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Problem Based Learning

(PBL) HAND BOOK


5th Semester

FOR TUTOR - CONFIDENTIAL

MKK MATA
Contributors,
dr. ANNY SULISTIYOWATI , Sp.M(K)
dr. AULIA ABDUL HAMID, M.Biomed.Sc., SpM
dr. DEBBY SHINTIYA DEWI, SpM(K)
dr. ELFINA G. SADONO, Sp.M(K)
dr. HARIWATI MOEHARIADI, Sp.M(K)
dr. HERA DWI NOVITA, Sp.M
dr. HERWINDO DICKY PUTRANTO, Sp.M
dr. LELY RETNO WULANDARI , Sp.M(K)
dr. M. MA’SUM EFFENDI, Sp.M(K)
dr. NADIA ARTHA DEWI , SpM(K)
dr. NANDA WAHYU ANANDITA, Sp.M(K)
dr. NINA HANDAYANI, Sp.M
dr. OVI SOFIA , Sp.M
dr. RETNANIADI SUPRIADI, Sp.M
dr. ROSY ALDINA, Sp.M(K)
dr. SAFARUDDIN REFA, Sp.M-KVR
dr. SESKOATI PRAYITNANINGSIH, Sp.M(K)
dr. TRIANA BUDI SULISTYA, SpM(K)
MEDICAL EDUCATION UNIT

Editor,
dr. YHUSI KARINA R., MSc.

Medical Faculty
Universitas Brawijaya
2016
PBL Semester V Tutor Hand Book
Academic Year 2016/2017

Belajar Sepanjang Hayat dengan Belajar Berbasis Masalah 7 Langkah


(Problem Based Learning 7 Jumps)
Oleh: MEU FKUB

Metode belajar berbasis masalah dengan 7 langkah (PBL 7 jumps) merupakan salah
satu metode belajar yang sering digunakan di dunia pendidikan kedokteran. Metode ini
pertama kali dikenalkan oleh Barrow (1980) sebagai bentuk pembelajaran yang diyakini
dapat menstimulus kemampuan penalaran klinis calon dokter. Barrow dan Tamblyn (1980),
yang dianggap sebagai Bapak-bapak PBL, mengatakan bahwa selama berpuluh-puluh tahun
pembelajaran di kedokteran terlalu menekankan pada hafalan yang seringkali tidak dapat
dimanfaatkan secara langsung untuk menyelesaikan masalah kedokteran riil. Mereka
berpikir alangkah baiknya bila pembelajaran mendekatkan masalah riil dengan ilmu yang
akan digunakan sehingga pada saat menjumpai masalah, ilmu, konsep dan teori dapat lebih
optimal digunakan. Oleh karena itu metode yang dikenalkan oleh Barrow dan Tamblyn ini
dilakukan dengan memberikan kepada mahasiswa masalah pasien untuk dipelajari dan
diselesaikan daripada menjejali dengan materi kuliah berjam-jam. Pendekatan belajar ini
dengan demikian memiliki dua tujuan utama, yaitu: 1) mengasah kemampuan pemecahan
masalah (problem solving) sekaligus 2) mendapatkan pengetahuan yang terintegrasi yang
relevan dengan masalah yang dihadapi. Dalam perkembangannya metode belajar PBL ini
ternyata juga berkontribusi positif pada peningkatan penguasaan pengetahuan,
kemampuan komunikasi kolaboratif serta aplikasi kedokteran berbasis bukti (evidence
based medicine).

Dalam dasawarsa terakhir, PBL telah menjadi salah satu trend setter pembelajaran
di fakultas kedokteran di dunia. Oleh karenanya, Standar Pendidikan Profesi Dokter
Indonesia menjadikan PBL sebagai pendekatan standar untuk Kurikulum Berbasis
Kompetensi di Pendidikan Dokter Indonesia. Metode pembelajaran PBL biasanya didisain
sebagai suatu pembelajaran dalam kelompok yang terdiri dari 10-15 mahasiswa yang sering
disebut kelompok diskusi kecil yang difasilitasi oleh seorang dosen yang disebut dengan
Tutor. Tutor dalam PBL bukanlah seorang pakar/narasumber dalam diskusi namun sebagai
penstimulus dinamika kelompok serta memonitor jalannya diskusi dalam mencapai sasaran
belajar yang telah ditetapkan. Diskusi PBL dimulai dengan paparan masalah yang biasanya
berupa deskripsi dari suatu fenomena yang membutuhkan penjelasan. Masalah ini sering
disebut dengan skenario pemicu. Kelompok diskusi kecil, tutor dan skenario pemicu
merupakan tiga unsur utama dalam pembelajaran PBL.

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Gambar 1 Tiga Unsur Utama dalam Pembelajaran PBL

Langkah-langkah dalam PBL 7 Jumps

PBL 7 jumps, seperti namanya terdiri dari 7 langkah sebagai berikut:

1. Reading the Case and Clarifing unclear terms or concepts


2. Define the problem
3. Analyze the problem using prior knowledge
4. Order Ideas and systematically analyze them in depth
5. Formulate learning objective
6. Seek additional information (individual learning)
7. Synthesize and test the new information by sharing

Pembelajaran PBL 7 jumps biasanya dibagi dalam dua sesi pembelajaran yang dilakukan
dalam hari yang berbeda. Langkah 1 s/d 5 dilakukan pada sesi pertama, dan langkah 7
dilakukan pada sesi kedua, sementara langkah 6 dilakukan diantara dua sesi sebagai bentuk
tugas individu. Dalam KBK Pendidikan Dokter, sesi I biasanya dilakukan pada hari Senin,
sementara untuk sesi II dilakukan pada hari Rabu atau Kamis. Sementara belajar individu
dilakukan dengan cara menggali informasi dari kuliah-kuliah terjadwal, wawancara
narasumber, praktikum, maupun mencari informasi dari literatur di internet maupun text
book di perpustakaan dilakukan diantara sesi I dan Sesi II. Pada sesi II setiap individu
melaporkan hasil belajarnya dalam kelompok diskusi untuk kemudian disusun menjadi hasil
diskusi kelompok dalam bentuk Laporan Diskusi PBL.

Langkah 1 : Membaca skenario pemicu (trigger scenario)

Hal pertama yang perlu dilakukan dalam menghadapi masalah adalah membuat segala yang
tidak jelas, terutama terhadap penggunaan istilah dalam masalah. Dengan melakukan hal ini
diharapkan setiap peserta diskusi memiliki pandangan yang sama tentang skenario yang
dihadapi serta ruang lingkupnya.

Setidaknya ada tiga aktivitas yang dilakukan langkah pertama ini, yaitu;

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1. Memastikan bahwa setiap peserta diskusi memiliki pemahaman yang sama


terhadap istilah (cue and clue) yang ada dalam skenario
2. Memastikan bahwa setiap peserta diskusi memiliki gambaran ruang lingkup yang
sama dari kasus yang akan didiskusikan
3. Memastikan bahwa setiap peserta diskusi menyepakati hal-hal apa yang diluar
ruang lingkup diskusi

Langkah 2: Define the problem (menentukan masalah)

Pada tahap ini, peserta diskusi harus memiliki kesepakatan terhadap masalah atau
fenomena yang membutuhkan penjelasan dan hubungan-hubungan teoritik yang ada
diantara masalah. Kadang masalah sudah jelas sejak awal sehingga kelompok dapat
langsung menuju langkah 3. Namun demikian pada beberapa kasus, hubungan variable
penting dalam kasus tidak selalu jelas dan membutuhkan penjelasan. Dalam langkah ini,
kelompok mengidentifikasi hal-hal yang kemungkinan menjadi masalah dalam kasus dari
cue and clue yang ada.

Langkah 3: Analyze the problem (menganalisa masalah, dengan brainstorming)

Langkah ini merupakan langkah untuk menggunakan pengetahuan yang telah didapatkan
sebelumnya untuk menjelaskan daftar masalah yang telah disepakati pada langkah kedua.
Masing-masing peserta tim diharapkan dapat berkontribusi menyumbangkan ide
konstruktifnya dalam menjelaskan masalah yang ditemukan berdasarkan pengetahuan
terbaik yang telah dimiliki.

Langkah 4: Order Ideas and systematically analyze them in depth

Pada tahap ini, peserta diskusi diharapkan telah memiliki kerangka konsep yang lebih jelas
dari masalah-masalah yang telah dijelaskan, termasuk hubungan antara pertanyaan dan
variabel baru yang muncul saat brainstorming. Pada tahap ini pemimpin diskusi diharapkan
mampu membuat anggota kelompok menyepakati urutan prioritas masalah yang akan
menjadi tujuan belajar.

Langkah 5 State Learning Objective (Menentukan Tujuan Belajar)

Langkah ini merupakan konklusi sementara dari langkah 4, dimana semua peserta diskusi
bersepakat terhadap masalah yang dapat dipahami (dapat dijelaskan secara logis dan
meyakinkan) serta masalah mana yang menjadi kebutuhan bersama untuk dipelajari baik
dari kuliah, baca literatur, diskusi dengan pakar serta aktivitas akademik lain yang mungkin
dilakukan pada langkah 6. Pada langkah ini anggota kelompok menyepakati rencana aksi
(action plan) dengan distribusi tugas masing-masing anggota.

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Langkah 6 Seek additional information (individual learning)

Masing-masing peserta diskusi mencari informasi terkait dengan teori, konsep, atau
penjelasan akademik yang relevan dengan daftar tujuan belajar yang telah ditetapkan pada
langkah 6.

Langkah 7 : Synthesize and test the new information by sharing

Anggota kelompok bertemu kembali untuk mendiskusikan informasi yang didapat masing-
masing sebagai tahap akhir dari PBL. Pada tahap ini peserta diskusi menyepakati bentuk
laporan bersama

Pembagian Peran dalam Diskusi PBL

Dalam pelaksanaan belajar kelompok kecil dalam PBL, mahasiswa membagi diri kedalam
peran-peran tertentu untuk melancarkan jalannya diskusi. Diantara peran yang dijalankan
antara lain:

A. Chair/leader (pemimpin diskusi)

Seperti namanya, tugas pemimpin diskusi adalah menjamin agar diskusi berjalan lancar
sesuai dengan tahap-tahapnya. Pemimpin bertanggung jawab mendistribusikan
kesempatan setiap anggota diskusi untuk berpendapat, menjaga dinamika diskusi dan
melakukan monitor terhadap waktu serta hasil diskusi. Tugas pemimpin diskusi juga
memastikan scribe dapat mengimbangi jalannya/dinamika diskusi serta melakukan
perekaman pendapat yang muncul dalam diskusi secara akurat. Pemimpin juga memiliki
tanggung jawab dalam memastikan pembagian tugas belajar kelompok.

B. Scribe (Sekretaris kelompok)

Tugas dari Scribe adalah mencatat jalannya diskusi, termasuk merekam sumber-sumber
belajar yang dikemukakan atau digunakan di dalam diskusi. Scribe mengumpulkan
catatan atau ide dari semua anggota dan menyarikannya sebagai hasil diskusi kelompok.

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C. Anggota Diskusi

Peran anggota diskusi adalah mengikuti langkah-langkah diskusi sesuai tahapannya dan
secara aktif berpartisipasi dalam diskusi. Kelancaran diskusi ditentukan oleh
keterbukaan masing-masing anggota kelompok untuk saling mendengar dan
menerima/berbagi informasi yang dimiliki serta saling menghargai pendapat yang
dikemukaan di dalam diskusi.

Peran Tutor dalam PBL


Secara umum, peran tutor dalam PBL adalah untuk memfasilitasi, menciptakan
pembelajaran aktif, serta mendorong seluruh anggota kelompok untuk berkolaborasi
mengembangkan ide-ide dan konsep yang relevan dengan masalah yang disajikan. Para
tutor harus dilatih, mereka tidak menyajikan informasi maupun memberikan jawaban.
Dalam grup yang baik, para siswa lah yang aktif mengidentifikasi masalah, berbagi informasi,
dan mencari kejelasan dari kesulitan yang mereka hadapi. Para tutor diharapkan dapat
menyesuaikan pendekatan pembelajaran mereka dengan tingkat pengetahuan siswa,
kualitas interaksi dalam grup PBL, dan konten dari permasalahan yang disajikan (Sefron &
Frommer, 2013).
Dalam PBL, tutor memiliki beberapa peran yang spesifik, yaitu :
1. The tutor as diagnostician
Tutor harus mampu menentukan dan mendiagnosis sejauh mana pengetahuan dan
keterampilan (prior knowledge) para siswa dalam konteks masalah yang disajikan.
Dengan mengetahui prior knowledge mereka, tutor akan dapat melihat secara
langsung bagaimana para siswa belajar, dan selanjutnya akan mempermudah tutor
dalam menfasilitasi proses belajar. Pada tahap ke tujuh (information sharing), tutor
juga diharapkan mengobservasi sampai sejauh mana para siswa mampu menguasai
materi, dan apakah mereka mampu mengaplikasikan pengetahuan mereka ke
dalam masalah yang disajikan.
2. The tutor as challenger
Siswa, baik secara individu maupun kelompok, tidak selalu dalam kondisi terdorong
untuk memaksa diri mereka sendiri untuk terlibat dalam proses belajar dan berpikir,
baik di dalam maupun di luar proses tutorial. Seringkali para tutor harus menantang
para siswa untuk bereksperimen dengan strategi belajar yang baru. Contohnya,
pada tahap diskusi (reporting), siswa cenderung hanya semata-mata menjawab
pertanyaan dari LO tanpa keinginan atau rasa penasaran tentang bagaimana
mengaplikasikannya pada kasus riil atau kasus lainnya. Disinilah tugas tutor untuk
merangsang mereka berpikir dan menvisualisasikannya.
3. The tutor as role model

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Pemberian contoh (modelling) bisa dilakukan secara lebih eksplisit atau kurang
eksplisit, tergantung dari problem yang dihadapi dalam dinamika kelompok. Dengan
mengembangkan berbagai keterampilan yang diperlukan untuk ber-PBL, tidak
hanya tutor, namun para siswa pun, juga dapat menjadi contoh yang efektif dalam
strategi belajar dan berpikir, serta mengembangkan keterampilan yang esensial
dalam problem-based learning.
4. The tutor as activator
Para siswa, terutama pada tingkat lanjut, seringkali sudah memiliki cukup prior
knowledge serta strategi belajar dan berpikir yang memadai, namun sayangnya
mereka belum berhasil untuk menggunakan modal ini dengan baik pada saat PBL.
Disinilah para tutor berperan sebagai activator, mengaktivasi para siswanya untuk
mengaplikasikan pengetahuan mereka secara efektif. Peran tutor sebagai activator
berbeda dengan peran tutor sebagai challenger, dimana pada peran ini siswa sudah
memiliki pengetahuan dan keterampilan namun belum mampu mengemasnya
secara optimal. Sedangkan peran challenger, lebih cenderung kepada mendorong
dan merangsang siswa untuk mencoba perilaku belajar yang baru serta memaksa
diri mereka sendiri untuk memaksimalkan potensi sesuai dengan konteks
permasalahan yang disajikan dalam PBL.
5. The tutor as monitor
Tugas ini mengharuskan tutor untuk melihat keseluruhan proses dan progress dari
grup tutorial serta masing-masing anggotanya selama PBL berlangsung. Selain itu,
tutor juga diharapkan mampu menentukan sejauh mana ketercapaian tujuan
belajar selama proses pembelajaran dalam PBL. Contohnya, jika tujuan belajar
kelompok yang disepakati terlalu simpel atau sedikit, maka tutor boleh
menambahkan atau menambah kompleksitas dari masalah. Pada tahap ini tentunya
tutor harus dapat menentukan terlebih dahulu tingkat pengetahuan siswanya,
sehingga tutor bisa menggiring para siswa sedekat mungkin dengan konteks kasus
sebenarnya.
6. The tutor as evaluator
Pada akhir sesi, para tutor akan diminta untuk berperan sebagai evaluator. Tahap
assessment ini akan memfokuskan terutama pada keterampilan profesional siswa
secara keseluruhan serta attitude mereka selama proses PBL berlangsung. Selain itu,
tutor diharapkan mampu menstimulasi refleksi dari para siswa selama proses PBL,
sehingga para siswa dan tutor sendiri bisa mengevaluasi kemampuan masing-
masing dalam proses pembelajaran.

OVERVIEW OF STUDENT SKILLS in PBL

STEP DESCRIPTION CHAIR SCRIBE

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1 Clarifying unfamiliar  Invites group members to read the  Divides the


terms problem blackboiard into
 Checks if everyone has read the three parts
Unfamiliar terms is the problem  Notes down the
problem text are  Checks if there are unfamiliar terms in unfamiliar terms
clarified the problem
 Concludes and proceeds to the next
phrase
2 Problem definition  Asks the group for possible problem  Notes down the
(cue and clue) definitions problem
 Paraphrases contributions of group definitions
The tutorial group members
defines the problem in  Checks if everyone is satisfied with the
a set of questions problem definitions
 Concludes and proceeds to the next
phrase
3 Brainstorming  Allows all group members to contribute  Makes brief and
(dari cue and clue one by one clear summaries
bisakah dibikin cerita  Summarizes contributions of group of contributions
sendiri) members  Distinguishes
 Stimulates all group members to between main
Preexisting knowledge contribute points and side
is activated and  Summarizes at the end of the issues
determined, hypothesis brainstorm
are generated  Makes sure that a critical analysis of all
contributions is postphoned until step
four
4 Analyzing the  Makes sure that all points from the  Makes brief and
problem(skala prioritas, brainstorm are discussed clear summaries
mana LO yg menjadi  Summarizes contributions of groups contributions
prioritas utama dst) members  Indicates
 Asks questions, promotes depth in the relations
Explanations and discussion between topics,
hypotheses are  Makes sure the group does not stray makes
discussed in depth and from the subject schemata
are systematically  Stimulates group members to find
analyzed to each other relations between topics
 Stimulates all group members to
contribute
5 Formulating learning  Asks for possible learning issues  Notes down the
issues  Paraphrases contributions of group learning issues
member
It is determined what  Checks if everyone is satisfied with the

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knowledge the group learning issues


lacks, and learning  Checks if all obscurities and
issues are formulated contradictions from the problem
on these topics analysis have been converted into
learning issues
7 Reporting  Prepares the structure of the reporting  Makes brief and
phase clear summaries
Findings from the  Makes an inventory ofa what sources of contributions
literature are reported have been used  Indicates
and answers to the  Repeats every learning issue and asks relations
learning issues are what has been found between topics,
discussed  Summarizes contributions of group makes
members schemata
 Asks questions, promotes depth in the  Distinguishes
discussion between main
 Stimulates group members to find points and side
relations between topics issues
 Stimualtes all group members to
contribute
 Concludes the discussion of each
learning issue with a summary

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CASES

SECTION

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PBL Tutorial
Monday, September 26, 2016 Wednesday, September 28, 2016 Session 1 -
(week IV)

Mata Kabur…

Seorang Laki-laki,bernama Tn. Paijo usia 65 tahun datang ke puskesmas diantar oleh
anaknya. Tn. Paijo merasa sejak 1 tahun ini penglihatan kedua matanya terasa kabur, kabur
dirasakan perlahan-lahan dan semakin memberat sejak 2 bulan ini mata kanan hanya bisa
melihat bayangan saja, dan mata kiri juga mengikuti seperti mata kanan. Awalnya mata
kanan terlebih dahulu kabur dirasakan seperti melihat tertutup oleh awan, silau, dan
kadang-kadang melihat double, kemudian diikuti oleh mata kiri. Tidak didapatkan mata
merah, nyeri ataupun gatal dan keluar kotoran. Dari riwayat kesehatan Tn. Paijo selama ini
tidak pernah memeriksakan diri ke dokter sehingga tidak tahu apa mempunyai Diabetes
Melitus ataupun Hipertensi. Sehari-hari Tn. Paijo bekerja sebagai petani yang sering
terpapar oleh sinar matahari. Tn. Paijo juga mempunyai kebiasaan merokok kira-kira 5
batang sehari, tetapi sudah 3 bulan ini Tn. Paijo berhenti merokok. Tn. Paijo juga tidak
pernah cedera ataupun mengalami kecelakaan sebelumnya didaerah mata dan kepala, dan
tidak pernah mengkonsumsi obat-obatan apapun atau jamu-jamuan serta tidak pernah
memakai kacamata sebelumnya. Tn. Paijo merasa sedih dan tidak berguna karena selama 3
bulan terakhir ini Tn. Paijo tidak dapat mandiri dan bekerja karena keadaan mata nya yang
semakin memburuk, sehingga keluarganya yang bergantian merawat Tn. Paijo
kesehariannya. Anak Tn. Paijo sebenarnya sudah sejak lama ingin membawa Tn. Paijo ke
dokter tetapi Tn. Paijo selalu menolak karena tidak ingin merepotkan anak-anaknya, karena
keadaan ekonomi keluarganya yang kekurangan, ditambah lagi ketakutan Tn. Paijo
mendengar cerita dari tetangganya yang mengalami kebutaan setelah dioperasi,sehingga Tn
Paijo bersikeras tidak mau untuk dibawa ke dokter. Didesa Tn. Paijo banyak penduduknya
yang sudah tua mengalami gangguan mata seperti Tn. Paijo, yang pekerjaan mereka
kebanyakan petani. Rumah Tn. Paijo didesa terpencil yang untuk pergi ke puskesmas
terdekat memerlukan waktu 3 jam memakai kendaraan bermotor. Akhirnya Tn. Paijo mau
untuk dibawa ke puskesmas dikarenakan cucunya akan menikah, sehingga Tn. Paijo
berkeinginan untuk bisa melihat kembali. Tn. Paijo berharap dokter dapat menjelaskan
penyakitnya dan bisa membuatnya melihat kembali. Setelah datang di puskesmas, dokter
puskesmas melakukan pemeriksaan mata dan didapati :
Dengan menggunakan Snellen chart :
Visus OD : 1/300
Visus OS : 1/60 Pinhole tetap
Segmen Anterior ODS mamakai penlight dan lup :

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Okuli Dextra Okuli Sinistra


Spasme -, edema - palpebra Spasme -, edema -
Hiperemi - Konjungtiva Hiperemi -
jernih Kornea jernih
dalam Kamera Okuli Anterior dalam
Radier line Iris Radier line
Reflek cahaya +, bulat+ Pupil Reflek cahaya +, bulat+
Keruh rata Lensa Keruh tidak rata
Tekanan Intra Okuli secara Digital didapatkan ODS normal palpasi
Keyword :
Usia tua, Kabur perlahan, kabur seperti tertutup awan, sering terpapar sinar matahari, lensa
keruh rata, lensa keruh tidak rata, iris shadow test - , Iris shadow test +
Permasalahan/pertanyaan:
1. Bagaimana Anatomi, fisiologi dan biokimia dari lensa?
2. Bagaimana Patofisiologi dari Katarak?
3. Apakah faktor resiko terjadinya katarak?
4. Apakah gejala dan tanda katarak?
5. Bagaimana patofisologi Katarak?
6. Bagaimana cara pemeriksaan dan Diagnosis Katarak?
7. Bagaimana managemen dan komplikasi katarak?
8. Bagaimana epidemiologi Katarak di Indonesia?
9. Apakah barrier katarak ?
Materi (brainstorming)  jawaban dari permasalahan
Introduction
Cataract is one of the most common eye disorder that causes significant visual
impairment. By definition, cataract is opacity of the lens. However, to be clinically
significant, the opacity should be in a certain degree to cause decrease of visual function. In
Indonesia, cataract is estimated to be responsible for 0.78% of blindness in the community.
Cataract is widely distributed in community throughout rural areas. Primary healthcare
providers are suitable pioneer case finders in the referral system. Basic examinations for

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screening and post surgical rehabilitation can also be done by medical doctors in these
settings. Through this module we will explore several aspects of cataract relevant for
general practitioners competency.
Anatomy of the lens
The lens is a transparent biconvex structure in the eye which lies in the visual axis. It
is located behind the iris and in front of the vitreous body, suspended by ligaments called
the zonule of Zinn. The central part of the lens can be seen through the pupil. In the adult
eye, the lens is about 4 mm thick and 9 mm in diameter. The lens is composed of cortex and
nucleus, covered by a semipermeable membrane known as the capsule. Zonular fibers are
attached to this capsule at the equatorial zone. Behind the anterior side of the capsule lies a
single layer epithelial cells. The epithelial cells performs regular metabolic activity and
mitosis. At the equatorial zone the epithelial cells differentiate into lens fibers. The main
function of the lens is to refract light and to provide accommodation. To maintain these
functions, the lens also has to keep its own clarity. The refractive power of the lens is about
20 diopters which is obtained from its curve and its refractive index difference from
aqueous humor and vitreus.

Picture 1. Illustration of the human lens (adapted from BCSC.AAO-2008/2009: Lens and
cataract)
Physiology
The lens is avascular and contains no nerve fibers. Control of water and electrolyte
balance is an important mechanism and critical to maintain lens transparency. The lens is
dehydrated and contains higher levels of potassium ions (K+) and amino acids than the
surrounding aqueous and vitreus. Conversely, the lens contains lower levels of sodium ions
(Na+) and chloride ions (Cl-) than the surrounding environment. The cation balance between
the inside and outside of the lens is the result of both the permeability of the lens cell
membranes and the activity of the sodium pump located within the cell membranes of the
epithelium and lens fiber. The mechanism by which the lens controls the state of water and
ions is termed the pump-leak theory. According to this theory, potassium and amino acids

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are actively transported into the anterior lens via the epithelium and then diffuse out with
concentration gradient through the back of the lens. Conversely, sodium flows through the
back of the lens with the concentration gradient and then is actively exchanged for
potassium by the epithelium. Active transport is energy dependant and critical in preserving
physiological condition of the lens.
Accommodation is another important feature of lens physiology. It is the
mechanism by which the eye changes focus from distance to near images. This ability is
produced by cillary muscle contraction which alters the tension of the zonules and changes
the shape of the lens. When cilliary muscle relaxes, the zonular tension increases and the
lens becomes less spherical, decreasing its dioptric power. On the other hand, when cillary
muscle contracts, the zonular tension is reduced and the power of the lens increases. The
capacity of accommodation diminishes with increasing age.
Biochemistry
The human lens is composed of 35% protein and 65% water. With increasing age,
more part of the proteins becomes water insoluble and scatter lights. The excess of
insoluble proteins can make the lens less transparent and become cataractous.
Energy production in the lens is dependant on glucose metabolism obtained from the
aqueous humor. Most of these glucose will enter the anaerobic metabolism and only a small
part of them undergoes aerobic metabolism in the lens. Hyperglycemic state can increase
glucose and its metabolites in the lens, which will increase the osmotic pressure and draw
water into the lens. This may result in swelling of lens fiber and opacification of the lens.
The lens is equipped with several enzymes that protect against free radical damage.
These include glutathione peroxidase, catalase, and superoxide dismutase. These enzyme
are valuable in preventing peroxidation of lens fiber which has been suggested as a factor
contributing to lens opacification.
Pathology
Cataracts may occur as a result of aging or secondary to hereditary factors, trauma,
inflammation, metabolic or nutritional disorders, or radiation. Congenital cataract are found
since birth. Cataracts found in young persons are termed juvenile cataract.
Age-related cataracts are the most common. The three common types of cataract
are nuclear, cortical, and posterior subcapsular (PSC). According to the level of opacity,
cataractous lens can be grossly classified as immature cataract when the opacity is not
homogen, and mature cataract when the lens opacity is total and homogen.
The mechanism of cataract formation is multifactorial and, therefore, difficult to
study. Oxidation of membrane lipids, structural or enzymatic proteins, or DNA by peroxides
or free radicals induced by UV light maybe early initiating events that lead to loss of
transparency in both the nuclear and cortical lens tissue. In cortical cataract, electrolyte
imbalance leads to overhydration of the lens, causing liquefaction of the lens fibers.

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Clinically, cortical cataract formation is manifested by the formation of vacuoles, clefts,


wedges, or lamellar separations that can be seen with the slit lamp. Nuclear cataracts
usually occur secondary to deamidation of the lens proteins by oxidation, proteolysis, and
glycation. The proteins aggregate into high-molecular-weight (HMW) particles that scatter
light. Colored products formed from amino acid residues in this process (urochrome)may be
present. The increasing optical density of the nucleus may cause index myopia that results
in myopic shift of the refractive error. In addition, the central region of the lens acquires a
murky, yellowish to brunescent appearance that is visible in optic section with the slit lamp.
Age-related PSCs are created by loss of lens fiber nuclei and replacement epithelial cells that
aberrantly migrate toward the posterior pole. These epithelial cells cluster, form balloon
cells, and interdigitate with adjacent lens fibers and the deeper cortical fibers, breaking
them down.

Picture 2. Lens with cataract (adapted from BCSC.AAO-2008/2009: Lens and cataract)
Risk factors for the development of cataract include:
Age. Prevalence of cataract increases in the aged people.
Diabetes mellitus. Persons with diabetes mellitus are at higher risk for cataracts, and
persons with diabetes who have cataracts have a higher morbidity than those without
cataracts.
Drugs. Certain medications have been found to be associated with cataractogenesis and
vision loss. There is an association between corticosteroids and posterior subcapsular
cataracts. Drugs such as phenothiazine or other thiazines and chlorpromazine have been
associated with the induction of cataract formation.
Ultraviolet radiation. Studies have shown that there is an increased chance of cataract
formation with unprotected exposure to ultraviolet (UV) radiation. Persons with higher
occupational exposure to UV light are at greater risk for cataract than those with lower
occupational exposure rates.
Smoking. An association between smoking and increased nuclear opacities has been
reported.
Alcohol. Several studies have shown increased cataract formation in patients with higher
alcohol consumption compared with patients who have lower or no alcohol consumption.

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Diagnosis and examination


Cataract patient can suffer decrease of visual acuity, glare, altered contrast
sensitivity, and diplopia. Reduction of visual acuity is gradual and painless. The glare can be
mild but can also be disabling, particularly during daylight or from car headlights. Contrast
sensitivity is measured by specially designed card and can provide a more comprehensive
measure of visual deterioration.
Examination
A flashlight is practical and valuable aid for examining the eye. Patient with suspected
cataract should be assessed for:
- Visual acuity, natural and best corrected.
- Anterior segment evaluation, including the eyelids, conjunctiva, cornea, anterior
chamber, iris, and pupil.
- Evaluation of the lens with pupillary dilatation (using pupillary dilating eye drops
such as Tropicamide / Mydriatyl). Iris shadow test can be useful in determining lens
opacities.
- Funduscopic evaluation.
Additional tests include:
- Intraocular pressure evaluation.
- Keratometry and biometry, (to estimate intraocular lens power).
- Potential acuity testing (e.g. retinometry).
- Posterior segment ultrasonography A/B scan.
Inquiry about systemic condition and other illness should be obtained. Blood pressure,
blood sugar level, and hemostasis function is a routine requirement when surgery is to be
planned.
Management
The mainstay of cataract management is surgery. However, nonsurgical management is
sometimes useful in the early stages of cataract.
Non-Surgical Management
During early cataract development, visual improvement may be achieved through a number
of means including:
• changes in spectacle lens prescription
• magnification or other visual aids
• appropriate illumination
Antioxidants supplements might have some beneficial effect for holding up cataract
development and are currently under investigation. No eye drops are currently available as
an effective treatment for cataract. Although pupillary dilating agents may give some visual
improvement for centrally located cataracts, they are not recommended for treatment.

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Surgical Management
The presence of a cataract does not itself indicate a need for surgery. Cataract surgery may
be indicated when the cataract reduces visual function to a level that interferes with
everyday activities of the patient and the patient desires surgical intervention to improve
vision. Most cataract surgery are elective. In cases with accompanying complication, such as
secondary glaucoma, the surgery can be urgent.
Indications for surgery
The following specific indications for cataract surgery are suggested:
1. The visual impairment produced by the cataract is responsible for the patient’s disability
in carrying out needed or desired activities (driving, reading, occupational needs), which can
be accompanied by the following symptoms:
• visual disability increases due to glare or dim illumination
• patient complains of monocular diplopia or polyopia
• visual disparity exists between the two eyes
2. Other indications for cataract removal
• Lens-induced disease: phacomorphic glaucoma, phacolytic glaucoma, and other lens-
induced disease may require cataract surgery and the need for extraction may be urgent.
• Concomitant ocular disease that requires clear media: cataract extraction may be required
to adequately diagnose other ocular conditions such as diabetic retinopathy.
Surgical Procedures
Under most circumstances, the standard of care in cataract surgery is removal of the
cataract by extracapsular cataract extraction (ECCE), using either phacoemulsification (PE)
or nuclear expression/ extraction. ECCE has replaced intracapsular cataract extraction (ICCE)
as the standard of care for primary cataract extraction although ICCE is still used under
certain special circumstances. Uncomplicated cataract surgery are usually done in less than
one hour and the patient may not need to be hospitalized. The following brief descriptions
show the nature as well as special indications and risks of each surgical procedure.
• Extracapsular cataract extraction by nuclear expression /extraction.
An incision of 8-10 mm is created at the corneo-scleral margin (limbal region). Following the
opening incision and anterior capsulotomy, the nucleus is expressed from the capsular bag
and removed in one piece through the incision. The residual cortex is removed by irrigation
and aspiration. This procedure requires a larger incision, usually necessitating several
sutures to close the wound. Modification of this procedure utilize a small incision (6-8 mm)
through a scleral tunnel that can self seal without suture or a single suture.
• Extracapsular cataract extraction by phacoemulsification.
An incision of 2-3 mm is created at the peripheral cornea. After the opening incision and
anterior capsulotomy, an ultrasonic probe emulsifies the hard nucleus, enabling the surgeon

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to remove the lens material using a suction device. This procedure maintains the normal
depth of the anterior chamber. The incision may be closed without sutures.
• Intracapsular cataract extraction.
A large incision is made at the limbal region (10 mm). Following the opening incision, the
entire lens is extracted in one piece, including its capsule. Because this procedure requires a
very large incision and carries a much higher risk of vitreous loss and postoperative
complications, it is seldom performed. However, it may be preferable to remove the
cataract by this procedure in special circumstances (e.g., dislocated lens).
Intraocular Lens Implantation
Current cataract surgery is almost always followed by intraocular lens (IOL)
implantation. The artificial lens can be made of solid material such as
polymethylmethacrylate or foldable material from silicone or acrylic. These lenses are
usually placed inside the capsular bag. When the capsular bag is not intact or removed (such
as in ICCE), the intraocular lens can be fixated by sutures to sclera. Visual rehabilitation
after IOL implantation can be satisfactory by reaching a 6/6 vision. Patient with implanted
IOL are termed pseudophakia as apposed to aphakia for those who does not have lens
implant. When IOL implantation is not feasible, visual rehabilitation can be achieved with
glasses or contact lens. However, thick glasses can cause image magnification and
anisometropia, and therefore cannot be used for monocular correction when the other eye
has a good visual acuity.
Post surgical rehabilitation and complication
Modern cataract surgery is considered as a safe and effective procedure.
Rehabilitation after surgery is relatively quick and complete wound healing and visual
stability can be achieved between 4-12 weeks (depending on surgical technique). However,
few complications can occur and must be cared with awareness. Some complication of
cataract surgery include:
Endophthalmitis, wound leak, iris prolapse, uveitis, increased intraocular pressure, corneal
edema, bullous keratopathy, dislocated IOL, vitreous lost, cystoid macular edema, retinal
detachment, and choroidal hemorrhage.
After surgery, the patient should be evaluated in the first day, followed by weekly
observation. Evaluation include patient’s complaint, visual acuity, anterior segment
condition, signs of inflammation, intraocular pressure and wound healing. Patient should be
advised to avoid load bearing and physical tasks until the wound is completely healed.
Personal hygiene, especially on the operated eye should be concerned. Topical eye drops of
antibiotics and antiinflamation are usually given for a few weeks. Spectacle correction or
reading adds can be prescribed after the visual function is stable.
Community Ophthalmology of Cataract

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The blindness rate in Indonesia is estimated around 1.5%, the highest in South East
Asia. This figure is higher than other countries such as Bangladesh, India, and Thailand. The
most common cause of blindness in Indonesia is cataract, which is categorized as treatable
blindness. According to WHO, a blindness rate over 1% is a social problem. Therefore, the
handling of the problem cannot be accomplished by the Department of Health alone, rather
by multidisciplinary approach, involvement of nongovernmental organizations and the
community itself. The high blindness rate is caused by low human resource capacity,
geographical factor, limited infrastructure, and socio-economic status. The number of
ophthalmologist in Indonesia is still small.
The incidence of cataract in Indonesia is around 1% or 210.000 people annually. On
the other hand, the surgical capacity is only 80,000 per year. Therefore, there would be an
additional number of cataract sufferer or backlog of 130,000 people every year. This high
backlog is affected by several factors, including the unawareness of the community, high
cost of surgery, shortage of ophthalmologist, and the reach of surgical capacity which is still
low.
One of the aim of community ophthalmology is elimination of cataract blindness.
The program consists of promotion (education), prevention, cure, and rehabilitation.
Execution of the programs may involve ophthalmologist, general healthcare workers, and
non healthcare personnel in the community. Through this approach it is expected that
cataract screening and surgery can be performed efficiently and effectively to reduce
cataract blindness.
Barrier Cataract
Although blindness in the developing world is usually curable, most patients do not
receive medical attention. One recent study found that “over two thirds of adults
over age 40 in a rural Indian population with low vision secondary to cataracts,
glaucoma, and refractive error had never sought eye care,” while another showed
that “90 % of the people seeking eye care in poverty-stricken areas in Sri Lanka had
similarly had no previous eye care.”Why is it that visually impaired people do not
seek eye care services even when care is available? The answer to this question is
multifold, and itis important to note that lack of awareness about treatment
availability and benefits is not the primary problem. Rather, patients face a variety
of barriers that combine to prevent them from seeking proper medical attention.
Cost
Financial barriers are commonly cited as reasons patients do not follow through
with ophthalmic surgery
Fear of Doctors

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For many patients, fear of doctors and of the unfamiliar is another barrier to obtaining eye
surgery
“Fear appears to be a major barrier in the region… Most patients expressed fear of the
hospital environment, staff and loss of pride and dignity… Fear of the unknown appears to
have played a major role in deciding on cataract surgery. In a study in Tanzania, it was
reported that fear of the city, where to stay, what is going to happen when left alone in the
hospital and similar fears far outweighed the perceived advantages of restored sight, among
cataract patients.”
“For many patients the fear of the unknown cannot be overcome. It has been said that for
every unsuccessful operation, five good operations have to be done to counter the effect in
the community
Fear of Treatment
All surgery entails some risk, and the fear of a poor outcome can be enough to cause
patients to forego treatment. This fear is frequently exacerbated by a poor understanding of
the procedure, or by hearsay of surgeries gone awry recently, or even decades prior.
“The main source of information about cataract surgery services was usually a fellow
patient, neighbor, or family member. The quality of this source of information varied widely,
with some patients perceiving cataract surgery as a cause of mortality, having heard of
someone who died after surgery.”
“The fear of pain or the fear of complications during or after surgery is so strong that
blindness and death appear preferable. They are simply not willing to come for cataract
surgery, even free of charge: ‘I would rather stay blind; I better die than going for the
operation.’”
Fatalism, Inevitability, or “God’s Will”
Cultural beliefs about medicine influence a patient’s willingness to seek medical care. In
cultures where diseases are believed to have non-medical causes, patients may not consider
medical treatment such as surgery. Patients who believe blindness is an inevitable
consequence of aging also fail to seek medical care.
“Rural patients often have a limited number of acquaintances and family members who
have undergone cataract surgery. Thus, blindness in the elderly is often an expected
condition. The main reasons that African patients offered cataract surgery did not proceed
were fear of surgery and a belief that blindness was a natural consequence of increasing
age, and could not be reversed.”
Lack of Transportation
Distance from clinics is a physical barrier to obtaining eye care, exacerbated by the lack of
transportation services. This is particularly true for those living in rural areas of Africa and
Asia.
“Surgical services are much more available in urban areas, while the majority of cataract
patients needing care are located in rural locations…In rural Africa, distance to the hospital
was cited by one third of patients as the most important barrier to surgery.”
Alternative Eye Care Services
In addition to the barriers listed above that “push” patients away from seeking eye care,
traditional and/or herbal eye care techniques “pull” patients away from eye surgeries by
offering an alternative treatment option.

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“The main alternatives to the regular eye-care service were chemical shops and indigenous
herbal medicine. This phenomenon of alternative/parallel care is not surprising partly
because of the relatively stronger numerical strength of chemical shops and herbalists in
this district and the negative barriers against uptake of hospital services. There is an
indication of relative inaccessibility of hospital eye services to the population. Reasons for
this inaccessibility include the consumers' concept of who could provide eye care and their
inability to distinguish between the different providers, and their perception of the hospital
and its staff.”
References
American Academy of Ophthalmology Staff. Basic And Clinical Science Course: Retina and
Vitreous. San Fransisco: American Academy of Ophthalmology. 2014-2015
Kanski JJ, Clinical Ophthalmology, A Systematic Approach. 8th ed. Edinburgh: Butterworth-
Heinemann. 2016
Vaughan D, Asbury T, Riordan-Eva P. General Ophthalmology. 18th ed. Stamford: Prentice
Hall. 2011
Willson F, Gurland JE, Hamed LM, Johnes KJ, Wilhelmus KR. Practical Ophthalmology, A
manual for Beginning Residence. San Fransisco: American Academy of Ophthalmology. 2016
Mitchell Paul,ForanSuriya (Australian Diabetes Society).Guidelines for the management of
Diabetic retinopathy. Commonwealth of Australia: National Health and medical Research
Council.2008

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PBL Tutorial Session 2 (Week V)


Monday, October 03, 2016 Wednesday, October 05, 2016

Bayangan Kabur…Hitam
TEMA
OD Non Proliferayive Diabetic Retinopathy
OS Proliferative Diabetic Retinopathy
LO PBL ( Learning Issues)
1. Anatomy of the retina in relation to diabetic retinopathy
2. Epidemiology diabetes mellitus and its complication to the eye
3. The risk factors and pathogenesis of diabetic retinopathy
4. Clinical features of diabetic retinopathy and its diagnosis
5. The prevention and the principles of diabetic retinopathy management
6. The role of general practicioners in the eradication of diabetic blindness

SKENARIO / PROBLEM
Seorang Laki-laki, usia 48 tahun datang ke puskesmas dengan keluhan mata kiri kabur. Mata
kiri kabur dirasakan sejak 3 bulan ini, perlahan-lahan dan semakin memberat. Sejak 2
minggu ini hanya bisa melihat bayangan. Awalnya kabur seperti melihat ada bayangan
seperti rambut melayang-layang mengikuti gerakan bola mata, kemudian memberat. Tidak
ada nyeri ataupun mata merah sebelumnya. Mata kanan juga kabur tetapi tidak lebih berat
dari mata kiri, kabur seperti melihat ada bayangan hitam, kabur perlahan, sejak 1 bulan ini,
tidak didaptkan mata nyeri atau merah. Riwayat penggunaan kacamata baca, tidak
didapatkan trauma sebelumnya. Riwayat penyakit yang lalu telah didiagnosis Diabetes
melitus oleh dokter sejak 8 tahunan yang lalu, pengobatan tidak rutin sehingga gula darah
naik turun. Penderita juga mengalami obesitas sejak usia muda, dan didapatkan riwayat
keluarga dengan obesitas dan Diabetes melitus. Tidak didapatkan riwayat tekanan darah
tinggi ataupun penyakit lainnya. Selama ini belum pernah memeriksakan mata ke dokter
mata. Pola makan masih tetap tidak terkontrol dan tidak pernah olahraga karena kesibukan
di tempat kerja. Riwayat pekerjaan sebagai pegawai kantor swasta. Riwayat merokok
kadang-kadang saja jika bersama teman-teman kantor. Setelah datang di puskesmas, dokter
puskesmas melakukan pemeriksaan mata dan didapati :
Dengan menggunakan Snellen chart :
Visus OD : 5/40 dengan koreksi S-1,50 5/30 pinhole tetap
Visus OS : 1/60 Pinhole tetap
Segmen Anterior ODS mamakai penlight dan lup :
Spasme -, edema - palpebra Spasme -, edema -
Hiperemi - Konjungtiva Hiperemi -
jernih Kornea jernih
dalam Kamera Okuli Anterior dalam
Radier line Iris Radier line
Reflek cahaya +, bulat+ Pupil Reflek cahaya +, bulat+
Kesan jernih Lensa Kesan jernih

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Tekanan Intra Okuli secara Digital didapatkan ODS normal palpasi


Pemeriksaan segmen posterior dengan oftalmoskopi didapatkan :

Funduskopi OD :
Fundus reflek +, papil N. II batas tegas, warna normal, Neovaskularisasi –
Media : jernih
Vasa : A/V ratio 2/3
Retina : perdarahan +, mikroaneurisma +, eksudat +
Makula : reflek +
Funduskopi OS :
Fundus reflek +, papil n II. Batas tegas, neovaskularisasi at disc + (NVD +), perdarahan
peripapil +
Media : kesan jernih
Vasa : sebagian tertutup perdarahan pre retina
Retina : perdarahan + (retina, pre retina), mikroaneurima +, eksudat +, neovaskularisasi
elsewhere + (NVE)
Makula : reflek -, sebagian tertutup perdarahan, edema +

CUE/CLUE :
1. What is the definition of diabetes mellitus
Diabetes mellitus is common metabolic disorder characterized by sustained
hyperglycemia of variable severity, secondary to lack, diminished efficacy, or both of
endogenous insulin. Diabetes may be insulin-dependent (IDDM) termed type 1 or
non-insulin-dependent (NIDDM) termed type 2.
Diabetescriteria : Symptoms of diabetes and a casual plasma glucose >200 mg/dL; or
Fasting plasma glucose (FPG) >126 mg/dL; or 2-hr plasma glucose > 200 mg/dl
2. Explain the pathogenesis of diabetes mellitus can cause retinopathy
Many biochemical pathways link the altered glucose metabolism of diabetes
directly to development and progression of diabetic retinopathy, which has a multifactorial
pathogenesis. This biochemical changes affecting retinal vasculature. Retinopathy exhibits
features of both microvascular occlusion and leakage.
 Microvascular occlusion

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Pathogenesis : Capillary changes consist of loss of pericytes, thickening of basement


membrane and damage and proliferation of endothelial cells. Haematological changes
consist of deformation and increased rouleaux formation of red blood cells and increased
platelet stickiness and aggregation leading to decrease oxygen transport. The consequences
of retinal capillary non-perfusion is retinal ischemia, and it can cause arteriovenous shunt
and neovascularization.
 Microvascular leakage
Pathogenesis : breakdown of the inner blood retinal barrier leads to leakage plasma
constituens into the retina. Physical weakening of the capillary wall results in localized
saccularoutpouchings of the vessel wall, termed microaneurisms. Consequences of
increased vascular permeability include the development of intraretinalhaemorrhage and
oedema which may be diffused or localized.

3. When we should perform eye examination for diabetes mellitus patients


Once diabetes mellitus is diagnosed, eye examination should be done.
4. What is diagnosis from the case ? Explain how to diagnosed diabetic retinopathy
Diagnosis : OD Non Proliferative Diabetic Retinopathy, OS Proliferative Diabetic
Retinopathy. To diagnosed diabetic Retinopathy from Fundus examination (with
direct or indirect ophthalmoscope) with dilated pupil or with fundus photographic
(standard examination), from laboratory (fasting glucose and 2 HPP).
5. Explain how diabetes mellitus can cause irreversible blindness in diabetic retinopathy
Chronic macular edema, macular ischemia (could be happened at NPDR + PDR),
vitreous bleeding, traction retinal detachment (PDR)
6. Explain how to prevent diabetic retinopathy as a primary health care provider
Reccomended eye examination
Diabetes type First examination Follow up
Type 1 3-5 years after diagnosed Annually
Type 2 At time of diagnosis Annually
Prior to pregnancy (type1 or Prior to conception and early in Every 1-3 months or at
type2) the first trimester discretion of ophthalmologist

7. In what condition you have to refer the diabetic retinopathy patients to the
ophthalmologist
If the reduced visual acuity has happened at the time we examine the patients, we have to
refer to ophthalmologist. Urgent referral to ophthalmologist must be done if there are
conditions like PDR, preretinal or vitreous haemorrhage, rubeosisiridis and retinal
detachment.
If the therapy is needed (clinical significan macular edema)
8. What are ocular manisfestation of Diabetes Mellitus?
9. What are risk factors and pathogenesis of Diabetic Retinopathy ?
10. What are clinical sign of Diabetic Retinopathy and how to diagnosed it?
11. How to prevent and principal managemen of Diabetic Retinopathy?
12. What are the general practitioners do to reduce Diabetic Retinopathy blindness in
primary health care?

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(BRAINSTORMING)
GLOBAL PREVALENCE OF DIABETES MELLITUS AND ITS COMPLICATION TO THE EYE
Diabetes mellitus is common metabolic disorder characterized by sustained
hyperglycemia of variable severity, secondary to lack, diminished efficacy, or both of
endogenous insulin. Diabetes may be insulin-dependent (IDDM) termed type 1 or non-
insulin-dependent (NIDDM) termed type 2. Diabetes mellitus among the leading cause of
death, disability, and economic loss throughout the world. WHO has estimated that there
were 171 million people worldwide with diabetes mellitus in 2000 and predicted that 366
million people will have diabetes mellitus by the year 2030. The increase will be due mainly
to increases in low and middle income countries.
There are many ocular manifestation of diabetes mellitus, like cataract, diabetic
retinopathy,and others. Diabetic retinopathy is a microvascular complication of
longstanding both type 1 and type 2 diabetes mellitus. It develops in nearly all persons with
type 1 diabetes and in more than 77% of those with type 2 who survive over 20 years with
the disease. The frightening thing about diabetic retinopathy that this diseases can cause
irreversible blindness.WHO has estimated that diabetic retinopathy is responsible for 4.8%
of the 37 million cases of blindness throughout the world.
In order to prevent vision loss due to diabetic retinopathy, primary health care
providers as a case finder have to be improved. The improvement include primary
prevention with specific attention of the risk factors, basic examination for screening, and
know when to refer.
BASIC ANATOMY OF THE RETINA
Retina is a light-sensitive , transparent tissue lining the inner surface of the
eye.Anatomically retina divided into a few general region. The posterior retina defined by
anatomist as the macula lutea, or yellow spot containing xantophyll (yellow) pigment. The
conventional boundary of the macula, as defined histologically, is that area with 2 or more
layers of ganglion cells that is 5-6 mm diameter and is centered vertically between the
temporal vascular arcades.
The central 1.5 mm of the macula is occupied by the fovea. Within the fovea is a region
devoid of retinal vessels known as the fovealavascular zone (FAZ).
The retina outside the macula is called peripheral retina.

Figure 1. Basic anatomy and posterior pole of the retina. Macula shown above is due to hisstologic definition.

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Figure 2. Anatomical ladmark of the macula (blue circle) and fovea (yellow circle)

In cross-sectional histologic preparation, the layers of the retina can be seen


easily. Several layers of neurons interconnected by synapses. They are listed here in order
from the inner to outer retina :
 Internal limiting membrane (ILM)
 Nerve fiber layer (NFL, the axon of ganglion cell layer)
 Ganglion cell layer
 Inner plexiform layer
 Inner nuclear layer
 Outer plexiform layer
 Outer nuclear layer (the nuclei of photoreceptors)
 External limiting membrane
 Rod and cone (photoreceptors)

Figure 3. Cross section of the fovea


Light striking the retina must travel through the full thickness of the retina to
reach the photoreceptors. The density and distribution of photoreceptors vary with
topographic location within retina. In the fovea is a densely packed arrangement of cones.
The central fovea has no rods. The number of cone photoreceptors decreases rapidly away
from the center. The periphery contains almost no cones.

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There are 2 sources blood supply to the retina. Central retinal artery that
vascularized 2/3 inner retina, and choroidal blood vessels that vascularized 1/3 outer
retina, particularly photoreceptor). Fovea avascular zone is vascularized by choroidal blood
vessels.

RISK FACTORS AND PATHOGENESIS OF DIABETIC RETINOPATHY


- RISK FACTORS
Diabetic retinopathy can happen to anyone who has diabetes. The risk is greater if
the patients has :
 Longer duration of diabetes : duration of diabetes predicts the prevalence and
severity of diabetic retinopathy. An earlier pre-pubertal diagnosis of diabetes may
predict earlier development of diabetic retinopathy. Diabetic retinopathy rarely
develops within 5 years of the onset of diabetes or before puberty, but about 5% of
type 2 diabetics have diabetic retinopathy at presentation.
 Poor glycaemic control: it relevant to the development and progression of diabetic
retinopathy.
 Blood pressure control: if poorly controlled is associated with worsening of diabetic
retinopathy
 Blood lipid control: Hyperlipidemia is well established as a risk factor for diabetic
retinopathy
 Others : smoking, pregnancy,nephropathy,genetic risk factor

- PATHOGENESIS
Many biochemical pathways link the altered glucose metabolism of diabetes
directly to development and progression of diabetic retinopathy, which has a multifactorial
pathogenesis. This biochemical changes affecting retinal vasculature. Retinopathy exhibits
features of both microvascular occlusion and leakage.
 Microvascular occlusion
Pathogenesis : Capillary changes consist of loss of pericytes, thickening of basement
membrane and damage and proliferation of endothelial cells. Haematological changes
consist of deformation and increased rouleaux formation of red blood cells and increased
platelet stickiness and aggregation leading to decrease oxygen transport. The consequences
of retinal capillary non-perfusion is retinal ischemia, and it can cause arteriovenous shunt
and neovascularization.
 Microvascular leakage
Pathogenesis : breakdown of the inner blood retinal barrier leads to leakage plasma
constituens into the retina. Physical weakening of the capillary wall results in localized
saccularoutpouchings of the vessel wall, termed microaneurisms. Consequences of
increased vascular permeability include the development of intraretinalhaemorrhage and
oedema which may be diffused or localized.

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Figure 4. Pathogenesis of diabetic retinopathy Figure 5. Consequences of retinal


ischemia in diabetic retinopathy

Figure 6. consequences of increased vascular permeability in diabetic retinopathy

DIAGNOSIS AND EXAMINATION


- DIAGNOSIS
Diabetic retinopathy can be asymptomatic. Involvement of the fovea by oedema
or hard exudates or ischemia is the most common cause of visual impairment. Reduction of
visual acuity is gradual and painless. It can be mild to severe. In more severe stage of
diabetic retinopathy, severe visual loss can happened.Ussualy it caused by sequelae from
ischemia-induced neovascularization. It could be bleeding on the vitreous, tractional retinal
detachment, and others.
Diabetic retinopathy is classified into an early stage, non proliferative diabetic
retinopathy (NPDR), and a more advanced stage, proliferative diabetic retinopathy (PDR).
This latter stage is a manifestasion of ischemia-induced neovascularization from diabetes.
Nonproliferative diabetic retinopathy
Characteristic findings in NPDR include microaneurysm , cotton wool spots (nerve
fiber layer infarcts), intraretinalhaemorrhages (dot blot), nerve fiber layer haemorrhages
(flame shaped), intraretinalmicrovascular abnormalities (IRMA), hard exudates, retinal
oedema, arterioral abnormalities, dilatation and beading retinal veins. NPDR divided into
mild,moderate, and severe.
Proliferative diabetic retinopathy

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The signs of NPDR with neovascularization.Neovascularization is the hallmark of


PDR. New vessel may proliferate on or within one disc diameter of the optic nerve
head(NVD=new vessel at disc), or along the course of major vessel (NVE=New vessel
elsewhere), or both. Diabetic macular oedema can happened at both stage of diabetic
retinopathy. The clinical sign are location of retinal thickening relative to the fovea,
presence and location of exudates.

Figure 7. Nonproliferative diabetic retinopathy (left), Neovascularized disc in Proliveratife


diabetic retinopathy (right)
EXAMINATION
Screening involves measurement of visual acuity and fundus examination. The gold standard
for screening diabetic retinopathy is with clinically examination and fundusphotographics
with dilated pupil. Pupil dilation using 0.5% to 1% tropicamide eye drop is safe and
markedly increases the sensitivity of diabetic retinopathy examination using direct or
indirect phthalmoscope or slit lamp biomicroscopy with special lens. Additional tests include
:FundusFluorescein Angiography (FFA), Optical Coherence Tomography (OCT)
PREVENTION AND MANAGEMENT OF DIABETIC RETINOPATHY
The only means of preventing diabetic retinopathy is by regulating blood sugar,
blood pressure and other factors under the control of the patient, as guided by their
primary care provider or endocrinologist.
In order to achieve the public health goal to minimizing visual loss, secondary
prevention is needed. Primary care provider (general practicioner, endocrinologist,
diabetologist, or anyone who care with diabetics patients) should do early detection and
screening for diabetic retinopathy. Once diabetes mellitus is diagnosed, eye examination
should be done.
Table 1. Reccomended eye examination
Diabetes type First examination Follow up
Type 1 3-5 years after diagnosed Annually
Type 2 At time of diagnosis Annually
Prior to pregnancy (type1 or Prior to conception and early Every 1-3 months or at
type2) in the first trimester discretion of ophthalmologist
Table 2. Timetable based on retinopathy findings
Retinal abnormality Suggested follow up
Normal or rare microaneurysms Annually
Mild NPDR Every 9 months
Moderate NPDR Every 6 months
Severe NPDR Every 2-4 months

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Clinical significant macular edema Every 2-4 months*


PDR Every 2-3 months*
*Consider laser surgery
If the reduced visual acuity has happened at the time we examine the patients,
we have to refer to ophthalmologist. Urgent referral to ophthalmologist must be done if
there are conditions like PDR, preretinal or vitreous haemorrhage, rubeosisiridis and retinal
detachment.
There are many ways to manage diabetic retinopathy : with laser
photocoagulation, surgical management (pars planavitrectomy), and intravitreal injection
for symptomatic treatment. The therapy for diabetic retinopathy are depend on the stage
and the indication.
ERADICATION OF DIABETIC BLINDNESS
It has been reported that 36% of those with type 2 diabetes mellitus have never had
their eyes examined . These patients tend to be older, less educated and to have had a more
recent diagnosis than those receiving regular eye care. They are also likely to live in rural
areas and receive health care from a family or general practitioner. Alarmingly, 32% of
patients with diabetes mellitus at high risk for vision loss never undergo an eye examination,
and less than 40% of those with high-risk characteristics for vision loss receive treatment.
When examined,almost 61% of these patients are found to have diabetic retinopathy,
cataract, glaucoma or another ocular manifestation of diabetes mellitus. These findings
have significant implications forthe personand forsociety. In order to reduce diabetic
blindness, primary health provider should know the principles in eye care for patients with
diabetes.
 Patients should know that they have diabetes mellitus and the condition requires
care
 Patients should receive adequate care for diabetes mellitus, as guided by the
general practitioner as the primary health provider, endocrinologist, or
diabetologist
 Patients should undergo eye examination for the presence of diabetic retinopathy
 If retinopathy is detected, or patients is referred to an ophthalmologist for an
examination, the society must deliver the necessary level of eye care
 Patients should be sufficiently aware and motivated that they not only undergo eye
examination but also return regularly for such examination
Through this approach that involve general practitioners as primary health
providers, endocrinologist, diabetologist, ophthalmologist, the awareness of patients with
diabetes mellitus, and society, it is expected that diabetic blindness can be reduced.
References
American Academy of Ophthalmology Staff. Basic And Clinical Science Course: Retina and
Vitreous. San Fransisco: American Academy of Ophthalmology. 2014-2015
Kanski JJ, Clinical Ophthalmology, A Systematic Approach. 8th ed. Edinburgh: Butterworth-
Heinemann. 2016
Vaughan D, Asbury T, Riordan-Eva P. General Ophthalmology. 18th ed. Stamford: Prentice
Hall. 2011

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Willson F, Gurland JE, Hamed LM, Johnes KJ, Wilhelmus KR. Practical Ophthalmology, A
manual for Beginning Residence. San Fransisco: American Academy of Ophthalmology. 2016
Mitchell Paul,ForanSuriya (Australian Diabetes Society).Guidelines for the management of
Diabetic retinopathy. Commonwealth of Australia: National Health and medical
Research Council.2008

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