TETANUS DR. Arun R Nair - PowerPoint Presentation

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TETANUS

DR.

Arun

R Nair

SKHMC

Definition

Tetanus

is a neurologic syndrome characterized by generalized rigidity

and convulsive

spasm of skeletal muscles caused by a neurotoxin elaborated at

the site

of injury by

Clostridium

tetani

.

The

Pathogen

C.

tetani

is an anaerobic, gram-positive, slender, motile bacillus. When

it

sporulates

, the terminal spore gives the organism a characteristic “

drumstick” or

“tennis racket” shape. The vegetative form produces

tetanospasmin

(

a neurotoxin

).

EPIDEMIOLOGY

C.

tetani

can be found in 2 to 23% of soil samples, with the highest yield

in manure-treated

soil.

The

organism can also be found in stool from a

variety of

domestic and farm animals and poultry.

Most common in warm climates and in highly cultivated rural areas.

The

greatest

problem occurs

in resource-limited countries because of high numbers of

unimmunized mothers

and unhygienic practices.

PATHOBIOLOGY

Tetanospasmin, also known as tetanus neurotoxin or

TeNT

. 2.5

ng/kg

is a

lethal human dose.

Clinical

tetanus usually results from entry of the

organism into

a wound and low oxygen conditions that allow spore germination

and

survival of the vegetative organism to produce toxin.

Entry

is

usually through

a traumatic or surgical wound, drug injection site, burn, skin

ulcer, or

infected umbilical

cord.

Tetanospasmin acts on both the

α

and

δ

motor systems at synapses, resulting in disinhibition.

Tetanospasmin

binds the peripheral nerve

terminals and

is then carried intra-

axonally

within membrane-bound vesicles

to spinal

neurons at a transport rate of approximately 75 to 250 mm/day.

The light chain passes to the presynaptic terminals, where it blocks the release of neurotransmitters in inhibitory afferent motor neurons.

Loss of the inhibitory influence results in sustained muscle contraction.

Binding of the toxin is irreversible, so recovery requires the generation of new axon terminals

.

It

also produces

neuromuscular blockade

and skeletal muscle spasm and acts

on the

sympathetic nervous system.

The

end result is

marked flexor

muscle spasm and autonomic dysfunction.

CLINICAL MANIFESTATIONS

The usual incubation period is 3 to

21 days

(mean, 8 days), depending largely on the distance between the site

of injury

and the central nervous system.

A

short incubation period is

associated with

more severe symptoms

.

Forms

of tetanus include generalized, local, cephalic, and neonatal. Generalized tetanus is characterized by a

persistent tonic

spasm with brief exacerbations.

The

neck and jaw are

almost always

involved.

Trismus

(lockjaw) is the initial complaint in 75% of

cases, so

the patient is often initially seen by a dentist or oral surgeon.

Other early features include irritability, restlessness, diaphoresis, and dysphagia with hydrophobia and drooling.

Persistent

spasm of the back musculature may cause

opisthotonos

.

These

early manifestations reflect involvement of

the

paraspinous

muscles.

With

progression, all muscles contract, with

stronger muscles

overtaking weaker muscles.

Noise

or tactile stimuli may

precipitate spasms

and generalized convulsions.

Involvement

of the autonomic

nervous system

may result in severe arrhythmias, blood pressure oscillation,

profound diaphoresis

, hyperthermia, rhabdomyolysis, laryngeal spasm, and

urinary retention

.

In most cases, the patient remains lucid and afebrile.

The condition may continue for 3 to 4 weeks, despite antitoxin therapy, because of the time required for intra-axonal toxin transport.

Complications include fractures from sustained contractions, pulmonary emboli, bacterial infections, and dehydration

.

.

Death results from aspiration, hypoxia, respiratory

failure, cardiac

arrest or exhaustion.

Mild

cases with rigidity

usually recover

.

Poor

prognostic indicators include short

incubation period

, short onset time and extremes of age.

Localized tetanus

is a milder form of the disease.

Pain and

stiffness are confined to the site of the wound,

with increased

tone in the surrounding muscles. Recovery

usually occurs.

Cephalic tetanus

is uncommon but invariably fatal.

It usually

occurs when the portal of entry of

C.

tetani

is

the middle

ear. Cranial nerve abnormalities, particularly of

the seventh

nerve, are usual. Generalized tetanus may or

may not

develop

.

Neonatal tetanus

is usually due to infection of the

umbilical stump

. Failure to thrive, poor sucking, grimacing

and irritability

are followed by the rapid development of

intenserigidity

and spasms. Mortality approaches 100%.

Diagnosis

Few diseases resemble tetanus in its fully developed

form and

the diagnosis is therefore usually clinical.

Rarely

,

C.

tetani

is isolated from wounds.

The differential diagnosis

depends

on the dominant clinical

features and

includes dystonic reactions as a result of neuroleptic toxicity,

seizure disorders

,

hypocalcemic

or alkalotic tetany, alcohol withdrawal, and

strychnine poisoning

.

Clostridial

Myonecrosis

(Gas Gangrene)

Definition

Clostridial

myonecrosis

, or gas gangrene, can be caused by several

Clostridium

species

, most commonly

C. perfringens

after trauma or tissue

injury.

Epidemiology

Gas

gangrene has historically been a complication of battlefield injuries

and of

trauma in noncombat settings.

Traumatic injuries, vehicular accidents, crush

injuries, industrial

accidents,gunshot

wounds, and burns.

Postoperative complications -the

appendix, biliary tract, or intestine.

Pathobiology

Clostridia

are widely distributed in nature and can be cultured from

nearly all

soil samples, from environmental sites in the hospital, and from the human intestine.

A

critical factor is a physiologic state of the wound with conditions

that support germination and toxin production by toxigenic clostridia.

Particularly critical

are a low oxidation-reduction potential, hypoxia,

appropriate substrates

, and calcium ions

.

C. perfringens elaborates at least 12 recognized toxins, most

importantly

α-

toxin and

θ-

toxin of C. perfringens type A.

α-

toxin, a

phospholipase C

, and

θ-

toxin or

perfringolysin

O, a cholesterol-dependent

cytolysin

, in

the extensive

cell death and disruption of microvascular perfusion that are

characteristic of

clostridial

myonecrosis

.

Clinical manifestations

Initial

symptoms of traumatic

myonecrosis

usually occur 1 to 4 days after

the precipitating

event, although the range is 8 hours to 3 weeks.

The initial symptom

is pain that is often sudden and severe at the

site.

The

involved skin has intense

edema

and is initially pale before

progressing to

a bronze or magenta

color

, followed by the formation of bullae.

The bullae contain fluid that may be clear or

hemorrhagic

.

The

discharge

has an

odor

that is described as “foul-sweet.”

About 15% of patients have

bacteremia

that is usually complicated

by rapid

hemolysis

with a dramatic drop in the

hematocrit

, which

maybeven

decrease to 0%.

Common

complications include jaundice,

hypotension, hepatic

failure, and renal failure.

The

renal failure is often due to

hemoglobulinuria

and

myoglobulinuria

, but it may also be due to acute tubular necrosis

from

hypotension.

Despite

the severity of the illness, the patient’s

mental status

is usually remarkably good until very late in the disease

.

Uterine gas gangrene,

which was once common after septic abortions,

is now

rare but may complicate normal delivery, amniocentesis,

caesarean section

, or abortion. The onset is usually sudden, with fever,

tachycardia, hypotension

, renal failure, and jaundice. Radiography may show gas in

the uterine

wall. The urine is often “port wine” in

color

as a result of

hemoglobulinuria

,

and there is often jaundice because of massive intravascular

hemolysis

.

DIAGNOSIS

The diagnosis of gas gangrene is usually based on a constellation of

characteristic clinical

features, including

myonecrosis

, shock, and renal failure.

The patient

typically complains of severe pain. Early recognition is

important because

early institution of treatment may strongly influence the prognosis.

The diagnosis is established by examination of skin and muscle, which

shows putrid

discharge, characteristic bullae,

and

crepitations

. Gram

stain

demonstrates abundant

gram-positive bacilli and no inflammatory cells.

Histopathologic examination

of the lesion shows

myonecrosis

without

polymorphonuclear

leukocytes, Gas

is present in the tissue and may be detected by physical

examination,radiography

, or other imaging methods.