PICU Doc On Call

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

Welcome to another insightful episode of PICU on Call, a podcast dedicated to current and aspiring intensivists. In this episode, our hosts, Dr. Pradip Kamat, Dr. Rahul Damania, and their colleague, Dr. Jordan Dent, delve into the complexities of managing pneumonia in pediatric patients. The discussion is anchored around a clinical case involving a 10-year-old girl presenting with difficulty breathing and a fever, suggestive of pneumonia. We will break down the key themes and insights from the case, providing a comprehensive guide to understanding and managing pediatric pneumonia.Case PresentationThe episode begins with a detailed case presentation:Patient: 10-year-old girl, 28-week preemie with chronic lung disease.Symptoms: Progressive respiratory distress over eight days, worsening cough, increased work of breathing, hypoxemia (oxygen saturation in the low 80s despite supplemental oxygen).Findings: Chest X-ray reveals bilateral lower lobe infiltrates and a left-sided pleural effusion. Lab results show elevated CRP and a positive respiratory PCR for a bacterial pathogen.This case sets the stage for an in-depth discussion on the various aspects of pediatric pneumoRisk Factors for PneumoniaUnderstanding the risk factors for pneumonia is crucial for early identification and prevention. These risk factors can be categorized into three main groups:Host FactorsIncomplete Immunization Status: Children who are not fully vaccinated are at higher riskYoung Age: Infants and young children have immature immune systems, making them more susceptibleLower Socioeconomic Status: Limited access to healthcare and poor living conditions can increase riskEnvironmental FactorsExposure to Tobacco Smoke: Secondhand smoke can damage the respiratory tract and impair immune functionSeasonal Variations: Pneumonia cases peak during fall and winter due to increased circulation of respiratory virusesContact with Other Children: Daycare settings and schools can facilitate the spread of infectionsHealthcare-Associated FactorsProlonged Mechanical Ventilation: Increases the risk of ventilator-associated pneumonia (VAP)Nasogastric Tube Placement: Can introduce pathogens into the respiratory tract.Neuromuscular Blockade: Impairs the ability to clear secretionsInadequate Humidification: Dry air can damage the respiratory mucosaPathogenesis of PneumoniaPneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid accumulation and white blood cell infiltration in the alveoli, resulting in:Decreased Lung Compliance: The lungs become stiffer and harder to expand.Increased Airway Resistance: Narrowing of the airways makes breathing more difficult.Ventilation-Perfusion (V/Q) Mismatch: Impaired gas exchange leads to hypoxia and tachypnea.Etiology by Age GroupThe causative pathogens of pneumonia vary by age group:Neonates: Group B Streptococcus, E. coli, Listeria, KlebsiellaChildren Under 5: Viral causes (50% of cases) such as RSV, human metapneumovirus, and influenza, with bacterial causes like Streptococcus pneumoniae and Haemophilus influenzaeOlder Children and Teens: Mycoplasma pneumonia, Chlamydia pneumonia, and Streptococcus pneumoniaeClassification of PneumoniaPneumonia can be classified based on the acquisition setting:Community-Acquired Pneumonia (CAP): Occurs in patients not hospitalized in the past monthHospital-Acquired Pneumonia (HAP): Develops after 48 hours of...

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: a...

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: a...

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.li...

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.