|
 
 |
| LETTER TO EDITOR |
|
| Year : 2021 | Volume
: 5
| Issue : 4 | Page : 177-178 |
|
Posterior reversible encephalopathy syndrome secondary to blood transfusion
Jamir Pitton Rissardo, Ana Leticia Fornari Caprara
Department of Medicine, Federal University of Santa Maria, Santa Maria, Brazil
| Date of Submission | 28-Dec-2021 |
| Date of Acceptance | 30-Dec-2021 |
| Date of Web Publication | 28-Feb-2022 |
Correspondence Address:
Dr. Jamir Pitton Rissardo
Av. Roraima, 1000 - Camobi, Santa Maria - RS 97105-900
Brazil
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ljms.ljms_62_21
How to cite this article:
Rissardo JP, Fornari Caprara AL. Posterior reversible encephalopathy syndrome secondary to blood transfusion. Libyan J Med Sci 2021;5:177-8 |
Dear Editor,
We read the article entitled “Posterior reversible encephalopathy syndrome: An acute neurological complication of blood transfusion” in the esteemed “Libyan Journal of Medical Sciences” with great interest. Karri et al. reported a case of a young-adult female presenting with headache and generalized tonic-clonic seizures after packed red blood cells transfusion.[1] A brain magnetic resonance imaging (MRI) showed hyperintense areas in the occipital, parietal, and frontal gray matter which were suggestive of posterior reversible encephalopathy syndrome (PRES).
PRES, also known as reversible posterior leukoencephalopathy syndrome, is characterized by reversible clinicoradiographic findings of white matter edema usually presents in the posterior cerebrum. The most common clinical manifestations associated with this neurologic disorder are headaches, seizures, visual disturbances, and confusion.
Herein, we would like to hypothesize a pathophysiological mechanism to PRES secondary to blood transfusion and discuss other cases already reported in the literature.
Two main hypotheses for the development of PRES [Figure 1] are proposed. They are based on the myogenic regulation (autoregulation) of cerebral blood flow.[2] Apparently, the assumptions are contradictory. However, the pathways may have a link that was not already described. | Figure 1: Schematic diagram of the mechanism proposed for PRES secondary to blood transfusion. The most commonly described pathophysiological mechanisms to PRES are related to the self-regulation of cerebral blood vessels. One proposes that volume overload hypertension exceeds the cerebral vessels' self-regulation capacity. The other suggests that cerebral vasoconstriction occurs due to excessive autoregulation. IL-1: Interleukin-1, TNF: Tumor necrosis factor, PRES: Posterior reversible encephalopathy syndrome
Click here to view |
In the last literature review published about PRES following blood transfusion, 25 case reports were found. Gurumukhani et al. reported interesting results about this association.[3] First, the most commonly affected population are middle-aged (mean age of 44.48 years) females (96%). Second, the indication for blood transfusion was menorrhagia in 44% of the cases. Third, chronic anemia of more than 1-month duration was the most prevalent disorder encountered. Fourth, more than half of the patients had anemia classified as severe. Fifth, the neurological symptoms occurred within 1 week of the blood transfusion. Sixth, the clinical manifestations reported were encephalopathy, seizures, headaches, visual symptoms, and focal neurological deficits. Seventh, hypertension was associated with almost half of the cases. Eighth, the most frequent type of cerebral edema was vasogenic, which only affected the white matter.
Based on the findings described by Gurumukhani et al., we can assume that PRES secondary to packed red blood cells transfusion probably occurs due to the inactivation of self-regulatory mechanisms leading to a hyperperfusion pathway. This can be supported by the fact that hypertension is less commonly encountered in individuals who develop PRES following blood transfusion when compared to eclampsia or other autoimmune diseases.[4] Moreover, the most common cerebral edema was vasogenic, which is well known to be caused by the release of free radicals and cytokines leading to increased vascular permeability. Thus, there may be a third pathophysiological process connecting the hypoperfusion and hyperperfusion pathways.
In the majority of the cases described by Gurumukhani et al., full recovery was noted. Canpolat et al. studied the long-term follow-up of subjects diagnosed with PRES.[5] They observed that the presence of gliosis on brain MRI and interictal epileptic discharges on electroencephalograms (EEGs) are major risk factors for the development of epilepsy. Therefore, the individuals that develop PRES should be closely monitored in the follow-up with brain MRI and EEGs to assess the necessity of antiepileptic drugs or further management.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Karri M, Ramasamy B, Perumal S, Kannan KT. Posterior reversible encephalopathy syndrome: An acute neurological complication of blood transfusion. Libyan J Med Sci 2021;5:90-2.  [Full text] |
| 2. | Carvalho EG, Peluso HG, Batista LL, Moreira CS, Protti JS, Soares MC, et al. Reversible posterior encephalopathy syndrome in a 10-year-old child. J Bras Nefrol 2019;41:436-9. |
| 3. | Gurumukhani JK, Patel HD, Patel DM, Patel MV, Patel MM, Mahuwala ZK, et al. Posterior reversible encephalopathy syndrome following blood transfusion: A rare case report with literature review. Open Neurol 2021;15:31-6. |
| 4. | Rissardo JP, Fornari Caprara AL. Posterior reversible encephalopathy syndrome and eclampsia: Neuroimaging features. J Curr Res Sci Med 2019;5:128-9. [Full text] |
| 5. | Canpolat M, Kaya Özçora GD, Poyrazoğlu H, Per H, Çoşkun A, Gümüş H, et al. Long-Term Follow-Up of Patients with a Diagnosis of Posterior Reversible Encephalopathy Syndrome. Turkish Archives of Pediatrics. 2021;56. |
[Figure 1]
|
Search Pubmed for