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Efusi Pleura

02

MondayJUL 2012

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BY ELISASIREGAR IN

DIAGNOSA KEPERAWATAN

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Diagnose, Efusi Pleura, Nursing General

Efusi Pleura
1.

Pengertian
Efusi pleura adalah suatu keadaan dimana terdapat penumpukan cairan dalam rongga pleura. Selain cairan
dapat juga terjadi penumpukan pus atau darah. Efusi pleura bukanlah suatu disease entity tapi suatu gejala
penyakit yang serius yang dapat mengancam jiwa penderita (Sarwono, 1995 Hal 786).
Efusi pleura adalah istilah yang digunakan bagi penimbunan cairan dalam rongga pleura (Sylvia, A. Price, 1995
Hal 704)
Efusi pleura adalah jumlah cairan nonpurulen yang berlebihan dalam rongga pleural; antara lapisan visera dan
parietal (Susan Martin Tucker, 1998 Hal 265).

1.

Etiologi
Secara umum penyebab efusi pleura adalah sebagai berikut :

1.

Pleuritis karena bakteri piogenik

2.

Pleuritis tuberkulos

3.

Efusi pleura karena kelainan intra abdominal, seperti sirosis hati, pankreatitis, abses ginjal, abses hati,
dll.

4.

Efusi pleura karena gangguan sirkulasi, seperti pada decompensasi kordis, emboli pulmonal dan
hipoalbuminemia.

5.

Efusi pleura karena neoplasma, seperti mesolioma, karsinoma bronkhus, neoplasma metastatik,
limfoma malignum.

6.

Efusi pleura karena trauma, yakni trauma tumpul, laserasi, luka tusuk pada dada, ruptur esophagus.
Efusi pleura dapat berupa transudat dan eksudat. Eksudat dibedakan dari transudat dari kadar protein yang
dikandungnya dan dari berat jenisnya. Transudat mempunyai berat jenis kurang dari 1.015 dan kadar
proteinnya kurang dari 3%, sedangkan eksudat mempunyai berat jenis dan kadar protein lebih tinggi, karena
banyak mengandung sel (Sylvia, A. Price, 1995 Hal 704).
Transudat terjadi pada :

1.

Peningkatan tekanan vena pulmonalis, misalnya payah jantung kongestif. Pada kasus ini
keseimbangan kekuatan menyebabkan pebgeluaran cairan dari pembuluh.

2.

Hipoproteinemia, seperti pada penyakit hati dan ginjal, atau penekanan tumor pada vena kava.
Sedangkan penimbunan eksudat dapat disebabkan oleh :

1.

Sekunder dari peradangan atau keganasan pleura.

2.

Peningkatan permeabilitas kapiler atau gangguan absorpsi getah bening.

3.

Patofisiologi
Dalam keadaan normal seharusnya tidak ada rongga kosong antara pleura tersebut, karena biasanya di sana
hanya terdapat sedikit (10-20 cc) cairan yang merupakan lapisan tipis serosa dan selalu bergerak secara
teratur. Cairan yang sedikit ini merupakan pelumas antara kedua pleura, sehingga mereka mudah bergeser
satu sama lain. Dalam keadaan patologis rongga antara kedua pleura ini dapat terisi dengan beberapa liter
cairan atau udara.
Diketahui bahwa cairan masuk ke dalam rongga melalui pleura parietal dan selanjutnya keluar lagi dalam
jumlah yang sama melalui membran pleura viseralis via sistem limfatik dan vaskuler. Pergerakan cairan dari
pleura parietal ke pleura visceralis dapat terjadi karena adanya perbedaan tekanan hidrostatik dan tekanan
koloid osmotic. Cairan kebanyakan diabsorbsi oleh sistem limfatik dan hanya sebagian kecil yang diabsorbsi
oleh sistem kapiler pulmonal. Hal yang memudahkan penyerapan cairan pada pleura viseralis adalah
terdapatnya banyak mikrovili di sekitar sel-sel mesotelial

1.

Gambaran klinik
Keluhan-keluhan yang sering didapat adalah berupa sesak nafas, rasa berat pada dada serta keluhan/gejala
lain penyakit dasarnya seperti : bising jantung (pada payah jantung), lemas yang progresif disertai berat
badan yang menurun (pada neoplasma), batuk yang kadang kadang berdarah pada perokok (karsinoma
bronkus), tumor di organ lain (pada metastasis), demam subfebril (pada tuberkulosis), demam menggigil
(pada emfisema), asites (pada sirosis hati), asites dengan tumor di pelvis (pada sindrom Meig).
Pada pemeriksaan fisis akan ditemukan : fremitus yang menurun, perkusi yang pekak, tanda tanda
pendorongan mediastinum, suara nafas yang menghilang pada auskultasi.

1.
A.

Pemeriksaan laboratorium/diagnostik
Sinar tembus dada (x-ray)
Permukaan cairan yang terdapat dalam rongga pleura akan membentuk bayangan seperti kurva, dengan
permukaan daerah lateral lebih tinggi daripada bagian medial. Bila permukaannya horisontal dari lateral ke
medial, pasti terdapat udara dalam rongga tersebut yang dapat berasal dari luar atau dari dalam paru paru

sendiri. Kadang kadang sulit membedakan antara bayangan cairan bebas dalam pleura dengan adhesi karena
radang (pleuritis). Disini perlu pemeriksaan foto dada dengan posisi lateral dekubitus.
1.

Torakosentesis
Aspirasi cairan pleura (torakosentesis) berguna sebagai sarana untuk diagnostik maupun terapeutik.
Untuk diagnostik cairan pleura dilakukan pemeriksaan :
1.)

Warna cairan.

Biasanya cairan pleura berwarna agak kekuning-kekuningan (serous-xantho-chrome). Bila agak kemerahmerahan, ini dapat terjadi pada trauma, infark paru, keganasan, adanya kebocoran aneurisma aorta. Bila
kuning kehijauan dan agak purulen, ini menunjukkan adanya empiema. Bila merah tengguli, ini menunjukkan
adanya abeses karena ameba.
Characteristic

2.)

Significance

Bloody

Most likely an indication of malignancy in the absence


of trauma; can
also indicate pulmonary embolism, infection,
pancreatitis,
tuberculosis, mesothelioma, or spontaneous
pneumothorax

Turbid

Possible increased cellular content or lipid content

Yellow or whitish,
turbid

Presence of chyle, cholesterol or empyema

Brown (similar to
chocolate sauce
or anchovy paste)

Rupture of amebic liver abscess into the pleural space


(amebiasis
with a hepatopleural fistula)

Black

Aspergillus involvement of pleura

Yellow-green with debris

Rheumatoid pleurisy

Highly viscous

Malignant mesothelioma (due to increased levels of


hyaluronic acid)
long-standing pyothorax

Putrid odor

Anaerobic infection of pleural space

Ammonia odor

Urinothorax

Purulent

Empyema

Yellow and thick, with


metallic
(stainlike) sheen

Effusions rich in cholesterol (longstanding chyliform


effusion, eg,
tuberculous or rheumatoid pleuritis)

Biokimia.

Secara biokimia efusi pleura terbagi atas transudat dan eksudat.


Di samping pemeriksaan tersebut di atas, secara biokimia diperiksakan juga pada cairan pleura :
-

Kadar pH dan glukosa. Biasanya merendah pada penyakit-penyakit infeksi, arthritis rheumatoid, dan

neoplasma.
-

Kadar amilase. Biasanya meningkat pada pankreatitis dan metastasis adenokarsinoma.

Table 2. Specialized tests for detecting causes of pleural effusion

3.)

Test

Diagnosis

Triglycerides >110 mg/dL

Chylothorax

Amylase >200 U/dL

Esophageal perforation, malignancy, pancreatic disease, ruptured


ectopic pregnancy

Isoenzyme: salivary

Esophageal disease, malignancy (especially lung)

Isoenzyme: pancreatic

Pancreatitis, pancreatic pseudocyst

Rheumatoid factor >1:320 and > serum


titer

Rheumatoid effusion

Antinuclear antibodies >1:160


and > serum titer

Lupus pleuritis

Carcinoembryonic antigen >10 ng/mL

Malignancy

Adenosine deaminase >43 U/L

Tuberculous pleuritis

Sitologi

Pemeriksaan sitologi terhadap cairan pleura amat penting untuk diagnostik penyakit pleura, terutama bila
ditemukan sel-sel patologis atau dominasi sel-sel tertentu.
4.)

Bakteriologi

Biasanya cairan pleura steril, tapi kadang-kadang dapat mengandung mikroorganisme, apalagi bila cairannya
purulen, (menunjukkan empiema). Efusi yang purulen dapat mengandung kuman-kuman yang aerob ataupun
anerob.
Jenis kuman yang sering ditemukan dalam cairan pleuran adalah : pneumokok, E. coli, Kleibsiella,
Pseudomonas, Enterobacter.
Pada pleuritis tuberkulosa, kultur cairan terhadap kuman tahan asam hanya dapat menunjukkan yang positif
sampai 20 %.
1.

Biopsi pleura
Pemeriksaan histology satu atau beberapa contoh jaringan pleura dapat menunjukkan 50-75 % diagnosis
kasus-kasus pleuritis tuberkulosa dan tumor pleura. Bila ternyata hasil biopsy pertama tidak memuaskan,
dapat dilakukan beberapa biopsy ulangan. Komplikasi biopsy adalah pneumotoraks, hemotoraks, penyebaran
infeksi atau tumor padan dinding dada (Sarwono, 1995 Hal 788)

1.

Pemeriksaan cairan sitologi

2.

Pewarnaan gram, kultur, dan sensitivitas cairan pleura.

3.

Penanganan
Pada efusi yang terinfeksi perlu segera dikeluarkan dengan memakai pipa intubasi melalui sela iga. Bila cairan
pusnya kental sehingga kulit keluar atau bila empiemanya multikular, perlu tindakan operatif. Mungkin
sebelumnya dapat dibantu dengan irigasi cairan garam fisiologi atau larutan antiseptik (Betadine).
Pengobatan secara sistemik hendaknya segera diberikan, tetapi terapi ini tidak berarti bila tidak diiringi
pengeluaran cairan yang adekuat.

Untuk mencegah terjadinya lagi efusi pleura setelah aspirasi (pada efusi pleura maligna), dapat dilakukan
pleurodesis yakni melengketkan pleura viseralis dan pleura parietalis. Zat-zat yang dipakai adalah tetrasiklin
(terbanyak dipakai) Bleomycin, Corynebacterium parvum, Thio-tepa dan lain-lain.
Therapeutic thoracentesis may be done if the fluid collection is large and causing pressure or shortness of
breath. Treatment of the underlying cause of the effusion then becomes the goal.
For example, pleural effusions caused by congestive heart failure are treated with diuretics and other
medications that treat heart failure. Pleural effusions caused by infection are treated with antibiotics specific to
the causative organism. In patients with cancer or infections, the effusion is often treated by using a chest
tube to drain the fluid. Chemotherapy, radiation therapy, or instilling medication within the chest that prevents
re-accumulation of fluid after drainage may be used in some cases.

Tube thoracostomy
Definite indications include empyema (presence of pus in the pleural space); hemothorax;

large pneumothorax; and parapneumonic effusion with a positive finding with Gram staining of pleural fluid, pH
less than 7.0, or a glucose level less than 40 m/dL. A chest tube also might be indicated for parapneumonic
effusion with a pH between 7.00 and 7.20 or an LDH level above 1000 IU/L. Patients with these findings should
be admitted, and a pulmonologist should decide if chest tube placement is required. A chylothorax can be
managed with a chest tube, although placement of a pleuroperitoneal shunt is preferred because it prevents
malnourishment and immunologic compromise.

When chest tubes are inserted in the ED for the treatment of a spontaneous pneumothorax,

they initially should be connected to an underwater-seal drainage apparatus or a Heimlich valve rather than to
a suction device. Suction can create negative pleural pressures and increase the risk of reexpansion pulmonary
edema. A pulmonologist should be consulted when change to a suction device is considered.
1.

Komplikasi
Komplikasi yang sering terjadi antara lain :

1.

Pneumotoraks

2.

Pneumonia

3.

Emfisema

1.

Obat-Obatan
Drug Category: Antibiotics Expeditiously initiate empiric systemic antibiotic coverage for infections or
potentially septic conditions (eg, parapneumonic effusions, empyemas, esophageal perforation, intraabdominal
abscesses) in the ED. Base initial antibiotic selection on the microorganisms presumed present and the overall
clinical picture. Considerations include the patients age, comorbid conditions, duration of the illness (acute vs
subacute or chronic), setting (community vs nursing home), geographic location, and prevalence of resistance.
When available, results of pleural fluid Gram staining should help guide antibiotic selection.
Generally for parapneumonic effusions, initial antibiotics used in the ED should have a broad spectrum of
coverage for both aerobic microorganisms and anaerobic microorganisms. Various effective single and
combination antimicrobial therapies exist. A combination therapy may include a third-generation cephalosporin
such as ceftriaxone and a macrolide or alternatively monotherapy with a new generation antipneumococcal
fluoroquinolone. If the patient is immunosuppressed or has structural lung disease (eg, bronchiectasis), a
cephalosporin with enhanced antipseudomonal activity, such as ceftazidime (Fortaz) is recommended. If the
patient is in septic shock, a combination antimicrobial therapy may include vancomycin with a new generation
antipneumococcal fluoroquinolone (eg, levofloxacin) and gentamicin if recently hospitalized/nursing home
residence.

Drug Name

Ceftriaxone (Rocephin) Third-generation cephalosporin with broadspectrum, gram-negative activity; lower efficacy against gram-positive
organisms; higher efficacy against resistant organisms. Arrests bacterial growth
by binding to one or more penicillin-binding proteins.

Adult Dose

1-2 g IV qd

Pediatric Dose

50-75 mg/kg/d IV qd or divided q12h; not to exceed 4 g/d

Contraindications

Documented hypersensitivity; neonates (potential for causing kernicterus)

Interactions

Probenecid may increase levels; coadministration with ethacrynic acid,


furosemide, and aminoglycosides may increase nephrotoxicity

Pregnancy

B Usually safe but benefits must outweigh the risks.

Precautions

Adjust dose in renal impairment; caution in breastfeeding women and allergy


to penicillin

Drug Name

Clindamycin (Cleocin) Lincosamide for treatment of serious skin and softtissue staphylococcal infections. Also effective against aerobic and anaerobic
streptococci (except enterococci). Inhibits bacterial growth, possibly by
blocking dissociation of peptidyl t-RNA from ribosomes, arresting RNAdependent protein synthesis.

Adult Dose

450-900 mg IV q8h

Pediatric Dose

Not established

Contraindications

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic


impairment, antibiotic-associated colitis

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and


pancuronium; erythromycin may antagonize effects; antidiarrheals may delay
absorption

Pregnancy

B Usually safe but benefits must outweigh the risks.

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal


insufficiency; associated with severe and possibly fatal colitis; can cause
pseudomembranous enterocolitis secondary to Clostridium difficile infection

Drug Category: Diuretics Loop diuretics decrease plasma volume and edema by causing diuresis.

Drug Name

Furosemide (Lasix) Increases excretion of water by interfering with


chloride-binding cotransport system, which in turn inhibits sodium and
chloride reabsorption in ascending loop of Henle and distal renal tubule.

Adult Dose

20-40 mg/d IV; then 80 mg within 2 h prn

Pediatric Dose

1 mg/kg/dose IV slowly q6-12h with close supervision; not to exceed 6


mg/kg/dose; do not administer more frequently than q6h

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte (K, Mg,


Na) depletion

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of


antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine;
auditory toxicity appears to be increased with coadministration of
aminoglycosides; hearing loss of varying degrees may occur; anticoagulant
activity of warfarin may be enhanced when taken concurrently; increased
plasma lithium levels and toxicity are possible when taken concurrently

Pregnancy

C Safety for use during pregnancy has not been established.

Precautions

Frequently determine serum electrolyte, CO2, glucose, creatinine, uric acid,


calcium, and BUN levels during the first few months of therapy and
periodically thereafter; observe for blood dyscrasias and liver or kidney
damage

Drug Name

Spironolactone (Aldactone) For management of edema resulting from


excessive aldosterone excretion. Competes with aldosterone for receptor sites
in distal renal tubules, increasing water excretion while retaining potassium

and hydrogen ions.


Adult Dose

100 mg PO initial dose; adjust dose thereafter depending on individual


response

Pediatric Dose

Not established

Contraindications

Documented hypersensitivity; anuria, renal failure or hyperkalemia

Interactions

May decrease effect of anticoagulants; potassium and potassium sparing


diuretics may increase toxicity of spironolactone

Pregnancy

D Unsafe in pregnancy

Precautions

Caution in renal and hepatic impairment


DAFTAR PUSTAKA

Carpenito Lynda Juall, (1995), Buku Saku Diagnosa Keperawatan, Edisi 6,EGC. Jakarta.
C. Long Barbara, (1996), Perawatan Medikal Bedah, Buku 2,Alih bahasa Yayasan
Doenges E. Marilynn et all., (2000), Rencana Asuhan Keperawatan (Terjemahan Indonesia), Edisi 2 Jakarta.
Guyton dan Hall, (1997), Buku Ajar Fisiologi Kedokteran, Edisi 9 Penerbit EGC Ikatan Alumni Pendidikan
Keperawatan Padjajaran Banduing.
Price A. Sylvia, (1995), Patofisiologi, Buku II, Edisi IV, Cetakan I, EGC. Jakarta.
Sarwono Waspadji Suparman (1995), Ilmu Penyakit Dalam, Jilid II, FKUI, Jakarta.
Tucker Martin Susan, (1998),Standar Perawatan Pasien, Edisi 5 EGC. Jakarta.
www.emedicine.com/emerg/pulmonary.com
www.medicineplus.com
www.virtualrespiratorycenter.com
www.postgradmed.com
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1.

Nova Mckimsaid:

July 3, 2012 at 7:53 pm

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