DIAGNOSIS,MANAGEMENT OF LEPROSY DISEASE AND SURGICAL RECONSTRUCTION / diagnosa dan penataksanaan kusta serta rekontruksi bedah

INTRODUCTION

On the day of leprosy worldwide was falling on January 25, Indonesia was in the position of the 3rd world for new leprosy cases. The position of the two major populated by India and Brazil. The public stigma of leprosy is still not good where leprosy is a curse or karma disease. Leprosy recorded in Indonesia in 2010 showed as many as 17 200 new cases of leprosy and of that number as many as 1882 or about 10% in the second level of disability or handicap that is not visible, whereas in India the same year there were 126 600 new cases of leprosy sufferers, while Brazil there are 34 849 the new lepers. It is worried thing is as much as 1904 cases of leprosy in Indonesia suffered by children. This indicates that the transmission of leprosy still exists in society and the discovery of new cases there was delay. Ironic. The leaders scramble position and seat, while the people still continue to pick up from the development of leprosy.Here will be presented regarding the disease and how to handle and reconstruct the defect that caused the disease in the surgical field.

REVIEW REFERENCES

2.1. Definition of Leprosy. Leprosy is a chronic disease caused by the bacterium Mycobacterium leprae in the skin and peripheral nerves. Clinical manifestations of the disease varies greatly with the spectrum in between the two clinical forms of the lepromatous and tuberculoid. In patients with lepromatous leprosy attacks the type of upper respiratory tract and skin disorders-shaped nodules, papules, macules and in large quantities. In patients with tuberculoid type of leprosy skin lesions are usually single and rarely, the limit firmly lesions.

2.1.1. History of Disease Eradication Leprosy

According to the history of the eradication of leprosy in the world we can share in the three days are:

A. AncientLeprosy is known nearly 2000 years BC. It can be known from historical relics such as in Egypt, 1400 BC in India, the term leprosy was known in the Vedas, in China 600 BC, 400 BC in Mesopotamia.In the ancient times it has happened spontaneously exile people feel inferior and ashamed, as well as the public away from people because they feel disgusted and afraid.

2. Middle AgesAfter about the 13th century with the constitutional order and the prevailing feudal system in Europe resulted in the community is very obedient and fearful of the authorities and human rights do not receive attention. Similarly happened in the lepers who is usually a commoner. At that time the cause of diseases and drugs have not been found then the patient is more stringent and enforced exile living in Leprosaria / leper colony settlement for a lifetime.

3. Modern AgeWith leprosy germs ditemukannnya Amaeur by Gerhard Hansen in 1873, then begin a new era for the development of anti-leprosy drug seeking and mitigation efforts.Similarly in Indonesia dr. Sitanala has pioneered the treatment system changes that had been done in isolation, is gradually carried out by treatment of the road. Development of subsequent treatment were as follows:a. In 1951 used diamino Diphenyl sulfone (DDS) as a treatment for leprosy patients.b. In 1969 the eradication of leprosy began to be integrated in the clinic. c. Since 1982 Indonesia began using the drug combination of Multidrug Therapy (MDT) as recommended by WHO.

2.2. Leprosy Disease Etiology

The cause of the leprosy bacterium Mycobacterium leprae is a long rod-shaped, the sides parallel to the second round tip, size 0.3 to 0.5 micron x 1-8 microns. Basil is a rod-shaped gram-positive, not moving, not berspora, can be dispersed or in groups of varying sizes form. On direct examination microscopically, seemed typical of the formation of such bonds mengerombol bacilli cigar, so called packet of Cigars (globi) .12 capsulated but Basil was allegedly damaged on staining using carbon fukhsin. The organism does not grow on the seed buatan.13 leprosy is a chronic disease as leprosy bacteria take 12-21 days to divide and the average of 2-5 shoots year.12

2.2.1. ColourationFor staining leprosy germs (Basil Hold acid) is often used method of Ziehl Neelsen's by:

a. Preparations placed on the shelf and poured dye fukhsin carbon.b. Heated to steam out (not boiling) leave on for 3-5 minutes.c. Wash with water.d. Preparations included in the tube containing the acid alcohol for 3-5 seconds until the red color given off by alcohol.e. Wash with water ½ minutes.f. Preparations soaked or dipped in methylene blue 1% for ½ - 2 minutes. g. Wash with water. h. Allow to dry from the water, then preparations can be examined under a microscope.Readings: BTA (+): red coloredBTA (-): a blue colored

For the assessment of the results of the smear bacteria (preparations) used index Bacteria (Bacterial Index = BI) and Morphological Index (morphological index = MI).Bacterial Index is a semiquantitative measure of the density of AFB in smears.Usefulness of BI is to help determine the type of disease and assess treatment outcomes. Bacteria Mycobacterium leprae can be seen in the figure below:

 Figure 2.1. Mycobacterium leprae

 BACTERIAL INDEX (BI) 12:

(-): There are no AFB in 100 fields of view.(1 +): 1-10 BTA germs found in the 100 field of view.(2 +): 1-10 bacteria smear was found in 10 fields of view.(3 +): 1-10 bacteria smear was found in an average of one field of view.(4 +): 10-100 bacteria smear was found in an average of one field of view.(5 +): 100-1000 Kuma BTA was found in an average of one field of view.(6 +):> 1000 BTA bacteria found in an average of one field of view.

Morphological INDEX (MI):

The number of M. leprae in the form of whole or solid per 100 Mycobacterium lepraea. Intact form (solid) with an uninterrupted wall and absorb the dye evenlyb. Form of broken or discontinuous (fragmented) with walls partially or completely interrupted.c. Form of grains (granulated): like dots (points) arranged in a straight line or in groups.d. Form of globus: a germ of leprosy (50-200 bacteria) are intact (solid) or dashed (fragmented) or grain (granulated) clustered in a form of bond or a circle.e. Form groups (clumps): a form of leprosy germ grains (granulated)

 2.2.2. Antigen StructureLeprosy patients gave negative results on skin tests performed with the injection of the antigen intrakutan made from lepromatous nodules. This test is called the lepromin test.Lepromin test is specific and immunological tests are used to: find out hospes resistance against Mycobacterium leprae, leprosy determine prognosis, and know the results of treatment of leprosy.

The results of lepromin tests read as follows:a. Early Reaction Fernandez (read after 48 hours)Rapid reactions occur within 24-48 hours. Said to be positive if there were erythema (redness) and induration, and negative when it is said to arise only erythema (redness) alone or no change at the injection site.

b. Delayed Reaction Mitsuda (read after 4-6 weeks)Positive results if there are small papules that arise after 7-10 days, then turned into a large papules and nodules then become 1 cm in diameter. Negative results, if no local reaction, local reaction to a positive or a negative change. Delayed reactions (delayed reaction) is due to the presence of leprosy bacilli are intact.

 2.3. Epidemiology of Leprosy Disease2.3.1. Distribution and Frequency According to The Leprosy Patientsa. Distribution and Frequency by SexLeprosy can strike anyone. Males more affected than women, with a ratio of 2:1,12 except in Africa where women outnumber men. Physiological factors such as puberty, menopause, pregnancy, and the factor of infection and malnutrition may increase the clinical changes in leprosy disease .2 According to research conducted Posmaria Naibaho (2001) Leprosy HospitalSicanang island Belawan Medan North Sumatra found 108 leprosy patients, with the proportion of male patients 61.10% and 38.90% female patients .8 Results of research conducted Nurlaya Hutahayan (2008) Leprosy Hospital there Laguboti Hutasalem 125 lepers, the proportion of male patients 58.40% and 41.60% female patients .9

b. Distribution and Frequency According to AgeLeprosy can affect all umur.12 In Indonesia people with children under the age of 14 ± 13% available, but children under 1 year are rare. The highest frequency present in the age group between 25-35 years old.13According to research conducted Posmaria Naibaho (2001) Leprosy Hospital Sicanang Island Belawan Medan North Sumatra found 108 leprosy patients with the highest age group is 17-24 year age group (the proportion of 30.60%). 8

 Results of research conducted Nurlaya Hutahayan (2008) Leprosy Hospital Hutasalem Laguboti found 125 leprosy patients with the highest age group is 20-39 year age group (the proportion of 56.80%) 9

2.3.2. Frequency Distribution and Disease Leprosy According to Time and PlaceLeprosy around the world with different endemicity. Among the 122 endemic countries in 1985, 98 countries have achieved elimination of leprosy prevalence rate is <1/10.000 population. More than 10 million patients have been cured with Multidrug Therapy (MDT) at the end of 1999 and 641 091 cases still under treatment in 2000.2 In 2003, patients registered in Indonesia in late December 2003 as many as 18 312 patients consisting of 2814 patients with type PB leprosy (proportion of 15.36%) and 15 498 patients with leprosy type MB (the proportion of 84.64%) with a prevalence rate of 86 per 1 million population in 10 provinces, namely: East Java, West Java, Central Java, South Sulawesi, Papua , NAD, DKI Jakarta, North Sulawesi, North Maluku, and Nusa Tenggara Timur.2 In 2005 in North Sumatra, there were 286 recorded cases of leprosy patients comprised 254 people consisting of 32 patients with PB leprosy type (the proportion of 11.19%) and 254 patients with leprosy type MB (the proportion of 88.81%) .6According to research conducted Posmaria Naibaho (2001) Leprosy Hospital Sicanang Island Belawan Medan North Sumatra found 108 leprosy patients consisting of 33 patients with PB leprosy type (the proportion of 30.60%) and 75 patients with leprosy type MB (the proportion of 69.40% ) .

 Results of research conducted Nurlaya Hutahayan (2008) Leprosy Hospital Hutasalem Laguboti found 125 leprosy patients consisting of 48 patients with PB leprosy type (the proportion of 38.40%) and 77 patients with leprosy type MB (the proportion of 61.60%) .9

2.3.3. Determinant factors Kusta2 Diseasea. HostOnly humans only until recently regarded as a source of transmission of leprosy germs can even live in Armadillo, chimpanzees and in mice that have a foot Thymus gland (Athymic nude mouse).The entry of germs into the body of a host of leprosy has yet to be ascertained. It is estimated the entry way is through the upper respiratory tract and through skin contact that is not intact. A nasal scrapings from patients with untreated lepromatous type indicates the number of germs at 104-107. And has been shown that upper respiratory tract of patients with lepromatous type is the most important source of bacteria in the environment.Most humans are immune to leprosy (95%). From the research Directorate General of Communicable Disease Control & Environmental Health (P2M DG & PL) (1996) suggests the following picture:Of the 100 people who are exposed to: 95 people do not become ill, 3 people recover without treatment, two people became ill, it is not yet take into account the effect of treatment.

 A person in a particular environment will be included in one of the following three groups, namely:a. Hosts that have a high immunity which is the largest group that has been or will become resistant to leprosy germs.b. Hosts that have low immunity against leprosy germs, when suffering from leprosy type PB venom.c. Host is not immune to the leprosy germ is the smallest group and when suffering from leprosy type MB normally.

b. AgentThe cause of leprosy is Mycobacterium leprae was first discovered by Gerhard Amaeur Hansen in 1873. Mycobacterium leprae intracellular survival and have a great affinity to the nerve cells (Schwan Cell) and the cells of the reticulo endothelial system.Cleavage of a very long time, ie 2-3 weeks. Outside the human body (in the tropical conditions) leprosy germs can survive up to 9 days. Optimal growth of the leprosy germ is at a temperature of 270-300C.

 2.4. Classification of Leprosy DiseaseOnce someone is diagnosed with leprosy, the next step to determine the type / classification suffered from leprosy. Determination of the type of leprosy in a patient referred to the classification of leprosy. Classification of leprosy aims to determine the type and duration of treatment of disease, the patient stated Release from Treatment (RFT) .2

2.4.1. International Classification (Madrid, 1953): 12

a. Indeterminate (I)There is a skin disorder of the macula is round, amounting to 1 or 2. dipantat site boundary, legs, arms, back on the cheek. Smooth and slippery surface.

b. Tuberculoid (T)There is a thin round macules or patches of irregular lesions with the number 1 or number. Boundary locations are on the buttocks, back, arms, legs, cheeks. Surface dry, coarse often with healing in the middle.

c. Borderline (B)Somewhat thickened patches of skin disorders are disorganized and scattered.Boundary location with tuberculoid.

d. Lepromatous (L)Skin disorders in the form of thickened patches of diffuse, vague form. Shaped rash (nodule), the macula, a diffuse macular thin in body, evenly distributed throughout the body, large and small continued symmetric.2.4.2. Ridley-Jopling classification (1962) 15This classification is widely used in field studies of leprosy classified into 5 groups based on clinical, bacteriological, histopathological, and immunological.

a. Tuberculoid tuberculoid type (TT)Lesions in the form of patches of hypopigmentation makuloanestetik and contained in all places, particularly on the face and arms, except for: armpits, scalp (scalp), perineum and groin. Lesion boundary clearly different from the surrounding skin color.Hypopigmentation is a prominent symptom. Lesions can undergo spontaneous healing or the treatment for three years. 11

b. Borderline tuberculoid type (BT)BT leprosy symptoms in the same type with the type of TT, but smaller lesions, is not accompanied adamya hair loss, and neurological changes occur only pembengkakan.11

c. Type Mid Borderline (BB)On bacteriological examination found multiple results, and lepromin tests gave negative results. Irregularly shaped skin lesions, there are satellites that surrounds the lesion, and the asymmetrical distribution of lesions. The edges of the lesion can not be distinguished on the surrounding area. These symptoms are accompanied by adenopathi regional.10

d. Type Borderline lepromatous (BL)Lesions in this type of macular papules and nodules that tend to be asymmetrical.Neurological abnormalities occur at an advanced stage. There is no description as occurs in lepromatous type that is not accompanied madarosis, keratitis, and facies uslserasi leonine.9

e. Lepromatous type (LL)symmetrical diffuse lesions, shiny grayish. No change in the production of sweat glands, little change in sensation. In the advanced phase occurs madarosis (loss) and a face like a lion, bumpy face (facies Leo) 19Here is a picture of lepers according to Ridley-Jopling:

 Figure 2.2. Leprosy tuberculoid type & Bordeline



             2.3. Picture Study Leprosy Lepramatosa

 Figure 2.4. Patients with Leprosy Type L.L and B.L

 Figure 2.5. Patients with Leprosy Type B.B and B.T.

 2.4.3. WHO classification (1982), namely: 2

a. Type PB (Pausibasiler)Leprosy is a type of PB leprosy patients with Basil Hold acid (BTA) on smears, namely type I (indeterminate), TT (tuberculoid) and BT (borderline tuberculoid) according to the criteria of Ridley and Jopling and just have a number between 1-5 in the skin lesions .PB leprosy type is the type of leprosy is not contagious.

b. Type MB (multibacillary)MB leprosy patients kuta is all types of BB (mid borderline), BL (borderline lepromatous) and LL (lepromatous) according to the criteria of Ridley and Jopling with the number 6 or more lesions and skin smear positive. MB type of leprosy is a type that can be transmitted.Here is a picture of type PB leprosy and MB

 Figure 2.6. Type PB Leprosy

In determining the classification of types of PB and MB on criteria such as the table below:

No. Skin disorders and the results

inspection Pausi basilar (PB)Multi basilar (MB)A. Spots (macules) deadFlavora. Number 1-5> 5b. Small size and large-small Smallc. Unilateral distribution and

Bilateral asymmetry and bilateral symmetryd. Dry and rough consistency Smooth, shinye. Decisive is not expressly limitf. Loss of tasteThere is always spot on and certainly not clear Usually, If any, occurs at an advancedg.Lostability to sweat, hair falling out in patches patches do not sweating, there are patches of hair loss in patches still sweating, hair not fall on the spot.2. Infiltratesa. No skin There is, sometimes there is nob. Mucous membranes (nose, bleeding from the nose) There's never been there, sometimes there is no3. Central characteristics of healing (penyembuha in the ears) Punched out lesion (lesiondonut shape), madarosis, ginekomasti, saddle nose, and nasal voice4. No nodules Sometimes there5. Deformity (defects) usually occurs early Happens at an advanced stage6. Smear positive AFB smear-negative

2.5. Leprosy reactions2.5.1. Pengertian2The reaction of leprosy or leprosy reactions is an episode in the course of chronic leprosy is an immune response (cellular response) or antigen-antibody reaction (humoral response) with the result of patient harm, especially in the peripheral nerves that causes impaired function (disability).This reaction can occur in patients treated before and after treatment. But often occurs in the 6 months to 1 year after starting treatment.Things that facilitate the occurrence of leprosy reactions, for example:

A. Patients in poor condition2. Malnutrition

2.5.2. Types Reaksi2This type of reaction according to the process is divided into two types: type I reaction and the reaction of type II

a. Type I reaction (reserval Reaction, Reaction Up grading)Occur in patients with type PB and MB, and mostly occur in the first 6 months of treatment, type I reactions occur due to increased cellular immune response against bacteria rapidly in the skin and nerves of leprosy patients.Here there was a shift towards the type of PB leprosy.1) SymptomsSymptoms of the reaction can be seen in changes in skin lesions, neuritis (nerve tenderness), peripheral nerve dysfunction and sometimes the general state of disorder sufferers (constitution).2) According to the state of the reaction, leprosy tipee I can be divided into mild reactions and severe reactions.3) The journey of the reaction can last for 6-12 weeks or more.

b. Type II reactions (ENL reaction = reaction Nodosom leprosum Erythema)Tpe occur in patients with MB and a humoral response, where the leprosy germ is intact or not intact to an antigen. The body makes antibodies and complement (antigen + antibody + complement = immunokompleks).1) SymptomsSymptoms of the reaction can be seen in changes in lesions, neuritis (tenderness) and peripheral nerve dysfunction, disorders and complications in the constitution of the body organs2) According to the state of the reaction, the reaction can be differentiated mild and severe reactions.

3) Travel reactionUsually lasts for 3 weeks or more. Sometimes arise over and over and lasts longer.

2.6. Disability In Patients Kusta2Leprosy is a public health problem because of his disability. Defects caused by leprosy nerve function impairment in eyes, hands or feet. However, people with disabilities caused by leprosy "branded" for life as a "leper" while recovering from illness. While in fact almost all the defects can be prevented.

2.6.1. The process of defect kusta2The occurrence of defects depends on nerve function, and where the nerves are damaged. Disability in leprosy can occur through two processes:

a. Mycobacterium leprae kesusunan direct infiltration of peripheral nerve and organ(Eg the eye)b. By reaction of leprosy

2.6.2. Disability Level

WHO (1988) divide the defect rate of leprosy into three levels, namely:a. Level 0If the eye, hand or foot remains intact, then the stated level of defect 0b. Level 1If there are defects in the eyes, hands or feet due to nerve damage due to leprosy, but the defect was not visible, then the stated level of defect 1.Anesthetic eye examination is performed. Muscle weakness into one except eye defects.c. Level 2If there are defects caused by nerve damage and disability is seen (ulcers, sores, finger kiting, limp, shortening, the eyes can not close tightly, injury to the cornea), the stated level of disability 2.Is a matter which does not include any defects or abnormalities in the skin only, or that there was not a result of leprosy, namely: normal wound (on the hands or feet are not numb), thinning eyebrows (madarosis), saddle nose, numbness on the soles of other than (in general or on patches of skin); kiting, weakness of muscle or lose a finger caused by an accident.

2.7. Prevention and ControlLeprosy is a disease that gives big huge stigma in society, so that leprosy patients suffer not just because the disease course, also shunned or ostracized by society. It is actually more due to a disability that looks scary. Disability is actually caused more disability-looking body. The disability could be prevented if the diagnosis and treatment of disease is done early. Similarly, required knowledge of things that can cause disability and disability prevention, so as not to cause a visible disability.Identification and treatment of leprosy patients is the key to control. Children of parents who teinfeksi given chemoprophylaxis with sulfone up to the parents no longer infectious. If one family member in lepromatous leprosy, it is thus necessary for the prophylaxis of children within family.

2.7.1. Prevention Primodial10Primordial prevention ie prevention efforts on people who do not have risk factors for leprosy through counseling. Counseling about the disease is the process of improving knowledge, willingness and ability of community health workers so that people can maintain, enhance and protect the health of leprosy.

 2.7.2. Primary Prevention (Primary Prevention)Primary prevention is an attempt to defend someone who already have risk factors that are not sick .. 20 The purpose of primary prevention is to reduce the incidence of disease by controlling the causes of disease and risk factors. To prevent the occurrence of leprosy, efforts are noticed and maintain a healthy living environment, personal hygiene, early detection of leprosy and the mobilization of community participation to be checked out or encourage people who are suspected to check into the clinic.

2.7.3. Secondary Prevention (Secondary Prevention)Secondary prevention is the prevention of early disease that is preventing people who have been sick to heal, inhibiting the progression of the disease and avoid komplikasi.10 secondary prevention goal is to treat patients and reduce the consequences are more serious than the disease through early diagnosis and administration pengobatan.11 Secondary prevention can be done by early diagnosis and examination of neuritis, early detection of leprosy reactions, regular treatment with chemotherapy or surgery.

To establish the diagnosis of leprosy to look for signs of fundamental or "cardinal sign" in the body, namely:

a. Lesion (abnormality) skin numbnessSkin abnormalities / lesions can form whitish spots (hypopigmentasi) or reddish (eritematousa) the numbness (anesthesia).

b. Thickening of peripheral nerveCan be accompanied by pain and also can be with or without neurological dysfunction.Nerve function impairment is a result of chronic inflammation of peripheral nerves (peripheral neuritis). Disruption of this bias neural function in the form:a. Disruption of sensory function: numb

 b. Motor function disorders: muscle weakness (parese) or paralysis (Paralise)c. Autonomic function disorders: dry skin and cracked.

c. Non Acid Basil The presence of acid-resistant bacteria in the skin tissue scrapings (smear positive).Examination of scrapings only performed in cases of doubt.A person declared a leper if there is one of the major signs of the above. If the cardinal sign is found only the second and doubts should be referred to staff or expert leprosy, still unsure if the person is considered a suspected case of (suspected).

Signs of leprosy suspects (suspect)A. The signs on the skina. Spots / red skin disorders or white on the body b. Shiny skinc. Spots are not itchyd. The existence of the body parts that are not sweating or no hair.e. The blisters are not painful.

2. Signs of nervea. Tingling, stabbing, puncture and pain in the limbs or face. b. Movement disorders of limbs or the facec. The existence of defects (deformed)d. Wound (ulcer) that do not want to recover

2.7.4. Tertiary Prevention (Tertiary Prevention)Tertiary prevention goal is to reduce disability and rehabilitation is conducted rehabilitasi.20 efforts to restore a sick person so that a human being more efficient, productive, satisfying lifestyle to follow and to provide the best possible quality of life, according to the level of disease and disability tertiary prevention include:

a. Disability PreventionDefect prevention of leprosy is much better and more economical than handling.Prevention should be done as early as possible, either by medical personnel, as well as by patients themselves and their families.

Defect prevention efforts consist of:a. Primary defect prevention efforts, which include:1) Early diagnosis and treatment of neuritis2) Treatment on a regular basis and adequate3) Early detection of leprosy reactions4) The management of leprosy reactions

b. Secondary disability prevention efforts, which include:1) self care to prevent injuries2) physiotherapy exercises in the paralyzed muscles to prevent contractures.3) Reconstructive surgery for the correction of the paralyzed muscles in order not to get too much stress.4) Surgery to reduce the expansion of septic infection.5) Maintenance eyes, hands or feet and the anesthesia or muscle paralysis. 2.10

Prevention and correction of deformity and disabilityFollow the principle of surgicalTreatment aims to cure the patient in order to achieve full recovery of physical and mental defects which might be of bears. Thus, the patient is able to work for a living according to his ability and received back by the family and community environment.Treatment of physical disability should be followed by a course of education for people not able to return to its original position, but also acceptable to an assisted living and working back in the community.Follow surgery is part of the team work is one key to the success of treatment, ideally, the treatment team consists ata rehabilitation doctor, dermatologist physicians, orthopedic surgeons, psychologists, fsioterapis, medical social worker, nurse, occupational therapist, and expert prosthesis . Things to remember in the follow-loss surgery is that the flavor can not be repaired again. This happens because kerusahakan not only in axons, but also on the nerve endings in the skin. Having overcome a physical disability, then the response is rehabilitation. In accordance with its objectives, rehabilitation is divided into medical rehabilitation terdiir the physical and mental rehabilitation, work rehabilitation, social rehabilitation and education.

ACUTE CONDITIONPrevention of disability is shown to prevent primary defects and secondary disabilities.In terms of prevention, disability due to leprosy are also distinguished the early forms of disability and disability information. Early defects are often caused by acute leprosy reactions and neuritis can be recovered perfectly acute. Its action is to encourage the patient lying breaks while improving the general state Antilepra patients should be given and should not be stopped because it was feared the disease becomes progressive and resistant. Pain medications and anti-inflammatory class of regular NSAID dinajurkan. In the case of persistent pain may be used or carried neurolisis local anesthetic to relieve pressure on the axon due to inflammation and edema reajsu on the nerves. Fitted splint to rest the affected part, and strive for a more stable joint, then contractures prevented and eliminated with passive stretching. With this action is usually paralysis n.radialis (dropwrist) can be cured, while the paralysis n.poplitea lateralis (dropfoot) and sometimes it can n.medianus smebuh only, and are rarely cured paralysis n.ulnaris

CHRONIC CONDITIONLeprosy patients with chronic conditions generally occur due to anesthesia, paralysis, and dryness of skin ulceration, neuropathy and muscle paralysis. At this level seems dropfoot, clawtoes, dropwrist, claw hands, facial paralysis, saddle nose, or gynecomastia. Kelumpuhanyang there are settled.To prevent ulceration of neuropathy, patients need to be taught and given the knowledge to live with such a state body. Patients must wear footwear when walking and protective hand when lifting hot items. Chronic neuropathic ulceration and paralysis can be overcome by surgical acts for the purpose of prevention of secondary disabilities.

b. Rehabilitation Rehabilitation is conducted include medical rehabilitation, social rehabilitation, and economic rehabilitation. Medical rehabilitation efforts can be made for the disabled, among others, by the way is surgery and physiotherapy. Although the results were not perfect back to the origin, but its function and cosmetics can be repaired. Another way is the workmanship, which gives the appropriate disability employment body, so as to achieve and can boost your confidence, but it can be therapeutic psychological (mental).

2.8.Leprosy  Disease Eradication ProgrammIn 1991 the World Health Assembly has issued a resolution that is the elimination of leprosy in 2000. Indonesia as a member of the World Health Organization (WHO) has to fulfill the resolution. A fact that leprosy is spread unevenly in Indonesia and the prevalence rate (PR) varies widely by province, district / city / district. Patients enrolled in Indonesia until December 2003 as many as 18 312 people. Leprosy elimination target in Indonesia in 2000 was achieved nationally in mid-2000, but at provincial and district level is still much yet to achieve elimination. Until the end of December 2003, just 18 of 30 provinces and 325 of the 440 districts that could achieve elimination.

2.8.1. Goal

a. Long Term ObjectivesA. Decrease the transmission of leprosy in panyakit extent that leprosy is not a public health problem.2. prevent disability in all new cases were found through proper treatment and care.3. Provide care and appropriate rehabilitation services to people affected by leprosy.

b. Short Term GoalsA. Establish system of discovery and diagnosis of leprosy patients in the intensive high-endemic areas and in pockets of leprosy in low endemic areas so that the proportion of children and disability level 2 is less than 5%.2. Provide adequate treatment in order to reach the numbers healing (RFT Rate) of more than 90%.3. reduce the proportion of people with disabilities in the eyes of the hands and feet after RFT is less than 5%.4. Develop a health center with adequate disability care with the support of the referral system for general hospitals and special hospitals for cases with complications and need medical rehabilitation.5. Implement the management of leprosy eradication program in accordance with starategi endemicity area and supported by the supporting activities.

 2.8.2. Targets

A. The achievement of leprosy elimination at the provincial level in 2008.2. Achieving elimination of leprosy at the district level in 2010.3. The achievement of leprosy-free Indonesia by 2020.

2.8.3. Policies

A. Implementation of integrated leprosy eradication program in primary health care activities in health centers of services2. Treatment of leprosy patients with MDT according to WHO recommendations are given for free.3. Leprosy patients should not be isolated.

2.9. Treatment of PatientsThe main purpose of the leprosy eradication program is break the chain of transmission to reduce the incidence of disease, treat and cure patients and prevention onset of disability. To achieve that goal up to now the strategy that will be carried still based on early detection and treatment of patients, who apparently still needed even if later the effective leprosy vaccine has been available. Since reports of resistance to dapsone both primary and secondary, in 1977, WHO introduced a combination treatment comprising at least two effective drugs antikusta

Program Multi Drug Therapy (MDT) initiated in 1981, when WHO Chemotherapy study group was officially issued a recommendation of treatment of leprosy with MDT-WHO regimen. This regimen consists of a combination of drugs dapsone, rifampicin, and klofasimin. In addition to overcome the increasing resistance to dapsone, the use of MDT is also intended to reduce patient non-compliance and reduce dropout rates, drug (dro-out) is quite high in the dapsone monotherapy. Besides, it is expected also to be able to eliminate the persistence of MDT in leprosy germs tissuesMDT treatme nt regimens in Indonesia in accordance with the treatment regimen recommended by WHO regimen is as follows:

2.9.1. PB Type 2.12For PB leprosy type, consisting of rifampicin and dapsone kombisnasi.a. Types and drugs for adults:A. Rifampicin 600 mg / month and DDS 100 mg / day swallowed up in front of the officer.2. DDS 100 mg / day of drinking at home. b. The type and dose of medication for children:A. DDS 1-2 mg / kg body weight2. Rifampin 10-15 mg / kg body west c. Duration of treatmentDuration of treatment for patients with type PB is for 6-9 months.

2.9.2. MB Type 2.12To leprosy type MB, consisting of a combination of rifampicin, dapsone, clofazimine (lamprene).a. The type and dose of drugs for adults:A. Lamprene 300 mg / month2. Rifampicin 600 mg / month3. DDS 100 mg / month

The third drug is swallowed up in front of the clerk of each month.A. DDS 100 mg / day2. Lamprene 50 mg / dayBoth drugs are taken at home.

b. Lamprene dose for children:Age under 10 years: Monthly: 100 mg / monthDaily: 50 mg / 2 times / weekAge 11-14 years: Monthly: 200 mg / monthDaily: 50 mg / 3 times / week

Duration of treatment 2 yearsOnce treatment is stopped (Release from Treatment / RFT) patients included in the observation period (control), namely: the patient was clinically controlled and bakterioskopik least once a year for 5 years for multibacillary leprosy patients and controlled in the clinic once a year for 2 years for pausibasiler lepers. If at that time there was no activity, then the patient is declared free from observation (Release from Control / RFC) .

References

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2.     Ellard GA. Growing points in leprosy research 4 -  recent advances in chemotherapy of leprosy. Leprosy Rev 1974; 45:31.

3.     Shepard CC et al. Rapid bactericidal effect of rifampicin on M. leprae. Am

J Trop Med Hyg 1972; 21: 446.

4.     Cartel J et al. Hepatotoxicity of daily combination of 5  mg/kg prothio- namide and 10 mg/kg rifampicin. Intermit J Leprosy 1985; 53(1): 15.

5.     Chen  JK  et  al.  The  hepatotoxicity  of  combined  therapy  for  leprosy

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6.     Tan T. Hepatitis in leprosy patients treated by monthly rifampic in/dofa- zimine and daily combination of dapsone/clofazimine and a thionamide in Singapore. Abstracts of theist Asian Dermatological Conggress,Hongkong,

1986. p. 91.

7.     Chan  WC  et  al.  Renal  failure  during  interrnitent  rifampicin  therapy.

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8.     Cochran EM et al. Permanent renal damage with rifampicin. Lancet 1979;

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9.     Cordonnier D, Muller JM. Acute renal failure after  rifampicin. Lancet

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10.  Girling DI, Hitzke KL Adverse reactions to rifampicin. WHO Bull 1979;

57: 45.

11.  Dinkar DP. Do complications occur under multi-drug therapy? (editorial).

Indian J Leprosy 1987; 59: 369.

12.  Kosasih. Kusta. Ilmu Penyakit Kull' dan Kelamin. edisi  pertain*. FKUI

1987, 73.

13.  Richard AM. Leprosy. Principles of Internal Medicine 1. eleventh ed 1988,

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