|
Indian Pediatr 2011;48: 807-808 |
|
Transfusion Related Acute Lung Injury with
Intravenous Immunoglobulin |
V Gupta, P Gupta, and TP Yadav
From the Department of Pediatrics and Neonatology, PGIMER
and associate Dr Ram
Manohar Lohia Hospital, New Delhi, India.
Correspondence to: Dr T P Yadav, 16 LF Tansen Marg,
Bengali Market, Delhi 110 001, India.
Email: [email protected]
Received: March 04, 2010;
Initial review: May 7, 2010;
Accepted: July 20, 2010.
|
This case report describes transfusion related acute lung injury with
the use of intravenous immunoglobulin in a child with Guillain barre
syndrome.
Key words: Acute lung injury, Intravenous immunoglobulin,
Transfusion.
|
I ntravenous immunoglobulin (IVIG), a pooled
plasma derivative, has long been in clinical use and is considered a
safe drug. Serious complications of IVIG infusion are extremely
rare. We report a case of life threatening pulmonary edema in a
two-year old child following IVIG infusion.
Case Report
A 2-year (10 kg) female child was admitted with
complaints of progressively increasing weakness of both lower limbs
and trunk for last 10 days, and inability to speak and difficulty in
feeding for last 5 days. There was no prior medical history of
urinary retention, seizures, loss of consciousness, headache,
vomiting, rash, loose motion, cough, coryza, paresthesias,
hyperaesthesias or drug intake. The child did not suffer from any
medical illness or allergy in the past. There was decreased power in
lower limbs (3/5), trunk (3/5) and upper limbs(4/5), generalized
hypotonia with head lag, hyporeflexia with loss of gag reflex with
no pooling of secretions. All other cranial nerves were normal and
rest of the systemic examination was also unremarkable. CSF showed
albumino-cytological dissociation and nerve conduction velocity
revealed demyelinating pattern consistent with Guillain Barré
syndrome. Her serum levels of IgM, IgG and IgA were within normal
limits. She was started on IVIG at the dose of 400 mg/kg (2g/kg over
5 days) with infusion rate of 0.05 mL/kg/ min.
Nearly two hrs after IVIG infusion, child
developed signs of hypoxia in the form of increasing respiratory
distress with bilateral basal coarse crepts, air hunger and
irritability. Arterial blood gas on room air showed pH 7.36, PaO 2
of 53 mmHg, PaCO2 of 41
mmHg, and O2 saturation
of 88 percent. PaO2/FiO2
was = 252.38 mmHg (53/0.21). She was put on nasal oxygen. Her
respiratory distress worsened in next few minutes and blood pressure
started falling. She was intubated and kept on mechanical
ventilation in the intensive care unit. She was given one fluid
bolus of normal saline at 20 mL/kg over 1 hour. Chest X-ray
done after intubation revealed a normal cardiac silhouette and
bilateral interstitial and alveolar infiltrates consistent with
pulmonary edema. PaO2 /
FiO2 was 237.5mm Hg
(95/0.4). CVP was 7 cm. Echocardiography revealed normal left
ventricular function with ejection fraction of 60 %. In view of
falling BP with CVP of 7cm, no more fluids were administered and
child was started on inotropic support along with mechanical
ventilation. She maintained normal acid base balance with normoxia
(95% saturation) during the ventilation. After 72 hrs, she was
successfully extubated and maintained normoxia on minimal oxygen
support (FiO2 35%).
Repeat chest X-ray after 7 days of extubation was normal. She
did not receive any further dosages of IVIG. During the next 10 days
of hospitalization, her gag reflex and power in the trunk and lower
limbs improved.
Discussion
Our patient developed pulmonary edema and
hypotension within 2 hours of completion of first dose of IVIG. This
life threatening complication of acute lung injury is well known
after the administration of blood components but not after IVIG.
This usually presents within 1-6 h after transfusion and manifest as
clinical syndrome characterized by severe respiratory distress,
pulmonary edema, hypoxemia (PaO2/FiO2
<300 mmHg), normal left ventricular function and fever [1]. Our
patient fulfills the clinical criteria for transfusion related acute
lung injury (TRALI) as described by Kleinman, et al. [2].
TRALI after IVIG infusion has been reported only in two adult
patients so far described and not in pediatric patients as per
available English literature.
A large number of adverse reactions to IVIG have
been reported [4-7], including hypersensitivity reaction like
urticaria, angioedema and bronchospasm. Respiratory distress
following any infusion can also occur because of circulatory
overload or anaphylactic transfusion reactions.
Transfusion-associated circulatory overload develops within minutes
to hours of transfusion as congestive cardiac failure, cyanosis,
hypertension and it rapidly responds to aggressive diuresis and
ventilatory support. Anaphylactic transfusion reactions results in
laryngeal and bronchial spasm and manifest as tachypnea, wheezing,
cyanosis, erythma, edema and severe hypotension, during the
transfusion of any type of protein-containing blood component [8].
Akin to post blood component infusion TRALI, that
following IVIG infusion could have been due to immune mediated
mechanism [9] or neutrophil priming mechanism [2]. In our patient,
the possible mechanism could not be ascertained since the estimation
of antibody against neutrophils was not available.
It is suggested that clinician using IVIG should
closely monitor the patients to pick up this potential fatal
complication at the earliest and institute appropriate supportive
care timely.
Contributors: VG and TPY were involved in
active case management and review of literature. VG and PG revised
the paper for critically important intellectual content.
All authors approved the final version to be published.
Funding: None. Competing interest:
None stated.
References
1. Rizk A, Gorson KC, Kenney L, Weinstein R.
Transfusion-related acute lung injury after the infusion of IVIG.
Transfusion. 2001;41:264-8.
2. Kleinman S, Caulfield T, Chan P, Davenport R,
McFarland J, McPhedran S, et al. Toward an understanding of
transfusion-related acute lung injury: statement of a consensus
panel. Transfusion. 2004;44:1774-89.
3. Suassuna JHR, da Costa MADL, Faria RA,
Melichar AC. Noncardiogenic pulmonary edema triggered by intravenous
immunoglobulin in cancer – associated thrombotic thrombocytopenic
purpura- hemolytic uremic syndrome. Nephron. 1997;77:368-70.
4. Orbach H, Katz U, Sherer Y, Shoenfeld Y.
Intravenous immunoglobulin: adverse effects and safe administration.
Clin Rev Allergy Immunol. 2005;29:173-84.
5. Berkovitch M, Dolinski G, Tauber T, Aladjem M,
Kaplinsky C. Neutropenia as a complication of intravenous
immunoglobulin (IVIG) therapy in children with immune
thrombocytopenic purpura: common and non-alarming. Int J
Immunopharmacol. 1999;21:411-15.
6. Daphnis E, Stylianou K, Alexandrakis M,
Xylouri I, Vardaki E, Stratigis S, et al. Acute renal
failure, translocational hyponatremia and hyperkalemia following
intravenous immunoglobulin therapy. Nephron Clin Pract.
2007;106:c143-8.
7. Shorr AF, Kester KE. Meningitis and hepatitis
complicating intravenous immunoglobulin therapy. Ann Pharmacother.
1996;30:1115-6.
8. Silliman CC, Ambruso DR and Boshkov LK.
Transfusion – related acute lung injury. Blood. 2005:105:2266-73.
9. Moalic V, Vaillant C, Ferec C . Transfusion
related acute lung injury (TRALI): an unrecognised pathology. Pathol
Biol. 2005;53:111-5.
|
|
|
|