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| CASE REPORT |
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| Year : 2008 | Volume
: 52
| Issue : 6 | Page : 835 |
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Transfusion Related Acute Lung Injury -A Case Report
Anamika1, Vasanth Nayak2, Jose Chacko3, G Parameswara2
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 Acceptance | 26-Aug-2008 |
| Date of Web Publication | 19-Mar-2010 |
Correspondence Address:
G Parameswara
Department of Anaesthesia, Manipal Hospital, No: 98, Airport Road, Bangalore - 560017
India
 Source of Support: None, Conflict of Interest: None  | Check |
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 |
 Introduction | |  |
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 | | |
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 | | |
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 | | |
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[Figure 1], [Figure 2]
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