PICU Doc On Call podcast

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المحتوى المقدم من Dr. Pradip Kamat, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Rahul Damania. يتم تحميل جميع محتويات البودكاست بما في ذلك الحلقات والرسومات وأوصاف البودكاست وتقديمها مباشرة بواسطة Dr. Pradip Kamat, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Rahul Damania أو شريك منصة البودكاست الخاص بهم. إذا كنت تعتقد أن شخصًا ما يستخدم عملك المحمي بحقوق الطبع والنشر دون إذنك، فيمكنك اتباع العملية الموضحة هنا https://ar.player.fm/legal.

This Is Woman's Work with Nicole Kalil

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QUALIFIED: How Competency Checking and Race Collide at Work with Shari Dunn | 284 33:58

منذ 3 أيام33:58

التشغيل لاحقا

قوائم

إعجاب

احب

33:58

In this episode, we delve into the concept of being "qualified" in the workplace, examining who gets labeled as such, who doesn't, and the underlying reasons. We explore "competency checking"—the practice of scrutinizing individuals' abilities—and how it disproportionately affects underrepresented groups, often going unnoticed or unchallenged. Our discussion aims to redefine qualifications in a fair, equitable, and actionable manner. Our guest, Shari Dunn , is an accomplished journalist, former attorney, news anchor, CEO, university professor, and sought-after speaker. She has been recognized as Executive of the Year and a Woman of Influence, with her work appearing in Fortune Magazine, The Wall Street Journal, Ad Age, and more. Her new book, Qualified: How Competency Checking and Race Collide at Work , unpacks what it truly means to be deserving and capable—and why systemic barriers, not personal deficits, are often the real problem. Her insights challenge the narratives that hold so many of us back and offer practical solutions for building a more equitable future. Together, we can build workplaces and communities that don’t just reflect the world we live in, but the one we want to create. A world where being qualified is about recognizing the talent and potential that’s been overlooked for far too long. It’s not just about getting a seat at the table—it’s about building an entirely new table, one designed with space for all of us. Connect with Our Guest Shari Dunn Website& Book - Qualified: https://thesharidunn.com LI: https://www.linkedin.com/today/author/sharidunn TikTok: https://www.tiktok.com/@thesharidunn Related Podcast Episodes: How To Build Emotionally Mature Leaders with Dr. Christie Smith | 272 Holding It Together: Women As America's Safety Net with Jessica Calarco | 215 How To Defy Expectations with Dr. Sunita Sah | 271 Share the Love: If you found this episode insightful, please share it with a friend, tag us on social media, and leave a review on your favorite podcast platform! 🔗 Subscribe & Review: Apple Podcasts | Spotify | Amazon Music…

PICU Doc On Call

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PICU Doc On Call is the podcast for current and aspiring Intensivists. This podcast will provide protocols that any Critical Care Physician would use to treat common emergencies and the sudden onset of acute symptoms. Brought to you by Emory University School of Medicine, in conjunction with Dr. Rahul Damania and under the supervision of Dr. Pradip Kamat.

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#Science #Fitness #Biology #Podcasting Education #Medicine #Dr. Pradip Kamat, Dr. Rahul Damania #Dr. Pradip Kamat #Dr. Rahul Damania

PICU Doc On Call

updated منذ عام واحد

منزل السلاسل•Feed

95 حلقات

#Science #Fitness #Biology #Podcasting Education #Medicine #Dr. Pradip Kamat, Dr. Rahul Damania #Dr. Pradip Kamat #Dr. Rahul Damania

Alle afleveringen

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

منذ 7 weeks30:27

30:27

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

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

منذ 8 weeks26:25

26:25

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

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Inhalation Injury in the PICU 22:44

منذ 10 weeks22:44

22:44

In today’s episode, we explore a tragic but educational case involving a 15-year-old girl who suffered severe inhalation injury following a house fire. While heroically rescuing her brother and his friend, she endured prolonged cardiac arrest and severe multi-organ dysfunction. We’ll focus on the pathophysiology, investigation, and management of inhalation injuries, including the critical role of recognizing carbon monoxide and cyanide poisoning in these complex cases. Key Learning Points: Exposure to house fire and prolonged cardiac arrest Signs of inhalation injury and airway compromise Pathophysiology of inhalation injuries and their impact on multiple organ systems Management strategies for inhalation injury, including airway protection and ventilation Differentiating carbon monoxide and cyanide poisoning in pediatric fire victims Case Presentation A 15-year-old previously healthy girl is brought to the Pediatric Intensive Care Unit (PICU) after experiencing cardiac arrest during a house fire. She was found unconscious by firefighters after a heroic rescue attempt where she saved her brother and his friend. Upon arrival at the hospital, she was unresponsive, intubated, and in severe cardiovascular distress with signs of multi-organ dysfunction. Key findings include: Soot deposits and superficial burns on extremities Prolonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR) Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refill Metabolic acidosis, AKI, coagulopathy, transaminitis Severe hypoxic-ischemic encephalopathy on EEG These findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion. Pathophysiology of Inhalation Injury When a patient is exposed to smoke and hot gases during a fire, inhalation injury results in significant damage to the respiratory system. Inhalation injury has three main components: Upper airway involvement – Thermal injury can cause swelling and obstruction. Chemical pneumonitis – Noxious chemicals like carbon monoxide and cyanide trigger inflammation in the lungs. Systemic toxicity – Toxins such as carbon monoxide and cyanide can affect cellular oxygen utilization. The primary damage occurs in the lower respiratory tract, leading to airway edema, mucosal damage, and bronchial cast formation. This process can result in bacterial pneumonia, respiratory failure, and the need for aggressive intervention. Investigating Inhalation Injury A thorough diagnostic approach is essential when assessing patients with suspected inhalation injury: Basic Imaging: A chest X-ray (CXR) should be obtained, although a normal film doesn't rule out injury. Gold Standard – Bronchoscopy: Direct visualization allows for assessment and removal of bronchial casts. Laboratory Tests: Key labs include CBC, CMP, blood gas, lactate, co-oximetry (to assess CO levels), and toxicology screens. CO and Cyanide Testing: Critical for identifying toxic exposure, especially when a patient presents with altered mental status or unexplained metabolic acidosis. Managing Inhalation Injury: A Structured Approach Management revolves around three key pillars: Airway Protection: Intubation is essential for airway security. Signs such as progressive hoarseness, soot around the nose, or face burns should prompt early intervention. Ventilation Strategies: Use low tidal volumes and optimized PEEP for lung protection. In severe cases, consider advanced modalities like APRV, HFOV, or ECMO. Secretion Management: Aggressive pulmonary toilet and medications such as nebulized heparin, tPA, and N-acetylcysteine may help manage airway inflammation and obstructions. Recognizing and Treating Carbon Monoxide (CO) Poisoning In cases of suspected CO poisoning, the key is early recognition and treatment: CO Blood Levels: Measure carboxyhemoglobin levels immediately. Classic Symptoms: Look for the “cherry red” skin color and neurologic symptoms such as confusion or dizziness. First-Line Therapy: Administer 100% oxygen via a non-rebreather mask or endotracheal tube. Hyperbaric Oxygen: While 100% O2 works well, HBO therapy is crucial for preventing delayed neuropsychiatric complications. Fun Fact: CO has a much higher affinity for hemoglobin than oxygen, which leads to a "tissue oxygen famine," even with normal PaO2 levels. Identifying Cyanide Poisoning in Fire Victims Cyanide poisoning can be particularly challenging to diagnose but is crucial in fire victims. Look for: Classic Triad: Metabolic acidosis, elevated venous oxygen saturation, and CNS symptoms (confusion, mydriasis). Late Signs: Cardiovascular collapse, hypotension, and bradycardia. Treatment: Hydroxocobalamin is the first-line antidote (70 mg/kg IV), with the caveat that purple-red urine is a normal side effect. Avoid Nitrites: In burn victims, nitrite-based cyanide kits can worsen CO poisoning by forming methemoglobin. Clinical Tip: Unlike CO poisoning, cyanide poisoning presents with seizures and dilated pupils. Clinical Course of Our Patient The patient’s clinical course was marked by rapid deterioration despite aggressive treatment: Initially managed with high-frequency oscillatory ventilation (HFOV) due to pulmonary hemorrhage Developed severe PARDS, cardiac dysfunction, and multi-organ failure within 12 hours Ultimately, neuroimaging revealed anoxic brain injury with cerebral edema and herniation, leading to brain death This heartbreaking case highlights the importance of early intervention and recognition of inhalation injury in burn victims. Key Takeaways: Act quickly to protect the airway in pediatric fire victims—early intubation can be life-saving. Protect the lungs with proper ventilation strategies and aggressive secretion management. Time is critical when dealing with CO and cyanide poisoning. Immediate recognition and treatment are key to survival. Inhalation injuries can result in rapid multi-organ failure, and management requires a multi-disciplinary approach. Join Us for More Insights We hope this case-based discussion provides valuable insights into the complex management of inhalation injuries in pediatric burn victims. Stay tuned for our next episode and be sure to share your feedback and subscribe to the podcast! For more episodes, visit our website at picudoconcall.org . References: Tapking C., et al. "Burn and Inhalation Injury." Fuhrman & Zimmerman - Textbook of Pediatric Critical Care, Chapter 116, Pages 1347-1362. Bergman, et al. "Burns and Smoke Inhalation." Rogers Textbook of Pediatric Intensive Care, 6th edition, Chapter 33, Pages 484-497. Goh CT, Jacobe S. "Ventilation strategies in pediatric inhalation injury." Paediatr Respir Rev. 2016 Sep;20:3-9. Rodeberg DA, Housinger TA, et al. "Improved ventilatory function in burn patients using volumetric diffusive respiration." J Am Coll Surg. 1994 Nov;179(5):518-522.…

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Approach Toxic Alcohol Ingestion in the PICU 30:06

منذ 11 weeks30:06

30:06

Welcome and Episode Introduction Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital) Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol Case Presentation Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor Initial Labs & Findings: EtOH level: 420 mg/dL. Glucose: 50 mg/dL. Normal CXR and EKG. PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications Key Learning Points from the Case Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions Hypoglycemia and CNS depression are common features of ethanol toxicity in infants Management prioritizes glucose correction, airway support, and close neurological monitoring Deep Dive: Toxic Alcohols in the PICU 1. Ethanol Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia Diagnostic Workup: Focus on CNS and metabolic effects Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen Imaging (head CT) if indicated Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work 2. Methanol Sources: Windshield fluids, cleaning agents, moonshine Clinical Stages: Early: Dizziness, nausea, vomiting (0–6 hours) Latent: Asymptomatic (6–30 hours) Late: Vision disturbances, seizures, respiratory failure (6–72 hours) Key Symptoms: “Snowstorm blindness” from retinal toxicity Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases 3. Ethylene Glycol Sources: Antifreeze, brake fluids, household cleaners Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals) Red Flags: Hypocalcemia, renal failure, QT prolongation Management: Fomepizole, supportive care, and hemodialysis for severe toxicity 4. Propylene Glycol Sources: Medications like lorazepam and pentobarbital Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction Management: Discontinue offending agent, supportive care, and hemodialysis if severe 5. Isopropyl Alcohol Sources: Disinfectants, hand sanitizers Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis Management: Supportive care; fomepizole and ethanol are ineffective Key Laboratory Insights Osmolar Gap Formula: Measured Osmolality - Calculated Osmolality A high osmolar gap indicates unmeasured osmoles like toxic alcohols. Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference Management Pearls Ethanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe cases Methanol: Similar approach with additional focus on preventing blindness Propylene Glycol: Monitor lactate and renal function, discontinue offending medications Isopropyl Alcohol: Supportive care, no acidosis present Mnemonics for Toxic Alcohols MEGA GAP: Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis) Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses Takeaway Messages Early recognition of toxic alcohol ingestion is critical for successful management Differentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentation Engage poison control and social work early in the process Conclusion Pediatric toxic alcohol ingestions are rare but potentially life-threatening Fomepizole is a cornerstone therapy for methanol and ethylene glycol toxicity Supportive care remains essential across all toxic alcohol ingestions Connect with US! Twitter: @PICUDocOnCall Email: contact@picudoconcall.com…

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

منذ 14 weeks32:14

32:14

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

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Acute Hydrocephalus in the PICU 36:16

منذ 15 weeks36:16

36:16

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

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Approach Toxic Alcohol Ingestion in the PICU 30:06

منذ 20 weeks30:06

30:06

Introduction Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital) Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol Case Presentation Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor Initial Labs & Findings: EtOH level: 420 mg/dL. Glucose: 50 mg/dL. Normal CXR and EKG. PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications Key Learning Points from the Case Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions Hypoglycemia and CNS depression are common features of ethanol toxicity in infants Management prioritizes glucose correction, airway support, and close neurological monitoring Deep Dive: Toxic Alcohols in the PICU 1. Ethanol Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia Diagnostic Workup: Focus on CNS and metabolic effects Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen Imaging (head CT) if indicated Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work 2. Methanol Sources: Windshield fluids, cleaning agents, moonshine Clinical Stages: Early: Dizziness, nausea, vomiting (0–6 hours) Latent: Asymptomatic (6–30 hours) Late: Vision disturbances, seizures, respiratory failure (6–72 hours) Key Symptoms: “Snowstorm blindness” from retinal toxicity Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases 3. Ethylene Glycol Sources: Antifreeze, brake fluids, household cleaners Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals) Red Flags: Hypocalcemia, renal failure, QT prolongation Management: Fomepizole, supportive care, and hemodialysis for severe toxicity 4. Propylene Glycol Sources: Medications like lorazepam and pentobarbital Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction Management: Discontinue offending agent, supportive care, and hemodialysis if severe 5. Isopropyl Alcohol Sources: Disinfectants, hand sanitizers Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis Management: Supportive care; fomepizole and ethanol are ineffective Key Laboratory Insights Osmolar Gap Formula: Measured Osmolality - Calculated Osmolality A high osmolar gap indicates unmeasured osmoles like toxic alcohols. Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference Management Pearls Ethanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe cases Methanol: Similar approach with additional focus on preventing blindness Propylene Glycol: Monitor lactate and renal function, discontinue offending medications Isopropyl Alcohol: Supportive care, no acidosis present Mnemonics for Toxic Alcohols MEGA GAP: Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis) Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses Takeaway Messages Early recognition of toxic alcohol ingestion is critical for successful management Differentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentation Engage poison control and social work early in the process Conclusion Pediatric toxic alcohol ingestions are rare but potentially life-threatening Fomepizole is a cornerstone therapy for methanol and ethylene glycol toxicity Supportive care remains essential across all toxic alcohol ingestions Connect with US! Twitter: @PICUDocOnCall Email: contact@picudoconcall.com…

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

منذ 20 weeks29:35

29:35

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

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Hemostatis and Coagulation in the PICU 50:04

منذ 30 weeks50:04

50:04

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

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

منذ 44 weeks20:06

20:06

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

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PICU Management of Malignant Hyperthermia 29:32

منذ 46 weeks29:32

29:32

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

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Approach to Calcium Channel Blocker Overdose 26:01

منذ 1 year26:01

26:01

Show Introduction Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradip Kamat and Dr. Rahul Damania Case Presentation A 14-year-old female with a history of depression and oppositional defiant disorder presents with dizziness, slurring speech, and is pale appearance. The mother noticed symptoms of dizziness, stumbling, and sleepiness. The patient had a prior suicide attempt. Vital signs: HR 50 bpm, BP 75/40, GCS 10. The initial workup reveals hyperglycemia, and she is stabilized and admitted to the PICU. Key Aspects of Ingestion Work-up History and physical exam are crucial. Stratify acute or chronic ingestions. Consider baseline medications and coingestants. Perform initial screening examination to identify immediate measures for stabilization. Diagnostic Studies Pulse oximetry, continuous cardiac monitoring, ECG, capillary glucose measurement. Serum acetaminophen, ASA levels Consider extended toxicology screen. Differentiating CCB vs. Beta-Blocker Overdose ECG findings: PR interval prolongation and Bradydysrhythmia suggest CCB poisoning. Hyperglycemia in non-diabetic patients may indicate CCB overdose Approach to CCB Overdose Initial resuscitation and stabilization ABC approach Consult Poison Control Center Empiric use of glucagon, IV fluids, and vasopressors Consideration of orogastric lavage and activated charcoal Specific Medical Therapies Vasopressors: norepinephrine/epinephrine infusion Atropine for bradycardia IV calcium salts to overcome cardiovascular effects High-dose insulin and dextrose for myocardial function Investigational therapies: methylene blue, lipid emulsion Procedures Transvenous pacemaker placement if needed ECMO in refractory hypotension Key Takeaways Hypotension and bradycardia indicate life-threatening toxidromes. Differential includes CCB, BB, digoxin, clonidine, and CNS depressants. Stepwise approach includes close monitoring of ABCs and specific medical therapies. Thank you for listening to PICU Doc On Call. We would love for you to share your feedback, subscribe, and review our podcast. Visit picudoconcall.org for more information and resources. Stay tuned for our next episode! References Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 125 and 126. St-Onge M et al. Treatment for calcium channel blocker poisoning: a systematic review. DeRoos F. Calcium channel blockers. In: Goldfrank's Toxicologic Emergencies, 8th edition.…

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Acute Bronchiolitis in the PICU 29:57

منذ 1 year29:57

29:57

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

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The Modified Bohr Equation 18:09

منذ 1 year18:09

18:09

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

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Retropharyngeal Abscess in the PICU 20:42

منذ 1 year20:42

20:42

Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches. Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU. Case Presentation Patient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake. Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition. Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA). Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care. Key Elements Rapid Symptom Onset Neck Swelling & Drooling Limited Neck Mobility Problem Representation A previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy. Pathophysiology of RPA Anatomy of retropharyngeal space Rapid communication of infections via lymph nodes Infection sources: dental issues, trauma, localized infections (e.g., otitis, URI) Dangers of RPA Airway compromise and posterior mediastinitis Progression from cellulitis to abscess Microbial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulare Clinical Manifestations Seen predominantly in children aged 3-4 years Non-specific symptoms in the acute setting Pronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress Diagnostic Workup Thorough history and physical examination CT scan with contrast as the gold standard Blood culture, CRP, and procalcitonin for infection severity Clinical Pearls Limited neck mobility is the most specific physical exam finding Younger age and signs of airway obstruction indicate a complicated course Management of RPA Antibiotic therapy: Up to 50% cases can be treated with IV antibiotics Surgical drainage may be needed if no improvement or persistent respiratory distress Duration of therapy: 10 to 14 days Controversial use of steroids for reducing airway swelling Complications of RPA Upper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath rupture Mediastinitis: severe inflammation, infection of mediastinal tissues Patient's Clinical Course Respiratory viral panel: RSV, adenovirus, rhino/enterovirus Intubation due to worsening respiratory distress Incision and drainage (I&D) by ENT Cultures grew MRSA Extubation after air leak detection; discharged on oral Clindamycin Clinical Takeaways Maintain a low threshold for suspecting RPA Initiate broad-spectrum antibiotics early Prioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxia Consider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patients Conclusion Emphasize the critical nature of RPA in children and the importance of early intervention. Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications. References Villanueva-Fernández E, et al. (2022) Role of steroids in conservative treatment of parapharyngeal and retropharyngeal abscess in children. Eur Arch Otorhinolaryngol. Akhavan M. (2021) Ear, Nose, Throat: Beyond Pharyngitis: Retropharyngeal Abscess, Peritonsillar Abscess, Epiglottitis, Bacterial Tracheitis, and Postoperative Tonsillectomy. Emerg Med Clin North Am. Reilly BK, Reilly JS. (2012) Retropharyngeal abscess: diagnosis and treatment update. Infect Disord Drug Targets.…

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