This document discusses rational blood use and its components. It provides historical context on blood transfusions dating back to 1492. It then covers developments like the discovery of blood groups in 1901 and the establishment of the first blood bank in the 1930s. The document outlines the processing of donated blood into components like packed red blood cells, platelets, and plasma. It discusses indications for transfusions and special considerations like managing Rh-negative patients. Finally, it reviews potential complications of transfusions such as hemolytic and allergic reactions.
A PowerPoint presentation outlining the physiology of blood transfusion, and clinical precautions to take in preventing and managing blood transfusion reactions.
Blood transfusion - components , procedure , pre transfusion testing and comp...prasanna lakshmi sangineni
blod transfusion- introduction , procedure , pre transfusion tests , complications , characteristics of components and components usually used like packed red cells, FFP, platelet rich plasma, cryoprecipitate, albumin and other plasma derivatives
Autologous Blood Transfusion (ABT) means reinfusion of blood or blood products taken from the same patient
ABT is not a new concept, fear of transfusion- transmitted diseases stimulated the growth of autologous programme
A PowerPoint presentation outlining the physiology of blood transfusion, and clinical precautions to take in preventing and managing blood transfusion reactions.
Blood transfusion - components , procedure , pre transfusion testing and comp...prasanna lakshmi sangineni
blod transfusion- introduction , procedure , pre transfusion tests , complications , characteristics of components and components usually used like packed red cells, FFP, platelet rich plasma, cryoprecipitate, albumin and other plasma derivatives
Autologous Blood Transfusion (ABT) means reinfusion of blood or blood products taken from the same patient
ABT is not a new concept, fear of transfusion- transmitted diseases stimulated the growth of autologous programme
Teaching with Twitter: Is There A Place For Social Media In Higher Education?Kristopher Maday
This is a talk I gave at the 2015 University of Alabama System Scholars Institute Conference. In it I discuss how we as educators need to utilize social media to reach the "Millenial" generations and how we can use this medium as part of our promotion and tenure evidence for scholarly activity.
A number of groups have issued clinical practice guidelines for blood component therapy in an effort to improve transfusion practices, minimize the incidence of adverse transfusion reactions, and decrease costs. This slideshow by Dr Somnath Longani, Consultant, Midland Healthcare & Research Center Lucknow explains about the Blood Component Therapy in detail.
Blood products Transfusion and related complications,
Types of cell salvage, blood warming and autologous blood,
With intraoperative blood lots monitoring and transfusion
dr m laban
Tanta fever hospital scientific activity
sunday
12-8-2018
Blood transfusion
Aims of Transfusion Center
To care for the donor - ensure act of donation does not harm donor.
Provision of Blood of the best possible quality and safety for the patient receiving it.
Safe blood transfusion means:
Compatible and without transmission of infection
The Safest blood transfusion is No
transfusion
Blood donation
Careful donor selection with donor interview.
Age: not less than 17 years.
Pulse: between 50-100 beat / minute without irregularities.
Blood pressure: systole<180mmHg, diastolic <100mmHg.
Temperature: <37.5C
Hemoglobin:>12g/dl, Hct>38%
Site of vein puncture must be free of lesions and infections.
ABO grouping.
Rh typing.
Cross matching
Laboratory screening test for:-
HBsAg.
HCV Ab.
HIV.
HTLV1.
HTLV2.
Blood grouping means:-
the determination of the antigens of a specific group on the red cells
and the antibodies relevant to this group in the normal serum.
General information about DLBCL treatment and care for internists. Not meant for hematologist, though.
Sorry for lagging of explanation but what in the slide should be sufficient.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
4. THE FIRST BLOOD
TRANSFUSION ATTEMPT
• In1492 "the harrowing story was told that, at
the suggestion of a Jewish physician, the blood
of three boys was infused into the dying
pontiff ’s mouth (the concept of circulation
and methods for intravenous access did not
exist at that time). They were ten years old,
and had been promised a ducat each. All
three died."
Diario della città di Roma di Stefano Infessura scribasenato. 15th cent.
5. BLOOD AND CIRCULATION
• In 1628 William Harvey
published De Motu Cordis (On
the Motion of the Heart and
Blood) revealed the action
of the heart pumping blood
around the body in a circuit.
6. TRANSFUSION ATTEMPTS
• In
1667 Jean-Baptiste Denys, French
physician, performed transfusion with
sheep's and calf's blood.
• In
1818 James Blundell, successfully
performed transfusion for postpartum
hemorrhage, using patient's husband's blood.
• In1905 George Washington Crile, co-
founder of Cleveland Clinic, was the first
surgeon who used direct blood transfusion
in surgery.
7. BLOOD GROUPING
• In
1901, Karl Landsteiner discovered human blood groups.
Blood transfusion had become a lot safer since then.
8. DEVELOPMENT OF BLOOD
BANKING
• Anticoagulant was discovered in 1910, making the way to
blood banking.
• First stored blood was successfully transfused in 1916
by Oswald Hope Robertson, an English-born medical
scientist, during World War I.
• The first academic transfusion institution was found by
Alexander Bogdanov in Moscow.
• After Bogdanov's death Soviet established the world's first
blood bank in 1930s by Sergei Sergeevich Yudin at Nikolay
Sklifosovskiy Institute.
10. HOW IS DONATED BLOOD
PROCESSED?
• Blood and blood components come from potential donors.
• Wholeblood was used in first era of transfusion but blood
components are now wildly used for better efficient
management.
11.
12. LEUKOCYTE REDUCTION
• WBC less than 5 x 106/unit*
• Reduced febrile reaction risk yte
oc !
Le uk d!
duce
• Reduced CMV transmission re
• ReducedHLA-
alloimmunization risk
13. IRRADIATION
• Inactivate donor’s T-cells
• Reduced GVHD risk
• Reduce shelf life to 28 days
• Increased K+ leak
16. WHOLE BLOOD
•Volume 350 or 450 ml
•Contain red cell, white cells,
platelets, and plasma
•Stored at 2-6°c
•No functional platelets and
labile factors
•May indicated in neonatal
blood exchange
17. PACKED RED
BLOOD CELL
•Volume ~300 ml
•Hct ~75%
•Contain red cells, white
cells, small of plasma
•Stored at 2-6°c
•10ml/kg raise Hct ~10%
18. PACKED RED
BLOOD CELL
•Volume ~300 ml
•Hct ~75%
•Contain red cells, white
cells, small of plasma
•Stored at 2-6°c yte
oc !
Le uk d!
•10ml/kg raise Hct ~10% ce
re du
19. PACKED RED
BLOOD CELL
•Volume ~300 ml
•Hct ~75%
•Contain red cells, white
cells, small of plasma
•Stored at 2-6°c yte
oc !
Le uk d!
•10ml/kg raise Hct ~10% ce
re du
20. PLATELET
CONCENTRATE
•Volume ~50 ml
• Contain platelet 5.5 x 1010
RBC 0.5 ml and white cells
•Stored at 20-26°c with
continuous rocking shelf
•1 unit/10 kg raise platelet
20,000-50,000 ml/mcL
21. POOLED
LEUKOCYTE-
POOR PLATELET
•Made of 4 unit of whole
blood
•Contain platelet 3 x 1011 and
RBC 5 ml
•Comparable to Plt. conc. 4-6
units (6 - 8 units for SDP)
22. POOLED
LEUKOCYTE-
POOR PLATELET
•Made of 4 unit of whole
blood
•Contain platelet 3 x 1011 and yte
oc !
RBC 5 ml Le uk d!
duce
•Comparable to Plt. conc. 4-6 re
units (6 - 8 units for SDP)
23. POOLED
LEUKOCYTE-
POOR PLATELET
•Made of 4 unit of whole
blood
•Contain platelet 3 x 1011 and yte
oc !
RBC 5 ml Le uk d!
duce
•Comparable to Plt. conc. 4-6 re
units (6 - 8 units for SDP)
27. THRESHOLD FOR RBC
TRANSFUSION
• Hb < 7 g/dL in general patient
• Hb < 10 g/dL in patient with ischemic heart disease
• Hb < 10 g/dL in pre-operative patient or bleeding patient*
• In symptomatic or frail patient*
28. PATIENT WHO SHOULD NOT
BE TRANSFUSED
• Nutritional anemia
• Autoimmune hemolytic anemia
• Patient with high peripheral blast count
29. PLATELET REQUIREMENT
• In bleeding patient: keep platelet > 50,000 - 80,000/mcL
• Bleeding in vital organ: keep platelet > 100,000/mcL
• In chronic thrombocytopenia: keep > 10,000/mcL
• In DIC keep platelet > 20,000/mcL
• In APL keep platelet > 30,000 - 50,000/mcL
31. FRESH FROZEN PLASMA
• Ingeneral each milliliter of plasma count as 100% factor
activity
100% + 0% = 50% Hemostat level = 40%
• Ifcoagulogram ≤1.5 times of normal, other causes of abnormal
bleeding should be sought
35. RH NEGATIVE
• Rh negative is determined by absence of D antigen
• Antibody occur 4 - 8 wks after expose to D antigen
• Rh negative person should receive only Rh negative blood
• Platelets
have no Rh antigen but contaminated RBC can
induce antibody
36. PLATELET TRANSFUSION IN
RH NEGATIVE
• Check if patient already have Rh
antibody
• Give anti-D IgG before or within 72
hr after platelet transfusion
• 100 units can neutralize RBC 5 ml
• 300 units can neutralize Plt. conc. 30
units or LPPC 3 units
37. MISMATCH TRANSFUSION
• Transfuse
packed red cell without foreign antigen to avoid
major mismatch reaction
• Transfuse
plasma without offending antibody to avoid minor
mismatch reaction
• Platelet is considered as plasma due to high plasma content
• Platelet recovery will be less than expected
38. TRANSFUSION
COMPATIBILITY
Blood group Compatible Compatible
A RBC
A, O Plt. & FFP
A, AB
B B, O B, AB
AB AB, A, B, O AB
O O O, A, B, AB
39. PLATELET REFRACTORINESS
• Corrected count increment (CCI) < 3,000/mcL
• Corrected count increment = (Pre - Post) x Body surface area
Transfused platelet
41. MASSIVE TRANSFUSION
• 1 Total blood volume within 24 hr.
• Keep platelet > 50,000/mcL
• Keep coagulogram less than 1.5 times
• Not recommend 1:1:1 transfusion protocol
43. TRANSFUSION PRACTICE
• Check if bags are in good condition
• No leakage
• No fibrin clot
• Recordvital sign at before, start, 15 min after, 1 hr after,
and 4 hr after transfusion
46. IMMEDIATE HEMOLYTIC
TRANSFUSION REACTION
• ABO incompatibility is the most common cause
• Can be fatal even 30 ml of incompatible blood
• Intravascular hemolysis
• Renal failure
• Shock
57. IMMEDIATE HEMOLYTIC
TRANSFUSION REACTION
• IV fluid maintain urine output 100 ml/hr
• Furosemide or mannitol if needed
• Maintain blood pressure
• Check label
• Re-crossmatch on pre- and post-transfusion samples
• Prevention future event
58. DELAYED HEMOLYTIC
TRANSFUSION REACTION
• Occur 1 wk after transfusion
• Anamnestic immune response
• Extravascular hemolysis
• Usually subtle symptoms
• Antibody gradually decrease after expose to antigen
59. BACTERIAL CONTAMINATION
• Platelet
prone to have
bacterial overgrowth
enterocollitca can
• Yersinia
grow at 6°c etc.
• Antibioticshould be started
if suspected bacterial
contamination
60. ALLERGIC REACTION
• Allergic to plasma protein of donor
• Can give antihistamine to relieve symptoms
• In IgA deficiency patient should avoid plasma product
61. FEBRILE NONHEMOLYTIC
TRANSFUSION REACTION
• Fever
• Caused by alloantibody to HLA antigen on Plt. or WBC
• No specific treatment
• Must differentiate from other causes of fever
62. TRANSFUSION RELATED
ACUTE LUNG INJURY
• TRALI
• Causeby alloantibody from
donor to WBC of recipient
• Occur within 6 hours after
transfusion
• Symptoms is the same as
ARDS
63. TRANSFUSION RELATED
GRAFT-VERSUS-HOST DISEASE
• Cause by engraftment of donor T-cells
• Damage to epithelium and bone marrow
• Fatal condition
• Prevent with irradiation of blood component with T-cells
64. Recognize
T T
Engraft Reject Recipient
tissue
HLA antigen
T T-cells Transfusion related GVHD
65. PATIENT IN RISK OF GVHD
FROM TRANSFUSION
• Bone marrow transplant patient
• Intrauterine transfusion
• Hx of fludarabine use (follicular lymphoma, CLL, AML)
• HLA matched transfusion
• Transfusion from relatives
• Severe congenital immunodeficiency
66. PROTOCOL FOR
COMPLICATION EPISODE
Chill, fever, rash, flank pain, chest tightness,
vital sign change, alteration of consciousness,
dark urine
Stop transfusion!
Check vital sign, load IV fluid
maintain BP and urine output
Aware of renal complication
67. PROTOCOL FOR
COMPLICATION EPISODE
Check label and patient’s identification
Draw blood from patient Examine transfusing blood
Centrifuge for serum color Blood group
Coomb test Re-crossmatch with pre- and
Blood group post-transfusion samples
Hemoculture Hemoculture