Transcription
For so, this is the first case. A 56-year-old man was brought to the emergency department because of shortness of breath and abdominal pain. The emergency doctor on examination noticed that there is suspected pleural effusion, which he confirmed on the X-ray. There was hepatosplenomegaly as well.
The full blood count shows hemoglobin of 110, white cell count of 10.3, and platelet count of 110. So, this is the blood picture. And I would request any of the lab staff to comment on the blood picture. How would they report the blood picture for a clinical hematologist? Do we have any lab staff? You comment on the blood film. I'm asking from the lab staff because I was told that I should give equal opportunities to both lab staff and clinical hematologist. So, if there is any lab staff available, he can come up and comment on the blood film, please.
Right. So, I think you mean to say lab hematologist. Yes, any biomedical scientist, medical technologist, anyone like that, because the blood film is first seen by them, and then they escalate us to escalate the film to us. And in previous sessions, many of the lab staff messaged me that we need equal opportunities. So, I want lab staff first to comment on the film, and then obviously, this will go to clinical hematologist, and then we will ask from the clinical hematologist to comment. Right. So, we should wait for them. Right.
So, if the lab staff is not available, then I will act as a lab staff for this slide. That the blood film shows leukocytosis. The lymphocytes are the white cells are small in size with some projections from the cytoplasm. The red cells show few schistocytes and there is thalassaemia, but no platelet clumping seen. Refer to clinical hematologist for further opinion, for further opinion due to suspicion of acute leukemia. So, these are the comments that are made by the lab staff.
So, now this film has come to you. You are the clinical hematology registrar and you are sitting in the part two exam. The first question is, report this film. I will make it to 10 again. All right. So, now I need a clinical hematologist to comment on this film and report the film. Anyone? I can try. Yes. So, this is power 10. I'm giving you a general overview of the film.
Right. And now move to power 50 oil lens. Yes. So, let's see few slides and then you can start reporting the blood film. Sure.
Yes. So, report the blood film. You are sitting in the exam. How would you report this one? The film shows prom shows mainly small in size, having high N:C ratio, condensed nuclear chromatin, and some of these atypical cells, they have granular cytoplasm. Granules in them, inconspicuous nuclei. The RBC morphology shows mild anemia and few fragmented and poikilocytes are seen, and there is marked and there is thrombocytopenia. And okay, the peripheral film findings are consistent with a lymphoproliferative disorder, most likely T-cell prolymphocytic leukemia. And I would like to confirm my diagnosis with flow cytometry on peripheral blood for lineage specificity. I don't know whether I have to comment on the basis of this morphology that these may be T-cell prolymphocytic leukemia cells. They look like T-cell prolymphocytic leukemia cells because they are small, mature, and have cytoplasmic granules, which is a feature of T-cell prolymphocytic leukemia. You would not say definitely that this is T-cell prolymphocytic leukemia. You would say most likely it is consistent with T-cell prolymphocytic leukemia. So, I need flow cytometry to confirm my suspicion or to confirm this diagnosis.
So, what is the expected flow here? Um, usually these cells are CD2 positive, CD3 weak, they are CD5 and CD7 positive. Any other significant marker that is important for treatment purpose is CD52, I guess, to give alemtuzumab. Yes, CD52 is positive, and that determines the treatment as well, which is. Are you aware of any genetic mutation? Yeah, mostly they have inversion 14 and also the abnormalities of chromosome 8 and on CY, and on molecular genetics, they have I'm not sure there is something MMTCP1 or TCL1 A mutation also. They are also associated with ataxia telangiectasia and they have ATM gene rearrangement abnormalities. Yes, ATM gene mutation is associated with multiple things like mantle cell lymphoma and multiple myeloma as well. But here, more than 90% of the patients show MMTCP1 rearrangement. And the flow cytometry, you have mentioned treatment, you have mentioned which is alemtuzumab. This is sorry, more than 90% have which rearrangement? MMTCP1. MMTCP1. Okay. Yeah. So, this is T-cell prolymphocytic leukemia, mature T-leukemia, and it comes as a short case in the part two exam where they ask, what is the report the blood film, which carries six marks, and then expected flow, two marks, expected cytogenetics, two marks, sometimes one mark. And then they ask you what is the treatment of choice for these patients, which is alemtuzumab and transplant and interferon if they are symptomatic. If not symptomatic, then watch and wait is the policy. The T-cell prolymphocytic leukemia cells are small and their characteristic features in morphology are these granules. They carry a lot of granules like that. Some people call them Mickey Mouse cells, but I think this is not correct. Sometimes they have many granules, not two granules. So, anything that can help you in retaining the information for the exam purpose. Use.
All right, sir. How do you comment on the chromatin of these cells? Says, for me, it is difficult to pick. Is it a blast or a mature cell? A blast is usually large in size with open chromatin and nucleoli visible in it. While these cells were very small and the chromatin material was very dark blue and nucleoli were not visible here. So, this is a feature of mature leukemia. You see these features in CLL as well, in PCL lymphoma as well. They are very small, their nuclear material is very dark blue in color, and nucleoli are not visible. You will compare it with another malignancy which has a large blast with prominent nucleoli, open chromatin, and some have multiple nucleoli as well. So, you will see it in the second case now.
Sir, how do we differentiate it from megakaryoblasts which also have granules? Again, megakaryoblasts, they are a bit bigger than these T-cell prolymphocytic leukemia cells, and they have a specific appearance. I will bring that film next time. I have one film for acute megakaryoblastic leukemia as well. We call it as bloody AML. I will bring this film next time and I will also show the T-cell prolymphocytic leukemia to you as well to see the difference between the two. The megakaryoblasts, they are not as deeply blue colored like these cells, and they are bigger than the T-cell prolymphocytic leukemia cells and they are not that much in number as these T-cell prolymphocytic leukemia cells were. T-cell prolymphocytic leukemia, one of the features of T-cell prolymphocytic leukemia is that they are very high in number. Usually, when they present, they cross the mark of 100 in the peripheral blood, while the megakaryoblasts, they are not that much. They are big in size, not that deeply blue colored or basophilic colored, and they have quite a lot of granules and irregular markings of the cell. We will see that in the next assessment, the acute megakaryoblastic leukemia. Thank you. Thank you very much.
All right. So, this is the second case. This is again a 56-year-old man presented to ED with significant weight loss and night sweats, decreased appetite. He has anginal and axillary lymphadenopathy on examination, and he looked very tired and fatigued. This is the blood film from the patient. His white cell count shows hemoglobin of 98, platelet count of 93, and white cell count of 60. So, again, I would need a lab staff first to comment on this film.
So, the peripheral film of this patient. Are you the lab staff? Sir, I'm a lab hematologist. Lab hematologist. Okay. Right. So, so this peripheral film is showing leukocytosis, predominantly lymphocytes are seen of small to medium size, and there is thrombocytopenia on this power of lens. Okay. So, this is the power 50 now, and this is a Nia slide. So, the quality is a little bit low as compared to other. Right. So, these are not lymphocytes. They appear to me as monoblasts. Okay. These are large cells with low N:C ratio. These are large cells with low ratio, open chromatin, few having conspicuous nuclei, and the cytoplasm is agranular. There is moderate to copious amount of cytoplasm. You see cells having indentation, nuclear indentation. So, this is a blast, most probably of myeloid series. You said that this is a granular? At that power, I can say granular. Yes, there are granules, but very few. You can see these blasts have multiple nuclei, some small nuclei, some large nuclei, but the nucleus is multiple, and they are quite large as well. Yes, most probably the monoblasts. No, they are lymphoblasts because we cannot see any indentation. The monoblasts have very few indentations, but the cytoplasm here is not blue. There is no vacuole, and monoblasts do not have this clear nucleus like this cell has. This is a lymphoblast.
Sir, are these large granular lymphocytes? No, no. They may have very few granules, but most of them are without granules. Yes, sir. Like this one. I will make it to 100 power again. You can see they have multiple nuclei. Usually, lymphoblasts, they don't have nucleoli. Initially, we used to classify them on the basis of FAB when they were L2, then the L2 cells, they have nucleoli, but usually nucleoli are not a feature of lymphoblast. There is one lymphoma whose feature is having large blasts in the blood film with multiple nuclei. So, they have nucleoli here. This one, this one. So, the patient has features of B symptoms, lymphadenopathy, large lymphocytes, lymphoblasts with multiple nuclei. I will try to find out you lymphoblasts which carry vacuoles as well. Blastoid variant of some NHL. How are you going to differentiate between the blastoid variant of some NHL and the lymphoblast on morphology? So, the blastoid variant of mantle cell lymphoma has blasts, but they are not that much big. They are medium-sized. These blasts are very large in size with multiple nucleoli, and the patient has full-blown symptoms of lymphoma. So, a lab staff would report it like this: The blood film shows leukocytosis. There are multiple blasts which have basophilic cytoplasm with open chromatin and multiple nuclei. There are few small cells as well. Red cells show anisocytosis, as you can see their shapes and sizes are different as well, and there is thrombocytopenia and no platelet clumping. So, this is the report for the lab scientist or biomedical scientist, and then they would say, refer to clinical hematologist.
Now, this film is with you as a clinical hematologist, and you are sitting in an exam. You have seen this. What comes in your mind as a differential diagnosis? Large lymphoblasts with multiple nucleoli, lymphadenopathy in the patient. Say something. LGL? Sorry, large granular lymphocytes. LGL. The patient does not have the B symptoms like this severe. This patient has lymphadenopathy everywhere. LGL comes in context of SLE, rheumatoid arthritis, Sjögren's syndrome in the presence of any other autoimmune disease. This patient has all the symptoms of lymphoma. DLBCL? Yes, this is the feature of DLBCL. Their blasts are very large and they have multiple nucleoli in their chromatin, which is visible. Mantle cell lymphoma or blastoid variant of mantle cell lymphoma, they carry blasts as well, but they are medium-sized and they carry only one nucleolus. This patient has large blasts with multiple nucleoli. You say some cells have three or four nucleoli, and these cells have a lot of multiple nuclei, smaller in size. This is the feature of DLBCL. So, if you are working in NHS and you have lab access, go to your lab and see the film number 2302. So, this film must be present in your lab in NHS lab 2302, and you can see the full comment of the Babra Ban on this film. He has mentioned as well that these are large blasts with multiple nuclei, features of this is most likely a high-grade lymphoma. We need to send blood for urgent flow cytometry and other investigations to look for any lymph node which is amenable to biopsy.
All right. So, this is a high-grade lymphoma, and you have sent blood for flow cytometry. What is the expected flow here? Immunophenotyping. Expected. These as if they are DLBCL, then they should be CD10 and CD20 positive and should be CD5 negative. And also, we ask for the IgH gene rearrangement. If it is positive, then we go for BCL6 and BCL2 to label whether it's a double hit or a triple hit. For yes. Okay. And let's say this patient is fit for treatment, and you want to assess this patient for CNS prophylaxis. What will you do to assess whether he is fit for CNS prophylaxis or not? For CNS prophylaxis, you will do the CNS-IP. Okay. Who are the patients to whom you will offer CNS prophylaxis? I don't remember exactly, but maybe those who have stage three or four with extranodal disease involving the testes, the breast, the uterus. Okay. Those patients who have CNS-IP high (4-6) or if they have three or more extranodal sites involved, or they have specific anatomical sites involvement like testicular, adrenal gland, renal involvement, or even intravascular DLBCL as well. And especially in a case of female, if breast involvement and uterus involvement is there, then you offer the patient CNS prophylaxis. What do you offer in CNS prophylaxis? Intrathecal methotrexate. It's not always intrathecal methotrexate. Yes, it is high-dose methotrexate. If the patient has any contraindication for high-dose intravenous methotrexate, like effusions or poor renal function, then you go for intrathecal methotrexate. Otherwise, you just give them high-dose methotrexate. In any sort of effusions or infusions, you also avoid high-dose methotrexate because there is a chance that the patient will accumulate methotrexate over there and can lead to toxicity in the future. So, these are the big cells of DLBCL. If you are working in NHS, go to your lab and see the film number 2302, and you should see this high-grade lymphoma.
Right. So, this is the third case. This case is directly for the clinical hematologist. This is again a 56-year-old male who is complaining of low back pain. The full blood count shows anemia and thrombocytopenia. Hemoglobin is 90 and platelet count is 90 as well. On examination, he has some splenomegaly as well. So, low back pain, anemia, thrombocytopenia, and splenomegaly. Because of the persistent thrombocytopenia and anemia, a bone biopsy was done, and this is the trephine. Anyone who is a volunteer for this case? Anyone? Anas Al Basher on the list? Noha Omar, Iman Usman? Hi, hi Amir. So, I have told you the scenario. Yeah, and this is power 4. I will just go through the trephine to see whether this is a good size or not, and whether there are enough trabecular spaces or not. This is power 4 to give you an overview. Okay. So, trephine usually has some features that you should remember for the exam, and once you see them, the diagnosis should be very clear to you. Like follicular lymphoma has specific features, CLL trephine has specific features, myelomonocytic leukemia has specific features, DLBCL is very easy to pick. Hairy cell leukemia, if you are able to see the over-the-cell, it is good. So, this is you can see a Giemsa stain. This is one clue to you. Why I have brought a Giemsa stain? Similarly, myelofibrosis trephine has very specific features as well. So, now you have seen the length, you have seen the trabecular spaces, and you have seen the trabeculae as well. I will go to power 10 now. Okay. So, this is power 10, and again, you have to comment on all the lineages if you know the if you know the diagnosis, it doesn't matter, but you have to report it as it should be for the exam purpose, including length, cellularity, trabecular spaces, all lineages, any abnormal features, and then your impression, and suggesting flow cytometry or immunohistochemistry. If you have seen such trephine before, the diagnosis will be very, very clear to you. All right. Do you want me to go to power 50, or you have found enough features here? Sorry, my internet had a full network. I was disconnected and came back again. Yeah. So, do you want me to go to power 50, or you have found enough features here? No, can we go to power 50, please? Because if I go to power 50, most of the people will get the diagnosis on the spot. Those who know should get the diagnosis now, just from this view. No, not so. Now you can. Okay, all right. No, no problem. You can report the trephine. How would you report? Okay. Um, so is that similar to the aspirate? Like to comment on the initially on the low power on the cellularity? Um, oh, the same approach for the aspirate. First, comment on the length and adequacy, whether the sample is adequate or not. So, this is a good length sample. A good length and adequate sample. Sometimes you will find a trephine slide which is fully crushed or the end of the trephine is crushed like this. Trephine is crushed at this point. Yeah. So, good. So, this is a good length sample with crushing at one end, but the rest of the trabeculae are preserved. The trabeculae. Yeah, they are thickened. They are thickened because of the underlying disease. Okay. Yes, megakaryocytes are present. You have seen a lot of megakaryocytes here. There are. Yeah, yes. We cannot comment here on the myeloid lineage because the stain is Giemsa for that. H&E stain is better, but you have seen there is peritrabecular fibrosis, and there are a lot of spindle-shaped cells in the peritrabecular area, which gives a suspicion of systemic mastocytosis. But that needs to be confirmed on immunohistochemistry and blood level of tryptase. So, these are all the spindle-shaped cells. These are all the mast cells. All right. Yes. And mast cells are better seen on Giemsa stain. So, if in the exam, if you see any Giemsa stain, it will be for the purpose of systemic mastocytosis. But presence of Giemsa stain does not mean that you jump to systemic mastocytosis. See other features as well. Patients usually have bony pains, they can have neuropsychiatric problems as well, hepatosplenomegaly, anemia, because in systemic mastocytosis, we have either indolent form or smoldering form or advanced systemic mastocytosis. Advanced systemic mastocytosis usually comes with symptoms. Okay. Sorry, but just for the spindle shape like cells, for me, the cells look like more, you know, like it's like elliptical side or something, you know, like it's elongated. But is that like where where is like the characteristic is spindle shape of mast cells? Yes, most cells are spindle-shaped cells, mostly. And um, I don't have aspirate for this one. And aspirates, they are usually elongated as well. All right. Yeah. You see mast cells in Waldenström's as well. The nuclei of Waldenström's lymphocytes and trephine are surrounded by mast cells. This is the feature of Waldenström's. If I get, I need to find for that. I will. Okay. Dr. Amir, if they have given you the Giemsa stain for systemic mastocytosis, we don't comment on the granulocytic lineage and erythropoiesis. We just comment on the length adequacy, the length, the cellularity, and the trabeculae, and the main abnormality. We don't comment on neutrophils or lymphocytes. If you are good in Giemsa staining, then you can. But I am not good in Giemsa staining trephine reporting. I always use H&E for trephine report. But if you are asking for the exam, yes, ideally we should comment on the myeloid lineage and the erythroid lineage as well. But if you are confident whatever you are writing is correct, it is okay. But if this was H&E, I would have commented on myeloid lineage as well on the lineage. Megakaryocytes were visible here. Sir, is there any other differential that should come in mind except systemic mastocytosis if bone marrow trephine is given with Giemsa stain for the exam purpose? It is only systemic mastocytosis. But in real life, I'm not sure whether there is any other diagnosis which we made from Giemsa stain. And in the lab, we make both slides, H&E stains and Giemsa stains for every disease. But for the exam purpose, it is the Giemsa stain that comes for systemic mastocytosis. Like if you have any bone marrow for myelofibrosis, for MDS, for AML, they both would have Giemsa stain and H&E stain. But the reporting is more on the H&E for exam purpose. The lab staff, they are histopathologists and consultants. They know what to pick from Giemsa stain in those cases. But I'm just talking about exam purpose. Right. What is the criteria of systemic mastocytosis diagnosis? There are major and minor criteria. The major criteria includes the presence of dense clusters composed of more than 15% mast cells in aggregates in the marrow or in any extracutaneous tissue. The minor criteria include more than 25% mast cells which are either spindle-shaped or having an abnormal morphology, the presence of KIT mutation, and CD117 and CD25 expression on mast cells, and serum tryptase. CD four things in minor criteria. More than 25% abnormal spindle-shaped mast cells. Second would be the KIT mutation. Third would be the expression of CD25 or I think CD117 on the mast cells. Sorry, CD30 on the mast cells. And the fourth would be the serum tryptase, which would be more than I think 20 nanograms per ml. Right. If this patient has KIT D816V mutation plus PDGFRA mutation as well, what is the drug of choice? Mutation and PDGFRA mutation. This is a lot of eosinophils here. So, the patient has PDGFRA and KIT mutation both together. What drug do you usually give? I don't remember exactly the name. It's pretentiously. Recently. Okay.
So, this is the fourth case. This is a 25-year-old male with recurrent fevers. He didn't respond to antibiotics prescribed by GP, and despite three days of antibiotics, he is spiking high temperature. His full blood count shows hemoglobin of 98, white cell count of 9, and platelet count of 180. This is the blood film, and I want any lab staff to comment on the blood film. Plus, any biomedical scientist, medical lab technologist, if you have any in the audience. Sir, I can't comment on this power. So, this is power 10. I will go through the film to show you an overview of the film, and then I will move to power 50, and if required, power 100 as well. Okay. So, you have seen few slides on power 10. Now let's move to power 50. I put some oil on it. Right, sir. So, the blood smear of a 25-year-old male with low hemoglobin and normal platelet and white cell count is showing normocytic, normochromic red cells, and the ring, single delicate or single or multiple. I can see the two ring forms also infiltrating the red cells. Yes, sir. Ring form of most probably Plasmodium falciparum. Yeah. So, mostly. And you need to confirm this on RDT and microscopy. You mentioned that you are the lab staff, right? Yes, sir. I'm a trainee for FCPS in Pakistan. I completed my training. All right. So, then I would request you to report this film as well for the exam purpose, like you are sitting in part two exam or FCPS 2 exam. How would you report? So, the ring forms of Plasmodium falciparum are seen. So, we write like that. These are normocytic, normochromic red cells infiltrated by forms of Plasmodium that are delicate in shape with the. You don't know yet that these are falciparum. You need to confirm that on RDT and microscopy testing because ring forms can be present in many other things. Yes, sir. It can. Does it affect the diagnosis? Affect the treatment options? Yes, why not? We will discuss the treatment in a second. Now, Giemsa. Sir, okay. So, yes, comment on the blood film, please. Um, sir, I have commented already and I don't know how to comment. So, the blood film shows multiple ring trophozoites of malarial parasite. The red blood cell size is normal. There are few red blood cells with multiple rings in it. In some of the red cells, the ring is near to the red cell membrane. So, this is a feature which is a feature of Plasmodium falciparum. There are few schizonts in the blood film as well with low platelet count and the white cell count is normal. The features of malarial parasite is most likely consistent with Plasmodium falciparum. We need to confirm this on RDT and microscopy testing. You're right, sir. Okay. Okay. Why this is not vivax, sir? The differentiating points for the vivax are importantly that they invade the early precursors of the red blood cells, that are reticulocytes, and that are large in size. So, we can. And also, the ring is not delicate, it is with thickened cytoplasmic membrane. And in this case, Plasmodium falciparum invades almost all kinds of cells and also the mature red blood cells. This is the double dot appearance. So, the red cell size in vivax is large and the ring trophozoite form of the malarial parasite is thick as well. So, you must comment in your report about the red cell size, the ring features if they are thick or thin, near to the red cell membrane, multiple or single. And usually gametocytes are not seen in the blood films. If you are lucky, you will be able to see that. But in this film, I searched for gametocytes but could not see the crescent form or banana shape form of the malarial parasite. Right. What is RDT? Rapid Diagnostic Test. Right. And what is the principle of RDT? Rapid Diagnostic Test. Sir, it is based on the. We use ICT kits, and there are two types of kits. Either the film is coated by antibodies against the parasites, or they are coated with the antigens. So, they detect the presence of the parasite. And in case of falciparum, there is histidine-rich protein that is detected, and in case of vivax and other parasites, there is LDH. Okay. So, it is a lateral flow immunochromatographic antigen detecting test. Like it is a based on lateral flow method. It is an immunochromatographic antigen detection test which uses a labeled antibody to bind to the parasite antigen. Okay. And this complex makes a line in the result window. Just say it is an immunochromatographic antigen detection test which uses a labeled antibody against parasite antigen and this complex forms a line in the result. Is there any condition which gives you a false positive RDT? Rheumatoid factor, if present in a patient, can give you a false positive. So, we have seen even in the treated cases when there is no parasitemia, we cannot find any parasite in the blood. In the treated cases, even ICT gives a positive result. Yes, correct. Right. So, what is the indication of exchange transfusion in malaria? It's heavy parasitemia. I don't remember, but more than 30%. I think more than 30%. And cerebral malaria, or if the patient is very ill because of the parasite infestation, and the clinician decides that this should be treated by exchange transfusion. Usually, the patient is referred to infectious disease team or tropical medicine team. They deal with the malaria. And yes, parasite index for. Sorry, can you repeat? And the parasite index is 10% for exchange transfusion. 30%. 30%. Oh, thank you. And initially, we do not deal with the treatment of malaria in terms of drugs, but if they ask in the exam, then they are the artemisinin-based medication for Plasmodium falciparum. So, remember the name of the drug for cerebral malaria or severe malaria or falciparum. They will be asked in the exam. In real life, you do not deal with them, but for the exam purpose, remember the name of the drugs for these few infections: falciparum, trichinosis, leishmaniasis, and malaria. Right. The last case of the day. E. Okay. So, this is again a 56-year-old man presented to ED with severe shortness of breath, fever, extreme tiredness. He is febrile as well. The full blood count shows hemoglobin of 70, platelet count of 45, and white cell count of 12. This is the blood film, and I want any biomedical scientist or lab staff to comment on the blood film first, then I will go to clinical hematologist. Sir, sorry, how much was the white cell count? 12. Okay. Thanks. Ignore these things. These are not parasites. This is just the oil related stuff moving here and there. Okay. So, there is no biomedical staff or lab staff to comment, sir. The paper film of the male patient is showing anisocytosis in the red blood cells. There is polychromasia, macrocytes. Mhm. There are occasional tear drop cells. Okay. I want to see spherocytes, but there is central pallor in I can identify the central pallor in many of them. You look like microcytes. Some of them don't have. Okay. So, as a biomedical scientist, I will report it as the blood film shows anisocytosis with multiple polychromatic macrocytes, spherocytes, Howell-Jolly bodies, and high platelet count. No platelet clumping seen. The neutrophils are hypergranulated. Suspicion of hemolysis secondary to any infection. The film is referred to hematology registrar for expert opinion. Now, I need a clinical hematologist to report it for the purpose of the exam. Yes, anyone want to report it? Yeah, I can try. Yes. So, you are sitting in FCPS exam, but not now. Yeah. And this is the blood film for you. Yeah, yeah. And they want you to report it for six months. Okay. That is anisocytosis. The two rather two morphological populations present. One is macrocytes, and the other is spherocytes. There are ovalocytes in some of the cells. Yeah. And the poikilocytosis, I could see in the previous fields, some teardrop cells as well. The neutrophils were having toxic granulation. So, probably spherocytosis in a splenectomized patient. Sir, if this is there are nucleated red blood cells, and I could not see any polychromasia. If there is, these are all polychromasia. Oh, yes, yes. Large reticulocytes. Yeah. So, probably there is hemolysis also going on. And the poikilocytosis might be due to the hemolysis or maybe transfusion in a splenectomized patient. The toxic granulation might point towards an infectious trigger as a cause of hemolysis. Hope. Yeah, the red cells are agglutinated. These red cells are agglutinated. Oh, yes, there is not there is no marked agglutination. Yeah, this one here. Yeah, yeah. So, this question in an exam can come in two ways. One is the standard way, which is report the blood film, and second one is enumerate six points in this blood film. So, you would say for reporting the blood film shows severe red cell anisocytosis. If you are saying anisocytosis, mention red cell because there can be anisocytosis as well. Okay. Thank you. Containing multiple polychromatic macrocytes, microcytes, or spherocytes, teardrop cells, Howell-Jolly bodies. The neutrophils are hypergranulated. Multiple red cell agglutinations are noted. The platelet count looks increased, but there is no anisocytosis in platelets. The blood film is most likely consistent with hemolysis secondary to infection. We need hemolytic screen and infection screen on this patient to rule out whether this is autoimmune hemolytic anemia secondary to any infection or not. You commented on the blood film features, you give your suspected impression that this is hemolytic anemia secondary to infection, and you suggested hemolytic screen and infection screen. This can be autoimmune or this can be non-immune as well. But looks like this is autoimmune secondary to infection. Okay. And the Howell-Jolly bodies, hypohypersplenism. Okay. The patient, the patient may have hypoplenic or low splenic function because of many reasons, because of ongoing hemolysis. Maybe this is not the first time he's coming to the hospital with hemolysis. Maybe he had hyposthenic function because of other reasons. But there are Howell-Jolly bodies. There is increased platelet count as well in hypersplenic patient. You see Howell-Jolly bodies and increased platelet count, and this platelet count can be secondary to infection as well. Okay. Yeah. Thank you very much. Thank you. What are the secondary causes of autoimmune hemolytic anemia? Secondary to the connective tissue disorders or other autoimmune conditions. Yeah. So, yeah, go on. Categorize it in four groups. Secondary autoimmune causes of secondary causes of autoimmune hemolytic anemia can be because of four reasons: cancers, blah blah blah, CLL, lymphoma, infection, CMV, EBV, bacterial infection, neoplasms, then immune-related arthritis, etcetera, and then post-transplant. Okay. Post-transplant. Post-stem cell transplant, autoimmune hemolytic anemia is very common. Yes, yes. Thank you. And what would be the treatment of this patient? Treatment of the underlying infection. Underlying cause. Underlying cause. Yeah. Treat the underlying cause, the hemolysis will settle. So, Dr. Amir, in reporting of this case, you will say your peripheral findings are consistent with the hemolytic process, and here we have to mention what would be the most probable cause, or just we can say it's peripheral findings are consistent with the hemolytic process, and then we advise the hemolytic screen. So, as I mentioned in reporting that this patient has the blood film is most likely consistent with hemolysis secondary to infection because this patient has red cell agglutination and hypergranulation of neutrophils, and the patient was febrile as well in the history. The agglutinations, they are not very marked. Yes, they are not very marked because the patient is very anemic, and there are only few agglutinations, but they are all. And usually when we see agglutination, we think of cold autoimmune hemolytic anemia. Yes, but agglutination can be because of infections as well. Agglutination has a lot of causes. So, the lab staff will confirm this and then he can repeat the blood if there is a quite significant. And the non-immune causes of hemolytic anemia also includes infections as well as the autoimmune and the non-immune causes. Yes. First, you will do a hemolytic screen to find out whether that test is positive or not. If that is positive, it is immune. If that is not positive, it is non-immune. And then according to the guidelines, you will ask, you will think about few things. Whether first thing, first question according to the guideline is, is there any hemolysis? Yes, this patient has hemolysis. Is this hemolysis immune? Confirmed by that. So, if that is positive, now whether this patient has any blood transfusion in the last three months and any drug that he has recently taken that can induce autoimmune hemolytic anemia. Any other cause? In case of infant, we think about HDFN as well. And if it is anemia, okay, what type? So, that will tell you whether it is warm or whether it is a cold, whether it is a mixed. Okay. Now, thank you.
Okay, so this was the last case. And sir, I have a question. After splenectomy, the patient's peripheral blood may have nucleated red blood cells. What is the reason for this? How can we explain this? Because normally, if the patient has not had a splenectomy, he has no nucleated red blood cells. But after splenectomy, I have seen patients, they have a lot of nucleated red blood cells. So, sir, what? So, nucleated red blood cells can be present in severe hemolysis, like in the last few sessions when we had autoimmune hemolytic anemia patients, there were a lot of nucleated red blood cells. But this autoimmune hemolytic anemia does not have any nucleated red blood cells. If you have severe DIC and your bone marrow is under stress, you will have nucleated red blood cells in the peripheral blood film as well. If you have a leukoblastic blood film picture, MDS, or blastoid CML, or blastoid mantle cell lymphoma, the bone marrow is under stress, you will see multiple nucleated red blood cells in the blood film as well. And splenectomized patients, which is usually in thalassemia and in sickle cell disease, the spleen is the area of extramedullary hematopoiesis. When you remove the spleen, the bone marrow becomes under stress, and then the blood film is packed with nucleated red blood cells. So, nucleated red blood cells are not only in the peripheral blood film of splenectomy. They can appear in the peripheral blood film after many reasons, because of many reasons: severe hemolysis, severe infection, MDS, blastoid CML, also the leukemic phases of follicular lymphoma, they all have nucleated red blood cells in the peripheral blood. And thalassemia patients, because there is extramedullary hematopoiesis going on, it is very large, that's why you have nucleated red blood cells in the peripheral blood. And in babies, in two days old baby, if you see the blood film of a two days old baby, they will have a lot of nucleated red blood cells in the peripheral blood, which is normal for them because their spleen is not yet mature, and the bone marrow is producing everything, and bone marrow is under stress. So, any reason which makes the bone marrow under stress, you will get nucleated red blood cells in the peripheral blood. Sir, thank you.
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