A. IDENTITAS PASIEN Nama : Tn. M Umur : 54thn Suku : Melayu Jenis Kelamin : Laki-laki Alamat : Jayapura lor B.

ANAMNESA a. The main complaint difficult to open the mouth b. Additional complaints defence muscular (+), stiff neck (+). c. History of present illness Tn. M come to the emergency room because of he feel difficult to open his mouth since 3 days ago, 15 days ago he got an motorcycle accident and he fell to the asphalt so he got injury on his left knee but he not cured it that day. Stiff neck (+), defence muscular (+), spastic (+), fever (-), nausea (-), vomit (-), pus (+), C. STATUS PRAESENS Status Internus Kesadaran : GCS = 15 Gizi : cukup Suhu Badan : 36,5 C Tekanan Darah : 140/100 mmHg Nadi : 86 x/m Pernapasan : 26 x/m D. PROVISIONAL DIAGNOSIS Suspect Tetanus Differential Diagnosis : 1. meningitis 2. effect of phenotiazine theraphy 3. rabies

4. epilepsi E. LABORATORIUM WBC 11 x RBC 4,92 x HGB 16,5 g/dl PLT 382 x DGS 77 mg/dl TETANUS Definition Tetanus is an acute disease induced by an exotoxin of the bacteria Clostridium tetani, which grows anaerobically at the site of an injury. Tetanus spores are usually introduced into the body through a contaminated puncture, laceration, or other wound or by injected contaminated drugs. Tetanus is not transmissible from person to person. Tetanus is an acute, toxin-mediated disease caused by Clostridium tetani. Under favourable anaerobic conditions, such as in dirty, necrotic wounds, this ubiquitous bacillus may produce tetanospasmin, an extremely potent neurotoxin. Tetanus toxin blocks inhibitory neurotransmitters in the central nervous system, resulting in muscular stiffness and spasms that are typical of tetanus. The disease can affect any age group and case-fatality rates are high (10-80%) even where modern intensive care is available. There is no natural immunity against tetanus; protection can be provided by active immunization with tetanus toxoidcontaining vaccine*, (TT: formalininactivated tetanus toxin) or administration of an antitetanus antibody (tetanus-specific immunoglobulin, TIG). Tetanus is an acute, often fatal, disease caused by an exotoxin produced by the bacterium Clostridium tetani. It is characterized by generalized rigidity and convulsive spasms of skeletal muscles. The muscle stiffness usually involves the jaw (lockjaw) and neck and then becomes generalized. Although records from antiquity (5th century BCE) contain clinical descriptions of tetanus, it was Carle and Rattone in 1884 who first produced tetanus in animals by injecting them with pus from a fatal human tetanus case. During the same year, Nicolaier produced tetanus in animals by injecting them with samples of soil. In 1889, Kitasato isolated the organism from a human victim, showed that it produced disease when injected into animals, and reported that the toxin could be neutralized by specific antibodies. In 1897, Nocard demonstrated the protective effect of passively transferred antitoxin, and passive immunization in humans was used for treatment and prophylaxis during World War I. A method for inactivating tetanus toxin with formaldehyde was developed by Ramon in the early 1920's which led to the development of tetanus toxoid by Descombey in 1924. It was first widely used during World War II. l l l

Epidemiology Occurrence Tetanus occurs worldwide but is most frequently encountered in densely populated regions in hot, damp climates with soil rich in organic matter. Reservoir Organisms are found primarily in the soil and intestinal tracts of animals and humans. Mode of Transmission Transmission is primarily by contaminated wounds (apparent and inapparent). The wound may be major or minor. In recent years, however, a higher proportion of patients had minor wounds, probably because severe wounds are more likely to be properly managed. Tetanus may follow elective surgery, burns, deep puncture wounds, crush wounds, otitis media (ear infections), dental infection, animal bites, abortion, and pregnancy. Communicability Tetanus is not contagious from person to person. It is the only vaccine-preventable disease that is infectious but not contagious. Clinical description Most commonly presents with gradual onset of muscular rigidity and painful spasms, starting in the jaw (lockjaw, trismus) then spreading to the neck, trunk and extremities. Tetanus may cause laryngeal spasms, respiratory failure and autonomic dysfunction (fluctuations in pulse and blood pressure), leading to death, even with modern intensive care. In less than 20 percent of cases, muscle rigidity and spasms are limited to a confined area close to the site of injury. Transmission and clinical characteristics Tetanus is not transmitted from person to person. Infection occurs when C. tetani spores are introduced into acute wounds from trauma, surgeries and injections, or chronic skin lesions and infections. Cases have resulted from wounds that were considered too trivial to warrant medical attention. The incubation period of tetanus is usually between three and 21 days (median 7 days). Shorter incubation periods (<7 days) along with delays in seeking treatment are associated with fatal outcomes. Outbreaks of tetanus related to injuries associated with natural disasters such as earthquakes and tsunamis have been documented. Tetanus is characterized by muscle rigidity and painful muscle spasms. In generalized tetanus (the most common form), stiffness and pain often begin in the jaw muscles (trismus or lock jaw) and/or neck, shoulder and abdominal muscles. Early in the disease course, spasms are triggered by sensory stimuli such as touch, loud noises and bright lights. As the disease progresses, muscle groups throughout the body are affected and spontaneous generalized seizure-like tetanospasms develop. In the absence of the ability to provide ventilatory support, death is usually due to respiratory failure. Autonomic dysfunction, including

hypertension and tachycardia alternating with bradycardia and hypotension can be present in more severe tetanus cases and is associated with a poorer prognosis. Clostridium tetani C. tetani is a slender, gram-positive, anaerobic rod that may develop a terminal spore, giving it a drumstick appearance. The organism is sensitive to heat and cannot survive in the presence of oxygen. The spores, in contrast, are very resistant to heat and the usual antiseptics. They can survive autoclaving at 249.8F (121C) for 1015 minutes. The spores are also relatively resistant to phenol and other chemical agents. The spores are widely distributed in soil and in the intestines and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil may contain large numbers of spores. In agricultural areas, a significant number of human adults may harbor the organism. The spores can also be found on skin surfaces and in contaminated heroin. C. tetani produces two exotoxins, tetanolysin and tetanospasmin. The function of tetanolysin is not known with certainty. Tetanospasmin is a neurotoxin and causes the clinical manifestations of tetanus. On the basis of weight, tetanospasmin is one of the most potent toxins known. The estimated minimum human lethal dose is 2.5 nanograms per kilogram of body weight (a nanogram is one billionth of a gram), or 175 nanograms for a 70-kg (154lb) human. Pathogenesis C. tetani usually enters the body through a wound. In the presence of anaerobic (low oxygen) conditions, the spores germinate. Toxins are produced and disseminated via blood and lymphatics. Toxins act at several sites within the central nervous system, including peripheral motor end plates, spinal cord, and brain, and in the sympathetic nervous system. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with release of neurotransmitters, blocking inhibitor impulses. This leads to unopposed muscle contraction and spasm. Seizures may occur, and the autonomic nervous system may also be affected. Clinical Features The incubation period ranges from 3 to 21 days, usually about 8 days. In general the further the injury site is from the central nervous system, the longer the incubation period. The shorter the incubation period, the higher the chance of death. In neonatal tetanus, symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. On the basis of clinical findings, three different forms of tetanus have been described. Local tetanus is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. These contractions may persist for many

weeks before gradually subsiding. Local tetanus may precede the onset of generalized tetanus but is generally milder. Only about 1% of cases are fatal. Cephalic tetanus is a rare form of the disease, occasionally occurring with otitis media (ear infections) in which C. Tetani is present in the flora of the middle ear, or following injuries to the head. There is involvement of the cranial nerves, especially in the facial area. The most common type (about 80%) of reported tetanus is generalized tetanus. The disease usually presents with a descending pattern. The first sign is trismus or lockjaw, followed by stiffness of the neck, difficulty in swallowing, and rigidity of abdominal muscles. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes. Spasms continue for 34 weeks.Complete recovery may take months. Neonatal tetanus is a form of generalized tetanus that occurs in newborn infants. Neonatal tetanus occurs in infants born without protective passive immunity, because the mother is not immune. It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with an unsterile instrument. Neonatal tetanus is common in some developing countries (estimated more than 257,000 annual deaths worldwide in 2000-2003), but very rare in the United States. Complications Laryngospasm (spasm of the vocal cords) and/or spasm of the muscles of respiration leads to interference with breathing. Fractures of the spine or long bones may result from sustained contractions and convulsions. Hyperactivity of the autonomic nervous system may lead to hypertension and/or an abnormal heart rhythm. Nosocomial infections are common because of prolonged hospitalization. Secondary infections may include sepsis from indwelling catheters, hospital-acquired pneumonias, and decubitus ulcers. Pulmonary embolism is particularly a problem in drug users and elderly patients. Aspiration pneumonia is a common late complication of tetanus, found in 50%70% of autopsied cases. In recent years, tetanus has been fatal in approximately 11% of reported cases. Cases most likely to be fatal are those occurring in persons 60 years of age and older (18%) and unvaccinated persons (22%). In about 20% of tetanus deaths, no obvious pathology is identified and death is attributed to the direct effects of tetanus toxin.

Diagnosis Tetanus diagnosis is strictly clinical; there are no confirmatory laboratory tests. The WHO definition of adult tetanus requires at least one of the following signs: trismus (inability to open the mouth) or risus sardonicus (sustained spasm of the facial muscles); or painful muscular contractions. Although this definition requires a history of injury or wound, tetanus may also occur in patients who are unable to recall a specific wound or injury.

Laboratory test for diagnosis There are no laboratory findings characteristic of tetanus. The diagnosis is entirely clinical and does not depend upon bacteriologic confirmation. C. tetani is recovered from the wound in only 30% of cases and can be isolated from patients who do not have tetanus. Laboratory identification of the organism depends most importantly on the demonstration of toxin production in mice. Isolation of Clostridium tetani from culture of the wound site supports the diagnosis but yield is poor, and a negative culture does not rule out tetanus. In general, laboratories have a reduced role in the diagnosis of tetanus. Case classification classify it as confirmed. practitioner. definition. Medical Management All wounds should be cleaned. Necrotic tissue and foreign material should be removed. If tetanic spasms are occurring, supportive therapy and maintenance of an adequate airway are critical. Tetanus immune globulin (TIG) is recommended for persons with tetanus. TIG can only help remove unbound tetanus toxin. It cannot affect toxin bound to nerve endings. A single intramuscular dose of 3,000 to 5,000 units is generally recommended for children and adults, with part of the dose infiltrated around the wound if it can be identified. Intravenous immune globulin (IVIG) contains tetanus antitoxin and may be used if TIG is not available. Because of the extreme potency of the toxin, tetanus disease does not result in tetanus immunity. Active immunization with tetanus toxoid should begin or continue as soon as the persons condition has stabilized. Wound Management Antibiotic prophylaxis against tetanus is neither practical nor useful in managing wounds; proper immunization plays the more important role. The need for active immunization, with or without passive immunization, depends on the condition of the wound and the patients immunization history (see MMWR 2006;55[RR-17] for details). Rarely have cases of tetanus occurred in persons with a documented primary series of tetanus toxoid.

Persons with wounds that are neither clean nor minor, and who have had 02 prior doses of tetanus toxoid or have an uncertain history of prior doses should receive TIG as well as Td or Tdap. This is because early doses of toxoid may not induce immunity, but only prime the immune system. The TIG provides temporary immunity by directly providing antitoxin. This ensures that protective levels of antitoxin are achieved even if an immune response has not yet occurred. Treatment of tetanus disease General measures: if possible a separate ward/location should be designated for tetanus patients. Patients should be placed in a quiet shaded area and protected from tactile and auditory stimulation as much as possible. All wounds should be cleaned and debrided as indicated. Immunotherapy: if available, administer human TIG 500 units by intramuscular injection or intravenously (depending on the available preparation) as soon as possible; in addition, administer age-appropriate TT-containing vaccine, 0.5 cc by intramuscular injection at a separate site. [Tetanus disease does not induce immunity; patients without a history of primary TT vaccination should receive a second dose 12 months after the first dose and a third dose 612 months later.] Antibiotic treatment: metronidazole is preferred (500 mg every six hours intravenously or by mouth); Penicillin G (100,000200,000 IU/kg/day intravenously, given in 24 divided doses). Tetracyclines, macrolides, clindamycin, cephalosporins and chloramphenicol are also effective. Muscle spasm control: benzodiazepines are preferred. For adults, intravenous diazepam can be given in increments of 5 mg, or lorazepam in 2 mg increments, titrating to achieve spasm control without excessive sedation and hypoventilation (for children, start with doses of 0.1 0.2 mg/kg every 26 hours, titrating upward as needed). Large amounts may be required (up to 600 mg/day). Oral preparations could be used but must be accompanied by careful monitoring to avoid respiratory depression or arrest. Magnesium sulphate can be used alone or in combination with benzodiazepines to control spasm and autonomic dysfunction: 5 gm (or 75mg/kg) intravenous loading dose, then 23 grams per hour until spasm control is achieved. To avoid overdose, monitor patellar reflex as areflexia (absence of patellar reflex) occurs at the upper end of the therapeutic range (4mmol/L). If areflexia develops, dose should be decreased. Other agents used for spasm control include baclofen, dantrolene (12 mg/kg intravenous or by mouth every 4 hours), barbiturates, preferably short-acting (100150 mg every 14 hours in adults; 610 mg/kg in children; by any route), and chlorpromazine (50150 mg by

intramuscular injection every 48 hours in adults; 412 mg every by intramuscular injection every 48 hours in children). Autonomic dysfunction control: magnesium sulphate as above; or morphine. Note: blockers such as propranolol were used in the past but can cause hypotension and sudden death; only esmalol is currently recommended. Airway / respiratory control: drugs used to control spasm and provide sedation can result in respiratory depression. If mechanical ventilation is available, this is less of a problem; if not, patients must be carefully monitored and medication doses adjusted to provide maximal spasm and autonomic dysfunction control while avoiding respiratory failure. If spasm, including laryngeal spasm, is impeding or threatening adequate ventilation, mechanical ventilation is recommended when possible. Early tracheostomy is preferred as endotracheal tubes can provoke spasm and exacerbate airway compromise. Adequate fluids and nutrition should be provided, as tetanus spasms result in high metabolic demands and a catabolic state. Nutritional support will enhance chances of survival. Prior to the availability of a vaccine and mechanical ventilation (during the 1920s30s), careful monitoring and nursing care improved survival. If patients can be supported through one to two weeks of spasm and other complications, the chances of complete recovery greatly increase, particularly in non-elderly and previously healthy patients. Immunogenicity and Vaccine Efficacy After a primary series (three properly spaced doses of tetanus toxoid in persons 7 years of age and older, and four doses in children younger than 7 years of age) essentially all recipients achieve antitoxin levels considerably greater than the protective level of 0.1 IU/mL. Efficacy of the toxoid has never been studied in a vaccine trial. It can be inferred from protective antitoxin levels that a complete tetanus toxoid series has a clinical efficacy of virtually 100%; cases of tetanus occurring in fully immunized persons whose last dose was within the last 10 years are extremely rare. Antitoxin levels decrease with time. While some persons may be protected for life, by 10 years after the last dose, most persons have antitoxin levels that only approach the minimal protective level. As a result, routine boosters are recommended every 10 years. In a small percentage of individuals, antitoxin levels fall below the minimal protective level before 10 years have elapsed. To ensure adequate protective antitoxin levels, persons who sustain a wound that is other than clean and minor should receive a tetanus booster if more than 5 years have elapsed since their last dose. (See Wound Management for details on persons who previously received fewer than three doses).

Vaccination Schedule and Use DTaP (diphtheria and tetanus toxoids and acellular pertussis vaccine) is the vaccine of choice for children 6 weeks through 6 years of age. The usual schedule is a primary series of four doses at 2, 4, 6, and 1518 months of age. The first, second, and third doses of DTaP should be separated by a minimum of 4 weeks. The fourth dose should follow the third dose by no less than 6 months and should not be administered before 12 months of age. If a child has a valid contraindication to pertussis vaccine, pediatric DT should be used to complete the vaccination series. If the child was younger than 12 months old when the first dose of DT was administered (as DTaP or DT), the child should receive a total of four primary DT doses. If the child was 12 months of age or older at the time that the first dose of DT was administered, three doses (third dose 612 months after the second) completes the primary DT series. If the fourth dose of DTaP, DTP, or DT is administered before the fourth birthday, a booster dose is recommended at 46 years of age. The fifth dose is not required if the fourth dose was given on or after the fourth birthday. Because of waning antitoxin titers, most persons have antitoxin levels below the optimal level 10 years after the last dose of DTaP, DTP, DT, or Td. Additional booster doses of tetanus and diphtheria toxoids are required every 10 years to maintain protective antitoxin titers. The first booster dose of Td may be given at 11 or 12 years of age if at least 5 years have elapsed since the last dose of DTaP, DTP, or DT. The Advisory Committee on Immunization Practices (ACIP) recommendsthat this dose be administered as Tdap. If a dose is given sooner as part of wound management, the next booster is not needed for 10 years thereafter. More frequent boosters are not indicated and have been reported to result in an increased incidence and severity of local adverse reactions. Td is the vaccine of choice for children 7 years and older and for adults. A primary series is three or four doses, depending on whether the person has received prior doses of diphtheriacontaining vaccine and the age these doses were administered. The number of doses recommended for children who received one or more doses of DTP, DTaP, or DT before age 7 years is discussed above. For unvaccinated persons 7 years and older (including persons who cannot document prior vaccination), the primary series is three doses. The first two doses should be separated by at least 4 weeks, and the third dose given 6 to 12 months after the second. ACIP recommends that one of these doses (preferably the first) be administered as Tdap. A booster dose of Td should be given every 10 years. Tdap is approved for a single dose at this time (i.e., it should not be used for all the doses of Td in a previously unvaccinated person 7 years or older). Refer to the Pertussis chapter for more information about Tdap.

Interruption of the recommended schedule or delay of subsequent doses does not reduce the response to the vaccine when the series is finally completed. There is no need to restart a series regardless of the time elapsed between doses. Tetanus disease does not confer immunity because of the very small amount of toxin required to produce illness. Persons recovering from tetanus should begin or complete active immunization with tetanus toxoid (Td) during convalescence.

Contraindications and Precautions to Vaccination A severe allergic reaction (anaphylaxis) to a vaccine component or following a prior dose of tetanus toxoid is a contraindication to receipt of tetanus toxoid. If a generalized reaction is suspected to represent allergy, it may be useful to refer an individual for appropriate skin testing before discontinuing tetanus toxoid immunization. A moderate or severe acute illness is reason to defer routine vaccination, but a minor illness is not. If a contraindication to using tetanus toxoid-containing preparations exists, passive immunization with tetanus immune globulin (TIG) should be considered whenever an injury other than a clean minor wound is sustained. See the Pertussis chapter for additional information on contraindications and precautions to Tdap.

Adverse Reactions Following Vaccination Local adverse reactions (e.g., erythema, induration, pain at the injection site) are common but are usually self-limited and require no therapy. A nodule may be palpable at the injection site of adsorbed products for several weeks. Abscess the site of injection has been reported. Fever and other systemic symptoms are not common. Exaggerated local (Arthus-like) reactions are occasionally reported following receipt of a diphtheria- or tetanuscontaining vaccine. These reactions present as extensive painful swelling, often from shoulder to elbow. They generally begin from 2 to 8 hours after injections and are reported most often in adults, particularly those who have received frequent doses of diphtheria or tetanus toxoid. Persons experiencing these severe reactions usually have very high serum antitoxin levels; they should not be given further routine or emergency booster doses of Td more frequently than every 10 years. Less severe local reactions may occur in persons who have multiple prior boosters. Severe systemic reactions such as generalized urticaria (hives), anaphylaxis, or neurologic complications have been reported after receipt of tetanus toxoid. A few cases of peripheral neuropathy and Guillain-Barr syndrome (GBS) have been reported following tetanus toxoid administration. The Institute of Medicine has concluded that the available evidence favors a causal relationship between tetanus toxoid and both brachial neuritis and GBS, although these reactions are very rare. Vaccine Storage and Handling All tetanus-toxoid-containing vaccines should be stored at 3546F (28C). Freezing reduces the potency of the tetanus component. Vaccine exposed to freezing temperature should never be administered.

DAFTAR PUSTAKA 1. Epidemiological Record. Tetanus vaccine: WHO position paper. 2006, 81, 197208. 2. Aceh epidemiology group. Outbreak of tetanus cases following the tsunami in Aceh Province, Indonesia. Glob Public Health. 2006;1(2):173-7. 3. Sutiono AB, Qiantori A, Suwa H, Ohta T. Characteristic tetanus infection in disasteraffected areas: case study of the Yogyakarta earthquakes in Indonesia. BMC Res Notes. 2009 Mar 6;2:34. 4. Atkinson W, ed. Tetanus. In: Epidemiology and Prevention of Vaccine-Preventable Diseases. 12th ed. Washington DC: Public Health Foundation, 2011:291-300 http://www.cdc.gov/vaccines/pubs/pinkbook/pink-chapters.htm 5. http://herrysetyayudha.files.wordpress.com/2011/11/tetanus-pathogen2.jpg 6. http://www.dokterbedahherryyudha.com/2012/02/tetanus.html