83 yo male - anwresidency.comanwresidency.com/hospitalists/case_conf/heme/transfusion...

83 yo male PMH

Diverticulosis

HTN

DM II

Hyperchol

AVR 1997, EF 60% recently

CVA 1997, aphasia, R-sided

GI Bleeds

Meckel’s 1998

Hemicolectomy

UGIB 3mo PTA, 2mo PTA &

1mo PTA

Gastric erosions

DNR code status

HPI Hutch 2 wks ago w/ melena & Hgb

7.4, INR 2.4

FFP for reversal, 3u PRBCs

EGD= gastric erosions, Last

colonoscopy 1998

Hgb stable, coumadin resumed and

lovenox to bridge @ Discharge

Recurrent Melena on lovenox and

coumadin

Presented to Hutch INR 2.8 on lovenox and coumadin, Hgb

6.7

Pulse 110, 110/65, 98% RA

6u FFP, 2u prbcs given prior to transfer

transferred to ANW

83 yo male PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy

UGIB 3mo PTA, 2mo PTA & 1mo PTA

Gastric erosions

DNR code status

HPI Hutch 2 wks ago w/ melena & Hgb 7.4, INR

2.4


EGD= gastric erosions, Last colonoscopy

1998

Hgb stable, coumadin reversed and lovenox

to bridge @ Discharge

Recurrent Melena on lovenox and coumadin

still

Presented to Hutch and transferred to ANW

INR 2.8 on lovenox and coumadin, Hgb 6.7

Pulse 110, 110/65, 98% RA


Hgb 6.9, 2u PRBCs

ordered w/ lasix btwn

units

Difficulty matching, delayed

6 hours

Hgb 8.9, melanotic

diarrhea continues

Pulse 120s, BP 105/50

EGD negative

Plan prep for colonoscopy

in AM

Melena/diarrhea

increases

140 32101

3.9 21 1.1110

83 yo male

Hgb 8.4 still w Melena

1u prbc ordered

Needs leukoreduced units

for transfusions

Delayed secondary to

aby incompatabilities

Infusion started at

1pm

144 44108

3.9 18 1.699

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male 45min into infusion…

Patient shaky/cold

Temp 36.7

Resp rate to 40 acutely,

diffuse wheeze new,

labored breathing

Rapid response called

Blood pressure 160/110,

pulse 140s

Sats 92 > 80% on 100%

facemask over 10min

144 44108

3.9 19 1.699

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male Solumedrol 100mg IV

Benadryl 50mg IV

Lasix 40mg IV

Albuterol Neb

Bipap

MSO4

DNR confirmed

Developed abdominal pain

Transferred to ICU

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male Ntg gtt started

Lines placed

Lasix = brown urine

First 2 lab draws hemolyzed

3rd lab draw & Transf Rxn labs

Hgb 7.2 < 1u+8.4

INR 1.9 <1.2

Plts 102 < 235

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male Forced diuresis with

bicarb and lasix/ivf

Quick echo at bedside:

global hypokinesis-

severe

Repeat TTE after acidosis

improved with bolus

bicarb, EF 55%, no wma.

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male Cr 3.0 next morning

UA large blood, 2 rbcs

Off Bipap, sob resolved

Cr climbed to 4.6

Dialysis initiated, pulled line out

that night

Hgb dropped to 7.1 < 8.6

Colonoscopy: 2 avms in ileum

at anastamosis, clipped

Coumadin resumed

Cr climbed to 5.3 then leveled

out and started to fall

PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA


83 yo male PMH

Diverticulosis

HTN

DM II

Hyperchol



GI Bleeds

Meckel’s 1998

Hemicolectomy


Gastric erosions

DNR code status


2.4



1998




still



Pulse 110, 110/65, 98% RA

6u FFP given prior to transfer

Discharged to rehab

Blood Bank Path Report:

1. Probable ongoing delayed hemolytic

transfusion reaction

2. Possible component of acute

hemolysis without demonstrable

immunologic basis

INTERPRETATION

Of significance is that this patient

received multiple red blood cell

transfusions prior to his admission to

Abbott Northwestern Hospital on 8/21/07.

Serologic evaluation at Abbott

Northwestern Hospital and at American

Red Cross North Central Blood Services

revealed four red cell alloantibodies with

anti-e anti-Kell, anti-S, and anti-Duffy A

specificities. All three units transfused at

Abbott Northwestern Hospital were

negative for the corresponding red cell

antigens and all three units were

demonstrated to be crossmatch

compatible through the antiglobulin

phase in both saline and albumin media.

The patient's direct Coombs test was positive on the

pretransfusion specimen and the plasma free

hemoglobin was elevated on a pretransfusion

specimen to 46 mg/dl. Accordingly, ongoing hemolysis

was likely present prior to the transfusion of the

implicated unit, and presumably represents an

evolving delayed hemolytic transfusion reaction to the

units transfused at the outside facility. A post

transfusion plasma free hemoglobin, however, was

more significantly elevated at 177 mg/dl suggesting an

element of acute hemolysis with the third unit. This

correlates with a serum haptoglobin of less than 6

mg/dl. Nevertheless, a repeat serological evaluation

including complete crossmatch through the

antiglobulin phase in both saline and albumin did not

demonstrate evidence for serological incompatibility

with this third unit. Accordingly, the possibility of

nonimmunologic/mechanical hemolysis might also be

considered, possibly reflecting the presence of the

prosthetic heart valve.

An eluate from red cells in the post transfusion sample

demonstrates specificity for anti-S which would

support the diagnosis of delayed hemolytic

transfusion reaction associated with red cell units

transfused at the outside facility.

If additional transfusions are needed for this

individual, he should be cross matched with units

negative for the e, Kell, S, and Duffy-A antigens, and

complete crossmatch through the anti-globulin phase

will be necessary.

Transfusion Reactions

Staff Case Conference

2.1.2008

FEBRILE NONHEMOLYTIC REACTIONS

Most common

Clinically:

Fever, chills, mild dyspnea, muscle cramps

Time course:

1-6 hrs after transfusion

Cause:

Cytokines generated during storage

Donor leukocytes

FEBRILE NONHEMOLYTIC REACTIONS

Treatment:

Stop the transfusion and determine that a

hemolytic reaction is not taking place

Symptomatic tx:

Administration of antipyretics

Meperidine in patients with severe chills and

rigors

Prevention:

Leukoreduced transfusion

ACUTE HEMOLYTIC REACTIONS

Emergency

Etiology: pre-existing RBC antibodies in the

recipient to the donor erythrocyte: ABO (clerical error), preexisting antibodies not detectable:

Kell, Duffy, and Kidd

Signs and symptoms: Triad: fever, flank pain, and red or brown urine

(hemoglobinuria)

hypotension

Coomb’s Test: positive

Pink serum (hemoglobinemia) Plasma free hemoglobin

Complications: oliguria 33%, DIC 4%, death 20%

ACUTE HEMOLYTIC REACTIONS

Stop the transfusion

Maintain the patient's airway, blood pressure, and heart rate.

Begin an infusion of normal saline immediately to initiate a diuresis and avoid hypotension

From the other arm, obtain a sample for a direct antiglobulin test, plasma free hemoglobin, and repeat type and cross-match. Save a urine sample for hemoglobin testing

The blood bank should be alerted immediately, and a search for clerical error should be instituted.

This is of critical importance, since if blood samples or blood bags have been switched in error, there may be a second patient at risk for a similar event

Follow coagulation, plts, renal function

DELAYED HEMOLYTIC REACTIONS

2-10 days after transfusion

Aby against previously seen antigen

Usually Kidd, Rho system

Diagnosis is often made by the blood bank

new positive direct antiglobulin test and a new

positive antibody screen are found when more

blood is ordered

Slow decrease in Hgb, low grade fever,

spherocytes on smear

Treatment: none, unless brisk hemolysis

ANAPHYLACTIC REACTIONS

Associated with IgA Antibodies

Anti-IgA antibodies of IgG type that are

capable of binding complement

Selective IgA deficiency 1:300-500 persons

Treatment:

conventional anti-anaphylactic management

0.3-0.6cc 1:1000 Epi IM

0.5-1cc 1:10,000 Epi IV

Glucagon if on Bbl and refractory

1mg IV, can repeat up to 5mg qmin

URTICARIAL REACTIONS

Pre-existing IgE aby to substances in blood

Mast cells and basophils to release histamine,

leading to hives or urticaria

Only transfusion reaction in which the blood

product can be continued

Stop first and assure no further sx develop

Benadryl 25-50mg iv

Do not need to send to blood bank

TRALI – transfusion related acute lung injury

Clinical symptom spectrum:

Cough

Acute resp distress, hypoxemia, hypotension,

fever, and pulmonary edema

Donor aby to leukocytes

1:5000 transfusions (tip o’)

2-4 hrs after initiation of transfusion

Treatment: supportive

Usually fully recover in 48-72hrs

POSTTRANSFUSION PURPURA Patient antibodies directed against human platelet

antigens (developed through pregnancy or

previous transfusion)

Thrombocytopenia = hemorrhages in the skin and

mucous membranes, purplish spots or patches 5-

12 days following transfusion

Management:

avoid transfusion of plts

steroids, IVIG and possibly plasma exchange

washed cells or HPA-1a negative cells in the future

If untreated may persist for several weeks

Transfusion of Infectious DiseasesInfection

Hepatitis B

HTLV I

Hepatitis C

HIV I

Smoking 20 cig/d

Automobile driving

Soccer/Football

Canoeing

• Risk

1:205,000 transfusions

1:641,000 transfusions

1:1,935,000 transfusions

1:2,135,000 transfusions

1:200 risk of death/yr

1:5,900

1:25,000

1:100,000

<1:million = babesia, bartonella, borrelia, brucella,

leishmania, parvo, toxo, EBV, W. Nile, Malaria.

Types of PRBCs

Washed

Removes proteins left in small amt

of plasma

Used in: Patients with severe or recurrent

allergic reactions (eg, hives) associated

with red cell transfusion

Certain patients with IgA deficiency

when IgA deficient donors are not

available (although frozen

deglycerolized red cells may be the

component of choice; see below);

patients with IgA deficiency may have

circulating anti-IgA antibodies that react

with IgA in the donor plasma

In the rare patient with a complement-

dependent autoimmune hemolytic

anemia to prevent complement

infusion.

Irradiated red cells

Prevent the donor T lymphocytes from

dividing in the recipient

Used in:

patients who have hereditary

immune deficiency states

Prevents GVHD in

immunosuppressed pts and

related T-lymphocytes

Types of PRBCs

CMV Negative

Donors are CMV negative

Doesn’t pick up infected sero-negative “Window Period”

40-60% of donors are CMV positive

Used in: immunocompromised oncology patients,

individuals undergoing hematopoietic or solid

organ transplantation,

low birth weight CMV-seronegative neonates

Leukoreduced

Removes leukocytes

Prevents HLA alloimmunization, febrile

reactions

Used in:

Chronically transfused patients

Potential transplant recipients

Patients with previous febrile

nonhemolytic transfusion

reactions

CMV seronegative at-risk patients

for whom seronegative

components are not available

Transfusion reaction workup…

determine whether the correct unit of blood was

administered

repeat type, crossmatch, antibody screen, and

direct and indirect Coombs.

Other considerations with a hemolytic

transfusion:

Free serum hemoglobin appears as a pink color of the

serum in a clotted centrifuged specimen. This may be

observed with as little as 5-10 mL of hemolyzed blood.

Serum bilirubin level peaks in 3-6 hours as the free

hemoglobin is metabolized.

83 yo male - anwresidency.comanwresidency.com/hospitalists/case_conf/heme/transfusion...

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