The Fellow on Call: The Heme/Onc 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

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 first hematologic emergency: immune thrombocytopenic purpura (ITP).Immune thrombocytopenic purpura (ITP):Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!Specific instances where there may be close to undetectable platelet count: * Lab artifact (clumping)* Very severe DIC* Thrombotic thrombocytopenic purpura - though usually higher platelets in these cases * Heparin induced thrombocytopenia (in very severe cases) - though usually higher platelets in these cases * ITP ITP: Diagnosis of exclusion How to confirm it is ITP?* Post-transfusion CBC - a repeat CBC 30-60 mins after a platelet transfusion. In ITP, the platelet count will likely not budge. (Not perfect test!)* Immature platelet fraction (if available) - this will be elevated if mature platelets are being destroyed. (Again - not a perfect test) Treatment in acute cases: IVIG 1g/kg daily x2 days + Dexamethasone 40mg daily x4 daysReference:https://ashpublications.org/blood/article/106/7/2244/21649/How-I-treat-idiopathic-thrombocytopenic-purpura - 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

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 oncologic emergency: new brain mets. Cord compression:- If someone has a pathologic fracture, think about the following differential as underlying etiologies: - Females: rule out breast cancer - Males: Prostate cancer- Others: multiple myeloma, lymphoma, lung cancer, renal cell carcinoma, bladder - If cord compression, administer steroids; may require radiation to help with shrinking; also may need involvement of neurosurgery if there is lack of spine stability. Role of radiation in cord compression: -MRI is beneficial to help with radiation planning-Where is the disease in proximity to the spinal cord? In the bone? In the epidural space? Or pushing against the spinal cord +/- blocking CSF?-Is the spine stable? Use SINS scoring (https://radiopaedia.org/articles/spinal-instability-neoplastic-score-sins-2?lang=us) -If good spine stability (low SINS) or is not surgical candidate or radio-sensitive tumor: radiation up front-If poor spine stability (high SINS) then may need surgery up frontRadiosensitive tumors examples:LymphomaGerm cell tumors Small cell lung cancer Radio-resistant tumor examples (resistant does not mean that radiation cannot be used, however):MelanomaColorectal Renal cell Continue steroids as they are undergoing radiation to prevent flare up from inflammation and acute worsening from the mass on the spinal cordRole of neurosurgery: - What is a reasonable time that we can wait before operating for a new cord compression?- As noted above, cord compression has various degrees- Questions to ask: What neurologic symptoms? Over what time period? - Asymptomatic: You have time! Perhaps investigate why mass may be there. - Progressive over a couple of weeks: You have a little bit of time (a few days to get them to surgery)- Acutely having symptoms: You should intervene. - Spinal stability: are the weight-bearing components (ligaments) intact? Assessed via upright X-rays - If the tumor is radio-sensitive, may opt for radiation first (if diagnosis is known)A HUGE thank you to our special guests:Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PAJoshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC 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 second oncologic emergency: new brain mets. Brain mets:Strongly consider steroids, particularly with the presence of vasogenic edema associated with brain mets Stereotactic radiosurgery (SRS): use of high dose radiation delivered in a single treatment (“fraction”) that is delivered focally to the area of disease seen on imaging (typically MRI); great option for brain mets; can be performed by radiation oncology What to do to expedite Rad Onc planning: Thin-cut MRIStart patient on steroids Interpreting MRI imaging: T1 post-contrast sequence: to look for brain massT2 sequence: looking for vasogenic edema surrounding brain massMidline shift is an issue more so when it is acute; this is very different than slow changes over timeWho to operate on? Functional status prior to surgery; not in an area that can cause other harm; no other good alternative treatment optionsWhat to tell your NSGY colleague during a consult: A quick neuro exam (consciousness, strength, sensation, focal neurologic issues)Brief cancer historyUnderlying organ dysfunction Antiplatelet/anticoagulants A HUGE thank you to our special guests:Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PAJoshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC 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 first oncologic emergencies: superior vena cava (SVC) syndrome.Superior vena cava syndrome: Important: although we focus on a possible malignant mass in this discussion about SVC, other things can also cause SVC syndrome. How do you know about the chronicity of someone’s possible SVC syndrome? Compare to a recent picture!Image of patient with collateralization with SVC syndrome: DOI: 10.1056/NEJMicm1311911Workup: Need to determine the etiology; imaging is important: CT of chest (CT venogram)Consider ultrasound to rule out thrombosis Get biopsy (eventually) if this is malignancy DDx of mediastinal masses: 5Ts:ThymomaTerrible lymphoma (B or T-cell)Testicular cancerTeratoma Thyroid malignancies Central line (causing occlusion) +/- clotSo now what? Yes, an answer to what is causing the issue is important, but we need to ensure that patient has a stable airway and temporize the situationOften requires input of specialists, such as Interventional Radiology or Radiation Oncology How to treat patients with SVC syndrome?- Chemotherapy: Important in chemo-responsive tumors (ex. germ cell tumors, lymphomas, small cell lung cancer); This can take a while to work -Placement of stents: Provides more immediate relief, but more invasive -Radiation treatment: Not always possible - Laryngeal edema/cerebral edema: steroids for life-threatening complications; Can affect diagnostic yield of sample and affect diagnosis, but may be required in emergent situations When is more emergent treatment indicated and consultants definitely need to be called (TELL YOUR CONSULTANT IF ANY OF THESE ARE SEEN!):Hemodynamic instabilityWorsening respiratory statusWorsening neurological status Final decision for what to do is often a multi-disciplinary discussion Stents: Provides quick reliefDoes not prohibit a diagnosis and curative treatment for the underlying malignancy Radiation: Takes several days or weeks; depending on underling histologyIf they have received prior radiation, they may not be eligible for more radiation A HUGE thank you to our special guests:Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA (https://www.jefferson.edu/university/jmc/departments/radiation_oncology/education/residency/residents/miller.html)Rupal Parikh, MD: PGY6 in Diagnostic/Interventional Radiology at the Hospital of the University of Pennsylvania, Philadelphia, PA (https://www.pennmedicine.org/departments-and-centers/department-of-radiology/education-and-training/residency-programs/current-residents/ir-integrated-residents/ir-dr-fifth-year/rupal-parikh-md)Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

In our final stop in our Cytopenias series, we discuss the ins and outs of neutropenia. This is another very commonly seen issue in the clinic and in the hospital so most definitely high yield!Why is neutropenia dangerous?Prone to infections, especially gut translocation of bacteriaDefinition of neutropenia:NORMAL: WBC 4400-11000 cells/microL; neutrophils make up 40-70% of thatNeutropenia defined by ANC: WBC (cells/microL) x percent (PMNs  +  bands) ÷ 100 Breakdown:Neutropenia: ANC <1500 cells/microLMild: ANC ≥1000 and <1500 cells/microLModerate: ANC ≥500 and <1000 cells/microLSevere: ANC <500 cells/microLAgranulocytosis: ANC <200 cells/microLApproach to workup: HISTORY IS KEY!Medications; examples of common culprits-  Chemotherapy Methimazole Clozapine InfectionsAny infections due to bone marrow suppression Toxins Less common causes: CongenitalSevere congenital neutropenia:Diagnosed in childhood; used to be fatal, but now patients living longer because of G-CSF support10-30% risk of AML in lifetimeMutations in neutrophil elastase (ELANE) gene or mitochondrial HAX1 gene Cyclic neutropenia:Self-limiting neutropenia that occurs every 2-5 weeksSpectrum of symptoms: none or oral ulcers/mild infectionsConstitutional/ethnic neutropenia:Mild neutropenia (ANC >1000)No history of infectionsMore common in people of Mediterranean and African descentDuffy Antigen Receptor Complex (DARC) gene mutations in patients of African originBenign Familial:Mild neutropeniaNot linked to particular ethnic groupUnclear underlying etiologyAutoimmunePrimary autoimmune neutropenia rare in adultsTypically secondary autoimmune neutropeniaDue to underlying autoimmune disorderSeen with SLE and can worsen with flare of diseaseTypically mild, seldom needs treatment unless ANC <500Felty syndrome:  Rheumatoid arthritis, splenomegaly, and neutropeniaNeutropenia improves with treatment of RA MalignancyLarge granular lymphocyte (LGL) leukemia:Often associated with RA and shares features of Felty syndrome (RA, splenomegaly)Caused by monoclonal population of large granular lymphocytesIn contrast, in Felty’s: polyclonal or oligoclonalT-cell LGL is more commonly associated with neutropeniaRequires treatment with methotrexate or cyclophosphamideDietaryB12 and folate rarely cause isolated neutropeniaCopper deficiency (gastric bypass): Zinc excess can cause copper deficiencies – ask about denture creams in your history!  Workup:History:Prior CBCsHistory of recurrent infections (pneumonia, sinusitis, skin/soft tissue, dental caries)Ethnic backgroundFamily historySocial historyDietary historySurgical history (gastric bypass)Physical exam:AdenopathySplenomegalySkin findings suggesting recent ulcersAphthous ulcersexample: https://en.wikipedia.org/wiki/Aphthous_stomatitisTesting:CBC with differentialCMP – assess liver and renal function Peripheral smearHIV, Hepatitis serologiesSpecial scenariosANA – if autoimmune disease expectedRF – if autoimmune disease expectedESR – if autoimmune disease expected; probably not great for inpatient workupCRP – if autoimmune disease expected; probably not great for inpatient workupFlow cytometry for LGLBone marrow biopsy – mainly for unexplained neutropenia to rule out neoplastic process, such as leukemia, lymphoma, myeloma; if longstanding, likely negativeManagement:Treat the underlying causeAutoimmune neutropenia –When to suspect? Workup is negative, but their counts still continue to worsenTreatment if they have serious complicationsTreat with rituximabLGL-Responds to low dose methotrexate or cyclophosphamideDo you give G-CSF?For patients with recurrent/severe infections or mucosal erosionsDo not treat based on the number aloneTakes time for the growth factors to workReferences: https://doi.org/10.1182/blood-2014-02-482612 - Great “How I Treat” article from Blood! https://www.uptodate.com/contents/approach-to-the-adult-with-unexplained-neutropenia - UpToDate article written by same author as Blood article Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast