Rev. Bras. Anestesiol. vol.64 número3

(1)

RevBrasAnestesiol.2014;64(3):195---198

REVISTA

BRASILEIRA

DE

ANESTESIOLOGIA

OfficialPublicationoftheBrazilianSocietyofAnesthesiology

www.sba.com.br

CLINICAL

INFORMATION

Syndrome

of

inappropriate

antidiuretic

hormone

secretion

to

Guillain---Barré

syndrome

after

laparoscopic

cholecystectomy

Mensure

Yılmaz

C

¸akırgöz

a

_,

_Esra

_Duran

b

_,

_Cem

_Topuz

a

_,

_Deniz

_Kara

a

_,

_Namigar

_Turgut

a

_,

Ülkü

Aygen

Türkmen

a

_,

_Bülent

_Turanc

_¸

c

_,

_Mustafa

_Önder

_Dolap

d

_,

_Volkan

_Hancı

e,∗

a_Department_of_{Anesthesiology}_and_Reanimation,_Okmeydani_Training_and_Research_Hospital,_Istanbul,_Turkey b_¸ehit_S _Kamil_State_Hospital,_Gaziantep,_Turkey

c_Department_of_{Anesthesiology}_and_Reanimation,_C_¸orlu_Vatan_Private_Hospital,_Tekirda˘_g,_Turkey d_Department_of_General_Surgery_C_¸orlu_Vatan_Private_Hospital,_Tekirda˘_g,_Turkey

e_Department_of_{Anesthesiology}_and_Reanimation,_School_of_Medicine,_Dokuz_Eylül_University,_Konak,_Turkey

Received2November2012;accepted20March2013 Availableonline11October2013

KEYWORDS

Syndromeof inappropriate antidiuretichormone secretion;

Guillain---Barré syndrome; Laparoscopic cholecystectomy

Abstract

Backgroundandobjectives: Guillain---Barré Syndrome isone of themost common causes of

acute polyneuropathy inadults. Recently, theoccurrence ofGuillain---Barré Syndromeafter majorandminorsurgicaloperationshasbeenincreasinglydebated.InGuillain---Barrésyndrome, syndrome of inappropriate antidiuretic hormone secretion and dysautonomy are generally observedaftermaximalmotordeficit.

Casereport: A44-year-oldmalepatientunderwentalaparoscopiccholecystectomyforacute

cholecystitis.Afterthedevelopmentofasevereheadache,nausea,diplopia,andattacksof hypertensionintheearlypostoperativeperiod,acomputertomographyofthebrainwas nor-mal.Laboratorytestsrevealedhyponatremialinkedtosyndromeofinappropriateantidiuretic hormone secretion,thepatient’s fluids wererestricted,andfurosemideand3% NaCl treat-mentwasinitiated.Ontheseconddaypostoperative,thepatientdevelopednumbnessmoving upward fromthehandsandfeet,lossofstrength,difficultyswallowingandrespiratory dis-tress.Guillain---Barrésyndromewassuspected,andthepatientwasmovedtointensivecare. Cerebrospinalfluidexaminationshowed320mg/dLprotein,andacutemotor-sensorialaxonal neuropathywasidentifiedbyelectromyelography.Guillain---Barrésyndromewasdiagnosed,and intravenousimmuneglobulintreatment(0.4g/kg/day,5days)wasinitiated.After10daysinthe intensivecareunit,atwhichtherespiratory,hemodynamic,neurologicandlaboratoryresults returnedtonormal,thepatientwastransferredtotheneurologyservice.

Conclusions: Our case report indicates that although syndrome of inappropriate

antidi-uretichormonesecretionandautonomicdysfunctionarerarely theinitialcharacteristicsof

∗_{Corresponding}_author.

E-mail:vhanci@gmail.com(V.Hancı).

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196 M.Y.C¸akırgözetal.

Guillain---Barré syndrome,the possibility ofpostoperativesyndromeofinappropriate antidi-uretichormonesecretionshouldbekeptinmind.Thepresenceofsecondaryhyponatremiain thistypeofclinicalpresentationmaydelaydiagnosis.

Introduction

Theprevalenceofhyponatremiainthepostoperativeperiod is 4.4%.1 _Syndrome _of _{inappropriate} _antidiuretic_hormone

secretion (SIADH) develops due to the insufficient

inhibi-tion of antidiuretic hormone secretion linked to plasma

hypotonia. Hyponatremia after surgical intervention is a

well-knowncause.2_In_case_studies_in_the_literature,

SIADH-linkedacute hyponatremia develops in the first few days

aftersurgicalintervention,maycausedeathandisrelated

togeneralsurgicalstressand/orpainresponse.2---5_Only_one

case related to Guillain---Barré syndrome (GBS) has been

cited.6

InGBS,SIADH anddysautonomyaregenerallyobserved

aftermaximalmotordeficit.7---9_In_this_case_report,_the_rare

clinicalprogressionofGBSisreportedinadysautonomous

patient,causing SIADH-linkedserioushyponatremia inthe

early postoperative period before definite weakness and

areflexiaafteralaparoscopiccholecystectomy.

Case

report

A 44-year-old male patient presented to the emergency

service with a complaint of abdominal pain. On

physi-cal examination, sensitivity in the left subcostal region,

reboundandmusclerigiditywerediagnosed,andthe

‘Mur-phy’ sign was positive. An abdominal ultrasound showed

thickening of the bile duct wall, dilatation of the

bil-iarytractandhighvalues ofAlanin aminotransferaz(ALT)

(145(0---45)IU/L) andGama glutamil transferaz (GGT)(73

(0---50)IU/L). The patient was admitted to the surgical

servicewithadiagnosisofacutecholecystitis.Preoperative

examinationshowedthat thepatienthadbeen monitored

for ulcerative colitis (UC) for the previous ten years,

used no medications and had no previous operative

his-tory.Exceptforthepreoperativephysicalexaminationand

highALTandGGTvaluesfromthelaboratoryexamination,

the patient had no other symptoms. After 8h of fasting,

the 85kg ASA II-E risk group patient was given 3mg IM

dormicumpremedicationandtakentotheoperatingtable.

Hiselectrocardiograph(ECG),non-invasivebloodpressure,

end-tidalCO2(etCO2)andSpO2weremonitored.

Anesthe-siawasinducedwithintravenous(iv)propofol(2.5mg/kg),

fentanyl (1␮g/kg), and rocuronium (0.6mg/kg), and the

patientwassubsequentlyintubated.Anesthesia was

main-tained with1---2%sevoflurane and60---40% N2O---O2. During

the laparoscopic cholecystectomy, his hemodynamic

val-uesandoxygensaturationwerestable,andsupplementary

musclerelaxantsandivanestheticagentswerenot

admin-istered. During the nearly 50-min operation, 8mL/kg/h

Isolyte-S was given, and 200cc urine was passed. Our

patient was monitored in the recovery room and moved

totherelevantservicebeforepostoperativecomplications

arose.

At 12h postoperative, the patient developed a severe

headache,nausea,lethargy,diplopia,urineretention,and

attacks of hypertension; however, computed tomography

(CT)ofthebrainwasnormal.Laboratorytestsprovidedthe

following results: Na: 120mmol/L (135---148mmol/L);

K: 3.8mmol/L (3.5---5.1mmol/L); Cl: 98mmol/L

(101---109mmol/L); uric acid: 1.9mg/dL (3.5---7.2mg/dL);

Bloodureanitrogen(BUN):20mg/dL(17---43mg/dL);

creati-nine: 0.5mg/dL; and White blood cells (WBC):

24.0×103/mm3.Hisplasma osmolaritywas240mOsm/kg,

urine osmolarity was 515mOsm/kg and urinary sodium

was 89mmol/L. Adrenal functions (Adrenocorticotropes

hormon (ACTH): 30.6pg/mL [0---46]; cortisol: 20.02␮g/dL

[6.7---22.6]; Antidiuretic hormon(ADH):4.9pmol/L;

aldos-terone: 20.0pg/mL; and aldosterone/renin ratio: 2.38),

thyroidfunctiontests,vitaminB12andfolatevalueswere

normal.Inlightoftheseresults,thepatientwasdiagnosed

withSIADH, fluid restrictions were applied,and fusemide

and3%NaCltreatmentwasinitiated.

Ontheseconddaypostoperative,thepatientdeveloped

back pain, numbness starting at the hands and feet and

moving upwards from both extremities, loss of strength,

difficulty swallowingandrespiratory difficulty. After

eval-uationbytheneurologyunit,adiagnosisofGBSwasmade,

andthepatientwasmovedtotheintensivecareunit.

Phys-icalexamination showed limitedneck extensionand back

pain during neck movement. Knee, hip, and ankle

move-mentswererestrictedduetopain.Thesensitivityofjoint

regions increased on touch and during movement;

how-ever, there was no swelling or temperature increase in

thejoints.Neurologicexaminationshowedgoodorientation

andcooperation.Dysarthria,dysphagiaanddysphoniawere

present. Stiffneckand othersigns ofmeningeal irritation

were not present. In addition, bilateral ptosis, isochoric

pupil IR +/+, normal eye movement along the midline

globeandnonystagmuswerepresent.Hearingwasnormal.

Therewasbilateralcentralfacialparalysis.Theupperand

lowerextremitieshadlongsocks,shortgloves-stylesensory

defects.Afterbecomingcomfortablewithopioidanalgesics,

examinationshowedascoreof5/5onthe‘ModifiedResearch

Council(MRC)’scaleformusclestrength;theupper

extrem-ity proximal and distal muscles were 3/5, and the lower

extremityproximalanddistalmuscleswere2/5.Deep

ten-donreflexeswerehypoactiveabove,andnovaluewasfound

below. There was no pathologic reflex. Fundus

examina-tion was normal. His temperature (axillary) was 36.6◦_C,

heartratewas78/min,andrespirationwas24/min.Arterial

bloodgas(ABGs)werepH:7.48;PaCO2:36.9mmHg;PaO2:

115mmHg;SaO2:96%;andHCO3:22mmol/L.Hisrespiratory

difficultywasnotbadenoughtorequirearespirator.

A detailed history obtained from the patient’s family

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SIADHrelatedtoGuillain---Barrésyndromeafterlaparoscopiccholecystectomy 197

the patient had suffered from an upper respiratory tract

infection.Onthepatient’sfirstdayinintensivecare,a

lum-barpuncture wasperformed to obtain cerebrospinalfluid

for biochemical, culture and viralserology investigations.

Cerebrospinalfluid(CSF)examinationshowednormal

pres-sure, clear liquid, no cells, protein of 320mg/dL and all

otherparametersnormal.Therewasnobacterialproduction

fromtheCSFculture.Onthepatient’ssecondday,anEMG

was performed. Acute motor-sensorial axonal neuropathy

(AMSAN)wasobservedin theupperandlowerextremities

ontheelectromyograph.AdiagnosisofGBSwasmade,and

treatmentwasinitiatedwithintravenousimmunoglobulins

(0.4g/kg/day, 5 days). Symptomatic treatment was given

for hypertension attacks.Opioid analgesics weregiven to

treatpain.Paincontinueduntilthe10thdaybutdecreased

over time. The patient was monitored in the intensive

careunitfor 10days.When hyponatremiaandswallowing

improved, respiratory difficulties resolved,hemodynamics

werestable,upperextremitymotordeficitsresolved,and

lowerextremitysurficialpainandheatsensitivityreturned

to normal, the patient was transferred to the neurology

service. On final physical examination, his upper

extrem-ity distal and proximal muscle strength was 4 (MRC) and

3(MRC) forlowerextremities.Deep tendonreflexes were

normal.

Discussion

SIADHwasfirstdiagnosedin1957bySchwartzetal.,Bartter

andSchwartzre-examinedtheconditionin1967andlisted

thecardinalsymptomsofSIADHas(a)plasma

hypoosmolar-itywithsimilarhyponatremia,(b)plasmaosmolarityhigher

than urinary osmolarity, (c) excessive renal excretion of

sodium,(d)clinicalabsenceoffactorscausingedemaor

vol-umedepletion,and(e)normalrenalandadrenalfunction.

Currently,SIADHis knowntobecaused bymanydiseases,

malignantandotherwise.1

Postoperative SIADH is reported to occur after major

surgeries, such as abdominal and open heart operations,

is lesscommon afterminorsurgeries, andmayalso occur

aftercataractextractionunderlocalanesthetic.2---5_Nausea

associatedwithincreasedserumADHmayberelatedto

post-operativeSIADH,anditmaybepartofthestressresponse

tosurgeryandpain.2,3

GBS is the one of the most common causes of acute

polyneuropathy in adults. The incidence is thought to be

1---2/100,000.Itcanoccuratanyage,andthereisaslight

predominance inmales.10 _The_disease _begins_in _the_lower

extremities,andoverthecourseofhoursordays,itascends,

characterizedby weaknessinthearm andfacialmuscles.

The majority of patients have a history of upper

respira-tory tractor gastrointestinalsystem infections in the1---4

weekspriortosymptoms.11_While_the_pathogenesis_of_GBS_is

unknown,itisacceptedasahypersensitivehumoraland

cel-lularimmuneresponse,generallyattackingperipheralnerve

systemcomponents.10

Recently, theoccurrenceofGBSaftermajorandminor

surgicaloperationshasbeenincreasinglydebated.The

rel-evant literature is limited to case reports.10,12 _There _is

noinformationonincreased riskafter certainoperations.

The majority of cases have a history of bacterial or viral

infection,surgery,pregnancy,inflammatoryboweldiseases

(IBDs),connectivetissuediseases, suchaslupus,or other

malignancies.ThesedataindicatethatGBSmaybetriggered

byanunidentifiedpathogenoreventaffectingtheimmune

system.10

Our patient developed postoperative GBS clinical

fea-turesduringUCremission.IBDmayprogressrelatedtothe

patient’sclinical course or canoccur ascompletely

inde-pendentextraintestinal symptoms.UC patientshave been

identified with both central and peripheral nerve system

indications.14_There_are_three_case_reports_of_patients_with

a history of UC developing GBS in the literature. Two of

thepatients were in remission, andone wasin a relapse

period.13---15_In_these_cases,_it_was_thought_that_GBS_may_be

asymptomofextraintestinalUC.13_Our_patient_had_a_history

ofupperrespiratorytractinfectionthreeweeksprior.

Com-binedwiththetriggerofsurgicalstressandconsideringthe

lowincidenceofbothdiseasesandwithoutotherapparent

causesofacuteperipheralpolyneuropathy,afoundationof

anautoimmunediseasesuchasUCmayberesponsiblefor

changedimmunefunction,causingGBS.

SIADHmaydevelopduringoraftermaximalmotordeficit

in 30% of GBS patients and generally 65% of

dysauton-omycases.7,9,12,16 _Hoffmann _et_al.7 _noted _an _isolated_GBS

patientwithno signsof dysautonomy or initial symptoms

of SIADH. Our patient initially had normal strength and

reflexeswithinitial symptomsof SIADH anddysautonomy,

makinghim thesecondcase withtheseclinical

character-istics in the literature.12 _Visceral _afferent _fibers _may _be

affectedtogetherwithautonomicdysfunctionand

parasym-pathetic and sympathetic fibers, leading to sympathetic

andparasympatheticinsufficiencyandhyperactivitylinked

toneuropathy. Thesefactors combinedwithvascular

ten-sionreceptorsaffectingperipheralautonomicfiberscausing

abnormalADH secretionfromtheneurohypophysis reduce

theeffects of vagal inhibition.12 _However,_without

dysau-tonomy, therelationship between GBS and SIADH hasnot

beenclearlyexplained.

The pathogenesis of GBS-related SIADH is uncertain.

Among the hypotheses, pathogenesis may be linked

to changed osmoreceptor responses due to new lower

thresholdvaluesintheosmoregulatorysystem,

vasopressin-increased tubular sensitivity or ADH secretion affecting

cardiacvolumeandafferentperipheralautonomic

neurop-athyofosmolarityreceptors.7,12_Recently,_publications_have

proposedthatamultifunctionalcytokine,interleukin6

(IL-6),mayplay acentralrole inthe immunopathogenesisof

SIADHlinkedtoGBS.17

Onexamination,thebackpainanddistalsensorial

symp-tomsexperiencedbyourpatientwereinitialsignsofGBS;

however,theywereovershadowedbyacutemedical

man-agementproblemsofhyponatremiaanddysautonomy.The

patient’smentalchanges,secondarysymptomsto

hypona-tremia,made it difficult to evaluate daily symptoms and

delayed the definite diagnosis of weakness. In spite of

thecomplications,late-developingareflexiawasidentified

early,and the initial conservation of reflexes and normal

strengthshowedthepossibilityofimportantperipheral

neu-romusculardysfunctiontobelow.

OurcasereportindicatesthatalthoughSIADHand

auto-nomic dysfunctionare rarely the initial characteristics of

(4)

198 M.Y.C¸akırgözetal.

bekeptinmind.Thepresenceofsecondaryhyponatremia

in this type of clinical presentation may delay diagnosis.

It should not be forgotten that early GBS diagnosis and

appropriate treatment principles can lead to important

treatmentresultsincasessuchasthis.

Conflicts

of

interest

Theauthorsdeclarenoconflictsofinterest.

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