In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat discuss the resurgence of measles in the United States. They explore the virus's pathophysiology, clinical features, diagnostic methods, treatment options, and complications. They emphasize the critical role of vaccination in preventing measles outbreaks and address the historical context and public health challenges related to vaccine hesitancy. The speakers highlight the severe complications of measles, especially in immunocompromised patients, and advocate for robust vaccination efforts to protect vulnerable populations and prevent the spread of this preventable disease. Tune in to hear more!

Show Highlights:

• Resurgence of measles in the United States
• Historical context of measles outbreaks and vaccination impact
• Current statistics and recent cases of measles
• Pathophysiology of the measles virus
• Clinical features and progression of measles infection
• Diagnostic approaches for confirming measles
• Differential diagnosis considerations for fever and rash
• Treatment options and the role of vaccination
• Complications associated with measles, including severe outcomes
• Public health challenges related to vaccine hesitancy and advocacy for immunization

Resources:

CDC Measles Info Page

WHO Measles Global Surveillance

References:

Fuhrman & Zimmerman. Textbook of Pediatric Critical Care, Ch. 52

Long S et al. Principles and Practice of Pediatric Infectious Diseases, Ch. 227

Moss WJ. Measles. Lancet. 2017;390(10111):2490-2502

Paules CI, Marston HD, Fauci AS. NEJM. 2019;380(23):2185-2187

In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat chat about a challenging case involving a 15-year-old girl dealing with acute myocarditis and worsening respiratory failure. They explore the intricate dance between the heart and lungs, especially how positive pressure ventilation can affect heart function. They cover important topics like cardiac output, preload, and afterload, and discuss the delicate balance needed to manage myocarditis effectively. The episode offers practical tips for optimizing care for critically ill children, underscoring the importance of personalized treatment plans and teamwork in pediatric critical care. Tune in!

Show Highlights:

• Clinical case of a 15-year-old girl with acute myocarditis and respiratory failure
• Importance of understanding cardiopulmonary interactions in pediatric critical care
• Effects of positive pressure ventilation on cardiac function
• Key concepts of cardiac output, preload, and afterload in the context of myocarditis
• Challenges of managing hemodynamic instability in critically ill pediatric patients
• Differences between spontaneous breathing and positive pressure ventilation
• Strategies for optimizing preload and fluid management in myocarditis patients
• Tailoring ventilatory support and transitioning to invasive mechanical ventilation
• Monitoring for arrhythmias and managing myocardial function with inotropic support
• Importance of frequent assessments and collaboration with cardiac ICU teams for patient care

Optimizing Preload:

• Volume depletion is common in patients with hypotension and tachycardia. A careful fluid challenge is important to restore circulatory volume, but fluid overload should be avoided, especially with impaired left ventricular function.

Tailoring Ventilatory Support:

• Adjust BiPAP settings to improve oxygenation without overloading the heart with excessive positive pressures.
• Use the optimal level of PEEP to recruit alveoli while maintaining adequate venous return to the heart.

Supporting Myocardial Function:

• Inotropic support (e.g., milrinone) may be necessary to improve myocardial contractility. Milrinone also provides vasodilation, which can reduce afterload but must be used cautiously due to its potential to lower blood pressure.

Frequent Reassessments:

• Bedside echocardiography and regular monitoring of biomarkers (lactate, BNP) and clinical status are essential for ongoing evaluation.
• In severe cases, advanced therapies like ECMO may be required if the patient’s hemodynamic status continues to deteriorate.

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!

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.

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.