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Anemia in Pregnancy .ppt

This document discusses anemia in pregnancy. It provides trimester-specific cutoffs for defining anemia recommended by WHO and CDC. Iron deficiency anemia is the most common type of anemia in pregnancy due to increased iron requirements. Anemia can be detrimental for both mothers and children by increasing risks of issues like postpartum hemorrhage, preterm birth, and impaired development. The three pillars of patient blood management for optimizing outcomes are outlined as optimizing haemopoiesis through screening and treatment of anemia, minimizing blood loss and bleeding, and harnessing anaemia tolerance. Oral iron supplementation is recommended but intravenous iron may be needed for more severe cases.

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Anemia in Pregnancy Dr. Carol Lim Maternal Fetal Medicine Consultant Ampang Hospital
Anemia in Pregnancy WHO & CDC recommendation: Trimester-specific cutoffs for anemia • 1st trimester <110g/L (8% prevalence) • 2nd trimester <105g/L (12% prevalence) • 3rd trimester <110g/L (34% prevalence) Women at higher risk of IDA due to increased iron requirements. WHO recommendations on antenatal care for a positive pregnancy experience, 2016 Postpartum <100g/L Male Hb13; Non Pregnant Female Hb12
Anemia – a Global Public Health Problem! IDA – among the most important contributing factors to the global burden of diseases
~35% of women & older adults
ID & IDA in Pregnant Msian Women
Maternal Anemia (antenatal anemia + postpartum anemia) Women at risk include: • Pre-existing anemia • Grandmultipara • Poor spacing • Multiple pregnancy • Obesity • Poor socio-economic status • following Postpartum hemorrhage
Risk factors for Anemia = Risk factors for PPH Anemia itself is a risk factor for PPH Anemia is also a risk factor for VTE
Type of Anemia
This lecture will cover… • Iron Deficiency Anemia (IDA) • Anemia of Chronic Disease (ACD) / Anemia of Inflammation (AI) • Thalassemia Main focus – IDA, the most common type of anemia
ID / IDA is detrimental for mothers Camaschella C. Iron Deficiency Anemia. N Engl J Med 2015;372:1832-43. Breymann 2015 Iron deficiency anaemia in pregnancy; 18. Ponikowski, 2014 JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019 • Inability to tolerate blood loss • Risk of severe maternal morbidity or mortality after PPH • Increased risk in heart failure • Reduced milk production • Shorter lactation periods • Perinatal Mental Health • Impaired physical function • Reduced quality of life
ID / IDA is detrimental for children Camaschella C. Iron Deficiency Anemia. N Engl J Med 2015;372:1832-43. Breymann 2015 Iron deficiency anaemia in pregnancy; 18. Ponikowski, 2014 JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019 • Perinatal mortality, SB • Premature birth and low birth weight • IUGR / FGR, SGA • ID or IDA in newborn • Long-term adverse effects on brain development and behavior: ASD, ADHD, ID Maternal hemoglobin concentrations across pregnancy and maternal and child health: a systematic review and meta-analysis. Ann.N.Y.Acad.Sci.1450(2019)47-68
ASD: autism spectrum disorder ADHD: attention-deficit/hyperactivity disorder ID: intellectual disability JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019
Back to basic – ANEMIA… • Addressing Maternal Anemia –to protect Mothers & Newborns Bread & Butter !!
Iron Requirement during Pregnancy Ref: 1. Nils Milman. Prepartum anaemia: prevention and treatment. Ann Hematol (2008) 87:949–959. 2. Nils Milman. Iron and pregnancy—a delicate balance. Ann Hematol (2006) 85: 559–565
Serum Ferritin • Ferritin – most frequently used test for evaluating iron stores • Various cutoffs eg 70ug/L or 100ug/L have been used • <30 ug/L : low iron status (92% sen, 98% spec for absolute ID with or without anemia) • <15 ug/L : iron depletion • <12 ug/L : associated with IDA • Ferritin – acute-phase reactant, levels affected by inflammation
Transferrin Saturation (TSat) • TSat – iron available for tissue • Low TSat – insufficient iron supply to support normal erythropoiesis • If TSat <20% & Ferritin >100 – Functional ID (Iron Sequestration) eg anemia of chronic disease (ACD) / anemia of inflammation (AI) Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017
Ferritin >100 ng/mL plus TSAT >20% Definitions Ferritin 30-100 ng/mL plus TSAT >20% Low Iron Stores Ferritin <100 ng/mL plus TSAT <20% Ferritin <30 ng/mL Absolute ID Ferritin >100 ng/mL plus TSAT <20% Iron Sequestration (functional ID) Iron Replete Munoz et al, Blood Transfus. 2017 Sep;15(5):422-437. Defining Iron Deficiency ID accounts for 75% of non- physiologic anemia during pregnancy.
Non-Anemic Iron Deficiency (NAID) • Even in the absence of anemia, ID has negative impact for both mother & neonate:  Mother: cognitive ability, physical performance, PPH, transfusion, etc  Neonate: low APGAR, PTB, behavioral problems, etc • Hb not suitable to assess iron status, esp when there is various degree of hemodilution (ID on functional level) • Ferritin provides info on capacity of body iron reserves (ID on cellular level) • Iron deficiency is often seen in first trimester
Non-Anemic Iron Deficiency (NAID) • “Mild anemia” (Hb 11-12 or 13) – a misnomer • ID already advanced by the time anemia is detected. • IV iron replacement for NAID-associated fatigue (runners - *blood doping) • How about post-blood donation iron replacement? Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017 Hb concentrations for the diagnosis of Anemia & Assessment of Severity. WHO 2011
Non-Anemic Iron Deficiency (NAID) • Cancer, inflammatory bowel disease – NAID may induce 20 thrombocytosis (>350)  independent risk factor for thromboembolic event. • ID a preventable cause of thrombosis, especially in the elderly. • Obst VTE – adjusted odds ratio (aOR): o Anemia: 1.6-2.6 o >Parity 1: 1.5-2.4 o >35yr: 1.2-1.4 Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017 Reducing the Risk of VTE during Pregnancy & the Puerperium, RCOG 2015
Iron Homeostasis in Pregnancy Plasma volume expansion 50% RBC mass 25% i.e. Plasma Volume Expansion > RBC mass  Hb   Hematocrit  Nadir at end of T2 till beginning of T3  Normal physiologic anemia of pregnancy Hemodilution PVE > RBC
Severe antenatal anemia (<60g/L) Has been associated with: • Abnormal fetal oxygenation (20 to impaired O2 transport to uterus / placenta / fetus) -FGR • Non-reassuring fetal heart rate patterns • Reduced amniotic fluid volume • Fetal cerebral vasodilatation • Fetal mortality Patient Blood Management in Obstetrics: Management of Anemia & Hematinic Deficiencies in Pregnancy and in the post-partum period: NATA consensus statement Transfusion Medicine, 2018, 28,22-39 Sifakis & Pharmakides, 2000 Carles et al., 2003
High Hb Concentrations • Failure for plasma volume expansion (PVE) • Chronic renal impairment (eg lupus nephritis, advanced diabetes) Reduced plasma volume expansion Hemoconcentration • NOT indicator for good iron status • Increased blood viscosity low uterine arterial blood flow, reduced placental perfusion Reduced O2 delivery to the fetus Emerging understanding and measurement of plasma volume expansion in pregnancy Am J Clin Nutr 2017;106(Suppl):1620S-5S
U-shaped relation U-shaped relation between maternal Hb conc and adverse pregnancy outcomes. Hb Hb* * Hb >13 Maternal Hemoglobin Levels during Pregnancy and their Associations with Birth Weight of Neonates Iranian Journal of Pediatric Hematology Oncology Vol5.No4 Hb concentrations & adverse birth outcome in South Asia pregnant women: findings from a Prospective Maternal & Neonatal Health Registry. Reproductive Health 2020 IUGR, SGA, PTB, LBW, SB, Preeclampsia* Hb Adverse Pregnancy outcome
How to protect the mother & baby? Prevent / treat antenatal anemia, to avoid: • Neonatal outcomes (LBW, SGA, PTB, FGR, etc), & • Maternal outcomes (PPH, maternal sepsis, etc) ...by practicing Patient Blood Management
The Urgent Need to implement Patient Blood Management, WHO Policy Brief, 2021
The Urgent Need to implement Patient Blood Management, WHO Policy Brief, 2021
3 Pillars of PBM in Obstetrics 1. Optimise haemopoiesis 2. Minimise blood loss and bleeding 3. Harness and optimise tolerance of anaemia •Screen for red cell antibodies •Screen for & treat anemia (Hb, Ferritin) •Iron – oral, parenteral •?ESA •Pharmocologic/ haemostatic agents •Uterine tamponade •Cell salvage •MTP •Iron – oral, parenteral
1st Pillar of PBM: optimise haemopoiesis • Improve diagnosis & treatment of ID / IDA • Resort to Parenteral /IV Iron, if oral hematinics are not increasing Hb as targeted • Good response: Hb < 10g/L in 2w or <20g/L in 4w Optimise red cell mass
Anemia during Pregnancy • Routine screening for Iron Deficiency? (Hb, Ferritin, KIV TSat) • Replenish iron stores before one progresses to anemia
Oral Iron Therapy (Malaysia) Iron Product Content per tablet (mg) Elemental Iron per tablet (mg) Absorbed Iron per tablet (mg) Ferrous Fumarate 200 60 7.5 Zincofer (FF) 350 115 14.4 Iberet Folic (FS) 525 105 13.1 Maltofer + FA (IPC) - 100 12.5 Obimin (FF) 90 30 3.8 10- 15% Daily vs EOD ?
Hepcidin in Iron Metabolism • Major regulator of systemic iron bioavailability • Produced by liver • Synthesis of Hepcidin is regulated by 3 signals – 1. Need for increased erythropoiesis:  hepcidin 2. Increased plasma iron & iron store: hepcidin 3. Inflammation: hepcidin • Hepcidin blocks iron absorption & prevent iron overload  iron sequestration • Hepcidin effect lasts for 48hr (hence EOD dosing)
Ferroportin & Hepcidin • Ferroportin – transmembrane iron transporter found in duodenal enterocytes and macrophages • Hepcidin degrades ferroportin  preventing enteral iron absorption and transport of iron from liver
• EOD Iron is associated with increased absorption • Second trimester – still reasonable to continue oral iron if Hb is at least 10g/L • For Hb<10 or in third trimester – IV iron should be given to ensure adequate iron gets to the fetus. Michael Auerbach, MD
Every Other Day (EOD) Dosing Alternate days dosing may: -maximize fractional iron absorption, -increase dosage efficacy -reduce GI exposure to unabsorbed iron -improve tolerance of iron supplements Blood, 22 October 2015. Volume 126, Number 17
Regimes for Oral Hematinics Iron Deficiency (Prophylaxis) 1/1 EOD Iron Deficiency Anemia (Treatment) 1/1 Daily (Maltofer may go as high as 2-3 Tablet OD) NO Split dosing NO Double / triple hematinics NO Weekly intermittent dosing Prophylaxis 30-60mg Iron / day Treatment 120-180mg Iron / day
Fehr J et al. Praxis 2009;98:1445–1451; Gordeuk VR et al. Am J Clin Nutr 1987;46:1029–1034; Aapro M et al. Ann Oncol 2012;23:1954–1962 Iron Replacement Therapy Iron preparations in Malaysia Oral iron* Intravenous iron Iron(III) carbohydrate complexes • Iron sucrose (Venofer) • Iron dextran (Cosmofer) • Iron isomaltoside (Monofer) Iron(III) complexes: • Iron(III)-hydroxide polymaltose complex Iron(II) compounds: • Ferrous sulfate • Ferrous fumarate • Ferrous gluconate • Others Do not administer via IM Iron (uncertain absorption, painful, stain) Parenteral Iron is contraindicated in 1st trimester
“The feared anaphylactic reaction is extremely rare and occurs mainly with the high-molecular-weight ID (iron dextran)”* “Thus, it seems that the newer formulations are safer to administer and no test dose is required” 103 trials included 10,390 patients. IS= Iron sucrose; FCM= Ferric carboxymaltose; FG= Ferric gluconate Avni et al. Mayo Clin Proc. 2015 Jan;90(1):12-23. Risks of reactions with IV Iron *IMFERON (high molecular weight Iron Dextran) is not available in Msian market since ?2005
Reactions (1) Infusion Reaction / Fishbane Reactions • Self-limited; 1:100-250 administrations • Due to labile free iron • Acute chest / back tightness, myalgia, flushing, diarrhea, swelling of hand / feet • No BP, wheezing or stridor • Minor reactions; • hypersensitivity • Re-challenge with lower infusion rate or switch to other IV iron formulation • If urticaria - Antihistamine &/or Corticosteroid
Reactions (2) Hypotension • Hypersensitivity, or vascular reaction • Self-limited • Related to: Rapidity of administration Labile iron content • If hypotension - lie horizontally with leg elevation, IV fluid load (500ml), antihistamine, corticosteroid
Reactions (3) Anaphylaxis • IgE mediated • CARPA (complement activation related pseudoallergy) • Related to rapidity of administration • Exceedingly rare (<1:250,000 administrations) • With CVS & RS manifestations • Rx: epinephrine, fluid, corticosteroid • Antihistamine may delay efficacy of epinephrine *Delayed reaction – can’t be predicted by test dose Gomez-Ramirez et al. Prevention & Management of Acute Reactions to IV Iron in Surgical Patients. Blood Transfus 2019
Various IV Iron Preparations LMWID IS FDI/IIM FCM Molecular wt (Daltons) 103000 43300 1000 150000 Structure Iron core, CHO shell Iron core, CHO shell Linear, non- branched CHO Iron core, CHO shell Labile iron(%) 2% 3.5% 1% 0.5% Stability High Medium High High Maximum single dose 20mg/kg 7mg/kg (200mg boluses or 500mg TDI) 20mg/kg (1000-2000mg) 15mg/kg (1000mg) Max admin time 4-6hr 10-30min (bolus) 15-30min 15min Issues Longer time Lower dose Higher dose, Faster Hb Faster Hb Name of Iron Product Cosmofer Venofer Monofer Ferinject LMWID: Low Molecular Weight Iron Dextran (Cosmofer®); IS: Iron Sucrose (Venofer®) FDI/IIM: Ferric Derisomaltose / Iron Isomaltoside (Monofer®) FCM: Ferric Carboxymaltose (Ferinject®)
IV iron is indicated with or without trial of oral iron IV iron may be indicated when rapid increase of Hb and iron stores are required Camaschella C. Iron-Deficiency Anemia. N Engl J Med. 2015 Jul 30;373(5):485-6.
…early IV Iron therapy is recommended in postoperative period if iron is necessary. Where possible, it should be administered using a single high- dose preparation for the repletion of iron stores
When should we consider IV Iron? • When not responding to oral hematinics • When there is an urgency to top up Hb (before surgery / delivery) • When massive bleeding is anticipated. • Surgery / O&G: Pre-operatively / Antenatally Post-operatively / Postnatally – after PPH has been controlled & patient stabilized Intraoperatively
Iron Requirement Calculation • Oxygen Delivery (Iron for Hb) ~200-250gm Iron per g/dL Hb Target Hb >13g/dL • Oxygen Utilization (Iron for store & other non-haem functions) 1g/L Ferritin = ~8mg stored iron Target serum Ferritin >100g/L Munoz etal. Blood Transfus 2017; 15:422-37 Ganzoni formula Total iron dose = BW in kg x Hb deficit x 2.4 + Iron stores in mg *IV Iron is CONTRAINDICATED in 1st Trimester
How about ESA? Anemia of Chronic Disease (ACD) / Anemia of Inflammation (AI) – 2nd most common (after IDA) Typically: NcNc (may progress to Mc); Serum iron; TSat; reticulocytes; Ferritin may be  (acute phase protein); Hepcidin • Impaired EPO production • Blunted marrow erythroid response to EPO • Iron-restricted erythropoiesis • Pool of EPO-responsive cells Hypoproliferative anemia / functional ID
IDA vs ACD Iron Deficiency Anemia Anemia of Chronic Disease Hb Low Low MCV Low Normal (low in 30% pts) Ferritin Low High Serum Iron Low Low TIBC High / Normal Normal / Low TSat Low Low Erythropoietin level High Inappropriate low for degree of anemia Inflammatory markers Negative Raised Hepcidin Low Raised
Perinatal Care Manual 4th Ed, 2020
Investigate for ID
Iron Therapy - Oral
Iron Therapy – Intravenous (IV) • Uncertain absorption • Painful injection • Staining of injection site
Thalassemia • Most common genetic disorder, 4.5% of world population • 4-6% of Malaysians are carriers • Sabah has the highest carrier rate of Beta Thalassemia (more than national rate)
Beta Thalassemia Impaired production of beta globin chains 1.Beta thalassemia minor/trait/silent carrier 2.Beta thalassemia intermedia 3.Beta thalassemia major
Beta Thalassemia Minor / Trait • During pregnancy, women with beta thalassemia trait sometimes exhibit a tendency to develop a more profound "physiologic" anemia of pregnancy than normal mothers, and may require transfusion • However, pregnancy outcomes are generally favorable
Beta Thal Minor vs IDA Beta Thal Minor Iron deficiency anemia PBF •Microcytosis •Hypochromia •Target /tear drop cells +++ + +++ + +++ + RBC count +++ + Hematocrit >30% MCV <75 fL >80 fL RDW Normal Increased
Beta Thalassemia Intermedia • Usually do not require transfusion during at least the first few years of life, and are able to survive into the second decade of life without chronic hypertransfusion therapy • While they may not require transfusion therapy at all, or as often as those with thalassemia major, have increased absorption of dietary iron, and may ultimately develop signs and symptoms of iron overload • They may also suffer from the complications of chronic hypoxia, such as high cardiac output, increased pulmonary vascular resistance, pulmonary hypertension and heart failure
Beta Thalassemia Major • Characteristic clinical features • Transfusion dependant • Iron overload
Alpha Thalassemia Impaired production of alpha globin chains 1. Alpha thalassemia minima: loss of one of the four alpha globin genes 2. Alpha thalassemia minor: loss of two of the four alpha globin genes 3. Hemoglobin H disease: loss of three of the four alpha globin loci 4. Hydrops fetalis with Hb Barts:loss of all four alpha globin loci
Alpha Thalassemia Minima • essentially asymptomatic • Adult patients are not anemic, their red cells are not microcytic, and their hemoglobin electrophoresis pattern is normal. The complete blood count and peripheral smear are usually normal, although very slight hypochromia and microcytosis might be evident by microscopic examination • The diagnosis of alpha thalassemia minima can be reliably made only via DNA analysis
Alpha Thalassemia Minor • Resembles mild beta thalassemia trait • Adult patients may have mild anemia, their red cells are hypochromic and microcytic and target cells are present • Hemoglobin electrophoresis pattern is normal • The diagnosis can be reliably made only via DNA analysis
Alpha Thalassemia: HbH Disease • HbH disease exhibit all of the stigmata of chronic hemolytic anemia, including hepatosplenomegaly, indirect hyperbilirubinemia, elevated LDH, reduced haptoglobin, leg ulcers, and premature biliary tract disease • Resembles patients with beta thalassemia intermedia. Even though transfusion support is not necessary early in life, splenectomy or institution of transfusion support during the second or third decade of life is often necessary • Iron overload due to increased iron absorption is also a significant issue
Thalassemia: Prenatal screening/diagnosis PCR of fetal DNA extracted from: 1. Amniotic cells via amniocentesis 2. Trophoblast via chorionic villi sampling (CVS) 3. Erythroblast from cordocentesis
Thalassemia in Pregnancy
General Mx Outline • If pt is a carrier, screen partner • If both are carrier – counsel & offer prenatal diagnosis • Cascade screening if not done yet (including other children yet to be screened) • Thal carrier pt – can be under KK / O&G follow up (monitor Hb) • Thal major pt – under MFM / O&G combined follow up with Hematologist (iron overload complications) • Iron therapy only for Thal carrier with concurrent IDA • Keep Hb >7
Bring-to-Work Message • ID / IDA is important modifiable factor– early investigation, Rx of ID before progressing to IDA • Consider screening ferritin / TSat beside Hb – diagnose ID / IDA • EOD Oral Iron for prophylaxis, daily oral iron for Rx. • Resort to IV Iron if patient does not respond to oral hematinics (Treat mother & prevent anemia in fetus / newborn) • Postpartum anemia – use IV Iron for faster response • Consider ESA for ACD / AI (consultation with Hematologist)
Bring-to-Work Message • Anemia is a risk factor for PPH • Addressing Maternal Anemia –to Protect Mothers & Newborns • PBM prevents / reduces / manages PPH • Start providing IV Iron in KK setting • Thal Carrier couple – screen partner, prenatal diagnosis if indicated
THANK YOU carolkklim@yahoo.com

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Anemia in Pregnancy .ppt

  • 1.
    Anemia in Pregnancy Dr.Carol Lim Maternal Fetal Medicine Consultant Ampang Hospital
  • 2.
    Anemia in Pregnancy WHO& CDC recommendation: Trimester-specific cutoffs for anemia • 1st trimester <110g/L (8% prevalence) • 2nd trimester <105g/L (12% prevalence) • 3rd trimester <110g/L (34% prevalence) Women at higher risk of IDA due to increased iron requirements. WHO recommendations on antenatal care for a positive pregnancy experience, 2016 Postpartum <100g/L Male Hb13; Non Pregnant Female Hb12
  • 3.
    Anemia – a GlobalPublic Health Problem! IDA – among the most important contributing factors to the global burden of diseases
  • 4.
  • 5.
    ID & IDAin Pregnant Msian Women
  • 6.
    Maternal Anemia (antenatal anemia+ postpartum anemia) Women at risk include: • Pre-existing anemia • Grandmultipara • Poor spacing • Multiple pregnancy • Obesity • Poor socio-economic status • following Postpartum hemorrhage
  • 7.
    Risk factors forAnemia = Risk factors for PPH Anemia itself is a risk factor for PPH Anemia is also a risk factor for VTE
  • 8.
  • 9.
    This lecture willcover… • Iron Deficiency Anemia (IDA) • Anemia of Chronic Disease (ACD) / Anemia of Inflammation (AI) • Thalassemia Main focus – IDA, the most common type of anemia
  • 10.
    ID / IDAis detrimental for mothers Camaschella C. Iron Deficiency Anemia. N Engl J Med 2015;372:1832-43. Breymann 2015 Iron deficiency anaemia in pregnancy; 18. Ponikowski, 2014 JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019 • Inability to tolerate blood loss • Risk of severe maternal morbidity or mortality after PPH • Increased risk in heart failure • Reduced milk production • Shorter lactation periods • Perinatal Mental Health • Impaired physical function • Reduced quality of life
  • 11.
    ID / IDAis detrimental for children Camaschella C. Iron Deficiency Anemia. N Engl J Med 2015;372:1832-43. Breymann 2015 Iron deficiency anaemia in pregnancy; 18. Ponikowski, 2014 JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019 • Perinatal mortality, SB • Premature birth and low birth weight • IUGR / FGR, SGA • ID or IDA in newborn • Long-term adverse effects on brain development and behavior: ASD, ADHD, ID Maternal hemoglobin concentrations across pregnancy and maternal and child health: a systematic review and meta-analysis. Ann.N.Y.Acad.Sci.1450(2019)47-68
  • 12.
    ASD: autism spectrumdisorder ADHD: attention-deficit/hyperactivity disorder ID: intellectual disability JAMA Psychiatry. Dol:10.1001/jamapsychiatry.2019.2309 Published online September 18, 2019
  • 13.
    Back to basic– ANEMIA… • Addressing Maternal Anemia –to protect Mothers & Newborns Bread & Butter !!
  • 14.
    Iron Requirement duringPregnancy Ref: 1. Nils Milman. Prepartum anaemia: prevention and treatment. Ann Hematol (2008) 87:949–959. 2. Nils Milman. Iron and pregnancy—a delicate balance. Ann Hematol (2006) 85: 559–565
  • 15.
    Serum Ferritin • Ferritin– most frequently used test for evaluating iron stores • Various cutoffs eg 70ug/L or 100ug/L have been used • <30 ug/L : low iron status (92% sen, 98% spec for absolute ID with or without anemia) • <15 ug/L : iron depletion • <12 ug/L : associated with IDA • Ferritin – acute-phase reactant, levels affected by inflammation
  • 16.
    Transferrin Saturation (TSat) •TSat – iron available for tissue • Low TSat – insufficient iron supply to support normal erythropoiesis • If TSat <20% & Ferritin >100 – Functional ID (Iron Sequestration) eg anemia of chronic disease (ACD) / anemia of inflammation (AI) Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017
  • 17.
    Ferritin >100 ng/mL plusTSAT >20% Definitions Ferritin 30-100 ng/mL plus TSAT >20% Low Iron Stores Ferritin <100 ng/mL plus TSAT <20% Ferritin <30 ng/mL Absolute ID Ferritin >100 ng/mL plus TSAT <20% Iron Sequestration (functional ID) Iron Replete Munoz et al, Blood Transfus. 2017 Sep;15(5):422-437. Defining Iron Deficiency ID accounts for 75% of non- physiologic anemia during pregnancy.
  • 18.
    Non-Anemic Iron Deficiency(NAID) • Even in the absence of anemia, ID has negative impact for both mother & neonate:  Mother: cognitive ability, physical performance, PPH, transfusion, etc  Neonate: low APGAR, PTB, behavioral problems, etc • Hb not suitable to assess iron status, esp when there is various degree of hemodilution (ID on functional level) • Ferritin provides info on capacity of body iron reserves (ID on cellular level) • Iron deficiency is often seen in first trimester
  • 19.
    Non-Anemic Iron Deficiency(NAID) • “Mild anemia” (Hb 11-12 or 13) – a misnomer • ID already advanced by the time anemia is detected. • IV iron replacement for NAID-associated fatigue (runners - *blood doping) • How about post-blood donation iron replacement? Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017 Hb concentrations for the diagnosis of Anemia & Assessment of Severity. WHO 2011
  • 20.
    Non-Anemic Iron Deficiency(NAID) • Cancer, inflammatory bowel disease – NAID may induce 20 thrombocytosis (>350)  independent risk factor for thromboembolic event. • ID a preventable cause of thrombosis, especially in the elderly. • Obst VTE – adjusted odds ratio (aOR): o Anemia: 1.6-2.6 o >Parity 1: 1.5-2.4 o >35yr: 1.2-1.4 Current misconceptions in diagnosis & management of iron deficeincy. Munoz, Blood Transfus 2017 Reducing the Risk of VTE during Pregnancy & the Puerperium, RCOG 2015
  • 21.
    Iron Homeostasis inPregnancy Plasma volume expansion 50% RBC mass 25% i.e. Plasma Volume Expansion > RBC mass  Hb   Hematocrit  Nadir at end of T2 till beginning of T3  Normal physiologic anemia of pregnancy Hemodilution PVE > RBC
  • 22.
    Severe antenatal anemia(<60g/L) Has been associated with: • Abnormal fetal oxygenation (20 to impaired O2 transport to uterus / placenta / fetus) -FGR • Non-reassuring fetal heart rate patterns • Reduced amniotic fluid volume • Fetal cerebral vasodilatation • Fetal mortality Patient Blood Management in Obstetrics: Management of Anemia & Hematinic Deficiencies in Pregnancy and in the post-partum period: NATA consensus statement Transfusion Medicine, 2018, 28,22-39 Sifakis & Pharmakides, 2000 Carles et al., 2003
  • 23.
    High Hb Concentrations •Failure for plasma volume expansion (PVE) • Chronic renal impairment (eg lupus nephritis, advanced diabetes) Reduced plasma volume expansion Hemoconcentration • NOT indicator for good iron status • Increased blood viscosity low uterine arterial blood flow, reduced placental perfusion Reduced O2 delivery to the fetus Emerging understanding and measurement of plasma volume expansion in pregnancy Am J Clin Nutr 2017;106(Suppl):1620S-5S
  • 24.
    U-shaped relation U-shaped relationbetween maternal Hb conc and adverse pregnancy outcomes. Hb Hb* * Hb >13 Maternal Hemoglobin Levels during Pregnancy and their Associations with Birth Weight of Neonates Iranian Journal of Pediatric Hematology Oncology Vol5.No4 Hb concentrations & adverse birth outcome in South Asia pregnant women: findings from a Prospective Maternal & Neonatal Health Registry. Reproductive Health 2020 IUGR, SGA, PTB, LBW, SB, Preeclampsia* Hb Adverse Pregnancy outcome
  • 25.
    How to protectthe mother & baby? Prevent / treat antenatal anemia, to avoid: • Neonatal outcomes (LBW, SGA, PTB, FGR, etc), & • Maternal outcomes (PPH, maternal sepsis, etc) ...by practicing Patient Blood Management
  • 26.
    The Urgent Needto implement Patient Blood Management, WHO Policy Brief, 2021
  • 27.
    The Urgent Needto implement Patient Blood Management, WHO Policy Brief, 2021
  • 28.
    3 Pillars ofPBM in Obstetrics 1. Optimise haemopoiesis 2. Minimise blood loss and bleeding 3. Harness and optimise tolerance of anaemia •Screen for red cell antibodies •Screen for & treat anemia (Hb, Ferritin) •Iron – oral, parenteral •?ESA •Pharmocologic/ haemostatic agents •Uterine tamponade •Cell salvage •MTP •Iron – oral, parenteral
  • 29.
    1st Pillar ofPBM: optimise haemopoiesis • Improve diagnosis & treatment of ID / IDA • Resort to Parenteral /IV Iron, if oral hematinics are not increasing Hb as targeted • Good response: Hb < 10g/L in 2w or <20g/L in 4w Optimise red cell mass
  • 30.
    Anemia during Pregnancy •Routine screening for Iron Deficiency? (Hb, Ferritin, KIV TSat) • Replenish iron stores before one progresses to anemia
  • 31.
    Oral Iron Therapy(Malaysia) Iron Product Content per tablet (mg) Elemental Iron per tablet (mg) Absorbed Iron per tablet (mg) Ferrous Fumarate 200 60 7.5 Zincofer (FF) 350 115 14.4 Iberet Folic (FS) 525 105 13.1 Maltofer + FA (IPC) - 100 12.5 Obimin (FF) 90 30 3.8 10- 15% Daily vs EOD ?
  • 32.
    Hepcidin in IronMetabolism • Major regulator of systemic iron bioavailability • Produced by liver • Synthesis of Hepcidin is regulated by 3 signals – 1. Need for increased erythropoiesis:  hepcidin 2. Increased plasma iron & iron store: hepcidin 3. Inflammation: hepcidin • Hepcidin blocks iron absorption & prevent iron overload  iron sequestration • Hepcidin effect lasts for 48hr (hence EOD dosing)
  • 33.
    Ferroportin & Hepcidin •Ferroportin – transmembrane iron transporter found in duodenal enterocytes and macrophages • Hepcidin degrades ferroportin  preventing enteral iron absorption and transport of iron from liver
  • 35.
    • EOD Ironis associated with increased absorption • Second trimester – still reasonable to continue oral iron if Hb is at least 10g/L • For Hb<10 or in third trimester – IV iron should be given to ensure adequate iron gets to the fetus. Michael Auerbach, MD
  • 36.
    Every Other Day(EOD) Dosing Alternate days dosing may: -maximize fractional iron absorption, -increase dosage efficacy -reduce GI exposure to unabsorbed iron -improve tolerance of iron supplements Blood, 22 October 2015. Volume 126, Number 17
  • 37.
    Regimes for OralHematinics Iron Deficiency (Prophylaxis) 1/1 EOD Iron Deficiency Anemia (Treatment) 1/1 Daily (Maltofer may go as high as 2-3 Tablet OD) NO Split dosing NO Double / triple hematinics NO Weekly intermittent dosing Prophylaxis 30-60mg Iron / day Treatment 120-180mg Iron / day
  • 38.
    Fehr J etal. Praxis 2009;98:1445–1451; Gordeuk VR et al. Am J Clin Nutr 1987;46:1029–1034; Aapro M et al. Ann Oncol 2012;23:1954–1962 Iron Replacement Therapy Iron preparations in Malaysia Oral iron* Intravenous iron Iron(III) carbohydrate complexes • Iron sucrose (Venofer) • Iron dextran (Cosmofer) • Iron isomaltoside (Monofer) Iron(III) complexes: • Iron(III)-hydroxide polymaltose complex Iron(II) compounds: • Ferrous sulfate • Ferrous fumarate • Ferrous gluconate • Others Do not administer via IM Iron (uncertain absorption, painful, stain) Parenteral Iron is contraindicated in 1st trimester
  • 39.
    “The feared anaphylacticreaction is extremely rare and occurs mainly with the high-molecular-weight ID (iron dextran)”* “Thus, it seems that the newer formulations are safer to administer and no test dose is required” 103 trials included 10,390 patients. IS= Iron sucrose; FCM= Ferric carboxymaltose; FG= Ferric gluconate Avni et al. Mayo Clin Proc. 2015 Jan;90(1):12-23. Risks of reactions with IV Iron *IMFERON (high molecular weight Iron Dextran) is not available in Msian market since ?2005
  • 40.
    Reactions (1) Infusion Reaction/ Fishbane Reactions • Self-limited; 1:100-250 administrations • Due to labile free iron • Acute chest / back tightness, myalgia, flushing, diarrhea, swelling of hand / feet • No BP, wheezing or stridor • Minor reactions; • hypersensitivity • Re-challenge with lower infusion rate or switch to other IV iron formulation • If urticaria - Antihistamine &/or Corticosteroid
  • 41.
    Reactions (2) Hypotension • Hypersensitivity,or vascular reaction • Self-limited • Related to: Rapidity of administration Labile iron content • If hypotension - lie horizontally with leg elevation, IV fluid load (500ml), antihistamine, corticosteroid
  • 42.
    Reactions (3) Anaphylaxis • IgEmediated • CARPA (complement activation related pseudoallergy) • Related to rapidity of administration • Exceedingly rare (<1:250,000 administrations) • With CVS & RS manifestations • Rx: epinephrine, fluid, corticosteroid • Antihistamine may delay efficacy of epinephrine *Delayed reaction – can’t be predicted by test dose Gomez-Ramirez et al. Prevention & Management of Acute Reactions to IV Iron in Surgical Patients. Blood Transfus 2019
  • 43.
    Various IV IronPreparations LMWID IS FDI/IIM FCM Molecular wt (Daltons) 103000 43300 1000 150000 Structure Iron core, CHO shell Iron core, CHO shell Linear, non- branched CHO Iron core, CHO shell Labile iron(%) 2% 3.5% 1% 0.5% Stability High Medium High High Maximum single dose 20mg/kg 7mg/kg (200mg boluses or 500mg TDI) 20mg/kg (1000-2000mg) 15mg/kg (1000mg) Max admin time 4-6hr 10-30min (bolus) 15-30min 15min Issues Longer time Lower dose Higher dose, Faster Hb Faster Hb Name of Iron Product Cosmofer Venofer Monofer Ferinject LMWID: Low Molecular Weight Iron Dextran (Cosmofer®); IS: Iron Sucrose (Venofer®) FDI/IIM: Ferric Derisomaltose / Iron Isomaltoside (Monofer®) FCM: Ferric Carboxymaltose (Ferinject®)
  • 44.
    IV iron isindicated with or without trial of oral iron IV iron may be indicated when rapid increase of Hb and iron stores are required Camaschella C. Iron-Deficiency Anemia. N Engl J Med. 2015 Jul 30;373(5):485-6.
  • 45.
    …early IV Irontherapy is recommended in postoperative period if iron is necessary. Where possible, it should be administered using a single high- dose preparation for the repletion of iron stores
  • 47.
    When should weconsider IV Iron? • When not responding to oral hematinics • When there is an urgency to top up Hb (before surgery / delivery) • When massive bleeding is anticipated. • Surgery / O&G: Pre-operatively / Antenatally Post-operatively / Postnatally – after PPH has been controlled & patient stabilized Intraoperatively
  • 48.
    Iron Requirement Calculation •Oxygen Delivery (Iron for Hb) ~200-250gm Iron per g/dL Hb Target Hb >13g/dL • Oxygen Utilization (Iron for store & other non-haem functions) 1g/L Ferritin = ~8mg stored iron Target serum Ferritin >100g/L Munoz etal. Blood Transfus 2017; 15:422-37 Ganzoni formula Total iron dose = BW in kg x Hb deficit x 2.4 + Iron stores in mg *IV Iron is CONTRAINDICATED in 1st Trimester
  • 49.
    How about ESA? Anemiaof Chronic Disease (ACD) / Anemia of Inflammation (AI) – 2nd most common (after IDA) Typically: NcNc (may progress to Mc); Serum iron; TSat; reticulocytes; Ferritin may be  (acute phase protein); Hepcidin • Impaired EPO production • Blunted marrow erythroid response to EPO • Iron-restricted erythropoiesis • Pool of EPO-responsive cells Hypoproliferative anemia / functional ID
  • 50.
    IDA vs ACD IronDeficiency Anemia Anemia of Chronic Disease Hb Low Low MCV Low Normal (low in 30% pts) Ferritin Low High Serum Iron Low Low TIBC High / Normal Normal / Low TSat Low Low Erythropoietin level High Inappropriate low for degree of anemia Inflammatory markers Negative Raised Hepcidin Low Raised
  • 51.
  • 52.
  • 53.
  • 54.
    Iron Therapy –Intravenous (IV) • Uncertain absorption • Painful injection • Staining of injection site
  • 57.
    Thalassemia • Most commongenetic disorder, 4.5% of world population • 4-6% of Malaysians are carriers • Sabah has the highest carrier rate of Beta Thalassemia (more than national rate)
  • 58.
    Beta Thalassemia Impaired productionof beta globin chains 1.Beta thalassemia minor/trait/silent carrier 2.Beta thalassemia intermedia 3.Beta thalassemia major
  • 59.
    Beta Thalassemia Minor/ Trait • During pregnancy, women with beta thalassemia trait sometimes exhibit a tendency to develop a more profound "physiologic" anemia of pregnancy than normal mothers, and may require transfusion • However, pregnancy outcomes are generally favorable
  • 60.
    Beta Thal Minorvs IDA Beta Thal Minor Iron deficiency anemia PBF •Microcytosis •Hypochromia •Target /tear drop cells +++ + +++ + +++ + RBC count +++ + Hematocrit >30% MCV <75 fL >80 fL RDW Normal Increased
  • 61.
    Beta Thalassemia Intermedia •Usually do not require transfusion during at least the first few years of life, and are able to survive into the second decade of life without chronic hypertransfusion therapy • While they may not require transfusion therapy at all, or as often as those with thalassemia major, have increased absorption of dietary iron, and may ultimately develop signs and symptoms of iron overload • They may also suffer from the complications of chronic hypoxia, such as high cardiac output, increased pulmonary vascular resistance, pulmonary hypertension and heart failure
  • 62.
    Beta Thalassemia Major •Characteristic clinical features • Transfusion dependant • Iron overload
  • 63.
    Alpha Thalassemia Impaired productionof alpha globin chains 1. Alpha thalassemia minima: loss of one of the four alpha globin genes 2. Alpha thalassemia minor: loss of two of the four alpha globin genes 3. Hemoglobin H disease: loss of three of the four alpha globin loci 4. Hydrops fetalis with Hb Barts:loss of all four alpha globin loci
  • 64.
    Alpha Thalassemia Minima •essentially asymptomatic • Adult patients are not anemic, their red cells are not microcytic, and their hemoglobin electrophoresis pattern is normal. The complete blood count and peripheral smear are usually normal, although very slight hypochromia and microcytosis might be evident by microscopic examination • The diagnosis of alpha thalassemia minima can be reliably made only via DNA analysis
  • 65.
    Alpha Thalassemia Minor •Resembles mild beta thalassemia trait • Adult patients may have mild anemia, their red cells are hypochromic and microcytic and target cells are present • Hemoglobin electrophoresis pattern is normal • The diagnosis can be reliably made only via DNA analysis
  • 66.
    Alpha Thalassemia: HbHDisease • HbH disease exhibit all of the stigmata of chronic hemolytic anemia, including hepatosplenomegaly, indirect hyperbilirubinemia, elevated LDH, reduced haptoglobin, leg ulcers, and premature biliary tract disease • Resembles patients with beta thalassemia intermedia. Even though transfusion support is not necessary early in life, splenectomy or institution of transfusion support during the second or third decade of life is often necessary • Iron overload due to increased iron absorption is also a significant issue
  • 69.
    Thalassemia: Prenatal screening/diagnosis PCRof fetal DNA extracted from: 1. Amniotic cells via amniocentesis 2. Trophoblast via chorionic villi sampling (CVS) 3. Erythroblast from cordocentesis
  • 70.
  • 71.
    General Mx Outline •If pt is a carrier, screen partner • If both are carrier – counsel & offer prenatal diagnosis • Cascade screening if not done yet (including other children yet to be screened) • Thal carrier pt – can be under KK / O&G follow up (monitor Hb) • Thal major pt – under MFM / O&G combined follow up with Hematologist (iron overload complications) • Iron therapy only for Thal carrier with concurrent IDA • Keep Hb >7
  • 72.
    Bring-to-Work Message • ID/ IDA is important modifiable factor– early investigation, Rx of ID before progressing to IDA • Consider screening ferritin / TSat beside Hb – diagnose ID / IDA • EOD Oral Iron for prophylaxis, daily oral iron for Rx. • Resort to IV Iron if patient does not respond to oral hematinics (Treat mother & prevent anemia in fetus / newborn) • Postpartum anemia – use IV Iron for faster response • Consider ESA for ACD / AI (consultation with Hematologist)
  • 73.
    Bring-to-Work Message • Anemiais a risk factor for PPH • Addressing Maternal Anemia –to Protect Mothers & Newborns • PBM prevents / reduces / manages PPH • Start providing IV Iron in KK setting • Thal Carrier couple – screen partner, prenatal diagnosis if indicated
  • 74.