in setting of severe infection, as this is already a relatively immunosuppressed state. However, this depends heavily on the time from transplant, and the organ transplanted.
12. Mycophenolate levels (or mercaptopurine levels for the older azathioprine) tend not to fluctuate as much; the metabolism (via glucuronidation) is not as sensitive to hepatic function, so monitoring levels is rarely needed.
13. Most of our immunosuppressants are not significantly renally cleared, so renal injury (even dialysis) usually require no dose adjustment. However, they can be nephrotoxic, so high levels may CAUSE renal injury, not vice versa.
14. Tacrolimus is available in either immediate release capsule (taken twice daily) or a long-acting form (taken once daily). The latter helps to decrease peaks and some of the neurotoxicity (seizure, tremors), but cannot be opened. There is an 80% conversion between formulations (multiply the long-acting dose by 1.2, then divide by half to get the short-acting BID equivalent). Levels checked should always be troughs.
15. Short-acting tacrolimus capsules should not be opened and put down tubes, but can be opened and given sublingually (50% dose reduction)—just dribbled under the tongue—although nurses need to take special precautions like gowning and double gloving. There is also a liquid tacrolimus formulation available.
16. IV tacro exists, but has substantially higher nephrotoxicity, and the dose conversion is tricky; other routes are preferred.
17. Cyclosporine is available in suspension which can go down a feeding tube, or via IV form (dose reduction needed).
18. IV mycophenolate is available (1:1 conversion), as well as a liquid suspension.
19. Steroids can be used in the ICU as usual (e.g. stress dosing), and indeed temporarily converting transplant patients to a pure steroid regimen is a reasonable approach during critical illness (remember: 20 mg hydrocortisone is equivalent to 5 mg prednisone).
20. It’s generally sound to touch base with someone who knows a patient’s transplant history, even years out (often just their normal nephrologist, pulmonologist, etc in that case, not necessarily the original transplant team), when these patients are admitted for critical illness.
21. Calcineurin inhibitors can cause headaches, seizures, even PRES, hyperkalemia and hypomagnesemia, and hypertension, hypercholesterolemia, hyperglycemia/diabetes. Attributing these effects to the drug is usually a diagnosis of exclusion.

References

From: Fishman JA. Infection in Organ Transplantation. Am J Transplant. 2017 Apr;17(4):856-879. doi: 10.1111/ajt.14208. Epub 2017 Mar 10. PMID: 28117944.

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We discuss assessing patients prior to intubation or other airway management, including both elective and emergent circumstances, with Dr. Jed Wolpaw, anesthesiologist and intensivist from Johns Hopkins, anesthesiology residency program director, and host of the ACCRAC podcast.

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Takeaway lessons

1. Edentulous (toothless) patients are usually easier to intubate, but harder to mask ventilate. Heavy beards are harder to mask (can you trim it, or cover it with a Tegaderm?), larger neck circumferences, and larger tongues likewise.
2. Consider the history, particularly involving the head and neck anatomy. Is there surgical history here? Jaw or oral surgery? Prior trachs or oral/neck radiation? Rheumatoid arthritis or Down syndrome (which can cause atlanto-occipital instability and may warrant trying to limit any forced neck extension)?
3. Start by looking into the patient’s mouth (mouth open, sitting up, no “aah”):
   • Mallampati score (do you see the entire uvula, part of it, soft palate, or hard palate only?)
   • How is the dentition? Remove dentures if present. Are there loose teeth?
   • Is there an excess of soft tissue in the mouth (large tongue, etc)?
4. Evaluate the thyromental distance (thyroid bump to chin); <3 cm (or fingerwidths) suggests a more “anterior” airway.
5. Evaluate neck flexion and extension (passively if necessary) to appreciate limitations in neck mobility.
6. If the patient is able, evaluate how well the jaw can protrude/prognath: ability to bite more of the upper lip with the lower teeth is a good thing. This is probably the single most predictive test for airway difficult, although it usually requires patient cooperation.
7. Review the chart (or ask the patient) for prior documentation of intubation or anesthesia to determine if they have a history of a difficult airway. This can require some interpretation of the context and who was intubating previously. Good practice when documenting: write exactly what you did, and if it was difficult, write why! If you used a technique like awake intubation, a bougie, etc for elective or training reasons, document that reason so they don’t earn a label of a difficult airway forever.
8. The STOP-BANG score is used to predict post-anesthesia airway obstruction (i.e. OSA), and probably has some association with faster deoxygenation and difficult mask ventilation, but is generally not super relevant for intubation.
9. A patient with any concern for difficult intubation warrants consideration for factors also contributing to difficult LMA placement or cricothyrotomy. LMAs are difficult to place when the mouth opening is very small (about 2 inches) or the oral-laryngeal anatomy is unusual, and crics are difficult when the neck anatomy is impossible (eg a superimposed tumor, goiter, or heavily distorted anatomy). A patient who cannot have a cric may warrant an awake intubation to avoid the risk of inducing a patient who cannot be rescued.
10. Obesity is not a predictor of anatomically difficult intubation. Mask ventilation may be a little harder if there is increased oropharyngeal soft tissue. It is a predictor of physiologic difficulty (faster desat), though.
11. For emergent intubations: confirm code status, briefly evaluate the head/neck/mouth, use video laryngoscopy. Use hemodynamically stable agents for induction and reduce the dose, and ensure the team knows to subsequently sedate any patient who received a long-acting paralytic. Have a vasopressor drip ready, or better yet, running. Always set up everything and be prepared for every eventuality before you take away a patient’s ability to breathe.
12. Either RSI with paralytics, or perform awake intubation. Otherwise, never RSI the critically ill without neuromuscular blockade, which will reliably reduce your chances of success. Short-acting paralytics (succinylcholine) are brief—i.e. not much longer than the apneic period of a short-acting sedative—and long-acting paralytics (eg rocuronium) can be reversed with suggamedex, in the rare situations where letting the patient wake up and resume breathing is a smart move.
13. The one exception might be a ketamine-only intubation, which generally keeps the patient breathing, allowing you to either proceed to paralyzing or not depending on what you see, or maybe allow them to wake up.
14. While it’s nice if an emergent intubation has been NPO, it probably won’t change your technique; changes in gut motility in the critically ill mean almost anybody can have stomach contents. Treat most ICU patients as if they have a full stomach, i.e. RSI. The one exception: the PREVENT trial showed that mask ventilation during induction (usually a no-no for RSI) of critically ill patients does not increase aspiration risk and does reduce hypoxemia, so should probably usually be done.
15. In the highest aspiration risk patients like SBO or upper GI bleeding, keep the head of bed elevated, ensure ample/multiple suctions catheters, and be ready/willing to intubate the esophagus intentionally with your ETT and place it to suction to divert the stomach contents while you use a fresh ETT to intubate the glottis. Placing an NG beforehand to decompress the stomach is hit or miss as it can induce vomiting; it works better in a fully awake patient (who can manage any vomiting).
16. We should probably still learn and teach direct laryngoscopy, but do so using a video scope with regular-geometry blade.

References

1. PREVENT trial

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We discuss head and neck surgery with Dr. Alexandra Kejner, otolaryngologist at the Medical University of South Carolina specializing in transoral robotic surgery, reconstructive surgery including microvascular free tissue transfer, salivary neoplasms, and sialoendoscopic procedures.

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Takeaway lessons

1. Robotics has enabled much less invasive approaches to many head and neck procedures.
2. Major airway procedures create edema, and there is always risk for bleeding, so patients often remain intubated overnight.
3. The other common ICU indication is a free flap, a portion of tissue (potentially including skin, subcutaneous tissue, muscle, even bone) removed from a remote site and transplanted into the head and neck area, with vessels anastomosed. These are at risk of failure and require close monitoring.
4. Most of these procedures will involve placing a tracheostomy, and potentially a PEG (or NG). This facilitates both surgical access and early recovery.
5. Tumors are superficially resected with adequate margins, then reconstruction begins. Meanwhile, exposure of deeper structures and deeper resection occur, which may involve a jig to guide the removal (prepared in advance from imaging), and a matching cut to prepare the flap tissue. Lymph nodes are removed en bloc. Then the flap is transplanted and vessels anastomosed (at least one robust artery and vein), using microsurgery and teeny sutures (often 8-0 nylon).
6. As a supplement to the clinical exam, an implantable Doppler monitor is occasionally left in place to augment post-op monitoring of perfusion, as well as sometimes a Vioptix near-infrared spectroscopy device which performs real-time tissue oximetry.
7. On POD 0-1, hourly nursing monitoring of the flap is usually needed, with periodic provider checks. Changes in the exam (swelling, turgor, cap refill, color), signal, or bleeding may require return to the OR for revision. A single ICU night is the norm, although comorbidities are common and may require a longer stay if the stress of surgery unmasks other problems.
8. Laryngectomy may be performed, involving removal of the larynx (voice box), leaving a blind pouch; the lungs no longer connect to the upper airway in this case, and the entire team should be aware of this anatomy, as the patient cannot be intubated or their airway otherwise managed from above.
9. Most flaps will be on a baby aspirin and enoxaparin, but occasionally may use a heparin drip.
10. Most will receive three doses of dexamethasone, both to reduce edema and to treat any adrenal insufficiency.
11. Chlorhexadine or salt water oral rinses are performed to keep the operative site clean.
12. Multimodal pain management is needed for both the oral site and the donor flap site.
13. A drop in the Vioptix signal from the initial post-op reader, neck swelling, or difficulty breathing (dyspnea, hypoxia, etc) all warrant immediate involvement of the surgical team for danger to the airway or the flap. Flaps might also turn purple from venous congestion, sometimes a little later, also a surgical emergency.
14. A questioned flap might be scratched to see if it bleeds (which is good).
15. A patient in shock might need vasopressors, fluid, or to be hypotensive, none of which are great for a flap. A balanced approach is probably best. A low-dose phenylephrine drip may be the most appealing pressor, and vasopressin might be the riskiest. MAP >65 is a minimum, some prefer higher (>80).
16. Intro-operative feeding has been used in some centers due to the prolonged procedure times.
17. Flap failure historically was most often from a venous clot, but this has reduced over time; nowadays it’s often late failures due to a salivary fistula contaminating the area and creating a region of digestion, clot, and breakdown.
18. Surgeons will occasionally request deeper sedation (or even forcing the patient to maintain a specific neck position) to avoid dislodging monitors, disrupting a very delicate anastomosis, etc.
19. A swollen or firm anterior tongue, ooziness in the mouth, or a difficult airway on the initial intubation may lead a surgeon to request delaying extubation.
20. The immediate post-op appearance usually heals into a better eventual aesthetic result. Occasionally measures like prosthetics can be used.

References

1. Vasopressors improve outcomes in autologous free tissue transfer: A systematic review and meta-analysis
2. Postoperative Use of Vasopressors in Head and Neck Microvascular Reconstruction

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We learn about liver transplant with Dr. Meera Gupta, transplant surgeon at the University of Kentucky Healthcare Transplant Center, and surgical director of the Kidney and Pancreas Transplant Program. We discuss eligibility, triage, the peri-operative course, and important post-op complications.

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Takeaway lessons

1. Liver transplant eligibility is based on need, not time on the list. The MELD score (MELD 3 now, including albumin) is used for this, with MELD >9 (historically >15) considered the cutoff for transplant potentially exceeding the risk of not transplanting.
2. Livers can now be placed on warm perfusion pumps, allowing continued viability for much longer. This is mainly used in donors who died from cardiac death, those with high BMI or similar risks for primary non-function (i.e. the transplanted liver never starts working), and longer transport distances or expected operative times.
3. Incision is a large right subcostal incision, extended as needed. The liver hilum is dissected, preserving the feeding vessels. Caval clamping may be tested, then the liver is removed. This anhepatic phase in minimized to <60 minutes, preferably <45 minutes. The new liver is then anastomosed to the portal veins, vena cava, hepatic artery, and the bile duct. Some instability can occur during reperfusion, such as right heart strain, electrolyte abnormalities, or volume shifts.
4. Patients will usually remain intubated post-op, lines in place. Sedation ideally is limited so the patient can rouse and confirm the absence of encephalopathy. Systolic BP is closely watched (goal >90), as diastolic BP tends to be low in most liver failure patients. Hepatopulmonary patients can rest on the vent a little longer and are expected to remain on oxygen for the time being. Patients can be fed once extubated and stable.
5. High-dose steroids are loaded up front and then tapered, and oral immunosuppression initiated soon after.
6. Some AKI is common. Colloid like albumin is favored early.
7. Chronic thrombocytopenia is common and is monitored to determine when DVT prophylaxis can be started. Platelets >20k are targeted.
8. If INR >2, vitamin K is given empirically. FFP is usually not given prophylactically. Bleeding is usually considered a little preferable to clotting, in terms of ease of treatment.
9. A liver duplex is performed in the first 24 hours to ensure the new vascular supply is patent.

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We learn about pancreaticoduodenectomy (the Whipple) with Michael Cavnar (@DrMikeCavnar), surgical oncologist at University of Kentucky, with a fellowship in Complex General Surgical Oncology from Sloan Kettering. He specializes in GI surgical oncology (liver, pancreas, stomach, etc), with ongoing research in GI stromal tumors and hepatic artery infusion pump chemotherapy.

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Takeaway lessons

1. The Whipple involves an aggressive resection and reconstruction of pancreatic head tumors. Along with the head of the pancreas, the entire duodenum, the bile duct (up to near the entry of the cystic duct), the gallbladder, and usually the distal third of the stomach, along with the nearby lymph nodes, are all removed. There are then anastomoses at the small intestine, the bile duct, and the stomach.
2. The pylorus of the stomach is generally removed, but can be left in a pylorus-sparing Whipple. The benefit of this is not well-established.
3. It is almost always done for malignancy (or occasionally for other conditions like pre-malignant changes or pancreatitis with stricture). Mortality in high-volume centers is a few percent, and usually involves deaths in the first 90 days due to various complications more than death in the OR.
4. Hypotension in the first 24 hours is a poor sign, as it may lead to bowel ischemia, portal vein thrombosis, anastomotic ischemia, or other injuries to vulnerable areas. If getting behind on hemodynamics, consider holding an epidural if present.
5. NG tubes are often placed to around 55 cm. They should not be advanced or replaced by the ICU staff, as the stomach has been shortened, and advancing the tube may traumatize the anastomosis. Bilious gastric drainage is normal in anyone with post-Whipple anatomy. Patients will generally remain NPO for several days.
6. Patients will emerge with 1-2 surgical drains. Output should be serosanguinous (sparsely bloody at most), less than 200ml/hr or so. It may occasionally be lymphatic (clear to lightly serosanguinous), which can be somewhat higher volume. Output should not be bilious or feculent.
7. Early bleeding requiring surgical take-back is uncommon and usually obvious in the drains, unless they clot, which can occur. A pancreatic leak can also dribble onto the stump of the gastroduodenal artery, causing erosion, and subsequent bleeding usually tracks back up into the bowel lumen and hence GI bleeding.
8. Respiratory distress can be treated with oxygen or high-flow nasal cannula, but positive pressure (eg. BiPAP) should be used with caution and consultation with the surgical team, particularly within the first two weeks post-op, as aerophagy can apply pressure to the bowel anastomosis.
9. A leaking pancreatic anastomosis causing fistula will tend to marinate the gastroduodenal artery’s anastomosis in pancreatic juices, creating a pseudoaneurysm; this can be managed early before it turns into massive hemorrhage. Any streak of fresh blood in the drainage should be considered a sentinel marker of this and immediately evaluated, usually involving CTA or pancreas-protocol CT. The treatment of choice is IR embolization and stent, not open repair.
10. Glucose control in diabetics will usually be worse post-operatively, both due to stress and due to removing a portion of the pancreas. SGLT inhibitors can cause strange metabolic effects as well if not fully washed out.
11. Exocrine pancreatic insufficiency can be discovered once feeding begins, usually manifesting as diarrhea (steatorrhea), and can be treated with pancreatic enzyme supplements.
12. A proton pump inhibitor should generally be used post-operatively.

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We explore aortic dissection with Travis Hughes, vascular surgery fellow from the University of Kentucky, including classification, medical management, and nuances of the surgical perspective.

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Takeaway lessons

1. Type B dissections do not involve the heart or coronaries, but Type A vs B nomenclature is falling out of favor versus more anatomically specific labeling; this system helps characterize the gray area between the innominate and the left subclavian.
2. The main sequelae of concern in type B dissection in end organ ischemia. This may be dynamic, due to movement of the flap to obstruct the feeding artery, or static, due to occlusion by thrombosis.
3. Hypotension is unusual in type B dissection and should be a red flag for another factor, such as involvement of the heart (coronary dissection, tamponade), or rupture.
4. Rupture is not a common event in dissection (as compared to aortic aneurysm), but can occur.
5. Medical management of type B dissection involves controlling the impulse against the dissection flap by reducing heart rate and blood pressure. SBP <120 and HR <80 are reasonable standard goals, but should be customized somewhat to the patient; allowing higher goals in a pain-free patient, particularly one who is experiencing sequelae of relative hypotension may be reasonable.
6. During initial presentation, impulse control may prevent dissection from extending over a period of hours. Later, once it has thrombosed and scarred, risk may be somewhat less.
7. Dissection involving the renal arteries can be explored using doppler ultrasound in skilled hands.
8. Focal neurologic deficit should prompt concern for both stroke, and (in the lower extremities) thrombosis.
9. First line is usually an IV beta blocker for heart rate and either IV beta or calcium channel blocker for BP. Esmolol is a classic beta blocker, although involves a large volume of infusate, and is not always very effective. Labetalol and nicardipine are nice choices. Nitroprusside is usually a rescue.
10. Favor the right radial artery for an arterial catheter, as the left arm will sometimes be needed for the repair.
11. Transition to oral agents as they stabilize. A repeat CTA 5-7 days from admission (often prior to discharge) is usually appropriate.
12. The most common indication for repair is aneurysmal degeneration at the dissection site. Extension of the dissection, in the setting of appropriate medical management, is less common although possible, and may also indicate the need for repair.
13. The primary goal of repair is to cover the entry to the dissection, and potentially stenting to expand the true lumen. When there is involvement of the iliac arteries, stenting is usually needed there. Malperfusion to visceral vessels is often corrected with these maneuvers, but they can be specifically stented or thrombectomy performed if needed.
14. Open repair of type B dissection has become vanishingly rare due to high morbidity and rare indication.
15. Stenting of the aorta creates risk for spinal cord ischemia, so keep BP higher. Extremity neuro changes should prompt driving the MAP >90, naloxone, and IV steroids.
16. Lumber drain placement probably reduces this risk, and can be placed either reactively or proactively. Neurosurgery and/or anesthesiology or interventional radiology may do this.
17. Shorter ischemic time to organs or extremities, and baseline vasculopathy (which gives time for the body to develop a tolerance to it), portend better recovery after revascularization. Prolonged ischemia to extremities may require amputation or at least fasciotomies to prevent compartment syndrome.
18. Aspirin and perhaps clopidogrel (with or without a load) will usually be needed post-operatively.
19. Infection of long-standing grafts are not common but can occur. Contrast imaging and perhaps tagged WBC scans (nuclear scintigraphy) can identify these. Surgical removal may or may not be possible and tends to be morbid.

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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.

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Takeaway lessons

1. 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.
2. 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.
3. 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.
4. Try to get a urine sample before giving antibiotics.
5. 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.
6. Obstructing stone + UTI + unstable with sepsis = emergent decompression within hours. Overnight cases should generally be drained overnight. Stable patients can potentially wait longer.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. Stent removal can sometimes precipitate instability as well if there is some degree of infection present.