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Residency > Tetanus > Flashcards

Tetanus Flashcards

1
Q

What is usually the first cause of death?

A

Respiratory muscle dysfunction leading to hypoxia, hypoventilation and death

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2
Q

If patients survive the acute phase of the disease, what is the likely cause of death?

A

Autonomic dysfunction leading to dysrhythmias, MI, hypertension, hyperthermia

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3
Q

What is the classic inciting event that leads to tetanus?

A

A penetrating wound, although sometimes this is such a minor event that the patient cannot recall an injury

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4
Q

Apart from lacerations, abrasions, puncture wounds, what other scenarios can cause tetanus?

A

Childbirth, otitis media, corneal abrasions, dental procedures
Post-operative tetanus can occur because up to 10% of humans have C. tetani in the colon

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5
Q

Where is C. tetani found in the world?

A

Ubiquitous in soil and also found in feces of humans and animals

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6
Q

Is C. tetani aerobic or anearobic?

A

Obligate anaerobic

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7
Q

Can germination and replication of C. tetani happen without clinical findings of an infected wound?

A

Yes

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8
Q

What is the way that C. tetani causes disease?

A

Produces a neurotoxin that prevents vesicles from fusing to the presynaptic membrane and releasing inhibitory neurotransmitters such as glycine and GABA

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9
Q

What is the name of the neurotoxin?

A

tetanospasmin

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10
Q

How does tetanospasmin spread through the body?

A

Retrograde axonal transport and trans-synaptic spread to the CNS

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11
Q

What are the first neurons affected?

A

Interneurons that are afferent to alpha motor neurons which leads to the classic muscle spasms of tetanus

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12
Q

Are the effects of tetanospasmin reversible?

A

No, recovery only happens when a new axonal terminal is produced

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13
Q

What is the incubation period of tetanus?

A

1 day to several months

Shorter incubation period has a worse prognosis

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14
Q

What are the four types of tetanus clinical presentations?

A

Generalized: most common
Localized
Cephalic
Neonatal

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15
Q

Describe generalized tetanus

A

Most common presentation
First presents with lockjaw in 50-75% of patients
Early symptoms: irritability, weakness, myalgias, muscle cramps, dysphagia, hydrophobia, drooling
More advanced disease: spasms triggered by even minor stimuli, laryngeal spasm leading to respiratory failure, autonomic dysfunction leading to unchecked sympathetic tone with hypertension, tachycardia, dysrhythmias, MI, hyperthermia
Patient remains lucid throughout

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16
Q

How are tetanus and meningitis different?

A

Tetanus patients have no alteration in their mental state

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17
Q

Describe cephalic tetanus

A

Rare variant
Usually an injury to the face or otitis media
Cranial nerve palsies usually precede spasms, making it easy to misdiagnose this
Most commonly involves CNVII, mimicking Bell’s Palsy
Will have trismus and palsies

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18
Q

Describe neonatal tetanus

A

Generalized disease of the newborn
In developing countries where mom is not vaccinated or dirty instruments used on the umbilical cord
Symptoms in first week of life with irritability and poor feeding
Almost 100% fatal without intervention

19
Q

What are some of the complications of disease other than respiratory compromise and cardiovascular complications?

A

Fractures or dislocations from forceful contractures
Rhabdomyolysis and renal injury
Renal injury from dehydration and sympathetic overload
Hyperthermia
Peptic ulcers, ileus, intestinal perforation, constipation
SIADH
Hemolysis

20
Q

How is tetanus diagnosed?

A

Clinically
There are no lab tests
Wound cultures are not reliable
Other differential diagnoses are ruled out

21
Q

What is the spatula test?

A

Tongue depressor to the back of the throat
Gag and expulsion of the blade is negative
Reflex masseter spasm and biting the blade is positive
94% sensitive and 100% specific

22
Q

Poising from what substance has a similar presentation to tetanus?

A

Strychnine

Comes from rat poison, but can also be in street drugs

23
Q

What is another more likely cause of trismus?

A

Dental or intraoral infections

24
Q

Apart from intraoral infections, what other process can cause trismus and should be ruled out?

A

TMJ dislocation or TMJ syndrome

25
Q

What other diagnosis should be considered when a patient has dysphagia and respiratory dysfunction?

A

Rabies

26
Q

How is rabies unique from tetanus?

A

Rabies does not cause trismus

27
Q

What should be in the differential when a patient is presenting with CNVII palsy?

A 
Tetanus
Bell's palsy
Stroke
Botulism
CN palsies
Facial cellulitis with facial nerve compression
28
Q

What are the main treatment strategies for tetanus?

A

Supportive care
Elimination of unbound toxin
Active immunization
Prevention of further toxin production

29
Q

How are spasms managed?

A

Avoid touch and sounds as these can trigger spasms
Benzos are first line as they are GABA agonists (Diazepam most commonly used, but ativan and midazolam also good)
Propofol infusion works
Dantrolene can be adjunct as muscle relaxant
Mg infusion often advocated but no evidence
If no improvement with the above, paralyze, and intubate

30
Q

Which IV benzos can cause lactic acidosis and why?

A

IV lorazepam and diazepam have propylene glycol which can cause lactic acidosis at high doses

31
Q

What neuromuscular blocker should be used for paralysis?

A

Succinylcholine can be used in the first few days, but carries the risk of hyperkalemia and otherwise should be avoided
Rocuronium/Vecuronium are good but require continuous infusion, they lack hemodynamic side effects
Pancuronium is long acting but can worsen the autonomic instability because of catecholamine reuptake inhibition

32
Q

How is the autonomic and subsequent hemodynamic instability managed?

A

Combined alpha/beta blockers: labetalol or propranolol
Beta blockers alone should be avoided (unopposed alpha)
Clonidine has variable effect
Morphine, Mg, or spinal baclofen can help
Diuretics should be avoided (dehydration worsens autonomic instability)
Bradydysrhythmias treated with pacing, not atropine, as there is already too much sympathetic tone

33
Q

How is elimination of unbound toxin achieved?

A

Give HTIG (human tetanus immune globulin) and immunize with Td

34
Q

How does HTIG work?

A

Binds and eliminates all free toxin and toxin at the inoculation site
Does not bind toxin in the nervous system
Does reduce mortality
Does not treat any existing symptoms

35
Q

How and where should HTIG be given?

A

As soon as possible
Separate site from Td
Proximal to the wound is logical but not proven
Not approved for intrathecal in the US

36
Q

Wound debridement and antibiotics can decrease future release of toxin, but should not be done until what else has been done first?

A

Must give HTIG first as debridement and antibiotics can cause a transient release of toxin

37
Q

What is the antibiotic of choice and why?

A

Metronidazole 500 Q6h

Better penetration into devitalized tissue and abscesses and superior in recovery time and mortality benefit

38
Q

Why is penicillin not a first choice antibiotic?

A

Has GABA antagonist activity and can potentiate the effects of tetanospasm

39
Q

Who gets a prophylactic Tdap shot in the ED?

A

Anyone with an unknown or less than full series of three shots regardless of the wound type

40
Q

When does a person with a completed Tdap series need a prophylactic Tdap in the ED?

A

Never, not even with more extensive wounds

But can consider updating if they are immune compromised, IV drug users, elderly, or long time since last booster

41
Q

When is HTIG given prophylactically?

A

Only to patients with high risk wounds and unknown or incomplete vaccination history

42
Q

What are high risk wounds for tetanus?

A 
>6hrs old
>1cm deep
Stellate
Contaminated
Denervated
Ischemic
Infected
43
Q

What prophylactic medications are appropriate for pregnant patients?

A

Td and HTIG

44
Q

What should be given to patients that are reportedly allergic to tetanus?

A

Tetanus anaphylaxis is rare

But can give HTIG to these patients and should be referred to an allergist for immunization and further treatment

Residency (19 decks)

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