Acute tetanus: Difference between revisions
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==Background== | ==Background== | ||
*''Clostridium tetani'' spores enter skin through wound, make tetanospasmin toxin | |||
*2001-2008 in US, 233 cases, 26 deaths | |||
*Mortality as high as 45% | |||
*Incubation is 2 to 56d | |||
*Spores found in soil and human and animal feces | |||
**Tetanus prone wounds include contaminated lacerations, abrasions, puncture wounds; crush, avulsion, or frostbite injuries are also vulnerable to tetanus <ref>Auerbach PS. Wilderness Medicine. Philadelphia: Mosby Elsevier; 2007.</ref> | |||
**Preferentially binds GABA and glycinergic neurons and blocks pre-synaptic release | |||
***Motor neurons undergo sustained excitatory discharge, producing spasms | |||
*The majority of clinical tetanus happen in the elderly.<ref>Talan DA, et al. Tetanus immunity and physician compliance with tetanus prophylaxis practices among emergency department patients presenting with wounds. Ann Emerg Med. 2004 Mar;43(3):305-14.[http://www.ncbi.nlm.nih.gov/pubmed/14985655 Pubmed]</ref> | |||
== | ==Clinical Features== | ||
===Neonatal=== | ===Neonatal=== | ||
*From umbilical stump infection. Usually protected by passive maternal Abs | |||
*Symptoms - poor suck and failure to nurse, irritability, crying, grimacing | |||
*Usually with in 10 d of birth | |||
===Local=== | ===Local=== | ||
*Rigidity of muscles near wound- may progress to generalized | |||
===Generalized=== | ===Generalized=== | ||
*Most common form of tetanus | |||
*Usually begins with trismus (spasm of the masticator muscle group) with gradual onset of spasm of muscle groups in the trunk and extremities | |||
*Spasms exacerbated by external stimuli (light or sudden sound) | |||
*Patients can lose ability to breath during prolonged spasms | |||
*Respiratory failure is main cause of death | |||
*Patients are conscious and alert | |||
*Hypersympathetic state with sweating, hypertension, tachycardia, fever | |||
===Cephalic=== | ===Cephalic=== | ||
*Follow injuries to head or [[otitis media]] | |||
*Get cranial nerve dysfunction- usually cranial nerve 7 | |||
==Diagnosis== | ==Differential Diagnosis== | ||
{{Jaw spasms DDX}} | |||
== | ==Evaluation== | ||
*Diagnosis is clinical | |||
*Progressive symptoms<ref>Fernandez-Frackelton M: Bacteria, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 127:p 1681-1686</ref> | |||
**Alert and able to communicate | |||
**Trismus - lockjaw (50%-75% of patients) | |||
**Sardonic smile (risus sardonicus) - other facial muscles become involved | |||
**Minor stimuli such as touch or noise start tetanic contractions | |||
**Difficulty swallowing | |||
**Long bone fractures, tendon rupture | |||
**Opisthotonus - lumbar lordosis with the neck and legs extended and the arms flexed at the elbows | |||
**Laryngospasm | |||
**Autonomic instability | |||
**Sympathetic nervous system hyperactivity, including tachycardia, sweating, arrhythmias, and hypertension | |||
*No laboratory testing is used to diagnose tetanus; wound cultures are often negative | |||
== | ==Management== | ||
*Before wound debridement, immunoglobulin (TIG) directly into the wound and IM | |||
**Dose: 3000-6000 units IM with adequate mL to wound | |||
**Does not reverse toxin already bound to CNS. Binds circulating toxin | |||
*Tetanus toxoid; patients do NOT develop immunity after tetanus infection | |||
===Supportive Care=== | |||
*Place patient in a quiet room | |||
*Provide sedation with [[Benzodiazepines]] or phenobarbital | |||
*Airway management via intubation or tracheostomy should be performed when patient exhibits dysphagia or respiratory difficulties | |||
*Autonomic dysfunction management with magnesium sulfate or labetalol, morphine and clonidine | |||
*Magnesium sulfate has several desirable attributes for control of spasticity and autonomic dysfunction in tetanus<ref>Wangmo KP, Teng M, Henker R, Kinnear S, Tshering J, Wang NE. Survival of a Patient With Tetanus in Bhutan Using a Magnesium Infusion Managed Only by Clinical Signs. Wilderness & Environmental Medicine. 2014;25(2):194-197. doi:10.1016/j.wem.2013.11.006.</ref> | |||
**Acts as a presynaptic neuromuscular blocker by antagonizing calcium in the neuromuscular junction and myocardium | |||
**Blocks the release of catecholamines and has anticonvulsant properties | |||
**Often available in low-resource settings | |||
===[[Antibiotics]]=== | |||
{{Tetanus Antibiotics}} | |||
==See Also== | |||
*[[Tetanus (Prophylaxis)]] | |||
*[[Clostridium]] | |||
==References== | |||
<references/> | |||
Moll JL, Carden DL. Tetanus. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com/content.aspx?bookid=1658§ionid=109435736. Accessed December 01, 2017. | |||
[[Category:ID]] | [[Category:ID]] |
Revision as of 23:58, 27 April 2018
Background
- Clostridium tetani spores enter skin through wound, make tetanospasmin toxin
- 2001-2008 in US, 233 cases, 26 deaths
- Mortality as high as 45%
- Incubation is 2 to 56d
- Spores found in soil and human and animal feces
- Tetanus prone wounds include contaminated lacerations, abrasions, puncture wounds; crush, avulsion, or frostbite injuries are also vulnerable to tetanus [1]
- Preferentially binds GABA and glycinergic neurons and blocks pre-synaptic release
- Motor neurons undergo sustained excitatory discharge, producing spasms
- The majority of clinical tetanus happen in the elderly.[2]
Clinical Features
Neonatal
- From umbilical stump infection. Usually protected by passive maternal Abs
- Symptoms - poor suck and failure to nurse, irritability, crying, grimacing
- Usually with in 10 d of birth
Local
- Rigidity of muscles near wound- may progress to generalized
Generalized
- Most common form of tetanus
- Usually begins with trismus (spasm of the masticator muscle group) with gradual onset of spasm of muscle groups in the trunk and extremities
- Spasms exacerbated by external stimuli (light or sudden sound)
- Patients can lose ability to breath during prolonged spasms
- Respiratory failure is main cause of death
- Patients are conscious and alert
- Hypersympathetic state with sweating, hypertension, tachycardia, fever
Cephalic
- Follow injuries to head or otitis media
- Get cranial nerve dysfunction- usually cranial nerve 7
Differential Diagnosis
Jaw Spasms
- Acute tetanus
- Akathisia
- Conversion disorder
- Drug toxicity (anticholinergic, phenytoin, valproate, carbamazepine)
- Dystonic reaction
- Electrolyte abnormality
- Hypocalcemic tetany
- Magnesium
- Mandible dislocation
- Meningitis
- Peritonsillar abscess
- Rabies
- Seizure
- Strychnine poisoning
- Stroke
- Temporomandibular disorder
- Torticollis
Evaluation
- Diagnosis is clinical
- Progressive symptoms[3]
- Alert and able to communicate
- Trismus - lockjaw (50%-75% of patients)
- Sardonic smile (risus sardonicus) - other facial muscles become involved
- Minor stimuli such as touch or noise start tetanic contractions
- Difficulty swallowing
- Long bone fractures, tendon rupture
- Opisthotonus - lumbar lordosis with the neck and legs extended and the arms flexed at the elbows
- Laryngospasm
- Autonomic instability
- Sympathetic nervous system hyperactivity, including tachycardia, sweating, arrhythmias, and hypertension
- No laboratory testing is used to diagnose tetanus; wound cultures are often negative
Management
- Before wound debridement, immunoglobulin (TIG) directly into the wound and IM
- Dose: 3000-6000 units IM with adequate mL to wound
- Does not reverse toxin already bound to CNS. Binds circulating toxin
- Tetanus toxoid; patients do NOT develop immunity after tetanus infection
Supportive Care
- Place patient in a quiet room
- Provide sedation with Benzodiazepines or phenobarbital
- Airway management via intubation or tracheostomy should be performed when patient exhibits dysphagia or respiratory difficulties
- Autonomic dysfunction management with magnesium sulfate or labetalol, morphine and clonidine
- Magnesium sulfate has several desirable attributes for control of spasticity and autonomic dysfunction in tetanus[4]
- Acts as a presynaptic neuromuscular blocker by antagonizing calcium in the neuromuscular junction and myocardium
- Blocks the release of catecholamines and has anticonvulsant properties
- Often available in low-resource settings
Antibiotics
- Metronidazole 500mg IV (7.5mg/kg) q6hrs OR
- Clindamycin 600mg IV (7.5mg/kg) q6hrs
Penicillin
- Although once the drug of choice it is now no longer recommended since it may potentiate the effect of tetanus toxin by inhibiting the GABA receptors[5]
See Also
References
- ↑ Auerbach PS. Wilderness Medicine. Philadelphia: Mosby Elsevier; 2007.
- ↑ Talan DA, et al. Tetanus immunity and physician compliance with tetanus prophylaxis practices among emergency department patients presenting with wounds. Ann Emerg Med. 2004 Mar;43(3):305-14.Pubmed
- ↑ Fernandez-Frackelton M: Bacteria, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 127:p 1681-1686
- ↑ Wangmo KP, Teng M, Henker R, Kinnear S, Tshering J, Wang NE. Survival of a Patient With Tetanus in Bhutan Using a Magnesium Infusion Managed Only by Clinical Signs. Wilderness & Environmental Medicine. 2014;25(2):194-197. doi:10.1016/j.wem.2013.11.006.
- ↑ Ganesh Kumar AV. Benzathine penicillin, metronidazole and benzyl penicillin in the treatment of tetanus: a randomized, controlled trial .Ann Trop Med Parasitol. 2004 Jan;98(1):59-63 PMID 15000732
Moll JL, Carden DL. Tetanus. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com/content.aspx?bookid=1658§ionid=109435736. Accessed December 01, 2017.