SMART IMAGINATION

Detik-detik Terakhir Rasulullah SAW

Pagi itu, meskipun langit telah mulai menguning,burung-burung gurun enggan mengepakkan sayap. Pagi itu, Rasulullah dengan suara terbata memberikan petuah, “Wahai umatku, kita semua ada dalam kekuasaan Allah dan cinta kasih-Nya. Maka taati dan bertakwalah kepada-Nya. Kuwariskan dua hal pada kalian, sunnah dan Al Qur’an. Barang siapa mencintai sunnahku,bererti mencintai aku dan kelak orang-orang yang mencintaiku, akan bersama-sama masuk syurga bersama aku.”

Khutbah singkat itu diakhiri dengan pandangan mata Rasulullah yang teduh menatap sahabatnya satu persatu. Abu Bakar menatap mata itu dengan berkaca-kaca, Ummar dadanya naik turun menahan napas dan tangis nya. Uthman menghela napas panjang dan Ali menundukkan kepalanya dalam-dalam. Isyarat itu telah datang, saatnya sudah tiba." Rasulullah akan meninggalkan kita semua,” desah hati semua sahabat kala itu. Manusia tercinta itu, hampir usai menunaikan tugasnya di dunia. Tanda-tanda itu semakin kuat, tatkala Ali dan Fadhal dengan sigap menangkap Rasulullah yang limbung saat turun dari mimbar. Saat itu, seluruh sahabat yang hadir di sana pasti akan menahan detik - detik berlalu, kalau bisa.

Matahari kian tinggi, tapi pintu Rasulullah masih tertutup. Sedang di dalamnya, Rasulullah sedang terbaring lemah dengan keningnya yang berkeringat dan membasahi pelepah kurma yang menjadi alas tidurnya. Tiba-tiba dari luar pintu terdengar seorang yang berseru mengucapkan salam. “Bolehkah saya masuk?” tanyanya. Tapi Fatimah tidak mengizinkannya masuk, “Maafkanlah, ayahku sedang demam,” kata Fatimah yang membalikkan badan dan menutup pintu. Kemudian ia kembali menemani ayahnya yang ternyata sudah membuka mata dan bertanya pada Fatimah, “Siapakah itu wahai anakku?” “Tak tahulah aku ayah, sepertinya ia baru sekali ini aku melihatnya,” tutur Fatimah lembut. Lalu, Rasulullah menatap putrinya itu dengan pandangan yang menggetarkan. Satu-satu bagian wajahnya seolah hendak di kenang. “Ketahuilah, dialah yang menghapuskan kenikmatan sementara, dialah yang memisahkan pertemuan di dunia. Dialah malakul maut,” kata Rasulullah,

Fatimah pun menahan ledakkan tangisnya. Malaikat maut datang menghampiri, tapi Rasulullah menanyakan kenapa Jibril tak ikut menyertai. Kemudian dipanggilah Jibril yang sebelumnya sudah bersiap diatas langit dunia menyambut roh kekasih Allah dan penghulu dunia ini. “Jibril, jelaskan apa hakku nanti dihadapan Allah?” ,Tanya Rasululllah dengan suara yang amat lemah. “Pintu-pintu langit telah terbuka, para malaikat telah menanti rohmu. Semua syurga terbuka lebar menanti kedatanganmu,”kata jibril. Tapi itu ternyata tak membuat Rasulullah lega, matanya masih penuh kecemasan.

“Engkau tidak senang mendengar kabar ini?”Tanya Jibril lagi.”Kabarkan kepadaku bagaimana nasib umatku kelak?”. “Jangan khuawatir, wahai Rasul Allah, aku pernah mendengar Allah berfirman kepadaku: ‘Kuharamkan syurga bagi siapa saja, kecuali umat Muhammad telah berada didalamnya,” kataJibril.

Detik - detik semakin dekat, saatnya Izrail melakukan tugas. Perlahan roh Rasulullah ditarik nampak seluruh tubuh Rasulullah bersimbah peluh, urat-urat lehernya menegang. “Jibril, betapa sakit sakaratul maut ini.” Lirih Rasulullah mengaduh. Fatimah terpejam, Ali yang di sampingnya menunduk semakin dalam dan Jibril membuang muka. “Jijikkah kau melihatku, hinggakaupalingkan wajahmu Jibril?” Tanya Rasulullah pada Malaikat penghantar wahyu itu. “Siapakah yang tega, melihat kekasih Allah direnggut ajal,” kata Jibril. Sebentar kemudian terdengar Rasulullah memekik, kerana sakit yang tak tertahankan lagi. “Ya Allah, dahsyat niat maut ini, timpakan saja semua siksa maut ini kepadaku, jangan pada umatku. “

Badan Rasulullah mulai dingin, kaki dan dadanya sudah tak bergeraklagi. Bibirnya bergetar seakan hendak membisikkan sesuatu, Ali segera mendekatkan telinganya. “Uushiikum bis shalati, wa maa malakat aimanuku, peliharalah solat dan santuni orang-orang lemah di antaramu” Di luar pintu tangis mulai terdengar bersahutan, sahabat saling berpelukan. Fatimah menutupkan tangan diwajahnya, dan Ali kembali mendekatkan telinganya ke bibir Rasulullah yang mulai kebiruan. “Ummatii, ummatii, ummatiii?” – “Umatku,umatku, umatku” Dan, pupuslah kembang hidup manusia mulia itu.

Kini, mampukah kita mencintanya seperti Rosulullah mencintai kita semua? Allahumma sholli ‘ala Muhammad wa baarik wasalim ‘alaihi. wallohu’alam.

Osteoarthritis

Author: Carlos J Lozada, MD, Director of Rheumatology Fellowship Program, Associate Professor, Department of Medicine, Division of Rheumatology and Immunology, Jackson Memorial Medical Center, University of Miami School of Medicine
Coauthor(s): Eli Steigelfest, MD, Consulting Staff, Department of Rheumatology, The Consultant Group, PC
Updated: Apr 28, 2009

Introduction

Background

Osteoarthritis (OA) is the most common articular disease worldwide, affecting over 20 million individuals in the United States alone. Its high prevalence entails significant costs to society. Direct costs of osteoarthritis include clinician visits, medications, and surgical intervention. Indirect costs include such items as time lost from work. Costs associated with osteoarthritis can be particularly significant for elderly persons, who face potential loss of independence and who may need help with daily living activities. As the populations of developed nations age over the next few decades, the need for better understanding of osteoarthritis and for improved therapeutic alternatives will continue to grow.

Pathophysiology

Traditionally, osteoarthritis has been considered a disease of articular cartilage. The current concept holds that osteoarthritis involves the entire joint organ, including the subchondral bone and synovium.

Osteoarthritis has always been classified as a noninflammatory arthritis; however, increasing evidence has shown that inflammation occurs as cytokines and metalloproteinases are released into the joint. Therefore, the term degenerative joint disease is no longer appropriate when referring to osteoarthritis.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hands.

Cartilage is grossly affected. Focal ulcerations eventually lead to cartilage loss and eburnation. Subchondral bone formation also occurs, with development of bony osteophytes.

Frequency

United States

Osteoarthritis affects over 20 million individuals in the United States. Based on the radiologic definition of osteoarthritis, more than half of adults older than 65 years are affected.

International

Osteoarthritis is the most common articular disease. Estimates vary among different populations.

Mortality/Morbidity

• The disease progression of osteoarthritis is characteristically slow, occurring over several years or decades.
• Pain is usually the initial and principal source of morbidity in osteoarthritis. The patient can become progressively less active, leading to morbidities related to decreasing physical activity (including potential weight gain).

Race

The prevalence of osteoarthritis differs among different ethnic groups. Knee osteoarthritis appears to be more common in African American women than in other groups.

Sex

• The likelihood of developing osteoarthritis increases with age. The disease is equally common among men and women aged 45-55 years. After age 55 years, the disease becomes more common in women.
• DIP and PIP joint involvement that results in Heberden and Bouchard nodes is more common in women.

Age

• Osteoarthritis can be defined epidemiologically (ie, using radiographic criteria) or clinically (eg, radiography findings plus clinical symptoms). Based on radiographic criteria, osteoarthritis occurs in 30% of affected individuals aged 45-65 years and in more than 80% by their eighth decade of life, although most are asymptomatic.

Clinical

History

• Pain
• Pain is the main reason persons with osteoarthritis (OA) seek medical attention.
• Initially, symptomatic patients incur pain during activity, which can be relieved by rest and may respond to simple analgesics.
• Morning joint stiffness usually lasts for less than 30 minutes.
• Stiffness during rest (gelling) may develop.
• Joints may become unstable as the osteoarthritis progresses; therefore, the pain may become more prominent (even during rest) and may not respond to medications.

Physical

• Physical examination findings are mostly limited to the affected joints.
• Malalignment with a bony enlargement (depending on the disease severity) may occur.
• Most cases of osteoarthritis do not involve erythema or warmth over the affected joint(s); however, an effusion may be present.
• Limitation of joint motion or muscle atrophy around a more severely affected joint may occur.
• Sources of pain in osteoarthritis include the following:
• Joint effusion and stretching of the joint capsule
• Increased vascular pressure in subchondral bone
• Torn menisci
• Inflammation of periarticular bursae
• Periarticular muscle spasm
• Psychological factors
• Crepitus (a rough or crunchy sensation) may be palpated during motion of an involved joint.

Causes

• Risk factors of osteoarthritis include the following:
• Increasing age
• Obesity
• Female sex
• Trauma
• Infection
• Repetitive occupational trauma
• Genetic factors
• History of inflammatory arthritis
• Neuromuscular disorder
• Metabolic disorder
• The etiopathogenesis of osteoarthritis has been divided into the following 3 stages:
• Stage 1: Proteolytic breakdown of the cartilage matrix occurs. Chondrocyte metabolism is affected, leading to an increased production of enzymes, which includes metalloproteinases (eg, collagenase, stromelysin) that destroy the cartilage matrix. Chondrocytes also produce protease inhibitors, including tissue inhibitors of metalloproteinases (TIMP) 1 and 2 but in amounts insufficient to counteract the proteolytic effect.
• Stage 2: This stage involves the fibrillation and erosion of the cartilage surface, with a subsequent release of proteoglycan and collagen fragments into the synovial fluid.
• Stage 3: The breakdown products of cartilage induce a chronic inflammatory response in the synovium. Synovial macrophage production of cytokines, such as interleukin 1 (IL-1), tumor necrosis factor-alpha, and metalloproteinases, occurs. These can diffuse back into the cartilage and directly destroy tissue or stimulate chondrocytes to produce more metalloproteinases. Other pro-inflammatory molecules (eg, nitric oxide [NO], an inorganic free radical) may also be a factor. Eventually, these events alter the joint architecture, and compensatory bone overgrowth occurs in an attempt to stabilize the joint. As the joint architecture is changed and further mechanical and inflammatory stress occurs on the articular surfaces, the disease progresses unchecked.

Differential Diagnoses

Rhinosporidiosis

Other Problems to Be Considered

Osteoarthritis (OA) can usually be diagnosed on clinical grounds. The history and physical examination findings are sufficient. Radiographic findings confirm the initial impression (see Imaging Studies), and laboratory values are typically within the reference range. The initial goal is to differentiate osteoarthritis from other arthritides (eg, rheumatoid arthritis).

Rheumatoid arthritis predominately affects the wrists and the metacarpophalangeal (MCP) and PIP joints. Rheumatoid arthritis rarely, if ever, involves the DIP joints or lumbosacral spine. Rheumatoid arthritis is associated with prominent prolonged (>1 h) morning stiffness. Radiographic findings of rheumatoid arthritis include bone erosion (eg, periarticular osteopenia, marginal erosions of bone) rather than formation. Laboratory findings that further differentiate rheumatoid arthritis include systemic inflammation, positive rheumatoid factor results, joint fluid with polymorphonuclear cell predominance, and a substantially elevated WBC count.

Clinical history and characteristic radiographic findings can be used to differentiate spondyloarthropathy from sacroiliac and lumbosacral spine involvement.

Secondary osteoarthritis must be considered in individuals with chondrocalcinosis, joint trauma, metabolic bone disorders, hypermobility syndromes, and neuropathic diseases.

Reactive arthritis is another problem that may be considered.

Workup

Laboratory Studies

• No specific laboratory abnormalities are associated with osteoarthritis (OA).
• Levels of acute-phase reactants and erythrocyte sedimentation rate are within the reference range.
• Synovial fluid analysis usually indicates a WBC count below 2000/µL with a mononuclear predominance.

Imaging Studies

• Radiography
• Conduct imaging studies of the affected joint.
• The presence of osteophytes (ie, spurs at the joint margins) is the most characteristic findings.
• Other findings in osteoarthritis include asymmetric joint-space narrowing, subchondral sclerosis, and subchondral cyst formation.
• Roentgenographic findings are often poor predictors of the degree of symptomatology in a particular patient.

Procedures

Arthrocentesis of the affected joint can help exclude inflammatory arthritis, infection, and/or crystal arthropathy.

Histologic Findings

Histologically, the earliest changes occur in the cartilage. Proteoglycan staining is diminished, and, eventually, irregularity of the articular surface with clefts and erosions occurs.

Treatment

Medical Care

Nonpharmacologic interventions are the cornerstones of osteoarthritis (OA) therapy and include patient education, temperature modalities, weight loss,¹ exercise, physical therapy, occupational therapy, and joint unloading in certain joints (eg, knee, hip).

• Reduction of joint stress
• Instruct the patient to avoid aggravating stress to the affected joint.
• Implement correction procedures if the patient illustrates poor posture.
• Encourage obese patients to lose weight, thus relieving stress on the affected knees or hips.
• Occupational adjustments may be necessary.
• Physical therapy
• Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. These muscles help protect the articular cartilage from further stress.
• Instruct the patient to perform aerobic and muscle-strengthening exercises.
• Chaipinyo and Karoonsupcharoen (2009) found no significant difference between home-based strength training and home-based balance training for knee pain caused by osteoarthritis. However, more improvement was noted in the strength group in terms of knee-related quality of life (improved 17 points out of 100 [95% CI, 5-28] more than the balance group).²
• Hydrotherapy may be beneficial.
• Some patients with osteoarthritis benefit from heat and capsaicin cream placed locally over the affected joint, and a minority of patients report relief with ice.³
• Pharmacologic therapy
• The goals of osteoarthritis treatment include pain alleviation and improvement of functional status. Presently, no practical medication-based disease or structure-modifying intervention has been proven.
• Begin treatment with acetaminophen for mild or moderate pain without apparent inflammation.
• If the clinical response to acetaminophen is not satisfactory or if the clinical presentation is inflammatory, consider nonsteroidal anti-inflammatory drug (NSAIDs). Use the lowest effective dose or intermittent dosing if symptoms are intermittent and then try full doses if the patient's response is insufficient.
• Options in patients at an elevated risk for GI toxicity due to NSAIDs include the addition of a proton-pump inhibitor or misoprostol to the treatment regimen or the use of a selective cyclooxygenase inhibitor instead of the nonselective NSAID.
• In patients with highly resistant pain, consider the analgesic tramadol.
• Muscle relaxants may benefit patients with evidence of muscle spasm.
• Contemplate intra-articular injections of glucocorticoids to improve symptoms. No more than 4 glucocorticoid injections should be administered to a single joint per year because of the risk of long-term damage to cartilage. Systemic glucocorticoids have no role in the management of osteoarthritis. Intra-articular injections of hyaluronic acid (HA) are approved as symptomatic therapy of osteoarthritis in the knee. Prescribe as a series of 3 or 5 injections (depending on the product). Each injection is administered one week apart.
• Judicious use of narcotics (eg, acetaminophen with codeine) is reserved for patients with severe osteoarthritis.

Surgical Care

• Joint lavage: Closed-needle joint lavage may benefit a small subgroup of patients with osteoarthritis.
• Arthroscopy: Arthroscopy may help patients with osteoarthritis of the knee that in whom imaging reveals specific structural damage (eg, for repairing meniscal tears, removing fragments of torn menisci that are producing symptoms). Overall, arthroscopy is not recommended for nonspecific "cleaning of the knee" in osteoarthritis.
• Osteotomy
• Consider this procedure in patients with a malaligned hip or knee joint.
• The procedure is usually recommended in younger patients with osteoarthritis.
• Osteotomy can lessen the pain, although it can lead to more challenging surgery later if the patient requires arthroplasty.
• Arthroplasty
• Perform this procedure if all other modalities are ineffective and osteotomy is not viable or if a patient cannot perform his or her daily activities despite maximal therapy.
• This procedure alleviates pain and may improve function. Approximately 8-15 years of viability are expected from the joint replacement in the absence of complications.

Consultations

• A physiatrist may help in formulating a nonpharmacologic management plan.
• A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan.
• A nutritionist may help the patient lose weight.

Diet

A diet to achieve some degree of weight loss may be beneficial.

Activity

Osteoarthritis may severely hinder the patient's ability to work or even to perform daily living activities, depending on the joints involved and the degree of involvement.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Pay careful attention to a particular pharmacologic regimen's adverse-event profile.

Analgesic agents

Pain control is essential in the management of osteoarthritis (OA). The goals of treatment include pain alleviation and improvement of functional status. Currently, disease/structure-modifying intervention has been proven

Acetaminophen (Tylenol, Panadol, Aspirin-Free Anacin)

Initial trial warranted in patients with mild-to-moderate symptoms from osteoarthritis who fail to get sufficient relief with nonpharmacologic measures. DOC for patients with documented hypersensitivity to aspirin or NSAIDs, history of upper GI disease, or on anticoagulants.

Adult

1000 mg PO tid/qid; not to exceed 4 g/d

Pediatric

Disease state not seen in pediatrics

Rifampin may reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Documented hypersensitivity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity can occur with various dose levels in persons with chronic alcoholism; severe or recurrent pain or high or continued fever may indicate a serious illness; contained in many OTC products, and combined use with these products may result in cumulative doses exceeding recommended maximum dose/d

Nonsteroidal anti-inflammatory drugs (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. They are used for to relieve osteoarthritis pain when the clinical response is unsatisfactory to acetaminophen. The mechanism of action is nonselective inhibition of cyclooxygenases 1 and 2, resulting in reduced synthesis of prostaglandins and thromboxanes. Other mechanisms may also exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

In more inflammatory presentations of osteoarthritis, such as knee involvement with effusion, these agents may be used as first-line pharmacologic therapy.

Use the lowest effective dose or intermittent therapy if symptoms are intermittent.

Patients at high risk for GI toxicity may consider adding misoprostol or a proton pump inhibitor to the regimen or substituting a COX-2–specific inhibitor for the NSAID.

Ibuprofen (Ibuprin, Advil, Motrin)

Relieves pain and inflammation. Widely available. Relatively inexpensive as a generic drug.

Adult

400 mg PO tid prn; not to exceed 2400 mg/d

Pediatric

Disease state not seen in pediatrics

May decrease effects of loop diuretics; coadministration of anticoagulants may increase PT (monitor and watch for signs of bleeding); may increase serum lithium levels and risk of methotrexate toxicity; probenecid may increase toxicity of NSAIDs

Documented hypersensitivity to ibuprofen, other NSAIDs, or aspirin; avoid in peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and high risk of bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, decreased renal and hepatic function, anticoagulation abnormalities, or during anticoagulant therapy; adjust dose in renal insufficiency
NSAID labeling carries a warning about increased risk of hypertension, stroke, and cardiovascular events, including myocardial infarction

Meloxicam (Mobic)

To some extent, more selective for COX-2 receptors, compared to traditional NSAIDs. Decreases activity of cyclooxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Adult

7.5 mg PO qd prn; may increase to 15 mg PO qd prn

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; active GI bleeding

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia)
NSAID labeling carries a warning about increased risk of hypertension, stroke, and cardiovascular events, including myocardial infarction

COX-2 inhibitors

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is less in nonaspirin users receiving COX-2 inhibitors than with traditional NSAIDs.

Celecoxib (Celebrex)

COX-2–specific inhibitor. At therapeutic concentrations, COX-2 (inducible by cytokines at sites of inflammation such as the joints) is inhibited and COX-1 isoenzyme (present in platelets and GI tract) is spared; therefore, in nonaspirin users, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, is decreased when compared to nonselective NSAIDs. COX-2 is expressed in the kidney; however, the renal safety profile is not significantly superior to that of NSAIDs.

Adult

100 mg PO bid or 200 mg PO qd

Pediatric

Disease state not seen in pediatrics

Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations

Documented hypersensitivity to celecoxib, sulfonamides, NSAIDs or aspirin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in late pregnancy to avoid closure of ductus arteriosus; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, presence of existing controlled infections, severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; evaluate symptoms suggesting liver dysfunction or in abnormal liver lab results; adjust dose in renal insufficiency
NSAID labeling carries a warning about increased risk of hypertension, stroke, and cardiovascular events, including myocardial infarction

Follow-up

Deterrence/Prevention

• Overweight patients who have early signs of osteoarthritis (OA) or who are at high risk should be encouraged to lose weight.
• Recommend quadriceps-strengthening exercises in patients with osteoarthritis of the knees, except in those with pronounced valgus or varus deformity at the knees.

Prognosis

The prognosis of osteoarthritis depends on joints involved and severity. No proven disease/structure-modifying drugs for osteoarthritis currently exist; thus, the medication-based regimen is directed at symptom relief.

Patient Education

• Educate the patient on the natural history of and management options for osteoarthritis. Explain the differences between osteoarthritis and other more rapidly progressive arthritides such as rheumatoid arthritis.
• For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Osteoarthritis.

Miscellaneous

Medicolegal Pitfalls

• The risk of medications used to treat osteoarthritis (OA) include, but are not limited to, GI toxicities and potential cardiac toxicities of NSAIDs and potential complications of arthrocentesis. Discuss these risks with the patient.
• Complete a procedure note in the patient's chart for each arthrocentesis.

Jangan Langkahi Otoritas Tuhan

oleh Abdul Mutaqin

Sebagai mahluk terbaik, manusia telah berhasil mengubah wajah dunia. Fitur kehidupan berhasil didisain dengan berbagai kemudahan yang memukau. Manusia zaman ini seakan-akan tidak lagi memiliki kendala mobilitas. Seolah jarak tempuh berhasil diperpendek. Jarak waktu berhasil dipersingkat. Jarak pandang dan jarak dengar berhasil disederhanakan. Manusia sekarang seperti ”siluman”. Detik ini ia nongkrong di bumi Indonesia, tetapi dalam beberapa jam saja, ia sudah asik nyantai di belahan negara lain.

Manusia berhasil merevolusi hidupnya dari waktu ke waktu tanpa henti. Sesuatu yang tadinya mustahil, menjadi hal yang nyata terjadi. Sesuatu yang dulunya sama sekali tak terpikirkan, sekarang menjadi realitas kebiasaan hidupnya.

Di satu sisi, hampir semua kita merasakan manisnya buah teknologi rekayasa manusia tersebut. Tetapi di balik semua kemajuan yang telah digenggam, ada banyak hal yang menggelisahkan nurani manusia beriman. Manusia mulai berani bermain-main hampir di luar wilayah otoritasnya. Dengan kasat mata, kemajuan teknologi dijadikan alat propaganda yang sangat epektif bagi sebuah nilai, sikap dan perilaku yang dapat mengubah mindset orang dalam hitungan detik menuju kekafiran.

Lihatlah penomena tingginya intensitas acara sulap di media enterteinment. Sekarang, para pesulap bukanlah dominasi orang tua. Tetapi anak kecil yang ngomongnya saja belum jalas sudah pandai memainkan trik-trik ilmu magis. Terlepas dari bisa dijelaskan secara logika atau tidak, tetapi pada sisi tertentu sulap bisa menghadirkan “kemustahilan” yang dalam ranah keyakinan sangat sensitif. Maka sisi rawannya adalah ketakjuban pemirsa yang berlebihan kepada seorang pesulap yang mengantarkannya pada kekeliruan sikap dan penilaian terhadapnya. Terutama bagi masyarakat pemirsa yang pemahaman dan intensitas penghayatan agama yang minim.

Teknologi juga memperkenalkan ramalan elektronik jarak jauh. Kalau dahulu orang mendatangi dukun atau peramal yang tinggal di pelosok, sekarang setiap orang dituntun hanya dengan memencet tombol dan mengirim pesan pada nomor yang disediakan. Maka transaksi layanan kosultasi tentang masa depan, karir, jodoh, rizki dan peruntungan dapat terjadi dalam hitungan detik, massif dan terkesan modern. Entah, apakah para penyelia jasa tersebut sadar atau tidak, bahwa mereka telah ”menginjak” wilyah Tuhan. Mereka telah menumpulkan iman pemirsa dengan senjata teknologi.

Yang paling spektakuler, manusia dengan teknologinya berani memastikan bahwa tahun 2012 nanti akan terjadi kiamat dunia. Ini jauh melampaui sekedar persoalan jodoh, rizki, masa depan dan peruntungan yang tidak sekedar menginjak wilayah Tuhan, tetapi telah berani ”merebut” otoritas Tuhan.

Manusia memang memiliki sisi keunggulan sebagai mahluk Tuhan, tetapi manusia tetaplah manusia. Andaikan ada manusia yang diizinkan Tuhan tahu dengan pasti kapan kiamat terjadi, maka yang paling pantas tahu adalah Muhammad shallallaahu ’alaihi wa sallam. Nyatanya, manusia paling mulia itu; Imam para anbiya dan mursalin itu pun tidak mengetahui kapan kiamat akan terjadi. Oleh sebab itu, seorang muslim tidak sepatutnya gamang dalam menyikapi segala penomena kemajuan teknologi. Juga tidak sepatutnya jatuh dalam praduga yang hanya berdasar asumsi dan perkiraan semu. Jika seorang muslim masih menggantungkan nasib kepada dukun, masih larut dalam ketakjuban kepada kharisma seorang tokoh, atau seolah putus asa dengan prediksi kiamat yang jelas-jelas menjadi hak Yang Maha Kuasa, maka apa bedanya dengan orang-orang kafir yang tidak memiliki pegangan itu?

Jika disejajarkan dengan sesama mahluk, makhluk mana yang bisa mengungguli manusia? Tapi jika diperhadapkan dengan Sang Khalik, manusia bukanlah apa-apa. Manusia hanyalah setitik air di lautan jika dibandingkan dengan ilmu dan kekuasan Tuhan.

Manusia memang sanggup menguasai daratan, lautan dan antariksa. Tapi sampai detik ini, manusia tetap tak kuasa menolak bencana.

Dengan teknologinya, manusia mampu merekayasa yang keriput menjadi kencang atau yang buruk menjadi cantik. Tapi hingga kini tak ada satupun dari mereka yang dapat mengobati penyakit tua dan kematian.

Rekayasa genetika manusia memang mencengangkan. Ia dapat menentukan gen mana yang bagus, sehat, unggul, cerdas dan kemudian dipilihnya. Tetapi hingga kini, manusia tetap tak sanggup meniupkan ”ruh” kehidupan bagi proyek raksasanya itu. Buktinya, ”Dollly” si Domba rekayasa itu tak mampu ditolongnya dari kematian di usia yang sangat singkat.

Sadarlah wahai manusia. Kembalilah wahai manusia beriman. Jika teknologi memudahkan hidupmu, maka agama menyelamatkan hidupmu. Jika persaingan hidup menakutkanmu, maka iman menentramkan hatimu. Jika kemajuan tidak mengenal belas kasih, maka Islam mengajarkanmu kedamaian. Dan jika sain mengajarkanmu bebas nilai, maka ihsan mengingatkanmu akan kehadiran Tuhan. So, jangan langkahi otoritas Tuhan.

Depok, Oktober 2009