PICU Doc On Call

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

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

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

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

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

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

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

Welcome to another insightful episode of PICU on Call, a podcast dedicated to current and aspiring intensivists. In this episode, our hosts, Dr. Pradip Kamat, Dr. Rahul Damania, and their colleague, Dr. Jordan Dent, delve into the complexities of managing pneumonia in pediatric patients. The discussion is anchored around a clinical case involving a 10-year-old girl presenting with difficulty breathing and a fever, suggestive of pneumonia. We will break down the key themes and insights from the case, providing a comprehensive guide to understanding and managing pediatric pneumonia.Case PresentationThe episode begins with a detailed case presentation:Patient: 10-year-old girl, 28-week preemie with chronic lung disease.Symptoms: Progressive respiratory distress over eight days, worsening cough, increased work of breathing, hypoxemia (oxygen saturation in the low 80s despite supplemental oxygen).Findings: Chest X-ray reveals bilateral lower lobe infiltrates and a left-sided pleural effusion. Lab results show elevated CRP and a positive respiratory PCR for a bacterial pathogen.This case sets the stage for an in-depth discussion on the various aspects of pediatric pneumoRisk Factors for PneumoniaUnderstanding the risk factors for pneumonia is crucial for early identification and prevention. These risk factors can be categorized into three main groups:Host FactorsIncomplete Immunization Status: Children who are not fully vaccinated are at higher 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 FactorsExposure 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 FactorsProlonged Mechanical Ventilation: Increases the risk of ventilator-associated pneumonia (VAP).Nasogastric Tube Placement: Can introduce pathogens into the respiratory tract.Neuromuscular Blockade: Impairs the ability to clear secretions.Inadequate Humidification: Dry air can damage the respiratory mucosa.Pathogenesis of PneumoniaPneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid...

In today's episode, we explore a tragic but educational case involving a 15-year-old girl who suffered severe inhalation injury following a house fire. While heroically rescuing her brother and his friend, she endured prolonged cardiac arrest and severe multi-organ dysfunction. We'll focus on the pathophysiology, investigation, and management of inhalation injuries, including the critical role of recognizing carbon monoxide and cyanide poisoning in these complex cases.Key Learning Points:Exposure to house fire and prolonged cardiac arrestSigns of inhalation injury and airway compromisePathophysiology of inhalation injuries and their impact on multiple organ systemsManagement strategies for inhalation injury, including airway protection and ventilationDifferentiating carbon monoxide and cyanide poisoning in pediatric fire victimsCase PresentationA 15-year-old previously healthy girl is brought to the Pediatric Intensive Care Unit (PICU) after experiencing cardiac arrest during a house fire. She was found unconscious by firefighters after a heroic rescue attempt where she saved her brother and his friend. Upon arrival at the hospital, she was unresponsive, intubated, and in severe cardiovascular distress with signs of multi-organ dysfunction.Key findings include:Soot deposits and superficial burns on extremitiesProlonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR)Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refillMetabolic acidosis, AKI, coagulopathy, transaminitisSevere hypoxic-ischemic encephalopathy on EEGThese findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion.Pathophysiology of Inhalation InjuryWhen a patient is exposed to smoke and hot gases during a fire, inhalation injury results in significant damage to the respiratory system. Inhalation injury has three main components:Upper airway involvement – Thermal injury can cause swelling and obstruction.Chemical pneumonitis – Noxious chemicals like carbon monoxide and cyanide trigger inflammation in the lungs.

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

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

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

IntroductionHosts: Dr. Pradip Kamat (Children's Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children's Hospital)Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric managementFocus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcoholCase PresentationPatient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodkaKey Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odorInitial Labs & Findings:EtOH level: 420 mg/dL.Glucose: 50 mg/dL.Normal CXR and EKG.PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depressionInitial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complicationsKey Learning Points from the CaseToxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventionsHypoglycemia and CNS depression are common features of ethanol toxicity in infantsManagement prioritizes glucose correction, airway support, and close neurological monitoringDeep Dive: Toxic Alcohols in the PICU1. EthanolTypical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermiaDiagnostic Workup:Focus on CNS and metabolic effectsLabs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screenImaging (head CT) if indicatedManagement: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work2. MethanolSources: Windshield fluids, cleaning agents, moonshineClinical Stages:Early:...

Introduction:Today, Dr. Rahul Damania, Dr. Pradip Kamat, and their guest, Dr. Jordan Dent, discuss a critical case involving a 15-year-old male who collapsed during football practice due to exertional heat stroke. The discussion emphasizes the clinical presentation, risk factors, pathophysiology, and evidence-based management of heat stroke and other heat-related illnesses in pediatric patients. The episode also delves into the role of rapid cooling interventions and long-term care to minimize mortality and morbidity.Case Summary: A 15-year-old male with ADHD collapsed during football practice on a hot, humid day. He presented with:Normotension (BP: 101/67 mmHg)Tachycardia (HR: 157 bpm)Tachypnea (RR: 40 breaths/min)Febrile (Rectal temp: 41.8°C/107.2°F)Dry, hot skin, GCS of 9Lab abnormalities: hyponatremia, hypokalemia, hypoglycemia, elevated creatinine, liver enzymes, lactate, CK, and troponinAfter suffering cardiac arrest and undergoing resuscitation, the patient developed multiorgan dysfunction, including seizures, encephalopathy, and cerebral edema. Despite severe initial complications, the patient demonstrated neurological improvement with left-side hemiparesis before discharge.Key Discussion Points:Etiology and Pathophysiology of Heat Stroke:Heat stroke occurs when the body's thermoregulatory mechanisms fail, leading to dangerous elevations in core body temperature. Exertional heat stroke is common during strenuous physical activity in hot, humid environments.Key physiological breakdowns include inadequate sweating, vasodilation dysfunction, and subsequent cellular damage due to hyperthermia.Risk Factors for Exertional Heat Stroke:Environmental factors: High temperature, humidity, lack of hydration, and breaks.Athlete-related factors: Hypohidrosis, dehydration, medical conditions, and medications (e.g., Adderall).Heat illness is the third leading cause of death in high school athletics, with American football players particularly at risk.Spectrum of Heat-Related Illness:Heat Cramps: Involuntary muscle contractions due to dehydration and electrolyte imbalance.Heat Syncope: Transient loss of consciousness due to heat exposure.Heat Exhaustion: Milder heat illness with core temperature < 104°F, potentially progressing to heat stroke if untreated.

IntroductionWelcome to PICU Doc On Call, a podcast dedicated to current and aspiring pediatric intensivists. I'm Dr. Pradip Kamat from Children's Healthcare of Atlanta/Emory University School of Medicine, and I'm Dr. Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about medical education in the PICU. This podcast focuses on interesting PICU cases and their management in the acute care pediatric setting.Episode OverviewIn today's episode, we are excited to welcome Dr. Karen Zimowski, Assistant Professor of Pediatrics at Emory University School of Medicine and a practicing pediatric hematologist at Children's Healthcare of Atlanta at the Aflac Blood & Cancer Center. Dr. Zimowski specializes in pediatric bleeding and clotting disorders.Case PresentationA 16-year-old female with a complex medical history, including autoimmune thyroiditis and prior cerebral infarcts, was admitted to the PICU with acute chest pain and difficulty breathing. Despite being on low-dose aspirin, her oxygen saturation was 86% on room air. A CT angiography revealed a pulmonary embolism (PE) in the left lower lobe and signs of right heart strain. The patient was hemodynamically stable, and thrombolytic therapy was deferred in favor of anticoagulation. She was placed on BiPAP to improve her respiratory status. Her social history was negative for smoking, illicit drug use, or oral contraceptive use.Key Case PointsDiagnosis: Pulmonary embolism (PE)Hemodynamics: Stable with no right ventricular (RV) strain on echocardiogramManagement Focus: Anticoagulation and consultation with the hematology/thrombosis teamExpert Discussion with Dr. Karen ZimowskiRisk Factors and Epidemiology of VTE in PediatricsPathophysiology: Venous thromboembolism (VTE) in children involves components of Virchow's triad: stasis of blood flow, endothelial injury, and hypercoagulability.Incidence: VTE is rare in the general pediatric population but increases significantly in hospitalized children.Age Distribution: Bimodal peaks in infants and adolescents aged 15-17 years.Risk Factors: Central venous lines, infections, congenital heart disease, cancer, and autoimmune disorders.Clinical Manifestations of DVTSymptoms: Swelling, pain, warmth, and skin discoloration in the affected extremity.Specific Presentations:SVC syndrome from superior vena cava thrombosisAbdominal pain from portal vein thrombosisHematuria from renal vein thrombosisNeurological symptoms...

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

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.Hosts:Dr. Pradip Kamat: Children's Healthcare of Atlanta/Emory University School of MedicineDr. Rahul Damania: Cleveland Clinic Children's HospitalIntroduction:Pediatric Intensive Care Unit (PICU) physicians passionate about medical education in the acute care pediatric settingEpisode focus: A case of a 23-month-old ex-28 week premie presenting with sudden high fever and rapidly rising ETCO2 during surgeryCase Presentation:Presented by Dr. Rahul Damania23-month-old ex-28 week premie intubated during hernia repair surgeryNoticed rapidly rising ETCO2, unprovoked tachycardia, and elevated temperatureTransferred to PICU, exhibiting rigidity, clenched jaw, metabolic acidosis, and elevated lactate.Consideration of Malignant Hyperthermia (MH) crisisKey Points:Elevated temperature, hypercapnia, metabolic acidosis, and unprovoked tachycardia raise concern for MHOrganized discussion on pathophysiology, clinical signs, symptoms, and managementMultiple Choice Question:Diagnosis of MH crisis during scoliosis repairCorrect Answer: D) Sarcoplasmic reticulumDantrolene acts on the sarcoplasmic reticulum to inhibit calcium release, crucial in MH managementClinical Presentation of MH Crisis:Tachycardia, acidosis, muscle stiffness, and hyperthermia are hallmark featuresPotential life-threatening complications underscore the urgency of recognition and treatmentTriggers and Pathophysiology of MH Crisis:Triggered by inhalational agents and depolarizing neuromuscular blocking agentsPathophysiology involves defective Ryanodine receptor leading to uncontrolled calcium releaseDifferential Diagnosis:Includes sepsis, thyroid storm, pheochromocytoma, and neuroleptic malignant syndromeDifferentiation from similar conditions crucial for accurate managementDiagnostic Approach:High clinical suspicionGenetic testing (ryanodine...

Show IntroductionWelcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists.Hosted by Dr. Pradip Kamat and Dr. Rahul DamaniaCase PresentationA 14-year-old female with a history of depression and oppositional defiant disorder presents with dizziness, slurring speech, and is pale appearance.The mother noticed symptoms of dizziness, stumbling, and sleepiness.The patient had a prior suicide attempt.Vital signs: HR 50 bpm, BP 75/40, GCS 10.The initial workup reveals hyperglycemia, and she is stabilized and admitted to the PICU.Key Aspects of Ingestion Work-upHistory and physical exam are crucial.Stratify acute or chronic ingestions.Consider baseline medications and coingestants.Perform initial screening examination to identify immediate measures for stabilization.Diagnostic StudiesPulse oximetry, continuous cardiac monitoring, ECG, capillary glucose measurement.Serum acetaminophen, ASA levelsConsider extended toxicology screen.Differentiating CCB vs. Beta-Blocker OverdoseECG findings: PR interval prolongation and Bradydysrhythmia suggest CCB poisoning.Hyperglycemia in non-diabetic patients may indicate CCB overdoseApproach to CCB OverdoseInitial resuscitation and stabilizationABC approachConsult Poison Control CenterEmpiric use of glucagon, IV fluids, and vasopressorsConsideration of orogastric lavage and activated charcoalSpecific Medical TherapiesVasopressors: norepinephrine/epinephrine infusionAtropine for bradycardiaIV calcium salts to overcome cardiovascular effectsHigh-dose insulin and dextrose for myocardial functionInvestigational therapies: methylene blue, lipid emulsionProceduresTransvenous pacemaker placement if neededECMO in refractory...

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

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

Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches.Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU.Case PresentationPatient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake.Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition.Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA).Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care.Key ElementsRapid Symptom OnsetNeck Swelling & DroolingLimited Neck MobilityProblem RepresentationA previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy.Pathophysiology of RPAAnatomy of retropharyngeal spaceRapid communication of infections via lymph nodesInfection sources: dental issues, trauma, localized infections (e.g., otitis, URI)Dangers of RPAAirway compromise and posterior mediastinitisProgression from cellulitis to abscessMicrobial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulareClinical ManifestationsSeen predominantly in children aged 3-4 yearsNon-specific symptoms in the acute settingPronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress

Today, Dr. Pradip Kamat (Children's Healthcare of Atlanta/Emory University School of Medicine) and Dr. Rahul Damania (Cleveland Clinic Children's Hospital), are excited to speak with Matthew Kirschen, MD, PhD, FAAN, FNCS, regarding a very sensitive topic involving pediatric brain death guidelines published in 'Neurology' in October 2023. Dr. Matthew Kirschen, a leader in pediatric neurocritical care and one of the authors of the new guidelines.Guest Introduction:Dr. Matthew Kirschen is an Assistant Professor of Anesthesiology and Critical Care Medicine, Pediatrics, and Neurology at the Children's Hospital of Philadelphia. A proud alumnus of Brandeis University and Stanford, where he secured both his MD and PhD in neuroscience. Dr. Kirschen's journey includes a residency at Stanford followed by a unique dual fellowship in neurology and pediatric critical care at CHOP. Notably, he's among the rare professionals dual-boarded in both PCCM and Neurology.Dr. Kirschen's tireless endeavors in pediatric neuro-critical care, especially his work on multimodal neuro-monitoring to detect and prevent brain injuries in critically ill children, have garnered significant attention. His expertise also extends to predicting recovery post-severe brain injuries. Pertinent to today's discussion, Dr. Kirschen has displayed a keen interest in the precise diagnosis of brain death and proudly stands as one of the authors of the new guidelines on the topic of Pediatric and Adult Brain death/death by neurologic criteria.Discussion:1. Understanding Brain Death Criteria:Brain Death/Death by Neurologic Criteria (BD/DNC) declared with permanent cessation of all brain functions, including brainstemImportant considerations before BD/DNC determination:No evaluation in infants < 37 weeks corrected gestational ageAbsence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC2. Who Can Perform BD/DNC Evaluations:Attending clinicians must be credentialed and trained in BD/DNC evaluation.Two attending clinicians are needed for evaluation, with exceptions for advanced practice providers.3. Prerequisites for BD/DNC Determination:Importance of identifying the etiology of BD/DNC to avoid reversible processesObservation periods based on age and type of brain injuryMaintaining core body temperature before evaluation4. Blood Pressure Management:Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors.Specific blood pressure targets for different ECMO support types5. Medication Considerations:Excluding...

Today's case presentation involves a 2-year-old girl who was previously healthy and was admitted to the Pediatric Intensive Care Unit (PICU) for acute respiratory distress characterized by increased work of breathing and wheezing.Case PresentationA 2-year-old girl with acute respiratory distress due to RSV infectionPresented with increased work of breathing, wheezing, and no feverStarted on High Flow Nasal Cannula (HFNC) therapy in the PICUKey Elements:Prodrome of URI symptomsIncreased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry)HFNC improved the work of breathing and oxygen saturationPhysiology of HFNCMechanisms of ActionWashout of Nasopharyngeal Dead Space:HFNC clears nasopharyngeal dead space, improving oxygen efficiency.Reduces re-breathing of CO2 from the anatomical dead space.Enhances ventilation efficiency and oxygenation.Reduction in Upper Airway Resistance:HFNC reduces resistance in the upper airway.Delivers rapid gas flow matching or exceeding natural inhalation rate.Eases breathing, especially in neonates and infants with narrow airways.Optimal Conditioning of Gas:HFNC delivers heated and humidified oxygen, matching the body's conditions.Reduces energy expenditure and risk of airway irritationMore comfortable and effective compared to cold, dry air deliveryDebunking the PEEP Theory (Positive End-Expiratory Pressure) HFNC generates minimal and variable PEEP.Amount of PEEP depends on factors like flow rate and cannula sizeNot as high or consistent as other respiratory support devicesResearch FindingsA 2022 CHEST study by Khemani et al. on children with bronchiolitis challenged the conventional understanding of HFNC's mechanisms.HFNC primarily reduces breathing effort but does not consistently increase lung volume (EELV) or tidal volume (VT).Reduction in the pressure rate product (PRP) indicates decreased breathing effort, but not significant alterations in EELV or VT.

Welcome to PICU Doc on Call, a podcast dedicated to current and aspiring intensivists. I'm Pradeep Kumar coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two pediatric ICU physicians passionate about all things medical education in the PICU.Episode Overview: PICU.com call focuses on interesting PICU cases and management in the acute care Pediatric setting. In this episode, we discuss the case of an eight-year-old boy with chest pain, fatigue, and shortness of breath. This case presentation by Rahul highlights the complexity of pediatric care in the PICU.Case Presentation: An eight-year-old boy with up-to-date immunizations and no recent travel or pet exposure presented to the PICU with chief complaints of chest pain, fatigue, and decreased oral intake. His history over the preceding two weeks included a diminishing appetite, episodes of vomiting, and shortness of breath.On examination, he exhibited various cardiac findings, including a hyperdynamic left ventricle, murmurs, and a noted gallop. Abdominal and neurological findings were also concerning. Diagnostic studies revealed an enlarged heart, and sinus tachycardia with left ventricular hypertrophy, and echocardiography confirmed severe valvular and ventricular abnormalities.Laboratory Findings:Laboratory findings included elevated BNP, slightly elevated troponin, and elevated inflammatory markers (ESR and CRP). Strep throat culture was negative, but ASO and anti-DNAse B titers were markedly elevated. MRI confirmed multiple punctate infarctions, likely due to valvular heart disease.Diagnosis: Given the complex multisystem presentation, the child was admitted to the PICU for intensive monitoring and comprehensive management of this multisystem pathology. The working diagnosis is rheumatic fever.The episode is organized into three parts:Pathophysiology of Acute Rheumatic FeverApproach to Diagnosis and InvestigationsManagement and PreventionPathophysiology of Acute Rheumatic Fever: Acute rheumatic fever is an autoimmune disease initiated by a response to group A strep infection, primarily due to molecular mimicry. The streptococcal M protein has structural similarities with host proteins, leading to organ damage, especially in the heart.Epidemiology: Acute rheumatic fever is most prevalent in low to middle-income areas, affecting over 80% of cases. It mainly affects children between 5 to 14 years of age, and overcrowded households and limited healthcare access increase the risk. Globally, rheumatic heart disease affects millions of people annually and claims many lives.Jones Criteria for Diagnosis: The Jones criteria help diagnose acute rheumatic fever. For

Introduction: Welcome to "PQ Doc On Call," a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradeep Kamar from Children's Healthcare of Atlanta, Emory University School of Medicine, and Dr. Rahul Damia from Cleveland Clinic Children's Hospital, both passionate PICU physicians.You will hear:This episode dives into the management of pediatric drowning cases in the PICU, providing valuable insights into assessment, pathophysiology, and practical management strategies.Case Presentation: An 18-month-old girl was admitted to the PICU following a submersion incident in a residential pool. The child's initial unresponsiveness and subsequent clinical deterioration presented challenges for the PICU team, including respiratory distress, electrolyte imbalances, and potential neurological complications.Key Elements from the Case:Severe acute respiratory failure following submersionAbnormal electrolytes (hyponatremia)Neurological insult requiring ongoing monitoringDefinitions and Terminology:Clarification of drowning terminology, emphasizing uniform definitions and avoiding outdated terms like "near drowning." Key terms include primary vs. secondary drowning, saltwater vs. freshwater, intentional vs. non-intentional, and fatal vs. non-fatal drowning incidents.Pathophysiology:Airway Reflexes: Initial reflex laryngospasm triggered by liquid penetration, followed by relaxation due to hypoxia, hypercarbia, and acidosis.Gas Exchange Compromise: Decreased functional residual capacity leading to impaired oxygen uptake and CO2 elimination.Pulmonary Complications: Pulmonary edema, surfactant washout, increased pulmonary vascular resistance, and shunting, impacting oxygen delivery.Management Strategies:Out-of-Hospital: Aggressive on-site CPR and advanced life support are crucial for favorable outcomes. Swift control of hypoxia and acidosis is vital.In-PICU: Ventilation strategies resembling ARDS management (low tidal volume, low plateau pressures, high PEEP). Consider neurological exam, continuous EEG, and neuromuscular blockade if needed.Prognostic Factors: Duration of submersion, time to effective CPR, initial GCS, apnea persistence, pH levels, and neurologic status.Prevention:Empowering prevention through measures like fencing around pools, teaching children to swim, and vigilant adult supervision can significantly reduce the risk of pediatric drowning incidents.Conclusion:"PQ Doc On Call" underscores the importance of timely, effective CPR, swift management...

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

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

In this episode PICUDoc On Call, we discuss the case of a six-month-old ex-preemie with bacterial meningitis who presents with symptoms of cerebral sinus venous thrombosis. We explore the anatomy of the venous distribution in the brain and the clinical syndromes associated with sinus venous thrombosis. Our focus is on the imaging techniques, laboratory tests, and management strategies involved in diagnosing and treating this challenging condition.You will learn:A six-month-old ex-preemie presents with persistent fever, recurrent emesis, and increased somnolence.The patient experiences eye rolling and decreased oxygen saturation, prompting a visit to the emergency department.Physical examination reveals rigidity in all four limbs, and a head CT shows dilated ventricles and encephalomalacia.Lumbar puncture confirms an infection, and the patient is admitted to the hospital.After a 14-day course of antibiotics, the patient's clinical status worsens, leading to intubation and neurosurgery consultation.An MRI confirms cerebral venous sinus thrombosis.Anatomy of Venous Distribution in the Brain:Dural venous sinuses serve as conduits for venous blood return from the brain to the internal jugular veins.The superior sagittal sinus, cortical veins, transverse sinus, sigmoid sinus, and internal jugular vein are key components of the venous drainage system.Clinical Syndromes of Sinus Venous Thrombosis:Symptoms can be related to elevated intracranial pressure or focal brain damage from venous ischemia, infarction, or hemorrhage.Headache, seizures, focal neurologic deficits, and cranial nerve paralysis are common presentations.Cavernous sinus thrombosis can cause periorbital pain, ocular chemos, and paralysis of cranial nerves passing through the sinus.Risk Factors for Cerebral Sinus Venous Thrombosis:Dehydration, CNS or sinus infections, intracranial surgery, autoimmune disorders, genetic syndromes, metabolic syndromes, medications, and genetic thrombophilic states can predispose children to thrombosis.Thorough evaluation for risk factors, including thrombophilia, is recommended in children with cerebral venous thrombosis.Imaging and Laboratory Tests:CT and MRI with contrast-enhanced venography are preferred imaging tools to detect cerebral sinus venous thrombosis.Non-enhanced CT scans and T1/T2-weighted MRI scans show characteristic signs of thrombosis.Lab tests include CBC with differential, DIC panel, comprehensive metabolic panel, ESR, and specific thrombophilia tests.Management...

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

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

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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.In today's episode, we're bringing together some of the best content from our previous podcasts to present a comprehensive clinical case. We're also excited to share with you some of the most highly cited articles from the past year, presented in a practical, case-based format. This episode will offer you valuable insights into the latest research findings while also highlighting the real-world application of this knowledge in a clinical setting.We'll start by presenting an interesting case of a toddler who was transferred to the PICU due to increasing respiratory distress:A 2-year-old male was brought to the emergency department with a chief complaint of increased work of breathing and URI symptoms, including a cough and runny nose. The child had no significant past medical history, was not taking any medications, and had no known allergies. The child was up-to-date on immunizations, and there were no significant sick contacts.The family brought the child to the emergency department after noticing a significant increase in work of breathing, including the use of accessory muscles, nasal flaring, and chest retractions. The initial physical exam revealed tachypnea and decreased breath sounds on the right side. The child's vital signs were concerning for respiratory distress, with a heart rate of 170 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% on room air. Chest X-ray revealed right lower lobe pneumonia.The child was started on supplemental oxygen, and broad-spectrum antibiotics, and trialed with albuterol. Despite initial treatment, the child's respiratory distress worsened, and the decision was made to transfer the child to the PICU and place the patient on HFNC 1.5 L/kg. Upon admission to the PICU, the child's vital signs were still concerning, he was afebrile, with a heart rate of 180 beats per minute, respiratory rate of 60 breaths per minute, and oxygen saturation of 85% on 1.5L/kg HFNC at 75% FiO2. Given the persistent respiratory distress, the decision was made to intubate the child in the PICU for acute hypoxemic respiratory failure. Shortly after intubation, a central line is placed in the R internal jugular vein.To summarize key elements from this case:2-year-old with a prodrome of URI symptomsIs otherwise previously healthy with no significant medical history or allergiesDeveloped respiratory distress and diagnosed with pneumoniaTransferred to PICU, intubated for respiratory failureLet's fast forward in the case and talk about a scenario that frequently arises in the PICU. It's hospital day 2, and the patient's RSV swab is positive, and we're seeing some improvement on the X-ray....

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

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.Today, we are going to discuss the management of the postoperative patient admitted to the PICU. Our discussion will focus on the non-cardiac and non-transplant admission. Our objective in this episode is to create a framework on what areas of care to focus on when you have a patient admitted to the PICU post-operatively. Each surgery and patient is unique; however, we hope that you will garner a few pearls in this discussion so you can be proactive.in your management. Without any further delay, let's get started with today's case:We begin with a 13-year-old child, Alexa, with h/o of a genetic syndrome, who presents today with a history of thoracolumbar kyphoscoliosis. Over the years, Alexa's curvature has progressively worsened, resulting in difficulty breathing and chronic back pain. The decision was made to proceed with a complex spinal surgery, including posterior spinal fusion and instrumentation.In the weeks leading up to the surgery, Alexa underwent a thorough preoperative evaluation, including consultations with specialists and relevant imaging studies. Pulmonary function tests revealed a restrictive lung pattern, while the echocardiogram showed no significant cardiac abnormalities. Preoperative labs, including CBC, electrolytes, and coagulation profile, were within normal limits.During the surgery, Alexa was closely monitored by the anesthesia team, who administered general anesthesia with endotracheal intubation. The surgery was performed by the pediatric neurosurgery and orthopedics, with intra-operative neuromonitoring to assess spinal cord function. The surgical team encountered an unexpected dural tear, which was repaired using sutures and a dural graft. Due to the prolonged surgical time, a temporary intra-operative loss of somatosensory evoked potentials was noted. However, signals were restored after adjusting the patient's position and optimizing blood pressure. The posterior spinal fusion and instrumentation were completed successfully, but the surgery lasted 8 hours. Total intra-operative blood loss was 800 mL, and Alex received 2 units of packed red blood cells and was on NE for a little over half the case before weaning off.Alexa was admitted to the PICU intubated and sedated for postoperative care. The initial assessment showed stable vital signs, with a systolic blood pressure of 100 mmHg, heart rate of 90 bpm, and oxygen saturation of 99% on mechanical ventilation. Postoperative pain was managed with a continuous morphine infusion. The surgical team placed a closed suction drain near the surgical site and a Foley catheter for urinary output monitoring. You are now at the bedside for OR to PICU handoff…To summarize key components from this case:This is a patient with thoracolumbar kyphoscoliosis, underwent complex spinal surgery (posterior spinal fusion and instrumentation) due to progressive curvature, breathing difficulties, and chronic pain.

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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 of a 12-week-old girl old who is limp and seizing presented by Rahul.Chief Complaint: A 12-week-old previously healthy female infant was found limp in her crib and developed generalized tonic-clonic seizures on the way to the hospital.History of Present Illness: The mother returned from work on a Saturday to find her daughter unresponsive in her crib. The infant had been left in the care of her mother's boyfriend, who stated that the daughter had been sleeping all day and had a small spit up. As the patient continued to have low appetite throughout the day and continued to be unresponsive in her crib, mother called EMS to bring her to the emergency department. En route, the patient had tonic movement that did not resolve with intranasal benzodiazepines.ED Course: The infant presents to the ED being masked. Upon arrival at the ED, the infant was in respiratory distress, with a heart rate of 190 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% with bagging. She was intubated for seizure control upon arrival at the ED. Physical examination in the ED revealed bruising on the right neck region but was otherwise unremarkable. A non-contrast head CT showed no acute intracranial abnormalities. The initial diagnostic workup revealed normal CBC, mildly elevated hepatic enzymes, and pancreatic enzymes which were within normal limits. The blood gas showed metabolic acidemia with PCO2 in the 60s.Admission to PICU: Upon admission to the PICU, neurosurgery and trauma teams were consulted. A skeletal survey and ophthalmology consult for a fundoscopic examination were ordered, as there were concerns of non-accidental trauma. Further investigation is underway to determine the cause of the infant's condition.To summarize key elements from this case, this patient has:Patient left with mother's boyfriendInfant found limp and had seizures requiring intubationNeck bruiseAll of these bring up a concern for Non-Accidental Trauma (NAT) the topic of our discussion.Let's start with a short multiple-choice question:Which imaging modality is the most appropriate for establishing a diagnosis of abusive head trauma (AHT) in a 12-week-old infant with an open fontanelle on the exam?A. CT scan of the brain without contrast B. MRI of the brain without contrast C. Skull X-ray D. Doppler ultrasound of the headRahul, the correct answer is A. Though

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 and I'm Rahul Damania, from Cleveland Clinic Children's Hospital. 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:Welcome to our Episode about a 14-year-old male who collapsed on the baseball field.Here's the case presented by Rahul:A 14-year-old male athlete was playing in a high school baseball tournament when he was hit in the chest with a pitched ball. The impact caused him to collapse on the field. Bystander CPR was begun given his unresponsiveness and emergency medical services were immediately called. The patient was transported to the hospital. Upon arrival, he was unresponsive and had no pulse. An electrocardiogram (ECG) showed ventricular fibrillation, and advanced cardiac life support was initiated. After several shocks and cardiac compressions, the patient regained a pulse and was transferred to the pediatric intensive care unit for further evaluation and management.To summarize key elements from this case, this patient has:Been struck by a high-velocity object in the chestSuffered a cardiac arrest, likely due to an arrhythmia from the blunt chest traumaThe presentation brings up a concern for Commotio Cordis, our topic of discussion today!We wanted to create this educational episode in light of the recent medical event experienced by the Buffalo Bill's safety Damar Hamlin. His blunt chest trauma, which led to cardiac arrest, has been postulated to be due to commotio cordis. At the date of this record, we are glad that Damar Hamlin is on the road to recovery.Absolutely, let's dive in more into this topic, Let's start with a short multiple-choice question:The 14-year-old described in our case suffered cardiac arrest after blunt chest trauma. Based on the working diagnosis of comottio cordis, what is the most likely EKG finding which may be seen in this patient?A. Ventricular fibrillationB. Ventricular tachycardiaC. Complete heart blockD. AsystoleThe correct answer is A. In a study published in JAMA (2002; 287(9):1142-1146) which used data from the US Commotio Cordis registry maintained by the Minneapolis Heart Institute Foundation, reported that the most common arrhythmia out of the 128 confirmed cases, 82 of which had EKGs which could be analyzed was ventricular fibrillation. Three patients had Vtach, 3 had Bradyarrhythmia and 1 had complete heart block. Although 40 patients had asystole, this was unlikely to be the initial rhythm after impact. Interestingly, the majority of these rhythms were recorded at the scene.Rahul, What is the definition of Commotio...

Approach to Pediatric Trauma 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 and I'm Rahul Damania, from Cleveland Clinic Children's Hospital. 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.Welcome to our Episode today of a 7 yo M who presents to the PICU after a severe Motor Vehicle Accident.Here is the case presented by RahulA 7-year-old male child is admitted to the PICU after sustaining severe trauma. The patient was brought to the emergency department after a motor vehicle accident that involved an 18-wheeler truck & the family's car; in this severe accident the 7 yo was noted to be restrained however upon impact was ejected from the vehicle. He was unconscious and had multiple injuries, including a laceration on the head and bruising on the chest. The EMS was activated and the patient presented to the ED for acute stabilization. Upon examination, the patient was found to have a Glasgow Coma Scale score of 8, indicating a serious head injury. He had multiple bruises and abrasions on the chest and arms, and his pulse was rapid and weak. The patient was resuscitated with colloid and blood products, intubated, and transferred to the pediatric intensive care unit for further management.Notably, a CT scan of the head showed a skull fracture and a subdural hematoma. A chest X-ray showed multiple rib fractures and bilateral pulmonary opacities with no evidence of pneumothorax. The patient was also found to have a grade 2 liver laceration and a splenic injury. Pelvic x-ray and cardiac FAST exam were unrevealing.To summarize key elements from this case, this patient has:A traumatic brain injuryPulmonary contusions and is at risk for PARDSLiver and spleen injuryAnemiaPertinent negative includes: No pelvic injuries or injuries to great vessels in the chestRahul, let's approach the PICU medical management of this case based on a culmination of various guidelines published in the Pediatric Critical Care literature. Namely, let's use this case to dive deep into guidelines for:Traumatic brain injury (TBI)****Transfusion and Anemia Expertise Initiative (****TAXI)pediatric blunt liver and spleen injury management, are also known as the ATOMAC protocol, as well as general PICU management of acute trauma.As we take the management of this pediatric trauma patient in a systems-based fashion let's first go into the Management of Pediatric Traumatic Brain Injuries, can you start us off with some key management considerations?Based on the March 2019 TBI guidelines published in Pediatric Critical Care Medicine in 2019 (PCCM20(3S):p S1-S82, March 2019)This patient should have an ICP monitor or even an EVD placed for CSF diversion in consultation with the NS and trauma team. A CPP of at least >50 in our 7 yo patient and ICP < 20 mm Hg has been shown to improve outcomes and reduce mortality.Just as a quick review, CPP stands for cerebral perfusion pressure, which is the pressure that maintains blood flow to the brain. The formula for CPP is:CPP = MAP (mean arterial pressure) - ICP (intracranial pressure)Monitoring does not affect outcomes directly; rather the information from monitoring can be used to direct treatment decisions. Treatment informed by data from monitoring may result in better outcomes than treatment informed solely by data from clinical assessment. In short, it is important to have qualitative and quantitative data to optimize your decision-making.As we talked about ICP control is so crucial for

Dear Listeners & Peds ICU community, WE are back on air!Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.I'm Pradip Kamat coming BACK to you from Children's Healthcare of Atlanta/Emory University School of Medicineand 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.As we turn into a new year, we would like to introduce Season 2 of PICU Doc on Call. Yes Pradip, I am super excited for this year & I want to take this moment to thank YOU all, our listener community for making PICU Doc on Call such a success as we share our passion for medical education thru this forum!This episode will give you a quick layout of how we will be organizing each episode of PICU doc on call this year. We will also highlight some tips and tricks on how to best learn from a medical podcast. Our goal in this episode is to provide you a framework on some best practices in medical podcasting and how to retain information from a podcast. Especially for our past & future episodes, we hope you can use this audio learning platform to assist you in applying the knowledge at the bedside when you are working in the acute care setting.Let's get into our first learning objective,Rahul, did you know that learning via podcasts can actually benefit your brain & change the neural chemistry.In fact, a 2016 med ed study published out of UC Berkeley concluded that listening to narrative stories from podcasts can stimulate multiple parts of your brain such as the limbic system and can enhance mood as it modulates dopamine and serotonin driven neural pathways. Think about listening to your favorite true-crime podcast — the suspense actually allows for you to stimulate centers in your medulla that increase the amount of endorphines, dopamine and serotonin that keep you on the edge of your seat.That is so unique, so based on this, I do want to highlight some of the key elements which will make our podcast or any medical podcast you listen to beneficial. These pearls will also help you if you are developing a medical podcast of your own!The first concept here is that many podcasts provide narratives.When it comes to medical podcasts, narratives are in the form of medical cases which allow for you to retain content knowledge as a patient case invokes emotion and this can help you remember information more robustly.When listening to a podcast, you have to use your imagination to picture what's going on. For example, if I painted a 2 yo M with a history of rhinorrhea at home for about a week who now presents to the ED with subcostal & intercostal retractions that then progresses to intubation in the PICU, you not only are envisioning a patient in front of you, but also are shifting your mind across settings. Our brain has to work at the pace of the audio, so hopefully your mind doesn't wander off like it does when reading a textbook page. And because you have to...

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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: Welcome to our Episode a three-year-old girl with altered mental status and acute respiratory failure Here's the case presented by Rahul— A three-year-old presents to the PICU with altered mental status and difficulty breathing. Per the mother, the patient was in the usual state of health on the day prior to admission when the mother left her in the care of her maternal grandmother. When mom arrived home later in the afternoon, mom was unable to wake her and reported that she seemed "stiff". She did not have any abnormal movements or shaking episodes. Mom called 911 and the patient was brought to our ED. No known head trauma, though the patient is in the care of MGM throughout the day. No emesis. Nhttp://emesis.no/ (o) recent sick symptoms. No witnessed ingestion, however, the patient's mother reports that MGM is on multiple medications (Xarelto, zolpidem, Buspar, gabapentin, and acetaminophen) and uses THC-containing products specifically THC gummies. In the ED: The patient had waxing and waning mentation with decreased respiratory effort. GCS was recorded at 7. Arterial blood gas was performed showing an initial pH of 7.26/61/31/0. The patient was intubated for airway protection in the setting of likely ingestion. The patient has no allergies, immunizations are UTD. BP 112/52 (67) | Pulse 106 | Temp 36.2 °C (Tympanic) | Resp (!) 14 | Ht 68.5 cm | Wt 14.2 kg | SpO2 100% | BMI 30.26 kg/m² Physical exam was unremarkable-pupils were 4-5mm and sluggish. There was no rash, no e/o of trauma Initial CMP was normal with AG of 12, CBC was unremarkable, and Respiratory viral panel was negative. Serum toxicology was negative for acetaminophen, salicylates, and alcohol. Basic Urine drug screen was positive for THC To summarize key elements from this case, this patient has: Altered mental status: - waxing and waning with GCS less than 8 suggestive of decreased ventilatory effort pre-intubation impending acute respiratory failure Dilated but reactive pupils All of which brings up a concern for possible ingestion such as THC (but cannot rule out other ingestion) This episode will be organized… Pharmacology of Cannabis Clinical presentation of Cannabis toxicity Workup & management of Cannabis toxicity The Cannabis sativa plant contains over 500 chemical components called cannabinoids, which exert their psychoactive effect on specific receptors in the central nervous system and immune system. The 2 best-described cannabinoids are THC and cannabidiol (CBD)—and are the most commonly used for medical purposes. Patients with intractable epilepsy or chronic cancer pain may be using these drugs. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication. The term cannabis and the common name, marijuana, are often used interchangeably). Rahul, can you shed some light on the pharmacokinetics/pharmacodynamics of cannabis? Cannabis exists in various forms: marijuana (dried, crushed flower heads, and leaves), hashish (resin), and hash oil (concentrated resin extract), which can be smoked, inhaled, or ingested. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication, in contrast to CBD, the main non-psychoactive component of cannabis. The potency of cannabis is usually based on the THC content of the preparation. The THC is lipid soluble and highly protein bound and has a volume of distribution of 2.5 to 3.5...

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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: Welcome to our Episode: A Somnolent Toddler. Here's the case: A 2 yo M presents to the PICU after being found increasingly sleepy throughout the day. The toddler is otherwise previously healthy and was noted to be in his normal state of health prior to today. The mother dropped the toddler off at his Grandmother's home early this morning. Grandmother states that he was playing throughout the day, and she noticed around lunchtime the toddler stumbles around and acts more sleepy. She states that this was around his nap time so she did not feel it was too out of the ordinary. The toddler 1 hr later was still very sleepy, and the grandmother noticed that the toddler had some shallow breathing. She called mother very concerned as she also found her purse open where she typically keeps her pills. The grandmother has a history of MI and afib as well as hypertension. She is prescribed a multitude of medications. Given the child's increased lethargy, the grandmother presents the patient to the ED. In the ED, the child is noted to be afebrile with HR 55 & RR of 18. His blood pressure is 78/40. On exam he has minimal reactivity to his pupils, he has shallow breathing and laying still on the bed. A POC glucose is 68 mg/dL. Acute resuscitation is begun and the patient presents to the PICU. To summarize key elements from this case, this patient has: Drowsiness Bradycardia Normotension This is in the setting of being at grandma's home and having access to many medications Given the hemodynamic findings and CNS obtundation, this patient's presentation brings up concern for a clonidine or beta-blocker ingestion. This episode will be organized: Beta-Blocker poisoning We will also examine other medications that potentially can be toxic to a toddler (one pill can kill) present in Grandma's purse which include: TCA, CCB, Opioids, oral anti-diabetic agents, digoxin, etc. The presence of a grandparent is a risk factor for unintentional pediatric exposure to pharmaceuticals commonly referred to as the Granny Syndrome. Grandparents' medications account for 10% to 20% of unintentional pediatric intoxications in the United States. To kids, all pills look like candy. Let's start with a multiple choice. An overdose of which of the following medications may mimic the presentation of Metoprolol overdose? A. Verapamil toxicity B. Ketamine toxicity C. Valium toxicity D. Lithium toxicity The correct answer is A, verapamil toxicity. Verapamil is a non DHP CCB. It acts at the level of the SA and AV node similar to Metoprolol, a beta-1-specific antagonist. Both cause bradycardia and AV node block. Valium though a CNS depressant, can cause CV depression as well, however, would have fewer changes on the conduction system compared to a non-DHP CCB.  What is the mechanism of toxicity with beta-blockers? Beta-blockers are competitive inhibitors at beta-adrenergic binding sites, which results in decreased production of intracellular cyclic adenosine monophosphate (cAMP) with a resultant blunting of multiple metabolic and cardiovascular effects of circulating catecholamines. They attenuate the effect of adrenergic catecholamines on the heart Decrease inotropic and chronotropic response. Some drugs like Propranolol can act as Na channel blockers (myocyte membrane stabilizing activity) at high doses resulting in arrhythmias and seizures. Toxic doses of drugs like Sotalol can result in K channel blockade giving rise to prolonged QT and risk for...

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 and 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: Welcome to our Episode of a 4-day-old with jaundice and vomiting. Here's the case presented by Rahul: A full-term 4-day-old boy presents to the ED after recently being discharged from the newborn nursery. Per mom, the patient "look yellow" and was having difficulty with feeding. The mother states that the patient would be increasingly sleepy, and will only latch to the breast for five minutes. The patient has been having decreased wet diapers, and the stool is loose and non-bloody. Mother was concerned today as the child continue to look yellow, especially in the eyes, had four episodes of vomiting, and overall was acting lethargic. The patient presented to the emergency room afebrile, tachypneic, and tachycardic. The patient was noted to have initial serum glucose of 70. As the patient was increasingly dehydrated, laboratory testing was difficult to obtain. The infant was fussy for the caregivers. The patient was resuscitated with 2 x 10 per kilo boluses and responded well. Point of care ultrasound noted normal four-chamber cardiac anatomy and squeeze. Given the instability of the patient, a RAM cannula was initiated, and the patient presented to the PICU. To summarize key elements from this case, this 4-day-old infant has: an acute presentation of jaundice and poor feeding Prominent GI symptoms and dehydration A sepsis-like presentation with hemodynamic instability responsive to fluids All of which brings up a concern for inborn error of metabolism, likely galactosemia. This episode will be organized… Clinical Presentation Laboratory Findings & Biochemistry Management of Galactosemia Rahul, let's start with a short multiple choice question: Of the following biochemical enzymes, which of the following is deficient in classic galactosemia? A. UDP Glucoronyl Transferase B. Aldolase B C. Galactose 1 Uridyl Transferase D. Galactokinase The correct answer is C. Galactose 1 Uridyl Transferase aka GALT. Classic galactosemia is caused by a complete deficiency of galactose-1-phosphate uridyl transferase (GALT). We should contrast this with galactokinase deficiency. These two present quite differently — GALT deficiency presents like our patient with jaundice, vomiting, hepatomegaly, renal dysfunction, and sepsis. Galactokinase deficiency has less of systemic symptoms and these patients similar to GALT deficiency have cataracts that are usually bilateral and resolved with dietary therapy. To go through our other answer choices, remember that Aldolase B is the rate-limiting enzyme in fructose metabolism, thus a deficiency in this enzyme would cause hereditary fructose intolerance. With this lead in question, let's pivot into the biochemistry of galactose and review key lab findings in our patient with galactosemia. Rahul, can you give us a quick summary of how galactose is metabolized in our body? Galactose is a sugar found primarily in human milk and milk products as part of the disaccharide lactose. Lactose is hydrolyzed to glucose and galactose by the intestinal enzyme lactase. The galactose then is converted to glucose for use as an energy source, however it needs a series of reactions: Galactokinase → which catalyzes the rxn galactose to galactose 1 PO4 Our rate limiting enzyme Galactose-1-phosphate uridyl transferase (GALT). GALT helps place a sugar moiety on galactose 1 PO4 to turn it into glucose 1 Phos which can then be utilized in glycolysis or glycogenesis. A complete deficiency in GALT is known as classic...

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...

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. Today we are joined by two wonderful clinical pharmacists — Whitney Moore & Stephanie Yasechko. Whitney is a Clinical Pharmacy Specialist at Children's Healthcare of Atlanta. She is on Twitter at @MoorephinRx. Stephanie is a Pediatric Lung Transplant Clinical Pharmacy Specialist at Cincinnati Children's Hospital Medical Center. We are so excited to have you both on today. My name is Rahul Damania and I am a Pediatric Intensivist at Cleveland Clinic Children's Hospital; Welcome to PICU Doc On Call where we focus on all things MED-ED in the PICU. Our podcast focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: Welcome to our Episode an 18 yo immunocompromised patient with headache & sore throat Here's the case presented by Rahul: An 18-year-old female (40 kg) with PMH significant for fibrolamellar carcinoma of the liver, presents to the ED with headache and sore throat. She is febrile to 38.3, tachycardic, tachypneic, and has a WBC of 27K on her CBC. She is markedly hypotensive with BP on the arrival of 99/65. Cultures were drawn, the patient was given x1 doses of vancomycin and meropenem, and she was transported to the PICU for further workup and management. Due to her progressive hemodynamic instability, increased inflammatory markers, and marked immunocompromised state, the team is considering broadening her anti-microbial coverage. To summarize key elements from this case, this patient has: Fibrolamellar carcinoma of the liver A presentation of headache, sore throat, and hemodynamic instability with concern for sepsis A current regimen of just antibacterials, which brings up the consideration of adding anti-fungal coverage in her clinically ill state. Our episode today will be covering anti-fungal agents in the PICU. We will review general mycology, understand different classes of antifungals, and highlight practical clinical pearls in the acute care setting. As mentioned, this patient has risk factors for an immunocompromised state due to her underlying liver condition. As we dive deeper into antifungals, Whitney, can you please give us an overview of common fungal pathogens in the PICU? Before we discuss the major drugs, it's important that we take some time to briefly review the most common fungi we encounter clinically since it's hard to choose the right agent when you don't know exactly what you are treating. Clinically, Candida is probably the most common fungal pathogen encountered, especially in warm, moist environments. It is important to determine what type of species is growing. The three major species known to cause infection are C. albicans, C. glabrata, and C. krusei, but it is important to differentiate these species when identified since they have different resistance patterns. Cryptococcus is another type of fungus that is known to cause meningitis or fungemia, especially in immunocompromised or cirrhotic patients. Both Candida and Cryptococcus are classified as yeast on Gram stain. Treating cryptococcus will require the use of an agent that has good penetration to the CNS. Endemic fungi known as Coccidia, Histoplasma, and Blastomyces are known to cause disseminated infections in immunocompromised hosts; however, each fungus is associated with a different geographic region in the United States. With any type of infection, it is always very important to consider your patients' exposures and recent travel history. And finally, there are two major molds that have the potential to be pathogenic. The first is Aspergillus which is identified via hyphae (tall filaments) on Gram stain well known to cause invasive pulmonary infections in the immunocompromised, specifically those who are neutropenic and/or received a lung transplant.

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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: Welcome to our Episode about a 4-year-old girl with a chief complaint of headache and vomiting Here's the case: A 4-year-old presents to the PICU with headaches + vomiting and abnormal CT scan findings. The patient presented to the ED with h/o abdominal pain X 5 days with nonbilious, non-bloody emesis. Initial CBC, UA was normal. The patient was given some pain meds and IV fluids. Further history revealed that the patient has been having severe headaches for the last 5 days and had emesis secondary to the headaches resulting in generalized, non-specific abdominal pain. No h/o of trauma or seizures, no h/o of fever or diarrhea, no h/o toxic ingestions h/o recent travel, exposure to sick contacts, COVID test negative. No family h/o migraines, her immunizations are UTD. Besides the normal UA and CBC, her CMP was also normal. A CT scan of the head revealed right frontoparietal mass with moderate surrounding edema, 6 mm leftward midline shift, diffuse sulcal narrowing, and right cisternal narrowing. Imaging of the abdomen (US and CT w/ contrast) was unremarkable. An MRI done revealed: Right parietal diffusion restricting lesion, most compatible with abscess. Moderate surrounding vasogenic edema. Given her abdominal pain- Abdominal KUB as well as contrast CT scan of abdomen and pelvis were performed and revealed no abdominopelvic pathology. In the ED her vitals were normal and the patient was afebrile. On her PE: the patient appeared sleepy but woke up and answered questions appropriately. No focal deficits, PERRL, normal tone and strength. The rest of her physical exam was completely normal. She now is transferred to the PICU for serial neurological exams. To summarize key elements from this case, this patient has: Headache with altered mental status No focal deficits Vomiting surprisingly no fever Imaging showing right frontoparietal mass. All of which brings up a concern for brain abscess This episode will be organized… Epidemiology and pathogenesis Diagnosis Management Rahul, can you inform our listeners about the epidemiology of brain abscesses? Only about 25% of brain abscesses occur in children. Incidence in developed countries is about 1-2% while in developing countries it's about 8%. Peak incidence in children is seen between the ages of 4-7 years and is more common in males. Brain abscess in the neonatal age group is rare but are associated with a higher risk of complications and mortality. Risk factors for brain abscess include Otologic infections (ear, sinus, and dental infections), Congenital heart disease (30% of patients with BA have an underlying heart defect) with intra-cardiac or intrapulmonary shunting (pulmonary AV malformations in hemorrhagic telangiectasis), immunodeficiencies (solid organ transplantation, HIV, etc), prolonged steroid use, diabetes, alcoholism neurosurgical procedures, trauma. Other rare causes can be airway foreign bodies, congenital dermal sinuses, and esophageal procedures (such as dilatations). Brain abscess typically begins with a localized area of cerebritis which evolves through various stages (typically 10-14 days) to develop into an encapsulated collection of purulent material with peripheral gliosis or fibrosis. 40-50% of the spread of infection is via a contiguous site of infection such as otitis, sinusitis or mastoiditis or from head trauma or neurosurgical procedure. 30-40% is spread through the hematogenous route from endocarditis, pulmonary infections, or dental abscess. 90% of brain...

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 and 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: Welcome to our Episode an 18 -year old with sore throat, and unilateral L-sided neck pain for ~2 weeks. Here's the case presented by Rahul: An 18-year-old female presents to the ED with cough, fever, fatigue, sore throat, and unilateral L-sided neck pain for ~2 weeks. The patient also has been having non-specific chest pain, weight loss, and decreased appetite for ~ 1 month. Patient has no recent travel h/o, no h/o of vaping or illicit drug use, and there were no sick contacts at home. Vitals revealed an HR 105, BP 116/66, Temp 38.3, and respiratory rate 35, She was 65 Kg and SPO2 on 2L NC was 100%. Physical exam was negative except (L) neck tender to palpation. There was no goiter, lymphadenopathy or hepatosplenomegaly. An initial chest x-ray was significant for possible multi-lobar pneumonia versus metastases. A Chest CT revealed multifocal septic emboli in the lungs. Echo did not show any gross vegetation. She has no rash or any trauma to the neck or difficulty swallowing, no oral ulcers, joint pain, or diarrhea. She had no recent dental work or drinking of unpasteurized milk or eating raw fish or meat. She was admitted to the PICU as she had hypotension requiring fluid boluses, and lab works significant for hyponatremia, rhabdomyolysis, worsening AKI, elevated ferritin, and elevated D-dimer. Her serum uric acid was 9.9, LDH = 230 (normal) ,ESR 78 (normal = 20 or less). Her serum lactate and serum troponin and BNP were all normal. Pertinently, US neck revealed an occlusive thrombus in the (L) IJ vein (done so as to avoid contrast in face of AKI), and blood cultures sent. To summarize key elements from this case, this 18-year-old female presents with fever +cough+sore throat Fatigue + Weight loss (L) neck pain Hypotension with abnormal labs including a concerning WBC with (L) shift, anemia, AKI, elevated uric acid, and ESR Chest CT with possible pulmonary emboli US showing occlusion. All of which brings up a concern for possible malignancy or pulmonary emboli from a septic focus in the neck and a possible diagnosis of Lemierre syndrome This episode will be organized… Definition Diagnosis (physical, laboratory) Management Rahul: What is the definition of Lemierre's syndrome? Lemierre's syndrome, also known as post-anginal septicemia or necrobacillosis, is characterized by bacteremia, internal jugular vein thrombophlebitis, and metastatic septic emboli secondary to acute pharyngeal infections. All of which are seen in our above case presentation. Previously called as the forgotten disease as its incidence was decreasing due to the increasing use of antibiotics especially penicillin for URI. However, recently there is an increase in Lemierre's disease cases with decreased use of antibiotics due to antibiotic stewardship. The recent increase in Lemierre disease due to decreased antibiotic use has not been proven and remain controversial. Rahul what are some of the causative organisms of Lemierre syndrome? The most common causative agent of Lemierre's syndrome is Fusobacterium necrophorum, followed by Fusobacterium nucleatum and anaerobic bacteria such as streptococci, staphylococci, and Klebsiella pneumoniae. Rahul: Can you tell our listeners about the pathophysiology of Lemierre's syndrome? Lemierre syndrome can occur in health adults (more common in males in the age group of 14-24 years). Risk factors include immunocompromised patients, organisms, and environmental conditions. Lipopolysaccharides in F. necrophorum have endotoxic...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. Welcome to our Episode a 16-year-old who is coughing up blood. Here's the case: A 16-year-old female with h/o SLE was transferred to the PICU due to hypoxia requiring increasing FIO2. A few hours prior to admission to the PICU patient also started coughing up blood and had difficulty breathing. The patient was admitted to the general pediatric floor 2 days earlier for pneumonia requiring an IV antibiotic and O2 via NC. Once transferred to the PICU, she had a rapid deterioration with progressive hematemesis, worsening respiratory distress, and saturations in the low 70s requiring escalating FIO2. The patient was emergently intubated using ketamine + fentanyl and rocuronium. Chest radiograph showed: Worsening bibasilar alveolar and interstitial airspace disease concerning pulmonary hemorrhage. The patient was initially placed on HFOV Paw 26, FIO2 70%, Hz 8, Dp 70, and later transitioned to airway pressure release ventilation or APRV. The patient was also started on inhaled tranexamic acid or TXA and high-dose pulse steroids. The patient initially continued to have some blood coming out from the ETT with suctioning but secretions became clear in ~24 hours. The mother reported that the patient has never had hematemesis/hemoptysis before, or bleeding from any site in the past. Denied history of frequent respiratory infections or recent URI symptoms. The patient has been vaccinated/boosted x3 vs covid. Her COVID PCR is negative. The mother states that she does not engage in tobacco products or alcohol. A physical exam revealed a well-developed teenage girl laying supine in bed deeply sedated and mechanically ventilated. There was decreased AE at lung bases and coarse breath sounds throughout. There was no hepatosplenomegaly and exams of the heart, abdomen and other systems were normal. There was no skin rash and extremities were well perfused with no clubbing in the fingers. The pulmonary team was consulted and a workup was started for pulmonary hemorrhage. To summarize key elements from this case, this patient has: Autoimmune disease: Systemic lupus erythematosus Respiratory Failure warranting MV 2/2 Pulmonary hemorrhage Her presentation and deterioration bring up a concern for diffuse alveolar hemorrhage our topic of discussion for today. This episode will be organized… Definition Etiology Pathophysiology Diagnosis Management Rahul: How do we define pulmonary hemorrhage (PH): PH is defined as the extravasation of blood into airways and/or lung parenchyma. Blood in the airways produces a diffusion barrier resulting in hypoxemia. Due to the reduction of airway diameter from accumulated blood, there is increased airway resistance and even airway obstruction. Subsequently, ventilation can be impaired leading to increased WOB as well as myocardial work required for O2 delivery. Repeated episodes of PH can result in interstitial fibrosis thus changing lung compliance. Hemoptysis by definition is any bleeding from below the vocal cords. PH can be classified as focal or diffuse. Diffuse is further classified as diffuse immune or diffuse nonimmune. Loss of 10% of a patient's circulating blood volume into the lungs, regardless of age, causes a significant alteration in cardiorespiratory function and should be considered massive. In adults, massive pulmonary hemorrhage is defined as blood loss of 600mL or more in 24 hours. In infants, the involvement of at least two pulmonary lobes by confluent foci of extravasated RBCs constitutes as massive PH. “Enough bleeding to make one nervous is probably massive.” Let's pivot and talk about etiologies. Pradip, What are some of the causes of pulmonary hemorrhage in the PICU? Non-immune diffuse PH is usually seen in patients with congenital heart disease (TAPVR, pulmonary atresia, mitral stenosis, hypoplastic left heart syndrome to name a few) neonates (secondary to sepsis, HIE, BW < 1500...

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 and I'm Rahul Damania from Cleveland Clinic Children's Hospital. 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: In today's episode, we discuss about a 12-year-old male with lethargy after ingestion. Here's the case presented by Rahul: A 12-year-old male is found unresponsive at home. He was previously well and has no relevant past medical history. The mother states that he was recently in an argument with his sister and thought he was going into his room to “have some space.” The mother noticed the patient was in his room for about 1 hour. After coming into the room she noticed him drooling, minimally responsive, and cold to the touch. The patient was noted to be moaning in pain pointing to his abdomen and breathing fast. Dark red vomitus was surrounding the patient. The mother called 911 as she was concerned about his neurological state. With 911 on the way, the mother noticed a set of empty vitamins next to the patient. She noted that these were the iron pills the patient's sister was on for anemia. EMS arrives for acute stabilization, and the patient is brought to the ED. En route, serum glucose was normal. The patient presents to the ED with hypothermia, tachycardia, tachypnea, and hypertension. His GCS is 8, he has poor peripheral perfusion and a diffusely tender abdomen. He continues to have hematemesis and is intubated for airway protection along with declining neurological status. After resuscitation, he presents to the Pediatric ICU. Upon intubation, an arterial blood gas is drawn. His pH is 7.22/34/110/-6 — serum HCO3 is 16, and his AG is elevated. To summarize key elements from this case, this patient has: Lethargy and unresponsiveness after acute ingestion. His hematemesis is most likely related to his acute ingestion. And finally, he has an anion gap metabolic acidosis, as evidenced by his low pH and low HCO3. All of these salient factors bring up the concern for acute iron ingestion! In today's episode, we will not only go through acute management pearls for iron poisoning, but also go back to the fundamentals, and cover ACID BASE disorders. We will break this episode down into giving a broad overview of acid base, build a stepwise approach, and apply our knowledge with integrated cases. We will use a physiologic approach to cover this topic! Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic? Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving. When we conceptualize acid base today, we will focus on pH, HCO3, and CO2. As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient. Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3? Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is attributed to a variation in the bicarbonate concentration. Now that we have some fundamentals down, let's move into definitions. Can you define acidemia and alkalemia and comment on how...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 3rd-year pediatric critical care fellow and we are coming to you from Children's Healthcare of Atlanta Emory University School of Medicine Today's episode is dedicated to the transition between NICU & PICU. We will focus on the ventilation of the ex-premature infant who graduated from NICU care and transitioned to the PICU. I will turn it over to Rahul to start with our patient case. Case: A 4-month-old ex-27 week baby boy is transferred to our PICU after an echo at an outside hospital showed elevated pulmonary pressures. The infant was born via a stat C-section due to maternal complications during pregnancy. His birth weight was 560 g. The patient was intubated shortly after delivery and had a protracted course in the NICU which included a sepsis rule out, increased ventilator settings, and a few weeks on inhaled nitric oxide (iNO). The intubation course was complicated pulmonary hemorrhage on day 1 after intubation. After such an extensive NICU course, thankfully, the infant survived & was sent home on 1/2 LPM NC, diuretics, albuterol, inhaled corticosteroids, Synthroid, multivitamin with iron as well as Vitamin D. The patient was able to tolerate breast milk via NG tube and had a home apnea monitor with pulse oximetry. After about a week's stay at home, the mother noted that the patient's SPO2 was in the low 80s. The mother took the patient to the local hospital, where the patient was started on HFNC which improved his saturations. An echo done at the OSH showed elevated RV pressures (higher than the prior echo). The patient was subsequently transferred to our hospital for further management. At our hospital, the patient presented hypoxemic, tachycardic, and tachypneic. On physical exam: Baby appeared well developed, had a systolic murmur heard throughout the precordium, and there was increased WOB with significant intercostal retraction. There was no hepatosplenomegaly. Due to worsening respiratory distress, and increasing FIO2 requirement despite maximum RAM cannula, the patient was intubated and placed on conventional MV. A blood gas prior to intubation revealed a pH of 7.1/PCO2 of 100. An arterial line and a central venous line were also placed for better access and monitoring. Initial vent settings post intubation PRVC ventilation: TV 32cc, (25/10), 0.7 time, rate 0 (patient sedated/paralyzed). To summarize, What are some of the features in H&P that are concerning for you in this case: Ex-27 week prematurity with a birth weight of 560 gms Prolonged MV in the NICU Home O2 requirement Abnormal echo showing high pulmonary pressures hypercarbia despite the use of RAM cannula As mentioned, our patient was intubated, can you tell us pertinent diagnostics which were obtained? CXR revealed: Hazy airspace opacification in the right upper lung concerning developing pneumonia. Streaky airspace opacity in the left lung base medially may represent atelectasis. I do want to highlight that the intubation of an ex-premie especially with elevated RV pressures is a high-risk scenario, it is best managed by a provider with experience, in a very controlled setting with optimal team dynamics. Adequate preparation to optimize the patient prior to the intubation as well as the knowledge to manage the post intubation cardiopulmonary interactions are essential. I would highly advise you to re-visit our previous podcast on intubation of the high-risk PICU patient by Dr. Heather Viamonte. Like many Peds ICU conditions, the management of the EX-NICU graduate in the PICU is a multidisciplinary team sport. Our patient likely has the diagnosis of Bronchopulmonary Dysplasia or BPD, Pradip, can you comment on the evolving definition of this diagnosis? Let me first define BPD — Clinically, BPD is defined by a requirement of oxygen supplementation either at...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. I am Pradip Kamat. I am Rahul Damania, a current 3rd year pediatric critical care fellow. I am Kate Phelps- a second year pediatric critical care medicine. We come to you from Children's Healthcare of Atlanta Emory University School of Medicine. We are delighted to be joined by guest expert Dr Stephanie Jernigan Assistant Professor of Pediatric-Pediatric nephrology, Medical Director of the Pediatric Dialysis Program at Children's Healthcare of Atlanta. She is the Chief of Medicine and Campus Medical Director at Children's Healthcare of Atlanta, Egleston Campus. Her research interests include chronic kidney disease, and dialysis. She is on twitter @stephaniejern13 I will turn it over to Rahul to start with our patient case... A 3 year old previously healthy male presents with periorbital edema. Patient was initially seen by a pediatrician who prescribed anti-histamines for allergy. After no improvement in the eye swelling after a two week anti-histamine course, the patient was given a short course of steroids, which also did not improve his periorbital edema. The patient progressed to having abdominal distention and was prescribed miralax for constipation. Grandparents subsequently noticed worsening edema in his face, eyes, and feet. The patient subsequently had low urine output, low appetite and lack of energy patient was subsequently brought to an ED and labs were obtained. Grandparents denied any illness prior to presentation, fever, congestion, sore throat, cough, nausea, vomiting, gross hematuria, or diarrhea. In ED patient was noted to be hypertensive (Average systolic 135-highest 159mm HG), tachycardic (HR 130s-140s), breathing ~20-30 times per minute on RA with SpO2 92%. Admission weight was recorded at 16.5Kg. Physical exam showed periorbital edema, edema of ankles, there was mild abdominal distention (no tenderness and no hepatosplenomegaly), heart and lung exams were normal. There were no rashes on extremities. Labs at the time of transfer to the PICU: WBC 10 (62% neutrophils, 26% lymphocytes) Hgb 7.2, Hct 21, Platelets 276. BMP: Na 142/K 8.4/Cl 102/HCO3 19/BUN 173/creatinine 5.8. Serum phosphorus was 10.5, Total Ca 6.4 (ionized Ca= 3.4), Mag 2.0, albumin 2.6, AST/ALT were normal. An urine analysis showed: 1015, ph 7.5, urine protein 300 and rest negative. Chest radiograph revealed small bilateral pleural effusions. After initial stabilization of his hyperkalemia-patient was admitted to the PICU. PTH intact 295 (range 8.5-22pg/mL). Respiratory viral panel including for SARS-COV-2 was negative. C3 and C4 were normal. A nephrotic syndrome/FSGS genetic panel was sent. A renal US showed: bilateral echogenic kidneys and ascites (small volume). Pradip: Dr Phelps what are the salient features of the above case presented? Kate Phelps: This patient has a subacute illness characterized by edema, anemia, and proteinuria. His labs show that he has severe acute kidney injury with significantly elevated BUN and Creatinine, hyperkalemia, hyperphosphatemia, and hypocalemia. Rahul: Dr Jernigan welcome to PICU Doc on Call Podcast. Thanks Kate, Rahul and Pradip for inviting me to your podcast. This is a such a great way to provide education and it is my pleasure to come today to speak about one of my favorite topics, pediatric dialysis. I have no financial disclosures or conflicts of interest and am ready to get started. Rahul: Dr Jernigan as you get that call from the ED and then subsequently from the PCCM docs, as a nephrologists whats going on in your mind ? When I get the call from the outside hospital my first job is to make sure the patient is safe and stable for transfer to a tertiary care center. This includes concern about airway, breathing and level of alertness. From a renal standpoint, I am worried about elevated blood pressure, electrolyte abnormalities, in this case primarily the hyperkalemia, and fluid...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat I'm Rahul Damania, a third-year PICU fellow. I'm Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing gastrointestinal bleeding. Kate: Let's start with a case: A 4-year-old, previously healthy male presents to the emergency room after a large, bloody stool at home. He notably had an episode of dark emesis and an episode of blood-tinged emesis on the day prior. In triage, he is altered and unable to answer questions coherently. Initial vital signs are temperature 36.1 C, RR 24, HR 146, BP 110/54. Point-of-care labs show hemoglobin to be 5.1 with hematocrit 15. His venous blood gas is reassuring against respiratory disease, and he is in no respiratory distress. Further labs are sent and a massive transfusion protocol is initiated before transfer to the PICU. Before arrival in the PICU, he receives two aliquots of RBCs, 1 aliquot of FFP, and 1 aliquot of platelets. Additional labs are sent from the PICU, post-transfusion. His post-transfusion hemoglobin is 8.8. Other labs are notable for normal MCV, elevated total bilirubin to 4.1 (with direct component 3.4), and elevated AST and ALT to 309 and 495 respectively. Rahul: To summarize key elements from this case, this patient has: An undifferentiated gastrointestinal bleed with both hematemesis and hematochezia. He has symptomatic anemia, as evidenced by tachycardia Altered mental status. He is initially stabilized via transfusion of several blood products and liver function labs are shown to be very abnormal — which we will get more into later! PK: Let's get into important parts of the history and physical. Kate, can you tell me what some key history items in this patient are — and what are some areas to make sure to touch on when a patient has a GI bleed? Kate: Yeah! I'd love to. First - in our patient, some important elements are his rather acute onset. His parents mention he has had one day of bleeding symptoms - first with emesis yesterday, with components of old, partially digested blood, as well as some fresh blood. Second, he has a frankly bloody stool at home. Given his clinical instability, history taking was probably limited at first, so it's important to ask follow-up questions and really dig into the case after stabilization! I like to put my questions about gastrointestinal bleeding into buckets based on the questions I need to answer. I need to answer: is this active bleeding or old blood? Is this slow, insidious bleeding or fast, life-threatening bleeding? Is this an upper GI bleed or a lower GI bleed? Bright red blood in emesis tells us that bleeding is active, whereas coffee-ground or dark emesis tells us that, while recent, the blood has been partially digested in the stomach and may not be ongoing. Similarly, melena (dark, tarry stool), tells us blood has come through the colon. While coffee-ground emesis and melena don't rule out an active bleed, they do tell us the bleeding may be slower, as large volume, active bleedy is irritating to the stomach and gastrointestinal tracks and moves through the system quickly. The next question I want to answer is: what is the cause of this bleed? Easy bruising, petechiae and mucosal bleeding may point to a coagulation disorder. Abdominal cramping, frequent stooling, and weight loss may point to inflammatory bowel disease. Past medical history, family history, and a thorough review of systems are key here. Rahul: Yeah, that's great! Let's talk about your question of upper GI vs lower GI bleed. First, a definition: an upper GI bleed is bleeding that occurs above the ligament of Treitz — which is ligamentous tissue that supports the end of the duodenum and beginning of the jejunum at their junction. While not 100% specific, some...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kama and I'm Rahul Damania, a third-year PICU fellow. I'm Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing rhabdomyolysis and associated acute kidney injury in the ICU. Rahul: Here's the case, a 7-year-old female presents to the ED with three days of fever, poor PO, and diffuse myalgia. In the ED, her vital signs are T 39.1C, HR 139, BP 82/44, RR 32. She is pale and diaphoretic, complaining weakly about how much her legs hurt. Her parents note that she has not been peeing very well since yesterday, and when she does pee it is “very concentrated, almost brown.” She's also been spending all her time on the couch and has asked to be carried to the bathroom when she does need to go. An IV is placed by the emergency room team, and she is given a fluid bolus, acetaminophen, and initial labs are drawn (CMP, CBC, RSV/Flu swab) before she is admitted to the PICU. In the PICU, her fever is better and her vitals have improved to T 37.7, HR 119, BP 115/70, and RR 25. Her respiratory swab has just resulted positive for Influenza A. Further labs are sent, including creatine kinase (CK), coagulation studies, and a urinalysis. Labs are notable for K 3.9, Bicarb 22, BUN 15, Cr 0.8, and CK 5768 IU/L. Her urinalysis is notable for 1 WBC, 2 RBC, +3 blood, negative nitrites, and leukocyte esterase. Kate: To summarize key elements from this case, this patient has: Influenza A, as evidenced by her respiratory swab, as well as her clinical prodrome. She has diffuse myalgias, as well as fevers, diaphoresis, and hypotension. Labs are most notable for elevated creatinine and elevated creatine kinase, as well as an abnormal urinalysis. All of which brings up a concern for rhabdomyolysis and myoglobin-induced acute kidney injury. Before we get into this episode — let's create a mental framework for this episode — we will dissect our case by highlighting key H&P components, visit a differential diagnosis, pivot to speaking about pathophysiology, and finally, speak about management! Rahul: Let's transition into some history and physical exam components of this case. The classic presentation of rhabdomyolysis is myalgias, muscle weakness, and tea-colored urine, all of which our patient has. Decreased urinary output can also accompany, a variety of reasons, but most notably if the patient has myoglobin-induced acute kidney injury. In our patient, poor PO is also probably contributing to her decrease in urine output. Red flag signs or symptoms will include anuria, hypotension, and altered mental status (which is rare but may indicate severe acidemia and deterioration) Pradip: As we think about our case, what other disease processes might be in our differential? As we dive in a bit more, we'll come up with ways to distinguish between rhabdo and other things! Viral myositis - inflammation in the muscles in the setting of a viral illness, which can definitely happen with influenza and other common viruses Some other things which may cause reddish-brown urine, including hematuria, hemoglobinuria, porphyria, some specific foods or drugs (like rifampin, beets, food coloring — even ibuprofen) We also have to investigate a bit more to convince ourselves that our patient's AKI is due to rhabdomyolysis, as it could be from dehydration, sepsis, NSAIDS, etc. Kate: Let's dive further into rhabdomyolysis! Rhabdomyolysis affects over 25,000 adults and children every year. While toxins (including prescription drugs, alcohol, and illicit drugs) and trauma are two common causes of rhabdo in adults (and teens), infections, especially viruses, are the most common cause in young children. Influenza, EBV, and CMV are three most commonly reported. What's the pathophysiology of...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode about a 14- year- old female who presented with hypotension after a suicide attempt. Here's the case: A 14 yo F with PMH of depression and oppositional defiant disorder presents with dizziness. Her mother states she was in her normal state of health when on the day of admission she noticed the patient to be dizzy, slurring speech, and pale. The mother became very concerned about the dizziness as the patient was stumbling and a few hours prior to presentation, became increasingly sleepy. The patient does have a history of depression and is controlled on sertraline. Other medications in the home include Metformin, Amlodipine, and Clonidine. The patient denies ingesting any substance. She does have a prior attempt two years prior, after an argument with her mother; however, her mother was able to “stop” her prior to the attempt. She presents to the ER via EMS. Her vital signs are notable for HR 50 bpm with occasional PACs and non-conducted QRS complexes on telemetry; BP of 75/40. A physical exam is notable for AMS and GCS of 10. She is noted to have clear breath sounds, with a cardiac exam notable for slowed and delayed pulses. Initial laboratory work is notable for serum glucose 180 mg/dL and B HCG negative. Initial resuscitation is begun with IV fluids and atropine. Serum acetaminophen and ASA levels are sent and upon stabilization, the patient presents to the PICU for admission. To summarize key elements from this case, this patient has: A history of depression with prior attempt An acute bout of altered mental status Bradycardia, hypotension, and hyperglycemia. All of which brings up a concern for an acute ingestion Let's take a step back and talk about the approach to ingestions in the PICU. What are key aspects to consider in the work-up of these patients? History and physical are key: Stratifying acute or chronic ingestions Baseline prescription medications a patient may be taking or have access to in the household Whether the ingestion involves a single drug or co-ingestants are all first steps in evaluating your patient. In an undifferentiated patient, management is paramount. Initial management is focused on pattern recognition and acute stabilization. A brief initial screening examination should be performed on all patients to identify immediate measures required to stabilize and prevent deterioration of the patient. Assess the airway, vital signs, mental status, pupil size, and skin temperature and moisture. These components of your physical exam should help allude to a toxidrome, and these syndromes are frequently tested on board examinations. Any time a patient has hypotension and bradycardia other drugs that should be considered include beta blockers, digoxin, clonidine, as well as ingestion of barbiturates, opioids, and even benzodiazepines. What are some diagnostic studies you will want to send immediately in a patient with suspected ingestion? Immediate diagnostic studies to be performed include pulse oximetry, continuous cardiac monitoring, an electrocardiogram (ECG), and a capillary glucose measurement (in altered patients). Intravenous (IV) access should be obtained in all cases of serious ingestion. You also want to send beta-hcg and acetaminophen and salicylate levels. an extended toxicology screen may be required on a case-by-case basis. One study found detectable serum acetaminophen concentrations in 9.6 percent of all overdose patients; almost one-third of this subset denied ingestion of acetaminophen. Now that you've focused on ABCs are there more detailed laboratory studies to send in patients with toxidromes? Symptomatic patients and those with an unreliable or unknown history should, at a minimum, undergo...