Anemias - H/O Flashcards
Anemia Intro
- Hematopoesis: the process of making of formed elements in the blood (90% water, 10% solute)
- Occurs in the bone marrow after birth, liver & spleen in utero
- RBCs provide O2 to the tissues
- Core causes of anemia
1. Increased destruction of red blood cells (RBCs)
2. Decreased production
3. Blood loss
Anemia=level hb (WHO)
- Males < 13 g/dL
- Females <12 g/dL
Microcytic
Iron Deficiency
Thalassemias
Anemia of Chronic Disease (ACD)
Normocytic
ACD
Early Fe deficiency
Renal failure
Macrocytic
B12
Folic acid
Liver disease
Hypothyroid
Hypochromic
(RBC color)
Iron deficiency
Low hgb amount in each cell
Low MCH (mean cell hgb; average content of hgb per RBC)
Low MCHC (mean cell hgb concentration, average volume of hgb in a given volume of packed RBCs)
Symptoms/Signs of Anemia
Symptoms
- Asymptomatic
- Weakness
- Headache, dizziness
- Palpitations
- Exercise Intolerance due to SOB
- Dyspnea
- Claudication
Signs
- Pallor (skin, oral mucosa, conjunctiva, palms)
- Jaundice (hemolytic)
- Tachycardia, tachypnea
- Edema
- Ecchymosis, petechiae: Platelet dysfunction
- ACUTE VS CHRONIC
- Acute: more severe sxs
- Chronic: more gradual onset and therefore less severe sxs
Iron Deficiency
Pathophysiology
- Microcytic, hypochromic anemia
- Iron helps make hgb functional
- Max absorption in duodenum, decreased in proximal jejunum
Epidemiology: Most common type of anemia US (CDC 2013)
- 9% of the overall US population, MC Females & children <2
- Children 1-2 yo: 14%
- Females 12-49 yo: 9%
Risk Factors
-Early childhood, adolescence, pregnancy, menses/blood loss, renal disease, impaired absorption, chronic alcoholism, poor nutrition
Iron Deficiency - dx
Etiology
- Blood loss (e.g. menorrhagia, gastric ulcers)
- increased demand (growth, pregnancy)
- decreased iron absorption, decreased iron intake, celiac disease, gastric bypass or morbid obesity
Presentation
- Pica: craving for non-edible substances (e.g clay, dirt, ice, paper products, or starch)
- Severe chronic deficiency: Plummer-Vinson Syndrome
- Brittle nails, cheilosis, smooth tongue, esophageal webs
Diagnosis
- Microcytic (MCV < 75), Hypochromic on smear
- Hgb < 13 males, <12 in females,
- Labs: CBC, serum iron, ferritin
Iron deficiency labs
- decreased Hgb (Normal: 12-16 Fem, 13-17.5 g/dL- Male)
- decreased Hematocrit (35-50%)
- decreased MCV –Microcytic (80-100fL)
- decreased MCHC- Hypochromic (31-37%)
- decreased Ferritin (15-150 ng/mL) - a protein that helps store iron
- increased TIBC -Total iron binding capacity (250-400 mcg/dL), TIBC: Indirect measure of free transferrin (no Fe), Transferrin: Protein that carries iron in the blood
- decreased Total serum iron (50-150 mcg/dL) –Amount of iron in blood
- Reticulocyte count (0.5-1.5 nl)
- Stool sample looking for occult blood
Fe Deficiency Management
-Differential Dx: Thalassemia, ACD
Management of Anemia
- Find underlying cause (Fe will not work if not Fe def)
- Iron vs dietary supplementation
- Recheck hgb q 4 weeks until normal, sooner is not as useful unless worried of worsening hgb
Diet
-RDA 8mg men; 18mg women
-Heme iron in meat, fish, poultry is absorbed 3x that of
non-heme iron in veggies, supplements
-Iron hearty food: see above, broccoli, raw tofu, Total cereal, lentils
Fe Replacement
-Ferrous gluconate : 325mg tid
-Fe sulfate 325 (65mg elemental iron), Fe fumarate 325 (107), Fe gluconate 325 (39)
-200mg of elemental iron daily in 2-3 divided doses/day
-If intolerable due to AE, decrease dose by half
-If tolerating-should see increase by 2-4 g/dL q 3-4 weeks
-Parenteral Iron-via IV for those unable
to tolerate PO Fe or with chronic profound losses
-Continue Fe therapy x 3-6 months after normal hgb/hct to replete tissue stores
-Acute bleed-one month
Fe deficiency - education
-Adherence is important to stress given likelihood for AE
-Peds: delay of motor or mental function
-Pregnancy: risk for small or preterm baby with risk of health problems
-Teens: memory, mental function decreased
Iron supplementation:
-Empty stomach with vitamin C. Avoid taking with coffee, tea. Food decreases absorption by 50%
-Breast fed babies—Fe fortified cereal after 6 m.o.
Potential AE of Fe:
-Nausea, GI upset, stools may be black and tarry, constipation
B12 Deficiency Anemia
Pathophysiology
- Cobalamin=Vitamin B12, Macrocytic (MCV > 100)
- Water soluble, stored in the liver
- Maintains CNS function, several biochemical functions, and needed for DNA synthesis
- Max absorption in stomach and terminal ileum
- Humans cannot make B12-MUST be consumed regularly
- Comes from animal proteins: beef, poultry, fish, eggs, & dairy
- Unfortified plant-based foods do not contain vitamin B12
Epidemiology
- MC in older adults >51 yo (1/31 individuals)
- Atrophic gastritis and pernicious anemia MC in elderly
Risk Factors
- Cohn’s, gastric bypass surgery, pernicious anemia, vegan, strict vegetarian diet
- Pernicious anemia : Chronic atrophic gastritis– Decreased production of IF (Intrinsic factor), Autoimmune– Antibodies attack gastric cells -> impaired production of IF that is critical for absorption of vitamin B12
Etiology
-Inadequate intake, malabsorption (IF deficiency, PPIs, H2 blockers), Inadequate utilization
B12 deficiency - signs, sxs, dx
Presentation/symptoms
- Glossitis, dysphagia
- Neurologic: Peripheral neuropathy, paresthesias, irritability, dementia, depression, ataxia, and weakness
- If neuro sxs present > 6 months decreases chance of reversibility
Diagnosis
- Labs: Serum cobalamin, CBC, peripheral smear
- Low serum B12 (nl 100-900), +/- low hb
- Peripheral smear: macrocytosis with hypersegmented polymorphonuclear leukocytes
- May have falsely normal serum B12 in presence of liver disease, myeloproliferative disorders, and renal insufficiency—f/u on sxs!
B12 Deficiency - Management
-Patient education, generally well tolerated, normalizing hgb within one week
-Recheck CBC and B12 level after 1-2 months after tx start and again 3-6 months to ensure stable levels
pElderly with malabsorption-need lifelong tx!
-Iron demands may decrease due to erythropoiesis
PO Vitamin B12
- Preferred for mild, moderate anemia, & maintenance
- 1-2 mg (1,000-2,000 mcg) PO daily
- 1% of PO doses of vitamin absorbed in small intestine
Parenteral (IM)
- 1000 mcg daily x 1 week, then 1000mcg q week x 1 month, then 1000 mcg q month
- Requires office visit. Consider if severe B12 deficiency or neuro sxs, vomiting, diarrhea, bowel resection
Nasal Spray
- Absorption erratic, limited data, $$$
B12 Deficiency Management - education/diet
- Generally supplementation is well tolerated
- Possible AE (rare) : hypokalemia, hyperuricemia, sodium retention, rebound thrombocytosis
- If needing lifelong tx due to malabsorption, Prep the pt for this!
Diet
- RDA B12: 2.4 micrograms daily for adults
- Fish, poultry, beef, dairy
B12 Must Knows!
1) Vitamin B12 deficiencies occur in adults 51 years of age or older at a frequency of 1 (3.2%) in every 31 persons, and manifest as serum vitamin B12 levels below the cutpoint of 200 pg/mL.
2) All patients with unexplained hematologic or neurologic signs or symptoms should be evaluated for a vitamin B12 deficiency. If found, the cause should be determined.
3) Today, megaloblastic anemia is most likely due to vitamin B12 deficiency and needs prompt evaluation. In the United States, folic acid fortification has made folate deficient megaloblastic (macrocytic) anemia a very rare condition.
4) Although the body’s ability to absorb naturally occurring vitamin B12 decreases with age, most people can readily use the synthetic form of cobalamin.
5) All people 51 years of age and older should get most of their daily vitamin B12 through supplements containing vitamin B12 or foods fortified with vitamin B12.
Folic Acid Deficiency Anemia
Pathophysiology: Macrocytic
- Water soluble and heat labile
- Found in green leafy vegetables, fruits
- Folic acid= synthetic form of folate
- Absorbed in proximal 3rd of small of intestine
- Necessary for production of nucleic acids, proteins, amino acids as well as DNA synthesis
Epidemiology
< 1% of US population -down from 10-12%, Why??
-1998 FDA mandated fortification in cereal products
Risk Factors
- Alcoholism, malnutrition
- Alcohol directly interferes with erythropoiesis as well as decreased absorption of folic acid
Etiology
- Decreased dietary intake, Increased usage (hemolytic anemia), Decreased absorption
- Medications: Folate antagonists: methotrexate, trimethoprim, triamterene
Folic Acid Deficiency Anemia - sxs, dx
Presentation
-No neurologic sxs, general sxs of anemia, fatigue, HA
Diagnosis
-Macrocytic anemia, decreased serum folate
Management
- Symptomatic improvement is within 1-2 weeks
- Hgb should normalize within 2 months
FA Deficiency Management
Medication Management
-PO folic acid 1-5mg PO daily x 4 months
Patient education
- Should be educated on dietary needs
- Neural tube defects in pregnancy
- Breastfeeding mothers should continue PNV while breastfeeding
- 3 month prior to pregnancy take PNV or folic acid to build stores
Diet
-RDA is 4 mg daily, 6 mg in pregnancy
Anemia of Chronic Diseases (ACD)
Pathophysiology
- Infectious, inflammatory, or neoplastic disease that is more than 6-8 weeks
- During chronic disease, RBC lifespan is shortened
- May be release of cytokines during illness that inhibit RBC production
Risk Factors and potential etiologies
- Any chronic disease that puts physiologic stress on the body
- Infections: Osteomyelitis, HIV, hepatitis
- Autoimmune disease: SLE, RA
Anemia of Chronic Diseases (ACD) - sxs, dx
Presentation
- Symptoms of anemia
- May be combined with sxs of underlying disease
Diagnosis
- Rule out other treatable forms of anemia
- Labs, studies, focused exam based on pt’s sxs that may lead to underlying disease dx
Management
- Will improve with improvement of underlying disease
- Rarely severe enough to need transfusion
Anemia of Chronic Diseases (ACD) - education, diet
Patient education
- Counsel on underlying disease state and its relation to anemia sxs
- Can be frustrating in chronic state of fatigue-offer psychosocial support and resources if medically limited
Diet
-Encourage general balanced diet with fruits, vegetables, and lean meats
Hemoglobinopathies
- Multiple types—all result in abnormal hgb
- Acquired (toxins, methemoglobinemia) or inherited, structural, thalassemias, hereditary persistence of fetal hgb
- Over 1,000 different mutations in globin changes
- 300,000 children born each year with severe inherited hemoglobinopathies worldwide
Hemolytic Anemia
- Anemia from destruction of RBCs
- May be inherited or acquired
Classic features
- Jaundice
- Splenomegaly (primary site of hemolysis)
- Colored urine
Labs
- Reticulocytosis (usually > 2.5%)
- Hgb is normal to profoundly low
- Hyperbilirubinemia (mostly unconjugated)
- Reduced/absent haptoglobin
- The liver destroys haptoglobin & free hgb complex
- LDH may increased
Hemoglobin Types
- Hemoglobin F (fetal): Found in fetuses and newborns: Replaced by Hb A shortly after birth - this is Normal
- Hemoglobin A (adult):Normal Hb in adults - this is Normal
- Hemoglobin A2: Normal hb found in adults (smaller quants)- this is Normal
- Hemoglobin S: Present in Sickle Cell Disease (SCD)
- Hemoglobin C: Hexagonal crystals-Doesn’t carry O2 well
- Hemoglobin D: May be present in SCD
- Hemoglobin E: Frequent in India and SE Asia (60%): Homozygotes have minimal anemia, sxs
- Hemoglobin H (heavy): Present in certain thalassemia
Sickle Cell Anemia
- A condition of hemoglobin that results in a “sickle” or “crescent” shape when deoxygenated
- Painful episodes known as “sickle cell crisis” occur as a result of vaso-occlusion in microcirculation from sickle shaped hemoglobin
- Sickle cell disease has potential for serious complications, damage to organs, premature death, and psychosocial implications
- Individuals with SCD should always have a hematologist on their care team
Sickle Cell Types
- Sickle Cell Trait
- Hb A and S (HbAS), Heterozygous
- Benign carrier state without hematologic disturbance - HbSC
- Symptomatic condition to a lesser extent than HbSS - Sickle Cell Anemia or Sickle Cell Disease (SCD)
- HbSS, Homozygous
- Most severe
Sickle Cell Disease
Pathophysiology
- Autosomal recessive, (HbSS)
- Abnormal hgb S due to mutation in beta globin chain—when deoxygenated may sickle
Epidemiology(CDC 2012)
- SCD affects an estimated 90,000-100,000 in US
- 3 million have Sickle cell trait
- 1/500 black and AA births, 1/36,000 Hispanic-American
Risk Factors
- African decent (MC), Middle East, Mediterranean
- Worse prognosis: less HbF, those with increased episodes
Sickle Cell Disease - sxs
Presentation
- Newborn screening
- Generally sickle cell episode (SC crisis) prompts investigation & dx
Course
- Acute episode (SC crisis): Peak of episodes between 19-39 yo, may start after 2 yo
- Is the first sx in 25% of patients
- Increased mortality rate associated with higher frequency of episodes in those older than 19 yo
SCD - dx
-Hemoglobin electrophoresis
Newborn screen (hemoglobinopathies)-done @ 24-48 h old
- Two confirmation tests done if positive findings
- In MN includes: HbSS, HbSC, S-Beta thalassemia, variant hemoglobinopathies
SCD Management
- Referral to hematologist upon dx
- If positive newborn screen, should be seen by Heme by 8 weeks of age
- Hgb electrophoresis to confirm at 12 months old
- F/u q 3-6 months with SC specialist
- Reticulocyte count and CBC done at first visit
- Routine childhood vaccines including those for High Risk pts!!
SCD Management - tx
-Infants with hgb SS require penicillin prophylaxis for pneumococcal sepsis
InfantsPenVK dose62.5 mg PO bid
- 3 months of age: Increase to 125mg PO bid
- 3 years: Increase to 250mg PO bid
- Stop at age 5 : Or continue for 5 years post splenectomy
Splenectomy indicated if splenic sequestration occurs (recurrence likely) –can be life threatening
- RBC trapped in spleen causing enlargement, drop in hgb, and potentially hypovolemic shock
- Dx: Hgb drops min 2 g/dL, increased retic count, & splenomegaly. May have rapid breathing, abd pain, tachy
- 1st occurrence MC between 3 months and 5 years of age
Management of Sickle Cell Crisis
Painful episodes of vasoocclusion with potential organ complications that may lead to disability and even death
- May last 2 hours to 2 weeks
- Rehydration (PO or IV)
- Pain control
Chronic pain may develop as a result of tissue injury related to acute episode vs neuropathic pain
- Care team approach recommended
- Likely to have multiple specialists involved due to effects on other organs
- Greater than 3 episodes per year correlated with lower life expectancy
SCD Pain
Non pharmacologic
-Music, reading, distraction, stretching muscles, massage, warm bath/shower
- Significant increase in water!
- Stepwise pain control: Tylenol, ibuprofen, tramadol, and oxycodone
- Severe pain- Seek urgent medical help
SCD - meds
Medication Management
- Hydroxyurea-disease modifying therapy: Once daily dosing, Monitoring: CBC q 2 wks, titrated q 12 wks, Pg cat D
- Increases HbF, decreased acute episodes, and hemolysis
- AE: Rash, HA, neutropenia, thrombocytopenia, severe anemia
Potential complications of SCD
- Average life expectancy is 45, 50% live over 50 yo
- MCC death in adults is CVI, ACS
- MCC children is PNA
Acute Chest Syndrome
-Leading cause of death for patients with SCD
Diagnosis
- Temp >38.5 C, respiratory sxs, new density on x-ray
- 55% present with CP, new pulmonary infiltrate, Chest pain, and respiratory sxs (tachypnea, wheezing, cough)
- May have pain in arms, legs, ribs, sternal pain
- Adults more likely to require mechanical ventilation, prolonged hospital stay, and greater risk of death compared to children (UTD, 2012)
SCD - education
- Educate family on when to seek prompt medical care (within 4 h of sx onset)
- Temp > 101.5, respiratory sxs, newly palpable spleen, severe abdominal pain, jaundice, neurologic sxs, pallor, fatigue, priapism (> 4 h), uncontrolled pain at home
- More likely to experience muscle breakdown & heatstroke than others not afflicted with SCD
- Rest, hydration, avoid excessive heat during athletics
- Adherence to meds, AE of meds, potential long term risks, teratogenic effects
- Early recognition of pain signs in kids (decreased activity, appetite)
- Pain management at home (Non pharm and pharm)
- Coordination with teachers and support structure to respond to episodes
Sickle Cell Long Term
Children
- Growth failure
- Splenic dysfunction (lifelong)
- Prone to more serious infections
- Splenic infarction
Teens
- Neurodevelopment and MS delay
- Psychosocial difficulties
Adults
- Chronic pain
- Depression
- Potential for chemical dependency
Thalassemia
-A hemoglobinopathy that is an inherited autosomal recessive genetic defect that results in inability to produce normal hgb
Types
- Alpha thalassemia minor
- Alpha thalassemia major-incompatible w/ life outside womb
- Beta thalassemia minor/intermedia
- Beta thalassemia major-Most severe (Cooley’s anemia)
Pathophysiology
- Defective globin chain synthesis
- Microcytic, normal smear vs nucleated red cells (accelerated erythropoiesis) vs target cells, schistocytes
- Hemolysis occurs due to intracellular inclusions of unpaired globin chains that remain from deleted globin chains
Thalassemia - etiology
Epidemiology (CDC, 2011)
- Most commonly inherited genetic disorder in the world
- Beta thalassemia is MC
- Cooley’s: 1,000 affected in US
Risk Factors
-Asian, Chinese, Mediterranean, African, African American ethnicity
Etiology
- Alpha MINOR: Genetic mutation of alpha globin
- Alpha MAJOR: Results in stillbirth
- Beta MINOR: Genetic deletion of 1-2 beta globin chains
- Beta INTERMEDIA: Mild homozygous or combined heterozygous mutations. Dependent upon severity of globin chain production
- Beta MAJOR (Cooley’s): genetic defect inherited from both parents
Thalassemia - Presentation
- Alpha Minor: Asymptomatic to Mild anemia: Carrier status is important given Hydrops fetalis risk
- Beta Minor: Asymptomatic to Mild anemia
- Beta Intermedia: Between mild and severe-usually do not need regular transfusions
Beta Major (Cooley’s anemia)
- Severe anemia that develops in first year of life
- Bone deformities (bone marrow expansion), jaundice, growth delay/FTT, splenomegaly
- Early death due to HF, avg 20-30 yo
Thalassemia - dx and prognosis
Diagnosis
-Hemoglobin electrophoresis
Prognosis
-Asymptomatic course vs mild anemia
Beta Thalassemia Major
-Chronic hemolysis due to excess unpaired chains that result from mutations
-Heart failure due to chronically increased CO to maintain perfusion to tissues
-Splenomegaly
-Gallstones, gout, jaundice
Thalassemia - management
-Mild alpha or beta thalassemia: No treatment required
Severe beta thalassemia (major)
- Referral to hematologist
- May need blood transfusions, Folic acid, avoid excess Fe (liver)
- May consider stem cell transplant, splenectomy
- Deferoxamine, deferiprone and deferasirox-chelate iron in serum
- Used in transfusion dependent patients, improves life expectancy
MONITORING —Beta Thalassemia Major (Hematologist)
Kids
-Q 3 months LFTs, serum ferritin, sxs, QOL
-Q 6 months growth, development, eyes, heart, endocrine, liver U/S
Adults
-Same as above, bone density scan, liver dz monitoring-iron overload
Thalassemia - Support/Education
Diet
-Increased Fe absorption in intestine due to ineffective erythropoiesis
Patient Education
- Disease, chronicity, adherence to tx, quality of life goals, education for family, available support, flu vaccine q year
- May consider genetic counseling prior to becoming pregnant
- Severe dz: Avoid EtOH, iron supplementation
Glucose-6-Phosphate Dehydrogenase Deficiency - Pathophysiology
- X-linked recessive enzyme deficiency that results in a hemolytic anemia when oxidative stress occurs on RBC
- The Pentose Shunt is the only source of NADPH to RBC
- Very important in glutathione metabolism which protects RBC from oxidative damage
- Hgb becomes rigid due to oxidative stress resulting in hemolysis in spleen- also some intravascular hemolysis
- Heinz bodies and bite cells develop resulting in episodes of hemolysis
- May be asymptomatic until exposure to trigger which causes hemolytic episode
G6PD Smear
Heinz Bodies: Denatured hgb Precipitate
Bite Cells: Spleen’s process of removing the membrane with hgb inclusions
G6PD - epidemiology
Epidemiology
- 400 million people worldwide-MC inherited enzyme deficiency
- MC Mediterranean descent
- Males mostly affected
- Females with lyonization (inactivation of x-chromosome in various cells)
Risk Factors
-Originating from Mediterranean, India, SE Asia, Central South America, and Africa
Etiology
- X-linked Deficiency of an enzyme called glucose–6-phosphate dehydrogenase
- Males generally more symptomatic than females
G6PD - sxs
Presentation
- Most often asymptomatic
- Prolonged jaundice, peaks 2nd-3rd day-rarely present at birth
- Most serious complication—Kernicterus
- Adulthood-hemolytic episodes may occur if triggered: Present with jaundice, pallor, dark urine, splenomegaly, back pain
Diagnosis
- Measure G6PD levels in RBCs as prompted by Hx & PE-Referral to Heme
- Note: May be falsely elevated after hemolytic episode due to reticulocytosis– Wait several weeks
Differential dx
-Hemolytic anemia, SCD, Hereditary Spherocytosis
G6PD - labs
Labs
- CBC with diff, platelet count, reticulocyte count if jaundiced, peripheral smear
- Hemolysis labs: Bilirubin, Direct coombs, G6PD tests, Plasma free hb, urine hb, urine hemosiderin
- KNOW What your ordering-otherwise refer!
- Generally retic count > 2.5% in hemolytic anemia
- May consider ferritin, hb electrophoresis if microcytic
Diet
-Avoid Fava Beans
G6PD - Triggers
- Glutathione whose production is facilitated by G6PD and maintained by NADPH, prevents oxidative damage to hb
- Hemolysis is precipitated when hb is oxidized by offending agent
Drug Induced
- Antimalarials (primaquine),
- sulfonamides (sulfamethoxazole), sulfones (dapsone)
- Antibiotics with sulfa or nitrofurantoin
Infections (MC)
-Hepatitis, PNA, systemic viral or bacterial infections
Foods
-Fava Beans (contain beta-glycosides and oxidants)
G6PD - management
Management
-Fluids, treat any infections, eliminate offending agent, supportive cares, rarely require transfusion
Patient Education
- Symptom recognition of hemolysis-when to seek help
- Foods and meds to avoid, annual flu shot
- May consider genetic counseling if pregnancy planning
Hereditary Spherocytosis
Pathophysiology
- Heterogeneous recessive or dominant mutation
- 1 of 6 genes that result in this protein defect of the cellular membrane causing instability in cytoskeleton
Epidemiology
- Approximately 1/5,000 affected
- MC form of hemolytic anemia
Risk Factors
-Eastern European, affected parent
Etiology
- Hemolytic anemia from a defect that leads to cytoskeletal instability -> sphere shaped RBC
- Spleen is a core site of destruction of RBC
Hereditary Spherocytosis - sxs, dx
Presentation
- Common features: Anemia, jaundice, splenomegaly
- May be asymptomatic-> mild -> life threatening
- Majority: 60-75% of cases have Moderate HS
- 20-30% Mild, 5% Severe
Diagnosis
- Osmotic Fragility Test (Test of choice)
- Confirmatory test after 12 mo of age when hgb matures
Labs
- Beware of pseudohyperkalemia
- CBC, retic count, bilirubin, LDH
Hereditary Spherocytosis - Management
- Acute hemolytic episodes : Supportive, fluids, Some may require transfusions
- Routine monitoring of hgb at wcc through 6 mo: Recheck hgb with viral illness, increased fatigue, pallor
- Splenectomy -> if chronic transfusion requirement due to anemia or growth failure: Goal of waiting until after age 4-6 yo due to risk of sepsis
- Appropriate vaccines for kids: (MCV, PCV, HIB, flu…)
- Cholecystectomy case by case : Children less likely to have bilirubin stones
