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GAS GANGRENE

Dr Mohammed Akbar Khan

DEFINITION

Gangrene - Massive necrosis of tissue, superadded


by putrefaction
Gas gangrene - Clostridial myonecrosis
Myonecrosis - Bacterial infection - Necrotic damage
specific to muscle tissue - Gas tissues in gangrene.
Deadly form of gangrene - Clostridium perfringens.
Medical emergency

Microorganisms - opportunistic - Skin breakage - Body


Myonecrosis - Bacteria - Specific exotoxins.
Envenomation by snakes of the Bothrops genus
(family Viperidae),
Ischemic necrosis - vascular blockage (II Diabetes)
Tumours that block or hoard blood supply
Disseminated intravascular coagulation (DIC) or other
thromboses

ORGANISMS
Anaerobic - Gram-positive - Spore-forming bacillus
Genus Clostridium
C. perfringens - Most common etiologic agent
Other common clostridial species
Clostridium bifermentans
Clostridium septicum
Clostridium sporogenes
Clostridium novyi
Clostridium fallax
Clostridium histolyticum
Clostridium tertium

Gram stain of cysts with large rod-shaped bacteria

True saprophytes - soil and dust.


Mucous membranes GI tract & Female genital tract.
Clostridia - Colonize in skin- mainly around perineum.
Obligate anaerobes- some species - Aerotolerant.
Bacterial multiplication & production of soluble
proteins called exotoxins require a low oxygen
tension.

Non-clostridial organisms - 60-85% cases


Recent clinical series -gas gangrene in wound cultures
-83.3% of aerobic gram-negative bacilli
-4.5% anaerobic gram-positive bacilli- Clostridium sp
Aerobic gram-negative bacteria
Escherichia coli
Proteus species
Pseudomonas aeruginosa
Klebsiella pneumoniae

C perfringens - 20 exotoxins.
Alpha toxin-lecithinase,necrotizing,hemolytic,cardiotoxic

Beta toxin - necrotizing


Epsilon toxin - permease
Iota toxin - necrotizing
Delta toxin - hemolysin
Phi toxin - Hemolysin, cytolysin
Kappa toxin - collagenase, gelatinase, necrotizing
Lambda toxin - Protease
Mu toxin - Hyaluronidase
Nu toxin - Deoxyribonuclease, hemolytic necrotizing

ALPHA-TOXIN

Zinc metalloenzyme - Phospholipase-c activity


(lecithinase)
Cell destruction - hydrolysis of key cell membrane
Lysis of erythrocytes- leukocytes- platelets- fibroblasts
& muscle cells.
Strains that do not produce alpha-toxin are less
virulent
Purified alpha-toxin has a myocardial suppressant
effect - shock

PREDISPOSING FACTORS

Contamination - clostridial spores - posttraumatic or


postoperative lesions
Local wound conditions > degree of clostridial
contamination
Disrupted or necrotic tissue provides the necessary
enzymes and a low oxidation/reduction potential,
allowing for spore germination.
Foreign bodies, premature wound closure& devitalized
muscle reduce the spore inoculum necessary to cause
infection
Local effects - necrosis of muscle, subcutaneous fat
&thrombosis of blood vessels.
Marked edema - compromise blood supply

Incubation period - short (<24 h) -1 hour to 6 weeks


Self-perpetuating destruction of tissue - locally &
systemically acting exotoxins.
Fermentation of glucose - gas production
C septicum spontaneous gas gangrene
Nitrogen is the predominant gas component (74.5%), oxygen (16.1%), H2 (5.9%), & CO2 (3.4%).
Production of hydrogen sulfide and CO2 gas begins
late and dissects along muscle bellies & fascial
planes.
Local effects - rapid spread of the infection.
Systemic effects - exotoxins - severe hemolysis.
Hemoglobin levels - very low levels
Hypotension- acute tubular necrosis and renal failure

Very high mortality rate - 25%


spontaneous gas gangrene/ Delay treatment -100%

Injury
Dead tissue, blood clots, foreign matter aerobic organisms

Develop Anaerobic Condition


(Exogenous infection) Germination of spores
Gas gangrene
Oedema, Necrosis, Gas production,
Toxaemia, Myositis
Crepitus

CLASSIFICATION
POST-TRAUMATIC
POST-OPERATIVE
SPONTANEOUS

POSTTRAUMATIC

60% of all gas gangrene


automobile collisions.
Other complications of trauma
Crush injuries,
Compound fractures,
Gunshot wounds,
Thermal
Electrical burns,
Frostbite.
Farm or industrial injuries contaminated with soil
Rare causes- IM or SC injections with insulin,
epinephrine, quinine, or cocaine

POSTOPERATIVE

clostridial infections
colon resection
ruptured appendix
bowel perforation
biliary or other GI surgery, including laparoscopic
cholecystectomy and colonoscopy.
Septic back-street abortions - uterine gas gangrene.

SPONTANEOUS

without external wound or injury - serious underlying


conditions.
Colorectal adenocarcinoma
Hematologic malignancy
Children - Neutropenia
chemotherapy
spontaneous C septicum infections.
Diabetes or neutropenic colitis.
Many cases - no predisposing condition
C perfringens
C septicum

SYMPTOMS

Posttraumatic gas gangrene - serious injury - skin or


soft tissues or have experienced open fractures.
Postoperative gas gangrene - undergone recent
surgery of the GI or biliary tract.
History is usually unremarkable - occult malignancy
associated spontaneous gas gangrene.
Sudden onset of pain is usually the first symptom
Pain gradually worsens but spreads only as the
underlying infection spreads.
Feeling of heaviness in the affected extremity.
Low-grade fever and apathetic mental status

SIGNS

Local swelling & serosanguineous exudate - onset of


pain.
skin - bronze color - blue-black color with skin blebs
and hemorrhagic bullae.
Within hours, entire region - markedly edematous.
Nonodorous or may have a sweet mousy odor.
Crepitus follows gas production
crepitus may not be detected with palpation owing to
brawny edema.
Pain and tenderness to palpation disproportionate to
wound appearance
Tachycardia disproportionate to body temperature is
common, - feeling of impending doom.
Late signs - include hypotension, renal failure, and a
paradoxical heightening of mental acuity.

SUMMARY C/P

Air under the skin (subcutaneous emphysema)


Blisters filled with brown-red fluid
Drainage from the tissues, foul-smelling brownred or bloody fluid (serosanguineous discharge)
Increased heart rate (tachycardia)
Moderate to high fever
Moderate to severe pain around a skin injury
Pale skin color, later becoming dusky and
changing to dark red or purple
Progressive swelling around a skin injury
Sweating
Vesicle formation, combining into large blisters
Yellow color to the skin (jaundice)

Laboratory Studies

Hemolytic anemia
Increased lactate dehydrogenase (LDH)
White blood cell No leukocytosis.
Toxic shock syndrome - C sordellii or C septicum
Hemoconcentration & leukocytosis.
Gram stain - exudate or infected tissues
Box-car & large gram-positive bacilli without neutrophils

< 1% of blood cultures - grow clostridial species.


Metabolic abnormalities
metabolic acidosis & renal failure
with tissue injuries and hypotension.

Gas gangrene C. perfringens typeA(Principal),


Capsulated, non-motile

LecithinaseC- toxaemia

Nagler reaction
Colonies withhaloes
Colonies without
haloes
Incorporatedwith
Antitoxins

C Perfringens
C histolyticum
C septicum
C novyii
C Perfringens

Alpha toxin
(lecithinase)

IMAGING STUDIES
Radiograph
Delineate the typical feathering pattern of gas in
soft tissue
Gas may not be present in patients
Gas in soft tissue does not confirm diagnosis

Gas feathering in the arm soft tissue

Extension of gas gangrene to the chest wall after initial debridement

CT SCAN

Abdominal cases

OTHER TESTS

Rapid detection of alpha-toxin or sialidases - ELISA


In vitro amplification of alpha-toxin or DNA - PCR

PROCEDURES

Surgical exploration confirms diagnosis


muscle appears pale
No contractile function -incised or electrically stimulated
Bedside biopsy with immediate frozen section under LA

Develop massive hemolysis, shock, ARDS &R F


Require invasive procedures
Right-sided heart catheterization
Mechanical ventilation
Hemodialysis.

HISTOLOGIC FINDING

Destruction of other connective tissues and a paucity


of neutrophils - infected area
Leukocyte aggregates - border regions

ANTIBIOTIC THERAPY

DOC - penicillin G - 10-24 million U/d


Combination of penicillin and clindamycin
Protein synthesis inhibitors
clindamycin, chloramphenicol, rifampin, tetracycline
Inhibit synthesis of clostridial exotoxins
Allergic to penicillin - Clindamycin & Metronidazole
Combination of penicillin and metronidazole
antagonistic and is not recommended.
Daptomycin, linezolid, and tigecycline not be used as
primary antibiotics

INTENSIVE CARE

End-organ failure
Other concomitant serious medical conditions that
require intensive supportive care.

ADJUVANT THERAPY

Recombinant human activated protein C


Drotrecogin alfa activated
Adjuvant therapy for patients with severe sepsis
Serious bleeding
Drotrecogin alfa activated &repeated surgical
debridement
Frequent interruption of the continuous infusion
Not recommend this adjuvant therapy

Hyperbaric oxygen (HBO) therapy


important adjunct to surgery and antimicrobial therapy
increased survival - treatment with surgery & antibiotics
Direct bactericidal effect on most clostridial species
inhibits alpha-toxin production
enhance the demarcation of viable & nonviable tissue
prior to surgery.
100% oxygen at 2.5-3 absolute atmospheres for 90-120
minutes 3 times
Potential risks
Pressure-related trauma-barotraumatic otitis pneumothorax

Oxygen toxicity (myopia, seizures).


Claustrophobia.
Most adverse effects - self-limiting & resolve after
termination therapy

SURGICAL CARE

Fasciotomy for compartment syndrome - not be


delayed in patients with extremity involvement.
Perform daily debridement - necrotic tissue.
Amputation of the extremity may be necessary and
life-saving.
Abdominal involvement requires excision of the body
wall musculature.
Uterine gas gangrene following septic abortion
usually necessitates hysterectomy.

Hemipelvectomy

SUMMARY

Most devastating infections.


extremity amputation or massive loss of muscles, skin, and soft
tissues, requiring extensive reconstructive surgery and physical
rehabilitation.
spontaneous gas gangrene may have occult malignancies of
the GI tract.
Aggressive surgical debridement and intensive medical therapy
are the mainstays of treatment
HBO therapy has become an important adjunctive therapy
compartment syndrome - do not delay fasciotomy
Deterrence/Prevention
Avoid suturing wounds due to a crush injury or open fractures
with devitalized muscle and soil contamination.
Provide warnings and instructions of wound care to rescuers
and health care workers - clostridial infections, -tetanus and gas
gangrene, in injured victims of natural disasters such as
earthquake or tsunami.

COMPLICATIONS

Massive hemolysis - repeated blood transfusion


DIC- Severe bleeding Complicate aggressive surgical
debridement
Acute renal failure
Acute respiratory distress syndrome
Shock
Prognosis Failure to provide an early diagnose and inadequate surgical
intervention
dictate the outcome.
better if the incubation period is shorter than 30 hours,
Spontaneous gas gangrene worse prognosis than other
forms of gas gangrene.

TETANUS

EPIDEMOLOGY

International health problem, as C. tetani spores are ubiquitous.


Persons who are unvaccinated or inadequately immunized.
More common in hot, damp climates with soil rich in organic
matter.
Spores introduced into the body through puncture wounds.
Agricultural areas, a significant number of human adults may
harbor the organism.
Spores can also be found on skin surfaces and in contaminated
heroin.
Tetanus particularly the neonatal form remains a significant
public health problem in non-industrialized countries.
WHO estimated59,000 newborns worldwide died in 2008
neonatal tetanus.
Tetanus is the only vaccine-preventable disease that is
infectious but is not contagious.

History

Ancient people -relationship between wounds and fatal


muscle spasms.
Greek - (tetanos) taut & (teinein) - Stretch
1884
Isolated strychnine-like toxin of tetanus from free-living,
anaerobic soil bacteria.
Etiology of the disease - demonstrated transmissibility
of tetanus for first time.
produced tetanus in rabbits by injecting pus from a
patient with fatal tetanus into their sciatic nerves.
1889,
Kitasato Shibasabur -C. tetani was isolated from a
human victim
organism could produce disease when injected into
animals
toxin could be neutralized by specific antibodies

History

1897,
Edmond Nocard - tetanus antitoxin induced
passive immunity in humans
could be used for prophylaxis and treatment.
1924
P. Descombey - Tetanus toxoid vaccine was
developed
used to prevent tetanus induced by battle
wounds during World War II

INTRODUCTION

Tetanus - Prolonged contraction of skeletal muscle


fibers.
Primary symptoms tetanospasmin
neurotoxin - Gram-positive, obligate anaerobic
bacterium Clostridium tetani.
Infection - wound contamination
Cut or deep puncture wound.
muscle spasms - jaw (lockjaw) and elsewhere in the
body
Infection can be prevented by proper immunization
and by post-exposure prophalysis

INTRODUCTION

Skeletal muscle
Cardiac or heart muscle cannot be tetanized - Intrinsic
electrical properties.
Mortality rates - 48% to 73%.
Highest mortality rates - Unvaccinated & > 60 years
Shorter the incubation period -More severe symptoms
Neonatal tetanus,
symptoms usually appear from 4 to 14 days after
birth
averaging about 7 days

Types
Basis of clinical findings, four different forms of tetanus
Generalized tetanus
Neonatal tetanus
Local tetanus
Cephalic tetanus

GENERALIZED TETANUS

Most common type of tetanus - 80% of cases.


Descending pattern.
First sign - trismus or lockjaw & facial spasms called risus
sardonicus,
Stiffness of the neck,
Difficulty in swallowing,
Rigidity of pectoral and calf muscles.
Other symptoms - elevated temperature, sweating,
elevated blood pressure, and episodic rapid heart rate.
Spasms may occur frequently and last for several minutes
with the body shaped into a characteristic form called
opisthotonos.
Spasms continue for up to 4 weeks, and complete
recovery may take months

NEONATAL TETANUS
Generalized tetanus that occurs in newborns.
Infants - Not acquired passive immunity mother has never been immunized - risk.
Infection of the unhealed umbilical stump stump is cut with a non-sterile instrument.
Neonatal tetanus - developing countries
-Responsible for about 14% neonatal deaths,
-Very rare in developed countries

LOCAL TETANUS

Uncommon
Persistent contraction of muscles - same anatomic
area as the injury.
Contractions may persist for many weeks before
gradually subsiding.
Local tetanus is generally milder- 1% fatal
Generalized tetanus.

CEPHALIC TETANUS

Rare form
Otitis media (ear infections) in which C. tetani is
present in the flora of the middle ear,
Injuries to the head.
Cranial nerves -Facial area.

ETIOLOGY

Tetanus Rust- rusty nails,


Objects with rust outdoors or harbor anaerobic
bacteria
Rust - not cause tetanus /contain more C. tetani
bacteria.
Rough surface of rusty metal merely provides a prime
habitat for a C. tetani endospore to reside, & nail puncture skin & deliver endospore into the wound.
Endospore is a non-metabolizing survival structure metabolize and cause infection once in an adequate
environment - Anaerobic
Stepping on a nail (rusty or not) - tetanus infection
puncture wound, delivering endospores to a
suitable environment for growth.

PATHOPHYSIOLOGY

Clostridium tetani,
obligate nonencapsulated anaerobic gram-positive bacillus
Rod-shaped bacteria

spores

resistant to heat, desiccation, and disinfectants.


soil, house dust, animal intestines, and human feces.
gain entry can persist in normal tissue for months to years.
anaerobic conditions, geminate & elaborate tetanospasmin
and tetanolysin.

Tetanolysin - no role - clinical course of tetanus


Tetanospasmin

neurotoxin
causes the clinical manifestations of tetanus.

Tetanospasmin

Toxin is inactive inside the bacteria, - Bacteria dies Released and activated by proteases
Active tetanospasmin - Retrograde axonal transport to
the spinal cord and brain stem
Lymphatic & vascular circulations - End plates of all nerves.
Enters nervous system peripherally - Myoneural jn.
Transported centripetally into neurons of the CNS

Most potent toxins


Minimum lethal dose - 2.5 nanograms per kilogram of
body weight or 175 nanograms for a 70-kg
Neurons - incapable of neurotransmitter release GABA and Glycine - Major inhibitory neurotransmitters

Tetanospasmin

Failure of inhibition of motor reflex responses to sensory


stimulation.
Generalized contractions of the agonist and antagonist
musculature characteristic of a tetanic spasm.
Shortest peripheral nerves - first to deliver the toxin to the CNS,
- early symptoms of facial distortion & back & neck stiffness
Damaged UMN
cannot inhibit LMN ( Renshaw cells),
cannot control reflex responses to afferent sensory stimuli.

Both mechanisms hallmark - muscle rigidity and spasms.


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.

SYMPTOMS

Tetanus are seen in

either never vaccinated or


completed primary series but no booster in preceding 10 yrs.

Patients with clinical manifestations occurring within 1


week of an injury have more severe clinical courses.
Patients with generalized tetanus present with trismus
(lockjaw)
Stiffness,
Neck rigidity- Muscle rigidity - Major manifestation
Descending pattern - jaw & facial muscles over the
next 24-48 hours to extensor muscles of the limbs
Dysphagia - pharyngeal muscle spasms

SYMPTOMS

Restlessness,
Reflex spasms

Triggered by minimal external stimuli - Noise, light, or touch.


Last seconds to minutes
More intense
Increase in frequency with disease progression
Cause apnea, fractures, dislocations, and rhabdomyolysis.
Laryngeal spasms can occur - Asphyxia.

Other symptoms
Elevated temperature, sweating, elevated blood pressure,
and episodic rapid heart rate.

Sustained contraction of facial musculature produces


a sneering grin expression known as risus sardonicus.

RISUS SARDONICUS.

SIGNS

Site of antecedent acute injury


Lower Extremity 52%
Upper Extremity 34%,
Head or Trunk 5%
Autonomic dysfunction
extremes in blood pressure, dysrhythmias, and cardiac
arrest.
Neonatal tetanus
Inability to suck 3-10 days after birth.
Presenting symptoms include irritability, excessive crying,
grimaces, intense rigidity, and opisthotonus.
Tetanic seizures may occur and portend a poor prognosis.
Frequency and severity of seizures are related to severity of the
disease.
Seizures resemble epileptic seizures with the presence of a
sudden burst of tonic contractions.

SIGNS
& experiences severe pain.

No LOC
Seizures - muscle groups
Opisthotonos, flexion and abduction of the arms
Clenching of the fists against the thorax
Extension of the lower extremities
Localized tetanus
Painful spasms muscles in close proximity to the site of
injury.
Disorder may persist for several weeks but is usually selflimiting.
Cephalic tetanus
Characterized by variable cranial nerve (CN) palsies
CN VII is most frequently involved
Untreated progress to generalized tetanus
Ophthalmoplegic tetanus - variant
Develops after penetrating eye injuries
Results in CN III palsies and ptosis

SIGNS

Abdominal tenderness and guarding,


Mimicking an acute abdomen.
Exploratory laparotomies have been performed .
Tetanospasmin
Disinhibitory effect on the ANS
level of toxin in the CNS increases.
ANS disturbances,
Sweating, fluctuating blood pressure,
Episodic tachydysrhythmia,
Increased release of catecholamines
Drugs with beta-blocker effects
Cardiovascular manifestations of ANS instability,
Associated with increased risk of sudden death.

TESTS

No blood tests that can be used to diagnose tetanus.


Diagnosis - presentation of tetanus symptoms
Laboratory identification of C. tetani can only be
demonstrated by production of tetanospasmin in mice.
Spatula test
Touching the posterior pharyngeal wall with a sterile, softtipped instrument,
Positive test -involuntary contraction of the jaw (biting down
on the "spatula"),
Negative test - gag reflex attempting to expel the foreign
object.
High specificity and a high sensitivity

PREVENTION

Recovery from naturally acquired tetanus does not


result in immunity to tetanus.
Extreme potency of the tetanospasmin toxin; even a
lethal dose of tetanospasmin is insufficient to provoke
an immune response.
Tetanus can be prevented by vaccination with tetanus
toxoid
The CDC recommends that adults receive a booster
vaccine every ten years

PREVENTION

Standard care practice


booster to any patient with a puncture wound who is
uncertain last vaccinated,
he or she has had fewer than 3 lifetime doses of the vaccine

Booster
not prevent a potentially fatal case of tetanus from the
current wound
It take up to two weeks for tetanus antibodies to form

children under the age of seven,


tetanus vaccine is often administered as a combined
vaccine,-DPT/DTaP diphtheria and pertussis.

Adults and children >7,


Td vaccine (tetanus and diphtheria)
Tdap (tetanus, diphtheria, and acellular pertussis)

TETANUS IMMUNE GLOBULIN

Recommended for treatment of tetanus.


Remove unbound tetanus toxin, but it cannot affect toxin bound
to nerve endings.
A single intramuscular dose of 3000-5000 units is generally
recommended for children and adults, with part of the dose
infiltrated around the wound if it can be identified.
WHO recommends
TIG 500 units by intramuscular injection or intravenously immediatly
administer age-appropriate TT-containing vaccine (Td, Tdap, DT, DPT,
DTaP, or TT depending on age or allergies), 0.5 cc by intramuscular
injection at 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 6-12 months later.

TREATMENT

The wound must be cleaned.


Dead and infected tissue should be removed by surgical
debridement.
Administration of the antibiotic metronidazole decreases
the number of bacteria but has no effect on the bacterial
toxin.
Penicillin was once used to treat tetanus, but is no longer
the treatment of choice, owing to a theoretical risk of
increased spasms. - Metronidazole is not available.
Passive immunization with human anti-tetanospasmin
immunoglobulin or tetanus immunoglobulin is crucial.
If specific anti-tetanospasmin immunoglobulin is not
available, then normal human immunoglobulin may be
given instead.
All tetanus victims should be vaccinated against the
disease or offered a booster shot.

MILD TETANUS

Muscle spasms - Diazepam or Other muscle relaxants


Extreme cases - Paralyze the patient with curare-like
drugs and use a mechanical ventilator.
Maintenance of an airway and proper nutrition
Total parenteral nutrition
Intake of 3500-4000 C & at least 150 g of protein per day
liquid form -tube directly into stomach (Percutaneous
endoscopic gastrostomy)
drip into a vein
high-caloric diet maintenance - increased metabolic strain
brought on by the increased muscle activity.

Full recovery takes 4 to 6 weeks because the body


must regenerate destroyed nerve axon terminals

SEVERE TETANUS

Admission to intensive care.

Lockjaw symptoms are caused due to Clostridium tetani infection.


Damaged upper motor neurons cause muscular rigidity leading to Lock-jaw

SURGICAL THERAPY

Debridement of wounds to remove organisms


and to create an aerobic environment.
Excise at least 2 cm of normal viable-appearing
tissue around the wound margins.
Incise and drain abscesses.
Delay wound manipulation - several hours after
administration of antitoxin - risk of releasing
tetanospasmin into the bloodstream.

DRUGS

Muscle spasm, rigidity, and tetanic seizures


sedative-hypnotic agents,
general anesthetics,
centrally acting muscle relaxants,
neuromuscular blocking agents.
Antibiotics are used to prevent multiplication of C
tetani, thus halting production and release of toxins.

Antibiotics - prevent multiplication of C tetani,


thus halting production and release of toxins

ANTICONVULSANTS

Sedative-hypnotic agents - mainstays of tetanus


treatment.
Benzodiazepines - primary agents for muscle spasm
prevention and work by enhancing GABA inhibition.
Diazepam is the most frequently studied and used drug.
Diazepam reduces anxiety, produces sedation, and
relaxes muscles.
Lorazepam is an effective alternative. Large amounts (up
to 600 mg/d).
Phenobarbital is another anticonvulsant that may be used
to prolong effects of diazepam.
Phenobarbital is also used to treat severe muscle spasms
and provide sedation when neuromuscular blocking
agents are used.

OTHER AGENTS

Spasm control

baclofen,
Dantrolene,
Short-acting barbiturates
Chlorpromazine.

Magnesium sulphate can +/- benzodiazepines


Control spasm and autonomic dysfunction
5 g (or 75 mg/kg) intravenous loading dose, then 2-3 g/h until
spasm controlled
Monitor patellar reflex, - Areflexia - Upper end of the therapeutic
range (4 mmol/L).
Areflexia develops, dose should be decreased to avoid overdose.
Does not reduce need for mechanical ventilation in adults with
severe tetanus,
Reduce requirement for other drugs to control muscle spasms and
cardiovascular instability.

COMPLICATIONS

Prior to 1954, asphyxia from tetanic spasms was the usual


cause of death.
Advent of neuromuscular blockers, mechanical ventilation, and
pharmacologic control of spasms, sudden cardiac death has
become the leading cause of death.
Sudden cardiac death has been attributed to excessive
catecholamine productions, direct action of tetanospasmin, or
tetanolysin on the myocardium.
Nosocomial infections are common when hospitalization is
prolonged.
Secondary infections may include sepsis from decubitus ulcers,
hospital-acquired pneumonias, and indwelling catheters.
Pulmonary embolism is particularly a problem in drug users and
elderly patients.

Further complications include the following:


Long bone fractures
Glenohumeral joint and temporomandibular joint
dislocations
Hypoxic injury and aspiration pneumonia is a common
late complication of tetanus, found in 5070% of
autopsied cases.
Adverse effects of autonomic instability, including
hypertension and cardiac dysrhythmias
Paralytic ileus, pressure sores, and urinary retention
Malnutrition and stress ulcers
Coma, nerve palsies, neuropathies, psychological
aftereffects, and flexion contractures

PROGNOSIS

Dependent on incubation period, time from spore


inoculation to first symptom, and time from first
symptom to first tetanic spasm.
shorter intervals indicate more severe tetanus and a
poorer prognosis.
Survive tetanus and return to their predisease state of
health.
Recovery is slow and usually occurs over 2-4 months.
Some patients remain hypotonic.
Clinical tetanus does not produce a state of immunity;
patients who survive the disease require active
immunization with tetanus toxoid to prevent a
recurrence.

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