Referat Efusi PleuraPatofisiologi

D-FURQONITA/26-3-2007*

D-FURQONITA/26-3-2007

Fisiologi PleuraNormalnya cairan pleura dibentuk secara lambat sbg filtrasi dari pembuluh darah kapiler pleura parietal, dr interstitial pleura visceral, dan peritoneum via small holes in diaphragm Filtrasi terjadi karena perbedaan tekanan osmotik plasma dan jaringan interstitial, kemudian melalui sel mesotelial masuk ke rongga pleuraVolumenya dipertahankan melalui drainase limfatikVolume cairan pleura normal 5 15 cc*IPD FKUI jilid 3

Tek. onkotikTek. hidrostatik

Efusi Pleurapengumpulan cairan di dalam rongga pleura akibat transudasi atau eksudasi yang berlebihan dari permukaan pleura.

Jenis EfusiTransudatBukan penyakit primer paruCHF, sirosis hati, sindrom nefrotik, dialisis peritoneum, hipoalbumin, perikarditis konstriktiva, keganasan, atelektasis, pneumotoraksEksudat Proses peradangan permeabilitas kapiler pleura meningkat sel mesotelial menjadi bulat pengeluaran cairan ke dlm rongga pleuraTB, pneumonia, keganasan paru, proses imunologis (SLE, sarkoidosis,dll)IPD FKUI jilid 3

Transudat vs EksudatNormal : cairan pleura transudatEfusi transudat : hubunan normal antara tekanan kapiler hidrostatik dg koloid osmotik terganggu produksi cairan pleura > reabsorbsiTerdapat pd :Peningkatan tek.kapiler sistemikPeningkatan tek.kapiler pulmonalMenurunnya tek. Koloid osmotik dlm pleuraMenurunnya tek. Intra pleura( gagal jantung kiri, sindrom nefrotik, obstr. Vena cava superior, asites, sindrom Meig, efek dialisis peritoneal, pneumotoraksIPD FKUI jilid 3

Efusi eksudatCairan yg terbentuk melalui membran kapiler yang abnormal dan berisi protein berkonsentrasi tinggi dibandingkan protein pd cairan transudat terjadi krn peradanganProtein dlm cairan pleura berasal dari sal. Getah beningKegagalan aliran limfatik peningkatan konsentrasi protein cairan pleuraIPD FKUI jilid 3

Gamba patofis efusi ipd 2331

Harrison internal medicine

PATOFISIOLOGI

CHF : tekanan vena pulmonalis akan meningkat Peningkatan tekanan hidrostatikPerikarditir konstriktif : berkurangnya fx diastolic kongesti vena pulmonal dan sistemikSirosis : penurunan tekanan onkotik plasma serta adanya kebocoran diafragmaSindrom nefrotik : peningkatan tekanan hidrostatik dan penurunan tekanan onkotik Peritoneal dialisis : perpindahan cairan dialisat ke rongga pleura melalui celah diafragma

Malignancy : Tumor sekunderThe three tumors that cause approximately 75% of all malignant pleural effusions are lung carcinoma, breast carcinoma, and lymphoma Patofis :Menumpuknya sel tumor meningkatkan permeabilitas pleura thd air dan proteinMassa tumor : tersumbatnya vena dan pb. Limfe gagalreabsorbsiTumor mudah infeksi hipoproteinemiaMesotelioma (tumor primer pleura)Emboli pulmonal : menurunnya aliran A. pulmonal iskemik & kerusakan parenkim paru serta penumpukan cairan di proksimal emboli

Parapneumonic EffusionTahap eksudatifFocus infeksi peningkatan permeabilitas kapiler paruTahap fibropurulenperluasan / pecahnya focus infeksi cairan yang berakumulasi di rongga pleura sudah lebih banyak dan sudah berisi bakteriTahap organisasiPada tahap ini fibroblast bermigrasi ke cairan pleura membentuk membrane inelastic sehingga paru tidak bisa mengembangTB : fokus subpleura yg robek / obstruksi b. limfe akibat peradangan sal.&kel. Limfe

Emboli parupeningkatan permeabilitas kapiler di paru atau pleura akibat iskemik atau inflamasi

Sindrom Meigasites dan efusi pleura akibat tumor ovarium

DIAGNOSIS

The first step is to determine whether the effusion is a transudate or an exudate.A transudative pleural effusion occurs when systemic factors that influence the formation and absorption of pleural fluid are altered. Theleading causes of transudative pleural effusions in the United States are left ventricular failure, pulmonary embolism, and cirrhosisexudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered. The leading causes of exudative pleural effusions are bacterial pneumonia, malignancy, viral infection, and pulmonary embolismTransudative and exudative pleural effusions are distinguished by measuring the lactate dehydrogenase (LDH) and protein levels in the pleural fluidEksudat : 1. pleural fluid protein/serum protein 0.52. pleural fluid LDH/serum LDH 0.63. pleural fluid LDH more than two-thirds normal upper limit forserum

Thin membrane that lines the outside of the lungs and the inside of the chest wallVisceral pleura-adheres to the lungs, hilar bronchi and major fissuresParietal pleura-lines the inner surface of chest wall and mediastinumSeparated by airtight space that contains a lubricating fluid that allows the two pleura to glide against each other during breathing

*Normally, fluid enters the pleural spacefrom the capillaries in the parietal pleura and is removed via the lymphaticssituated in the parietal pleura. Fluid can also enter the pleuralspace from the interstitial spaces of the lung via the visceral pleura orfrom the peritoneal cavity via small holes in the diaphragm. The lymphaticshave the capacity to absorb 20 times more fluid than is normallyformed. Accordingly, a pleural effusion may develop when thereis excess pleural fluid formation (from the interstitial spaces of thelung, the parietal pleura, or the peritoneal cavity) or when there isdecreased fluid removal by the lymphatics*Chf The effusion occurs because the increased amounts of fluid in the lung interstitial spaces exit in part across the visceral pleura.

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