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.
3. Systemic...

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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