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Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 10  |  Issue : 2  |  Page : 370-372  

Recurarization in a successfully managed case of posterior reversible encephalopathy syndrome (PRES) for emergency caesarean section


Department of Anaesthesia, Padmashree Dr. DY Patil Medical College, Nerul, Navi Mumbai, India

Date of Web Publication26-Apr-2016

Correspondence Address:
Suchita Parikh
Department of Anaesthesia, Padmashree Dr. DY Patil Medical College, Nerul, Navi Mumbai, India
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0259-1162.167833

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   Abstract 


Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiologic syndrome of headache, visual changes, altered mental status and seizures with radiologic findings of posterior cerebral white matter edema. It is seen in hypertensive encephalopathy, renal failure, and autoimmune disorders or in patients on immunosuppressants. We report a case of 24-year-old primigravida who presented at term with sudden onset hypertension, neurological deficits, and an episode of the visual blackout. Magnetic resonance imaging showed features suggestive of PRES. She was posted for emergency lower segment cesarean section. General anesthesia was administered and blood pressure managed with antihypertensives. Postoperatively, she developed acute respiratory depression after prophylactic administration of injection magnesium sulfate. This case highlights that good clinical acumen along with early neuroimaging helps in prompt diagnosis, treatment and prevention of long-term neurological sequelae in PRES and the anesthetic implications of administering magnesium sulfate in the immediate post neuromuscular block reversal phase.

Keywords: Eclampsia, magnesium sulfate, neuromuscular monitoring, posterior reversible encephalopathy syndrome, recurarization


How to cite this article:
Parikh S, Tavri S, Mohite S. Recurarization in a successfully managed case of posterior reversible encephalopathy syndrome (PRES) for emergency caesarean section. Anesth Essays Res 2016;10:370-2

How to cite this URL:
Parikh S, Tavri S, Mohite S. Recurarization in a successfully managed case of posterior reversible encephalopathy syndrome (PRES) for emergency caesarean section. Anesth Essays Res [serial online] 2016 [cited 2019 Nov 20];10:370-2. Available from: http://www.aeronline.org/text.asp?2016/10/2/370/167833




   Introduction Top


Posterior reversible encephalopathy syndrome (PRES) was first described by Hinchey in 1996 with headache, visual changes, altered mental status, seizures, and hyperintensities in the white matter of parietooccipital lobes.[1] This is seen in diverse clinical situations like hypertension, eclampsia, preeclampsia, immunosuppressive and cytotoxic medications, severe hypercalcemia, autoimmune disorders, hemolytic uremic syndrome, renal failure, and sepsis.[2],[3]

We report, a successfully managed case of a full term primigravida with PRES posted for emergency lower uterine segment cesarean section [LSCS] with emphasis on avoiding magnesium sulfate (MgSO4) in immediate postreversal phase.


   Case Report Top


A full term 26-year-old antenatal registered primigravida weighing 50 kg, presented with sudden onset weakness of the right side of the body and an episode of diminution of vision. Her blood pressure (BP) which had remained normal was now 200/110 mmHg. Injection labetalol 100 mg was given intravenously (IV) and an urgent magnetic resonance imaging (MRI) showed ill-defined hyperintensities involving bilateral basal ganglia, periventricular white matter, and parietal cortex suggestive of PRES [Figure 1].
Figure 1: (a and b) Cerebral magnetic resonance imaging our patient which showed ill-defined hyperintensities in the basal ganglia, periventricular white matter and parietal lobes suggestive of posterior reversible encephalopathy syndrome

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On systemic examination, the patient was conscious, drowsy with involuntary movements, normal tone, the power of 3/5 in right and 5/5 on the left upper and lower limbs. Reflexes were normal with equivocal plantars. Coordination, gait, sensory examination, vision, and fundoscopy were normal. There were no signs or symptoms of meningism. Other systems and blood investigations were normal. Urinary albumin was +2. Ultrasonography showed single intrauterine pregnancy with cord loops around the neck and tocography recorded intermittent bradycardia.

A decision to perform an emergency LSCS under general anesthesia was taken in view of her hypertensive crisis, neurological symptoms, sonographic findings, and fetal bradycardia.

After confirming an informed valid consent and starvation, pantoprazole 40 mg and ondansetron 4 mg were given IV for aspiration prophylaxis. Routine monitors were attached. The neuromuscular monitor was used for administration of relaxants. Preoperatively pulse: 104/min BP: 170/110 mmHg, respiratory rate: 25/min, oxygen saturation (SpO2): 98% on room air. After preoxygenation for 3 min and premedication with glycopyrrolate 0.2 mg and 2% lignocaine 60 mg IV, modified rapid sequence induction was done with thiopentone sodium 3 mg/kg and rocuronium 0.8 mg/kg. Intubated with a 7.5 cuffed endotracheal tube at the train of four (TOF) score of 0. Anesthesia maintained with oxygen-air and isoflurane 0.8–1%. A 2 kg baby was delivered with APGAR score of 6/10 at 1 min and 8/10 at 5 min. IV oxytocin 20 units infusion, midazolam 1 mg and fentanyl 60µg given after baby delivery. The intraoperative course was uneventful with adequate urine output. BP was maintained between 150/100–140/90 mmHg with labetalol 0.1–0.3 mg/kg/min infusion.

The patient was reversed when TOF score was 90% with neostigmine 0.05 mg/kg and glycopyrrolate 8 µg/kg and was extubated after she fulfilled all criteria for extubation. She was conscious, responding to verbal commands with BP of 150/100 mmHg.

MgSO4 10 g intramuscularly and 4 g IV was given 10 min postextubation by the gynaecologist as a prophylaxis against convulsions.

Immediately, the patient developed respiratory depression and became unresponsive. Monitoring showed heart rate (HR) 98/min, BP 180/100 mmHg and SpO2 95% and TOF score 20%. The patient was reintubated after administering IV propofol 100 mg. 10 cc 10% calcium gluconate was given IV to antagonize the effects of magnesium. IV hydrocortisone 100 mg was given to prevent laryngeal edema.

It was decided to shift the patient to Intensive Care Unit (ICU) for ventilatory support, control of BP, and to maintain a stable intracerebral milieu till reversal of recurarization. The patient was sedated with midazolam-fentanyl infusion. Blood counts and blood gases showed normal values; BP maintained at 140/90 mmHg with IV labetalol 0.1–0.3 mg/kg/min and nitroglycerin 0.1 mg/kg/min. She was weaned and extubated on confirming extubation criteria.

Postextubation vitals: HR 96/min, BP 140/90 mmHg, SpO2 98%. However, her neurological motor deficits persisted for which a neurological reference was done. She was observed in ICU for 2 days. A repeat MRI done on the 10th postoperative day showed a decrease in the extent of the disease [Figure 2]. The patient improved symptomatically by day 20 and discharged on day 24.
Figure 2: (a and b) Cerebral magnetic resonance imaging our patient after supportive treatment showed decrease in extent of disease as compared to the previous report

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   Discussion Top


PRES or reversible posterior leucoencephalopathy occurs in 5% of eclamptic patients.[1],[3]

Among the several theories for the pathophysiology of PRES, leading hypothesis is a rise in BP above the baseline causing breakdown of brain vascular autoregulation and dilatation of cerebral arterioles with leakage through the endothelial junctions resulting in vasogenic edema.[4],[5],[6] The posterior brain is at a greater risk because of its less extensive innervation, which makes it unable to adjust to BP fluctuations hence decreasing its threshold for vasogenic edema.[4],[7]

Reversibility of PRES is not spontaneous; hence, complete resolution depends on prompt intervention although partial resolution and fatality have been reported.[5],[8] Control of BP, seizures, and withdrawal of causative factor is the treatment of choice.[5],[9]

It is advisable to reduce BP only by 15–25% to maintain cerebral perfusion as there is a loss of autoregulation.[5]

In pregnant or postpartum patients, MgSO4 is the anticonvulsant drug of choice. It has a depressant effect on the central nervous system and neuromuscular junction (NMJ), reduces hyperreflexia, prevents onset and recurrence of seizures, improving maternal and neonatal outcome.[5]

Our patient went into immediate respiratory depression after administration of MgSO4 postreversal of neuromuscular blockade. MgSO4 inhibits prejunctional acetylcholine release and postjunctional action potentials, potentiating effect of nondepolarizing neuromuscular blocking drugs.

Some amount of neuromuscular blocking drug present at the NMJ in synergism with magnesium could have caused recurarization, muscle weakness, and respiratory depression which were also documented by the reduction in the TOF ratio.[10],[11]

An MRI ruled out other causes such as eclampsia, cerebral venous sinus thrombosis, and pregnancy-related stroke. Infectious or autoimmune inflammatory disorders were ruled out by the clinical course, negative blood culture, and serological studies.


   Conclusion Top


PRES is often an unsuspected condition which is commonly precipitated by an acute elevation of BP, such as in preeclampsia. Early recognition and prompt radiological diagnosis along with prompt control of BP has important therapeutic and prognostic implications. Thus, clinicians should be aware of the spectrum of imaging findings in PRES. MgSO4 is an anticonvulsant of choice in pregnancy but should be used cautiously after reversal to prevent potentiation of residual muscle relaxant effect. Neuromuscular monitoring intraoperatively helps titrate relaxant dose and postoperatively confirms a complete reversal.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500.  Back to cited text no. 1
    
2.
Alparslan M, Bora U, Hüseyin K, Ayhan D, Gültekin S. Posterior reversible encephalopathy syndrome in a renal transplanted patient. Am J Case Rep 2013;14:241-4.  Back to cited text no. 2
    
3.
Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: Fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008;29:1036-42.  Back to cited text no. 3
    
4.
Nuwer JM, Eshaghian S. Late postpartum eclampsia with posterior reversible encephalopathy syndrome. Hosp Physician 2007;43:45-9.  Back to cited text no. 4
    
5.
Pedraza R, Marik PE, Varon J. Posterior reversible encephalopathy syndrome: A review. Crit Care Shock 2009;12:135-43.  Back to cited text no. 5
    
6.
Achar SK, Shetty N, Joseph TT. Posterior reversible encephalopathy syndrome at term pregnancy. Indian J Anaesth 2011;55:399-401.  Back to cited text no. 6
[PUBMED]  Medknow Journal  
7.
Raina S, Mahesh D, Rajendra G, Chauhan NS. Reversible posterior leukoencephalopathy syndrome. J Neurosci Rural Pract 2012;3:222-4.  Back to cited text no. 7
[PUBMED]  Medknow Journal  
8.
Pugliese S, Finocchi V, Borgia ML, Nania C, Della Vella B, Pierallini A, et al. Intracranial hypotension and PRES: Case report. J Headache Pain 2010;11:437-40.  Back to cited text no. 8
    
9.
Iwama M, Takahashi H, Takagi R, Hiraoka M. Permanent bilateral cortical blindness due to reversible posterior leukoencephalopathy syndrome. J Nippon Med Sch 2011;78:184-8.  Back to cited text no. 9
    
10.
Fawcett WJ, Stone JP. Recurarization in the recovery room following the use of magnesium sulphate. Br J Anaesth 2003;91:435-8.  Back to cited text no. 10
    
11.
Hans GA, Bosenge B, Bonhomme VL, Brichant JF, Venneman IM, Hans PC. Intravenous magnesium re-establishes neuromuscular block after spontaneous recovery from an intubating dose of rocuronium: A randomised controlled trial. Eur J Anaesthesiol 2012;29:95-9.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2]



 

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