SECTION ON CRITICAL CARE

Transcription

1 SECTION ON CRITICAL CARE CRITICAL RESULTS JUNE 2014 EDITOR: Carley Riley, MD, MPP CONTENT MANAGER: Jyoti Assudani, MD What s Happening Now? SOCC Celebrates 30 Years during AAP 2014 NCE - San Diego, October by Brad Poss, MD, FAAP The Section on Critical Care (SOCC) will be hosting its annual scientific and educational session on Sunday and Monday October 12 and 13 in beautiful downtown San Diego as part of the American Academy of Pediatrics (AAP) 2014 National Conference & Exhibition. Come celebrate the SOCC 30-year anniversary in America s Finest City with education, networking, and pediatric critical care trivia and history. An additional highlight this year will be the AAP s social event, San Diego Experience At the USS Midway Aircraft Carrier, that will be held on the evening of Saturday, October 11. The SOCC will host a full day of educational programming on Sunday, October 12 to consist of a half day of abstract presentations (oral and poster format) that focus on clinical and laboratory research topics that impact the clinical care of critically ill and injured infants, children and adolescents. The forum represents an excellent opportunity for trainee presentations; awards for best overall abstract, best physician in training abstract, and a physician in training travel grant will be given. The afternoon will be a ticketed event where attendees will have the opportunity to participate in simulation experiences in improving team communication, managing patient scenarios, and increasing their procedural competency. The format will be a series of patient cases using simulation technology in a team-based format as well as utilizing procedural stations and interactive questions. The day will conclude with the section s brief business meeting and presentation of the Distinguished Career Award. Monday, October 13 will be a highly educational joint morning session with the Section on Hospital Medicine entitled Post-Intensive Care Syndrome (PICS): Are They Really OK When They Leave the ICU? Post-intensive care syndrome, or PICS, consists of the multiple health problems that are present when the patient is in the ICU and may persist after the patient returns home. These physical and behavioral problems can affect the patient and their family and includes weakness, cognitive brain dysfunction, anxiety, and depression. Please join us to learn more about the latest research and prevention strategies regarding PICS. Page 1

2 2014 World Congress on Pediatric Intensive & Critical Care: A Unique Conference of Great Value by Brad Poss, MD, FAAP The World Federation of Pediatric Intensive and Critical Care Societies (WFPICCS) held its 7th World Congress on Pediatric Intensive and Critical Care (PICC 2014) on May 5 to 7 in historic and exciting Istanbul, Turkey with pre-conference workshops held May 3 and 4. I can personally attest to the fantastic and broad-reaching educational and networking opportunities that this unique conference provided. The focus of PICC 2014 was the crossroads to the future of pediatric intensive and critical care which fit perfectly with beautiful Istanbul, known for its enchanting blend of Eastern and Western culture. Each day included 9 different tracks ranging from The Illness to The Organization and each track included multi-disciplinary presentations from around the globe with time built in for sharing lessons learned. In addition, there were superb research presentations woven throughout the entire program. Personal highlights included a fun filled evening cruise on the Bosphorus with old and new friends, superb presentations on pediatric intensive care international network collaboration and humor in the Pediatric Intensive Care Unit (PICU), and a thought-provoking movie and discussion on moral distress in PICU teams. Our chosen field of pediatric critical care is often full of daily challenges and stresses, so it was rewarding to see the passion and innovation that units and healthcare team members across the world are bringing to the challenges of advancing patient care, quality outcomes, scientific advances, and taking care of each other. Make plans now to attend the next World Congress on Pediatric Intensive and Critical Care to be held in Toronto, Canada in 2016 Who s Advocating How? AAP Helps Pediatricians & Pediatric Subspecialists Advocate for Children s Safety The AAP believes that children deserve a safe environment in which to grow and learn and provides resource to the many pediatricians and pediatric subspecialists who want to help. The AAP understands that unique and powerful position from which pediatricians may advocate for children's health issues. For more information on how pediatricians can make changes, visit How Pediatricians Can Advocate for Children s Safety in Their Communities. Page 2

3 AAP Supports World Sepsis Day on September 13 The AAP remains an active supporter of the Global Sepsis Alliance (GSA) and World Sepsis Day (WSD). The third annual WSD will take place on September 13, For more information, view the most recent WSD Newsletter. What Opportunities Exist? Community Access to Child Health (CATCH) Grants - Application Deadline July 31 Grants of up to $10,000 for pediatricians and fellowship trainees and $2,000 for pediatric residents are available from the Community Access to Child Health (CATCH) program for innovative initiatives that will ensure all children, especially underserved children, have medical homes and access to health services not otherwise available in their communities. Applications for Planning, Implementation, and Resident Grants accepted until July 31. PREP ICU Q&A Each AAP SOCC Critical Results will include a question and answer courtesy of PREP ICU The AAP s Premier Critical Care Self-Assessment. For a free trial or subscription to the PREP ICU Self- Assessment programs, visit Question An 18-month-old boy who was found face down in a swimming pool without respiratory effort or a heartbeat was resuscitated by paramedics and had return of spontaneous circulation before arrival in the emergency department. On arrival, he has decorticate response to painful stimuli, hypoxemia (SaO2 of 85% during bag-valve-mask ventilation), tachycardia (heart rate of 170/min), and hypotension (blood pressure of 68/35 mmhg). His blood pressure decreases further after intubation, requiring volume resuscitation and initiation of an epinephrine infusion at 0.05 micrograms/kg/min. He is transported to your hospital and admitted to the pediatric intensive care unit. He has a mean arterial blood pressure of 60 mmhg, central venous pressure of 6 mmhg, 2+ pulses in his extremities, and approximately 2-second capillary refill. He receives mechanical ventilation because of progressive acute respiratory distress syndrome, currently on a rate of 24, FiO2 of 0.8, peak inspiratory pressure of 32 cmh2o, and positive end-expiratory pressure (PEEP) of 12 cmh2o. His most recent arterial blood gas shows the following: ph 7.38, PaCO2 55 mmhg, PaO2 61 mmhg, HCO3 31 meq/l (31 mmol/l), base excess +6 meq/l, SaO2 90%. Thirty-six hours after admission, while receiving a decreasing epinephrine infusion (currently 0.03 micrograms/kg/min), the boy develops liver dysfunction, with serum alanine aminotransferase of 2670 U/L and aspartate aminotransferase of 3255 U/L. He is not jaundiced. Page 3

4 Of the following, the MOST likely cause of his elevated liver enzyme values is: A. centrilobular hepatocyte necrosis due to hypoxemia and ischemia B. diffuse hepatocellular injury due to epinephrine-induced hepatic artery constriction C. diffuse hepatocellular injury due to persistent hypoxemia D. periportal hepatocyte injury due to decreased liver perfusion pressure from high PEEP E. hepatic artery thrombosis with periportal infarction Answer The liver has a dual blood supply. Approximately two-thirds of the blood supply is from the portal vein and is rich in nutrients and hormones from the gastrointestinal tract but relatively desaturated; under normal conditions, the remainder is highly saturated blood that arrives via the hepatic artery. The two mix in the periportal area of the liver lobule. As blood flows through the sinusoids from the periportal area (zone 1) toward the central venules (zone 3), oxygen and nutrient content progressively decrease. As a consequence, hepatocytes in the pericentral area are significantly more vulnerable to ischemic injury and necrosis than those in the periportal area. In this scenario, therefore, the most likely cause of his elevated liver enzyme values is centrilobular hepatocyte necrosis due to hypoxemia and ischemia. Ischemic injury to the liver is relatively common in children when perfusion is compromised and there is an imbalance between metabolic demand and oxygen supply. During very low perfusion states, the limited cardiac output is shunted preferentially from the splanchnic bed to the brain and heart. Children who have undergone cardiopulmonary arrest, such as the boy described in the vignette, are at obvious risk, but others who have low cardiac output states (even without hypotension) or asphyxia also are at risk. Patients at risk include those who have hypoplastic left heart syndrome, coarctation, shock from any cause, and prolonged seizure activity, among others. Patients experiencing ischemic hepatitis commonly have markedly elevated transaminase values 24 to 48 hours after the compromising event, often reaching concentrations of 5000 to 10,000 U/ L. If the perfusion and oxygenation are corrected, serum enzyme concentrations decrease to normal over the next 3 to 11 days, and functional recovery is good. Although biopsy usually is not necessary, pathology evaluation reveals primarily centrilobular (pericentral) hepatocyte necrosis. Vasoactive agents, especially vasopressors, may alter splanchnic blood flow, including flow to the liver, but the dose reported for this patient would be expected to have primarily a β-agonist effect. The epinephrine dose would likely be insufficient to contribute to hepatic injury. In fact, maintaining adequate cardiac output is important for allowing resolution of ischemic hepatitis. Page 4

5 Though this child has severe lung disease, as evidenced by marginal oxygenation at high mean airway pressure and a high concentration of inspired oxygen, mild desaturation (90%) is unlikely to cause ongoing injury in the face of adequate cardiac output. Hypoxia at the time of the initial insult no doubt contributed to the currently apparent hepatocellular injury, but the small decrement in oxygen content associated with this saturation when the blood is mixed 2-to-1 with portal venous blood would not be expected to cause continuing injury. To the extent that hypoxemia does contribute to hepatocellular injury, it would be concentrated in the centrilobular (pericentral) zone. Inadequate perfusion pressure across the hepatic vascular bed can contribute to hepatic injury and likely is one of the reasons for hepatic dysfunction and elevated transaminases in patients who have right heart failure. Elevated central venous pressure (CVP) results in increased resistance to systemic venous return and decreased hepatic perfusion pressure (ie, mean arterial pressure [MAP] hepatic venous pressure). To the extent that airway pressure is transmitted to the vasculature, positive-pressure ventilation also may decrease hepatic perfusion pressure by increasing the CVP and, secondarily, hepatic venous pressure. In this patient, however, airway pressure does not appear to be significantly referred to the vasculature. Perfusion pressure in this infant is approximately 54 mmhg (MAP-CVP), which is probably close to normal at this age. Hepatic artery thrombosis is very uncommon in children, except after liver transplantation, when it often is associated with loss of the graft. In other patients, hepatic artery thrombosis does not predictably lead to infarction because blood flow from the portal circulation is usually sufficient to sustain liver viability. Suggested Readings: McLin VA, Yazigi N. Developmental anatomy and physiology of the liver and bile ducts. Pediatric Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 3rd ed. Philadelphia, Pa: Saunders Elsevier; 2006: Stocker JT, Husain AN, Dehner LP, Chandra RS. The liver, gallbladder, and biliary tract. Pediatric Pathology. 2nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001: American Board of Pediatrics Content Specifications: Understand the factors affecting hepatic blood flow Know the anatomy and physiology of the hepatic/portal circulation Page 5