PICU Doc On Call

In this episode of PICU Doc on Call, Dr. Monica Gray and Dr. Pradip Kamat chat about flexible fiberoptic bronchoscopy (FFB) in the pediatric ICU. They walk through a case involving an eight-year-old who’s dealing with respiratory failure after a stem cell transplant. Along the way, they talk about when and why you might use bronchoscopy both for diagnosis and treatment—plus how to approach sedation and what effects the procedure can have on the heart and lungs. They also dive into important topics like managing hypoxia, handling increased airway and pulmonary vascular resistance, and what to keep in mind if your patient has a traumatic brain injury. The episode wraps up with tips for managing fever after the procedure and a quick look at how rigid bronchoscopy compares.Show Highlights:Use of flexible fiberoptic bronchoscopy (FFB) in the pediatric ICU (PICU)Indications for performing bronchoscopy (diagnostic and therapeutic)Management of sedation and analgesia during bronchoscopyCardiovascular effects associated with bronchoscopy proceduresRespiratory effects and complications during bronchoscopySpecial considerations for bronchoscopy in patients with traumatic brain injury (TBI)Post-procedure complications, including fever and its managementOverview of rigid bronchoscopy and its indicationsImportance of understanding physiological changes during bronchoscopyEducational focus on acute pediatric care for current and aspiring PICU internsReferences:Reference 1: Sachdev A, Chhawchharia R. Flexible Fiberoptic Bronchoscopy in Pediatric Practice. Indian Pediatr. 2019 Jul 15;56(7):587-593. PMID: 31333214.Reference 2: Li SX, Tao XF, Wu HJ, Jin F, Zhu GH, Wang YS, Tang LF, Chen ZM, Wu L. Advances in pediatric flexible bronchoscopy. World J Pediatr. 2025 Oct;21(10):945-956. doi: 10.1007/s12519-025-00967-7. Epub 2025 Oct 4. PMID: 41045338; PMCID: PMC12578761.Reference 3: Truitt BA, Kasi AS, Kamat PP, Fundora MP, Simon DM, Guglani L. Cryoextraction via flexible bronchoscopy in children with tracheobronchial obstruction. Pediatr Pulmonol. 2023 Sep;58(9):2527-2534. doi: 10.1002/ppul.26540. Epub 2023 Jun 23. PMID: 37350368.

In this episode of "PICU Doc on Call," Drs. Monica Gray and Pradip Kamat from Children's Healthcare of Atlanta dive into the use of inhaled anesthetics, especially isoflurane, in the pediatric ICU. We’re focusing on those tough cases: refractory status asthmaticus and status epilepticus. We’ll chat about why isoflurane is our go-to over other agents like sevoflurane, desflurane, or nitrous oxide, and break down its bronchodilatory and anticonvulsant properties. We’ll also touch on important pharmacology concepts, such as MAC and the blood-gas partition coefficient, and discuss how we approach dosing and ventilator management when using isoflurane.Of course, we’ll also discuss the potential adverse effects that can come with prolonged use, and why it’s important to stop other sedatives and beta-agonists once you start isoflurane. Join us as we walk through the practical aspects and pearls for using inhaled anesthetics in the PICU!Show Highlights:Use of inhaled anesthetics in pediatric intensive care units (PICU)Focus on isoflurane for managing refractory status asthmaticus and status epilepticusComparison of inhaled anesthetic agents: isoflurane, sevoflurane, nitrous oxide, and desfluraneImportance of minimum alveolar concentration (MAC) and blood-gas partition coefficient in anesthetic pharmacodynamicsMechanism of action of isoflurane in airway management and bronchodilationClinical administration techniques for isoflurane in critically ill childrenVentilator management principles for intubated children with status asthmaticusRole of isoflurane in refractory and super-refractory status epilepticusPotential adverse effects and considerations for prolonged isoflurane useSummary of pharmacologic concepts essential for safe isoflurane therapy in pediatric patientsReferences:Rogers Text Book of Pediatric Intensive Care: Chapter 47: Acute Severe Asthma. Stewart C, Brilli RJ. pages 763-775Reference 1: Stetefeld HR, Schaal A, Scheibe F, Nichtweiß J, Lehmann F, Müller M, Gerner ST, Huttner HB, Luger S, Fuhrer H, Bösel J, Schönenberger S, Dimitriadis K, Neumann B, Fuchs K, Fink GR, Malter MP; IGNITE Study Group, with support from the German Neurocritical Care Society (DGNI). Isoflurane in (Super-) Refractory Status Epilepticus: A Multicenter Evaluation. Neurocrit Care. 2021 Dec;35(3):631-639. doi: 10.1007/s12028-021-01250-z. Epub 2021 Jul 20. PMID: 34286464; PMCID: PMC8692280.Reference 2: Zeiler FA, Zeiler KJ, Teitelbaum J, Gillman LM, West M. Modern inhalational anesthetics for refractory status epilepticus. Can J Neurol Sci. 2015 Mar;42(2):106-15. doi: 10.1017/cjn. 2014.121. Epub 2015 Jan 9. PMID: 25572922.Reference 3: Werner HA. Status asthmaticus in children: a review. Chest. 2001 Jun;119(6):1913-29. doi: 10.1378/chest. 119.6.1913. PMID: 11399724.Reference 4: Gill B, Bartock JL, Damuth E, Puri N, Green A. Case report: Isoflurane therapy in a case of status asthmaticus requiring extracorporeal membrane oxygenation. Front Med (Lausanne). 2022 Nov 8;9:1051468. doi: 10.3389fmed. .2022.1051468. PMID: 36425104; PMCID: PMC9679515.

In this episode of *PICU Doc on Call*, Drs. Monica Gray, Pradip Kamat, and Rahul Damania chat about a 17-year-old girl who ended up with acute liver failure after she intentionally took 22.5 grams of acetaminophen. She came in 48 hours later with really high transaminases and an INR of 5.5, so she was admitted to the PICU. The hosts break down how acetaminophen affects the body, walk through its four clinical stages, and discuss how to manage it—focusing on N-acetylcysteine as the primary antidote. They also touch on other treatments, like fomepizole. Thankfully, this patient recovered without needing a liver transplant, which really shows how important it is to have a team approach with intensivists, hepatologists, toxicologists, and psychiatry all working together.Show Highlights:Clinical case presentation of a 17-year-old girl with acetaminophen ingestion leading to acute liver failureMechanism of acetaminophen toxicity and its metabolic pathwaysEpidemiology of acetaminophen toxicity in pediatric populationsPathophysiology of acetaminophen overdose and its effects on liver functionClinical manifestations and progression of acetaminophen toxicity through various stagesEvaluation and diagnostic criteria for assessing acetaminophen toxicityManagement strategies for acetaminophen overdose, including the use of N-acetylcysteine (NAC).Discussion of adjunctive therapies such as fomepizole in severe cases.Importance of supportive care in managing complications of acute liver failureAn interdisciplinary approach to treatment involving various medical specialtiesReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.Reference 1: 2019 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 37th Annual Report. Gummin DD, Mowry JB, Beuhler MC, Spyker DA, Brooks DE, Dibert KW, Rivers LJ, Pham NPT, Ryan ML. Clin Toxicol (Phila). 2020;58(12):1360.Reference 2: Pepin L, Matsler N, Fontes A, Heard K, Flaherty BF, Monte AA. Fomepizole Therapy for Acetaminophen-Induced Liver Failure in an Infant. Pediatrics. 2023 Oct 1;152(4):e2022061033. doi:10.1542/peds. 2022-061033. PMID: 37681263.Reference 3. Chiew AL, Buckley NA. Acetaminophen Poisoning. Crit Care Clin. 2021 Jul;37(3):543-561.Reference 4. Squires JE, Alonso EM, Ibrahim SH, Kasper V, Kehar M, Martinez M, Squires RH. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Position Paper on the Diagnosis and Management of Pediatric Acute Liver Failure. J Pediatr Gastroenterol Nutr. 2022 Jan 1;74(1):138-158. doi: 10.1097/MPG.0000000000003268. PMID: 34347674.

In this episode of "PICU Doc on Call," Drs. Monica Gray, Pradip Kamat, and Rahul Damania discuss the use of intranasal medications in pediatric intensive care. Using the case of a four-month-old infant needing an MRI, they explore when and why intranasal drugs are preferred over IV access, the science behind nasal drug delivery, safe administration techniques, and common medications used. The episode highlights the benefits of intranasal sedation—such as rapid onset and needle-free delivery—while emphasizing teamwork and careful monitoring for safe, effective pediatric care.Show Highlights:Use of intranasal medications in pediatric intensive care settingsCase study of a four-month-old infant requiring sedation for an MRI.Advantages of intranasal delivery over IV accessPharmacokinetics and neuroanatomy related to intranasal drug absorptionTechniques for safe and effective administration of intranasal medicationsComparison of intranasal dosing to oral and IV routesCommon intranasal medications used in the pediatric ICUImportance of timing and monitoring during sedation proceduresTeamwork and communication in administering intranasal medicationsClinical applications and implications for patient comfort and care deliveryReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.Reference 1: Tsze DS, Woodward HA, McLaren SH, Leu CS, Venn AMR, Hu NY, Flores-Sanchez PL, Stefan BR, Shen ST, Ekladios MJ, Cravero JP, Dayan PS. Optimal Dose of Intranasal Midazolam for Procedural Sedation in Children: A Randomized Clinical Trial. JAMA Pediatr. 2025 Sep 1;179(9):979-986. doi: 10.1001/jamapediatrics. 2025.2181.Reference 2: Prescott MG, Iakovleva E, Simpson MR, Pedersen SA, Munblit D, Vallersnes OM, Austad B. Intranasal analgesia for acute moderate to severe pain in children - a systematic review and meta-analysis. BMC Pediatr. 2023 Aug 18;23(1):405. doi: 10.1186/s12887-023-04203-x.Reference 3: Chabowski L, Mahboobi Z, Navolokina A. Intranasal ketamine for procedural sedation in children. Am J Emerg Med. 2023 Jun;68:195. doi: 10.1016/j.ajem.2023.04.013.Reference 4: Sulton C, Kamat P, Mallory M, Reynolds J. The Use of Intranasal Dexmedetomidine and Midazolam for Sedated Magnetic Resonance Imaging in Children: A Report From the Pediatric Sedation Research Consortium. Pediatr Emerg Care. 2020 Mar;36(3):138-142. doi: 10.1097/PEC.0000000000001199.

In this special “PICU Doc On Call Shorts” episode, pediatric ICU physicians Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania break down the concept of Mean Arterial Pressure (MAP). Using a case of a six-year-old in septic shock, they discuss how to calculate MAP, normal pediatric values, and the physiological determinants and clinical significance of MAP. The hosts highlight MAP’s role in guiding management of critically ill children, review autonomic and endothelial regulation, and reinforce learning with a board-style question. This episode emphasizes practical bedside application for pediatric interns and ICU providers.Show Highlights:Overview of Mean Arterial Pressure (MAP) and its clinical significance in pediatric critical care.Introduction of a clinical case involving a 6-year-old child in septic shock.Explanation of the formula for calculating MAP and its application to the clinical case.Discussion of normal reference values for MAP in children and their clinical implications.Physiological determinants of MAP, including cardiac output and systemic vascular resistance.Role of the autonomic nervous system in regulating MAP through baroreceptor reflexes.Importance of maintaining adequate MAP for organ perfusion, particularly in critically ill patients.Clinical applications of MAP monitoring and management strategies in the PICU.Summary of key takeaways regarding MAP calculation, physiological determinants, and clinical relevance.Mention of related topics, such as invasive versus non-invasive blood pressure monitoring.References:DeMers D, Wachs D. Physiology, Mean Arterial Pressure. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.Pediatric Blood Pressure Metrics and Hypotension Thresholds (details the task force data used to derive the 5th and 50th percentile MAP estimation formulas for children)Berlin DA, Bakker J. Starling curves and central venous pressure. Crit Care. 2015 Feb 16;19(1):55.Magder S. Volume and its relationship to cardiac output and venous return. Crit Care. 2016 Sep 10;20(1):271

In this episode of "PICU Doc on Call," Drs. Pradip Kamat and Rahul Damania dive into a pediatric ICU case involving a 4-year-old girl who presents with severe anemia and bleeding, ultimately diagnosed with von Willebrand disease (VWD). They chat about the causes and different types of VWD, walk through the key clinical features, and break down how to diagnose and manage this condition. Drs. Kamat and Damania highlight the important roles of desmopressin and factor concentrates in treatment. Throughout the episode, they stress the need to recognize VWD in kids who have mucosal bleeding and offer practical tips for intensivists on lab evaluation and treatment strategies for this common inherited bleeding disorder.Show Nighlights: Clinical case discussion of a 4-year-old girl with severe anemia and bleeding symptomsDiagnosis of von Willebrand disease (VWD) and its significance in pediatric critical careEtiology and pathogenesis of von Willebrand diseaseClassification of von Willebrand disease into types (Type 1, Type 2 with subtypes, Type 3)Clinical manifestations and symptoms associated with VWDDiagnostic approach for identifying von Willebrand disease, including laboratory testsManagement strategies for VWD, including desmopressin and von Willebrand factor concentratesRole of adjunctive therapies such as antifibrinolytics and hormonal treatmentsImportance of multidisciplinary collaboration in managing complex bleeding disordersOverview of the pathophysiology of von Willebrand factor and its role in hemostasisReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.Reference 1: Leebeek FW, Eikenboom JC. Von Willebrand's Disease. N Engl J Med. 2016 Nov 24;375(21):2067-2080.Reference 2: Ng C, Motto DG, Di Paola J. Diagnostic approach to von Willebrand disease. Blood. 2015 Mar 26;125(13):2029-37.Platton S, Baker P, Bowyer A, et al. Guideline for laboratory diagnosis and monitoring of von Willebrand disease: A joint guideline from the United Kingdom Haemophilia Centre Doctors' Organisation and the British Society for Hematology. Br J Haematol 2024 May;204(5):1714-1731.Mohinani A, Patel S, Tan V, Kartika T, Olson S, DeLoughery TG, Shatzel J. Desmopressin as a hemostatic and blood-sparing agent in bleeding disorders. Eur J Haematol. 2023 May;110(5):470-479. doi: 10.1111/ejh.13930. Epub 2023 Feb 12. PMID: 36656570; PMCID: PMC10073345.

In this episode of "PICU Doc On Call," Drs. Pradip Kamat and Rahul Damania discuss the acute management of a 14-year-old boy with severe rectal bleeding and hypertension, ultimately diagnosed with inflammatory bowel disease (IBD). They review the approach to pediatric lower GI bleeding, diagnostic workup, and imaging, emphasizing early recognition and resuscitation. They outline IBD management, including steroids, biologics such as infliximab, and nutritional support, while highlighting the importance of screening for infections before immunosuppression. The episode provides practical insights for PICU physicians on handling acute GI emergencies in children.Show Nighlights: Clinical case of a 14-year-old male with hypertension and rectal bleeding.Diagnosis of inflammatory bowel disease (IBD) following significant blood loss.Approach to pediatric rectal bleeding and its implications.Diagnostic workup including laboratory tests and imaging modalities.Management strategies for IBD in acute pediatric care.Importance of early recognition and resuscitation in cases of shock.Physiological principles related to blood loss and shock in children.Differential diagnoses for lower gastrointestinal bleeding in pediatrics.Initial evaluation and stabilization protocols for pediatric patients.Nutritional support and multidisciplinary care in managing IBD. References:Romano C, Oliva S, Martellossi S, et al. Pediatric gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric Gastroenterology. World J Gastroenterol. 2017;23(8):1326-1337.Pai AK, Fox VL. Gastrointestinal bleeding and management. Pediatr Clin North Am. 2017;64(3):543-561.Padilla BE, Moses W. Lower gastrointestinal bleeding and intussusception. Surg Clin North Am. 2017;97(1):63-80.Kaur M, Dalal RL, Shaffer S, Schwartz DA, Rubin DT. Inpatient management of inflammatory bowel disease-related complications. Clin Gastroenterol Hepatol. 2020;18(11):2417-2428.Ashton JJ, Ennis S, Beattie RM. Early-onset paediatric inflammatory bowel disease. Lancet Child Adolesc Health. 2017;1(2):147-158.Bouhuys M, Lexmond WS, van Rheenen PF. Pediatric inflammatory bowel disease. Pediatrics. 2022;150(6):e2022059341.Rosen MJ, Dhawan A, Saeed SA. Inflammatory bowel disease in children and adolescents. JAMA Pediatr. 2015;169(11):1053-1060.Conrad MA, Rosh JR. Pediatric Inflammatory Bowel Disease. Pediatr Clin North Am. 2017 Jun;64(3):577-591.Turner D, Ruemmele FM, Orlanski-Meyer E, et al. Management of Paediatric Ulcerative Colitis, Part 1: Ambulatory Care-An Evidence-based Guideline From European Crohn's and Colitis Organization and European Society of Paediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr. 2018 Aug;67(2):257-291, correction can be found in J Pediatr Gastroenterol Nutr 2020 Dec;71(6):794.

In this episode of "PICU Doc on Call," Dr. Pradip Kamat and Dr. Rahul Damania dive into a fascinating case of a 9-month-old infant who comes in with hypoglycemia and seizures. Together, they break down the basics of glucose metabolism, walk through the causes of hypoglycemia, and discuss the best diagnostic strategies and acute management steps. They put a special spotlight on using diazoxide for hyperinsulinemic hypoglycemia, discussing not only how it works but also its potential side effects. The conversation also discusses dietary interventions for metabolic disorders and highlights the importance of rapid diagnosis and personalized treatment.Show Highlights:Pediatric hypoglycemia and its implications in infantsCase study of a 9-month-old infant with hypoglycemia and seizuresPhysiology of glucose metabolism and its regulationCauses of hypoglycemia, categorized into primary and secondary etiologiesDiagnostic approaches for identifying the cause of hypoglycemiaInitial management strategies for acute hypoglycemiaLong-term treatment options based on underlying causesImportance of timely diagnosis and intervention in the PICU settingPharmacologic management of hyperinsulinemic hypoglycemia, including the use of diazoxideMultidisciplinary care and follow-up for pediatric patients with hypoglycemiaReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 84 Alder M et al. Pediatric Sepsis. Pages 1293-1309Honarmand K, Sirimaturos M, Hirshberg EL, Bircher NG, Agus MSD, Carpenter DL, Downs CR, Farrington EA, Freire AX, Grow A, Irving SY, Krinsley JS, Lanspa MJ, Long MT, Nagpal D, Preiser JC, Srinivasan V, Umpierrez GE, Jacobi J. Society of Critical Care Medicine Guidelines on Glycemic Control for Critically Ill Children and Adults 2024. Crit Care Med. 2024 Apr 1;52(4):e161-e181. doi: 10.1097/CCM.0000000000006174. Epub 2024 Jan 19. PMID: 38240484.Rosenfeld E, Thornton PS. Hypoglycemia in Neonates, Infants, and Children. 2023 Aug 22. In: Feingold KR, Ahmed SF, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hofland J, Kalra S, Kaltsas G, Kapoor N, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Singer F, Sperling MA, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000–. PMID: 37665756.Rayas MS, Salehi M. Non-Diabetic Hypoglycemia. 2024 Jan 27. In: Feingold KR, Ahmed SF, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hofland J, Kalra S, Kaltsas G, Kapoor N, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Singer F, Sperling MA, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000–. PMID: 27099902.Nakrani MN, Wineland RH, Anjum F. Physiology, Glucose Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560599/Chen X, Feng L, Yao H, Yang L, Qin Y. Efficacy and safety of diazoxide for treating hyperinsulinemic hypoglycemia: A systematic review and meta-analysis. PLoS One. 2021 Feb 11;16(2):e0246463. doi: 10.1371/journal.pone.0246463. PMID: 33571197; PMCID: PMC7877589.Kucharczyk P, Albano G, Deisl C, Ho TM, Bargagli M, Anderegg M, Wuest S, Konrad D, Fuster DG. Thiazides Attenuate Insulin Secretion Through Inhibition of Mitochondrial Carbonic Anhydrase 5b in β -Islet Cells in Mice. J Am Soc Nephrol. 2023 Jul 1;34(7):1179-1190. Doi: 10.1681/ASN.0000000000000122. Epub 2023 Apr 17. PMID: 36927842; PMCID: PMC10356162.

Today, Dr. Monica Gray, Dr. Pradip Kamat, and Rahul Damania discuss a critical case involving a 10-year-old boy who developed post-intubation desaturation. Using the DOPE mnemonic (Displacement, Obstruction, Pneumothorax, Equipment failure), they systematically troubleshoot the emergency, highlighting the importance of teamwork, capnography, and manual ventilation. The team emphasizes structured approaches, simulation training, and essential bedside tools to ensure rapid, effective management of acute deterioration in intubated children, turning a life-threatening crisis into a controlled, solvable situation.Show Highlights:Clinical case discussion of a ten-year-old boy with post-intubation desaturation in the pediatric ICUUse of the "DOPE" mnemonic (Displacement, Obstruction, Pneumothorax, Equipment failure) for troubleshootingSystematic approaches in emergency situations in pediatric critical careAssessment and management of sudden desaturation in intubated patientsEvaluation of potential causes of desaturation, including tube displacement and obstructionRole of equipment failure in acute deterioration and strategies to address itSignificance of continuous capnography and manual ventilation techniquesPrevention strategies for unplanned extubation in pediatric ICU settingsEmphasis on teamwork, communication, and simulation training in crisis managementReview of literature insights related to hypoxemia and equipment issues in pediatric intubationReferences:Topjian AA, et al. Part 4: Pediatric Basic and Advanced Life Support—2020 AHA PALS Guidelines. Circulation. 2020.Foundational pediatric resuscitation guidance endorsing early switch to manual ventilation and structured troubleshooting for the deteriorating intubated child.Cook TM, et al. Major complications of airway management in the UK: NAP4. British Journal of Anaesthesia. 2011.Seminal audit highlighting ICU/ED airway failures and the critical role of waveform capnography in preventing unrecognized esophageal intubation.Volpicelli G, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Medicine. 2012. High-impact consensus placing lung ultrasound at the bedside to rapidly diagnose pneumothorax during post-intubation deterioration.Prekker ME, et al. Video vs direct laryngoscopy for ED intubation—randomized trial. New England Journal of Medicine. 2023.NEJM RCT showing higher first-pass success with video laryngoscopy—relevant to preventing displacement/misplacement drivers of desaturation.Chrimes N, et al. Preventing unrecognised oesophageal intubation: consensus guideline. Anaesthesia. 2022.Modern, practice-changing guidance: sustained waveform capnography is the mainstay to exclude esophageal placement and avert catastrophic hypoxemia.

Welcome to "PICU Doc on Call," the podcast where the world of pediatric critical care comes alive! Today, Dr. Monica Gray, Dr. Pradip Kamat, and Rahul Damania delve into a fascinating case involving a 16-year-old male presenting with headache, photophobia, anemia, and cerebral venous thrombosis. After some detective work, the diagnosis? Paroxysmal nocturnal hemoglobinuria, or PNH.Join us as we break down the pathogenesis and clinical features of PNH, walk through the diagnostic workup, and discuss management strategies, especially the game-changing role of complement inhibitors like Eculizumab. We’ll also review this patient’s clinical journey, highlighting the key pearls for recognizing and treating PNH in the pediatric intensive care unit.So, tune in to hear more!Show Highlights:Clinical case presentation of a 16-year-old male with symptoms including headache, photophobia, and anemiaDiagnosis of paroxysmal nocturnal hemoglobinuria (PNH) and its clinical significancePathogenesis of PNH, including the role of the PIGA gene mutation and GPI-anchored proteinsClinical features and complications associated with PNH, such as thrombosis and hemolysisDiagnostic workup for PNH, including laboratory tests and flow cytometryManagement strategies for PNH, focusing on complement inhibitors like EculizumabImportance of supportive care in the PICU for patients with PNHDiscussion of emerging therapies and advancements in PNH treatmentPatient outcome and clinical course following treatment for PNHKey takeaways regarding the diagnosis and management of PNH in pediatric intensive careReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care.Reference 1: Brodsky RA. Paroxysmal nocturnal hemoglobinuria. Blood. 2014 Oct 30;124(18):2804-11.Reference 2 Waheed A, Shammo J, Dingli D. Paroxysmal nocturnal hemoglobinuria: Review of the patient experience and treatment landscape. Blood Rev. 2024 Mar;64:101158.Reference 3: Kokoris S, Polyviou A, Evangelidis P, Grouzi E, Valsami S, Tragiannidis K, Gialeraki A, Tsakiris DA, Gavriilaki E. Thrombosis in Paroxysmal Nocturnal Hemoglobinuria (PNH): From Pathogenesis to Treatment. Int. J. Mol. Sci. 2024 Nov 11;25(22):12104.

In today’s episode, Dr. Monica Gray and Dr. Pradip Kamat sit down with neurosurgeon Dr. Neal Laxpati, MD, PhD, to chat about intracranial pressure (ICP) monitoring in pediatric critical care. Using real case studies, they dive into how and when to use external ventricular drains (EVDs) and ICP bolts, walking listeners through setup, potential risks, and everyday challenges. The group discusses device complications, ways to prevent infections, how to interpret waveforms, and shares practical bedside tips. It’s a must-listen for intensivists looking for hands-on advice and key insights to help optimize care for kids with brain injuries or hydrocephalus.Show Highlights:Pediatric critical care unit (PCU) case discussionsIntracranial pressure (ICP) monitoring in pediatric patientsCase studies involving a 10-year-old girl with diffuse midline glioma and a 16-year-old male with a ruptured arteriovenous malformation (AVM)Cerebrospinal fluid (CSF) physiology and its role in ICP managementTypes of ICP monitoring devices: external ventricular drains (EVDs) and intraparenchymal monitorsIndications and complications associated with ICP monitoringInterpretation of ICP waveforms and their clinical significanceManagement strategies for elevated ICP and CSF drainageRisks and challenges of ICP monitoring, including infection and device malfunctionImportance of interdisciplinary communication and meticulous bedside care in pediatric critical care settingsReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 118. Traumatic brain injury. Kochaneck et al. Page 1375 -1400Rogers textbook:Reference 1: Forsyth RJ, Parslow RC, Tasker RC, Hawley CA, Morris KP; UK Paediatric Traumatic Brain Injury Study Group; Paediatric Intensive Care Society Study Group (PICSSG). Prediction of raised intracranial pressure complicating severe traumatic brain injury in children: implications for trial design. Pediatr Crit Care Med. 2008 Jan;9(1):8-14. doi: 10.1097/01.PCC.0000298759.78616.3A. PMID: 18477907.Reference 2: Appavu B, Burrows BT, Foldes S, Adelson PD. Approaches to Multimodality Monitoring in Pediatric Traumatic Brain Injury. Front Neurol. 2019 Nov 26;10:1261. doi: 10.3389/fneur.2019.01261. PMID: 32038449; PMCID: PMC6988791.

Ever wondered how PICU teams make those critical calls about blood pressure and vasoactive meds? On this episode, Dr. Monica Gray and Dr. Pradip Kamat dive into the real-world questions that come up during pediatric intensive care rounds. They break down the pros and cons of arterial line versus non-invasive cuff measurements, talk through blood pressure targets for tough cases like sepsis and brain injury, and share practical tips for weaning kids off vasoactive drugs. With a focus on the latest guidelines and research, Monica and Pradip offer actionable advice to help you fine-tune hemodynamic management for your sickest patients. Tune in!Show Highlights:Relationship between blood pressure and cardiac output in pediatric patientsComparison of arterial line (invasive) versus non-invasive cuff measurements for blood pressure monitoring in the PICUBlood pressure targets for critical illnesses such as sepsis, traumatic brain injury, and respiratory failure in childrenStrategies for weaning vasoactive medications in critically ill pediatric patientsImportance of accurate blood pressure measurement and monitoring in the PICUDiscussion of organ autoregulation and its impact on blood pressure managementClinical assessment and individualized care in setting blood pressure goalsRecommendations for initial vasoactive agents in pediatric septic shockChallenges and considerations in vasoactive medication selection and weaningNeed for further research on pediatric vasoactive medication management strategiesReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 110. Alder M et al. Pediatric Sepsis. Pages 1293-1309.Rogers Textbook of Pediatric Critical Care Medicine. Chapter 88. Fitzgerald J et al. Bacterial Sepsis.Pages 1469-1485.Reference 1 Weiss S. Vasoactive Selection for Pediatric Septic Shock-Where to begin. JAMA Network Open, 2025;8(4):e254726.Reference 2 Schlapbach LJ, Watson RS, Sorce LR, Argent AC, Menon K, Hall MW, Akech S, Albers DJ, Alpern ER, Balamuth F, Bembea M, Biban P, Carrol ED, Chiotos K, Chisti MJ, DeWitt PE, Evans I, Flauzino de Oliveira C, Horvat CM, Inwald D, Ishimine P, Jaramillo-Bustamante JC, Levin M, Lodha R, Martin B, Nadel S, Nakagawa S, Peters MJ, Randolph AG, Ranjit S, Rebull MN, Russell S, Scott HF, de Souza DC, Tissieres P, Weiss SL, Wiens MO, Wynn JL, Kissoon N, Zimmerman JJ, Sanchez-Pinto LN, Bennett TD; Society of Critical Care Medicine Pediatric Sepsis Definition Task Force. International Consensus Criteria for Pediatric Sepsis and Septic Shock. JAMA. 2024 Feb 27;331(8):665-674.

Welcome to PICU Doc on Call, the podcast where we break down real-life cases from the pediatric intensive care unit and share practical insights for clinicians everywhere! I’m Dr. Monica Gray, and I’m joined by my co-host, Dr. Pradip Kamat.Today, we’re diving into a fascinating case: a 13-year-old boy who suddenly developed muscle weakness and was found to have severe hypokalemia. After some detective work, he was diagnosed with familial hypokalemic periodic paralysis, a rare but important condition to recognize in the PICU.We’ll discuss the genetic underpinnings, classic clinical features, and common triggers associated with this disorder. Additionally, we’ll guide you through the differential diagnosis, key management strategies, such as potassium supplementation, and explain why genetic testing is so crucial. We’ll also cover essential considerations for anesthesia and cardiac monitoring in these patients.Whether you’re a pediatric intensivist or just interested in acute neuromuscular care, stick around for some practical pearls you can use on your next shift!Show Highlights:Clinical case discussion of a 13-year-old male patient with muscle weakness and hypokalemiaDiagnosis and management of familial hypokalemic periodic paralysisGenetic basis and mutations associated with hypokalemic periodic paralysis (CACNA1S and SCN4A)Physiological mechanisms underlying hypokalemic periodic paralysisCommon clinical presentations and triggers for episodes of muscle weaknessDifferential diagnoses for muscle weakness and hypokalemia in pediatric patientsLaboratory investigations to confirm hypokalemic periodic paralysisTreatment options for hypokalemic periodic paralysis, including potassium supplementation and prophylactic medicationsImportance of avoiding triggers and coordinating care with anesthesiaReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 68: Weimer M et al. Acute neuromuscular disease and disorders page 840Rogers Textbook of Pediatric Intensive Care Medicine: Management of Sodium and Potassium Disorders. Pages 1876- 1883Reference 1: Weber F, Lehmann-Horn F. Hypokalemic Periodic Paralysis. 2002 Apr 30 [Updated 2018 Jul 26]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025. Available from: https://www.ncbi.nlm.nih.gov/books/NBK1338/Reference 2: Channelopathies. Clin Exp Pediatr. 2014;57(1):1-18.   Published online January 31, 2014**DOI: https://doi.org/10.3345/kjp.2014.57.1.1**Reference 3: Statland JM, Fontaine B, Hanna MG, Johnson NE, Kissel JT, Sansone VA, Shieh PB, Tawil RN, Trivedi J, Cannon SC, Griggs RC. Review of the Diagnosis and Treatment of Periodic Paralysis. Muscle Nerve. 2018 Apr;57(4):522-530.

Learn how to sharpen your pediatric intubation skills and make evidence-based decisions at the bedside. Today, Dr. Pradip Kamat, Dr. Monica Gray, and Dr. Rahul Damania expertly dissect the nuances of selecting optimal induction agents for critically ill children in the PICU. Through engaging, real-world case scenarios, our hosts guide you through drug choices in complex situations such as cardiogenic shock, septic shock, and elevated intracranial pressure—always prioritizing hemodynamic stability and patient safety. Gain valuable insights into the advantages, limitations, and clinical pearls of agents like propofol, fentanyl, ketamine, and midazolam, along with practical strategies for rapid sequence intubation, neuromuscular blockade, and individualized patient care. Don’t miss this high-yield discussion, packed with actionable knowledge!Show Highlights:Induction agents for endotracheal intubation in critically ill childrenClinical scenarios highlighting optimal choices of induction agents and neuromuscular blockersImportance of maintaining hemodynamic stability during intubationPharmacology and clinical considerations of various induction agents (e.g., propofol, ketamine, fentanyl, etomidate)Use of neuromuscular blocking agents (NMBAs) in pediatric intubationDifferences between depolarizing and non-depolarizing neuromuscular blockersRisks associated with specific induction agents in patients with cardiac dysfunction or septic shockModified rapid sequence intubation (RSI) techniques for unstable patientsKey takeaways for managing critically ill pediatric patients requiring intubationPractical tips for optimizing intubation conditions and minimizing complicationsReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care 6th Edition. Chapters 127 - 135, Pages 1510 - 1610Hendrix JM, Regunath H. Intubation Endotracheal Tube Medications. [Updated 2025 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459276/Agrawal, Dewesh. Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis. UpToDate. Last updated Dec 4, 2024.Vanlinthout LE, Geniets B, Driessen JJ, Saldien V, Lapré R, Berghmans J, Uwimpuhwe G, Hens N. Neuromuscular-blocking agents for tracheal intubation in pediatric patients (0-12 years): A systematic review and meta-analysis. Paediatr Anaesth. 2020 Apr;30(4):401-414. doi: 10.1111/pan.13806. Epub 2020 Mar 9. PMID: 31887248.Tarquinio KM, Howell JD, Montgomery V, Turner DA, Hsing DD, Parker MM, Brown CA 3rd, Walls RM, Nadkarni VM, Nishisaki A; National Emergency Airway Registry for Children; Pediatric Acute Lung Injury and Sepsis Investigators Network. Current medication practice and tracheal intubation safety outcomes from a prospective multicenter observational cohort study. Pediatr Crit Care Med. 2015 Mar;16(3):210-8. doi: 10.1097/PCC.0000000000000319. PMID: 25581629.Conway JA, Kharayat P, Sanders RC Jr, Nett S, Weiss SL, Edwards LR, Breuer R, Kirby A, Krawiec C, Page-Goertz C, Polikoff L, Turner DA, Shults J, Giuliano JS Jr, Orioles A, Balkandier S, Emeriaud G, Rehder KJ, Kian Boon JL, Shenoi A, Vanderford P, Nuthall G, Lee A, Zeqo J, Parsons SJ, Furlong-Dillard J, Meyer K, Harwayne-Gidansky I, Jung P, Adu-Darko M, Bysani GK, McCarthy MA, Shlomovich M, Toedt-Pingel I, Branca A, Esperanza MC, Al-Subu AM, Pinto M, Tallent S, Shetty R, Thyagarajan S, Ikeyama T, Tarquinio KM, Skippen P, Kasagi M, Howell JD, Nadkarni VM, Nishisaki A; National Emergency Airway Registry for Children (NEAR4KIDS) and for the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI). Ketamine Use for Tracheal Intubation in Critically Ill Children Is Associated With a Lower Occurrence of Adverse Hemodynamic Events. Crit Care Med. 2020 Jun;48(6):e489-e497. doi: 10.1097/CCM.0000000000004314. PMID: 32317603.Zanza C, Piccolella F, Racca F, Romenskaya T, Longhitano Y, Franceschi F, Savioli G, Bertozzi G, De Simone S, Cipolloni L, La Russa R. Ketamine in Acute Brain Injury: Current Opinion Following Cerebral Circulation and Electrical Activity. Healthcare (Basel). 2022 Mar 17;10(3):566. doi: 10.3390/healthcare10030566. PMID: 35327044; PMCID: PMC8949520.Zeiler FA, Teitelbaum J, West M, Gillman LM. The ketamine effect on ICP in traumatic brain injury. Neurocrit Care. 2014 Aug;21(1):163-73. doi: 10.1007/s12028-013-9950-y. PMID: 24515638.

Ready for a deep dive into a real-life pediatric ICU situation? Today,  Dr. Pradip Kamat, Dr. Monica Gray, and Dr. Rahul Damania will walk you through the case of a seven-year-old girl with Hemoglobin SC (HbSC) disease, who presents with abdominal swelling, pneumonia, low oxygen, and pain.In this episode, our team unpacks the spleen’s anatomy and its crucial role in immunity, then zooms in on how sickle cell disease can throw a wrench in splenic function. You’ll hear how they approach the diagnosis and management of acute splenic sequestration crisis, sharing clinical pearls along the way. Plus, they’ll break down why quick recognition is so important and discuss strategies for both immediate and long-term care in pediatric sickle cell patients. Don’t miss these practical insights from the frontlines of pediatric critical care!Show Highlights:Case study of a seven-year-old girl with hemoglobin SC diseasePresentation of symptoms: abdominal distension, pneumonia, hypoxia, and body painDiscussion of acute splenic sequestration crisis as a complication of sickle cell diseaseAnatomy and physiology of the spleenThe role of the spleen in sickle cell disease and how sickled cells affect splenic functionAcute splenic sequestration crisis, including clinical features and laboratory evaluationsManagement strategies for acute splenic sequestration crisis in the ICUImportance of blood transfusions and supportive care in treatmentProphylactic measures to prevent recurrence of splenic sequestrationEducational emphasis on recognizing clinical signs and the need for timely interventionReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 88. Hemoglobinopathies. Baender, MA, Marsh Anne. Pages: 1457-1470Rogers' textbook of pediatric intensive care: Hematologic Emergencies. McCory MC, Bhar S, and Blaine E. Pages 2003-2005Brousse V, Buffet P, Rees D. The spleen and sickle cell disease: the sick(led) spleen. Br J Haematol. 2014 Jul;166(2):165-76. doi: 10.1111/bjh 12950. Epub 2014 May 26. PMID: 24862308.Waleed S, Aldabsa M, Gouher S. Splenic Sequestration Induced by Parvovirus B19: A Case Report. Cureus. 2024 May 23;16(5):e60937. doi: 10.7759/cureus. 60937. PMID: 38915956; PMCID: PMC11195323.Solanki DL, Kletter GG, Castro O. Acute splenic sequestration crises in adults with sickle cell disease. Am J Med. 1986 May;80(5):985-90. doi: 10.1016/0002-9343(86)90649-2. PMID: 3706382.Karna B, Jha SK, Al Zaabi E. Hemoglobin C Disease. [Updated 2023 May 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559043/

Welcome to "PICU Doc on Call," the podcast where real cases meet real expertise at the bedside! Join Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania as they unravel the mysteries of pediatric critical care. In today’s episode, our team dives into the compelling case of a previously healthy seven-year-old girl who arrives with seizures, right arm weakness, and sudden respiratory failure. Together, they’ll break down the diagnosis and management of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, also known as MOGAD. This autoimmune demyelinating disorder can challenge even the most seasoned clinicians. Tune in as our experts walk you through the clinical features, essential diagnostic workup, and the critical importance of early immunosuppressive therapy. Whether you’re at the bedside or on the go, this episode is packed with practical pearls and a multidisciplinary approach to recognizing and treating acute pediatric neuroimmunological emergencies in the PICU. Let’s get started!Show Highlights:Presentation of a complex pediatric case involving a seven-year-old girl with new-onset seizures and acute respiratory failureDiscussion of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) as an autoimmune demyelinating disorderOverview of the clinical presentation and diagnostic criteria for autoimmune encephalitisImportance of a broad differential diagnosis, including infectious and autoimmune causes, in pediatric patients with seizures and neurological deficitsDiagnostic approach involving MRI, lumbar puncture, and antibody testing for MOGADManagement strategies for MOGAD, including stabilization, seizure control, and immunosuppressive therapyNeurocritical care considerations for monitoring and treating elevated intracranial pressureLong-term management challenges and the need for multidisciplinary care in pediatric patients with MOGADDiscussion of potential outcomes and the risk of relapse in children with MOGAD.Emphasis on the importance of early and comprehensive diagnostic testing to avoid misdiagnosisReferences:Fuhrman & Zimmerman - Pediatric Critical Care 6th Edition, Chapter 64Gole S, Anand A. Autoimmune Encephalitis. [Updated 2023 Jan 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK578203/Salama S, Khan M, Pardo S, Izbudak I, Levy M. MOG antibody-associated encephalomyelitis/encephalitis. Mult Scler. 2019 Oct;25(11):1427-1433. doi: 10.1177/1352458519837705. Epub 2019 Mar 25. PMID: 30907249; PMCID: PMC6751007Lancaster E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016 Jan;12(1):1-13. doi: 10.3988/jcn.2016.12.1.1. PMID: 26754777; PMCID: PMC4712273.Fisher KS, Illner A, Kannan V. Pediatric neuroinflammatory diseases in the intensive care unit. Semin Pediatr Neurol. 2024 Apr;49:101118. Doi: 10.1016/j.spen.2024.101118. Epub 2024 Feb 1. PMID: 38677797.Hébert J, Muccilli A, Wennberg RA, Tang-Wai DF. Autoimmune Encephalitis and Autoantibodies: A Review of Clinical Implications. J Appl Lab Med. 2022 Jan 5;7(1):81-98. Doi: 10.1093/jalm/jfab102. PMID: 34996085.Lopez JA, Denkova M, Ramanathan S, Dale RC, Brilot F. Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody-associated disease. Clin Transl Immunology. 2021 Jul 26;10(7):e1316. doi: 10.1002/cti2.1316. PMID: 34336206; PMCID: PMC8312887.

Have you ever wondered what happens when a toddler gets into something they definitely shouldn’t? Today, Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania discuss the case of an 18-month-old boy who accidentally ingested concentrated bleach, presenting with stridor, drooling, and vomiting. They review the clinical approach to caustic ingestions in children, including airway management, diagnostic workup, and the roles of endoscopy, steroids, and multidisciplinary care. The episode also highlights potential complications such as esophageal strictures and cancer, emphasizes prevention strategies, and provides key takeaways for intensivists managing similar pediatric emergencies. If you’re an intensivist or just want to know what to do in a pediatric emergency, don’t miss these essential takeaways for managing one of the scariest situations in the ER.Show Highlights:Case study of an 18-month-old boy who ingested concentrated bleachClinical presentation including symptoms like stridor, drooling, and vomitingManagement strategies for caustic ingestions in childrenImportance of airway management and monitoring in cases of caustic ingestionDiagnostic workup including imaging and endoscopyDifferential diagnosis considerations for similar presentations (e.g., button batteries, laundry detergent pods)Mechanism of injury caused by alkaline substances like bleachLong-term complications associated with caustic ingestions, such as esophageal strictures and cancerMultidisciplinary approach to treatment involving various medical specialtiesPrevention strategies to reduce the incidence of accidental caustic ingestions in childrenReferences:American Academy of Pediatrics – Pediatric Care Online: Esophageal Caustic Injury (AAP clinical guidance on caustic ingestions).Fuhrman & Zimmerman’s Pediatric Critical Care textbook – Chapters on toxicology and gastrointestinal emergencies (covering caustic injury management and critical care approach).Hoffman RS, et al. “Ingestion of Caustic Substances.” New England Journal of Medicine. 2020; 382(18):1739-1748. A comprehensive review of caustic ingestion injuries and management.Arnold M, Numanoglu A. “Caustic ingestion in children – a review.” Semin Pediatr Surg. 2017;26(2):95-104. Review of epidemiology, pathophysiology, and treatment of caustic injuries in kids.Johnson CM, Brigger MT. “The public health impact of pediatric caustic ingestion injuries.” Arch Otolaryngol Head Neck Surg. 2012;138(12):1111-1115. (Epidemiology study showing declining incidence).Pediatric Critical Care Medicine (PCCM) Journal – various case reports and series on caustic ingestion (for case-based insights), and annual National Poison Data System reports (for statistics on pediatric poisonings).Tringali A, et al. ESGE/ESPGHAN Pediatric GI Endoscopy Guidelines (Endoscopy, 2017) – Includes recommendations for endoscopy timing and steroid use in caustic ingestions.Usta M, et al. “High doses of methylprednisolone in the management of caustic esophageal burns.” Pediatrics. 2014;133(6):E1518-24. (Key study demonstrating steroids benefit in grade 2b injuries).Royal Children’s Hospital Melbourne – Clinical Practice Guidelines: Caustic Ingestions (2019) – Practical hospital guidelines emphasizing early intubation for airway threat, endoscopy within 24h, IV PPI, and supportive care.

Today, Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania discuss two real-life pediatric cases of hyponatremia in the PICU. They talk through a case of a six-month-old baby with severe sodium depletion and a teenager dealing with cancer-related hyponatremia. The team breaks down the pathophysiology, walks us through the diagnostic workups, and discusses the careful management needed for these cases. They emphasize the importance of correcting sodium levels gradually and addressing the root cause of the problem. They share practical tips for intensivists and highlight why staying vigilant and following evidence-based care is so crucial when managing critically ill kids with electrolyte disturbances. Tune in to hear more!Show Highlights:Discussion of hyponatremia in pediatric patients, particularly in the PICUPresentation of two case studies illustrating different presentations of hyponatremiaExamination of the pathophysiology of hyponatremia, including its classification into hypovolemic, euvolemic, and hypervolemic typesOverview of diagnostic investigations for hyponatremia, including volume status assessment and serum/urine electrolyte measurementsManagement strategies for hyponatremia, emphasizing the importance of gradual correction of sodium levelsRisks associated with rapid correction of hyponatremiaImportance of fluid management in different types of hyponatremiaRole of pharmacological interventions in specific cases, such as SIADHClinical presentation and symptoms associated with hyponatremia in pediatric patientsEmphasis on continuous monitoring of sodium levels and clinical status during treatmentReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 71. Fluid and electrolyte issues in pediatric critical illness. Evans I, Joyce E. Page 866-872Rogers' textbook of Pediatric Intensive Care Chapter 108: Disorders of Water, Sodium and Potassium homeostasis: Schneider J & Glater-Welt L. Pages 1868-1880Harrison’s Principles of Internal Medicine Volume 1. Chapter 53: Fluid and Electrolyte Disturbances. Mount D. Pages 338-347

Today, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray, pediatric intensivists, sit down to chat about the diagnosis and management of acute myocarditis in children. They focus on a real-life case involving a one-month-old infant who presented with poor feeding, respiratory distress, and fever. Together, they break down the possible causes, key clinical signs, diagnostic approaches, and treatment options for pediatric myocarditis. Throughout the discussion, they highlight the importance of early recognition, a multidisciplinary team approach, and supportive care in improving outcomes for these critically ill infants. This episode is packed with practical insights and is designed to help pediatric intensivists tackle this challenging and potentially life-threatening condition. Tune in to hear more!Show Highlights:Definition and etiology of acute myocarditis in pediatric patientsClinical case presentation of a one-month-old infant with acute myocarditisSymptoms and clinical manifestations of acute myocarditis in childrenDiagnostic approaches for identifying acute myocarditis, including echocardiography and laboratory testsManagement strategies for acute myocarditis, including intensive care and medicationImportance of recognizing atypical presentations in infantsPrognosis and risk factors associated with acute myocarditisRole of multidisciplinary collaboration in managing acute myocarditisImpact of viral infections on the development and severity of myocarditisOutcomes and potential complications related to acute myocarditis in pediatric patientsReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 108. Life-threatening viral diseases and their treatment. Vora S et al. Pages 1273-1278Rogers’ textbook of Pediatric Intensive Care. Chapter 74: cardiomyopathy, myocarditis, and mechanical circulatory support. Harmon WG et al. Pages 1247-1255Robinson J, Hartling L, Vandermeer B, Sebastianski M, Klassen TP. Intravenous immunoglobulin for presumed viral myocarditis in children and adults. Cochrane Database Syst Rev. 2020 Aug 19;8(8): CD004370. Doi: 10.1002/14651858.CD004370.pub4. PMID: 32835416

In this episode of "PICU Doc on Call," pediatric intensivists Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray discuss a critical case involving a 16-year-old male who experienced severe carbon monoxide poisoning after being found unresponsive in a garage. They chat about the pathophysiology, clinical manifestations, diagnostic workup, and management of carbon monoxide toxicity. Furthermore, they cover the importance of early oxygen administration, recognizing potential delayed neurological sequelae, and keeping an eye out for cardiac complications. Tune in and hear more about a comprehensive approach to treatment and the significance of multidisciplinary support for achieving the best patient outcomes.Show Highlights:Case presentation of a 16-year-old male with severe carbon monoxide poisoningPathophysiology of carbon monoxide toxicity and its effects on hemoglobinClinical manifestations and symptoms associated with carbon monoxide poisoningDiagnostic workup for suspected carbon monoxide exposureManagement principles for treating carbon monoxide poisoning in pediatric patientsSources and scenarios leading to carbon monoxide poisoningComplications arising from carbon monoxide exposure including neurological injuriesImportance of early oxygen administration and monitoring in treatmentDiscussion of hyperbaric oxygen therapy and its indicationsKey takeaways for clinicians regarding the management and follow-up of carbon monoxide poisoning casesWe welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org.References:Tapking, C., et al. (2021). Burn and inhalation injury. In J. J. Zimmerman & A. T. Rotta (Eds.), Fuhrman and Zimmerman’s Pediatric Critical Care (6th ed., pp. 1347–1362). Elsevier.Nañagas KA, Penfound SJ, Kao LW. Carbon Monoxide Toxicity. Emerg Med Clin North Am. 2022 May;40(2):283-312. doi: 10.1016/j.emc.2022.01.005. Epub 2022 Apr 5. PMID: 35461624.Smollin C, Olson K. Carbon monoxide poisoning (acute). BMJ Clin Evid. 2010 Oct 12;2010:2103. PMID: 21418677; PMCID: PMC3217756.Palmeri R, Gupta V. Carboxyhemoglobin Toxicity. [Updated 2023 Apr 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan.

Welcome to another exciting episode of PICU Doc on Call! Today, we're diving deep into the world of pediatric critical care with our expert hosts, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray. Get ready to unravel the mysteries of the oxygen extraction ratio (O2ER) and its pivotal role in managing pediatric acute respiratory distress syndrome (ARDS) and multi-organ dysfunction.Picture this: a seven-year-old girl battling severe pneumonia that spirals into ARDS and septic shock. Our hosts walk you through this gripping case, shedding light on calculating O2ER and why central venous oxygen saturation (ScvO2) is a game-changer. They'll share their top strategies for optimizing oxygen delivery and cutting down on oxygen demand.But that's not all! This episode is all about the holistic approach to managing critically ill pediatric patients. Tune in to discover how these insights can lead to better outcomes for our youngest and most vulnerable patients. Don't miss out on this vital conversation!Show Highlights:Clinical significance of the oxygen extraction ratio (O2ER) in pediatric critical careImportance of understanding oxygen delivery and consumption in critically ill patientsCalculation and interpretation of O2ER and its relationship to central venous oxygen saturation (ScvO2)Physiological concepts related to oxygenation, including intrapulmonary shunting and ventilation-perfusion mismatchManagement strategies for increasing oxygen delivery and reducing oxygen demand in ARDS and septic shockInterventions such as blood transfusions, sedation, and optimization of cardiac outputImplications of lactic acidosis and anaerobic metabolism in the context of inadequate oxygen deliveryHolistic approach to patient management, focusing on both numerical values and overall metabolic needsWe welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org.References:Fuhrman B.P. & Zimmerman J.J. (Eds.). Pediatric Critical Care, 6th ed. Elsevier; 2021. (Key concepts of oxygen delivery, consumption, and extraction in shock states are discussed in Chapter 13) .Nichols D.G. (Ed.). Roger’s Textbook of Pediatric Intensive Care, 5th ed. Wolters Kluwer; 2016. (Comprehensive review of oxygen transport and utilization in critically ill children, including ARDS and shock).Lucking S.E., Williams T.M., Chaten F.C., et al. Dependence of oxygen consumption on oxygen delivery in children with hyperdynamic septic shock and low oxygen extraction. Crit Care Med. 1990;18(12):1316–1319. doi:10.1097/00003246-199012000-00002.Ronco J.J., Fenwick J.C., Tweeddale M.G., et al. Pathologic dependence of oxygen consumption on oxygen delivery in acute respiratory failure. Chest. 1990;98(6):1463–1466. doi:10.1378/chest.98.6.1463 .Carcillo J.A., Davis A.L., Zaritsky A. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock. Crit Care Med. 2002;30(6):1365–1378. (ACCM guidelines emphasizing ScvO₂ targets in shock) .Emeriaud G, López-Fernández YM, Iyer NP, et al; PALICC-2 Group; PALISI Network. Executive summary of the second international guidelines for the diagnosis and management of pediatric ARDS (PALICC-2). Pediatr Crit Care Med. 2023;24(2):143–168. doi:10.1097/PCC.0000000000003147.

In this episode, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray dive into a critical case involving a five-week-old baby facing acute respiratory failure due to pertussis. They chat about how this condition shows up, how it's diagnosed, and the best ways to manage it, especially considering the serious complications it can cause in infants, like pulmonary hypertension and the potential need for ECMO. The conversation underscores the importance of catching it early and providing supportive care, while also highlighting how crucial vaccination is in preventing pertussis. Tune in to learn how severe this disease can be and why staying alert in pediatric care is so important.Show Highlights:Clinical case of a five-week-old infant with acute respiratory failure and pertussis diagnosisEpidemiology and public health impact of pertussis, including vaccination rates and outbreak patternsPathophysiology of pertussis and its effects on respiratory health, particularly in infantsClinical presentation of pertussis, including stages of the disease and atypical symptoms in infantsDiagnostic approaches for pertussis, including laboratory findings and PCR testingManagement strategies for severe pertussis, including supportive care and antibiotic therapyPotential complications associated with pertussis, especially in young infantsDifferential diagnosis considerations for pertussis and distinguishing features from other infectionsImportance of vaccination in preventing pertussis and reducing morbidity and mortalityECMO as a treatment option for severe cases and its associated challenges, and outcomesWe welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org.References:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter and Rogers texbook of Pediatric intensive care -both do not have any Pertussis mentioned in their index.Rowlands HE, Goldman AP, Harrington K, Karimova A, Brierley J, Cross N, Skellett S, Peters MJ. Impact of rapid leukodepletion on the outcome of severe clinical pertussis in young infants. Pediatrics. 2010 Oct;126(4):e816-27. doi: 10.1542/peds.2009-2860. Epub 2010 Sep 6. PMID: 20819895.Lauria AM, Zabbo CP. Pertussis. [Updated 2022 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519008/Berger JT, Carcillo JA, Shanley TP, Wessel DL, Clark A, Holubkov R, Meert KL, Newth CJ, Berg RA, Heidemann S, Harrison R, Pollack M, Dalton H, Harvill E, Karanikas A, Liu T, Burr JS, Doctor A, Dean JM, Jenkins TL, Nicholson CE; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Collaborative Pediatric Critical Care Research Network (CPCCRN). Critical pertussis illness in children: a multicenter prospective cohort study. Pediatr Crit Care Med. 2013 May;14(4):356-65. doi: 10.1097/PCC.0b013e31828a70fe. PMID: 23548960; PMCID: PMC3885763.Cousin, V.L., Caula, C., Vignot, J. et al. Pertussis infection in critically ill infants: meta-analysis and validation of a mortality score. Crit Care 29, 71 (2025). https://doi.org/10.1186/s13054-025-05300-2Domico M, Ridout D, MacLaren G, Barbaro R, Annich G, Schlapbach LJ, Brown KL. Extracorporeal Membrane Oxygenation for Pertussis: Predictors of Outcome Including Pulmonary Hypertension and Leukodepletion. Pediatr Crit Care Med. 2018 Mar;19(3):254-261. doi: 10.1097/PCC.0000000000001454. PMID: 29319632.Centers for Disease Control: https://www.cdc.gov/schoolvaxview/data/index.html; https://www.cdc.gov/pertussis/php/surveillance/pertussis-incidence-by-age-group-and-year.html; https://www.cdc.gov/pertussis/media/pdfs/2025/01/pertuss-surv-report-2024_PROVISIONAL-508.pdf (various links)Tuan, Ta Anh MD, PhD1; Xoay, Tran Dang MD1; Nakajima, Noriko MD, PhD2; Nakagawa, Satoshi MD3; Phuc, Phan Huu MD, PhD1; Hung, Dau Viet MD, PhD1; Dung, Nguyen Trong MD1; Dong, Ngo Tien MD1; Dung, Tran Ba MD1; Thuy, Phung Thi Bich PhD4; Hai, Le Thanh MD, PhD5; Dien, Tran Minh MD, PhD6. Pertussis Infants Needing Mechanical Ventilation and Extracorporeal Membrane Oxygenation: Single-Center Retrospective Series in Vietnam. Pediatric Critical Care Medicine 22(9):p e471-e479, September 2021. | DOI: 10.1097/PCC.0000000000002723

In today’s episode, Dr. Rahul Damania and Dr. Pradip Kamat welcome their new co-host, Dr. Monica Gray. They’ll dive into the topic of upper airway obstruction in children and explore a case involving a 12-month-old girl who presents with stridor and fever. Throughout the discussion, they delve into the underlying causes, possible diagnoses, and management strategies. Key takeaways include the significance of keeping the child calm, ensuring proper positioning, and utilizing treatments such as dexamethasone and Racemic epinephrine. They’ll also touch on advanced therapies and serious infections like epiglottitis. The episode highlights the importance of recognizing stridor, knowing when to consider PICU admission, and the effectiveness of low-dose dexamethasone. Tune in to learn more!Show Highlights:Overview of upper airway obstruction in pediatric patientsCase presentation of a 12-month-old girl with stridor and feverDiscussion on the pathophysiology of stridor and its clinical significanceDifferential diagnoses for stridor, including croup, epiglottitis, and foreign body aspirationManagement strategies for upper airway obstruction, including stabilization and medicationImportance of calming the child and optimal positioning during treatmentUse of dexamethasone and racemic epinephrine in managing croupAdvanced therapies, such as Helios, for specific casesIndicators for pediatric intensive care unit (PICU) admissionKey clinical points and takeaways for healthcare professionals managing airway emergenciesReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 47 Otteson T, Richardson C, Shah J: Diseases of the upper Airway. Pages 524-535Rogers Textbook of Pediatric Intensive Care: Chapter 25; Ong May Soo Jacqueline, Tijssen J, Bruins BB and Nishisaki A: Airway management. Pages 341-365Reference: Asmundsson AS, Arms J, Kaila R, Roback MG, Theiler C, Davey CS, Louie JP. Hospital Course of Croup After Emergency Department Management. Hosp Pediatr. 2019 May;9(5):326-332. doi: 10.1542/hpeds.2018-0066. PMID: 30988017; PMCID: PMC6478427.Reference: Aregbesola A, Tam CM, Kothari A, Le ML, Ragheb M, Klassen TP. Glucocorticoids for croup in children. Cochrane Database Syst Rev. 2023 Jan 10;1(1):CD001955. doi: 10.1002/14651858.CD001955.pub5. PMID: 36626194; PMCID: PMC9831289.Previous Episode Mentioned:PICU Doc On Call Episode 80

In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat discuss the resurgence of measles in the United States. They explore the virus's pathophysiology, clinical features, diagnostic methods, treatment options, and complications. They emphasize the critical role of vaccination in preventing measles outbreaks and address the historical context and public health challenges related to vaccine hesitancy. The speakers highlight the severe complications of measles, especially in immunocompromised patients, and advocate for robust vaccination efforts to protect vulnerable populations and prevent the spread of this preventable disease. Tune in to hear more!Show Highlights:Resurgence of measles in the United StatesHistorical context of measles outbreaks and vaccination impactCurrent statistics and recent cases of measlesPathophysiology of the measles virusClinical features and progression of measles infectionDiagnostic approaches for confirming measlesDifferential diagnosis considerations for fever and rashTreatment options and the role of vaccinationComplications associated with measles, including severe outcomesPublic health challenges related to vaccine hesitancy and advocacy for immunizationResources:CDC Measles Info PageWHO Measles Global SurveillanceReferences:Fuhrman & Zimmerman. Textbook of Pediatric Critical Care, Ch. 52Long S et al. Principles and Practice of Pediatric Infectious Diseases, Ch. 227Moss WJ. Measles. Lancet. 2017;390(10111):2490-2502Paules CI, Marston HD, Fauci AS. NEJM. 2019;380(23):2185-2187

In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat chat about a challenging case involving a 15-year-old girl dealing with acute myocarditis and worsening respiratory failure. They explore the intricate dance between the heart and lungs, especially how positive pressure ventilation can affect heart function. They cover important topics like cardiac output, preload, and afterload, and discuss the delicate balance needed to manage myocarditis effectively. The episode offers practical tips for optimizing care for critically ill children, underscoring the importance of personalized treatment plans and teamwork in pediatric critical care. Tune in!Show Highlights:Clinical case of a 15-year-old girl with acute myocarditis and respiratory failureImportance of understanding cardiopulmonary interactions in pediatric critical careEffects of positive pressure ventilation on cardiac functionKey concepts of cardiac output, preload, and afterload in the context of myocarditisChallenges of managing hemodynamic instability in critically ill pediatric patientsDifferences between spontaneous breathing and positive pressure ventilationStrategies for optimizing preload and fluid management in myocarditis patientsTailoring ventilatory support and transitioning to invasive mechanical ventilationMonitoring for arrhythmias and managing myocardial function with inotropic supportImportance of frequent assessments and collaboration with cardiac ICU teams for patient careManagement StrategiesOptimizing Preload:Volume depletion is common in patients with hypotension and tachycardia. A careful fluid challenge is important to restore circulatory volume, but fluid overload should be avoided, especially with impaired left ventricular function.Tailoring Ventilatory Support:Adjust BiPAP settings to improve oxygenation without overloading the heart with excessive positive pressures.Use the optimal level of PEEP to recruit alveoli while maintaining adequate venous return to the heart.Supporting Myocardial Function:Inotropic support (e.g., milrinone) may be necessary to improve myocardial contractility. Milrinone also provides vasodilation, which can reduce afterload but must be used cautiously due to its potential to lower blood pressure.Frequent Reassessments:Bedside echocardiography and regular monitoring of biomarkers (lactate, BNP) and clinical status are essential for ongoing evaluation.In severe cases, advanced therapies like ECMO may be required if the patient’s hemodynamic status continues to deteriorate.

Today,  pediatric intensivists Dr. Pradip Kamat and Dr. Rahul Damania discuss a complex case of a 12-year-old girl who suffered a seizure and unresponsiveness due to a subarachnoid hemorrhage from a ruptured aneurysm. They explore the multi-system effects of traumatic brain injury (TBI) and intracranial hemorrhage, focusing on non-neurologic organ dysfunction. They’ll also highlight the impact on cardiovascular, respiratory, renal, and hepatic systems, emphasizing the importance of understanding these interactions for better patient management. Tune in to hear relevant studies and management strategies to improve outcomes in pediatric TBI cases.In This Episode:Clinical case of a 12-year-old girl with seizure and unresponsiveness due to subarachnoid hemorrhage from a ruptured aneurysmManagement of non-neurologic organ dysfunction in traumatic brain injury (TBI) and intracranial hemorrhageMulti-system effects of brain injuries, including cardiovascular, respiratory, renal, and hepatic complicationsImportance of recognizing non-neurologic organ dysfunction in pediatric patientsEpidemiology and prevalence of non-neurologic organ dysfunction in patients with aneurysms or subarachnoid hemorrhageMechanisms of organ dysfunction following brain injury, including inflammatory responses and cytokine releaseManagement strategies for cardiovascular complications in TBI patients.Discussion of respiratory complications, such as acute lung injury and ARDS, in the context of TBIRenal and hepatic dysfunction associated with traumatic brain injury and their managementEmphasis on the need for a comprehensive understanding of organ interactions to improve patient outcomes in pediatric critical careConclusionIn summary, the episode underscores the complex interplay between brain injury and multi-system organ dysfunction. The hosts emphasize the need for a comprehensive understanding of these interactions to improve patient outcomes in pediatric TBI cases. They advocate for a team-based approach to management, focusing on individual patient physiology and the delicate balance required to address the challenges posed by non-neurologic organ dysfunction.Connect With Us!We hope you found value in this case-based discussion. Please share your feedback, subscribe, and leave a review on our podcast. For more resources, visit our website at PICUoncall.org.Thank you for joining us, and stay tuned for our next episode!

Welcome to another insightful episode of PICU on Call, a podcast dedicated to current and aspiring intensivists. In this episode, our hosts, Dr. Pradip Kamat, Dr. Rahul Damania, and their colleague, Dr. Jordan Dent, delve into the complexities of managing pneumonia in pediatric patients. The discussion is anchored around a clinical case involving a 10-year-old girl presenting with difficulty breathing and a fever, suggestive of pneumonia. We will break down the key themes and insights from the case, providing a comprehensive guide to understanding and managing pediatric pneumonia.Case PresentationThe episode begins with a detailed case presentation:Patient: 10-year-old girl, 28-week preemie with chronic lung disease.Symptoms: Progressive respiratory distress over eight days, worsening cough, increased work of breathing, hypoxemia (oxygen saturation in the low 80s despite supplemental oxygen).Findings: Chest X-ray reveals bilateral lower lobe infiltrates and a left-sided pleural effusion. Lab results show elevated CRP and a positive respiratory PCR for a bacterial pathogen.This case sets the stage for an in-depth discussion on the various aspects of pediatric pneumoRisk Factors for PneumoniaUnderstanding the risk factors for pneumonia is crucial for early identification and prevention. These risk factors can be categorized into three main groups:Host FactorsIncomplete Immunization Status: Children who are not fully vaccinated are at higher riskYoung Age: Infants and young children have immature immune systems, making them more susceptibleLower Socioeconomic Status: Limited access to healthcare and poor living conditions can increase riskEnvironmental FactorsExposure to Tobacco Smoke: Secondhand smoke can damage the respiratory tract and impair immune functionSeasonal Variations: Pneumonia cases peak during fall and winter due to increased circulation of respiratory virusesContact with Other Children: Daycare settings and schools can facilitate the spread of infectionsHealthcare-Associated FactorsProlonged Mechanical Ventilation: Increases the risk of ventilator-associated pneumonia (VAP)Nasogastric Tube Placement: Can introduce pathogens into the respiratory tract.Neuromuscular Blockade: Impairs the ability to clear secretionsInadequate Humidification: Dry air can damage the respiratory mucosaPathogenesis of PneumoniaPneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid accumulation and white blood cell infiltration in the alveoli, resulting in:Decreased Lung Compliance: The lungs become stiffer and harder to expand.Increased Airway Resistance: Narrowing of the airways makes breathing more difficult.Ventilation-Perfusion (V/Q) Mismatch: Impaired gas exchange leads to hypoxia and tachypnea.Etiology by Age GroupThe causative pathogens of pneumonia vary by age group:Neonates: Group B Streptococcus, E. coli, Listeria, KlebsiellaChildren Under 5: Viral causes (50% of cases) such as RSV, human metapneumovirus, and influenza, with bacterial causes like Streptococcus pneumoniae and Haemophilus influenzaeOlder Children and Teens: Mycoplasma pneumonia, Chlamydia pneumonia, and Streptococcus pneumoniaeClassification of PneumoniaPneumonia can be classified based on the acquisition setting:Community-Acquired Pneumonia (CAP): Occurs in patients not hospitalized in the past monthHospital-Acquired Pneumonia (HAP): Develops after 48 hours of hospitalizationVentilator-Associated Pneumonia (VAP): Occurs within 48 hours of intubationAspiration Pneumonia: Results from inhaling gastric or oral contentsNecrotizing Pneumonia: Caused by aggressive bacteria, often requiring CT imaging for diagnosisClinical PresentationWhen a child presents with suspected pneumonia, clinicians should look for:Systemic Symptoms: Fever, lethargy, poor appetiteRespiratory Symptoms: Tachypnea, hypoxia, and classic findings like cracklesKey Indicators: Moderate hypoxemia (SpO2 < 96%) and increased respiratory effort (nasal flaring, intercostal retractions)Diagnostic ApproachThe diagnostic workup for bacterial pneumonia typically includes:Basic Labs: CBC, inflammatory markers (CRP, procalcitonin), and a comprehensive metabolic panelCultures: Blood cultures have low yield; pleural fluid cultures are more definitiveImaging: Chest X-rays can overestimate pneumonia; point-of-care ultrasound may help identify effusionsManagement FrameworkManagement begins with assessing whether the child can be treated at home or requires hospitalization. Key considerations for admission include:Hypoxemia: SpO2 < 92%Rapid Respiratory Rates: Indicative of severe respiratory distressToxic Appearance or Poor Oral Intake: Suggests a need for closer monitoring and supportive careIn the PICU, management involves:Respiratory SupportNasal Cannula: For mild casesHigh-Flow Nasal Cannula (HFNC): For moderate casesMechanical Ventilation: For severe cases of respiratory failureAntibiotic TherapyEmpiric Therapy: Based on age, severity, and local resistance patternsTargeted Therapy: Adjusted based on culture results and clinical responseSupportive CareFluid Management: To maintain hydration and electrolyte balanceNutrition: Ensuring adequate caloric intakeFever Control: Using antipyretics to manage feverComplications of PneumoniaComplications occur in about 3% of pneumonia cases and include:Pleural Effusion: Managed with chest tube placement and fibrinolytic therapyNecrotizing Pneumonia: May require drainage if abscesses developSystemic Complications: Such as ARDS, sepsis, and multi-organ dysfunctionConclusionEarly diagnosis and management of bacterial pneumonia are crucial to prevent complications and mortality. Key indicators include moderate hypoxemia and increased work of breathing. Diagnostic imaging findings such as large pleural effusions and cavitation strongly suggest bacterial infection.

In today’s episode, we explore a tragic but educational case involving a 15-year-old girl who suffered severe inhalation injury following a house fire. While heroically rescuing her brother and his friend, she endured prolonged cardiac arrest and severe multi-organ dysfunction. We’ll focus on the pathophysiology, investigation, and management of inhalation injuries, including the critical role of recognizing carbon monoxide and cyanide poisoning in these complex cases.Key Learning Points:Exposure to house fire and prolonged cardiac arrestSigns of inhalation injury and airway compromisePathophysiology of inhalation injuries and their impact on multiple organ systemsManagement strategies for inhalation injury, including airway protection and ventilationDifferentiating carbon monoxide and cyanide poisoning in pediatric fire victimsCase PresentationA 15-year-old previously healthy girl is brought to the Pediatric Intensive Care Unit (PICU) after experiencing cardiac arrest during a house fire. She was found unconscious by firefighters after a heroic rescue attempt where she saved her brother and his friend. Upon arrival at the hospital, she was unresponsive, intubated, and in severe cardiovascular distress with signs of multi-organ dysfunction.Key findings include:Soot deposits and superficial burns on extremitiesProlonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR)Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refillMetabolic acidosis, AKI, coagulopathy, transaminitisSevere hypoxic-ischemic encephalopathy on EEGThese findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion.Pathophysiology of Inhalation InjuryWhen a patient is exposed to smoke and hot gases during a fire, inhalation injury results in significant damage to the respiratory system. Inhalation injury has three main components:Upper airway involvement – Thermal injury can cause swelling and obstruction.Chemical pneumonitis – Noxious chemicals like carbon monoxide and cyanide trigger inflammation in the lungs.Systemic toxicity – Toxins such as carbon monoxide and cyanide can affect cellular oxygen utilization.The primary damage occurs in the lower respiratory tract, leading to airway edema, mucosal damage, and bronchial cast formation. This process can result in bacterial pneumonia, respiratory failure, and the need for aggressive intervention.Investigating Inhalation InjuryA thorough diagnostic approach is essential when assessing patients with suspected inhalation injury:Basic Imaging: A chest X-ray (CXR) should be obtained, although a normal film doesn't rule out injury.Gold Standard – Bronchoscopy: Direct visualization allows for assessment and removal of bronchial casts.Laboratory Tests: Key labs include CBC, CMP, blood gas, lactate, co-oximetry (to assess CO levels), and toxicology screens.CO and Cyanide Testing: Critical for identifying toxic exposure, especially when a patient presents with altered mental status or unexplained metabolic acidosis.Managing Inhalation Injury: A Structured ApproachManagement revolves around three key pillars:Airway Protection: Intubation is essential for airway security. Signs such as progressive hoarseness, soot around the nose, or face burns should prompt early intervention.Ventilation Strategies: Use low tidal volumes and optimized PEEP for lung protection. In severe cases, consider advanced modalities like APRV, HFOV, or ECMO.Secretion Management: Aggressive pulmonary toilet and medications such as nebulized heparin, tPA, and N-acetylcysteine may help manage airway inflammation and obstructions.Recognizing and Treating Carbon Monoxide (CO) PoisoningIn cases of suspected CO poisoning, the key is early recognition and treatment:CO Blood Levels: Measure carboxyhemoglobin levels immediately.Classic Symptoms: Look for the “cherry red” skin color and neurologic symptoms such as confusion or dizziness.First-Line Therapy: Administer 100% oxygen via a non-rebreather mask or endotracheal tube.Hyperbaric Oxygen: While 100% O2 works well, HBO therapy is crucial for preventing delayed neuropsychiatric complications.Fun Fact: CO has a much higher affinity for hemoglobin than oxygen, which leads to a "tissue oxygen famine," even with normal PaO2 levels.Identifying Cyanide Poisoning in Fire VictimsCyanide poisoning can be particularly challenging to diagnose but is crucial in fire victims. Look for:Classic Triad: Metabolic acidosis, elevated venous oxygen saturation, and CNS symptoms (confusion, mydriasis).Late Signs: Cardiovascular collapse, hypotension, and bradycardia.Treatment: Hydroxocobalamin is the first-line antidote (70 mg/kg IV), with the caveat that purple-red urine is a normal side effect.Avoid Nitrites: In burn victims, nitrite-based cyanide kits can worsen CO poisoning by forming methemoglobin.Clinical Tip: Unlike CO poisoning, cyanide poisoning presents with seizures and dilated pupils.Clinical Course of Our PatientThe patient’s clinical course was marked by rapid deterioration despite aggressive treatment:Initially managed with high-frequency oscillatory ventilation (HFOV) due to pulmonary hemorrhageDeveloped severe PARDS, cardiac dysfunction, and multi-organ failure within 12 hoursUltimately, neuroimaging revealed anoxic brain injury with cerebral edema and herniation, leading to brain deathThis heartbreaking case highlights the importance of early intervention and recognition of inhalation...

Welcome and Episode IntroductionHosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital)Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric managementFocus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcoholCase PresentationPatient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodkaKey Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odorInitial Labs & Findings:EtOH level: 420 mg/dL.Glucose: 50 mg/dL.Normal CXR and EKG.PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depressionInitial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complicationsKey Learning Points from the CaseToxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventionsHypoglycemia and CNS depression are common features of ethanol toxicity in infantsManagement prioritizes glucose correction, airway support, and close neurological monitoringDeep Dive: Toxic Alcohols in the PICU1. EthanolTypical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermiaDiagnostic Workup:Focus on CNS and metabolic effectsLabs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screenImaging (head CT) if indicatedManagement: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work2. MethanolSources: Windshield fluids, cleaning agents, moonshineClinical Stages:Early: Dizziness, nausea, vomiting (0–6 hours)Latent: Asymptomatic (6–30 hours)Late: Vision disturbances, seizures, respiratory failure (6–72 hours)Key Symptoms: “Snowstorm blindness” from retinal toxicityManagement: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases3. Ethylene GlycolSources: Antifreeze, brake fluids, household cleanersPathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals)Red Flags: Hypocalcemia, renal failure, QT prolongationManagement: Fomepizole, supportive care, and hemodialysis for severe toxicity4. Propylene GlycolSources: Medications like lorazepam and pentobarbitalPresentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunctionManagement: Discontinue offending agent, supportive care, and hemodialysis if severe5. Isopropyl AlcoholSources: Disinfectants, hand sanitizersPresentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosisManagement: Supportive care; fomepizole and ethanol are ineffectiveKey Laboratory InsightsOsmolar Gap Formula:Measured Osmolality - Calculated OsmolalityA high osmolar gap indicates unmeasured osmoles like toxic alcohols.Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interferenceManagement PearlsEthanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe casesMethanol: Similar approach with additional focus on preventing blindnessPropylene Glycol: Monitor lactate and renal function, discontinue offending medicationsIsopropyl Alcohol: Supportive care, no acidosis presentMnemonics for Toxic AlcoholsMEGA GAP:Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar GapIsopropyl Alcohol: Isolated Osmolar Gap (no acidosis)Propylene Glycol: Mimics ethylene glycol with HAGMA at high dosesTakeaway MessagesEarly recognition of toxic alcohol ingestion is critical for successful managementDifferentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentationEngage poison control and social work early in the processConclusionPediatric toxic alcohol ingestions are rare but potentially life-threateningFomepizole is a cornerstone therapy for methanol and ethylene glycol toxicitySupportive care remains essential across all toxic alcohol ingestionsConnect with US!Twitter: @PICUDocOnCallEmail: [email protected]

Did you know that Multi-Organ Dysfunction Syndrome (MODS) can result from both infectious and non-infectious causes? In our latest episode, we delve deep into the pathophysiology of MODS, exploring how different organs interact and fail in sequence. We discuss key concepts like organ functional reserve and the kinetics of organ injury, which aren’t as straightforward as they seem. Tune in to learn about the non-linear progression of organ damage and how it impacts management strategies in pediatric critical care.We break down the case into key elements:Patient Background: A 15-year-old girl with chronic TPN dependence and a PICC line presented with septic shock and respiratory failure.Initial Presentation: Blood cultures confirmed Gram-negative rod bacteremia. She developed multi-system complications, including acute kidney injury (AKI), thrombocytopenia, and cardiac dysfunction.Management: Broad-spectrum antibiotics, mechanical ventilation, vasoactive agents, and supportive care for MODS.Key Case Highlights:Clinical case of a 15-year-old girl with sepsis from a gram-negative rodDependence on total parenteral nutrition (TPN) and prolonged PICC line useDiscussion of septic shock, acute respiratory failure, and acute kidney injuryOverview of multiple organ dysfunction syndrome (MODS) and its definitionsPathophysiology of MODS, including organ functional reserve and kinetics of organ injuryMolecular mechanisms involved in MODS, such as mitochondrial dysfunction and immune responsesSpecific phenotypes of sepsis-induced MODS, including TAMOF and IPMOFManagement strategies for MODS, emphasizing multidisciplinary approachesRole and complications of therapeutic plasma exchange (TPE) in treating MODSImportance of recognizing signs of MODS and timely intervention in pediatric patientsSegment 1: MODS Definitions and PhenotypesKey Definition: MODS is the progressive failure of two or more organ systems due to systemic insults (infectious or non-infectious).Phenotypes:TAMOF (Thrombocytopenia-Associated Multi-Organ Failure): Characterized by thrombocytopenia, hemolysis, and decreased ADAMTS13 activity.Immunoparalysis: Persistent immunosuppression and risk of secondary infections.Sequential Liver Failure: Often associated with viral triggers.Segment 2: Pathophysiology of MODSMolecular Insights:Mitochondrial dysfunction and damage-associated molecular patterns (DAMPs)Innate and adaptive immune dysregulationMicrocirculatory dysfunction and ischemia-reperfusion injuryOrgan Interactions: MODS evolves through complex multi-organ interdependenciesSegment 3: Diagnosis and Evidence-Based ManagementKey Diagnostic Pearls:MODS is not solely infection-driven; it requires a shared mechanism and predictable outcomes.Use biomarkers like ADAMTS13 and TNF-α response for phenotypic classification.Management Highlights:Supportive Care: Multisystem approach including lung-protective ventilation, renal replacement therapy, and hemodynamic support.Therapeutic Plasma Exchange (TPE): Especially effective in TAMOF by restoring ADAMTS13 and removing inflammatory mediators.Segment 4: Practical Tips for IntensivistsEarly recognition of MODS phenotypes for targeted therapyImportance of multidisciplinary teamwork in critical care settingsMonitoring for complications like TMA and immunoparalysis during prolonged ICU staysFollow Us:Twitter: @PICUDocOnCallEmail: [email protected]

In this episode, we discuss the case of a 15-year-old girl who presents with progressive headache, nausea, vomiting, and difficulty ambulating. Her condition rapidly evolves into altered mental status and severe hydrocephalus, leading to a compelling discussion about the evaluation, diagnosis, and management of hydrocephalus in pediatric patients.We break down the case into key elements:A comprehensive look at acute hydrocephalus, including its pathophysiology and causesEpidemiological insights, clinical presentation, and diagnostic approachesManagement strategies, including temporary and permanent CSF diversion techniquesA review of complications related to shunts and endoscopic third ventriculostomyKey Case Highlights:Patient Presentation:A 15-year-old girl with a 3-day history of worsening headaches, nausea, vomiting, and difficulty walkingAltered mental status and bradycardia upon PICU admissionCT scan revealed severe hydrocephalus without a clear mass lesionManagement Steps in the PICU:Hypertonic saline bolus improved her mental status and pupillary reactionsNeurosurgery consultation recommended MRI and close neuro checksInitial management included dexamethasone, keeping the patient NPO, and hourly neuro assessmentsDifferential Diagnosis:Obstructive (non-communicating) vs. non-obstructive (communicating) hydrocephalusConsideration of alternative diagnoses like intracranial hemorrhage and idiopathic intracranial hypertensionEpisode Learning Points:Hydrocephalus Overview:Abnormal CSF buildup in the ventricles leading to increased intracranial pressure (ICP)Key distinctions between obstructive and non-obstructive typesEpidemiology and Risk Factors:Congenital causes include genetic syndromes, neural tube defects, and Chiari malformationsAcquired causes: post-hemorrhagic hydrocephalus (e.g., from IVH in preemies), infections like TB meningitis, and brain tumorsClinical Presentation:Infants: Bulging fontanelles, sunsetting eyes, irritabilityOlder children: Headaches, vomiting, papilledema, and gait disturbancesManagement Framework:Temporary CSF diversion via external ventricular drains (EVD) or lumbar cathetersPermanent interventions include VP shunts and endoscopic third ventriculostomy (ETV)Complications of Shunts and ETV:Shunt infections, malfunctions, over-drainage, and migrationETV-specific risks, including delayed failure years post-procedureClinical Pearl:Communicating hydrocephalus involves symmetric ventricular enlargement and is often linked to inflammatory or post-treatment changes affecting CSF reabsorption.Hosts’ Takeaway Points:Dr. Pradip Kamat emphasizes the importance of timely recognition and intervention in hydrocephalus to prevent complications like brain herniation.Dr. Rahul Damania highlights the need for meticulous neurological checks in PICU patients and an individualized approach to treatment.Resources Mentioned:Hydrocephalus Clinical Research Network guidelines.Recent studies on ETV outcomes in pediatric populations.Call to Action:If you enjoyed this discussion, please subscribe to PICU Doc On Call and leave a review. Have a topic you’d like us to cover? Reach out to us via email or on social media!Follow Us:Twitter: @PICUDocOnCallEmail: [email protected] tuned for more cases that challenge and inspire us as PICU clinicians!

IntroductionHosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital)Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric managementFocus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcoholCase PresentationPatient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodkaKey Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odorInitial Labs & Findings:EtOH level: 420 mg/dL.Glucose: 50 mg/dL.Normal CXR and EKG.PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depressionInitial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complicationsKey Learning Points from the CaseToxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventionsHypoglycemia and CNS depression are common features of ethanol toxicity in infantsManagement prioritizes glucose correction, airway support, and close neurological monitoringDeep Dive: Toxic Alcohols in the PICU1. EthanolTypical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermiaDiagnostic Workup:Focus on CNS and metabolic effectsLabs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screenImaging (head CT) if indicatedManagement: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work2. MethanolSources: Windshield fluids, cleaning agents, moonshineClinical Stages:Early: Dizziness, nausea, vomiting (0–6 hours)Latent: Asymptomatic (6–30 hours)Late: Vision disturbances, seizures, respiratory failure (6–72 hours)Key Symptoms: “Snowstorm blindness” from retinal toxicityManagement: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases3. Ethylene GlycolSources: Antifreeze, brake fluids, household cleanersPathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals)Red Flags: Hypocalcemia, renal failure, QT prolongationManagement: Fomepizole, supportive care, and hemodialysis for severe toxicity4. Propylene GlycolSources: Medications like lorazepam and pentobarbitalPresentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunctionManagement: Discontinue offending agent, supportive care, and hemodialysis if severe5. Isopropyl AlcoholSources: Disinfectants, hand sanitizersPresentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosisManagement: Supportive care; fomepizole and ethanol are ineffectiveKey Laboratory InsightsOsmolar Gap Formula:Measured Osmolality - Calculated OsmolalityA high osmolar gap indicates unmeasured osmoles like toxic alcohols.Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interferenceManagement PearlsEthanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe casesMethanol: Similar approach with additional focus on preventing blindnessPropylene Glycol: Monitor lactate and renal function, discontinue offending medicationsIsopropyl Alcohol: Supportive care, no acidosis presentMnemonics for Toxic AlcoholsMEGA GAP:Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar GapIsopropyl Alcohol: Isolated Osmolar Gap (no acidosis)Propylene Glycol: Mimics ethylene glycol with HAGMA at high dosesTakeaway MessagesEarly recognition of toxic alcohol ingestion is critical for successful managementDifferentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentationEngage poison control and social work early in the processConclusionPediatric toxic alcohol ingestions are rare but potentially life-threateningFomepizole is a cornerstone therapy for methanol and ethylene glycol toxicitySupportive care remains essential across all toxic alcohol ingestionsConnect with US!Twitter: @PICUDocOnCallEmail: [email protected]

Introduction:Today, Dr. Rahul Damania, Dr. Pradip Kamat, and their guest,  Dr. Jordan Dent, discuss a critical case involving a 15-year-old male who collapsed during football practice due to exertional heat stroke. The discussion emphasizes the clinical presentation, risk factors, pathophysiology, and evidence-based management of heat stroke and other heat-related illnesses in pediatric patients. The episode also delves into the role of rapid cooling interventions and long-term care to minimize mortality and morbidity.Case Summary: A 15-year-old male with ADHD collapsed during football practice on a hot, humid day. He presented with:Normotension (BP: 101/67 mmHg)Tachycardia (HR: 157 bpm)Tachypnea (RR: 40 breaths/min)Febrile (Rectal temp: 41.8°C/107.2°F)Dry, hot skin, GCS of 9Lab abnormalities: hyponatremia, hypokalemia, hypoglycemia, elevated creatinine, liver enzymes, lactate, CK, and troponinAfter suffering cardiac arrest and undergoing resuscitation, the patient developed multiorgan dysfunction, including seizures, encephalopathy, and cerebral edema. Despite severe initial complications, the patient demonstrated neurological improvement with left-side hemiparesis before discharge.Key Discussion Points:Etiology and Pathophysiology of Heat Stroke:Heat stroke occurs when the body’s thermoregulatory mechanisms fail, leading to dangerous elevations in core body temperature. Exertional heat stroke is common during strenuous physical activity in hot, humid environments.Key physiological breakdowns include inadequate sweating, vasodilation dysfunction, and subsequent cellular damage due to hyperthermia.Risk Factors for Exertional Heat Stroke:Environmental factors: High temperature, humidity, lack of hydration, and breaks.Athlete-related factors: Hypohidrosis, dehydration, medical conditions, and medications (e.g., Adderall).Heat illness is the third leading cause of death in high school athletics, with American football players particularly at risk.Spectrum of Heat-Related Illness:Heat Cramps: Involuntary muscle contractions due to dehydration and electrolyte imbalance.Heat Syncope: Transient loss of consciousness due to heat exposure.Heat Exhaustion: Milder heat illness with core temperature < 104°F, potentially progressing to heat stroke if untreated.Heat Stroke: Life-threatening with core temperature ≥ 104°F, CNS dysfunction, and risk of multiorgan failure.Management of Heat Stroke:Rapid Cooling: Immediate cooling to bring core temperature down to 39°C within 30 minutes is critical. Methods include ice packs, cold water immersion, and core cooling techniques (cold IV fluids, gastric lavage).Supportive Care: Management of shock, electrolyte imbalances, rhabdomyolysis, DIC, and ARDS.Monitoring and Long-Term Care: Continuous EEG, fluid management, and rehabilitation are key in managing neurological and systemic complications.Differentiating Heat Stroke from Fever:Fever results from a reset of the hypothalamic setpoint due to pyrogens, while heat stroke involves the failure of thermoregulation without a change in the hypothalamic setpoint.Case Outcome:The patient initially suffered significant neurological damage but improved with intensive care and rehabilitation. By discharge, the patient showed notable recovery, though with some lasting deficits.Key Takeaways:Heat stroke is a medical emergency with a high risk of mortality and long-term complications if not treated promptly.Early recognition, rapid cooling, and a multidisciplinary approach are critical to improving outcomes.Athletes and children engaging in strenuous activities in hot environments should be closely monitored for signs of heat-related illness.References:Fuhrman, B., & Zimmerman, J. J. (2020). Hyperthermic Injury. In Textbook of Pediatric Critical Care (pp. 1327-1331).Rogers, M. C., et al. (2016). Thermoregulation. In Rogers' Textbook of Pediatric Intensive Care (pp. 546-552).Ishimine, P. (2022). Heat Stroke in Children. UpToDate. Retrieved from www.uptodate.com/contents/heat-stroke-in-children.Jardine, D. S. (2007). Heat Illness and Heat Stroke. Pediatrics in Review, 28(7), 249–258. https://doi.org/10.1542/pir.28-7-249.Patel, J., et al. (2023). Critical illness aspects of heatstroke: A hot topic. Journal of Intensive Care Society, 24(2), 206-214. https://doi.org/10.1177/17511437221148922.Ramirez, O., Malyshev, Y., & Sahni, S. (2018). It’s Getting Hot in Here: A Rare Case of Heat Stroke in a Young Male. Cureus, 10(12), e3724. https://doi.org/10.7759/cureus.3724.

IntroductionWelcome to PICU Doc On Call, a podcast dedicated to current and aspiring pediatric intensivists. I'm Dr. Pradip Kamat from Children’s Healthcare of Atlanta/Emory University School of Medicine, and I’m Dr. Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about medical education in the PICU. This podcast focuses on interesting PICU cases and their management in the acute care pediatric setting.Episode OverviewIn today’s episode, we are excited to welcome Dr. Karen Zimowski, Assistant Professor of Pediatrics at Emory University School of Medicine and a practicing pediatric hematologist at Children’s Healthcare of Atlanta at the Aflac Blood & Cancer Center. Dr. Zimowski specializes in pediatric bleeding and clotting disorders.Case PresentationA 16-year-old female with a complex medical history, including autoimmune thyroiditis and prior cerebral infarcts, was admitted to the PICU with acute chest pain and difficulty breathing. Despite being on low-dose aspirin, her oxygen saturation was 86% on room air. A CT angiography revealed a pulmonary embolism (PE) in the left lower lobe and signs of right heart strain. The patient was hemodynamically stable, and thrombolytic therapy was deferred in favor of anticoagulation. She was placed on BiPAP to improve her respiratory status. Her social history was negative for smoking, illicit drug use, or oral contraceptive use.Key Case PointsDiagnosis: Pulmonary embolism (PE)Hemodynamics: Stable with no right ventricular (RV) strain on echocardiogramManagement Focus: Anticoagulation and consultation with the hematology/thrombosis teamExpert Discussion with Dr. Karen ZimowskiRisk Factors and Epidemiology of VTE in PediatricsPathophysiology: Venous thromboembolism (VTE) in children involves components of Virchow’s triad: stasis of blood flow, endothelial injury, and hypercoagulability.Incidence: VTE is rare in the general pediatric population but increases significantly in hospitalized children.Age Distribution: Bimodal peaks in infants and adolescents aged 15-17 years.Risk Factors: Central venous lines, infections, congenital heart disease, cancer, and autoimmune disorders.Clinical Manifestations of DVTSymptoms: Swelling, pain, warmth, and skin discoloration in the affected extremity.Specific Presentations:SVC syndrome from superior vena cava thrombosisAbdominal pain from portal vein thrombosisHematuria from renal vein thrombosisNeurological symptoms from cerebral sinus venous thrombosisDiagnostic Approach for DVTImaging:Compression Doppler Ultrasonography: Primary method for diagnosing DVT in pediatric patients.MR Venography (MRV) and CT Venography (CTV): Used for abdominal and cerebral sinus thrombosis.Laboratory Studies:D-dimer: Useful in adults; limited specificity in children.Other Labs: Renal and liver function tests, CBC with differential, DIC panel.Management of DVTAnticoagulation StrategiesUnfractionated Heparin (UFH):Targets factors IIa and Xa; requires frequent monitoring.Adverse events: Bleeding and thrombocytopenia.Low Molecular Weight Heparin (LMWH):More predictable pharmacokinetics than UFH.Advantages include ease of administration and lower risk of HIT.Vitamin K Antagonists (VKAs):Used for long-term anticoagulation.Requires regular INR monitoring.Direct Oral Anticoagulants (DOACs):Dabigatran, Rivaroxaban, and Apixaban used in pediatric VTE.Advantages: No routine monitoring required, predictable effects.ConclusionIn this episode, we discussed the intricacies of VTE diagnosis and management in pediatric patients. We thank Dr. Karen Zimowski for sharing her expertise on anticoagulation and hemostasis in the PICU. For more episodes and our Doc on Call management cards, visit picudoconcall.org.Stay tuned for our next episode, and thank you for listening!ReferencesFuhrman & Zimmerman - Textbook of Pediatric Critical Care: Thrombosis in Pediatric Critical Care.American Society of Hematology 2018 Guidelines for Management of Venous Thromboembolism: Treatment of Pediatric Venous Thromboembolism.Antithrombotic Therapy in Neonates and Children: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.O’Brien, SH, Stanek JR, Witmer CM, Raffini L. The Continued Rise of Venous Thromboembolism Across US Children’s Hospitals. Pediatrics (2022).

Welcome to PICU Doc On Call, where Dr. Pradip Kamat from Children’s Healthcare of Atlanta/Emory University School of Medicine and Dr. Rahul Damania from Cleveland Clinic Children’s Hospital delve into the intricacies of Pediatric Intensive Care Medicine. In this special episode of PICU Doc on Call shorts, we dissect the Alveolar Gas Equation—a fundamental concept in respiratory physiology with significant clinical relevance.Key Concepts Covered:Alveolar Gas Equation Demystified: Dr. Rahul explains the Alveolar Gas Equation, which calculates the partial pressure of oxygen in the alveoli (PAO2). This equation, PAO2 = FiO2 (Patm - PH2O) - (PaCO2/R), is essential in understanding hypoxemia and the dynamics of gas exchange in the lungs.Calculating PAO2: Using the Alveolar Gas Equation, the hosts demonstrate how to calculate PAO2 at sea level, emphasizing the influence of atmospheric pressure, fraction of inspired oxygen (FiO2), water vapor pressure, arterial carbon dioxide pressure (PaCO2), and respiratory quotient (R) on oxygenation.A-a Gradient and Hypoxemia: The A-a gradient, derived from the Alveolar Gas Equation, is discussed in the context of hypoxemia evaluation. Understanding the causes of hypoxemia, including ventilation/perfusion (V/Q) mismatch, anatomical shunt, diffusion defects, and hypoventilation, is crucial for clinical diagnosis and management.Clinical Scenarios and A-a Gradient Interpretation: Through a clinical scenario, the hosts elucidate how different conditions affect the A-a gradient and oxygenation, providing insights into respiratory pathophysiology and differential diagnosis.Clinical Implications and Management Strategies: The hosts highlight the clinical significance of the Alveolar Gas Equation in assessing oxygenation status, diagnosing gas exchange abnormalities, and tailoring respiratory management strategies in the pediatric intensive care setting.Key Takeaways:Utility of the Alveolar Gas Equation: Understanding and applying the Alveolar Gas Equation is essential for evaluating oxygenation and diagnosing respiratory abnormalities.Interpreting A-a Gradient: A normal A-a gradient suggests alveolar hypoventilation as the likely cause of hypoxemia, whereas elevated gradients indicate other underlying pathologies.Clinical Relevance: Recognizing the clinical implications of the Alveolar Gas Equation aids in accurate diagnosis and optimal management of respiratory conditions in pediatric intensive care patients.Conclusion:Join Dr. Kamat and Dr. Damania as they unravel the complexities of the Alveolar Gas Equation, providing valuable insights into respiratory physiology and its clinical applications. Don’t forget to subscribe, share your feedback, and visit picudoconcall.org for more educational content and resources.References:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter: Physiology of the respiratory system. Chapter 42. Khemani et al. Pages 470-481Rogers textbook of Pediatric intensive care: Chapter 44. Respiratory physiology. Akong K et al. Pages 691-721Respiratory Physiology for the Anesthesiologist. Bigatello L and Pesenti A, Anesthesiology 2019; 130: 1064-77

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.Hosts:Dr. Pradip Kamat: Children’s Healthcare of Atlanta/Emory University School of MedicineDr. Rahul Damania: Cleveland Clinic Children’s HospitalIntroduction:Pediatric Intensive Care Unit (PICU) physicians passionate about medical education in the acute care pediatric settingEpisode focus: A case of a 23-month-old ex-28 week premie presenting with sudden high fever and rapidly rising ETCO2 during surgeryCase Presentation:Presented by Dr. Rahul Damania23-month-old ex-28 week premie intubated during hernia repair surgeryNoticed rapidly rising ETCO2, unprovoked tachycardia, and elevated temperatureTransferred to PICU, exhibiting rigidity, clenched jaw, metabolic acidosis, and elevated lactate.Consideration of Malignant Hyperthermia (MH) crisisKey Points:Elevated temperature, hypercapnia, metabolic acidosis, and unprovoked tachycardia raise concern for MHOrganized discussion on pathophysiology, clinical signs, symptoms, and managementMultiple Choice Question:Diagnosis of MH crisis during scoliosis repairCorrect Answer: D) Sarcoplasmic reticulumDantrolene acts on the sarcoplasmic reticulum to inhibit calcium release, crucial in MH managementClinical Presentation of MH Crisis:Tachycardia, acidosis, muscle stiffness, and hyperthermia are hallmark featuresPotential life-threatening complications underscore the urgency of recognition and treatmentTriggers and Pathophysiology of MH Crisis:Triggered by inhalational agents and depolarizing neuromuscular blocking agentsPathophysiology involves defective Ryanodine receptor leading to uncontrolled calcium releaseDifferential Diagnosis:Includes sepsis, thyroid storm, pheochromocytoma, and neuroleptic malignant syndromeDifferentiation from similar conditions crucial for accurate managementDiagnostic Approach:High clinical suspicionGenetic testing (ryanodine receptor gene sequencing) and Caffeine Halothane Contracture Test (CHCT) for diagnosisImmediate workup during crisis includes blood gas, lactate, CPK, CMP, and urine analysisGeneral Management Framework:MH crisis is a medical emergency requiring rapid interventionDantrolene Na administration, supportive measures, and continuous monitoring in PICUUtilization of Malignant Hyperthermia carts and involvement of specialized hotlinesClinical Pearls and Pitfalls:Early recognition is crucial.Proper administration of Dantrolene Na without delayExtended monitoring period in PICU to ensure stabilityConclusion:Importance of recognizing and managing MH crisisFeedback, subscription, and reviews encouragedWebsite picudoconcall.org for additional resourcesReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care ChapterMalignant Hyperthermia Association of the United StatesWhat is MH?[Managing a crisis](https://www.mhaus.org/ healthcare-professionals/managing-a-crisis/)Rosenbaum HK, Rosenberg H. UpToDate: Malignant hyperthermia: diagnosis and management of acute crisis.

Show IntroductionWelcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists.Hosted by Dr. Pradip Kamat and Dr. Rahul DamaniaCase PresentationA 14-year-old female with a history of depression and oppositional defiant disorder presents with dizziness, slurring speech, and is pale appearance.The mother noticed symptoms of dizziness, stumbling, and sleepiness.The patient had a prior suicide attempt.Vital signs: HR 50 bpm, BP 75/40, GCS 10.The initial workup reveals hyperglycemia, and she is stabilized and admitted to the PICU.Key Aspects of Ingestion Work-upHistory and physical exam are crucial.Stratify acute or chronic ingestions.Consider baseline medications and coingestants.Perform initial screening examination to identify immediate measures for stabilization.Diagnostic StudiesPulse oximetry, continuous cardiac monitoring, ECG, capillary glucose measurement.Serum acetaminophen, ASA levelsConsider extended toxicology screen.Differentiating CCB vs. Beta-Blocker OverdoseECG findings: PR interval prolongation and Bradydysrhythmia suggest CCB poisoning.Hyperglycemia in non-diabetic patients may indicate CCB overdoseApproach to CCB OverdoseInitial resuscitation and stabilizationABC approachConsult Poison Control CenterEmpiric use of glucagon, IV fluids, and vasopressorsConsideration of orogastric lavage and activated charcoalSpecific Medical TherapiesVasopressors: norepinephrine/epinephrine infusionAtropine for bradycardiaIV calcium salts to overcome cardiovascular effectsHigh-dose insulin and dextrose for myocardial functionInvestigational therapies: methylene blue, lipid emulsionProceduresTransvenous pacemaker placement if neededECMO in refractory hypotensionKey TakeawaysHypotension and bradycardia indicate life-threatening toxidromes.Differential includes CCB, BB, digoxin, clonidine, and CNS depressants.Stepwise approach includes close monitoring of ABCs and specific medical therapies.Thank you for listening to PICU Doc On Call. We would love for you to share your feedback, subscribe, and review our podcast. Visit picudoconcall.org for more information and resources.Stay tuned for our next episode!ReferencesFuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 125 and 126.St-Onge M et al. Treatment for calcium channel blocker poisoning: a systematic review.DeRoos F. Calcium channel blockers. In: Goldfrank's Toxicologic Emergencies, 8th edition.

Hosts:Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of MedicineRahul Damania, Cleveland Clinic Children’s HospitalIntroductionToday, we discuss the case of an 8-month-old infant with severe bronchospasm and abnormal blood gas. We'll delve into the epidemiology, pathophysiology, and evidence-based management of acute bronchiolitis.Case SummaryAn 8-month-old infant presented to the ER with decreased alertness following worsening work of breathing, preceded by URI symptoms. The infant was intubated and transferred to the PICU, testing positive for RSV. Initial blood gas showed 6.8/125/-4, and CXR revealed massive hyperinflation. Vitals: HR 180, BP 75/45, SPO2 92% on 100% FIO2, RR 12 (prior to intubation), now around 16 on the ventilator, afebrile.Discussion PointsEtiology & Pathogenesis: Bronchiolitis is primarily caused by RSV, with other viruses and bacteria playing a role. RSV bronchiolitis is the most common cause of hospitalization in infants, particularly in winter months. Immuno-pathology involves an unbalanced immune response and can lead to various extra-pulmonary manifestations.Diagnosis: Diagnosis is clinical, based on history and examination. Key signs include upper respiratory symptoms followed by lower respiratory distress. Blood gas, chest radiography, and viral testing are generally not recommended unless warranted by severe symptoms or clinical deterioration.Management Framework: For patients requiring PICU admission, focus on oxygenation and hydration. High-flow therapy and nasal continuous positive airway pressure (CPAP) can be used. Hydration and feeding support are crucial. Antibiotics, steroids, and bronchodilators are generally not recommended. Mechanical ventilation and ECMO may be necessary in severe cases.Immunoprophylaxis & Nosocomial Infection Prevention: Palivizumab and nirsevimab are used for RSV prevention in high-risk infants. Strict infection control measures, including hand hygiene and isolation, are essential to prevent nosocomial infections.ConclusionRSV bronchiolitis is a common and potentially severe respiratory illness in infants. Management focuses on supportive care, with a careful balance between oxygenation and hydration. Immunoprophylaxis and infection control are crucial in preventing the spread of the virus.Thank you for listening to our episode on acute bronchiolitis. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more resources. Stay tuned for our next episode!ReferencesRogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823Reference 1: Dalziel, Stuart R; Haskell, Libby; O'Brien, Sharon; Borland, Meredith L; Plint, Amy C; Babl, Franz E; Oakley, Ed. Bronchiolitis. The Lancet. , 2022, Vol.400(10349), p.392-406. DOI: 10.1016/S0140-6736(22)01016-9; PMID: 35785792Reference 2: Schroeder AR, Destino LA, Ip W, Vukin E, Brooks R, Stoddard G, Coon ER. Day of Illness and Outcomes in Bronchiolitis Hospitalizations. Pediatrics. 2020 Nov;146(5):e20201537. doi: 10.1542/peds.2020-1537. PMID: 33093138.

Hosts:Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of MedicineRahul Damania, Cleveland Clinic Children’s HospitalCase Introduction:6-year-old patient admitted to PICU with severe pneumonia complicated by pediatric Acute Respiratory Distress Syndrome (pARDS).Presented with respiratory distress, hypoxemia, and significant respiratory acidosis.Required intubation and mechanical ventilation.Despite initial interventions, condition remained precarious with persistent hypercapnia.Physiology Concept: Dead SpaceDefined as the volume of air that does not participate in gas exchange.Consists of anatomic dead space (large airways) and physiologic dead space (alveoli).Physiologic dead space reflects ventilation-perfusion mismatch.Pathological Dead Space:Occurs due to conditions disrupting pulmonary blood flow or ventilation.Common in conditions like pulmonary embolism, severe pneumonia, or ARDS.Clinical Implications:Increased dead space fraction (DSF) in PARDS is a prognostic factor linked to severity and mortality.Elevated DSF indicates worse lung injury and inefficient gas exchange.DSF can be calculated using the formula: DSF = (PaCO2 – PetCO2) / PaCO2.Practical Management:Optimize Mechanical VentilationEnhance PerfusionConsider Positioning (e.g., prone positioning)Summary of Physiology Concepts:Bohr equation for physiologic dead space.Importance of lung-protective ventilation strategies.Monitoring and trending dead space fraction.Strategies to improve airway patency and mucociliary clearance.Connect with us!PICU Doc on Call provides concise explanations of critical concepts in pediatric intensive care.Feedback, subscriptions, and reviews are encouraged.Visit picudoconcall.org for episodes and Doc on Call infographics.Hosted by Dr. Pradip Kamat and Dr. Rahul Damania.Reference:Yehya N, Bhalla AK, Thomas NJ, Khemani RG. Alveolar Dead Space Fraction Discriminates Mortality in Pediatric Acute Respiratory Distress Syndrome. Pediatr Crit Care Med. 2016 Feb;17(2):101-9. doi: 10.1097/PCC.0000000000000613. PMID: 26669646; PMCID: PMC4740261.

Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches.Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU.Case PresentationPatient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake.Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition.Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA).Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care.Key ElementsRapid Symptom OnsetNeck Swelling & DroolingLimited Neck MobilityProblem RepresentationA previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy.Pathophysiology of RPAAnatomy of retropharyngeal spaceRapid communication of infections via lymph nodesInfection sources: dental issues, trauma, localized infections (e.g., otitis, URI)Dangers of RPAAirway compromise and posterior mediastinitisProgression from cellulitis to abscessMicrobial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulareClinical ManifestationsSeen predominantly in children aged 3-4 yearsNon-specific symptoms in the acute settingPronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distressDiagnostic WorkupThorough history and physical examinationCT scan with contrast as the gold standardBlood culture, CRP, and procalcitonin for infection severityClinical PearlsLimited neck mobility is the most specific physical exam findingYounger age and signs of airway obstruction indicate a complicated courseManagement of RPAAntibiotic therapy: Up to 50% cases can be treated with IV antibioticsSurgical drainage may be needed if no improvement or persistent respiratory distressDuration of therapy: 10 to 14 daysControversial use of steroids for reducing airway swellingComplications of RPAUpper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath ruptureMediastinitis: severe inflammation, infection of mediastinal tissuesPatient's Clinical CourseRespiratory viral panel: RSV, adenovirus, rhino/enterovirusIntubation due to worsening respiratory distressIncision and drainage (I&D) by ENTCultures grew MRSAExtubation after air leak detection; discharged on oral ClindamycinClinical TakeawaysMaintain a low threshold for suspecting RPAInitiate broad-spectrum antibiotics earlyPrioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxiaConsider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patientsConclusionEmphasize the critical nature of RPA in children and the importance of early intervention.Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications.ReferencesVillanueva-Fernández E, et al. (2022) Role of steroids in conservative treatment of parapharyngeal and retropharyngeal abscess in children. Eur Arch Otorhinolaryngol.Akhavan M. (2021) Ear, Nose, Throat: Beyond Pharyngitis: Retropharyngeal Abscess, Peritonsillar Abscess, Epiglottitis, Bacterial Tracheitis, and Postoperative Tonsillectomy. Emerg Med Clin North Am.Reilly BK, Reilly JS. (2012) Retropharyngeal abscess: diagnosis and treatment update. Infect Disord Drug Targets.

Today, Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University School of Medicine) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital), are excited to speak with Matthew Kirschen, MD, PhD, FAAN, FNCS, regarding a very sensitive topic involving pediatric brain death guidelines published in 'Neurology' in October 2023. Dr. Matthew Kirschen, a leader in pediatric neurocritical care and one of the authors of the new guidelines.Guest Introduction:Dr. Matthew Kirschen is an Assistant Professor of Anesthesiology and Critical Care Medicine, Pediatrics, and Neurology at the Children's Hospital of Philadelphia. A proud alumnus of Brandeis University and Stanford, where he secured both his MD and PhD in neuroscience. Dr. Kirschen’s journey includes a residency at Stanford followed by a unique dual fellowship in neurology and pediatric critical care at CHOP. Notably, he's among the rare professionals dual-boarded in both PCCM and Neurology.Dr. Kirschen’s tireless endeavors in pediatric neuro-critical care, especially his work on multimodal neuro-monitoring to detect and prevent brain injuries in critically ill children, have garnered significant attention. His expertise also extends to predicting recovery post-severe brain injuries. Pertinent to today's discussion, Dr. Kirschen has displayed a keen interest in the precise diagnosis of brain death and proudly stands as one of the authors of the new guidelines on the topic of Pediatric and Adult Brain death/death by neurologic criteria.Discussion:1. Understanding Brain Death Criteria:Brain Death/Death by Neurologic Criteria (BD/DNC) declared with permanent cessation of all brain functions, including brainstemImportant considerations before BD/DNC determination:No evaluation in infants < 37 weeks corrected gestational ageAbsence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC2. Who Can Perform BD/DNC Evaluations:Attending clinicians must be credentialed and trained in BD/DNC evaluation.Two attending clinicians are needed for evaluation, with exceptions for advanced practice providers.3. Prerequisites for BD/DNC Determination:Importance of identifying the etiology of BD/DNC to avoid reversible processesObservation periods based on age and type of brain injuryMaintaining core body temperature before evaluation4. Blood Pressure Management:Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors.Specific blood pressure targets for different ECMO support types5. Medication Considerations:Excluding medications affecting CNS function before BD/DNC evaluationRecommendations for drug level monitoring and metabolic derangement exclusion6. Performing the BD/DNC Neurologic Examination:Two independent examinations by different clinicians with a minimum 12-hour intervalCentral components including assessing irreversible coma and brainstem reflexes7. Apnea Testing:Two apnea tests after each neurologic examinationProcedures, complications, and baseline PCO2 and pH considerations 8. Ancillary Tests:BD/DNC remains a clinical evaluation; ancillary tests are used in specific circumstances.Conditions and circumstances for using or not using ancillary tests9. Case Presentation and Family Communication:Real-life case presented and discussed following the new AAN guidelines.No need for consent before evaluation; communication with the family emphasized.Maintaining transparency and involvement in the BD/DNC process10. Public Trust in BD/DNC:Building trust through education, transparency, public involvement, and ethical considerationsContinuous improvement, professional collaboration, and legal frameworksWe welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!References:Greer D, Kirschen MP et al. Pediatric and Adult Brain Death/Death by Neurologic Criteria Consensus Guideline Report of the AAN Guidelines Subcommittee, AAP, CNS, and SCCM. Neurology 2023; 101:1-21. doi:10.1212/WNL.0000000000207740Pediatric Neurocritical Care Educational Series - Lecture_ Brain Death 2023 Guidelines

Today’s case presentation involves a 2-year-old girl who was previously healthy and was admitted to the Pediatric Intensive Care Unit (PICU) for acute respiratory distress characterized by increased work of breathing and wheezing.Case PresentationA 2-year-old girl with acute respiratory distress due to RSV infectionPresented with increased work of breathing, wheezing, and no feverStarted on High Flow Nasal Cannula (HFNC) therapy in the PICUKey Elements:Prodrome of URI symptomsIncreased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry)HFNC improved the work of breathing and oxygen saturationPhysiology of HFNCMechanisms of ActionWashout of Nasopharyngeal Dead Space:HFNC clears nasopharyngeal dead space, improving oxygen efficiency.Reduces re-breathing of CO2 from the anatomical dead space.Enhances ventilation efficiency and oxygenation.Reduction in Upper Airway Resistance:HFNC reduces resistance in the upper airway.Delivers rapid gas flow matching or exceeding natural inhalation rate.Eases breathing, especially in neonates and infants with narrow airways.Optimal Conditioning of Gas:HFNC delivers heated and humidified oxygen, matching the body's conditions.Reduces energy expenditure and risk of airway irritationMore comfortable and effective compared to cold, dry air deliveryDebunking the PEEP Theory (Positive End-Expiratory Pressure) HFNC generates minimal and variable PEEP.Amount of PEEP depends on factors like flow rate and cannula sizeNot as high or consistent as other respiratory support devicesResearch FindingsA 2022 CHEST study by Khemani et al. on children with bronchiolitis challenged the conventional understanding of HFNC's mechanisms.HFNC primarily reduces breathing effort but does not consistently increase lung volume (EELV) or tidal volume (VT).Reduction in the pressure rate product (PRP) indicates decreased breathing effort, but not significant alterations in EELV or VT.Physiological EffectsHR, RR, and SpO2 are key indicators of HFNC efficacy.HR and RR should approach normal ranges for the child's age.Improvement in SpO2 levels while maintaining or reducing FiO2 indicates a positive response.ConclusionHFNC is a valuable tool in pediatric care for alleviating respiratory distress.Not a one-size-fits-all solution; vigilant monitoring and reassessment are crucialRecognizing HFNC's mechanisms allows for optimized bedside application.Closing Remarks:Subscribe, share feedback, and leave a review on the podcast.Visit picudoconcall.org for more episodes and management cards.Hosted by Dr. Pradip Kamat and Dr. Rahul DamaniaReferencesMiller AG, Gentle MA, Tyler LM, Napolitano N. High-Flow Nasal Cannula in Pediatric Patients: A Survey of Clinical Practice. Respir Care 2018; 63:894.Wraight TI, Ganu SS. High-flow nasal cannula use in a pediatric intensive care unit over 3 years. Crit Care Resusc 2015; 17:197.Hutchings FA, Hilliard TN, Davis PJ. Heated humidified high-flow nasal cannula therapy in children. Arch Dis Child 2015; 100:571.Lee JH, Rehder KJ, Williford L, et al. Use of high flow nasal cannula in critically ill infants, children, and adults: a critical review of the literature. Intensive Care Med 2013; 39:247.Wing R, James C, Maranda LS, Armsby CC. Use of high-flow nasal cannula support in the emergency department reduces the need for intubation in pediatric acute respiratory insufficiency. Pediatr Emerg Care 2012; 28:1117.Bressan S, Balzani M, Krauss B, et al. High-flow nasal cannula oxygen for bronchiolitis in a pediatric ward: a pilot study. Eur J Pediatr 2013; 172:1649.Mayfield S, Bogossian F, O'Malley L, Schibler A. High-flow nasal cannula oxygen therapy for infants with bronchiolitis: pilot study. J Paediatr Child Health 2014; 50:373.Kelly GS, Simon HK, Sturm JJ. High-flow nasal cannula use in children with respiratory distress in the emergency department: predicting the need for subsequent intubation. Pediatr Emerg Care 2013; 29:888.

Welcome to PICU Doc on Call, a podcast dedicated to current and aspiring intensivists. I'm Pradeep Kumar coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two pediatric ICU physicians passionate about all things medical education in the PICU.Episode Overview: PICU.com call focuses on interesting PICU cases and management in the acute care Pediatric setting. In this episode, we discuss the case of an eight-year-old boy with chest pain, fatigue, and shortness of breath. This case presentation by Rahul highlights the complexity of pediatric care in the PICU.Case Presentation: An eight-year-old boy with up-to-date immunizations and no recent travel or pet exposure presented to the PICU with chief complaints of chest pain, fatigue, and decreased oral intake. His history over the preceding two weeks included a diminishing appetite, episodes of vomiting, and shortness of breath.On examination, he exhibited various cardiac findings, including a hyperdynamic left ventricle, murmurs, and a noted gallop. Abdominal and neurological findings were also concerning. Diagnostic studies revealed an enlarged heart, and sinus tachycardia with left ventricular hypertrophy, and echocardiography confirmed severe valvular and ventricular abnormalities.Laboratory Findings:Laboratory findings included elevated BNP, slightly elevated troponin, and elevated inflammatory markers (ESR and CRP). Strep throat culture was negative, but ASO and anti-DNAse B titers were markedly elevated. MRI confirmed multiple punctate infarctions, likely due to valvular heart disease.Diagnosis: Given the complex multisystem presentation, the child was admitted to the PICU for intensive monitoring and comprehensive management of this multisystem pathology. The working diagnosis is rheumatic fever.The episode is organized into three parts:Pathophysiology of Acute Rheumatic FeverApproach to Diagnosis and InvestigationsManagement and PreventionPathophysiology of Acute Rheumatic Fever: Acute rheumatic fever is an autoimmune disease initiated by a response to group A strep infection, primarily due to molecular mimicry. The streptococcal M protein has structural similarities with host proteins, leading to organ damage, especially in the heart.Epidemiology: Acute rheumatic fever is most prevalent in low to middle-income areas, affecting over 80% of cases. It mainly affects children between 5 to 14 years of age, and overcrowded households and limited healthcare access increase the risk. Globally, rheumatic heart disease affects millions of people annually and claims many lives.Jones Criteria for Diagnosis: The Jones criteria help diagnose acute rheumatic fever. For a definitive diagnosis, evidence of a preceding group A strep infection is required. Major manifestations include carditis, arthritis, erythema marginatum, subcutaneous nodules, and Sydenham's chorea. Minor criteria include fever, elevated inflammatory markers, prolonged PR interval on EKG, and mild joint issues.Differentiating Low and High-Risk Populations: The criteria differentiate between low and high-risk populations based on the epidemiology of acute rheumatic fever. The presentation of arthritis varies, and the thresholds for fever or inflammatory marker elevation are lower in high-risk populations.Diagnostic Approach:Diagnosis includes throat swab, anti-streptolysin O antibody titers, anti-DNAse B titers, CBC with differential, blood cultures, inflammatory markers, EKG, chest X-ray, and echocardiography. Joint analysis may be performed if needed.Sydenham's Chorea:Sydenham's chorea is marked by involuntary movements, primarily in the trunk and limbs, and it often resolves within 12 to 15 weeks with treatment.Management of Acute Rheumatic Fever: Management includes eradicating the remaining strep infection, controlling inflammation, and preventing recurrence. Penicillin or amoxicillin is used to treat the infection, while aspirin or NSAIDs are used to manage inflammation. In severe cases, systemic steroids may be considered. Cardiac surgery should be delayed until acute inflammation resolves. Prophylactic antibiotics are used for prevention.Conclusion: Rheumatic fever management requires a holistic approach, encompassing infection control, inflammation management, and long-term prevention. Early recognition, thorough diagnostics, and prophylactic antibiotics play essential roles in managing this condition.Future Directions: Research is needed for early detection using biomarkers and the development of a group A strep vaccine.Closing Remarks: As pediatric intensivists, we play a pivotal role in primary prevention by advocating for awareness and prompt treatment of group A strep infections.Thank you for listening to PICU Doc on Call. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more information. Stay tuned for our next episode.

Introduction: Welcome to "PQ Doc On Call," a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradeep Kamar from Children's Healthcare of Atlanta, Emory University School of Medicine, and Dr. Rahul Damia from Cleveland Clinic Children's Hospital, both passionate PICU physicians.You will hear:This episode dives into the management of pediatric drowning cases in the PICU, providing valuable insights into assessment, pathophysiology, and practical management strategies.Case Presentation: An 18-month-old girl was admitted to the PICU following a submersion incident in a residential pool. The child's initial unresponsiveness and subsequent clinical deterioration presented challenges for the PICU team, including respiratory distress, electrolyte imbalances, and potential neurological complications.Key Elements from the Case:Severe acute respiratory failure following submersionAbnormal electrolytes (hyponatremia)Neurological insult requiring ongoing monitoringDefinitions and Terminology:Clarification of drowning terminology, emphasizing uniform definitions and avoiding outdated terms like "near drowning." Key terms include primary vs. secondary drowning, saltwater vs. freshwater, intentional vs. non-intentional, and fatal vs. non-fatal drowning incidents.Pathophysiology:Airway Reflexes: Initial reflex laryngospasm triggered by liquid penetration, followed by relaxation due to hypoxia, hypercarbia, and acidosis.Gas Exchange Compromise: Decreased functional residual capacity leading to impaired oxygen uptake and CO2 elimination.Pulmonary Complications: Pulmonary edema, surfactant washout, increased pulmonary vascular resistance, and shunting, impacting oxygen delivery.Management Strategies:Out-of-Hospital: Aggressive on-site CPR and advanced life support are crucial for favorable outcomes. Swift control of hypoxia and acidosis is vital.In-PICU: Ventilation strategies resembling ARDS management (low tidal volume, low plateau pressures, high PEEP). Consider neurological exam, continuous EEG, and neuromuscular blockade if needed.Prognostic Factors: Duration of submersion, time to effective CPR, initial GCS, apnea persistence, pH levels, and neurologic status.Prevention:Empowering prevention through measures like fencing around pools, teaching children to swim, and vigilant adult supervision can significantly reduce the risk of pediatric drowning incidents.Conclusion:"PQ Doc On Call" underscores the importance of timely, effective CPR, swift management of hypoxia and acidosis, and vigilant neurological assessment in pediatric drowning cases. Prevention remains paramount in avoiding such incidents.Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

In this episode of PICU Doc On Call, your hosts Pradip Kamat and Rahul Damania, experienced Pediatric ICU physicians, take you on an enlightening journey through the intricate landscape of lactic acidosis. Join us as we unravel the complexities, share clinical insights, and provide practical guidance on diagnosing and managing this critical condition in the acute care pediatric setting.You will hear:Case Presentation:4-year-old boy with hypotension, fatigue, rash, and respiratory distressRecent COVID-19 exposure, concerning respiratory symptomsHypotensive, tachycardic, tachypneic, low pulse oximetry readingSwollen red lips, erythematous rash, hepatomegalyHigh-flow nasal cannula, resuscitation, epinephrine infusionInitial arterial blood gas: pH 7.22, lactate 4.5 mMol/LDefinition of Lactic Acidosis:Hyperlactatemia and lactic acidosis criteriaCauses: impaired tissue oxygenation or mitochondrial dysfunctionTypes of Lactic Acidosis:Type A: Impaired O2 delivery, shock-relatedType B: Impaired O2 utilization, toxins, infectionsLactate Measurement:Comparability between POCT and central lab analysisRole of lactate measurement in pediatric sepsisLactic Washout:Rising lactate with re-established oxygen deliveryImpaired clearance in microcirculation, liver, kidneyMonitoring trends with clinical exams and lab surrogatesBicarbonate Therapy:Role in Type A lactic acidosisControversy, indications, and potential complicationsConclusion:PICU Doc On Call podcast explores the intriguing case of a 4-year-old boy with lactic acidosis, highlighting the clinical intricacies of diagnosing and managing this condition. The hosts, Pradip Kamat and Rahul Damania provide insightful discussions on the different types of lactic acidosis, the physiological mechanisms behind it, and the role of bicarbonate therapy. The episode emphasizes the importance of addressing underlying causes and offers valuable clinical pearls for managing pediatric patients with lactic acidosis.Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

In this episode of PICU Doc On Call, Dr. Pradip Kamat and Dr. Rahul Damania discuss a case of a 4-year-old girl with bite marks and swelling of her foot, presenting with concerning vital signs and abnormal labs. They explore snake envenomation and its management in the pediatric critical care setting.Classifying Snake EnvenomationSnakes with venom-delivering fangs, primarily Elapidae and Viperidae, are responsible for most human envenomations and fatalities. We're focusing on Pit Vipers today, including rattlesnakes, cottonmouths, and the copperhead. Elapids, such as the coral snake, differ by having round pupils, short fangs, and no facial pit.Risk Factors for Pediatric SnakebitesSnakebite incidents can happen when toddlers unintentionally disturb snakes, particularly in low-light conditions or grassy areas. Teenagers trying to capture snakes are another frequent group presenting with upper extremity bites. Pathophysiology of Snake EnvenomationSnake venoms contain toxic proteins that affect various physiological systems, leading to neurotoxic, hemotoxic, myotoxic, or cytotoxic effects. Envenomation can happen immediately or be delayed, presenting with various clinical and laboratory anomalies.Syndromes Observed After Snake EnvenomationThe impact of a snakebite depends on the snake type, fang size, and venom injection site. Effects may include cytotoxicity, lymphatic system damage, platelet dysfunction, neurotoxicity, cardiotoxicity, hypotension, and nephrotoxicity.General Management FrameworkIn snakebite cases, prehospital care involves immediate EMS call and ensuring airway, breathing, and hemodynamic stability. In the hospital, general supportive care is crucial, and antivenin administration depends on clinical presentation and snake type.Antivenin ConsiderationsAntivenin dosage is challenging due to unknown venom load, and its choice depends on safety, kinetics, cost, and the specific snake involved. Smaller fragments of antivenin have larger distribution volumes and shorter half-lives. Recurrence, anaphylaxis, and serum sickness are potential side effects of antivenin.Clinical PearlsA high index of suspicion is required to diagnose snake envenomation.Antivenin is the mainstay of therapy, and rapid transport to a facility with antivenin is crucial.Patients should be educated about recurrence, serum sickness, and lifestyle adjustments after a pit viper bite.Thank you for listening to this episode on snake envenomation in the PICU. For more episodes, visit our website picudoconcall.org. Stay tuned for our next episode! Don't forget to share your feedback and subscribe to our podcast.

In this episode PICUDoc On Call, we discuss the case of a six-month-old ex-preemie with bacterial meningitis who presents with symptoms of cerebral sinus venous thrombosis. We explore the anatomy of the venous distribution in the brain and the clinical syndromes associated with sinus venous thrombosis. Our focus is on the imaging techniques, laboratory tests, and management strategies involved in diagnosing and treating this challenging condition.You will learn:A six-month-old ex-preemie presents with persistent fever, recurrent emesis, and increased somnolence.The patient experiences eye rolling and decreased oxygen saturation, prompting a visit to the emergency department.Physical examination reveals rigidity in all four limbs, and a head CT shows dilated ventricles and encephalomalacia.Lumbar puncture confirms an infection, and the patient is admitted to the hospital.After a 14-day course of antibiotics, the patient's clinical status worsens, leading to intubation and neurosurgery consultation.An MRI confirms cerebral venous sinus thrombosis.Anatomy of Venous Distribution in the Brain:Dural venous sinuses serve as conduits for venous blood return from the brain to the internal jugular veins.The superior sagittal sinus, cortical veins, transverse sinus, sigmoid sinus, and internal jugular vein are key components of the venous drainage system.Clinical Syndromes of Sinus Venous Thrombosis:Symptoms can be related to elevated intracranial pressure or focal brain damage from venous ischemia, infarction, or hemorrhage.Headache, seizures, focal neurologic deficits, and cranial nerve paralysis are common presentations.Cavernous sinus thrombosis can cause periorbital pain, ocular chemos, and paralysis of cranial nerves passing through the sinus.Risk Factors for Cerebral Sinus Venous Thrombosis:Dehydration, CNS or sinus infections, intracranial surgery, autoimmune disorders, genetic syndromes, metabolic syndromes, medications, and genetic thrombophilic states can predispose children to thrombosis.Thorough evaluation for risk factors, including thrombophilia, is recommended in children with cerebral venous thrombosis.Imaging and Laboratory Tests:CT and MRI with contrast-enhanced venography are preferred imaging tools to detect cerebral sinus venous thrombosis.Non-enhanced CT scans and T1/T2-weighted MRI scans show characteristic signs of thrombosis.Lab tests include CBC with differential, DIC panel, comprehensive metabolic panel, ESR, and specific thrombophilia tests.Management Strategies:Supportive care, including airway management, hemodynamics, and neurologic monitoring, is crucial.Consultation with a multidisciplinary team (neurosurgeons, neuro-interventional radiologists, hematologists, etc.) is necessary.Anticoagulation therapy with heparin is initiated and closely monitored.Surgical interventions (e.g., EVD placement, ventricular peritoneal shunt, decompressive hemicraniectomy) may be required in severe cases.Long-term rehabilitation may be necessary for neurological deficits.In summary:Cerebral sinus venous thrombosis in pediatric patients requires a multidisciplinary approach for prompt diagnosis and management. Recognizing the clinical signs, conducting appropriate imaging and laboratory tests, and initiating timely interventions are crucial for improved outcomes.

Welcome to PICU Doc on Call, a podcast dedicated to intense wisdom in the field of pediatric critical care. In this episode, hosts Pradeep Kama and Rahul Damania, both pediatric ICU physicians, discuss the case of a five-year-old male who presents to the emergency department with unexplained fatigue and fever. The patient's symptoms include fatigue, intermittent fevers, tachycardia, and significantly low hemoglobin levels.The hosts delve into the possible causes of the patient's condition, considering a blood cell disorder and the potential for severe anemia due to aplastic crisis. They explain the physiological adaptations that occur in severe acute anemia, including the shifting of the oxyhemoglobin curve to the right and the increase in cardiac output through tachycardia and increased stroke volume.The podcast episode also covers different forms of hemolytic anemia, including extravascular and intravascular hemolysis, autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria. The hosts discuss the workup for hemolytic anemias, such as complete blood count, peripheral smear, LDH levels, haptoglobin levels, and Coombs tests. They emphasize the importance of involving hematology and infectious disease specialists for accurate diagnosis and management.The case of the five-year-old with hereditary spherocytosis is explored, highlighting the characteristic spherocytic shape of red blood cells and potential complications like hemolytic crisis, splenic sequestration, and aplastic crisis. The hosts provide insights into the pathophysiology and presentations of these complications, emphasizing the need for prompt recognition and appropriate interventions.In summary, this episode of PICU Doc on Call provides valuable information on the evaluation and management of a pediatric patient with fatigue, fever, and anemia, shedding light on different forms of hemolytic anemias and their associated complications.

Welcome to "PICU Doc On Call," a podcast dedicated to current and aspiring intensivists. In this episode, Dr. Pradip Kamat and Dr. Rahul Damania discuss an interesting case of a 16-year-old male with high-grade fever and abdominal pain. The patient also presents with a rash and other concerning symptoms, leading to urgent medical attention. They provide a summary of the key elements from the case, including vital signs, physical examination findings, and laboratory and imaging results.Dr. Kamat then shares his thought process regarding the working diagnosis for this patient, considering several possibilities such as severe bacterial infection, atypical appendicitis or cholecystitis, toxic shock syndrome, and systemic inflammatory processes like Multisystem Inflammatory Syndrome in Children (MIS-C) and atypical Kawasaki disease.Moving on to the topic of vasopressors, Dr. Damania explains the importance of understanding how these medications work and their specific pharmacological properties. They discuss the classification of shock as cold or warm and the limitations of relying solely on clinical signs to categorize septic shock in children.They highlight the challenges in selecting the appropriate vasopressor, such as a lack of standardization in clinical examination and individual variability in response to medications. They emphasize the need for a comprehensive approach when evaluating and managing pediatric shock patients, considering multiple factors beyond traditional bedside signs.The hosts then engage in a rapid review of pressors, starting with a multiple-choice question regarding the choice of vasoactive infusion for a patient with toxic shock syndrome. They discuss the pros and cons of using norepinephrine (NE) in distributive shock and highlight its vasoconstrictive effects, inotropic activity, and potential side effects.They proceed to compare NE with epinephrine, explaining the differences in their actions on adrenergic receptors and their effects on various circulations. They mention that epinephrine acts on all adrenergic receptors and has hemodynamic and metabolic effects, redirecting cardiac output and increasing myocardial oxygen demand.Lastly, the hosts touch on phenylephrine, a vasopressor that acts on the alpha-1 receptor and elevates systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). They stress the importance of securing central line access when administering vasopressors to avoid harm to peripheral and systemic tissues.In conclusion, this episode provides valuable insights into the diagnosis and management of a complex pediatric case involving high-grade fever, abdominal pain, and shock. The hosts also offer a rapid review of common vasopressors, highlighting their mechanisms of action, pros, and cons.

Today’s episode of "PICU Doc On Call," with Dr. Pradip Kamat and Dr. Rahul Damania, pediatric ICU physicians, delves into intriguing case and management strategies within the acute care pediatric setting.This episode focuses on a 2-year-old child transferred to the PICU due to pneumonia-induced respiratory distress. As the child's condition deteriorates, intubation becomes necessary to address acute hypoxemic respiratory failure.We discuss the significance of minimizing unnecessary blood cultures in febrile patients with central lines in the PICU. A study implementing a quality improvement program is referenced, which successfully reduces blood culture rates, broad-spectrum antibiotic usage, and CLABSI rates without impacting mortality or length of stay.Next, we’ll explore the comparison between a high-flow nasal cannula (HFNC) and continuous positive airway pressure (CPAP) in pediatric patients experiencing respiratory distress. Findings from a randomized controlled trial revealed that HFNC is non-inferior to CPAP in terms of time required for liberation from respiratory support.We further investigate the application of pediatric early warning scores (PEWS) and automated clinical prediction models to identify patients at risk of deterioration and transfer to the PICU. The importance of employing clinical judgment and a combination of assessment tools to determine the need for transfer is emphasized.Lastly, we’ll highlight the significance of screening for social determinants of health in critically ill children and their families. A study demonstrates that a substantial number of participants had unmet social needs, underscoring the importance of screening to provide appropriate interventions and resources.To summarize, this podcast episode covers key topics such as reducing unnecessary blood cultures, comparing HFNC and CPAP in respiratory distress, utilizing PEWS and clinical prediction models for patient identification, and the importance of screening for social determinants of health.Be sure to listen in entirety as we discuss the case.