Maryland CC Project

Welcome to a momentous occasion for MCCP. Today we have Dr. Rahul Nanchal, the co-Chair of both the SCCM and ESICM task force on hepatic failure in the ICU; making him one of the world’s foremost experts in the field of liver failure! Dr. Nanchal visits from the Medical College of Wisconsin where he has both an Associate Professorship in Pulmonary and Critical Care Medicine and acts as the medical ICU director. Dr. Nanchal is also well published in the field and is currently the principle investigator for the novel use of extracorporeal liver assist devices in acute decompensated alcohol induced liver failure. We are very fortunate that even with his busy schedule he was able to stay in Baltimore long enough to impart his many years of knowledge and wisdom in one amazing lecture. If you ever plan to correctly treat the cirrhotic in your ICU you CANNOT MISS this talk! #1 Principle: Vasodilated State * ↑ portal venous pressure → ↑ splanchnic vasodilation → ↑ splanchnic flow → ↑ splanchnic pressure → ↑ splanchnic shunts  → ↑ portal venous pressure…. and repeat to decompensation….   #2 Principle: Complicated Hemodynamic State * Significantly decreased effective blood volume * Any additional loss of vascular tone/volume (sepsis, GIB, overdiuresis) leads to SIGNIFICANT organ dysfunction! * Baseline MAP is decreased * difficult to define sepsis, shock, hypotension * Abnormal lactic acid and ScVO2 values are the norm * Cirrhotic cardiomyopathy with depressed systolic and diastolic function is common * Adrenal insufficiency is nearly expected with significant liver dysfunction further complicating management #3 Principle: You must recognize Acute decomposition of Chronic disease! * An acute drop in baseline liver function should start the investigation for infection (#1 cause!) * If caught early and treated aggressively there is reversibility (but never to baseline!) Jalan, et al. Journal of Hepatology 2012 57, 1336-1348 * Diagnosis * Worsened coagulopathy (INR >1.5) * Encephalopathy (NO cerebral edema!) * Pre-existing liver disease * Illness duration < 26 weeks * New organ failure (AKI is #1)  * Mortality at 3 months is 33% compared to 2% at baseline (source) #4 Principle: Infections are the #1 cause of mortality * UTI: #1 infectious cause of decompensation * most nosocomial and preventable (catheter hygiene) * SBP: Traditionally > 250 PMNs in ascites, however <250 PMNs diagnostic if gram positive is source! * Hemorrhagic (>10k RBCs): subtract 1 PMN for each 250 RBCs * Nosocomial SBP (>48 hours hospitalization) needs abx escalation as MDR bacteria is common * C. diff: #1 infectious cause of mortality  * Antibiotic choice is important! (source) * 1/4 of patients are placed on wrong initial antibiotic (8% never get proper abx!) * Median time to abx: ~7.5 hours! * Mortality >75% if incorrect abx chosen! #5 Principle: Acute Kidney Injury is just the beginning * AKI: most common extra hepatic injury and a major contributor to mortality * Most commonly caused by infection (#1 SBP)

It’s an unbelievable honor to have Dr. Sam Tisherman come and join our critical care faculty at the Shock Trauma Center and University of Maryland.  Dr. Tisherman is a Professor of Surgery & Critical Care and heavily involved our fellowship education.  He has won numerous education awards, and was inducted into the University of Pittsburgh School of Medicine’s Academy of Master Educators.  He is well-known for his research in traumatic shock and cardiac arrest – and is responsible for the development of Emergency Preservation and Resuscitation (EPR). A true intensivist interested in all things critical care, Dr. Tisherman came to discuss an incredibly important (and often overlooked) topic: Nutrition. Nutrition assessment * Traditional nutrition markers such as albumin, prealbumin, and retinol-binding protein have a limited role in the ICU * Inaccurate measurements are partly due to the fact that most of these are acute phase reactants! Timing of Nutrition * Start feeds within 24-48 hrs – nutrition decreases infection rates, length of stay, and possibly mortality. * Beware feeding the patient too early.  Shocked patients or those in the  resuscitation phase can develop bowel ischemia with feeding. * Feeding patients on low-dose pressors is probably ok. * Early fascial closure and less fistula formation has been found in patients who receive early feeding with a traumatic open abdomen. * Feeding early in pancreatitis is better for gut epithelium integrity and can reduce complication rates. Caloric and Protein Goals * Protein intake: 1-1.2 g/kg/d to keep nitrogen balance + for wound healing and immune system function. * Caloric goals are 25-30 cal/kg/day * Harris Benedict equation calculates energy expenditure based on age, gender, weight, and height, and takes into account stress factor. * Indirect calorimetry measures carbon dioxide production directly * No difference in mortality shown between under feeding and full feeding. Feeding Obese Patients in the ICU * Obese patients may require less calories per Kg, but higher protein intake per Kg. * Calories: approximately 25cal/kg/d * Protein: approxmiately1.5-2 g/kg/d Location – Enteral vs parenteral * Contraindications for enteral feeding: shock, GI obstruction,  short gut, fistula,  ileus. * Jejunostomy compared to gastrostomy, has higher risk of obstruction and torsion. * G tube indicated if its use us anticipated for more than 6 weeks. * Diarrhea in patients receiving enteral feeding warrants meds review( abx, laxatives), investigation of fecal impaction, kwashiorkor. Enteral Access * Bowel sounds, flatus, and bowel movement are overrated parameters for post operative feeding. * Consider post-pyloric feeding tube for vomiting despite pro-kinetic and high risk for aspiration. * No difference between post-pyloric and gastric in vent associated conditions. * In acute pancreatitis, early enteral feeding is recommended. Still debatable whether  gastric or post-pyloric/ligament of Treitz is better. Evidence about Residuals & Feeding * Prone positioning does not increase residuals in one study  but there is a higher risk of regurgitation. * Multi-center trial in France showed no difference in VAP upon not checking residuals. (Reignier et al., 2013) Parenteral Feeding * TPN is indicated for anticipated NPO more than a week,

Dr. Hong Kim is back – this time to discuss two classic hemoglobinopathies. Do you you know the common iatragenic causes of methemoglobinemia?  How about when to send a patient for hyperbaric oxygen for carbon monoxide exposure?  If not, this is a can’t miss lecture. Written summary by Ahmad Aswad Carbon Monoxide Toxicity * In the U.S. common sources of exposure include residential fire (with cyanide as a potential co-exposure), engine exhaust, natural gas appliances, propane-powered engines, & paint stripper ingestion. * Normal: Physiologic carboxyhemoglobin (COHb) levels: 1-2% in healthy individuals, up to 5-10% in smokers! * Pathophysiology: Once inhaled/absorbed it binds to hemoglobin with 250 times higher affinity than oxygen causing “functional” anemia. Mitochondrial dysfunction also a major cause of clinical decompensation. * Symptoms: At about 10%: Begins with headache, dizziness at level >10%, can progress to unconsciousness, death with levels above 50% * Diagnosis * Lab: CO-oximetry * Radiology: CT head shows basal ganglia lesions * Treatment * Primary treatment: Removal from exposure, 100% FiO2 by non-rebreather mask * t1/2: CO half-life is 5 hours * Hyperbaric Oxygen (HBO) Therapy: causes dissociation of CO from Hb, myoglobin, and cytochrome oxidase in the mitochondria * Decreases half-life to 23 minutes * HBO may also antagonize lipid peroxidation and decrease leukocyte adhesion, minimizing the inflammatory response. * Survivors may develop delayed neuropsychiatric sequelae and cognitive impairment weeks after exposure. * Risk factors of delayed reactions include LOC, age> 30 & duration of CO exposure. * Case reports suggest that HBO initiated within 6 hours from exposure may prevent delayed neurologic sequelae * Indications for HBO * Levels of CO Hb >25 %, ( >15 % in pregnant and pediatric population, expert opinion) * Clinical symptoms: Chest pain, dizziness, syncope, seizures, coma, focal neurological findings, pregnancy * Cochrane review: insufficient evidence to support HBO use * American college of emergency physicians (ACEP): HBO a therapeutic option, cannot be mandated Methemoglobin (MetHb) * Both hereditary & toxic forms of methemoglobinemia exist * Normal levels are 1-3% * Pathophysiology: Oxidizes iron moiety to Fe3+ in hemoglobin leading to inability to carry oxygen. * Clinical findings * May not be symptomatic up until levels above 20%, with death occurring at levels above 70% * Pulse oximetry shows hypoxemia with saturation levels <90% * SpO2 usually stays around 85% as levels of MetHb increase * Precipitants * Common drugs: Dapsone, benzocaine, phenazopyridine, amyl nitrites and anti-malarials. * Chemicals such as aniline dye, organic nitrites, and nitrates food preservatives. * Treatment: Methylene blue * Indication: Symptomatic patients and MetHb >25%. Response is seen within minutes and dose may be repeated once. * Mechanism: Fe3+ oxidized to Fe2+ via NADPH dependent pathway * Can cause hemolysis, decreased pulse-oximetry, and can potentially cause serotonin syndrome. * Can be considered in patients with G6PD deficiency only in very life threatening cases, as hemolysis will often be seen 24 hours later. * Alternative treatment options: Exchange transfusion, HBO, and ascorbic acid (slow response)   Suggested Reading * Scheinkestel CD, Bailey M, Myles PS, et al.

Dr. Daniel Herr is the Chief of Surgical ICU Services and also the Director of our Cardiac Surgery ICU at the University of Maryland.  Dr. Herr is known internationally for his contributions in the management of ICU delirium, but is also an incredible leader.  Adding to our leadership series, Dr. Herr gave this phenomenal talk on how find the right job and be an effective leader.  Once you do find the right job, what next?  Regardless of your administrative responsibilities, if your job requires you manage a team of people, this is a CAN’T MISS discussion that is jam packed with leadership pearls and pitfalls. Finding & Starting a New Job  * Rule #1: Be introspective – know what you want to do * Rule #2: Cast a wide net, start early, and be patient * Rule #3: Have goals, and stand out.  Every year, come up with 3 goals: one for yourself, one for the ICU, and one for the hospital. * Rule #4: Start HUMBLE, learn the culture, & listen. Take notes on a daily basis. * Rule #5: Meet key players, learn names, make connections quickly How to be an Effective Boss * Listen first, act second. * Build a team. It’s not about YOU, its all about US * Be a role model.  EVERYONE is watching. The front desk clerk, nurse, resident, fellow, maintenance staff. * Empower your staff to contribute to clinical and administrative decision making. * Thixotrophy: Certain gels or fluids that are thick (viscous) under static conditions will flow (become thin, less viscous) over time when shaken, agitated, or otherwise stressed (time dependent viscosity) * Apply the concept of thixotrophy to administrative change.   Change takes time and reinforcement.  Be patient and get used to delayed gratification. * Adopt first, then reinvent, then refine. * Be LEAN. Give options, but minimize them.  Become an expert at a few things, and do them very well. * Address Conflict.  Be aggressive with addressing interpersonal conflict in your ICU.  It is the most common cause of burnout which leads to staff turnover. * Be Present.  Know everything that’s happening in your ICU. Don’t be the person who lives in their office. Suggested Reading * St andre A. The formation, elements of success, and challenges in managing a critical care program: part I. Crit Care Med. 2015;43(4):874-9. [PubMed Link] * St andre A. The Formation, Elements of Success, and Challenges in Managing a Critical Care Program: Part II. Crit Care Med. 2015;43(5):1096-101. [PubMed Link] * Manthous CA, Hollingshead AB. Team science and critical care. Am J Respir Crit Care Med. 2011;184(1):17-25. [PubMed Link]

Dr. Deborah Stein is the Chief of Trauma at the R Adams Cowley Shock Trauma Center, Medical Director of the Neurotrauma Intensive Care Unit at STC, and an expert in renal replacement therapy – To be honest that barely touches her level of expertise, and we’re not really sure what she can’t do… In this session, Dr. Stein breaks down some advanced concepts related to continuous renal replacement therapy (CRRT) and at the end, introduces a novel extracorporeal therapy for acute liver failure – MARS (Molecular Adsorbent Recirculating System). Written Summary by Dr. Neil Christopher Modalities of RRT * Intermittent hemodialysis (IHD) – rapid removal, minimal breaks in therapy, low cost BUT can cause hypotension, dialysis disequilibrium, catabolism, & cerebral edema * Cerebral edema – diffusion of CO2 with bicarbonate creates an intracellular acidosis which increases water uptake by the brain * CRRT – continuous removal, preserves hemodynamic stability, simple BUT expensive * Peritoneal Dialysis – simple, low cost, hemodynamic stability BUT limited volume removal, risk for peritonitis * Cochrane Review – No mortality benefit for CRRT over IHD * BUT – trials rarely included hemodynamically unstable patients.  There was significant heterogeneity in patient characteristics, had variable mortality and did not consider subgroups that may specifically benefit from CRRT Advanced Concepts in CRRT * AKI results in a stepwise increase in relative risk of death when going from risk->injury->failure * Indications for renal replacement therapy (RRT) – life threatening changes in fluid, electrolyte and acid-base balance * Not a BUN /creat cut off – consider trends and broader clinical context * Alternative indications – Severe Sepsis / Rhabdomyolysis * Convection vs. Diffusion * Convection moves solutes through filter across pressure gradient (solute drag) * Diffusion moves solutes through filter down concentration gradient * Adsorption – Molecules can Adsorb to the filter – Polyacrylonitrile (high adsorption) * Can be an additional modality for solute removal * Filter Flux  – determined by CRRT filter pore size. In general, high-flux membranes have larger pores, that allow more solutes and ultrafiltrate to move across the membrane. * Sieving coefficient is capacity of solute to pass through filter (Sc = Concentration in ultrafiltrate / concentration in plasma) * Determined by Molecular weight, protein binding, filter porosity, adsorption onto filter * High Sc = freely filtered * Clinical relevance: Antibiotics and other therapies’ dosing regimens dosing may be significantly impacted by RRT. * Filtration Fraction = amount of ultrafiltrate removed relative to plasma flow * Higher FF can lead to clotting, while lower FF can result in excessive shearing forces/hemolysis from higher flow of plasma * Higher FF results in a decreased Sieving coefficient * Substitution fluid – PRE vs. POST * PRE-dilution is theoretically less efficient – solutes diluted prior to their removal * POST-dilution leads to increased viscosity / shear within filter which limits ultrafiltrate production (25% of Qb) * PRE-dilution is practically more effective, not limited by filter constraints Clinical Considerations * Timing – early vs. late initiation of CRRT – no significant benefit in mortality * Dose of RRT – measured by Kt/V or URR * Kt/V of 3.9/week roughly equivalent to delivered effluent volume of 20-25ml/kg/h (actual g...

Dr. Munish Goyal is an Emergency Medicine trained Intensivist who has been a leader in resuscitation science over the past decade.  Dr. Goyal is returning to the University of Maryland where he did his fellowship at the Shock Trauma Center to discuss the importance of early, aggressive resuscitation and why he believes our current system needs to improve in order  to meet the rising demand for critical care outside of the traditional walls of the ICU. Written Summary by Dr. Nikki Naderi Intensive Care Delivery Outside the ICU * The number of patients being admitted to the intensive care unit (ICU) from the emergency department (ED) has significantly increased * In a study, between 2002-03 there were 2.79 million ICU admissions from the ED to the ICU and between 2008-09 the number increased to 4.14 million * Overall, the total number of ED visits increased by 18% during that time frame, but the number of ICU admissions increased by 48% * Nationwide 2.1% of ED patients are admitted to the ICU Mortality Effects * Multiple factors have been studied in patients with sepsis to understand their effect on mortality * Antibiotics delivery within 1 hour of presentation * If the patient is hypotensive, for every hour antibiotics are not given, mortality increases by 7.6% * This effect is not seen in non-hypotensive patients * Colloid vs. Crystalloid: no difference in 28-day mortality with resuscitation with 4% albumin vs. crystalloids  * MAP target: no difference in mortality when MAP goal was 65-70 vs. 80-85, normally hypertensive patients had decreased need for RRT with the higher MAP goal * Length of time spent in the ED: * Retrospective cross-sectional study of project IMPACT: ICU mortality increased by 2% in patients whose ER length of stay (LOS) was 6 hours or greater before transfer to the ICU, in hospital mortality increased by 4% * In a study of blunt trauma patients, for those patients intubated in the ER, for each 1 hour stay in the ER the risk of pneumonia increased by 20%’ * Case volume: the number of cases seen, directly correlated with in patient mortality Models Adapting to Increase in Volume of Critically Ill * Increasing the focus on phase of critical illness over the patient’s physical location * Improving the ED’s ability to manage critically ill patients * University of Michigan Model (EC3): Resuscitation rooms proximal to transitional ICU beds – paradigm shift away from traditional ED to ICU transfer model. * Resuscitation Units – University of Maryland Critical Care Resuscitation Unit   Additional Reading  * Chalfin DB, Trzeciak S, Likourezos A, Baumann BM, Dellinger RP. Impact of delayed transfer of critically ill patients from the emergency department to the intensive care unit. Crit Care Med. 2007;35(6):1477-83. [PubMed Link] * Mullins PM, Goyal M, Pines JM. National growth in intensive care unit admissions from emergency departments in the United States from 2002 to 2009. Acad Emerg Med. 2013;20(5):479-86. [PubMed Link]

Managing complex patients with ARDS can be challenging.  Many believe the Berlin criteria we use to identify ARDS are largely confounded and often identify the disease too late. Additionally, how do you manage the patient who’s intravascularly depleted but is drowning from pulmonary edema? (Classic – they are wet and dry!!)  What if there was a way to identify the patient developing ARDS before a blood gas or chest x-ray? Or even better, objectively treat their excessive extravascular lung water?  We were fortunate enough to have Dr. Nielsen return to speak on this interesting topic. Dr. Nielsen is an intensivist who has a great deal of experience PiCCO and using extravascular lung water estimates to guide complex therapies in patients with ARDS. Extravascular Lung Water (EVLW) & Transpulmonary Thermodilution (TPTD) Written summary by Dr. Nikki Naderi Definition and Measurement * EVLW: all the fluid in the lungs that is not intravascular or intrapleural i.e. surfactant, edema * Consists of 20-25% of the total fluid in the lungs * Normal: < 7 ml/kg * Measured by: * Gravimetry- gold standard for measurement, however can be only done ex-vivo, the lung is weighed both wet and dry, the difference in the weight is EVLW * TPTD: both double indicator (thermo-dye) and single indicator (thermos) methods correlate closely with gravimetry and can by down in-vivo * In a single indicator thermodilution, cold water is injected through an internal jugular or subclavian veins. An intrarterial thermister placed in the femoral artery measures the change in blood temperature and plots it against time. * From these measurements EVLW can be calculated PiCCO Parameters * Cardiac output (CO) & index (CI) * Volumetric Preload (GEDV) & Index (GEDI) * Lung water (EVLW) * Afterload (SVRI) * Contractility (CFI) * Volume responsiveness (SVV/PPV) Clinical Applications * Diagnosis, prognosis and treatment guidance in ARDS * In multiple studies EVLW has been found to have a linear correlation with lung weight * An EVLW of about 15 mL/kg was 99% specific for diffuse alveolar damage * Predicts onset of acute lung injury (ALI) before traditional parameters to diagnose ALI/ARDS such as hypoxia and CXR findings * EVLW when indexed to pulmonary blood volume can discriminate hydrostatic edema (due to cardiac causes) from ARDS Prognosis * For every increase of 1 mL/kg of EVLW, there is a 7% increase risk of death and an EVLW of greater than 21 mL/kg has a mortality of >70% Treatment * EVLW has been shown to be a better surrogate for degree of pulmonary edema in ARDS than wedge pressure, thereby a more accurate guide in treatment and diuresis of patients with ARDS Limitations * The measurement of EVLW can be underestimated in patients with underlying lung disease, focal lung disease, shunt, high PEEP on the ventilator, pulmonary vascular obstruction and a cardiac index of less than 1.5 * Hemodynamic monitoring unreliable in patients with arrhythmias, right heart failure, and require controlled ventilation   Additional Reading * Tagami T, Sawabe M, Kushimoto S, et al. Quantitative diagnosis of diffuse alveolar damage using extravascular lung water. Crit Care Med. 2013;41(9):2144-50. [PubMed Link] * Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent prognostic factor in patients with acute respiratory distress syndrome. Crit Care Med. 2013;41(2):472-80. [Open Access Link] * Sánchez M, García-de-lorenzo A,

Dr. Burton Lee is BACK!  It’s always an honor to have Dr. Lee return to the US from Kenya and take a break from his critical care clinical and academic duties across the Atlantic Ocean.  This time, Dr. Lee brought with him another thought provoking lecture about ethics in evidence based medicine and how it may be impacting the way we practice on a day-to-day basis. This talk takes a deeper dive into the scientific literature studying decision making, bias, human nature, and the conflicts that exist within, “Conflict of interest”. Concepts There are only a few sociopaths out there who will lie all the way, and a few who remain completely honest.  A majority fall somewhere in between. Reciprocity: The act of exchanging something for mutual benefit is a normal behavior (Harvey, 2010), but can have a profound effect on published outcomes, choice of research question, etc. The Token Effect: The concept that objects gained dishonestly have less of a consequence then if cash is exchanged. (Mazar, 2008) May have a major impact on medical care and medical decision making. * How often are data points dropped, modified, or changed in scientific research?  It’s actually quite common. (Fanelli, 2009) * The peer-review process is partially broken, and a soft stop at best (Bohannon, 2013) * Guidelines seem to be susceptible to bias and conflict of interest as well (Neuman, 2011) Conflict of Interest * Moral licensing: Disclosure does not remove bias (Cain (2005) Dirt on Coming Clean) * Burden of disclosure: The recipient of advice from a biased source, often doesn’t know how to navigate the advice which still has a significant impact on decision making. The result of these ethical dilemmas is that medical reversals will not be rare.   Additional Reading * Dunn AG, Arachi D, Hudgins J, Tsafnat G, Coiera E, Bourgeois FT. Financial conflicts of interest and conclusions about neuraminidase inhibitors for influenza: an analysis of systematic reviews. Ann Intern Med. 2014;161(7):513-8. [PubMed Link] * Als-nielsen B, Chen W, Gluud C, Kjaergard LL. Association of funding and conclusions in randomized drug trials: a reflection of treatment effect or adverse events?. JAMA. 2003;290(7):921-8. [PubMed Link]

Today we are in for a real treat! We have two of the smartest doctors to ever grace the stage here at the University of Maryland. First you will hear from Dr. Mark Walsh, an Emergency Medicine and Internal Medicine physician from Memorial Hospital, deep in Notre Dame territory of South Bend, Indiana. In addition to dominating the world of Emergency Medicine AND running his own medicine ward at Memorial Hospital, Dr. Walsh also maintains one of the largest independent coagulopathy research groups in the country. And, as you will hear, when he is not saving the trauma world one guided transfusion at a time, Dr. Walsh spends every moment he can assisting in the development of a hospital teaching service near Port-au-Prince, Haiti. Also here to talk about his experience filling the gaps in the anesthetic management of the Haitian population is Dr. Rick Skupski. Dr Skupski is dually trained in both Anesthesia and Medicine, a rare find. This has led him down a very academic path in life as he works beside Dr. Walsh performing coagulopathy research at Memorial Hospital. He is also the main nidus behind taking the average EM doc and making them an anesthesia guru! I assure you, the next 60 minutes will both touch your heart and stimulate your intellect. PART 1: TEG/ROTEM * Pearl #1: Why choose TEG (or ROTEM?) * Shows even early alterations in coagulopathy (TIC!) * Results available within 20 minutes! * PT/PTT/INR can take 90+ minutes… * Pearl #2: TEG= easy to understand!  * And abnormalities can be seen across the room:                                 * Pearl #3: TEG can guide treatment modalities in REAL time (Heres a FULL LECTURE!) * Add in platelet mapping allows identification of TxA2 vs ADP inhibition (ASA and Clopidigrel use) * Extremely important to assist in corrective treatments! * Pearl #4: Regardless of which modality, TEG or ROTEM, the same information can be gathered (though TEG is SO much easier!) PART 2: Emergency Physician General Anesthesia Syllabus (EP GAS) *   1/12/2010: 7.0 earthquake led to the loss of approximately 240,000 human lives * a number close to 3,000,000 were affected in total, many injured and without access to water, food, or healthcare * An issue arose immediately: we have the surgeons, “we can’t find enough anesthesiologists” * A unique thought came to the team from Memorial Hospital, Indiana: crash course for EM physicians * An expedited Anesthesia Boot Camp * A similar thought process to the training done during WWII to boost anesthesiologist numbers * Extremely simple process * Rule #1: KISS (keep it simple stupid!) * Always start in the same drug order * Always use the same syringe volumes * Rule #2: BVM skills > Intubation skills * Until you can prove that you control the airway, you don’t own the airway! * Rule #3: Always use the simple algorithm: MS MAID (and you will forget nothing) * Machine check * Suction * Monitor * Airway supplies * IV line * Drugs

Today we are once again excited to have Dr./LtCol/All-around critical care guru Sam Galvagno. In addition to publishing in multiple major journals, defending the country, maintaining FOUR board certifications, AND maintaining a PhD in Clinical Research; Dr. Galvagno somehow finds time away from his job as Associate Director of the University of Maryland SICU to do what he does best: share his advanced knowledge of critical care. It is an honor and a privilege to share with you a lecture topic that Dr. Galvagno has spent many years researching: Osmotherapy. I assure you, no matter what your level of exposure is to this topic I GUARANTEE you will take away a TON of new clinical pearls!! Key points * Pearl #1: Egress of water = Loss of volume in the cranial vault * Monroe-Kelley Doctrine! * This is a BRIDGE to definitive therapy! * Pearl #2: Water movement in the brain is NOT PASSIVE * Need to physically alter the osmotic equilibrium with: * A non-toxic, inert, object with COMPLETE exclusion from the brain * Pearl #3: A 1.6% reduction in brain volume = 90 ml of brain tissue saved!!  * An Osm of 300-320 will: * Allow active egress of water from the brain tissue → decreased intracranial volume * Improve elasticity of the cranial vault * Pearl #4: There is NO JUSTIFICATION in withholding an osmolar agent due to lack of central access * NO study shows significant harm is caused by using PIV * Pearl #5: Osmotherapy agent effects extend beyond simply osmotic action: Mannitol * 1100 mOsm/L * Dose: 0.25-1.5g/kg * Takes 15-30 minutes for full effect, i.e.: takes time to lower ICP * Lasts 2-4 hours * Effects: * Concentration gradient → egress of intracranial fluid * Volume expansion (detrimental in CHF) → increased CO → improved CPP * Vasoconstriction + decreased viscosity → improved CBF * Proximal tubule diuretic (detrimental in AKI/CKD) * Free radical scavenger * Goal: * DO NOT worry about a desired serum osm goal (i.e. <320…) * Calculate Serum Osm Gap  * Renal failure rare with Osm Gap < 55!! * Adverse effects: * #1 side effect- diuresis → hypovolemia and hypotension * Pulmonary edema, metabolic acidosis, hemolysis, AKI, hyperkalemia Hypertonic Saline * 3% 1027 mOsm/L, 5% 1711 mOsm/L, 23.4% 8000 mOsm/L * Dose: 1-2 cc/kg/hr 3% or 4-6cc/kg/hr 2% (Ideal Body Weight) * Lasts 48 to 72 hours * Rise in Sodium can be augmented with simultaneous use of loop diuretic * CAUTION: * Chloride load leads to SEVERE hyperchloremic metabolic acidosis * Sudden rise in sodium can lead to Central Pontine Myelinolysis (but…. only one documented case) * Effects: * Goal: * Na level 145-160 (i.e. Osm 300-320) * Adverse effects: * In addition to acidosis and CPM, a rapid ICP drop can tear bridging veins and lead to a SDH Hypertonic Saline vs. Mannitol * No study has ever shown a remarkable difference (yet….) Suggested Readings * Vincent Cottenceau, Francoise Masson, Eugenia Mahamid, Laurent Petit, Venyamin Shik, Francois Sztark, Menashe Zaaroor, and Jean Francois Soustiel.

Dr. Giora Netzer (@GioraNetzer) is one of our esteemed faculty who is trained in clinical epidemiology as well as pulmonary critical care.  He has done an extensive amount of research in ARDS but also has a passion for how we take care of patient’s families in the ICU.  In this talk Dr. Netzer presents some of his innovative research and opinions about a phenomenon he’s described as Family ICU Syndrome (FICUS) that significantly impacts the care we provide to the critically ill.  While you may often hear Dr. Netzer describe himself as a, “simple country lung doctor” I think all of us agree that the potential impact of this work is much greater then he lets on. Key Points Surrogate decision-making is common for the critically ill! Making decisions for a loved one is HARD. In fact, many family members of the critically ill: * Suffer from clinical depression * Have high levels of anxiety & stress * May go on to develop post-traumatic stress disorder as well * Anticipitory grief * Learned helplessness * Sleep deprivation * Cognitive bias Family ICU Syndrome defined FICUS affects all of US * Family conflict has a strong impact on feelings of burnout * Futile care carries an opportunity cost for other patients * “We need to communicate better” may not be the complete problem Cognitive biases that affect surrogate decision-making * Optimism bias * Surrogate’s opinion about prognosis correlates less and less as the patient’s prognosis worsens. * Qualitative expression of prognosis does not significantly impact the surrogate’s reception of the message. * Framing effect * People react to a particular choice in different ways depending on whether it is presented as a loss or as a gain * Presenting a scenario as a chance of dying vs. surviving makes a difference! * Clinical decision aids may be the solution to reducing the framing effect ant helping not only families, but also clinicians become more clear with treatment strategies. * Base rate fallacy * An error in thinking that can cause a surrogate to ignore the probability of a potential outcome when given specifics regarding their own family member. * Example: The mortality of ARDS is high, but given my family members circumstances their chance of survival is different. Family centered ICU care can significantly impact both the patient and surrogate’s hospital course. * A must read piece by Mark Attiah (@MarkAttiah) in JAMA – A Piece of My Mind. Treat Me Like a Child Strongly consider including family participation in daily rounds. Great way to be efficient and improve communication. Suggested Readings * Netzer G, Sullivan DR. Recognizing, naming, and measuring a family intensive care unit syndrome. Ann Am Thorac Soc. 2014;11(3):435-41. [PubMed Link] * Verceles AC, Corwin DS, Afshar M, et al. Half of the family members of critically ill patients experience excessive daytime sleepiness. Intensive Care Med. 2014;40(8):1124-31. [PubMed Link] * Davidson JE, Jones C, Bienvenu OJ. Family response to critical illness: postintensive care syndrome-family. Crit Care Med. 2012;40(2):618-24. [PubMed Link]

Dr. Sam Galvagno is a Lieutenant Colonel in the US Air Force who is an expert in anesthesia critical care, airway management, critical care education, published in JAMA, and a black belt in Tae Kwon Do to boot. Did I mention he earned a PhD in Clinical Investigation?  This short talk is JAM PACKED with clinical pearls.  Needless to say, Dr. Galvagno owns the resuscitation room in more ways than one and we were lucky enough to have him come and give us his opinions on induction agents for the critically-ill. Key points * “Earning the anesthetic,” applies to the concept that a patient’s physiology must be able to handle the prescribed dose of induction agent.  Shocked patients usually require a significantly reduced dose of anesthetic to avoid adverse effects of hypotension and cardiac depression. * Critical for anyone involved in airway management to do at least 3 things * BEFORE you begin your RSI, commit to a definitive airway * Gather extra hands and delegate tasks.  Focus on doing one thing and one thing only. * Your equipment should be prepared and proximal If it isn’t within 3 feet of you, it might as well be on MARS   STC Airway Algorithm Paralytics * The Roc vs. Sux debate goes on… * Personal preference for Rocuronium, but you still need to know how to effectively use Sux (and even Vecuronium!) as a back up plan (drug shortages) * Sux vs. Roc Cochrane Review – Rocuronium was underdosed in a majority of these studies, which is why sux may have looked better. Induction Agents Etomidate * Dose: 0.2 – 0.3 mg/kg Ideal Body Weight * Adverse reactions: Emetic, really not as hemodynamically neutral as we think. * Adrenal insufficiency? * May be a signal, but unsure if there is clinical significance.  Studies indicating AI reasonably criticized. * Wagner, 2014 – Probably one of the most well done studies showing no AI. Propofol * Dose: 0.5 mg/kg or LOWER * Dose highly dependent on hemodynamic status. * Known to highly reduce SVR, BP, ICP, and is a cardiac depressant. * Probably should administer in 10 mg boluses if giving to a critically ill patient * Bottom line: Probably shouldn’t be using in the acutely-ill patient due to known side effects. Ketamine * Dose: 0.5 – 2 mg/kg IV, standard dose of 1 mg/kg usually adequate * Prepare those around you for the patient to dissociate, not fall asleep. * Benefits: Patient continues spontaneous breathing * Pitfalls * Ketamine is a direct myocardial depressant, so be cautious when inducing with ketamine in the patient with a low EF. Effects are usually balanced by increased catecholamine release. * Beware the patient with prolonged shock or who is catecholamine deplete – you won’t see that BP bump you’re used to. * Primary drug of choice for a majority of emergency airways today Suggested Readings * El-orbany M, Connolly LA. Rapid sequence induction and intubation: current controversy. Anesth Analg. 2010;110(5):1318-25. * Stollings JL, Diedrich DA, Oyen LJ, Brown DR. Rapid-sequence intubation: a review of the process and considerations when choosing medications. Ann Pharmacother. 2014;48(1):62-76. * Sikorski RA, Koerner AK, Fouche-Weber, LY, Galvagno SM. Choice of General Anesthetics for Trauma Patients.

Dr. Megan Brenner is currently one of the leaders in the development of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA).  As a trained trauma, critical care, and vascular surgeon Dr. Brenner is actively developing the integration of REBOA here at the Shock Trauma Center and the University of Maryland for both trauma and medical patients experiencing massive hemorrhage.  During this talk Dr. Brenner discusses her experience with REBOA, its indications, potential uses, and why she believes this is a critically important tool for all resuscitationists to learn. Lecture Key Points Indication:  Exsaguinating hemorrhage below the diaphragm (blunt/penetrating trauma, non-traumatic bleeding) Problem:  Cross-clamping the Aorta does not usually end well Solution:  Endovascular occlusion (REBOA) prevents a morbid surgery and buys time for definitive repair.  Needs to be performed by bedside providers! * We’re behind in the US!  Currently, REBOA can only be inserted by femoral cutdown since the FDA has only approved a vascular catheter that can fit through a 12 Fr arterial sheath.  This size sheath requires a surgical vascular repair. For the trauma patient, you only need 3 diagnostic tests prior to considering REBOA * CXR * Pelvic XR * FAST exam Current algorithm here at STC   Balloon Landing Zones   The BEST Course: If you are a surgeon interested in coming to Baltimore and attending the Basic Endovascular Skills for Trauma course at the Shock Trauma Center, email BEST@umm.edu for dates and information.   Suggested Readings & Additional References * White JM, Cannon JW, Stannard A, Markov NP, Spencer JR, Rasmussen TE. Endovascular balloon occlusion of the aorta is superior to resuscitative thoracotomy with aortic clamping in a porcine model of hemorrhagic shock. Surgery. 2011;150(3):400-9. * Brenner ML, Moore LJ, Dubose JJ, et al. A clinical series of resuscitative endovascular balloon occlusion of the aorta for hemorrhage control and resuscitation. J Trauma Acute Care Surg. 2013;75(3):506-11. * Brenner M, Hoehn M, Pasley J, Dubose J, Stein D, Scalea T. Basic endovascular skills for trauma course: bridging the gap between endovascular techniques and the acute care surgeon. J Trauma Acute Care Surg. 2014;77(2):286-91. * Megan Brenner & Scott Weingart discuss REBOA * LITFL Critical Care Compendium reviews the nuts & bolts of REBOA

Carl Shanholtz, MD is medical director of the Medical Intensive Care Unit at the University of Maryland Medical Center. After a fellowship in critical care medicine at Johns Hopkins University he did further training in Hematology and Oncology at the University of Maryland Medical Center. He specializes in the care of hematologic and solid malignancy patients and shares his wisdom for the treatment of ICU complications of these cancers and their therapy.   I. Acute Tumor Lysis Syndrome Epidemiology * More common with hematologic leukemias and high tumor burden lymphomas such as Burkitt’s lymphoma * The solid tumors in which it is encountered are most commonly breast and small cell carcinoma of the lung * Any malignancy, with enough tumor burden or aggressive therapy, can develop tumor lysis Presentation * Marked by intracellular lysis of cells * Hyperkalemia, Hyperuricemia, Hyperphosphatemia, and a reactive hypercalcemia (due to binding of phosphate) Pathogenesis * Uric acid crystals precipitate in the renal tubules creating an obsructive nephropathy Treatment * Prophylaxis before treatment, if possible * Crystalloid hydration * Allopurinol inhibits the formation of uric acid * Urate Oxidase (rasburicase) oxidizes uric acid to allantoin, which is 10-fold more soluble * Biologically active for 18-21 hours * Evidence that it is effective at lowering uric acid levels * No evidence that it prevents renal failure or lowers mortality * Urinary alkalinization and forced diuresis with furosemide are OUT * They cause calcium phosphate precipitation in the renal tubules which is worse than urate nephropathy II. Acute Myeloid Leukemia (AML) Hyperleukocytosis: * Defined as WBC >100,000, but this is not an absolute cutoff. *depends on the type of cancer: CLL cells are mature. APL may be symptomatic with WBC > 10,000 because the granules are thrombotic * Initial therapy may be cytoreduction with hydroxyurea * Leukapheresis can be used for certain AML to rapidly decrease circulating WBCs * High WBC on presentation is a poor prognostic indicator Acute Promyelocytic Leukemia (APL) – A disease every intensivist should know! * Due to a chromosomal translocation (15;17) * Treated with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) * Even in the absence of respiratory failure or shock, these patients may have treatment initiated in the ICU due to expected course of illness * Affects the young and is CURABLE with the differentiation agents listed above   1. Hemorrhage * 30-60% of deaths are from hemorrhage * ICH is a known complication * DIC is commonly seen; check fibrinogen daily * Manage with FFP, cryoprecipitate, and platelets to maintain fibrinogen > 100 and plt >30-50 * Aminocaproic acid and transexamic acid are controversial and not recommended    2. Thrombosis * Less common than hemorrhage * Heparin is no longer recommended    3. Differentiation syndrome * Manifests as ARDS-like respiratory failure * Treated with Dexamethasone 10mg IV bid and temporary discontinuation of ATRA or ATO III. Hypercalcemia of Malignancy Etiology * 80% PTHrp seen in squamous cell carcinoma and lymphoma * 20% Osteoclast activating factor seen in multiple myeloma * <1% endogenous calcitriol production seen in lymphomas, esp. Hodgkins Clinical Manifestations * Constitutional: dehydration, polydipsia * Neurological: fatigue, lethargy, hyporeflexia, confusion * Gastrointestinal: nausea, vomiting,

Lewis Rubinson, MD, PhD is Director of the Critical Care Resuscitation Unit at R Adams Cowley Shock Trauma Center at the University of Maryland. He recently spent a month in Sierra Leone providing clinical care to patients with Ebola as a WHO consultant. At Kenema Government Hospital, he was one of only two physicians providing daily care for upwards of 130 patients with confirmed Ebola. During his talk, he will dispel myths about the disease that have been propagated by the lay press and describe what lessons we can bring back from resource-limited settings to help provide care to these patients in the United States. History of Ebola Outbreaks Ebolavirus was first discovered and diagnosed in 1976 in Uganda. This was part of the Gulu outbreak where 425 patients were infected. Since that time there have been over 20 documented outbreaks. These outbreaks have been small, and were typically in rural environments where control measures were effective at limiting the extent of disease spread. Vaccination and novel therapeutics were created but their development was stalled due to the lack of a potential economic marketplace. Ebola in West Africa in 2014 is different. It has been largely a disease of the inner city, where control measures were not in place and healthcare infrastructure is lacking. Initial cases were noted last December. The disease seem to take hold when, in March, infected patients from Gueckedou, Guinea returned west and brought the disease to Conakry, the country’s capital. The spread of disease has since affected Sierra Leone, Liberia, and now Mali. Pillars of EBV Control I. Contact tracing and case finding II. Early isolation III. Clinical care IV. Safe treatment of the dead How is Ebola Transmitted? * Ebola is transmitted through infectious body fluids such as emesis, diarrhea, sweat * The sicker patients are typically more infectious * Casual contact can transmit the disease, but is probably the wrong message to be spreading. Casual contact can result in transmission when the patient is seriously ill. Casual contact in early stages is unlikely to result in spread of disease       (see Table 2 below, from Dowell SF, Mukunu R, Ksiazek TG, Khan AS, Rollin PE, Peters CJ. Transmission of Ebola hemorrhagic fever: a study of risk factors in family members, Kikwit, Democratic Republic of the Congo, 1995. Commission de Lutte contre les Epidémies à Kikwit. J Infect Dis. 1999;179 Suppl 1:S87-91.) * Fomite transmission is less likely, but precautions should be taken * Airborne transmission is unconfirmed; many patients in west Africa are not receiving administration of high flow oxygen, endotracheal intubation, and suctioning that they might receive in resource-able settings. * We don’t know how Ebola will be transmitted in modern health care settings. * Close contacts and HCW are most at risk. Most transmission is DIRECT CONTACT Principles of Personal Protective Equipment (PPE) 1. Don’t go in and out of the care area frequently 2. High levels of PPE early in disease and during severe illness 3. 100% discipline in donning and doffing – active safety officer 4. Chest, abdomen, gloves, and boots are most likely to be contaminated Making the Diagnosis Screening – CDC guidelines, a starting point Diagnosis –  requires special handling. Done by PCR at state lab or CDC. Need more sensitive tests for rule outs Isolation – No travelling or diagnostic studies. Limited POC labs. Diagnostic imaging with bedside US Treatment – Oral rehydration, ACT for malaria, antibiotics (ceftriaxone or Cipro) for possible bacterial translocation Rubinson’s Principles for Ebola Care 1. The number of personnel entering the room should be minimized.