Case Report Mine

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CASE REPORT

SENIOR CLINICAL CLERKSHIP

Periode of January 17th 2011February 14th 2011

Intan Noor Indah S. Ked (04061001120)

Said Syabri Albana (04061001087)

Advisor:

Dr. H. A. Rachman Toyo, Sp.S (K)

DEPARTMENT OF NEUROLOGY

FACULTY OF MEDICINE SRIWIJAYA UNIVERSITY / RSMH

PALEMBANG

2011


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NEUROLOGY MEDICAL RECORD

Identification

Name : Mr YAge : 23th years old

Sex : Male

Address : Ogan Ilir

Religion : Islam

Admission date : February 28th, 2013

Anamnesis (Autoanamnesis)

The patient was admitted to RSMH Neurology ward because he complained of

difficulty to open his mouth and sudden seizure.+ 1 day before admitted to the hospital, the patient complain that he could not

open his mouth at all and suffered from tonic seizure especially when stimulated. There

was no difficulty of breathing reported. The patient also complained stomach and neck

stiffness.

+ 10 days ago patient had history of being pricked by a nail on his left foot.

Patient was not given any antitetanus injection on his left foot, and has history of tooth

decay. The patient suffered from this illness for the first time.

PHYSICAL EXAMINATION

PRESENT STATE

Internal State

Sense : compos mentis

Nutrition : Sufficient

Pulse : 72 beats/min

Respiratory rate : 18 times/min

Blood pressure : 130/60 mmHg

Psychiatric stateAttitude : cooperative

Attention : present

Neurological stateHead

Shape : brachiocephaly

Size : normal

Symetric : symetricHematome : no

GCS = 15 (E4 M6 V5)

Heart :72 x/m,murmur(-),gallop (-)

Lungs :vesikuler(+)N,ronkhi(-),

wheezing (-)

Abdomen : muscle stiffness (+)

Liver : no abnormality

Spleen : no abnormalityExtremities : (see neurological state)

Genital : was not examined

Facial Expression : naturally

Physical contact : present

Deformity : no

Fracture : noFracture pain : no


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Tumor : no

Neck

Position : straight

Torticolis : no

Nape of neck stiffness : yes (+)

Vessel : no widening

Pulsation : no disorder

Deformity : no

Tumor : noVessels : no widening

CRANIAL NERVES

Olfaktorius nerve

Smelling

Anosmia

Hyposmia

Parosmia

Opticus nerve

Visual acuityCampus visi (cannot determine)

Anopsia Hemianopsia

Oculi fundus

Edema papil Atrophy papil Retina bleeding

Occulomotorius,Trochlearis

and Abducens nerves

Diplopia

Eyes gap

Ptosis

Eyes position

Strabismus

Exophtalmus Enophtalmus Deviation conjugae

Eyes movement

Pupil

Shape Size Isochor/anisochor Midriasis/miosis

Light reflex

direct consensuil

Right

no abnormality

-

-

-

Right

6/6V.O.D

-

-

was not examined

was not examined

was not examined

Right

-

symetric

-

NoNo

No

No

Good to all direction

Round

3mm

isochor

No

++

Left

no abnormality

-

-

-

Left

6/6V.O.S

-

-

was not examined

was not examined

was not examined

Left

-

symetric

-

NoNo

No

No

Good to all direction

Round

3mm

isochor

No

++


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accommodationArgyl Robertson

Trigeminus nerveMotoric

Biting Trismus Corneal reflex

Sensory

Forehead Cheek Chin

Facialis nerveMotoric

Frowning

Eyes closingGiggling

Nasolabial fold

Facial shape

rest Speaking/whistling

Sensory

2/3 anterior toungeAutonomy

Salivation Lacrimation Chvosteks sign

Statoacusticus nerve

Cochlearis nerveWhispering

Hour ticking

Weber test

Rinne test

Vestibularis nerveNystagmus

Vertigo

Glossopharingeus and Vagus

nervesPharyngeal arch

Uvula

Swallowing disorder

Hoarsing/nasalising

Heart beat

Reflex Vomiting

+

No

Right

no abnormalityno abnormality

no abnormality

no abnormality

no abnormality

no abnormality

Right

no abnormality

no abnormality

no lagophtalmusno abnormality

no abnormality

symetric

symetric

no abnormality

no abnormality

no abnormality

no abnormality

Right

no abnormality

no abnormality

was not examined

was not examined

No

-

Right

symetric

Centre

(-)

no abnormality

no abnormality

was not examined

+

No

Left

no abnormalityno abnormality

no abnormality

no abnormality

no abnormality

no abnormality

Left

no abnormality

no abnormality

no lagophtalmusno abnormality

no abnormality

symetric

symetric

no abnormality

no abnormality

no abnormality

no abnormality

Left

no abnormality

no abnormality

was not examined

was not examined

No

-

Left

Symetric

Centre

(-)

no abnormality

no abnormality

was not examined


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Coughing Occulocardiac Caroticus sinus

Sensory

1/3 posterior tounge

was not examined was

was not examined

was not examined

no disorder

was not examined

was not examined

was not examined

No disorder

Accessorius NerveShoulder Raising

Head Twisting

Hypoglossus NerveTounge Showing

Fasciculation

Papil AthrophyDysarthria

MOTORICArms:

Motion

Power

Tones

Physiological Reflex

Biceps Triceps Radius Ulna

Pathological Reflex

Hoffman Tromner Leri Meyer

Trofik

Legs:

Motion

PowerTones

Clonus

Tigh Foot

Physiological reflex

K P R A P R

Pathological reflex

Babinsky Chaddock Oppenheim Gordon

Right

symetris

no abnormality

Right

no deviation

no

nono

Right

Sufficient

5

Increased

Normal

Normal

Normal

Normal

None

None

None

None

Right

Sufficient

5Normal

-

-

Normal

Normal

-

-

--

Left

symetris

no abnormality

Left

no deviation

no

nono

Left

Sufficient

5

Increased

Normal

Normal

Normal

Normal

None

None

None

None

Left

Sufficient

5Normal

-

-

Normal

Normal

-

-

--


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Schaeffer Rossolimo Mendel Bechterew

Abdominal skin reflex

Upper Middle Lower Trofik

-

-

-

++

+

Normotrofik

-

-

-

++

+

Normotrofik

SENSORY No abnormalities

PICTURE


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VEGETATIVE FUNCTIONMicturition : normal

Defecation : normal

Erection : normal

VERTEBRAL COLUMNKyphosis : no Tumor : no

Lordosis : no Meningocele : no

Gibbus : no Hematome : no

Deformity : no Tenderness : no

SYMPTOMS OF MENINGEAL IRRITATION

Nape of neck stiffness

Kerniq

Lasseque

Brudzinsky Neck Cheek Symphisis Leg I Leg II

Right

-

-

-

-

-

-

-

-

Left

-

-

-

-

-

-

-

-

GAIT AND EQUILIBIRIUM

Gait

Ataxia : couldnt be assessed

Hemiplegic : couldnt be assessed

Scissor : couldnt be assessed

Propulsion : couldnt be assessed

Trunk Ataxia :couldnt be assessed

Limb Ataxia :couldnt be assessed

Equilibirium and CoordinationRomberg :couldnt be assessed

Dysmetri :couldnt be assessed

fingerfinger :couldnt be assessed

finger nose :couldnt be assessed

Histeric : couldnt be assessedheel - heel :couldnt be assessed

Limping : couldnt be assessed

Reboundphenomenon :couldnt be assessed

Steppage : couldnt be assessed

Dysdiadochokinesis :couldnt be assessed

Astasia-Abasia: -

MOTION ABNORMALTremor : no

Chorea : noAthetosis : no


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Ballismus : no

Dystoni : no

Myoclonus : no

LIMBIC FUNCTION

Motoric aphasia : -Sensoric aphasia : -

Apraksia : -

Agraphia : -

Alexia : -

Nominal aphasia : -

LABORATORY FINDINGS

BLOOD (1st

March 2013)Hb : 14.3 gr/dl

Leucocyte : 12.500/mm3

Erytrocyte : 4.44x 106/mm3Hematocrit : 42 vol%

Diff Count : 0/2/0/68/20/10

Thrombocyte : 184.000/mm3

BSS : 84 mg/dl

URINE

Colour : Not performed Sedimen:

Reaction : Not performed - Eritrocyte : Not performed

Protein : Not performed - Leukocyte : Not performed

Glucose : Not performed - Epithel : Not performed

Reduction : Not performed - Bacteria : Not performed

Urobilin : Not performed - Crystal : Not performed

Bilirubin : Not performed

FECES

Consistency : not performed Erytrocyte : not performed

Slime : not performed Leucocyte : not performed

Blood : not performed Worm egg : not performed

Amoeba coli/ : not performedHystolitica : not performed

CEREBRO SPINAL FLUID

Colour : not performed Protein : not performed

Clarity : not performed Glucose : not performed

Pressure : not performed NaCl : not performed

Cell : not performed Queckensted : not performed

Nonne : not performed Celloidal : not performed

Pandy : not performed Culture : not performed


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SPECIFIC EXAMINATION

Cranium X- Ray : not performed

Chest X- Ray : not performed

Vertebral column X- Ray : not performed

Electroencephalography : not performed

Electroneuromyography : not performedElectrocardiography : not performed

Arteriography : not performed

Pneumography : not performed

CT-Scan : not performed

RESUME

IDENTIFICATION

Name : Mr YAge : 23 years old

Sex : Male

Occupation : Employee

Address : Ogan Ilir

Religion : Islam

Admission date: 28th February 2013, 15.02 pm

ANAMNESIS

The patient was admitted to RSMH Neurology ward because he complained of

difficulty to open his mouth and sudden seizure.

+ 1 day before admitted to the hospital, the patient complain that he could not

open his mouth at all and suffered from tonic seizure especially when stimulated. There

was no difficulty of breathing reported. The patient also complained stomach and neck

stiffness.

+ 10 days ago patient had history of being pricked by a nail on his left foot. Patient was

not given any antitetanus injection on his left foot, and has history of tooth decay. The

patient suffered from this illness for the first time.

EXAMINATION

Present State

Sense : compos mentis (GCS 15: E4M6V5)

Blood pressure : 120 / 80 mmHg

Pulse : 72x/minute

Respiratory rate : 18x/minute

Temperature : 36,7o C

Nutrition : sufficient

Neurological state

Nn. Craniales :n.III: round pupil, ischor, 3 mm, light reflex +/+


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n.V : Trismus was found on finger

n. XII: no abnormalities

Motoric function

Motoric function Arm Leg

Right Left Right LeftMotion Sufficient Sufficient Sufficient Sufficient

Power 5 5 5 5

Tones Normal Normal Normal Normal

Clonus - -

Physiological reflex Increased Increased Increased Increased

Pathological reflex - - - -

Sensory function : no abnormality

Vegetative function : no abnormality

Limbic function : no abnormality

Abnormal Movement : (-)

Gait & Stability : no abnormality

Meningeal Irritation : stiffed neck(-), kernigs sign (-), lasseques sign (-)

LABORATORY FINDINGS

(1st

March 2013)

Hb : 14.3 gr/dl

Leucocyte : 12.500/mm3

Hematocrit : 42 vol%

Diff Count : 0/2/0/68/10/4Thrombocyte : 184.000/mm3

BSS : 84 mg/dl

HEART

CK-NAC : 223 U/L

URINE

Was not examine

FAECES

Was Not examine

DIAGNOSIS

Clinical diagnostic : Tetanus

Diagnosis topic : Neuromuscular junction (NMJ)

Diagnosis etiology : Infection

MANAGEMENTTreatment :

Medicine : IVFD RL gtt XX/menit

Ceftriaxone injection 2x 2 gr IV (skin test should be done)Anti-tetanus 20,000 for 5 days ( skin test should be done)


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Diazepam injection

Assesment prodebridement surgery

PROGNOSIS : Quo ad vitam : dubia ad bonam

Quo ad functionam : dubia

BAB II

2,1 DEFINITIONTetanus is a neurologic disorder, characterizied by increased muscle tone and spasms,

that is caused by tetanospasmin, a powerful proteintoxin elaborated by Clostridiumtetani. Tetanus occurs in several clinical forms, including generalized, neonatal and

localized disease. It is an illness characterized by an acute onset of hypertonia, painful

muscular contractions (usually of the muscles of the jaw and neck), and generalized

muscle spasms without other apparent medical causes. Despite widespread

immunization of infants and children in the United States since the 1940s, tetanus still

occurs in the United States. Currently, tetanus is a severe disease primarily of older

adults who are unvaccinated or inadequately vaccinated.

2.2 CLASSIFICATION

Tetanus may be categorized into the following 4 clinical types:

Generalized Localized Cephalic Neonatal

2.3 SIGN AND SYMPTOMPS

Generalized tetanus, the most common form of the disease, is characterized by

increased muscle tone and generalized spasms. The median time of onset after injury is7 days: 15% of cases occurs within 3 days and 10% after 14 days. Typically, the patient

first notices increased tone in the masseter muscles (trimus or lockjaw). Dysphagia or

stiffness or pain in the neck, shoulder and back muscles appears concurrently or soon

there after subsequent involvement of other muscles procedure a rigid abdomen and

stiff prozimal limb muscles, the hands and feet are relatively spared. Sustained

contraction of the facial muscles results in a grimace or sneer, and contraction of the

back muscles produces an arched back (opisthotonos). Some patients develop

paroxysmal, violent, painful, generalized muscle spasms that may cause cyanosis and

threaten ventilation. These spasms occur repetitively and may be spontaneous or

provoked by even the slightest stimulation. A constant threat during generalized spasms

is reduced ventilation or apnea or laryngospasm. The severity of illness may be mild (muscle rigidity and spasms), or moderate (trismus, dysphagia, rigidity and spasms) or


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severe (frequent explosive paroxysms). The patient maybe febrile, although many

patients have no fever; mentation is unimpaired. Deep tendon replaced may be

increased. Dysphagia or ileus may preclude oral feeding.

Autonomic dysfunction commonly complicates severe cases and is characterized by

labile or sustained hypertension, tachycardia, dysrhythma, hyperpyrexia, profusesweating, peripheral vasoconstriction, and increased plasma and urinary catecholamine

levels. Periods of bradycardia and hypotension may also be documented. Sudden

cardiac arrest sometimes occurs, bt uts bases is unknown. Other complications include

aspiration pneumonia, fractures, muscle rupture, deep-vein thrombophlebitis,

pulmonary emboli, decubitus ulcer and rhabdomyolysis.

Approximately 50-75% of patients with generalized tetanus present with trismus

(lockjaw), which is the inability to open the mouth secondary to masseter muscle

spasm. Nuchal rigidity and dysphagia are also early complaints that cause risus

sardonicus, the scornful smile of tetanus, resulting from facial muscle involvement.[1]

As the disease progresses, patients have generalized muscle rigidity with intermittent

reflex spasms in response to stimuli (e.g. noise, touch). Tonic contractions cause

opisthotonos (ie, flexion and adduction of the arms, clenching of the fists, and extension

of the lower extremities). During these episodes, patients have an intact sensorium and

feel severe pain. The spasms can cause fractures, tendon ruptures, and acute respiratory

failure.

Patients with localized tetanus present with persistent rigidity in the muscle group close

to the injury site. The muscular rigidity is caused by a dysfunction in the interneurons

that inhibit the alpha motor neurons of the affected muscles. No further central nervous

system (CNS) involvement occurs in this form, and mortality is very low.

Cephalic tetanus is uncommon and usually occurs after head trauma or otitis media.

Patients with this form present with cranial nerve (CN) palsies. The infection may be

localized or may become generalized.

i) Generalized tetanusGeneralized tetanus is the most commonly found form of tetanus in the United States,

accounting for 85-90% of cases. The extent of the trauma varies from trivial injury to

contaminated crush injury. The incubation period is 7-21 days, largely depending on thedistance of the injury site from the central nervous system (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 these structures

are innervated by the shortest axons. The condition may progress for 2 weeks despite

antitoxin therapy because of the time needed for intra-axonal antitoxin transport.

ii) Localized tetanus


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Localized tetanus involves an extremity with a contaminated wound and is of highly

variable severity. It is an unusual form of tetanus, and the prognosis for survival is

excellent.

iii) Cephalic tetanusCephalic tetanus generally follows head injury or develops with infection of the

middle ear. Symptoms consist of isolated or combined dysfunction of the cranial

motor nerves (most frequently CN VII). Cephalic tetanus may remain localized or

may progress to generalized tetanus. It is an unusual form of tetanus with an

incubation period of 1-2 days. The prognosis for survival is usually poor

iv) Neonatal tetanus

Neonatal tetanus (tetanus neonatorum) is generalized tetanus that results from infection

of a neonate. It primarily occurs in underdeveloped countries and accounts for as many

as one half of all neonatal deaths. The usual cause is the use of contaminated materialsto sever or dress the umbilical cord in newborns of unimmunized mothers.

The usual incubation period after birth is 3-10 days, which explains why this form of

tetanus is sometimes referred to as the disease of the seventh day. The newborn usually

exhibits irritability, poor feeding, rigidity, facial grimacing, and severe spasms with

touch. Mortality exceeds 70%.

2.4 ETIOLOGY

The etiologic agent of tetanus, C tetani, is an anaerobic, motile, gram-positive rod that

forms an oval, colorless, terminal spore and assumes a shape that resembles a tennis

racket or a drumstick. The spores may survive for years in some environments and are

resistant to disinfectants and to boiling for 20 minutes. Vegetative cells are easily

inactivated and are susceptible to several antibiotics.

Tetanus can be acquired outdoors as well as indoors. The source of infection usually is

a wound (approximately 65% of cases), which often is minor (eg, from wood or metal

splinters or thorns). Frequently, no initial medical treatment is sought. Chronic skin

ulcers are the source in approximately 5% of cases, and in the remainder of cases, no

obvious source is identified.

Tetanus can also develop as a complication of chronic conditions such as abscesses and

gangrene, and it may complicate burns, frostbite, middle ear infections, dental or

surgical procedures, abortion, childbirth, and intravenous (IV) or subcutaneous drug

use. In addition, possible sources not usually associated with tetanus include otitis

media, intranasal and other foreign bodies, and corneal abrasions.

Under immunization is an important cause of tetanus. Tetanus affects nonimmunized

persons, partially immunized persons, or fully immunized individuals who do not

maintain adequate immunity with periodic booster doses.

Only 12-14% of patients with tetanus in the United States have received a primaryseries of tetanus toxoid. During 1998-2000, only 6% of all patients with tetanus were


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known to be current with tetanus immunization, with no fatal cases reported among this

group.[8] Surveillance data from this period revealed the following:

In 73% of patients with tetanus in the United States, tetanus occurred after anacute injury, including puncture wounds (50%), lacerations (33%), and

abrasions (9%) Of those who obtained medical treatment of their injury in the United States

from 1998 to 2000, 96% received tetanus immune globulin (TIG) as part of their

treatment; 55% of patients required assisted ventilation, and 31% of these

patients died

Stepping on a nail accounted for 32% of the puncture wounds Tetanus was found to occur in burn victims; in patients receiving intramuscular

injections; in persons obtaining a tattoo; and in persons with frostbite, dental

infections (eg, periodontal abscesses), penetrating eye injuries, and umbilical

stump infections

Other reported risk factors included diabetes, chronic wounds (eg, skin ulcers,abscesses, or gangrene), parenteral drug abuse, and recent surgery (4% of UScases)

During 1998-2000, 12% of patients with tetanus in the United States haddiabetes (with mortality, 31%), compared with 2% during 1995-1997; of these

patients, 69% had acute injuries and 25% had gangrene or a diabetic ulcer

The median time interval between surgery and onset of tetanus was 7 days Tetanus was reported after tooth extractions, root canal therapy, and intraoral

soft tissue trauma

World wide risk factors for neonatal tetanus include the following:

Unvaccinated mother, home delivery, and unhygienic cutting of the umbilicalcord increase susceptibility to tetanus

A history of neonatal tetanus in a previous child is a risk factor for subsequentneonatal tetanus

Potentially infectious substances applied to the umbilical stump (eg, animaldung, mud, or clarified butter) are risk factors for neonates

Immunity from tetanus decreases with advancing age. Serologic testing for immunity

has revealed a low level among elderly individuals in the United States. Approximately

50% of adults older than 50 years are nonimmune because they never were vaccinated

or do not receive appropriate booster doses. The prevalence of immunity to tetanus inthe United States exceeds 80% for persons aged 6-39 years but is only 28% for those

older than 70 years.

2.5 EPIDEMIOLOGY

I) International statistics


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C tetani is found worldwide in soil, on inanimate objects, in animal feces, and,

occasionally, in human feces. Tetanus is predominantly a disease of underdeveloped

countries. It is common in areas where soil is cultivated, in rural areas, in warm

climates, during summer months, and among males. In countries without a

comprehensive immunization program, tetanus predominantly develops in neonates and

young children.[10, 11]

Developed nations have incidences of tetanus similar to those observed in the United

States. For instance, only 126 cases of tetanus were reported in England and Wales in

1984-1992.

Although tetanus affects all ages, the highest prevalence is in newborns and young

people.[12] In 1992, an estimated 578,000 infant deaths were attributed to neonatal

tetanus. In 1998, 215,000 deaths occurred, more than 50% of them in Africa. Tetanus is

a target disease of the World Health Organization (WHO) Expanded Program on

Immunization. Overall, the annual incidence of tetanus is 0.5-1 million cases. WHO

estimated that in 2002, there were 213,000 tetanus deaths, 198,000 of them in childrenyounger than 5 years.

ii) Age Related

Neonatal tetanus is rare, occurring most frequently in countries without comprehensive

vaccination programs.

The risk for development of tetanus and for the most severe form of the disease is

highest in the elderly population. In the United States, 59% of cases and 75% of deaths

occur in persons aged 60 years or older. From 1980 through 2000, 70% of reported

cases of tetanus in the United States were among persons aged 40 years or older. Of all

these patients, 36% are older than 59 years and only 9% are younger than 20 years.

iii) Sex- related

Tetanus affects both sexes. No overall gender predilection has been reported, except to

the extent that males may have more soil exposure in some cultures. In the United

States from 1998 to 2000, the incidence of tetanus was 2.8 times higher in males aged

59 years and younger than in females in the same age range.

A difference in the levels of tetanus immunity exists between the sexes. Overall, menare believed to be better protected than women, perhaps because of additional

vaccinations administered during military service or professional activities. In

developing countries, women have an increased immunity where tetanus toxoid is

administered to women of childbearing age to prevent neonatal tetanus.

2.5 PATHOPHYSIOLOGY


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Clostridium tetani, an obligate anaerobic gram-positive bacillus, is the pathogen

responsible for tetanus. This bacterium is nonencapsulated and forms spores that are

resistant to heat, desiccation, and disinfectants. The spores are ubiquitous and are found

in soil, house dust, animal intestines, and human feces. Spores that gain entry can

persist in normal tissue for months to years.

To germinate, the spores need tissue with the proper anaerobic conditions.[4] Wounds

with low oxidation-reduction potential, such as those with dead or devitalized tissue, a

foreign body, or active infection, are ideal for germination of the spores and release of

toxin. Infection by C tetani results in a benign appearance at the portal of entry because

of the inability of the organism to evoke an inflammatory reaction (unless coinfection

with other organisms develops).

When the proper anaerobic conditions are present, the spores germinate and produce the

following 2 toxins:

Tetanolysin This substance is a hemolysin with no recognized pathologicactivity

Tetanospasmin This toxin is responsible for the clinical manifestations oftetanus; by weight, it is one of the most potent toxins known, with an estimated

minimum lethal dose of 2.5 ng/kg body weight

Tetanospasmin is synthesized as a 150-kd protein consisting of a 100-kd heavy chain

and a 50-kd light chain joined by a disulfide bond.The heavy chain mediates binding of

tetanospasmin to the presynaptic motor neuron and also creates a pore for the entry of

the light chain into the cytosol. The light chain is a zinc-dependent protease that cleaves

synaptobrevin.

After the light chain enters the motor neuron, it travels by retrograde axonal transport

from the contaminated site to the spinal cord in 2-14 days. When the toxin reaches the

spinal cord, it enters central inhibitory neurons. The light chain cleaves the protein

synaptobrevin, which is integral to the binding of neurotransmitter containing vesicles

to the cell membrane.

As a result, gamma-aminobutyric acid (GABA)-containing and glycine-containing

vesicles are not released, and there is a loss of inhibitory action on motor and autonomic

neurons.With this loss of central inhibition, uncontrolled muscle contractions (spasms)

occur in response to normal stimuli such as noises or lights and autonomichyperactivity.

Once the toxin becomes fixed to neurons, it cannot be neutralized with antitoxin.

Recovery of nerve function from tetanus toxins requires sprouting of new nerve

terminals and formation of new synapses.

Localized 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.

PREVENTION


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Active inmmunizationAll partially immunised and unimmunized adults should receive vaccine, as should

those recovering from tetanus. The primary series for adults consists f three doses: the

first and second doeses are given 4-8 week apart, and the third doses: is given 6-12

months after the second. A booster dose is required every 10 years and may be given at

mid-decade ages- 35, 45 and so on. Combined tetanus and diphtheria toxoid, absorbed.Adsorbed vaccine is preferred because it produced tetanus/diphtheria/ attenuated

pertussis vaccines have recently been approved.

PROGNOSISThe application of methods to monitor and support oxygenation has markedly improved

the prognosis in the tet


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CASE ANALYSIS

Differensial diagnosis

Topical Differensial diagnosis

topic of pain manifestation On this patient

Infratentorium (1/3

posterior of cranium)

Pain is projected to back

of head and neck by

cervical nerves IX and X

Pain on the right side of

head and not speard to

neck

So, the possibility that topic of pain is come from infratentorium structures cannot be

excluded.

topic of pain manifestation On this patientSupratentorium (2/3 on

the front side of cranium)

Pain is projected to

frontal, parietal dan

temporal areas by nerve

V

Pain on the right side of

head and not speard to

neck

So, the possibility that topic of pain is come from Supratentorium structures cannot be

excluded.

Conclusion: the topic of pain in this patient may be come from Supratentorium and

infratentorium structures.


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Etiologic Differensial diagnosis:

1. Cluster Headache2. Tension Headache3. Traction and inflammatory headache4. Vascular Headache

- Cluster HeadacheManifestation On this patient

- Intense, nonthrobbing- Unilateral and common onOrbitotempora areas.

- The mode of onset usually nocturnal,12 hours after falling asleep and maybeassociated with rapid eye movement.

- Pain can be appear on cheek andsometimes with redness on the cheek

- Predisposition factor : stress, weather

Throbbing

No

No

No

No

So, the possibility that etiology of pain is Cluster Headache can be excluded.

- Tension HeadacheManifestation On this patient- Pressure (nonthrobbing),

- tightness, aching

- pressure on occipitocervical areas

- Continuous, variable intensity, for days, weeks, or

months

- Common with Depression, worry, anxiety

No

No

No

No

No

So, the possibility that etiology of pain is tension Headache can be excluded.

- Traction and inflammatory headacheManifestation On this patient

Mass : tumor, edema, blood clot, abscess

hematoma

- the pain became more frequent and moresevere

-throbbing

-deafness on one side

-Vertigo

-Oftalmoplegia-nausea and vomit

Yes

Yes

No

No

NoNo


21/21

-Infection :Meningitis, encephalitis, sinusitis,

infection of nose, teeth, and eyes Yes

So, the possibility that etiology of pain is Traction and inflammatory headache

cannot be excluded.

- Vascular HeadacheManifestation On this patient

Migraine

- Headache with at less 2 from 4 sign :- Unilateral- Throbbing- the intensity of pain is from

moderate to severe

- pain can be more severe on dailyactivity

- on duration of pain, 1 of two sign appear:

nausea and vomit , fotofobia and fonofobia.

yes

yes

yes

yes

no

So, the possibility that etiology of pain is vascular headachecannot be excluded.

Conclusion: the etiology of pain in this patient may be vascular headache and Traction

and inflammatory headache.

Documents

Case Report Mine