Maryland CC Project

h1, h2, h3, h4, p, li {font-family: 'Noto Serif', serif;} p, li {font-size:1.8rem; color:black;} Rory Spiegel, MD, Critical Care Medicine Fellow, Division of Pulmonary & Critical Care Medicine and Clinical Instructor, Department of Emergency Medicine at the University of Maryland SOM, presents the weekly multi-departmental critical care fellows’ lecture on “Starling, Guyton, and Ultrasonographic Findings of Venous Excess.” Lecture summary written by Robert Brown, MD A growing body of evidence is calling for thoughtful use of IV fluids * The FEAST trial from Andrews et al. Effect of an early resus protocol on in-hospital mortality among adult with sepsis and hypotension. JAMA. 2017;318(13):1233-1240* The CLASSIC trial from Hjortrup et al. Restricting volumes of resus fluid in adults with septic shock after initial management. Intensive Care Med 2016 42:1695-1705* Comparison of two fluid management strategies in acute lung injury by the national heart lung and blood institute acute respiratory distress syndrome clinical trials network N Engl J Med 2006;354:2564-75.* ANDROMEDA trial from Hernandez et al. Effect of a resus strategy targeting peripheral perfusion status. JAMA. 2019;321(7):654-664 Moving from the concept of fluid responsiveness to the concept of fluid tolerance * A healthy person is fluid responsive but driving fluid volume high enough to no longer be responsive is to overload them* IVF do not stay intravascular for long. Only 15-30 minutes* Giving fluid quickly corresponds to 3rd spacing even faster. The physiologic basis for fluid tolerance * Mean systemic pressure is 7mmHg on the venous side (that’s the pressure exerted by the walls of the veins pressing on the blood and it competes with the pressure in the right ventricle)* Therefore, the right ventricle changes shape to accommodate volume without changing pressure* In sepsis you lose venous tone, and thus pressors can help* Most of the filling of the right atrium occurs during right ventricular systole but when you have venous excess, you end up with more backflow into the venous system instead of forward flow Measuring with Ultrasound * Hepatic vein – blood is flowing away from the probe and toward the heart until the atrial kick briefly sends it retrograde* The hepatic flow waveform looks just like the CVP tracing, you can see the atrial kick, filling during right ventricular systole, and then diastolic filling* With venous congestion the systolic filling decreases and diastolic filling increases. When severe, the waves fuse and all forward flow is happening in right ventricular diastole* Portal vein – thicker walls, also flows away from the probe, toward the heart* Flow is monophasic until you get venous excess – then you see pulsatility and when very severe there is backflow* Portal pulsatility index = (peak – trough)/peak and there is a continuum, but 20% is a sign of pronounced pulsatility* Renal vein* Normal wave form shows increase in flow with systole and flow decreases in diastole but with greater congestion there is biphasic venous flow

Dr. Deborah M. Stein, MD, MPH, R Adams Cowley Professor in Shock & Trauma and Chief of Trauma at the R Adams Cowley Shock Trauma Center and University of Maryland SOM presents the weekly multi-departmental critical care fellows’ lecture on ”What kills you in the first 20 minutes after injury.”

Jonathan Chow, MD, Assistant Professor and Director, Critical Care Fellowship in the Division of Critical Care Medicine, Department of Anesthesiology at the University of Maryland SOM presents the weekly multi-departmental critical care fellows’ lecture on “When All Else Fails – Rescue Medications for Vasodilatory Shock.” Lecture Summary by Dr. Jason Nam Types of shock * Obstructive Shock (2%)* Hypovolemic Shock (16%)* Cardiogenic Shock (16%)* Distributive Shock (66%)* Septic (62%) – most common shock in the ICU* Non-septic (4%) Why is shock so deadly? * Low BP increases likelihood of AKI and myocardial injury. * Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension.* Increased mortality and norepinephrine-refractory vasoplegic syndrome. * Prolonged post-op vasoplegic syndrome leads to multiorgan failure and increased mortality. Vasoplegic syndrome after off-pump coronary artery bypass surgery: a rising threat.* Other complications* Ischemic skin lesions developing in 30% of ICU patients with catecholamine-resistant vasodilatory shock. Catecholamine Resistance * Other adjuncts (see below)* Novel vasopressors such as angiotensin II When All Else Fails: Novel Use of Angiotensin II for Vasodilatory Shock: A Case Report. Rescue Medications for Vasodilatory Shock * Methylene Blue:* Methylene blue decreased nitric oxide by inhibiting nitric oxide-stimulated soluble guanylyl cyclase.* May reduce mortality after cardiac surgery. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery.* May reduce ICU length of stay. Preoperative methylene blue administration in patients at high risk for vasoplegic syndrome during cardiac surgery.* No real Level 1 evidence on MB. Use of methylene blue in sepsis: a systematic review.* Vitamin B12* Thought to be due to NO scavenging. Use of Hydroxocobalamin (Vitamin B12a) in Patients With Vasopressor Refractory Hypotension After Cardiopulmonary Bypass: A Case Series.* Thiamine and Vitamin C* Combination of vitamin C and thiamine is being used to treat septic shock Hydrocortisone, Vitamin C, and Thiamine for the Treatment of Severe Sepsis and Septic Shock: A Retrospective Before-After Study. * Vitamin C is a potent antioxidant and free radical scavenger. It also increases sensitivity to glucocorticoids.* Thiamine deficiency also common in sepsis. * The above retrospective study showed that: NE requirements decreased, SOFA scores improved, and over 30% reduction in mortality.* VICTAS: an enrolling clinical trial to study the above Angiotensin II * Angiotensin II decreases NE requirements. Kidney releases renin in low perfusion states. Occurs in pulmonary and renal endothelium. Angiotensin II causes ADH secretion and increases MAP. * ATHOS is a study on

Please welcome back an old friend of Baltimore, Karen G. Hirsch, MD. Dr. Hirsch is an Assistant Professor of Neurology and the Director of Neurocritical Care at the Stanford University Medical Center. She is also one of the guru’s and experts in the field of neuroprognostication after cardiac arrest leading to a multitude of publications and numerous grants. Today we are exceedingly fortunate to have her grace the halls of The University of Maryland to give us a crash course on what we SHOULD be doing for our cardiac arrest patients. I assure you, this is a lecture all of us need to hear!

Today we welcome back Samuel Tisherman, MD, Professor of Surgery and Director of the Center for Critical Care and Trauma Education and the Director of the Surgical ICU of the University of Maryland Medical Center. Dr. Tisherman recently joined UMMC directly from The University of Pittsburgh, where he was the Director of the Multidisciplinary Critical Care Training Program and program director for the Surgical Critical Care Fellowship. In his 20 years at the University of Pittsburgh he held several other titles, including Associate Director of the Safar Center for Resuscitation Research, Professor in the Departments of Critical Care Medicine and Surgery, and Director of the Neurotrauma Intensive Care Unit. Today we are fortunate to have Dr. Tisherman speak on what he know’s best: the cursed surgical abdomen. Over the next 60 minutes he navigates this unstable mine-field and leaves you with a better understanding of the thought process used before opening someone’s abdomen!

Today we are fortunate to welcome Sam Hsu, MD, RDMS, Assistant Professor for the University of Maryland Medical School. Dr. Hsu is the acting Emergency Department Ultrasound Director at one of the UMMC satellite centers her in Baltimore, Mercy Medical Center. He also takes on command of medical student emergency ultrasound education for the medical school. I guess you could say, he lives and breaths ED ultrasound! Today he takes us through his algorithm on how to approach ultrasonography of the lungs. I have attending many lectures on the topic and have even performed lung US research, but this lecture is the best presentation I have ever seen on the topic. You NEED to watch this lecture.

Lewis Rubinson, MD, PhD, Professor of Medicine, Program in Trauma, R Adams Cowley Shock Trauma Center at the University of Maryland SOM and Vice President & Deputy Chief Clinical Officer at UMMC, presents the weekly multi-departmental critical care fellows’ lecture on “Status Asthmaticus.”  Lecture Summary by Dr. Jason Nam SA Background and Basics * Most ED visits (75%) for asthma do NOT require hospitalization. Inpatient mortality for asthma remains low (5%). * This talk will focus on patients who require mechanical support. Life threatening status asthmaticus. Mostly younger patients. * Historical predictors of life threatening asthma: HR >110, RR>25, PEF<50%, Pulsus Paradoxus >25. Not always best at predicting. Perhaps better predictor of risk is lack of peak flow improvement with albuterol. * 3Ss of Asthma. Airflow obstruction due to swelling, bronchospasm, and Secretions. * The immediate goals for life threatening asthma:* Improve airflow, reduce and avoid hyperinflation, and reduce inflammation. * The pharm mainstays: SABA, systemic corticosteroids, inhaled short-acting anticholinergic, may consider IV Mg or terbutaline or heliox. Mechanical ventilation? Non-invasive ventilation * Benefit in COPD well-established. * Potential benefits – improved mechanics without ETT, less HCAP. * Potential pitfalls – gastric inflation and worse mechanics, aspiration, harder to limit RR and min ventilation. * It requires proper patient selection and close monitoring. * Consider if pH>=7.2. Close monitoring. Set iPAP to get Vt 6-8cc/kg. Set ePAP (PEEP) for trigger sensitivity. Watch RR and monitor pt very closely. Avoid in non-verbal patients. * General recommendations to referring physicians: stop bagging patient esp at fast rate, NMBA paralysis, continuous SABA, VC-AC, set PIP alarm high, RR 8-12, Vt 6-7 cc/kg IBW.  How do patients with life-threatening SA die? Hemodynamic collapse, barotrauma, progression of anoxic CNS injury; most do NOT have irreversible sequelae from hypercapnia. Initiating invasive mechanical ventilation * Induction with ketamine or propofol is reasonable* May require intermittent NMBA. * Do not manually ventilate at high rate peri-intubation. * Anticipate high PIPs. PIP vs Pplat in practice High PIP w acceptable Pplat is generally not injurious; barotrauma tends to be correlated with elevated Pplat, not elev PIP with low Pplat. Elevated PaCO2 usually does NOT kill. But hyperinflation does: * Need sufficient expiratory time to allow lungs to empty to near FRC for next breath. Permissive hypercapnia. * In truly life-threatening SA, lecturer uses Vol-AC, RR-10, Vt 6-7 cc/kg. How to gauge when/how to modify settings Air trapping due to mucus plugging and bronchospasm, dynamic hyperinflation, Triggering with Auto-PEEP * To initiate gas flow, the patient must generate an effort that exceeds the amount of auto-PEEP. So can increase PEEP to reduce work of trigger. Is Extrinsic PEEP ok? * PEEP can reduce work of trigger. PEEP could increase resistance to airflow during expiration. * Permissive hypercapnia is not deliberate hypercapnia. Other adjuncts?

Edward Pickering, MD, Assistant Professor of Medicine, Division of Pulmonary & Critical Care Medicine at University of Maryland SOM and Director, Interventional Pulmonology at Baltimore VAMC, presents the weekly multi-departmental critical care fellows’ lecture on “Evaluation and Management of Hemoptysis: From a Trickle to Projectile.” Lecture summary by Dr. Jason Nam Definition of Massive Hemoptysis * No uniform cut off value or definition* Life threatening is a better term. Chronic respiratory failure- 50mL/hr can cause hypoxemia and instability. * Definition- airway obstruction from clots, hypoxemia, need for mechanical ventilation, or hemodynamic instability.* Don’t want to underestimate other factors- like ability to protect airway, rate of bleeding, and underlying co-morbidities. * Etiology- airway disease (bronchiectasis, neoplasm), parenchymal disease (infection, immunologic, neoplasm), or vascular causes (AVM, pseudoaneurysm, valvular disease, VTE). * 90% is bronchial artery in supply. Failed Bronchial artery embolization (BAE)- 25%. Either unsuccessful or non-bronchial system supply. * Diagnosis and localization: CXR, traditional CT, multi-detector CT, or bronchoscopy. Initial management- * Stabilize the patient, bad lung down if you know, airway protection, intubation.* Intubate with at least size>8 ETT clear airway of clot. Lung isolation- protect the good side. Selective mainstem intubation, Fogarty.  Selective mainstem intubation. Protect left side when right side is filling up with blood. * Fogarty balloons– available in multiple sizes. Except for 8Fr, must maintain manual inflation. Make sure to read insert- different volumes of air/saline for each size.* Bronchial blockers- available in 5, 7, 9Fr. Spherical or elliptical. 3 ports. Wire loop for guide via scope. Determine dimensions. Lubricate well. Attach multisport adaptor.   * Topical therapies-Iced saline aliquots- no randomized trials. Topical epinephrine- unpredictable absorption. Thrombin- promotes clot formation via fibrin activation. * Multidisciplinary approach. Most likely, interventional radiology will treat the cause. Post-tracheostomy bleeding * Incidence 5%. Timing narrows differential. First 2-3 days tend to be local factors. Weeks 1-6 tracheo-innominate fistula. * Minor oozing- due to submucosal vessel or coagulopathy. Treat with gauze, silver nitrate sticks, correct coagulopathy. More significant bleeding due to thyroid vein/artery, thyroid isthmus, or suction trauma. Tracheo-innominate fistula catastrophic and most feared complication. Peaks around week 3-4. 2 main causes: low tracheostomy (below 4th tracheal ring) or high-riding innominate artery. Discussion of various patient scenarios * Patient scenario #1 with life threatening hemoptysis. Bronchoscopy shows clots. Clot is your friend because it is causing tamponade. Bleeding probably distal to the clot. * You see no evidence of continued bleeding. Biopsy suspicious for squamous cell carcinoma. Patient gets BAE. 1/3 of patients especially those in malignancy have non-bronchial sources of bleeding. Good short term success. 2 weeks later- recurrent massive hemoptysis. Bronchial blocker placed. Patient never received a CTA. Now gets one, and you see massive RLL pseudo aneurysm. Gets IR coils placed. CTA very helpful for identifying cause and structure. 

Mojdeh S. Heavner, PharmD, BCPS, BCCCP, Assistant Professor, Critical Care, Department of Pharmacy Practice and Science at the U of Maryland School of Pharmacy and Jason J. Heavner, M.D., Chair, Department of Critical Care Medicine, University of Maryland Baltimore Washington Medical Center, present the weekly multi-departmental critical care fellows’ lecture on “Advances in Protocol-Driven Management of Alcohol Withdrawal Syndrome in the ICU.” Lecture Summary (by Dr. Jason Nam) Alcohol use disorders (AUD) include: * excessive alcohol intake* alcohol abuse* alcohol dependence Alcohol use disorders (AUD) are associated with: * 49% increased risk for mechanical ventilation* Chronic alcohol intake leads to immune dysregulation* Pneumonia is most common cause of sepsis in AUD patients* Delirium tremens develops in 24-33% of AWS patients Timeline of alcohol withdrawal Protocols in the ICU * Advantages – reduce harmful variations in care, maximize efficiency, improve outcomes* Disadvantages – minimize clinical judgment, encourage complacency, and stifle learning* CIWA-Ar* Symptom-triggered scoring. * Validated in outpatient detox unit. * Not studied in post-operative, medically complex, or ICU patients. The Yale New Haven Experience * Presenters’ experience of developing a novel ICU protocol at Yale New Haven. * The protocol utilizes an objective administered scoring system (Modified MINDS). Dosing regimens derived from pharmacokinetic profile of each drug. * Reiterates need for accurate diagnosis. Suggests adjuvant therapies specially to treat autonomic hyperactivity. Requires physician re-evaluation at critical times. * Outcomes of YAWP: * Significant reduction in ICU intubation and pneumonia. * Significant use of adjuvants like clonidine. * Annual cost-savings of $3.5M for the health system. * Overall, YAWP implementation associated with significant improvements. Conclusions * Patient with AWS in the ICU can experience serious complications.* Small, single center studies evaluating the use of ICU-specific AWS protocols, but more work is needed to establish a standard of care for ICU management.* YAWP implementation has been associated with decreased odds of MICU intubation as well as significant cost savings for patients with AWS. References * Heavner, Jason J., et al. “Implementation of an ICU‐Specific Alcohol Withdrawal Syndrome Management Protocol Reduces the Need for Mechanical Ventilation.” Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 38.7 (2018): 701-713. https://www-ncbi-nlm-nih-gov.proxy-hs.researchport.umd.edu/pubmed/29800507 * DeCarolis, Douglas D., et al. “Symptom‐driven lorazepam protocol for treatment of severe alcohol withdrawal delirium in the intensive care unit.” Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 27.4 (2007): 510-518. https://www-ncbi-nlm-nih-gov.proxy-hs.researchport.umd.edu/pubmed/17381377 * Littlefield, Audrey J., et al. “Correlation Between mMINDS and CIWA-Ar Scoring Tools in Patients With Alcohol Withdrawal Syndrome.” American Journal of Critical Care 27.4 (2018): 280-286. https://www.

David Hager, MD, PHD, Assistant Professor, Division of Pulmonary and Critical Care at the Johns Hopkins University School of Medicine presents on “Vitamin C in Sepsis: Rationale for the VICTAS Trial.” Clinical Pearls Summary by Dr. Andy Deitchman Background High dose vitamin C, Thiamine, and hydrocortisone. Marik. Chest 2017 Inclusion Criteria * Sepsis with respiratory support (e.g. HFNC, NiPPV, mechanical ventilation) and/or need for continuous vasopressors > 1 hr. Design * Intervention v placebo (+/- stress dose steroids) x 4 days or ICU discharge, whichever comes first.* Intervention consists of:* Vitamin C 1.5 g every 6 hours* Thiamine 100 mg every 6 hours* Hydrocortisone 50 mg every 6 hours Outcomes * Primary: ventilator and vasopressor free days* Key secondary outcomes: Mortality at 30 days Physiology * Humans and guinea pigs, only mammals that do not make vitamin C* Fun fact: Peppers are a better natural source of vit. C than oranges* Vitamin C is rapidly consumed in the setting of acute illness. Functions of vitamin C * Cofactor to produce dopamine, norepinephrine, vasopressin, and corticosteroids* Enhances sensitivity to catecholamines* Anti-oxidant, free radical scavenger* Attenuates acute lung injury in septic animal models* Improve endothelial vascular integrity* Improves WBC function* Thiamine* Improved lactate clearance by driving pyruvate into the TCA cycle* Reduces possible renal injury from oxalic acid formation caused by high dose vitamin C* Pitfalls* High dose vitamin C – erroneously high glucose readings on POC glucometer Selected References Marik, Paul E., et al. “Hydrocortisone, vitamin C, and thiamine for the treatment of severe sepsis and septic shock: a retrospective before-after study.” Chest 151.6 (2017): 1229-1238.[ScienceDirect] Marik, Paul E. “Vitamin C for the treatment of sepsis: the scientific rationale.” Pharmacology & therapeutics 189 (2018): 63-70.[ScienceDirect] Uploaded by Sami Safadi, MD

Today we welcome Zachary Kon, M.D., Assistant Professor in the Department of Cardiothoracic Surgery at NYU. In addition to acting as the Surgical Director of Pulmonary Hypertension/Pulmonary Thromboendarterectomy Program, Dr. Kon also acts as the Surgical Director of the NYU Lung Transplantation Program. In addition to > 70 peer-reviewed publications, he has been invited all over the world as an expert speaker in the field pulmonary embolism therapy. We are fortunate to have him in-house to share his knowledge of what to do when the PE is starting to become overwhelming!

Today we welcome Josh D King, MD, Assistant Professor of Medicine at the University of Virginia School of Medicine where he also serves as the associate program director for the nephrology fellowship program. Dr. King is a rare specimen, with board certifications in both Nephrology and Toxicology he focuses on critical care nephrology, acute treatment of drug overdoses, and addressing acute poisoning and envenomation. In addition to his clinical work, Dr King is a prolific academician, publishing numerous journal articles on the topic of acute care toxicology. Today he was kind enough to travel up Interstate 95 and donate an hour of his time to explain what we HAVE TO KNOW if we plan to work in the modern ICU!

Dr. Sanjeev Shah, Assistant Professor of Clinical Medicine at the University of Pennsylvania presents present the weekly multi-departmental critical care fellows’ lecture on “Lactate in the ICU – more than meets the eye” Uploaded by Sami Safadi, MD

Today with have the distinct pleasure to welcome a mentor of mine and a true expert in the field of critical care, Kevin K Chung, MD, FCCM, FACP, Colonel, Army. After finishing a fellowship in Critical Care Medicine at Walter Reed Army Medical Center, Dr. Chung was assigned to the US Army Institute of Surgical Research (USAISR) where he has served in the capacity of Medical Director of the Burn Intensive Care Unit, Task Area Manager of Clinical Trials in Burns and Trauma, and the Director of Research for the USAISR. We are exceedingly fortunate to have him in town to speak on ICU management of Burns. Dr. Chung is the WORLD EXPERT on this topic. I recommend everyone, no matter your practice, take 60 minutes to appreciate the depth of knowledge passed along in this lecture. Burns don’t just present to burn centers!

Today we have the distinct pleasure to welcome Neill Adhikari, MDCM, M.Sc., one of the world’s experts on critical care management in resource limited settings. Dr Adhikari is currently practicing as an intensivist at Sunnybrook Health Sciences Centre in the Interdepartmental Division of Critical Care at the University of Toronto. He also acts as an Associate scientist, Evaluative Clinical Sciences, Trauma, Emergency & Critical Care Research Program, at the Sunnybrook Research Institute where he focuses on critical care delivery in low-resource settings. Over his brief academic career Dr. Adhikari has been incredibly prolific in academic production, publishing over 180 peer-reviewed journal articles and accepting speaking engagements from around the globe. This afternoon we were fortunate to lure him down from Canada to speak on an exceedingly important topic: how can we address the devastation of sepsis in areas of the world where basic labs and clean water can often be a luxury and not a guarantee?