[HSF] A TRALI case
Ani Anyanwu
anianyanwu at hotmail.com
Thu Mar 15 22:40:14 EDT 2007
These cases are all a reminder that blood transfusion is not innocuous.
It puzzles me that we are prepared to accept death or near-death by transfusion in preference to (assuming it exists) renal failure by aprotinin.
Maybe one day the lawyers will hear of TRALI too. Someday we will be held accountable for our liberal application of blood transfusion (or our failure to take measures to prevent it).
Ani
----- Original Message -----
From: Mark Levinson<mailto:mmlevinson at hsforum.com>
To: OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com>
Sent: Wednesday, March 14, 2007 9:56 PM
Subject: [HSF] A TRALI case
On Mar 13, 2007, at 10:03 AM, prasannasimha wrote:
> 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.
Prasanna:
You may have clarified a puzzling complication affecting one of my
patients!
Routine mitral valve repair + RF Maze in 78 yo male with perfect
result. Extubated in OR with clear CXR and perfect hemodynamics.
On second post-op day, suddenly hypoxic with white-out of lungs,
worse on right. Patient had vomited earlier in the day, so
possible aspiration, but....
WBC count fell acutely from 15,300 to 1,900! and patient goes into
vasodilatory shock with renal failure and
mild hepatic injury (enzymes ~ 650, T Bili ~ 6.0).
Immediately stopped cordarone (which I have also seen cause acute
ARDS!). Intubated on 100% FiO2 with severe
bilateral pulmonary infiltrates. Emergency TEE: no change in
valve....no MR, MS, SAM. Moderately depressed LV function
(preop EF 70% with normal CAs and no CABG needed).
*Severe* metabolic acidosis, like someone with dead gut...but abdomen
soft and non-distended. No sign of leg ischemia.
6 amps of bicarb and continuous bicarb drip overnight. Supported
with pitressin, epinephrine, and as a wild guess...Steroids!
Within 48 hours, CXR back to normal, acidosis gone, FiO2 30%, and WBC
count up to 10,000 again. Off all pressors and inotropes.
But still in renal failure, now on dialysis.
I was at a total loss to explain this episode. I have never, ever
seen such a precipitous drop in WBC count, but I immediately suggested
to the family that the leukocytes were being sequested in the lung
and releasing toxins causing the systemic toxicity, acidosis, and
shock. But
I did not know how this all started, and I was reluctant to blame it
all on aspiration pneumonia. I felt that if the patient had an
aspiration pneumonia,
the leukocyte count would have gone up! and the CXR would not have
cleared so quickly.
Until now, I have not seen this syndrome, but the papers you quoted
below state exactly what happened to this man. I will search his
transfusion
records and see if he received any RBCs prior to his event, but I
suspect I will find he did....
Very serious problem for this person, but it must be rare as I have
not seen (or at least recognized) it in the past...
Thanks so much..
Mark M. Levinson, MD
Founder, Editor-in-Chief,
The Heart Surgery Forum
WWW: <http://www.hsforum.com<http://www.hsforum.com/>>
Email: <mmLevinson at hsforum.com<mailto:mmLevinson at hsforum.com>>
>
> 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<mailto:ebender001 at charter.net> wrote:
>> John, What's that?
>>
>> Ed
>> ---- jbflegejr at aol.com<mailto:jbflegejr at aol.com> wrote:
>>> Could this be TRALI? John Flege
>>>
>>> -----Original Message-----
>>> From: ebender001 at charter.net<mailto:ebender001 at charter.net>
>>> To: OpenHeart-L at hsforum.com<mailto: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
>>> _______________________________________________ OpenHeart-L
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