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 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:

1. Basic Imaging: A chest X-ray (CXR) should be obtained, although a normal film doesn't rule out injury.
2. Gold Standard – Bronchoscopy: Direct visualization allows for assessment and removal of bronchial casts.
3. Laboratory Tests: Key labs include CBC, CMP, blood gas, lactate, co-oximetry (to assess CO levels), and toxicology screens.
4. 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:

1. Airway Protection: Intubation is essential for airway security. Signs such as progressive hoarseness, soot around the nose, or face burns should prompt early intervention.
2. Ventilation Strategies: Use low tidal volumes and optimized PEEP for lung protection. In severe cases, consider advanced modalities like APRV, HFOV, or ECMO.
3. 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.

• 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

• 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

• 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

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

• 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

• 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

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

• 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

• 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: [email protected]

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

• 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.

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

• 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.

• 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: [email protected]

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!

Follow Us:

• Twitter: @PICUDocOnCall
• Email: [email protected]

Stay tuned for more cases that challenge and inspire us as PICU clinicians!

• 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

• 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

• 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

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

• 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

• 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

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

• 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

• 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: [email protected]

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.
• Heat Stroke: Life-threatening with core temperature ≥ 104°F, CNS dysfunction, and risk of multiorgan failure.

1. 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.

1. 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.

1. 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:

1. Heat stroke is a medical emergency with a high risk of mortality and long-term complications if not treated promptly.
2. Early recognition, rapid cooling, and a multidisciplinary approach are critical to improving outcomes.
3. Athletes and children engaging in strenuous activities in hot environments should be closely monitored for signs of heat-related illness.

References:

1. Fuhrman, B., & Zimmerman, J. J. (2020). Hyperthermic Injury. In Textbook of Pediatric Critical Care (pp. 1327-1331).
2. Rogers, M. C., et al. (2016). Thermoregulation. In Rogers' Textbook of Pediatric Intensive Care (pp. 546-552).
3. Ishimine, P. (2022). Heat Stroke in Children. UpToDate. Retrieved from www.uptodate.com/contents/heat-stroke-in-children.
4. 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.
5. 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.
6. 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.

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.

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.

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.

• Diagnosis: Pulmonary embolism (PE)
• Hemodynamics: Stable with no right ventricular (RV) strain on echocardiogram
• Management Focus: Anticoagulation and consultation with the hematology/thrombosis team

• 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.

• 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

• 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.

• 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.

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!

1. Fuhrman & Zimmerman - Textbook of Pediatric Critical Care: Thrombosis in Pediatric Critical Care.
2. American Society of Hematology 2018 Guidelines for Management of Venous Thromboembolism: Treatment of Pediatric Venous Thromboembolism.
3. Antithrombotic Therapy in Neonates and Children: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.
4. O’Brien, SH, Stanek JR, Witmer CM, Raffini L. The Continued Rise of Venous Thromboembolism Across US Children’s Hospitals. Pediatrics (2022).

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

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.

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.