PICU Doc On Call

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

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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: [email protected]

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

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.

Hosts:

• Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
• Rahul Damania, Cleveland Clinic Children’s Hospital

Introduction

Today, we discuss the case of an 8-month-old infant with severe bronchospasm and abnormal blood gas. We'll delve into the epidemiology, pathophysiology, and evidence-based management of acute bronchiolitis.

Case Summary

An 8-month-old infant presented to the ER with decreased alertness following worsening work of breathing, preceded by URI symptoms. The infant was intubated and transferred to the PICU, testing positive for RSV. Initial blood gas showed 6.8/125/-4, and CXR revealed massive hyperinflation. Vitals: HR 180, BP 75/45, SPO2 92% on 100% FIO2, RR 12 (prior to intubation), now around 16 on the ventilator, afebrile.

Discussion Points

• Etiology & Pathogenesis: Bronchiolitis is primarily caused by RSV, with other viruses and bacteria playing a role. RSV bronchiolitis is the most common cause of hospitalization in infants, particularly in winter months. Immuno-pathology involves an unbalanced immune response and can lead to various extra-pulmonary manifestations.
• Diagnosis: Diagnosis is clinical, based on history and examination. Key signs include upper respiratory symptoms followed by lower respiratory distress. Blood gas, chest radiography, and viral testing are generally not recommended unless warranted by severe symptoms or clinical deterioration.
• Management Framework: For patients requiring PICU admission, focus on oxygenation and hydration. High-flow therapy and nasal continuous positive airway pressure (CPAP) can be used. Hydration and feeding support are crucial. Antibiotics, steroids, and bronchodilators are generally not recommended. Mechanical ventilation and ECMO may be necessary in severe cases.
• Immunoprophylaxis & Nosocomial Infection Prevention: Palivizumab and nirsevimab are used for RSV prevention in high-risk infants. Strict infection control measures, including hand hygiene and isolation, are essential to prevent nosocomial infections.

Conclusion

RSV bronchiolitis is a common and potentially severe respiratory illness in infants. Management focuses on supportive care, with a careful balance between oxygenation and hydration. Immunoprophylaxis and infection control are crucial in preventing the spread of the virus.

Thank you for listening to our episode on acute bronchiolitis. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more resources. Stay tuned for our next episode!

References

Rogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823

Reference 1: Dalziel, Stuart R; Haskell, Libby; O'Brien, Sharon; Borland, Meredith L; Plint, Amy C; Babl, Franz E; Oakley, Ed. Bronchiolitis. The Lancet. , 2022, Vol.400(10349), p.392-406. DOI: 10.1016/S0140-6736(22)01016-9; PMID: 35785792

Reference 2: Schroeder AR, Destino LA, Ip W, Vukin E, Brooks R, Stoddard G, Coon ER. Day of Illness and Outcomes in Bronchiolitis Hospitalizations. Pediatrics. 2020 Nov;146(5):e20201537. doi: 10.1542/peds.2020-1537. PMID: 33093138.

Hosts:

• Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
• Rahul Damania, Cleveland Clinic Children’s Hospital

Case Introduction:

• 6-year-old patient admitted to PICU with severe pneumonia complicated by pediatric Acute Respiratory Distress Syndrome (pARDS).
• Presented with respiratory distress, hypoxemia, and significant respiratory acidosis.
• Required intubation and mechanical ventilation.
• Despite initial interventions, condition remained precarious with persistent hypercapnia.

Physiology Concept: Dead Space

• Defined as the volume of air that does not participate in gas exchange.
• Consists of anatomic dead space (large airways) and physiologic dead space (alveoli).
• Physiologic dead space reflects ventilation-perfusion mismatch.

Pathological Dead Space:

• Occurs due to conditions disrupting pulmonary blood flow or ventilation.
• Common in conditions like pulmonary embolism, severe pneumonia, or ARDS.

Clinical Implications:

• Increased dead space fraction (DSF) in PARDS is a prognostic factor linked to severity and mortality.
• Elevated DSF indicates worse lung injury and inefficient gas exchange.
• DSF can be calculated using the formula: DSF = (PaCO2 – PetCO2) / PaCO2.

Practical Management:

• Optimize Mechanical Ventilation
• Enhance Perfusion
• Consider Positioning (e.g., prone positioning)

Summary of Physiology Concepts:

• Bohr equation for physiologic dead space.
• Importance of lung-protective ventilation strategies.
• Monitoring and trending dead space fraction.
• Strategies to improve airway patency and mucociliary clearance.

Connect with us!

• PICU Doc on Call provides concise explanations of critical concepts in pediatric intensive care.
• Feedback, subscriptions, and reviews are encouraged.
• Visit picudoconcall.org for episodes and Doc on Call infographics.
• Hosted by Dr. Pradip Kamat and Dr. Rahul Damania.

Reference:

• Yehya N, Bhalla AK, Thomas NJ, Khemani RG. Alveolar Dead Space Fraction Discriminates Mortality in Pediatric Acute Respiratory Distress Syndrome. Pediatr Crit Care Med. 2016 Feb;17(2):101-9. doi: 10.1097/PCC.0000000000000613. PMID: 26669646; PMCID: PMC4740261.

Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches.

Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU.

• Patient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake.
• Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition.
• Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA).
• Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care.

• Rapid Symptom Onset
• Neck Swelling & Drooling
• Limited Neck Mobility

• A previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy.

• Anatomy of retropharyngeal space
• Rapid communication of infections via lymph nodes
• Infection sources: dental issues, trauma, localized infections (e.g., otitis, URI)

• Airway compromise and posterior mediastinitis
• Progression from cellulitis to abscess
• Microbial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulare

• Seen predominantly in children aged 3-4 years
• Non-specific symptoms in the acute setting
• Pronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress

• Thorough history and physical examination
• CT scan with contrast as the gold standard
• Blood culture, CRP, and procalcitonin for infection severity

• Limited neck mobility is the most specific physical exam finding
• Younger age and signs of airway obstruction indicate a complicated course

• Antibiotic therapy: Up to 50% cases can be treated with IV antibiotics
• Surgical drainage may be needed if no improvement or persistent respiratory distress
• Duration of therapy: 10 to 14 days
• Controversial use of steroids for reducing airway swelling

• Upper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath rupture
• Mediastinitis: severe inflammation, infection of mediastinal tissues

• Respiratory viral panel: RSV, adenovirus, rhino/enterovirus
• Intubation due to worsening respiratory distress
• Incision and drainage (I&D) by ENT
• Cultures grew MRSA
• Extubation after air leak detection; discharged on oral Clindamycin

• Maintain a low threshold for suspecting RPA
• Initiate broad-spectrum antibiotics early
• Prioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxia
• Consider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patients

• Emphasize the critical nature of RPA in children and the importance of early intervention.
• Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications.

• Villanueva-Fernández E, et al. (2022) Role of steroids in conservative treatment of parapharyngeal and retropharyngeal abscess in children. Eur Arch Otorhinolaryngol.
• Akhavan M. (2021) Ear, Nose, Throat: Beyond Pharyngitis: Retropharyngeal Abscess, Peritonsillar Abscess, Epiglottitis, Bacterial Tracheitis, and Postoperative Tonsillectomy. Emerg Med Clin North Am.
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