32

CASE REPORT

PEDIATRIC TETANUS

Presenters: Fadillah Akbar S (080100063)

Endah Galih Harina (080100086)

Day/ Date: Tuesday/ October 2 2012

Supervisor: Prof. dr. Hj. Bidasari Lubis, Sp.A(K)

CHAPTER 1

INTRODUCTION

1.1. Background

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.

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, or 175 nanograms for a 70-kg human.

1.2.Objective

This paper is done in order to complete the task in following the doctor's professional education program in the department of pediatrics. In addition, providing knowledge to the author and readers about empyema thoracicCHAPTER 2

LITERATURE REVIEW

PEDIATRIC TETANUS

2.1. Definition

Tetanus is an intoxication by increased muscle tone dan spams caused by the release of the neurotoxin tetanospasmin by Clostridium tetani following inoculation into a human host. Tetanus occurs in several clinical forms, including generalzed, cephalic, localized, and neonatal disease. 1

Tetanus is disease with a spasm without major accompanied by impaired consciousness. These symptoms caused directly, instead of germs but as impact exotoxin (tetanospasmin) produced by germs at a synapse ganglion, the spinal cord connection neuro muskular and nerve autonom. 2

Tetanus is an acute, spastic paralytic illness caused by tetanospasmin, a neurotoxin produced by Clostridium tetani 4 2.2.Epidemiology and Risk Factor

Although C. tetani is located everywhere, the disease is encountered largely in underdeveloped, overcrowded, and economically disadvantaged countries. Because immunization is totally eff ective in preventing tetanus, it is most frequently noted in countries or in ethnic groups in which effective immunization is less likely to be achieved. In the United States, tetanus is encountered more frequently in blacks in the rural South, where a combination of more extensive exposure to spores and incomplete immunity are predisposing factors. 3

Tetanus is an entirely preventable disease; the first vaccine was produced in 1924. Routine vaccination began in the UK in 1961. It is given as a combined vaccine along with diphtheria and pertussis (DPT). Unfortunately, immunity to tetanus may not be life-long and booster injections may be required after individuals sustain tetanus-prone wounds. Tetanus immunization guidelines are available in the British National Formulary. Poor access to a programme of immunization accounts for the high prevalence of the disease in the developing world. Implementation of global tetanus immunization has been a target of the World Health Organization since 1974. Recently there has been a cluster of tetanus cases amongst injecting drug-users in the UK. Twenty-four cases were reported between 2003 and 2004. The majority of these had no record of (or, at best, incomplete) immunization. This outbreak is thought to be a result of a batch of contaminated heroin.2 I.M or s.c. drug-use is a particularly high risk activity for developing tetanus. 5 A marked decrease in mortality from tetanus occurred from the early 1900s to the late 1940s. In the late 1940s, tetanus toxoid was introduced into routine childhood immunization and tetanus became nationally notifiable. At that time, 500600 cases (approximately 0.4 cases per 100,000 population) were reported per year. 6

After the 1940s, reported tetanus incidence rates declined steadily. Since the mid-1970s, 50100 cases (~0.05 cases per 100,000) have been reported annually. From 2000 through 2007 an average of 31 cases were reported per year. The death-to-case ratio has declined from 30% to approximately 10% in recent years. An all-time low of 18 cases (0.01 cases per 100,000) was reported in 2009. 6During 2001 through 2008, the last years for which data have been compiled, a total of 233 tetanus cases was reported, an average of 29 cases per year. Among the 197 caes with known outcomes the case-fatality rate was 13%. Age of onset was reported for all 233 cases, of which, 49% were among persons 50 years of age or older. The median age was 49 years (range 5-94 years). A total of 138 (59%) were male. Incidence was similar by race. The incidence among Hispanics was almost twice that among non-Hispanics. However, when intravenous drug users (IDUs) were excluded the incidence was almost the same among Hispanics compared with non-Hispanics. 6

Almost all reported cases of tetanus are in persons who have either never been vaccinated, or who completed a primary series but have not had a booster in the preceding 10 years. Heroin users, particularly persons who inject themselves subcutaneously, appear to be at high risk for tetanus. Quinine is used to dilute heroin and may support the growth of C. tetani. Neonatal tetanus is rare in the United States, with only two cases reported since 1989. Neither of the infants' mothers had ever received tetanus toxoid.6

Tetanus toxoid (TT) vaccination status was reported for 92 (40%) of the 233 patients. A total of 37 patients (41%) received no TT doses, 26 (28%) received 1 dose, five (5%) received 3 doses, and 24 (26%) received 4 or more doses. Seven (24%) of 29 patients with 3 or more doses of TT had received their last dose within 10 years, 18 (62%) from 10 to 54 years previously, and four (14%) reported an unknown interval since their last dose. 6Among 195 patients whose medical history was known, 30 (15%.) were reported to have diabetes. Twenty-seven (15%) of 176 patients whose status was known were IDUs, of whom 16 (59%) were Hispanic. An acute wound preceded disease onset in 167 (72%) patients. Of those patient wounds, 132 (79%) were punctures, or contaminated, infected, or devitalized wounds considered tetanus-prone and eligible to receive tetanus immune globulin (TIG). Case reports for 51 (84%) of those who sought care were sufficiently complete to evaluate prophylaxis received; 49 (96%) did not receive appropriate TT prophylaxis or TT plus TIG as is currently recommended. Among all 233 patients, 31 (13%) reported a chronic wound or infection before disease onset, including diabetic ulcers and dental abscesses. Twenty-two (9%) reported no wounds or infections; of these, 14 were IDUs. 62.3.Etiology

The tetanus bacillus is a long, thin (2 to 5 m 3 to 8 m), motile, gram-positive anaerobic rod. Older cultures of these organisms and smears from wounds frequently stain as gram-negative microbes, and this result may be confusing to the uninitiated. These organisms may develop a terminal spore that does not take the Gram stain and gives the bacterium a drumstick appearance. The spores are very resistant to heat and the usual antiseptics, and they may persist in tissues for many months in a viable, although dormant, state. Under anaerobic conditions the organisms are easily isolated on blood agar or in cooked meat broth. The organism does not ferment carbohydrates, does not usually liquefy gelatin, and produces little change in litmus milk. The bacilli are widely distributed in soil; street dust; and the feces of some horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Consequently, manure-containing soil may be highly infectious. In agricultural areas a significant number of normal human adults may harbor the organisms, and agricultural workers have a higher incidence of infection. The spores have also been found in contaminated heroin.Tetanus bacilli produce a potent neurotoxin that is one of the most toxic substances known; the mouse LD50 of highly purified preparations is between 0.1 and 1 ng/kg (Schiavo et al., 1995 ). Tetanus neurotoxin derives its potency by virtue of its absolute specificity for neuronal cells and its target intracellular catalytic activity. 102.4.Etiopathogenesis

Tetanus result from infection with Clostridium tetani. Clostridium tetani is an obligate of anaerobic gram positive bacteria, mobile, nonencapsulated, and forms spores, which are resistant to heat, desiccation, and disinfectants. The spores are found in soil, house dust, animal intestines, and human feces. They need tissue with the proper anaerobic conditions to germinate; the ideal media are wounds with tissue necrosis. And the bacillus are found in or on soil, manure, dust, clothing, skin, and 10-25% of human GI tracts.7Most cases of tetanus are caused by direct contamination of wounds with the clostridial spores (Tolan, 2012). But these spores can persist in normal tissue for months to years.4 Clostridium tetani is not a tissue-invasive organism and cannot evoke an inflammatory reaction, unless co-infection with other organisms develops, so it has a benign appearance.2 If the conditions become anaerobic caused of low oxidationreduction potential, such as dead or devitalized tissue, a foreign body, or active infection,the spores in the tissue germinate and elaborate toxins in low oxidation-reduction potential (Eh) of an infected injury site.8

2.5.Pathophysiology

There are two kind of toxins produced by C. tetani, they are tetanospasmin and tetanolysin. Tetanolysin is not believed to be of any significance in the clinical course of tetanus. Tetanospasmin is a neurotoxin and causes the clinical manifestation of tetanus. Tetanospasmin that is released by the maturing bacilli is distributed via the lymphatic and vascular circulation to the end plates of all nerves.12A plasmid carries the toxin gene; the toxin is released with vegetative bacterial cell death and subsequent lysis. Tetanus toxin (tetanospasmin) are 150-kd simple proteins consisting of a heavy (100 kd) and a light (50 kd) chain joined by a single disulfide bond. Tetanus toxin binds at the neuromuscular junction and enters the motor nerve by endocytosis, after which it undergoes retrograde axonal transport to the cytoplasm of the alpha-motoneuron. In the sciatic nerve, the transport rate was found to be 3.4mm/hr. The toxin exits the motoneuron in the spinal cord and next enters adjacent spinal inhibitory interneurons, where it prevents release of the neurotransmitter -aminobutyric acid (GABA) by cleaving proteins crucial for the proper functioning of the synaptic vesicle release apparatus. The phenomenal potency of tetanus is enzymatic in nature. The light chain of tetanus is a zinc-containing endoprotease (zinc metalloprotease) whose substrate is synaptobrevin, a constituent protein of the docking complex that enables the synaptic vesicle to fuse with the terminal cell membrane.5 This diminished inhibition result in an increase in the resting firing rate of the motor neuron, which is responsible for the observed muscle rigidity.1The lessened activity of reflexes limits the polysynaptic spread of impulses (a glycinergic activity). Agonists and antagonists may be recruited rather than inhibited, with consequent production of spasms. Loss of inhibition may also affect preganglionic sympathetic neurons in the lateral gray matter of the spinal cord and produce sympathetic hyperactivity and high levels of circulating catecholamines. Finally, tetanospasmin can block neurotransmitter release at the neuromuscular junction, causing weakness and paralysis. The autonomic nervous system is also rendered unstable in tetanus. 1Localized tetanus develops when only the nerves supplying the affected muscle are involved. Generalized tetanus develops when the toxin released at the wound spreads through the lymphatics and blood to multiple nerve terminals. The blood-brain barrier prevents direct entry of toxin to the CNS. 12.6.Diagnosis

The diagnosis of tetanus may be established clinically. History

Most cases occur in patients with a history of only partial immunization. Persons who inject drugs also constitute a high-risk group. Symptoms usually begin 8 days (2-14 days) after the infection, but it may be as long as months after the injury, then the onset may range from 3 days to 3 weeks (Hinfey,2011). Tetanus may be either generalized, which is more common, or localized (Nelson). Patients may report a sore throat with dysphagia (early sign). The initial manifestation may be local tetanus, in which the rigidity affects only 1 limb or area of the body where the clostridium-containing wound is located.7Generalized Tetanus

The extent of the trauma in generalized tetanus varies from trivial injury to contaminated crush injury. The incubation period is 7-21 days, largely depending on the distance of the injury site from the CNS. Trismus is the presenting symptom in 75% of cases; a dentist or an oral surgeon often initially sees the patient. Other early features include irritability, restlessness, diaphoresis, and dysphagia with hydrophobia, drooling, and spasm of the back muscles. These early manifestations reflect involvement of bulbar and paraspinal muscles, possibly because they are innervated by the shortest axons.1 Muscle rigidity spreads in a descending pattern from the jaw and facial muscles over the next 24-48 hours to the extensor muscles of the limbs.12The simptom called sardonic smile of tetanus (risus sardonicus) results from intractable spasm of facial and buccal muscles. When the paralysis extends to abdominal, lumbar, hip, and thigh muscles, the patient may assume an arched posture of extreme hyperextension of the body, opisthotonos, with the head and the heels bent backward and the body bowed forward with only the back of the head and the heels touching the supporting surface. Opisthotonos is an equilibrium position that results from unrelenting total contraction of opposing muscles, all of which display the typical boardlike rigidity of tetanus.8Because tetanus toxin does not affect sensory nerves or cortical function, the patient unfortunately remains conscious, in extreme pain, and in fearful anticipation of the next tetanic seizure. These seizures are characterized by sudden, severe tonic contractions of the muscles, with fist clenching, flexion, and adduction of the arms and hyperextension of the legs. Without treatment, the seizures range from a few seconds to a few minutes in length with intervening respite periods, but as the illness progresses, the spasms become sustained and exhausting. The smallest disturbance by sight, sound, or touch may trigger a tetanic spasm. The tetanic paralysis usually becomes more severe in the 1st wk after onset, stabilizes in the 2nd wk, and ameliorates gradually over the ensuing 1-4 wk (Nelson). The condition may progress for 2 weeks despite antitoxin therapy because of the time needed for intra-axonal antitoxin transport.1Localized Tetanus

Localized tetanus causes painful spasms of muscle at the site of contaminated wound where spore inoculate.7 This is an unusual form of tetanus and the prognosis for survival is excellent.1 But localized tetanus may precede generalized tetanus. Cephalic tetanus is a rare form of localized tetanus involving the bulbar musculature that occurs with wounds or foreign bodies in the head, nostrils, or face. It also occurs in association with chronic otitis media. Cephalic tetanus is characterized by retracted eyelids, deviated gaze, trismus, risus sardonicus, and spastic paralysis of tongue and pharyngeal musculature.8 The prognosis for survival is usually poor.1Tetanus Neonatorum

Neonatal tetanus (tetanus neonatorum), the infantile form of generalized tetanus, typically manifests within 3-12 days of birth as progressive difficulty in feeding (i.e., sucking and swallowing), with associated hunger and crying.8 The usual cause is the use of contaminated materials to sever or dress the umbilical cord in newborns of unimmunized mothers. The usual incubation period after birth is 3-10 days, which is why it is sometimes referred to as the disease of the seventh day. Paralysis or diminished movement, stiffness to the touch, and spasms, with or without opisthotonos, characterize the disease. The umbilical stump may hold remnants of dirt, dung, clotted blood, or serum, or it may appear relatively benign (Nelson). The mortality rate exceeds 70%.1

Physical diagnostic

Generilized tetanus

In the inspection, sardonic smile (risus sardonicus) in the face and persistent spasm of the back musculature (opisthotonus) are found. Waves of opisthotonus are highly characteristic of the disease. With progression, the extremities become involved in episodes of painful flexion and adduction of the arms, clenched fists, and extension of the legs. Noise or tactile stimuli may precipitate spasms and generalized convulsions. Involvement of the autonomic nervous system may result in severe arrhythmias, oscillation of the blood pressure, profound diaphoresis, hyperthermia,rhabdomyolysis, laryngeal spasm, and urinary retention. In most cases, the patient remains lucid. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate.12 Fever, occasionally with a temperature as high as 40C, is common because of the substantial metabolic energy consumed by spastic muscles. Laryngeal and respiratory muscle spasm can lead to airway obstruction and asphyxiation. Dysuria and urinary retention result from bladder sphincter spasm; forced defecation may occur.8Tetanus Neonatorum

This is generalized tetanus that results from infection of a neonate. It primarily occurs in underdeveloped countries and accounts for up to one half of all neonatal deaths. Physical examination findings are similar to generalized tetanus findings. The newborn usually exhibits irritability, poor feeding, rigidity, facial grimacing, and severe spasms with touch. 8Localized Tetanus

In mild cases, patients may have weakness of the involved extremity, presumably due to partial immunity. In more severe cases, intense painful spasms occur and usually progress to generalized tetanus. In cephalic tetanus, cranial nerve findings and rapid progression are typical. This form may remain localized or progress to generalized tetanus.1Laboratory test

Wounds should be cultured in suspected cases. However,C tetanican be cultured from wounds of patients without tetanus and frequently cannot be cultured from wounds of patients with tetanus.The leukocyte count may be high. Cerebrospinal fluid examination yields normal results.1Serum antitoxin levels of 0.01 or higher are considered protective and make tetanus unlikely, although rarely cases have been reported despite the presence of protective antitoxin levels. Serum muscle enzyme levels (eg, creatine kinase, aldolase) may be elevated. 12.7.Differential Diagnosis

Fully developed, generalized tetanus cannot be mistaken for any other disease. However, trismus may result from parapharyngeal, retropharyngeal, or dental abscesses, or rarely, from acute encephalitis involving the brainstem. Either rabies or tetanus may follow an animal bite, and rabies may present as trismus with seizures. However, rabies may be distinguished from tetanus by its hydrophobia, marked dysphagia, predominantly clonic seizures, and CSF pleocytosis. Although strychnine poisoning may result in tonic muscle spasms and generalized seizure activity, it seldom produces trismus, and unlike tetanus, general relaxation usually occurs between spasms. Hypocalcemia may produce tetany, characterized by laryngeal and carpopedal spasms, but trismus is absent. Occasionally, epileptic seizures, narcotic withdrawal, or other drug reactions may suggest tetanus.5 And, the other differential diagnosis are meningitis which found meningens signs and bacteria or different CSF composition.12.8.ManagamentManagement of tetanus requires eradication of C. tetani and the wound environment conducive to its anaerobic multiplication, neutralization of all accessible tetanus toxin, control of seizures and respiration, palliation and provision of meticulous supportive care, and, finally, prevention of recurrences.8 All patients should be admitted to a medical or neurological intensive care unit where they can be monitored and observed continuously. Some hospitals in which tetanus is frequently encountered have specially constructed, quiet, dark rooms to minimize extrinsic stimuli that might trigger paroxysmal spasms. Patients must be allowed to rest quietly to limit peripheral stimuli, and they must be positioned carefully to prevent aspiration pneumonia. Intravenous fluids should be instituted, and electrolytes and blood gases are essential to guide therapy.3Surgical wound excision and debridement is often needed to remove the foreign body or devitalized tissue that created anaerobic growth conditions. Surgery should be done promptly, after the administration of human tetanus immunoglobulin (TIG) and antibiotics. Excision of the umbilical stump in neonatal tetanus is no longer recommended.8Once tetanus toxin has begun its axonal ascent to the spinal cord, it cannot be neutralized by TIG. Accordingly, TIG is given as soon as possible to neutralize toxin that diffuses from the wound into the circulation before the toxin can bind at distant muscle groups. An optimal dose of TIG has not been determined. A single intramuscular injection of 500 U of TIG is sufficient to neutralize systemic tetanus toxin, but total doses as high as 3,000-6,000 U are also recommended. Infiltration of TIG into the wound is now considered unnecessary. If TIG is unavailable, use of human intravenous immunoglobulin (IVIG), which contains 4-90 U/mL of TIG, or of equine- or bovine-derived tetanus antitoxin (TAT), may be necessary. However, the optimal dosage of IVIG is not known, and it is not approved for this indication. The usual dose of TAT is 50,000-100,000 U, with half given intramuscularly and half intravenously, but as little as 10,000 U may be sufficient. TAT is not available in the United States. Approximately 15% of patients given the usual dose of TAT experience serum sickness. When using TAT, it is essential to check for possible sensitivity to horse serum and desensitization may be needed. The human-derived immunoglobulins are much preferred because of their longer half-life (30 days) and the virtual absence of allergic and serum sickness adverse effects. Intrathecal TIG, given to neutralize tetanus toxin in the spinal cord, is not effective.8Penicillin is the standard therapy for tetanus in most parts of the world, although antibiotics for C.tetani probably play a relatively minor role in the specific treatment of this disease. Recommended dose is 100,000200,000 IU/day intramuscularly or intravenously for 710 days. In 1945, it was first noted that intravenous administration of penicillin could produce convulsions. The animal models had myoclonic convulsions caused penicillin when applied directly to the cortex. Penicillin became the standard model for producing experimental focal epilepsy.3Metronidazole has been considered the first line of therapy and is a safe alternative to penicillin. Rectal administration of metronidazole is rapidly bioavailable and produces fewer spasms than repeated intravenous or intramuscular injections. Dose is 400 mg rectally or 500 mg intravenously every 6 hours for 710 days.3All patients with generalized tetanus need muscle relaxants. Diazepam provides both relaxation and seizure control; the initial dose of 0.1-0.2/kg q 3-6 hr given intravenously is then titrated to control the tetanic spasms, after which it is sustained for 2-6 wk before its tapered withdrawal. Magnesium sulfate, other benzodiazepines (e.g., midazolam), chlorpromazine, dantrolene, and baclofen are also used. Intrathecal baclofen produces such complete muscle relaxation that apnea often ensues; like most other agents listed, baclofen should be used only in an intensive care unit setting. The best survival rates in generalized tetanus are achieved with neuromuscular blocking agents such as vecuronium and pancuronium, which produce a general flaccid paralysis that is then managed by mechanical ventilation. Autonomic instability is regulated with standard - and - (or both) blocking agents; morphine has also proved useful.82.9.Prevention

Because there is essentially no natural immunity to tetanus toxin, the only effective way to control tetanus is by prophylactic immunization. Thus, universal primary immunization with subsequent maintenance of adequate antitoxin levels by means of appropriately timed boosters is necessary to protect all age groups.3Table 1 Clinical guideline for tetanus prophylaxis10History of

Full TT Course

or

TT BoosterSimple Wounds

(non-Tetanus prone)Complicated wounds

TTHTIGTTHTIG

No or unknownFull courseNoFull CourseConsider

Full TT course < 5 yearsNoNoNoNo

Full TT course 5 10 yearsNoNoBoosterNo

Full TT course > 10 yearsBoosterNoBoosterConsider

Human Tetanus Immune Globulin (HTIG) should be reserved for protecting non-immunised patients or patients having existing immune deficient conditions with wounds that are considered to be Tetanus-prone. Advice from senior medical staff should be sought when in doubt. HTIG is safe and indicated for patients with a contraindication to TT (such as anaphylaxis) and have a Tetanus-prone wound.11Table 2 Tetanus prone wounds and Non-tetanus prone wounds11Clinical FeaturesTetanus prone woundsNon-tetanus prone wounds

Age of wound

Configuration

Depth

Mechanism of injury

Signs of infection

Devitalized tissue

Contaminants

Denervated and/or ischemic tissue> 6 hours

Stellate wound, avulsion

> 1 cm

Missile, crush, burn, frostbite

Present

Present

Present

Present< 6 hours

Linear wound, abrasion

< 1 cm

Sharp surface

Absent

Absent

Absent

Absent

2.10. Complications

The seizures and the severe, sustained rigid paralysis of tetanus predispose the patient to many complications. Aspiration of secretions and pneumonia may have begun before the first medical attention was received. Maintaining airway patency often mandates endotracheal intubation and mechanical ventilation with their attendant hazards, including pneumothorax and mediastinal emphysema. The seizures may result in lacerations of the mouth or tongue, in intramuscular hematomas or rhabdomyolysis with myoglobinuria and renal failure, or in long bone or spinal fractures. Venous thrombosis, pulmonary embolism, gastric ulceration with or without hemorrhage, paralytic ileus, and decubitus ulceration are constant hazards. Excessive use of muscle relaxants, an integral part of care, may produce iatrogenic apnea. Cardiac arrhythmias, including asystole, unstable

blood pressure, and labile temperature regulation reflect disordered autonomic nervous system control that may be aggravated by inattention to maintenance of intravascular volume needs.82.11. PrognosisThe most important factor influencing outcome is the quality of supportive care. Mortality is highest in the very young and the very old. A favorable prognosis is associated with a long incubation period, with the absence of fever, and with localized disease. An unfavorable prognosis is associated with a week or less between the injury and the onset of trismus and with 3 days or less between trismus and the onset of generalized tetanic spasms. Sequelae of hypoxic brain injury, especially in infants, include cerebral palsy, diminished mental abilities, and behavioral difficulties. Most fatalities occur within the 1st wk of illness. Reported case fatality rates for generalized tetanus range between 5% and 35% and for neonatal tetanus extend from 75% without it. Cephalic tetanus has an especially poor prognosis because of breathing and feeding difficulties.CHAPTER III

CASE REPORT

Name

: Gilang Ramadhan

Age

: 3 tahun

Sex

: Male

Address

: Jl. L Sujono G Palapa I LK VIII Bandar Selamat Medan

Date of Admission: 1 September 2012

Major Complaint: difficulty in opening the mouth

History

: Patient has been experiencing this condition for the past 5 days, rigidity of abdominal muscle is found to be experiencing for past 5 days, rigidity of limbs muscle is found to be experiencing for past 5 days. Spasm after stimulation is found to be experiencing for past 5 days. Cough and shortness of breath is found to be experiencing for past 5 days. Fever is not found. Generalized spasticity is found, freq 1x, it is experiencing for past 1 day. History of tooth carries is found. History of wound on right sole of foot is found but patient doesnt know when and what caused.History of birth

: patient is single son in familyHistory of immunization: not completeHistory of nutrition

: 0-6 months : breast milk

History of medications: -

Physical examination

Presence Status:Sensorium: compos mentis. Temperature: 36,8(C.

Anemic (-), dyspnea (-), cyanotic (-), edema (-), icteric (-).

Body weight (BW): 12 kg. Body length (BL): 65 cm

CDC: BW/Age = 95.8%, BL/Age = 98.5%, BW/BL = 97.5%

Localized status :

Head: Eye: light reflex (+/+), isochoric pupil, pale inferior conjunctiva palpebra (-/-). Ear: within normal limit. Nose: within normal limit. Mouth: trismus (+) 0.5 cm. Face: risus sardonicus (+). Neck:Lymph node enlargement (-).

Thorax:symmetries fusiform, retraction (-)

HR: 112 bpm, regular, murmur (-)

RR : 22 x/minute, regular, ronkhi (-/-)

Abdomen: Peristaltic (+), muscular rigidity (+), liver and spleen not palpable.

Extremities : Pulse = 112 bpm, regular, adequate pressure/volume, warm axilla, capillary refill time (CRT) < 3, clubbing finger (-), BCG scar (-) right arm.Genitalia:Male, within normal limit and anus (+).

Laboratory Result: September 1st 2012

TestResultsNormal ValueUnit

Complete Blood Count

Hemoglobin (Hb)10.7011.3 14.1g %

Erytrocyte (RBC)4.824.40 4.48106/mm3

Leukocyte (WBC)16.314.5 13,5103/mm3

Hematocrite33.3037 41 %

Trombocyte (PLT)584150 450 103/mm3

MCV69.2081 - 95fL

MCH22.2025 29 pg

MCHC32.1029 31 g %

RDW17.4011.6 14.8 %

MPV9.507.0 10.2 fL

PCT8.30%

PDW8.6fL

Neutrofil84.3037 80%

Limfosit12.8020 40 %

Monosit2.802 8 %

Eosinophil0.001 6 %

Basophil0.1000 1 %

Neutrophil absolute13.752,4 7,3103/L

Limfosit absolute2.091.5 5,1103/L

Monosit absolute0.460.2 0.6103/L

Eosinophil absolute0.000.10 0.30103/L

Basophil absolute0.010 0.1 103/L

ParametersResultsNormal ValueUnit

Faal Hemostasis

PT + INR

Protombin Time

Control12.30Second

Pasient11.80Second

INR0.94

APTT

Control30.2Second

Patient28Second

Trombin Time

Control17.8Second

Patient18Second

Clinical Chemistry

Liver

AST/SGOT95