[HSF] CABG/Mitral Repair
Tea Acuff
tacuff at swbell.net
Tue Mar 13 21:40:59 EDT 2007
Thanks to all for the replies, but TRALI seems similar to PIMP to me.
tea
----- Original Message ----
From: prasannasimha <prasannasimha at gmail.com>
To: OpenHeart-L at lists.hsforum.com
Sent: Tuesday, March 13, 2007 10:03:20 AM
Subject: Re: [HSF] CABG/Mitral Repair
Here it is.
Prasanna
TRALI: Transfusion Related Acute Lung Injury
Vol. 3, No. 1 - April 2000
Provided by Your Independent, Nonprofit Community Blood Center in
conjunction with America's Blood Centers..
Transfusion related acute lung injury (TRALI) is best described as a
clinical constellation of signs and symptoms including dyspnea,
cyanosis, hypotension, fever and chills along with physical findings of
bilateral pulmonary edema. The symptoms typically begin within 1-2 hours
of transfusion and usually are present by 4-6 hours. The severity can
range from mild to severe but is related to the degree of hypoxia.^1
The syndrome is associated with significant morbidity and has been
reported as the third most common cause of a fatal transfusion reaction.
In a series of 36 patients with TRALI, all required oxygen support for a
mean of 40 hours.2 Mechanical ventilation was required in 72 percent;
TRALI was determined to contribute significantly to mortality in 6 percent.
TRALI most often is associated with transfusion of whole blood, packed
red blood cells (pRBCs) and fresh frozen plasma (FFP). There are rare
reports of TRALI following transfusion of granulocytes, cryoprecipitate,
platelet concentrates and apheresis platelets. Infusion of even very
small volumes of blood can trigger this reaction. Estimates of frequency
have ranged from 0.014 percent to 0.02 percent per unit transfused and
from 0.04 percent to 0.16 percent per patient transfused.^2,3
Radiographic Findings: The development of bilateral pulmonary
infiltrates after transfusion, without evidence of cardiac compromise or
acute volume overload, should lead to suspicion of TRALI. The pulmonary
infiltrates appear at the time of the reaction and resolve within 96
hours in about 80 percent of affected patients. Arterial blood gas
values typically show hypoxemia and respiratory alkalosis paralleling
the changes seen on chest x-ray and physical exam. Infiltrates may
persist for at least 7 days in the remaining 20 percent. Persistence of
infiltrates has been associated with difficulty weaning from mechanical
ventilation. The radiographic findings tend to be more remarkable than
the physical findings.
Etiology: Classically, the etiology of TRALI has been attributed to the
presence of leukocyte antibodies in the plasma of multiparous donors
directed against recipient white blood cells (WBCs). Granulocyte or HLA
class I antibodies are found in at least one donor in about 70 percent
of cases.^2 In some cases, HLA class II antibodies in donor plasma have
been detected against recipient cells.^4 The exact specificity of the
antibody involved and documentation of the presence of the corresponding
antigen in the recipient have been determined in only a few cases of
TRALI.^5,6
TRALI
Clinical Picture:
* Noncardiogenic pulmonary edema
* Dyspnea, cyanosis, hypotension, fever, chills
* Develops within 1-2 hours of transfusion. Usually present by 4-6 hours
* Difficult to distinguish from Acute Respiratory Distress Syndrome
Pathogenesis:
* Sequestration of WBCs in pulmonary microvasculature leads to
increased vascular permeability and pulmonary edema
Etiology:
* Antibodies against granulocyte, HLA class I or class II antigens
* Biologically active lipids in stored cellular blood components
* Pulmonary edema arises from capillary injury rather than volume
overload
Treatment:
* Supportive ventilatory assistance
* Maintenance of hemodynamic status (e.g., saline infusion)
Diuretics are contraindicated
Less often, leukocyte antibodies, directed against donor white blood
cells, are identified in the recipient. Interdonor reactions, caused by
the interaction in the recipient of leukocyte antibodies from one donor
with the leukocytes of another donor have also been reported. Popovsky
et al. have hypothesized that donor antibodies more commonly cause TRALI
than recipient antibodies because the former are able to react with the
entire circulating and marginating pool of WBCs in the recipient.^7
Antibodies in the recipient have a much smaller pool of donor WBCs in a
blood component with which to react.
The pulmonary edema in TRALI is attributed to WBC-antibody interaction,
with subsequent sequestration of WBCs in the pulmonary microvasculature,
leading to increased vascular permeability and accumulation of fluid and
protein in the alveoli.
Another hypothesis of the etiology of TRALI is that biologically active
lipids in stored blood components enhance polymorphonuclear cell (PMN)
NADPH oxidase activity.^8 This priming activity, however, is not present
in non-cellular blood components or fresh cellular blood components.
Silliman et al. advanced a two-event hypothesis to explain the etiology
of TRALI.^9 The first event consists of a predisposing condition. The
second is the infusion of biologically active lipids or antibodies to
leukocytes in stored cellular blood components. These researchers
demonstrated that there was significantly more PMN-priming activity
present in post-transfusion samples from 10 patients who had TRALI
reactions compared to their pre-transfusion samples or in pre- and
post-transfusion samples from 10 control patients with only febrile or
urticarial transfusion reactions. Additionally, all 10 patients with
TRALI had a predisposing condition including infection, cytokine
administration, recent surgery or massive transfusion. Only 2 of the 10
patients with febrile or urticarial reactions had a similar predisposing
condition.
Diagnosis: The diagnosis of TRALI is based primarily upon clinical signs
and symptoms, not laboratory findings. It is important to determine that
the pulmonary edema is noncardiogenic, because it is treated differently
than cardiogenic or volume overload types of pulmonary edema.
Noncardiogenic pulmonary edema is clinically distinguished from other
forms of pulmonary edema based upon normal to decreased pulmonary
capillary wedge pressure, normal pulmonary artery pressure, absence of
jugular venous distention, absence of murmurs or gallops, normal cardiac
silhouette, absence of pulmonary vascular congestion and no evidence of
myocardial infarction by EKG and enzyme testing.
Laboratory confirmation of the clinical diagnosis of TRALI, although
important, is performed at a later date. The donors of all components
transfused within 6 hours of initiation of the reaction should be
screened for the presence of granulocyte and HLA class I antibodies. If
a large number of donors are involved, female donors or multiparous
female donors can be screened for antibodies first. Then, if those
donors are negative for antibody, male donors should be screened. If all
of the implicated donors' units are negative, including for HLA class II
antibodies^4 , the patient should be tested for leukocyte antibodies. To
prove the diagnosis, the antibody present in the donor (or rarely the
recipient) should correspond to an HLA or granulocyte antigen present in
the recipient (or donor).
Treatment: Corticosteroids, epinephrine and diuretics traditionally have
been used to treat TRALI. However, since the pulmonary edema in TRALI is
not related to fluid overload or cardiac dysfunction, but to altered
vascular permeability in the lungs with exudation of fluid and protein
into the alveoli, it is logical that maintenance of adequate circulating
volume is the most beneficial and appropriate therapy.^10 Ventilatory
assistance and circulatory support are the mainstays of treatment of
TRALI; because the disease is self-limited, the majority of patients
will respond to these therapies alone. The use of corticosteroids
remains controversial. Since the pulmonary edema is due to capillary
leak syndrome and is not secondary to volume overloaddiuretic use may be
detrimental and could lead to hypotension, and decreased cardiac output.
Prevention: Several approaches to the prevention of TRALI have been
recommended. Most include limiting the amount of plasma transfused from
implicated donors by diverting plasma to recovered plasma and using
pRBCs with either washed or frozen-deglycerolized. Popovsky et al.
suggested that implicated donors should be told not to donate again.^7
Given the rarity of TRALI, a more moderate approach probably is more
realistic. The blood center that supplied the blood component should be
notified. Any remaining blood product should be returned for studies,
such as screening for HLA antibodies in the donor. HLA typing of the
recipient will assist in determining specificity. Plasma from implicated
donors should be diverted for protein fractionation. Transfusion of
pRBCs from such donors when preserved in an anticoagulant-preservative
solution like AS-2 probably is acceptable due to the small volume of
plasma present in this component.
References
1. Kopko PM and Holland PV. Transfusion-related acute lung injury. Br
J Haematol 1999;105:322-9.
2. Popovsky MA and Moore SB. Diagnostic and pathogenetic
considerations in transfusion-related acute lung injury.
Transfusion 1985;25:573-7.
3. Ausley MB. Fatal transfusion reactions caused by donor antibodies
to recipient leukocytes. Am J Forensic Med Pathol 1987;8:287-90.
4. Kopko PM, MacKenzie MR, Paglieroni TR et al. Can HLA class II
antibodies cause TRALI? Transfusion 1999;39:58(S).
5. Yomtovian R, Kline W, Press C et al. Severe pulmonary
hypersensitivity associated with passive transfusion of a
neutrophil-specific antibody. Lancet 1984;1:244-6.
6. Eastlund T, McGrath PC, Britten A, Propp R. Fatal pulmonary
transfusion reaction to plasma containing donor HLA antibody. Vox
Sang 1989;57:63-66.
7. Popovsky MA, Chaplin HC and Moore SB. Transfusion-related acute
lung injury: a neglected, serious complication of hemotherapy.
Transfusion 1992;32:589-592.
8. Silliman CC, Thurman GW and Ambruso DR. Stored blood components
contain agents that prime the neutrophil NADPH oxidase through the
platelet-activating-factor receptor. Vox Sang 1992;63:133-6.
9. Silliman CC, Paterson AJ, Dickey WO et al. The association of
biologically active lipids with the development of
transfusion-related acute lung injury: a retrospective study.
Transfusion 1997;37:719-726.
10. Levy GJ, Shabot MM, Hart ME et al. Transfusion-associated
noncardiogenic pulmonary edema. Transfusion 1986;26:278-81.
ebender001 at charter.net wrote:
> John, What's that?
>
> Ed
>
> ---- jbflegejr at aol.com wrote:
>
>> Could this be TRALI? John Flege
>>
>> -----Original Message-----
>> From: ebender001 at charter.net
>> To: OpenHeart-L at hsforum.com
>> Sent: Mon, 12 Mar 2007 10:27 PM
>> Subject: [HSF] CABG/Mitral Repair
>>
>> Ten days ago a 52 year old obese diabetic female was admitted with
>> unstable angina and class 3-4 heart failure. She had cardiac cath
>> showing a 25% EF, and tight LAD and Circ stenoses. LV gram also showed
>> severe MR. No right heart cath was performed. Echo showed severe MR
>> with a dilated annulus and central regurg. There was no flail. Her
>> creatinine went from 1.6 to 3.6 in three days, then came back down to
>> 1.3. She had been in pulmonary edema, and this resolved with diuretics.
>> After waiting until her creatinine improved as above, this past Friday
>> I did 2 vessel CABG and mitral annuloplasty with a 24 ETLogix ring and
>> a couple of cleft closures. No post-op MR on TEE. In the OR her initial
>> PA pressures were a little more than one-half systemic (systolic BP
>> around 100). After the operation her PA pressures were 30-15 with a
>> systemic BP of 120/70. Over the next 24 hours, she whited out both
>> lungs, her PA pressures have once again become high, she has required
>> very high doses of pressors. Any beta agonist drug causes horrific
>> ventricular and supraventricular arrhythmias (even with ongoing
>> cordarone and lidocaine). I have her on inocor, vasopressin, and
>> levophed. A balloon pump was also placed. Repeat echo shows LVEF about
>> 40%, no MR, trace AI, and a dilated RV. Her CVP is 20-25. I dialed in
>> Nitric oxide with some initial improvement in PA pressures, but not
>> long-lasting. Short of VAD therapy, anybody have any other tricks?
>>
>> Ed Bender, MD
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