[HSF] A TRALI case
Ben Bidstrup
benjamin.bidstrup at bigpond.com
Sat Mar 17 01:17:04 EDT 2007
Not if you don't see patients!
>You can get sued for not operating. John
>
>-----Original Message-----
>From: benjamin.bidstrup at bigpond.com
>To: OpenHeart-L at lists.hsforum.com
>Sent: Thu, 15 Mar 2007 11:35 PM
>Subject: Re: [HSF] A TRALI case
>
> It cost insurance companies and more importantly many people
>their lives when HIV was transmitted by transfusion. Arthur Ashe for
>one died as a result of AIDS received from a transfusion after CABG.
>There were many high profile suits about that. In some countries it
>is still going on. Hep C is still a worry - with more intense
>screening, the cost of blood products goes up.
> Whilst the safety of blood products has improved with increased
>screening, it still has its risks. This case of probable TRALI is
>but one example.
> So everything is a balance - get sued for giving blood, get sued
>for not giving blood, get sued for using a hemostatic agent, get
>sued for using the pump, get sued for not using it etc.
>Only way to avoid all of this is
>
>
>Don't operate!!
>
> >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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>-- Ben Bidstrup FRACS FRCSEd FEBCTS
>Consultant Cardiothoracic Surgeon
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