eMedicine Specialties > Emergency Medicine > Hematology & Oncology

Anemia, Acute: Treatment & Medication

Author: Daniel Kahsai, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Downey Regional Medical Center; Consulting Staff Per Diem, Department of Emergency Medicine, Kaiser Permanente-Bellflower
Coauthor(s): Craig N van Roekens, MD, MBA, MPH, FACEP, Director of Emergency Services, Vassar Brothers Medical Center
Contributor Information and Disclosures

Updated: Oct 22, 2009

Treatment

Prehospital Care

  • Initial care of patients includes supplemental oxygen, intravenous fluid resuscitation, applying direct pressure to any external hemorrhage, fracture splinting, and rapid transport.
  • Recent prehospital studies suggest that trauma patients should receive minimal fluid resuscitation. This remains unproven and controversial.
  • The military antishock treatment (MAST) suit is occasionally used in the prehospital setting for trauma patients with pelvis and lower extremity injuries. It is contraindicated in patients with pulmonary edema or a ruptured diaphragm. It is also contraindicated in pregnant patients.

Emergency Department Care

Evaluate ABCs and immediately treat any life-threatening conditions. Crystalloid is the initial fluid of choice.

  • Acute anemia due to blood loss
    • Monitor with pulse oximetry, cardiac monitor, and a sphygmomanometer.
    • Provide supplemental oxygen via nasal cannula or face mask.
    • Establish 2 large-bore intravenous lines and rapidly infuse 1-2 L of crystalloid while monitoring the patient carefully for signs and symptoms of iatrogenic congestive heart failure.
    • Consider type O or type-specific blood transfusion for patients who remain hypotensive after 2 L of crystalloid infusion for young healthy patients with a hematocrit level below 20 or for elderly patients with a hematocrit level below 30.
    • Vasopressors are relatively contraindicated in the treatment of hypovolemic shock.
    • Obtain fresh frozen plasma (FFP), coagulation factors, and platelets, if indicated.
    • Patients with hemophilia should have samples of the deficient factors sent for measurement.
    • Pregnant trauma patients in whom there is concern for feto-maternal blood transfer should be given Rh-immunoglobulin (RhoGAM) if they are Rh negative.
    • Once the patient is stabilized, begin specific measures to treat the underlying cause of bleeding.
  • Acute anemia due to hemoglobinopathy
    • The decision to transfuse depends on the rate of fall of the hemoglobin and the patient's clinical condition.
    • In sickle cell anemia, correction of simple anemia alone by transfusion is adequate. Hydroxyurea8 can be used to reduce sickle cell crisis. Recently, gene therapy and bone marrow transplant6 are considered potentially curative. However, these treatment modalities are not widely available.
    • For severe anemia (levels <5 g/dL), full-volume transfusion may lead to volume overload. These patients should be transfused cautiously, often with concurrent use of diuretics.
    • If the clinical picture is urgent, exchange transfusion, especially in vasoocclusive crisis, is the treatment of choice. This rapidly reduces the number of sickle cells while lowering blood viscosity.
    • In patients with aplastic crisis, a decrease in reticulocyte count indicates the need for transfusion.
  • Acute anemia due to acquired platelet disorder
    • Patients with thrombocytopenia who have clinical evidence of bleeding should receive a platelet transfusion.
    • Patients with platelet counts lower than 10,000/µL are at risk for spontaneous cerebral hemorrhage and require a prophylactic transfusion.
    • The preferred treatment for TTP and HUS is large-volume plasmapheresis with FFP replacement. Many patients require daily plasmapheresis. Increasing platelet count, decreasing lactate dehydrogenase (LDH), and decreasing red blood cell fragments indicate a positive response to treatment. Most patients also receive high-dose glucocorticoids as well as antiplatelet agents (aspirin). Patients who do not respond to plasmapheresis can be treated with splenectomy or immunosuppression.
    • Idiopathic thrombocytopenia purpura (ITP) is rarely treated with transfusion because the transfused platelets are destroyed rapidly. In stable patients, the initial treatment is supportive care. Patients with active bleeding are treated with high-dose immunoglobulin and steroids. Platelet transfusion is also indicated if active bleeding is present. Patients with chronic ITP who are not responsive to steroids may be candidates for immunosuppressive therapy, intravenous IgG, danazol, or splenectomy.
  • Acute anemia due to congenital bleeding disorder
    • Treat von Willebrand disease with cryoprecipitate. Each unit of cryoprecipitate will raise the VWF by 3%.
    • Treat hemophilia A with factor VIII concentrate.
    • Treat hemophilia B with factor IX concentrate. Dosage is based on the site of the bleeding.
  • Acute anemia due to disseminated intravascular coagulation
    • The role of heparin in treating DIC remains controversial. If heparin is used, it should be in conjunction with platelet transfusion.
    • Maintain platelet count above 50,000/µL. Use FFP and cryoprecipitate to correct coagulation factor and fibrinogen deficiency.
  • Blood products
    • Whole blood contains RBCs, platelets, and coagulation factors; however, it is rarely used as a treatment option.
    • Packed red blood cells (PRBCs) are the remaining components of whole blood after the plasma and platelets are removed. One unit of PRBCs is the product of 1 unit of whole blood and has a volume of 250-300 mL. Each unit of PRBCs is expected to raise the hematocrit level by 3 points.
    • Each unit of platelets contains 50 mL of plasma and has normal amounts of fibrinogen and coagulation factors. Some decrease in factors V and VII is noted compared with whole blood. Each unit of platelets raises the platelet count by approximately 10,000/µL. The usual adult dose is 1 U/10 kg.
    • FFP is the medium that suspends RBCs and platelets and contains all the coagulation factors. The coagulation factors are diluted. Patients with factor V and XI deficiency and those with coagulopathies due to liver disease are the best candidates, as most of the other coagulation factors are now available in concentrated forms.
    • Cryoprecipitate is derived from the precipitate collected from thawed FFP. It contains fibrinogen, factor VIII, VWF, and factor XIII. It is ideal for treatment of mild hemophilia A and conditions that lead to afibrinogenemia.
  • All blood products have the potential to transmit bacterial and viral diseases.
    • The rate of hepatitis B infection is estimated to be 1 infection per 200,000 units.
    • Prevalence of hepatitis C infection ranges from 1 infection per 2000 to 1 infection per 6000 units. This is a recent revision from the 1992 Centers for Disease Control and Prevention (CDC) estimate of 3.2 infections per 100,000 transfusions.
    • Other complications of transfusion therapy include volume overload, hypothermia, allergic reactions, anaphylaxis, DIC, hypocalcemia, and graft-versus-host disease.
    • In individuals who do not consent to blood transfusion (eg, Jehovah's Witnesses), crystalloid solutions in the acute phase and erythropoietin and iron supplements in the subacute phase may be beneficial. Currently, exciting research is underway to evaluate the effectiveness of inorganic compounds such as dodecafluoropentane emulsion (DDFPe) as a blood substitute. DDFPe is an inorganic fluorocarbon compound that expands at body temperature and has a strong affinity for oxygen.9 PolyHeme10 is an oxygen-carrying blood substitute made from human blood. While PolyHeme may not be appropriate for patients who are Jehovah's Witnesses, it is an excellent option for those willing to receive human-blood–derived products. PolyHeme does not require crossmatching, has a shelf life of more than 12 months, and has virtually no risk of transmitting infections.

Consultations

  • For admitted patients, surgical evaluation or hematologic consult may be indicated.
  • If a patient is expected to be discharged, notify the primary care physician to ensure adequate follow-up care.

Medication

Therapeutic approaches to treat anemia include blood and blood products, immunotherapies, hormonal/nutritional therapies, and adjunctive therapies.

The goal of therapy in acute anemia is to restore the hemodynamics of the vascular systems and to replace lost RBCs. To achieve this, the practitioner may use mineral and vitamin supplements, blood transfusions, vasopressors, histamine (H2) antagonists, and glucocorticosteroids.

Blood and blood products

Correction of acute anemia often requires blood and/or blood products. With significant ongoing hemorrhage or hemolysis, transfusion of blood alone is insufficient. Nonetheless, providing timely transfusion to restore hemoglobin to safe levels can prevent major complications of acute anemia.


Packed red blood cells (PRBCs)

Used preferentially to whole blood since they limit volume, immune, and storage complications. PRBCs have 80% less plasma, are less immunogenic, and can be stored about 40 d (versus 35 d for whole blood). PRBCs are obtained after centrifugation of whole blood. Leukocyte-poor PRBCs are used in patients who are transplant candidates/recipients or in those with prior febrile transfusion reactions. Washed or frozen PRBCs are used in individuals with hypersensitivity transfusion reactions.

Adult

1 U of PRBCs should raise hemoglobin level by 1 g/dL or hematocrit level by 3%
Rate of transfusion is dependent upon rate of hemorrhage or hemolysis and patient's initial condition; when massive rapid transfusions are anticipated, a blood warmer and use of fresh frozen plasma and platelets (1 U of FFP and 1 U of platelets for every 3-4 U of PRBCs) should be considered to prevent DIC and dilutional thrombocytopenia; massive transfusions can predispose patients to hypocalcemia and hyperkalemia, partly due to binding agents; with less immediately life-threatening hemorrhage, blood can be administered IV over 3-4 h, premedicating with acetaminophen and diphenhydramine to prevent febrile transfusion reactions

Pediatric

Whole blood preferred; IV boluses should be given as 10 mL/kg; if PRBCs are used, boluses should be 5 mL/kg
Total dose should be based on estimated blood volume loss; multiply estimated percent loss by total blood volumes: 100 mL/kg for premature, 90 mL/kg for term infant, and 80 mL/kg for children

Refusal of blood product by a competent adult or a legal guardian of a minor can be very difficult; immediate consultations with hospital ethical and legal staff mandated

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Volume overload may occur (monitoring urinary output and pulmonary status and judicious use of diuretics to treat important)
Major ABO incompatibility may occur and result in a hemolytic reaction (life-threatening complication that requires immediate cessation of transfusion); hypersensitivity reactions can occur, ranging from minor pruritus and rash to major bronchospasm, airway edema, and shock (reactions require cessation of transfusion); fever can occur, but does not require aborting transfusion when is only reaction observed
Massive transfusions can result in dilutional thrombocytopenia and coagulopathy, as well as hypothermia and hypocalcemia
Finally, transfusions can result in transmission of infectious diseases (eg, hepatitis B and C, HIV)


Fresh frozen plasma

FFP contains coagulation factors as well as protein C and protein S. Uses include treatment of coagulopathies, TTP, and reversal of Coumadin. FFP does not transmit infections.

Adult

1 U increases coagulation factor by approximately 2%

Pediatric

Administer as in adults

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Patients with IgA deficiency should receive FFP from donors who are IgA deficient to decrease risk of anaphylaxis


Cryoprecipitate

Used for the treatment of Von Willebrand disease. Contains fibrinogen, factor VIII, and von Willebrand factor. Can be used in lieu of factor VIII concentrate if latter is unavailable.

Adult

1 U will increase VWF by 3%

Pediatric

Administer as in adults

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Risk of contracting transfusion-related infections is a concern


Platelets

Patients who are thrombocytopenic and have clinical evidence of bleeding should receive a platelet transfusion. Patients with platelet counts of less than 10,000/mcL are at risk for spontaneous cerebral hemorrhage and require a prophylactic transfusion.
Preferred treatment for TTP and hemolytic-uremic syndrome is large-volume plasmapheresis with FFP replacement. ITP is rarely treated with transfusion as the transfused platelets are destroyed rapidly. In stable patients, initial treatment is with prednisone. High-dose immunoglobulin and splenectomy are very effective treatments.

Adult

1 U/10 kg IV; 1 U increases platelet count 5000-10,000/mcL

Pediatric

Administer as in adults

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Patients with multiple previous transfusions may undergo alloimmunization; risk exists of contracting transfusion-related infections


Factor IX concentrate

Hemophilia B is treated with factor IX concentrate. Recombinant factor IX currently is undergoing clinical trials (current treatment is FFP or prothrombin-rich plasma concentrate).

Adult

Dosage is based on site and amount of bleeding

Pediatric

Not established

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use of prothrombin-rich plasma concentrate may cause activation of the coagulation system; recombinant factor IX is not expected to be procoagulant


Recombinant factor VIII

Used to treat hemophilia A.

Adult

1 U raises factor VIII by 2% per kg when given IV bid
Uncomplicated soft tissue bleeding or mild hemarthrosis: Raise level by 15-20%
Severe hemarthrosis or retroperitoneal bleed: Raise level by 25-50%
CNS or life-threatening bleeding: Raise level by 50% or more

Pediatric

Administer as in adults

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Recombinant factor VII does not transmit infections

Vasopressors

These drugs decrease portal circulation pressure by diminishing blood flow due to vasoconstriction. Major indication is variceal bleeding.


Vasopressin (Pitressin)

Causes vasoconstriction of vascular smooth muscles and increases water permeability and reabsorption in the collecting tubules. Decreases portal pressure in patients with portal hypertension.

Adult

20 U initially, then 0.1-0.5 U/min IV for variceal esophageal bleeding; if bleeding stops, continue at same dose for 12 h, then taper off over 24-48 h

Pediatric

0.002-0.005 U/kg/min IV initially; titrate as needed to maximum 0.01 U/kg/min; if bleeding stops, continue at same dose for 12 h, then taper off over 24-48 h

Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects

Documented hypersensitivity; coronary artery disease

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia


Somatostatin (Zecnil)

Diminishes blood flow to portal system due to vasoconstriction, thus decreasing variceal bleeding. Has similar effects to vasopressin but does not cause coronary vasoconstriction.

Adult

250 mcg IV bolus followed by 250 mcg IV drip

Pediatric

Not established

Epinephrine, demeclocycline, and thyroid hormone supplementation may decrease effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate or cause gallbladder disease; alters balance in counterregulatory hormones and may cause hypothyroidism and cardiac conduction defects

Histamine (H2) antagonists

These agents produce blockade of H2 receptors.


Cimetidine (Tagamet)

The primary indication is to reduce symptoms and accelerate healing of gastric ulcers. In the acutely bleeding patient, they have limited benefit.

Adult

300 mg PO qid, or 800 mg hs, or 400 mg bid
50 mg/h IV/IM

Pediatric

Not established; suggested dose is 20-40 mg/kg/d PO/IV/IM in equally divided doses q4h

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur

Glucocorticoids

These agents are used to treat idiopathic and acquired autoimmune hemolytic anemias.


Prednisone (Deltasone, Sterapred, Meticorten)

Glucocorticoids inhibit phagocytosis of antibody-covered platelets. Treatment of ITP during pregnancy is conservative unless condition is severe. For severe cases, use lowest dose of glucocorticoids. In neonate, if platelet count drops below 50,000-75,000 platelets/µL, consider prednisone and exchange transfusions and immune globulin.

Adult

Autoimmune hemolytic anemias: 0.05-2 mg/kg/d PO divided bid/qid

Pediatric

4-5 mg/m2/d PO or 1-2 mg/kg/d PO

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Vitamin

Vitamin K deficiency causes elevation of prothrombin time and is commonly seen in patients with liver disease.


Vitamin K

Decrease in levels of vitamin-K–dependent factors (II, VII, IX, X, protein C, protein S) can lead to bleeding. Vitamin K is also used to treat hemorrhagic disease of the newborn, Coumadin-induced bleeding, and hypothrombinemia from other causes (eg, antibiotic, aspirin).

Adult

2.5-10 mg IM/SC

Pediatric

Hemorrhagic disease of the new born
Prophylaxis: 0.5-1 mg IM/SC
Treatment: 1 mg IM/SC

Effects of warfarin, sodium, and dicumarol are antagonized by vitamin K

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

IV infusion of vitamin K should be avoided, as cases of fatalities have been reported; rapid infusion may result in flushing and a feeling of constriction in chest

More on Anemia, Acute

Overview: Anemia, Acute
Differential Diagnoses & Workup: Anemia, Acute
Treatment & Medication: Anemia, Acute
Follow-up: Anemia, Acute
Multimedia: Anemia, Acute
References
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References

  1. Veng-Pedersen P, Chapel S, Schmidt RL, Al-Huniti NH, Cook RT, Widness JA, et al. An integrated pharmacodynamic analysis of erythropoietin, reticulocyte, and hemoglobin responses in acute anemia. Pharm Res. Nov 2002;19(11):1630-5. [Medline].

  2. Adamson JW, Longo DL. Anemia and polycythemia. In: Harrison's Principles of Internal Medicine. Vol 1. 15th ed. New York, New York: McGraw-Hill; 2001:348-354.

  3. Laks J, Pilon RN, Klovekorn WP, Anderson W, MacCallum JR, O'Connor NE. Acute hemodilution: its effect of hemodynamics and oxygen transport in anesthetized man. Ann Surg. Jul 1974;180(1):103-9. [Medline].

  4. Valenzuela JE, Schubert T, Fogel MR, et al. A multicenter, randomized, double-blind trial of somatostatin in the management of acute hemorrhage from esophageal varices. Hepatology. Dec 1989;10(6):958-61. [Medline].

  5. Gregg SG, Mazzeo RS, Budinger TF, Brooks GA. Acute anemia increases lactate production and decreases clearance during exercise. J Appl Physiol. Aug 1989;67(2):756-64. [Medline].

  6. Krishnamurti L, Bunn HF, Williams AM, Tolar J. Hematopoietic cell transplantation for hemoglobinopathies. Curr Probl Pediatr Adolesc Health Care. Jan 2008;38(1):6-18. [Medline].

  7. Blanchette V, Carcao M. Intravenous immunoglobulin G and anti-D as therapeutic interventions in immune thrombocytopenic purpura. Transfus Sci. Sep 1998;19(3):279-88. [Medline].

  8. Koren A, Segal-Kupershmit D, Zalman L, et al. Effect of hydroxyurea in sickle cell anemia: a clinical trial in children and teenagers with severe sickle cell anemia and sickle cell beta-thalassemia. Pediatr Hematol Oncol. May-Jun 1999;16(3):221-32. [Medline].

  9. Alayash AI, D'Agnillo F, Buehler PW. First-generation blood substitutes: what have we learned? Biochemical and physiological perspectives. Expert Opin Biol Ther. May 2007;7(5):665-75. [Medline].

  10. Jahr JS, Varma N. PolyHeme. Northfield Laboratories. IDrugs. May 2004;7(5):478-82. [Medline].

  11. Cone JB, Wallace BH, Caldwell FT, Smith SD, Searcey R. Beneficial effects of a hypertonic solution for resuscitation in the presence of acute hemorrhage. Am J Surg. Dec 1987;154(6):585-8. [Medline].

  12. Fortune JB, Feustel PJ, Saifi J, Stratton HH, Newell JC, Shah DM. Influence of hematocrit on cardiopulmonary function after acute hemorrhage. J Trauma. Mar 1987;27(3):243-9. [Medline].

  13. Gould SA, Rosen AL, Sehgal LR, et al. Fluosol-DA as a red-cell substitute in acute anemia. N Engl J Med. Jun 26 1986;314(26):1653-6. [Medline].

  14. Jan KM, Chien S. Effect of hematocrit variations on coronary hemodynamics and oxygen utilization. Am J Physiol. Jul 1977;233(1):H106-13. [Medline].

  15. Koskolou MD, Roach RC, Calbet JA, Radegran G, Saltin B. Cardiovascular responses to dynamic exercise with acute anemia in humans. Am J Physiol. Oct 1997;273(4 Pt 2):H1787-93. [Medline]. [Full Text].

  16. Lundgren CE, Bergoe GW, Tyssebotn I. The theory and application of intravascular microbubbles as an ultra-effective means of transporting oxygen and other gases. Undersea Hyperb Med. 2004;31(1):105-6. [Medline].

  17. Mintz P, ed. Transfusion medicine. Hematology Oncology Clinics. 1994;8(6):1045-1104.

  18. Sassetti B, Vizcarguenaga MI, Zanaro NL, et al. Hemolytic uremic syndrome in children: platelet aggregation and membrane glycoproteins. J Pediatr Hematol Oncol. Mar-Apr 1999;21(2):123-8. [Medline].

  19. Tintinalli J, Ruiz E, Krome RL. Emergency Medicine: A Comprehensive Study Guide. 4th ed. New York, New York: McGraw-Hill; 1996:1-7,447-53.

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Further Reading

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Keywords

anemia, acute anemia, treatment, symptoms, causes, hemorrhage, hemorrhagic shock, ectopic pregnancy, esophageal varices, sickle cell anemia, sickle cell disease, hemophilia, Cooley anemia, thalassemia, hemolytic-uremic syndrome, idiopathic thrombocytopenic purpura, ITP, thrombotic thrombocytopenic purpura, TTP, chronic anemia, blood loss, iron deficiency anemia, hemoglobinopathy, congenital coagulopathy, autoimmune hemolytic anemia, acquired platelet disorder, disseminated intravascular coagulation, DIC

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Contributor Information and Disclosures

Author

Daniel Kahsai, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Downey Regional Medical Center; Consulting Staff Per Diem, Department of Emergency Medicine, Kaiser Permanente-Bellflower
Daniel Kahsai, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Craig N van Roekens, MD, MBA, MPH, FACEP, Director of Emergency Services, Vassar Brothers Medical Center
Craig N van Roekens, MD, MBA, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Physician Executives, American Medical Association, Massachusetts Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Samuel M Keim, MD, Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine
Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jeffrey L Arnold, MD, FACEP, Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center
Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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