PICU Doc On Call

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 lymphomaAllogeneic 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.

Dr. Michael Wolf, PICU specialist, discusses an unstable neonate case. Highlights include diagnosing an acutely ill newborn, managing neonatal shock, assessing congenital heart disease, and stabilizing neonates in the PICU. Topics cover initial investigations, considerations for neonatal airway dynamics, and prostaglandin use in duct-dependent heart conditions.

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 @BabyBeanDocA 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/<80Stage 1 HTN is 130/80 to 139/89Stage 2 HTN is >/= 140/90That'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.

Dr. Roshan George discusses the acute management of hyperkalemia in the PICU, focusing on causes, symptoms, and clinical manifestations. Key topics include EKG findings, renal conditions, and management strategies like insulin therapy and dialysis. The importance of early detection and monitoring in high-risk patients is emphasized.

Dr. Heather Viamonte, a pediatric cardiac intensivist, discusses the management of high-risk intubations in the PICU. Topics include pathological derangements prior to intubation, systolic dysfunction, preparation, collaboration, equipment, and managing intubation of critically ill pediatric patients.

Dr. Lisa Lima and Dr. Tom Austin discuss the acute management of anterior mediastinal mass in the PICU. They cover key presentation features, diagnosing challenges, management strategies, Chamberlain procedure, and considerations for ECMO backup.

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 patientsWhen the tumor cells die or lyse, what’s inside those cells comes out into the bloodKey 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 tumorsPatients with fast-growing tumors, like lymphoma and leukemia, are at high riskKey pathophysiologic principles that drive TLS:The imbalance of electrolytes can impact heart functionTLS is characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and uric acid, which is a by-product of DNA breakdownIf untreated, the uric acid can lead to acute kidney injury and renal failureElectrolyte and metabolic disturbances can progress to renal insufficiency, cardiac arrhythmias, seizures, and deathTLS releases cytokines that can cause a systemic inflammatory response and multi-organ failureOther 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. 

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 teamA robust and experienced team for perioperative care and graft outcomeA comprehensive and multidisciplinary post-transplant teamThe process of organ procurement for cadaveric and living donor renal transplants includes the following:Multiple factors determine the points a patient receives toward transplant priorityDeceased donor kidneys are classified using the KDPI (kidney donor profile index)A thorough evaluation is performed for living donorsAdvantages to living donation include a shorter time on dialysis and waitlists, improved graft survival, and shorter ischemia time than from a deceased donorInformation 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 phaseHow immunosuppressive medications might be used for the pediatric renal transplant patientWhy the post-op transplant patient might need dialysisClinical 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.