LAPORAN PENDAHULUAN PNEUMONIA22.30FARIDARAHMAWATINO COMMENTSA.PengertianPneumonia adalah peradangan pada paru-.paru dan bronkiolus yang disebabkan oleh bakteri,jamur ,virus, atau aspirasi karna makanan atau benda asing.Pneumonia adalah infeksi pada parenkim paru, biasanya berhubungan dengan pengisian cairan didalam alveoli hal ini terjadi akibat adanya infeksi agen/ infeksius atau adanya kondisi yang mengganggu tekanan saluran trakheabronkialis. Adapun beberapa keadaan yang mengganggu mekanisme pertahanan sehingga timbul infeksi paru misalnya, kesadaran menurun, umur tua, trakheastomi, pipa endotrakheal dan lain-lain. Dengan demikian flora endogen yang menjadi pathogen ketika memasuki saluran pernapasan.(Ngasrial, Perawatan anak sakit, 1997).B.EtiologiBakteri : streptococus pneumoniae, staphylococus aureus.Virus : Influenza, parainfluenza, adenovirusJamur : Candidiasis, histoplasmosis, aspergifosis, coccidioido mycosis, cryptococosis,pneumocytis carini.Aspirasi : Makanan, cairan, lambung.Inhalasi : Racun atau bahan kimia, rokok, debu dan gas.Pneumonia virus bisa disebabkan oleh:Virus sinsisial pernafasan, Hantavirus, Virus influenza,Virus parainfluenza,Adenovirus, Rhinovirus, Virus herpes simpleks, Micoplasma (pada anak yang relatif besar)

Pada bayi dan anak-anak penyebab yang paling sering adalah:Virus sinsisial pernafasanAdenovirusVirus parainfluenzaVirus influenza.C.PatofisiologiPneumonia dapat terjadi akibat menghirup bibit penyakit di udara, atau kuman di tenggorokan terisap masuk ke paru-paru. Penyebaran bisa juga melalui darah dari luka di tempat lain, misalnya di kulit. Jika melalui saluran napas, agen (bibit penyakit) yang masuk akan dilawan oleh berbagai sistem pertahanan tubuh manusia. Misalnya, dengan batuk-batuk, atau perlawanan oleh sel-sel pada lapisan lendir tenggorokan, hingga gerakan rambut-rambut halus (silia) untuk mengeluarkan mukus (lendir) tersebut keluar. Tentu itu semua tergantung besar kecilnya ukuran sang penyebab tersebut.D.Menifestasi KlinikGejala penyakit pneumonia biasanya didahului infeksi saluran nafas atas akut selama beberapa hari. Selain didapatkan demam, menggigil, suhu tubuh meningkat dapat mencapai 40 derajat celsius, sesak nafas, nyeri dada, dan batuk dengan dahak kental, terkadang dapat berwarna kuning hingga hijau. Pada sebagian penderita juga ditemui gejala lain seperti nyeri perut, kurang nafsu makan, dan sakit kepala.

Tanda dan Gejala berupa:Batuk nonproduktif, Ingus (nasal discharge),Suara napas lemah, Retraksi intercosta, Penggunaan otot bantu nafas, Demam, Ronchii, Cyanosis, Leukositosis, Thorax photo menunjukkan infiltrasi melebar, Batuk, Sakit kepala, Kekakuan dan nyeri otot, Sesak nafas, Menggigil, Berkeringat, Lelah.

Gejala lainnya yang mungkin ditemukan:Kulit yang lembabMual dan muntahKekakuan sendi.E.KlasifikasiMenurut buku Pneumonia Komuniti, Pedoman Diagnosis dan Penatalaksanaan di Indonesia yang dikeluarkan Perhimpunan Dokter Paru Indonesia, 2003 menyebutkan tiga klasifikasi pneumonia.Berdasarkan klinis dan epidemiologis:

o Pneumonia komuniti (community-acquired pneumonia).o Pneumonia nosokomial, (hospital-acquired pneumonia/nosocomial pneumonia).o Pneumonia aspirasi.o Pneumonia pada penderita immunocompromised.

Berdasarkan bakteri penyebab:o Pneumonia bakteri/tipikal.Dapat terjadi pada semua usia. Pneumonia bakterial sering diistilahkan dengan pneumonia akibat kuman. Pneumonia jenis itu bisa menyerang siapa saja, dari bayi hingga mereka yang telah lanjut usia. Para peminum alkohol, pasien yang terkebelakang mental, pasien pascaoperasi, orang yang menderita penyakit pernapasan lain atau infeksi virus adalah yang mempunyai sistem kekebalan tubuh rendah dan menjadi sangat rentan terhadap penyakit itu.Pada saat pertahanan tubuh menurun, misalnya karena penyakit, usia lanjut, dan malnutrisi, bakteri pneumonia akan dengan cepat berkembang biak dan merusak paru-paru.Jika terjadi infeksi, sebagian jaringan dari lobus paru-paru, atau pun seluruh lobus, bahkan sebagian besar dari lima lobus paru-paru (tiga di paru-paru kanan, dan dua di paru-paru kiri) menjadi terisi cairan. Dari jaringan paru-paru, infeksi dengan cepat menyebar ke seluruh tubuh melalui peredaran darah. Bakteri Pneumokokus adalah kuman yang paling umum sebagai penyebab pneumonia bakteri tersebut.Gejalanya Biasanya pneumonia bakteri itu didahului dengan infeksi saluran napas yang ringan satu minggu sebelumnya. Misalnya, karena infeksi virus (flu). Infeksi virus pada saluran pernapasan dapat mengakibatkan pneumonia disebabkan mukus (cairan/lendir) yang mengandung pneumokokus dapat terisap masuk ke dalam paru-paru.Beberapa bakteri mempunyai tendensi menyerang seseorang yang peka, misalnya klebsiella pada penderita alkoholik, staphyllococcus pada penderita pasca infeksi influenza. Pneumonia Atipikal. Disebabkan mycoplasma, legionella, dan chalamydia.

o Pneumonia Akibat virus.Penyebab utama pneumonia virus adalah virus influenza (bedakan dengan bakteri hemofilus influenza yang bukan penyebab penyakit influenza, tetapi bisa menyebabkanpneumonia juga).GejalanyaGejala awal dari pneumonia akibat virus sama seperti gejala influenza, yaitu demam, batuk kering, sakit kepala, nyeri otot, dan kelemahan. Dalam 12 hingga 36 jam penderita menjadi sesak, batuk lebih parah, dan berlendir sedikit. Terdapat panas tinggidisertai membirunya bibir.Tipe pneumonia itu bisa ditumpangi dengan infeksi pneumonia karena bakteri. Hal itu yang disebut dengan superinfeksi bakterial. Salah satu tanda terjadi superinfeksi bakterial adalah keluarnya lendir yang kental dan berwarna hijau atau merah tua.o Pneumonia jamur,sering merupakan infeksi sekunder. Predileksi terutama pada penderita dengan daya tahan lemah (immunocompromised).

Berdasarkan predileksi infeksi:Pneumonia lobaris, pneumonia yang terjadi pada satu lobus (percabangan besar dari pohon bronkus) baik kanan maupun kiri.Pneumonia bronkopneumonia, pneumonia yang ditandai bercak-bercak infeksi pada berbagai tempat di paru. Bisa kanan maupun kiri yang disebabkan virus atau bakteri dan sering terjadi pada bayi atau orang tua. Pada penderita pneumonia, kantong udara paru-paru penuh dengan nanah dan cairan yang lain. Dengan demikian, fungsi paru-paru, yaitu menyerap udara bersih (oksigen) dan mengeluarkan udara kotor menjadi terganggu. Akibatnya, tubuh menderita kekurangan oksigen dengan segala konsekuensinya, misalnya menjadi lebih mudah terinfeksi oleh bakteri lain (super infeksi) dan sebagainya. Jika demikian keadaannya, tentu tambah sukar penyembuhannya. Penyebab penyakit pada kondisi demikian sudah beraneka macam dan bisa terjadi infeksi yang seluruh tubuh.

F.PenatalaksanaanPengobatan diberikan berdasarkan etiologi dan uji resistensi tapi karena halitu perlu waktu dan pasien pneumonia diberikan terapi secepatnya :Penicillin G: untuk infeksi pneumonia staphylococcus.Amantadine, rimantadine: untuk infeksi pneumonia virus.Eritromisin, tetrasiklin, derivat tetrasiklin: untuk infeksi pneumonia mikroplasma.Menganjurkan untuk tirah baring sampai infeksi menunjukkan tanda-tanda.Pemberian oksigen jika terjadi hipoksemia.Bila terjadi gagal nafas, diberikan nutrisi dengan kalori yang cukup.G.Pemeriksaan Penunjang1.Sinar X : mengidentifikasikan distribusi struktural (misal: lobar, bronchial); dapat juga menyatakan abses).2.Pemeriksaan gram/kultur, sputum dan darah: untuk dapat mengidentifikasi semua organisme yang ada.3.Pemeriksaan serologi: membantu dalam membedakan diagnosis organisme khusus.4.Pemeriksaan fungsi paru: untuk mengetahui paru-paru, menetapkan luas berat penyakit dan membantu diagnosis keadaan.5.Biopsi paru: untuk menetapkan diagnosis.6.Spirometrik static: untuk mengkaji jumlah udara yang diaspirasi.7.Bronkostopi: untuk menetapkan diagnosis dan mengangkat benda asing.LAPORAN PENDAHULUAN PNEUMONIA

a. Definisi

Pneumonia adalah peradangan paru dimana asinus paru terisi cairan radang dengan atau tanpa disertai infiltrasi dari sel radang kedalam dinding alveoli dan rongga interstisium. (secara anatomis dapat timbul pneumonia lobaris maupun lobularis / bronchopneumonia.

Pneumonia merupakan salah satu penyakit infeksi saluran pernafasan yang terbanyak didapatkan dan sering merupakan penyebab kematian hampir di seluruh dunia. Di Indonesia berdasarkan survei kesehatan rumah tangga tahun 1986 yang dilakukan Departemen Kesehatan, pneumonia tergolong dalam penyakit infeksi akut saluran nafas, merupakan penyakit yang banyak dijumpai.

b. Faktor-faktor yang menyebabkan terjadinya pneumonia :

Diketahui beberapa faktor yang mempengaruhi terjadinya pneumonia yaitu :

1. Mekanisme pertahanan paru

Paru berusaha untuk mengeluarkan berbagai organisme yang terhirup seperti partikel debu dan bahan-bahan lainnya yang terkumpul di dalam paru. Beberapa bentuk mekanisme ini antara lain: bentuk anatomis saluran pernafasan, reflek batuk, system mukosilier, juga system fagositosis yang dilakukan oleh sel-sel tertentu dengan memakan partikel-partikel yang mencapai permukaan alveoli.

Bila fungsi ini berjalan baik, maka bahan infeksi yang bersifat infeksius dapat dikeluarkan dare saluran nafas, sehingga pada orang sehat tidak akan terjadi infeksi serius. Infeksi saluran nafas berulang terjadi aakibat berbagai komponen system pertahanan paru yang tidak bekerja dengan baik.

2. Kolonisasi bakteri di saluran nafas

Di dalam saluran nafas atas banyak bakteri yang bersifat kosal. Bila jumlah mereka semakin meningkat dan mencapai suatu konsentrasi yang cukup, kuman ini kemudian masuk ke saluran nafas bawah dan paru, dan akibat kegagalan mekanisme pembersihan saluran nafas keadaan ini akan bermanifestasi sebagai penyakit.

Mikroorganisme yang tidak dapat menempel pada permukaan mukosa saluran nafas akan ikut dengan sekresi saluran nafas dan terbawa bersama mekanisme pembersihan, sehingga tidak terjadi kolonisasi. Proses penempelan organisme pada permukaan mukosa saluran nafas tergantung dare system pangemalan mikroorganisme tersebut oleh sel eputel.

3. Pembersihan saluran nafas terhadap bahan infeksius

Saluran nafas bawah dan paru berulangkali dimasuki oleh berbagai mikroorganisme dare saluran nafas atas, akan tetapi tidak menimbulkan sakit, ini meninjukkan adanya suatu mekanisme pertahanan paru yang efisien sehingga dapat menyapu bersih mikroorganisme sebelum mereka bermultiplikasi dan menimbulkan penyakit.

Pertahanan paru terhadap hal-hal yang berbahaya dan infeksius berupa reflek batuk, penyempitan saluran nafas dengan kontraksi otot polos bronkus pada awal terjadinya proses peradangan, juga dibantu oleh respon imunitas humoral.

c. Etiologinya

Sebagian besar disebabkan oleh mikroorganisme, akan tetapi dapat juga oleh bahan-bahan lain, sehingga dikenal:

1. Lipid pneumonia : oleh karena aspirasi minyak mineral

2. Chemical pneumonitis : inhalasi bahan-bahan organic atau uap kimia seperti berilium

3. Extrinsik Allergik Alveolitis : inhalasi bahan-bahan debu yang mengandung allergen, seperti debu dare parik-pabrik gula yang mengandung spora dare actynomicetes thermofilik.

4. Drug Reaction Pneumonitis : nitrofurantion, busulfan, methotrexate

5. Pneumonia karena radiasi sinar rontgen

6. Pneumonia yang sebabnya tidak jelas : desquamative interstitial pneumonia, eosinofilik pneumonia

7. Microorganisma

GROUP

PENYEBAB

TYPE PNEUMONIA

Bacteri

Aktinomyctes

Fungi

Riketsia

Klamidia

Mikoplasma

Virus

Protozoa

Streptococcos pneumonia

Streptococcus piogenes

Stafilococcus aureus

Klebsiella pneumonia

Eserikia koli

Yersinia pestis

Legionnaires bacillus

A. Israeli

Nokardia asteroids

Kokidioides imitis

Histoplasma kapsulatum

Blastomises dermatitidis

Aspergillus

Fikomisetes

Koksiella Burnetty

Chlamidia psittaci

Mikoplasma pneumonia

Infulensa virus, adenovirus respiratory syncytial

Pneumosistis karini

Pneumonia bacteri

Legionnaires disease

Aktinomikosis pulmonal

Nokardiosis pulmonal

Kokidioidomikosis

Histoplasmosis

Blastomikosis

Aspergilosis

Mukormikosis

Q Fever

Psitakosis,Ornitosis

Pneumonia mikoplasmal

Pneumonia virus

Pneumonia pneumistis (pneumonia plasma sel)

d. Gambaran Klinis

Gambaran klinis biasanya didahului olek infeksi saluran nafas akut bagian atas selama beberapa hari, kemudian diikuti dengan demam, suhu tubuh kadang-kadang melebihi 40 derajat C, sakit tenggorok, nyeri otot dan sendi. Juga disertai batuk, dengan sputum mukoid atau purulen, kadang-kadang berdarah.

Pada pemeriksaan fisik dada terlihat bagian sakit tertinggal waktu bernafas dengan suara nafas bronchial kadang-kadang melemah. Didapatkan ronki basah halus, yang kemudian menjadi ronki basah kasar pada stadium resolusi.

1. Community Acquired Pneumonia yaitu, pneumonia yang didapatkan di masyarakat, terjadinya infeksi di luar rumah sakit.

2. Hospital Acquirted Pneumonia yaitu, pneumonia yang didapat selama penderita dirawat di rumah sakit. Hampir 1 % dare penderita yang dirawat di rumah sakit mendapatkan pneumonia selama dalam perawatan dan 1/3nya mungkin akan meninggal. Demikian pula halnya dengan penderita yang dirawat di ICU lebih dare 60 % menderita pneumonia.

3. Pneumonia in the immunocompromised host yaitu, yang terjadi akibat terganggunya system kekebalan tubuh. Macula ini semakin meningkat dengan penggunaan obat-obatan sitotoksik dan imunosupresif, hal ini akibat dare merningkatnya kemajuan di bidang pengobatan penyakit keganasan dan transplantasi organ.

e. Gambaran Patogenesis

Dalam keadaan sehat, paru tidak akan terjadi pertumbuhan mikroorganisme, keadan ini disebabkan oleh adanya mekanismer pertahanan paru. Terdapatnya bakteri di dalam paru merupakan akibat ketidakseimbangan antara daya than tubuh, mikroorganisme, dan lingkuingan sehingga mikroorganisme dapat berkembang biak dan berakibat timbulnya sakit.

Masuknya mikroorganisme ke saluran nafas dan paru dapat melalui berbagai cara, yaitu :

- Inhalsi langsung dare udara

- Aspirasi dare bahan-bahan yang ada di nasofaring dan orfaring

- Perluasan langsung dare tempat-tempat lain

- Penyebaran secara hematogen

Gambaran patologis dalam batas-batas tertentu, tergantung pada penyebabnya. Di antaranya yaitu :

1. Pneumonia bakteri

Ditandai oleh eksudat intra alveolar supuratif disertai konsolidasi. Proses infeksi dapat diklasifikasikan berdasarkan anatomi. Terdapat konsolidasi dare seluruh lobus pada pneumonia lobaris, sedangkan pneumonia lobularis atau broncopneumonia menunjukkan penyebaran daerah infeksi yang berbecak dengan diameter sekitar 3-4 cm, mengelilingi dan mengenai broncus.

2. Pneumonia Pneumokokus

Pneumokokus mencapai alveolus-alveolus dalam bentuk percikan mucus atau saliva. Lobus paru bawah paling sering terserrang, karena pengaruh gaya tarik bumi. Bila sudah mencapai dan menetap di alveolus, maka pneumokokus menimbulkan patologis yang khas yang terdiri dare 4 stadium yang berurutan :

- kongesti (4-12 jam pertama)eksudat serusa masuk dalam alveolus-alveolus dare pembuluh darah yang bocor dan dilatasi

- hepatisasi merah (48 jam berikutnya) paru-paru tampak merah dan tampak bergranula karena sel darah merah, fibrin, dan leukosit polimorfonuklear mengisi alveolus-alveolus

- hepatisasi kelabu (3-8 hari) paru-parub tampak abu-abu karena leukosit dan fibrin mengalami konsolidasi dalam alveolus yang terserang.

- Resolusi (7-11 hari) eksudat mengalami lisis dan direabsorbsi oleh mikrofag sehingga jaringan kembali pada strukturnya semula.

Timbulnya pneumonia pneumokokus merupakan suatu kejadian yang tiba-tiba, disertai menggigil, demam, rasa sakit pleuritik, batuk dan sputum yang berwarna seperti karat. Pneumonia pneumokokus biasanya tidak disertai komplikasi dan jaringan yang rusak dapat diperbaiki kemabali. Komplikasi tentang sering terjadi adalah efusi plura ringan. Adanya bakterimia mempengaruhi prognosis pneumonia. Adanya bakterimia menduga adanya lokalisasi proses paru-paru yang tidak efektif. Akibat bakterimia mungkin berupa lesi metastatik yang dapat mengakibatkan keadaan seperti meningitis, endokariditis bacterial dan peritonitis. Sudah ada vaksin untuk merlawan pneumonia pneumokokus. Biasanya diberikan pada mereka yang mempunyai resiko fatal yang tinggi, seperti anemia sickle-sell, multiple mietoma, sindroma nefrotik, atau diabetes mellitus.

3. Pneumonia Stafilokokus

Mempunyai prognosis jelek walaupun diobati dengan antibiotika. Pneumonia ini menimbulkan kerusakan parenkim paru-paru yang berat dan sering timbul komplikasi seperti abses paru-paru dan empiema. Merupakan infeksi sekunder yang sering menyerang pasien yang dirawat di rumah sakit, pasien lemah dan paling sering menyebabkan broncopneumonia.

4. Pneumonia Klebsiella / Friedlander

Penderita ini berhasil mempertahankan hidupnya, akhirnya menderita pneumonia kronik disertai obstruksi progresif paru-paru yang akhirnya menimbulkan kelumpuhan pernafasannya. Jenis ini yang khas yaitu, pembentukan sputum kental seperti sele kismis merah (red currant jelly). Kebanyakan terjadi pada lelaki usia pertengahan atau tua, pecandu alcohol kronik atau yang menderita penyakit kronik lainnya.

5. Pneumonia pseudomonas

Sering ditemukan pada orang yang sakit parah yang dirawat di rumah sakit atau yang mnenderita supresi system pertahanan tubuh (misalnya mereka yang menderita leukemia atau transplantasi ginjal yang menerima obat imunosupresif dosis tinggi). Seringkali disebabkan karena terkontaminasi peralatan ventilasi.

6. Pneumonia Virus

Ditandai dengan peradangan interstisial disertai penimbunan infiltrat dalam dinding alveolus meskipun rongga alveolar sendiri bebas dare eksudat dan tidak ada konsolidasi. Pneumonia virus 50 % dare semua pneuminia akut ditandai oleh gejala sakit kepala, demam dan rasa sakit pada otot-otot yang menyeluruh, rasa lelah sekali dan batuk kering. Kebanyakan pneumonia ini ringan dan tidak membutuhkan perawatan di rumah sakit dan tidak mengakibatkan kerusakan paru-paru yang permanen. Pengobatan pneumonia virus bersifat sympomatik dan paliatif, karena antibiotik tidak efektif terhadap virus. Juga dapat mengakibatkan pneumonitis berbecak yang fatal atau pneumonitis difus.

7. Pneumonia Mikoplasma

Serupa dengan pneumonia virus influenza, disertai adanya pneumonitis interstitial. Sangat mudah menular tidak seperti pneumonia virus, dapat memberikan respon terhadap tetrasiklin atau eritromisin.

8. Pneumonia Aspirasi

Merupakan pneumonia yang disebabkan oleh aspirasi isi lambung. Pneumonia yang diakibatkannya sebagian bersifat kimia, karena diakibatkan oleh reaksi terhadap asam lambung, dan sebagian bersifat bacterial, karena disebabkan oleh organisme yang mendiami mulut atau lambung. Aspirasi paling sering terjadi selama atau sesudah anestesi (terutama pada pasien obstretik dan pembedahan darurat karena kurang persiapan pembedahan), pada anak-anak dan pada setiap pasien yang disertai penekanan reflek batuk atau reflek muntah. Inhalasi isi lambung dalam jumlah yang cukup banyak dapat menimbulkan kematian yang tiba-tiba, karena adanya obstruksi, sedangkan aspirasi isi lambung dalam jumlah yang sedikit dapat mengakibatkan oedema paru-paru yang menyebar luas dan kegagalan pernafasan. Beratnya respon peradangan lebih tergantung dare pH dare zaat yang diaspirasikan. Aspirasi pneumonia selalu terjadi apabila pH dan zat yang diaspirasi 2,5 atau kurang. Aspirasi pneumpnia sering menimbulkan kompliokasi abses, bronchiectase, dan gangrean. Muntah bukan sarat masuknya isi lambung kedalam cabang tracheobronchial, karena regurgitasi dapat juga terjadi secara diam-diam pada pasien yang diberi anestesi. Paling penting pasien harus ditempatkan pada posisi yang tepat agar secret orofarengeal dapat keluar dare mulut.

9. Pneumonia Hypostatik

Pneumonia yang sering timbul pada dasar paru yang disebabkan oleh nafas yang dangkal dan terus menerus dalam posisi yang sama.

Daya tarik bumi menyebabkan darah tertimbun pada bagian bawah paru dan infeksi membantu timbulnya pneumonia yang sesungguhnya

10. Pneumonia Jamur

Tidak sesering bakteri. Beberapa jamur dapat menyebabkan penyakit paru supuratif granulomentosa yang seringkali disalah tafsirkan sebagai TBC. Banyak dare infeksi jamur bersifat endemic pada daerah tertentu. Contohnya di US, hystoplasmosis (barat bagian tengah dan timur), koksibiodomikosis (barat daya) dan blastomikosis (tenggara). Spora jamur ini ditemukan dalam tanah dan terinhalasi. Spora yang terbawa masuk kebagian paru yang lebih difagositosis terjadi reaksi peradangan disertai pembentukan kaverne. Semua perubahan patologis ini mirip sekali dengan TBC sehingga perbedaan kurang dapat ditentukan dengan menemukan dan pembiakan jamur dare jaringan paru.tes serologi serta tes hypersensitifitas kulit yang lambat belum menunjukan tanda positif sampai beberapa minggu sesudah terjadi infeksi, bahkan pada penyakit yang berat tes mungkin negatif. Pneumonia jamur sering menimbulkan komplikasi pada stadium terakhir penyakit tersebut, terutama pada penyakit yang sangat berat, misalnya Ca atau leukemia, candida alicans adalah sejenis ragi yang sering ditemukan pada sputum orang yang sehat dan dapat menyerang jaringan paru. Penggunaan antibiotik yang lama juga dapat mengubah flora normal tubuh dan memungkinkan infasi candida. Amfotinsin B merupakan obat terpilih untuk infeksi jamur pada paru.

f. Pemeriksaan Laboratorium

Pada pemeriksaan laboratorium terdapat peningkatan jumlah leucosit, biasanya > 10.000/l kadang mencapai 30.000 jika disebabkan virus atau mikoplasma jumlah leucosit dapat normal, atau menurun dan pada hitung jenis leucosit terdapat pergeseran kekiri juga terjadi peningkatan LED. Kultur darah dapat positif pada 20 25 pada penderita yang tidak diobatai. Kadang didapatkan peningkatan ureum darah, akan tetapi kteatinin masih dalah batas normal. Analisis gas darah menunjukan hypoksemia dan hypercardia, pada stadium lanjut dapat terjadi asidosis respiratorik.

g. Gambaran Radiologi

Foto toraks merupakan pemeriksaan penunjang yang sangat penting. Foto toraks saja tidak dapat secara khas menentukan penyebab pneumonia, hanya merupakan petunjuk kearah diagnosis etiologi. Gambaran konsolidasi dengan air bronchogram (pneumonia lobaris), tersering disebabkan oleh streptococcus pneumonia. Gambaran radiologis pada pneumonia yang disebabkan clebsibella sering menunjukan adanya konsolidasi yang terjadi pada lobus atas kanan, kadang dapat mengenai beberapa lobus. Gambaran lainya dapat berupa bercak daan cavitas. Kelainan radiologis lain yang khas yaitu penebalan (bulging) fisura inter lobar. Pneumonia yang disebabkan kuman pseudomonas sering memperlihatkan adanya infiltrasi bilateral atau gambaran bronchopneumonia. Firus dan mycoplasma sering menyebabkan pneumonia interstisial terutama radang sptum alveola. Pada pemeriksaan radiologis terlihat gambaran retikuler yang difus.

h. Penatalaksanaan

1 Koreksi kelainan yang mendasari.

2 Tirah baring.

3 Obat-obat simptomatis seperti: parasetamol (pada hipereksia), morfin (pada nyeri hebat).

4 Jaga keseimbangan cairan dan elektrolit dengan batuan infus, dekstrose 5%,normal salin atau RL.

5 Pemilihan obat-obat anti infeksi: tergantung kuman penyebab.

6 Pertahankan jalan nafas

7 oksigenasi

DIAGNOSA KEPERAWATAN

1. Bersihan jalan nafas tidak efektif berhubungan dengan inflamasi trakeobronkial, pembentukan edema, peningkatan produksi sputum. (Doenges, 1999 : 166)

2. Gangguan pertukaran gas berhubungan dengan perubahan membran alveolus kapiler, gangguan kapasitas pembawa aksigen darah, ganggguan pengiriman oksigen. (Doenges, 1999 : 166)

3. Pola nafas tidak efektif berhubungan dengan proses inflamasi dalam alveoli. (Doenges, 1999 :177)

4. Gangguan keseimbangan cairan dan elektrolit berhubungan dengan kehilangan cairan berlebih, penurunan masukan oral. (Doenges, 1999 : 172)

5. Nutrisi kurang dari kebutuhan tubuh berhubungan dengan kebutuhan metabolik sekunder terhadap demam dan proses infeksi, anoreksia yang berhubungan dengan toksin bakteri bau dan rasa sputum, distensi abdomen atau gas.( Doenges, 1999 : 171)

6. Intoleransi aktifitas berhubungan dengan insufisiensi oksigen untuk aktifitas sehari-hari. (Doenges, 1999 : 170)

FOKUS INTERVENSI

1. Bersihan jalan nafas tidak efektif berhubungan dengan inflamasi trakeobronkial, pembentukan edema, peningkatan produksi sputum

Tujuan :

- Jalan nafas efektif dengan bunyi nafas bersih dan jelas

- Pasien dapat melakukan batuk efektif untuk mengeluarkan sekret

Hasil yang diharapkan :

- Mempertahankan jalan nafas paten dengan bunyi nafas bersih/ jelas

- Menunjukkan perilaku untuk memperbaiki bersihan jalan nafas

- Misalnya: batuk efektif dan mengeluarkan sekret.

Intervensi :

a. Auskultasi bunyi nafas, catat adanya bunyi nafas. Misalnya: mengi, krekels dan ronki.

Rasional: Bersihan jalan nafas yang tidak efektif dapat dimanifestasikan dengan adanya bunyi nafas adventisius

b. Kaji/ pantau frekuensi pernafasan, catat rasio inspirasi/ ekspirasi

Rasional: Takipnea biasanya ada pada beberapa derajat dan dapat ditemukan pada penerimaan atau selama stres/ adanya proses infeksi akut. Pernafasan dapat melambat dan frekuensi ekspirasi memanjang dibanding inspirasi.

c. Berikan posisi yang nyaman buat pasien, misalnya posisi semi fowler

Rasional: Posisi semi fowler akan mempermudah pasien untuk bernafas

d. Dorong/ bantu latihan nafas abdomen atau bibir

Rasional: Memberikan pasien beberapa cara untuk mengatasi dan mengontrol dipsnea dan menurunkan jebakan udara

e. Observasi karakteristik batik, bantu tindakan untuk memoerbaiki keefektifan upaya batuk.

Rasional: Batuk dapat menetap, tetapi tidak efektif. Batuk paling efektif pada posisi duduk tinggi atau kepala di bawah setelah perkusi dada.

f. Berikan air hangat sesuai toleransi jantung.

Rasional: Hidrasi menurunkan kekentalan sekret dan mempermudah pengeluaran.

2. Gangguan pertukaran gas berhubungan dengan perubahan membran alveolus kapiler, gangguan kapasitas pembawa oksigen darah, gangguan pengiriman oksigen.

Tujuan :

- Perbaikan ventilasi dan oksigenasi jaringan dengan GDA dalam rentang normal dan tidak ada distres pernafasan.

Hasil yang diharapkan :

- Menunjukkan adanya perbaikan ventilasi dan oksigenasi jaringan

- Berpartisispasi pada tindakan untuk memaksimalkan oksigenasi

Intervensi :

a. kaji frekuensi, kedalaman, dan kemudahan pernafasan

Rasional :Manifestasi distres pernafasan tergantung pada derajat keterlibatan paru dan status kesehatan umum

b. Observasi warna kulit, membran mukosa dan kuku. Catat adanya sianosis

Rasional :Sianosis menunjukkan vasokontriksi atau respon tubuh terhadap demam/ menggigil dan terjadi hipoksemia.

c. Kaji status mental

Rasional :Gelisah, mudah terangsang, bingung dapat menunjukkan hipoksemia.

d. Awsi frekuensi jantung/ irama

Rasional :Takikardi biasanya ada karena akibat adanya demam/ dehidrasi.

e. Awasi suhu tubuh. Bantu tindakan kenyamanan untuk mengurangi demam dan menggigil

Rasional :Demam tinggi sangat meningkatkan kebutuhan metabolik dan kebutuhan oksigen dan mengganggu oksigenasi seluler.

f. Tinggikan kepala dan dorong sering mengubah posisi, nafas dalam, dan batuk efektif

Rasional :Tindakan ini meningkatkan inspirasi maksimal, meningkatkan pengeluaran sekret untuk memperbaiaki ventilasi.

g. Kolaborasi pemberian oksigen dengan benar sesuai dengan indikasi

Rasional :Mempertahankan PaO2 di atas 60 mmHg.

3. Pola nafas tidak efektif berhubungan dengan proses inflamasi dalam alveoli

Tujuan:

- Pola nafas efektif dengan frekuensi dan kedalaman dalam rentang normal dan paru jelas/ bersih

Intervensi :

a. Kaji frekuensi, kedalaman pernafasan dan ekspansi dada.

Rasional :Kecepatan biasanya meningkat, dispnea, dan terjadi peningkatan kerja nafas, kedalaman bervariasi, ekspansi dada terbatas.

b. Auskultasi bunyi nafas dan catat adanya bunyi nafas adventisius.

Rasional :Bunyi nafas menurun/ tidak ada bila jalan nafas terdapat obstruksi kecil.

c. Tinggikan kepala dan bentu mengubah posisi.

Rasional :Duduk tinggi memungkinkan ekspansi paru dan memudahkan pernafasan.

d. Observasi pola batuk dan karakter sekret.

Rasional :Batuk biasanya mengeluarkan sputum dan mengindikasikan adanya kelainan.

e. Bantu pasien untuk nafas dalam dan latihan batuk efektif.

Rasional :Dapat meningkatkan pengeluaran sputum.

f. Kolaborasi pemberian oksigen tambahan.

Rasional :Memaksimalkan bernafas dan menurunkan kerja nafas.

g. Berikan humidifikasi tambahan

Rasional :Memberikan kelembaban pada membran mukosa dan membantu pengenceran sekret untuk memudahkan pembersihan.

h. Bantu fisioterapi dada, postural drainage

Rasional :Memudahkan upaya pernafasan dan meningkatkan drainage sekret dari segmen paru ke dalam bronkus.

4. Gangguan keseimbangan cairan dan elektrolit berhubungan dengan kehilngan cairan berlebih, penurunan masukan oral.

Tujuan : Menunjukkan keseimbangan cairan dan elektrolit

Intervensi :

a. Kaji perubahan tanda vital, contoh :peningkatan suhu, takikardi,, hipotensi.

Rasional :Untuk menunjukkan adnya kekurangan cairan sisitemik

b. Kaji turgor kulit, kelembaban membran mukosa (bibir, lidah).

Rasional :Indikator langsung keadekuatan masukan cairan

c. Catat lapporan mual/ muntah.

Rasional :Adanya gejala ini menurunkan masukan oral

d. Pantau masukan dan haluaran urine.

Rasional :Memberikan informasi tentang keadekuatan volume cairan dan kebutuhan penggantian

e. Kolaborasi pemberian obat sesuai indikasi.

Rasional :Memperbaiki ststus kesehatan

5. Nutrisi kurang dari kebutuhan tubuh berhubungan dengan peningkatan kebutuhan metabolik sekunder terhadap demam dan proses infeksi, anoreksia, distensi abdomen.

Tujuan :

- Menunjukkan peningkatan nafsu makan

- Mempertahankan/ meningkatkan berat badan

Intervensi :

a. Identifikasi faktor yang menimbulkan mual/ muntah.

Rasional :Pilihan intervensi tergantung pada penyebab masalah

b. Berikan wadah tertutup untuk sputum dan buang sesering mungkin, bantu kebersihan mulut.

Rasional :Menghilangkan bahaya, rasa, bau,dari lingkungan pasien dan dapat menurunkan mual

c. Jadwalkan pengobatan pernafasan sedikitnya 1 jam sebelum makan.

Rasional :Menurunkan efek mual yang berhubungan dengan pengobatan ini

d. Auskultasi bunyi usus, observasi/ palpasi distensi abdomen.

Rasional :Bunyi usus mungkin menurun bila proses infeksi berat, distensi abdomen terjadi sebagai akibat menelan udara dan menunjukkan pengaruh toksin bakteri pada saluran gastro intestinal

e. Berikan makan porsi kecil dan sering termasuk makanan kering atau makanan yang menarik untuk pasien.

Rasional :Tindakan ini dapat meningkatkan masukan meskipun nafsu makan mungkin lambat untuk kembali

f. Evaluasi status nutrisi umum, ukur berat badan dasar.

Rasional :Adanya kondisi kronis dapat menimbulkan malnutrisi, rendahnya tahanan terhadap infeksi, atau lambatnya responterhadap terapi

6. Intoleransi aktifitas berhubungan dengan insufisiensi oksigen untuk aktifitas hidup sehari-hari.

Tujuan : Peningkatan toleransi terhadap aktifitas.

Intervensi :

a. Evakuasi respon pasien terhadap aktivitas.

Rasional :Menetapkan kemampuan/ kebutuhan pasien dan memudahkan pilihan intervensi

b. Berikan lingkungan yang tenang dan batasi pengunjung selama fase akut.

Rasional :Menurunkan stres dan rangsangan berlebihan, meningkatkan istirahat

c. Jelaskan pentingnya istitahat dalam rencana pengobatan dan perlunya keseimbamgan aktivitas dan istirahat.

Rasional :Tirah baring dipertahankan untuk menurunkan kebutuhan metabolik

d. Bantu aktivitas perawatan diri yang diperlukan.

Rasional :Meminimalkan kelelahan dan membantu keseimbangan suplai dan kebutuhan oksigen

DAFTAR PUSTAKA

Barbara Engram (1998), Rencana Asuhan Keperawatan Medikal Bedah Jilid I, Peneribit Buku Kedokteran EGC, Jakarta.

Barbara C. Long (1996), Perawatan Medikal Bedah: Suatu Pendekatan Proses Keperawatan, The C.V Mosby Company St. Louis, USA.

Hudak & Gallo (1997), Keperawatan Kritis: Pendekatan Holistik Volume I, Penerbit Buku Kedoketran EGC, Jakarta.

Jan Tambayonmg (2000), Patofisiologi Unutk Keperawatan, Penerbit Buku Kedoketran EGC, Jakarta.

Marylin E. Doenges (2000), Rencana Asuhan Keperawatan: Pedoman Untuk Perencanaan dan Pendokumentasian Perawatan Pasien edisi 3, Penerbit Buku Kedoketran EGC, Jakarta.

Sylvia A. Price (1995), Patofisiologi: Konsep Klinis Proses-proses Penyakit Edisi 4 Buku 2, Penerbit Buku Kedoketran EGC, Jakarta

Guyton & Hall (1997), Buku Ajar Fisiologi Kedokteran Edisi 9, Penerbit Buku Kedoketran EGC, Jakarta

Abstract

The first point of a good diagnostic strategy for healthcare-associated pneumonia (HCAP) is correct classification of patients with specific criteria, as suggested by the last American Thoracic Society/ Infectious Diseases Society of America (ATS/IDSA) guidelines. However, clinical practice and recent literature have suggested new risk factors for multidrug-resistant infection (MRI): the presence of permanent indwelling devices, prior antibiotic use in the last 3 months, chronic and advanced pulmonary diseases (chronic obstructive pulmonary disease, bronchiectasis, etc.), history of alcoholism, and immunosuppression. The clinical presentation in HCAP patients is often unusual (mild respiratory symptoms and frequent extrapulmonary manifestations) due to different factors: advanced age, neurological disorders, and multiple chronic comorbidities. Moreover, HCAP commonly presents a worse clinical course than community-acquired pneumonia, a prolonged length of stay, and a mortality rate close to hospital-acquired pneumonia. Chest radiography and routine laboratory markers (including C-reactive protein) are always needed for clinical evaluation and severity assessment. The clinical use of new biomarkers of infection and sepsis (procalcitonin, etc.) is currently being investigated. Extensive microbiological testing to overcome the high prevalence of MRI in HCAP, including urinary antigens forLegionellaandStreptococcus pneumoniae; blood cultures; Gram staining and low respiratory tract secretions (sputum, tracheobronchial aspirate, fibrobronchial aspirate, protected specimen brush, bronchoalveolar lavage); and cultures for aerobic, anaerobic, mycobacterial, and fungal pathogens are recommended, whereas the indication for serology tests for respiratory viruses and atypical pathogens is low. By contrast, the new polymerase chain reaction-based techniques for the rapid identification (2 to 4 hours) of microbial pathogens in respiratory samples (nasopharyngeal swab, bronchoalveolar lavage) seem to be the most innovative future perspective in the diagnostics of HCAP

Definition of Healthcare-associated Pneumonia

Table 1 Risk Factors for Multidrug-Resistant Pathogens Causing Hospital-Acquired Pneumonia, Healthcare-Associated Pneumonia, and Ventilator-Associated Pneumonia

Antimicrobial therapy in preceding 90 days

Current hospitalization of 5 days or more

High frequency of antibiotic resistance in the community or in the specific hospital unit

Presence of risk factors for HCAP:

Hospitalization for 2 or more days in the preceding 90 days

Residence in a nursing home or extended care facility

Home infusion therapy (including antibiotics)

Chronic dialysis within 30 days

Home wound care

Family member with multidrug-resistant pathogen

Immunosuppressive disease and/or therapy

From Reference 6, with permission.

Table 2 Additional Risk Factors for Multidrug-Resistant Infections in Healthcare-Associated Pneumonia

Presence of chronic indwelling device

Prior antibiotic use in the last 3 months

Chronic and advanced pulmonary diseases (chronic obstructive pulmonary disease, bronchiectasis, etc.)

History of alcoholism and immunosuppression (i.e., systemic corticosteroids, immunosuppressive therapy, etc.

In the last 2 decades the literature has described a group of patients commonly residing in long-term care facilities (LTCFs) (nursing homes, hemodialysis centers, etc.) or with some contact with the healthcare environment, whose pneumonia usually shows a worse clinical course and outcomes [mortality, length of stay (LOS),[13]etc.] than that of patients with community-acquired pneumonia (CAP). These findings have led to the development of the new concept of healthcare-associated pneumonia (HCAP).

Nonetheless, it is uncertain whether the previous clinical conditions (older age, impaired functional status, high number of comorbidities, etc.) or a different microbiological etiology than CAP can be considered as the main cause of these findings.

Although the definition criteria for HCAP have not been clearly established, it is evident that more attention is needed on this issue because the number of patients attending outpatient health care settings (LTCFs, domiciliary care programs, etc.) is increasing worldwide.[4,5]The first point of a good diagnostic strategy, in the context of the initial evaluation (medical history collection and physical examination), is the correct classification of patients with HCAP.

The last American Thoracic Society/Infectious Diseases Society of North America (ATS/IDSA) guidelines for the management of hospital-acquired pneumonia (HAP) define specific criteria (Table 1) to identify HCAP patients and recommend antimicrobial therapy similar to that administered in cases of HAP.[6]However, clinical practice and recent literature have suggested that all patients with permanent indwelling devices (e.g., permanent urinary and other permanent catheters, gastrostomy, nasogastric tube, etc.) are at risk of multidrug-resistant infections (MRIs).[7]Therefore, it is likely that this additional criterion should be considered to identify HCAP patients because it represents a strong risk factor for MRI and could consistently influence the diagnostic and therapeutic approach.

Accordingly, to detect HCAP patients with tangible risk factors for MRI, it is strongly recommended to consider, alongside the ATS/IDSA criteria, the factors shown inTable 2.

Actually, due to the lack of information, awareness about HCAP seems inadequate and does not facilitate the recognition of MRI risk factors among patients fulfilling the ATS/IDSA criteria for HCAP. Indeed, despite the bad prognosis of pneumonia in this set of patients, not all HCAPs really have to be empirically treated for nosocomial microorganisms because this could lead to the overuse of antibiotics, with the resulting possibility of emergent resistances and inadequate antibiotic coverage of some community pathogens such asLegionellaspp.[8]andChlamydia pneumoniae.[9]Consequently, wide diagnostic testing is recommended to optimize the initiation and downscaling of antibiotic therapy, despite the frequent practical difficulties, such as the fact that many patients are not able to provide a good sputum specimen for analysis, and it is often impossible to distinguish between chronic airway colonization and a new infection causing pneumonia.

Clinical Presentation

The clinical presentation of HCAP patients is frequently unusual and nonclassical as a consequence of different conditioning factors, including advanced age, the presence of neurological disorders, and/or multiple chronic comorbidities.

In regard to pneumonia in elderly patients, it Osler described as "a painless and often lethal event";[10]indeed, the classic respiratory symptoms of pneumonia, such as cough, expectoration, dyspnea, and pleuritic chest pain, are commonly mild[11,12]and less frequent than in younger patients. On the other hand, extrapulmonary manifestations, including mental confusion and gastrointestinal disorders (anorexia, nausea, vomiting, abdominal pain, etc.), are very frequent and often predominate over respiratory symptoms.[13]It has also been observed that in older CAP patients many symptoms (cough, sputum, fatigue, anorexia, myalgias, etc.) are longer lasting than in younger patients.[14]Riquelme et al reported dyspnea to be the most frequent symptom in older patients with CAP, whereas 19% of the patients did not present cough, sputum, or pleuritic pain, and altered mental status was present in almost 45% of this group.[15]In addition, it is known that fever is less commonly present in older[15,16]compared with younger CAP patients, likely as a result of an altered thermoregulatory capacity to produce and respond to endogenous pyrogens.[17]In their recent review Niederman and Brito provide a very good description of the clinical features of pneumonia in the elderly.[18]A variable proportion of HCAP patients have neurological and cerebrovascular disorders with frequent impairment in swallowing or cough reflexes that implies an elevated incidence of bronchoaspiration.[19]The reported incidence of dysphagia, particularly in nursing homes, is between 50 and 75%.[20,21]The definition of bronchoaspiration implies the aspiration of a considerable inoculum of pathogens from a previous colonized oropharynx or of a little inoculum in the presence of predisposing conditions that make the clearance of the aspirated secretions difficult, such as a high virulent bacterial burden, forceless coughing, insufficient ciliary transport, or altered immunoresponse. Indeed, Vergis et al identified witnessed aspiration and sedative medications as the most important risk factors for pneumonia in LTCFs,[22]and Kikuchi and colleagues demonstrated the occurrence of aspiration in 71% of elderly patients with CAP compared with 10% in healthy age-matched control subjects.[23]Moreover, dysphasia can significantly hinder the interpretation of signs and symptoms during medical evaluation.

The clinical presentation of pneumonia in patients with multiple chronic comorbidities (chronic obstructive pulmonary disease, congestive heart failure, renal failure, etc.) may suggest an acute exacerbation of a comorbidity rather than pneumonia.[11,24]In conclusion, in patients with recent contact with the healthcare environment and with suspicion of pneumonia, prompt and well-oriented diagnostic testing is fundamental because an unusual clinical presentation (older age, neurological disorders, comorbid illnesses) and the frequent predominance of the symptoms of comorbidities can cause a considerable delay in the first dose of antibiotic,[11,25,26]the administration of which is generally considered a predictor of outcome[27,28]in pneumonia.

Clinical Course

Despite the great differences among the studies published on the microbial etiology of HCAP,[1,29,30]it has been unanimously described that, compared with CAP, HCAP patients commonly have a worse clinical presentation (hypoxemia, need for mechanical ventilation support, multilobar infiltration) but not a different incidence of complications (pleural effusion, myocardial infarction, etc.).[2,31,32]In addition, a prolonged LOS[1,3,34]and a mortality rate close to HAP are also reported.[1,2,12,31Diagnostic Tests

Radiology

Along with a correct history and an extensive clinical evaluation, chest radiography (preferably posteroanterior and lateral positions) is always needed to define the presence of a new pulmonary infiltrate, the severity of the disease, and the presence of complications.[33]It is important to be aware of the existence of different pathological conditions, such as the presence of atelectasis, pulmonary edema (cardiogenic and noncardiogenic), pleural effusion, hemorrhage, neoplastic lesions, infectious and malformative cysts, pulmonary infarction (i.e., pulmonary thromboembolism), drug-induced pulmonary lesions (oxygen, chemotherapy agents, amiodarone, etc.), diffuse alveolar damage [adult respiratory distress syndrome (ARDS)], organizing pneumonia [bronchiolitis obliterans organizing pneumonia (BOOP)], that can erroneously be interpreted as pneumonia. In case of doubt or relevant disagreement between the clinical presentation and the radiological findings, it is recommended to perform a computed tomographic (CT) scan.

Laboratory Tests

Routine laboratory markers are a fundamental part of the clinical evaluation for deciding the site of care and severity assessment. Recommended assessments include blood cell count, electrolytes, hepatic and renal function, arterial blood gases, C-reactive protein (CRP) and procalcitonin (PCT) levels.

CRP is an acute inflammatory mediator that is released from the liver by interleukin-6 (IL-6) stimulation, after tissue damage as part of systemic inflammatory response. It is a useful marker of sepsis, infection, and response to treatment.[34]Unfortunately, there are some limitations to its use: serum CRP levels slowly increase (at least 24 hours after the onset of infection) and do not reliably correlate with the severity of the disease. In addition, CRP levels also increase in noninfectious inflammatory processes such as coronary syndrome or postoperative periods. No specific evaluations have been made in HCAP patients but it has been demonstrated that high serum levels of CRP in elderly patients with pneumonia are a useful prognostic marker of disease severity.[35]PCT is a new marker of bacterial infection that has been widely investigated in the last decade since the first description in 1996 of elevated serum levels of PCT, the prohormone of calcitonin, in inhalational burn injury, in several sepsis syndromes, and in endotoxemia.[36]It is a peptide synthesized in monocytes undergoing adhesion processes but not in circulating polymorphonuclear cells. Tissue cells produce PCT only when interacting with activated monocytes. Different studies have demonstrated that PCT is helpful to differentiate bacterial infections from other inflammatory (i.e., ARDS, autoimmune diseases) or infectious (i.e., viral) diseases[3739]for its cytokine-like role in host defense versus bacterial infections.[37]PCT monitoring, therefore, cannot only limit the overuse of antibiotics[38,40,41]but can also contribute to an early evaluation of disease severity.[37]Furthermore, high levels of PCT at admission and at day 3 are a good predictor of treatment failure.[38]Indeed, in an attempt to improve current sepsis definitions, the PIRO (predisposition, insult infection, response, organ dysfunction) concept recommends the use of readily measurable circulating biomarkers as an additional tool for the timely assessment and severity classification of septic patients and the prediction of mortality.[42]No specific studies on the utility of PCT measurements in HCAP patients are available in the literature, but it is likely that in patients with an atypical clinical presentation [mild and unusual symptoms of lower respiratory tract infection (LRTI)], biological markers may have a greater role in achieving the diagnosis of pneumonia.

However, for the diagnosis of infections, the diagnostic accuracy of PCT has a primary importance: whereas PCT levels lower than 0.1 ng/dL suggest the absence of bacterial infection and interruption of antibiotic therapy (when previously initiated) and levels of PCT 0.5 ng/dL are clearly associated with bacterial infection, PCT levels between 0.26 and 0.5 ng/dL can still indicate a possible bacterial infection and can be of diagnostic value in conditions other than sepsis.[37,41]Kruger and colleagues indicate a cutoff level of 0.228 ng/mL to predict patients at low risk of death from CAP in all severity score classes.[43]As a consequence, very sensitive assays (with a functional detection limit less than 0.5 ng/mL) are recommended. Nonetheless, despite the evidence-based recommendation to monitor PCT levels in critically ill patients with sepsis,[44]it remains unclear whether an altered immunoresponse secondary to diseases, drugs, or aging can affect the expression of PCT in respiratory bacterial infections. Therefore, more information is needed on the pathophysiology of PCT and, consequently, on its diagnostic value in specific categories of patients, such as the very elderly and immunosuppressed individuals (chemotherapy, corticosteroids, hematopoietic disorders, etc.) who may be highly represented among HCAP.

Other new inflammatory biomarkers, including Pro-adrenomedullin, pro-atrial natriuretic peptide (ANP), carbamoyl phosphate sinthase-1 (CPS-1), pro-endothelin-1 (pro-ET-1), and copeptine (pro-vasopressine), are currently being investigated as possible helpful biomarkers for individual risk assessment and outcome prediction in sepsis and severe infection and to detect cardiovascular abnormalities in pneumonia patients.[37,4547]Etiologic Diagnosis

A variety of microbiological tests, with various indications and limitations, are commonly available to investigate the microbial etiology of pneumonia. Nevertheless, the diagnostic value of many specimens obtained routinely, as well as those achieved through more invasive procedures (fiber-bronchoscopy, etc.) is controversial even in critically ill patients.

Blood cultures are usually recommended for more severe patients[48]and for those who have not previously received antibiotics.[49]Metersky and colleagues demonstrated that in these patients false-positive results were less likely than in patients with mild illness and in those who had previously been administered antibiotics.[50]Different studies have evaluated the contribution of blood culture to clinical management of hospitalized patients with CAP and have found blood cultures to be of poor utility in directing antibiotic therapy, rarely cost saving, and weak from an epidemiological point of view.[51,52]By contrast, we should consider that HCAP patients are more similar to HAP patients in whom blood cultures are strongly recommended. Indeed, the microbial pattern can considerably differ from CAP (unusual antimicrobial resistance, presence of atypical/uncommon pathogens), and, as a consequence, the empirical antibiotic therapy is more likely to be inadequate. Thus a greater effort to achieve the etiological diagnosis is justified in HCAP, despite the possible increase in costs.

Sputum is the most common specimen obtained in LRTI, but it is also the most problematic. First, many patients do not have productive cough or are too weak to provide a deep respiratory sample. Second, very strict screening criteria for microscopic examination of sputum must be followed to ensure the quality of the microbiological determination (proportion of epithelial and polymorphonuclear (PMN) cells, etc.).[53,54]A variety of suggestions to improve sputum quality include no ingestion of food for 1 to 2 hours, rinsing the mouth with water or saline solution, rapid transport of specimens to the laboratory, and prompt inoculation of culture media.[55]However, there is no clear evidence that any of these procedures improve the utility of the sputum specimen. Sputum induction with a 3% NaCl solution, suggested in the past to obtain specimens less contaminated from the upper respiratory tract, is currently not recommended because no benefits have been demonstrated for the etiological investigation[56]and because of the risk of provoking bronchial obstruction.

Nonetheless, the visualization of a predominant bacterial morphology in Gram staining of lower respiratory tract (LRT) secretions may be useful in predicting the etiologic agent, especially in intensive care settings where the promptness in achieving an etiological diagnosis and in directing the antibiotic therapy toward gram-positive or -negative microorganisms is fundamental and may be life-saving in some circumstances.

Although the sensitivity and specificity of Gram staining of LRT secretions ranges widely between 57 and 95% and between 48 and 87%, respectively, according to the type and quality of specimens, negative Gram stains and cultures in patients who have not previously received antibiotics have a high negative predictive value (94%), suggesting that other noninfectious causes of pulmonary infiltrates should be investigated (pulmonary edema, neoplasia, etc.)

Whereas the importance of Gram staining and sputum culture in the evaluation of pneumonia in hospitalized patients is clear, their role in patients with pneumonia not severe enough to require hospitalization is debated because the overall yield is low and because the impact on clinical care is infrequent.[33,5761]However, a study by Musher and colleagues on pneumococcal pneumonia demonstrated that, with the exclusion of patients who have received antibiotics within the last 24 hours, the sensitivities of Gram staining and sputum culture were 80% and 93%, respectively, suggesting that, with proper management (no prior antibiotic use, good specimen quality, and rapid transport to the laboratory) these procedures have an increased utility.[62]These conclusions can be particularly true in HCAP patients with multiple risk factors for MRI because the ATS guidelines for the management of HAP, ventilator-associated pneumonia (VAP), and HCAP clearly delineate a specific indication for sputum culture when it could likely change the individual antibiotic management.[6]The retrospective analysis of Micek et al[32]in 639 culture-positive patients with pneumonia shows that the microbiological diagnosis was obtained more with sputum (63.5% of CAP patients, 73.8% of HCAP patients) more than with blood cultures (CAP, 37.5%; HCAP, 30.9%), BAL (CAP, 4.3%; HCAP, 4.9%) or urinary antigen forLegionella(CAP, 3.4%; HCAP, 0.2%). Despite the limitation of a retrospective analysis of only positive-culture pneumonia, these results are encouraging to consider sputum a good specimen, particularly from the epidemiological point of view.

Similarly, in El Solh et al's series of elderly patients with CAP, the microbial etiology was obtained in 59% of cases by sputum examination and in 41% by other techniques.[63]However, it is important to remember that HCAP patients, particularly those residing in LTCFs, have a high prevalence of colonization of the upper respiratory tract from pathogen microorganisms, and this finding can seriously hinder the etiological diagnosis and mislead antibiotic therapy.

Other more invasive but reliable respiratory specimens are tracheobronchial aspirates (TBAS), fibrobronchial aspirates (FBAS), protected specimen brush (PSB), and bronchoalveolar lavage (BAL), commonly preferred to sputum when available (intubated or tracheostomized patients), for better Gram stain sensitivity and specificity as well as the possibility of performing quantitative cultures that can differentiate pathogen infections from microbial colonization (cutoff value > 105CFU /mL).

The collection of TBAS is the simplest and least invasive technique to obtain respiratory samples in intubated patients at a relatively low cost. Qualitative culture has a limited value because, despite having acceptable sensitivity (90 to 100%), its specificity for infection is very poor (14 to 47%). However, quantitative cultures of TBAS, with a cutoff point of 105CFU/mL have shown an accuracy similar to that of bronchoscopic sampling methods[64]and with the advantage of a high negative predictive value in case of patients who have not previously received antibiotics. The study by El Solh and colleagues[65]analyzed the diagnostic value of TBAS cultures in comparison with PSB and BAL in 75 patients with severe nursing home-acquired pneumonia admitted to the intensive care unit (ICU). They obtained an etiological diagnosis in 49 patients (65%), either with BAL or with PSB, with an absolute concordance in 33 cases (67%) between the two techniques. In comparison, the accuracy of TBAS was favorable at a cutoff point of 104CFU/mL (sensitivity of 90% and specificity of 77%), with the results coinciding with PSB and BAL in 30 cases (61%).

Quantitative FBAS also seems to obtain results similar to invasive sampling methods in terms of diagnostic yield and clinical outcome.[66]The PSB technique allows LRT sampling by advancing a catheter containing a sealed sampling brush through the working channel of the bronchoscope allowing 0.01 mL of secretions to be collected for microbial investigation. The selected threshold to discriminate colonization and infections is 103CFU/mL, and PSB has shown a high sensitivity (above 70%) and specificity (80 to 90%) for infection. It should be pointed out that the diagnostic yield decreases markedly if the sample is obtained under antibiotic treatment. This technique is simple and the sampling fast, minimizing side effects of the procedure.

BAL is performed through the insertion of the bronchoscope and can collect samples from both distal bronchi and a large alveolar area. After blocking the tip of the bronchoscope in a segmental or subsegmental bronchus, 100 to 150 mL of saline are instilled and aspirated consecutively. Quantitative culture of BAL, with a cutoff point at 104CFU/mL, has very good sensitivity and specificity (approaching 100%). The utility of BAL in immunosuppressed patients with pulmonary infiltrates has been clearly demonstrated, with the early use of the information provided by this method in this specific population being related to a better outcome.[67]In CAP there is no firm information supporting its use and possible side effects, and contraindications are weighted individually in each patient.

Alternatively, there are "blind" techniques to obtain LRT secretions through the insertion of a catheter in a distal bronchus without the help of fibrobronchoscopy. In this case, the sensitivity and specificity are 74 to 97% and 74 to 100%, respectively, for BAS, and 63 to 100% and 66 to 96% for BAL.

El Solh and colleagues[30,68]studied the microbial etiology in older patients ( 75 years) with severe pneumonia admitted to the ICU: 57 individuals were residing in the community and 47 in nursing homes. A similar diagnostic yield (BAL, PSB performed blindly or via bronchoscopic guide) was described in both groups of CAP and nursing home-acquired pneumonia, suggesting that the accuracy and diagnostic value of the invasive techniques to obtain LRT secretions are comparable in both groups. In addition, invasive bronchial sampling in this series[68]led to a change in microbial therapy in 40% of cases and discontinuation of antibiotics in 10% of definite pneumonia, with no differences in mortality or in the incidence of complications between patients who underwent a bronchoscopy and those who did not.

However, due to the severity of underlying medical illnesses, the risks of invasive diagnostic approaches (bronchoscopy or needle aspiration) make their application in the practice more infrequent. Nevertheless, an LRT sample should always be collected in intubated or tracheostomized patients.

It is recommended to test all the respiratory samples for mycobacterial (Ziehl-Nielsen and auramine stains; mycobacterial culture) as well as fungal pathogens, particularly in patients with bronchiectasis or suspected immunosuppression because the number of immunosuppressed patients among HCAP cases can be considerably higher than in CAP cases, as shown in the large HCAP series from the group in St. Louis, Missouri, where immunosuppressed patients ranged between 23 and 39% of all HCAP patients with positive cultures.[2,32]A diagnostic thoracentesis should always be performed in patients with large pleural effusion to investigate parapneumonic effusion and empyema, complications that can make the treatment considerably difficult and delay the achievement of clinical stability.[6]Gram staining and culture for aerobic and anaerobic bacteria and pneumococcal antigen tests should be performed in the pleural liquid. A retrospective comparative study of empyema in 114 community-residing and 55 nursing home-residing patients[69]described that the latter patients had a delayed clinical presentation and a higher yield of anaerobic organisms compared with individuals from the community. These findings suggest that particular attention is necessary with HCAP patients because the clinical presentation is often misleading in defining the severity and etiology of the disease, and more extensive diagnostic procedures are needed in these patients.

Tests for the determination of urinary antigens forLegionella pneumophilaandStreptococcus pneumoniaeare usually available in emergency departments (EDs) at a low cost and with good feasibility. Pneumococcal testing (all serotypes) has a good sensitivity (70%) and specificity (90%), but it has some limitations: false-positive results have been reported in individuals who had received specific vaccination or with bronchial colonization. In addition, a positive result can be observed up to 25 weeks after the infection, therefore making more it difficult to differentiate acute infection fromS. pneumoniae. On the other hand, notwithstanding its high sensitivity (70 to 90%) and specificity (> 90%), the urinary antigen test forLegionella, which is positive from the third day of infection, is able to detect only serotype 1, accounting for 75 to 90% of all infections forLegionella, and not serotypes 4 and 6, which also cause infections in humans.[70]Alternative diagnostic tests forLegionellaare LRT culture, direct fluorescent antibody (DFA) staining in respiratory secretions and tissue samples (rapid but technically demanding), seroconversion (titers 1:128), or nucleic acid amplification.

Large epidemiological studies have clearly demonstrated that older adults living in LTCFs are at a higher risk for invasive pneumococcal disease and death than community-living older adults,[71]and outbreaks of multidrug-resistant (MDR) pneumococci[72,73]and ofLegionella[74]among nursing home residents have been widely described. These data confirm the relevance of low-cost and easy-to-perform determinations for pneumococcal andLegionellainfections in this population.

Nasopharyngeal swab is an additional easy-to-perform and low-cost test, useful for the determination of respiratory virus (influenza viruses A and B, parainfluenza virus, respiratory syncytial virus, adenovirus, coronavirus, and rhinovirus). Viral diagnostic methods include culture, rapid antigen detection, real time polymerase chain reaction (RT-PCR), and serologic testing, with availability and sensitivity varying on the basis of the specific virus. Respiratory secretions appropriate for testing include nasal swab or wash specimens, sputum specimens, and BAL fluid samples.[75]Studies on CAP in adults indicate a viral etiology in 1 to 23% of cases, with the influenza virus being the most common,[76]whereas the information about viruses in HCAP is reduced, with the frequency of viral detection ranging between 0 and 14% of all cases with a known etiological diagnosis.[30,77]Today, pure viral pneumonia is uncommon, perhaps because prior infection and vaccination have induced immunity among older persons. The true incidence of secondary bacterial pneumonia during influenza is unknown, but it is clear that dual viral-bacterial infections are more severe than viral infections alone, as evidenced by higher rates of intensive care use and morbidity.[75]An observational 3-year study in LTCFs investigated serology for viral infections in 382 patients. A total of 204 viral infections were identified in 157 subjects; the human metapneumovirus (13%) and coronavirus (11%) were the most frequently isolated viruses.[78]The presence of bronchitis, pneumonia, and any LRTIs was strongly associated with the presence of a viral infection. This work undoubtedly demonstrates that a wide range of respiratory viruses circulate among LTCFs, contributing to the morbidity of respiratory illnesses.

A specific nasopharyngeal swab is indicated for methicillin-resistantStaphylococcus aureus(MRSA) detection when suspected. Nonetheless, it may be difficult to distinguish between MRSA colonization (healthy carriers), which is relatively frequent in weakened patients, and new MRSA infections. Indeed, different authors have described thatS. aureusinfections as relatively common in the nursing home population,[79,80]especially in individuals with indwelling devices,[7]and these findings have reinforced the idea of new outbreaks of community-acquired MRSA. In our experience community MRSA infections are anecdotal, and contact with the healthcare environment should be investigated because it seems to be the most frequent source of such infections.

The suspicion of "atypical pneumonia" should be taken into account when dealing with older and nursing home patients because epidemic episodes have been described in these populations.[8,9,81]Serology testing is available forChlamydia pneumoniaeandMycoplasma pneumoniae,[82]accounting for a variable number of pneumonia cases (up to 21% of CAP,[83]2 to 27% of HCAP statistics[12,30]), but also for virus (see before). The utility of serology in routine testing is poor due to the delay in obtaining results, although it has an important role in populational studies and for epidemiological purposes.[84,85]However, the empirical antibiotic treatment of HCAP should always cover atypical pathogens (macrolides, quinolones, etc.).[33]Nasopharyngeal swab has also recently been used, when available, for PCR determination of an increasing number of microorganisms.[86]In view of such a wide panel of microbiological tests the decision of the physician is guided by specific clinical indications, procedural risks, the clinical conditions of patients, time to results, and so forth.

Indicators for more extensive diagnostic tests should be considered, including (1) early failure, (2) pleural effusion, (3) cavitation, (4) recent travel to exotic places, and (5) history of immunosuppression (urgent fiberbronchoscopy [FBS]).[18]Table 3 Main Causes of Recurrent Pneumonia

Sources of aspiration

Dysphagia and cough reflex disorders[19,89]

Hiatal hernia as a cause of repetitive nocturnal bronchoaspiration (gastric regurgitation)[90,91]

Dental plaque and pharyngeal colonization by pathogenic microorganisms[19,92,93]

Sleep apnea-related bronco-aspirations[94,95]

Bronchiectasis: idiopathic and secondary[96]

Humoral immunity disorders (i.e., common variable immunodeficiency[97]).

Middle lobe syndrome[98]

Obstructive pneumonia and cancer[99]

Healthcare-Associated Pneumonia

Faculty and DisclosuresCME/CE Released: 06/25/2007; Valid for credit through 06/25/2008

CME/CE InformationINTRODUCTION

Healthcare-associated pneumonia (HCAP), a newly recognized form of pneumonia, was included in the 2005 American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA) guidelines for nosocomial pneumonia.[1]HCAP refers to patients with pneumonia, at any time in their hospital stay (on admission or acquired in the hospital), who have a history of recent hospitalization in the past 90 days, residence in a nursing home or extended care facility, treatment with chronic hemodialysis, receipt of home wound care, or exposure to a family member with drug-resistant pathogen infection. There remains confusion about how to best define this entity, what the likely pathogens are, and how to optimally approach therapy and prevention. In addition, the guidelines considered that patients with HCAP are at risk for infection with multidrug-resistant (MDR) gram negatives and methicillin-resistantStaphylococcus aureus(MRSA). Thus, the current recommendation is to treat HCAP patients with multidrug broad-spectrum empirical therapy, a practice that may promote further antibiotic resistance, particularly if such broad-spectrum therapy is not needed for all affected individuals. At the 2007 ATS meeting, a symposium was held to discuss HCAP and the controversies in management and prevention. Topics discussed included defining HCAP epidemiology and bacteriology, the approach to diagnosis, therapy and prevention, and evaluation of the best way to use effective therapy while minimizing the promotion of antimicrobial resistance, leading to optimal patient outcomes.

Epidemiology and Bacteriology

Like community-acquired pneumonia (CAP), HCAP can be present when the patient is first admitted to the hospital, but unlike CAP, and similar to nosocomial pneumonia, the etiologic pathogens can be MDR gram negatives and MRSA. A study by Kollef and colleagues[2]noted that this difference in bacteriology is likely a consequence of the fact that HCAP patients have more comorbid illness than patients with CAP. These comorbidities include immunosuppression, diabetes, chronic renal disease, heart disease, and stroke. Marcos Il Restropo, MD, from the University of Texas, San Antonio, discussed unpublished data from his own institution where all HCAP patients had MDR risk factors, which included prior antibiotics, residence in a nursing home, chronic renal failure, and immunosuppression. One other unpublished study from Washington University in St. Louis, Missouri, found that HCAP was more common than CAP, and that 63% of these patients had been recently hospitalized; 31% were immunosuppressed; 18% were nursing home residents; and 6% were undergoing hemodialysis.

Dr. Restropo described studies documenting the bacteriology of HCAP to include a high frequency of MRSA andPseudomonas aeruginosa.[2]In one study, the frequency of MRSA was 57% but 25% hadP aeruginosa,[2]whereas in another study of patients with MDR gram negatives present on admission, there was a high frequency of HCAP risk factors, including recent antibiotics and residence in a long-term care facility.[3]When patients with MRSA were compared with those with methicillin-susceptibleS aureus(MSSA) infection in another study using a case-control methodology, once again, prior hospitalization, home nursing care, and transfer from a nursing home were all associated with the presence of MRSA.[4]The higher frequency of these difficult pathogens in patients with HCAP may explain why their mortality rate of 12% to 23% is higher than that of patients with CAP. To minimize this mortality risk, Dr. Restropo urged the use of early and aggressive appropriate empirical therapy, with a broad-spectrum antimicrobial approach followed by de-escalation to fewer drugs and narrower spectrum agents, as culture and clinical data become available. In addition, he recommended use of therapy at proper doses, as suggested in the ATS/IDSA guidelines, and he recommended linezolid over vancomycin for the therapy of MRSA ventilator-acquired pneumonia (VAP).[1]One additional suggestion that he discussed was to use short-duration therapy, citing a French study that documented the efficacy of 8-day therapy of VAP caused by organisms other than nonfermenting gram negatives, such asP aeruginosa.[5]Pathogenesis and Prevention of HCAP

David Ost, MD, from New York University School of Medicine, New York, NY, discussed the pathogenesis and use of risk factors to guide the prevention of VAP, in an effort to understand how to avoid other nosocomial pneumonia syndromes, including HCAP. He cited the impact of VAP on hospital stay, which increases stay by 7-9 days, while adding a cost of nearly $12,000 per episode.[6]Dr. Ost pointed out the imprecision of clinical definitions of VAP, showing that depending on the number of criteria used, the frequency of infection can vary from 8% to 30%, but that by any definition, VAP leads to adverse outcomes. In addition, the frequency, when expressed as a daily risk rate, falls with increasing duration of mechanical ventilation, emphasizing the need for prevention studies to stratify patients by the duration of mechanical ventilation. Given this important impact of VAP, prevention could have a high reward, and efforts should be based on an understanding of both modifiable and unmodifiable risk factors -- and might reduce the incidence by as much as 50%.[7]On the basis of an understanding of modifiable risks, the effective strategies for prevention that Dr. Ost recommended included rapid weaning from the ventilator, including daily interruption of sedation; use of noninvasive ventilation when possible; positioning patients with the head of the bed elevated; using open lung ventilation if possible; avoidance of nasotracheal intubation in favor of orotracheal intubation; treatment in an adequately staffed intensive care unit (ICU); careful consideration of selective digestive decontamination (with topical and systemic antibiotics, but not topical alone) to reduce the risk for gram-negative infection; consideration of chlorhexidine baths; and consideration of sucralfate for intestinal bleeding prophylaxis. Dr. Ost emphasized the difference between efficacy in clinical trials and true clinical effectiveness in "real-world" situations. He stated that the use of subglottic secretion drainage with special endotracheal tubes and specific enteral feeding methods could not be specifically recommended.

Diagnosing Nosocomial Pneumonia

Kenneth V. Leeper, MD, from the Emory School of Medicine in Atlanta, Georgia, discussed the controversies surrounding invasive vs noninvasive diagnosis of VAP. His major focus was to examine which approach could minimize the impact of VAP on mortality, length of stay, antibiotic use, antibiotic resistance, and duration of mechanical ventilation. He first discussed the recently published, Canadian, multicenter clinical trial comparing invasive and noninvasive diagnostic methods, and demonstrating no impact on mortality.[8]He criticized the trial because it did not enroll many patients with MDR pathogens.

In trying to define the most cost-effective approach to VAP diagnosis, Dr. Leeper first examined noninvasive strategies. He pointed out that the clinical definition of pneumonia has a relatively low sensitivity and specificity in some studies, but that if too sensitive a definition were used, it could lead to the overuse of antibiotics and a failure to recognize nonpneumonic causes of fever. He pointed out the potential value of the Clinical Pulmonary Infection Score (CPIS) to enhance the noninvasive diagnosis of VAP, and cited a study by Singh and colleagues[9]in which antibiotic cost, antibiotic resistance, and mortality were reduced when a protocol employing serial measurements of CPIS was used to guide antibiotic therapy, when compared with usual clinical management. He also showed how clinical management could be used to guide duration of therapy, and lead to less systemic antibiotic use.

Looking at the putative advantages of an invasive diagnostic approach, Dr. Leeper cited the potential to avoid unnecessary and inappropriate antibiotic therapy, and to be able to narrow and focus antibiotics once culture data from quantitative cultures of lower respiratory tract secretions become available. He discussed a review[10]that reported the sensitivity of bronchoscopic diagnosis to be between 42% and 93%, with a specificity varying between 45% and 100%. Early studies documented the safety of withholding therapy in patients with negative quantitative cultures and a low clinical suspicion of infection, but a large French multicenter study comparing an invasive bronchoscopic approach with a noninvasive strategy for antibiotic use showed a reduction in 14-day mortality and antibiotic use.[11]One alternative to bronchoscopic cultures is blind minibronchoalveolar lavage (BAL) done through an endotracheal tube, and one decision analysis showed that the best approach to maximize VAP survival, while minimizing cost and antibiotic use, was to give empirical therapy with 3 antibiotics and then adjust on the basis of mini-BAL culture data.[12]Dr. Leeper advocated this approach, but stated that at his institution the decision to start therapy was also guided by CPIS, but the decision to continue or modify therapy was, in part, based on the results of a repeat mini-BAL, done after 4 days of therapy.

Managing HCAP and Reducing the Risk for Antimicrobial Resistance

There are various ways to limit antibiotic resistance by managing risk factors in the patient with HCAP. Not only have the resistance rates in nosocomial pneumonia been rising in recent years, especially if infection is caused byP aeruginosaor MRSA, but in one recent German study, infection with these pathogens was an independent risk factor for mortality, using multiple logistic regression analysis.[13]A number of factors have led to rising rates of resistance, including inappropriate use of antibiotics, underdosing of key antimicrobial agents, using a broader spectrum of therapy than is needed, unnecessary treatment of airway colonization, excessively prolonged therapy, and failure of infection control methods. Common to many of these factors is the usage of antibiotics, and many investigations have shown that usage within 2 weeks of the onset of VAP is a risk for subsequent resistance to the previously used antibiotic.[14,15]In a discussion, which I led at this meeting, I highlighted a number of potentially effective strategies to limit resistance, which included infection control, surveillance respiratory cultures, avoiding monotherapy with certain antimicrobial agents, avoiding broader antimicrobial therapy than is necessary, antimicrobial "stewardship," de-escalation of therapy when possible, and more effective "up-front" therapy. Infection control is a universal need, and it can limit the spread of resistant pathogens from one patient to another. In addition, infection control practitioners can facilitate a good knowledge of local (specific for each ICU) microbiology. A study by the Duke University Infection Control Network, collecting such data and sharing best practices, led to a reduction in the frequency of VAP and of infections caused by MRSA.[16]A number of strategies have led to the use of fewer and more focused antibiotics, and because usage is the major factor driving resistance, these strategies could be very valuable. These have included the collection of tracheal aspirate surveillance cultures, which can be used to guide initial VAP empirical therapy, and in one study this practice led to the use of less broad-spectrum therapy than the use of international guidelines.[17]Careful selection of specific antimicrobials is also an effective strategy to limit resistance, because monotherapy with third-generation cephalosporins can promote the emergence of extended-spectrum beta-lactamases and the emergence of inducible type 1 chromosomal beta-lactamases during therapy.[1,18]In addition, quinolones can promote antimicrobial resistance, not only to quinolones, but also to multiple other agents, and, thus, I suggested that in the ICU, these agents should generally be reserved for a second episode of infection -- and not the first acquired infection -- because the latter practice may make it impossible to have any effective agents for subsequent infection.[15]In an effort to avoid the use of broader spectrum therapy than is absolutely necessary, we examined the recommendation of current guidelines to treat all HCAP patients with a 3-drug regimen geared at resistant gram negatives and MRSA.[1]Citing a study, from Buffalo, New York, of 88 patients with severe nursing home-acquired pneumonia, he pointed out that resistant organisms were only present in 19%, and that they were present only if patients had multiple risk factors, in addition to severe illness.[19]Because narrow-spectrum therapies have been effective for some nursing home populations, he recommended that triple therapy be reserved for patients with at least 2 of the 3 key risk factors, and that patients without these risks be treated with a narrower spectrum regimen. These risk factors were severe illness, recent antibiotic therapy, and poor functional status.

A recent IDSA publication examined the practices of antimicrobial stewardship, emphasizing the multidisciplinary nature of this effort, which can be done through prospective audits and interventions or by formulary restrictions.[20]The recommendation for formulary restrictions was not strong, but the study authors did recommend use of therapy guidelines that are based on local bacteriologic data, de-escalation of therapy when possible, and dose optimization. Antimicrobial cycling and antibiotic order forms were not strongly recommended.

In closing, I recommended a number of other strategies to limit resistance, including shorter durations of therapy. One way to facilitate this approach may be to follow serial measurements of biological markers, such as C-reactive protein and procalcitonin. One other promising strategy that was discussed is the use of adjunctive aerosolized aminoglycosides to optimize the initial therapy of MDR gram negatives. I described unpublished data from a multicenter study of aerosolized amikacin, given by a special proprietary nebulizer, in a blinded placebo-controlled fashion, along with systemic antimicrobials (all patients received this latter therapy). The data showed that at the end of 7 days, patients given aerosol antibiotic therapy were using less systemic antibiotics than patients given a placebo aerosol, raising the possibility that this approach can eradicate infection rapidly and minimize the need for prolonged systemic therapy.

Using Pathophysiology and Risk Factors to Optimize HCAP Outcomes

Richard G. Wunderink, MD, FCCP, from Feinberg School of Medicine, Northwestern University, Chicago, Illinois, focused on ways to improve the outcomes, especially mortality, duration of ICU stay, duration of mechanical ventilation, and the degree of organ dysfunction in patients with HCAP. He referred to a study of MRSA VAP in which the use of linezolid, rather than vancomycin, led to a reduction in mortality.[21]The major focus of the discussion was to evaluate antimicrobial treatment failure and recurrent infection as signs of immunosuppression in the critically ill patient, especially as a consequence of immune paralysis at the time of severe infection. Dr. Wunderink considered 2 possible types of explanations for this immune dysfunction, both with supporting data: temporary disease-related immune impairment and fixed immune impairment as a consequence of genetic polymorphisms in the immune response. He advocated the use of biomarkers to follow the course of the immune response to infection. He believed that the major focus for the future would be to understand this immune paralysis and recognize it when present, so that interventions could be made to improve outcomes. Currently, because we do not have such interventions, we are limited to changing antibiotics in the face of uncontrolled infection, finding unrecognized sites of infection, and replacing immunoglobulins in patients who are deficient.

Supported by an independent educational grant from GlaxoSmithKline

References[CLOSE WINDOW]

References

1. Niederman MS, Craven DE, Bonten MJ, et al. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388-416.Abstract2. Kollef MH, Shorr A, Tabak YP, et al. Epidemiology and outcomes of health-care-associated pneumonia: results from a large US database of culture positive patients. Chest. 2005;128:3854-3862.Abstract3. Pop-Vicas AE, D'Agata EM. The rising influx of multidrug-resistant gram-negative bacilli into a tertiary care hospital. Clin Infect Dis. 2005;40:1792-1798.Abstract4. Lescure FX, Locher G, Eveillard M, et al. Community-acquired infection with healthcare-associated methicillin-resistant Staphylococcus aureus: the role of home nursing care. Infect Control Hosp Epidemiol. 2006;27:1213-1218.Abstract5. Chastre J, Wolff M, Fagon JY, et al. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA. 2003;290:2588-2598.Abstract6. Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med. 2002;165:867-903.Abstract7. Bonten MJ, Kollef MH, Hall JB. Risk factors for ventilator-associated pneumonia: from epidemiology to patient management. Clin Infect Dis. 2004;38:1141-1149.Abstract8. The Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med. 2006;355:2619-2630.Abstract9. Singh N, Rogers P, Atwood CW, et al. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med. 2000;162:505-511.Abstract10. Torres A, El-Ebiary M. Bronchoscopic BAL in the diagnosis of ventilator-associated pneumonia. Chest. 2000;117:198S-202S.Abstract11. Fagon JY, Chastre J, Wolff M, et al. Invasive and noninvasive strategies for management of suspected ventilator-associated pneumonia: a randomized trial. Ann Intern Med. 2000;132:621-630.Abstract12. Ost DE, Hall CS, Joseph G, et al. Decision analysis of antibiotic and diagnostic strategies in ventilator-associated pneumonia. Am J Respir Crit Care Med. 2003;168:1060-1067.Abstract13. Gastmeier P, Sohr D, Geffers C, et al. Risk factors for death due to nosocomial infection in intensive care unit patients: findings from the Krankenhaus Infektions Surveillance System. Infect Control Hosp Epidemiol. 2007;28:466-472.Abstract14. Trouillet JL, Vuagnat A, Combes A, et al. Pseudomonas aeruginosa ventilator-associated pneumonia: comparison of episodes due to piperacillin-resistant versus piperacillin-susceptible organisms. Clin Infect Dis. 2002;34:1047-1054.Abstract15. Niederman MS. Reexamining quinolone use in the intensive care unit: use them right or lose the fight against resistant bacteria. Crit Care Med. 2005;33:443-444.Abstract16. Kaye KS, Engemann JJ, Fulmer FM, et al. Favorable impact of an infection control network on nosocomial infection rates in community hospitals. Infect Control Hosp Epidemiol. 2006;27:228-232.Abstract17. Michel F, Franceschini B, Berger P, et al. Early antibiotic treatment for BAL-confirmed ventilator-associated pneumonia: a role for routine endotracheal aspirate cultures. Chest. 2005;127:589-597.Abstract18. Paterson DL, Ko WC, Von Gooberg A, et al. International prospective study of Klebsiella pneumoniae bacteremia: implications of extended-spectrum beta-lactamase production in nosocomial infections. Ann Intern Med. 2004;140:26-32.Abstract19. El Solh AA, Pietrantoni C, Bhat A, et al. Indicators of potentially drug-resistant bacteria in severe nursing home-acquired pneumonia. Clin Infect Dis. 2004;39:474-480.Abstract20. Dellit TH, Owens RC, McGowan JE, et al. Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship. Clin Infect Dis. 2007;44:159-177.Abstract21. Wunderink RG, Rello J, Cammarata SK, et al. Linezolid vs vancomycin: analysis of two double-blind studies of patients with methicillin-resistant Staphylococcus aureus nosocomial pneumonia. Chest. 2003;124:1789-1797.Abstract