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Year : 2008  |  Volume : 52  |  Issue : 6  |  Page : 835 Table of Contents     

Transfusion Related Acute Lung Injury -A Case Report

1 P.G.Student, Department of Anaesthesia and Intensive Care, Manipal Hospital, Bangalore, India
2 Senior Consultant, Department of Anaesthesia and Intensive Care, Manipal Hospital, Bangalore, India
3 Consultant in Intensive Care, Department of Anaesthesia and Intensive Care, Manipal Hospital, Bangalore, India

Date of Acceptance26-Aug-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
G Parameswara
Department of Anaesthesia, Manipal Hospital, No: 98, Airport Road, Bangalore - 560017
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Source of Support: None, Conflict of Interest: None

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Transfusion related acute lung injury (TRALI) is a rare but life threatening complication of blood transfusion which is being increasingly recognized. It is caused by cross reaction between donor antibodies and host leucocytes or between donor leucocytes with host antibodies. TRALI usually presents as an Acute Lung Injury (ALI) resulting in pulmonary congestion and edema, often leading to Acute Respiratory Distress Syndrome (ARDS). We report a case of TRALI in a patient who underwent laparotomy for ruptured corpus luteal cyst requiring blood transfusion. She presented with acute pulmonary edema about an hour after commencing a blood transfusion .This was managed conservatively with oxygen, steroids and diuretics. Patient improved rapidly and later discharged without any residual complications.

Keywords: Transfusion, Acute lung injury, Pulmonary edema, Leucocyte antigen -antibody reaction, TRALI

How to cite this article:
Anamika, Nayak V, Chacko J, Parameswara G. Transfusion Related Acute Lung Injury -A Case Report. Indian J Anaesth 2008;52:835

How to cite this URL:
Anamika, Nayak V, Chacko J, Parameswara G. Transfusion Related Acute Lung Injury -A Case Report. Indian J Anaesth [serial online] 2008 [cited 2021 Mar 6];52:835. Available from: https://www.ijaweb.org/text.asp?2008/52/6/835/60697

   Introduction Top

Transfusion-related acute lung injury (TRALI) is a rare but often devastating complication of blood trans­fusion. TRALI is potentially life threatening and rank second only to ABO mismatch as a cause of transfu­sion related fatalities. The incidence of TRALI has been reported to be about 0.01 to 0.08 % per plasma con­taining unit transfused and an associated mortality rate of 5 - 14 % [1],[2] . The pathogenesis of acute lung injury is related to cross-reaction between donor anti­bodies and host leucocytes or less commonly, host an­tibodies and donor leucocytes [3] . Symptoms of TRALI generally develop within 6 hours of transfusion, most often occurring within first 2 hours after transfusion is started [4] . The presentation varies between mild pulmo­nary congestion to frank pulmonary edema and subse­quent acute respiratory distress syndrome. The diag­nosis is often by exclusion of other causes of pulmo­nary edema or ARDS. Clinical management consists mainly of supportive treatment with oxygen therapy and mechanical ventilation if needed. Most patients recover fully after acute episode and with timely management.

We report a case of TRALI in 19 year old female following whole blood transfusion which was recog­nized promptly and managed successfully.

   Case report Top

A 19-year-old female weighing 45 kg presented with severe spasmodic pain of her lower abdomen of 5 days duration. On initial examination in the emergency department, she was fully awake and communicative, with a pulse rate of 98/min, BP of 100/60mmHg and breathing comfortably at 16 breaths/min with oxygen saturation of 98% on room air. Apart from mild diffuse tenderness over her lower abdomen, the rest of her clinical examination was unremarkable. Initial investi­gations revealed hemoglobin of 9.3 gm%, white cell count of 10,330/cmm and platelet count 318,000/cmm. Her clotting parameters, renal and hepatic function were within normal limits. A routine chest X-ray done at this time did not reveal any abnormality. She was further investigated with an abdominal ultrasound scan that revealed extensive pelvic haematoma. She remained haemodynamically stable and an emergency exploratory laparotomy was planned. At pre-anaesthetic evalua­tion, she was found to have mild tachycardia (110/min) and a blood pressure of 120/76 mm of Hg. Her respi­ratory rate was 15 /min with oxygen saturations well maintained on room air. The rest of her systemic ex­amination was unremarkable. She was pre-medicated with glycopyrrolate 0.2 mg IV and induced with fenta­nyl 100 µg, ketamine 100 mg, and lidocaine 75 mg IV. After suxamethonium 75 mg, she was intubated with a 7.0 sized endotracheal tube. Anaesthesia was main­tained with 66% N 2 O in oxygen, sevoflurane and an atracurium infusion at 25 mg.hr -1 .

Intraoperatively, haemorrhagic corpus luteal cyst of the left ovary was noted with a haematosalpinx. Around 800 - 900 ml of clot was removed from the Pouch of Douglas. A left salpingo-oophorectomy was done. She was infused with 1.0 liter of Ringer's lactate and a unit of whole blood was also commenced intra­operatively. She remained haemodynamically stable and was easy to ventilate with a tidal volume of 400 ml generating a peak inspiratory pressure of 20 -22 cm of H 2 O. Her oxygen saturations were maintained between 98 -99% throughout the procedure. Reversal of neu­romuscular blockade was accomplished with neostig­mine 2.5 mg and glycopyrrolate 0.4 mg and she was extubated fully awake after suctioning of the endotra­cheal tube. No excessive secretions were noticed at this time. Shortly after arrival in recovery, about an hour following commencement of blood transfusion, she was noticed to be increasingly tachycardic (130/min) and tachypnoeic (40 - 45/ min) with use of accessory muscles. She was also coughing up pink frothy secre­tions and her oxygen saturations dropped low (85 - 90%) on 10 L/min of oxygen through a Hudson mask. Auscultation of the chest revealed bilateral coarse crepitations. Arterial blood gas analysis revealed a pH of 7.39, PCO2: 47.9, PO2: 74.2, BE: 2.9 and HCO3: 28.4.The blood transfusion was stopped and intrave­nous frusemide 60 mg was given at this time; this re­sulted in a copious diuresis; she was also given 100 mg hydrocortisone IV. With these measures her dyspnoea and oxygen saturation improved and she was trans­ferred to the intensive care unit. A chest X-ray done in ICU revealed bilateral fluffy infiltrates, [Figure 1] and a transthoracic echocardiogram done was normal. Over the next 6 - 8 hours she continued to improve; her respiratory rate settled down to 20 -25/min and she was able to maintain oxygen saturation of more than 95% on nasal prongs at 3L/min. The rest of her recov­ery was uneventful - she was transferred to the ward the next day and discharged home on day 5.

   Discussion Top

Our patient developed features of acute pulmo­nary oedema soon after a laparotomy and salpingo­oophorectomy for a ruptured corpus luteal cyst that had resulted in significant blood loss. Her symptoms began about an hour after starting a blood transfusion. The possibilities we considered initially were (1) pul­monary aspiration during the procedure - there was no evidence to suggest this or (2) negative pressure pul­monary edema - there were no signs of airway ob­struction at any stage to cause this. The other possibil­ity was of a pulmonary transfusion reaction. These can be (1) transfusion associated circulatory overload (TACO) (2) TRALI (3) allergic/anaphylactic reac­tions and (4) bacterial contamination and hemolytic transfusion reactions [1] . Circulatory overload was un­likely in our patient, as she had received just 1.0L of Ringer's lactate intraoperatively and had clearly lost more than 800 ml of blood. Her normal echocardiogram also ruled out a primary heart disease that could have resulted in pulmonary edema. An allergic or anaphy­lactic reaction was unlikely as there was no associated hypotension or urticarial rash and these reactions gen­erally occur almost immediately after commencing the transfusion. In our case, respiratory distress occurred about an hour after transfusion. Reactions due to mis-matched blood transfusion generally occur almost immediately of starting the transfusion and after as little as 10-50 ml of blood having been transfused. Mismatched blood transfusion also produces hypotension, tachy­cardia and importantly, hemoglobinuria. Our patient did not have any of these signs except tachycardia. Rapid improvement within a matter of hours without specific treatment also made haemolytic or allergic re­actions less likely. The onset of symptoms about an hour after beginning transfusion, hypoxemia, bilateral fluffy infiltrates on the X-ray and improvement within 6 to 8 hours with supportive treatment favour the diag­nosis of TRALI in this case. Although the diagnosis of TRALI is essentially clinical by exclusion of other likely possibilities, it can be confirmed by testing for anti-leu­kocyte antibodies in the donor blood. This test was not available to us; hence we couldn't positively confirm TRALI in our patient.

TRALI denotes development of acute lung injury and non-cardiogenic pulmonary edema in conjunction with transfusion of plasma containing blood products. It may be an important cause of transfusion associated death; however, lack of awareness may result in sig­nificant underreporting [2] . The National Heart, Lung and Blood Institute proposed a definition of TRALI as Acute Lung Injury (ALI) occurring during or within six hours of a transfusion in patients without preexisting ALI be­fore transfusion [5] . Acute Lung Injury can be distinguished from TRALI by the presence of risk factors [6] caused by direct lung injury such as aspiration, pneumonia, toxic inhalation etc. and by indirect injury such as due to se­vere sepsis, shock, multiple trauma, acute pancreatitis, cardiopulmonary bypass etc. The diagnosis of TRALI should be considered in all cases of respiratory dis­tress with significant hypoxemia with PaO 2 /FiO 2 ratio less than 300mmHg, [7] bilateral chest infiltrates on chest radiographs temporally related to transfusion. Other TRALI related signs reported are fever, tachycardia, hypotension, cyanosis and transient leucopenia. Plasma containing blood components such as whole blood [8] , aphaeretic platelet concentrates [9] , fresh frozen plasma, packed red cells, granulocytes [10] , cryoprecipitate [11] and intravenous immunoglobulin [12] have all been implicated. The pathophysiology is related to two predominant hypotheses [13] - increased pulmonary capillary perme­ability induced by (1) anti-leukocyte antibodies in the donor blood or (2) neutrophil activation induced by biologically active agents like lipids and cytokines [9],[10] . The former mechanism is through antileukocyte anti­-bodies that activate the recipient leukocytes and result in their sequestration within the lung and subsequent degranulation leading to increased pulmonary capillary permeability. The latter mechanism arises from the un­derlying problem (sepsis, inflammation etc) causing activation of the pulmonary endothelium leading to neu­trophil sequestration within the lung. Donor antibodies activate these "primed" neutrophils, leading to pulmo­nary capillary leak [Figure 2]. TRALI may also be pre­cipitated by agents that directly cause endothelial fen­estration, including high levels of vascular endothelial growth factor (VEGF) or high levels of HLA class II antibodies, directed against antigens on the pulmonary endothelium.

The management of TRALI is mainly supportive in nature with oxygen supplementation, mechanical ven­tilation and haemodynamic support as necessary. Since pulmonary edema in TRALI is not related to fluid over­load or cardiac dysfunction, but due to increased al­veolar vascular permeability in the lungs with exudation of fluid and proteins into the alveoli, it is logical that maintenance of adequate circulatory volume is the most beneficial therapy [14] . Diuretics may not be of use in this condition. Recently inhaled nitric oxide is shown to have little benefit in treatment of ALI [15] .

The outcome from TRALI is likely to be better than that associated with other conditions that result in acute lung injury and ARDS. TRALI may be associ­ated with a mortality of 5 - 14% 14% [1],[2] . Popovsky et al [4] reported 36 patients who developed TRALI. All pa­tients required oxygen support, 72%of them required mechanical ventilation. 20% of these patients had persistent hypoxia which lasted more than 7 days. Ulti­mately all these patients also improved. The mortality in this series was about 5-8% due to complications re­lated to acute lung injury. In another study, Clark et al [16] reported 46 patients, out of 14,602 transfusions, who developed severe TRALI. Most reactions were seen in patients with hematological malignancies and all these patients ultimately survived.

Our patient was a fit, 19 year old girl who did not have any incidental problems apart from a significant bleed from a ruptured corpus luteal cyst. She probably had a mild form of TRALI and improved rapidly with conservative measures. We would like to emphasize the importance of being aware of the possibility of TRALI in any patient who develops features of acute pulmonary oedema within 2 to 6 hours of a blood prod­uct transfusion. Such cases should be promptly reported to the local blood bank authorities; diagnosis may be confirmed by testing the donor for anti-leukocyte anti­bodies. As the TRALI occur due to donor leucocyte antigens and host cell antibodies reaction in most cases, there is a possibility of TRALI occurring when the same donor blood is transfused to other recipient as well. So timely tracing of implicated blood donor with granu­locytes reactive antibodies, and preventing the donor from future blood donation may prevent TRALI and potentially save the lives of future transfusion recipi­ents. The concurred blood donors should not donate blood for any future recipient.

   References Top

1.Looney MR, Groopper MA, Mathay MA. Transfusion related acute lung injury: a review. Chest 2004;126:249­-58.  Back to cited text no. 1      
2.Toy P, Gajic O. Transfusion related acute lung injury. Anesth Analg 2004;99: 1623-24.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Bux J, Becker F, Seeger W, et al. Transfusion related acute lung injury due to HLA -A2 specific antibodies in recipient and NBI specific antibodies in donor blood. Br J Hematol 1996; 93:707-13.  Back to cited text no. 3      
4.Popovsky MA. Transfusion related acute lung injury. In:Popovsky MA, ed: Transfusion Reactions. 2 nd Edi­tion, Bethesda, MD ; American Association of Blood Bank Press 2001;pp:55-170.  Back to cited text no. 4      
5.Toy P, Popovsky MA, Abraham E, et al. National Heart Lung and Blood institute Working Group on TRALI; Transfusion related acute lung injury: Definition and review. Crit Care Med 2005;33:721-6.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Kleinman S, Caulfield T, Chan P, et al. Towards an un­derstanding of transfusion related acute lung injury; statement of a consensus panel. Transfusion 2004; 44:1774-89.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Silliman CC, Boshkov LK, Mehdizadehkashi Z, et al. Transfusion related acute lung injury: epidemiology and a prospective analysis of etiological factors. Blood 2003; 101: 454-462.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Silliman CC. Transfusion related acute lung injury. Trans­fusion Med Rev 1999;13:177-186.  Back to cited text no. 8      
9.Boshkov LK, Maloney J, Bieber S, Silliman CC. Two cases of TRALI from the same platelet unit: Implica­tions for pathophysiology and the role of PMNs and VEGF. Blood 2000; 96: 655.  Back to cited text no. 9      
10.Bastit D, Cavelier B, Ropartz C. "White lung" during granulocyte transfusion: possible role of leukoagglutinins [in French]. Nouv Presse Med 1982;11: 2156-57.  Back to cited text no. 10  [PUBMED]    
11.Bray RA, Harris SB, Josephson CD, Hillyer CD, Gebel HM. Unappreciated risk factors for transplant patients: HLA antibodies in blood components. Hum Immunol 2004;65: 240-244.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Rizk A, Gorson KC, Kenney L, Weinstein R. Transfusion-related acute lung injury after the infusion of IVIG. Transfusion 2001; 41: 264-268.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Christopher C, Silliman, et al. Transfusion-related acute lung injury. Blood 2004 ;105:2266-2273.  Back to cited text no. 13      
14.Transfusion Medicine Bulletin 2000;3:1.  Back to cited text no. 14      
15.Adhikari NK, Burns KE, Friedrich JO, Granton JT, Cook DJ, Meade MO. Effect of nitric oxide on oxygenation and mortality in acute lung injury: Systematic review and meta-analysis. BMJ 2007;334:779.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]  
16.Clarke G, Podlosky L, and Petrie L, Boshkov L. Severe respiratory reactions to random donor platelets: An in­cidence and nested case-control study (Abstract). Blood 1994;84(Suppl 1):465.  Back to cited text no. 16      


  [Figure 1], [Figure 2]


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