Updated: Sep 29, 2009
The International Headache Society (IHS) began developing a classification system for headaches in 1985. Finalized in 1988, this system includes a tension-type headache category, further defined as either episodic or chronic. Headache categories also are defined by whether they are associated with pericranial muscle disorders.
Episodic tension headache usually is associated with a stressful event. This headache type is of moderate intensity, self-limited, and usually responsive to nonprescription drugs.
Chronic tension headache often recurs daily and is associated with contracted muscles of the neck and scalp. This type of headache is bilateral and usually occipitofrontal.
Tension-type headache is the most common type of chronic recurring head pain. In the past, pain etiology was presumed to be the muscular contraction of pain-sensitive structures of the cranium, but the IHS intentionally abandoned the terms muscular contraction headache and tension headache because no research supports muscular contraction as the sole pain etiology.
Both muscular and psychogenic factors are believed to be associated with tension-type headache.1
Headaches account for 1-4% of all emergency department (ED) visits and is the ninth most common reason for a patient to consult a physician. Physicians classify 90% of headaches reported to them as muscle contraction or migraine headaches.
No literature suggests that headache frequency is different in other regions of the world.
A female preponderance of migraine exists, 14-17%, compared with 5-6% in males.
All ages are susceptible, but most patients are young adults.
Pain onset in tension-type headache can have a throbbing quality and is usually more gradual than onset in migraines. Compared with migraines, tension-type headaches are more variable in duration, more constant in quality, and less severe.
The physical examination serves mainly to exclude the possibility of other headache causes.
Stress may cause contraction of neck and scalp muscles, although no evidence confirms that the origin of pain is sustained muscle contraction.
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Most patients with severe headache should not receive opiate analgesics until the responsible physician can complete an appropriate history and neurologic examination.
While the emergency physician must be able to identify patients with serious headache etiology, more than 90% of patients in the ED have migraine, tension, or mixed-type benign headache. Therefore, providing symptomatic relief should be a priority.
Various modalities are used in the treatment of tension headaches. These include hot or cold packs, ultrasound, electrical stimulation, improvement of posture, trigger point injections, occipital nerve blocks, stretching, and relaxation techniques.
Regular exercise, stretching, balanced meals, and adequate sleep may be part of a headache treatment program.4
These agents may alleviate headache pain by inhibiting prostaglandin synthesis, reducing serotonin release, and blocking platelet aggregation. Although the effects of NSAIDs in the treatment of headache pain tend to be patient specific, ibuprofen is usually the DOC for initial therapy. Other options include naproxen, ketoprofen, and ketorolac.
Usually DOC for treatment of mild to moderately severe headache, if no contraindications.
200-800 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 20-40 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate upward; not to exceed 2.4 g/d
>12 years: Administer as in adults
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; third trimester of pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderately severe pain. Inhibits inflammatory reactions and pain by decreasing enzyme cyclooxygenase activity, thus inhibiting prostaglandin synthesis.
500 mg PO, followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
For relief of mild to moderately severe pain and inflammation. Small dosages initially indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity; third trimester of pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors. PO form offers no advantage over other less expensive PO NSAIDs.
30 mg IV single dose; most common route used in ED
>65 years, renal impairment, or <50 kg: 15 mg IV single dose
30-60 mg IM initially, followed by 15-30 mg q6h prn
Not to exceed 5 d of treatment; consider only 1-2 days of treatment in elderly because of increased risk of GI bleed
Not established; suggested dose 0.4-1 mg/kg IM once
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; not for CNS administration
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts (rare) usually return to normal during ongoing therapy; discontinue therapy if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs
Absorbed rapidly; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Useful in diagnosis as it helps other headache syndromes (eg, chronic paroxysmal hemicrania).
Immediate release: 25-50 mg PO bid/tid
Sustained release: 75 mg PO bid; not to exceed 200 mg/d
1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding or renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists)
These agents alleviate headache, possibly by inhibiting prostaglandin synthesis.
Treats mild to moderately severe pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.
325-650 mg PO q4-6h; not to exceed 4 g/d
10-15 mg/kg/dose PO q4-6h; not to exceed 60-80 mg/kg/d
Antacids and urinary alkalinizers may increase effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increased bleeding time; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not use in children (<16 y) with flu
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
These agents are used in combination with aspirin and acetaminophen for pain relief and to induce sleep. Caffeine is used to increase its GI absorption. However, butalbital is associated with rebound headaches. Increasing use of these combination preparations may fail to provide pain relief and worsen headache symptoms.
Drug combination used to relieve tension headaches. Barbiturate component has generalized depressant effect on CNS.
1-2 tab/cap PO q4h; not to exceed 6 tab/cap in 24 h
Not established
Effects decreased by phenothiazines, quinidine, tricyclic antidepressants, theophylline, haloperidol, chloramphenicol, ethosuximide, corticosteroids, warfarin, doxycycline, and beta-blockers; effects increased by CNS depressants, methylphenidate, valproic acid, propoxyphene, and benzodiazepines
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Risk of rebound headache and overuse; caution in patients with history of substance abuse
Drug combination used to relieve tension headaches. Barbiturate component has generalized depressant effect on CNS.
1-2 tab PO at onset, repeat q4h; not to exceed 6 doses in 24 h
Not established
Effects decreased by phenothiazines, quinidine, tricyclic antidepressants, theophylline, haloperidol, chloramphenicol, ethosuximide, corticosteroids, warfarin, doxycycline, and beta-blockers; effects increased by CNS depressants, methylphenidate, valproic acid, propoxyphene, and benzodiazepines
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Risk of rebound headache and overuse; caution in patients with history of substance abuse
Patients with infrequent headaches can be treated with simple analgesics initially.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs or upper GI disease or taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h
Rifampin can reduce analgesic effects; barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; G-6-P deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholics who exceed 4000 mg/d; severe or recurrent pain or high or continued fever may indicate serious illness; acetaminophen contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding safe daily totals
Indicated for treatment of mild to moderately severe headache.
30-60 mg/dose based on codeine content PO q4-6h or 1-2 tab q4h; not to exceed 12 tab/d; not to exceed 4 g acetaminophen in 24 h
0.5-1 mg/kg/dose based on codeine content PO q4-6h; 10-15 mg/kg/dose based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen in 24 h
CNS depressants or tricyclic antidepressants increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
Indicated for relief of moderately severe to severe pain. DOC for aspirin-hypersensitive patients.
1-2 tab/cap PO q4-6h prn headache
0.05-0.15 mg/kg/dose oxycodone PO q4-6h prn; not to exceed 5 mg/dose of oxycodone
Phenothiazines may decrease analgesic effects; CNS depressants or tricyclic antidepressants increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Duration of action may increase in elderly persons; be aware of total daily dose of acetaminophen patient is receiving; do not exceed 4000 mg/24 h of acetaminophen; higher doses may cause liver toxicity
These agents are useful in aborting headache and treating emesis that results from acute pain.
Antidopaminergic agent effective in treating emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.
12.5 mg PO/PR tid and 25 mg hs
25 mg IV/IM, repeat in 2 h prn; switch to PO as soon as possible
<2 years: Contraindicated
>2 years: 0.25-1 mg/kg PO/IV/IM/PR q4-6h prn
Other CNS depressants or anticonvulsants may cause additive effects; with epinephrine, may cause hypotension
Documented hypersensitivity; children younger than 2 y (incidences of death due to respiratory depression)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, and asthma
May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine-receptors, through anticholinergic effects, and depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory response, acting as respiratory stimulant at high altitude.
Metoclopramide (Reglan) can be used as an alternative to prochlorperazine. Studies show prochlorperazine is better.
5-10 mg PO/IM tid/qid; not to exceed 40 mg/d
2.5-10 mg IV q3-4h prn; not to exceed 10 mg/dose or 40 mg/d
25 mg PR bid
2.5 mg PO/PR q8h or 5 mg q12h prn; not to exceed 15 mg/d
IV dosing not recommended for children
0.1-0.15 mg/kg/dose IM; change to PO as soon as possible
Other CNS depressants or anticonvulsants may cause additive effects; with epinephrine, may cause hypotension
Documented hypersensitivity; bone marrow suppression; narrow-angle glaucoma; severe liver or cardiac disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Drug-induced Parkinson syndrome or pseudoparkinsonism occurs quite frequently; akathisia is most common extrapyramidal reaction in elderly persons; lowers seizure threshold; caution in patients with history of seizures
Dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. Acts centrally on chemoreceptor triggers in the floor of the fourth ventricle, which provides important antiemetic activity.
10 mg IV
Not established
Anticholinergic agents may antagonize effects of metoclopramide; opiate analgesics may increase metoclopramide toxicity in CNS
Documented hypersensitivity; pheochromocytoma or GI hemorrhage, obstruction or perforation; history of seizure disorders
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in history of mental illness and Parkinson disease
These are direct vasoconstrictors of smooth muscle in cranial blood vessels. Their activity depends on the CNS vascular tone at the time of administration.
Alpha-adrenergic and serotonin antagonist. Causes constriction of peripheral and cranial blood vessels.
2 tabs PO at onset of attach, 1 tab q30min prn; not to exceed 6 tab per attack or 10 tab/wk
1 tab SL at first sign of attach and 1 tab q30min; not to exceed 3 tabs/d or 5 tabs/wk
1 suppository PR at first sign of attack with second dose after 1h prn; not to exceed 2 suppositories/attack or 5 suppositories/wk
Not established
Increases effects of heparin and toxicity of nitroglycerin, propranolol, erythromycin, and clarithromycin
Documented hypersensitivity hepatic or renal disease; peptic ulcer disease; sepsis; peripheral vascular disease
X - Contraindicated; benefit does not outweigh risk
Avoid using prolonged regimens due to danger of causing gangrene as well as dependency
Alpha-adrenergic blocking agent with direct stimulating effect on smooth muscle of peripheral and cranial blood vessels; depresses central vasomotor centers. Mechanism of action is similar to ergotamine; nonselective 5HT1 agonist with wide spectrum of receptor affinities outside 5HT1 system; also binds to dopamine. Thus, has alpha-adrenergic antagonist and serotonin antagonist effect. Indicated to abort or prevent vascular headache when rapid control needed or when other routes of administration not feasible.
Available in IV or intranasal preparations, tends to cause less arterial vasoconstriction than ergotamine tartrate.
1 mg IM at first sign of headache, repeat q1 h; not to exceed 3 mg total dose
2 mg IV maximum dose for faster effect; most commonly given at 0.5-1 mg IV with antiemetic; not to exceed 6 mg/wk
Intranasal: 1 spray into each nostril and repeat prn within 15 min; not to exceed 6 sprays/d or 8 sprays/wk
Not established
Increases effects of heparin and toxicity of nitroglycerin, propranolol, erythromycin, and clarithromycin
Documented hypersensitivity; has used sumatriptan or zolmitriptan within previous 24 h; within 2 wk of discontinuing MAO inhibitors
X - Contraindicated; benefit does not outweigh risk
Caution in angina, hypertension, impaired renal or hepatic function, or peripheral vascular disease
Deterrence and prevention of headache may include the following:
Complications of headache may include the following:
Fumal A, Schoenen J. Tension-type headache: current research and clinical management. Lancet Neurol. Jan 2008;7(1):70-83. [Medline].
Silver N. Headache (chronic tension-type). Am Fam Physician. Jul 1 2007;76(1):114-6. [Medline]. [Full Text].
[Guideline] Martin V, Elkind A. Diagnosis and classification of primary headache disorders. In: Standards of care for headache diagnosis and treatment. Chicago (IL): National Headache Foundation; 2004. [Full Text].
[Guideline] Ruoff G, Urban G. Treatment of primary headache: episodic tension-type headache. In: Standards of care for headache diagnosis and treatment. Chicago (IL): National Headache Foundation; 2004. [Full Text].
Arena JG, Bruno GM, Hannah SL, et al. A comparison of frontal electromyographic biofeedback training, trapezius electromyographic biofeedback training, and progressive muscle relaxation therapy in the treatment of tension headache. Headache. Jul-Aug 1995;35(7):411-9. [Medline].
Bogaards MC, ter Kuile MM. Treatment of recurrent tension headache: a meta-analytic review. ALYSIS. Sep 1994;10(3):174-90. [Medline].
Carlsson J, Augustinsson LE, Blomstrand C, et al. Health status in patients with tension headache treated with acupuncture or physiotherapy. Headache. Sep 1990;30(9):593-9. [Medline].
De Benedittis G, Lorenzetti A, Sina C, Bernasconi V. Magnetic resonance imaging in migraine and tension-type headache. Headache. May 1995;35(5):264-8. [Medline].
[Best Evidence] Detsky ME, McDonald DR, Baerlocher MO, et al. Does this patient with headache have a migraine or need neuroimaging?. JAMA. Sep 13 2006;296(10):1274-83. [Medline].
Ficek SK, Wittrock DA. Subjective stress and coping in recurrent tension-type headache. Headache. Sep 1995;35(8):455-60. [Medline].
Goldstein JN, Camargo CA Jr, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. Jun 2006;26(6):684-90. [Medline].
Iversen HK, Langemark M, Andersson PG, et al. Clinical characteristics of migraine and episodic tension-type headache in relation to old and new diagnostic criteria. Headache. Jul 1990;30(8):514-9. [Medline].
Landy S. Migraine throughout the life cycle: treatment through the ages. Neurology. Mar 9 2004;62(5 Suppl 2):S2-8. [Medline].
Silberstein SD. Tension-type headaches. Headache. Sep 1994;34(8):S2-7. [Medline].
Silberstein SD, Olesen J, Bousser MG, et al. The International Classification of Headache Disorders, 2nd Edition (ICHD-II)--revision of criteria for 8.2 Medication-overuse headache. Cephalalgia. Jun 2005;25(6):460-5. [Medline].
Tfelt-Hansen P. Acute pharmacotherapy of migraine, tension-type headache, and cluster headache. J Headache Pain. Apr 2007;8(2):127-34. [Medline].
tension headache, tension-type headache, chronic tension headache, episodic tension headache, chronic recurring head pain, cluster headache, migraine headache, muscle contraction headache
Michelle Blanda, MD, Chair, Department of Emergency Medicine, Summa Health System; Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine
Michelle Blanda, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Lori K Sargeant, MD, Consulting Staff, Summa Emergency Associates, Inc
Lori K Sargeant, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, and Ohio State Medical Association
Disclosure: Nothing to disclose.
Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland
Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
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