Dokter Blog: from the desk of Rahajeng Tunjungputri

Medicine et cetera by @ajengmd

Neglected people, unseen diseases

This article was published in The Jakarta Post 15 May 2011


– Rahajeng Tunjungputri, Contributor, Nijmegen

Most of us cannot imagine that there are hidden diseases that affect billions of the world’s population that have been neglected for so many years. Nevertheless, as hard as this may be to believe, this is indeed the case with neglected tropical diseases (NTDs)…

click here to read full article on The Jakarta Post


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Commentary: Professor Robot, psychiatrists, and overdosing CT-scans

I will add interesting news I stumble upon this week, and write short commentaries and thoughts about them. The original links to the news are available and I make no attempts to summarize these news.

Professor Robot

Kevin Warwick, a professor of cybernetics at the University of Reading, has a silicon chip implanted into his forearm to fire electrical impulses back to the brain and observe whether human could interpret and respond to stimulus sent by computers. The success of this self-experiment may be revolutionary for development of prosthesis. He basically has turned himself into bionic human purely for the sake of research.

If that sounds fascinating, try other examples of self-experimenting scientists in the article: Stubbins Ffirth drank the blackened vomit of yellow-fever patients in his attempts to prove that the disease was not an infectious one, while James Caroll and Jesse Lazear, US army physicians expose themselves to mosquito bites to prove that these vectors are transmitting the disease. Caroll had long-term complications and Lazear died during the course of this experiment.

These scientists have been regarded as either altruist or extremists. While it’s interesting what this may lead to discover, most research in the world of course are based on strict research protocol and recruit volunteers which safety are ensured.


This week, G. Harris on The New York Times brought us the story of how psychiatry is a transformed field. Psychiatrists, due to what they say a systemic shift in psychiatry care provision -that is payment by insurance companies-, now are “forced” to “talk less and prescribe more”. They no longer have the time for talk therapy and instead opt to examine and treat patients with high efficiency. This include only asking close ended questions relevant to their chief complaints, and prescribing drugs to allow them to function. The words “quality of life of patients” was not once mentioned in the article.

While this is perhaps the first time there is such exposure on the profession in US, I have sensed it since a few years ago, and this perhaps is already true for other fields of medicine in a country where doctors are paid on an out-of-pocket basis like Indonesia. You can’t afford a 45-minutes appointments when there are no appointments system, and you’re paid exactly the amount of money no matter how much time you spent on a patient. It’s still however, very much different from the practice of medicine in a well-insured country like The Netherlands for example, where it is mandatory to schedule your doctors appointments, and have longer appointments time for new patients and a fixed minimum time for every following appointments.

The article was closed on the note that a physician said, “I’m concerned that I may be put in a position where I’d be forced to sacrifice patient care to make a living, and I’m hoping to avoid that.”. But that is not the truth. The truth is that they are already in that position, and they know it, and it’s not just to make a living, it’s to make up the lifestyle that they want.

Click here for the original story

Overdosing CT-Scans

Cabell Huntington Hospital in Huntington, West Virginia are under scrutiny after they were found to perform CT-scan with radiation dose of 10x the necessary dose. This result in serious and dangerous medical side effects for patients as a result of over-radiation. The hospital was not responding adequately to this serious events, while the manufacturer of the CT-scan have filed a report to the FDA that this error was caused by medical technician who had manually increased the radiation to obtain sharper image, which was not necessary to detect pathology on the scans.

I can imagine that this events are not being regularly monitored in many parts of the world, and patient safety are relatively neglected. It’s time that we bring more awareness on this matter.

Click here for the original story

Rahajeng. Nijmegen, 7 March 2011

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My article, “Facing the challenge of climate change in health issues” has been published in Agora, L’Oréal-UNESCO For Women in Science website


Below is a short excerpt of the article,

“During my training as a medical student with overnight shifts in the wards of a government hospital, new patients admitted with severe leptospirosis or dengue fever means that there may be another long night without sleep. Infectious diseases wards are often overcrowded and a new patient can be admitted only when a patient is discharged. As medical students with clinical responsibilities at the hospital, we rarely have the chance to think beyond the hospital walls: about why the diseases these patients come in with had happened in the first place.

Climate change as a major cause of infectious diseases in Indonesia

In Indonesia, infectious diseases are still the main health problem. Diarrhoeal diseases, dengue haemorrhagic fever, typhoid fever, malaria, tuberculosis and respiratory infections are the most common infectious diseases (World Health Organization, 2010). Most of these are vector-borne and water-borne diseases which have been known to be influenced by climate change. The IPCC (Intergovernmental Panel on Climate Change) has concluded that “climate change is projected to increase threat to human health, particularly in lower income populations, predominantly within tropical/subtropical countries.” Climate change has affected the incidence and pattern of infectious diseases through environmental change, increased flooding, drought, changes in weather patterns and increasing incidence of natural disasters (IPCC, 2001)…” Read the rest of the article in Agora, L’Oréal-UNESCO For Women in Science website

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Letter: Proper antibiotic use (The Jakarta Post)

My letter on proper antibiotic use (previously published in The Jakarta Post, 1 September 2010)

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Identification PPT for Parasitology Students

For students,

The following is now available on slideshare:

And a very informative video on Schistosomiasis, this is the last of 3 videos:

Wish you all the best for your exams!


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Trematodes presentation

The short version of the powerpoint presentation of trematodes we use for response discussion was just uploaded. This only consists selected (and most important) slides.

You can click the pic below (or click here) to see the presentation on slideshare.

There is an interesting case report on trematode infection on NEJM:

Do Hyun Park, M.D., Ph.D.
Hyun-Young Son, M.D.
University of Ulsan College of Medicine
138-736, Seoul, South Korea

A 62-year-old man reported having had fatigue, fever, and cramping abdominal pain for 7 days. He also reported that he had recently eaten raw pond smelt (Hypomesus olidus). The results of liver-function tests were abnormal, showing elevated levels of aspartate aminotransferase (350 IU per liter), alanine aminotransferase (352 IU per liter), alkaline phosphatase (204 IU per liter), {gamma}-glutamyltransferase (434 IU per liter), total bilirubin (6.4 mg per deciliter [109 µmol per liter]), and conjugated bilirubin (3.9 mg per deciliter [67 µmol per liter]). The white-cell count was also elevated (13,000 per cubic millimeter), and there was eosinophilia (27%). A computed tomographic scan of the abdomen showed dilatation of the common bile duct without definite filling defects. Given our concern that the patient might have acute cholangitis, a duodenoscopy was performed, and a prominent major papilla was discovered. After cannulation of the common bile duct, numerous leaf-shaped worms popped out (see video) and were subsequently identified as Clonorchis sinensis (also called Opisthorchis sinensis). The patient was given praziquantel and had a quick and uneventful recovery. The clinical manifestations of clonorchiasis tend to reflect the worm burden and the duration of infection. Clonorchis may persist in the biliary tree for decades, and prolonged infestation is associated with the development of cholangiocarcinoma. Acute cholangitis and pancreatitis are rare but important complications of C. sinensis infestation.

Good luck for your exams!
Images used in the presentations are not mine, no copyright infringement intended.

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Parasitology Identification 1


Dear Students,

Due to request of the parasitology tutorial I had with my student groups today, I decided to share this with you. Not the file itself obviously, but as usual, it is now available for your viewing pleasure and your studying on Slideshare.

Today we spent about 1 hour in class for “practice-exam” and discussion about these parasites.

Please study, and good luck for your exams. I wish you nothing but the best!

For the powerpoint slides click here



Some extra pics from today’s session:

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Videos of worm in intestine!!!

Dear all,



Video 1:


Video 2:



Video 3:


Jae Hak Kim, M.D.
Jin Ho Lee, M.D.
Dongguk University College of Medicine
Goyang, South Korea



Video 4:





Other source:

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Choosing Medical Specialty (and more on Internal medicine, infectious disease, and academic medicine)

By: Dr. Rahajeng

I recently stumbled on a very interesting publication of Lange, The Ultimate Guide to Choosing Medical Specialty by Brian Freeman.

For many, the decision of taking up a specialty is easy, for others it’s much more complicated. The best thing is of course to be able to choose based on your interest and the kind of life you want for yourself. I realized very early on that a certain medical specialty is not just about the kind of work that you have to do, but also about the commitment you have to make to a certain lifestyle. I was lucky to have had a real life experience about the field I am going to take up, as well as to have several mentors to introduce me to it.

What is sometimes not immediately anticipated for us Indonesian young medical doctors is that choosing a medical specialty is a decision of the family (and family sometimes means the whole extended family). This means you can’t really make your own decision. There’s mum, dad, grandparents (if they’re around), and maybe others that will have a say about the decision, and for some unlucky ones, the decision is not even yours anymore. For some, they never had a say in what they like, it’s always about what they have to take.

For example, a friend of mine had been pursuing his interest in surgery for a long time during medical school. Dad is a pediatrician, and mom is an ophthalmologist. He did express his interest of surgery to his parents, but dad took over the decision-making and told him that ob-gyn was the best choice for him. He agreed to it despite the fact that he had another choice. He thought that it was what’s best for the family.

For another guy, ob-gyn is a no-question choice, as many in the family (grandpa, uncles) was ob-gyn specialist and they already establish their own private hospital and clinics. Neither a bright nor dedicated student, by circumstances that many call luck, he is to take over the family business.

My own experience is by situation a more liberated one despite the family medical legacy. Grandpa from dad’s side was an orthopedic surgery professor, uncle is also an orthopedic surgeon and his son is now an orthopedic surgery resident. My father was briefly in surgical residency but he resigned and decided that being a company’s medical manager and acupuncture was more enjoyable. He worked for 25 years in a national oil mining company as medical manager and have started and now runs the first dermatology/ aesthetic acupuncture clinic in the city. Uncle from mom’s side is a psychiatrist. I had ob-gyn and pediatrics in mind for a short period. I was finally exposed to the wonders of internal medicine and infectious disease and eventually choosing infectious disease for myself two years ago, preferably in academic setting.

Back to the book, it also offers looking to MBTI personality types to see if you cut-out to be in certain specialty although for internal medicine, it is very flexible on who it is most suited for (Introverted–Intuitive–Feeling– Judging INFJ, Extroverted–Sensing–Feeling– Judging ESFJ, Introverted–Intuitive–Thinking– Judging INTJ, Extroverted–Intuitive–Thinking– Judging ENTJ). It doesn’t really matter I guess, as long as you have good access to yourself, knowing what you like and what you can be passionate about. I happen to be an ENFJ (sorry, you gotta find out what that is yourself).

I started thinking about these 4 years ago when I was still doing my preclinical years (naturally, without having a book to guide my thinking):

• What do you want to get out of your medical career? (intellectual and spiritual satisfaction)

• For whom do you want to work? (international academic institutions)

• Do you want to be a leader in your specialty? (i’d like that very much, so yes)

• How much time do you want to devote to research, teaching, or administrative work? (research and teaching: a lot of time. Administrative: naaah, not really into it)

And knowing that I’ve explored answers to these questions has definitely made me confident in the choices I make.

I have a vision of what career I want for myself, as well as very personal reasons of why I choose a certain path. But the thing is I always know what I like, not just the science but also the lifestyle. I like international travel, I like discussions, I like challenges of pursuing knowledge of the unknown. I like reading, writing and facing cerebral challenges. And I definitely like giving presentations in front of international audience, preferably about something I know a lot about. Those reasons above are part of the things that shape my choices.

And surprise surprise, my Keirsey profiling ended up being “teacher”.


These are selected excerpt from the book “The Ultimate Guide to Choosing Medical Specialty” by Brian Freeman


Before considering their practice options, residents in every specialty have to decide whether or not to subspecialize. The additional time spent in fellowship training gives them advanced knowledge and skills—both of which are essential for practicing as an expert in a focused variety of specialty medicine.

Residents who become inspired by a particular organ system or a complex problem within their specialty should seriously consider pursuing a fellowship. The training provides sophisticated knowledge and skills, making you an expert to whom colleagues look for advice and teaching. Knowing one narrow area very well can enhance your career satisfaction and build your professional confidence. With an emphasis on research and scholarly endeavors, fellowships are also great preparation for careers in academic medicine.

Are there any disadvantages to pursuing a fellowship? Just one—the temporary financial sacrifice. You will have to wait several more years before paying off all those big educational debts hanging over your head.

Private Practice: Delivering the Best Patient Care

Most of you will enter private practice after completing residency or fellowship. In the private sector, physicians either work by themselves or with others, providing high-quality medical care to all types of patients. Because they are not tied strictly to the large academic medical centers, private practitioners have the flexibility to set up shop anywhere in the country—urban, suburban, or rural. Depending on the specialty, you may be working in the office-clinic (dermatology, rheumatology, allergy medicine), the hospital (anesthesiology, radiology, pathology), or both (internal medicine, surgery, pediatrics). Some private practitioners also make rounds at other places, like nursing homes (geriatricians, internists), state facilities (psychiatrists), and prisons (internists, family practitioners).

Academic Medicine: Shaping the Future of Your Specialty

Medical students who want to be leaders in their specialty should consider a career in academic medicine. A much smaller percentage of physicians work at university hospitals than in the private sector. Academicians serve as medical school faculty members in their specialty’s department and also provide patient care at their affiliated teaching hospital. With less emphasis on patient volume and turnover, the pace of academic medicine is more relaxed than that of private practice. Although the job market for new faculty physicians is quite strong, the tertiary care medical centers are usually in major metropolitan areas. This limitation means that academic physicians—whether pediatricians or interventional radiologists—have less geographic flexibility than their counterparts in the private


Whereas private practitioners deliver patient care to the masses, academic physicians in every specialty and subspecialty have a set of three universal—and equally important—responsibilities.

1. Teaching: Every doctor receives residency training in a teaching hospital. By staying there to practice, academic physicians instruct generation after generation of specialists. Much of this time is spent supervising and teaching fellows, residents, and medical students. Through hours of mentorship, academic physicians can make a meaningful difference in their charges’ professional lives by shaping their formative years of clinical training. These inexperienced young doctors will pepper you with lots of probing questions, keeping you sharp in your specialty. Most faculty members recruited out of residency or fellowship start teaching at the level of Assistant Professor. Promotion and tenure—just like in nonmedical fields—are directly related to your ability to teach and conduct ground-breaking research.

2. Research: Through cutting-edge clinical and basic science research, academic physicians are responsible for advancing their specialty. They generate new knowledge, develop procedures and drugs, and evaluate the efficacy of different types of treatment. For instance, a general surgeon might conduct a study looking at the best time to take out a chest tube, and an internist investigates the outcomes of treating diabetic and renal failure patients with ACE inhibitors. Academic physicians also have to teach their colleagues in private practice about the latest advances in their specialty.

They do so by writing up their findings in medical journals and giving lectures at national conferences. To carry out any research project, academic physicians have to obtain the necessary funding—by submitting grants themselves or by receiving money from their department. In the world of academia, the number of papers published and amount of federal research grants received confers prestige on a university medical center. (In a certain weekly news magazine, the formula used to rank US hospitals and medical schools gives the greatest weight to research awards from the National Institutes of Health.)

3. Patient care: In every specialty, academic physicians provide the latest and most innovative medical care. Tertiary medical centers draw a diverse mix of patients, from the indigent (most teaching hospitals are historically located in underserved city neighborhoods) to the very wealthy (e.g., Saudi princes who fly in for the most advanced treatment). Most patients receive care directly from residents and fellows, who are supervised by their attending physicians, of course. Compared to private practitioners, full-time faculty members generally take less call, devote fewer hours to patient care, and earn less money. All revenue generated from clinical practice goes directly to the medical center instead of counting as personal income. In turn, the hospital pays each faculty physician a fixed salary that is directly proportional to the type and volume of medicine he or she practices. This is why academic pediatricians earn less than an academic cardiothoracic surgeon.

Academic medicine is perfect for doctors inspired by working with some of medicine’s greatest minds the authors of well-known textbooks, the renowned researchers who develop new drugs and vaccines, the innovators who figured out how to surgically separate two newborns sharing the same brain. Because teaching hospitals are part of major referral centers, academic physicians are the ones who manage most of the rare and complicated cases. You will take care of diseases and conditions on a level that few physicians ever surpass. This career path, therefore, gives you the autonomy to become a true leader in your specialty.

The book also features profiles of every specialty. And here I will only put up what is obviously my pick: Internal medicine (and a little bit more about infectious disease).


Internal medicine is perhaps the most cerebral of all specialties. It requires a high level of critical thinking. Many students are drawn to internal medicine for the intellectual stimulation. There are always interesting cases that require a lot of problem solving and interpretation of signs, symptoms, and other pieces of data.

Internists are very intellectually curious doctors. They always like to ask questions of themselves and others during the differential diagnosis process. Fascinated by the science of medicine, internists love exploring details—like the mechanisms of drug therapy or the pathophysiology of disease. To make the best diagnosis, internists tend to read quite a bit. Keeping abreast of the latest advances in general medicine requires a career-long commitment to reading journals such as JAMA or The New England Journal of Medicine.

Critical thinking is necessary because internists take a scientific approach to being master diagnosticians. They thrive on making a great diagnosis, analyzing a fascinating big case, and solving complex medical problems. Internists love to sit around and discuss disease. They get excited by putting together a patient’s signs, symptoms, and laboratory findings and trying to come up with a long list of possible differential diagnoses. Unfortunately, sometimes the daily activity in internal medicine is perceived as lots of thinking and talking but little action. In particular, academic inpatient rounds can perpetuate the stereotype of internal medicine as mental masturbation. This is because internists are thorough individuals who make sure not to leave out any possible diagnoses. Students who love to solve problems and mental puzzles find internal medicine a fascinating specialty. Internists are experts at taking patient histories and performing physical examinations. It is with the information derived from the H&P that they make most diagnoses. After talking to the patient, the internist constructs a list of differential diagnoses for each of the patient’s problems. This process allows them to clearly organize in their minds what is going on with the patient and how to address each issue; many patients have multiple medical problems or complaints. To finalize a diagnosis from a list of many, the internist relies on a great deal of critical thinking and deductive reasoning from the data at hand. They take pieces of evidence from the history, physical, laboratory data, and imaging studies to rule in or rule out various disease states. It is kind of like mental detective work. An internist in academics commented that “figuring out how all the pieces to a patients’ clinical puzzle fit together is extremely rewarding.” With a confident diagnosis in hand, the internist then moves on to treating the patient. Across the subspecialties of internal medicine, therapeutic interventions take the form of either pharmacologic agents or procedures. General internists, for instance, keep up with the advances in treating high blood pressure with the newest medications and are experts at figuring out the proper antibiotic for a patient with bacterial meningitis. Although this specialty requires thorough, organized thought, internists are more than just thinkers; they are also proficient in many technical skills essential for the diagnosis and treatment of illness. These skills include a number of inpatient procedures, such as thoracentesis, paracentesis, lumbar puncture, and central line placement, and outpatient procedures like flexible sigmoidoscopy, endometrial biopsy, and intra-articular injections.


Likes physical diagnosis, pharmacology, and physiology.

Is a thorough, cautious problem- solver.

Can interact well with people and maintain long-term relationships.

Likes working with his or her mind.

Is a good, patient listener.


Internal medicine is comprised of many subspecialties. In 2000, roughly half of

all graduates from internal medicine residency programs sought fellowship training.

Currently there are 10 possible areas of subspecialization. Before jumping into one of these disciplines, take a moment for some honest self-evaluation. It is essential that you give some thought to

your field of interest and the type of personality most suited to it.

For aspiring physicians who prefer direct primary patient care, general internal

medicine is the place to be. Specialists tend to be much more scientifically oriented

and enjoy more complex and difficult cases. They serve as consultants to the general internist, directing medical care for a specific organ system and often teaching the general internist about the patients’ disease process. For certain specialties, like cardiology, gastroenterology, and critical care, more time is spent caring for patients in the hospital environment than in the office setting. No matter whether you choose cardiology or rheumatology, all subspecialists are, at heart, excellent general internists. You will still be required to have high-quality history and physical examination skills, as well as the ability to interpret laboratory and radiographic findings, to produce a comprehensive differential diagnosis. In every subspecialty, all internists take care of very sick adult patients who have many medical problems.

Infectious Disease

If you love studying bacteria, viruses, parasites, and fungi, then the subspecialty of infectious disease is for you. These physicians take the basic science of microbiology and apply it to clinical situations. In their diagnostic workup, they approach the patient’s disease process by taking into consideration recent travel, geographic region, country of origin, and cultural practice. They are experts in the proper collection and analysis of culture specimens, plus a variety of laboratory tests, such as antibiotic sensitivity tests, CD4 counts, and infectious serologies.

Their treatment regimens are largely pharmacologic and draw on the latest developments in antibiotic therapy. Through the use of vaccines, they practice a great deal of preventive medicine. Most patients who require the expertise of these clinicians have diseases that are short-term in nature. Thus, infectious disease specialists typically serve as consultants for other physicians. In the summer of 2002, they were on the front lines of the West Nile virus outbreak in the United States. They consult on patients in the hospital for diagnostic challenges (e.g., fever of unknown origin) and for treatment regimens of specific infectious diseases (e.g., bacterial endocarditis, meningitis, cellulitis, sepsis). Many infectious disease physicians maintain longer relationships with patients suffering from chronic diseases, such as HIV/AIDS and tuberculosis, who require extensive follow up. Some practice travel medicine, serving as consultants to patients preparing for international travel and to those who acquired illnesses while overseas. Other areas of expertise include infection control within health care settings, international public health, and the prevention of antibiotic resistance through education and research. They also are involved in the tracking and epidemiology of certain communicable diseases. As the threat of biological attack becomes a growing concern, the prevention, recognition, and treatment of bioterrorism are now focal points of infectious disease. Fellowships require 2 years of training after residency.

Semarang, 7-6-2009



Freeman B. The Ultimate Guide to Choosing Medical Specialty. Lange 2007.

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Stratifikasi Risiko, Antibiotika Empirik dan Evaluasi Pasien PPOK Eksaserbasi Akut

Oleh: Dr. Rahajeng

Artikel ini adalah diskusi lanjutan dari Penggunaan Rasional Antibiotik pada PPOK Eksaserbasi Akut di blog ini. Silakan menuju ke artikel tersebut untuk pembahasan awal yang lebih lengkap.


Salah satu tujuan dari GOLD, Global Initiative for Chronic Obstructive Lung Disease, adalah meningkatkan kesadaran dokter dan masyarakat mengenai gejala penyakit paru obstruktif kronik (PPOK). Klasifikasi derajat PPOK berdasarkan pemeriksaan spirometri dibagi menjadi 4 stage. Pesan kesehatan masyarakat yang penting adalah bahwa batuk dan produksi sputum kronik adalah hal yang tidak normal dan membutuhkan pemeriksaan lebih lanjut mengenai penyebabnya.

Klasifikasi PPOK berdasarkan GOLD adalah (1):

Stage 1: PPOK ringan

Keterbatasan airflow ringan (FEV1/FVC < 70%, FEV1 ≥ 80% predicted), dan kadang, tapi tidak selalu, batuk dan produksi sputum kronik.

Pada tahap ini individu tidak menyadari bahwa fungsi parunya abnormal.

Stage 2: PPOK Sedang

Keterbatasan airflow memburuk (FEV1/FVC < 70%, 50% ≤ FEV1 < 80% predicted), timbul sesak napas setelah aktivitas (exertion)

Pada tahap ini individu biasanya mulai mencari pengobatan karena gejala pernapasan kronik atau eksaserbasi.

Stage 3: PPOK berat

Keterbatasan airflow makin memburuk (FEV1/FVC < 70%, 30% ≤ FEV1 < 50% predicted), sesak napas makin berat, kemampuan latihan menurun, dan eksaserbasi berulang yang berdampak pada kualitas hidup pasien.

Stage 4: PPOK sangat berat

Keterbatasan airflow sangat berat (FEV1/FVC < 70%, FEV1 < 30% predicted) atau FEV1<50% dengan gagal napas kronik.

Pada tahap ini kualitas hidup sangat berkurang dan eksaserbasi dapat menyancam jiwa.

Sebuah studi multicenter menyimpulkan bahwa stratifikasi GOLD dan kebutuhan akan terapi oksigen jangka panjang (Long term oxigen therapy/ LTOT) merupakan prediktor penting untuk perawatan di rumah sakit (2).

Berdasarkan GOLD 2008, indikasi untuk perawatan PPOK eksaserbasi akut di rumah sakit adalah (1):

–          Peningkatan mendadak dari beratnya gejala (misalnya tiba-tiba muncul gejala sesak napas saat istirahat)

–          PPOK berat

–          Timbulnya tanda baru (edema, sianosis)

–          Eksaserbasi yang tidak berespon terhadap penanganan awal

–          Komorbiditas yang signifikan

–          Eksaserbasi yang sering

–          Aritmia

–          Ketidakpastian dalam diagnosis

–          Usia tua

–          Perawatan di rumah yang kurang memadai

GOLD menyarankan pemakaian antibiotik pada kasus-kasus dengan peningkatan volume atau purulensi sputum, peningkatan derajat sesak napas, dan pada kasus yang membutuhkan ventilasi mekanik. Antibiotika diberikan secara empirik dan rasional, dengan memperhatikan stratifikasi faktor risiko yang dimiliki pasien.


Pada eksaserbasi, secara klinis untuk memutuskan antibiotik apa yang digunakan secara empiris dapat digunakan algoritma di atas. Pasien dibedakan menjadi PPOK tanpa komplikasi dan dengan komplikasi (3).

PPOK tanpa komplikasi adalah pasien PPOK dengan usia > 65 tahun, FEV1 > 50% predicted, < 3 eksaserbasi per tahun, tanpa penyakit jantung. Untuk kelompok ini digunakan makrolid advance (azithromycin, clarithromycin), cephalosporin (cefuroxime), Doxycycline, Trimepthoprim-sulfamethoxazole, dan pada paparan antibiotik yang baru terjadi (< 3 bulan) perlu dipilih antibiotik alternatif.

PPOK dengan komplikasi adalah pasien usia ≥ 65 tahun, FEV1 ≤ 50%, ≥ 3 eksaserbasi/tahun, atau adanya penyakit jantung. Digunakan antibiotika: Floroquinolone (levofloxacin, moxifloxacin), amoxicilin-calvulanate, atau pada paparan antibiotik yang baru terjadi dapat dipilih antibiotik alternatif.

Antibiotik yang dipilih berdasarkan berat gejala dan pengelompokan risiko di atas diberikan selama menunggu hasil kultur dan uji sensitivitas atau dilakukan evaluasi dalam 72 jam. Kondisi klinis yang memburuk atau respon yang tidak adekuat dalam 72 jam merupakan indikasi untuk penyelidikan lebih lanjut.

Biasanya pengobatan diberikan selama 7-10 hari. Respon biasanya tampak dalam waktu 3-5 hari dan penggantian antibiotik dapat dipertimbangkan bila respon tidak memuaskan. Jika dilakukan pemberian antibiotik iv, maka penggantian antibiotik oral dilakukan setelah 72 jam (4).

Berbagai perkumpulan ahli pulmonologi di dunia memiliki panduan yang berbeda mengenai stratifikasi risiko dan pengelompokan pasien serta antibiotik apa yang dapat digunakan (5),(6). Namun pada dasarnya dapat disimpulkan bahwa pemberian antibiotika pada pasien PPOK merupakan keputusan yang didasarkan atas situasi klinis pasien. Kebanyakan antibiotika baru merupakan modifikasi dari struktur yang telah ada, sehingga pemilihan antibiotika secara cermat harus dilakukan untuk mempertahankan sensitivitas antibiotika yang telah ada dan mencegah resistensi.


(1). Global Initiative for Chronic Obstructive Lung Disease (GOLD). Pocket Guide to COPD Diagnosis, Treatment and Management 2008.

(2). Lusuardi  M., Lucioni C., De Benedetto F., Mazzi S., Sanguninetti C. M., Donner C. F.GOLD severity stratification and risk of hospitalisation for COPD exacerbations. Monaldi archives for chest disease  2008, vol. 69, no 4, pp. 164-169.

(3). Sethi S. Murphy T. Infection in the Pathogenesis and Course of Chronic Obstructive Pulmonary Disease. N Engl J Med 2008;359:2355-65.

(4). The Australian and New Zealand COPD Reference Site. COPD acute exacerbation plan.

(5).Wilson R. Bacteria, antibiotics and COPD. Eur Respir J 2001; 17: 995–1007.

(6) Stoller J. Acute Exacerbations of Chronic Obstructive Pulmonary Disease. N Engl J Med, Vol. 346, No. 13.


Bagan adalah milik New England Journal of Medicine, diunduh dari

Terima kasih kepada Dr. Nur Farhanah Sp.PD, staf bagian Infeksi Tropik FK Undip atas masukan yang berharga.

Filed under: miscelaneous, , , ,

Tinjauan Pustaka: Profilaksis Malaria

Tinjauan pustaka oleh: Dr. Rahajeng

Malaria adalah penyakit endemis di lebih dari 100 negara. Tiap tahun pengunjung daerah endemis terjangkit malaria akibat tidak adanya imunitas terhadap malaria. Imigran dari daerah endemis yang pindah untuk tinggal di daerah non-endemis kemudian berkunjung ke area endemis juga dapat tertular malaria akibat berkurang atau tidak adanya imunitas. Demam yang terjadi dalam waktu 3 bulan setelah meninggalkan daerah endemis harus diselidiki untuk kemungkinan malaria. 95% kasus malaria pengunjung daerah endemis terjadi dalam waktu 30 hari setelah kembali dari daerah endemis.

Orang yang kembali dari daerah endemis ke daerah non-endemis dapat mengalami masalah akibat dokter yang tidak familier dengan gejala malaria; diagnosis tertunda, pengobatan tidak tersedia dan menyebabkan tingkat kematian yang tinggi.

Orang yang non-imun di daerah endemis yang terpapar gigitan nyamuk berisiko terkena malaria. Ini termasuk orang semi-imun yang yang kehilangan seluruh atau sebagian imunitasnya akibat tinggal di area non-endemis selama 6 bulan atau lebih.


Malaria dapat timbul dengan gejala influenza-like, termasuk nyeri kepala dan nyeri punggung. Muntah, diare, nyeri perut dan batuk dapat merupakan gejala yang mirip penyakit infeksi lainnya. Buku ajar menggambarkan demam dengan episode antara beberapa jam sampai 2-3 hari, namun pada orang non-imun demam dapat terjadi dengan pola ireguler dalam 1 hari.


Kemoprofilaksis lini pertama didesain untuk mencegah kematian akibat malaria falciparum berat. Obat-obatan ini juga mencegah serangan primer dari spesies non-falciparum. Resistensi P. falciparum terhadap chloroquine hampir universal; chloroquine hanya efektif di Meksiko, area Amerika Tengah di sebelah barat Terusan Panama, Kariba, Asia Timur dan beberapa negara Timur Tengah. Di area endemis lain, WHO dan CDC merekomendasikan atovaquone-proguanil, mefloquine, dan doksisiklin; obat-obatan ini menunjukkan 95% efikasi terhadap P. falciparum.

Resistensi mefloquine terjadi di area rural terbatas di Asia Tenggara. Pilihan obat untuk orang yang bepergian ke area dengan malaria yang resisten chloroquin bergantung pada faktor seperti lama tinggal, usia dan riwayat penyakit, kehamilan dan apakah ada intoleransi obat sebelumnya serta pertimbangan ekonomi. Berikut informasi tentang pilihan obat:



Chloroquine, mefloquine dan doksisiklin tidak mencegah infeksi pertama pada manusia, namun bekerja terhadap parasit yang menginfeksi eritrosit setelahlepas dari fase maturasi awal di hepar. Akibatnya, obat ini harus diteruskan sampai 4 minggu setelah paparan terakhir terhadap nyamuk yang terinfeksi untuk menyingkirkan parasit yang masih mungkin dilepaskan dari hepar pada bulan berikutnya. Namun atovaquone-proguanil tidak hanya bekerja terhadap parasit yang ada di dalam darah namun juga terhadap parasit yang aktif bereplikasi di hepar sehingga dapat dihentikan 1 minggu setelah paparan.

Kemoprofilaksis dengan atovaquone-proguanil dan doksisiklin harus dimulai 1 atau 2 hari sebelum perjalanan ke daerah endemis, sementara chloroquine harus dimulai 1 minggu sebelum perjalanan.

Penggunaan mefloquine harus dimulai 3 minggu sebelum perjalanan, terutama untuk mengamati efek samping yang mungkin menyebabkan penghentian obat dan pemilihan obat lain. Indikasi untuk pemakaian obat jenis lain adalah kecemasan akut, depresi, kelelahan, dan confusio.

Infeksi malaria pada wanita hamil lebih berat dengan risiko untuk ibu dan janin. Tidak ada kemoprofilaksis yang efektif 100%. WHO dan CDC menyarankan wanita hamil tidak bepergian ke daerah endemis malaria. Jika terpaksa menggunakan kemoprofilaksis, mefloquine adalah obat pilihan untuk malaria resisten chloroquine.

Obat pilihan pada anak-anak sama dengan dewasa, namun doksisiklin direkomendasikan untuk tidak digunakan untuk anak kurang dari 8 tahun. Tersedia panduan dosis anak untuk agen antimalaria.


Skizont adalah tahap multinuklear parasit yang mengalami pembelahan mitotik di sel host. Skizontid tahap hepatik seperti atovaquone-proguanil dan primaquine membunuh parasit selama periode perkembangan aktif parasit di hepatosit, obat-obat ini membunuh keempat spesies malaria.

Hanya primaquine yang dapat membunuh hipnozoit sehingga dapat mencegah relaps malaria. Dibandingkan obat lain, atovaquone-proguanil dan primaquine bekerja pada dua titik berbeda dari siklus hidup parasit. Atovaquone-proguanil bekerja terhadap skizont hepar tapi tidak dapat membunuh hipnozoit.

Skizontid tahap darah seperti atovaquone-proguanil, doksisiklin, mefloquine, dan chloroquine menginterupsi perkembangan skizon dalam eritrosit sehingga mencegah manifestasi klinis infeksi malaria.


Freedman, D. Malaria Prevention in Short-Term Travelers. N Engl J Med 359;6. August 7, 2008.

WHO. International Travel and Health. 2009.


Disclaimer: Tabel dan gambar adalah milik New England Journal of Medicine, diunduh dari

Filed under: miscelaneous, , , , , ,


By: Dr. Rahajeng Tunjung





Alhamdu lillahi rabbil ‘aalamiin.












My colleagues in MFDU who have supported me.



  1. Able to live abroad independently for study purpose
  2. Able to perform well in the courses and rotation
  4. Learn about tropical medicine from The Netherland’s perspective
  5. Learn about public health from the international perspective
  6. Make use of the learning opportunities available in Radboud University
  8. Learn about the Infectious Disease Department in UMC Radboud
  9. Learn about the management of infectious disease in UMC Radboud
  10. Learn about the infectious disease commonly encountered in The Netherlands


1 February 2007: Course of Health and Disease in The Tropics

1 March 2007: Course of Public Health, International Perspective

1 April 2007: Rotation in Infectious Disease Department UMC Radboud




Monday, 5/2/07






  • Insight in design and structure of health system and it’s consequence
  • Geographical accessibility of health care


Two stages of the game:

  1. Planning stage : design and describe the health system



  • Delay in getting medical help may be caused by:

–          the distance between health care facilities and villages

–          limited transportation

–          people can’t leave their family or their village to seek medical help

Tuesday, 6/2/07




Wednesday, 7/2/07




  1. Malaria
  2. TB
  3. Lymphatic

While the order based on total death:

  1. TB
  2. Malaria
  3. Leishmaniasis

Epidemiological trends:

  1. Increase in mortality and drug resistance
  2. increase in epidemics

Burden of diseases can be calculated from:

  1. DALY
  2. Death
  3. Economic impact

–          Productivity lost

–          Reduction in annual economic growth rate

From the World Health Report 2003:

–          Communicable diseases are starting to decrease while non-communicable diseases are increasing.


WHO 2002:

DALY in developing countries:

  2. Lower respiratory tract infection
  3. Diarrhoeal diseases

The highest risk factors for health problems:

  1. Underweight
  2. Unsafe water, poor hygiene and sanitation
  3. Unsafe sex
  4. Indoor smoke and fume inhalation
  5. Zinc, iron, and Vitamin A deficiency




Thursday, 8/2/07



Friday, 9/2/07







Monday, 12/2/07





Tuesday, 13/2/07

  • Lecture on epidemiological aspect of malaria.

Wednesday, 14/2/07


–          Case management: diagnosis, therapy, intermittent preventive treatment (IPT)

–          Comparison of insecticide treated nets (ITN) and combination of ITN-IPT

–          Malaria and pregnancy

–          Drug resistance

Thursday, 15/2/07



Friday, 16/2/07


Wednesday, 21/2/07

  • Written test

Final version of the research proposal enclosed.


Research proposal preparation


Forum presentation of research proposal

Final version of presentation is enclosed


The strong points of this course the students find positive are:

–          the use of english (especially for the dutch students)

–          the topics of discussions and articles used as references are up to date and recent

–          the group works that allow interaction and exchange between the dutch and the international students

–          the professors were able to give the lectures clearly and with good structure

The weak points of this course are:






Monday, 5/3/07

Lecture: Opening and introduction of course

What is public health?


–Policy and planning – of health systems

–Prevention – of diseases

–Promotion – of healthy lifestyles

–Protection – against health hazards

–Partnership – to build coalitions

Aim of the course


–the main determinants of major public health problems

–efforts made within health systems to adress these

•for a wide range of situations


Lecture: Health and its determinants

Measure of disease

nMortality rates

•Historically important


nMeasure for burden of disease

nDisability-adjusted life years

nLoss of life years, adjusted for quality of these years lived

Disability adjusted life years

nPowerful instrument to compare chronic and fatal diseases

•E.g. depression and HIV/AIDS

nInfluential in policy and planning of health programs in developing countries

Child diseases (0-4 yr)

  • Enormous progression since ’70s
  • Especially in areas with economic progress
  • Progress in Africa offset by HIV/AIDS

Adult diseases

  • General mortality decline
  • Except in Africa: enormous increase because of HIV/AIDS
  • In other areas, non-communicable disease gain importance
  • Difference in burden of disease between countries is increasing
  • Determinants

The good…




nPolio is eridicated as epidemic

The bad…


nTuberculosis and malaria become more and more resistant against medical treatment

nIn 2002 10,5 million children died (< 5 jr)



The ugly….


nThe ratio of child mortality between developing and developed countries was

•5,5 in 1960

•10,3 in 1990

•13,0 in 2002

nAlso major differences between countries – also in eich countries

Tuesday, 6/3/07

Work group: Health and determinants

Wednesday, 7/3/07

Practical: Gapminder: exploring global health


We analyzed the following graphic series:

  1. Human development and income growth 2004
  2. Human development trends 2005
  3. Milenium Development Goal Achievement Graphs 2003



–          Region with the lowest is Sub-saharan Africa.

–          Singapore and Hongkong are Asian countries that perform as well as OECD countries.


–          Economic growth requires investing in human development first.

–          Indonesia, along with Srilanka and China progress in both income in 1975-2002.







Response lecture: Health and determinants


Lecture: Globalisation


Thursday, 8/3/07

Work group: Globalisation

Friday, 9/3/07


Response lectures: Globalisation

The elements of globalisation include:

  1. Economic growth
  2. Income distribution
  3. Social development

The phases of epidemiological transition:

  1. Hunger
  2. Pandemics
  3. Man made diseases
  4. Delayed chronic degenerative diseases
  5. Re-emerging infections

Monday, 12/3/07

Lecture: Health systems





  1. Financial accessibility
  2. Physical accessibility
  3. Availability of human resources
  4. Availability of material resources
  5. Organizational quality
  6. Relevance of services
  7. Technical quality
  8. Social accountability

Tuesday, 13/3/07

Discussions: what makes a good health system?

  • Objectives and impacts of the health system was discussed.

Health systems

Why need a organised health system by government?


•Need collective action

–for prevention

–to control communicable diseases

•Ensure equal access for rich and poor

–Good health is equally important for rich and poor

Health systems: evolved in past century


–Stimulated by industrial revolution

Eight steps to effective implementation of services

1. Financial Accessibility

•Typical problem

–Formal user fees are unaffordable

–Exemptions used for influential individuals

–Insurance serves only urban elite and formal sector workers

•Possible remedies

–Reduce user fees for basic services / strengthen exemption mechanisms

–Develop community financing arrangements   covering informal sector

2. Availability of Human Resources

•Typical problem

–Lack of trained and motivated staff in remote undesirable areas

•Poor deployment policies, wage gap between internal and global market

•Possible remedies

–Improved personnel policies, favoring hard-to-reach areas


3. Availability of Material Resources

•Typical problem

–Shortage of essential drugs, and low quality / fake drugs

•Poor management of drug supply

•Consumers have insuffient knowledge

•Possible remedies

–Improved drug management


4. Organizational Quality

•Typical problem

–Long queues / underutilization of facilities, lack of respectful care

•Social distance between provider and community

•Poor service management

•Possible remedies

–Train staff in planning and management

–Introduce community management committees

–Disseminate info about ‘patients rights’

–Include satisfaction measures in evaluation

5. Relevance of Service Mix

•Typical problem

–Ad-hoc, history based priority setting

•Disproportinate supply of curative services,

•Little relation between services ↔ burden of disease

•Public spending favors the least poor

•Possible remedies

–Rational priority setting of services

–Establish core package adressing basic  needs

6. Technical Quality

•Typical problem

–Inefficacious services delivered

•Lack of use of practical guidelines / diagnostic and treatment algorithms

•Poor training / supervision

•Possible remedies

–Improve drug management, with special focus on rational drug use

–Improve training and supervision

–Performance based payments / contracting out

7. Social Accountability

•Typical problem


•Community is not participating in management

•Possible remedies

–Establish and/or improve formal entities for community participation

•Actively promote participation of vulnrable groups

Wednesday, 14/3/07

Response lecture on “what makes a good health system”

Lecture: Choosing the right interventions



Thursday, 15/3/07

Discussion: Quality of Care


Perceived quality of care is how the

Friday, 16/3/07

Response lecture: Choosing the right interventions

Monday, 19/3/07

Lecture: Global Initiatives



–          sexual health

–          family planning

–          abortion

–          safe motherhood

Tuesday, 20/3/07

Working group: Global Initiatives

Wednesday, 21/3/07

Video: Millenium Development Goals

Thursday, 22/3/07

Working group: Primary Health Care

Friday, 23/3/07

Response lecture: Primary health care

Monday, 26/3/07

Lecture and video: Healthy cities

Tuesday, 27/3/07

Working group and lecture: healthy cities

Thursday, 28/3/07


Friday, 29/3/07

Presentation of paper




















Review of lecture:



–           Rejected asylum seekers

–          Ex-partners or family of legal immigrants

The effects of their undocumented status in The Netherlands are:

–          poor working and living conditions

–          little amount of money, and therefore stuck to stay in The Netherlands

–          in fear and uncertainty about their condition

–          vulnerability to violence, especially the women

–          no social network

–          pre-existing illness

The health problems in undocumented immigrants are:

–          anxiety

–          sleeping problems

–          contraception problems

–          abortion for economic reasons

–          more serious illness (delay in seeking treatment)

–          higher perinatal death

–          more problems in pregnancy

–          depression

–          HIV/AIDS

–          TB

Problems encountered causing limited access to care by undocumented immigrants are:

–          no health insurance

–          no money for paying treatment cost



Barriers from the doctors are:

–          financial reason (patients unable to pay)


–          practical difficulties (language, time, lack of knowledge due to different diseases

–          lack in the continuity of care (patient is homeless and live in poor condition)


–          spread of communicable disease (TB, STI)


–          inequity and inequality

Integrated approach for the health of undocumented migrants:


–          providing stability in supportive network

–          education for doctors (about the obligation to treat everyone)

–          education for migrants (about how to seek health care)


Review of lecture:

– Chronic poverty causes vulnerability to illness.


– People at risk for chronic poverty are:

– Those with low level of education

– land degradation

– large families with high dependency

– women and children

– widows, caste, ethnicities (related to ownership esp. in Africa)

– Type of poverty:

1. Income poverty

2. Asset poverty:

– absence of critical assets required for survival

– asset loss after occurrence of shocks (illness, death, natural disaster, marriage)

– There is need to search for risk-coping and insurance mechanism

1. Before events happen

2. After events happen

– The shocks, or critical life events, can be categorized as follows:




– Level of intervention:

1. Macro: economic growth of the country

2. Meso: development of insurance network









Food,  Health, and The Role of International Community




  1. Limited expenditures
  2. Introduction of user fees of public services
  3. Rejection of taxation as financing means
  4. Increasing inequities


Social capital consists of these elements:

–          Material resources

–          Immaterial resources

–          In network of social relations

–          Mobilized by individual or collective actors







Health in Urban Settings by Dr. Francoise Barten



























Filed under: miscelaneous, , , , ,

Reaksi Transfusi

Risiko transfusi darah ini dapat dibedakan atas reaksi cepat dan lambat.

Reaksi Akut

Reaksi akut adalah reaksi yang terjadi selama transfusi atau dalam 24 jam setelah transfusi. Reaksi akut dapat dibagi menjadi tiga kategori yaitu ringan, sedang-berat dan reaksi yang membahayakan nyawa. Reaksi ringan ditandai dengan timbulnya pruritus, urtikaria dan rash. Reaksi ringan ini disebabkan oleh hipersensitivitas ringan. Reaksi sedang-berat ditandai dengan adanya gejala gelisah, lemah, pruritus, palpitasi, dispnea ringan dan nyeri kepala. Pada pemeriksaan fisis dapat ditemukan adanya warna kemerahan di kulit,  urtikaria,  demam,  takikardia,  kaku otot. Reaksi ringan diatasi dengan pemberian antipiretik, antihistamin atau kortikosteroid, dan pemberian transfusi dengan tetesan diperlambat.

Reaksi sedang-berat biasanya disebabkan oleh hipersensitivitas sedang-berat, demam akibat reaksi transfusi non-hemolitik (antibodi terhadap leukosit, protein, trombosit), kontaminasi pirogen dan/atau bakteri.

Pada reaksi yang membahayakan nyawa ditemukan gejala gelisah, nyeri dada, nyeri di  sekitar tempat masuknya  infus, napas pendek, nyeri punggung, nyeri kepala, dan dispnea. Terdapat pula tanda-tanda kaku otot, demam, lemah, hipotensi (turun ≥20% tekanan darah sistolik), takikardia (naik ≥20%), hemoglobinuria dan perdarahan yang tidak jelas. Reaksi ini disebabkan oleh hemolisis intravaskular akut, kontaminasi bakteri, syok septik, kelebihan cairan, anafilaksis dan gagal paru akut akibat transfusi.

Hemolisis intravaskular akut

Reaksi hemolisis intravaskular akut adalah reaksi yang disebabkan inkompatibilitas sel darah merah. Antibodi dalam plasma pasien akan melisiskan sel darah merah yang inkompatibel. Meskipun volume darah inkompatibel hanya sedikit (10-50 ml) namun sudah dapat menyebabkan reaksi berat. Semakin banyak volume darah yang inkompatibel maka akan semakin meningkatkan risiko.

Penyebab terbanyak adalah inkompatibilitas ABO. Hal ini biasanya terjadi akibat kesalahan dalam permintaan darah, pengambilan contoh darah dari pasien ke tabung yang belum diberikan label, kesalahan pemberian label pada tabung dan ketidaktelitian memeriksa identitas pasien sebelum transfusi. Selain itu penyebab lainnya adalah adanya antibodi dalam plasma pasien melawan antigen golongan darah lain (selain golongan darah ABO) dari darah yang ditransfusikan, seperti sistem Idd, Kell atau Duffy.

Jika pasien sadar, gejala dan tanda biasanya timbul dalam beberapa menit awal transfusi, kadang-kadang timbul jika telah diberikan kurang dari 10 ml. Jika pasien tidak sadar atau dalam anestesia, hipotensi atau perdarahan yang tidak terkontrol mungkin merupakan satu-satunya tanda inkompatibilitas transfusi. Pengawasan pasien dilakukan sejak awal transfusi dari setiap unit darah.

Kelebihan cairan

Kelebihan cairan menyebabkan gagal jantung dan edema paru. Hal ini dapat terjadi bila terlalu banyak cairan yang ditransfusikan, transfusi terlalu cepat, atau penurunan fungsi ginjal. Kelebihan cairan terutama terjadi pada pasien dengan anemia kronik dan memiliki penyakit dasar kardiovaskular.

Reaksi anafilaksis

Risiko meningkat sesuai dengan kecepatan transfusi. Sitokin dalam plasma merupakan salah satu penyebab bronkokonstriksi dan vasokonstriksi pada resipien tertentu. Selain itu, defisiensi IgA dapat menyebabkan reaksi anafilaksis sangat berat. Hal itu dapat disebabkan produk darah yang banyak mengandung IgA. Reaksi ini terjadi dalam beberapa menit awal transfusi dan ditandai dengan syok (kolaps kardiovaskular), distress pernapasan dan tanpa demam. Anafilaksis dapat berakibat fatal bila tidak ditangani dengan cepat dan agresif dengan antihistamin dan adrenalin.

Cedera paru akut akibat transfusi (Transfusion-associated acute lung injury = TRALI)

Cedera paru akut disebabkan oleh plasma donor yang mengandung antibodi yang melawan leukosit pasien. Kegagalan fungsi paru biasanya timbul dalam 1-4 jam sejak awal transfusi, dengan gambaran foto toraks kesuraman yang difus. Tidak ada terapi spesifik, namun diperlukan bantuan pernapasan di ruang rawat intensif.

2. Reaksi Lambat

Reaksi hemolitik lambat

Reaksi hemolitik lambat timbul 5-10 hari setelah transfusi dengan gejala dan tanda demam, anemia, ikterik dan hemoglobinuria. Reaksi hemolitik lambat yang berat dan mengancam nyawa disertai syok, gagal ginjal dan DIC jarang terjadi. Pencegahan dilakukan dengan pemeriksaan laboratorium antibodi sel darah merah dalam plasma pasien dan pemilihan sel darah kompatibel dengan antibodi tersebut.

Purpura pasca transfusi

Purpura pasca transfusi merupakan komplikasi yang jarang tetapi potensial membahayakan pada transfusi sel darah merah atau trombosit. Hal ini disebabkan adanya antibodi langsung yang melawan antigen spesifik trombosit pada resipien. Lebih banyak terjadi pada wanita. Gejala dan tanda yang timbul adalah perdarahan dan adanya trombositopenia berat akut 5-10 hari setelah transfusi yang biasanya terjadi bila hitung trombosit <100.000/uL. Penatalaksanaan penting terutama bila hitung trombosit ≤50.000/uL dan perdarahan yang tidak terlihat dengan hitung trombosit 20.000/uL. Pencegahan dilakukan dengan memberikan trombosit yang kompatibel dengan antibodi pasien.

Penyakit graft-versus-host

Komplikasi ini jarang terjadi namun potensial membahayakan. Biasanya terjadi pada pasien imunodefisiensi, terutama pasien dengan transplantasi sumsum tulang; dan pasien imunokompeten yang diberi transfusi dari individu yang memiliki tipe jaringan kompatibel (HLA: human leucocyte antigen), biasanya yang memiliki hubungan darah. Gejala dan tanda, seperti demam, rash kulit dan deskuamasi, diare, hepatitis, pansitopenia, biasanya timbul 10-12 hari setelah transfusi. Tidak ada terapi spesifik, terapi hanya bersifat suportif.

Kelebihan besi

Pasien yang bergantung pada transfusi berulang dalam jangka waktu panjang akan  mengalami akumulasi besi dalam tubuhnya (hemosiderosis). Biasanya ditandai dengan gagal organ (jantung dan hati). Tidak ada mekanisme fisiologis untuk menghilangkan kelebihan besi. Obat pengikat besi seperti desferioksamin, diberikan untuk meminimalkan akumulasi besi dan mempertahankan kadar serum feritin <2.000 mg/l.


Infeksi yang berisiko terjadi akibat transfusi adalah Hepatitis B dan C, HIV, CMV, malaria, sifilis, bruselosis, tripanosomiasis)


WHO. The clinical use of blood: handbook. Geneva, 2002. Didapat dari URL:

HTA. Transfusi Komponen Darah: Indikasi dan Skrining. Jakarta, 2003.


Dr. Rahajeng

Filed under: miscelaneous, , , ,

Penggunaan Rasional Antibiotika Pada Pasien PPOK

Oleh: Dr. Rahajeng N. Tunjung


PPOK adalah penyakit yang menyebabkan kematian tertinggi ke-4 di Amerika Serikat. Diperkirakan bahwa morbiditas dan mortalitas akan terus meningkat. Diperkirakan 12 juta orang di AS didiagnosis dengan PPOK sementara 12 juta lainnya memiliki PPOK yang tidak terdiagnosis. Pada tahun 2003, PPOK di AS menyebabkan 15,4 juta kunjungan dokter ke rumah, dan pada tahun 2007, biaya tahunan total diperkirakan melebihi 42,6 juta dolar. Biaya ini lebih rendah dari keadaan sebenarnya karena tidak memperhitungkan biaya akibat penyakit yang tidak terdiagnosis maupun komorbiditas. PPOK menimbulkan beban kesehatan, sosial dan ekonomi yang besar. Hal ini dapat disebabkan karena kurangnya kesadaran mengenai penatalaksanaan yang tepat oleh dokter umum.[1]

Walaupun telah tersedia pedoman penatalaksanaan evidence-based, penelitian menunjukkan bahwa kesadaran dan pemahaman akan PPOK khususnya diantara dokter umum masih rendah. Penelitian yang dilakukan Tsagaraki et al menemukan bahwa walaupun pedoman penatalaksanaan PPOK telah tersedia, spesialis cenderung untuk mengikuti pedoman tersebut sementara dokter umum tidak. Hal ini dapat menyebabkan tingginya angka PPOK di masyarakat yang tidak terdiagnosis maupun yang tidak diobati, khususnya pada tahap awal di mana intervensi dini akan lebih menguntungkan.[2]


PPOK ditandai dengan pembatasan aliran udara dalam paru yang reversibel dan progresif. Berdasarkan Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2008, PPOK adalah penyakit yang dapat dicegah dan diobati dengan efek ekstrapulmoner yang signifikan yang dapat menyebabkan berbagai derajat keparahan pada tiap pasien. Komponen pulmonernya ditandai dengan pembatasan aliran udara yang tidak sepenuhnya reversibel. Pembatasan aliran udara biasanya progresif dan dihubungkan dengan  adanya respon inflamasi abnormal paru terhadap partikel noksius dan gas (‘COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles and gases’)1.

PPOK adalah penyakit yang progresif dan berkelanjutan, tidak ada tanda khusus pada tahap awal penyakit. Pada tahap selanjutnya, gejala dapat berkurang namun tidak sepenuhnya reversibel. PPOK biasanya terjadi akibat paparan yang lama terhadap partikel iritan di mana fungsi protektif dan perbaikan dari paru tidak optimal. Bukti-bukti menunjukkan bahwa rokok berefek toksik terhadap sel-sel di paru dan mengganggu mekanisme perbaikan jaringan paru. Namun tidak semua kasus PPOK disebabkan oleh rokok dan tidak semua perokok akan menderita PPOK. Paparan jangka panjang terhadap debu dan zat kimia, polusi dalam ruangan dari akibat asap kompor, serta polusi luar ruangan meningkatkan risiko terhadap PPOK1,2,[3].

PPOK dihubungkan dengan adanya komponen inflamasi di mana kaskade inflamasi menyebabkan kerusakan jaringan yang timbul pada penyakit ini. Inflamasi pada saluran napas pasien PPOK serupa dengan inflamasi yang terjadi pada saluran napas perokok yang tidak menderita PPOK namun jauh lebih berat2,3.

Inflamasi dan kerusakan jaringan paru pada PPOK ditemukan di jalan napas proksimal dan perifer, parenkim paru dan vaskuler paru. Ketidakseimbangan antara perbaikan paru dan mekanisme pertahanan diri menyebabkan fibrosis jalan napas perifer. Adanya kerusakan jalan napas menyebabkan terjadinya mekanisme perbaikan yang mengembalikan jaringan ke fungsi normal atau yang mendekati normal. Adanya kerusakan jaringan parenkim paru menyebabkan emfisema yang ditandai dengan melebarnya alveoli dan rusaknya struktur bronkiolus. Adanya perubahan struktur ini menyebabkan meningkatkan tahanan di jalan napas perifer, menyebabkan terjadinya obstruksi. Adanya edema dan hipersekresi mukus selanjutnya memperberat penyempitan jalan napas2.

Dengan makin progresifnya PPOK, perubahan patologis yang terus-menerus menyebabkan sesak yang makin berat, pada awalnya hanya saat pasien beraktivitas dan selanjutnya bahkan saat istirahat. Hipersekresi mukus dan disfungsi silia menyebabkan batuk produktif dengan sputum mukoid, lebih sering di pagi hari. selanjutnya terjadi hiperinflasi paru, pertukaran gas abnormal, hipertensi pulmonal, dan cor pulmonale. Hiperinflasi terjadi akibat ketidakseimbangan volume udara saat inhalasi dan ekshalasi. Pada pasien PPOK ekshalasi memanjang karena adanya hiperinflasi paru3.


Keluhan yang dapat timbul adalah sesak napas yang progresif, terus-menerus dan lebih berat dengan aktivitas. Batuk kronis dapat terjadi intermiten maupun tidak produktif. Sputum produktif dan faktor risiko (+) seperti merokok, iritasi gas dan asap pembakaran, juga menandakan adanya PPOK. PPOK ringan dapat timbul tanpa gejala. Anamnesis berupa riwayat paparan terhadap faktor risiko, riwayat penyakit sebelumnya, riwayat keluarga PPOK, riwayat eksaserbasi dan perawatan di RS sebelumnya, komorbiditas, dampak penyakit terhadap aktivitas.

Pemeriksaan fisik didapatkan:

–       Pernapasan pursed lips

–       Takipnea

–       Dada emfisematous atau barrel chest

–       Tampilan fisik blue boater atau pink puffer

–       Bunyi napas vesikuler melemah

–       Ekspirasi memanjang

–       Ronki kering atau wheezing

–       Bunyi jantung jauh

Diagnosis pasti dengan uji spirometri

–       FEV1/FVC < 70%

–       Uji bronkodilator: FEV1 pasca bronkodilator <80% prediksi

Analisis gas darah dilakukan pada pasien dengan gagal napas atau payah jantung kanan.

Pada PPOK dengan eksaserbasi akut didapatkan sesak napas yang lebih berat, kadang disertai mengi, bertambahnya batuk dan sputum, serta sputum lebih purulen atau berubah warna. Bisa didapatkan gejala non-spesifik seperti malaise, insomnia, fatigue, depresi. Pada uji spirometri didapatkan fungsi paru sangat menurun.


Tabel di atas menggambarkan bahwa gejala pada umumnya muncul hanya setelah terjadinya penurunan FEV1 (forced expiratory volume in one second). Gejala makin berat dengan semakin menurunnya fungsi paru3.

PPOK Dengan Eksaserbasi Akut

Eksaserbasi akut PPOK adalah peristiwa di mana pada perjalanan penyakit terdapat perubahan dalam beratnya sesak, batuk dan produksi sputum yang melebihi variasi harian, memiliki onset akut, dan membutuhkan pengobatan yang berbeda dari obat-obatan yang biasa digunakan oleh pasien PPOK (GOLD, 2008)1.

Penyebab paling sering dari eksaserbasi akut adalah infeksi trakeobronkial dan polusi udara. Penelitian dengan menggunakan data dari kultur sputum serta serologis menunjukkan bahwa 50% kejadian eksaserbasi akut disebabkan infeksi1,[5].



Infeksi bakteri menimbulkan perubahan jalan napas dan inflamasi sistemik yang menyebabkan peningkatan beratnya gejala PPOK. Respon inflamasi akan meningkatkan aktivitas enzim proteolitik yang jika berlanjut akan memperberat PPOK, menyebabkan cedera epitel jalan napas dan mengganggu mekanisme imun paru-paru. Gangguan mekanisme imun selanjutnya dapat mempermudah terjadinya kolonisasi bakteri5.

Penilaian derajat eksaserbasi dapat dilakukan dengan pemeriksaan1:

–       X foto thoraks: dapat membedakan dengan penyakit lain dengan gejala yang sama

–       EKG: membantu diagnosis hipertrofi ventrikel kiri, aritmia, dan iskemi miokard.

–       Pemeriksaan lain:

  • Kultur sputum dan uji sensitivitas antibiotik
  • Pemeriksaan elektrolit dan gula darah


PPOK Onset usia 40 tahun ke atasGejala progresifRiwayat merokok/terpapar faktor risiko

Sesak saat beraktivitas

Keterbatasan aliran udara yang irreversibel

Asma Onset pada masa anak-anakGejala hilang timbul

Gejala terutama di malam/pagi hari

Terdapat alergi, rhinitiis, dermatitis

RPK asma

Keterbatasan aliran udara yang reversibel

Gagal jantung kongestif Ronki basah halus di basal paruX foto thoraks: jantung melebar, edema paru
Bronkiektasis Sputum dalam jumlah besarBerhubungan dengan infeksi bakteriRonki kasar pada auskultasi

X foto thoraks menunjukkan dilatasi dan penebalan dinding bronkus

Tuberkulosis Onset pada semua usiaX foto thoraks menunjukkan infiltrat atau lesi noduler

Diagnosis: pemeriksaan mikrobiologis


Tujuan pengobatan PPOK adalah untuk1,2,3:

–       Meredakan gejala

–       Mencegah progresifitas penyakit

–       Meningkatkan toleransi terhadap aktivitas

–       Memperbaiki status kesehatan

–       Mencegah dan mengobati komplikasi

–       Mencegah dan mengobati eksaserbasi

–       Mengurangi mortalitas

–       Mencegah efek samping pengobatan

Tujuan ini dapat dicapai dengan1:

  1. Melakukan monitoring penyakit
  2. Mengurangi faktor risiko
  3. Menangani PPOK stabil
  4. Menangani eksaserbasi

Terapi PPOK Stabil3,4

Terapi Farmakologis

  1. Bronkodilator
  • Diberikan secara inhalasi
  • Dapat diberikan rutin untuk mencegah gejala timbul/memburuk, atau secara intermiten untuk meredakan gejala.
  • 3 Golongan:
    • Agonis beta-2: fenopterol, salbutamol, albuterol, terbutalin, salmeterol
    • Antikolinergik: ipratropium bromid, oksitroprium bromid
    • Metilxantin: teofilin lepas lambat bila β-2 dan steroid belum memuaskan.

Dianjurkan menggunakan kombinasi daripada meningkatkan dosis monoterapi.


2. Steroid pada:

–       PPOK yang menunjukkan respon uji steroid

–       PPOK stadium IIB dan III

–       PPOK dengan eksaserbasi akut

3. Obat-obatan lain:

  • Mukolitik: ambroxol, karbosistein
  • Antioksidan: N-asetil-sistein
  • Imunoregulator: tidak rutin
  • Antitusif: tidak rutin
  • Vaksinasi: influenza, pneumokok

Terapi non-farmakologis

  1. Rehabilitasi: latihan fisik, latihan ketahanan, latihan pernapasan, rehabilitasi psikososial
  2. Terapi oksigen jangka panjang (>15 jam sehari): pada PPOK stadium III

–       PaO2 < 55 mmHg atau SaO2 < 88% dengan/tanpa hiperkapnia

–       PaO2 55-60 mmHg atau Sa02 < 88% dengan hipertensi pulmonal, edema perifer karena gagal jantung, polisitemia.

  1. Nutrisi
  2. Pembedahan: pada PPOK berat (bila dapat memperbaiki fungsi paru atau gerakan mekanik paru).

Komponen terapi PPOK meliputi perawatan kesehatan, terapi medikamentosa dan suplemental. Karena pasien dengan penurunan fungsi paru bisa saja asimtomatis, maka uji spirometri dilakukan untuk mengetahui penurunan fungsi paru asimtomatis pada pasien dengan faktor risiko. Terapi dimulai jika terdapat penurunan fungsi paru, dengan atau tanpa adanya gejala. Kebiasaan merokok harus dihentikan pada semua pasien3.

Pasien pada awalnya hanya akan mendapatkan terapi sesuai keperluan, berupa monoterapi dengan antikolinergik atau β-agonis. Untuk pasien dengan sakit sedang-berat atau untuk pasien dengan gejala persisten atau memburuk diberikan bronkodilator long-acting (antikolinergik atau β-agonis) dengan jadwal teratur, atau kombinasi antikolinergik dengan β-agonis.

Pada pasien dengan bronkodilator long-acting, agen short-acting harus diberikan bersamaan untuk mengatasi gejala akut (lihat kotak dengan garis putus-putus). Diberikannya rehabilitasi paru akan mengurangi gejala dan meningkatkan toleransi aktivitas. Penambahan teofilin atau kortikosteroid inhalasi untuk mengoptimalkan terapi bronkodilator dapat menambah manfaat terapi. Pasien sakit sedang atau berat perlu diperiksa untuk kemungkinan adanya hipoksemia yang harus ditangani dengan agresif apabila ada. Pembedahan untuk mengurang volume paru dan transplantasi adalah pilihan untuk kelompok dengan penyakit yang sangat berat.

Terapi PPOK Eksaserbasi Akut

Indikasi rawat inap pada pasien eksaserbasi adalah1:

–       Gejala memburuk dengan cepat

–       PPOK berat

–       Terdapat tanda yang baru muncul (edema perifer, sianosis)

–       Penyakit komorbid yang signifikan

–       Eksaserbasi yang sering timbul

–       Aritmia

–       Usia tua

Antibiotik diberikan pada pasien1:

–       Dengan 3 gejala utama berupa sesak yang bertambah berat, sputum yang bertambah banyak, atau sputum yang lebih purulen.

–       Dengan sputum yang lebih purulen dan gejala lain.

–       Dengan pasien yang membutuhkan ventilasi mekanik.


Penatalaksanaan PPOK eksaserbasi akut di rumah1:

–       Bronkodilator seperti pada PPOK stabil, 4-6kali/hari, 2-4 hirup/kali.

–       Steroid oral dapat diberikan 10-14 hari.

–       Bila terdapat infeksi diberikan antibiotik spektrum luas (termasuk S. pneumonia, H. influenzae, M. catarrhalis).

Terapi PPOK eksaserbasi akut di rumah sakit1,4,5,[6]:

–       Terapi oksigen terkontrol

–       Bronkodilator, inhalasi agonis β-2 (dosis dan frekuensi ditingkatkan) + antikolinergik.

–       Pada eksaserbasi akut berat: ditambahkan aminofilin (0,5 mg/kgBB/jam)

–       Steroid: prednisolon 30-40 mg PO selama 10-14 hari.

Steroid intravena diberikan dalam keadaan berat.

–       Antibiotika pada infeksi

–       Ventilasi mekanik pada gagal napas.

Terapi awal berupa suplementasi oksigen agar kadar saturasi mencapai 90-92%. Terapi kombinasi bronkodilator tiap 4-6 jam. Nebulizer direkomendasikan jika diperkirakan tingkat distres pasien dapat mengurangi efektivitas pemakaian inhaler. Jika kondisi membaik, inhaler dapat digunakan untuk menggantikan nebulizer. Berdasarkan data dari randomized trial, penggunaan antibiotik spektrum sempit (trimeptoprim-sulfamethoxazole, doksisiklin, atau amoksisilin) diberikan selama 10 hari jika didapat peningkatan sesak, jumlah maupun purulensi sputum. Kultur dan pengecatan sputum dilakukan pada kasus yang refrakter terhadap terapi antibiotik oral. Steroid sistemik diberikan dengan dosis awal 40 mg dengan penurunan dosis 10 mg tiap 2 hari selama 8 hari. Kurangnya bukti mengenai mukolitik menyebabkan obat ini tidak digunakan secara rutin6.

Setelah pasien dipulangkan dari rumah sakit, pasien perlu mendapat edukasi untuk menghindari faktor risiko, menghentikan kebiasaan merokok, dan kontrol ke rumah sakit1.


Terdapat beberapa pedoman tatalaksana yang terangkum dalam bagan di bawah. Kebanyakan menganjurkan terapi singkat kortikosteroid sistemik dan antibiotik untuk eksaserbasi berat, serta penggunaan ventilator mekanik untuk eksaserbasi dengan gagal napas.

Berbeda dengan beberapa pedoman lain, GOLD memilih pemakaian β-agonis sebagai bronkodilator lini pertama, merekomendasikan penambahan antikolinergik jika tidak ada respon terhadap β-agonis, serta menyarankan pemakaian golongan metilxantin6.

[1] Global Initiative for Chronic Obstructive Lung Disease (GOLD). Pocket Guide to COPD Diagnosis, Treatment and Management 2008.

[2] Fromer L. Cooper C. A Review of the GOLD Guidelines for the Diagnosis and Treatment of Patients With COPD.

[3]Sutherland ER, Cherniack RM. Management of Chronic Obstructive Pulmonary Disease. N Engl J Med 2004;350:2689-97.

[4] PAPDI. Standar Pelayanan Medik.


[6] Stoller JK. Acute Exacerbations of Chronic Obstructive Pulmonary Disease. N Engl J Med, Vol. 346, No. 13.

[vii] August, P. Initial Treatment of Hypertension. N Engl J Med 2003;348:610-7.

[viii] NIH. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. August 2004.

[ix] Dart A et al. Treatment of systemic hypertension in asthma patients with pulmonary disease: COPD and asthma. Chest 2003;123;222-243


Gambar dan bagan pada tinjauan pustaka ini adalah milik New England Journal of Medicine

Pictures and charts in this article belongs to New England Journal of Medicine.

Filed under: miscelaneous, , , , ,

Seorang laki-laki dengan PPOK eksaserbasi akut dan Hipertensi stage 2



Nama                               : Tn. A

Umur                                : 63 tahun

Jenis kelamin                   : Laki-laki

Agama                             : Islam

Alamat                             : Desa Tanggul  Rt /Rw 004/001 Jepara

Masuk RS                        : 26 Desember 2008



Masalah Aktif



Masalah Pasif



Penyakit paru obstruktif kronik



Hipertensi stage 2



1. Anamnesis

Autoanamnesis dengan penderita di bangsal Anggrek pada tanggal 27 Desember 2008 pukul 11.00 WIB

  • Keluhan Utama : sesak
  • Riwayat Penyakit Sekarang :

–          1 minggu sebelum masuk RSUD Kartini penderita batuk (+), dahak warna putih, panas (-).

–          3 hari sebelum masuk RS penderita mengeluh batuk (+), dahak kental warna kekuningan, panas (-). Penderita merasa tubuh lemas.

–          1 hari sebelum masuk RS penderita mengeluh sesak terus-menerus, namun tidak mengganggu aktivitas. Dahak semakin banyak, kental, warna kuning. Panas (+).

Keringat malam hari (-), batuk darah (-), nyeri dada (-), dada berdebar-debar (-), mual (-), muntah (-), BAK dan BAB tidak ada keluhan.

–          ± 8 jam sebelum masuk RSUD Kartini, penderita mengeluh sesak nafas, dirasakan makin bertambah dan mengganggu aktivitas. Sesak makin berat dengan aktivitas.

–          Riwayat kaki bengkak (-), terbangun di malam hari karena sesak (-).

–          Riwayat kontak dengan penderita dengan batuk lama (+), yaitu adik penderita.

–          Riwayat merokok (+) 1 pak/hari, berhenti 6 tahun yang lalu.

  • Riwayat Penyakit Dahulu
    • Riwayat dirawat di RS (+) tahun 2007 karena sesak. Penderita dirawat kurang lebih 1 minggu, pulang dengan keadaan membaik.
    • Riwayat Hipertensi (+), tidak kontrol teratur
    • Riwayat Diabetes Melitus disangkal
    • Riwayat penyakit jantung disangkal
    • Riwayat asma disangkal
    • Riwayat pengobatan TB sebelumnya disangkal
  • Riwayat Penyakit Keluarga

Adik penderita yang tinggal 1 rumah, menderita batuk > 3 minggu.

  • Riwayat Sosial Ekonomi

Penderita tidak bekerja. Memiliki 4 orang anak yang sudah mandiri. Penderita tinggal 1 rumah dengan adiknya. Biaya pengobatan ditanggung ASKESKIN. Kesan sosial ekonomi : kurang.

2. Pemeriksaan fisik

Pemeriksaan fisik dilakukan tanggal  27 Desember 2008 pukul 11.15 WIB.

KU                 : sadar, tampak lemah, terpasang kanul oksigen, terpasang infus di lengan kanan bagian bawah.

Tanda Vital    : N    : 88 x / menit, isi dan tegangan cukup

T     :  170/100 mmHg

RR  :  24x / menit, reguler

t     : 38,2°C

Status Internus

BB = 46kg       PB = 162 cm     BMI= 17,6 (Underweight)

Kepala           : mesosefal, turgor dahi cukup

Rambut         : hitam, tidak mudah dicabut.

Kulit               : sianosis (-), ikterik (-).

Mata              : cekung (-), conjungtiva palpebra anemis (–/–), sklera ikterik (-/-)

Hidung           : epistaksis (-), nafas cuping (-)

Telinga           : discharge (–), nyeri tragus (-)

Mulut             :                         bibir kering (-), selaput lendir kering (-), sianosis (–)

Tenggorok     : T1-1, vaskuler injeksi (-),faring hiperemis (-),

Leher             : Deviasi trakea (-), pembesaran nnll (-/-), kaku kuduk (-/-)

Dada   : Inspeksi         : venektasi (-), barrel chest (+), sela iga melebar (+)

Paru       : Inspeksi           : simetris statis dinamis, retraksi (+), SIC melebar (+)

Palpasi            : stem fremitus kiri sama dengan kanan

Perkusi            : hipersonor seluruh lapangan paru

Auskultasi       :

Ka = SD Vesikuler menurun. Ronki kasar (+), wheezing (+), eksperium memanjang pada seluruh lapangan paru atas, tengah, bawah.


Ronki kasar +/+Wheezing +/+

Eksperium memanjang

Ronki kasar +/+Wheezing +/+

Eksperium memanjang

Jantung            :               Inspeksi             : Ictus cordis tak tampak

Palpasi            : Ictus cordis teraba di SIC V, 2 cm medial Linea midclavicularis sinistra, tidak kuat angkat, tidak melebar

Perkusi            : batas jantung kanan di linea parasternalis dx

batas jantung kiri di linea medio axillaris sinistra

Kesan konfigurasi jantung dalam batas normal

Auskultasi       : Bunyi jantung I-II normal, bising (-), gallop (-)

Abdomen                   : Inspeksi           : datar, venektasi (-)

Auskultasi       :  bising usus (+) normal

Perkusi            : timpani, pekak sisi (+)N, pekak alih (-)

Palpasi            : Hepar dan lien tak teraba, turgor kulit kembali cepat, nyeri tekan (-)

Genital           :dalam batas normal

Ekstremitas   :                  Superior                      Inferior

Sianosis                       – / –                              – / –

Akral dingin                 – / –                              – / –

Anemis                                    – / –                              – / –

Capillary refill              < 2 ”                             < 2”

  1. Pemeriksaan Penunjang

Lab. Darah (26 Desember 2008)

  1. Hb      : 11,4 g/dl                                Leuko  : 16.100 /mmk

Ht       : 31,7%                                    GDS    : 156

Trombosit : 406.000/mmk

Kesan     :  Leukositosis


Seorang laki-laki, usia 70 tahun dirawat di RSUD Kartini dengan keluhan utama sesak napas. 3 hari sebelum masuk RS penderita batuk (+), dahak kental warna kekuningan, panas (-). 1 hari sebelum masuk RS penderita mengeluh sesak terus-menerus, namun tidak mengganggu aktivitas. Karena sesak makin bertambah kemudian penderita berobat ke RSUD.

Pada pemeriksaan fisik didapatkan :



T     :  170/100 mmHg

RR  :  24x / menit, reguler

t     : 38,2°C


Palpasi            : stem fremitus kiri sama dengan kanan

Perkusi            : hipersonor seluruh lapangan paru

Auskultasi       :

Ka = SD Vesikuler, ronki kasar (+), wheezing (+), eksperium memanjang pada seluruh lapangan paru atas, tengah, bawah.


Jantung              :     tak ada kelainan

Abdomen           :     tak ada kelainan

Ekstremitas        :     tak ada kelainan

Pemeriksaaan Penunjang

Ht       : 31,7%                                    GDS    : 156

Trombosit : 406.000/mmk

Kesan     :  Leukositosis


  1. PPOK eksaserbasi akut
  2. Hipertensi stage 2


1. PPOK eksaserbasi akut

Assesment   : Mengetahui adanya infeksi sekunder

IP Dx    S     : –

O   : LED, diff count, sputum BTA 3x, X foto thoraks AP lateral

IP Tx            :  O2 3 L/m kanul

Infus asering 16 tpm + Aminofilin 1 amp/500 cc Asering

Injeksi Cefotaksim 2 x 1 gram iv

Injeksi Ranitidin 3 x 1 ampul


Salbutamol 3 x 2 mg

Ambroxol 3 x 1 tab

IP Mx           : keadaan umum, tanda vital, keluhan sesak

IP Ex            :

–          Menjelaskan pada penderita dan keluarga bahwa penderita memiliki PPOK yang sedang mengalami kekambuhan.

–          Menjelaskan pemeriksaan dan pengobatan yang akan dilakukan di RS.

–          Menjelaskan pada penderita untuk menjaga kesehatan, makan makanan dengan gizi seimbang, menghindari polusi udara dan asap rokok.

2. Hipertensi stage 2

Assesment   : Etiologi, komplikasi

IP Dx S        : –

O          : TG, Kolesterol, HDL, LDL, asam urat, GDS.

IP Tx            : Captopril 3 x 12,5 mg

IP Mx   :       Keadaan umum, tekanan darah

IP Ex     :

  • Menjelaskan bahwa penderita perlu mengkonsumsi diet kaya sayuran, buah, rendah lemak dan rendah garam.
  • Menjelaskan bahwa penderita perlu melakukan aktivitas fisik misalnya berjalan kaki setidaknya 30 menit/hari, 3x seminggu.
  • Menjelaskan bahwa penderita perlu kontrol teratur.


Pada kasus ini telah dilaporkan pria 63 tahun dengan PPOK eksaserbasi akut dan hipertensi stage II. Dasar diagnosis pada pasien ini adalah:


–       Sesak napas

–       Batuk berdahak yang makin berat 3 hari terakhir

–       Malaise

Pemeriksaan fisik

–       Kesadaran compos mentis, tampak sesak

–       Tanda vital RR = 24x/menit (takipnea)

–       Dada emfisematous

–       Suara napas vesikuler melemah

–       Ekspirasi memanjang

–       Ronki kasar dan wheezing

Pemeriksaan penunjang didapatkan leukositosis yang menandakan adanya infeksi, yang kemungkinan menyebabkan atau memperberat eksaserbasi akut dari PPOK.

Diagnosis hipertensi stage 2 didapatkan dari pemeriksaan tekanan darah yaitu 170/100 mmHg.


Prinsip pengelolaan meliputi aspek keperawatan, medikamentosa dan dietetik.

  1. Aspek keperawatan

Pasien dengan PPOK eksaserbasi akut ini dirawat inap karena terjadi eksaserbasi akut dengan perburukan gejala sesak napas dan batuk yang makin purulen. Selain itu rawat inap juga berguna untuk melakukan pengawasan dan pemeriksaan lebih lanjut.

Dilakukan tirah baring, posisi tubuh setengah duduk atau sesuai kenyaman pasien untuk bernapas, pengawasan keadaan umum, tanda vital, serta perkembangan gejala.

  1. Aspek medikamentosa

Di UGD pasien mendapat:

–       O2 3L/menit kanul

–       Nebulizer yang terdiri dari Bisolvon, Berotec, Atrovent

–       Infus Asering 16 tpm + Aminofilin 1 ampul

–       Injeksi Cefotaxim 2 x 1 gram iv

–       Injeksi Ranitidin 3 x I ampul

–       Salbutamol 3 x 1 tablet

–       Ambroksol 3 x 1 tablet

Nebulizer sebagaimana dijelaskan dalam GOLD bermanfaat jika terjadi eksaserbasi yang diperkirakan dapat mengurangi efektivitas inhaler. Pasien diberikan nebulizer dengan kombinasi Bisolvon, Berotec, Atrovent.

Aminofilin diberikan sesuai anjuran GOLD sebagai bronkodilator pada eksaserbasi akut yang berat. Sementara itu β-agonis tetap diberikan sebagai preparat oral.

Pemakaian Ambroksol sebagai mukolitik selama pasien mengalami eksaserbasi akut masih dipertanyakan, namun kegunaannya terbukti efektif untuk mengurangi eksaserbasi, meredakan gejala penderita bronkitis kronik. Efek ini kemungkinan disebabkan karena mukolitik dapat mengurangi hipersekresi, dan kemungkinan, jumlah bakteri di jalan napas. Namun peneliti masih mengingatkan bahwa mukolitik bisa jadi tidak cost-effective untuk semua pasien PPOK dan bisa jadi hanya menguntungkan pada pasien dengan penyakit berat atau eksaserbasi yang sering[i],[ii].

Pemberian antibiotik pada pasien ini sesuai indikasi berdasarkan algoritme pemberian antibiotik pada pasien PPOK. Gejala yang timbul menunjukkan bahwa pasien mengalami eksaserbasi sedang, tanpa komplikasi sehingga dapat diberikan preparat golongan Cefalosporin berupa Cefotaxim.

  1. Aspek dietetik dan edukasi

Diet yang diberikan pada penderita ini adalah 3 kali nasi. Edukasi yang diberikan mengenai PPOK adalah:

–       Anjuran untuk kontrol teratur

–       Anjuran agar pasien patuh dengan jadwal minum obat/menggunakan inhaler

–       Anjuran agar pasien menghindari faktor risiko seperti asap pembakaran, asap rumah tangga dari kompor, merokok maupun asap rokok dari perokok di sekitarnya.

Edukasi yang diberikan berhubungan dengan hipertensi adalah mempertahankan berat badan dalam rentang ideal, melakukan aktivitas fisik aerobik setidaknya 30 menit per hari, mengkonsumsi buah-buahan dan sayuran dan makanan rendah lemak, serta mengurangi asupan garam dalam makanan sehari-hari.


Prognosis untuk kehidupan (quo ad vitam) adalah ad bonam, karena tidak adanya kegawatan selama pasien berada di rumah sakit. Prognosis terhadap kesembuhan (quo ad sanam) dan fungsi (quo ad fungsionam) adalah ad bonam, dengan penanganan yang berkelanjutan untuk memperbaiki kualitas hidup pasien.

[i] White, C. Mucolytic useful for COPD, guidelines say. BMJ. 2004 February 28; 328 (7438): 486.

[ii] Marton KI. Oral Mucolytic Drugs Help with COPD. Journal Watch General Medicine, June 26, 2001.

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Regards, Rahajeng

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