The Fellow on Call: The Heme/Onc Podcast

Lung cancer specialized testing in NSCLC: What do we do if we biopsy a suspected metastatic lesion?* Immunohistochemistry (IHC): **Confirm if it is metastatic NSCLC **Confirms the histology of the NSCLC (such as adenocarcinoma vs. squamous cell)**Used to determine the type of chemotherapy that can be administered for treatment *PDL1 testing: **PDL1 is a protein expressed by certain cancer cells allowing them to evade the immune system (“fake mustache analogy”).**Also confirmed by IHC**This protein is targetable!**Often measured as:***Total protein expression (TPS): The number of positive tumor cells divided by the total number of viable tumor cells multiplied by 100%***Composite protein expression (CPS): The number of positive tumor cells, lymphocytes and macrophages, divided by the total number of viable tumor cells multiplied by 100%*Molecular testing: **We discuss this in detail in Episode 005**Genetic information from the tissue sample**Always better to get sample from soft tissue than from bone**Why is this important?***To be able to identify “driver mutations”****What is it? Important mutations that may be “driving” oncogenesis****Many of these have drugs that directly target these mutationsPrognostic vs. predictive biomarkers:*Prognostic biomarkers: Mutations or changes that give information about the cancer’s overall outcome regardless of therapy*Predictive biomarkers: Mutations that provide information about how a cancer may respond to a particular drug Cell-free DNA (AKA “liquid biopsy”):*Special tests that can detect microscopic amounts of cancer cell DNA within the patient’s blood which may also be used to find prognostic/predictive biomarkers*Ongoing studies to see if this can be used to find relapse of diseasePlease visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Lung Cancer Histology and Staging*Workup for a nodule that is concerning: **Ensure there is a dedicated CT scan of the chest to evaluate **Try to obtain old imaging; the rate of change is important **Can get PET, but even if a lesion if not FDG-avid, but growing quickly we should consider biopsy anyway**Referral to pulmonary medicine, who can assist with biopsy and also regional lymph node evaluation (important – more below)**PFTs are often ordered because it provides information about lung function in anticipation of possible surgery for treatment Lung Cancer Histology: *Non-small cell lung cancer (NSCLC)**Umbrella term for a variety of cancers**Increased risk in smokers**More common types: ***Adenocarcinoma (~50% of all lung cancers)****Most common overall; cancer of the mucus producing cells****IHC: TTF-1, NapsinA, CK7 positive***Squamous Cell Carcinoma (22.7%)****More often seen in patients with a smoking history ****IHC: p63 positive and cytokeratin pearls***Remaining ~15% are the other types of lung cancer / mixed histologies**Small cell lung cancer (SCLC)***Neuroendocrine tumor with very different pathology***Much more aggressive than NSCLC***Oncologic emergency***IHC: Chromogranin and synaptophysin positive IHC pearls: TTF-1 usually means lung cancer (but can be negative in squamous cell lung cancer). This will be important in the future (we promise :])*Staging for NSCLC:**Nodal evaluation: lymph node evaluation is part of the workup for NSCLC**Single digit = central/mediastinal nodes (higher risk)**Double digit = peripheral/hilar/intrapulmonary lymph nodes (lower risk)**“R” vs. “L” is direction *Pearl: Why is this important? If there is nodal involvement, systemic therapy is going to be necessary *Putting it all together: **T: Tumor size: T1-4**N: Nodal involvement***N0: no nodal involvement ***N1: Nodes closest to the primary tumor (double digits)****Ipsilateral peribronchial, hilar, intrapulmonary ***N2: Further away (single digit)****Ipsilateral mediastinal and/or subcarinal LN***N3: Contralateral any node or supraclavicular LN **M: Metastasis – in lung cancer, patients with certain patterns of metastatic disease are still curable! ***M0: no mets***M1a: Contralateral lobe, pleural effusion or pericardial effusion à these are generally still curable!***M1b: single site of metastatic disease à these are generally still curable!***M1c: multiple sites of metastatic disease à these are generally not curable*Staging for SCLC: **Limited stage - meaning it can fit in “one radiation field”**Extensive stage - does not fit in “one radiation field”*Once lung cancer is diagnosed:**Go to NCCN to learn the flow of ongoing management**Complete staging (if not already done):***CT C/A/P (don’t necessarily need if a PET scan is done)***PET Scan***MRI brain à in general this is needed, but there are some exception to this (see NCCN)**Referral to pulmonary for nodal evaluationReferences: NCCN.orghttps://doi-org.proxy.library.vanderbilt.edu/10.1016/j.semcancer.2017.11.019-Article about IHC markers for lung cancer Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we sit down with guest pulmonologist Dr. Greta Dahlberg to discuss how she thinks about and works up lung nodules concerning for malignancy.Lung nodules: * For discussions about incidental lung nodules and lung cancer screening, check out Episode 197 from our friends, The Curbsiders (link: https://thecurbsiders.com/podcast/197) * Nodule vs. mass:** “Micronodule” is <3mm** “Nodule” is <3 cm** “Mass” is anything bigger *Characteristics of “benign” vs. “malignant” nodule** Most important thing is change over time; therefore always good to have old imaging if possible. ** If growing overtime, even if slowly, that should raise red flags for malignancy** Volume doubling time (link: https://radcalculators.org/volume-doubling-time-vdt-calculator-for-pulmonary-nodules-volume-based/)*** If doubling time <20 days, it’s often infectious*** Average lung cancer doubling times is 100 days* Benign: ** Smooth** Calcifications (diffusely or popcorn calcifications)** Internal fat appearance * What about a spiculated nodule? ** This is when there are nodules with “little hairs” coming off, often thought to be malignant** Dr. Dahlberg reports that odds ratio of it being malignant is 2.5, so it is high, but not that high. So spiculated does NOT necessarily mean malignant. * Workup before referring to Pulmonary: ** Dedicated CT scan of the chest ** Obtain old imaging ** PET CT*** Expert tip: If growing, whether it’s hot or not, it warrants a biopsy*** PET can help identify spread and/or nodal involvement* Biopsy approaches (we don’t know approach which one is better … There are studies ongoing!):** Transthoracic biopsy (CT guided):*** Performed by IR*** Major risk: pneumothorax (20-25% have one after procedure!)*** Benefit: Does not need general anesthesia**Transbronchial biopsy: *** Performed by Pulmonary*** Requires general anesthesia and paralyzing *** Options while doing biopsy:**** EBUS**** Fluoroscopy *** Major risks: Pneumothorax (1.5% have one, less than half need chest tube)*** Benefit: You can also do EBUS to stage mediastinum. Remember- we always look to upstage a cancer and by looking at the mediastinum, this helps to accomplish that* What if someone has two lung nodules on contralateral sides?** Likely both will be sampled** If PET has one nodule that is more FDG-avid than the other, they will go after that first. But they can sample both if safe. * Does PET help with bronchoscopy?** It can help, but appearance during bronchoscopy is more important* When is something NOT amenable to bronchoscopy?** The middle third of the lung is hardest and most technically challenging** Lower lobes of lungs, made difficult by atelectasis** Contrary to common belief, peripheral lesions are easier due to anatomy of the lungsAbout our guest: Dr. Greta Dahlberg (link: https://medicine.vumc.org/person/greta-dahlberg-md) is a pulmonary/critical care fellow at Vanderbilt University Medical Center in Nashville, TN. Thank you so much for joining us! Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

We have now covered the fundamentals of pharmacology. This week, we sit down with Renee McAlister, PharmD, BCOP to learn more about the nuances of pharmacology from an expert that does this day in and day out. *The products/resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities. Pharmacology Capstone: * Irritant vs. Vesicant:** For extravasation, what to do?*** Not a great general source; would recommend checking institutional guidelines. *** Different drugs may require a cold vs. warm compress.*** Some drugs have antidotes - it is best to just look this up when it happens* Why is there a “cut off time” to get in chemotherapy orders?** Many hospital pharmacies are not 24 hours, therefore need prep time. ** Many drugs take a long time to prepare!** A lot verification goes into ensuring that the drugs are correctly ordered, prepared, and handled. Therefore this requires adequate staff to do this safely. * What does "ideal body weight” mean?** Calculated by the patient’s sex, height, and the calculated body weight based on this information ** Helps with drug-dosing to ensure that drugs are not over/under-dosed* What does “AUC” mean?** Incorporates renal function and the amount of exposure you want the patient to have to the drug. Based on the Calvert equation.** It is important to re-calculate each time with a new Cr to ensure that this is updated.** Example: https://reference.medscape.com/calculator/169/carboplatin-auc-dosing-calvert* What is the role of granulocyte colony-stimulating factor (GCSF)?** Helps to prevent the risk of infection, especially from endogenous bacteria.** GCSF helps to minimize the window of neutropenia related to treatment with chemotherapy** NCCN guidelines (www.nccn.org) provides guidelines about febrile neutropenia risk. A risk >20% means that we build in GCSF administration into the treatments. *** If risk 10-20% with certain risk factors, we may consider adding GCSF*** Always look at the paper that was what the approval of the regimen was based off of - they will comment on if/how GCSF was used during the study. *** If patient develops neutropenic fever during a cycle, if even the drug is not traditionally one that we consider GCSF for, it would be appropriate to consider GCSF for future cycles to decrease the risk of febrile neutropenia. * What are the different “types” of GCSF?** Examples:*** Filgrastim (“Neupogen”) - daily dosing, short-acting GCSF*** Pegylated-filgrastim (“Neulasta”) - don’t have to give daily dosing; one time shot because it lasts for longer*** On-body injector (OBI) - a device put on the arm that delivers pegylated- filgastrim at approximately 26 hours after chemotherapy ** Dosing: Very different dosing for all of these medications; pay attention to the dosing! * Supportive care: ** How do you decide what anti-emetics to include?*** NCCN supportive care guidelines is a great place to start*** Regimens with >90% emetic potential should get at least three agents (for example: ddACT, cisplatin based regimens)**** Example: 5-HT3 receptor antagonists, dexamethasone, olanzapine, and aprepetant*** Moderate emetic potential (30-90%), add at least 2 drugs**** Example: 5-HT3 receptor antagonists and dexamethasone*** Lower risk (30%): usually one one drug**** Example:5-HT3 receptor antagonists** If patients have refractory nausea in a cycle, add another agent. When adding drugs, always ensure you are incorporating the patient’s other medical history AND drug-drug interactions* Pharmacists are an amazing source of information! Please reach out with questions!Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips! In this episode, we discuss important considerations, including “does my patient need a port?”, “what if drugs extravasate?”, “how do I keep side effects of drug classes straight?!” *The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities. Pharmacology 101: * Irritant vs. Vesicant:** Each drug is deemed one of these based on the degree of tissue damage that can result if drug extravasates under skin. 
** Vesicant: needs central access
** Irritant: can be given peripherally 
* Does my patient need a port/picc?** If vesicant; for continuous infusions over several days (e.g. 5-FU); some patients with difficult access may request. 
*Advantages of ports: ** Easy access for labs
** Easy access for chemotherapy/fluids
* Disadvantages: ** Risk of infection
** Risk of thrombosis 
* General overview of chemotherapy side effects: ** Going to target the fastest growing cells in the body, which includes cells that line the GI tract, skin, hair/nails, and blood cells
** Therefore side effects are related: *** GI: nausea/vomiting, diarrhea (sometimes constipation), decreased appetite, taste changes
*** Low blood counts **** WBC nadir ~10-14 days (generally), and recover 21-28 days after chemo
* What about unique side effects of chemotherapy classes? How do we keep them straight?** We love keeping “Chemoman” from the USMLE study days in mind!
* Anthracycline*** MOA: Topoisomerase inhibitors
*** Ends in “rubicin”
*** You might hear people call doxorubicin the “red devil”
*** Used in lots of cancers
*** Hair loss occurs with this one
*** Known to cause cytopenias and associated with higher nausea potential 
*** Unique side effects: **** Heart failure (always get baseline echo!)
**** Development of MDS and leukemia 
* Alkylating agents** MOA: Drugs add alkyl group to the guanine base of the DNA molecule, preventing linking of strands
** End in “fosfamide”
** fosfamide or cyclophosphamide (AKA cytoxan)
** Used in lots of cancers
** Known to cause cytopenias and hair loss
** Unique side effects:*** Secondary MDS or leukemia possible 
*** Ifosfamide = neurotoxicity = methylene blue antidote
*** Cyclophosphamide = hemorrhagic cystitis due to acrolein byproduct accumulation = prevent by giving mesna to protect bladder
* Antimetabolites** MOA: Purine analog, pyrimidine analog, folate antagonists; therefore prevent production of base pairs or binds instead of normal base pairs
** End in “abine” - capecitabine, cytarabine, gemcitabine, cladribine, fludarabine
** Also 5-FU and 6-MP in this category so “number followed by dash”
 ** Unique side effects:*** Think bone marrow suppression in this category  
* Platinum agents** MOA: Believed to cause cross-linking of DNA
** End in “platin”
** Associated with high risk of neuropathy 
** Unique side effects: *** Cisplatin: **** Nephrotoxicity 
**** Ototoxicity 
**** High risk of nausea; need special prophylaxis 
*** Carboplatin: cytopenias
*** Oxaliplatin: higher rates GI side effects 
* Microtubule agents** MOA: Impair microtubule function, therefore impacting cell division
** End in “taxel” or vincristine/vinblastine (“V-stine”)
** Unique side effects: Neuropathy
Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips! In this episode, we discuss the fundamentals and some of our favorite resources. *********The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities. *********1) How do you know what regimen to use for a disease?* www.NCCN.org : ** National Comprehensive Cancer Network** Free resource, but need to make an account!** Provides stepwise approach to workup, choosing a regimen, and surveillance information, treatment for refractory disease* www.HemOnc.org : **Organized by disease type with long lists of treatment options** Provides a breakdown of regimen, but also provides the primary literature that lead to the regimen’s approval for use!**We cannot highlight how important it is to remember to check out the primary literature!2) Patient education: Use these to drive discussion; you still want to walk your patients through these* www.Oncolink.org : Ronak’s favorite resource * www.Chemocare.com : Vivek and Dan’s favorite resource3) Basic Terminology: * Cycle: The number of days between one round of treatment until the start of the next; abbreviated with “C”* Days: Counts the actual days within a cycle; abbreviated with “D”* Example: C1D1: Cycle 1 of a regimen, day 1 of this cycle4) Dosing:* Always have updated height and weight for patients** Many drugs are dosed based on body surface area (BSA)** Other drugs use area under the curve (AUC)* Always get a CMP and CBC prior to giving treatment 5) General categories of cancer therapies:* Cytotoxic: Kills cells in the body** Analogous to antibiotics killing bacteria ** Relatively non-specific in terms of what cells they target; but they’re often specific for parts of the cell replication cycle * Immune therapy: Harness the immune system to attack cancer** More specific than cytotoxic agents* Targeted therapy: Drugs made specifically for known mutations ** A cancer with a distinct mutation in a protein is then a target for this drug** In general:***“Mab”- antibody targeted for phenotypic expression***“ib”- small molecule for driver mutation** Targeted cytotoxic chemotherapy: a monoclonal antibody specific for a mutation linked to very potent chemotherapyPlease visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we’ll talk about one of the key hematologic malignancies that you’ll encounter as a fellow, one that requires immediate action to reduce mortality: acute promyelocytic leukemia (APL or APML)- Acute Promyelocytic leukemia (APL or APML):**Stay tuned for our upcoming “part two” and “chemotherapy basics” episodes for more information on non-acute management of this disease**APL is a true hematologic emergency! Although this is a very curable form of leukemia, it is associated with high rates of severe DIC and high mortality in the period immediately following diagnosis***Untreated, can see pulmonary or cerebrovascular hemorrhage in up to 40% of patients***10-20% incidence of hemorrhage-related mortality in the initial period***Statistically significant increase in mortality at 30 days with just a 12-hour delay in initial hematologist consultation- Disease basics:** Rare subtype of AML( <10% of cases)** Driven by translocations involving the retinoic acid receptor alpha (RARA) on chromosome 17, classically with the promelocytic leukemia gene (PML) on chromosome 15 [i.e. t(15;17)]***Other non-classical translocations exist, but nearly all involve RARA**Because of this driver mutation, treatment with a specific isoform of vitamin A: all-trans retinoic acid (ATRA) forces promyelocytes to differentiate and ultimately apoptose - Initial work up:**Standard CBC with differential, CMP** Review smear for characteristic features:** Large nuclei and scant cytoplasm** “Folded” appearance to nuclei (like a peach emoji 🍑)** Auer rods (which tells you blasts are myeloid lineage)** Heavily granulated cytoplasm (hypergranular form - most common)***Also a “hypogranular variant,” so like always, make sure to discuss any findings with your friendly neighborhood hematopathologist**Stat DIC labs:**PT/aPTT**Fibrinogen**Stat PML-RARA FISH (see next section) to look for classic driver mutation and clinch diagnosis** “Tumor lysis syndrome (TLS) labs”***LDH*** Uric acid**Peripheral flow cytometry***CD33+, CD 117+***CD34-, HLA-DR-, CD11a/b/c-*** Increased side scatter (esp in hypergranular type)- Acute Management** Start ATRA: immediate treatment is so important in this disease, and side effect profile is minimal enough that empiric treatment when disease is on the differential is standard of care**Correct coagulopathies as you detect them ***Keep fibrinogen > 110 mg/dL*** Keep INR < 2.0*** Keep plt > 30k/uLReferences:Gulam Abbas Manji, Samira Khan Manji, Sheetal Karne, and Jeff Chao “Time to ATRA in suspected newly diagnosed acute promyelocytic leukemia and association with early death rate at a non-cancer center institution: Are we meeting the target?” Journal of Clinical Oncology 2012 30:15_suppl, 6615-6615 - impact of treatment delay on 30-day mortalityEytan M. Stein, Neerav Shukla, Jessica K. Altman “Chapter 20: Acute Myeloid Leukemia” section on acute promyelocytic leukemia ASH SAP 7th Ed pp588-590. DOI: 10.1182/ashsap7.chapter20Warrell RP Jr, de Thé H, Wang ZY, Degos L. Acute promyelocytic leukemia. N Engl J Med. 1993 Jul 15;329(3):177-89. doi: 10.1056/NEJM199307153290307. PMID: 8515790. - Great review of the basics in NEJM from the early 2000sSanz MA, Fenaux P, Tallman MS, Estey EH, Löwenberg B, Naoe T, Lengfelder E, Döhner H, Burnett AK, Chen SJ, Mathews V, Iland H, Rego E, Kantarjian H, Adès L, Avvisati G, Montesinos P, Platzbecker U, Ravandi F, Russell NH, Lo-Coco F. Management of acute promyelocytic leukemia: updated recommendations from an expert panel of the European LeukemiaNet. Blood. 2019 Apr 11;133(15):1630-1643. doi: 10.1182/blood-2019-01-894980. Epub 2019 Feb 25. PMID: 30803991. - Updated treatment guidelines (more on this in “Part 2” to come)Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our fourth hematologic emergency: thrombotic thrombocytopenic purpura (TTP). Thrombotic thrombocytopenic purpura (TTP):- Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!- New anemia and thrombocytopenia should raise concerns for TTP! Workup: - Peripheral smear - concern for schistocytes. Look at this first! Example of these cells from ASH image bank here- ADAMTS13 level - always draw ASAP before any intervention- Repeat CBC- Reticulocyte count - will have elevated retic count- Citrated platelet count - CMP- PT, PTT, INR- Fibrinogen- Haptoglobin - LDH- Viral serologies Clinical manifestations: - Fever, Anemia, Thrombocytopenia, Renal (AKI), Altered Mental Status- If you see this - the patient is in bad shapeMechanism:- Tiny blood clots form in the body, causing platelet shearing- Loss of ADAMTS13 - This protein normally is responsible for chopping up von Willebrand’s factor (vWF)- In the absence of ADAMTS13, vWF multimers are extra long, therefore interacting with platelets/collagen more and causing activation of platelets and clotting system- This causes red blood cell shearing due to small vessel microthrombi (brain, kidneys, heart)- Cytokine release causes fevers Management:- Do not reflexively transfuse platelets; can make situation worse - PLASMIC Score: helps to stratify likelihood of TTP; MDCalc link (https://www.mdcalc.com/plasmic-score-ttp)Treatment: - Plasma exchange: replacing ADATMS13-deficient plasma with ADAMTS13-rich plasma- This is different than plasmapheresis, where we replace plasma with albumin- Steroids: 1mg/kg prednisone daily to stop auto-antibody (against ADAMTS13) production- Confirm with ADAMTS13 levels; if <10%, this is confirmatory. This is why this is the FIRST step that we just send off as soon as TTP is suspected - IF YOU DON’T HAVE ACCESS TO PLASMA EXCHANGE: can administer FFP until you can get them to a center than can do plasma exchange - Caplacizumab: reserved for patients with severe neurological dysfunction, stroke, or myocardial infarction. Check out the NEJM paper on this (below)!Microangioathic hemolytic anemia (MAHA): - Umbrella term for red blood cells shearing in the small blood vessels; TTP is one example of a MAHAReferences:https://ashpublications.org/blood/article/129/21/2836/36273/Thrombotic-thrombocytopenic-purpura - great review article from ASH on TTPhttps://www.nejm.org/doi/10.1056/NEJMoa1806311 - NEJM paper on caplacizumab Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our third hematologic emergency: heparin-induced thrombocytopenia (HIT)!Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!HIT:- Any time a patient with heparin exposure and now with a new thrombotic event, you need to think about HIT!What is HIT?- Type 1: a transient drop in platelets after heparin is started- Type 2: **The scary one! Antibody-mediated process**Heparin molecules bind to platelet-factor 4 (PF4)**This complex activates platelets, which then further releases more PF4 from the plateletsWhat is the difference between HIT and HITT?- HITT is when there is also thrombosis (HIT + Clot) Why is this more common in the cardiac ICU?- It is believed that IgM interacts with ultra-long complexes, which heparin is- Lots of heparin is required for cardiac surgery- Therefore lots of exposure to heparin increases likelihood, increasing likelihood for IgM to IgG class-switching; HIT is IgG-mediated process** Remember - since this is antibody-mediated, therefore it takes a few days for the antibodies to form in patient with a new diagnosis of HIT!How to stratify?4-T score (MDCalc Link: https://www.mdcalc.com/4ts-score-heparin-induced-thrombocytopenia)Workup: - Sent HIT ELISA test in patient with high suspicion - ELISA just suggests if the HIT antibody is present- If ELISA positive, then do confirmatory assay, i.e., is this antibody actually doing anything, is the "serotonin-release assay” - Send 4 extremity dopplers to look for thrombosis - STOP heparin/heparin-derived products and SWITCH anticoagulant, such as argatroban, fondaparinux, bivalirudin (do not wait for a positive test if your suspicion is high enough!)If HIT positive: - Add heparin to their allergy list- Continue anticoagulation until platelets are recovered (>150K)- Continue anticoagulation for 3-6 months for patients with HITTWords of wisdom: If patient comes from outside hospital and starts having decreasing platelets, consider HIT in your differential! References: https://ashpublications.org/blood/article/119/10/2209/29530/How-I-treat-heparin-induced-thrombocytopenia- great review article from ASH on HITPlease visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second hematologic emergency: disseminated intravascular coagulation (DIC) with an added bonus of an intro to thrombotic microangiopathic anemias (TMAs).Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!Disseminated intravascular coagulation (DIC):Workup: CBCCMPPT, PTT, INRFibrinogenPeripheral smear - concern for schistocytes. Example of these cells from ASH image bank: https://imagebank.hematology.org/image/60306/schistocytes?type=upload#:~:text=A%20schistocyte%20is%20present%20in,angles%20and%2For%20straight%20borders.Basic mechanism of DIC is consumption of clotting factors leading to coagulopathy Need to be weary of thrombotic microangiopathy: Small blood clots forming in the small vessels leading to endothelial damage, which cause shear stress on the RBCs, which then break down into a schistocyte (AKA triangulocyte or helmet cell) Examples: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)Management (our opinion!): - Repeat coags q4-6 hours initially (but base interval based on patient) NOTE: INR Is NOT a good assessment of “clotting status” in these situations- Repeat fibrinogen q4-6 hours initially (but base interval based on patient); keep fibrinogen >100 with cryoprecipitate in more stable patients; consider higher thresholds for more acutely ill patients (such as >150) - Repeat CBC q6-8 hours initially; can provide platelets if low, especially if they are bleeding - Workup and treatment for trigger of DIC (infection, trauma, medications, etc.)How does cirrhosis affect data interpretation?- Use clinical context to determine if labs are acutely abnormal or if they have signs/symptoms to suggest underlying liver dysfunction- In the acute setting, always just replace what is missing! How can you tell the difference between nutritional deficiencies vs. consumption (as in with DIC?)- Factor activity levels! Consider checking: Factor 8 (made in endothelium), Factor 5 (Vit K independent), Factor 7 (vitamin K dependent) - If all down, then consider DIC- If Vit K-dependent low, then nutritional deficiency Reference:https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation - Great How I Treat article from Blood Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast