Arch Gynecol Obstet DOI 10.1007/s00404-015-3800-4

REVIEW

Therapy and differential diagnosis of posterior reversible encephalopathy syndrome (PRES) during pregnancy and postpartum Mauro Cozzolino1 • Claudia Bianchi1 • Giulia Mariani1 • Laura Marchi1 Massimiliano Fambrini1 • Federico Mecacci1

•

Received: 6 March 2015 / Accepted: 17 June 2015 Ó Springer-Verlag Berlin Heidelberg 2015

Abstract Purpose Posterior reversible encephalopathy syndrome (PRES) is an usually reversible neuro-radiological clinical entity characterized by headache, confusion, visual disturbances or blindness and seizures. It rarely occurs without seizures. Methods We conducted a literature review in MEDLINE about PRES during post partum and pregnancy, focusing on differential diagnosis and therapy. We reviewed 28 articles (case reports, original articles and reviews) describing PRES as well as a case of a severe, immediate postpartum HELLP syndrome (haemolysis, elevated liver enzyme levels, low platelet count) with PRES without generalized seizure. Results The development of PRES after delivery is unusual. Magnetic resonance imaging represents the gold standard for the diagnosis of this condition. White matter oedema in the posterior cerebral hemispheres is typical on neuroimaging. PRES is reversible when early diagnosis is established and appropriate treatment is started without delay. The pathogenesis of PRES is discussed and the importance of a prompt diagnosis is emphasized, as the crucial role of rapid blood press reduction. Conclusion MRI is the diagnostic gold standard and it may be useful in the differential diagnosis. The goal of the therapy is to control elevated blood pressure and to prevent seizures or promptly manage it.

Keywords Pregnancy  Eclampsia  HELLP syndrome  Hypertension  Imaging

& Mauro Cozzolino [email protected]

Methods

1

Department of Biomedical, Experimental and Clinical Sciences, Division of Obstetrics and Gynecology, University of Florence, Largo Brambilla, 350134 Florence, Italy

Introduction Posterior reversible encephalopathy syndrome (PRES) or reversible posterior leukoencephalopathy syndrome (RPLS) is a rare clinical and neuro-radiological condition first described by Hinchey et al. in 1996 [1]. PRES is often associated with hypertensive encephalopathy, preeclampsia, eclampsia, renal failure, immunosuppressive therapy or chemotherapy [1]. More rarely it can be related to autoimmune disorders, thrombotic thrombocytopenic purpura, HIV syndrome, acute intermittent porphyria, blood transfusion and electrolyte disturbances [2, 3]. This syndrome is typically characterized by a variable combination of clinical conditions such as headaches, visual disturbances, nausea, vomiting, disorders of consciousness and generalized seizures. Laboratory results can vary, depending on the different associated conditions. The typical neuro-radiological finding, however, is cortical and subcortical oedema, especially in posterior cerebral regions [4, 5]. PRES is usually considered a reversible condition if promptly diagnosed and properly treated. However, a delayed or incorrect diagnosis may lead to irreversible damage [6].

We reported the case of a patient who developed PRES in the post partum period, complicated by HELLP syndrome. We also reviewed the currently available literature

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concerning differential diagnosis and therapeutical options for PRES. Literature research We conducted a review of the literature using MEDLINE and searching for articles published in English from April 2003 to August 2014. The following terms were used: PRES (Posterior reversible encephalopathy syndrome), RPLS (reversible posterior leukoencephalopathy syndrome), HELLP syndrome, Pre-eclampsia, Eclampsia, Pregnancy. We found a total of 33 articles but only 28 of them were in written English. Among these 28 articles, 22 were case reports, 3 were original articles and the remaining 3 were reviews. All the articles that were taken into account concerned PRES during pregnancy or postpartum period. Case presentation A gravida 2 para 1, 32-year-old woman, at 38 weeks gestation, was admitted to our clinic due to spontaneous labour. At the time of admission to hospital, her blood pressure was 142/90 mmHg and laboratory tests were normal. There was no past history of hypertension nor other diseases. Both the current and the previous pregnancy were physiological. During the second stage of delivery, the woman began complaining of headaches. A healthy male child, weighting 3.010 g, Apgar index 10 9, 50 10, was born with normal vaginal delivery. One hour after delivery, the headaches rapidly increased in intensity, followed by severe epigastric pain and vomiting; blood pressure was 169/110–187/109 mmHg. I.v. MgSO4 was immediately administered, beginning with a loading dose of 4 g in 20 min, followed by a maintenance dose (i.v. 2 g per hour). Calcium channel blockers were administered per os. Vital parameters were monitored every 15 min. ECG registered a sinus rhythm at 86 bpm. Laboratory tests reported increased liver enzymes—AST = 355 U/L, ALT = 217 U/L, CPK = 381 U/L, LDH = 677 U/L, and a reduction in platelet count to 126 9 109/L. Renal function tests, haematocrit level, serum bilirubin and electrolytes were within normal limits. Findings were suggestive of postpartum preeclampsia complicated by HELLP syndrome. Dexamethasone was promptly administered. Despite antihypertensive medications the patient continued complaining of an occipital headache, as well as visual disturbances such as blurred vision. Due to the persistent headache and the decreased patient’s alertness, brain CT was performed. The CT showed a diffuse hypodensity in the right cerebellar lobe without evidence of intracranial bleeding. Thereafter, brain MR-imaging and MR-angiography of the circle of Willis were performed,

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which showed cortical and sucbortical hyperintense lesions in both cerebellar lobes with elevated diffusion and no angiopaty; imaging features related to vasogenic oedema consistent with PRES syndrome (Fig. 1). Neurological examination showed a drowsy patient in a confused state. With the neurologists’ recommendation, the woman was transferred to the Subintensive Care Unit (SCU) for monitoring. Anticoagulant therapy, antiedemigenic agents (such as mannitol–dexamethasone), diuretic agent (furosemide) were administrated in addition to MgSO4 infusion; we witnessed a progressive state of consciousness improvement with neurological deficit resolution, biochemical analysis and blood pressure normalization. The patient remained for 3 days in the SCU; then she came back to the Obstetric Department and on the 15th day after delivery she was discharged home without any symptom. The follow-up brain MRI performed 3 weeks later showed the complete resolution of brain oedema and no vascular imaging of abnormalities (Fig. 1). The resolution further supported the diagnosis of PRES.

Discussion The incidence of PRES has not been established to date. Hinchey et al. first described this condition, which was associated with other diseases, including eclampsia. Eclampsia and pre-eclampsia are common clinical conditions described in association with PRES during pregnancy and the postpartum period. Pre-eclampsia can be complicated by HELLP syndrome and in about one-third of cases it occurs in the immediate post-partum period. This clinical condition is responsible for maternal and perinatal death and early diagnosis and appropriate treatment can reduce both these events [7]. PRES was defined as a various combination of acute neurologic clinical manifestation including consciousness disturbance, seizure, headache, visual abnormalities, nausea/vomiting and focal neurological signs associated with neuroimaging findings consistent with PRES. Focal neurological signs consist of symptoms or signs related with the damage or the dysfunction of a specific anatomic site in the central nervous system. These signs were categorized as unifocal or multifocal, and as transient or persistent. Seizures, frequently the most common symptom, are usually generalized, tonic–clonic and often preceding other manifestations [8]. Visual abnormalities due to the involvement of the occipital lobe range from cortical blindness, homonymous hemianopsia, blurred vision, visual neglect and visual hallucinations [9]. Encephalopathy caused confusion, lethargic behaviour with slowed motor responses or deep stupor [10].

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Fig. 1 The MRI study shows the presence of bright alteration in the T2 weighted images in correspondence of both cerebellar hemispheres. It indicates the presence of vasogenic oedema. a FLAIR,

axial and b corresponding DWI image. FLAIR sequences, acquired after 3 weeks, show the complete resolution of brain oedema (c)

PRES is usually associated with increased blood pressure, but it may occur with a mild elevation in blood pressure even in normotensive patients. Pathophysiology of PRES remains controversial and there are multiple theories. The preferred theory suggests that a rapid rise in blood pressure leads to a breakdown in cerebral autoregolation with cerebral arterioles dilatation. The disruption of the blood–brain barrier results in the shifting of the fluid from the intravascular compartment to the interstitial space with a consequent vasogenic oedema [11, 12]. An alternative theory suggests that the spasm of cerebral vessels in response to acute hypertension causes a decrease in cerebral blood flow and cytotoxic oedema [13]. Neuroimaging is essential for the diagnosis of PRES. CT scan must be performed as first investigation for patients with acute neurological disorders, complicated pregnancy and postpartum, in order to rule out an haemorrhagic or an ischaemic stroke. Unfortunately, CT scans may show lesions in only about 50 % of cases of PRES [10]. The disorder appears as areas of low density involving the posterior cranial fossa and the occipital lobe. MRI is the gold standard for diagnosis of PRES (Table 1) [14], because it can both provide information about cerebral involvement earlier than CT and, it can also be a useful tool in the differential diagnosis. MRI shows bright lesions on T2 weighted imaging, especially on fluid attenuated inversion recovery (FLAIR) acquisition: they may be rarely isolated, usually patchy or confluent. Both hemispheres are affected, sometimes asymmetrically, involving subcortical white matter especially in the posterior cerebellar fossa and the parieto-occipital regions. However, T2- imaging could not distinguish vasogenic oedema (reversible) from citotoxic oedema (irreversible): these can be differentiated only by

diffusion weighted imaging (DWI) [15, 16]. Sometimes small intracranial haemorrhage occurs close to the typical PRES lesion [17]; susceptibility weighted MRI is very sensitive in detection. The MRI also plays a central role in the follow-up: MRI scans must be acquired at 24–48 h after the acute event and then repeated until the disappearance of imaging and clinical features. Differential diagnosis of PRES in pregnancy and puerperium may be difficult and challenging. It includes severe neurological conditions such as cerebrovascular disorders, particularly ischaemic and haemorrhagic stroke or cerebral venous sinus thrombosis (CVTS), cerebral artery dissection [15, 18–25]. Other differential diagnosis are partial seizure, migraine, infection (encephalitis and meningitis) [15, 20], inflammatory or autoimmune diseases like vasculitis [15, 19, 24], metabolic and demyelinating disorders [19, 23] (Table 1). Clinical features and MRI findings lead to correct diagnosis of PRES in most of cases, so further investigations are rarely required. CT imaging is primarily used to exclude a haemorrhagic event, but it is insufficient to distinguish PRES from other neurologic conditions such as infarction, vasculitis and demyelinating disorders; cerebrospinal examination is necessary when a neurological infectious disease is suspected. MRI in the evaluation of the circle of Willis can show stenosis or occlusion as evidence in the cases of cerebral venous sinus trombosis. The goal of the therapy is to control elevated blood pressure, seizures, minimize vasospasm and risk of secondary infarct or haemorrhage [18]. Magnesium sulphate (MgSO4) is the first choice for the treatment of PRES: it improves both seizures and hypertension (Table 1). Actually in the central nervous system MgSO4 protects blood

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Arch Gynecol Obstet Table 1 Diagnosis, differential diagnosis, hypertension therapy, seizures therapy during PRES References

Diagnosis

Roth [15]

Hypertension therapy

Seizures therapy

Magnesium sulphate, antihypertensive

Differential diagnosis Stroke, encephalitis, intracranial venous thrombosis, intoxication with anticholinergic drugs, vasculitis

DominguesFuentes [19]

Lumbar puncture, CT, MRI

Sulphate magnesium, labetalol, hydralazine

Diazepam and phenytoin; sedation, intubation and mechanical ventilation; midazolam and valproic acid

Stroke, intracranial venous sinus thrombosis, demielinizantes diseases, vasculitis, metabolic alterations, encephalitis

Pinzon [20]

CT, lumbar puncture

Magnesium sulphate, hydralazine, labetalol, sodium nitroprusside

Magnesium sulphate benzodiazepines and phenytoin

Hemorrhagic strokes cerebral venous thrombosis, migraine, cerebral artery dissection, encephalitis, ischaemic stroke, cerebral venous, sinus thrombosis, cerebral artery dissection

Krishnamoorthy [21]

CT, lumbar puncture, MRI, MRV

Labetalol

Endotracheal intubation magnesium sulphate

Phaeochromocytoma, iatrogenic meningitis, subarachnoid haemorrhage, venous sinus thrombosis and ischemia

Nasr [22]

CT, Fundoscopy, MRI

Magnesium sulphate, hydralazine, labetalol

Magnesium sulphate

Intracerebral haemorrhages venous sinus thrombosis

Vijayalakshmi [23]

CT, MRI

Magnesium sulphate, labetalol

Aygun [24]

CT

Magnesium sulphate, nifedipine

Haemorrhage, venous thrombosis, vasculitis, pontine and extrapontine myelinosis Magnesium sulphate

Postma [25]

MRI

Magnesium sulphate

Magnesium sulphate

Servillo [27]

MRI

Calcium antagonists labetalol, nifedipine

Magnesium sulphate, nimodipine

Tsukimori [28]

MRI/MRA

Magnesium sulphate, sodium nitroprusside, nicardipine

Magnesium sulphate

Gimovsky [33]

CT, MRI/ MRA

Amagada [34]

CT

Magnesium sulphate, labetalol, hydralazine

Diazepam magnesium sulphate

Maccora [35]

EEG, CT, MRI

Magnesium sulphate, sodium nitroprusside

Levetiracetam, magnesium sulphate

Fujiwara [36]

Lumbar puncture, ECG, EEG, CT, MRI/ MRA –

Magnesium sulphate, nifedipine

Diazepam, phenytoin, magnesium sulphate

Powel [37]

Wei-Xia Peng [38]

MRI

Oehm [39] Torrillo [40]

MRI

Marano [41]

MRI, EEG

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Phenytoin

Magnesium sulphate, labetolol, nifedipine Magnesium sulphate, nifedipine

Magnesium sulphate and diazepam gabexate mesilate

Magnesium sulphate Magnesium sulphate, nicardipine, labetalol

Magnesium sulphate Magnesium sulphate

Phenobarbital

Arch Gynecol Obstet Table 1 continued References

Diagnosis

Hypertension therapy Magnesium sulphate

Seizures therapy

Differential diagnosis

Intracranial haemorrhage

Ural [42]

MRI

Thakur [43]

CT

Labetalol, magnesium sulphate

Diazepam, magnesium sulphate

Ekawa [44]

MRI, CT

Magnesium sulphate, hydralazine, nifedipine

Magnesium sulphate

Ondergoglu [45]

MRI

Magnesium sulphate, hydralazine

Diazepam, phenytoin, magnesium sulphate

Blindness during pregnancy

Youssoufa [46]

CT, MRI

Nicardipine, magnesium sulphate

Wagner [47]

MRI, CT

Magnesium sulphate

Schusse [48]

EEG, MRI

Labetalol, magnesium sulphate

Magnesium sulphate

Progressive multifocal leukodystrophy

Magnesium sulphate, labetalol, hydralazine, nicardipine

Magnesium sulphate

Hydralazine

Magnesium sulphate

Brewer [49] Siddiqui [50]

MRI, MRA, MRV

brain barrier, this way limiting cerebral edema formation [26]. In the peripheral and cerebral vasculature, MgSO4 may act as a vasodilator to reduce vasoconstriction or decrease peripheral resistance [26]. Generally, MgSO4 is administered with initial intravenous bolus followed by continuous infusion for 48 h after the acute event. During therapy with MgSO4, patients should be monitored closely checking for deep tendon reflexes, respirations, urine output and magnesemia. Other antiepileptic agents, alone or together with MgSO4, such as diazepam, phenytoin and valproic acid, are used for seizure control but their use is not approved by all authors because of their side effects (respiratory depression, cardiac effects, vigilance effects) [27]. Patients should be treated concomitantly with antihypertensive therapy: the blood pressure should be gradually corrected to target levels of 140–155 mm Hg systolic and 90–105 mm Hg diastolic. Higher blood pressure levels indeed have been associated with incomplete oedema resolution. Parenterally administered calcium antagonists or orally labetolol and nifedipine are usually preferred [27]. Intravenous hydralazine can be also used for the treatment of severe hypertension. Vasodilators such as nitroglycerin are excluded because they can worsen clinical manifestations of PRES [28]. An antioedema agent which can be successfully used to decrease intracranial pressure is mannitolo. Demir et al. [29] proved that the treatment with mannitolo is not superior to the treatment with MgSO4 in achieving neurological recovery. The corticosteroids can be used to treat concurrent haemolysis, elevation of liver enzymes and lowering of platelet count that occur in HELLP syndrome [30]. Theoretically, corticosteroids should reduce vasogenic oedema even if in literature there are no reports about steroids usage in patients with PRES [15].

Intracranial sinus thrombosis

The prognosis of PRES is good after an appropriate treatmen; symptoms generally resolve in about 3–8 days. Imaging abnormalities disappear within a few weeks. However, 5–12 % of cases can take a negative course with irreversible brain damages culminating in persistent severe neurologic deficits or death [31, 32]. The early diagnosis and the prompt treatment of PRES are very important to avoid irreversible neurological injury. In conclusion, this neurological syndrome should be considered in patients with headaches, visual abnormalities, altered consciousness and increased blood pressure. Seizures, as in our case, may not occur. MRI is the diagnostic gold standard and it may be useful in the differential diagnosis. The goal of the therapy is to control elevated blood pressure and to prevent seizures or promptly manage it. MgSO4 therapy should be initiated as soon as preeclampsia, eclampsia or PRES is suspected because it resolves both hypertension and seizures. We believe early recognition of symptoms and immediate diagnosis, can guarantee a good prognosis with a complete resolution of neurological symptoms and cerebral lesions.

Conflict of interest The authors did not report any potential conflicts of interest. I would like to warmly thank Joel Contreras and Giovanna Carriero for reviewing the English of the manuscript and for valuable advice.

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