PICU Doc On Call

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 which interfere with the Krebs cycle and specifically uncouple oxidative phosphorylation. This leads to acidosis, heat production, and hypoglycemia.
• Although not common, neuromuscular irritability manifested as paratonia (inability to relax muscles) and extreme muscle rigidity can develop, further contributing to hyperthermia and increasing the risk of rhabdomyolysis.
• Salicylates induce fatty acid metabolism resulting in ketone production which can further compound the anion gap metabolic acidosis.
• Disruption of the electron transport chain causes a dissociative shock picture in which there is adequate oxygen delivery, however, the tissues are unable to uptake the oxygen.
• Considerations in the diagnostic approach to our patient with salicylate poisoning:
• Salicylate poisoning can happen acutely (usually in young adults with suicidal ideation) or chronically, which often happens in the elderly who are taking aspirin therapeutically but have an inadvertent overdose. Because the pathways for salicylate elimination are fully saturated in those taking the drug chronically, a higher toxicity can occur at even a lower dose. 
• The plasma level of salicylate required to elicit symptoms tends to be lower in chronic than in acute salicylate poisoning. In cases of acute salicylate toxicity, rising plasma levels are roughly correlated with the development of expected clinical manifestations, but such correlations are notoriously absent with chronic toxicity. 
• Salicylate poisoning should be suspected in any patient with the following:
• Possible ingestion of known or unknown drug
• Tinnitus, nausea, vomiting, tachypnea, and altered mental status
• Elevated anion gap metabolic acidosis; remember that the patient can present with a mixed respiratory alkalosis and an anion gap metabolic acidosis
• Any elderly patient on chronic aspirin therapy who presents with agitation, confusion, hallucinations, slurred speech, seizures, and coma; “salicylate jag” refers to restlessness and mental aberrations that resemble alcohol intoxication
• Your diagnosis will likely be confirmed by elevated serum salicylate concentration!
• It is important to check salicylate levels with serial measurements every three hours because toxicity can be delayed. Once you get the level, you can stratify the level of toxicity:
• Generally, a level of 15-30 mg/dL is considered therapeutic for inflammatory conditions, but levels can exceed 40-50 within 1-2 hours of a single ingestion.
• Significant toxicity begins to manifest at a level >45 with tinnitus, vertigo, nausea, vomiting, and hyperventilation.
• A level of 50-70 indicates severe intoxication; the patient can have fever, sweating, listlessness, and incoordination.
• At levels exceeding 75, patients are at risk for hallucinations, seizures, cerebral edema, coma, noncardiogenic pulmonary edema, and cardiovascular collapse. 
• Other major testing to consider include acetaminophen level, acid-base status with electrolytes, blood gas, urine pH, and pregnancy test, renal and liver function tests, and possible head CT if there are signs of cerebral edema or persistent altered mental status. 
• If the history, physical exam, and diagnostic investigation lead us to a salicylate poisoning diagnosis, the general management framework would be as follows:
• Management is based on supportive care and elimination of salicylate, including gastric decontamination with activated charcoal and possibly polyethylene glycol via a nasogastric tube.
• The airway should be protected with intubation for respiratory failure, in the obtunded or delirious patient, or for a procedure such as dialysis access catheter placement. Avoid a low respiratory rate because any decrease in pH from a rising PCO2 can enhance movement of salicylate into tissues, and the patient can worsen.
• In fluid management, use Lactated Ringer’s solution since normal saline can cause normal anion gap acidosis and lower pH. A hallmark of therapy for salicylate ingestion is the alkalinization of the patient’s urine until the serum salicylate level is <40 mg/dL, metabolic acidosis is resolved, and the patient is asymptomatic with a normal respiratory rate. It is recommended to give one meQ/Kg initial bolus of NaHCO3 followed by three ampules of NaHCO3 added to one liter of D5W, with the goal of keeping the urine pH above 7.5. Add some KCL to this as hypokalemia can occur. Check serial blood gases, along with ionized calcium and magnesium, and avoid a serum pH above 7.5. 
• Hemodialysis should be considered for the patient because the water solubility, small size, low volume of distribution, and absence of tissue binding make salicylate an ideal substance to dialyze. 
• Urinary alkalinization is NOT a substitute for dialysis and can be stopped once dialysis is initiated. 
• Hemodialysis should be considered for any patient with severe signs or symptoms, including severe fluid and electrolyte disturbances, altered mental status, cerebral edema, acute respiratory distress syndrome, and acute kidney injury. 
• Hemodialysis is recommended if the plasma salicylate level is greater than 90 mg/dL or greater than 80 if kidney function is impaired. 
• Conventional hemodialysis is preferred, but hemoperfusion or CVVH is acceptable if hemodialysis is not available or the patient is unstable.
• Keep close communication with poison control and the clinical toxicologist because of the life-threatening complications that can occur.
• Repeat the salicylate level at least every three hours until the level is down-trending. 
• Learn more about salicylate toxicity from these sources:
• The review of salicylate toxicity by Palmer and Clegg from the New England Journal of Medicine, June 2020
• Chapter 126, p. 1503 of the latest edition of Fuhrmanns and Zimmerman’s textbook of Pediatric Critical Care
• Clinical pearls:
• A salicylate level of 300 mg/kg can result in severe toxicity and even death. Salicylate toxicity must be suspected in any patient presenting with fever, diaphoresis, mixed respiratory alkalosis, and metabolic acidosis.
• Urinary alkalinization using NaHCO3 in IV fluids is the hallmark of therapy to prevent systemic absorption of the drug. Serial measurements of serum K, Magnesium, and a blood gas are required during the process of alkalinization, and urinary pH should be maintained at 7.5 or greater.
• Despite normal serum glucose, the CSF glucose can be low. Dextrose can be used for acute delirium. 
• Indications for dialysis include plasma salicylate level >90 mg/dL or >80 mg/dL if kidney function is impaired. Any severe signs or symptoms, including severe fluid and electrolyte disturbances, cerebral edema, acute respiratory distress syndrome, and acute kidney injury are indications for dialysis. 

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. Both of these medications block thyroid peroxidase.

 In terms of differential in our case, you want to think about other causes of fever, tachycardia, and CNS dysfunction, including, but not limited to sepsis, serotonin syndrome, neuroleptic malignant syndrome, heatstroke, and drug intoxication. 

The diagnostic approach for our patient should focus on her history and physical examination. Be sure to include thyroid function tests, cardiac evaluation via EKG or Echo, chest x-ray, blood culture, urine analysis, and lateral neck radiographs to assess airway compression. 

The general management framework for the diagnosis of thyroid storm should include a multimodal approach to block thyroid hormone production and action quickly, reverse systemic decompensation, and identify and treat any underlying causes and precipitants of thyroid storm. The key components are:

• Optimal communication between the pediatric endocrinology team and ICU staff
• Acute resuscitative measures in the PICU, such as aggressive cooling measures, IV fluids, and stress-dose steroids
• Management of thyroid storm is characterized by the “Five Bs”:
• Block synthesis of new thyroid hormone with antithyroid medications like PTU or methimazole
• Block release of thyroid hormone with inorganic iodine
• Block conversion of T4 into T3
• Block peripheral effects of thyroid hormone with beta-blockers like atenolol and [propranolol
• Block iodine uptake with the use of cholestyramine

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 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 be. If a matched sibling donor is not available (or in some inherited conditions that may not be an option as a donor), then matched unrelated donors or matched cord blood units of appropriate size can provide a good option to proceed.
• Then come considerations of mismatched unrelated donors, and haplo-identical related donors.
• The type of donor and degree of match dictates the type of GVHD prophylaxis we will use and further immunosuppression.

 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. 

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 premature infants and those with HTN or other risk factors for bleeding. 
• Diagnostics needed prior to consulting on a patient with venous occlusion include Doppler US, CT or MRI to visualize central vessels, cone-beam CT (CBCT), and hematology consult.
• General principles of venous recanalization for acute venous occlusion:
• Acute venous occlusions are typically related to acute thromboembolism.
• Intravascular ultrasound (IVUS) is a valuable tool.
• CDT with a catheter dripping tPA overnight.
• Balloon angioplasty followed by systemic anticoagulation.
• Treatment options for chronic venous occlusions range from endovascular angioplasty and stenting to surgical bypass grafts or prosthetic graft reconstruction. Endovascular techniques are more widely accepted in pediatrics.
• Post-procedure patients in the PICU should have neurological monitoring and pain management, along with careful monitoring of the heparin infusion and tPA management. Worsening conditions may point to surgical interventions. 
• Dr. Gill explains the protocol developed for heparin and tPA dosage and monitoring.
• Precautions needed by the PICU doctor for patients getting tPA and heparin include no arterial sticks, intramuscular injections, rectal temperatures, catheters, NSAIDs, or other platelet drugs. The key is a collaborative approach between interventional radiology, anesthesia, and hematology.
• Once the IR physician is satisfied with clot removal and blood flow in the previously occluded vessel, a decision is made to stop the tPA infusion.
• IR also provides other services like chest tube, PICC line, and GT placements, lumbar punctures, biopsies of liver/kidneys, and thermal ablation of solid tumors or painful bony metastases.
• Takeaway clinical pearls include the collaborative team of anesthesia, hematology, PICU, and IR for optimal outcomes. IR should be called early and often. Labs should be followed closely, especially Fibrinogen, platelets, and hemoglobin/hematocrit. 

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. 

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 aware of the pharmacology and relevant side effects of these agents in efforts to choose the best drug for the patients condition. Early consultation with nephrology is warranted in these patients along with monitoring of end organ function.

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.

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. Viamonte shares her perspectives on sedation and other medications to consider with intubation.
• Takeaway clinical pearls regarding intubation of the critically-ill, high-risk patient include maintaining the patient’s cardiopulmonary reserve, leveraging team potential and resources, and mitigating chaos. “Advance preparation is the key to success.”