Acute Hydrocephalus In The PICU PICU Doc On Call podcast

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PICU Doc On Call

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Emerging Neurologic Autoimmune Disorders (MOGAD) in the PICU 27:42

11 days ago27:42

27:42

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 failure Discussion of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) as an autoimmune demyelinating disorder Overview of the clinical presentation and diagnostic criteria for autoimmune encephalitis Importance of a broad differential diagnosis, including infectious and autoimmune causes, in pediatric patients with seizures and neurological deficits Diagnostic approach involving MRI, lumbar puncture, and antibody testing for MOGAD Management strategies for MOGAD, including stabilization, seizure control, and immunosuppressive therapy Neurocritical care considerations for monitoring and treating elevated intracranial pressure Long-term management challenges and the need for multidisciplinary care in pediatric patients with MOGAD Discussion of potential outcomes and the risk of relapse in children with MOGAD. Emphasis on the importance of early and comprehensive diagnostic testing to avoid misdiagnosis References: Fuhrman & Zimmerman - Pediatric Critical Care 6th Edition, Chapter 64 Gole 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: PMC6751007 Lancaster 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.…

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PICU Doc On Call

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Cardiopulmonary Interactions in the PICU 20:24

25 days ago20:24

20:24

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 bleach Clinical presentation including symptoms like stridor, drooling, and vomiting Management strategies for caustic ingestions in children Importance of airway management and monitoring in cases of caustic ingestion Diagnostic workup including imaging and endoscopy Differential diagnosis considerations for similar presentations (e.g., button batteries, laundry detergent pods) Mechanism of injury caused by alkaline substances like bleach Long-term complications associated with caustic ingestions, such as esophageal strictures and cancer Multidisciplinary approach to treatment involving various medical specialties Prevention strategies to reduce the incidence of accidental caustic ingestions in children References: 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.…

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PICU Doc On Call

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Approach to Bleach Ingestion in the PICU 31:19

6 weeks ago31:19

31:19

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 bleach Clinical presentation including symptoms like stridor, drooling, and vomiting Management strategies for caustic ingestions in children Importance of airway management and monitoring in cases of caustic ingestion Diagnostic workup including imaging and endoscopy Differential diagnosis considerations for similar presentations (e.g., button batteries, laundry detergent pods) Mechanism of injury caused by alkaline substances like bleach Long-term complications associated with caustic ingestions, such as esophageal strictures and cancer Multidisciplinary approach to treatment involving various medical specialties Prevention strategies to reduce the incidence of accidental caustic ingestions in children References: 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.…

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PICU Doc On Call

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Salty Saga of Hyponatremia and Hypotension in the PICU 39:31

8 weeks ago39:31

39:31

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 PICU Presentation of two case studies illustrating different presentations of hyponatremia Examination of the pathophysiology of hyponatremia, including its classification into hypovolemic, euvolemic, and hypervolemic types Overview of diagnostic investigations for hyponatremia, including volume status assessment and serum/urine electrolyte measurements Management strategies for hyponatremia, emphasizing the importance of gradual correction of sodium levels Risks associated with rapid correction of hyponatremia Importance of fluid management in different types of hyponatremia Role of pharmacological interventions in specific cases, such as SIADH Clinical presentation and symptoms associated with hyponatremia in pediatric patients Emphasis on continuous monitoring of sodium levels and clinical status during treatment References: Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 71. Fluid and electrolyte issues in pediatric critical illness. Evans I, Joyce E. Page 866-872 Rogers' textbook of Pediatric Intensive Care Chapter 108: Disorders of Water, Sodium and Potassium homeostasis: Schneider J & Glater-Welt L. Pages 1868-1880 Harrison’s Principles of Internal Medicine Volume 1. Chapter 53: Fluid and Electrolyte Disturbances. Mount D. Pages 338-347…

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PICU Doc On Call

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Cardiopulmonary Interactions (basics) in the PICU 28:40

10 weeks ago28:40

28:40

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 patients Clinical case presentation of a one-month-old infant with acute myocarditis Symptoms and clinical manifestations of acute myocarditis in children Diagnostic approaches for identifying acute myocarditis, including echocardiography and laboratory tests Management strategies for acute myocarditis, including intensive care and medication Importance of recognizing atypical presentations in infants Prognosis and risk factors associated with acute myocarditis Role of multidisciplinary collaboration in managing acute myocarditis Impact of viral infections on the development and severity of myocarditis Outcomes and potential complications related to acute myocarditis in pediatric patients References: Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 108. Life-threatening viral diseases and their treatment. Vora S et al. Pages 1273-1278 Rogers’ textbook of Pediatric Intensive Care. Chapter 74: cardiomyopathy, myocarditis, and mechanical circulatory support. Harmon WG et al. Pages 1247-1255 Robinson 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…

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PICU Doc On Call

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Approach to Carbon Monoxide (CO) Poisoning in the PICU 22:57

13 weeks ago22:57

22:57

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 poisoning Pathophysiology of carbon monoxide toxicity and its effects on hemoglobin Clinical manifestations and symptoms associated with carbon monoxide poisoning Diagnostic workup for suspected carbon monoxide exposure Management principles for treating carbon monoxide poisoning in pediatric patients Sources and scenarios leading to carbon monoxide poisoning Complications arising from carbon monoxide exposure including neurological injuries Importance of early oxygen administration and monitoring in treatment Discussion of hyperbaric oxygen therapy and its indications Key takeaways for clinicians regarding the management and follow-up of carbon monoxide poisoning cases We 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.…

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PICU Doc On Call

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Oxygen Extraction Ratio (O₂ ER) in the PICU 25:26

15 weeks ago25:26

25:26

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 care Importance of understanding oxygen delivery and consumption in critically ill patients Calculation and interpretation of O2ER and its relationship to central venous oxygen saturation (ScvO2) Physiological concepts related to oxygenation, including intrapulmonary shunting and ventilation-perfusion mismatch Management strategies for increasing oxygen delivery and reducing oxygen demand in ARDS and septic shock Interventions such as blood transfusions, sedation, and optimization of cardiac output Implications of lactic acidosis and anaerobic metabolism in the context of inadequate oxygen delivery Holistic approach to patient management, focusing on both numerical values and overall metabolic needs We 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.…

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PICU Doc On Call

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A Case of Pertussis in the PICU 34:06

17 weeks ago34:06

34:06

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 diagnosis Epidemiology and public health impact of pertussis, including vaccination rates and outbreak patterns Pathophysiology of pertussis and its effects on respiratory health, particularly in infants Clinical presentation of pertussis, including stages of the disease and atypical symptoms in infants Diagnostic approaches for pertussis, including laboratory findings and PCR testing Management strategies for severe pertussis, including supportive care and antibiotic therapy Potential complications associated with pertussis, especially in young infants Differential diagnosis considerations for pertussis and distinguishing features from other infections Importance of vaccination in preventing pertussis and reducing morbidity and mortality ECMO as a treatment option for severe cases and its associated challenges, and outcomes We 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/s13054-025-05300-2 Domico 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…

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PICU Doc On Call

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Management of Upper Airway Obstruction | Croup in the PICU 32:34

19 weeks ago32:34

32:34

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 patients Case presentation of a 12-month-old girl with stridor and fever Discussion on the pathophysiology of stridor and its clinical significance Differential diagnoses for stridor, including croup, epiglottitis, and foreign body aspiration Management strategies for upper airway obstruction, including stabilization and medication Importance of calming the child and optimal positioning during treatment Use of dexamethasone and racemic epinephrine in managing croup Advanced therapies, such as Helios, for specific cases Indicators for pediatric intensive care unit (PICU) admission Key clinical points and takeaways for healthcare professionals managing airway emergencies References: Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 47 Otteson T, Richardson C, Shah J: Diseases of the upper Airway. Pages 524-535 Rogers Textbook of Pediatric Intensive Care: Chapter 25; Ong May Soo Jacqueline, Tijssen J, Bruins BB and Nishisaki A: Airway management. Pages 341-365 Reference: 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…

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PICU Doc On Call

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Measly Business - A Guide for the Pediatric Intensivist 30:38

21 weeks ago30:38

30:38

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 States Historical context of measles outbreaks and vaccination impact Current statistics and recent cases of measles Pathophysiology of the measles virus Clinical features and progression of measles infection Diagnostic approaches for confirming measles Differential diagnosis considerations for fever and rash Treatment options and the role of vaccination Complications associated with measles, including severe outcomes Public health challenges related to vaccine hesitancy and advocacy for immunization Resources: CDC Measles Info Page WHO Measles Global Surveillance References: Fuhrman & Zimmerman. Textbook of Pediatric Critical Care , Ch. 52 Long S et al. Principles and Practice of Pediatric Infectious Diseases , Ch. 227 Moss WJ. Measles . Lancet . 2017;390(10111):2490-2502 Paules CI, Marston HD, Fauci AS. NEJM . 2019;380(23):2185-2187…

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PICU Doc On Call

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Cardiopulmonary Interactions (basics) in the PICU 20:37

24 weeks ago20:37

20:37

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 failure Importance of understanding cardiopulmonary interactions in pediatric critical care Effects of positive pressure ventilation on cardiac function Key concepts of cardiac output, preload, and afterload in the context of myocarditis Challenges of managing hemodynamic instability in critically ill pediatric patients Differences between spontaneous breathing and positive pressure ventilation Strategies for optimizing preload and fluid management in myocarditis patients Tailoring ventilatory support and transitioning to invasive mechanical ventilation Monitoring for arrhythmias and managing myocardial function with inotropic support Importance of frequent assessments and collaboration with cardiac ICU teams for patient care Management Strategies Optimizing 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.…

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PICU Doc On Call

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Traumatic Brain Injury in the PICU | Non-Neurological Organ Dysfunction (NNOD) 30:27

32 weeks ago30:27

30:27

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 aneurysm Management of non-neurologic organ dysfunction in traumatic brain injury (TBI) and intracranial hemorrhage Multi-system effects of brain injuries, including cardiovascular, respiratory, renal, and hepatic complications Importance of recognizing non-neurologic organ dysfunction in pediatric patients Epidemiology and prevalence of non-neurologic organ dysfunction in patients with aneurysms or subarachnoid hemorrhage Mechanisms of organ dysfunction following brain injury, including inflammatory responses and cytokine release Management strategies for cardiovascular complications in TBI patients. Discussion of respiratory complications, such as acute lung injury and ARDS, in the context of TBI Renal and hepatic dysfunction associated with traumatic brain injury and their management Emphasis on the need for a comprehensive understanding of organ interactions to improve patient outcomes in pediatric critical care Conclusion In 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!…

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PICU Doc On Call

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Little Lungs Big Bugs: Approach to Bacterial PNA 26:25

33 weeks ago26:25

26:25

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 Presentation The 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 Pneumonia Understanding the risk factors for pneumonia is crucial for early identification and prevention. These risk factors can be categorized into three main groups: Host Factors Incomplete Immunization Status: Children who are not fully vaccinated are at higher risk Young Age: Infants and young children have immature immune systems, making them more susceptible Lower Socioeconomic Status: Limited access to healthcare and poor living conditions can increase risk Environmental Factors Exposure to Tobacco Smoke: Secondhand smoke can damage the respiratory tract and impair immune function Seasonal Variations: Pneumonia cases peak during fall and winter due to increased circulation of respiratory viruses Contact with Other Children: Daycare settings and schools can facilitate the spread of infections Healthcare-Associated Factors Prolonged 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 secretions Inadequate Humidification: Dry air can damage the respiratory mucosa Pathogenesis of Pneumonia Pneumonia 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 Group The causative pathogens of pneumonia vary by age group: Neonates: Group B Streptococcus, E. coli, Listeria, Klebsiella Children Under 5: Viral causes (50% of cases) such as RSV, human metapneumovirus, and influenza, with bacterial causes like Streptococcus pneumoniae and Haemophilus influenzae Older Children and Teens: Mycoplasma pneumonia, Chlamydia pneumonia, and Streptococcus pneumoniae Classification of Pneumonia Pneumonia can be classified based on the acquisition setting: Community-Acquired Pneumonia (CAP): Occurs in patients not hospitalized in the past month Hospital-Acquired Pneumonia (HAP): Develops after 48 hours of hospitalization Ventilator-Associated Pneumonia (VAP): Occurs within 48 hours of intubation Aspiration Pneumonia: Results from inhaling gastric or oral contents Necrotizing Pneumonia: Caused by aggressive bacteria, often requiring CT imaging for diagnosis Clinical Presentation When a child presents with suspected pneumonia, clinicians should look for: Systemic Symptoms: Fever, lethargy, poor appetite Respiratory Symptoms: Tachypnea, hypoxia, and classic findings like crackles Key Indicators: Moderate hypoxemia (SpO2 < 96%) and increased respiratory effort (nasal flaring, intercostal retractions) Diagnostic Approach The diagnostic workup for bacterial pneumonia typically includes: Basic Labs: CBC, inflammatory markers (CRP, procalcitonin), and a comprehensive metabolic panel Cultures: Blood cultures have low yield; pleural fluid cultures are more definitive Imaging: Chest X-rays can overestimate pneumonia; point-of-care ultrasound may help identify effusions Management Framework Management 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 distress Toxic Appearance or Poor Oral Intake: Suggests a need for closer monitoring and supportive care In the PICU, management involves: Respiratory Support Nasal Cannula: For mild cases High-Flow Nasal Cannula (HFNC): For moderate cases Mechanical Ventilation: For severe cases of respiratory failure Antibiotic Therapy Empiric Therapy: Based on age, severity, and local resistance patterns Targeted Therapy: Adjusted based on culture results and clinical response Supportive Care Fluid Management: To maintain hydration and electrolyte balance Nutrition: Ensuring adequate caloric intake Fever Control: Using antipyretics to manage fever Complications of Pneumonia Complications occur in about 3% of pneumonia cases and include: Pleural Effusion: Managed with chest tube placement and fibrinolytic therapy Necrotizing Pneumonia: May require drainage if abscesses develop Systemic Complications: Such as ARDS, sepsis, and multi-organ dysfunction Conclusion Early 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.…

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Inhalation Injury in the PICU 22:44

35 weeks ago22:44

22:44

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 arrest Signs of inhalation injury and airway compromise Pathophysiology of inhalation injuries and their impact on multiple organ systems Management strategies for inhalation injury, including airway protection and ventilation Differentiating carbon monoxide and cyanide poisoning in pediatric fire victims Case Presentation A 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 extremities Prolonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR) Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refill Metabolic acidosis, AKI, coagulopathy, transaminitis Severe hypoxic-ischemic encephalopathy on EEG These findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion. Pathophysiology of Inhalation Injury When 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 Injury A 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 Approach Management 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) Poisoning In 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 Victims Cyanide 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 Patient The patient’s clinical course was marked by rapid deterioration despite aggressive treatment: Initially managed with high-frequency oscillatory ventilation (HFOV) due to pulmonary hemorrhage Developed severe PARDS, cardiac dysfunction, and multi-organ failure within 12 hours Ultimately, neuroimaging revealed anoxic brain injury with cerebral edema and herniation, leading to brain death This heartbreaking case highlights the importance of early intervention and recognition of inhalation injury in burn victims. Key Takeaways: Act quickly to protect the airway in pediatric fire victims—early intubation can be life-saving. Protect the lungs with proper ventilation strategies and aggressive secretion management. Time is critical when dealing with CO and cyanide poisoning. Immediate recognition and treatment are key to survival. Inhalation injuries can result in rapid multi-organ failure, and management requires a multi-disciplinary approach. Join Us for More Insights We hope this case-based discussion provides valuable insights into the complex management of inhalation injuries in pediatric burn victims. Stay tuned for our next episode and be sure to share your feedback and subscribe to the podcast! For more episodes, visit our website at picudoconcall.org . References: Tapking C., et al. "Burn and Inhalation Injury." Fuhrman & Zimmerman - Textbook of Pediatric Critical Care, Chapter 116, Pages 1347-1362. Bergman, et al. "Burns and Smoke Inhalation." Rogers Textbook of Pediatric Intensive Care, 6th edition, Chapter 33, Pages 484-497. Goh CT, Jacobe S. "Ventilation strategies in pediatric inhalation injury." Paediatr Respir Rev. 2016 Sep;20:3-9. Rodeberg DA, Housinger TA, et al. "Improved ventilatory function in burn patients using volumetric diffusive respiration." J Am Coll Surg. 1994 Nov;179(5):518-522.…

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PICU Doc On Call

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Approach Toxic Alcohol Ingestion in the PICU 30:06

36 weeks ago30:06

30:06

Welcome and Episode Introduction Hosts: 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 management Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol Case Presentation Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor Initial Labs & Findings: EtOH level: 420 mg/dL. Glucose: 50 mg/dL. Normal CXR and EKG. PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications Key Learning Points from the Case Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions Hypoglycemia and CNS depression are common features of ethanol toxicity in infants Management prioritizes glucose correction, airway support, and close neurological monitoring Deep Dive: Toxic Alcohols in the PICU 1. Ethanol Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia Diagnostic Workup: Focus on CNS and metabolic effects Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen Imaging (head CT) if indicated Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work 2. Methanol Sources: Windshield fluids, cleaning agents, moonshine Clinical 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 toxicity Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases 3. Ethylene Glycol Sources: Antifreeze, brake fluids, household cleaners Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals) Red Flags: Hypocalcemia, renal failure, QT prolongation Management: Fomepizole, supportive care, and hemodialysis for severe toxicity 4. Propylene Glycol Sources: Medications like lorazepam and pentobarbital Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction Management: Discontinue offending agent, supportive care, and hemodialysis if severe 5. Isopropyl Alcohol Sources: Disinfectants, hand sanitizers Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis Management: Supportive care; fomepizole and ethanol are ineffective Key Laboratory Insights Osmolar Gap Formula: Measured Osmolality - Calculated Osmolality A high osmolar gap indicates unmeasured osmoles like toxic alcohols. Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference Management Pearls Ethanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe cases Methanol: Similar approach with additional focus on preventing blindness Propylene Glycol: Monitor lactate and renal function, discontinue offending medications Isopropyl Alcohol: Supportive care, no acidosis present Mnemonics for Toxic Alcohols MEGA GAP: Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis) Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses Takeaway Messages Early recognition of toxic alcohol ingestion is critical for successful management Differentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentation Engage poison control and social work early in the process Conclusion Pediatric toxic alcohol ingestions are rare but potentially life-threatening Fomepizole is a cornerstone therapy for methanol and ethylene glycol toxicity Supportive care remains essential across all toxic alcohol ingestions Connect with US! Twitter: @PICUDocOnCall Email: contact@picudoconcall.com…

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PICU Doc On Call

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Multisystem Organ Dysfunction Syndrome (MODS) in the PICU 32:14

39 weeks ago32:14

32:14

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 rod Dependence on total parenteral nutrition (TPN) and prolonged PICC line use Discussion of septic shock, acute respiratory failure, and acute kidney injury Overview of multiple organ dysfunction syndrome (MODS) and its definitions Pathophysiology of MODS, including organ functional reserve and kinetics of organ injury Molecular mechanisms involved in MODS, such as mitochondrial dysfunction and immune responses Specific phenotypes of sepsis-induced MODS, including TAMOF and IPMOF Management strategies for MODS, emphasizing multidisciplinary approaches Role and complications of therapeutic plasma exchange (TPE) in treating MODS Importance of recognizing signs of MODS and timely intervention in pediatric patients Segment 1: MODS Definitions and Phenotypes Key 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 MODS Molecular Insights: Mitochondrial dysfunction and damage-associated molecular patterns (DAMPs) Innate and adaptive immune dysregulation Microcirculatory dysfunction and ischemia-reperfusion injury Organ Interactions: MODS evolves through complex multi-organ interdependencies Segment 3: Diagnosis and Evidence-Based Management Key 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 Intensivists Early recognition of MODS phenotypes for targeted therapy Importance of multidisciplinary teamwork in critical care settings Monitoring for complications like TMA and immunoparalysis during prolonged ICU stays Follow Us: Twitter: @PICUDocOnCall Email: contact@picudoconcall.com…

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PICU Doc On Call

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Acute Hydrocephalus in the PICU 36:16

40 weeks ago36:16

36:16

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 causes Epidemiological insights, clinical presentation, and diagnostic approaches Management strategies, including temporary and permanent CSF diversion techniques A review of complications related to shunts and endoscopic third ventriculostomy Key Case Highlights: Patient Presentation: A 15-year-old girl with a 3-day history of worsening headaches, nausea, vomiting, and difficulty walking Altered mental status and bradycardia upon PICU admission CT scan revealed severe hydrocephalus without a clear mass lesion Management Steps in the PICU: Hypertonic saline bolus improved her mental status and pupillary reactions Neurosurgery consultation recommended MRI and close neuro checks Initial management included dexamethasone, keeping the patient NPO, and hourly neuro assessments Differential Diagnosis: Obstructive (non-communicating) vs. non-obstructive (communicating) hydrocephalus Consideration of alternative diagnoses like intracranial hemorrhage and idiopathic intracranial hypertension Episode Learning Points: Hydrocephalus Overview: Abnormal CSF buildup in the ventricles leading to increased intracranial pressure (ICP) Key distinctions between obstructive and non-obstructive types Epidemiology and Risk Factors: Congenital causes include genetic syndromes, neural tube defects, and Chiari malformations Acquired causes: post-hemorrhagic hydrocephalus (e.g., from IVH in preemies), infections like TB meningitis, and brain tumors Clinical Presentation: Infants: Bulging fontanelles, sunsetting eyes, irritability Older children: Headaches, vomiting, papilledema, and gait disturbances Management Framework: Temporary CSF diversion via external ventricular drains (EVD) or lumbar catheters Permanent interventions include VP shunts and endoscopic third ventriculostomy (ETV) Complications of Shunts and ETV: Shunt infections, malfunctions, over-drainage, and migration ETV-specific risks, including delayed failure years post-procedure Clinical 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: @PICUDocOnCall Email: contact@picudoconcall.com Stay tuned for more cases that challenge and inspire us as PICU clinicians!…

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PICU Doc On Call

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Approach Toxic Alcohol Ingestion in the PICU 30:06

44 weeks ago30:06

30:06

Introduction Hosts: 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 management Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol Case Presentation Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor Initial Labs & Findings: EtOH level: 420 mg/dL. Glucose: 50 mg/dL. Normal CXR and EKG. PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications Key Learning Points from the Case Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions Hypoglycemia and CNS depression are common features of ethanol toxicity in infants Management prioritizes glucose correction, airway support, and close neurological monitoring Deep Dive: Toxic Alcohols in the PICU 1. Ethanol Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia Diagnostic Workup: Focus on CNS and metabolic effects Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen Imaging (head CT) if indicated Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work 2. Methanol Sources: Windshield fluids, cleaning agents, moonshine Clinical 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 toxicity Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases 3. Ethylene Glycol Sources: Antifreeze, brake fluids, household cleaners Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals) Red Flags: Hypocalcemia, renal failure, QT prolongation Management: Fomepizole, supportive care, and hemodialysis for severe toxicity 4. Propylene Glycol Sources: Medications like lorazepam and pentobarbital Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction Management: Discontinue offending agent, supportive care, and hemodialysis if severe 5. Isopropyl Alcohol Sources: Disinfectants, hand sanitizers Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis Management: Supportive care; fomepizole and ethanol are ineffective Key Laboratory Insights Osmolar Gap Formula: Measured Osmolality - Calculated Osmolality A high osmolar gap indicates unmeasured osmoles like toxic alcohols. Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference Management Pearls Ethanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe cases Methanol: Similar approach with additional focus on preventing blindness Propylene Glycol: Monitor lactate and renal function, discontinue offending medications Isopropyl Alcohol: Supportive care, no acidosis present Mnemonics for Toxic Alcohols MEGA GAP: Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis) Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses Takeaway Messages Early recognition of toxic alcohol ingestion is critical for successful management Differentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentation Engage poison control and social work early in the process Conclusion Pediatric toxic alcohol ingestions are rare but potentially life-threatening Fomepizole is a cornerstone therapy for methanol and ethylene glycol toxicity Supportive care remains essential across all toxic alcohol ingestions Connect with US! Twitter: @PICUDocOnCall Email: contact@picudoconcall.com…

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PICU Doc On Call

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It’s Getting Hot in Here | Heat Stroke in the PICU 29:35

45 weeks ago29:35

29:35

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 9 Lab abnormalities: hyponatremia, hypokalemia, hypoglycemia, elevated creatinine, liver enzymes, lactate, CK, and troponin After 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.…

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PICU Doc On Call

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Hemostatis and Coagulation in the PICU 50:04

1 year ago50:04

50:04

Introduction Welcome 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 Overview In 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 Presentation A 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 Points Diagnosis: Pulmonary embolism (PE) Hemodynamics: Stable with no right ventricular (RV) strain on echocardiogram Management Focus: Anticoagulation and consultation with the hematology/thrombosis team Expert Discussion with Dr. Karen Zimowski Risk Factors and Epidemiology of VTE in Pediatrics Pathophysiology: 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 DVT Symptoms: Swelling, pain, warmth, and skin discoloration in the affected extremity. Specific Presentations: SVC syndrome from superior vena cava thrombosis Abdominal pain from portal vein thrombosis Hematuria from renal vein thrombosis Neurological symptoms from cerebral sinus venous thrombosis Diagnostic Approach for DVT Imaging: 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 DVT Anticoagulation Strategies Unfractionated 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. Conclusion In 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! References Fuhrman & 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).…

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PICU Doc on Call Shorts: Alveolar Gas Equation 20:06

1 year ago20:06

20:06

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 470-481 Rogers textbook of Pediatric intensive care: Chapter 44. Respiratory physiology. Akong K et al. Pages 691-721 Respiratory Physiology for the Anesthesiologist. Bigatello L and Pesenti A, Anesthesiology 2019; 130: 1064-77…

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PICU Management of Malignant Hyperthermia 29:32

1 year ago29:32

29:32

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 Medicine Dr. Rahul Damania: Cleveland Clinic Children’s Hospital Introduction: Pediatric Intensive Care Unit (PICU) physicians passionate about medical education in the acute care pediatric setting Episode focus: A case of a 23-month-old ex-28 week premie presenting with sudden high fever and rapidly rising ETCO2 during surgery Case Presentation: Presented by Dr. Rahul Damania 23-month-old ex-28 week premie intubated during hernia repair surgery Noticed rapidly rising ETCO2, unprovoked tachycardia, and elevated temperature Transferred to PICU, exhibiting rigidity, clenched jaw, metabolic acidosis, and elevated lactate. Consideration of Malignant Hyperthermia (MH) crisis Key Points: Elevated temperature, hypercapnia, metabolic acidosis, and unprovoked tachycardia raise concern for MH Organized discussion on pathophysiology, clinical signs, symptoms, and management Multiple Choice Question: Diagnosis of MH crisis during scoliosis repair Correct Answer: D) Sarcoplasmic reticulum Dantrolene acts on the sarcoplasmic reticulum to inhibit calcium release, crucial in MH management Clinical Presentation of MH Crisis: Tachycardia, acidosis, muscle stiffness, and hyperthermia are hallmark features Potential life-threatening complications underscore the urgency of recognition and treatment Triggers and Pathophysiology of MH Crisis: Triggered by inhalational agents and depolarizing neuromuscular blocking agents Pathophysiology involves defective Ryanodine receptor leading to uncontrolled calcium release Differential Diagnosis: Includes sepsis, thyroid storm, pheochromocytoma, and neuroleptic malignant syndrome Differentiation from similar conditions crucial for accurate management Diagnostic Approach: High clinical suspicion Genetic testing (ryanodine receptor gene sequencing) and Caffeine Halothane Contracture Test (CHCT) for diagnosis Immediate workup during crisis includes blood gas, lactate, CPK, CMP, and urine analysis General Management Framework: MH crisis is a medical emergency requiring rapid intervention Dantrolene Na administration, supportive measures, and continuous monitoring in PICU Utilization of Malignant Hyperthermia carts and involvement of specialized hotlines Clinical Pearls and Pitfalls: Early recognition is crucial. Proper administration of Dantrolene Na without delay Extended monitoring period in PICU to ensure stability Conclusion: Importance of recognizing and managing MH crisis Feedback, subscription, and reviews encouraged Website picudoconcall.org for additional resources References: Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter Malignant Hyperthermia Association of the United States What 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.…

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Approach to Calcium Channel Blocker Overdose 26:01

1 year ago26:01

26:01

Show Introduction Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradip Kamat and Dr. Rahul Damania Case Presentation A 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-up History 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 Studies Pulse oximetry, continuous cardiac monitoring, ECG, capillary glucose measurement. Serum acetaminophen, ASA levels Consider extended toxicology screen. Differentiating CCB vs. Beta-Blocker Overdose ECG findings: PR interval prolongation and Bradydysrhythmia suggest CCB poisoning. Hyperglycemia in non-diabetic patients may indicate CCB overdose Approach to CCB Overdose Initial resuscitation and stabilization ABC approach Consult Poison Control Center Empiric use of glucagon, IV fluids, and vasopressors Consideration of orogastric lavage and activated charcoal Specific Medical Therapies Vasopressors: norepinephrine/epinephrine infusion Atropine for bradycardia IV calcium salts to overcome cardiovascular effects High-dose insulin and dextrose for myocardial function Investigational therapies: methylene blue, lipid emulsion Procedures Transvenous pacemaker placement if needed ECMO in refractory hypotension Key Takeaways Hypotension 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! References Fuhrman & 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.…

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Acute Bronchiolitis in the PICU 29:57

2 years ago29:57

29:57

Hosts: Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine Rahul Damania, Cleveland Clinic Children’s Hospital Introduction Today, 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 Summary An 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 Points Etiology & 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. Conclusion RSV 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! References Rogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823 Reference 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: 35785792 Reference 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.…

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The Modified Bohr Equation 18:09

2 years ago18:09

18:09

Hosts: Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine Rahul Damania, Cleveland Clinic Children’s Hospital Case 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 Space Defined 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 Ventilation Enhance Perfusion Consider 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.…

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PICU Doc On Call

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Retropharyngeal Abscess in the PICU 20:42

2 years ago20:42

20:42

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 Presentation Patient: 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 Elements Rapid Symptom Onset Neck Swelling & Drooling Limited Neck Mobility Problem Representation A 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 RPA Anatomy of retropharyngeal space Rapid communication of infections via lymph nodes Infection sources: dental issues, trauma, localized infections (e.g., otitis, URI) Dangers of RPA Airway compromise and posterior mediastinitis Progression from cellulitis to abscess Microbial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulare Clinical Manifestations Seen predominantly in children aged 3-4 years Non-specific symptoms in the acute setting Pronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress Diagnostic Workup Thorough history and physical examination CT scan with contrast as the gold standard Blood culture, CRP, and procalcitonin for infection severity Clinical Pearls Limited neck mobility is the most specific physical exam finding Younger age and signs of airway obstruction indicate a complicated course Management of RPA Antibiotic therapy: Up to 50% cases can be treated with IV antibiotics Surgical drainage may be needed if no improvement or persistent respiratory distress Duration of therapy: 10 to 14 days Controversial use of steroids for reducing airway swelling Complications of RPA Upper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath rupture Mediastinitis: severe inflammation, infection of mediastinal tissues Patient's Clinical Course Respiratory viral panel: RSV, adenovirus, rhino/enterovirus Intubation due to worsening respiratory distress Incision and drainage (I&D) by ENT Cultures grew MRSA Extubation after air leak detection; discharged on oral Clindamycin Clinical Takeaways Maintain a low threshold for suspecting RPA Initiate broad-spectrum antibiotics early Prioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxia Consider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patients Conclusion Emphasize the critical nature of RPA in children and the importance of early intervention. Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications. References Villanueva-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.…

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Pediatric Neurocritical Care | Unveiling the Brain Death Guidelines 41:43

2 years ago41:43

41:43

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 brainstem Important considerations before BD/DNC determination: No evaluation in infants < 37 weeks corrected gestational age Absence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC 2. 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 processes Observation periods based on age and type of brain injury Maintaining core body temperature before evaluation 4. Blood Pressure Management: Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors. Specific blood pressure targets for different ECMO support types 5. Medication Considerations: Excluding medications affecting CNS function before BD/DNC evaluation Recommendations for drug level monitoring and metabolic derangement exclusion 6. Performing the BD/DNC Neurologic Examination: Two independent examinations by different clinicians with a minimum 12-hour interval Central components including assessing irreversible coma and brainstem reflexes 7. Apnea Testing: Two apnea tests after each neurologic examination Procedures, 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 tests 9. 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 process 10. Public Trust in BD/DNC: Building trust through education, transparency, public involvement, and ethical considerations Continuous improvement, professional collaboration, and legal frameworks We 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.0000000000207740 Pediatric Neurocritical Care Educational Series - Lecture_ Brain Death 2023 Guidelines…

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Physiology of High-Flow Nasal Cannula (HFNC) 19:08

2 years ago19:08

19:08

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 Presentation A 2-year-old girl with acute respiratory distress due to RSV infection Presented with increased work of breathing, wheezing, and no fever Started on High Flow Nasal Cannula (HFNC) therapy in the PICU Key Elements: Prodrome of URI symptoms Increased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry) HFNC improved the work of breathing and oxygen saturation Physiology of HFNC Mechanisms of Action Washout 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 irritation More comfortable and effective compared to cold, dry air delivery Debunking the PEEP Theory (Positive End-Expiratory Pressure) HFNC generates minimal and variable PEEP. Amount of PEEP depends on factors like flow rate and cannula size Not as high or consistent as other respiratory support devices Research Findings A 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 Effects HR, 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. Conclusion HFNC is a valuable tool in pediatric care for alleviating respiratory distress. Not a one-size-fits-all solution; vigilant monitoring and reassessment are crucial Recognizing 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 Damania References Miller 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.…

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A Case of Rheumatic Fever in the PICU 23:11

2 years ago23:11

23:11

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 Fever Approach to Diagnosis and Investigations Management and Prevention Pathophysiology 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.…

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PICU Doc On Call

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Submersion injury 23:47

2 years ago23:47

23:47

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 submersion Abnormal electrolytes (hyponatremia) Neurological insult requiring ongoing monitoring Definitions 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 .…

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PICU Doc On Call

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75: Lactic Acidosis in the PICU 28:07

2 years ago28:07

28:07

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 distress Recent COVID-19 exposure, concerning respiratory symptoms Hypotensive, tachycardic, tachypneic, low pulse oximetry reading Swollen red lips, erythematous rash, hepatomegaly High-flow nasal cannula, resuscitation, epinephrine infusion Initial arterial blood gas: pH 7.22, lactate 4.5 mMol/L Definition of Lactic Acidosis: Hyperlactatemia and lactic acidosis criteria Causes: impaired tissue oxygenation or mitochondrial dysfunction Types of Lactic Acidosis: Type A: Impaired O2 delivery, shock-related Type B: Impaired O2 utilization, toxins, infections Lactate Measurement: Comparability between POCT and central lab analysis Role of lactate measurement in pediatric sepsis Lactic Washout: Rising lactate with re-established oxygen delivery Impaired clearance in microcirculation, liver, kidney Monitoring trends with clinical exams and lab surrogates Bicarbonate Therapy: Role in Type A lactic acidosis Controversy, indications, and potential complications Conclusion: 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 .…

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PICU Doc On Call

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Snakebite Care in the PICU: Beneath the Fangs 20:32

2 years ago20:32

20:32

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 Envenomation Snakes 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 Snakebites Snakebite 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 Envenomation Snake 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 Envenomation The 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 Framework In 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 Considerations Antivenin 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 Pearls A 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.…

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PICU Doc On Call

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Cerebral Sinus Venous Thrombosis | An Infant with Eye Rolling 27:39

2 years ago27:39

27:39

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.…

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PICU Doc On Call

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Hereditary Spherocytosis 21:29

2 years ago21:29

21:29

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.…

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PICU Doc On Call

3 years ago17:04

17:04

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode: Here's the case presented by Rahul: A 21-month-old girl was brought to an OSH ED for somnolence and difficulty breathing, which developed after she accidentally ingested an unknown amount of liquid medicine that was used by her grandfather. Per the mother, the patient’s grandfather was given the liquid medication for the treatment of his opioid addiction. The patient took some unknown amount from the open bottle that was left on the counter by the grandfather. Immediately after ingestion of the medicine, the patient initially became irritable and had some generalized pruritus. The patient subsequently became sleepy followed by difficulty breathing and her lips turned grey. The patient was rushed to an outside hospital ED for evaluation. OSH ED: The patient arrived unresponsive and blue, she was noted to be sleepy and difficult to arouse on arrival, with pinpoint pupils and hypoxic to 88%. , but After receiving Naloxone, however, she became awake and interactive. Her glucose on presentation was 58 mg/dL and Her initial VBG resulted 7.3/49.6/+2. She continued to have intermittent episodes of somnolence without apnea. Poison control called and recommend starting a naloxone infusion; she was also given dextrose bolus. The patient was admitted to the PICU. To summarize key elements from this case, this patient has: Accidental ingestion of an unknown medication Altered mental status Difficulty breathing—with grey lips suggestive of hypoventilation/hypoxia All of which brings up a concern for a toxidrome which is our topic of discussion for today The typical symptoms seen in our patient of pinpoint pupils, respiratory depression, and a decreased level of consciousness is known as the “opioid overdose triad” Given the history of opioid addiction in the grandfather, the liquid medicine given to him is most likely methadone.In fact, in this case, the mother brought the bottle of medicine, which was subsequently confirmed to be prescription methadone given to prevent opioid withdrawal in the grandfather. To dive deeper into this episode, let’s start with a multiple choice question: Which of the following opioids carries the greatest risk of QTc prolongation? A. Methadone B. Morphine C. Fentanyl D. Dilaudid The correct answer is methadone. Methadone prolongs QT interval due to its interactions with the cardiac potassium channel (KCNH2) and increases the risk for Torsades in a dose-dependent manner. Besides the effect on cardiac repolarization, methadone is also associated with the development of bradycardia mediated via its anticholinesterase properties and through its action as a calcium channel antagonist. Hypokalemia, hypocalcemia, hypomagnesemia, and concomitant use of other drugs belonging to the family of CYP3A4 system inhibitors such as erythromycin can prolong Qtc. Even in absence of these risk factors, methadone alone can prolong QTc. Thanks for that, I think it is very important to involve your Pediatric Pharmacy team to also help with management as children may be concurrent qt prolonging meds. Rahul, what are some of the pharmacological and clinical features of methadone poisoning? Methadone is a synthetic opioid analgesic made of a racemic mixture of two enantiomers d-methadone and l-methadone. besides its action on mu and kappa receptors, it is also an NMDA receptor antagonist. Due to its long action, methadone is useful as an analgesic and to suppress opioid withdrawal symptoms (hence used for opioid detoxification). Methadone causes constipation, nausea, and vomiting (due to its effect on the chemoreceptor trigger zone). Methadone is well absorbed in the GI tract and can be detected in the plasma within 30 minutes. Although its half-life is 10-18 hours, it can be as high as 25 hours or longer in acute overdoses. In infants and children, a single dose of methadone clinical manifestations can last X 72 hours. The action of methadone is similar to morphine and is primarily on mu, delta, and kappa receptors. It causes drowsiness, respiratory depression, hypotension, and miosis. Cerebral edema has been associated with severe toxicity. Pradip, If you had to work up this patient with methadone ingestion, what would be your diagnostic approach? The classic triad of miosis + respiratory depression and altered mental status with a quick response to Naloxone is diagnostic of opioid poisoning. History of methadone exposure such as in our case above will help clinch the diagnosis. Blood gas, CMP, CBC, Routine and comprehensive drug screens (may help with co-existing toxins). Methadone is usually not tested on a standard drug screen unless specifically requested. Standard urine immunoassays are not able to detect synthetic opioids such as methadone. Methadone ingestion is confirmed when both methadone and methadone metabolite (EDDP) are detected in the urine using high-performance liquid chromatography. However such testing is costly and may take time. The window of methadone detection can range from 3-4 days (rarely up to 14 days). EKG beta-HCG in a female teenager. Always follow your state's poison control recommendations. If our history, physical, and diagnostic investigation led us to methadone ingestion as our diagnosis, what would be your general management of framework? Symptomatic and good supportive PICU care with continuous monitoring of airway patency is the mainstay of treatment in patients who present with mild to moderate methadone toxicity. Charcoal lavage may be tried in mild intoxication in a patient who is not altered. Administer oxygen and assist ventilation for respiratory depression. Naloxone is an opioid antagonist and the antidote of choice, especially in severe toxicity. For children under 5years of age (or < 20Kg): Use 0.1mg/kg. For children > 5 years or over 20Kg 2mg IV every 2-3hours. Naloxone can be administered SC, IM, IV, via the endotracheal tube or even intranasally. Continuous infusion is likely to be necessary for patients who have ingested methadone, as the duration of action of Naloxone is 1 to 2 hours, compared with a duration of action of 24 hours for methadone. The infusion should be started at a rate such that two-thirds of the dose effective for initial reversal is administered each hour, and titrated as needed. Naloxone can potentiate withdrawal in opioid-dependent patients. A side effect of naloxone use can be transient hypertension or pulmonary edema (both rare) and such risks should not preclude its use. Early intubation and ventilation assistance should be performed if respiratory depression does not respond to naloxone. Adequate circulatory support with IV fluids and vasopressors (if needed) should be assured if a patient presents with a circulatory collapse that does not reverse with naloxone. Treat seizures with benzodiazepines, propofol, and/or barbiturates. Monitor for QT prolongation and dysrhythmias. Torsades de pointes Correct electrolyte abnormalities. Intravenous magnesium and overdrive pacing as indicated Very rarely ECMO may be required if life-threatening pulmonary edema refractory to standard measures. Pradip, it was found in our case that the patient had significant hypoglycemia. Can you shed some light on this in relation to the methadone overdose? Blood glucose needs to be carefully monitored. Most studies report hypoketotic, hyperinsulinemic, and hypoglycemia after an acute, unintentional methadone exposure, especially with high doses. Possible etiologies of hypoglycemia may include promotion of pancreatic insulin release, suppression of counter-regulatory mechanisms such as glucagon, epinephrine, and sympathoadrenal responses to hypoglycemia as well as impairment of glycogenolysis and gluconeogenesis. As we wrap up today, let’s also go through the criteria for observation, admission, and ICU-level care. All patients who develop CNS or respiratory depression should be admitted for observation (for at least 24 hours) even after adequate response to naloxone therapy. Patients who require intubation or a naloxone infusion will obviously require an intensive care unit admission. Patients should not be discharged until they have remained awake and alert for 4 to 6 hours after the Naloxone infusion has been discontinued. Patients with mild toxicity who do not require Naloxone should be observed for at least 8 hours. Please also work closely with toxicologists and local poison control as well! Pradip, what are some clinical pearls or pitfalls to avoid? Remember the triad of pinpoint pupils+respiratory depression+altered mental status is highly suggestive of opioid poisoning Naloxone is the drug of choice in opioid overdose, an infusion may be needed for longer-acting agents such as methadone. In addition to Naloxone, close attention to airway patency and maintenance of respiration is required in the PICU So today we learned about the management of methadone ingestion in a toddler. Liquid methadone is highly toxic and even as one little teaspoon can lead to fatality in a toddler. Besides appropriate storage of methadone to prevent accidental ingestion by toddlers, early recognition of the classic opioid triad (AMS+Pinpoint pupils+respiratory depression) and prompt medical intervention can be life-saving. This concludes our episode on Methadone ingestion. We hope you found value in our short, case-based podcast. We 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 myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you! References: Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 126 Toxidromes and Their treatment by Prashant Joshi. Page 1497. Reference 1: Sachdeva DK, Stadnyk JM. Are one or two dangerous? Opioid exposure in toddlers. J Emerg Med. 2005 Jul;29(1):77-84. doi: 10.1016/j.jemermed.2004.12.015. PMID: 15961014. Reference 2: Boyer EW, McCance-Katz EF, Marcus S. Methadone and buprenorphine toxicity in children. Am J Addict. 2010 Jan-Feb;19(1):89-95. doi: 10.1111/j.1521-0391.2009.00002.x. PMID: 20132125. Reference 3: Glatstein M, Finkelstein Y, Scolnik D. Accidental methadone ingestion in an infant: case report and review of the literature. Pediatr Emerg Care. 2009 Feb;25(2):109-11. doi: 10.1097/PEC.0b013e318196faff. PMID: 19225381.…

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