DDAVP is the appropriate initial therapy for this patient with von Willebrand's disease, Type I presenting with gastrointestinal bleeding. DDAVP causes release of von Willebrand factor and factor VIII from endothelial cells and is effective for type I von Willebrand's disease.
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
ITP is immune mediated acquired hemorrhagic disorder of adults and children characterized by transient or persistent thrombocytopenia and depending upon severity of thrombocytopenia, increased risk of bleeding
Epidemiology of Acute Kidney Injury (AKI)
By Dr. Usama Ragab
Lecturer of Internal Medicine
I have discussed the epidemiology, etiology of acute kidney injury
GEMC- Hemostasis: Platelet and Coagulation Disorders- Resident TrainingOpen.Michigan
This is a lecture by Dr. Joseph Hartmann from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Sickle Cell Disease: Special Considerations in Pediatrics- Resident Tra...Open.Michigan
This is a lecture by Hannah Smith, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
ITP is immune mediated acquired hemorrhagic disorder of adults and children characterized by transient or persistent thrombocytopenia and depending upon severity of thrombocytopenia, increased risk of bleeding
Epidemiology of Acute Kidney Injury (AKI)
By Dr. Usama Ragab
Lecturer of Internal Medicine
I have discussed the epidemiology, etiology of acute kidney injury
GEMC- Hemostasis: Platelet and Coagulation Disorders- Resident TrainingOpen.Michigan
This is a lecture by Dr. Joseph Hartmann from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Sickle Cell Disease: Special Considerations in Pediatrics- Resident Tra...Open.Michigan
This is a lecture by Hannah Smith, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
01.09.09(b): Complications of TransfusionOpen.Michigan
Slideshow is from the University of Michigan Medical
School's M2 Hematology / Oncology sequence
View additional course materials on Open.Michigan: openmi.ch/med-M2Hematology
GEMC - Communicable and Infectious Disease Emergencies - for NursesOpen.Michigan
This is a lecture by Katherine A Perry from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Dr. Joseph Hartmann from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Slideshow is from the University of Michigan Medical School's M2 Endocrine sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Endo
Slideshow is from the University of Michigan Medical
School's M2 Hematology / Oncology sequence
View additional course materials on Open.Michigan: openmi.ch/med-M2Hematology
Slideshow is from the University of Michigan Medical School's M2 Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Resp
Slideshow is from the University of Michigan Medical
School's M1 Immunology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Immunology
This is a lecture by Dr. Jessica Holly from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Abdominal Compartment Syndrome- for ResidentsOpen.Michigan
This is a lecture by Alison Haddock from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Katherine A Perry from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: Recognition and Management of Shock: Resident TrainingOpen.Michigan
This is a lecture by Dr. Jim Holliman from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Jim Holliman, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Alterations in Body Temperature: The Adult Patient with a Fever- Reside...Open.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Rapid Sequence Intubation & Emergency Airway Support in the Pediatric E...Open.Michigan
This is a lecture by Michele Nypaver, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Disorders of the Pleura, Mediastinum, and Chest Wall- Resident TrainingOpen.Michigan
This is a lecture by Andrew Barnosky, DO from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Dental Emergencies and Common Dental Blocks- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Arthritis and Arthrocentesis- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Bursitis, Tendonitis, Fibromyalgia, and RSD- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Right Upper Quadrant Ultrasound- Resident TrainingOpen.Michigan
This is a lecture by Jeff Holmes from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: Nursing Process and Linkage between Theory and PracticeOpen.Michigan
This is a lecture by Jeremy Lapham from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
2014 gemc-nursing-lapham-general survey and patient care managementOpen.Michigan
This is a lecture by Dr. Jeremy Lapham from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: The Role of Radiography in the Initial Evaluation of C-Spine TraumaOpen.Michigan
This is a lecture by Dr. Stephen Hartsell from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Dr. Jim Holliman from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Ghana Grab Bag Pediatric Quiz- Resident TrainingOpen.Michigan
This is a lecture by Hannah Smith, MD and Ruth S. Hwu, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
How to Make a Field invisible in Odoo 17Celine George
It is possible to hide or invisible some fields in odoo. Commonly using “invisible” attribute in the field definition to invisible the fields. This slide will show how to make a field invisible in odoo 17.
Unit 8 - Information and Communication Technology (Paper I).pdfThiyagu K
This slides describes the basic concepts of ICT, basics of Email, Emerging Technology and Digital Initiatives in Education. This presentations aligns with the UGC Paper I syllabus.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
Normal Labour/ Stages of Labour/ Mechanism of LabourWasim Ak
Normal labor is also termed spontaneous labor, defined as the natural physiological process through which the fetus, placenta, and membranes are expelled from the uterus through the birth canal at term (37 to 42 weeks
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
Dive into the world of AI! Experts Jon Hill and Tareq Monaur will guide you through AI's role in enhancing nonprofit websites and basic marketing strategies, making it easy to understand and apply.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
Safalta Digital marketing institute in Noida, provide complete applications that encompass a huge range of virtual advertising and marketing additives, which includes search engine optimization, virtual communication advertising, pay-per-click on marketing, content material advertising, internet analytics, and greater. These university courses are designed for students who possess a comprehensive understanding of virtual marketing strategies and attributes.Safalta Digital Marketing Institute in Noida is a first choice for young individuals or students who are looking to start their careers in the field of digital advertising. The institute gives specialized courses designed and certification.
for beginners, providing thorough training in areas such as SEO, digital communication marketing, and PPC training in Noida. After finishing the program, students receive the certifications recognised by top different universitie, setting a strong foundation for a successful career in digital marketing.
GEMC: Hematologic and Oncologic Emergencies: Resident Training
1. Project: Ghana Emergency Medicine Collaborative, 2013
Document Title: Hematologic and Oncologic Emergencies
Author(s): Joe Lex, MD, FACEP, FAAEM, MAAEM (Temple University)
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2
3. Hematologic and Oncologic
Emergencies
Joe Lex, MD, FACEP, FAAEM, MAAEM
Associate Professor of Emergency Medicine,
Department of Emergency Medicine
Temple University School of Medicine
Philadelphia, PA USA
3
8. Who Needs Blood?
• Most patients uncomfortable if
hemoglobin concentration <7 g/dL
• Patients with heart or pulmonary
disease may need hemoglobin
concentration of ≥10 g/dL to
safeguard adequate oxygen
transport
8
9. What’s Available?
• Packed Red Blood Cells:
centrifuged whole blood with 80%
of plasma removed
• Adult: 1 unit PRBC raises
hemoglobin by 1 gm/dL
• Child: Each mL/kg raises
hemoglobin by 1 gm/dL
9
10. What’s Available?
• Platelets: shelf life ~5 days
– ABO / Rh checks are needed
– “Six pack” raises count by ~30,000
• Fresh Frozen Plasma: ~1 year
– 1 unit / mL of each coagulation factor
– No cellular components
– 10–15 mL / kg (3–4 250 mL bags)
10
11. Special Needs
• All blood products now leukocytedepleted
• Washed cell products in patients
with confirmed deficiency of IgA
• Irradiated cell products used to
prevent graft-versus-host reactions
in immunosuppressed patients
11
17. Febrile Nonhemolytic
• Multiple prior transfusions or
multiparous women
• Fever, chills shortly after start
• Same workup as acute
intravascular hemolytic reaction
• Diagnosis of exclusion
17
18. Febrile Nonhemolytic
• Stop transfusion
• IV fluid through new tubing
• Antipyretic
• Broad-spectrum antibiotic(s)
• Future transfusions: probably
leukoreduced
18
19. Febrile Nonhemolytic
• MILD: if patient responds to
antihistamine, may resume
transfusion
• SEVERE: antihistamine, steroids,
epinephrine, IVF
19
21. Delayed Hemolytic
• Extravascular: antibodies react to
non-ABO antigens
• Antibody-coated RBCs removed
from circulation by liver and spleen
before they are lysed è
extravascular è no
hemoglobinemia, hemoglobinuria
21
22. Delayed Hemolytic
• Typically asymptomatic, may have
fever
• Same workup as acute
intravascular hemolytic reaction
22
23. TRALI
• Transfusion-associated acute lung
injury (TRALI)
• Increasingly recognized event
• Acute respiratory distress, often
associated with fever, noncardiogenic pulmonary edema, and
hypotension
• ~1 in 2000 transfusions
23
24. Transfusion-Associated Graftversus-Host Disease
• Donor lymphocytes recognize
immunocompromised recipient as
foreign, attack host tissues
• Usually 4–10d post transfusion
• Fever, N-V, rash, diarrhea
24
27. Other Complications
• Hypothermia from cold blood
• Volume overload
• Breakdown of citrate into
bicarbonate è metabolic alkalosis
• Citrate / serum calcium complex è
hypocalcemia
27
28. 8. Your patient is profoundly anemic
and you believe she would benefit from
a blood transfusion. In weighing
benefits against risks, you tell her that
the most common adverse effect is:
a. hepatitis C transmission.
b. hepatitis B transmission.
c. human immunodeficiency virus (HIV)
transmission.
d. febrile nonhemolytic reaction.
e. graft versus host reaction.
28
29. 8. Your patient is profoundly anemic
and you believe she would benefit from
a blood transfusion. In weighing
benefits against risks, you tell her that
the most common adverse effect is:
a. hepatitis C transmission.
b. hepatitis B transmission.
c. human immunodeficiency virus (HIV)
transmission.
d. febrile nonhemolytic reaction.
e. graft versus host reaction.
29
30. 8. Most common transfusion adverse
Febrile non-hemolytic reaction is
estimated to occur once for every 200
units transfused. During the
transfusion or within a few hours after
its completion, the patient has a
temperature elevation of at least 1°C
and usually has chills. The usual
cause of this febrile reaction is an
antigen-antibody reaction involving the
plasma, platelets, or white blood cells
that are passively transfused to the
recipient along with the RBCs.
30
31. 8. Most common transfusion adverse
Once a febrile transfusion reaction is
recognized, the current transfusion
should be terminated because there is
not sufficient clinical evidence to
differentiate the simple febrile
nonhemolytic reaction from the more
serious immediate hemolytic reaction.
31
33. Thrombus Formation
• Damaged epithelium è collagen
and tissue factor (TF) exposed to
flowing blood è adherence /
activation of platelets (relies on von
Willebrand Factor [vWF])
33
34. Thrombus Formation
• Tissue factor activates coagulation
cascade è generates thrombin è
converts fibrinogen to fibrin è
forms long, cross-linking strands
that trap platelets and RBCs to
form insoluble clot
34
35. Thrombus Formation
• Thrombin also triggers tissue
plasminogen activator è activates
plasmin
• Plasmin, anti-thrombin III, protein C
& protein S cause fibrinolysis
35
36. Warfarin
• Inhibits Vitamin K-dependent
coagulation factors II, VII, IX, X
– Half-lives 7h (FVII) to 50h (FII)
• Inhibits Vitamin K-dependent
anticoagulants Protein C & S
– Half-lives up to 40h
• 1st few days: may be procoaguable
36
37. Warfarin Overdose: No Bleed
• INR <5: omit next warfarin or ê
dose
• INR 5 – 9: omit next 1-2 doses,
give oral vitamin K (1 – 2.5 mg)
• INR >9: omit warfarin, give oral
vitamin K (2.5 – 5 mg)
• Avoid subcutaneous vitamin K
37
38. Warfarin Overdose: Bleed
• Vitamin K 10 mg slow IV infusion
• Fresh frozen plasma (FFP): start
with 4 – 6 units
– Each ml of FFP contains 1unit of
each coagulation factor
– INR will not correct beyond ~1.5
• Prothrombin complex concentrate
– Rapid, expensive, procoaguability
38
39. Heparin Overdose
• Heparin activates antithrombin III
• Short half-life: stopping drip will
normalize in few hours
• Can reverse with protamine sulfate:
1mg IV for every 100u heparin
unfractionated given in prior 2 hrs
– Works a little for LMWH
39
40. Liver Disease
• Liver synthesizes nearly all clotting
factors
• é PT/INR do not correlate well with
risk of bleeding
• Can reverse with FFP if active
bleeding, require invasive
procedure
• ± vitamin K
40
42. Hemophilias
• Inherited: sex-linked recessive
• Factor VIII: hemophilia A (more
common)
• Factor IX: hemophilia B
• Clinically indistinguishable
• PTT elevated in both
42
43. Clinical Severity
• Related to activity level of factor
<1% - severe à frequent
spontaneous bleeds
1 – 5% - moderate à occasional
spontaneous, lots in trauma
>5% - mild à no spontaneous,
excessive in trauma, surgery
43
44. Presentation
• Vast majority in ED have known
disease, present with complications
• Most common: intramuscular, intraarticular bleeds
44
45. Treatment: Based on Complaint
• Minor bleeding: replace 25%
• Severe bleeding: replace 50%
• Life-threatening: replace 100%
• FVIII: 1U/kg é plasma level ~2%
• FIX: 1U/kg é plasma level ~1%
• In ED, assume baseline plasma
level to be zero
45
46. Replacement Factors
• Can be recombinant or derived
from human plasma
• Hemophilia A: mild to moderate à
start with DDAVP
– Causes release of vWF and FVIII
from endothelial cells
• Arthrocentesis rarely indicated
46
47. 5. The initial dose of factor VIII required
for a 60-kg male with severe
hemophilia A in whom you suspect a
ruptured spleen is:
a. 1,500 units
b. 2,850 units
c. 3,000 units
d. 6,000 units
e. 5,700 units
47
48. 5. The initial dose of factor VIII required
for a 60-kg male with severe
hemophilia A in whom you suspect a
ruptured spleen is:
a. 1,500 units
b. 2,850 units
c. 3,000 units
d. 6,000 units
e. 5,700 units
48
49. 5. …initial dose of factor VIII … severe
hemophilia A … ruptured spleen … 3,000
units.
A 60-kg patient with a life threatening
hemorrhage who requires 100%
correction will need 50 mL/kg = 3000
units of factor VIII
49
50. von Willebrand Disease
• Mucocutaneous bleeding more
likely
• Hemarthrosis less likely
• Humate F®: FVIII-vWF concentrate
• DDAVP only effective in Type 1
50
51. 15. A 38-year-old woman has von
Willebrand’s disease, Type I. She
complains of blood-tinged emesis and
epigastric pain. Her stool tests weakly
positive for blood. Appropriate initial
therapy includes:
a. vitamin K.
b. 6 units platelet concentrate.
c. factor IX concentrate.
d. desmopressin (DDAVP).
e. plasmapheresis.
51
52. 15. A 38-year-old woman has von
Willebrand’s disease, Type I. She
complains of blood-tinged emesis and
epigastric pain. Her stool tests weakly
positive for blood. Appropriate initial
therapy includes:
a. vitamin K.
b. 6 units platelet concentrate.
c. factor IX concentrate.
d. desmopressin (DDAVP).
e. plasmapheresis.
52
53. 15. von Willebrand’s disease, Type I ...
blood-tinged emesis … initial therapy…
Treatment of von Willebrand’s disease
depends on the type of disease that is
present and the severity of bleeding.
Desmopressin (DDAVP) treatment has
benefit in patients with mild to
moderately severe von Willebrand’s
disease, but should be given in
consultation with a hematologist.
Factor VIII (cryoprecipitate) or fresh
frozen plasma may be used in patients
with severe bleeding.
53
54. Disseminated Intravascular
Coagulation (DIC)
• Many potential causes: infection,
malignancy, trauma, OB
• Loss of hemostasis regulatory
mechanisms
• Thrombin overproduced è
promotes clotting
• Fibrin obstructs small vessels
• Consumed platelets and factors
54
55. Presentation
• May be lab abnormalities only: no
overt clinical signs
• Bleeding, organ dysfunction
possible
55
57. Treatment
• Treat underlying cause
• Bleeding-predominant: FFP,
platelets, cryoprecipitate
• Clotting-predominant: heparin
– More common in chronic DIC
– Not appropriate for acute DIC
57
58. 3. The most helpful lab study in diagnosing
disseminated intravascular coagulation is
the:
a. D-dimer, which is elevated.
b. partial thromboplastin time (PTT), which
is decreased.
c. fibrinogen level, which is elevated.
d. prothrombin time, which is prolonged.
e. fibrin degradation products (FDP), which
are diminished.
58
59. 3. The most helpful lab study in diagnosing
disseminated intravascular coagulation is
the:
a. D-dimer, which is elevated.
b. partial thromboplastin time (PTT), which
is decreased.
c. fibrinogen level, which is elevated.
d. prothrombin time, which is prolonged.
e. fibrin degradation products (FDP), which
are diminished.
59
60. 3. Useful labs in DIC
MOST USEFUL:
• PT / INR – é
• Platelet count – usually ê
• Fibrinogen level – ê
HELPFUL:
• aPTT – usually é
• Thrombin clot time – é
• Fragmented RBCs – present
• FDP and D-dimers – é
60
61. 10. The cornerstone of Emergency
Department management of DIC is:
a. hemodynamic stabilization and
treatment of the underlying disorder.
b. rapid correction of thrombocytopenia.
c. aggressive resuscitation with colloid.
d. pan-culture and broad-spectrum
antibiotic coverage.
e. rapid intubation and hyperventilation.
61
62. 10. The cornerstone of Emergency
Department management of DIC is:
a. hemodynamic stabilization and
treatment of the underlying
disorder.
b. rapid correction of thrombocytopenia.
c. aggressive resuscitation with colloid.
d. pan-culture and broad-spectrum
antibiotic coverage.
e. rapid intubation and hyperventilation.
62
63. 10. Cornerstone of managing DIC
The primary cause of the DIC needs to be
determined and treated. The high
mortality rate in severe DIC is primarily
due to the underlying disorder. Many
patients with DIC require no specific
therapy if there is no evidence of
bleeding, or if thrombosis and laboratory
studies are not deteriorating. The first
principle of management is to stabilize
the patient hemodynamically, providing
oxygen, fluids, and life support as
needed.
63
66. Platelets
• Platelet life-span: 10 days
• Each day marrow produces /
releases ~10% of platelets
• Platelet count <20,000:
spontaneous bleed
• Platelet count >50,000: minimal
needed to avoid bleeding in
trauma / surgery
66
67. Platelets
• Aspirin blocks COX receptors for
life of platelet
• Withhold aspirin for 1 day è
~25,000 active platelets
• Withhold aspirin for 2 days è
~50,000 active platelets
• NSAIDs block COX receptors for
life of NSAID (~4 – 8 hours)
67
70. Presentation
• More common in women, adults in
4th decade of life
• 40% have URI / flu-like symptoms
prior to presentation
• Fatigue, malaise
• Fever
• Neurologic symptoms: headache,
confusion, seizure, stroke, coma
70
72. Treatment
• Plasma exchange: very effective
• Platelet transfusion CONTRAINDICATED (é thrombus
formation)
• Last resort: steroids, splenectomy
72
73. 6. A 44-year-old woman with a history of
TTP, in remission for 30 days, presents to
the ED complaining of lethargy. Laboratory
results would likely show:
a. é LDH, é reticulocyte count, é red
blood cell count.
b. é LDH, é reticulocyte count, é
creatinine.
c. ê platelet count, ê red blood cell
count, ê reticulocyte count.
d. ê platelet count, ê reticulocyte
count, ê LDH.
73
74. 6. A 44-year-old woman with a history of
TTP, in remission for 30 days, presents to
the ED complaining of lethargy. Laboratory
results would likely show:
a. é LDH, é reticulocyte count, é red
blood cell count.
b. LDH, reticulocyte count,
creatinine.
c. ê platelet count, ê red blood cell
count, ê reticulocyte count.
d. ê platelet count, ê reticulocyte
count, ê LDH.
74
75. 6. TTP – Laboratory results
In TTP, laboratory studies will show an
anemia of variable degree, LDH,
reticulocytosis, indirect bilirubin,
negative Coombs’ test, and
schistocytes on peripheral smear.
Thrombocytopenia is often severe with
the count <20,000/mL in 50% of
patients. BUN and creatinine are
typically .
75
76. Hemolytic Uremic Syndrome (HUS)
• Similar to TTP, but worse renal
dysfunction, less severe neurologic
symptoms
– ~60% require hemodialysis
• “Typical” or “childhood”: follows
acute bloody diarrhea
– Most common: E coli O157:H7
– Usually 5 years and younger
76
78. 1. A patient with anemia, thrombocytopenia,
renal failure, normal coagulation tests and a
clear sensorium probably has:
a.
b.
c.
d.
e.
idiopathic thrombocytopenic anemia.
thrombotic thrombocytopenic purpura.
hemolytic-uremic syndrome.
disseminated intravascular coagulation.
autoimmune hemolytic anemia.
78
79. 1. A patient with anemia, thrombocytopenia,
renal failure, normal coagulation tests and a
clear sensorium probably has:
a.
b.
c.
d.
e.
idiopathic thrombocytopenic anemia.
thrombotic thrombocytopenic purpura.
hemolytic-uremic syndrome.
disseminated intravascular coagulation.
autoimmune hemolytic anemia.
79
80. 1. Hemolytic Uremic Syndrome
ITP generally presents with isolated
thrombocytopenia. TTP causes
neurologic symptoms in addition to the
other symptoms. DIC will have
abnormal coagulation studies.
Autoimmune hemolytic anemia may
cause severe rapid anemia, which may
present with angina or congestive heart
failure.
80
81. 4. Hemolytic-uremic syndrome is most
commonly seen in:
a. neonates.
b. infants and children 6 months to 4
years of age .
c. adolescents.
d. women age 30 to 50.
e. both sexes, over age 75.
81
82. 4. Hemolytic-uremic syndrome is most
commonly seen in:
a. neonates.
b. infants and children 6 months to
4 years of age.
c. adolescents.
d. women age 30 to 50.
e. both sexes, over age 75.
82
83. 4. Hemolytic-uremic syndrome is most
commonly seen in infants and children.
Hemolytic-uremic syndrome (HUS) is a
disease mainly of infancy and early
childhood, with a peak incidence
between 6 months and 4 years of age.
83
84. Heparin-Induced
Thrombocytopenia (HIT)
• More common with unfractionated
• Heparin-dependent antibody
activates platelets
• Signs / symptoms occur 5 to 7 days
after starting heparin
• ~50% develop thrombosis
– Venous or arterial
– Life- and limb-threatening
84
85. Diagnosis & Treatment
• Moderate thrombocytopenia (~50%
reduction)
• HIT antibodies in serum
• Discontinue all heparins, avoid in
future
• Avoid warfarin: can progress to
gangrene
• Other medicines can also cause
85
86. 11. Heparin-induced thrombocytopenia:
a. does not occur with low molecular
weight heparins.
b. requires a minimum number of units,
so a heparin “flush” is always safe.
c. can paradoxically cause thrombosis,
ischemia, and amputation.
d. never occurs during the first 24 hours
of infusion.
e. is easily treated with warfarin and
fresh-frozen plasma.
86
87. 11. Heparin-induced thrombocytopenia:
a. does not occur with low molecular
weight heparins.
b. requires a minimum number of units,
so a heparin “flush” is always safe.
c. can paradoxically cause
thrombosis, ischemia, and
amputation.
d. never occurs during the first 24 hours
of infusion.
e. is easily treated with warfarin and
fresh-frozen plasma.
87
88. 11. HIT thrombosis
Heparin-induced thrombocytopenia
(HIT) is due to an antibody, usually
IgG, which attaches to and stimulates
platelets. This platelet activation
produces both thrombocytopenia and a
tendency for thrombosis. The
incidence of HIT is between 1 and 3%
in patients treated with unfractionated
heparin but significantly less in patients
treated with LMW products.
88
89. 11. HIT thrombosis
The onset of HIT is usually 5 to 12 days
after heparin treatment is started but
may be sooner for patients who
developed the antibody from a previous
exposure. Thrombosis may involve the
skin (similar to warfarin-induced
cutaneous necrosis), the arteries (e.g.,
femoral artery thrombosis), or the veins
(e.g., recurrent DVT or PE).
89
91. Signs and Symptoms
• Easy bruising, prolonged menses,
mucosal bleeding
• Petechiae, purpura
• Diagnosis: thrombocytopenia on
CBC
91
92. Treatment
• Steroids (?)
• If refractory: splenectomy or
immunosuppressive therapy
• Platelet transfusion ONLY if serious
bleeding
• Intravenous immunoglobulin G
(IVIG) in children with intracranial
hemorrhage (rare)
92
93. 14. A 5-year-old girl complains of weakness
and fatigue. Two weeks ago she saw her
family doctor and was diagnosed with an
upper respiratory infection. She received no
medicine at that time. Physical examination
shows only a scattered petechial rash
located in areas where her clothing is snug
against her skin, such as underwear elastic
lines. Laboratory studies show a white
blood cell count 11,000/mm3 , Hgb 10.5 mg/
dL, and platelet count of 16,000/mm3.
Appropriate management of this patient
should be:
93
94. 14. Recent URI … petechial rash …
platelet count of 16,000/mm3.
a. platelet concentrate transfusion.
b. discharge home with instructions to
limit contact sports.
c. admit for salicylate therapy.
d. admit for splenectomy.
e. admit for observation.
94
95. 14. Recent URI … petechial rash …
platelet count of 16,000/mm3.
a. platelet concentrate transfusion.
b. discharge home with instructions to
limit contact sports.
c. admit for salicylate therapy.
d. admit for splenectomy.
e. admit for observation.
95
96. 14. Recent URI … petechial rash …
platelet count of 16,000/mm3.
Acute idiopathic thrombocytopenic
purpura (ITP) is seen most often in
children 2 to 6 years old. A viral
prodrome is common, usually within 3
weeks of the onset. The platelet count
falls, usually to <20,000/mm3. The
course is self-limited, with a greater
than 90% rate of spontaneous
remission. Morbidity and mortality are
low. Treatment is supportive. Steroid
therapy does not alter disease course.
96
100. Non-Hodgkin Lymphoma
• Proliferation of lymphoid cells from
lymph nodes OR lymphatic tissue
other than bone marrow
• B-Cell, T-Cell, NK-Cell: can be
indolent or aggressive
• Diagnosis: biopsy
• Treatment: chemotherapy /
radiation
100
101. Pancytopenia
• Anemia + thrombocytopenia +
neutropenia
• Bone marrow diseases: myelodysplasia, myelofibrosis, some
leukemias and lymphomas
• Systemic diseases: lupus, severe
infection, sarcoidosis, alcohol,
tuberculosis, êvitamin B12, folate
101
103. Aplastic Anemia
• Pancytopenia with hypocellular
bone marrow
– Acquired: marrow stem cells
damaged by drugs, radiation, virus,
chemical, immune-related
– Inherited: Fanconi’s anemia,
dyskeratosis congenita
103
104. Signs & Symptoms
• Bleeding, easy bruising
• Fatigue, malaise, anemia è short
of breath
• Infection common
104
105. Diagnosis / Treatment
• CBC, reticulocyte count
• Bone marrow biopsy
• Immediate: depends on severity of
anemia / thrombocytopenia /
neutropenia ± complications
• Bone marrow transplant
105
106. Red Blood Cells (RBC)
• Normal life: ~120 days
• Marrow releases ~1% total count
daily
– “baby red cells” = nucleated =
reticulocytes
106
107. 7. The most helpful laboratory study to
differentiate poor red blood cell production
from increased red cell destruction is the:
a. sedimentation rate.
b. sideroblast level.
c. serum iron level.
d. total to direct bilirubin ratio.
e. reticulocyte count.
107
108. 7. The most helpful laboratory study to
differentiate poor red blood cell production
from increased red cell destruction is the:
a. sedimentation rate.
b. sideroblast level.
c. serum iron level.
d. total to direct bilirubin ratio.
e. reticulocyte count.
108
109. 7. ê production vs destruction
Reticulocytes are RBCs of intermediate
maturity. They are an index of the
production of mature RBCs by the bone
marrow (reported as a percent of total
RBCs). ê reticulocyte count reflects
impaired RBC production; seen with
low levels of iron, vitamin B12, folate,
bone marrow failure. reticulocyte
count reflects accelerated
erythropoeisis, the normal marrow
response to anemia; seen with blood
loss and hemolytic anemias.
109
111. Sickle Cell Disease
• Inherited mutated hemoglobin: HbS
• Recessive gene: both parents need
to pass to offspring
• HbS + HbA: trait è asymptomatic
• HbS + HbC (beta-thalassemia):
chronic anemia + recurrent painful
crises
111
112. Sickle Cell Disease
• RBC life span 10 – 15 days
• Marrow on constant “overdrive”
• Reticulocyte “normal” 8 – 10%
• WBC “normal” at 15 – 20K
• Hemoglobin “normal” at 8 – 10
• Platelets “normal” >500K
112
113. Vaso-Occlusive Crisis
• AKA acute painful episode
• Pain in extremities, chest,
abdomen, back
• No lab test can confirm
• No vital sign can confirm
• Treatment: analgesia
– Avoid meperidine
113
114. Acute Chest Syndrome
• New infiltrate on chest x-ray +
fever, cough, ésputum, dyspnea,
tachypnea, hypoxia
• Many causes: fat embolism from
marrow ischemia, pulmonary vasoocclusion, infection, venous
thromboembolism, pulmonary
edema
114
115. Acute Chest Syndrome
• Children: fever & cough most
common
• Adults: fever & chest pain as
presenting complaint
– Some develop 2 – 3 days into
hospital stay
• ± hypoxemia
115
116. Acute Chest Syndrome
• Chest x-ray normal in ~50%
• Treatment supportive
• Empiric antibiotic: 3rd / 4th
generation cephalosporin +
macrolide
• Severe è exchange transfusion
116
117. Splenic Sequestration
• Etiology: unknown
• Typically occurs in infants
– Tender, enlarged spleen
– Signs of hypovolemia, shock
– Concurrent infection common
• Diagnosis: worsening anemia,
persistent reticulocytisis, tender
large spleen
117
119. Aplastic Crisis
• Marrow shuts down
• Abrupt ê hemoglobin
• Abrupt ê reticulocytes (<2%)
• Causes: folate deficiency, human
parvovirus B19 (in children)
• Blood transfusion: severe anemia,
cardiorespiratory symptoms
119
120. Hemolytic Crisis
• Abrupt ê hemoglobin
• Major increase reticulocyte
production
• May see worsening jaundice
120
121. Other Complications
• Functional asplenia: infected by
encapsulated organisms
• Strokes: CNS occlusive events
• Priapism: low-flow due to corpora
cavernosa occlusion
121
122. 2. The viral agent implicated in an aplastic
crisis of patients with sickle cell disease is:
a.
b.
c.
d.
e.
adenovirus (atypical).
herpes simplex.
parvovirus.
coxsackie virus.
HTLV-IV.
122
123. 2. The viral agent implicated in an aplastic
crisis of patients with sickle cell disease is:
a.
b.
c.
d.
e.
adenovirus (atypical).
herpes simplex.
parvovirus.
coxsackie virus.
HTLV-IV.
123
124. 2. Parvovirus & Sickle cell
Aplastic crises can be precipitated by
viral infections (particularly parvovirus
B19), folic acid deficiency, or the
ingestion of bone marrow toxins such
as phenylbutazone. Bone marrow
erythropoiesis is slowed or stopped.
The hematocrit falls to as low as 10%,
and the reticulocyte count falls to as
low as 0.5%. The white blood cell
count and platelet counts usually
remain stable.
124
125. 9. A 12-year-old girl with sickle cell disease is
brought by her mother after she passed out
twice. She was kept home from school the
last few days for a “cold.” When you ask
the child to stand, you must catch her to
prevent her from falling to the ground. This
is suspicious for:
a. salmonella sepsis.
b. sequestration crisis.
c. acute chest syndrome.
d. aplastic crisis.
e. hemolytic crisis.
125
126. 9. A 12-year-old girl with sickle cell disease is
brought by her mother after she passed out
twice. She was kept home from school the
last few days for a “cold.” When you ask
the child to stand, you must catch her to
prevent her from falling to the ground. This
is suspicious for:
a. salmonella sepsis.
b. sequestration crisis.
c. acute chest syndrome.
d. aplastic crisis.
e. hemolytic crisis.
126
127. 9. Sequestration crisis
Sequestration crisis occurs primarily in
children and is the second most
common cause of death in children with
SCD under the age of 5 years. Often
preceded by viral infections, sickled
cells block the splenic outflow, causing
pooling of peripheral blood and sickled
cells in the spleen. Such patients
present in hypovolemic shock with an
enlarged spleen.
127
128. Hemolytic Anemia
• RBC destruction
• Intravascular
– Smear à fragmented RBCs
(schistocytes)
– More acute than extravascular
• Extravascular
– Occurs in liver or spleen
– Smear à spherocytes
128
131. Signs & Symptoms
• Vary depending on disease
• Symptoms related to anemia
• Jaundice
• Hepatosplenomegaly
131
132. Diagnosis
• Smear à schisto-, spherocytes
• Reticulocytes should be é
• Haptoglobin: binds free Hgbà ê
• Bilirubin é
• LDH é (released from RBCs)
• Hemoglobinemia, hemoglobinuria
• Autoimmune è direct Coombs +
132
133. Hypochromic Microcytic Anemia
• ê iron à iron deficiency
• ê globin à thalassemia
• ê porphyrin à sideroblastic, lead
toxicity
• Chronic disease
133
134. 13. A healthy 12-year-old AfricanAmerican female complains of
weakness and fatigue 3 days after
starting a course of trimethoprimsulfamethoxasole and pyridium for
a urinary tract infection. Her
hemoglobin is 4.8 mg/dl, and her
urine is tea-colored, but you see no
red blood cells on microscopic
exam. She probably has
undiagnosed:
134
135. 13. 12-year-old African-American
female…weakness and fatigue… TMP/
SMZ … hgb 4.8 mg/dl … no RBCs in
urine. Undiagnosed:
a. hemolytic uremic syndrome.
b. G6PD deficiency.
c. idiopathic thrombocytopenic purpura.
d. thrombotic thrombocytopenic
purpura.
e. sickle cell disease.
135
136. 13. 12-year-old African-American
female…weakness and fatigue… TMP/
SMZ … hgb 4.8 mg/dl … no RBCs in
urine. Undiagnosed:
a. hemolytic uremic syndrome.
b. G6PD deficiency.
c. idiopathic thrombocytopenic purpura.
d. thrombotic thrombocytopenic
purpura.
e. sickle cell disease.
136
137. 13. G6PD
Deficiency of the RBC enzyme
glucose-6-phosphate dehydrogenase
(G-6-PD) is the most common human
enzyme defect, affecting nearly onetenth of the world’s population. The
RBC is unable to protect itself against
oxidant stress. Acute hemolytic crises
occur that are incited by bacterial and
viral infections, exposure to oxidant
drugs, metabolic acidosis (such as
diabetic ketoacidosis), and ingestion of
fava beans in some patients.
137
138. 13. G6PD
Within 1 to 3 days following oxidant
stress, the patient can develop
hemoglobinuria and the potential for
vascular collapse. These hemolytic
crises are generally well tolerated and
self-limited because only the older
RBCs will hemolyze. The drugs most
commonly associated with oxidant
stress are sulfa drugs, antimalarials,
phenazopyridine, and nitrofurantoin.
138
139. Diagnosis / Treatment
• ê serum iron level
• ê serum ferritin level
• é total iron binding capacity (TIBC)
• Treatment: iron supplements,
outpatient workup
139
140. Macrocytic Anemia
• Most important: megaloblastic
• ê folate (green vegetables, fruit,
cereals) or ê vitamin B12 (meat)
è impaired DNA synthesis
140
141. Macrocytic Anemia
• Petechiae, mucosal bleeding,
infections, sore mouth / tongue,
diarrhea, weight loss
• B12 can also have paresthesias,
ataxia
• Diagnosis: send levels
• Treatment: replace
141
142. Polycythemia
• éHct: >51% in M, >48% in F
• Apparent: ê plasma volume
• Secondary
– Appropriate: hypoxia
– Inappropriate: é erythropoietin
• Polycythemia vera: é production
RBCs, WBCs, platelets
– Can progress to myelofibrosis,
leukemia
142
145. 16. A 68-year-old man complains of
headache, dizziness, and blurred
vision. His blood pressure is
190/118 mmHg. He has a florid
face, normal fundi, and marked
splenomegaly. His hematocrit is
67%. Reasonable therapy
includes:
145
146. 16. … florid face … splenomegaly …
hematocrit = 67%. Therapy:
a. 250cc salt-poor albumin.
b. intravenous nitroprusside.
c. phlebotomy.
d. plasmapheresis.
e. sublingual nifedipine.
146
147. 16. … florid face … splenomegaly …
hematocrit = 67%. Therapy:
a. 250cc salt-poor albumin.
b. intravenous nitroprusside.
c. phlebotomy.
d. plasmapheresis.
e. sublingual nifedipine.
147
148. 16. … florid face … splenomegaly …
hematocrit = 67%. Therapy:
Emergency treatment of any form of
symptomatic polycythemia is
phlebotomy. Usually not more than
500 ml of blood is slowly removed as
the volume is replaced with a
comparable amount of normal saline.
148
149. Methemoglobinemia
• éproduction or êreduction
• Causes discussed in toxicology
• Cyanosis with normal oxygen
saturation
• Treatment:
– Congenital: usually none
– Toxic è symptomatic è treat with
intravenous methylene blue
149
151. Leukemia
• éproduction undifferentiated
hematopoietic stem cells
• Acute Lymphocytic (ALL)
• Signs & symptoms: protean
– Related to abnormal cells crowding
out normal cells à êRBC, êWBC,
êplatelets
– Bacterial infections in 1/3 at time of
diagnosis
151
152. Leukemia
• Chronic Lymphocytic (CLL): most
common in patients >50 years
• Often no symptoms: may have
fatigue, large lymph nodes,
infections (esp. respiratory)
• Diagnosis: absolute lymphocyte
count >5000 cells/ml
• Treatment: monitor, chemo
152
153. Multiple Myeloma
• Abnormal éplasma cells
• Fatigue from anemia
• Bone pain from osteolytic lesions or
pathologic fractures
• Diagnosis: écalcium, écreatinine
• Bone marrow: >10% plasma cells
• Serum / urine protein electrophoresis (SPEP, UPEP)
153
154. Treatment
• Chemotherapy
• Plasmapheresis for hyperviscosity
syndrome
• If comatose: temporize by removing
1 liter blood, replace with normal
saline
• écalcium: IV saline, steroids
154
157. Hyperviscosity Syndrome
• éabnormal serum proteins
• Waldenstrom macroglobulinemia
• Multiple myeloma (less common)
• Most common symptoms:
neurologic, visual
• May see mucosal or GI bleeding
• CHF from é plasma volume
• Plasmapheresis, exchange
157
158. Leukostasis
• WBC sludging in microcirculation
• Usually acute leukemia
• Can be seen with chronic, NHL
• Neurologic symptoms
• Can see respiratory failure
• Treatment: leukapheresis,
hydroxyurea, chemotherapy
158
159. Neutropenic Fever
• Absolute neutrophil count (ANC) =
neutrophils + bands
• ANC <500 cells/ml
• Signs and symptoms: fever
• Treatment: IV antibiotics
– Ceftazidime or cefepime ± aminoglycoside or –penem
– Add vancomycin if appropriate
159
160. Spinal Cord Compression
• Lymphoma, metastasis, primary
• S&S: back pain, weakness,
numbness, bowel / bladder / sexual
dysfunction
• Diagnosis: MRI
– CT myelogram if MRI not available
• Treatment
– Dexamethasone
– Radiation therapy
160
161. Superior Vena Cava Syndrome
• Tumor obstructs SVC è venous
hypertension, congestion
• Early signs: face edema that
improves through day
• SOB, cough, chest pain
• Distension of chest, neck veins
• Cyanosis
• Diagnosis: chest CT
• Treatment: radiation therapy
161
162. Acute Tumor Lysis Syndrome
• Usually after chemotherapy
• Lysed cells è metabolic changes
• Hyperuricemia: N/V, renal failure
due to renal precipitation
• Hyperphosphatemia: N/V, lethargy,
seizures, renal impair
– Also binds with Ca+ à êcalcium
• Hypocalcemia: tetany, arrhythmia
162
163. Acute Tumor Lysis Syndrome
• Hyperkalemia: N/V, muscle
weakness, cramps, arrhythmias,
heart block è asystole
• Acute renal failure: possible
hemodialysis; do NOT alkalinize
urine, worsens éphosphorus and
êcalcium
163
164. Others
• Hypercalcemia: see EndocrineMetabolic Emergencies
• Pericardial Effusion / Tamponade:
see Cardiovascular Emergencies
164
165. 12. A 42-year-old woman with adult T-cell
lymphoma-leukemia complains of back pain,
abdominal pain, and confusion. Laboratory
evaluation shows a total calcium of 15.8 mg/
dl. Appropriate management of this patient
should include:
a. plasmapheresis.
b. IV bicarbonate.
c. IV hypertonic saline / oral
Kayexalate®.
d. IV normal saline and IV furosemide.
e. glucagon.
165
166. 12. A 42-year-old woman with adult T-cell
lymphoma-leukemia complains of back pain,
abdominal pain, and confusion. Laboratory
evaluation shows a total calcium of 15.8 mg/
dl. Appropriate management of this patient
should include:
a. plasmapheresis.
b. IV bicarbonate.
c. IV hypertonic saline / oral Kayexalate®.
d. IV normal saline and IV
furosemide.
e. glucagon.
166
167. 12. Hypercalcemia of malignancy
Patients with severe hypercalcemia
(>14 mg/dl) require immediate
treatment regardless of symptoms.
The four basic goals of therapy are
(1) restore intravascular volume,
(2) enhance renal calcium elimination
(3) reduce osteoclastic activity
(4) treat primary disorder.
167
168. 12. Hypercalcemia of malignancy
Isotonic saline is the first step. Once
volume is restored, the calcium will
usually have ê by 1.6 to 2.4 mg/dl, but
hydration alone rarely leads to
complete normalization. Loop diuretics
inhibit resorption of calcium in the thick
ascending loop of Henle, é the
calciuric effect of hydration. Volume
expansion must precede administration
of furosemide, because the drug’s
effect depends on the delivery of
calcium to the distal nephron.
168
169. Pearls
• The first step in managing any
transfusion reaction to to stop the
transfusion
• Hemarthrosis in hemophiliacs:
factor replacement, never
arthrocentesis
• Minor head injury in hemophilia:
replace factor, head CT, admit for
observation
169
170. Pearls
• Initial treatment in mild-moderate
hemophilia A: DDAVP
• NO PLATELET TRANSFUSION in
patients with TTP, HUS
• Once a patient has HIT, no heparin
can ever again be used, including
LMWH
170