Abstract immo b ili t y t o c om p ression of th e re c urren t - PDF document

P a g e | 87 ’ R.M. S .P. K arunara t ne 1 , S .R. Jaya w i c kreme 1 , G. M ayura th an 1 , N.M.T. C . Jayasekara 1 , B.M. D ayananda 1 , T. Jeyakan th 1 , S .K.G.P.H.K. Sooriyagoda 1 , M. A marasing h e 1 , I . S . W i c krama t unga 1 , A.H.M.T.B. Ab eysing h e 1 1 . T ea ch ing H os p i t al K andy Corres p onding au th or R.M. S .P. K arunara t ne E -mail: s h anike@ymail .c om Abstract : M ore th an a c en t ury ago a c ardio v o c al syndrome w as des c ri b ed b y O r t ner wh ere h e a tt ri b u t ed a c ase of lef t v o c al fold Abstract immo b ili t y t o c om p ression of th e re c urren t laryngeal ner v e b y a dila t ed lef t a t rium in a p a t ien t w i th mi t ral v al v e s t enosis . Curren t ly th e term Ortner’s syndrome has come to encompass any nonmalignant, cardiac, intrathoracic process that results in em b arrassmen t of ei th er re c urren t laryngeal ner v e-usually b y s t re tch ing , p ulling , or c om p ression ; th ere b y c ausing v o c al fold p aralysis . N o t sur p risingly , th e lef t re c urren t laryngeal ner v e w i th i t s longer c ourse around th e aor t i c ar ch is more fre q uen t ly in v ol v ed th an th e rig ht ner v e , wh i ch p asses around the subclavian artery. Here we discuss Ortner’s syndrome as an un c ommon p resen t a t ion of idio p a th i c p ulmonary ar t erial h y p er t ension . Introduction O n examina t ion , s h e h ad a regular p ulse . B lood H oarseness of v oi c e due t o lef t re c urren t laryngeal p ressure w as 100/80mm h g . JV P w as 10 c m , w i th ner v e p aralysis w as firs t des c ri b ed in 1897 b y p rominen t CV w a v es . O n p al p a t ion th ere w as a N or b er t O r t ner , an A us t rian ph ysi c ian , in a p a t ien t p rominen t rig ht v en t ri c ular h ea v e and p al p a b le w i th mi t ral v al v e disease (mi t ral s t enosis and lef t p ulmonary ar t ery im p ulse . O n aus c ul t a t ion th ere a t rial enlargemen t ) . Various c ardio p ulmonary w as loud P 2 and a p ulmonary flo w murmur . Signs c ondi t ions asso c ia t ed w i th lef t re c urren t laryngeal of t ri c us p id regurgi t a t ion w ere p resen t, w i th a ner v e p alsy h a v e b een des c ri b ed , o v er th e las t 100 p ulsa t ing li v er and s h if t ing dullness indi c a t ing years . Th us , th e syndrome is no w also t ermed as as c i t es . R es p ira t ory examina t ion w as no t c ardio v o c al syndrome . sugges t i v e of a p i c al lung p a th ology . Th e neurologi c al examina t ion re v ealed no fea t ures of Here we report a case o f Ortner’s syndrome H orner’ s syndrome . o cc urring due t o idio p a th i c p ulmonary ar t erial h y p er t ension (I PAH ) .Th e findings of our re v ie w H er p ulse oxime t ry w as lo w a t 8 3 % sa t ura t ion on of li t era t ure rela t ing t o c ardio v as c ular disorders room air w i th ar t erial h y p oxaemia c onfirmed b y affe ct ing th e re c urren t laryngeal ner v e and th e b lood gas analysis . H er C h es t x-ray s h o w ed p a th ogenesis of h oarseness are also dis c ussed . enlargemen t of th e h ear t and main p ulmonary ar t eries w i th p eri ph eral oligaemia of b o th lung fields b u t h ad no signs of lef t a t rial enlargemen t Case report (Figure 01) . Th e ele ct ro c ardiogram ( E C G ) s h o w ed rig ht axis de v ia t ion , rig ht b undle b ran ch b lo c k and A 24 year old unmarried female w as admi tt ed w i th rig ht a t rial and rig ht v en t ri c ular h y p er t ro ph y a 12 mon th h is t ory of p rogressi v e dys p noea , (Figure 02) . Th e lef t h ear t w as normal on c oug h, fa t igue , and w eig ht loss . S h e h ad no t i c ed e ch o c ardiogra ph y w i th normal mi t ral and aor t i c p rogressi v e h oarseness of v oi c e 3 mon th s v al v es .H er rig ht v en t ri c le w as dila t ed , w i th se pt al dura t ion . S h e h ad no t h ad ch es t p ain , h aemo pt ysis , p aradox and e v iden c e of R V v olume o v erload or ankle s w elling . S h e h ad no p re v ious h is t ory of (Figure 0 3 ) . r h euma t i c v al v ulo p a th y , c onne ct i v e t issue S h e h ad se v ere t ri c us p id regurgi t a t ion & disorders or ch roni c lung disease . S h e h ad no p as t p ulmonary regurgi t a t ion w i th in c reased rig ht h is t ory t o sugges t any p ro v oked or un p ro v oked dee p v ein th rom b osis or p ulmonary em b olism v en t ri c ular p ressures and p ulmonary ar t erial fea t ures . S h e denied any p as t or c urren t use of p ressures . Th ere w ere no c ardia c s h un t s . D ire ct re c rea t ional drugs or w eig ht redu ct ion laryngos c o p y c onfirmed lef t v o c al c ord p alsy . medi c a t ions . Sri Lankan Journal of Cardiology Volume 1: Issue 2 - January 2019

P a g e | 88 Bronchoscopy studies were negative. Routine Br Bronchoscopy studies were negative. Routine hae haematology, haematology, autoantibody autoantibody profile profile and and inf inflammatory markers were unremarkable. Liver inflammatory markers were unremarkable. Li v er fun function tests were slightly abnormal with function tests were slightly abnormal with moderate elevation of transaminases. Abdom moderate elevation of transaminases. Abdominal mo inal ultrasound confirmed moderate ascites and dilated ult ultrasound confirmed moderate ascites and dilated hepatic veins. There were no space occurring hep hepatic veins. T h ere w ere no s p a c e o cc urring lesions. les lesions. Right heart catheterization confirmed severe Rig Right heart catheterization confirmed severe pulmonary arterial hypertension without any intra pulmonary arterial hypertension without any intra pu car cardiac shunts. CT Pulmonary angiography cardiac shunts. CT Pulmonary angiography sho showed dilated central pulmonary arteries, with showed dilated central pulmonary arteries, with F i g u r e 3 - 2 D echo showing severe RA, RV volume M P A per peripheral pruning (Figure 04). Further contrast CT peripheral pruning (Figure 04). Further contrast CT overload. chest excluded any tumoral compression or chest excluded any tumoral compression or aortic h aor t i c arch pathology and clearly demonstrated the ar ch p a th ology and c learly demons t ra t ed th e compression nature of the left recurrent laryngeal c om p ression na t ure of th e lef t re c urren t laryngeal nerve by the grossly dilated pulmonary trunk. ner v e b y th e grossly dila t ed p ulmonary t runk . F i g u r e 4- CT Pulmonary Angiography (CTPA) showing F i g u r e 1- Chest X ray peripheral oligemia/ reduced grossly dilated M ain Pulmonary Artery without any vascular marking of underline pulmonary hypertension. obvious paranchymal/interstitial lung disease. RPA Discussion The causes of recurrent laryngeal nerve paralysis have been classified as non-surgical paralysis, surgical paralysis (thyroid/oesophageal operations and intubation) or a combination of the two (1) . In 1897, Ortner described a series of 3 cases of mitral stenosis with concomitant hoarseness of voice because of left recurrent laryngeal nerve palsy. The cause was attributed to compression of the left recurrent laryngeal nerve by an enlarged left atrium (2) . Since then various authors have recorded their F i g u r e 2- E C G showing tall P waves of underline experiences of recurrent laryngeal nerve pulmonary hypertension. involvement in various cardiac disorders such as E isenmenger complex ( 3 ) , left ventricular failure (4) , atrial septal defect ( 5 ) , patent ductus arteriosus (P D A) ( 6 ,7) , primary pulmonary hypertension Sri Lankan Journal of Cardiology Volume 1: Issue 2 - January 2019