Intensive Care Med (2007) 33:230–236

DOI 10.1007/s00134-006-0459-0 REVIEW

Giuseppe Servillo
Francesca Bifulco
Posterior reversible encephalopathy syndrome
Edoardo De Robertis in intensive care medicine
Ornella Piazza
Pasquale Striano
Fabio Tortora
Salvatore Striano
Rosalba Tufano

Received: 26 February 2006
Accepted: 19 October 2006
Published online: 21 November 2006
© Springer-Verlag 2006
G. Servillo (u) · F. Bifulco ·
E. De Robertis · O. Piazza · R. Tufano
Department of Surgical and
Anesthesiological Sciences, Medical
Intensive Care Unit,
Naples, Italy
e-mail: servillo@unina.it
Tel.: +39-081-7463554
Fax: +39-081-5456338
P. Striano · S. Striano
Federico II University, Epilepsy Centre,
Department of Neurological Sciences,
Naples, Italy
F. Tortora
Federico II University, Service of
Neuroradiology,
Naples, Italy
Abstract Background: Posterior
reversible encephalopathy syndrome
(PRES) is a well-recognized clinico-
neuroradiological transient condition.
Early recognition is of paramount im-
portance for prompt control of blood
pressure or removal of precipitating
factors and treatment of epileptic
seizures or status epilepticus. Delay
in the diagnosis and treatment may in
fact results in death or in irreversible
neurological sequelae. Discussion:
PRES is characterized by headache,
altered mental status, seizures, and
visual disturbances and is associated
with a number of different causes,
most commonly acute hyperten-
sion, preeclampsia/eclampsia, and
immunosuppressive agents. Clinical
symptoms and neuroradiological find-
ings are typically indistinguishable
among the cases of PRES, regard-
less of underlying cause. Magnetic
resonance studies typically show
edema involving the white matter of
cerebral posterior regions, especially
parieto-occipital lobes but frontal
and temporal lobes, and other en-
cephalic structures may be involved.
Conclusions: Intensivists and other
physicians involved in the evaluation
of patients with presumed PRES must
be aware of the clinical spectrum
of the associated conditions, the
diagnostic modalities, and the correct
treatment.
Keywords Posterior reversible en-
cephalopathy syndrome · Intensive
care · Magnetic resonance imaging ·
Encephalopathy · Eclampsia

Introduction Clinical features

In 1996 Hynchey et al. [1] first described a reversible PRES is a clinicoradiological syndrome associated with
syndrome characterized by headache, altered mental the following clinical conditions [1, 2, 3, 4, 5, 6]:
functioning, seizures, and blurred vision, associated with
neuroimaging findings indicating predominantly poster- • Hypertensive encephalopathy
ior leukoencephalopathy. The authors coined the term • Preclampsia/eclampsia/HELLP (hemolysis, elevated
“posterior reversible leukoencephalopathy syndrome” liver enzymes, low platelet count) syndrome
for this condition. However, this term was considered • Immunosuppressive/cytotoxic drugs (e.g., cyclosporin,
misleading by other authors, as the involvement of gray antineoplastic drugs, interferon-α, antiretroviral ther-
matter is also observed, and the term posterior reversible apy)
encephalopathy syndrome (PRES) was therefore intro- • Acute or chronic renal diseases (e.g., glomerulonephri-
duced [2]. tis, dialysis disequilibrium syndrome)

• Thrombotic thrombocytopenic purpura/haemolytic
uraemic syndrome
• High-dose steroid therapy
• Liver failure (e.g., drug-induced)/transplantation
• Endocrine dysfunctions (e.g., primary aldosteronism,
pheochromocitoma)
• Hypercalcemia/hyperparathyroidism
• Bone marrow transplantation
• Massive blood transfusion/erythropoietin therapy
• Porphyria
• Other causes (e.g., intravenous globulin, contrast media
exposure, scorpion poison, stimulants abuse, digitoxin
intoxication, Averrhoa carambola ingestion)
The clinical picture is characterized by an acute en-
cephalopathy with headache, vomiting, confusion,
seizures, and visual impairment [1, 2, 3, 4]. Patients have
an acute or subacute neurological presentation, often
heralded by convulsions. Seizures may begin focally but
usually become generalized. Multiple seizures are more
common than single events, sometimes presenting a true
status epilepticus. Alertness and behavior disturbances
range from somnolence and lethargy to stupor and frank
coma; restlessness and agitation may alternate with
lethargy. Visual disturbances are almost always present
ranging from hemianopsia and visual neglect to cortical
blindness. Tendon reflexes are usually brisk and some
patients may also present weakness and incoordination of
the limbs [1, 2, 3, 4].
Radiographic findings
Recognition of the characteristic imaging findings by
radiologists is the key to diagnosing this syndrome and
preventing deleterious workups or therapies. Computed
Fig. 1 a Noncontrast computed
tomography showing diffuse
hypodensity in posterior regions
bilaterally. b Fluid-attenuated
inversion recovery MRI showing
increased white/gray matter
affecting predominantly the
parieto-occipital and frontal
areas. c Diffusion-weighted
image showing elevated regional
apparent diffusion coefficient in
a pattern typical of posterior
reversible encephalopathy
syndrome
231
tomography can be used preliminarily to detect hypo-
dence lesions of posterior encephalopathy, but magnetic
resonance imaging (MRI) is the gold standard [1, 2, 3, 7].
Due to the widespread use of MRI this syndrome is being
diagnosed more frequently. During the acute phase MRI
usually reveals hyperintence on both echoes of a dual-echo
T2-weighted sequences and either iso- or hypointence
on T1-weighted images brain abnormalities, including
both gray and white matter. Mainly involved are the
parietal-occipital lobes; however, cerebellar hemispheres,
basal ganglia, frontal lobes, and brainstem are also often
involved [1, 2, 8]. Fluid-attenuated inversion recovery
sequences significantly improve the ability to diagnose
and detect subcortical and cortical lesions in PRES over
proton density and T2-weighted spin-echo images and
therefore should be performed in patients with suspected
PRES to allow more confident recognition of the often
subtle imaging abnormalities (Fig. 1) [2]. Diffusion-
weighted MRI has been demonstrated to be particularly
sensitive to changes in distribution of water in the brain
and can detect white matter edema early and reliably
differentiate between vasogenic and cytotoxic edema in
these patients (Fig. 1) [7, 8]. A spectrum of severity has
been hypothesized, ranging from an initially reversible
phase of vasogenic edema formation to a later phase of
ischemic damage and hemorrhage, which carries a worse
prognosis [9]. Magnetic resonance spectroscopy has been
also suggested having a prognostic value during the acute
phase, when high lactate levels may be present probably
due to transient derangement of energy metabolism [3,
4]. Finally, the use of perfusion computed tomography
with stable xenon, a technique providing a quantitative
measure of cerebral perfusion, has been recently proposed
in the early stage to monitor the degree of cerebral
perfusion and to guide titration of antihypertensive
therapy [10].
232

Pathophysiology and pathological features Otherwise, delayed diagnosis and therapy can result in
permanent damage to affected brain tissues [2, 25, 26, 27,
The exact pathogenesis of PRES remains incompletely 28, 29]. Sometimes, even with adequate therapy, recovery
understood but is probably related to the failure cerebral is not complete [30, 31, 32]. In particular, posterior
autoregulation and endothelial damage. The favored encephalopathy can be complicated by ischemia, with or
pathogenetic theory suggests autoregulatory disturbance without vasospasm, and infarcts, typically in a posterior
with hyperperfusion, resulting in blood-brain barrier borderzone distribution between the middle and posterior
breakdown with reversible edema, without infarction [11, cerebral arteries [10]. The interruption of a status epilep-
12, 13, 14]. In particular, in conditions accompanied by ticus seems to be of particular importance since patients
high blood pressure (e.g., hypertensive encephalopathy) it with multiple seizures have major evidence of cerebral
has been suggested that the increased systemic pressure infarction [30]. It can also be thought that despite the
exceeds the autoregulatory mechanisms of the cere- benign course during the acute phase some patients may
bral vasculature, sufficient to overcome the blood-brain later develop chronic neurological sequaele, for example,
barrier, and hence allowing extravasation of fluid and focal epilepsy. Cases of hypertensive encephalopathy
blood into the brain parenchyma [4, 15]. Thus there is or eclampsia followed by later development of chronic
a “breakthrough” of autoregulation and increasing blood epilepsy have been reported in the literature [31, 32].
pressure, an upper limit of autoregulation is surpassed, Recurrent seizures starting from weeks to years after
causing focal dilatation of cerebral vessels. Regions of the acute encephalopathy and neuroradiological study
both vasoconstriction and vasodilatation (“sausage-string reveal lateralized hyppocampal sclerosis or posterior brain
pattern”) develop [16, 17], especially in arterial boundary lesions. In these patients posterior encephalopathy acted
zones, resulting in brain hyperperfusion. This leads to as a precipitating injury leading to a permanent cerebral
focal areas of breakdown of the blood-brain barrier and damage and possibly triggering a chronic epileptic focus.
extravasation of fluid. MRI findings suggest the development of the transient,
Autopsy studies in patients with hypertensive en- “edema” lesions into malacic areas. However, as acute
cephalopathy or eclampsia show varying degrees of neuroimaging study is not available for any of these cases,
vascular (fibrinoid necrosis and of thrombosis arterioles this mechanism remains speculative [31, 32].
and capillaries) and parenchymal (microinfarcts, cerebral
edema) alterations [18, 19]. However, brain biopsy find-
ings have been reported that show edematous white matter Differential diagnosis
with no evidence of vessel wall damage or infarction,
thus supporting the concept that the imaging changes The differential diagnosis of PRES covers a wide spectrum
on MRI represent vasogenic edema [20]. It is not well of neurological and extraneurological diseases:
known why the posterior circulation is preferentially
affected. A possible explanation is the lower sympathetic • CNS vasculitis
innervation of posterior cerebral arterial circulation than
in the internal carotid artery territory, with a consequent – Granulomatous angiitis
reduced autoregulation of already impaired cerebral – Systemic lupus erythematosus
areas [21, 22]. – Polyarteritis nodosa
An alternative theory for PRES suggests spasm of cere-
bral arteries in response to acute hypertension, resulting in • Acute or subacute neurological diseases
decreased cerebral blood flow and ischemia and cytotoxic
edema, especially in the border zones between arterial ter- – Ischemic stroke
ritories (“watershed zones”) [23]. Finally, cytotoxic thera- – Progressive multifocal leukoencephalopathy
pies may have direct toxicity on the vascular endothelium, – Acute disseminated encephalomyelitis
leading to brain capillary leakage, and blood-brain barrier – Infective encephalitis
disruption which triggers vasogenic edema [1, 24]. How- – Cerebral venous thrombosis
ever, further research is needed for a better comprehension – Cerebral autosomal dominant arteriopathy with
of pathophysiology of this complex condition. stroke and ischemic leukoencephalopathy
(CADASIL)

Outcome • Mithocondrial diseases

One of the distinctive characteristics of PRES is the – Mitochondrial encephalomyopathy, lactic acidosis
reversibility of the clinical and radiological abnormali- and stroke-like episodes (MELAS)
ties once treatment is instituted [1, 3, 6]. Most patients – Myoclonic epilepsy and ragged red fibers syndrome
usually make a complete recovery within few weeks [1]. (MERRF)

• CNS collagen diseases
• Hypoglycemia/hyponatremia
Principal differential diagnoses include sinus/cerebral
vein thrombosis and acute cerebral ischemia, which are
ruled out by MRI examinations. Infectious/autoimmune-
inflammatory disorders are usually excluded because of
the clinical course, negative findings on multiple blood
and CSF cultures, no significant increase in CSF white
blood cells, and negative serological studies. Moreover,
the distinction between PRES and extensive ischemic
stroke has very relevant therapeutic as well as prognostic
implications for the approach to controlling the hyperten-
sion and the possible reversibility of neurological deficit
in PRES. Generally, special investigations (e.g., CSF
examination) are not necessary except from a clinical
suspect of infectious/autoimmune-inflammatory disorders
(e.g., primary angiitis of brain) in which a reactive CSF
picture is observed [33].
Treatment and critical care management
Lowering blood pressure, removal or significant reduction
of the causative immunosuppressive medication, and treat-
ment of seizures are mandatory. Most of these problems
are best managed in the intensive care setting [34, 35].
Stepwise treatment of PRES is as follows:
• Removal/significant reduction in the causative fac-
tors/medications
• Maintenance of hydration (intravenous crystalloid flu-
ids), adequate arterial oxygenation, correction of elec-
trolyte disturbances
• Monitoring of airways and ventilation. Intubation (if
insufficient oxygenation)
• Insertion of central venous catheter (if cardiac dysfunc-
tion)
• Delivery or cesarean section in pregnant women
• Lowering of blood pressure (mean arterial blood pres-
sure: 105–125 mmHg with not more that 25% reduc-
tion within the first hour)
– Intravenous therapy preferred (first agents:
nicardipine at 5–15 mg/h, labetalol at 2–3 mg/min,
or nimodipine; second-line agents: sodium nitro-
prussiate, hydralazine, and diazoxide)
– Avoid angiotensin-converting enzyme inhibitors in
pregnant women
• Treatment of status epilepticus
– Intravenous anticonvulsants (first agents: lo-
razepam, initial dose 0.1 mg/kg in 2-mg boluses
over 2–5 min or diazepam at 10–20 mg over 2 min;
233
second-line agents: phenytoin (or fosphenytoin)
at 15 mg/kg or phenobarbital at 15–20 mg/kg,
infusion speed: 50 mg/min)
– In pregnant women: magnesium sulfate 5–6 bolus
intravenously in 20–30 min; 1–2 g/h intravenous
continuous infusion
– Refractory status epilepticus: propofol, midazolam,
or pentobarbital
– Continuous electroencephalographic monitoring (if
available)
General guidelines treatment
The initial evaluation of patients with PRES should
focus on rapid correction of mean arterial blood pressure,
hydration using intravenous crystalloid fluids, mainte-
nance of adequate arterial oxygenation, and correction
of coagulopathies and electrolyte disturbances [22, 34].
Attention should first be given to monitoring airways and
ventilation. Intubation may be initially avoided, but it is
necessary to maintain adequate oxygenation if aspiration,
hypoxemia, or pulmonary edema occurs. Insertion of
a central venous catheter may be sometimes required
to guide treatment if cardiac dysfunction is present [34,
35]. Over recent decades the termination of pregnancy
in women in the setting of ICU has been considered
standard practice [22]. Nowadays the wide availability of
intravenous antihypertensive and antiepileptic medications
permits many pregnancies to be carried to term, with
delivery of a healthy infant.
Treatment of hypertension
Correction of systemic blood pressure abnormalities is
crucial since, if untreated, it may lead to development
or exacerbation of cerebral edema. On the other hand,
too rapid correction of systemic hypertension in pregnant
women may result in compromised uteroplacental blood
flow. In general, the goal of treatment should be to reduce
mean blood pressure to approximately premorbid levels;
it should be monitored with a radial arterial catheter
and maintained between 105–125 mmHg, preferably by
intravenous antihypertensive medications. Nicardipine
(5–15 mg/h) or labetalol (2–3 mg/min) are usual first-line
agents. Angiotensin-converting enzyme inhibitors should
be avoided in obstetric patients due to their toxic effect on
the fetal kidney [21, 22]. Fenoldopam mesylate is a se-
lective dopamine 1 agonist, with no effect on dopamine 2
or α1 -receptors, producing a selective renal vasodilation.
This drug is potentially extremely useful as it may favor
the kidney oxygen supply/demand ratio and prevent
acute renal failure. In critically ill patients a continuous
infusion of fenoldopam at 0.1 µg/kg per minute does not
cause any clinically significant hemodynamic impairment
234

and improves renal function compared with renal dose
dopamine [36].
Nitroglycerin is often used; however, it has been
reported to aggravate edema in these patients, probably
by further enhancing brain vasodilatation [37]. Sodium
nitroprussiate, hydralazine, and diazoxide may be used
although they are difficult to titrate. Parenterally admin-
istrated nimodipine, a cerebral selective calcium-channel
blocker, may be useful in preventing cerebral vasospasm,
a pathogenetic mechanisms demonstrated in pregnant
patients with hypertensive leukoencephalopathy [38]. In
addition, a putative neuroprotective effect of nimodipine
has been also suggested [39].
Treatment of status epilepticus
Status epilepticus, defined as recurrent epileptic seizures
without complete recovery between seizures, is a neuro-
logical complication demanding immediate interventa-
tion [22, 40]. As there is often an association between
prolonged seizures and poor outcome, the importance of
early treatment must be stressed. Continuous electroen-
cephalographic monitoring, if available, is essential to
detect subtle or purely electrical seizures. Moreover, if
the patient does not recover after therapy, monitoring
of seizures should involve electroencephalography to
avoid overlooking persistence of clinically silent status
epilepticus [40].
As a general rule the intensity of treatment should
reflect the risk to the patient from status epilepticus, and
drugs likely to depress blood pressure and respiration
should be avoided [21, 22]. In addition to general sys-
temic support (airway, circulation), magnesium sulfate
is considered the mainstay of treatment in pregnant
women. This drug acts by increasing vasodilatation by
countering calcium-dependent arterial vasoconstriction,
thus increasing cerebral blood flow and thereby preventing
the ischemic insult that would engender seizures [21].
Recently an international study confirmed the efficacy of
this drug without harmful effects [41]. For treatment of
status epilepticus in PRES related to other causes than
pregnancy, intravenous administration of benzodiazepines
(lorazepam or diazepam) is recommended as first-line
therapy. Lorazepam is administrated at the initial dose of
0.1 mg/kg given in repeated 2-mg boluses slowly over
2–5 min; alternatively, 10–20 mg diazepam may be given
at 2–5 mg/min [22]. If status epilepticus persists, second-
line drugs include phenytoin, fosphenytoin, and third-line
drugs the barbiturate phenobarbital, or the anesthetics
thiopental or propofol, or possibly ketamine. Phenytoin
is given in bolus at the dose of 15 mg/kg. Phenobarbital
may be administered at 15–20 mg/kg (50–100 mg/min)
with a daily maintenance dose of 1–3 mg/kg. However,
benzodiazepines and phenobarbital may worsen the
vigilance or cause respiratory depression, and phenytoin
may induce cardiac adverse effects (i.e., hypotension,
cardiac dysrhytmias). Fosphenytoin, a prodrug of pheny-
toin, has a lower incidence of local side effects (e.g.,
thrombophlebitis, “purple glove”) but equivalent cardiac
risks [21]; in addition, it is not available in many countries.
Although not approved by the United States Food and
Drug Administration for the treatment of status epilepti-
cus, intravenous valproate is an emerging option for this
purpose. Recent observations report its efficacy and safety
in patients with cardiovascular failure, in the elderly and in
neurointensive care unit [42]. Moreover, in our experience
valproate has led to seizure remission without adverse ef-
fects in obstetric patients with PRES [26, 32]. However, the
possible occurrence of thrombocytopenia should be con-
sidered, and careful hematological monitoring is thus re-
quired. To remain cases of refractory status epilepticus,
continuously infused anesthetic medication may be nec-
essary, usually either midazolam, propofol, or pentobarbi-
tal. In particular, propofol has been recently shown to be
highly effective in course of intensive care in patients with
refractory status epilepticus [43].
Conclusions
Although it is a well known condition among neuroradiol-
ogists, PRES is still unfamiliar to many clinicians working
in critical areas. Delay in diagnosis of this condition may
lead to additional morbidity and prolonged ICU stay. Thus
it is very important that intensivists and all physicians be
well aware of this syndrome since prompt recognition and
precocious treatment have prognostic implications.

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