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EDUARDO V. BONGAT JR.

, PTRP, RM, RN(USRN)


Tetanus
Also called lockjaw
An acute, preventable, and often
fatal disease
Caused by exotoxin of Clostridium
tetani
Characterized by muscle rigidity
involving the masseter and neck
muscles
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Four Requirements for
Developing Lockjaw
Presence of tetanus spores or
vegetative forms of the bacillus
Injury to the tissues
Wound conditions that
encourage multiplication of the
organism
A susceptible host
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Tetanus
Spores are found in soil, dust, and GI
tract of humans and animals
Bacteria enter body through wound,
especially puncture or crush wound or
burn
May enter through scratch, bee sting,
thorn, or needle prick
Exposure greater during outdoor
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Pathophysiology of Tetanus
Exotoxin spreads from wound to
CNS by way of neurons or
bloodstream
Toxin becomes fixed on nerve
cells of brainstem and spinal cord
Toxin produces muscle stiffness

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2003 by Mosby, Inc., an affiliate of Elsevier
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Clinical Manifestations of
Tetanus
Initially: progressive stiffness and
tenderness of neck and jaw muscles,
difficulty in opening the mouth, facial
muscle spasm
Progressive: opisthotonos, difficulty
swallowing, laryngospasm, and
tetany of respiratory muscles
Rigid abdominal and limb muscles
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Clinical Manifestations of Tetanus
(cont.)
Respiratory: accumulated secretions,
atelectasis, pneumonia, respiratory arrest
Patient anxious but alert; mentation
unaffected
Rapid HR, diaphoresis, mild or absent
fever
Incubation: 3 to 10 days
Mortality approximately 30%; usually fatal
in newborn
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Therapeutic Management of
Tetanus
Prevention by tetanus toxoid or
tetanus antitoxin after exposure
Treatment of wounds contaminated
with dirt, feces, soil, saliva, puncture
wounds, avulsions, crushing, burns,
and frostbite should include tetanus
immune globulin if patient
inadequately immunized
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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 8
Therapeutic Management of
Tetanus (cont.)
ICU for constant observation and respiratory
support availability
Monitor fluid and electrolyte status
Tetanus immune globulin therapy to
neutralize toxins
Wound care to decrease organism
proliferation
Muscle relaxants, sedatives, pancuronium
(Pavulon)
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2003 by Mosby, Inc., an affiliate of Elsevier
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Nursing Considerations
Control environmental stimuli
Careful monitoring of respiratory
status
Attempt to reduce anxiety of
child and family

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 10
Nursing Considerations
Control environmental stimuli
Careful monitoring of respiratory
status
Attempt to reduce anxiety of
child and family

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 11
Botulism
Food poisoning resulting from ingestion
of toxin produced by the anerobic
bacillus Clostridium botulinum
Sources:
Improperly sterilized home canned
foods for older children
Infant sources: honey and light or
dark corn syrup
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Clinical Manifestations of
Botulism
CNS symptoms appear abruptly
12 to 36 hours after ingestion
General signs
Weakness, dizziness, headache,
diplopia, speech difficulties
Vomiting
Progressive, life-threatening
respiratory paralysis
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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 13
Treatment of Botulism
IV botulism antitoxin
Supportive measures—
respiratory support
Continue therapy until paralysis
abates

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 14
Infant Botulism
Caused by ingestion of spores or
vegetative cells of C. botulinum and
subsequent release of toxin
Source of botulism in infants: honey,
and light or dark corn syrup fed to
them
Wide variation in severity of disease:
mild constipation to respiratory failure
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2003 by Mosby, Inc., an affiliate of Elsevier
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Infant Botulism (cont.)
Constipation is often the presenting symptom
Generalized weakness, decreased movement,
diminished deep tendon reflexes
Loss of head control, feeding difficulty, weak
cry, diminished gag reflex, hypotonia
Do not treat infants with botulism antitoxin
Prognosis generally good but very slow (weeks
to months)

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2003 by Mosby, Inc., an affiliate of Elsevier
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Spinal Cord Injuries
Generally result of indirect trauma
Especially in MVC without child
restraints
Vertebral compression from blows to
the head or buttocks (diving, surfing,
falls from horses)
Birth injuries from traction force on
spinal cord during breech delivery
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Levels of Spinal Cord
Injuries
Higher injury—more extensive damage
Paraplegia: complete or partial paralysis of
lower extremities
Tetraplegia: lacking functional use of all
four extremities (formerly called
quadriplegia)
High cervical cord injury affects phrenic
nerve, paralyzes diaphragm → ventilatory
dependency
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Relationships of Spinal
Cord Segments and Spinal
Nerves to Vertebral Bodies

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Spinal Cord Injury
Therapeutic management: stabilization
and transport to pediatric trauma center
environment
Management is complex and controversial
Nursing considerations
Stabilization, careful assessment,
prevention of complications, maintain
maximum function

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2003 by Mosby, Inc., an affiliate of Elsevier
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Nursing Management
of Spinal Cord Injuries
Respiratory care
Temperature regulation
Skin care
Physiotherapy
Neurogenic bladder
Bowel training
Autonomic dysreflexia
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2003 by Mosby, Inc., an affiliate of Elsevier
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Dermotomes and
Innervation of Major
Muscles

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Rehabilitation
Evaluation and support
Remobilization
Physical rehabilitation
Psychosocial rehabilitation
Sexuality issues

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2003 by Mosby, Inc., an affiliate of Elsevier
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Muscular Dystrophies (MDs)
Largest group of muscular diseases
in children
All have genetic origin with gradual
degeneration of muscle fibers,
progressive weakness, and wasting
of skeletal muscles
All have increasing disability and
deformity with loss of strength
Mosby items and derived items © 2007,
2003 by Mosby, Inc., an affiliate of Elsevier
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Initial Muscle Groups Involved
in MDs

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2003 by Mosby, Inc., an affiliate of Elsevier
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Duchenne Muscular
Dystrophy (DMD)
Also called pseudohypertrophic
muscular dystrophy
Most severe and most common of
the MDs in childhood
X-linked inheritance pattern; one
third are fresh mutations
Incidence: 1 in 3500 male births

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2003 by Mosby, Inc., an affiliate of Elsevier
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Characteristics of DMD
Onset between ages 3 and 5 years
Progressive muscle weakness, wasting,
and contractures
Calf muscles hypertrophy in most
patients
Progressive generalized weakness in
adolescence
Death from respiratory or cardiac failure
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2003 by Mosby, Inc., an affiliate of Elsevier
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Diagnostic Evaluation of
DMD
Suspected based on clinical appearance
Confirmation by EMG, muscle biopsy, and
serum enzyme measurement
Serum CPK and AST levels high in first
2 years of life, before onset of weakness;
levels diminish as muscle deterioration
continues

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 28
DMD: Clinical Manifestations
Waddling gait, frequent falls, Gower sign
Lordosis
Enlarged muscles, especially thighs and upper
arms
Profound muscular atrophy in later stages
Mental deficiency common

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 29
Therapeutic Management of
DMD
No effective treatment has been established
Primary goal: maintain function in unaffected
muscles as long as possible
Keep child as active as possible
ROM, bracing, performance of ADLs, surgical
release of contractures prn
Genetic counseling for family

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 30
DMD: Nursing
Considerations
Help child and family cope with chronic,
progressive, debilitating disease
Help design a program to foster independence
and activity as long as possible
Teach child self-help skills
Arrange for appropriate health care assistance
as child’s needs intensify (home health, skilled
nursing facility, respite care for family, etc.)

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2003 by Mosby, Inc., an affiliate of Elsevier
Inc. Slide 31

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