Case 129 – update 1

Thanks for everyone’s thoughts So far we have now established the following:

No Anticoagulants
No ETOH excess
Normal liver function
No previous coagulation results available for this lady
No personal history of bleeding
No FHx of bleeding disorder

The lab performed the following extra tests at your request:

Repeat Coag results:

PT 12.4, APTT 49.6, APTT 50:50 Mix 46, Fib 2.9, DRVVT Ratio 1.5 (0.8-1.2)

Anticardiolipin and Anti beta 2 glycoprotein 1 Ab are pending
What is the likely cause for prolonged APTT?
Is it safe to proceed with planned LP on the basis of the above tests?
Anything further to recommend to the clinical team?

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Case 129 – The beginning

You are the haematology registrar on call and you get contacted regarding a 28 year old lady who presented to the A&E department on Saturday evening. She presented with a sudden onset severe headache that had been present for 12 hours with associated vomiting. Her CT Head has been provisionally reported over the phone to A&E as “normal” and  the medical registrar wants to perform an urgent lumbar punctureto investigate for possible subarachnoid haemorrhage.

Blood tests so far (Ref range in brackets):

Wcc 11.6 (3.6 – 11), Hb 140 (115-165), Plt 400 (140-400), Neu 10.2 (1.7-7.5)

PT 12.6 (10-14)

APTT 49 (22-36)

Fib 3 (1.5-4)

Is it safe to proceed with the planned lumbar puncture?

What other history would you ask the registrar on the phone?

Any further tests you would request from the lab?

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Case 128 – Summary!

Thank you for everyone’s contributions with case 128!

We discussed a complex case of a 65 year who was critically unwell with severe pancreatitis. During her admission she developed anaemia and marked thrombocytopenia. Our discussions centred upon the potential differential diagnoses, focusing in more detail on pancreatitis associated thrombotic thrombocytopenia purpura (TTP) and post transfusion purpura (PTP). At a later stage she also had a further complication of bilateral pulmonary emboli and portal vein thrombosis directing our thoughts to the management of these in the setting of her thrombocytopenia. This case highlighted the challenges (and frustrations!) that we are often faced with in our clinical roles where the diagnosis is not clear cut but immediate management is essential prior to confirmation of the diagnosis – if this can be achieved! Please see below for information on the main topics we discussed throughout this case.

Potential differential diagnosis of bi-cytopenia (Hb + Plts) with acute onset includes:

  1. Severe acute illness
    1. Rx: underlying cause. Transfusion support as required
  2. DIC (with either bleeding / acute illness to account for anaemia)
    1. Rx: underlying cause. Transfusion support for coagulopathy /thrombocytopenia if bleeding / surgery
  3. Drug-induced immune mediated thrombocytopenia
    1. Rx: Stop causative agent. Consider IVIg +/- steroids. Transfusion support as required.
  4. Drug-related marrow suppression
    1. Rx: Stop causative agent. Transfusion support as required.
  5. Microangiopathic haemolytic anaemia (including TTP)
    1. Rx see below for pancreatitis-associated TTP
  6. Post-transfusion purpura
    1. Rx see below for PTP
  7. Acute haematological malignancies e.g acute leukaemia
  8. Marrow infiltration

 

Pancreatitis-associated TTP

  • Rare complication of pancreatitis. Typically occurs during acute episode but can occur shortly after resolution
  • ADAMTS13 is only moderately reduced
  • Good outcomes following plasma exchange and steroids

Post-transfusion purpura (PTP)

  • Extremely rare complication of transfusions with blood components containing platelets and should be considered in those who have developed thrombocytopenia within 14 days of a transfusion.
  • Since leucodepletion has been introduced the incidence of PTP is <1 in 700,000.
  • PTP occurs when a blood transfusion stimulates an anamnestic response of HPA antibodies in a previously sensitised patient. The most common initial sensitising event is pregnancy but immunisation by HPA alloantigen can also occur from previous transfusions.
  • The marked thrombocytopenia associated with PTP is secondary to the antibody mediated destruction of both the donor platelets AND patients own platelets.
  • The presence of IgG allo-HPA antibodies confirms the diagnosis of PTP. Anti-HPA-1a is most frequent antibody implicated in PTP. If PTP is strongly suspected management should be initiated prior to serological confirmation.
  • Management
    • IVIg 2g/kg over 2-5 consecutive days
    • Consider plasma exchange if IVIG alone not effective
    • During acute episode of PTP no benefit of transfusing blood components from HPA compatible donors. Unfortunately random platelet transfusions are also not effective and multiple transfusions are often required in setting in haemorrhage.
    • Following acute episode transfusion of blood components should be from HPA compatible donors.
  • Report to SHOT / MHRA

 

Potential differential diagnosis of acute onset thrombocytopenia and macrovascular venous thromboembolism includes:

  1. Critical illness
  2. Malignancy
  3. PNH
  4. Antiphospholipid syndrome
  5. HITT

 

Management of venous thromboembolism in context of marked thrombocytopenia

  • Individualised approach as always! Assessment of risk of VTE vs bleeding
  • Management of thrombosis
    • Optimise risk reduction of VTE by non-pharmacological means i.e hydration, mobilisation
  • Anticoagulation options
    • consider bleeding risk, renal / liver function
    • In our case with marked thrombocytopenia and low eGFR unfractionated heparin (UFH) likely to be the safest option due to short half life and reversal agent available. However UFH needs regular monitoring of anti-Xa levels (or APTTr levels if baseline APTT within normal range) and if this can not be achieved than its use is often unsafe and a twice daily low molecular weight heparin may be better option
  • Management of bleeding risk
    • Need close monitoring of platelets and manage cause of thrombocytopenia
    • Consider platelet transfusions to maintain platelet count >50 (depending on cause of thrombocytopenia – avoid unless bleeding in HITT / TTP / PTP / ITP etc)

References:

1. Scully et al. Guidelines on the diagnosis and management of TTP and other thrombotic microangiopathies. British Journal of Haematology. 2012.

1. Massey E. NHS Blood and Transplant clinical guidelines. Post transfusion purpura.  2011. https://nhsbtdbe.blob.core.windows.net/umbraco-assets-corp/14873/inf153-post-transfusion-purpura.pdf

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Case 128 – Update 4!

Thank you for everyone’s ongoing contributions!

The patient underwent further intra-abdominal surgery without significant bleeding complications following the management below:

  1. Vitamin K 10mg IV
  2. Co-trimoxazole stopped
  3. IVIg 2g/kg over 2 days
  4. Platelet transfusion (random ABO and D compatible with good 15 minute increment – plt count went from 25 to 51)
  5. 2 units packed red cells

Unfortunately 3 days later our 65 year old patient has deteriorated and is now on critical care having been intubated and ventilated. A CTPA and CT abdo-pelvis was performed and this has shown:

  • Bilateral segmental PEs
  • Fully occluded portal vein thrombosis
  • Mild improvement regarding appearance of pancreatitis

Repeat bloods are as follows:

  • Hb 78 Plts 39 WCC 5
  • PT 18 APTT 39 Clauss fib 3
  • eGFR 31 Bili 125 ALT 320 Alk phos 110 CRP 265

Questions:

  1. How would you manage our patient now (from haem perspective)?

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

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Case 128 – Update 3!

I think we’re all in agreement that we currently can’t give a definitive diagnosis as is frequently the case in complex critically unwell individuals. From your responses the most likely differentials for our patient’s bi-cytopenias include the following (or combination of the following):

  1. Severe sepsis / critical illness (marrow suppression, consumptive coagulopathy, liver dysfunction etc)
  2. Drug induced immune mediated thrombocytopenia
  3. Post transfusion purpura

Repeat bloods:

Hb 74 Plts 25 WCC 6 PT 20 APTT 41 Clauss fib 3

Questions:

  1. How would you manage our patient generally and also if planned for further surgery (laparotomy)

 

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 128 – Update 2!

Thank you for everyone’s ongoing contributions!

We now have the outstanding results to help diagnose our patients bi-cytopenias (and old results for reference) and some additional history as requested:

Her bloods from this morning are as follows:

  • Hb 71 (several transfusions required throughout this admission)
  • Plts 20 (plt count was within normal range upto 3 days ago)
  • PT 19, APTT 40, Clauss fib 5.2
  • DAT negative. LDH 326
  • Stage 2 AKI, bilirubin 84 (ULN 21), ALT 250 (0-40), Alk phos normal

 

Outstanding results now in:

  • Blood film: Normocytic normochromic anaemia with unremarkable red cell morphology including NO red cell fragments or features of haemolysis. Thrombocytopenia appears genuine with no plt clumps. Plts morphologically normal. left shifted neutrophils with toxic granulation.
  • Retics: upper level of normal.
  • HIT assay: negative (and intermediate 4Ts score)
  • B12 / folate: normal
  • Autoimmune screen: negative
  • HIV / hep B / C: negative
  • Serum electropheresis: no paraprotein.
  • The patient has received 10 units packed red cells over the past 2 weeks for support several surgeries but has also been given appropriate associated FFP / platelet support.
  • (NB: an ADAMST13 has not been requested given the above findings and plasma exchange had not been initiated.)

Questions:

  1. What are the most likely differentials now?
  2. Any others related to the transfusion history and how could you investigate?
  3. Can you give a definitive diagnosis for cause of anaemia / thrombocytopenia?

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 128 – Update 1!

Thank you for everyone’s contributions so far!

Below is the additional information you requested to help determine the cause of our 65 year old patients anaemia and marked thrombocytopenia.

  • Her severe pancreatitis is secondary to gallstones.
  • She has a previous history of cholecystitis (due to gallstones) and well controlled hypertension.
  • She has no significant alcohol history.
  • She has been on amlodipine for years and takes no other medications or OTC treatments. She has however been on multiple new medications this admission including starting prophylactic low molecular weight heparin throughout admission and co-trimoxazole started approximately 5 days ago.
  • A CT abdo-pelvis this admission has demonstrated pancreatitis with marked necrosis, cholecystitis. The liver and spleen appear normal. Low volume lymphadenopathy (~2cm) in the porta hepatis but nil elsewhere.

 

Her bloods from this morning are as follows:

  • Hb 71 (several transfusions required throughout this admission)
  • Plts 20 (plt count was within normal range upto 3 days ago)
  • PT 19, APTT 40, Clauss fib 5.2
  • DAT negative. LDH 326
  • Stage 2 AKI, bilirubin 84 (ULN 21), ALT 250 (0-40), Alk phos normal
  • Blood film, retics, serum electropheresis, autoimmune screen, viral screen all pending

With this new information what are your differential diagnoses?

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

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Case 128 – The beginning!

You are the haematology registrar oncall and are contacted by the surgical team regarding a 65 year old woman with severe pancreatitis. The patient is critically ill. They are after some advice regarding the following FBC results:

Hb 72, Plts 31, WCC 5.5, Neuts 4.4

Questions:

  1. What other information would you want to ascertain from the clinical team?
  2. What initial investigations would you want to review/perform to look into the cause of her cytopenias?

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

TeamHaem are not a position of authority.  It is an educational platform to allow discussion and learning.

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Case 127 – the summary

Thanks for all your input this week, as we worked through the investigation and management of CML; highlighting a few areas for discussion as we went!

See below summary notes on CML – mainly taken from the European Leukaemia Network (ELN) and ESMO guidelines. Any mistakes are my own!

Screen Shot 2020-04-30 at 19.23.13Screen Shot 2020-04-30 at 19.23.30Screen Shot 2020-04-30 at 19.23.39

Key references:

Hochhaus, A., Baccarani, M., Silver, R.T. et al. European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia. Leukemia 34, 966–984 (2020). https://doi.org/10.1038/s41375-020-0776-2

Hochhaus, A. et al. Chronic myeloid leukaemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-upAnnals of Oncology, Volume 28, iv41 – iv51

 

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to evolve over the coming week so keep checking #TeamHaem on Twitter for more information. 

Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 127 – Update 2

Our 31 year old female patient with newly diagnosed CML in chronic phase is commenced on dasatinib 100 mg OD with the aim of gaining a faster deep molecular response (DMR).

3 years later (patient is now 34)…..

  • She has tolerated the drug well – no evidence of pleural effusions
  • She has had a complete haematological response (CHR)
  • Her BCR-ABL1 to ABL1 ratio has been hovering around 0.05% for the last 2 years. She is now asking to stop the drug to start trying for a family

What is the evidence around stopping TKI therapy? How would you counsel the patient in the best way forward?

 

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

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Case 127 – update 1

Our 31 year old patient has repeat bloods including a few extra. FBC confirms leucocytosis with WCC 38, and basophilia 3.8. Platelets are normal. U&Es and LFTs are normal. No organomegaly on clinical exam.

Cytogenetics confirms the Ph chromosome t(9;22) and RT-PCR demonstrates BCR-ABL1 to ABL1 transcript ratio as 56%

This confirms a diagnosis of CML in chronic phase

On further questioning, this 31 year old female patient has no relevant PMH. She has a FH of familial hypercholesterolaemia but maintains regular exercise, good diet and doesn’t smoke. She works as a primary school teacher, has been married for 2 years and has no children, but is planning a family in the near future.

How would you explain the disease/prognosis to this young patient? What would be the options for 1st line treatment?

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Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 127 – The beginning

You are the haematology SpR reviewing routine blood films in the lab at 4pm when you come across the following FBC differential and film from a GP request. The patient is a 31 year old female. Clinical details state ‘for bloods.’

FBC:

  • Hb 115 g/l
  • MCV 90 fl
  • Plt 152 x 109/L
  • WCC 19.3 x 109/L
  • Neuts 10.4 x 109/L
  • Lymph 1.4 x 109/L
  • Monocytes 4.2 x 109/L
  • Eosinophils 1.1 x 109/L
  • Basophils 2.2x 109/L

Blood film as shown below:

CML

What does the FBC and blood film demonstrate? What are the next actions you would take?

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Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 126 – Update 3!

Thank you for everyone’s contributions so far!

As advised by yourselves we have commenced our 57 year old gentleman who has newly diagnosed T-PLL on Alemtuzumab with the aim of consolidating with an allogenic stem cell transplant. He had been tolerating it well having only  experienced mild infusion reactions with cycle 1 and 2. However he has now presented with marked diarrhoea post his 4th cycle of treatment.

Questions:

  1. What is the differential diagnosis for this?
  2. What investigations would you perform?

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to  evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 126 – Update 2!

Thank you for everyone’s thoughts on the blood film. Think we’re all in agreement that blood film shows small to medium sized lymphocytes with high nuclear/cytoplasmic ratio and folded nucleoli. There are also occasional forms with nucleolus and cytoplasmic protrusions.

The flow plots are now available. Can you help interpret to ascertain the immunophenotype and ??diagnosis.

TPLL Flow1

TPLL Flow2TPLL Flow3

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Case 126 – Update 1!

 

We advised the GP to repeat the asymptomatic 57 year old patient FBC (with film) in 4-6 weeks and to refer to haematology if absolute lymphocyte count was >10 or if he had associated cytopenias / B symptoms / lymphadenopathy / hepatosplenomegaly.

Unfortunately after 4 weeks the GP contacts you again to say the patient re-presented with drenching night sweats. On examination he has an macular rash over his thorax and the spleen is now palpable 3cm below the costal margin.

Repeat FBC: Hb 125 Plts 110 WCC 62 Neuts 4 Lymphocytes 56

Blood film:

TPLL1

TPLL2

Questions:

  1. What does the blood film show? Diagnosis??
  2. What further investigations would you request?

 

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

 Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 126 – The beginning!

You are the on-call haematology registrar who has been contacted by a conscientious GP regarding a fit and well 57 year old man who has an incidental finding of lymphocytosis. The FBC was performed as part of his monitoring for hypothyroidism.

Hb 131 MCV 90 Plts 180 WCC 13 Neutrophils 4.5 Lymphocytes 7

Questions:

  1. What further information would you want to clarify with the GP?
  2. How would you advise the GP regarding the lymphocytosis?

 

Please reply to us (@TeamHaem) on Twitter and always include #TeamHaem to allow others to follow your comments. Please join in the debate and learn about haematological problems along the way. The case will continue to evolve over the coming week so keep checking #TeamHaem on Twitter for more information.

 Please note – all cases on TeamHaem are entirely fictional to protect patient confidentiality.

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Case 125 – Summary

Thanks for all your input in managing this case or iron deficiency anaemia in pregnancy.   Case 45 previously discussed anaemia in pregnancy and this case highlights changes in recommendations for oral iron replacement as well as indications and complications associated with intravenous iron.

Blood parameters and pregnancy

In pregnancy there is a physiological reduction in haemoglobin due to the dilutional effect from expansion of plasma volume as well as increased use of iron for foetal growth and maternal erythropoiesis. As such there are different thresholds used to define anaemia in pregnancy which are:

  • Hb <110 g/l in the first trimester
  • Hb <105 g/l in the second and third trimester 
  • Hb< 100g/L immediately postpartum

Other factors which may contribute towards anaemia are many and include iron, vitamin B12 and folate deficiency, haemoglobinopathies,  inflammatory disorders, haemolysis and bleeding.

Other changes to blood parameters which occur in pregnancy include a 20% increase in red cell mass with increase in MCV of up to 6fL, which may mask the reduced MCV which may be seen in iron deficiency. There may be a neutrophilia and monocytosis. The blood film may be left shifted. 

Risks of iron deficiency in pregnancy

Risks to the mother which may be associated with iron deficiency include fatigue, increased infection, reduced cognition, postpartum haemorrhage and possible need for blood transfusion.

Risks to the baby may include increased perinatal and neonatal mortality, pre‐term birth and low birth weight and less clear cut – possible neurodevelopmental issues. Haemoglobinopathy screening

Haemoglobinopathy screening

All pregnant women are offered a FBC and group and save as well as screening for haemoglobinopathy via the family origin questionnaire at their booking appointment (usually 8-12 weeks). All women in high risk areas (foetal prevalence of sickle cell disease >1.5/10 000) will have a haemoglobinopathy screen as well as those with risk identified from their family origin questionnaire and blood count. The screening programme looks for sickle cell disease, thalassaemia and some unusual haemoglobin variants.  It is not designed to pick up HbH disease in the foetus, although it may do.  

Oral iron replacement

If the routine blood count shows microcytic anaemia it is reasonable to assume this is due to iron deficiency and give a trial of iron whilst awaiting a haemoglobinopathy screen. If there is evidence of haemoglobinopathy, check a ferritin level before starting a trial of iron to avoid exacerbating iron overload.

Recent BSH guidelines for iron deficiency in pregnant women now recommend 40-80mg of elemental iron daily as once daily dosing or alternate day dosing has been found to lower hepcidin levels and maximise fractional absorption of iron whilst reducing adverse effects.  Daily dosing is suggested as a practical compromise aiming for optimum compliance and more rapid response. Alternate day dosing is suggested if nausea and epigastric discomfort is experienced. 

To optimise use of oral iron:  

  • Take with vitamin C to increase absorption
  • Take early in the morning on an empty stomach
  • Warn about potential adverse effects and how to manage them
  • Avoid taking with tannins (tea, red wine etc.)
  • Don’t take with PPIs or H2 receptor blockers

After starting oral iron treatment, the full blood count should be checked at 2-3 weeks and should demonstrate a rise in Haemoglobin if the anaemia is due to iron deficiency.

Once the Hb is in the normal range, replacement should continue for 3 months and until at least 6 weeks postpartum to replenish iron stores.

IV iron replacement

Consider IV iron replacement if:

  • Unable to tolerate different preparations of oral iron
  • Need quick increase in haemoglobin e.g. nearing delivery. BSH guidelines suggest it should be considered in women presenting after 34 weeks gestation with confirmed iron deficiency anaemia and an Hb of <100 g/L
  • No response to oral iron/malabsorption issues

IV iron is contraindicated in the first trimester and can rarely cause transient fetal bradycardia so the manufacturers recommend monitoring of the foetus during administration. It is also contraindicated in bacteraemia or decompensated liver disease or if there is a history of anaphylaxis or serious hypersensitivity following any IV iron preparation and suggested use with caution. The manufacturers recommend monitoring for 30 minutes after the infusion for any reactions, although the risk is low (<1/200,000). Extravasation can cause haemosiderin skin staining which may be permanent and any discomfort at the infusion site should be reviewed, the infusion stopped, and plastics advice sought if concern.

When to refer to specialist care

BSH guidelines recommend referral to specialist care if Hb <70 g/L and/or associated with significant symptoms or gestation >34 weeks, or if the Hb is failing to respond after 2–3 weeks of oral iron correctly taken. They state that iron deficiency anaemia should not affect decisions on the mode of delivery, but anaemia is associated with increased risk of PPH, hence women with Hb <100 g/l approaching birth should have an individualised plan. This should include consideration of IV access, birth in an obstetrician‐led unit and active management of third stage of labour.

Women with uncorrected anaemia antenatally should have a Hb check within 48 h of birth, as should those who have had blood loss >500 ml, or symptoms suggestive of postpartum anaemia.

References:

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Update 5

After 2 weeks the patient stopped taking the iron tablets as she was struggling with abdominal discomfort and constipation.  She is prescribed an IV iron infusion for later that week and attends for this but unfortunately she notices some discomfort and some brown discolouration spreading in her anticubital fossa a few minutes into the infusion.  The infusion is stopped. 

Questions:

  • What has happened here?
  • Are there any contraindications for iron infusions?
  • Are there any further steps which need to be taken to prepare for her labour?
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Update 4

The patient did not attend any further appointment for follow up FBC or her 28 week appt.  At 36 weeks she finally attended her midwife appointment and her FBC was as follows:

  • Hb 80g/L
  • MCV 76fL
  • MCH 22.7pg
  • MCHC 31.2%
  • PLT 154×10*9/L
  • WCC 9.2×10*9/L

Given your comments on the previous film, the following were added:

  • Ferritin 8μg/l
  • Vitamin B12 168pmol/L
  • Folate 5.2μg/L
  • LDH 118U/L (normal)
  • Reticulocytes 74 × 10*9/L
  • Bilirubin 9μmol/L

Questions:

  • What are your thoughts on the results?
  • What management might be appropriate?
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Update 3

As most of you told us the film shows microcytic red cells with occasional pencil cells and target cells. Some of you mentioned variable haemoglobinisation, some macrocytic cells, occasional spherocytes and suggested we check folate and vitamin B12 levels and investigate for hamolysis. 

As you told us the HPLC is normal. It shows no variant haemoglobin and the HbA2 is within normal limits suggesting no evidence of beta thalassaemia. 

The patient was given dietary advice as you suggested and we opted for a trial of daily dosing of 200mg ferrous sulphate. Recent BSH guidelines for iron deficiency in pregnant women now recommend 40-80mg of elemental iron daily as once daily dosing or alternate day dosing has been found to lower hepcidin levels and maximise fractional absorption of iron whilst reducing adverse effects.  Daily dosing is suggested as a practical compromise aiming for optimum compliance and more rapid response. 

We invited her to attend for a repeat full blood count 2 weeks later which was as follows:

  • Hb 91g/L
  • MCV 74fL
  • PLT 151×10*9/L
  • WCC 9.9×10*9/L

Questions:

  • What are your thoughts on the FBC now/?
  • Would you continue iron replacement? If so for how long?
  • What are the risks associated with iron deficiency in pregnancy?
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