Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat

My name is Rahul Damania, a current 2nd year pediatric critical care fellow. We come to you from Children's Healthcare of Atlanta and the Emory University School of Medicine Atlanta, GA

Today's episode is dedicated to How to Read And Critically Review a Paper not only for the Journal club presentation at the fellows conferences but also for use in your clinical practice as a pediatric intensivist.

We are delighted to be joined by Jocelyn Grunwell, MD, PhD. Dr. Grunwell is an Assistant Professor of Pediatrics-Pediatric Critical Critical Care at Emory University School of Medicine in Atlanta, GA. She is a K-scholar with research interests in mitochondrial dysfunction in critical illness, the airway immune response in pediatric acute respiratory distress syndrome, and near-fatal asthma. She is on twitter @GrunwellJocelyn.

Rahul: Dr Grunwell welcome to picu doc on call. We are delighted to have you on our podcast today to discuss how to read & critically review a manuscript.

Grunwell: Thank you Rahul and Pradip for having me on PICU DOC on Call. I have no conflicts of interest or financial disclosures.

Q1. Rahul: Dr Grunwell: Why should a pediatric intensivist (whether in training or as a faculty) read journal articles?

Grunwell: There are several reasons you might want to read journal articles, and your reading should be tailored to your goals. For example, first, you may want to learn more about a clinical topic to understand how to diagnose, treat or manage a disease. 2nd you may want to find the best evidence for how to treat a patient. 3rd, you may want to learn about the basic biology or mechanisms of a disease. Finally, you may want to identify gaps in a particular field of research to develop a research plan and write a proposal to explore a new research area.

Q2: Dr Grunwell: Where do you find manuscripts relevant to intensivists?

First, I would like to suggest that the learners and faculty in pediatric critical care make a habit of reading at the very least the abstracts in various pediatric journals even if they don't have the time to read an entire article. I generally go to Pediatric Critical Care Medicine, Critical Care Medicine, Critical Care Explorations, Pediatrics, Journal of Pediatrics, NEJM, JAMA Pediatrics, and the family of American Thoracic Society journals on a weekly basis. You can set-up your account so that the table of contents of these journals will be emailed to you. There are apps available, such as ReadQxMD, where you can be alerted to new content of interest to you. You can sign up and follow the accounts of several journals of interest to you on Twitter. There is also a useful, free website sponsored by Dr. Hari Krishnan called picujournalwatch.com in which Dr Krishnan has journal articles well-organized. The website is constantly updated to show the latest manuscripts relevant to our field. You can keep your articles organized by topic in software such as EndNote. Also doing a search on PubMed, OVID etc. can also be helpful to find latest information on a topic. Talking to a medical library scientists is very useful to structure a systematic search for articles or to get a article from a journal that is not available at your institution.

Q3: Dr Grunwell can you define the term level of evidence?

Grunwell: the term level of evidence - or traditional hierarchy of evidence - refers to what degree that information can be trusted based on the study design.

The most common question is related to therapy or an intervention. Levels of therapy are typically represented as a pyramid with systematic reviews or meta-analyses positioned at the top of the pyramid followed by well-designed randomized control...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of a 9 year old girl with worsening seizures in the setting of an electrolyte abnormality.

Here's the case:

A 9 year old girl presents to the ED with increased frequency of seizures, dehydration and listlessness. She has h/o of global developmental delay, congenital hydrocephalous (with VP shunt in place with her last revision 3 years prior, and seizure d/o treated with Leviteracetam. She usually has one or two focal seizures per day but on day of admission she had multiple prolonged seizures which were also generalized tonic clonic in semiology. Per her caregiver, the patient usually eats by mouth and mother typically gives her 3 cups of water daily. There is no history of diarrhea but patient has had 2-3 bouts of non-bloody non-bilous emesis on day of presentation. Looking at her growth chart, the patient has also lost ~ 2KG of her weight in the last 3 months and has had poor follow up with her PCP. In the ED she has a hypovolemic shock picture as she is hypothermic, tachycardic, tachpneic, and hypotensive with appropriate saturations. Blood gas is notable for a mild metabolic acidosis. Patient receives abortive seizure rescue. A head CT showed no increased in hydrocephalus, no mass or hemorrhage and a shunt series confirms patency of her VP shunt. Most pertinently to this case, her serum sodium on her RFP was undetectable at a value of = >200mEQ/dL; this was confirmed by a repeat lab draw and POC value. Other notable findings included an elevated Cr for age, an elevated BUN and a microcytic anemia. Patient was given a NS bolus, had cultures drawn, was started on broad spectrum abx therapy, stabilized and sent to the PICU.

To summarize key elements from this case, this patient has:

• A history of GDD with epilepsy and shunted hydrocephalus.
• A stigmata of cachexia.
• And a presentation of hypovolemic shock secondary to decreased intake, increased loss, and potential underlying concern for sepsis.
• The most important element of this case is her extreme hypernatremia
• All of these factors in this case point to our topic of discussion today → the approach to hypovloemic hypernatremia 2/2 to dehydration.
• Let's transition into some history and physical exam components of hypovolemic hypernatremia?

1. Key history features in patients who present with Hypovolemic HyperNa include:

• Increased losses such as emesis
• Decreased intake, and in this setting potentially lack of access to free water
• Listlessness which could be related to cerebral hypoperfusion
• Increase in seizure frequency due to increased rapid depolarization of Na channels in the brain and fluid shifts

Welcome to the first episode of our podcast for current and aspiring intensivists. Our panel of medical professionals and students will examine specific patient cases, symptoms, and treatments. Today’s episode focuses on anaphylaxis. Join us!

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our case: a four-year-old is admitted to PICU, and TPN has been administered.
• Symptoms: dyspnea, wheezing, strider, and urticaria
• Vitals: hypotensive, tachycardic, with stats dropping rapidly
• What is anaphylaxis? An acute, life-threatening, systemic allergic reaction that can lead to death by airway obstruction or cardiovascular collapse.
• Anaphylaxis symptoms include skin, mucosal, respiratory, cardiovascular, and gastrointestinal symptoms that develop within one hour of exposure to the allergen.
• Anaphylaxis triggers can include allergens, biologics, immunotherapy, and radio-contrast media.
• The anaphylaxis reaction ends with distributive shock, manifested by low cardiovascular output, low systemic vascular resistance, and high pulmonary vascular resistance.
• Acute management of an anaphylaxis reaction includes airway, circulation, and breathing management, and epinephrine (the dosing is different from code dose).
• Watch out for hypotension and lower airway obstruction as possible complications, which can be managed with fluids and nebulized albuterol.
• Adjunctive therapies include histamine blockers and steroids.
• Post-anaphylaxis care:
• Focus on observation of the patient for 10-24 hours.
• Watch for a biphasic reaction.
• At discharge, provide two prescriptions for epinephrine, education for the patient and family, and a medical alert bracelet for the patient to wear. 

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:...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode about a 4-year-old girl with a chief complaint of headache and vomiting

Here's the case:

A 4-year-old presents to the PICU with headaches + vomiting and abnormal CT scan findings. The patient presented to the ED with h/o abdominal pain X 5 days with nonbilious, non-bloody emesis. Initial CBC, UA was normal. The patient was given some pain meds and IV fluids. Further history revealed that the patient has been having severe headaches for the last 5 days and had emesis secondary to the headaches resulting in generalized, non-specific abdominal pain. No h/o of trauma or seizures, no h/o of fever or diarrhea, no h/o toxic ingestions h/o recent travel, exposure to sick contacts, COVID test negative. No family h/o migraines, her immunizations are UTD. Besides the normal UA and CBC, her CMP was also normal.

A CT scan of the head revealed right frontoparietal mass with moderate surrounding edema, 6 mm leftward midline shift, diffuse sulcal narrowing, and right cisternal narrowing. Imaging of the abdomen (US and CT w/ contrast) was unremarkable. An MRI done revealed: Right parietal diffusion restricting lesion, most compatible with abscess. Moderate surrounding vasogenic edema. Given her abdominal pain- Abdominal KUB as well as contrast CT scan of abdomen and pelvis were performed and revealed no abdominopelvic pathology.

In the ED her vitals were normal and the patient was afebrile. On her PE: the patient appeared sleepy but woke up and answered questions appropriately. No focal deficits, PERRL, normal tone and strength. The rest of her physical exam was completely normal. She now is transferred to the PICU for serial neurological exams.

To summarize key elements from this case, this patient has:

• Headache with altered mental status
• No focal deficits
• Vomiting
• surprisingly no fever
• Imaging showing right frontoparietal mass.
• All of which brings up a concern for brain abscess
• This episode will be organized…
• Epidemiology and pathogenesis
• Diagnosis
• Management

Rahul, can you inform our listeners about the epidemiology of brain abscesses?

Only about 25% of brain abscesses occur in children. Incidence in developed countries is about 1-2% while in developing countries it's about 8%. Peak incidence in children is seen between the ages of 4-7 years and is more common in males. Brain abscess in the neonatal age group is rare but are associated with a higher risk of complications and mortality.

Risk factors for brain abscess include Otologic infections (ear, sinus, and dental infections), Congenital heart disease (30% of patients with BA have an underlying heart defect) with intra-cardiac or intrapulmonary shunting (pulmonary AV malformations in hemorrhagic telangiectasis), immunodeficiencies (solid organ transplantation, HIV, etc), prolonged steroid use, diabetes, alcoholism neurosurgical procedures, trauma. Other rare causes can be airway foreign bodies, congenital dermal sinuses, and esophageal procedures (such as dilatations).

Brain abscess typically begins with a localized area of cerebritis which evolves through various stages (typically 10-14 days) to develop into an encapsulated collection of purulent material with peripheral gliosis or fibrosis.

40-50% of the spread of infection is via a contiguous site of infection

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our discussion today on airway clearance in the critically-ill patient in the PICU. We will focus on the use of pharmacological as well as non-pharmacological techniques in critically ill children admitted to the ICU. This episode will be a general overview as specific clinical scenarios such as NM disease may warrant specific therapeutics.

Let’s get started with the case:

We have an 8-month old ex-34 week premie intubated for acute respiratory failure secondary to RSV bronchiolitis. The patient is on a conventional mechanical ventilator receiving a TV of 6ml/kg, rate of 20, PEEP 6, 40% FiO2 inspiratory time of 0.7

CXR shows a pattern suggestive of viral pneumonia with minimal hyperinflation and atelectasis of the right middle lobe. The patient has excessive secretions when the suction catheter is assessed. The patient is hemodynamically stable and is on feeds via a NG tube.

Rahul, Can you comment on how a child clears his/her pulmonary secretions normally when not ill?

That's an excellent question. Normally some baseline secretions are produced by all humans. Normal bronchial secretions are made up of contributions from mucus-secreting (goblet)cells as well as cells secreting serous fluid. The ciliary epithelium made of columnar cells line the entire tracheobronchial tree up to the alveolar ducts. This ciliary epithelium provides the coordinated rhythmic force that propels the overlying “mucus blanket” towards the central airways and upper respiratory tract.

Primary mechanisms of tracheobronchial clearance of these secretions consist of (1) The mucociliary (MC) escalator in the smaller airways and (2) Cough in central and larger airways. The co-ordinating activity of the beating cilia and their interaction with the overlying viscoelastic layer of mucus makes up the mucociliary escalator. The MC escalator helps remove both healthy and pathologic secretions from the airways as well as the removal of inhaled particles. This MC transport can be affected by mycoplasma, influenza and other viruses as well as exposure to toxins (cigarette smoke, vaping) as well as in CF, asthma, COPD, and ciliary dyskinesia just to name a few.

Once the secretions are in large or central airways they are coughed out or swallowed.

Let’s transition and talk a little on how one generates an effective cough:

1. For an effective cough one needs firstly to take a sufficiently deep breath in.
2. The glottis needs to close briefly to allow an increase in intrathoracic pressure
3. This is followed by expulsive glottic opening together with abdominal contraction, which results in air being forcibly expelled.

 Individuals with neuromuscular disease, bulbar insufficiency, obtunded patients, those on MV with chemical neuromuscular blockade, severe skeletal deformity may have decreased cough expiratory airflow. Reduced ability to cough results in secretion retention, mucus...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. Today we are joined by two wonderful clinical pharmacists — Whitney Moore & Stephanie Yasechko.

Whitney is a Clinical Pharmacy Specialist at Children’s Healthcare of Atlanta. She is on Twitter at @MoorephinRx.

Stephanie is a Pediatric Lung Transplant Clinical Pharmacy Specialist at Cincinnati Children’s Hospital Medical Center.

We are so excited to have you both on today. My name is Rahul Damania and I am a Pediatric Intensivist at Cleveland Clinic Children’s Hospital; Welcome to PICU Doc On Call where we focus on all things MED-ED in the PICU. Our podcast focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode an 18 yo immunocompromised patient with headache & sore throat

Here's the case presented by Rahul:

An 18-year-old female (40 kg) with PMH significant for fibrolamellar carcinoma of the liver, presents to the ED with headache and sore throat. She is febrile to 38.3, tachycardic, tachypneic, and has a WBC of 27K on her CBC. She is markedly hypotensive with BP on the arrival of 99/65. Cultures were drawn, the patient was given x1 doses of vancomycin and meropenem, and she was transported to the PICU for further workup and management. Due to her progressive hemodynamic instability, increased inflammatory markers, and marked immunocompromised state, the team is considering broadening her anti-microbial coverage.

To summarize key elements from this case, this patient has:

• Fibrolamellar carcinoma of the liver
• A presentation of headache, sore throat, and hemodynamic instability with concern for sepsis
• A current regimen of just antibacterials, which brings up the consideration of adding anti-fungal coverage in her clinically ill state.

Our episode today will be covering anti-fungal agents in the PICU.

We will review general mycology, understand different classes of antifungals, and highlight practical clinical pearls in the acute care setting.

As mentioned, this patient has risk factors for an immunocompromised state due to her underlying liver condition. As we dive deeper into antifungals, Whitney, can you please give us an overview of common fungal pathogens in the PICU?

Before we discuss the major drugs, it’s important that we take some time to briefly review the most common fungi we encounter clinically since it’s hard to choose the right agent when you don’t know exactly what you are treating.

Clinically, Candida is probably the most common fungal pathogen encountered, especially in warm, moist environments. It is important to determine what type of species is growing. The three major species known to cause infection are C. albicans, C. glabrata, and C. krusei, but it is important to differentiate these species when identified since they have different resistance patterns.

Cryptococcus is another type of fungus that is known to cause meningitis or fungemia, especially in immunocompromised or cirrhotic patients. Both Candida and Cryptococcus are classified as yeast on Gram stain. Treating cryptococcus will require the use of an agent that has good penetration to the CNS.

Endemic fungi known as Coccidia, Histoplasma, and Blastomyces are known to cause disseminated infections in immunocompromised hosts; however, each fungus is associated with a different geographic region in the United States. With any type of infection, it is always very important to consider your patients’ exposures and recent travel history.

And finally, there are two major molds that have the potential to be pathogenic. The first is Aspergillus which is identified via hyphae (tall...

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.

Key Case Highlights:

• Clinical case of a 15-year-old girl with sepsis from a gram-negative rod
• Dependence on total parenteral nutrition (TPN) and prolonged PICC line use
• Discussion of septic shock, acute respiratory failure, and acute kidney injury
• Overview of multiple organ dysfunction syndrome (MODS) and its definitions
• Pathophysiology of MODS, including organ functional reserve and kinetics of organ injury
• Molecular mechanisms involved in MODS, such as mitochondrial dysfunction and immune responses
• Specific phenotypes of sepsis-induced MODS, including TAMOF and IPMOF
• Management strategies for MODS, emphasizing multidisciplinary approaches
• Role and complications of therapeutic plasma exchange (TPE) in treating MODS
• Importance of recognizing signs of MODS and timely intervention in pediatric patients

Segment 1: MODS Definitions and Phenotypes

• Key Definition: MODS is the progressive failure of two or more organ systems due to systemic insults (infectious or non-infectious).
• Phenotypes:
• TAMOF (Thrombocytopenia-Associated Multi-Organ Failure): Characterized by thrombocytopenia, hemolysis, and decreased ADAMTS13 activity.
• Immunoparalysis: Persistent immunosuppression and risk of secondary infections.
• Sequential Liver Failure: Often associated with viral triggers.

Segment 2: Pathophysiology of MODS

Molecular Insights:

• Mitochondrial dysfunction and damage-associated molecular patterns (DAMPs)
• Innate and adaptive immune dysregulation
• Microcirculatory dysfunction and ischemia-reperfusion injury
• Organ Interactions: MODS evolves through complex multi-organ interdependencies

Segment 3: Diagnosis and Evidence-Based Management

• Key Diagnostic Pearls:
• MODS is not solely infection-driven; it requires a shared mechanism and predictable outcomes.
• Use biomarkers like ADAMTS13 and TNF-α response for phenotypic classification.
• Management Highlights:
• Supportive Care: Multisystem approach including lung-protective ventilation, renal replacement therapy, and hemodynamic support.
• Therapeutic Plasma Exchange (TPE): Especially effective in TAMOF by restoring ADAMTS13 and removing inflammatory mediators.

Segment 4: Practical Tips for Intensivists

• Early recognition of MODS phenotypes for targeted therapy
• Importance of multidisciplinary teamwork in critical care settings
• Monitoring for complications like TMA and immunoparalysis during prolonged ICU stays

Follow Us:

• Twitter: @PICUDocOnCall
• Email:

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode with a 15 year old Male having hypotension and bradycardia.

Here's the case presented by Rahul:

A 15 year old M presents to the PICU after sustaining an acute trauma. The patient was brought to the ER by his family after being on a boat and lifting a heavy object. He did not fall, sustain any head or extremity trauma, but did feel an achy non-radiating back pain shortly after the event. His grandmother states that the patient kept complaining about the back-pain and over the next few hours the patient became increasingly fatigued and flushed in the face. The patient was able to move his arms and legs and still walk, however family became concerned when the patient had abdominal fullness and was unable to urinate properly. He presents to the emergency department for further evaluation. In the emergency department he is noted to be awake however intermittently sleepy. His vital signs are notable for a HR of 58 bpm and a blood pressure of 85/60. He has 3/5 motor strength in his lower extremities with decreased sensation in his feet. Patellar reflexes are 1+ bilaterally. Rectal tone is normal. Acute resuscitation is begun for this patient.

To summarize key elements from this case, this patient has:

• Acute trigger
• Back pain
• Vital sign instability and lower motor neuron signs.
• All of which bring up a concern for a spinal cord injury.
• Let's transition and discuss some history and physical exam components of this presentation:

1. What are key history features in a child who presents with hypotension and bradycardia?

• As our worry is primarily spinal cord in etiology you would want to ask about trauma — this could be blunt or penetrating trauma
• You also would like to ask about the nature of the injury and scene. It is especially important to inquire with the pre-hospital providers about the nature of the injury and the patient course in transport. Besides our normal ABCs, it is important to ask the care taken regarding spinal cord restriction (such as use of a cervical collar or backboard)
• Another high yield history component when you think about hypotension and bradycardia is to assess for Numbness, weakness, or changes in bowel or bladder habits. In this case the patient had abdominal fullness which maybe due to bladder dysfunction.

This is a great summary of key history findings for patients who present with hypotension and bradycardia as it relates to spinal cord issues. Remember that patients who have Down's syndrome may have a predilection to have lax ligaments especially in the upper verterbrae. As a result, you should have an increased index of suspicion if a Down's Syndrome patient presents with hypotension and bradycardia in the presence or absence of trauma. In a study published in 2017 in Neurocrit Care it was estimated that about 20% of patients with Trisomy 21 may have atlantoaxial instability.

A great point which you just highlighted. Remember that when you approach hypotension and bradycardia, it is also important to focus on cardiac etiologies:

Bradycardia directly pulls down the cardiac output, potentially causing shock, and especially if you have a blunted vasoconstrictor response you can couple this bradycardia with hypotension.I do not want to delve too much out of the scope of today's episode but there is a wide differential for bradycardia but specifically related to history you should consider intoxication as a cause of bradycardia and hypotension.

• This includes:
• Beta-blocker or...

Today’s episode is dedicated to pediatric acute liver failure. Join us as we discuss the patient case, symptoms, and treatment. 

 Joining the conversation is Dr. Rene Romero, Professor of Pediatrics at Emory University School of Medicine and the Medical Director of the Liver Transplant Program at Children’s Healthcare of Atlanta. 

>>Click here to download the PICU card for this episode<<

Show Highlights: 

• Our case, symptoms, and diagnosis: a three-year-old child presents in the PICU with decreased arousal; the patient is hypoglycemic. The coagulation panel is significant for increased PTT and INR, and AST and ALT are significantly elevated. The patient is hyperammonemic, and the acetaminophen level is normal. The diagnosis is acute liver failure.
• Basic functions of the liver, the “workhorse of the body” that plays major roles in interactions with other organs
• Why pediatric acute liver failure is more difficult to diagnose than in adults; key indicators are coagulopathy along with biochemical disruptions
• The most important contributing factors to pediatric acute liver failure, and why most pediatric cases are children under four years of age
• Causes of pediatric acute liver failure in the US include HSV, adenovirus, enterovirus, metabolic causes, and acetaminophen, especially in older children
• The diagnostic approach considers infectious etiologies, toxins, vascular issues, and immune dysregulation
• In treatment, care should be given to the correction of abnormal lab values and possible renal replacement therapy
• Why the use of prophylactic antifungal antibiotics is controversial and varies from institution to institution
• How to discern hyperammonemia and neurologic status
• The role of intracranial pressure monitoring for cerebral edema, which is the mode of death for these patients
• Key Clinical Pearls: acute liver failure is a systemic disease that requires a broad diagnostic approach, and the need for standardized approaches still exists.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode.

Today, we are going to discuss the management of the postoperative patient admitted to the PICU. Our discussion will focus on the non-cardiac and non-transplant admission. Our objective in this episode is to create a framework on what areas of care to focus on when you have a patient admitted to the PICU post-operatively. Each surgery and patient is unique; however, we hope that you will garner a few pearls in this discussion so you can be proactive.

in your management. Without any further delay, let’s get started with today’s case:

We begin with a 13-year-old child, Alexa, with h/o of a genetic syndrome, who presents today with a history of thoracolumbar kyphoscoliosis. Over the years, Alexa's curvature has progressively worsened, resulting in difficulty breathing and chronic back pain. The decision was made to proceed with a complex spinal surgery, including posterior spinal fusion and instrumentation.

In the weeks leading up to the surgery, Alexa underwent a thorough preoperative evaluation, including consultations with specialists and relevant imaging studies. Pulmonary function tests revealed a restrictive lung pattern, while the echocardiogram showed no significant cardiac abnormalities. Preoperative labs, including CBC, electrolytes, and coagulation profile, were within normal limits.

During the surgery, Alexa was closely monitored by the anesthesia team, who administered general anesthesia with endotracheal intubation. The surgery was performed by the pediatric neurosurgery and orthopedics, with intra-operative neuromonitoring to assess spinal cord function. The surgical team encountered an unexpected dural tear, which was repaired using sutures and a dural graft. Due to the prolonged surgical time, a temporary intra-operative loss of somatosensory evoked potentials was noted. However, signals were restored after adjusting the patient's position and optimizing blood pressure. The posterior spinal fusion and instrumentation were completed successfully, but the surgery lasted 8 hours. Total intra-operative blood loss was 800 mL, and Alex received 2 units of packed red blood cells and was on NE for a little over half the case before weaning off.

Alexa was admitted to the PICU intubated and sedated for postoperative care. The initial assessment showed stable vital signs, with a systolic blood pressure of 100 mmHg, heart rate of 90 bpm, and oxygen saturation of 99% on mechanical ventilation. Postoperative pain was managed with a continuous morphine infusion. The surgical team placed a closed suction drain near the surgical site and a Foley catheter for urinary output monitoring. You are now at the bedside for OR to PICU handoff…

To summarize key components from this case:

This is a patient with thoracolumbar kyphoscoliosis, underwent complex spinal surgery (posterior spinal fusion and instrumentation) due to progressive curvature, breathing difficulties, and chronic pain.

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...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine in Atlanta, GA.Today we are going to present a case of a 3 year old presenting with bilateral hyper-flexed wrists.

Here is Rahul with our case:

A 3 yo previously healthy M presents to the emergency department after his mother noted his wrists becoming completely stiff and flexed. Despite several attempts to stretch out his wrist, his mother was unable to place them back into position. She brought him to the ED for further evaluation. Importantly, mother denies any trauma or injury. Mom notes that this happened once before one month ago. The episode lasted 10 min and self-resolved. She did not seek medical attention at that time. Patient has no history of bleeding, bruising or chronic medical conditions. His immunizations are UTD. Family hx was relatively unremarkable however the mother states that she gets admitted to the hospital for Kidney Stones 4-5 times per year. She usually follows with a urologist. Though she is on diuretic therapy for recurrent renal stones, she denies that her son has any access to these medications & also denies any ingestion. She does state that patient is a picky eater and does not drink milk but will eat cheese often with 4-5 cups of juice. Mother denies any recent upper respiratory tract symptoms, vomiting, constipation, urinary abnormalities or changes in gait.

Upon presentation to the ED, his vital signs were stable. His physical exam is normal except for Bilateral hands in flexion with digits on flexion as well. After some resistance the examiner was able to extend hands. There were no abrasions or signs of cutaneous injury in his bilateral hands. Full range of motion of elbow and shoulder as well as full range of motion of ankle and knee as well as hip. Prior to drawing blood for a diagnostic work-up the patient undergoes an EKG which shows some artifact but is notable for a prolonged QTc interval of 560.

To summarize key elements from this case so far, we have a toddler with

• Bilateral hyper-flexion of the wrists which seem to be in a tonic state and is recurrent
• A family history of renal metabolic disease.
• and finally, an EKG abnormality.
• Rahul one key pertinent negative at this stage is that there is no trauma & patient has full range of motion at other large joints
• Rahul, let's transition to key history and physical elements when you think about bilateral wrist flexion.

1. This is an interesting chief complaint, however I would tailor my history to assess for trauma as this seems to be a primary MSK issue.

• The key feature here is that the patient has bilateral wrist involvement which brings up the concern for an underlying systemic cause such as an electrolyte abnormality, connective tissue disorder, or muscular abnormality. The family history of recurrent kidney stones points more towards a familial renal or electrolyte problem.
• I would ask about any trauma related to skin wounds. As this patient is in a tonic state, I would worry about tetanus.
• I would also get a good dietary history as excessive juice consumption may have limited nutritional value.

1. On physical exam, I would look for any other MSK abnormalities with this bilateral wrist flexion. Especially if we are heading down the route of nutritional abnormality, electrolyte disturbance or renal anomaly, I would like to assess for any bowing of the legs, joint flaring, any metacarpal shortening, or rib abnormality.

Pradip, I would love to hear more about the emergency room diagnostic work-up in this patient...

• To continue with

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania, from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode about a 14-year-old male who collapsed on the baseball field.

Here’s the case presented by Rahul:

A 14-year-old male athlete was playing in a high school baseball tournament when he was hit in the chest with a pitched ball. The impact caused him to collapse on the field. Bystander CPR was begun given his unresponsiveness and emergency medical services were immediately called. The patient was transported to the hospital. Upon arrival, he was unresponsive and had no pulse. An electrocardiogram (ECG) showed ventricular fibrillation, and advanced cardiac life support was initiated. After several shocks and cardiac compressions, the patient regained a pulse and was transferred to the pediatric intensive care unit for further evaluation and management.

To summarize key elements from this case, this patient has:

• Been struck by a high-velocity object in the chest
• Suffered a cardiac arrest, likely due to an arrhythmia from the blunt chest trauma

The presentation brings up a concern for Commotio Cordis, our topic of discussion today!

We wanted to create this educational episode in light of the recent medical event experienced by the Buffalo Bill’s safety Damar Hamlin. His blunt chest trauma, which led to cardiac arrest, has been postulated to be due to commotio cordis. At the date of this record, we are glad that Damar Hamlin is on the road to recovery.

Absolutely, let’s dive in more into this topic, Let's start with a short multiple-choice question:

The 14-year-old described in our case suffered cardiac arrest after blunt chest trauma. Based on the working diagnosis of comottio cordis, what is the most likely EKG finding which may be seen in this patient?

A. Ventricular fibrillation

B. Ventricular tachycardia

C. Complete heart block

D. Asystole

The correct answer is A. In a study published in JAMA (2002; 287(9):1142-1146) which used data from the US Commotio Cordis registry maintained by the Minneapolis Heart Institute Foundation, reported that the most common arrhythmia out of the 128 confirmed cases, 82 of which had EKGs which could be analyzed was ventricular fibrillation. Three patients had Vtach, 3 had Bradyarrhythmia and 1 had complete heart block. Although 40 patients had asystole, this was unlikely to be the initial rhythm after impact. Interestingly, the majority of these rhythms were recorded at the scene.

Rahul, What is the definition of Commotio...

Today’s episode is dedicated to acute management of hyperkalemia in the PICU. Join us as we discuss the patient case, symptoms, and treatment. 

We are delighted to be joined by Dr. Roshan George, Associate Professor of Pediatrics, a practicing Pediatric Nephrologist at Children’s Healthcare of Atlanta, and the Program Director of Pediatric Nephrology Fellowship at Emory University School of Medicine. 

Show Highlights:

• Our case, symptoms, and diagnosis: A two-year-old male with a history of focal segmental glomerulosclerosis controlled on chronic prednisone therapy presents to the PICU for respiratory failure. The patient is noted to be hypotensive and tachycardic. Potassium is elevated at 6.4 with no hemolysis noted. The EKG is notable for peak T waves, and the patient is also noted to be anuric. 
• Definition of hyperkalemia: a potassium serum level higher than 5.5 (Be sure to correlate your lab sample with clinical and telemetry changes to rule out pseudohyperkalemia)
• Common causes of hyperkalemia:
• Increased intake of potassium
• Transcellular shift
• Decreased renal excretion
• Inborn error of metabolism, especially adrenal problems
• Why it’s important to be vigilant about hyperkalemia in patients with chronic kidney disease, end-stage renal disease, acute kidney injury, and those with a transplanted kidney
• Clinical manifestations of hyperkalemia:
• The risk is for cardiac conduction abnormalities and muscle weakness/paralysis.
• Adverse events can occur with levels > 5.5mEq/L, and the risk increases as levels rise.
• Any serum K level > 6mEq/L is significant, regardless of EKG changes.
• Two hallmarks that can drive effective management of hyperkalemia are EKG findings and laboratory confirmation of elevated serum potassium.
• Other important labs for patients with hyperkalemia include a basic electrolyte panel to assess kidney function, CBC, and serum blood gas to assess acid/base balance. (A medication check for K supplements or ACE inhibitors should also be done.)
• Steps in the management of hyperkalemia:
• First, caution should be exercised that any K level > 5.5 is a medical emergency and should be addressed immediately without finding the etiology. 
• Stabilize the cardiac membrane.
• Shift potassium with insulin and glucose, bicarbonate, and B2 adrenergic agents.
• The long-term goal should be to improve excretion with Kayexalate or Furosemide (Remember the mnemonic: “Loops lose K.”)
• General considerations about dialysis are:
• CVVH vs. HD
• Severe hyperkalemia is a key indication for RRT in acutely ill patients.
• Hemodialysis can be used in an emergency.
• Takeaway clinical pearls regarding hyperkalemia: 
• Make sure the potassium level is accurate.
• Consider the next steps in potassium removal.
• Remember that etiology is the last step.

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

Management Strategies

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’s episode of "PICU Doc On Call," with Dr. Pradip Kamat and Dr. Rahul Damania, pediatric ICU physicians, delves into intriguing case and management strategies within the acute care pediatric setting.

This episode focuses on a 2-year-old child transferred to the PICU due to pneumonia-induced respiratory distress. As the child's condition deteriorates, intubation becomes necessary to address acute hypoxemic respiratory failure.

We discuss the significance of minimizing unnecessary blood cultures in febrile patients with central lines in the PICU. A study implementing a quality improvement program is referenced, which successfully reduces blood culture rates, broad-spectrum antibiotic usage, and CLABSI rates without impacting mortality or length of stay.

Next, we’ll explore the comparison between a high-flow nasal cannula (HFNC) and continuous positive airway pressure (CPAP) in pediatric patients experiencing respiratory distress. Findings from a randomized controlled trial revealed that HFNC is non-inferior to CPAP in terms of time required for liberation from respiratory support.

We further investigate the application of pediatric early warning scores (PEWS) and automated clinical prediction models to identify patients at risk of deterioration and transfer to the PICU. The importance of employing clinical judgment and a combination of assessment tools to determine the need for transfer is emphasized.

Lastly, we’ll highlight the significance of screening for social determinants of health in critically ill children and their families. A study demonstrates that a substantial number of participants had unmet social needs, underscoring the importance of screening to provide appropriate interventions and resources.

To summarize, this podcast episode covers key topics such as reducing unnecessary blood cultures, comparing HFNC and CPAP in respiratory distress, utilizing PEWS and clinical prediction models for patient identification, and the importance of screening for social determinants of health.

Be sure to listen in entirety as we discuss the case.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our episode, A Three-Year-Old with recent cough and leg weakness.

Here's the case presented by Rahul.

A 3-year-old previously healthy female presented to the hospital with a 2-week history of productive cough and congestion and the new 1-day onset of bilateral weakness. Today, the mother noticed weakness and inability to stand/walk following after shower as well as her voice becoming hoarse. She also noticed her lying more limp sitting on her lap, unable to sit up fully without her mother supporting her. She had no trouble holding up her head. The mother endorses increased fussiness but is able to be consoled. Decreased p/o intake, last meal was yesterday. About 1-2 weeks prior to this patient also had non-bloody diarrhea that resolved spontaneously after a few days.

UOP normal with 2-3 wet diapers. No difficulty breathing. No history of head trauma or trauma to lower extremities, no erythema/swelling to joints. No pain associated with leg movement. No previous difficulty with walking - developing normally otherwise. No fever, recent travel, H/O sick contact at home (sibling with URI). No allergies, immunization UTD. CMP largely unremarkable. CBC with leukocytosis to 19.72 with L shift and platelets of 647. CRP 0.3, ESR 12.

Afebrile, RR 24/min, HR 130, BP 140/86.

On PE: Patient was coughing, had a hoarse voice heart and lung exam was normal. Normal abdominal exam. No rash

Neurological exam: PERRL, (A+O) X3, 3-4/5 strength at ankles and knees and 5/5 in arms, +UE DTR's but none at patella or ankles. Has a wide-based ataxic gait and needs to hold on to the wall/furniture to ambulate.

Rahul, to summarize key elements from this case, this patient has:

• A cough with a hoarse voice
• No fever
• Inability to stand/walk (i.e. lower extremity weakness) with no DTRs in patellae or ankle
• Normal mental status
• Diarrhea (non-bloody) preceding neurological weakness
• All of these bring up a concern for Guillain-Barré syndrome-An immune-mediated disease possibly triggered by a recent infection and targeting the peripheral nervous system.

Let's transition into some history and physical exam components of this case?

1. What are key history features in this 3-year-old child

• Acute (B) leg weakness
• Cough with hoarse
• Diarrheal illness
• No fever, no /o rash or trauma

1. Pradip, Are there some red-flag...

Welcome to PICU Doc on Call, a podcast dedicated to current and aspiring intensivists. I'm Pradeep Kumar coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two pediatric ICU physicians passionate about all things medical education in the PICU.

Episode Overview: 

PICU.com call focuses on interesting PICU cases and management in the acute care Pediatric setting. In this episode, we discuss the case of an eight-year-old boy with chest pain, fatigue, and shortness of breath. This case presentation by Rahul highlights the complexity of pediatric care in the PICU.

Case Presentation: 

An eight-year-old boy with up-to-date immunizations and no recent travel or pet exposure presented to the PICU with chief complaints of chest pain, fatigue, and decreased oral intake. His history over the preceding two weeks included a diminishing appetite, episodes of vomiting, and shortness of breath.

On examination, he exhibited various cardiac findings, including a hyperdynamic left ventricle, murmurs, and a noted gallop. Abdominal and neurological findings were also concerning. Diagnostic studies revealed an enlarged heart, and sinus tachycardia with left ventricular hypertrophy, and echocardiography confirmed severe valvular and ventricular abnormalities.

Laboratory Findings:

Laboratory findings included elevated BNP, slightly elevated troponin, and elevated inflammatory markers (ESR and CRP). Strep throat culture was negative, but ASO and anti-DNAse B titers were markedly elevated. MRI confirmed multiple punctate infarctions, likely due to valvular heart disease.

Diagnosis: 

Given the complex multisystem presentation, the child was admitted to the PICU for intensive monitoring and comprehensive management of this multisystem pathology. The working diagnosis is rheumatic fever.

The episode is organized into three parts:

• Pathophysiology of Acute Rheumatic Fever
• Approach to Diagnosis and Investigations
• Management and Prevention

Pathophysiology of Acute Rheumatic Fever: 

Acute rheumatic fever is an autoimmune disease initiated by a response to group A strep infection, primarily due to molecular mimicry. The streptococcal M protein has structural similarities with host proteins, leading to organ damage, especially in the heart.

Epidemiology: 

Acute rheumatic fever is most prevalent in low to middle-income areas, affecting over 80% of cases. It mainly affects children between 5 to 14 years of age, and overcrowded households and limited healthcare access increase the risk. Globally, rheumatic heart disease affects millions of people annually and claims many lives.

Jones Criteria for Diagnosis: 

The Jones criteria help diagnose acute rheumatic fever. For

In this episode of PICU Doc On Call, Dr. Pradip Kamat and Dr. Rahul Damania discuss a case of a 4-year-old girl with bite marks and swelling of her foot, presenting with concerning vital signs and abnormal labs. They explore snake envenomation and its management in the pediatric critical care setting.

Classifying Snake Envenomation

Snakes with venom-delivering fangs, primarily Elapidae and Viperidae, are responsible for most human envenomations and fatalities. We're focusing on Pit Vipers today, including rattlesnakes, cottonmouths, and the copperhead. Elapids, such as the coral snake, differ by having round pupils, short fangs, and no facial pit.

Risk Factors for Pediatric Snakebites

Snakebite incidents can happen when toddlers unintentionally disturb snakes, particularly in low-light conditions or grassy areas. Teenagers trying to capture snakes are another frequent group presenting with upper extremity bites. 

Pathophysiology of Snake Envenomation

Snake venoms contain toxic proteins that affect various physiological systems, leading to neurotoxic, hemotoxic, myotoxic, or cytotoxic effects. Envenomation can happen immediately or be delayed, presenting with various clinical and laboratory anomalies.

Syndromes Observed After Snake Envenomation

The impact of a snakebite depends on the snake type, fang size, and venom injection site. Effects may include cytotoxicity, lymphatic system damage, platelet dysfunction, neurotoxicity, cardiotoxicity, hypotension, and nephrotoxicity.

General Management Framework

In snakebite cases, prehospital care involves immediate EMS call and ensuring airway, breathing, and hemodynamic stability. In the hospital, general supportive care is crucial, and antivenin administration depends on clinical presentation and snake type.

Antivenin Considerations

Antivenin dosage is challenging due to unknown venom load, and its choice depends on safety, kinetics, cost, and the specific snake involved. Smaller fragments of antivenin have larger distribution volumes and shorter half-lives. Recurrence, anaphylaxis, and serum sickness are potential side effects of antivenin.

Clinical Pearls

• A high index of suspicion is required to diagnose snake envenomation.
• Antivenin is the mainstay of therapy, and rapid transport to a facility with antivenin is crucial.
• Patients should be educated about recurrence, serum sickness, and lifestyle adjustments after a pit viper bite.

Thank you for listening to this episode on snake envenomation in the PICU. For more episodes, visit our website picudoconcall.org. Stay tuned for our next episode! Don't forget to share your feedback and subscribe to our podcast.

Today, we welcome Dr. Stella Shin, Assistant Professor of Pediatrics-Pediatric Nephrology at The Emory University School of Medicine. Dr Shin is also the Director of General Pediatric Nephrology and the Director of Acute Kidney Replacement Therapy at The Children's Healthcare of Atlanta in Atlanta, GA. Her interests include nephrotoxic medication stewardship, health informatics and healthcare quality improvement. She is on twitter @BabyBeanDoc

A 17 year old previously healthy thinly built male teenager is brought to the emergency department for sudden development of blurred vision. Patient has a h/o headaches for the last few months accompanied by abdominal pain and relieved by vomiting. He has also felt his heart racing during such episodes and accompanied by profuse sweating. Patient had tried various over the counter pain medications without much improvement in his headaches or abdominal pain. An initial CT scan of the head reveled no intracranial pathology. ED physician noted a a blood pressure of 200/120 mm HG and a pulse of 132beats/minute. He is started on nicardipine in the ICU.

• Definitions for normal and high blood pressure come from the AAP clinical practice guidelines for screening and management of high blood pressure. According to these guidelines:
• Normal BP is a blood pressure reading that is < 90%ile for children 1-12 yrs of age: A normal BP for teenagers 13 years and older = <120/<80.
• High blood pressure is divided into three categories: Elevated BP, Stage 1 HTN, and Stage 2 HTN. This is further delineated into categories for children 1-12 yo and 13 or older.
• For children 1-12 yo:
• Elevated BP is a BP that is >/= 90%ile but <95%ile, or a BP of 120/80 up to <95%ile, whichever is lower.
• Stage 1 HTN is a BP that is ≥95%ile to <95%ile+12 mmHg, or a BP of 130/80 to 139/89, whichever is lower.
• Stage 2 HTN is a BP that is ≥95%ile+12 mmHg, or a BP that is ≥140/90, whichever is lower.
• It's much more simple for children 13 and older:
• Elevated BP is 120/<80 to 129/<80
• Stage 1 HTN is 130/80 to 139/89
• Stage 2 HTN is >/= 140/90
• That's a lot of numbers and cut offs to remember. To make it easy, in general, hypertension in children and adolescents is defined as a sustained systolic and/or diastolic blood pressure elevation ≥ 95%ile for age, gender, and height. And adult BP cut offs are used for teenagers 13 years or older.

Acute severe hypertension is defined as significant blood pressure elevation with or without of acute target-organ damage from the hypertension.

This is further classified based on target organ involvement into hypertensive urgency and hypertensive emergency. The key difference between the two is whether target organ injury is present.

Hypertensive Urgency is acute severe hypertension WITHOUT acute target-organ damage. Hypertensive urgency is not associated with adverse short-term outcomes and can be managed in the ambulatory setting.

Hypertensive Emergency is acute severe hypertension that is accompanied by acute target-organ injury. It is a medical emergency with substantial morbidity and mortality requiring immediate treatment in an ICU.

It is important to note for our listeners that acute sever hypertension is on a spectrum with hypertensive urgency and emergency, and these diagnoses exist on a spectrum!

Our discussion focused on acute severe hypertension, which is a medical emergency especially when there is target organ injury. A titratable infusion of an antihypertensive such as nicardipine should be the first line to lower the BP by 25% in first 8 hours as precipitous drop may cause cerebral ischemia. While there are multiple IV antihypertensives, the pediatric critical care team should be should be

Today’s episode is dedicated to acute metabolic emergencies. Join us as we discuss the patient case, symptoms, and treatment. 

Joining us is Dr. Lori-Anne Schillaci, trained in clinical pediatric genetics with additional training in metabolism. She had a dual appointment in the Department of Pediatric Emergency Medicine at Rainbow Babies and Children’s Hospital, as well as an appointment in the Department of Genetics and Metabolism. Dr. Schillaci is currently embarking on a fellowship in Pediatric Emergency Medicine at Wake Forest Brenner Children’s Hospital. 

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our case: A three-month-old infant presents with seizures and decreased oral intake
• History, symptoms, and treatment: The child is hypothermic and tachypneic. Blood gas is notable for anion-gap metabolic acidosis. Blood cultures are drawn, and antibiotics are started. Urine organic acids and serum ammonia are both pending. 
• A metabolic emergency is defined as a defect in the breakdown or storage of the body’s energy sources (sugar, fat, and protein) at the cellular level
• Why metabolic conditions can be inherited or result from a spontaneous mutation
• How the toxic products form in the body and can affect children in three categories (protein, fat, and sugar metabolism)
• Common lab tests would be for ammonia, gas, and blood sugar
• Why the physician should save a purple top tube before any transfusion
• General management should include treatment of the underlying acute issues, early dextrose fluids, normal saline fluid boluses, IV lipid emulsion (except in patients with known fatty acid oxidation defects)
• Advice to colleagues in managing a patient with inborn error:
• Keep in mind that the presentation can occur in older kids
• Get early labs when they are sick
• Start high dextrose fluids
• Keep the patient NPO
• Treat fever, hypoglycemia, seizures, infection, etc. 
• The goal is to prevent catabolism and be aggressive early in treatment
• Dr. Schillaci’s final thoughts: “Be vigilant. Assume an inborn error of metabolism unless proven otherwise. Be aware of late presentations of inborn errors of metabolism.”

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.

Case Presentation

• 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.

Key Elements

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

Problem Representation

• 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.

Pathophysiology of RPA

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

Dangers of RPA

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

Clinical Manifestations

• 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

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I’m Kate Phelps, a second-year pediatric critical care fellow joining Pradip and Rahul today!

I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Today we are honored to have Dr. John Berkenbosch- senior author of the Prevention and Management of Pain, Agitation, Neuromuscular Blockade, and Delirium in Critically Ill Pediatric Patients with consideration of the ICU Environment and Early Mobility (PANDEM) guidelines recently published in February 2022 issue of the Pediatric Critical Care journal.

Dr. Berkenbosch is a Professor of Pediatrics and Pediatric Critical Care at the University of Louisville School of Medicine, and continues to be nationally recognized as an expert in pediatric procedural sedation with multiple publications relating to sedation practices, particularly novel uses of procedural sedation medications and regimens. He currently also serves as co-chair for the American College of Critical Care Medicine’s Task Force guidelines for sedation and analgesia in critically ill children which we will be discussing in today’s episode. Dr. Berkenbosch’s research interests have primarily focused on pediatric procedural sedation and implementation of technology advances in Pediatric Critical Care and have resulted in 57 publications as well as several book chapters

Rahul: Dr. Berkenbosch welcome to the PICU Doc ON call podcast. I would also like to point out that the free full access to the PANDEM guidelines is available online at pccmjournal.org

Dr. Berkenbosch: Thanks Rahul and Pradip. I am excited to be on the PICU Doc on Call Podcast to discuss the PANDEM guidelines. I want to first start by giving a huge shout-out to all the team members who contributed to these guidelines’ development. This is a topic about which I am quite passionate but also one that provides much-needed guidance regarding pain/agitation/delirium to our entire pediatric critical care community!

KATE: Dr. Berkenbosch, the rationale for the development of the PANDEM guidelines was the high variability in pediatric sedation and analgesia. Can you speak to this variability and why it was important to address that variability?

That is a great question, the variability has been one of the key motivators in the creation of these guidelines. We also wanted to develop a guideline that was broader in scope than what was currently available. The ICU Liberation bundle provided a paradigm for liberating critically ill patients from mechanical ventilation and the ICU environment and as we delved into developing these guidelines, we realized that many elements of the ICU liberation bundle aligned very closely with PICU sedation and analgesia so it made imminent sense to incorporate all of these topics into the guidelines, an acknowledgment if you will, that PICU liberation & sedation go hand in hand!

Absolutely, as we have stated in our prior episodes, the paradigm is: intubate → ventilate → liberate, and sedation/analgesia is intertwined in each of these processes.

Dr. Berkenbosch, as we get into the guidelines, can you please highlight how the search strategy for these guidelines...

Today’s episode is dedicated to the acute management of pediatric stroke. Join us as we discuss the patient case, symptoms, and treatment. 

Joining us is Dr. Elissa Ortolani, Assistant Professor of Pediatrics in the Division of Child Neurology and Assistant Professor of Neurology at Emory University School of Medicine. Dr. Ortolani has a strong clinical interest in pediatric vascular disease and is one of the few pediatric neurologists who has completed a formal adult stroke fellowship. She is actively helping to develop a pediatric stroke program at Children’s Healthcare of Atlanta.

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our case: a five-year-old male, previously healthy, has had cold symptoms for two days; he presents to the ER with possible stroke symptoms
• Symptoms: the patient has had left arm and left leg weakness during the past day, and his mother noticed a subtle left side lip droop with drooling
• Acute management: In the ER, a CT revealed a subtle hypodensity in the right basal ganglia region; the patient was admitted to PICU for further monitoring and workup
• Causes of an acute pediatric vascular event can include stroke, seizure, migraine, and toxidrome
• Definition of stroke: an acute neurologic change identified by advanced imaging
• Practical tools in evaluating stroke include F-facial droop, A-arm weakness, S-speech difficulty, T-time. (Now, amended to FASTER to include stability and eyes/vision)
• Risk factors for pediatric stroke include vascular issues like sickle cell disease, congenital heart problems, thrombophilia, and mitochondrial, inflammatory, or connective tissue disease
• In pinpointing pediatric stroke or stroke mimic, which is very common, MRI is the preferred imaging method 
• Important considerations in the diagnosis of pediatric stroke are that mild sedation is sufficient for the 10-12 minutes needed for MRI
• In the management of pediatric stroke, TPA should be administered within 4.5 hours, and endovascular therapy (if needed) should be administered within 24 hours
• Why the diagnosis and management of pediatric stroke is delayed, and how ER and ICU physicians can change that
• Developing a pediatric stroke program is a collaborative effort among emergency care providers, radiologists, pharmacists, adult neuro interventionalists, ICU team, neurosurgeons, hematologists, and rehab physicians
• A key in the diagnosis of pediatric stroke is recognizing altered mental status

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...

 Today's episode is dedicated to the approach to the unstable neonate. Join us as we discuss the anatomic and physiological considerations for the neonate, initial investigations, and management framework on stabilizing a child. 

We are delighted to be joined by Dr. Michael Wolf, Associate Professor of Pediatrics at Emory University School of Medicine, and Associate Medical Director of the Cardiac Intensive Care Unit at Children's Healthcare of Atlanta. The CICU at Children’s is one of the highest volume pediatric heart centers in the nation. Dr. Wolf is also Chair of the "You Matter Program" at Children's Healthcare of Atlanta, which addresses physician resilience and second victim syndrome in providers.

Show Highlights:

•  Our case, symptoms, and diagnosis: A 4-day-old former full-term neonate delivered via C-section for non-reassuring fetal heart tones is to be discharged from the well-child nursery. On the day of discharge, the child is noted to have progressive tachypnea, tachycardia, and progressive acrocyanosis. The extremities are cool, and the child has delayed capillary refill. Pulse-oximetry is notable for a discordance between upper and lower extremity saturations. Femoral pulses are poorly palpable. Blood gas is significant for metabolic acidosis. The patient is rushed to the NICU, and the process to transfer the baby to a pediatric cardiac intensive care facility is initiated.
• Important considerations to keep in mind for the neonatal or infant population are according to the traditional Airway-Breathing-Circulation model:
• Airway--The infant airway is prone to dynamic obstruction due to a larger tongue and epiglottis, compliant soft tissues, and their obligatory nose breathing.
• Breathing--Differences in chest wall dynamics, oxygen metabolism, and respiratory musculature place the small infant at greater risk for respiratory failure than the older child.
• Cardiac--Considerations focus on key events in the transition from fetal to neonatal circulation, and include the initiation of prostaglandins and calcium administration to drive contractility..
• Shock categories to consider for the neonate include hypovolemic shock from hemorrhage, obstructive entities like severe pulmonary hypertension, and septic shock. 
• Initial stabilization of the neonate includes the following lab testing and imaging: blood gas and glucose determination, basic electrolytes, vital signs and clinical exam data, and prostaglandin infusions to reestablish blood flow. The loop of intervention and reassessment is imperative as you acutely stabilize a child with neonatal shock!
• Other key diagnostics include four extremity blood pressure and low extremity pulses, pre- and post-ductal saturations, bedside echocardiography, and delving into the history with prenatal screening. 
• The management framework focuses on prostaglandins and dosage protocols, the availability of intubation equipment, and the risk of necrotizing enterocolitis (NEC).
• Besides congenital heart defects, other considerations for the unstable neonate are sepsis, infusions of ionotropes, cardiac catheterizations, and possible balloon valvuloplasty. 
• Takeaway clinical pearls regarding the unstable neonate:
• Always think about prostaglandins when approaching the neonate with shock.
• Use a physical exam to check pulses and blood pressure.
• Remember that a focused, rapid, bedside echocardiogram can help diagnose shock. 
• We hope you learned something from today’s discussion of the importance of a broad differential, key presentation features of congenital heart disease, and the importance of early PG initiation in the management of an unstable neonate. 

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode an 8-year-old admitted for PRESS syndrome with altered mental status secondary to seizures.

Here's the case presented by Rahul:

Our patient today is an eight-year-old who was admitted to the floor with a diagnosis of MIS-C. On his initial echo, his EF had mildly depressed systolic function, dilatation of coronaries, and worsening of inflammatory markers. As a result, the care team increased the dosing of the methylprednisolone administered to this patient. Since the initiation of methylprednisone, The patient's SBP had been steadily increasing with the latest systolic values approaching 140s-150s.

On hospital day 3 patient had a generalized tonic-clonic seizure and became unresponsive for which a rapid response on the floor was called. The patient was emergently bagged and brought to the PICU for airway protection and intubation

Initial vitals on PICU admission: He was afebrile, mildly tachycardic, and hypertensive to 160s even after sedation.

In the PICU an initial head CT scan done after intubation and stabilization of the patient showed no bleeding or mass. cEEG monitoring was initiated, neurology consulted and an MRI was ordered for the following day. As his AMS was thought to be related to his BP, the team pursued BP control with Nicardipine.

To summarize key elements from this case, this patient has:

• Seizure
• Altered mental status
• Hypertension
• Acute respiratory failure
• All of which brings up a concern for an acute CNS pathology.

Absolutely, the differential is broad, however, right now I am thinking of an acute stroke categorized as hemorrhagic, ischemic, or venous thrombotic; a meningoencephalitis, CNS vasculitis, acute demyelinating encephalomyelitis, metabolic encephalopathy, tumor, or AMS related to hypertension.

Pradip, let's transition into some history and physical exam components of this case?

What are key history features in this child?

• MIS-C with cardiac dysfunction and coronary anomalies
• Increase in steroid dosage
• Progressive increase in BP as a result of this increase

Rahul, are there some red-flag symptoms or physical exam components which you could highlight?

• The patient's physical exam was relatively normal. Of note, the fundoscopic exam did not reveal papilledema and no renal bruit was auscultated.
• His Pupils were equal, round, and reactive to light. The face was...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of a 16 year old with fever and a rash.

Here's the case:

A 16 year old F presents to the PICU with generalized weakness, fever and a diffuse rash**.** Three days prior to admission she stated that she was feeling lightheaded and the day after she started having frequent non-bloody diarrhea. She states that she has otherwise been healthy, no sick contacts or travel, and the only change in her life was her menstrual cycle which ended a few days before her symptoms started. She says that about two weeks ago, she went to her primary care physician to get an in-grown toe nail drained, but was able to recover after some analgesia and antibiotics for a week. On day of admission her mother brings her into the ED as she says her rash continues to progress. Her mother states that the rash looks like a sunburn. Mother noticed on day of admission that her daughter now had red injected eyes bilaterally without discharge, and was becoming increasingly confused with her fevers. Of note, the patient has also has had decreased oral intake as she says her mouth quote hurts when she swallows. She has had no sore throat, congestion, dysuria, or headache. She presents to the ED febrile to 39 C and tachycardic to 130 bpm. She is ill appearing and has orthostatic vital signs. Her exam is notable for palpable diffuse myalgia, oropharyngeal hyperemia, diffuse erythroderma, and conjunctival injection. She is noted to have a hyperdynamic precordium and faint crackles bilaterally. Her L toe is mildly erythematous with no discharge, necrosis or pain to palpation. Acute resuscitation and diagnostics are begun and patient is transferred to the pediatric intensive care unit.

To summarize key elements from this case, this patient has:

• Hx of a fever and multisystem involvement including GI manifestations, myalgias, confusion, mucositis, and rash
• This is in the setting of a local drainage procedure and course of antibiotics.
• In addition, she presents now with fever, hypotension, and tachycardia.
• These elements so far bring up a broad differential but for now we can agree that it seems that she has signs of acute inflammation or infection throughout her body.

nsition into some history and physical exam components of this case.

1. If we take a step back, what are key history features in a child who presents with fever & rash?

• Understanding the characteristics of the rash, the evolution, and progression of the rash is important.
• In the setting of myalgias, fever, headache, and rash you should think of assessing for any recent travel as tick-borne illnesses commonly present with this symptomatology.
• You also want to assess for recent antibiotic exposures, sexual history, and surgical history - in our case, our patient had a recent procedure on her...

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

Key Learning Points:

• Exposure to house fire and prolonged cardiac arrest
• Signs of inhalation injury and airway compromise
• Pathophysiology of inhalation injuries and their impact on multiple organ systems
• Management strategies for inhalation injury, including airway protection and ventilation
• Differentiating carbon monoxide and cyanide poisoning in pediatric fire victims

Case Presentation

A 15-year-old previously healthy girl is brought to the Pediatric Intensive Care Unit (PICU) after experiencing cardiac arrest during a house fire. She was found unconscious by firefighters after a heroic rescue attempt where she saved her brother and his friend. Upon arrival at the hospital, she was unresponsive, intubated, and in severe cardiovascular distress with signs of multi-organ dysfunction.

Key findings include:

• Soot deposits and superficial burns on extremities
• Prolonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR)
• Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refill
• Metabolic acidosis, AKI, coagulopathy, transaminitis
• Severe hypoxic-ischemic encephalopathy on EEG

These findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion.

Pathophysiology of Inhalation Injury

When a patient is exposed to smoke and hot gases during a fire, inhalation injury results in significant damage to the respiratory system. Inhalation injury has three main components:

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

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamatand I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of a 19 month old female with bloody stool, petechiae and no urine output

Here's the case presented by Rahul:

A 19 month old previously healthy female was brought to the pediatric emergency department for blood in her stool. Patient was at daycare the previous day where she developed a low grade fever, congestion and URI symptoms along with non-bloody-non-bilious vomiting and diarrhea. Patient had a rapid COVID test which was negative and was sent home with instructions for oral hydration. That evening, patient began having vomiting/diarrhea which worsened. She was unable to retain anything by mouth and her parents also noted blood in her stool.

Due to this, she was rushed to the Emergency Department. In the ED here, she was hypertensive for age BP of 124/103 mm Hg, febrile, and ill. Specks of blood were noted on the diarrheal stool in the diaper.

On her physical exam she was noted to be pale with petechiae on neck and chest. Her abdomen was soft, ND, with some hyperactive bowel sounds, and no hepatosplenomegaly. The rest of her physical examination was normal.

In the ED, initial labs were significant for WBC 19, Hgb 8.8, and Platelets 34. CMP was significant for BUN of 74mg/dL and Cr of 3.5mg/dL, Na 131 mmol/L, and K of 5.5mmol/L, Ca 8.3mg/dL (corrected for albumin of 2.2g/dL), Phosphorous 8.5 AST 413, and ALT of 227, LDH > 4000. BNP was 142 and troponin negative. She was given 1 dose of CTX 50mg/kg and a 20cc/kg NS bolus. Stool PCR was sent. She was given labetalol for her hypertension, started on maintenance IV fluids and transferred to the PICU for further management.

Rahul to summarize key elements from this case, this patient has:

• We have a 19-month old child with
• Diarrhea and emesis X 2 days
• No urine output for over 24 hours
• Bloody stool
• Petechiae on the neck and chest
• Anemia and thrombocytopenia

All of which bring up a concern for hemolytic uremic syndrome the topic of our discussion today

Let's transition into some history and physical exam components of this case.

What are the key historical features in this child who presents with above?

• Bloody stool which alludes to an invasive diarrhea
• No urine output and an ill appearing state which points to a systemic inflammatory condition and end organ dysfunction.

Are there some red-flag symptoms or physical exam components which you could highlight?

• Presence of petechiae which are physical exam features of thrombocytopenia

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat.

My name is Rahul Damania, a current 3rd year pediatric critical care fellow. We come to you from Emory University School of Medicine-Children's Healthcare of Atlanta.

Today's episode is very special as we are going to be discussing 7 Habits of Highly Effective PICU fellows. As many trainees, both residents and fellows are settling into the year, We wanted to make a special podcast which highlights some key, high value habits Which can make the pediatric critical care experience very fruitful longitudinally!

We are delighted to be joined by Dr. Kevin Kuo and Dr. Paige Stevens.

Dr. Kuo is a Clinical Associate Professor, Pediatrics - Critical Care as well as the Program Director, Pediatric Critical Care Fellowship at Stanford University. Notably, Dr. Kuo is also the site creator and editor of the informational & well-known PICU website learnpicu.com- which accumulates over 10K views a month. Dr. Paige Stevens is a PCCM fellow at Stanford University and is here to provide the trainee perspective.

Dr. Kuo and Dr Stevens - we are delighted to have you. Welcome to PICU doc on call podcast.

• Dr Kuo or Stevens: Thank You Pradip and Rahul for having us on PICU Doc on Call. We have no relevant financial disclosures or conflicts of interest.

Our episode will be a series of actionable steps which can optimize your passion and performance in the PICU. This episode was inspired by the very famous book: The 7 Habits of Highly Effective People by Steven Covey which is an international bestseller.

To start with our episode, Dr. Kuo, do you mind highlighting the 7 Habits which we will cover:

• KK: Sure, here they are:
• From Dr. Covey's book we wanted to start with Begin with the End in Mind as the first habit
• Second, Embrace a Growth Mindset
• Third, Eat a Piece of Humble Pie Daily
• Fourth, Remember the ABCs
• Fifth, Put on Your Own Oxygen Mask First
• Sixth, Be Aware of the Meta
• Seventh, Sing in the Rain

Awesome, I can't wait to get into each of these. Dr. Kuo can you start us off with the first habit — Begin with the End in Mind?

• Dr. Kuo: sure
• 3 years goes by very quickly - what do you want your career to look like, what skills do you want to have gained, what things do you want to accomplish by the end of your three years, where do you want to work when you finish (academic vs community)?
• Be honest with...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Here's the case:

A 6-year-old child with a known h/o craniopharyngioma who has been endocrinologically intact with exception of needing thyroid replacement was admitted to the PICU prior to craniotomy to proceed with further tumor resection as well as the removal of a secondary cyst impacting his brainstem. The patient is receiving Keppra for seizures and per mother, he has recently been significantly more sleepy at school.

On POD Op day 5: the PICU the bedside nurse notices increased urine output (6cc/kg/hr to as high as 10cc/kg/hr). Initially, there was an increase in Na to 157mEq/L within 48-72 hours the serum Na dropped to 128mEq/L

To summarize key elements from this case, this patient has:

• Increase UOP
• Rapidly increasing Na initially followed by a drop
• All of which brings up a concern for Na abnormality post craniotomy

In today’s episode, we will be breaking down all things Sodium & the Brain. We will discuss diagnostic & management frameworks related to three pathologies:

1. Central Diabetes Insipidus
2. Syndrome of inappropriate Anti-Diuretic Hormone or SIADH
3. Cerebral Salt Wasting

These diagnoses can certainly be seen individually inpatients or as a spectrum of diseases — as we go through each of these diagnoses, pay particular attention to patient characteristics and lab abnormalities. Namely, serum sodium, serum osm, and urine osm.

To build the fundamentals, lets first start with classic nephrology saying: Serum Na represents Hydration

This takes us into a brief review of normal physiology — talking about three important hormones:

1. ADH
2. Aldosterone
3. Atrial Natriuretic Peptide (ANP)

Let’s go through a quick multiple-choice question.

A patient is recently started on DDAVP for pan-hypopituitarism. The medication acts similarly to a hormone that is physiologically synthesized in which of the following from which are in the body?

A. Paraventricular Nucleus of the Hypothalamus

B. Supraoptic Nucleus of the Hypothalamus

C. Anterior Pituitary

D. Vascular Endothelium

The correct answer here is B the Supraoptic Nucleus of the Hypothalamus. Remember that ADH is synthesized in the hypothalamus and released from the posterior pituitary.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our episode, which is Part 2 of our acute severe asthma management. Today we discuss invasive mechanical ventilation of the acute asthmatic.

A patient with a history of asthma presents to the PICU with decreased air entry. Somnolence. Hypercarbia and drooling. The patient is hypoxemic and has see-saw breathing.

Rahul: Let’s dive right into this. What are the indications for intubating a child with acute severe asthma?

Absolute indications include:

• Altered mental status which may be preceded by obtundation, agitation
• Cardiac and respiratory arrest

Relative indications decided on a case by case basis:

Progressive exhaustion-despite, despite maximal therapy. Profound hypoxemia refractory to supplemental oxygen administration, and respiratory failure.

The decision to intubate should not be solely determined based on blood gas results.

Pradip, can you shed light on how we prepare for the intubation of the patient with acute severe asthma?

Rahul, first and foremost- we take the intubation of an asthmatic very seriously. In fact we try the whole “kitchen sink” to avoid intubation. But there will be times when we have to intubate especially for the indications you mentioned above.

The intubation will worsen the patient’s bronchospasm, put the patient at risk for barotrauma as well as cardiovascular collapse.

Preparation is the key- A team huddle and mapping prior to proceeding to intubate is the key. Every person in the room should have clear roles and responsibilities. Scenarios of what to do if “X” happens should be clearly laid out to the team by the team leader (preferably the attending or a senior fellow). The senior-most experienced person should manage the airway. At least two dedicated RTs to provide bag-mask ventilation as well as manage the ventilator are required. Nursing roles to push meds, chart the vitals and other activities as well a role for the resource nurses to help in case of cardiac arrest should be clearly laid out. Additionally, facilities that have access to isoflurane should have that ready to go. We typically give a heads up to our ECMO team to be on stand-by.

Prior to Intubation: Have central access or multiple large-bore PIVs if possible. Keep crystalloids boluses ready for hypotension. We also have peri-arrest epinephrine as well as an epinephrine infusion ready for any hypotension, bradycardia, or cardiac arrest. For intubation, we typically use Ketamine, fentanyl, and rocuronium (some centers may use succinylcholine). We use cuffed endotracheal tube. We don't bag-mask at fast rates but rather wait for a full expiration prior to the next breath being delivered. These patients require slow respiratory rates with very prolonged expiratory times to allow for adequate gas exchange and lung volumes. A helpful technique is to use a stethoscope to auscultate at...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode a 2-year-old with severe pallor and O2 desaturation.

Here's the case presented by Rahul:

A two-year-old presents to the PICU with severe pallor + O2 requirement. The patient went for a routine check with her primary care who noted the patient appeared severely pale. He sent the patient to the ED. An initial Hgb check revealed a Hgb of 1.5gm/dL. Per mother, she is otherwise healthy but a very picky eater. She also reports the patient drinks milk as a soothing adjunct at night, consuming between 12 - 36oz a day. No family h/o of anemia or any other blood disorders.

No h/o recent illness. Mother had a normal spontaneous full-term delivery. The patient is up to date on her immunizations. Per mother, developmental milestones are normal. The mother also denies any history of decreased activity in the child. Given the low Hgb, the patient was admitted to the PICU.

Let's transition into some history and physical exam components of this case?

What are key history features in this child?

• Severe pallor in a 2-year-old
• H/o being a picky eater
• H/o excessive milk consumption
• Pertinent negatives include: No obvious blood loss, No petechia, bruising, or jaundice

What did the physical exam show?

• The patient was hypertensive, tachycardic to the 140s, and 10th% weight for growth percentiles
• On physical exam, the patient was in no acute distress. Her lips, gums, and conjunctiva were pale. She had a systolic ejection murmur. As a pertinent negative, she had no hepatosplenomegaly. She also has no rash, bruising, or petechiae.

The lack of hepatosplenomegaly may indicate that the patient has no signs of extramedullary hematopoiesis. Patients with hemolytic processes resulting in anemia may present with signs of scleral icterus, jaundice, and hepatosplenomegaly resulting from increased red cell destruction. In fact, in an emergency department setting, the clinical detection of jaundice was found to have sensitivity and specificity of only approximately 70 percent.

To continue with our case, then what were the patient's labs consistent with:

• Initial CBC showed: WBC 8.5K, RBC 1.14 (L), Hgb 1.5gm/dL; Hct 6.1, MCV 53.5, and an elevated RDW 37.7. Initial platelet count was 50K, reticulocyte count 1.1%
• Peripheral smear revealed no blasts, thrombocytopenia - with occasional medium-sized platelets - ghost cells and anisocytosis/poikilocytosis- which appears most consistent with iron deficiency.
• It was interesting that the patient had...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat. I’m Dr. Ali Towne, a rising 3rd-year pediatrics resident interested in a neonatology fellowship, and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode a 5-month-old, ex-28 week female with abdominal distention.

Here's the case:

A 5-month-old, ex 28 week, female with a past medical history of severe BPD, pulmonary hypertension, home oxygen requirement, and G-tube dependence presents with hypoxemia and increased work of breathing.

The patient has a history of prolonged NICU stay with 8 weeks of intubation. The patient developed worsening respiratory distress requiring increased support and eventual intubation for hypoxemic respiratory failure. Echo showed worsened pulmonary hypertension with severe systolic flattening of the ventricular septum and a markedly elevated TR jet. The patient had poor peripheral perfusion, and upon intubation was started on milrinone and epinephrine. The patient improved, but the patient then developed abdominal distention and increasing FiO2 requirements prompting an abdominal x-ray. X-ray showed diffuse pneumatosis with portal venous gas. The patient was made NPO and antibiotic therapy was initiated.

To summarize key elements from this case, this patient has NEC.

• NEC is not a homogenous disease, but rather a collection of diseases with similar phenotypes.
• Some people split NEC into two categories: Cardiac NEC and Inflammatory NEC.
• Babies who develop cardiac NEC tend to be significantly older than babies who develop inflammatory NEC (about 1 month vs 2 weeks).
• There are three main contributory factors to the development of NEC: gut prematurity, abnormal bacterial colonization, and ischemia-reperfusion injury.
• Many cases result from an ischemic insult to the bowel, resulting in translocation of intra-luminal bacteria into the wall of the bowel, but the etiology and course of NEC can be very variable.
• This translocation can cause sepsis and death; the ischemia of the bowel can result in intestinal perforation and/or necrosis.

Necrotizing enterocolitis (NEC) is one of the most common gastrointestinal emergencies in the newborn infant. It is estimated to occur in 1 to 3 per 1000 live births. More than 90 percent of cases occur in very low birth weight (VLBW) infants (BW <1500 g) born at <32 weeks gestation, and the incidence of NEC decreases with increasing gestational age (GA) and BW.

What are key risk factors for the development of NEC?

• Prematurity and Birth Weight
• NEC incidence is inversely proportional to gestational age.
• Congenital Heart Disease
• Puts children at risk for NEC due to (1) decreased stroke volume, and (2) improperly oxygenated blood which...

Today’s episode is dedicated to the acute management of anterior mediastinal mass in the PICU. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Lisa Lima and Dr. Tom Austin. 

Dr. Tom Austin is the Director of General Pediatric Anesthesiology at Children’s Healthcare of Atlanta-Egleston. He is also an Associate Professor of Anesthesiology and Pediatrics at Emory University School of Medicine.

Dr. Lisa Lima is a Fourth Year Advanced Technology Fellow in the Division of Critical Care at Children’s Healthcare of Atlanta. She’s also the Senior Associate in the Department of Pediatrics at Emory University School of Medicine. She’s one of the only pediatric-trained ECMO Fellows in the country. 

Show Highlights:

• Our case, symptoms, and diagnosis: A 17-year-old female has facial swelling and shortness of breath. She recently went to her primary care physician and received a steroid burst and Benadryl for the facial swelling. On the day of admission, her mother noticed that the patient had a deep voice and a “funny” inspiratory sound. The patient presented to the ER and was noted to have a widened mediastinum on a chest x-ray, bringing up concern for an anterior mediastinal mass.
• Key presentation features for mediastinal masses
• What defines a widened mediastinum?
• Important differentials to consider with mediastinal masses:
• Take the patient’s history and presentation into context, like if there was a high-impact motor vehicle collision, history of congestive heart failure, lupus, transplant, leukemia, or lymphoma
• Pay attention to the Four T’s: thymoma, teratoma, ATLL(lymphoma), and thyroid masses
• Key principles that might put pediatric patients with mediastinal masses at risk for anesthetic agents
• Important pathophysiologic issues for patients with mediastinal mass include compressed trachea, blocked access to lungs, and right ventricular failure; these effects can be magnified under general anesthesia
• Why we need to have great appreciation of the risk of cardiovascular collapse in patients in a tenuous physiological state
• General management strategies for those patients who are unable to lie flat or may not tolerate a diagnostic scan: patient history, personal physical exam, determining a rescue position
• Key considerations for the patient in the PICU:
• Keep the patient spontaneously breathing
• Have adequate access with large-bore IVs in sites with no anatomic compression
• Have a rescue position
• Have a backup plan for rapid deterioration
• Communicate with others on the patient care team
• Why the Chamberlain procedure is used to obtain a tissue biopsy when there isn’t another primary biopsy site
• Key anesthesia principles for patients needing intrathoracic biopsies:
• Have clear role assignments in the multidisciplinary team approach
• Keep the patient spontaneously breathing
• Manage the patient’s pain
• Employ liberal use of local anesthetics
• Avoid intubation if possible
• If necessary, use fiber optic intubation
• Keep large-bore IVs in extremities
• Why it’s important to stress interdisciplinary involvement early in management
• Key factors to consider in patients headed to the OR about airway compression and vascular compression
• Takeaway clinical pearls regarding anterior mediastinal masses:
• Remember the Four T’s
• The pathophysiology of local compression
• Emphasize a streamlined...

Today’s episode is dedicated to the differentiation and management of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)

We are delighted to be joined by Dr. Eric Felner. Dr. Felner is a Professor of Pediatrics/Pediatric Endocrinology at the Emory University School of Medicine and is an Adjunct Professor of Chemical and Biomedical Engineering at Georgia Tech.

Show Highlights:

• Our case, symptoms, and diagnosis: A 15-year-old male presents with a one-week history of increased urination. He is otherwise healthy except for a viral URI last week. He is found to be disoriented and tachycardic, with an exam notable for delayed peripheral capillary refill and cool extremities. The patient has deep, labored respirations upon examination, and labs confirm hyperglycemia with a serum glucose of 850, mild acidosis, and 2+ ketones. His CPK level is elevated, and a crystalloid fluid bolus is started. 
• Hyperosmolar hyperglycemic state is defined as a serum glucose greater than 600 mg/dL, serum osmolality of 330 mOsm/kg, and the absence of ketosis and acidosis.
• The key difference between HHS and DKA is that DKA is characterized by the presence of ketones in the blood and acidosis, but HHS means these are completely absent.
• Even though DKA and HHS are similar, their management strategies have their own nuances.
• In DKA, the lack of insulin leads to management strategies, while HHS is marked by complete dehydration and excessive urination. 
• Factors that point to HHS will be a very overweight child, family history, and ethnicity; Type-2 diabetes is much more common in African-American, Latin-American, and Native-American children, while Type-1 is more common in Caucasians. 
• Specific labs for patients with suspected DKA or HHS include a comprehensive metabolic panel (CMP), blood gas, and CPK for HHS.
• For both conditions, management strategies focus on insulin and fluid administration, but there are key differentiations:
• DKA is managed using the triple bag therapy that was pioneered by Dr. Felner.
• There is a risk for cerebral edema with administering fluid.
• The most important data relating to fluid administration with regard to neurological outcomes is what we have learned in calculating fluids with the “2x maintenance formula” to guard against mistakes that could result in cerebral edema.
• Key considerations regarding low-dose vs. standard-dose insulin therapy revolve around the weight and age of the pediatric patient.
• For HHS, the key is to manage fluids and give insulin; for Type-1 diabetics, the key is to eliminate acidosis.
• Key PICU management pearls in minimizing cerebral edema risks are to determine the level of sickness by the PCO2 level, high BUN, and by not giving bicarbonate. Remember that children under age 5 have a higher risk for cerebral edema.
• In the management of both DKA and HHS, remember that it comes down to how sick a patient is and not necessarily following the numbers. 
• In general pediatrics, managing a sick DKA patient means giving an IV, administer fluids, and call a specialist management team right away.
• Dr. Felner discusses the association between COVID-19 and Type 1 diabetes based on his experience. 
• As intensivists and endocrinology teams work together to transition patients to an intermittent insulin regimen, it’s important to remember how to convert from IV insulin to subQ insulin. 
• Takeaway clinical pearls include the key diagnostic elements between DKA and HHS. In HHS, patients will have higher glucose levels, milder acidosis, mild ketosis, and increased dehydration. Both conditions will have insulin and fluid management, and HHS patients may require increased fluid resuscitation. 

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat

and my name is Rahul Damania and we come to you from Children's Healthcare of Atlanta Emory University School of Medicine. Today's episode is dedicated to optimizing your Pediatric Critical Care Knowledge and study skills by utilizing your medical librarian.

We are delighted to be joined by Ms. Carrie Price a health Professions librarian. Carrie was formerly at the Welch Medical Library, serving the faculty, students and staff of Johns Hopkins Medical Institutions. Ms Price is currently at the Albert S. Cook Library of Towson University in Towson, Maryland.

Ms Price is an expert searcher with a strong interest in user-centered and instructional design, evidence-based medicine, and inter-professional education.

Ms Price also maintains and updates a YouTube Channel with videos about citation management, searching, and evidence-based medicine. Carrie is on twitter @carrieprice78

Q1. Carrie welcome to PICU DOC on Call Podcast. Our topic today— Value of the librarian in PedsICU education and it is one of the first in our series of how learners can organize their study habits while rotating in the PEDS ICU.

Carrie: Thanks Rahul and Pradip for having me on PICU DOC on Call podcast. I have no conflicts of interest or financial disclosures.

Q2. Carrie tell us your story and how you came to be an expert medical librarian ?

Carrie: I came into librarianship as a second career, after a first career in nonprofit development. I was fortunate to start my work in libraries at Johns Hopkins University, where I worked as a library assistant in access services while getting my masters degree in library science. During this time my mom was diagnosed with appendix cancer, a rare cancer, (she's okay now), and through the time we spent together in the hospital, I noticed there was a medical library in the building. I had this epiphany that librarians weren't limited by traditional career paths. From then I started focusing on health and consumer health classes. Later, at a work all-staff meeting, I literally bumped into the former director of the Welch Medical Library, and the rest is history! I applied for an open position, was hired, and started working at the Welch Medical Library in 2012. It has been an incredible experience. I am fortunate to work extensively with a number of departments and divisions at Johns Hopkins and now at Towson University, so my experiences have been really multidisciplinary. In the past I worked as a physical therapy technician, which was awesome and helped inform the knowledge I brought to the profession. I've taken a lot of professional development in the field. I just never stop learning, and I love sharing information on Twitter, YouTube, and on my website, which is carrieprice78.github.io.

This is such an amazing story!

Q3: Carrie the practice of critical care medicine requires that learners in the Peds ICU remain current in their knowledge of the literature. Given an overwhelming amount of information out there how should these learners drink from that fire hydrant without being blown away?

Carrie: I think that's an excellent question. Prior to the arrival of internet, most additional knowledge was acquired from physically going to a library and perusing through peer reviewed journals and textbooks. Now, things are digital and even "born-digital" — and there is so much information available online and on your phone.... I understand that given how much information is out there, a learner can feel overwhelmed and have difficulty trusting the information they see. That's why critical appraisal is a key part of evidence-based practice. Studies have shown the value of readily-available information in patient care and have highlighted the role of the library and...

Today’s episode is dedicated to the approach to thyroid storm. It’s the first in our Mini-Case series.

Show Highlights:

Our case, symptoms, and diagnosis: A 12-year-old female presents to the PICU with chest discomfort. She was noted to be anxious by her parents over the past few days. They felt she was a bit "off," as she would constantly drop items and have a tremor. A few weeks prior to these symptoms, she was noted to have rhinorrhea, congestion, and progressive neck swelling. Her parents became increasingly concerned this morning as her temperature was 104F. Per her parents, she was agitated throughout the night and became increasingly somnolent in the early morning. 

To summarize key elements from this case, this patient has:

• Chest pain likely due to a cardiac etiology or musculoskeletal cause.
• Tremor likely due to a primary neurologic cause or increased metabolic drive.
• Neck swelling with fever after a prodrome of URI symptoms which could be concerning for lymphadenitis or thyroid goiter.
• Synthesizing these symptoms together, this patient likely has a systemic etiology such as hyperthyroidism, with the most severe manifestation being thyroid storm, a toxidrome, or a pheochromocytoma. Given the fever and altered mental status, considering sepsis is key.

Key history features in this child with tachycardia and signs of hyperthyroidism:

• High fevers up to 104F
• Altered mental status
• Neck swelling 

Red flag symptoms and physical exam components in a patient with severe hyperthyroidism include:

• Airway
• Check for dyspnea or stridor when the patient is supine.
• Do a Mallampati assessment.
• Auscultate for a bruit in the neck. 
• Cardiovascular system
• Concerns include congestive heart failure and cardiac dysrhythmias.
• Widened pulse pressure is common 

The American Thyroid Association has advocated for the Burch-Wartofsky Point Scale (BWPS) for severe thyrotoxicosis. A score of 45 or higher indicates thyroid storm. A case-control study published in 2015 in the Journal of Endocrinology noted that the BWPS may overdiagnose up to 20% of patients. Clinical criteria on the BWPS include the following:

• Thermoregulatory dysfunction
• Central nervous system effects
• Gastrointestinal-hepatic dysfunction
• Cardiovascular dysfunction
• Congestive heart failure
• Presence or absence of a precipitant history of URI or underlying thyroid condition

Back to our specific case, the patient's labs are consistent with low TSH and elevated free T4, indicating primary hyperthyroidism, positive for TSH-receptor antibodies, and the diagnosis of thyroid storm was confirmed.

• Other lab findings included elevated WBC, high ALT and AST, elevated glucose, and elevated cortisol. Her cardiac evaluation was notable for sinus tachycardia with occasional PACs.
• Other important labs include a coagulation panel, BNP and lactate, CRP, procalcitonin, blood cultures, and basic blood chemistries.

Let’s quiz ourselves with a multiple choice question:

• A patient with thyroid storm is admitted to the PICU. He is started on thyroid modulating therapy. Which of the following mechanisms of action does this medication likely work by?
•  A. Activate Thyroid Peroxidase
•  B. Inhibit Thyroid Peroxidase
•  C. Inhibit Iodine Uptake within the Thyroid
•  D. Increase conversion from T4 to T3

   The correct answer is B. The most likely medication which is used in thyroid storm is methimazole or propylthiouracil.

Introduction

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.

Episode Overview

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.

Case Presentation

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.

Key Case Points

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

Expert Discussion with Dr. Karen Zimowski

Risk Factors and Epidemiology of VTE in Pediatrics

• 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.

Clinical Manifestations of DVT

• 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...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania, and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode a 24-month-old girl with increased seizure frequency.

Here's the case:

A 24-month old girl presents to the ED with h/o shaking/jerking episodes in her sleep. The patient was in the care of her aunt when this acute episode occurred. When the father arrived from work, he saw his daughter having episodes of her body shaking alternating with heavy breathing. The patient would not wake up in between episodes. There was pertinently no history of trauma. 911 was called and when EMS arrived, she was starting to arouse and respond to stimuli. The patient was transported to the ED. In the ambulance, the patient continued to have similar shaking and jerking episodes and was given rectal diazepam. On arrival to ED, the patient had a fever of 38.5 Centigrade. Due to ongoing seizures, the patient was loaded with Fosphenytoin, after having been given a total of two doses of IV Lorazepam. The patient was subsequently intubated for airway protection and respiratory failure. A respiratory viral panel was negative for SARS-COV-2 but positive for Rhino-enterovirus. The patient was admitted to the PICU with cEEG monitoring and placed on mechanical ventilation with fentanyl + dexmedetomidine infusions with as needed Midazolam administrations

Her physical examination on arrival to the PICU was unremarkable. She wasn't interactive as she had just received sedation after intubation. On her neuro-examination, Pupils are equal and punctiform. The face is symmetric. The tongue is midline. Normal bulk and tone. No spontaneous movements were noted. No withdrawal to painful stimuli. Tendon reflexes were equal throughout. No clonus is noted.

Rahul, to summarize key elements from this case, this patient has:

• Fever
• Viral infection with Rhinoentero virus
• Generalized Tonic clonic seizure lasting > 5minutes
• Acute respiratory failure
• All of which brings up a concern for status epilepticus

Absolutely, we will get to this later on in the episode; however, remember that Status epilepticus is historically defined as single epileptic seizure of >30 minutes duration or a series of epileptic seizures during which function is not regained between ictal events in a 30-minute period

• Let's transition into some history and physical exam components of this case?

1. What are key history features in this child who presents with status epilepticus?

• Prolonged Seizures
• Fever with viral symptomatology which may act as a trigger
• A pertinent negative is that this patient had no history of trauma or co-morbid conditions such as a genetic syndrome.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode: A Somnolent Toddler.

Here's the case:

A 2 yo M presents to the PICU after being found increasingly sleepy throughout the day. The toddler is otherwise previously healthy and was noted to be in his normal state of health prior to today. The mother dropped the toddler off at his Grandmother’s home early this morning. Grandmother states that he was playing throughout the day, and she noticed around lunchtime the toddler stumbles around and acts more sleepy. She states that this was around his nap time so she did not feel it was too out of the ordinary. The toddler 1 hr later was still very sleepy, and the grandmother noticed that the toddler had some shallow breathing. She called mother very concerned as she also found her purse open where she typically keeps her pills. The grandmother has a history of MI and afib as well as hypertension. She is prescribed a multitude of medications. Given the child’s increased lethargy, the grandmother presents the patient to the ED. In the ED, the child is noted to be afebrile with HR 55 & RR of 18. His blood pressure is 78/40. On exam he has minimal reactivity to his pupils, he has shallow breathing and laying still on the bed. A POC glucose is 68 mg/dL. Acute resuscitation is begun and the patient presents to the PICU.

To summarize key elements from this case, this patient has:

• Drowsiness
• Bradycardia
• Normotension
• This is in the setting of being at grandma’s home and having access to many medications
• Given the hemodynamic findings and CNS obtundation, this patient’s presentation brings up concern for a clonidine or beta-blocker ingestion.
• This episode will be organized:
• Beta-Blocker poisoning
• We will also examine other medications that potentially can be toxic to a toddler (one pill can kill) present in Grandma's purse which include: TCA, CCB, Opioids, oral anti-diabetic agents, digoxin, etc.

The presence of a grandparent is a risk factor for unintentional pediatric exposure to pharmaceuticals commonly referred to as the Granny Syndrome. Grandparents’ medications account for 10% to 20% of unintentional pediatric intoxications in the United States. To kids, all pills look like candy.

• Let’s start with a multiple choice.
• An overdose of which of the following medications may mimic the presentation of Metoprolol overdose?
• A. Verapamil toxicity
• B. Ketamine toxicity
• C. Valium toxicity
• D. Lithium toxicity

The correct answer is A, verapamil toxicity.

• Verapamil is a non DHP CCB.
• It acts at the level of the SA and AV node similar to Metoprolol, a beta-1-specific antagonist.
• Both cause bradycardia and AV node block.
• Valium though a CNS depressant, can cause CV depression as well, however, would have fewer changes on the conduction system compared to a non-DHP CCB.

 What is the mechanism of toxicity with beta-blockers?

Beta-blockers are competitive inhibitors at beta-adrenergic binding sites, which results in decreased production of intracellular cyclic adenosine monophosphate (cAMP) with a resultant blunting of multiple metabolic and cardiovascular effects of circulating catecholamines.

• They attenuate the effect of adrenergic catecholamines on the heart
• Decrease inotropic and chronotropic...

Acute pulmonary Hypertensive Crises.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode a 7 month old boy ex-26 week premature infant with acute hypoxemia, bradycardia episodes, poor perfusion

Here's the case:

A 7 month old ex-26 week male was transferred from the outside hospital to our PICU for tracheostomy evaluation. Patient was intubated on second day of life. He had a prolonged course, on inhaled Nitric Oxide for first 2-3 months of life in the setting of severe pulmonary hypertension, requiring HFOV for a prolonged period of time. Failed extubation attempts multiple times. Received steroid burst x2. BPD settings trialed (lower rate, longer iTime, high PEEP, larger TV) without improvement. At time of transfer he was in PRVC mode on the ventilator — TV ~10ml/kg, 50%, PEEP 8, rate 28 (Peak pressures 27-32). Patient received albuterol Q4 for bronchospasm/wheezing and pulmicort BID. Patient was deeply sedated with morphine and midazolam. Interstitial lung disease panel was negative. ECHO showed: systolic septal flattening, moderate RV hypertrophy with normal systolic functioning. Patient was not on any PH medications at transfer. Patient is also on furosemide, hydrochlorothiazide and spironolactone.

Patient has completed a course of antibiotics for klebsiella tracheitis from a ETT CX a week prior to admission to our picu. Patient tolerated feeds via an NJ tube.

The team continues to evaluate his case as the Patient continues to have episodes of acute desaturation, tachycardia, cool extremities and poor perfusion.

To summarize key elements from this case, we have a 7month old who is ex-26 week premie

• Patient has BPD and is on high vent settings and failing extubation
• Abnormal echocardiogram with flat septum and hypertrophied Right ventricle
• Episodes of cold shock-tachycardia, poor perfusion, and cool extremities
• Hypoxia

All of which bring up a concern for acute pulmonary hypertensive crisis

Rahul Let's transition into some history and physical exam components of this case?

What are key history features in this infants who presents with an acute pulmonary hypertensive crisis

• Prematurity
• BPD

Remember BPD is defined by a requirement of oxygen supplementation either at 28 days postnatal age or 36 weeks postmenstrual age.

Are there some red-flag symptoms or physical exam components which you could highlight?

• Presence of cold shock: tachycardia, cool extremities and poor...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode a three-year-old girl with altered mental status and acute respiratory failure

Here's the case presented by Rahul—

A three-year-old presents to the PICU with altered mental status and difficulty breathing.

Per the mother, the patient was in the usual state of health on the day prior to admission when the mother left her in the care of her maternal grandmother. When mom arrived home later in the afternoon, mom was unable to wake her and reported that she seemed "stiff". She did not have any abnormal movements or shaking episodes. Mom called 911 and the patient was brought to our ED. No known head trauma, though the patient is in the care of MGM throughout the day. No emesis. No recent sick symptoms. No witnessed ingestion, however, the patient's mother reports that MGM is on multiple medications (Xarelto, zolpidem, Buspar, gabapentin, and acetaminophen) and uses THC-containing products specifically THC gummies. In the ED: The patient had waxing and waning mentation with decreased respiratory effort. GCS was recorded at 7. Arterial blood gas was performed showing an initial pH of 7.26/61/31/0. The patient was intubated for airway protection in the setting of likely ingestion. The patient has no allergies, immunizations are UTD.

BP 112/52 (67) | Pulse 106 | Temp 36.2 °C (Tympanic) | Resp (!) 14 | Ht 68.5 cm | Wt 14.2 kg | SpO2 100% | BMI 30.26 kg/m²

Physical exam was unremarkable-pupils were 4-5mm and sluggish. There was no rash, no e/o of trauma

Initial CMP was normal with AG of 12, CBC was unremarkable, and Respiratory viral panel was negative. Serum toxicology was negative for acetaminophen, salicylates, and alcohol.

Basic Urine drug screen was positive for THC

To summarize key elements from this case, this patient has:

• Altered mental status: - waxing and waning with GCS less than 8 suggestive of decreased ventilatory effort pre-intubation
• impending acute respiratory failure
• Dilated but reactive pupils
• All of which brings up a concern for possible ingestion such as THC (but cannot rule out other ingestion)
• This episode will be organized…
• Pharmacology of Cannabis
• Clinical presentation of Cannabis toxicity
• Workup & management of Cannabis toxicity

The Cannabis sativa plant contains over 500 chemical components called cannabinoids, which exert their psychoactive effect on specific receptors in the central nervous system and immune system. The 2 best-described cannabinoids are THC and cannabidiol (CBD)—and are the most commonly used for medical purposes. Patients with intractable epilepsy or chronic cancer pain may be using these drugs. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication. The term cannabis and the common name, marijuana, are often used interchangeably).

Rahul, can you shed some light on the pharmacokinetics/pharmacodynamics of cannabis?

Cannabis exists in various forms: marijuana (dried, crushed flower heads, and leaves), hashish (resin), and hash oil (concentrated resin extract), which can be smoked, inhaled, or ingested. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication, in contrast to CBD, the main...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat.

My name is Rahul Damania, a current 2nd-year pediatric critical care fellow. We come to you from Children’s Healthcare of Atlanta-Emory University School of Medicine.

Today's episode is dedicated to pediatric post-cardiac arrest care.

We are going to split this topic into two episodes, part one of pediatric post-cardiac arrest syndrome will address the epidemiology, causes, and pathophysiology.

I will turn it over to Rahul to start with our patient case...

• 11 yo previously healthy M who is admitted to the PICU after cardiac arrest.
• The patient was noted to be found unresponsive and submerged in a neighborhood pool.
• He was pulled out by bystanders and CPR was started for 5 minutes with two rounds of epinephrine prior to achieving ROSC.
• During transport to the OSH, the patient developed hypotension requiring a continuous epinephrine infusion.
• His initial blood gas was notable for a mixed respiratory and metabolic acidosis:
• 7.0/60/-20
• His initial serum lactate was 6.8 mmol/L.
• He presents to the PICU with a temperature of 36.6, HR 130s, MAPs 50s on Epinephrine infusion at 0.03mcg/kg/min
• He is mechanically ventilated with notable settings PEEP of 10, FiO2 65%.
• The patient is taken to head CT which shows diffuse cerebral edema and diffusely diminished grey-white differentiation most pronounced in the basal ganglia.

Great Rahul, can you please comment on his physical exam & PMH?

• Important physical exam findings include an unresponsive intubated patient with a cervical collar and bilateral non-reactive pupils at 4mm. The patient received mechanical ventilation with coarse breath sounds. A heart exam revealed tachycardia with no murmur or gallop. The patient does not respond to stimuli, intermittent jerking movements of arms and legs were observed. There was no evidence of rash or trauma. No past medical history of seizures or any heart disease. No home medications or toxic ingestions are suspected.

So now he is transferred to the ICU, what did we do?

• An arterial line, central venous line, urinary catheter, esophageal temperature probe was placed. The patient was ventilated using a TV of 6cc/kg and a PEEP of 10 (FIO2 ~65%) to keep SPO2 >94%. The patient initially had runs of ventricular tachycardia for which lidocaine was used. Although the initial EKG showed mild QTc prolongation, it subsequently normalized and was considered to be due to his cardiac arrest and resuscitation. An echocardiogram revealed normal biventricular systolic function (on epinephrine) and also showed normal origins of the coronary arteries. Comprehensive Arrhythmia Panel did not identify a specific genetic cause for the patient's sudden cardiac arrest. The patient was placed on continuous EEG, which demonstrated...

Welcome to PICU Doc on Call, a podcast dedicated to intense wisdom in the field of pediatric critical care. In this episode, hosts Pradeep Kama and Rahul Damania, both pediatric ICU physicians, discuss the case of a five-year-old male who presents to the emergency department with unexplained fatigue and fever. The patient's symptoms include fatigue, intermittent fevers, tachycardia, and significantly low hemoglobin levels.

The hosts delve into the possible causes of the patient's condition, considering a blood cell disorder and the potential for severe anemia due to aplastic crisis. They explain the physiological adaptations that occur in severe acute anemia, including the shifting of the oxyhemoglobin curve to the right and the increase in cardiac output through tachycardia and increased stroke volume.

The podcast episode also covers different forms of hemolytic anemia, including extravascular and intravascular hemolysis, autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria. The hosts discuss the workup for hemolytic anemias, such as complete blood count, peripheral smear, LDH levels, haptoglobin levels, and Coombs tests. They emphasize the importance of involving hematology and infectious disease specialists for accurate diagnosis and management.

The case of the five-year-old with hereditary spherocytosis is explored, highlighting the characteristic spherocytic shape of red blood cells and potential complications like hemolytic crisis, splenic sequestration, and aplastic crisis. The hosts provide insights into the pathophysiology and presentations of these complications, emphasizing the need for prompt recognition and appropriate interventions.

In summary, this episode of PICU Doc on Call provides valuable information on the evaluation and management of a pediatric patient with fatigue, fever, and anemia, shedding light on different forms of hemolytic anemias and their associated complications.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode of a 4-day-old with jaundice and vomiting.

Here's the case presented by Rahul:

A full-term 4-day-old boy presents to the ED after recently being discharged from the newborn nursery. Per mom, the patient "look yellow" and was having difficulty with feeding. The mother states that the patient would be increasingly sleepy, and will only latch to the breast for five minutes. The patient has been having decreased wet diapers, and the stool is loose and non-bloody. Mother was concerned today as the child continue to look yellow, especially in the eyes, had four episodes of vomiting, and overall was acting lethargic. The patient presented to the emergency room afebrile, tachypneic, and tachycardic. The patient was noted to have initial serum glucose of 70. As the patient was increasingly dehydrated, laboratory testing was difficult to obtain. The infant was fussy for the caregivers. The patient was resuscitated with 2 x 10 per kilo boluses and responded well. Point of care ultrasound noted normal four-chamber cardiac anatomy and squeeze. Given the instability of the patient, a RAM cannula was initiated, and the patient presented to the PICU.

To summarize key elements from this case, this 4-day-old infant has:

• an acute presentation of jaundice and poor feeding
• Prominent GI symptoms and dehydration
• A sepsis-like presentation with hemodynamic instability responsive to fluids
• All of which brings up a concern for inborn error of metabolism, likely galactosemia.
• This episode will be organized…
• Clinical Presentation
• Laboratory Findings & Biochemistry
• Management of Galactosemia

Rahul, let's start with a short multiple choice question:

• Of the following biochemical enzymes, which of the following is deficient in classic galactosemia?
• A. UDP Glucoronyl Transferase
• B. Aldolase B
• C. Galactose 1 Uridyl Transferase
• D. Galactokinase

The correct answer is C. Galactose 1 Uridyl Transferase aka GALT. Classic galactosemia is caused by a complete deficiency of galactose-1-phosphate uridyl transferase (GALT). We should contrast this with galactokinase deficiency. These two present quite differently — GALT deficiency presents like our patient with jaundice, vomiting, hepatomegaly, renal dysfunction, and sepsis. Galactokinase deficiency has less of systemic symptoms and these patients similar to GALT deficiency have cataracts that are usually bilateral and resolved with dietary therapy. To go through our other answer choices, remember that Aldolase B is the rate-limiting enzyme in fructose metabolism, thus a deficiency in this enzyme would cause hereditary fructose intolerance.

With this lead in question, let’s pivot into the biochemistry of galactose and review key lab findings in our patient with galactosemia. Rahul, can you give us a quick summary of how galactose is metabolized in our body?

Galactose is a sugar found primarily in human milk and milk products as part of the disaccharide lactose.

Lactose is hydrolyzed to glucose and galactose by the intestinal enzyme lactase.

The galactose then is converted to glucose for use as an energy source, however it needs a series of reactions:

1. Galactokinase → which catalyzes the rxn galactose to galactose 1 PO4
2. Our rate limiting enzyme Galactose-1-phosphate uridyl transferase

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode.

Here's the case of a 12-week-old girl old who is limp and seizing presented by Rahul.

• Chief Complaint: A 12-week-old previously healthy female infant was found limp in her crib and developed generalized tonic-clonic seizures on the way to the hospital.
• History of Present Illness: The mother returned from work on a Saturday to find her daughter unresponsive in her crib. The infant had been left in the care of her mother's boyfriend, who stated that the daughter had been sleeping all day and had a small spit up. As the patient continued to have low appetite throughout the day and continued to be unresponsive in her crib, mother called EMS to bring her to the emergency department. En route, the patient had tonic movement that did not resolve with intranasal benzodiazepines.
• ED Course: The infant presents to the ED being masked. Upon arrival at the ED, the infant was in respiratory distress, with a heart rate of 190 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% with bagging. She was intubated for seizure control upon arrival at the ED. Physical examination in the ED revealed bruising on the right neck region but was otherwise unremarkable. A non-contrast head CT showed no acute intracranial abnormalities. The initial diagnostic workup revealed normal CBC, mildly elevated hepatic enzymes, and pancreatic enzymes which were within normal limits. The blood gas showed metabolic acidemia with PCO2 in the 60s.
• Admission to PICU: Upon admission to the PICU, neurosurgery and trauma teams were consulted. A skeletal survey and ophthalmology consult for a fundoscopic examination were ordered, as there were concerns of non-accidental trauma. Further investigation is underway to determine the cause of the infant's condition.

To summarize key elements from this case, this patient has:

• Patient left with mother's boyfriend
• Infant found limp and had seizures requiring intubation
• Neck bruise
• All of these bring up a concern for Non-Accidental Trauma (NAT) the topic of our discussion.

Let's start with a short multiple-choice question:

Which imaging modality is the most appropriate for establishing a diagnosis of abusive head trauma (AHT) in a 12-week-old infant with an open fontanelle on the exam?

• A. CT scan of the brain without contrast B. MRI of the brain without contrast C. Skull X-ray D. Doppler ultrasound of the head

Rahul, the correct answer is A.

Though

Dear Listeners & Peds ICU community, WE are back on air!

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming BACK to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU.

PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting.

As we turn into a new year, we would like to introduce Season 2 of PICU Doc on Call. 

Yes Pradip, I am super excited for this year & I want to take this moment to thank YOU all, our listener community for making PICU Doc on Call such a success as we share our passion for medical education thru this forum!

This episode will give you a quick layout of how we will be organizing each episode of PICU doc on call this year. We will also highlight some tips and tricks on how to best learn from a medical podcast. Our goal in this episode is to provide you a framework on some best practices in medical podcasting and how to retain information from a podcast. Especially for our past & future episodes, we hope you can use this audio learning platform to assist you in applying the knowledge at the bedside when you are working in the acute care setting.

Let’s get into our first learning objective,

Rahul, did you know that learning via podcasts can actually benefit your brain & change the neural chemistry.

In fact, a 2016 med ed study published  out of UC Berkeley concluded that listening to narrative stories from podcasts can stimulate multiple parts of your brain such as the limbic system and can enhance mood as it modulates dopamine and serotonin driven neural pathways. Think about listening to your favorite true-crime podcast  — the suspense actually allows for you to stimulate centers in your medulla that increase the amount of endorphines, dopamine and serotonin that keep you on the edge of your seat.

That is so unique, so based on this, I do want to highlight some of the key elements which will make our podcast or any medical podcast you listen to beneficial. These pearls will also help you if you are developing a medical podcast of your own!

The first concept here is that many podcasts provide narratives.

When it comes to medical podcasts, narratives are in the form of medical cases which allow for you to retain content knowledge as a patient case invokes emotion and this can help you remember information more robustly.

When listening to a podcast, you have to use your imagination to picture what’s going on. For example, if I painted a 2 yo M with a history of rhinorrhea at home for about a week who now presents to the ED with subcostal & intercostal retractions that then progresses to intubation in the PICU, you not only are envisioning a patient in front of you, but also are shifting your mind across settings. Our brain has to work at the pace of the audio, so hopefully your mind doesn’t wander off like it does when reading a textbook page. And because you have to...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure.

Here's the case presented by Rahul:

A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil.

4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH.

At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management.

Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol.

She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam.

Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur.

Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted.

To summarize key elements from this case, this patient has:

• H/o of lupus and is on immunosuppressive medications
• New onset fever/malaise
• This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation.

Rahul: Lets pause right here and take a look at key history and physical exam components in a patient who has a chronic auto-immune condition:

• Fever, malaise and feeling tired all signs of constitutional symptoms.
• She has abdominal pain and vomiting that could again be related to systemic inflammation but also an intro-hepatic lesion.

Are there some red-flag symptoms or physical exam components which you could highlight?

• This patient has signs of shock!
• Tachycardia with delayed cap refill and cool extremities
• Tachypnea
• & hepatomegaly which could indicate increased central venous pressures.
• Initially her outside presentation of...

Approach to Pediatric Trauma 

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania, from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode.

Welcome to our Episode today of a 7 yo M who presents to the PICU after a severe Motor Vehicle Accident.

Here is the case presented by Rahul

A 7-year-old male child is admitted to the PICU after sustaining severe trauma. The patient was brought to the emergency department after a motor vehicle accident that involved an 18-wheeler truck & the family’s car; in this severe accident the 7 yo was noted to be restrained however upon impact was ejected from the vehicle. He was unconscious and had multiple injuries, including a laceration on the head and bruising on the chest. The EMS was activated and the patient presented to the ED for acute stabilization. Upon examination, the patient was found to have a Glasgow Coma Scale score of 8, indicating a serious head injury. He had multiple bruises and abrasions on the chest and arms, and his pulse was rapid and weak. The patient was resuscitated with colloid and blood products, intubated, and transferred to the pediatric intensive care unit for further management.

Notably, a CT scan of the head showed a skull fracture and a subdural hematoma. A chest X-ray showed multiple rib fractures and bilateral pulmonary opacities with no evidence of pneumothorax. The patient was also found to have a grade 2 liver laceration and a splenic injury. Pelvic x-ray and cardiac FAST exam were unrevealing.

To summarize key elements from this case, this patient has:

• A traumatic brain injury
• Pulmonary contusions and is at risk for PARDS
• Liver and spleen injury
• Anemia
• Pertinent negative includes: No pelvic injuries or injuries to great vessels in the chest

Rahul, let's approach the PICU medical management of this case based on a culmination of various guidelines published in the Pediatric Critical Care literature. Namely, let's use this case to dive deep into guidelines for:

Traumatic brain injury (TBI)

****Transfusion and Anemia Expertise Initiative (****TAXI)

pediatric blunt liver and spleen injury management, are also known as the ATOMAC protocol, as well as general PICU management of acute trauma.

As we take the management of this pediatric trauma patient in a systems-based fashion let's first go into the Management of Pediatric Traumatic Brain Injuries, can you start us off with some key management considerations?

• Based on the March 2019 TBI guidelines published in Pediatric Critical Care Medicine in 2019 (PCCM20(3S):p S1-S82, March 2019)
• This patient should have an ICP monitor or even an EVD placed for CSF diversion in consultation with the NS and trauma team. A CPP of at least >50 in our 7 yo patient and ICP < 20 mm Hg has been shown to improve outcomes and reduce mortality.

Just as a quick review, CPP stands for cerebral perfusion pressure, which is the pressure that maintains blood flow to the brain. The formula for CPP is:

CPP = MAP (mean arterial pressure) - ICP (intracranial pressure)

Monitoring does not affect outcomes directly; rather the information from monitoring can be used to direct treatment decisions. Treatment informed by data from monitoring may result in better outcomes than treatment informed solely by data from clinical assessment. In short, it is important to have qualitative and quantitative data to optimize your decision-making.

As we talked about ICP control is so crucial for

In this episode of PICU Doc On Call, your hosts Pradip Kamat and Rahul Damania, experienced Pediatric ICU physicians, take you on an enlightening journey through the intricate landscape of lactic acidosis. Join us as we unravel the complexities, share clinical insights, and provide practical guidance on diagnosing and managing this critical condition in the acute care pediatric setting.

You will hear:

Case Presentation:

4-year-old boy with hypotension, fatigue, rash, and respiratory distress

Recent COVID-19 exposure, concerning respiratory symptoms

Hypotensive, tachycardic, tachypneic, low pulse oximetry reading

Swollen red lips, erythematous rash, hepatomegaly

High-flow nasal cannula, resuscitation, epinephrine infusion

Initial arterial blood gas: pH 7.22, lactate 4.5 mMol/L

Definition of Lactic Acidosis:

• Hyperlactatemia and lactic acidosis criteria
• Causes: impaired tissue oxygenation or mitochondrial dysfunction

Types of Lactic Acidosis:

• Type A: Impaired O2 delivery, shock-related
• Type B: Impaired O2 utilization, toxins, infections

Lactate Measurement:

• Comparability between POCT and central lab analysis
• Role of lactate measurement in pediatric sepsis

Lactic Washout:

• Rising lactate with re-established oxygen delivery
• Impaired clearance in microcirculation, liver, kidney
• Monitoring trends with clinical exams and lab surrogates

Bicarbonate Therapy:

• Role in Type A lactic acidosis
• Controversy, indications, and potential complications

Conclusion:

PICU Doc On Call podcast explores the intriguing case of a 4-year-old boy with lactic acidosis, highlighting the clinical intricacies of diagnosing and managing this condition. The hosts, Pradip Kamat and Rahul Damania provide insightful discussions on the different types of lactic acidosis, the physiological mechanisms behind it, and the role of bicarbonate therapy. The episode emphasizes the importance of addressing underlying causes and offers valuable clinical pearls for managing pediatric patients with lactic acidosis.

Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kama and I'm Rahul Damania, a third-year PICU fellow. I’m Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing rhabdomyolysis and associated acute kidney injury in the ICU.

Rahul: Here's the case, a 7-year-old female presents to the ED with three days of fever, poor PO, and diffuse myalgia. In the ED, her vital signs are T 39.1C, HR 139, BP 82/44, RR 32. She is pale and diaphoretic, complaining weakly about how much her legs hurt. Her parents note that she has not been peeing very well since yesterday, and when she does pee it is “very concentrated, almost brown.” She’s also been spending all her time on the couch and has asked to be carried to the bathroom when she does need to go.

An IV is placed by the emergency room team, and she is given a fluid bolus, acetaminophen, and initial labs are drawn (CMP, CBC, RSV/Flu swab) before she is admitted to the PICU. In the PICU, her fever is better and her vitals have improved to T 37.7, HR 119, BP 115/70, and RR 25. Her respiratory swab has just resulted positive for Influenza A. Further labs are sent, including creatine kinase (CK), coagulation studies, and a urinalysis. Labs are notable for K 3.9, Bicarb 22, BUN 15, Cr 0.8, and CK 5768 IU/L. Her urinalysis is notable for 1 WBC, 2 RBC, +3 blood, negative nitrites, and leukocyte esterase.

Kate: To summarize key elements from this case, this patient has:

• Influenza A, as evidenced by her respiratory swab, as well as her clinical prodrome.
• She has diffuse myalgias, as well as fevers, diaphoresis, and hypotension.
• Labs are most notable for elevated creatinine and elevated creatine kinase, as well as an abnormal urinalysis.
• All of which brings up a concern for rhabdomyolysis and myoglobin-induced acute kidney injury.

Before we get into this episode — let's create a mental framework for this episode — we will dissect our case by highlighting key H&P components, visit a differential diagnosis, pivot to speaking about pathophysiology, and finally, speak about management!

• Rahul: Let's transition into some history and physical exam components of this case.
• The classic presentation of rhabdomyolysis is myalgias, muscle weakness, and tea-colored urine, all of which our patient has. Decreased urinary output can also accompany, a variety of reasons, but most notably if the patient has myoglobin-induced acute kidney injury. In our patient, poor PO is also probably contributing to her decrease in urine output. Red flag signs or symptoms will include anuria, hypotension, and altered mental status (which is rare but may indicate severe acidemia and deterioration)
• Pradip: As we think about our case, what other disease processes might be in our differential? As we dive in a bit more, we’ll come up with ways to distinguish between rhabdo and other things!
• Viral myositis - inflammation in the muscles in the setting of a viral illness, which can definitely happen with influenza and other common viruses
• Some other things which may cause reddish-brown urine, including hematuria, hemoglobinuria, porphyria, some specific foods or drugs (like rifampin, beets, food coloring — even ibuprofen)
• We also have to investigate a bit more to convince ourselves that our patient’s AKI is due to rhabdomyolysis, as it could be from dehydration, sepsis, NSAIDS, etc.

Kate: Let’s dive further into rhabdomyolysis!

Rhabdomyolysis affects over 25,000 adults and children every year. While toxins (including prescription drugs, alcohol, and illicit drugs) and trauma are two common causes of...

Today’s episode is dedicated to post-operative management of liver transplant patients in PICU. Join us as we discuss the patient case, symptoms, and treatment. 

Joining us is Dr. Joe Magliocca, Associate Professor of Surgery in the Department of Surgery at Emory University School of Medicine. He is also the Surgical Director of Adult and Pediatric Liver Transplantation at Children’s Healthcare of Atlanta. 

Also joining the conversation is Dr. Rene Romero, Professor of Pediatrics at Emory University School of Medicine and Medical Director of the Liver Transplant Program at Children’s Healthcare of Atlanta, which is one of the largest liver transplant programs in the country with over 600 pediatric liver transplants to date. 

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our patient, symptoms, and treatment: An 18-month-old with a history of biliary atresia is admitted to PICU after an orthotopic whole liver transplant. The patient is intubated, and Doppler ultrasound shows vascular patency post-operatively. AST and ALT are pending. 
• Common indications for pediatric liver transplantation:
• 500-700 pediatric liver transplants are performed annually in the US
• 40% of the transplants are done on children born with biliary atresia
• 10-15% of the transplants are due to acute liver failure
• 5% of the transplants are due to malignancies
• The rest of the transplants are due to different childhood diseases and metabolic diseases
• How the PELD (Pediatric End-Stage Liver Disease in children under 12) score relates to prioritization for liver transplant
• Criteria for the PELD score are bilirubin, albumin, age, growth parameters, and INR
• The major differences between whole organ vs. split liver transplantation (long-term outcomes are similar and good for both situations)
• Why liver transplantation requires less immunosuppression than other organ transplants
• Three phases of the liver transplant process are the hepatectomy phase, anhepatic phase, and reperfusion phase
• Specifics of the time intervals during the transplant process, where the major risk is for primary non-function during cold ischemia and warm ischemia times
• Major red flags to look for during the immediate post-operative period
• Acute post-op management includes extubation in the OR, CV monitoring, pain management, checking urine and electrolyte levels, and communication with the transplant surgeon and liver team
• How treatment and management have evolved over time with standardized post-op management, protocols, and parameters
• Two important aspects of post-op management are nutrition and immunosuppression
• Clinical pearls of wisdom:
• The need for organ donors is great. 
• Teamwork and collaboration are essential for good patient outcomes. 
• The transformation in the field of liver transplantation has saved many children’s lives.

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

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode about a 14- year- old female who presented with hypotension after a suicide attempt.

Here's the case:

A 14 yo F with PMH of depression and oppositional defiant disorder presents with dizziness. Her mother states she was in her normal state of health when on the day of admission she noticed the patient to be dizzy, slurring speech, and pale. The mother became very concerned about the dizziness as the patient was stumbling and a few hours prior to presentation, became increasingly sleepy. The patient does have a history of depression and is controlled on sertraline. Other medications in the home include Metformin, Amlodipine, and Clonidine. The patient denies ingesting any substance. She does have a prior attempt two years prior, after an argument with her mother; however, her mother was able to “stop” her prior to the attempt. She presents to the ER via EMS. Her vital signs are notable for HR 50 bpm with occasional PACs and non-conducted QRS complexes on telemetry; BP of 75/40. A physical exam is notable for AMS and GCS of 10. She is noted to have clear breath sounds, with a cardiac exam notable for slowed and delayed pulses. Initial laboratory work is notable for serum glucose 180 mg/dL and B HCG negative. Initial resuscitation is begun with IV fluids and atropine. Serum acetaminophen and ASA levels are sent and upon stabilization, the patient presents to the PICU for admission.

To summarize key elements from this case, this patient has:

• A history of depression with prior attempt
• An acute bout of altered mental status
• Bradycardia, hypotension, and hyperglycemia.
• All of which brings up a concern for an acute ingestion
• Let’s take a step back and talk about the approach to ingestions in the PICU.

1. What are key aspects to consider in the work-up of these patients?

• History and physical are key:
• Stratifying acute or chronic ingestions
• Baseline prescription medications a patient may be taking or have access to in the household
• Whether the ingestion involves a single drug or co-ingestants are all first steps in evaluating your patient.
• In an undifferentiated patient, management is paramount. Initial management is focused on pattern recognition and acute stabilization.
• A brief initial screening examination should be performed on all patients to identify immediate measures required to stabilize and prevent deterioration of the patient. Assess the airway, vital signs, mental status, pupil size, and skin temperature and moisture.

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....

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat

and my name is Rahul Damania and we come to you from Children's Healthcare of Atlanta Emory University School of Medicine. Today's episode is dedicated to the rational use of antibiotics in the PICU

We are delighted to be joined by two brilliant Pediatric clinical pharmacists Ms Whitney Moore and Ms. Stephanie Yasechko from Children's Healthcare of Atlanta.

I will turn it over to Rahul to start with our patient case...

• Case

An 8-year-old female (24 kg, 130 cm) with PMH significant for severe persistent asthma and history of multiple PICU admissions presents to the ED with swelling, redness and inability to bear weight in her (L) lower leg.

Patient had just finished soccer practice the evening prior to her ED visit when she first noticed swelling and redness of her left lower leg. She also had a fever as well as some non-bloody, non-bilious emesis. Her past h/o is significant for poorly controlled asthma with multiple admissions to the PICU.

Upon arrival to the ED, patient's BP was hypotensive, tachycardic, and tachypneic. She was given two 20 mL/kg NS boluses, and blood cultures were drawn in addition to a CBC, BMP, and UA.

Labs were notable for an elevated white count, lactate, and serum Cr. Patient was given a dose of antibiotic, and transported to the PICU for further workup and management.

Whitney and Stephanie welcome to PICU Doc on call.

Thanks Rahul and Pradip for having us. Neither one of us have any financial disclosures or conflicts of interest.

We want to divide today's discussion into 3 segments- antibiotic selection, transition into dosing and end with therapeutic monitoring

Whitney, what are some of the factors to consider prior to choosing an antibiotic regimen in our patient case with a preliminary diagnosis of cellulitis of the left lower extremity with possible sepsis?

• Whitney: First and foremost you want to consider your host so really diving deep into the patient’s past medical history and secondly we should consider the likely pathogens that are causing the patient’s infection. In this case given the invasive nature of her infection and recent hospital admissions I would start Vancomycin and Cefepime. Once blood cultures results are back, we can then tailor or narrow her antibiotics based on susceptibilities.

Stephanie what are some of the other factors to consider prior to starting antibiotics in this patient?

• Other things to consider include her multiple previous hospitalizations, significant exposure to broad-spectrum antibiotics, whether or not she is immunocompromised, the presence of chronic conditions like lung disease, ventilator/trach dependency, and if patient was a resident of a long term care facility. Additionally any history of organ or bone marrow transplant or malignancy with use of chemotherapy/radiation, and/or a history of growth of multiple drug resistant organisms.

This is an important point - infectious disease is not just about the relevant pathogen or "bug" but it is also about understanding the host status!

Stephanie -why vancomycin and cefepime in this case?

• In this patient the major pathogens to consider include: P. aeruginosa (give her multiple previous PICU admissions).
• Also she has extensive cellulitis which necessitates antibiotic coverage against Methicillin resistant staph aureus (MRSA) and Streptococcus pyogenes . So our options in this case include vancomycin for broad-spectrum gram positive coverage, and generally either piperacillin/tazobactam or cefepime for broad-spectrum gram negative and pseudomonal...

Today’s episode is dedicated to PICU applications of lipid emulsion therapy. Join us as we discuss the patient case, symptoms, and treatment. 

Joining us is Dr. Ziad N. Kazzi, Associate Professor of Emergency Medicine at Emory University School of Medicine, Director of the International Toxicology Fellowship Program at Emory, and Assistant Medical Director of the Georgia Poison Center. Dr. Kazzi is also a board member of the American College of Medical Toxicology and current president of the Middle East North Africa Toxicology Association. 

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our case: a 14-year-old girl has been admitted to PICU after acute ingestion of the calcium channel blocker Amlodipine in a suicide attempt
• Symptoms: profound hypotension
• Acute management: After fluid resuscitation, norepinephrine infusion, and high-dose insulin therapy, lipid emulsion therapy is considered
• How lipid emulsion therapy began
• How lipids work in the toxicology realm
• Applications in PICU for indicators and efficient doses of lipid emulsion therapy
• Examples of cases that call for lipid emulsion therapy
• Considerations of propofol as a substitute for lipid emulsion therapy
• To minimize complications from lipid emulsion therapy, pay attention to dosing guidelines, limit the duration of the infusion, and focus on systemic toxicities
• Final thoughts: Know when to use (and when not to use) antidotes and be aware of publication bias with any studies

Resources:

Download the PICU Card for this episode here

www.lipidrescue.org  

Today’s episode is dedicated to acute management of laryngospasm. Join us as we discuss the patient case, symptoms, and treatment. 

Joining us is Dr. Tom Austin, director of General Pediatric Anesthesiology at Children’s Healthcare of Atlanta-Egleston. He’s also an associate professor of anesthesia and pediatrics at Emory University School of Medicine. 

>>Click here to download the PICU card for this episode<<

Show Highlights:

• Our case: a two-year-old male with a history of Wilms’ tumor presents in a sedation suite for post-surveillance MRI
• History, symptoms, and treatment: One-week history of nasal congestion with no active nasal discharge and clear lung sounds. Patient was placed on continuous pulse ox symmetry and CO2 monitoring. With sedation for the MRI, the patient had a sudden cough, which progressed to perioral cyanosis and loss of end-tidal CO2.
• How this case illustrates laryngospasm
• Definition of laryngospasm: complete or partial closure of the larynx due to some manner of external stimulation
• Why laryngospasm leads to acute respiratory failure in children
• How laryngospasm differs from airway obstruction
• Characteristic breathing pattern with laryngospasm
• Acute management of laryngospasm includes a bag-mask and positive pressure ventilation, followed by deepened sedation, and a breathing tube
• Why early recognition of laryngospasm is the key

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode a 15 mo F with respiratory distress and runny nose.

Here's the case:

A 15 mo F presents to the ED with cough, runny nose, and increased work of breathing. Her mother states that the patient has had these symptoms for the past three days, however, the work of breathing progressed. The patient has had 2 fevers during this course, with the highest 101F. She says that her 3 yo cousin who she visited for the holidays had similar symptoms. Mother notes decreased PO and wet diapers. The patient presented to the ED with the following vital signs: T 38.5C, HR 155, BP 70/48 (MAP 50), RR 48, 92% on RA. The patient on the exam was noted to be tachypneic with abdominal retractions, grunting, and nasal flaring. The patient was nasally suctioned and initiated on 12 L 40% of HFNC. The patient was then transferred to the PICU for further management.

To summarize key elements from this case, this patient has:

• Increased work of breathing indicates respiratory distress.
• She has a prodrome of symptoms that worsened prior to presentation
• And a sick contact.
• All of which brings up a concern for acute respiratory failure requiring non-invasive positive pressure ventilation in the form of HFNC.
• Let's transition into some history and physical exam components of this case?

1. What are key history features in this child who presents with respiratory distress & URI sx?

• Usually, children under the age of two with bronchiolitis will present with cough, respiratory distress, and crackles on lung exam.
• The crackles indicate atelectatic alveoli that are filled with fluid which occurs due to inflammatory processes in the lung triggered by respiratory viruses.
• Respiratory distress, increased work of breathing, respiratory rate, and oxygenation all can change rapidly with crying, coughing, and agitation.

1. Are there some red-flag symptoms or physical exam components in a child with acute respiratory distress which you could highlight?

• That is a great question. We really want to highlight the distinction between respiratory distress and respiratory failure.
• Children with respiratory failure in our case may have issues with oxygenation or ventilation as well as increased work of breathing that necessitates higher levels of respiratory support like HFNC.
• In a 2003 Journal of Pediatrics study, infants who were most severely affected with bronchiolitis were born prematurely, <12 weeks of age, or who have underlying...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our episode of a three-year-old girl presenting with a cough and difficulty breathing

Here's the case presented by Rahul:

A previously healthy 3-year-old girl presented to the OSH for difficulty breathing. She had a two-day h/o of cough (worse at night) and congestion but no fever. She has no h/o of emesis, h/o recent travel, or exposure to some/toxins. Initially, she received steroids, albuterol, and O2 but due to continued worsening of breathing and hypoxia-She was transferred to our PICU for initiation of High Flow Nasal Cannula. She has no allergies and her immunizations are up to date. There is a strong family history of asthma and atopic dermatitis. The mother also noted that the patient has h/o of coughing episodes while playing outside with her siblings.

Initial Vitals: Temp 37.9, HR 100, BP 97/73, respiratory rate 49, SPO2 98% on 15LPM HFNC at 60% FIO2 , weight 17.5kg

On PE: The child is awake, playful. she is tachycardic with no murmur. She has subcostal, intercostal, supra-sternal retractions. There is bilateral symmetric chest expansion. The air entry is decreased with diffuse (B) wheeze. There is atopic dermatitis in the flexor areas of the elbows/knees. The rest of the physical examination was normal. No hepatosplenomegaly.

Viral panel: positive for HMP, SARS COV-2 negative

CXR: Atelectasis superimposed upon viral pneumonitis versus multifocal bronchopneumonia. No evidence of parapneumonic effusion or air leak.

CBC and BMP are normal.

To summarize key elements from this case, this 3-year-old girl has:

• Cough and congestion
• Increased WOB and difficulty breathing
• Hypoxia
• No fever or rash
• No recent ingestions or exposure to tobacco smoke
• All of which brings up a concern for a lower airway obstructive process most likely acute asthma

Let's transition into some history and physical exam components of this case?

Rahul, what are key history features in this child who presents with increased work of breathing?

• Cough and congestion
• Difficulty breathing
• No h/o suggestive of atopic dermatitis
• Increased WOB: retractions (subcostal, intercostal, suprasternal). Important to note there is no nasal flaring, head bobbing or grunting.
• Decreased AE

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat

My name is Rahul Damania, a current 3rd-year pediatric critical care fellow and we are coming to you from Children’s Healthcare of Atlanta Emory University School of Medicine

Today's episode is dedicated to the transition between NICU & PICU. We will focus on the ventilation of the ex-premature infant who graduated from NICU care and transitioned to the PICU.

I will turn it over to Rahul to start with our patient case.

• Case: A 4-month-old ex-27 week baby boy is transferred to our PICU after an echo at an outside hospital showed elevated pulmonary pressures. The infant was born via a stat C-section due to maternal complications during pregnancy. His birth weight was 560 g. The patient was intubated shortly after delivery and had a protracted course in the NICU which included a sepsis rule out, increased ventilator settings, and a few weeks on inhaled nitric oxide (iNO).

1. The intubation course was complicated pulmonary hemorrhage on day 1 after intubation. After such an extensive NICU course, thankfully, the infant survived & was sent home on 1/2 LPM NC, diuretics, albuterol, inhaled corticosteroids, Synthroid, multivitamin with iron as well as Vitamin D. The patient was able to tolerate breast milk via NG tube and had a home apnea monitor with pulse oximetry.

• After about a week’s stay at home, the mother noted that the patient’s SPO2 was in the low 80s. The mother took the patient to the local hospital, where the patient was started on HFNC which improved his saturations. An echo done at the OSH showed elevated RV pressures (higher than the prior echo). The patient was subsequently transferred to our hospital for further management. At our hospital, the patient presented hypoxemic, tachycardic, and tachypneic. On physical exam: Baby appeared well developed, had a systolic murmur heard throughout the precordium, and there was increased WOB with significant intercostal retraction. There was no hepatosplenomegaly.
• Due to worsening respiratory distress, and increasing FIO2 requirement despite maximum RAM cannula, the patient was intubated and placed on conventional MV. A blood gas prior to intubation revealed a pH of 7.1/PCO2 of 100. An arterial line and a central venous line were also placed for better access and monitoring. Initial vent settings post intubation PRVC ventilation: TV 32cc, (25/10), 0.7 time, rate 0 (patient sedated/paralyzed).

To summarize, What are some of the features in H&P that are concerning for you in this case:

• Ex-27 week prematurity with a birth weight of 560 gms
• Prolonged MV in the NICU
• Home O2 requirement
• Abnormal echo showing high pulmonary pressures
• hypercarbia despite the use of RAM cannula

As mentioned, our patient was intubated, can you tell us pertinent diagnostics which were obtained?

• CXR revealed: Hazy airspace opacification in the right upper lung concerning developing pneumonia. Streaky airspace...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode an 18 -year old with sore throat, and unilateral L-sided neck pain for ~2 weeks.

Here's the case presented by Rahul:

An 18-year-old female presents to the ED with cough, fever, fatigue, sore throat, and unilateral L-sided neck pain for ~2 weeks. The patient also has been having non-specific chest pain, weight loss, and decreased appetite for ~ 1 month.

Patient has no recent travel h/o, no h/o of vaping or illicit drug use, and there were no sick contacts at home. Vitals revealed an HR 105, BP 116/66, Temp 38.3, and respiratory rate 35, She was 65 Kg and SPO2 on 2L NC was 100%. Physical exam was negative except (L) neck tender to palpation. There was no goiter, lymphadenopathy or hepatosplenomegaly.

An initial chest x-ray was significant for possible multi-lobar pneumonia versus metastases. A Chest CT revealed multifocal septic emboli in the lungs. Echo did not show any gross vegetation. She has no rash or any trauma to the neck or difficulty swallowing, no oral ulcers, joint pain, or diarrhea. She had no recent dental work or drinking of unpasteurized milk or eating raw fish or meat. She was admitted to the PICU as she had hypotension requiring fluid boluses, and lab works significant for hyponatremia, rhabdomyolysis, worsening AKI, elevated ferritin, and elevated D-dimer. Her serum uric acid was 9.9, LDH = 230 (normal) ,ESR 78 (normal = 20 or less). Her serum lactate and serum troponin and BNP were all normal. Pertinently, US neck revealed an occlusive thrombus in the (L) IJ vein (done so as to avoid contrast in face of AKI), and blood cultures sent.

To summarize key elements from this case, this 18-year-old female presents with

• fever +cough+sore throat
• Fatigue + Weight loss
• (L) neck pain
• Hypotension with abnormal labs including a concerning WBC with (L) shift, anemia, AKI, elevated uric acid, and ESR
• Chest CT with possible pulmonary emboli
• US showing occlusion.
• All of which brings up a concern for possible malignancy or pulmonary emboli from a septic focus in the neck and a possible diagnosis of Lemierre syndrome
• This episode will be organized…
• Definition
• Diagnosis (physical, laboratory)
• Management
• Rahul: What is the definition of Lemierre’s syndrome?
• Lemierre’s syndrome, also known as post-anginal septicemia or necrobacillosis, is characterized by bacteremia, internal jugular vein thrombophlebitis, and metastatic septic emboli secondary to acute pharyngeal infections. All of which are seen in our above case presentation. Previously called as the forgotten disease as its incidence was decreasing due to the increasing use of antibiotics especially penicillin for URI. However, recently there is an increase in Lemierre’s disease cases with decreased use of antibiotics due to antibiotic stewardship. The recent increase in Lemierre disease due to decreased antibiotic use has not been proven and remain controversial.
• Rahul what are some of the causative organisms of Lemierre syndrome?
• The most common causative agent of Lemierre’s syndrome is Fusobacterium necrophorum, followed by Fusobacterium nucleatum and anaerobic bacteria such as streptococci, staphylococci, and Klebsiella pneumoniae.
• Rahul: Can you tell our listeners about the pathophysiology of Lemierre’s syndrome?
• Lemierre syndrome can occur...

Today’s episode is dedicated to the intubation of the critically ill pediatric patient. Join us as we discuss the patient case, symptoms, and treatment.

We are delighted to be joined by Dr. Heather Viamonte. Dr. Viamonte is an Assistant Professor of Pediatrics at Emory University School of Medicine. She is a Pediatric Cardiac Intensivist at the Children’s Heart Center and the Director of Cardiac ECMO. The Children’s Heart Center is a 30-bed, dedicated cardiac intensive care unit at the Children’s Healthcare of Atlanta at Egleston. She is a newly published author whose book, Wilde Type, has already been released, and a second novel is on its way to publication. Dr. Viamonte is on Twitter as @hk_jacobs. 

Show Highlights:

• Our case, symptoms, and diagnosis: A four-month-old patient is admitted to the PICU from the emergency department for acute respiratory failure on high-flow nasal cannula. The child’s condition has slowly deteriorated over the last few hours and now requires intubation. An echo is performed pre-intubation due to enlarged cardiac silhouette on chest radiograph demonstrating left ventricular dysfunction with ejection fraction in the low 40s. The patient’s saturations are dipping to the mid-80s despite being on maximal HFNC support. 
• Common indications for intubation in the PICU or CICU include acute respiratory failure, upper airway obstruction, hemodynamic instability, management of increased ICP, mediastinal masses, protection of the airway, as well as for procedures and safe transport.
• Patient conditions with a high risk prior to endotracheal intubation include congenital or acquired heart disease, an infant or child with hemodynamic instability, pulmonary hypertension, upper airway obstruction, increased ICP, and mediastinal masses.
• Factors in infants and children with congenital heart disease that make them high risk for intubation include anatomical or physiologic issues that could lead to cardiac arrests, such as systemic ventricular dysfunction, single ventricle physiology, arrhythmias, pulmonary hypertension, and coronary artery anomalies.
• Why an understanding of the patient’s past medical history and overall physiology are important for risk stratification
• Anatomical concerns that should be assessed in infants and children prior to intubation include genetic syndrome heart defects that could interfere with bag-mask ventilation, airway visualization, or laryngoscopy. These could include morbid obesity and abnormalities of the face, mouth, and teeth. 
• In conceptualizing congenital heart defects prior to intubation, the overriding concern is blood flow to the heart and lungs. Three factors to consider are volume overload, pressure overload, and systemic hypoxemia.
• Patients can have anatomical and physiological difficulties with regards to airway management, especially in those who are critically ill and those with cardiac disease.
• Four important clinical scenarios for physiologic derangements are hypoxemia, hypotension, metabolic acidosis, and congenital heart lesion pathophysiology.
• Remember that infants and children have a higher fragility factor and are at a higher risk for rapid desaturation, hypoxic brain injury, and cardiac arrest. 
• Key factors for the intensivist are fine attention to detail, optimizing your monitoring equipment, and anticipating risk factors for peri-intubation cardiac arrest. 
• Special considerations with intubation for the patient with severe metabolic acidosis are necessary to prevent cardiovascular collapse and pulmonary hypertension.
• How systolic dysfunction from either ventricle plays into the process of intubation
• Factors to consider to mitigate risk in intubation include preparation, a multidisciplinary approach, intubation equipment nearby, and management of the post-intubation period.
• Dr....

Today’s case presentation involves a 2-year-old girl who was previously healthy and was admitted to the Pediatric Intensive Care Unit (PICU) for acute respiratory distress characterized by increased work of breathing and wheezing.

Case Presentation

A 2-year-old girl with acute respiratory distress due to RSV infection

• Presented with increased work of breathing, wheezing, and no fever
• Started on High Flow Nasal Cannula (HFNC) therapy in the PICU

Key Elements:

• Prodrome of URI symptoms
• Increased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry)
• HFNC improved the work of breathing and oxygen saturation

Physiology of HFNC

Mechanisms of Action

Washout of Nasopharyngeal Dead Space:

• HFNC clears nasopharyngeal dead space, improving oxygen efficiency.
• Reduces re-breathing of CO2 from the anatomical dead space.
• Enhances ventilation efficiency and oxygenation.

Reduction in Upper Airway Resistance:

• HFNC reduces resistance in the upper airway.
• Delivers rapid gas flow matching or exceeding natural inhalation rate.
• Eases breathing, especially in neonates and infants with narrow airways.

Optimal Conditioning of Gas:

• HFNC delivers heated and humidified oxygen, matching the body's conditions.
• Reduces energy expenditure and risk of airway irritation
• More comfortable and effective compared to cold, dry air delivery

Debunking the PEEP Theory (Positive End-Expiratory Pressure) 

• HFNC generates minimal and variable PEEP.
• Amount of PEEP depends on factors like flow rate and cannula size
• Not as high or consistent as other respiratory support devices

Research Findings

• A 2022 CHEST study by Khemani et al. on children with bronchiolitis challenged the conventional understanding of HFNC's mechanisms.
• HFNC primarily reduces breathing effort but does not consistently increase lung volume (EELV) or tidal volume (VT).
• Reduction in the pressure rate product (PRP) indicates decreased breathing effort, but not significant alterations in EELV or VT.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat

I'm Rahul Damania, a third-year PICU fellow.

I’m Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing gastrointestinal bleeding.

Kate: Let’s start with a case:

A 4-year-old, previously healthy male presents to the emergency room after a large, bloody stool at home. He notably had an episode of dark emesis and an episode of blood-tinged emesis on the day prior. In triage, he is altered and unable to answer questions coherently. Initial vital signs are temperature 36.1 C, RR 24, HR 146, BP 110/54. Point-of-care labs show hemoglobin to be 5.1 with hematocrit 15. His venous blood gas is reassuring against respiratory disease, and he is in no respiratory distress. Further labs are sent and a massive transfusion protocol is initiated before transfer to the PICU. Before arrival in the PICU, he receives two aliquots of RBCs, 1 aliquot of FFP, and 1 aliquot of platelets. Additional labs are sent from the PICU, post-transfusion. His post-transfusion hemoglobin is 8.8. Other labs are notable for normal MCV, elevated total bilirubin to 4.1 (with direct component 3.4), and elevated AST and ALT to 309 and 495 respectively.

Rahul: To summarize key elements from this case, this patient has:

• An undifferentiated gastrointestinal bleed with both hematemesis and hematochezia.
• He has symptomatic anemia, as evidenced by tachycardia
• Altered mental status.
• He is initially stabilized via transfusion of several blood products and liver function labs are shown to be very abnormal — which we will get more into later!

PK: Let’s get into important parts of the history and physical. Kate, can you tell me what some key history items in this patient are — and what are some areas to make sure to touch on when a patient has a GI bleed?

Kate: Yeah! I’d love to.

First - in our patient, some important elements are his rather acute onset. His parents mention he has had one day of bleeding symptoms - first with emesis yesterday, with components of old, partially digested blood, as well as some fresh blood. Second, he has a frankly bloody stool at home. Given his clinical instability, history taking was probably limited at first, so it’s important to ask follow-up questions and really dig into the case after stabilization!

I like to put my questions about gastrointestinal bleeding into buckets based on the questions I need to answer. I need to answer: is this active bleeding or old blood? Is this slow, insidious bleeding or fast, life-threatening bleeding? Is this an upper GI bleed or a lower GI bleed? Bright red blood in emesis tells us that bleeding is active, whereas coffee-ground or dark emesis tells us that, while recent, the blood has been partially digested in the stomach and may not be ongoing. Similarly, melena (dark, tarry stool), tells us blood has come through the colon. While coffee-ground emesis and melena don’t rule out an active bleed, they do tell us the bleeding may be slower, as large volume, active bleedy is irritating to the stomach and gastrointestinal tracks and moves through the system quickly.

The next question I want to answer is: what is the cause of this bleed? Easy bruising, petechiae and mucosal bleeding may point to a coagulation disorder. Abdominal cramping, frequent stooling, and weight loss may point to inflammatory bowel disease. Past medical history, family history, and a thorough review of systems are key here.

Rahul: Yeah, that’s great! Let’s talk about your question of upper GI vs lower GI bleed.

First, a definition: an upper GI...

Introduction: 

Welcome to "PQ Doc On Call," a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradeep Kamar from Children's Healthcare of Atlanta, Emory University School of Medicine, and Dr. Rahul Damia from Cleveland Clinic Children's Hospital, both passionate PICU physicians.

You will hear:

This episode dives into the management of pediatric drowning cases in the PICU, providing valuable insights into assessment, pathophysiology, and practical management strategies.

Case Presentation: 

An 18-month-old girl was admitted to the PICU following a submersion incident in a residential pool. The child's initial unresponsiveness and subsequent clinical deterioration presented challenges for the PICU team, including respiratory distress, electrolyte imbalances, and potential neurological complications.

Key Elements from the Case:

• Severe acute respiratory failure following submersion
• Abnormal electrolytes (hyponatremia)
• Neurological insult requiring ongoing monitoring

Definitions and Terminology:

Clarification of drowning terminology, emphasizing uniform definitions and avoiding outdated terms like "near drowning." Key terms include primary vs. secondary drowning, saltwater vs. freshwater, intentional vs. non-intentional, and fatal vs. non-fatal drowning incidents.

Pathophysiology:

• Airway Reflexes: Initial reflex laryngospasm triggered by liquid penetration, followed by relaxation due to hypoxia, hypercarbia, and acidosis.
• Gas Exchange Compromise: Decreased functional residual capacity leading to impaired oxygen uptake and CO2 elimination.
• Pulmonary Complications: Pulmonary edema, surfactant washout, increased pulmonary vascular resistance, and shunting, impacting oxygen delivery.

Management Strategies:

• Out-of-Hospital: Aggressive on-site CPR and advanced life support are crucial for favorable outcomes. Swift control of hypoxia and acidosis is vital.
• In-PICU: Ventilation strategies resembling ARDS management (low tidal volume, low plateau pressures, high PEEP). Consider neurological exam, continuous EEG, and neuromuscular blockade if needed.
• Prognostic Factors: Duration of submersion, time to effective CPR, initial GCS, apnea persistence, pH levels, and neurologic status.

Prevention:

Empowering prevention through measures like fencing around pools, teaching children to swim, and vigilant adult supervision can significantly reduce the risk of pediatric drowning incidents.

Conclusion:

"PQ Doc On Call" underscores the importance of timely, effective CPR, swift management...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our episode of a 14-year-old girl with sudden acute outbursts of aggression and severe agitation.

Here's the case presented by Dr. Damania:

A 14-year-old previously healthy teenager with no significant past h/o presents to the PICU with a three-day h/o of aggressive behavior, agitation, and screaming. Her mother reports that her daughter has recently developed insomnia, abnormal movements and is more irritable with temper tantrums and episodic unintelligible verbal output. Parents report no recent stressors at home or at school. She has been also complaining of headaches for the past week along with things "being too loud". She denies any vertigo symptoms or tinnitus. The patient is brought to the ER due to persistent auditory/visual hallucinations followed by agitation, aggressive behavior, and catatonia. There is no h/o of recent illnesses, head trauma, fevers, rash, abdominal pain, diarrhea, or vomiting. Social history is negative for drugs of abuse in the home. Family h/o negative for seizures, and psychiatric disorders.

The patient is sent to the ED and upon arrival has an unprovoked convulsive episode concerning a GTC seizure. The patient was initially admitted to the floor but transferred to the PICU for management of severe agitation, aggressive behavior, and fluctuations of blood pressure and heart rate.

Initial vitals in the PICU were notable for tachycardia. The patient was found to be afebrile, normotensive for age, and SpO2 96% on RA. Her physical exam though limited by her aggressive behaviors was normal. The heart, lung, and abdominal exams are normal with no rash or bruising on her body.

Initials lab work includes a negative:

• U preg
• Serum and Urine tox screen
• CBC, CMP, and UA are all within normal limits
• Inflammatory markers — including ESR CRP are unremarkable.
• A head CT which was normal and an A lumbar puncture revealed colorless CSF with 8 white and 0 red cells. Serum and CSF glucose were within normal limits and protein count in CSF was negligible.
• An extended multi-disciplinary work-up is initiated.

To summarize key elements from this case, Rahul this teenage girl has:

• Sudden outbursts of agitation, and aggression
• Recent difficulty in sleeping
• Irritability, and decreased verbal output
• Auditory and visual hallucinations
• Potential autonomic dysfunction as she has fluctuating BP and HR All of which brings up a concern for neuropsychiatric symptoms that could be organic in nature.
• Let's transition into some history and physical exam components of this...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. I am Pradip Kamat.

I am Rahul Damania, a current 3rd year pediatric critical care fellow.

I am Kate Phelps- a second year pediatric critical care medicine. We come to you from Children's Healthcare of Atlanta Emory University School of Medicine.

We are delighted to be joined by guest expert Dr Stephanie Jernigan Assistant Professor of Pediatric-Pediatric nephrology, Medical Director of the Pediatric Dialysis Program at Children’s Healthcare of Atlanta. She is the Chief of Medicine and Campus Medical Director at Children’s Healthcare of Atlanta, Egleston Campus. Her research interests include chronic kidney disease, and dialysis. She is on twitter @stephaniejern13

I will turn it over to Rahul to start with our patient case...

• A 3 year old previously healthy male presents with periorbital edema. Patient was initially seen by a pediatrician who prescribed anti-histamines for allergy. After no improvement in the eye swelling after a two week anti-histamine course, the patient was given a short course of steroids, which also did not improve his periorbital edema. The patient progressed to having abdominal distention and was prescribed miralax for constipation. Grandparents subsequently noticed worsening edema in his face, eyes, and feet. The patient subsequently had low urine output, low appetite and lack of energy patient was subsequently brought to an ED and labs were obtained. Grandparents denied any illness prior to presentation, fever, congestion, sore throat, cough, nausea, vomiting, gross hematuria, or diarrhea. In ED patient was noted to be hypertensive (Average systolic 135-highest 159mm HG), tachycardic (HR 130s-140s), breathing ~20-30 times per minute on RA with SpO2 92%. Admission weight was recorded at 16.5Kg. Physical exam showed periorbital edema, edema of ankles, there was mild abdominal distention (no tenderness and no hepatosplenomegaly), heart and lung exams were normal. There were no rashes on extremities.

Labs at the time of transfer to the PICU: WBC 10 (62% neutrophils, 26% lymphocytes) Hgb 7.2, Hct 21, Platelets 276. BMP: Na 142/K 8.4/Cl 102/HCO3 19/BUN 173/creatinine 5.8. Serum phosphorus was 10.5, Total Ca 6.4 (ionized Ca= 3.4), Mag 2.0, albumin 2.6, AST/ALT were normal. An urine analysis showed: 1015, ph 7.5, urine protein 300 and rest negative. Chest radiograph revealed small bilateral pleural effusions. After initial stabilization of his hyperkalemia-patient was admitted to the PICU. PTH intact 295 (range 8.5-22pg/mL). Respiratory viral panel including for SARS-COV-2 was negative. C3 and C4 were normal. A nephrotic syndrome/FSGS genetic panel was sent. A renal US showed: bilateral echogenic kidneys and ascites (small volume).

Pradip: Dr Phelps what are the salient features of the above case presented?

Kate Phelps: This patient has a subacute illness characterized by edema, anemia, and proteinuria. His labs show that he has severe acute kidney injury with significantly elevated BUN and Creatinine, hyperkalemia, hyperphosphatemia, and hypocalemia.

Rahul: Dr Jernigan welcome to PICU Doc on Call Podcast.

Thanks Kate, Rahul and Pradip for inviting me to your podcast. This is a such a great way to provide education and it is my pleasure to come today to speak about one of my favorite topics, pediatric dialysis. I have no financial disclosures or conflicts of interest and am ready to get started.

Rahul: Dr Jernigan as you get that call from the ED and then subsequently from the PCCM docs, as a nephrologists whats going on in your mind ?

When I get the call from the outside hospital my first job is to make sure the patient is safe and stable for transfer to a tertiary care center. This includes concern about airway, breathing and level of alertness. From a renal standpoint,...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Here's the case presented by Rahul:

A 21-month-old girl was brought to an OSH ED for somnolence and difficulty breathing, which developed after she accidentally ingested an unknown amount of liquid medicine that was used by her grandfather. Per the mother, the patient’s grandfather was given the liquid medication for the treatment of his opioid addiction. The patient took some unknown amount from the open bottle that was left on the counter by the grandfather. Immediately after ingestion of the medicine, the patient initially became irritable and had some generalized pruritus. The patient subsequently became sleepy followed by difficulty breathing and her lips turned grey. The patient was rushed to an outside hospital ED for evaluation.

OSH ED: The patient arrived unresponsive and blue, she was noted to be sleepy and difficult to arouse on arrival, with pinpoint pupils and hypoxic to 88%. , but After receiving Naloxone, however, she became awake and interactive. Her glucose on presentation was 58 mg/dL and Her initial VBG resulted 7.3/49.6/+2. She continued to have intermittent episodes of somnolence without apnea. Poison control called and recommend starting a naloxone infusion; she was also given dextrose bolus. The patient was admitted to the PICU.

To summarize key elements from this case, this patient has:

Accidental ingestion of an unknown medication

Altered mental status

Difficulty breathing—with grey lips suggestive of hypoventilation/hypoxia

All of which brings up a concern for a toxidrome which is our topic of discussion for today

The typical symptoms seen in our patient of pinpoint pupils, respiratory depression, and a decreased level of consciousness is known as the “opioid overdose triad” Given the history of opioid addiction in the grandfather, the liquid medicine given to him is most likely methadone.In fact, in this case, the mother brought the bottle of medicine, which was subsequently confirmed to be prescription methadone given to prevent opioid withdrawal in the grandfather.

To dive deeper into this episode, let’s start with a multiple choice question:

Which of the following opioids carries the greatest risk of QTc prolongation?

A. Methadone

B. Morphine

C. Fentanyl

D. Dilaudid

The correct answer is methadone. Methadone prolongs QT interval due to its interactions with the cardiac potassium channel (KCNH2) and increases the risk for Torsades in a dose-dependent manner. Besides the effect on cardiac repolarization, methadone is also associated with the development of bradycardia mediated via its anticholinesterase properties and through its action as a calcium channel antagonist. Hypokalemia, hypocalcemia, hypomagnesemia, and concomitant use of other drugs belonging to the family of CYP3A4 system inhibitors such as erythromycin can prolong Qtc. Even in absence of these risk factors, methadone alone can prolong QTc.

Thanks for that, I think it is very important to involve your Pediatric Pharmacy team to also help with management as children may be concurrent qt prolonging meds.

Rahul, what are some of the pharmacological and clinical features of methadone poisoning?

Methadone is a synthetic opioid analgesic made of a racemic mixture of two enantiomers d-methadone and l-methadone. besides its...

Welcome to "PICU Doc On Call," a podcast dedicated to current and aspiring intensivists. In this episode, Dr. Pradip Kamat and Dr. Rahul Damania discuss an interesting case of a 16-year-old male with high-grade fever and abdominal pain. The patient also presents with a rash and other concerning symptoms, leading to urgent medical attention. They provide a summary of the key elements from the case, including vital signs, physical examination findings, and laboratory and imaging results.

Dr. Kamat then shares his thought process regarding the working diagnosis for this patient, considering several possibilities such as severe bacterial infection, atypical appendicitis or cholecystitis, toxic shock syndrome, and systemic inflammatory processes like Multisystem Inflammatory Syndrome in Children (MIS-C) and atypical Kawasaki disease.

Moving on to the topic of vasopressors, Dr. Damania explains the importance of understanding how these medications work and their specific pharmacological properties. They discuss the classification of shock as cold or warm and the limitations of relying solely on clinical signs to categorize septic shock in children.

They highlight the challenges in selecting the appropriate vasopressor, such as a lack of standardization in clinical examination and individual variability in response to medications. They emphasize the need for a comprehensive approach when evaluating and managing pediatric shock patients, considering multiple factors beyond traditional bedside signs.

The hosts then engage in a rapid review of pressors, starting with a multiple-choice question regarding the choice of vasoactive infusion for a patient with toxic shock syndrome. They discuss the pros and cons of using norepinephrine (NE) in distributive shock and highlight its vasoconstrictive effects, inotropic activity, and potential side effects.

They proceed to compare NE with epinephrine, explaining the differences in their actions on adrenergic receptors and their effects on various circulations. They mention that epinephrine acts on all adrenergic receptors and has hemodynamic and metabolic effects, redirecting cardiac output and increasing myocardial oxygen demand.

Lastly, the hosts touch on phenylephrine, a vasopressor that acts on the alpha-1 receptor and elevates systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). They stress the importance of securing central line access when administering vasopressors to avoid harm to peripheral and systemic tissues.

In conclusion, this episode provides valuable insights into the diagnosis and management of a complex pediatric case involving high-grade fever, abdominal pain, and shock. The hosts also offer a rapid review of common vasopressors, highlighting their mechanisms of action, pros, and cons.

Today’s episode focuses on salicylate toxicity, specifically in the case of a teenager with abdominal pain and emesis. Join us in this discussion of symptoms, patient history, diagnosis, management, and treatment. 

Show Highlights:

• Our case: A 15-year-old female is admitted to the PICU for intentionally ingesting a large amount of aspirin tablets. She had epigastric abdominal pain with some non-biliary, non-bloody emesis when she presented to the outside emergency department twelve hours post-ingestion. She denies any neurological symptoms, including tinnitus but appears anxious and tachypneic. In the emergency department, her salicylate level was 45 mg/dL after her ingestion of about 250 aspirin tablets of 325 mg each. The patient is previously healthy, denies the use of illicit drugs and alcohol, is not sexually active, and has no allergies. 
• To summarize the key elements of this case and patient history, she has ingested potentially toxic amounts of aspirin and has suicidal ideation but has no tinnitus or other neurological symptoms. 
• Physical examination results show stable vital signs except for a temp of 38.8C; she has persistent tachypnea and mild epigastric tenderness but no rashes or previous cutting scars.
• Patient labs were consistent with a 12-hour salicylate level of 45 mg/dL, liver function, Bun/Creatinine, and coagulation profile are all normal. Her anion gap is slightly elevated, urine pH is 6, specific gravity is normal, and urine pregnancy test is negative. 
• Based on patient history, physical exam, and labs, it appears that the patient has GI symptoms of early salicylate toxicity. Ingesting potentially toxic amounts of aspirin brings concern for life-threatening injuries to organs and possible loss of life. Let’s quiz ourselves with a short multiple-choice question:
• A teenager with a previous history of suicidal attempt now presents with confusion, increased respiratory rate, fever, and diaphoresis. Her physical exam including the pupillary exam is normal. Her labs are remarkable for a pH of 7.45, CO2 of 19, HCO3 of 11, serum anion gap of 20meQ/L, serum K of 2.9, and serum glucose of 180 mg/dL. There are weakly positive ketones in the urine. The next step in management of this patient is:
• A) NaHCO3 infusion
• B) Insulin infusion
• C) Oral activated charcoal
• D) Hemodialysis dialysis
• The correct answer to this question is A) Sodium bicarbonate infusion.
• Insulin therapy is not the answer because serum glucose is low, and a patient with a pH>7.25 is unlikely to have DKA.
• While activated charcoal can be used, especially followed by sorbitol given with the first dose, we need to be cautious about its use with an altered mental status as in the patient above.
• Since we do not have a salicylate level at this stage, offering hemodialysis should not be the first step, although it can be considered later given the neurological symptoms. 
• Remember: Any patient with a previous history of suicidal ideation who presents with confusion, fever, and diaphoresis with the above labs is suggestive of mixed respiratory alkalosis with high anion gap metabolic acidosis is highly suggestive of aspirin poisoning. Always examine the pupils in any case of poisoning, as that may point one towards a possible toxidrome. 
• Let’s highlight how basic science correlates with ASA poisoning:
• Remember the mechanism of action. Aspirin is a cyclo-oxygenase inhibitor which blocks prostaglandin production and has an antithrombotic effect by inhibiting platelet generation of thromboxane A2.
• Salicylates are weak acids...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat

and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our PICU Mini-Series Episode a 10 month old who is intubated for acute respiratory failure secondary to RSV bronchiolitis.

Here's the case:

A 10-month-old full-term infant girl old is intubated for acute respiratory failure secondary to RSV bronchiolitis. Patient was brought to the ED by parents on day 3 of her illness with h/o cough, congestion and worsening respiratory distress. She has had increasing WOB and grunting. After assessment in the ED where the patient had a brief trial of HFNC, she was intubated with a 4.0 ETT due to persistent hypoxemia. Pertinently, her viral panel was positive for RSV, and the patient was transferred to the PICU. In the PICU, patient was ventilated using PRVC: Set TV of 90cc (patient is 11KG), PEEP 6, PS 10, and FIO2 40%. Throughout her course, she was mechanically ventilated and sedated for about a week. She required a continuous infusion of rocuronium due to decreased lung compliance and high peak pressures. Patient weaned on her ventilator settings by ICU day 7 and the decision to move towards extubation was made.

To summarize key elements from this case, this patient has:

• 10 month old with acute respiratory failure secondary to RSV infection and with a secondary bacterial infection due to H.Influenza.
• Had about a six day course on the ventilator requiring sedation and NMB
• and now we are at the discussion of extubation readiness.Rahul, do you mind summarizing the patient's peri-extubation course?

Sure Pradip, so on day 6 of hospitalization our patient was weaned to low mechanical ventilator settings. The chest radiograph, which initially showed evidence of interstitial pneumonitis and atelectasis now improved and the patient had improved secretion burden. The patient was on ceftriaxone throughout the hospital course as her ETT cx with which grew Hemophilus Influenzae.

• What about the patient's neurological status?
• The patient was initially on fentanyl, dexmedetomidine and a rocuronium infusion — a day prior to considering extubation, the patient was off of the continuous rocuronium infusion oxygenating and ventilating well. The patient prior to extubation was wide awake and appropriate during the morning sedation holiday.
• Any other important clinical markers?
• Yes, the patient's clinical exam including lung exam was reassuring. The patient underwent a pressure support trial PEEP 5, CPAP 10 and had a normal respiratory effort with exhaled of about 5 mL/kg. The RT, however mentioned that the patient did not have a "leak" when performing the leak test. The finally the patient was given a few doses of furosemide for diuresis prior to extubation.
• Awesome, today's episode we really want to focus on extubation readiness however prior to this discussion, can we take a step back and talk about some red-flag symptoms which led to intubation for this patient?
• This patient had severe respiratory distress which progressed to failure.
• The tachypnea, decreased mentation, and grunting were key signs that the patient was progressing to endotracheal intubation.
• Grunting is important to highlight as this refers to the child generating auto-PEEP to combat the atelectasis present in bronchiolitis.
• Remember that a child's chest wall has a high compliance and a decreased propensity for outward elastic recoil — this in essence reduces FRC and thus there is a more balance towards the inward recoil of the long (closing capacity). The highly compliant chest wall and the natural inward recoil of the infant lung creates a propensity towards atelectasis and subsequent impairments in breathing. Low FRC can also...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure.

Here's the case presented by Rahul:

A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil.

4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH.

At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management.

Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol.

She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam.

Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur.

Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted.

To summarize key elements from this case, this patient has:

• H/o of lupus and is on immunosuppressive medications
• New onset fever/malaise
• This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation.

Rahul: Lets pause right here and take a look at key history and physical exam components in a patient who has a chronic auto-immune condition:

• Fever, malaise and feeling tired all signs of constitutional symptoms.
• She has abdominal pain and vomiting that could again be related to systemic inflammation but also an intra-hepatic lesion.

Are there some red-flag symptoms or physical exam components which you could highlight?

• This patient has signs of shock!
• Tachycardia with delayed cap refill and cool extremities
• Tachypnea
• & hepatomegaly which could indicate increased central venous pressures.
• Initially her outside presentation of fluid refractory shock is of utmost concern!
• Fluid refractory shock with multi organ presentation involving liver, kidney and the blood/coagulation systems
• All of these elements bring up a concern for some acute life threatening process such as sepsis, or even immune dys-regulation due to her h/o of Lupus
• To continue with our case, the patients labs were consistent with:Acute liver dysfunction (Elevated AST and ALT in the thousands, Total bilirubin 1.6, GGT 56) although the total bilirubin is not elevated to a degree I would expect.
• AKI (creatinine 2.18)
• An uptrending Coagulopathy with elevated PT and INR: PT 120 and a peak INR of 16
• Thrombocytopenia: Platelets < 50K
• She had a peak lactate 9.2
• and concurrent Metabolic acidemia: serum HCO3 7, and pH 7.18.
• A Pertinent negative: Normal serum ammonia <38 micromol/L (nl < 50)
• Finally, she had an elevated WBC 20.5K/ Hgb 9.7, Platelet 42. CRP 4.2/ESR...

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

In today's episode, we discuss about a 12-year-old male with lethargy after ingestion.

Here's the case presented by Rahul:

A 12-year-old male is found unresponsive at home. He was previously well and has no relevant past medical history. The mother states that he was recently in an argument with his sister and thought he was going into his room to “have some space.” The mother noticed the patient was in his room for about 1 hour. After coming into the room she noticed him drooling, minimally responsive, and cold to the touch. The patient was noted to be moaning in pain pointing to his abdomen and breathing fast. Dark red vomitus was surrounding the patient. The mother called 911 as she was concerned about his neurological state. With 911 on the way, the mother noticed a set of empty vitamins next to the patient. She noted that these were the iron pills the patient’s sister was on for anemia. EMS arrives for acute stabilization, and the patient is brought to the ED. En route, serum glucose was normal. The patient presents to the ED with hypothermia, tachycardia, tachypnea, and hypertension. His GCS is 8, he has poor peripheral perfusion and a diffusely tender abdomen. He continues to have hematemesis and is intubated for airway protection along with declining neurological status. After resuscitation, he presents to the Pediatric ICU. Upon intubation, an arterial blood gas is drawn. His pH is 7.22/34/110/-6 — serum HCO3 is 16, and his AG is elevated.

To summarize key elements from this case, this patient has:

• Lethargy and unresponsiveness after acute ingestion.
• His hematemesis is most likely related to his acute ingestion.
• And finally, he has an anion gap metabolic acidosis, as evidenced by his low pH and low HCO3.
• All of these salient factors bring up the concern for acute iron ingestion! In today’s episode, we will not only go through acute management pearls for iron poisoning, but also go back to the fundamentals, and cover ACID BASE disorders.
• We will break this episode down into giving a broad overview of acid base, build a stepwise approach, and apply our knowledge with integrated cases.

We will use a physiologic approach to cover this topic!

• Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic?
• Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving.
• When we conceptualize acid base today, we will focus on pH, HCO3, and CO2.
• As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient.
• Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3?
• Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is...

Welcome and Episode Introduction

• Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital)
• Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management
• Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol

Case Presentation

• Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka
• Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor
• Initial Labs & Findings:
• EtOH level: 420 mg/dL.
• Glucose: 50 mg/dL.
• Normal CXR and EKG.
• PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression
• Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications

Key Learning Points from the Case

• Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions
• Hypoglycemia and CNS depression are common features of ethanol toxicity in infants
• Management prioritizes glucose correction, airway support, and close neurological monitoring

Deep Dive: Toxic Alcohols in the PICU

1. Ethanol

• Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia
• Diagnostic Workup:
• Focus on CNS and metabolic effects
• Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen
• Imaging (head CT) if indicated
• Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work

2. Methanol

• Sources: Windshield fluids, cleaning agents, moonshine

Clinical Stages:

1. Early: Dizziness, nausea, vomiting (0–6 hours)
2. Latent: Asymptomatic (6–30 hours)
3. Late: Vision disturbances, seizures, respiratory failure (6–72 hours)

• Key Symptoms: “Snowstorm blindness” from retinal toxicity
• Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases

3. Ethylene Glycol

• Sources: Antifreeze, brake fluids, household cleaners
• Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals)
• Red Flags: Hypocalcemia, renal failure, QT prolongation
• Management: Fomepizole, supportive care, and hemodialysis for severe toxicity

4. Propylene Glycol

• Sources: Medications like lorazepam and pentobarbital
• Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction
• Management: Discontinue offending agent, supportive care, and hemodialysis if severe

5. Isopropyl Alcohol

• Sources: Disinfectants, hand sanitizers
• Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis
• Management: Supportive care; fomepizole and ethanol are ineffective

Key Laboratory Insights

• Osmolar Gap Formula:
• Measured Osmolality - Calculated Osmolality
• A high osmolar gap indicates unmeasured osmoles like toxic alcohols.
• Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference

Management Pearls

• Ethanol and...

In this episode PICUDoc On Call, we discuss the case of a six-month-old ex-preemie with bacterial meningitis who presents with symptoms of cerebral sinus venous thrombosis. We explore the anatomy of the venous distribution in the brain and the clinical syndromes associated with sinus venous thrombosis. Our focus is on the imaging techniques, laboratory tests, and management strategies involved in diagnosing and treating this challenging condition.

You will learn:

• A six-month-old ex-preemie presents with persistent fever, recurrent emesis, and increased somnolence.
• The patient experiences eye rolling and decreased oxygen saturation, prompting a visit to the emergency department.
• Physical examination reveals rigidity in all four limbs, and a head CT shows dilated ventricles and encephalomalacia.
• Lumbar puncture confirms an infection, and the patient is admitted to the hospital.
• After a 14-day course of antibiotics, the patient's clinical status worsens, leading to intubation and neurosurgery consultation.
• An MRI confirms cerebral venous sinus thrombosis.

Anatomy of Venous Distribution in the Brain:

• Dural venous sinuses serve as conduits for venous blood return from the brain to the internal jugular veins.
• The superior sagittal sinus, cortical veins, transverse sinus, sigmoid sinus, and internal jugular vein are key components of the venous drainage system.

Clinical Syndromes of Sinus Venous Thrombosis:

• Symptoms can be related to elevated intracranial pressure or focal brain damage from venous ischemia, infarction, or hemorrhage.
• Headache, seizures, focal neurologic deficits, and cranial nerve paralysis are common presentations.
• Cavernous sinus thrombosis can cause periorbital pain, ocular chemos, and paralysis of cranial nerves passing through the sinus.

Risk Factors for Cerebral Sinus Venous Thrombosis:

• Dehydration, CNS or sinus infections, intracranial surgery, autoimmune disorders, genetic syndromes, metabolic syndromes, medications, and genetic thrombophilic states can predispose children to thrombosis.
• Thorough evaluation for risk factors, including thrombophilia, is recommended in children with cerebral venous thrombosis.

Imaging and Laboratory Tests:

• CT and MRI with contrast-enhanced venography are preferred imaging tools to detect cerebral sinus venous thrombosis.
• Non-enhanced CT scans and T1/T2-weighted MRI scans show characteristic signs of thrombosis.
• Lab tests include CBC with differential, DIC panel, comprehensive metabolic panel, ESR, and specific thrombophilia tests.

Management...

Today, Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University School of Medicine) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital), are excited to speak with Matthew Kirschen, MD, PhD, FAAN, FNCS, regarding a very sensitive topic involving pediatric brain death guidelines published in 'Neurology' in October 2023. Dr. Matthew Kirschen, a leader in pediatric neurocritical care and one of the authors of the new guidelines.

Guest Introduction:

Dr. Matthew Kirschen is an Assistant Professor of Anesthesiology and Critical Care Medicine, Pediatrics, and Neurology at the Children's Hospital of Philadelphia. A proud alumnus of Brandeis University and Stanford, where he secured both his MD and PhD in neuroscience. Dr. Kirschen’s journey includes a residency at Stanford followed by a unique dual fellowship in neurology and pediatric critical care at CHOP. Notably, he's among the rare professionals dual-boarded in both PCCM and Neurology.

Dr. Kirschen’s tireless endeavors in pediatric neuro-critical care, especially his work on multimodal neuro-monitoring to detect and prevent brain injuries in critically ill children, have garnered significant attention. His expertise also extends to predicting recovery post-severe brain injuries. Pertinent to today's discussion, Dr. Kirschen has displayed a keen interest in the precise diagnosis of brain death and proudly stands as one of the authors of the new guidelines on the topic of Pediatric and Adult Brain death/death by neurologic criteria.

Discussion:

1. Understanding Brain Death Criteria:

• Brain Death/Death by Neurologic Criteria (BD/DNC) declared with permanent cessation of all brain functions, including brainstem
• Important considerations before BD/DNC determination:
• No evaluation in infants < 37 weeks corrected gestational age
• Absence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC

2. Who Can Perform BD/DNC Evaluations:

• Attending clinicians must be credentialed and trained in BD/DNC evaluation.
• Two attending clinicians are needed for evaluation, with exceptions for advanced practice providers.

3. Prerequisites for BD/DNC Determination:

• Importance of identifying the etiology of BD/DNC to avoid reversible processes
• Observation periods based on age and type of brain injury
• Maintaining core body temperature before evaluation

4. Blood Pressure Management:

• Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors.
• Specific blood pressure targets for different ECMO support types

5. Medication Considerations:

• Excluding...

Introduction:

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.

We've got an exciting new series for the show and we can't wait to share with you our PICU Doc On Call Mini Case Series. Coming this weekend!

Today’s episode is dedicated to post-operative management in the PICU of the pediatric renal transplant patient. Join us as we discuss the patient case, symptoms, and treatment. 

 Joining the conversation is Dr. Rouba Garro, Associate Professor of Pediatrics at Emory University School of Medicine and the Medical Director of the Kidney Transplant Program at Children’s Healthcare of Atlanta. Children’s Healthcare of Atlanta has one of the largest kidney transplant programs in the country and is the largest in the Southeast US with excellent patient and graft survival. 

Show Highlights: 

• Our case, symptoms, and diagnosis: a five-year-old is transferred to the PICU after a related living kidney transplant for end-stage renal disease due to obstructive uropathy. The patient has a history of post-urethral valves and is on room air, IV fluids, an arterial line, and a Foley catheter is in place.
• The top indicators for renal transplant in pediatrics vary according to age, but congenital anomalies are the most common in children younger than six.
• The criteria for being considered for kidney transplantation include several factors, including when kidney function drops below 20%.
• The keys for successful transplantation:
• An experienced pre-transplant team
• A robust and experienced team for perioperative care and graft outcome
• A comprehensive and multidisciplinary post-transplant team
• The process of organ procurement for cadaveric and living donor renal transplants includes the following:
• Multiple factors determine the points a patient receives toward transplant priority
• Deceased donor kidneys are classified using the KDPI (kidney donor profile index)
• A thorough evaluation is performed for living donors
• Advantages to living donation include a shorter time on dialysis and waitlists, improved graft survival, and shorter ischemia time than from a deceased donor
• Information from the operating team that is vital for the PICU team to know for post-op success includes patient history, transplant details, ischemia time, and transplant complications.
• Red flags for the critical care post-op team are in the three categories of blood pressure, urine output, and kidney function/electrolytes. 
• The need to watch for signs of infection in the post-op phase
• How immunosuppressive medications might be used for the pediatric renal transplant patient
• Why the post-op transplant patient might need dialysis
• Clinical pearls for post-op care of the pediatric renal transplant patient in the PICU:
• Teamwork and collaboration are key elements for success.
• The most important task is to monitor blood pressure, urine output, and electrolytes. 

Today’s episode is dedicated to Tumor Lysis Syndrome management in the PICU. Join us as we discuss the patient case, symptoms, and treatment.

We are delighted to be joined by Dr. Himalee Sabnis, Assistant Professor of Pediatrics at Emory University School of Medicine. She is also a pediatric hematologist/oncologist and the Co-Director of the High-Risk Leukemia Team at the AFLAC Cancer & Blood Disorders Center at Children’s Healthcare of Atlanta. 

Show Highlights:

• Our case, symptoms, and diagnosis: A three-year-old female with pre-B ALL presents on Day 2 of chemotherapy to the PICU. She is admitted with telemetry findings of arrhythmia, decreased urine output, and an EKG notable for peaked T waves. Her labs are notable for elevated WBC, hyperkalemia, hyperphosphatemia, and low ionized calcium.
• Tumor Lysis Syndrome is a life-threatening medical emergency stemming from rapid tumor cell destruction that overwhelms the usual metabolic and excretory pathways. 
• Why TLS is the most common pediatric oncologic emergency for pediatric cancer patients
• When the tumor cells die or lyse, what’s inside those cells comes out into the blood
• Key metabolic abnormalities that affect organ function are too much potassium and phosphorus, low calcium, and uric acid buildup.
• Those metabolic abnormalities can result in cardiac arrhythmia and kidney failure.
• Certain patient populations have an increased risk for TLS:
• Hematological cancers have a higher risk than solid tumors
• Patients with fast-growing tumors, like lymphoma and leukemia, are at high risk
• Key pathophysiologic principles that drive TLS:
• The imbalance of electrolytes can impact heart function
• TLS is characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and uric acid, which is a by-product of DNA breakdown
• If untreated, the uric acid can lead to acute kidney injury and renal failure
• Electrolyte and metabolic disturbances can progress to renal insufficiency, cardiac arrhythmias, seizures, and death
• TLS releases cytokines that can cause a systemic inflammatory response and multi-organ failure
• Other lab markers in patients with TLS include uric acid, LDH, CBC, DIC panel, and daily blood gas (these are typically trended every 4-6 hours).
• Key factors in TLS management are to understand the risk and know your resources.
• Steps taken would be continuous cardiac monitoring, uric acid control, administering Allopurinol to combat uric acid formation, and managing electrolyte disturbances in conjunction with an intensivist.
• Chemotherapy would not be delayed due to TLS because the patient’s condition won’t improve until the cancer is treated.
• How the complications of TLS are treated:
• Hyperphosphatemia should be treated by using oral phosphate binders such as aluminum hydroxide.
• Hypocalcemia does not require therapy unless cardiac function is affected.
• How renal replacement therapy might be required and indications are similar to other forms of acute kidney injury.
• Besides Allopurinol being given at the initiation of chemotherapy, patients at high risk for TLS may receive low-intensity initial therapy to prevent rapid cell lysis.
• Takeaway clinical pearls regarding TLS:
• Know what you’re dealing with because every cancer is different.
• Fluid management is important and will vary from patient to patient.
• Be proactive in monitoring. Intervene early and quickly.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

I will turn it over to Rahul to start with our patient case...

A 2 yo Asian M presents with difficulty feeding. He has a history of epilepsy and recently was switched to Valproic Acid for seizure control as well as OTC deficiency diagnosed at birth. He has had a 3-day history of URI, cough, which now progressed to this difficulty feeding. His parents state he was initially very fussy however in the past few hours he has been more sleepy. He has not had any fevers. They have noticed that while he is sleeping he has been breathing "fast." Prior to arrival at the emergency room, he was noted to have a large non-bloody, non-bilious emesis. Upon transfer to the trauma bay, the patient suddenly has a seizure. A quick POC glucose is normal. His care is escalated & diagnostic workup is initiated.

Pradip, our case had two key elements in his history, namely the h/o OTC deficiency & VPA use, which place him, particularly at high risk to have hyperammonemia. As this is our topic of discussion today, would you mind starting with a general background & definition of hyperammonemia?

Sure, this is a classic case of not only hyperammonemia but also a metabolic crisis in this case related to a urea cycle defect.

As background, the urea cycle is the metabolic pathway that transforms nitrogen to urea for excretion from the body. We get nitrogen sources from a few areas in the body:

• from peripheral (muscle)
• enteral sources (protein ingestion)

The urea cycle occurs in the liver and once the ammonia is converted to urea in the hepatocyte, it is excreted into the kidney as urea. We will dive into this deeper soon, however, pathologies that impair adequate hepatocyte function, can impair the urea cycle and thus lead to hyperammonemia.

This is a great basic science summary, would you mind commenting about this patient's enzyme defect — the OTC deficiency?

• Yes, Ornithine transcarbamylase, or OTC for short, is one of the first few enzymes in the urea cycle.
• As a background, the inheritance pattern of majority, all of the urea-cycle-defects (UCD) is autosomal recessive, however, OTC deficiency is different — it is X linked.
• In a 21-year, multi-center retrospective study, it was noted that only 34 % of patients with UCD presented during the neonatal period (<30 days of age) — and around 25% of cases present in the 2-12-year-old range. This is why I would like to drive home this clinical point to have a urea cycle defect or any inborn error of metabolism in your differential, especially in a child who presents in a critically ill, undifferentiated state.

Why do you think there are subsets of populations who present later?

• This is a great question and the cause may be multi-factorial — it is worth noting that patients may have partial enzyme...

Today's episode is dedicated to Critical Illness In Children With Hematopoietic Stem Cell Transplants.

We are delighted to be joined by Dr. Muna Qayed, Associate Professor of Pediatrics Emory University School of Medicine , Atlanta, GA. She is also the Director of the Blood and Marrow Transplant Program at the Aflac Cancer and Blood Disorders Center at Children's Healthcare of Atlanta.

Our Case: A 10 year old female with refractory high-risk ALL s/p mismatched unrelated donor transplantation T+13 days presents as a transfer to the PICU with abdominal distention, worsening jaundice, and escalating nasal cannula requirements. The patient's post-transplant course was complicated by gram-negative bacteremia requiring fluid resuscitation. A CXR upon transfer to the PICU is notable for bilateral airspace disease, a right sided pleural effusion, and hypoexpanded lung fields. The patient is promptly intubated, sedated and started on renal replacement therapy. Echo labs, and further imaging are pending.

What are the classic pediatric indications for BMT?

• Autologous BMT (where donor cells are from the patient/recipient) is used as consolidation in some solid tumors such as High risk neuroblastoma, brain tumors like medulloblastoma, and germ cell tumors, and are a standard treatment approach in relapsed Hodgkin lymphoma
• Allogeneic BMT-where in the donor cells are derived from another individual are typically used for hematologic malignancies. ALL and AML are most common pediatric indications.
• Also allogeneic BMT are used for wide spectrum of nonmalignant hematology conditions such as hemoglobinopathies ( Sickle cell disease, Thalassemia), and severe aplastic anemia, and inherited bone marrow failure syndromes, as well as some metabolic disorders and immune-deficiency disorders such as SCID, HLH and other primary immune regulatory disorders.

The sources of graft in BMT?

• Stem cells (which give rise to different types of blood cells - red cells, white cells and platelets are derived from the bone marrow. Thus the overall process is known as Bone Marrow Transplantation.
• Stem cells can be also derived from peripheral blood - when the donor is treated with granulocyte colony stimulating factor or G-CSF.
• There are some key advantages here, which include the ability to collect a much higher stem cell dose, with faster hematopoietic recovery.
• However the downside is a higher T cell content of the graft with subsequent increased risk of graft versus host disease.
• Umbilical cord blood is also used as a source of stem cells.
• Mega doses of stem cells are used to overcome histocompatibility barriers of mismatched transplantation. Majority of T cells have to be removed from donor pool to prevent severe GVHD., Increase risk of infection and relapse of patients original disease.

Explain the human leucocyte antigen (HLA) and its role in BMT?

• The Major Histocompatibility complex (MHC) system known as the human leukocyte antigen (HLA) in humans is located on the short arm of chromosome 6 and contains the most polymorphic gene cluster of the entire human genome.
• The HLA consists of regions designated as "classes". Class I and class II are relevant to stem cell transplant.
• The main function of HLA class I gene products (HLA-A, -B, and -C) is to present endogenous peptides to responding CD8+ T Cells, HLA class I antigens are expressed on all nucleated cells and platelets.
• While the class II coded molecules HLA-DR, -DP, and –DQ have restricted expression and process exogenous peptides for presentation to CD4+ helper T Cells, and are expressed on antigen presenting cells. HLA-A, HLA-B, HLA-C and HLA-DR are traditionally the loci critical for matching for stem cell donor.
• In addition to deciding on the source of the graft, we have to make decisions on who the donor will...

Today’s episode is dedicated to venous/arterial thrombi, also known as catheter directed thrombolysis.

We are delighted to be joined by Dr. Anne E. Gill, Assistant Professor of Radiology and Imaging Sciences at Emory University School of Medicine. She is a pediatric interventional radiologist at Children’s Healthcare of Atlanta. Her areas of expertise include pediatric thromboembolic disease, vascular malformations, enteric feeding tube access, and interventional oncology. Dr. Gill is on Twitter @AnneGillMD. 

Show Highlights:

• Our case, symptoms, and diagnosis: A 17-year old girl with antithrombin III deficiency presented with bilateral leg pain to an outside ED. Duplex ultrasound of the bilateral lower extremities revealed extensive acute bilateral deep vein thrombosis. A CT scan of the abdomen and pelvis showed an extensive occlusive clot in the inferior vena cava involving the infrarenal and suprarenal IVC. She was transferred to our hospital and admitted to the ICU for thrombolysis and initiation of catheter-directed TPA infusion. In interventional radiology, an IVC filter was placed in the suprarenal IVC; additionally, the venogram in IR showed complete thrombosis of the right upper femoral, external iliac, common iliac, and IVC, with collateral veins in the right lower extremity draining into the thrombosed upper femoral vein. Interventional radiology performed pharmacomechanical thrombolysis and balloon angioplasty of right external iliac, common iliac, and IVC and placed infusion catheter to drip tPA from right femoral vein to the IVC filter. The patient was also placed on continuous heparin drip for systemic anticoagulation management. Morphine and Dexmedetomidine were used for pain management.
• The overall prevalence of systemic venous occlusion in children is difficult to ascertain due to their asymptomatic quality.
• Congenital SVOs in children can be due to developmental hypoplasia or agenesis of major conducting veins; they can happen in utero or manifest as neonatal thrombosis. 
• Acquired causes of SVOs can include catheter acquired obstruction, hypercoagulability/thrombophilia, mechanical obstruction, and trauma.
• A careful history is necessary to determine whether the occlusion was a congenital or acquired SVO.
• This is challenging because symptoms of venous obstruction in children may not present until later in life.
• This distinction is important as it affects the procedures that can be done.
• Better outcomes are possible if a native pathway is present, even if it’s diminished from chronic obstruction and scarring. 
• Clinical presentations of systemic venous occlusions in children include head and neck swelling coupled with shortness of breath. In patients with acute DVT, venous congestion can manifest as prolonged capillary refill, coolness of extremities, and bluish discoloration to frank venous ischemia with loss of pulses. 
• Chronic DVT in extremities can present with a sense of heaviness, aching pain, and fatigue with activity; these symptoms are collectively described as post-thrombotic syndrome.
• Remember that obstruction to flow can compromise oxygen delivery!
• Common causes of venous occlusions are mal-positioned or wrongly sized central venous catheters, May-Turner syndrome, and long-standing central venous access lines in dialysis patients. 
• CDT is not recommended for DVTs below the inguinal ligament, based on the ATTRACT trial in 2017 that showed that CDT is most beneficial in veins above the inguinal ligament.
• Contraindications for CDT in children include allergy to tPA, active bleeding, surgery within the last 14 days, any invasive procedures in the last three days, recent seizures, recent trauma, or coagulopathy which can’t be easily corrected. Caution is needed with...

Introduction

• Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital)
• Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management
• Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol

Case Presentation

• Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka
• Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor
• Initial Labs & Findings:
• EtOH level: 420 mg/dL.
• Glucose: 50 mg/dL.
• Normal CXR and EKG.
• PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression
• Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications

Key Learning Points from the Case

• Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions
• Hypoglycemia and CNS depression are common features of ethanol toxicity in infants
• Management prioritizes glucose correction, airway support, and close neurological monitoring

Deep Dive: Toxic Alcohols in the PICU

1. Ethanol

• Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia
• Diagnostic Workup:
• Focus on CNS and metabolic effects
• Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen
• Imaging (head CT) if indicated
• Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work

2. Methanol

• Sources: Windshield fluids, cleaning agents, moonshine
• Clinical Stages:

1. Early:...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat.

And my name is Rahul Damania, we come to you from Children's Healthcare of Atlanta/Emory University School of Medicine. Today's episode is dedicated to Noninvasive and Invasive ventilation in children post-hematopoietic cell transplantation.

We are delighted to be joined by Dr. Courtney Rowan, MD, MSCR, Associate Professor of Pediatrics, and the Director of the Pediatric Critical care Fellowship at Indiana University School of Medicine/Riley Children’s Health.

Dr. Rowan's research interest is in improving the outcomes of immunocompromised children with respiratory failure. She is active in this field of research and has led and participated in multi-centered studies. She is the co-chair of the committee of the hematopoietic cell transplantation subgroup of the Pediatric acute lung injury and sepsis investigators network. In our podcast today we will be asking Dr. Rowan about the findings of her recent study published in the journal-Frontiers in Oncology reporting on the risk factors for noninvasive ventilation failure in children post hematopoietic cell transplant.

She is on twitter @CmRowan.

Patient Case

I will turn it over to Rahul to start with our patient case...

• A 15-year-old female with a history of AML s/p Allogeneic hematopoietic stem cell transplantation T+15 days presents with tachypnea and a new O2 requirement. She has been on the BMT floor for 48 hrs after being admitted for respiratory distress and fevers. Her blood cultures are negative but she is febrile intermittently. Her CXR shows nonspecific haziness, no focal opacity, and underinflation. Her weight is up 2KG in the last 48 hours. She is found to have increased work of breathing and mild desaturations to 88%. She is placed on HFNC and continued on broad-spectrum antibiotics. A respiratory viral panel and Sars-CoV-2 PCR is sent. Transfer to the Pediatric ICU is initiated.

Episode Dialogue

Dr. Rowan, welcome to our PICU Doc on-call podcast.

Dr. Rowan: Thanks Rahul & Pradip for having me. I am delighted to be here to discuss one of my favorite topics. I have no conflicts of interest but I have funding from the NHLBI.

Today we will be discussing the up-to-date evidence for NIV (HFNC and NIPPV) use in children who have had BMT. Additionally, we will also be discussing the use of invasive MV strategies including HFOV in the pediatric BMT population. To start us off, Dr. Rowan, why is the BMT cohort different from other patients admitted to the PICU?

There is an increase in the # of patients undergoing BMT as indications for BMT are being expanded to different disease processes. The Etiologies for lung disease in BMT patients can be infectious (common organisms as well as opportunistic organisms). They can have lung disease from non-infectious causes and even fluid overload from renal dysfunction/medications given and there is a constant threat of alloreactivity which can manifest as GVHD or engraftment syndrome. 75% of PICU admits of immunocompromised children come from the heme-onc inpatient services. BMT patients have a higher risk to progress to ARDS. Recent reports show the incidence of ARDS in the...

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 PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our PICU Doc On Call Mini-Case series. In this episode, we present a 15 year old girl who is admitted for shock after returning from her recent travel to NIgeria.

Here's the case:

13y F with no significant past medical history presents with 4 days of fever, headache, watery, non-bloody diarrhea, non-bloody, non-bilious emesis, decreased PO intake with worsening myalgias, fatigue, and weakness. She had traveled with her mother to Nigeria earlier this month and returned a week ago. Over the weekend mom consulted her pediatrician who prescribed an antiemetic without significant improvement of her symptoms. Once patient progressed to becoming light headed and weak, the mom decided to bring her to ED where she was found to be have tachycardia and hypotension. She required 3 L of crystalloid resuscitation was started an epinephrine continuous infusion and transferred to the PICU. Patient was found to have acute kidney injury with an elevated Cr, as well as a primarily direct hyperbilirubinemia and associated anemia and thrombocytopenia.

Her other history elements were notable for fever and difficulty breathing. Prior to traveling to Nigeria she did receive travel vaccinations and took mefloquine prophylaxis. She also had a negative COVID screen. While in Nigeria she denies exposure to animals, raw food intake, and only recalls that she may have had a few mosquito bites but this was well after returning from Nigeria until 7 days prior to presentation to the ED.

She presents to the PICU with hypotension, tachycardia at 160 bpm, tachypnea, and normal saturations. Her physical exam is notable for cool peripheral extremities, RUQ tenderness, and bilateral crackles.

She had no murmurs or gallops on her initial exam. Pertinently, she had no rash, lymphadenopathy or scleral icterus.

• This is a teenage girl who has fever and constitutional symptoms after returning from travel abroad
• She now presents with fluid refractory shock, tachycardia that is out of proportion to dehydration and signs of end-organ failure.
• Notable negatives include: No LNadenopathy, hepatosplenomegaly, or a rash
• Synthesizing these symptoms together → we are thinking that this picture may be related to a contracted infection or inflammatory condition related to her travel.
• Let's transition into some history and physical exam components of this case.

1. What are key history features in this child who presents with fever and shock after a recent travel outside the US (Nigeria-West Africa)

• Diarrhea and emesis days before presentation
• High Fever with no rash
• Mental status is maintained although she did have an headache
• Light headed and weakness are symptoms suggestive of dehydration and even shock
• Physical exam findings of importance here include- patient presenting with tachycardia, signs of poor perfusion such as delayed cap refill, cool extremities, hypotension. It is unique that even though she has RUQ pain there is no jaundice.

2. Are there some red-flag symptoms or physical exam components which you could highlight in a

patient with the above history and recent travel.

• Weakness, light-headedness, shock, tachycardia, poor perfusion, fever and evidence of multi-organ dysfunction are suggestive of an acute and possibly life threatening infection acquired during travel. Given her travel to West Africa: I would be worried about falciparum malaria, dengue fever, typhoid fever, and cholera. Other diseases to be...

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

Key Case Highlights:

• 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

Episode Learning Points:

• 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.

Resources Mentioned:

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

Call to Action:

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

Welcome to our Episode a 16-year-old who is coughing up blood.

Here's the case:

A 16-year-old female with h/o SLE was transferred to the PICU due to hypoxia requiring increasing FIO2. A few hours prior to admission to the PICU patient also started coughing up blood and had difficulty breathing. The patient was admitted to the general pediatric floor 2 days earlier for pneumonia requiring an IV antibiotic and O2 via NC. Once transferred to the PICU, she had a rapid deterioration with progressive hematemesis, worsening respiratory distress, and saturations in the low 70s requiring escalating FIO2. The patient was emergently intubated using ketamine + fentanyl and rocuronium. Chest radiograph showed: Worsening bibasilar alveolar and interstitial airspace disease concerning pulmonary hemorrhage. The patient was initially placed on HFOV Paw 26, FIO2 70%, Hz 8, Dp 70, and later transitioned to airway pressure release ventilation or APRV. The patient was also started on inhaled tranexamic acid or TXA and high-dose pulse steroids. The patient initially continued to have some blood coming out from the ETT with suctioning but secretions became clear in ~24 hours.

The mother reported that the patient has never had hematemesis/hemoptysis before, or bleeding from any site in the past. Denied history of frequent respiratory infections or recent URI symptoms. The patient has been vaccinated/boosted x3 vs covid. Her COVID PCR is negative. The mother states that she does not engage in tobacco products or alcohol.

A physical exam revealed a well-developed teenage girl laying supine in bed deeply sedated and mechanically ventilated. There was decreased AE at lung bases and coarse breath sounds throughout. There was no hepatosplenomegaly and exams of the heart, abdomen and other systems were normal. There was no skin rash and extremities were well perfused with no clubbing in the fingers. The pulmonary team was consulted and a workup was started for pulmonary hemorrhage.

To summarize key elements from this case, this patient has:

• Autoimmune disease: Systemic lupus erythematosus
• Respiratory Failure warranting MV 2/2 Pulmonary hemorrhage
• Her presentation and deterioration bring up a concern for diffuse alveolar hemorrhage our topic of discussion for today.
• This episode will be organized…
• Definition
• Etiology
• Pathophysiology
• Diagnosis
• Management
• Rahul: How do we define pulmonary hemorrhage (PH):
• PH is defined as the extravasation of blood into airways and/or lung parenchyma. Blood in the airways produces a diffusion barrier resulting in hypoxemia. Due to the reduction of airway diameter from accumulated blood, there is increased airway resistance and even airway obstruction. Subsequently, ventilation can be impaired leading to increased WOB as well as myocardial work required for O2 delivery. Repeated episodes of PH can result in interstitial fibrosis thus changing lung compliance. Hemoptysis by definition is any bleeding from below the vocal cords. PH can be classified as focal or diffuse. Diffuse is further classified as diffuse immune or diffuse nonimmune.

Loss of 10% of a patient’s circulating blood volume into the lungs, regardless of age, causes a significant alteration in cardiorespiratory function and should be considered massive. In adults, massive pulmonary hemorrhage is defined as blood loss of 600mL or more in 24 hours. In infants, the involvement of at least two pulmonary lobes by confluent foci of extravasated RBCs constitutes as massive PH. “Enough bleeding to make one nervous is probably massive.”

Let's pivot and talk about etiologies.

• Pradip, What are some of the causes of pulmonary hemorrhage in the...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat

My name is Rahul Damania, a current 2nd year pediatric critical care fellow. We come to you from Emory University,School of Medicine, Children’s Healthcare of Atlanta, Atlanta, GA.

Today's episode is dedicated to O2 delivery in the PICU. We would like to highlight in this episode Stanford University School of Medicine Pediatric Critical Care's LearnPICU website. The LearnPICU.com website Is dedicated to reviewing clinical topics related to pediatric critical care, and is an open access resources which Is widely accessed worldwide. The website has over 10,000 visits each month, and is managed by Dr. Kevin Kuo - Clinical associate professor of pediatrics pediatric critical care at Stanford University. Dr. Kuo has Been featured on our prior episode entitled seven habits of highly effective Picu fellows, and we are very excited to collaborate with his educational resources to provide you the listener a comprehensive educational experience.

Rahul, let's go ahead and get into today's case.

A 17-year old boy is admitted after he was struck by a car at slow speed while crossing the street.

He is has SPO2 of 98%, HR 98 bpm with a normal capillary refill and perfusion.

His blood gas at admission to the PICU reveals a ph of 7.3/PCO2 35/PaO2 196 mm Hg on 50% NRB with 100% O2 flowing at 12LPM.

His admission hgb is 10.5 gm%.

4 hours post admission, the nurses noticed that the patient is tachycardic to 150s, with a drop in his BP, delayed capillary refill, with cool extremities and increased output from the chest tube.

His SpO2 has decreased to 86% and PaO2 on his blood gas is now 65mm HG. He is found to have a POC Hgb of 6.8 mg/dL.

Let’s take this case and highlight key components of O2 delivery and O2 consumption.

Lets focus on O2 delivery first. Rahul What are the components of O2 delivery ?

 Pradip, O2 delivery is made of O2 content X Cardiac output

Simply put, O2 content is the amount of blood present in 100ml of arterial or venous blood. Its is denoted by CaO2 or CvO2 and its unit is mL O2 / dL blood or mL O2 per 100 mL of blood.

Before we introduce the complicated formula, let's just appreciate the variables within the equation.

Oxygen content is going to be a function of three variables:

This is going to be Hgb, Saturations on the hemoglobin also known as SaO2, and the amount of oxygen that is dissolved within the blood also known as your PaO2.

Pradip, Can you elucidate further about O2 content?

O2 content is given by the formula: CaO2 = (1.34X Hgb gm/dl X SaO2) + (0.003X PaO2)

Important points to remember about above formula is that the constant 1.34 (or 1.36 as given by

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. My name is Rahul Damania and we come to you from Children’s Healthcare of Atlanta-Emory University School of Medicine.

Today's episode Is part two of our pediatric post-cardiac arrest care syndrome

If you have not yet listened to part one, I would highly encourage you to visit that episode prior to delving into this one.

Part 1 addressed the epidemiology, causes, and pathophysiology of POST CARDIAC ARREST SYNDROME.

Part 2 Today will discuss management and complications related to post-cardiac arrest syndrome in the ICU.

To revisit our index case we had a:

• 11 yo previously healthy M who was admitted to the PICU after cardiac arrest. After stabilization: The patient was taken to head CT which showed diffuse cerebral edema and diffusely diminished grey-white differentiation most pronounced in the basal ganglia. He is now 18-24 hours post-cardiac arrest and the team is dealing with hemodynamic changes, arrhythmias, and difficulty with ventilation. The patient’s neurological exam still remains poor with fixed 5 mm pupils and upper motor neuron signs in the lower extremities.

Let’s get right into it:

• What are some of the principles in management of patients with post cardiac arrest syndrome (PCAS)? Where do we keep the patients blood pressure?
• Hypotension after ROSC is commonly encountered in children with PCAS. Early hypotension occurred in 27% of children after cardiac arrest is associated with lower survival to hospital discharge and unfavorable neurological outcome. When post-cardiac arrest hypotension is present, it is not clear whether increasing the blood pressure through administration of fluids and inotropes/vasopressors can mitigate harm, despite this 41% of patients under 18 receive vasopressor therapy within the first 6 hours after ROSC. Currently, there is no high-quality evidence to support any single specific strategy for post-cardiac arrest hemodynamic optimization in children. Treatment of post-cardiac arrest hypotension and myocardial dysfunction may be assisted by monitoring and evaluating arterial lactate and central venous oxygen saturation. Parenteral fluids, inotropes, and vasoactive drugs are to be used as needed to maintain a systolic blood pressure greater than the fifth percentile for age. Appropriate vasoactive drug therapies should be tailored to each patient and adjusted as needed.
• What about cardiac arrhythmia's such as Vtach seen in our patient?
• The rhythm disturbances observed during the post-cardiac arrest period include premature atrial and ventricular contractions, supraventricular tachycardias, and ventricular tachycardias. Heart block is unusual but can be observed as a manifestation of myocarditis. There is inadequate evidence in adults and no published studies in children to support the routine administration of prophylactic antiarrhythmics after ROSC, but rhythm disturbances during this period may warrant therapy. Treatment depends on the cause and hemodynamic consequences of the arrhythmias. Premature depolarizations, both atrial and ventricular, usually do not require therapy other than maintenance of adequate perfusion and normal fluid and electrolyte balance. Ventricular arrhythmias may...

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.

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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...