Empyema due to Ventriculopleural Shunt

Empyema due to Ventriculopleural Shunt

thalliurn-201 seintigraphy : a marker of severe and extensive diseast' . JAm \.oil Cardiol 19117; 9:7.52-.59 Okada R, (;Jm·ural effusions were not pro...

1MB Sizes 0 Downloads 78 Views

thalliurn-201 seintigraphy : a marker of severe and extensive diseast' . JAm \.oil Cardiol 19117; 9:7.52-.59 Okada R, (;Jm·<'r D. Williams S, Gaffney T. Myocardial kinetics of t..<.:hrwtium99m hexakis 2methoxy 2methylpropyl isonitrile. Cir<'ulation 191\/l; 77:491-911 Rf'ryeh SK, Scholz PM, Newman GE, Sahiston DC, Jones RH. Cardiae function at rt·st and during exercise in normals and in patit-nts with <.:oronarv artt-ry disease: evaluation with radionu· <'lid!' angiography. Ann Surg 19711; 1117:449-64 Rozanski A, Rt-rman D, Gray R. Diamond G, Raymond M, Prause J, et al. Prt'operative prediction of reversible myocardial asynPr~· hy postt'x<'rdst- radionudidt' ventriculography. N Eng! J Mt-d 191!2; .107:212-lfi D\·mond D. Fostt-r C , (;rt-nit-r R. Carpenter J, Schimidt D. Peak t'Xt-rdse and immediatt' postexercise imaging li>r the detection of left vt'ntrkular funetional abnormalities in coronary artery dist-ast- . Am J Cardin! 19114; .'5.1: 1.512-17 Matsuzaki M, (:allagher KP. Kemper WS, White F. Ross J Jr. Sustaint-d rt-gional dysfum·tion prodm~ed hy prolonged coronary stt-nosis: gradual rt-<·m·ery after reperfusion. Circulation 1983; fiR: 170-112 llomans DC, SuhiPtt E. Dai XZ, Hache RJ. Persistence of n•gional lt-ft ventricular dysfunction after exercise induced myo<'ardial isehemia. JClin Invest 19Rfi; 77:66-71 Robertson WS , Ft-igenhaum H , Armstrong WF, Dillon JC, O'Donnell J, Md1t•nr,· PW Exercise echocardiography: a clini· eally practical addition in the evaluation of coronary artery diseast-. J Am Coli Cardiol IAA1; 2:1011.5-91 <-~>ronarv

1

4

.')

fi

7

II

9

Empyema due to Ventriculopleural Shunt* C'.rmum lusif I\I.D. ;t Jmn Flrisrhuum , 1\I.D., F.C .C.P.;:j:. and Rajindrr Chitkara. 1\l.n .. FC.C . P.~

Empyema developing seven weeks after craniotomy in a 62-year-old black woman with an ipsilateral ventriculopleural (V-PL) shunt is described. Infection of the pleural space presumably resulted from transfer of organisms from a proximal V-PL shunt infection to the thorax. Empyema resulting from V-PL shunt infection has not previously been reported. Pleural effusions in patients with V-PL shunts must he considered as a potential site of infection with possible development of empyema.

(Chest 1991; 99:15.'18-39) V- PI.= ventriculopleural

V

entriculopleural shunting was introduced by Ransohofll for the treatment of hydrocephalus. In this early report, significant plt>ural effusions were not problematic, presumably due to the absorptive capacity of the pleural surfaces; however, latt>r studies documented the frequent occurrence of plt•ural effusions, particularly in children}·• Antisiphon devices, as well as the inclusion of valves to ensure more regular CSF Row, were designed to enable more reliable

*From the Division of Pulmonarv and Critical Care Medicine , Department of Medicine, Queens Hospital Center Affiliation of l•mg Island Jewish Medical Center and the Albert Einstein Collegt' of Medicine , Yeshiva University of New York, New York. tPulmonarv Ft-llow. :j:.lnstnrdo; in Medidne . ~Associate Professor of Medicine. Rt·print n •qursts: Or. Flrisr.lrmnn. /)jl'ision of fulmmuJry Mrdicine,

82-fi!i lfHth Strpc•t. JanUiica, .'VPw York 11492

1538

Ftr.l'RF. I . Chest rOt>ntgenogram taken on admission, demonstrating left-sided effusion and V-PL shunt catheter des~·ending into pleural space with contralateral mediastinal shift. pleural absorption of CSF. These devices have resulted in significant decreases in the incidence of large pleural effusions complicating V-PL shunts. 2 ·' While infection of the V-PL shunt following such procedures is a known complication, occurring in II of 59 cases in a recent report,' subsequent infection of the pleural Ruid with development of empyema has not been dt>scribed. We present a case of empyema which developed ipsilateral to an infected V-PL shunt. CASE REPORT A 62-year-old black woman presented with altered mental status and fever of one week's duration. She denied any con~h. sputum production, or pleuritic pain. Nine years prior to admission, decrea~ed ri~ht-sided auditory acuity led to the discovery of a cerebellar pontine angle tumor. Further evaluation was refused until four years prior to admission, when progression of symptoms occurred . Tumor enlargement was noted, which was believed to he consistent with an acoustic neuroma. A craniotomy was performed , with subtotal resection of htmor, hecause of the patient:~ desire to spare facial nerve function . After surgery, obstructive hydrocephalus developed , requiring V-PL shunting to the left hemithorax . Seven weeks prior to the current hospitalization, tumor recurrence was noted, and a second craniotomy was performed, a~ain with suhtotal excision of tumor. On admission the patient was found to he in moderate respiratory distress, with a respiratory rate nf 2R/min and a temperature of .19.4°C (l03°F}. She was confused and disoriented. Decreased breath sounds were noted in the left hemithorax, with dullness to percussion. The findings from the remainder of the physical examination were unremarkable. Laboratory examination revealed a white blood cell count of 33,600/cu mm. with Rfi percent PMNs and 12 percent band cells. The hemoglobin level was 13 wdl, and the platelet count was 4.59.000/cn mm . Findin~s from blood chemistries and urinalysis were within normal limits. Arterial blood gas analysis on room air Empyema due to Ventriculopleural Shunt (losif, Fleischman, Chitkara)

rt'\'Pal ..d a pH of 7.51, PaCO, of 3.'5 mm Hg, PaO, of 61 mm Hg, and 90 p..rcent saturation. A chest x-ray film (Fig I) demonstrated a V-PI. shunt cath..ter in thP lt•ft pleural spaee, with hoth free and lt><:ulated fluid. Pleural fluid revealed pumlent material with a white hlood <'<'II munt of 110.000/en mm . with 7R percent PMNs, glucose level of7 rng/dl , pH < 7.0, LDH level of7,600 units/L, and Grampositive eocd in pairs and <:ram-positive rods seen on Gram stain. Tuhe thoramstorny was performed , with removal of I,ROO ml of pumlent material; and antimiernhial therapy with ceftriaxone and vaneomydn was hegun. No eviden<·e of underlying pulmonary parenehymal infiltrates was noted. Culture of plt>ural fluid revealed Staphylot·occus PJ>idennidis and Streptococcti-V mitis. Thirty-six hours aftt>r the institution of antihiotk therap}: the patient was hrought to the operating morn for exteriori7.ation of the proximal end and rt•moval of tht• distal end of the V-PL shunt. A sample of turhid CSF with a white hlood eell <.1>tlllt of 480/cn mm was ohtained at that tirnf'. Culturps ofCSF. hl()(>t' wt>eks of et>ftriaxone therapy. A small amount of l()(·nlated pleural Huid persisted until discharge. DtscusstoN The present report describes the development of empyema due to Staph epidennidis and Strep mitis ipsilateral to a V-PL shunt, prest>nting with altered mental status, fever, and leukocytosis. Pleocytosis ofCSF was observed, although cultures were negative, presumably because this specimen was obtained after administration of antimicrobials. The absence of roentgenographically demonstrable pulmonary parenchymal infiltrates suggests that the pleural infection was not spcondary to pneumonitis. Furthermort', the organisms prespnt on culturt> are among those frequently reported to cause V-PL shunt infections" and are not often a primary canst' of pnt>umonia. These factors suggest that the shunt catheter was tht> most likely source of pleural infection. Vt>ntriculopleural shunts are conduits from the ventricles to tht> plt>ural space. In particular, transfer of glioblastoma ct>lls to the plt•ural space via a V-PL shunt has been reported in two patients. 1. 7 It would thert>fore seem reasonable that infection originating proximally in a V-PL shunt could also he transferred to the pleural space, producing empyema by direct delivery of organisms via the shunt catheter. To our knowledgt•, infection of pleural effusions resulting from V-PL shunts causing frank empyema has not been previously reportt•d . As shunt infection is a known complication of this procedure , ' a high index of suspicion must be maintained for infection in both tht> CSF and any associated pleural effusion whf'n thesf' patients present with fevers without another obvious source. Early sampling of the CSF and pleural fluid will diret·t prompt institution of antimicrobial therapy and shunt extt>rinri;r.ation, which may prevent the development of frank t>mpyema . REFERENCES

2 3 4 .'5

RansohoffJ. Ventriculopleural anastomosis in treatment of midline ohstrncft>d masses. J Neurosurg 19.'54;11 :295-301 Vt>nes JL. Pleural effusion and eosinophilia following ventriculopleural shunting. Dev Med Child Neurol 1976; 16:72-6 Venes JL. Shaw RK. Ventriculopleural shunting in the managemt>nt of hydrocephalus. Childs Brain 1979: 4:45-.'50 Hoffman JH, Hennick EB. Humphreys RP: Experience with ventrienlopleural shunts. Childs Brain 19&'3; 10:404-13 Nixon Hll. Vt>ntricnlo-plenral drainage with a valve. Dev Med

Child Neur 1962; 4:301-02 6 Venes JL. Control of shunt infection: report of 1.'50 <.1msecntive cases. J Neurosurg 1976; 45:311-14 7 Wakamatsu T, Matsuo T, Kawano S, Teramoto S, Matsumura H. Glioblastoma with extracranial metastasis through ventriculopleural shunt: case report . J Neurosurg 1971; 34:697-701

Chylothorax After Childbirth* Sue IGllion Cammarata , M.D.;t

Robert E. Brush, Jr., M.D., F.C.C .P.;* and Robert C. Hyzy, M.D.§

We report a case of chylothorax which appeared in a mother after childbirth. Disruption of the thoracic duct occurred with the high intrathoracic pressures generated by the Valsalva maneuver used by the patient during labor to "push." No evidence of other trauma or malignancy were fOund and the patient did well after use of total parenteral nutrition, thoracotomy with thoracic duct ligation, and (Che11t 1991; 99:1539-40) pleurodesis.

T

raumatic events precipitating chylothorax are usually obvious, but minor trauma has been noted to result in chylothorax. We recently treated a mother who presented with chylothorax after prolonged labor, ultimately requiring thoracotomy for ligation of the thoracic duct. CASE REPORT

The patient was a 20-yeaN>Id nulliparous white woman who went into labor at the end of an uneventful pregnancy. More than three hours were spent in the second stage with the fetal head remaining at I + station despite repeated pushing by the mother. Variable deceleration of the fetal heart rate and meconium staining of amniotic fluid were noted, necessitating a low transverse ceasarean section without complications. Achest roentgenogram after delivery documented a right pleural effusion (Fig 1) hut no other diagnostic work-up was pursued. The patient was discharged home without further complications. Three weeks after the ceasarean section, the patient noted a dry cough and dyspnea. Chest roentgenogram demonstrated opacification of the right hemithorax. Thoracentesis yielded 3 L of milky fluid, which was found to be chylous with a protein level of 3.8 g/dl, triglycerides, 2,730 mwdl, and large chylomicron hand of 40 percent on lipoprotein electrophoresis. The fluid white hlood cell munt was 6,015/cu mm with 97 percent monocytes and 3 percent neutrophils. Pleural fluid glucose value was 98 mg/dl with an LDH level of 197 lUlL. Her dyspnea resolved, but three days later, she was admitted for recurrent effusion. Except for her ceasarean section, the patient had no significant past medical history, no history of trauma, and no constitutional complaints. Physical examination revealed a healthy appearing female at 60.0 kg (132 lhs). There was no lymphadenopathy on examination and lung findings were consistent with a right pleural effusion. Admitting laboratory data included a nonnal white blood cell count, semm total protein value of 6.4 gldl; albumin, 3.4 g/dl; and cholesterol , 184 mg/dl. A PPD was not reactive and culh1res of pleural fluid were negative for Mycobacteria and bacteria. *From the Department of Pulmonary and Critical Care Medicine, Henry Ford Hospital, Detroit, and Michigan State University Kalamazoo Center For Medical Studies, Kalamaz()(l. tFellow. *Associate Clinical Professor. §Senior Staff Physician . CHEST I 99 I 6 I JUNE. 1991

1539