Selasa, November 24, 2009

Baru Kusadari.....

Ternyata Seperti ini.....

Tak terasa, hidup bergulir begitu cepat..., aku pun semakin dewasa, dan umurku pu tak begitu lama lagi, tapi apa yang telah aku perbuat......NOL Besar!!!!
sesungguhnya, aku tahu belum terlambat tuk merubah semua itu, dan belum terlambat untuk menjadi yang terbaik.....
sekarang q baru menyadari, sekarang q baru tau, inilah hidup, begitu kejam, keras, yang kalo orang gak kuat akan frustasi, bahkan sampai mati, subhanallah......itulah kuasa Allah, ....
mari kita ubah semuanya, menjadi manusia baru, yang lebih baik, jangan takut, dan jangan menyerah (kayak lagunya D'masiv....hehehe ^^)....Allahuakbar!!!!!

Minggu, Juni 21, 2009

Aku Tak Butuh Cinta

“Cuuy gw balik dulu yaaah”ucap gw ketemen temen gw yang lagi pada nongkrong di depan kampus,waktu menunjukan pukul empat sore,mata kuliah bahasa inggris udah bener bener bikin perut gw yang kroncongan tambah melilit,akhirnya gw putsin usai kuliah gw mau langsung ke kostan temen gw,karna gw pikir semoga dikostannya ada sesuatu yang bisa mengganjal perut gw yang kroncong protol,yang cuma baru di isi dua buah kueh pancong tadi pagi,hari ini gw bener bener boke,miskin,pakir,kere,ntah apa lagi istilah lain yang lebih daramatis,yang hanya bermodalkan duit gopean yang nyelip di kantong celana yang kemudian gw beliin kueh pancong yang terletak disamping kampus sewaktu gw mau berangkat kuliah,setelah itu ta ada lagi Sesutu yang masuk ke dalam perut gw,mungkin untuk saat ini gw adalah seseorang yang berhak mendapatkan pundi amal SCTV,karna emang gw bener bener ga megang duit sama sekali,bahkan pengemispun jauh lebih kaya ketimbang gw,makanya setelah pulang kuliah gw lebih memilih balik ketimbang nongkrong nongkrong yang paling Cuma di sodori rorko doang yang sama sekali ga bisa membuat perut gw merasa sedikit bahagia,di sepanjang perjalanan menuju kostan temen gw,gw Cuma bisa tertunduk simpul menahan perasaan melihat serentetan pedagang pecel lele,seefood,surabimod,dan gorengan yang terjejer manis di kawasan panorama yang terletak di kota bandung,godaan dan rintanganpun gw hadepin sampai akhirnya gwpun sampai juga di kostan temen gw,rasa bahagia,sedih,,harupun bercampur aduk dalam perasaan gw saat ini,sekalipum gw belum mendapatkan apa apa,setidaknya gw merasa bahagia telah berada tepat di depan pintu kostan temen gw,tak sabar rasanya untuk masuk dan menikmati makanan makanan yang terjejer manis di dapur,dengan antusias gw pun mengetuk pintu kostannya,
“hallo,,smlikum”ucap gw sambil mengetuk pintu kostannya,taklama kemudian muncul seseorang di balik pintu “eeh lo nang,,”ucapnya kaget ngeliat gw “ayo masuk”printahnya.
“giman kabar lo deen”Tanya gw sambil masuk kamarnya dan duduk di depan televisi..
“maksud loo…?”
“ngga,, kabar lo sehat ga?”Tanya gw lagi sembari mengambil remot yang ada di depan gw
“sehat.!!”ucapnya santai
Gw bingung harus ngomong apa lagi,sesaat kami terdiam,gw hanya bisa ngutak ngatik remot TV yang membuat ga jelas acaranya,akhirnya sidenipun kesal ngeliat gw yang ga jelas mau nonton apa,
“nyari apaan siih lo nang?”ucapnya kesel
“ga tau niiih acaranya ga ada yang bagus” jawab gw tanpa menoleh ke arahya.
“ohya,,ngomong ngomong kebeneran nih lo kesini”
Akhirnya tanda tanda dia akan nawarin makanan pun sudah terdengar jelas di telinga
“yaiyalaaah,,gw kan punya radar”ucap gw cengengesan “sinyal kuat indosat” ucap gw lagi
Si deni malah geleng geleng kepala “gila emeng temen gw yang satu ini tau aja kalo gw lagi butuh pertolongan”
Gw terdiam sejenak,ntah apa maksud dari omonganya itu,kalo dia sekarang lagi butuh pertolongan,Aaah paling paling itu Cuma masalah nganter dia kewarnet,ucap gw dalam hati
“maksud lo den?lo minta gw nganter lo ke warnet lagi,,,!!”
“bukan itu maksud gw nang,,”kali ini dengan tempang melas
“Oooh masalah yang itu!!”ucap gw so yakin
Kali ini ia sedikit tersenyum mendengar ucapan gw “ iya nang masalah itu,,lo paham kan?”
“he,,he,,tenang aja msalah itu mah,nanti gw bakal bilang sama si rini kalo lo cowo baik baik,,bukan gay dan tida homo..”
Tampangnya kini memelas lagi “bukan itu maksud gw nang,,!!”
Sebuah pertanyaaan yang telah membut gw ternganga “laah terus masalah apa dong??”
“gini nang”desahnya “dari tadi pagi gw belum makan apa apa tau,,!gw mau beli makan ga ada duit mau masak di dapur ga da yang bisa di masak sama sekali,,makanya kebeneran lo kesini,,gw mau minjem duit sama lo nang..!!!ada ga??”
Sebuah ungkapan yang telah membuat gw tersipu,gw hanya terdiam mendengar keluhanya yang ternyata lebih parah ketimbang gw,akhirnya gw jadi lebih sadar ternyata di bawah langit ada langit lagi,
“untuk masalah ini gw ga bisa bantu lo den”ucap gw tega
“jadi lo ga mau minjemin gw niih..?”tanyanya dengan mimik super melas,gw jadi tambah ga tega ngeliatnya,namun apalah daya diri ini tak bisa berbuat apa apa.
“bukanya gitu cuuy,,”ucap gw sembari menepuk pundaknya, “untuk masalah ini kita senasib,,gw kesini sebenarnya tida lain dan tida bukan mau numpang makan sama lo,,yang tadinya gw pikir kali aja lo ada makanan yang bisa gw makan,,nyatanya kita senasib den,,sama den gw juga belum makan apa apa dari pagi Cuma dua buah kueh pancong yang baru masuk kedalam perut gw,,”
Sideni juga melongo mendengar pernyataan gw yang juga menyedihkan
“trus gimana doong,,??”tanyanya
“yaudahlah den,,klo gitu gw mau balik aja,,gw mau tidur”ucap gw yang kemudian berdiri dan berbalik menuju pintu
“yaudah deh,,kalo gitu gw juga mau tidur”
“oke den,,gw cabut yaah”ucap gw setelah beres memakai sepatu
“hati hati yaa,,moga kita mimpi makan besar nang,,,nanti awas jangan pelit lo yaah”
“siap”ucap gw sambil meninggalkan kostannya.
Heeh,,tenyata bayangan makanan itu hanya ada dalam negri dongeng,beginilah keadaan anak kost yang belum dapet kiriman,hanya bisa berharap bisa bermimpi indah.setelah itu gw pun pulang ketempat di mana gw tinggal,sebuah kamar kost yang gw harap mengeluarkan keajaiban berubah menjadi sebuah mall besar atau seengganya alfamart,atau kalo ga warung juga ga apa apa,,,namun itu tadi !!
itu hanyalah sebuah hayalan tingkat tinggi,tak ada yang berubah dari kostan gw,setibanya gw di kostan waktu menunjukan pukul enam sore,kayanya kurang lazim kalo gw harus tidur magrib magrib kaya gini,kemudian gw pun menengok ke kostan temen gw yang berada tepat di samping kostan gw,boris namanya,mahsiswa asal medan yang merantau ke bandung untuk mencari kebahagiaan untuk masa depan katanya,untuk saat ini gw butuh pertolonganya,gw perhatikan kostanya pintunya terbuka lebar,gw lihat dia tengah asik tidur tiduran sembari melihat TV,gw pun berjalan menghampirinya
“eeh kou,,nang”ucapnya kaget yang ternyata sedang menonton bokep,lalu aku duduk di sampingnya
“nang,,kou sudah makan belum?”pertanyaan itu membuatku tersenyum “aku belum makan ris,,”
Ia malah tersenyum mendengar kata kata gw barusan, “kalo gitu kita sama nang,,kau mau makan tak??”ucap siboris sembari memukul paha gw
“ya mau laah”jawab gw antusias
“kalo gitu,,aku..teraktir yaah nang?”ucapnya antusias pula
Gw tersenyum mendengarnya“waah yang bener lo,,boleh boleh”
“tapi aku mau salat magrib dulu yaah nang,,”
“Oke siap,,berarti abis magrib kita makan niiih”
“yaudah mending kamu salat magrib dulu sanah”ucapnya sembari mengusir gw dari kostannya.
Akhirnya keajaiban datang juga,cacing cacing yang ada dalam perut gw langsung pada cengengesan mendengar kalo abis magrib gw akan makan.
Lima menit telah berlalu dimana gw juga udah kelar melaksankan salat magrib,siboris yang katanya mau nraktir gw itu pun udah manggil manggil di depan kamar gw
“Naang,,anang,,ayolah kita jalaan aku sudah lapar kali niiih”
“iya,,iya sabar”ucap gw sembari membuka pintu kostan
“kau mau makan apa nang?”ucapnya santai,gw hanya terdiam sesaat Gila niih temen gw yang satu ini bener bener pengertian sampai sampai nawarin gw mau makan apa segala,batin gw!
“gw maah ga mau muluk muluk ris,,gw cukup pengen makan mie kocok aja,,emang lo mau makan apa?”
“yaah aku terserah kau,,?”
Gw sedikit bingung mendengarnya“yaudah terserah lo aja deeh,,yang penting gw makan”
Lalu kami pun turun dan berangkat menuju warung terdekat,sesampainya di warung siborispun dengan penuh antusias memanggil manggil si pemilik warung
“halloo spada,,!!bang,,aku mau beli niih”ucapnya untuk ketiga kalinya
Kemudian muncul si pemilik warung “yaah beli apa yaah de,,?”
“aku amu beli miee kocok dua bang,,buat aku satu buat temen aku satu”
Si pemilik warung itupun mencarinya kemudian balik lagi dengan membawa satu buah mie kocok
“waah de,,mie kocoknya tinggal satu!!”
Si boris pun berbalik ke arah gw dan meminta persetujuan gw, “yaah terserah loo,,tapi mending nyari warung lain aja laah!!”karna mengutamaka kebersamaan gw pun menyuruhnya untuk membatalakannya,
“waah kayanya aku tak jadi beli bang soalnya kata temen aku ta usahlah kalo Cuma ada satu”
Dengan sedikit perasaan kecewa kamipun meninggalkan warung itu, segera kami pun menuju ke warung berikutnya namun apalah daya sial lagi lagi tak bisa di hadang,sesampainya disana ternyata warung itu tutup,boris pun berinisiatip untuk balik lagi kewarung sebelumya dan mengalah untuk tida harus dapat yang mie kocok
“sudah laah nang aku cape,,lebih baik kou beli mie yang disana saja laah,,ta apalah bukan aku yang mie kocok”ucapnya melirik kerah warung yang pertama
“yaudaah kalo gitu,,biar gw aja yang beli,,sini uangnnya”ucap gw sambil menyodorkan tangan
Boris malah kaget “loooh ko minta duit sama aku”
“laah katanya lo yang mau neraktir gw”
“yaah aku sudah bilang sama kou ,,aku ,,”menujuk kearah dirinya “teraktir yaah”lanjutnya lagi
Aku tersenyum lemes mendengarnya “kirain gw lo yang mau neraktir gw”
“berarti tadi,,”ucap kami serentak,celingukan sambil menunjuk kearah warung itu.
Dan kami pun tertawa terbahak bahak,sambil bergantian menjendulkan kepala,
“untung ajaa mie kocoknya ga ada,,coba kalo ada,di Tanya duit,celingukan kita!!”ucap gw sambil tertawa
Akhirnya kami pun kembali ke kostan dengan tangan kosong,perut memeng melilit namun meski begitu gw seneng bisa merasakan ternyata perbedaan itu indah,si boris yang bermaksud begini ternyata gw anggap begitu.tapi buat gw sekarang yang penting hati senang walau pun tak punya uang. iya ga?

Selasa, Juni 09, 2009

Sebagian Polewali Terserang Wabah Diare

Liputan6.com, Polewali: Pemerintah Polewali Mandar, Sulawesi Barat, menetapkan sejumlah kecamatan masuk kategori kejadian luar biasa (KLB) diare. Sebab, hanya dalam sepekan, sekitar 300 anak dilarikan ke petugas kesehatan. Bahkan, enam di antaranya meninggal dunia sebelum mendapat penanganan medis.

Berdasarkan pantauan SCTV, Ahad (7/6), faktor kemiskinan dan jauhnya akses pelayanan kesehatan dari permukiman warga diduga menjadi penyebab satu keluarga terserang diare akut. Seorang anaknya meninggal dunia, sedangkan satu lainnya dilarikan ke rumah sakit setelah kakaknya dikebumikan.

Kepala Bidang Pengendalian Masalah Penyakit Dinas Kesehatan Polewali Mandar, Hartini Asis mengatakan, selain menggelar penyuluhan kesehatan di sejumlah lokasi yang terjangkit, Dinkes juga telah mengirim bantuan obat-obatan seperti oralit dan cairan infus. Langkah ini ditempuh demi mengantisipasi jatuhnya korban baru.

Meski demikian, jika kecenderungan diare terus meningkat hingga beberapa hari mendatang, Dinkes akan melakukan uji sampel kotoran korban diare. Terutama, untuk memastikan jenis bakteri yang menyerang warga.(UPI)

Minggu, Juni 07, 2009

Herpes Zoster dan lain2

Herpes Zoster

Laboratory Studies

  • Diagnosis of herpes zoster is based primarily on clinical findings, specifically the characteristic location and appearance of the skin eruption in association with localized pain. However, in some patients, the presentation of herpes zoster can be atypical and may require additional testing. This is particularly true in immunocompromised patients.
  • Varicella-zoster virus can be cultured successfully; this has limited use in the ED due to the long time required for viral growth.
  • If necessary, a definitive diagnosis can be confirmed by sending swabs to the laboratory.
    • Lift the top of the lesion and swab the exposed base. The swab should then be rolled across a sterile glass side, which is air dried and sent to the laboratory for staining with immunofluorescent antibodies.
    • The swab can also be placed in viral transport medium for detection of viral DNA by polymerase chain reaction.
  • Tzanck smear can be obtained from the vesicular lesions; however, the smear does not differentiate between varicella-zoster virus and other herpes virus infections such as herpes simplex.
    • A Tzanck smear is a simple test that may be performed by the clinician or in a laboratory.
      • A fresh blister is unroofed and material from the base is smeared on a slide.
      • Wright stain is applied, and the smear is examined under the microscope.
      • A positive result shows distinctive giant cells with multiple nuclei.
      • This test has a significant false-negative rate of at least 20%. Therefore, a negative result does not rule out a herpes virus infection and should not preclude empiric treatment.
  • Empiric treatment, when indicated, should not be delayed pending the results of diagnostic tests.

Imaging Studies

No imaging tests are indicated in typical cases of cutaneous VZ infection.

Other Tests

  • Monoclonal antibody tests
  • Blood mononuclear cell testing for viral DNA (research)

Procedures

  • Biopsy for direct immunofluorescence testing (rarely performed)

Treatment

Symptomatic treatment

  • Patients with herpes zoster usually experience pain. Antiviral and steroid therapy provides relatively minor relief of pain, and analgesics are often needed.
    • Initial therapy may include nonsteroidal anti-inflammatory drugs (NSAIDs).
    • In many cases, narcotic analgesia is necessary.
    • A randomized clinical trial of oral analgesics for acute pain in patients with herpes zoster was conducted (n-87; age 50 years or older). Treatment was begun within 6 days of rash onset and with worst pain within 24 hours. Patients were initiated on a 7-day course of famciclovir with controlled-release (CR) oxycodone, gabapentin, or placebo for 28 days. Discontinuing participation, primarily associated with constipation, occurred most frequently in patients randomized to CR-oxycodone (27.6%) compared with placebo (6.9%). Mean worst pain was reduced the first week with CR-oxycodone compared with placebo (p=0.01). Gabapentin did not provide significantly greater pain relief than placebo, although the first week provided a modest reduction of pain.2
    • A randomized, double-blind, placebo-controlled study of extended-release gabapentin (gabapentin ER) demonstrated improvement in average daily pain score in patients with acute herpes zoster. In those taking gabapentin, a reduction of pain of 50% or greater from baseline was reported by 25.5-28.8% compared with 11.8% of patients taking placebo.3
  • Wet to dry dressings with tap water or 5% aluminum acetate (Burow solution). Apply to the affected skin for 30-60 minutes 4-6 times per day.
  • Bland lotions (ie, Calamine) may help relieve discomfort.

Antiviral therapy for uncomplicated herpes zoster

The goals of antiviral therapy are to decrease pain, to promote healing of skin lesions, and to prevent or reduce the severity of postherpetic neuralgia. Acyclovir and the newer antivirals valacyclovir and famciclovir have been shown to be effective if given within 48-72 hours of the appearance of the rash. The newer agents have better bioavailability and do not need to be given as frequently. Outcomes studied have included time to crusting of skin lesions, duration and severity of acute pain, and duration and incidence of postherpetic neuralgia.

Acyclovir has been the most studied and widely recommended, but in a blinded, randomized comparison trial, valacyclovir was shown to be superior to acyclovir.5,6 The trial included more than 1100 patients with uncomplicated zoster who were 50 years or older. Adverse effects were similar in both groups. Outcomes evaluated included resolution of acute pain and the duration of postherpetic neuralgia.

The duration of antiviral treatment in studies has varied from 7-21 days. Based on current literature, for immunocompetent patients, acyclovir for 7-10 days or a 7-day course of the newer agents is appropriate. Longer courses may be needed in immunocompromised patients.

Combined antiviral and corticosteroid therapy for uncomplicated herpes zoster

The addition of corticosteroids has been evaluated in patients treated with acyclovir. The benefit of steroids included accelerated healing of lesions and more rapid resolution of acute pain.7 Though statistically significant, the benefits were small. There was no effect on the development or duration of postherpetic neuralgia.

Steroids have not been studied with valacyclovir of famciclovir, so the benefit is unknown. The addition of steroids should be considered only in patients with severe symptoms. Steroids should not be given alone (without antiviral therapy) due to concern about promotion of viral replication. The effect of steroids on the incidence of secondary skin infection is unknown. Some authors have suggested that they may increase the risk. Prednisone, 40-60 mg/day, is a reasonable choice if steroids are used. The optimal duration of steroid therapy is not known. If prescribed, it seems reasonable for steroids to be used concurrently with antiviral therapy. The duration of steroid use should not extend beyond the period of antiviral therapy.

Treatment of complicated herpes zoster

Patients who are immunosuppressed are at risk for extensive skin involvement or disseminated disease. Although strong evidence is lacking, the following are highlights of some of the current recommendations for treating zoster in these patients.

  • Treat all immunosuppressed patients with antivirals, even when the onset of symptoms is more than 72 hours.
  • Valacyclovir should be used if oral therapy is selected.
  • Consider treatment with intravenous acyclovir for the following patients:
    • Transplant patients soon after transplantation or when being treated for rejection
    • Patients with advanced HIV
    • Patients with widespread skin involvement or visceral disease

Treatment of herpes zoster ophthalmicus

Two trials comparing oral acyclovir to famciclovir or valacyclovir in patients with ophthalmic zoster showed comparable outcomes with any of the regimens. Patients with diagnosed or suspected ophthalmic zoster should receive antivirals and be referred to an ophthalmologist.

Post exposure prophylaxis

Varicella-zoster immune globulin (VZIG) prevents or modifies clinical illness in susceptible, persons who are exposed to varicella or zoster. It should be reserved for patients at risk for complications such as those who are immunocompromised, pregnant, and for neonates.

Risk Factors for Chickenpox (Varicella)

Between 75 - 90% of chickenpox cases occur in children under 10 years of age. Before the introduction of the vaccine, about 4 million cases of chickenpox were reported in the U.S. each year. Since a varicella vaccine became available in the U.S. in 1995, however, the incidence of disease and hospitalizations due to chickenpox has declined by nearly 90%.

The disease usually occurs in late winter and early spring months. It can also be transmitted from direct contact with the open sores. (Clothing, bedding, and such objects do not usually spread the disease.)

A patient with chickenpox can transmit the disease from about 2 days before the appearance of the spots until the end of the blister stage. This period lasts about 5 - 7 days. Once dry scabs form, the disease is unlikely to spread.

Most schools allow children with chickenpox back 10 days after onset. Some require children to stay home until the skin has completely cleared, although this is not necessary to prevent transmission.

Risk Factors for Shingles (Herpes Zoster)

About 500,000 cases of shingles occur each year in the U.S. Anyone who has had chickenpox has risk for shingles later in life, which means that 90% of adults in the U.S. are at risk for shingles. Shingles occurs, however, in 10 - 20% of these adult over the course of their lives, so certain factors must exist to increase the risk for such outbreaks.

The Aging Process. The risk for herpes zoster increases as people age, and the overall number of cases will undoubtedly increase as the baby boomer generation gets older. One study estimated that a person who reaches age 85 has a 50% chance of having herpes zoster. The risk for postherpetic neuralgia (PHN) is also highest in older people with the infection and increases dramatically after age 50. PHN is persistent pain and is the most feared complication of shingles.

Immunosuppression. People whose immune systems are impaired from diseases such as AIDS or childhood cancer have a risk for herpes zoster that is much higher than those with healthy immune systems. Herpes zoster in people who are HIV-positive may be a sign of full-blown AIDS. Certain drugs used for HIV, called protease inhibitors, may also increase the risk for herpes zoster.

Cancer. Cancer places people at risk for herpes zoster. At highest risk are those with Hodgkin's disease (13 - 15% of these patients develop shingles). About 7 - 9% of patients with lymphomas, and between 1 - 3% of patients with other cancers, have herpes zoster. Chemotherapy itself increases the risk for herpes zoster.

Immunosuppressant Drugs. Patients who take certain drugs that suppress the immune system are at risk for shingles (as well as other infections). They include:

  • Azathioprine (Imuran)
  • Chlorambucil (Leukeran)
  • Cyclophosphamide (Cytoxan)
  • Cyclosporine (Sandimmune, Neoral)
  • Cladribine (Leustatin)

These drugs are used for patients who have undergone organ transplantation and are also used for severe autoimmune diseases caused by the inflammatory process. Such disorders include rheumatoid arthritis, systemic lupus erythematosus, diabetes, multiple sclerosis, Crohn's disease, and ulcerative colitis.

Lack of Exposure to Children Infected with Chickenpox. Interestingly, one study suggested that previously infected adults who are exposed to children with chickenpox may receive an extra boost in antibody production, which can actually help them fight off herpes zoster. This means that as more children are vaccinated against chickenpox, more adults may be at risk for herpes zoster.

Risk Factors for Shingles in Children. Although most common in adults, shingles occasionally develops in children. One study reported that only 5% of cases occur in those under age 15. Children with immune deficiencies are at highest risk. Children with no immune problems but who had chickenpox before they were 1 year old also have a higher risk for shingles.

Deterrence/Prevention

  • Theoretically, current varicella vaccines will reduce zoster incidence.
  • Vaccines are being tested for prevention of herpes zoster in individuals previously infected with wild varicella-zoster virus.
  • Patients with zoster may transmit the virus, causing infections in susceptible persons (who have not had prior infection).
    • Discharge instructions should include patient education to avoid contact with susceptible individuals, especially if they are pregnant (due to concerns about congenital varicella) or immunocompromised.
    • Transmission is by direct contact, and lesions are considered infectious until they are all crusted over.

Complications

Complications of herpes zoster may include the following:

Prognosis

  • Rash usually resolves within 14-21 days.
  • Postherpetic neuralgia is defined as pain persisting at least 1 month after the rash has healed. Its incidence increases dramatically with age (ie, 4% in those aged 30-50 years, 50% in those older than 80 years).

Shingles ( Herpes Zoster ) Stages

There are two stages of shingles:

1.The prodromal stage - at this stage symptoms occur about 2 to 5 days before the rash appears.

2.The eruptive stage - at this stage of shingles skin rash (lesions) appears.

How is impetigo diagnosed?

Diagnosing impetigo is mostly straightforward, though occasionally other conditions may look something like it, such as tinea (fungus, "ringworm") or scabies (mites). It is important to note that not every blister or ooze means infection. At times, other infected and noninfected skin diseases produce blister-like skin inflammation. Such conditions include herpes cold sores, chickenpox, poison ivy, other skin allergies, eczema, and insect bites. Secondary infection of these diseases does occur sometimes, but often blistering comes from the original condition and does not mean that actual impetigo has developed. Medical judgment -- helped by culture tests, when necessary -- is needed to decide whether antibacterial creams or pills should be used in addition to the remedies suitable for the original condition.

Diagnosis of Herpes Simplex

The herpes simplex virus is usually identifiable by its characteristic lesion: A thin-walled blister on an inflamed base of skin. However, other conditions can resemble herpes, and doctors cannot base a herpes diagnosis on visual inspection alone. In addition, some patients who carry the virus may not have visible genital lesions. Laboratory tests are essential for confirming herpes diagnosis. These tests include virologic tests (which examine samples of skin taken from the lesion) and serologic tests (blood tests that detect antibodies).

In its 2006 guidelines for sexually transmitted diseases, the U.S. Centers for Disease Control (CDC) recommends that both virologic and serologic tests be used for diagnosing genital herpes. Patients diagnosed with genital herpes should also be tested for other sexually transmitted diseases.

According to the CDC, up to 50% of first-episode cases of genital herpes are now caused by herpes simplex virus 1 (HSV-1). However, recurrences of genital herpes, and viral shedding without overt symptoms, are much less frequent with HSV-1 infection than herpes simplex virus 2 (HSV-2). It is important for doctors to determine whether the genital herpes infection is caused by HSV-1 or HSV-2, as the type of herpes infection influences prognosis and treatment recommendations.

How is Contact Dermatitis Diagnosed?

The diagnosis of contact dermatitis should be considered when a person has any acute or chronic rash that typically itches, but may also sting or burn. The rash classically has small blisters containing clear fluid, but can swell, crust, ooze or peel in other cases.

The diagnosis is made with a patch test, which involves the placement of various chemicals on the back for approximately 48 hours (it is not the same as allergy testing). This typically is done with a paper tape system, such as the TRUE test. The TRUE test is the only FDA approved test for contact dermatitis in the United States, although some allergists and dermatologists will develop more extensive patch test panels with chemicals purchased from Canada or Europe.

The results of the test are interpreted at 48 hours after placement, and again at 72 or 96 hours after placement. A positive test is confirmed when there are blisters, redness, and mild swelling at the site of the particular chemical in question. The site of the positive test usually itches, although the reaction size is typically limited to the site of contact, and therefore is usually smaller than a dime.

Senin, Mei 18, 2009

Katarak

Cataract

A cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in degree from slight to complete opacity and obstructing the passage of light. Early in the development of age-related cataract the power of the lens may be increased, causing near-sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially blinding if untreated. The condition usually affects both the eyes, but almost always one eye is affected earlier than the other.

A senile cataract, occurring in the aged, is characterized by an initial opacity in the lens, subsequent swelling of the lens and final shrinkage with complete loss of transparency.[2] Moreover, with time the cataract cortex liquefies to form a milky white fluid in a Morgagnian cataract, which can cause severe inflammation if the lens capsule ruptures and leaks. Untreated, the cataract can cause phacomorphic glaucoma. Very advanced cataracts with weak zonules are liable to dislocation anteriorly or posteriorly. Such spontaneous posterior dislocations (akin to the historical surgical procedure of couching) in ancient times were regarded as a blessing from the heavens, because some perception of light was restored in the cataractous patients.

Cataract derives from the Latin cataracta meaning "waterfall" and the Greek kataraktes and katarrhaktes, from katarassein meaning "to dash down" (kata-, "down"; arassein, "to strike, dash"). As rapidly running water turns white, the term may later have been used metaphorically to describe the similar appearance of mature ocular opacities. In Latin, cataracta had the alternate meaning "portcullis",[4] so it is also possible that the name came about through the sense of "obstruction". Early Persian physicians called the term nazul-i-ah, or "descent of the water"—vulgarised into waterfall disease or cataract—believing such blindness to be caused by an outpouring of corrupt humour into the eye. In dialect English a cataract is called a pearl, as in "pearl eye" and "pearl-eyed".

Causes

Cataracts develop from a variety of reasons, including long-term exposure to ultraviolet light, exposure to radiation, secondary effects of diseases such as diabetes, hypertension and advanced age, or trauma (possibly much earlier); they are usually a result of denaturation of lens protein. Genetic factors are often a cause of congenital cataracts and positive family history may also play a role in predisposing someone to cataracts at an earlier age, a phenomenon of "anticipation" in pre-senile cataracts. Cataracts may also be produced by eye injury or physical trauma. A study among Icelandair pilots showed commercial airline pilots are three times more likely to develop cataracts than people with non-flying jobs. This is thought to be caused by excessive exposure to radiation coming from outer space.[7] Cataracts are also unusually common in persons exposed to infrared radiation, such as glassblowers who suffer from "exfoliation syndrome". Exposure to microwave radiation can cause cataracts. Atopic or allergic conditions are also known to quicken the progression of cataracts, especially in children.

Cataracts may be partial or complete, stationary or progressive, hard or soft.

Some drugs can induce cataract development, such as corticosteroids[9] and Ezetimibe and Seroquel.

There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also classified by their location, e.g. posterior (classically due to steroid use) and anterior (common (senile) cataract related to aging).

Symptoms

As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted. Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare can be a problem as light is scattered by the cataract into the eye. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is demonstrated an eye specialist consultation is recommended.

In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon appears to be confined to one eye only.

Epidemiology

Age-related cataract is responsible for 48% of world blindness, which represents about 18 million people, according to the World Health Organization (WHO). In many countries surgical services are inadequate, and cataracts remain the leading cause of blindness. As populations age, the number of people with cataracts is growing. Cataracts are also an important cause of low vision in both developed and developing countries. Even where surgical services are available, low vision associated with cataracts may still be prevalent, as a result of long waits for operations and barriers to surgical uptake, such as cost, lack of information and transportation problems.

In the United States, age-related lenticular changes have been reported in 42% of those between the ages of 52 to 64, 60% of those between the ages 65 and 74, and 91% of those between the ages of 75 and 85.

Historical

The earliest records are from the Bible as well as early Hindu records. Early cataract surgery was developed by the Indian surgeon, Sushruta (6th century BCE). The Indian tradition of cataract surgery was performed with a special tool called the Jabamukhi Salaka, a curved needle used to loosen the lens and push the cataract out of the field of vision. The eye would later be soaked with warm butter and then bandaged. Though this method was successful, Sushruta cautioned that it should only be used when necessary. Greek physicians and philosophers traveled to India where these surgeries were performed by physicians. The removal of cataract by surgery was also introduced into China from India.

The first references to cataract and its treatment in Ancient Rome are found in 29 AD in De Medicinae, the work of the Latin encyclopedist Aulus Cornelius Celsus. The Romans were pioneers in the health arena—particularly in the area of eye care.

The Iraqi ophthalmologist Ammar ibn Ali of Mosul performed the first extraction of cataracts through suction. He invented a hollow metallic syringe hypodermic needle, which he applied through the sclerotic and extracted the cataracts using suction. In his Choice of Eye Diseases, written in circa 1000, he wrote of his invention of the hypodermic needle and how he discovered the technique of cataract extraction while experimenting with it on a patient.

Prevention

Although cataracts have no scientifically proven prevention, it is sometimes said that wearing ultraviolet-protecting sunglasses may slow the development of cataracts. Regular intake of antioxidants (such as vitamin A, C and E) is theoretically helpful, but taking them as a supplement has been shown to have no benefit.

Recent research

Although statins are known for their ability to lower lipids, they are also believed to have antioxidant qualities. It is believed that oxidative stress plays a role in the development of nuclear cataracts, which are the most common type of age-related cataract. To explore the relationship between nuclear cataracts and statin use, a group of researchers took a group of 1299 patients who were at risk of developing nuclear cataracts and gave some of them statins. Their results suggest that statin use in an at-risk population may be associated with a lower risk of developing nuclear cataract disease.

Research is scant and mixed but weakly positive for the nutrients lutein and zeaxanthin. Bilberry extract shows promise in rat models and in clinical studies.

In the past few years, eye drops containing acetyl-carnosine have been used by several thousands cataract patients across the world. The drops are believed to work by reducing oxidation and glycation damage in the lens, particularly reducing cristallin cross-linking, The use of these drops remains controversial due to lack of large properly designed trials.

Types of cataracts

Bilateral cataracts in an infant due to Congenital rubella syndrome

The following is a classification of the various types of cataracts. This is not comprehensive and other unusual types may be noted.

  • Classified by etiology

· Age-related cataract

· Immature senile cataract (IMSC): partially opaque lens, disc view hazy

· Mature senile cataract (MSC): Completely opaque lens, no disc view

· Hypermature senile cataract (HMSC): Liquefied cortical matter: Morgagnian cataract

· Congenital cataract

· Sutural cataract

· Lamellar cataract

· Zonular cataract

· Total cataract

· Secondary cataract

Slit lamp photo of anterior capsular opacification visible a few months after implantation of Intraocular lens in eye, magnified view

· Drug-induced cataract (e.g. corticosteroids)

· Traumatic cataract

· Blunt trauma (capsule usually intact)

· Penetrating trauma (capsular rupture & leakage of lens material—calls for an emergency surgery for extraction of lens and leaked material to minimize further damage)

  • Classified by location of opacity within lens structure (However, mixed morphology is quite commonly seen, e.g. PSC with nuclear changes & cortical spokes of cataract)

· Anterior cortical cataract

· Anterior polar cataract

· Anterior subcapsular cataract

Slit lamp photo of posterior capsular opacification visible a few months after implantation of Intraocular lens in eye, seen on retroillumination

· Nuclear cataract—Grading correlates with hardness & difficulty of surgical removal

· 1: Grey

· 2: Yellow

· 3: Amber

· 4: Brown/Black (Note: "black cataract" translated in some languages (like Hindi) refers to glaucoma, not the color of the lens nucleus)

· Posterior cortical cataract

· Posterior polar cataract (importance lies in higher risk of complication—posterior capsular tears during surgery)

· Posterior subcapsular cataract (PSC) (clinically common)

· After-cataract: posterior capsular opacification (PCO) subsequent to a successful extracapsular cataract surgery (usually within three months to two years) with or without IOL implantation. Requires a quick & painless office procedure with Nd:YAG laser capsulotomy to restore optical clarity.

KATARAK

Katarak merupakan penyakit mata yang dicirikan dengan adanya kabut pada lensa mata. Lensa mata normal transparan dan mengandung banyak air, sehingga cahaya dapat menembusnya dengan mudah. Walaupun sel-sel baru pada lensa akan selalu terbentuk, banyak faktor yang dapat menyebabkan daerah di dalam lensa menjadi buram, keras, dan pejal. Lensa yang tidak bening tersebut tidak akan bisa meneruskan cahaya ke retina untuk diproses dan dikirim melalui saraf optik ke otak.

Penyakit katarak banyak terjadi di negara-negara tropis seperti Indonesia. Hal ini berkaitan dengan faktor penyebab katarak, yakni sinar ultraviolet yang berasal dari sinar matahari. Penyebab lainnya adalah kekurangan gizi yang dapat mempercepat proses berkembangnya penyakit katarak.

Apakah Penyebab Katarak ?

Sebagian besar katarak terjadi karena proses degeneratif atau bertambahnya usia seseorang. Katarak kebanyakan muncul pada usia lanjut. Data statistik menunjukkan bahwa lebih dari 90% orang berusia di atas 65 tahun menderita katarak. Sekitar 550% orang berusia 75— 85 tahun daya penglihatannya berkurang akibat katarak. Walaupun sebenarnya dapat diobati, katarak merupakan penyebab utama kebutaan di dunia.

Sayangnya, Seorang penderita katarak mungkin tidak menyadari telah mengalami gangguan katarak. Katarak terjadi secara perlahan-perlahan sehingga penglihatan penderita terganggu secara berangsur. karena umumnya katarak tumbuh sangat lambat dan tidak mempengaruhi daya penglihatan sejak awal. Daya penglihatan baru terpengaruh setelah katarak berkembang sekitar 3—5 tahun. Karena itu, pasien katarak biasanya menyadari penyakitnya setelah memasuki stadium kritis.

Pada awal serangan, penderita katarak merasa gatal-gatal pada mata, air matanya mudah keluar, pada malam hari penglihatan terganggu, dan tidak bisa menahan silau sinar matahari atau sinar lampu. Selanjutnya penderita akan melihat selaput seperti awan di depan penglihatannya. Awan yang menutupi lensa mata tersebut akhirnya semakin merapat dan menutup seluruh bagian mata. Bila sudah sampai tahap ini, penderita akan kehilangan peng­lihatannya.

Secara umum terdapat 4 jenis katarak seperti berikut.

1. Congenital, merupakan katarak yang terjadi sejak bayi lahir dan berkembang pada tahun pertama dalam hidupnya. Jenis katarak ini sangat jarang terjadi.

2. Traumatik, merupakan katarak yang terjadi karena kecelakaan pada mata.

3. Sekunder, katarak yang disebabkan oleh konsumsi obat seperti prednisone dan kortikosteroid, serta penderita diabetes. Katarak diderita 10 kali lebih umum oleh penderita diabetes daripada oleh populasi secara umum.

4. Katarak yang berkaitan dengan usia, merupakan jenis katarak yang paling umum. Berdasarkan lokasinya, terdapat 3 jenis katarak ini, yakni nuclear sclerosis, cortical, dan posterior subcapsular. Nuclear sclerosis merupakan perubahan lensa secara perlahan sehingga menjadi keras dan berwarna kekuningan. Pandangan jauh lebih dipengaruhi daripada pandangan dekat (pandangan baca), bahkan pandangan baca dapat menjadi lebih baik. Penderita juga mengalami kesulitan membedakan warna, terutama warna birru. Katarak jenis cortical terjadi bila serat-serat lensa menjadi keruh, dapat menyebabkan silau terutama bila menyetir pada malam hari. Posterior subcapsular merupakan terjadinya kekeruhan di sisi belakang lensa. Katarak ini menyebabkan silau, pandangan kabur pada kondisi cahaya terang, serta pandangan baca menurun.

Gejala umum gangguan katarak meliputi :

· Penglihatan tidak jelas, seperti terdapat kabut menghalangi objek.

· Peka terhadap sinar atau cahaya.

· Dapat melihat dobel pada satu mata.

· Memerlukan pencahayaan yang terang untuk dapat membaca.

· Lensa mata berubah menjadi buram seperti kaca susu.

katarak dapat pula terjadi pada bayi karena sang ibu terinfeksi virus pada saat hamil muda. Penyebab katarak lainnya meliputi :

· Faktor keturunan.

· Cacat bawaan sejak lahir.

· Masalah kesehatan, misalnya diabetes.

· Penggunaan obat tertentu, khususnya steroid.

· Mata tanpa pelindung terkena sinar matahari dalam waktu yang cukup lama.

· Operasi mata sebelumnya.

· Trauma (kecelakaan) pada mata.

· Faktor-faktor lainya yang belum diketahui.

Klasifikasi Katarak

Katarak dapat diklasifikasikan menjadi :
- katarak Kongenital: Katarak yang sudah terlihat pada usia di bawah 1 tahun
- Katarak Juvenil : katarak yang terjadi sesudah usia 1 tahun
- Katarak Senil: katarak setelah usia 50 tahun
- Katarak Trauma: Katarak yang terjadi akibat trauma pada lensa mata

Etiologi Katarak

Sebagian besar katarak terjadi karena proses degeneratif atau bertambahnya usia seseorang. Usia rata-rata terjadinya katarak adalah pada umur 60 tahun keatas. Akan tetapi, katarak dapat pula terjadi pada bayi karena sang ibu terinfeksi virus pada saat hamil muda.
Penyebab katarak lainnya meliputi :

  1. Faktor keturunan.
  2. Cacat bawaan sejak lahir.
  3. Masalah kesehatan, misalnya diabetes.
  4. Penggunaan obat tertentu, khususnya steroid.
  5. gangguan metabolisme seperti DM (Diabetus Melitus)
  6. gangguan pertumbuhan,
  7. Mata tanpa pelindung terkena sinar matahari dalam waktu yang cukup lama.
  8. Rokok dan Alkohol
  9. Operasi mata sebelumnya.
  10. Trauma (kecelakaan) pada mata.
  11. Faktor-faktor lainya yang belum diketahui.


Patofisiologi Katarak

Lensa mata mengandung tiga komponen anatomis an: nukleus korteks & kapsul.nukleus mengalami perubahan warna coklat kekuningan seiring dengan bertambahnya usia.disekitar opasitas terdapat densitas seperti duri dianterior & posterior nukleus. Opasitas pada kapsul posterior merupakan bentuk katarak yang paling bermakna.perubahan fisik & kimia dalam lensa mengakibatkan hilangnya transparansi.salah satu teori menyebutkan terputusnya protein lensa normal terjadi disertai infulks air kedalam lensa proses ini mematahkan serabut lensa yang tegang & mengganggu transmisi sinar.teori lain mengatakan bahwa suatu enzim mempunyai peranan dalam melindungi lensa dari degenerasi.jumlah enzim akan menurun dg bertambahnya usia dan tidak ada pada kebanyakan pasien menderita katarak.


Manifestasi Klinik Katarak

Biasanya gejala berupa keluhan penurunan tajam pengelihatan secara progresif (seperti rabun jauh memburuk secara progresif). Pengelihatan seakan-akan melihat asap dan pupil mata seakan akan bertambah putih. Pada akhirnya apabila katarak telah matang pupil akan tampak benar-benar putih ,sehingga refleks cahaya pada mata menja di negatif (-). Bila Katarak dibiarkan maka akan mengganggu penglihatan dan akan dapat menimbulkan komplikasi berupa Glaukoma dan Uveitis.


Gejala umum gangguan katarak meliputi :

  1. Penglihatan tidak jelas, seperti terdapat kabut menghalangi objek.
  2. Peka terhadap sinar atau cahaya.
  3. Dapat melihat dobel pada satu mata.
  4. Memerlukan pencahayaan yang terang untuk dapat membaca.
  5. Lensa mata berubah menjadi buram seperti kaca susu.


Pemeriksaan Diagnostik Katarak

  1. Keratometri.
  2. Pemeriksaan lampu slit.
  3. Oftalmoskopis.
  4. A-scan ultrasound (echography).
  5. Penghitungan sel endotel penting u/ fakoemulsifikasi & implantasi.

Pengobatan Katarak

Satu-satunya adalah dengan cara pembedahan ,yaitu lensa yang telah keruh diangkat dan sekaligus ditanam lensa intraokuler sehingga pasca operasi tidak perlu lagi memakai kaca mata khusus (kaca mata aphakia). Setelah operasi harus dijaga jangan sampai terjadi infeksi.
Pembedahan dilakukan bila tajam penglihatan sudah menurun sedemikian rupa sehingga mengganggu pekerjaan sehari-hari atau bila telah menimbulkan penyulit seperi glaukoma dan uveitis.


Tekhnik yang umum dilakukan adalah ekstraksi katarak ekstrakapsular, dimana isi lensa dikeluarkan melalui pemecahan atau perobekan kapsul lensa anterior sehingga korteks dan nukleus lensa dapat dikeluarkan melalui robekan tersebut. Namun dengan tekhnik ini dapat timbul penyulit katarak sekunder. Dengan tekhnik ekstraksi katarak intrakapsuler tidak terjadi katarak sekunder karena seluruh lensa bersama kapsul dikeluarkan, dapat dilakukan pada yang matur dan zonula zinn telah rapuh, namun tidak boleh dilakukan pada pasien berusia kurang dari 40 tahun, katarak imatur, yang masih memiliki zonula zinn. Dapat pula dilakukan tekhnik ekstrakapsuler dengan fakoemulsifikasi yaitu fragmentasi nukleus lensa dengan gelombang ultrasonik, sehingga hanya diperlukan insisi kecil, dimana komplikasi pasca operasi lebih sedikit dan rehabilitasi penglihatan pasien meningkat.

Komplikasi Katarak

  • Penyulit yg terjadi berupa : visus tdk akan mencapai 5/5 à ambliopia sensori
  • Komplikasi yang terjadi : nistagmus dan strabismus


Pencegahan Katarak
Disarankan agar banyak mengkonsumsi buah-buahan yang banyak mengandung vit.C ,vit.A dan vit E

II. ANATOMI DAN FISIOLOGI LENSA

A. Anatomi Lensa

Lensa adalah suatu struktur bikonveks, avaskular tak berwarna dan transparan. Tebal sekitar 4 mm dan diameternya 9 mm. Dibelakang iris lensa digantung oleh zonula ( zonula Zinnii) yang menghubungkannya dengan korpus siliare. Di sebelah anterior lensa terdapat humor aquaeus dan disebelah posterior terdapat viterus.
Kapsul lensa adalah suatu membran semipermeabel yang dapat dilewati air dan elektrolit. Disebelah depan terdapat selapis epitel subkapsular. Nukleus lensa lebih keras daripada korteksnya. Sesuai dengan bertambahnya usia, serat-serat lamelar subepitel terus diproduksi, sehingga lensa lama-kelamaan menjadi kurang elastik. Lensa terdiri dari enam puluh lima persen air, 35% protein, dan sedikit sekali mineral yang biasa ada di jaringan tubuh lainnya. Kandungan kalium lebih tinggi di lensa daripada di kebanyakan jaringan lain. Asam askorbat dan glutation terdapat dalam bentuk teroksidasi maupun tereduksi. Tidak ada serat nyeri, pembuluh darah atau pun saraf di lensa.


B. Fisiologi Lensa

Fungsi utama lensa adalah memfokuskan berkas cahaya ke retina. Untuk memfokuskan cahaya yang datang dari jauh, otot-otot siliaris relaksasi, menegangkan serat zonula dan memperkecil diameter anteroposterior lensa sampai ukurannya yang terkecil, daya refraksi lensa diperkecil sehingga berkas cahaya paralel atau terfokus ke retina. Untuk memfokuskan cahaya dari benda dekat, otot siliaris berkontraksi sehingga tegangan zonula berkurang. Kapsul lensa yang elastik kemudian mempengaruhi lensa menjadi lebih sferis diiringi oleh peningkatan daya biasnya. Kerjasama fisiologik tersebut antara korpus siliaris, zonula, dan lensa untuk memfokuskan benda dekat ke retina dikenal sebagai akomodasi. Seiring dengan pertambahan usia, kemampuan refraksi lensa perlahan-lahan berkurang. Selain itu juga terdapat fungsi refraksi, yang mana sebagai bagian optik bola mata untuk memfokuskan sinar ke bintik kuning, lensa menyumbang +18.0- Dioptri.

C. Metabolisme Lensa Normal

Transparansi lensa dipertahankan oleh keseimbangan air dan kation (sodium dan kalium). Kedua kation berasal dari humour aqueous dan vitreous. Kadar kalium di bagian anterior lensa lebih tinggi di bandingkan posterior. Dan kadar natrium di bagian posterior lebih besar. Ion K bergerak ke bagian posterior dan keluar ke aqueous humour, dari luar Ion Na masuk secara difusi dan bergerak ke bagian anterior untuk menggantikan ion K dan keluar melalui pompa aktif Na-K ATPase, sedangkan kadar kalsium tetap dipertahankan di dalam oleh Ca-ATPase. Metabolisme lensa melalui glikolsis anaerob (95%) dan HMP-shunt (5%). Jalur HMP shunt menghasilkan NADPH untuk biosintesis asam lemak dan ribose, juga untuk aktivitas glutation reduktase dan aldose reduktase. Aldose reduktse adalah enzim yang merubah glukosa menjadi sorbitol, dan sorbitol dirubah menjadi fructose oleh enzim sorbitol dehidrogenase. Gangguan lensa adalah kekeruhan, distorsi, dislokasi, dan anomali geometrik. Pasien yang mengalami gangguan-gangguan tersebut akan menderita kekaburan penglihatan tanpa nyeri.

References:

www.yahoo.com

www.wikipedia.com

http://kinton.multiply.com/reviews/item/5

http://info.g-excess.com/id/info/PengertiandanDefinisiKatarak.info