Gas Gangrene Dr Akbar

8/10/2019 Gas Gangrene Dr Akbar

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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 damagespecific 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 otherthromboses





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 suppressanteffect - shock



PREDISPOSING FACTORS

Contamination - clostridial spores - posttraumatic orpostoperative lesions

Local wound conditions > degree of clostridialcontamination

Disrupted or necrotic tissue provides the necessary

enzymes and a low oxidation/reduction potential,allowing for spore germination.

Foreign bodies, premature wound closure& devitalizedmuscle 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 & fascialplanes.

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 laparoscopiccholecystectomy and colonoscopy.

Septic back-street abortions - uterine gas gangrene.



SPONTANEOUS without external wound or injury - serious underlying

conditions. Colorectal adenocarcinoma

Hematologic malignancy

Children - Neutropenia

chemotherapyspontaneous 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 theunderlying 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 blebsand 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 brown-

red 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 andchanging 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.

Gasgangrene CperfringenstypeA(Principal)



Gas gangrene C. perfringens type A (Principal),

Capsulated, non-motile

Lecithinase C - toxaemia

Nagler reaction

Colonies with haloes

Colonies withouthaloes

Incorporated withAntitoxins



C Perfringens

C histolyticumC 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 asprimary 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 surgicaldebridement

– Frequent interruption of the continuous infusion

– Not recommend this adjuvant therapy

H b i (HBO) th



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 tissueprior to surgery.

100% oxygen at 2.5-3 absolute atmospheres for 90-120minutes 3 times

Potential risks

Pressure-related trauma-barotraumatic otitis pneumothorax

Oxygen toxicity (myopia, seizures). Claustrophobia.

Most adverse effects - self-limiting & resolve aftertermination therapy



SURGICAL CARE

Fasciotomy for compartment syndrome - not bedelayed 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

http://upload.wikimedia.org/wikipedia/commons/b/b1/Hemipelvectomy_gas_gangrene.jpg




Hemipelvectomy

SUMMARY






SUMMARY Most devastating infections.

extremity amputation or massive loss of muscles, skin, and soft

tissues, requiring extensive reconstructive surgery and physicalrehabilitation.

spontaneous gas gangrene may have occult malignancies ofthe 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 fractureswith devitalized muscle and soil contamination.

Provide warnings and instructions of wound care to rescuersand health care workers - clostridial infections, -tetanus and gasgangrene, in injured victims of natural disasters such asearthquake or tsunami.

COMPLICATIONS



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 otherforms of gas gangrene.



TETANUS

EPIDEMOLOGY



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 organicmatter.

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 isinfectious but is not contagious.

History



History Ancient people -relationship between wounds and fatal

muscle spasms.

Greek - τέτανο(tetanos) – taut & τείνειν(teinein) - Stretch 1884

– Isolated strychnine-like toxin of tetanus from free-living,anaerobic soil bacteria.

– Etiology of the disease - demonstrated transmissibilityof tetanus for first time.

– produced tetanus in rabbits by injecting pus from apatient with fatal tetanus into their sciatic nerves.

1889,

– Kitasato Shibasaburō -C. tetani was isolated from ahuman victim

– organism could produce disease when injected intoanimals

– toxin could be neutralized by specific antibodies



History 1897,

– Edmond Nocard - tetanus antitoxin inducedpassive immunity in humans

– could be used for prophylaxis and treatment.

1924

– P. Descombey - Tetanus toxoid vaccine wasdeveloped

– used to prevent tetanus induced by battlewounds during World War II

O C O



INTRODUCTION Tetanus - Prolonged contraction of skeletal muscle

fibers. Primary symptoms – tetanospasmin

– neurotoxin - Gram-positive, obligate anaerobicbacterium Clostridium tetani .

Infection - wound contamination Cut or deep puncture wound.

muscle spasms - jaw (lockjaw) and elsewhere in thebody

Infection can be prevented by proper immunizationand 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



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 minuteswith the body shaped into a characteristic form calledopisthotonos.

Spasms continue for up to 4 weeks, and complete

recovery may take months



NEONATAL TETANUS



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



ETIOLOGY Tetanus – Rust- rusty nails,

Objects with rust –outdoors or harbor anaerobicbacteria

Rust - not cause tetanus /contain more C. tetanibacteria.

Rough surface of rusty metal merely provides a primehabitat 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 asuitable environment for growth.

PATHOPHYSIOLOGY



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 tetanospasminand tetanolysin.

Tetanolysin - no role - clinical course of tetanus Tetanospasmin

– neurotoxin

– causes the clinical manifestations of tetanus.



http://www.dreamstime.com/register?jump_to=http%3A%2F%2Fwww.dreamstime.com%2Froyalty-free-stock-image-tetanus-bacteria-image11898406



Tetanospasmin





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 ofbody weight or 175 nanograms for a 70-kg

Neurons - incapable of neurotransmitter release -

GABA and Glycine - Major inhibitory neurotransmitters

Tetanospasmin



Tetanospasmin Failure of inhibition of motor reflex responses to sensory

stimulation.

Generalized contractions of the agonist and antagonistmusculature 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 withantitoxin.

Recovery of nerve function from tetanus toxins requiressprouting of new nerve terminals and formation of newsynapses.

SYMPTOMS



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



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 producesa sneering grin expression known as risus sardonicus.



RISUS SARDONICUS.

SIGNS



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 thedisease.

Seizures resemble epileptic seizures with the presence of a

sudden burst of tonic contractions.

SIGNS

OC &



No LOC & experiences severe pain.

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 self-limiting.

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



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



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, soft-

tipped 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



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



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



US U G O U 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 doseinfiltrated 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 intramuscularinjection at separate site.

Tetanus disease does not induce immunity; Patients without a history of primary TT vaccination should

receive a second dose 1 –2 months after the first dose and athird dose 6-12 months later.

TREATMENT

The wound must be cleaned



The wound must be cleaned.

Dead and infected tissue should be removed by surgicaldebridement.

Administration of the antibiotic metronidazole decreasesthe number of bacteria but has no effect on the bacterialtoxin.

Penicillin was once used to treat tetanus, but is no longer

the treatment of choice, owing to a theoretical risk ofincreased spasms. - Metronidazole is not available.

Passive immunization with human anti-tetanospasminimmunoglobulin or tetanus immunoglobulin is crucial.

If specific anti-tetanospasmin immunoglobulin is notavailable, then normal human immunoglobulin may begiven instead.

All tetanus victims should be vaccinated against the

disease or offered a booster shot.

MILD TETANUS



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



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

http://upload.wikimedia.org/wikipedia/commons/d/d5/Lockjawsymptoms.jpg





Damaged upper motor neurons cause muscular rigidity leading to Lock jaw

SURGICAL THERAPY






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



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



ANTICONVULSANTS Sedative-hypnotic agents - mainstays of tetanus

treatment.

Benzodiazepines - primary agents for muscle spasmprevention and work by enhancing GABA inhibition.

Diazepam is the most frequently studied and used drug.

Diazepam reduces anxiety, produces sedation, andrelaxes muscles.

Lorazepam is an effective alternative. Large amounts (upto 600 mg/d).

Phenobarbital is another anticonvulsant that may be usedto prolong effects of diazepam.

Phenobarbital is also used to treat severe muscle spasmsand provide sedation when neuromuscular blockingagents are used.

OTHER AGENTS



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 therapeuticrange (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 andcardiovascular 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 hasbecome the leading cause of death.

Sudden cardiac death has been attributed to excessivecatecholamine productions, direct action of tetanospasmin, ortetanolysin on the myocardium.

Nosocomial infections are common when hospitalization isprolonged.

Secondary infections may include sepsis from decubitus ulcers,hospital-acquired pneumonias, and indwelling catheters.

Pulmonary embolism is particularly a problem in drug users andelderly 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 50 –70% ofautopsied cases.

Adverse effects of autonomic instability, includinghypertension and cardiac dysrhythmias

Paralytic ileus, pressure sores, and urinary retention Malnutrition and stress ulcers

Coma, nerve palsies, neuropathies, psychologicalaftereffects, and flexion contractures

PROGNOSIS



PROGNOSIS

Dependent on incubation period, time from spore

inoculation to first symptom, and time from firstsymptom to first tetanic spasm.

shorter intervals indicate more severe tetanus and apoorer prognosis.

Survive tetanus and return to their predisease state ofhealth.

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 activeimmunization with tetanus toxoid to prevent a

recurrence.



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Gas Gangrene Dr Akbar