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.

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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.

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:

• 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.

• 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.

• 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.

Pneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid...

In today’s episode, we explore a tragic but educational case involving a 15-year-old girl who suffered severe inhalation injury following a house fire. While heroically rescuing her brother and his friend, she endured prolonged cardiac arrest and severe multi-organ dysfunction. We’ll focus on the pathophysiology, investigation, and management of inhalation injuries, including the critical role of recognizing carbon monoxide and cyanide poisoning in these complex cases.

Key Learning Points:

• Exposure to house fire and prolonged cardiac 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:

1. Upper airway involvement – Thermal injury can cause swelling and obstruction.
2. Chemical pneumonitis – Noxious chemicals like carbon monoxide and cyanide trigger inflammation in the lungs.

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:

1. Early: Dizziness, nausea, vomiting (0–6 hours)
2. Latent: Asymptomatic (6–30 hours)
3. 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...

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:

1. Patient Background: A 15-year-old girl with chronic TPN dependence and a PICC line presented with septic shock and respiratory failure.
2. Initial Presentation: Blood cultures confirmed Gram-negative rod bacteremia. She developed multi-system complications, including acute kidney injury (AKI), thrombocytopenia, and cardiac dysfunction.
3. Management: Broad-spectrum antibiotics, mechanical ventilation, vasoactive agents, and supportive care for MODS.

• 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

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• Twitter: @PICUDocOnCall
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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

• 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

• 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.

• Hydrocephalus Clinical Research Network guidelines.
• Recent studies on ETV outcomes in pediatric populations.

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!

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• Twitter: @PICUDocOnCall
• Email:

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:

1. Early:...

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:

1. 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.

1. 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.

1. 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.