54 episodes

PICU Doc On Call is the podcast for current and aspiring Intensivists. This podcast will provide protocols that any Critical Care Physician would use to treat common emergencies and the sudden onset of acute symptoms. Brought to you by Emory University School of Medicine, in conjunction with Dr. Rahul Damania and under the supervision of Dr. Pradip Kamat.

PICU Doc On Call Dr. Pradip Kamat, Dr. Rahul Damania

    • Health & Fitness
    • 4.8 • 40 Ratings

PICU Doc On Call is the podcast for current and aspiring Intensivists. This podcast will provide protocols that any Critical Care Physician would use to treat common emergencies and the sudden onset of acute symptoms. Brought to you by Emory University School of Medicine, in conjunction with Dr. Rahul Damania and under the supervision of Dr. Pradip Kamat.

    53: GI Hemorrhage

    53: GI Hemorrhage

    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 bleed is bleeding that occurs above the ligament of Treitz — which is ligamentous tissue that supports the end of the duodenum and beginning of the jejunum at their junction. While not 100% specific, some..

    • 16 min
    Rhabdomyolysis

    Rhabdomyolysis

    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 HandP 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 rhabdo in adults (and teens), infections, especially viruses, are the most common cause in young children. Influenza, EBV, and CMV are three most commonly reported.
    What’s the pathophysiology of...

    • 14 min
    Approach to Calcium Channel Blocker Overdose

    Approach to Calcium Channel Blocker Overdose

    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.

    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.

    These components of your physical exam should help allude to a toxidrome, and these syndromes are frequently tested on board examinations. Any time a patient has hypotension and bradycardia other drugs that should be considered include beta blockers, digoxin, clonidine, as well as ingestion of barbiturates, opioids, and even benzodiazepines.


    What are some diagnostic studies you will want to send immediately in a patient with suspected ingestion?
    Immediate diagnostic studies to be performed include pulse oximetry, continuous cardiac monitoring, an electrocardiogram (ECG), and a capillary glucose measurement (in altered patients). Intravenous (IV) access should be obtained in all cases of serious ingestion.
    You also want to send beta-hcg and acetaminophen and salicylate levels. an extended toxicology screen may be required on a case-by-case basis.

    One study found detectable serum acetaminophen concentrations in 9.6 percent of all overdose patients; almost one-third of this subset denied ingestion of acetaminophen.


    Now that you’ve focused on ABCs are there more detailed laboratory studies to send in patients with toxidromes?
    Symptomatic patients and those with an unreliable or unknown history should, at a minimum, undergo...

    • 21 min
    All Things Sodium & the Brain in the PICU

    All Things Sodium & the Brain in the PICU

    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 and the Brain. We will discuss diagnostic and management frameworks related to three pathologies:
    Central Diabetes Insipidus
    Syndrome of inappropriate Anti-Diuretic Hormone or SIADH
    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:
    ADH
    Aldosterone
    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.
    What are the physiologic actions of ADH?
    ADH Increases H2O permeability by directing the insertion of aquaporin 2 (AQP2) H2O channels in the luminal membrane of the principal cells. Thus, as we will see with Central Diabetes insipidus, in the absence of ADH, the principal cells are virtually impermeable to water.
    Let's talk about our next hormone, aldosterone. What are the important physiologic considerations?
    Aldosterone is secreted from the adrenal cortex as a byproduct of the RAAS.
    Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure.
    It also helps in secreting K and H. This physiology is applied directly at the bedside when we have patients in the ICU who have a contraction alkalosis secondary to diuretics. The increase in aldosterone as these patients lose free water from their Lasix administration results in hypokalemia and metabolic alkalosis.

    Alright, what about the third hormone, ANP?
    Atrial natriuretic peptide (ANP) is released from the atria in response to an increase in blood volume and atrial pressure.
    ANP causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR.
    causes increased excretion of Na+ and water by the kidney, which reduces blood volume and attempts to bring arterial pressure down to normal.

    As ANP causes natriuresis, diuresis, and inhibition of renin, you can consider this hormone as having a complementary and opposite effect to ADH and aldosterone.
    Alright, now that we...

    • 21 min
    Necrotizing Enterocolitis (NEC)

    Necrotizing Enterocolitis (NEC)

    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 reduced oxygen supply to the SMA and decreases intestinal wall perfusion.
    On the repair of the cardiac lesion, patients develop reperfusion injury due to their now improved perfusion to their gut. This reperfusion causes hyper inflammation via neutrophil activation resulting in NEC.
    NEC primarily occurs in healthy, growing, and feeding VLBW preterm infants. It presents with sudden changes in feeding tolerance (increase in gastric residuals) with both nonspecific systemic signs (eg, apnea, respiratory failure, poor feeding, lethargy, or temperature instability) and abdominal signs (eg, abdominal distension, bilious gastric retention and/or vomiting, tenderness, rectal bleeding, and diarrhea). Physical findings may include abdominal wall erythema, crepitus, and induration.

    Other than the immediate risk of death, what are some consequences of NEC long-term?
    Higher risk of malnutrition and short gut.
    BPD
    Developmental delay.

    What are some areas of current research and development on the topic of NEC?
    Improved biomarkers for early recognition of NEC prior to the development of radiographic findings.
    Preventative...

    • 16 min
    Pediatric Pain, Agitation, Neuromuscular Blockade, and Delirium in Critically Ill Pediatric Patients (PANDEM)

    Pediatric Pain, Agitation, Neuromuscular Blockade, and Delirium in Critically Ill Pediatric Patients (PANDEM)

    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 athttp://pccmjournal.org ( 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 and 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 were derived?
    Of course, this was a remarkable group effort solicited by the Society of Critical Care Medicine. We were initially modeled after the adult PAD (pain, agitation, and delirium) guidelines task force but, as described already, extended beyond that to include Pediatric Pain, Agitation, Neuromuscular Blockade, and Delirium in addition to the PICU Environment and Early Mobility. It was comprised of 29 national experts who collaborated over a ten-year period. The full task force gathered annually in person during the Society of Critical Care Medicine Congress for progress reports and further strategizing with the final face-to-face meeting occurring in...

    • 34 min

Customer Reviews

4.8 out of 5
40 Ratings

40 Ratings

ATLPSL_owner ,

Excellent repository of knowledge!!

Regardless of your clinical level, RN, RRT, RPh, or MD - this podcast has high value for all!! Drs Kamat and Damania are clearly invested in disseminating useful clinical knowledge to promote the care of patients in the Intensive Care setting. I’ve already learned so much background on different management strategies, but I look forward to the many directions this podcast can go! It doesn’t hurt that I can gain knowledge while doing house chores, either! Keep up the knowledge share, gentlemen! Much appreciated!

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