WikEM - User contributions [en]

Pericarditis

2016-08-01T21:17:56Z

Peterdmorris: PR depression addition

==Background==
[[File:Pericarditis.jpg|thumbnail|Pericarditis compared with normal pericardium]]
===Etiology===
*Idiopathic (25-85%)
*Infection (up to 20%, including viral, bacterial, TB)
*Malignancy: heme, lung, breast
*[[Uremia]]
*Post radiation
*Connective tissue disease
*Drugs: [[procainamide]], [[hydralazine]], methyldopa, anticoagulants
*Cardiac injury (can see up to weeks later): post [[MI]] (Dressler's syndrome), [[thoracic trauma]], [[aortic dissection]]
*Troponin elevation may indicate a concurrent [[myocarditis]] which predispose to risk of [[CHF]] or [[arrhythmias|arrhythmia]]. <ref>LeWinter MM, et al. Clinical practice. Acute pericarditis. N Engl J Med. 2014 Dec 18;371(25):2410-6. PMID: 25517707.</ref>

==Clinical Features==
*Pleuritic [[chest pain]]
**Radiates to chest, back, left trapezius
**Diminishes with sitting up/leaning forward
*[[shortness of breath]]
**Especiallyif concommitant [[pleural effusion]]
*Hypotension/extremis if [[cardiac tamponade]]
*[[Fever]]
*Friction rub

==Differential Diagnosis==
*[[CHF]]
*[[PE]]
*[[Pneumothorax]]
*[[Aortic dissection]]
*[[Pneumomediastinum]]
*[[Pleuritis]]

{{ST elevation DDX}}

==Evaluation==
===Work-Up===
*ECG
*Labs
**WBC, ESR, trop
*CXR
*Bedside Ultrasound to rule out effusion

===ECG===
[[File:ECG000026-2.jpg|thumb|Acute pericarditis with clear diffuse ST elevation and some PTa depression]]
*Classically described to cause diffuse ST elevations
*PR depression is a very specific finding exclusive to viral pericarditis (or PR elevation in AVR)
*Less reliable in post-MI patients and those with baseline ECG abnormalities
*May see low voltage/alternans if effusion present
*If early repol confounding interpretation check ST:T ratio
**If (ST elev)/(T height) in V6 or I >0.25 likely pericarditis
*If predominantly inferior elevation, depression in aVL is sensitive for STEMI<ref>Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.</ref

====Stages of Progression====
[[File:Stadia pericarditis.png|thumb|Stages of pericarditis]]
[[File:Ptadepressie.png|thumb|PTa depression]]
*Stage I:
**Global concave up [[ST elevation]] in all leads (esp V4-6, I, II) in all leads except in aVR, V1 and III
**PTa depression (depression between the end of the P-wave and the beginning of the QRS- complex)
*Stage II:
**"pseudonormalisation," ST to baseline, big T's, PR dep
*Stage III:
**T wave flatten then inversion
*Stage IV:
**Return to baseline

===[[STEMI]] vs [[Pericarditis]]===
{| class="wikitable"
|-
| '''[[MI]]'''
| '''[[Pericarditis]]'''
|-
| no fever
|
fever

pain varies w/motion

|-
| focal ST chgs
| diffuse ST elev
|-
| reciprocal chgs
| no reciprocal chgs
|-
| Q waves
| no Q wave
|-
| +/- pulmonary edema
| clear lungs
|-
| wall motion abn
| nl wall motion
|}

==Management==
===Initial Treatment===
*'''NSAIDS or Aspirin (ASA)''' are usually first line treatment for viral or idiopathic pericarditis.<ref>Imazio M. A randomized trial of colchicine for acute pericarditis.N Engl J Med. 2013 Oct 17;369(16):1522-8 [http://www.nejm.org/doi/pdf/10.1056/NEJMoa1208536 PDF]</ref>
**[[Aspirin]] 800mg every 8 hours for 7 to 10 days, followed by tapering during a period of 3 to 4 weeks OR
**[[Ibuprofen]] 600mg every 8 hours for 7 to 10 days, followed by tapering during a period of 3 to 4 weeks
*'''Glucocorticoid therapy''' for patients with contraindications to [[NSAIDs]]
**[[Prednisone]] 0.2 to 0.5mg/kg of body weight per day for 2 weeks with gradual tapering<ref>Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericar- ditis: high versus low doses: a nonran- domized observation. Circulation 2008; 118:667-71.</ref>

===Recurrent or Refractory===
''For recurrent or refractory cases consider colchicine and or steroids although literature suggests it can be used as first line''<ref>Imazio M.Colchicine as first-choice therapy for recurrent pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial. Arch Intern Med. 2005 Sep 26;165(17):1987-91.</ref>

*'''[[Colchicine]]'''
**Patients >70kg - 0.6mg PO BID x 3 months
**Patients<70kg - 0.6mg PO Daily x 3 months
**If patients develop serious diarrhea decrease their dosing to the next weight class or stop treatment.

====Contraindications to Colchicine<ref>Imazio M. Controversial issues in the management of pericardial diseases.Circulation. 2010 Feb 23;121(7):916-28.[http://circ.ahajournals.org/content/121/7/916.long PDF] </ref>====
*Tuberculous
*Neoplastic pericarditis
*Liver disease or aminotransferase levels ≥1.5x upper limits of normal
*Creatinine >2.5mg/dL (>221 umol/L)
*Myopathy or CK > upper limits of normal
*Inflammatory bowel disease
*Life expectancy ≤18 months
*Pregnancy or lactation

===Uremic Pericarditis===
*The definitive treatment is dialysis

===[[Pericardial effusion and tamponade|Tamponade]]===
*Tamponade requires [[Pericardiocentesis]]

==Disposition==
*Hospitalization is not necessary in most cases
*Consider admission for:
**Subacute onset over weeks
**[[Fever]] >100.4
**Large effusion (echo-free space>20mm)
**Immunosupressed
**Anticoagulant use
**Failure to respond to [[NSAID]]s (>7dy)
**Elevated cardiac enzymes

==Complications==
*[[Pericardial Effusion and Tamponade]]
*Recurence
**Usually weeks to months after initial episode
**Management is same
*Contrictive Pericarditis
**Restrictive picture with pericardial calcifications on CXR, thickened on TTE
**Treat with pericardial window

==See Also==
*[[ST segment elevation]]
*[[STEMI]]
*[[Myocardial_Infarction_Complications|Myocardial Infarction Complications]]

==References==
<references/>

[[Category:Cardiology]]

Pericarditis

2016-08-01T21:15:09Z

Peterdmorris:

==Background==
[[File:Pericarditis.jpg|thumbnail|Pericarditis compared with normal pericardium]]
===Etiology===
*Idiopathic (25-85%)
*Infection (up to 20%, including viral, bacterial, TB)
*Malignancy: heme, lung, breast
*[[Uremia]]
*Post radiation
*Connective tissue disease
*Drugs: [[procainamide]], [[hydralazine]], methyldopa, anticoagulants
*Cardiac injury (can see up to weeks later): post [[MI]] (Dressler's syndrome), [[thoracic trauma]], [[aortic dissection]]
*Troponin elevation may indicate a concurrent [[myocarditis]] which predispose to risk of [[CHF]] or [[arrhythmias|arrhythmia]]. <ref>LeWinter MM, et al. Clinical practice. Acute pericarditis. N Engl J Med. 2014 Dec 18;371(25):2410-6. PMID: 25517707.</ref>

==Clinical Features==
*Pleuritic [[chest pain]]
**Radiates to chest, back, left trapezius
**Diminishes with sitting up/leaning forward
*[[shortness of breath]]
**Especiallyif concommitant [[pleural effusion]]
*Hypotension/extremis if [[cardiac tamponade]]
*[[Fever]]
*Friction rub

==Differential Diagnosis==
*[[CHF]]
*[[PE]]
*[[Pneumothorax]]
*[[Aortic dissection]]
*[[Pneumomediastinum]]
*[[Pleuritis]]

{{ST elevation DDX}}

==Evaluation==
===Work-Up===
*ECG
*Labs
**WBC, ESR, trop
*CXR
*Bedside Ultrasound to rule out effusion

===ECG===
[[File:ECG000026-2.jpg|thumb|Acute pericarditis with clear diffuse ST elevation and some PTa depression]]
*Classically described to cause diffuse ST elevations
*Less reliable in post-MI patients and those with baseline ECG abnormalities
*May see low voltage/alternans if effusion present
*If early repol confounding interpretation check ST:T ratio
**If (ST elev)/(T height) in V6 or I >0.25 likely pericarditis
*If predominantly inferior elevation, depression in aVL is sensitive for STEMI<ref>Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.</ref
*PR depression is common with viral pericarditis, or PR elevation in AVR

====Stages of Progression====
[[File:Stadia pericarditis.png|thumb|Stages of pericarditis]]
[[File:Ptadepressie.png|thumb|PTa depression]]
*Stage I:
**Global concave up [[ST elevation]] in all leads (esp V4-6, I, II) in all leads except in aVR, V1 and III
**PTa depression (depression between the end of the P-wave and the beginning of the QRS- complex)
*Stage II:
**"pseudonormalisation," ST to baseline, big T's, PR dep
*Stage III:
**T wave flatten then inversion
*Stage IV:
**Return to baseline

===[[STEMI]] vs [[Pericarditis]]===
{| class="wikitable"
|-
| '''[[MI]]'''
| '''[[Pericarditis]]'''
|-
| no fever
|
fever

pain varies w/motion

|-
| focal ST chgs
| diffuse ST elev
|-
| reciprocal chgs
| no reciprocal chgs
|-
| Q waves
| no Q wave
|-
| +/- pulmonary edema
| clear lungs
|-
| wall motion abn
| nl wall motion
|}

==Management==
===Initial Treatment===
*'''NSAIDS or Aspirin (ASA)''' are usually first line treatment for viral or idiopathic pericarditis.<ref>Imazio M. A randomized trial of colchicine for acute pericarditis.N Engl J Med. 2013 Oct 17;369(16):1522-8 [http://www.nejm.org/doi/pdf/10.1056/NEJMoa1208536 PDF]</ref>
**[[Aspirin]] 800mg every 8 hours for 7 to 10 days, followed by tapering during a period of 3 to 4 weeks OR
**[[Ibuprofen]] 600mg every 8 hours for 7 to 10 days, followed by tapering during a period of 3 to 4 weeks
*'''Glucocorticoid therapy''' for patients with contraindications to [[NSAIDs]]
**[[Prednisone]] 0.2 to 0.5mg/kg of body weight per day for 2 weeks with gradual tapering<ref>Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericar- ditis: high versus low doses: a nonran- domized observation. Circulation 2008; 118:667-71.</ref>

===Recurrent or Refractory===
''For recurrent or refractory cases consider colchicine and or steroids although literature suggests it can be used as first line''<ref>Imazio M.Colchicine as first-choice therapy for recurrent pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial. Arch Intern Med. 2005 Sep 26;165(17):1987-91.</ref>

*'''[[Colchicine]]'''
**Patients >70kg - 0.6mg PO BID x 3 months
**Patients<70kg - 0.6mg PO Daily x 3 months
**If patients develop serious diarrhea decrease their dosing to the next weight class or stop treatment.

====Contraindications to Colchicine<ref>Imazio M. Controversial issues in the management of pericardial diseases.Circulation. 2010 Feb 23;121(7):916-28.[http://circ.ahajournals.org/content/121/7/916.long PDF] </ref>====
*Tuberculous
*Neoplastic pericarditis
*Liver disease or aminotransferase levels ≥1.5x upper limits of normal
*Creatinine >2.5mg/dL (>221 umol/L)
*Myopathy or CK > upper limits of normal
*Inflammatory bowel disease
*Life expectancy ≤18 months
*Pregnancy or lactation

===Uremic Pericarditis===
*The definitive treatment is dialysis

===[[Pericardial effusion and tamponade|Tamponade]]===
*Tamponade requires [[Pericardiocentesis]]

==Disposition==
*Hospitalization is not necessary in most cases
*Consider admission for:
**Subacute onset over weeks
**[[Fever]] >100.4
**Large effusion (echo-free space>20mm)
**Immunosupressed
**Anticoagulant use
**Failure to respond to [[NSAID]]s (>7dy)
**Elevated cardiac enzymes

==Complications==
*[[Pericardial Effusion and Tamponade]]
*Recurence
**Usually weeks to months after initial episode
**Management is same
*Contrictive Pericarditis
**Restrictive picture with pericardial calcifications on CXR, thickened on TTE
**Treat with pericardial window

==See Also==
*[[ST segment elevation]]
*[[STEMI]]
*[[Myocardial_Infarction_Complications|Myocardial Infarction Complications]]

==References==
<references/>

[[Category:Cardiology]]

Myasthenia gravis

2016-05-21T15:06:17Z

Peterdmorris: NIF/FVC parameters

==Background==
*Autoantibody degradation, dysfunction, and blockade of acetylcholine receptor at the NMJ<ref>Medications and Myasthenia Gravis (A Reference for Health Care Professionals) [http://www.myasthenia.org/LinkClick.aspx?fileticket=JuFvZPPq2vg%3d PDF]</ref>
*Thymus is abnormal in 75% of pts
**Thymectomy resolves or improves symptoms in most pts, especially those with a thymoma
*No sensory, reflex, pupillary, or cerebellar deficits

===Drugs that may unmask or worsen myasthenia gravis===
*Antibiotics (Aminoglycosides, Clinda, Fluoroquinolones, Vancomyacin)<ref> UpToDate Clinical manifestations of myasthenia gravis may 2016</ref>
*Cardiovasular drugs (Beta blockers, procainamide)
*Other (Botox, quinines, Magnesium)

===Drugs Usually well-tolerated in myasthenia gravis but occasionally associated with an exacerbation===
*Local anesthetics
*Antibiotics (Tetracycline/doxy, Macrolides, Flagyl, nitrofurantoin)
*Anticonvulsants (carbamazepine, ethosuximide, gabapentin, phenobarbital, phenytoin)
*Butyrophenones (haldol)
*Phenothiazines (chlorpromazine/prochlorpromazine)
*Calcium Channel Blockers
*Steroids
*Opthalmic drugs (betaxolol/timolol/proparacaine)
*Other (Iodinated contrast agent)

==Clinical Features==
*Muscle weakness
**Proximal extremities
**Neck extensors
**Facial/bulbar muscles (dysphagia, dysarthria, dysphonia)
*Ocular weakness
**Ptosis
**[[Diplopia]]
**CN III, IV, or VI weakness

==Differential Diagnosis==

===Drug-induced myasthenia===
*[[Antibiotics]] ([[aminoglycosides]], [[fluroquinolones]], [[clindamycin]], [[metronidazole]], [[macrolides]])<ref>Sanders DB, Guptill JT. Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. Continuum. 2014 Oct;20(5)</ref>
*Steroids
*Anticonvulsants (phenytoin, barbiturates, lithium)
*Psychotropics (haloperidol)
*Beta-blockers / calcium-channel blockers
*Local anesthetics
*Narcotics
*Anticholinergics (diphenhydramine)
*NMJ blocking agents (roc, sux)

{{Weakness DDX}}

==Diagnosis==
*Symptoms worsen with repetitive use / as the day progresses<ref>Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e (2010), Chapter 167. Chronic Neurologic Disorders</ref>
**Ice Pack Test- should improve symptoms temporarily (usually ptosis; high specificity)
***Place ice-pack on eyes for 2 mins, if ptosis decreases by ≥2mm the test is positive
*Acetylcholine receptor antibodies (AcHR-Ab). Positive in 80-90% of generalized MG and 40-55% in Ocular MG.

==Myasthenic Crisis versus Cholinergic Crisis==
*Myasthenic Crisis
**Respiratory failure is feared complication
**Much more common
**D/t med non-compliance, infection, surgery, tapering of immunosuppressants, meds
*Cholinergic Crisis
**Excessive anticholinesterase medication may cause weakness and cholinergic symptoms
**Rarely if ever seen w/ dose limitation of pyridostigmine to less than 120mg q3hr
**If on usual dose of meds assume exacerbation due to MG even w/ cholinergic side effects
*Edrophonium (Tensilon) test to distinguish the two is controversial
**Give 1-2 mg IV slow push. If any fasciculations, resp depression, or cholinergic symptoms within a few minutes, problem is likely cholinergic crisis (no more edrophonium). If no evidence of cholinergic excess, give total of 10 mg and observe improvement in case of myasthenic crisis.
**Side effects of Edrophonium: Arrhythmias, Hypotension, Bronchospasm
**Thus, need to be on a monitor, with atropine on hand
**Treatment: Atropine

==Treatment==
#Always evaluate tidal volume, Forced Vital capacity (normal is 10-12cc/kg), FEV, negative inspiratory force (NIF) (normal is -80 to -100 and greater than +20 respiratory support indicated), ability to handle secretions <ref>Emergency Medicine Practice -- Weakness: A systemic approach to acute non-traumatic neurologic and neuromuscular causes Dec 2002</ref>

#Meds
#*Pyridostigmine
#**If pt's usual dose has been missed the next dose is usually doubled
#**PO route: 60-90mg q4hr
#**IV route: 1/30th of the PO dose (2-3mg) by slow IV infusion
#*Neostigmine
#**0.5mg IV
#[[Intubation]]
#*If possible avoid depolarizing AND non-depolarizing agents
#**If pt requires paralysis use non-depolarizing agent at smaller dose
#**If must use depolarizing agents, will need higher doses
#Plasmapherisis
#IVIG

==See Also==
*[[Weakness]]

==References==
<references/>

[[Category:Neurology]]

Myasthenia gravis

2016-05-18T17:13:55Z

Peterdmorris: /* Diagnosis */

==Background==
*Autoantibody degradation, dysfunction, and blockade of acetylcholine receptor at the NMJ<ref>Medications and Myasthenia Gravis (A Reference for Health Care Professionals) [http://www.myasthenia.org/LinkClick.aspx?fileticket=JuFvZPPq2vg%3d PDF]</ref>
*Thymus is abnormal in 75% of pts
**Thymectomy resolves or improves symptoms in most pts, especially those with a thymoma
*No sensory, reflex, pupillary, or cerebellar deficits

===Drugs that may unmask or worsen myasthenia gravis===
*Antibiotics (Aminoglycosides, Clinda, Fluoroquinolones, Vancomyacin)<ref> UpToDate Clinical manifestations of myasthenia gravis may 2016</ref>
*Cardiovasular drugs (Beta blockers, procainamide)
*Other (Botox, quinines, Magnesium)

===Drugs Usually well-tolerated in myasthenia gravis but occasionally associated with an exacerbation===
*Local anesthetics
*Antibiotics (Tetracycline/doxy, Macrolides, Flagyl, nitrofurantoin)
*Anticonvulsants (carbamazepine, ethosuximide, gabapentin, phenobarbital, phenytoin)
*Butyrophenones (haldol)
*Phenothiazines (chlorpromazine/prochlorpromazine)
*Calcium Channel Blockers
*Steroids
*Opthalmic drugs (betaxolol/timolol/proparacaine)
*Other (Iodinated contrast agent)

==Clinical Features==
*Muscle weakness
**Proximal extremities
**Neck extensors
**Facial/bulbar muscles (dysphagia, dysarthria, dysphonia)
*Ocular weakness
**Ptosis
**[[Diplopia]]
**CN III, IV, or VI weakness

==Differential Diagnosis==

===Drug-induced myasthenia===
*[[Antibiotics]] ([[aminoglycosides]], [[fluroquinolones]], [[clindamycin]], [[metronidazole]], [[macrolides]])<ref>Sanders DB, Guptill JT. Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. Continuum. 2014 Oct;20(5)</ref>
*Steroids
*Anticonvulsants (phenytoin, barbiturates, lithium)
*Psychotropics (haloperidol)
*Beta-blockers / calcium-channel blockers
*Local anesthetics
*Narcotics
*Anticholinergics (diphenhydramine)
*NMJ blocking agents (roc, sux)

{{Weakness DDX}}

==Diagnosis==
*Symptoms worsen with repetitive use / as the day progresses<ref>Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e (2010), Chapter 167. Chronic Neurologic Disorders</ref>
**Ice Pack Test- should improve symptoms temporarily (usually ptosis; high specificity)
***Place ice-pack on eyes for 2 mins, if ptosis decreases by ≥2mm the test is positive
*Acetylcholine receptor antibodies (AcHR-Ab). Positive in 80-90% of generalized MG and 40-55% in Ocular MG.

==Myasthenic Crisis versus Cholinergic Crisis==
*Myasthenic Crisis
**Respiratory failure is feared complication
**Much more common
**D/t med non-compliance, infection, surgery, tapering of immunosuppressants, meds
*Cholinergic Crisis
**Excessive anticholinesterase medication may cause weakness and cholinergic symptoms
**Rarely if ever seen w/ dose limitation of pyridostigmine to less than 120mg q3hr
**If on usual dose of meds assume exacerbation due to MG even w/ cholinergic side effects
*Edrophonium (Tensilon) test to distinguish the two is controversial
**Give 1-2 mg IV slow push. If any fasciculations, resp depression, or cholinergic symptoms within a few minutes, problem is likely cholinergic crisis (no more edrophonium). If no evidence of cholinergic excess, give total of 10 mg and observe improvement in case of myasthenic crisis.
**Side effects of Edrophonium: Arrhythmias, Hypotension, Bronchospasm
**Thus, need to be on a monitor, with atropine on hand
**Treatment: Atropine

==Treatment==
#Always evaluate tidal volume, FEV, negative inspiratory force (NIF), ability to handle secretions
#Meds
#*Pyridostigmine
#**If pt's usual dose has been missed the next dose is usually doubled
#**PO route: 60-90mg q4hr
#**IV route: 1/30th of the PO dose (2-3mg) by slow IV infusion
#*Neostigmine
#**0.5mg IV
#[[Intubation]]
#*If possible avoid depolarizing AND non-depolarizing agents
#**If pt requires paralysis use non-depolarizing agent at smaller dose
#**If must use depolarizing agents, will need higher doses
#Plasmapherisis
#IVIG

==See Also==
*[[Weakness]]

==References==
<references/>

[[Category:Neurology]]

Myasthenia gravis

2016-05-18T16:48:14Z

Peterdmorris: /* Diagnosis */

==Background==
*Autoantibody degradation, dysfunction, and blockade of acetylcholine receptor at the NMJ<ref>Medications and Myasthenia Gravis (A Reference for Health Care Professionals) [http://www.myasthenia.org/LinkClick.aspx?fileticket=JuFvZPPq2vg%3d PDF]</ref>
*Thymus is abnormal in 75% of pts
**Thymectomy resolves or improves symptoms in most pts, especially those with a thymoma
*No sensory, reflex, pupillary, or cerebellar deficits

===Drugs that may unmask or worsen myasthenia gravis===
*Antibiotics (Aminoglycosides, Clinda, Fluoroquinolones, Vancomyacin)<ref> UpToDate Clinical manifestations of myasthenia gravis may 2016</ref>
*Cardiovasular drugs (Beta blockers, procainamide)
*Other (Botox, quinines, Magnesium)

===Drugs Usually well-tolerated in myasthenia gravis but occasionally associated with an exacerbation===
*Local anesthetics
*Antibiotics (Tetracycline/doxy, Macrolides, Flagyl, nitrofurantoin)
*Anticonvulsants (carbamazepine, ethosuximide, gabapentin, phenobarbital, phenytoin)
*Butyrophenones (haldol)
*Phenothiazines (chlorpromazine/prochlorpromazine)
*Calcium Channel Blockers
*Steroids
*Opthalmic drugs (betaxolol/timolol/proparacaine)
*Other (Iodinated contrast agent)

==Clinical Features==
*Muscle weakness
**Proximal extremities
**Neck extensors
**Facial/bulbar muscles (dysphagia, dysarthria, dysphonia)
*Ocular weakness
**Ptosis
**[[Diplopia]]
**CN III, IV, or VI weakness

==Differential Diagnosis==

===Drug-induced myasthenia===
*[[Antibiotics]] ([[aminoglycosides]], [[fluroquinolones]], [[clindamycin]], [[metronidazole]], [[macrolides]])<ref>Sanders DB, Guptill JT. Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. Continuum. 2014 Oct;20(5)</ref>
*Steroids
*Anticonvulsants (phenytoin, barbiturates, lithium)
*Psychotropics (haloperidol)
*Beta-blockers / calcium-channel blockers
*Local anesthetics
*Narcotics
*Anticholinergics (diphenhydramine)
*NMJ blocking agents (roc, sux)

{{Weakness DDX}}

==Diagnosis==
*Symptoms worsen with repetitive use / as the day progresses<ref>Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e (2010), Chapter 167. Chronic Neurologic Disorders</ref>
**Ice Pack Test- should improve symptoms temporarily (usually ptosis; high specificity)
***Place ice-pack on eyes for 2 mins, if ptosis decreases by ≥2mm the test is positive
*Acetylcholine receptor antibodies (AcHR-Ab). While 85% of patients with generalized myasthenia gravis have serum antibodies, the sensitivity may be 45-60% but the specificity is near 100%.

==Myasthenic Crisis versus Cholinergic Crisis==
*Myasthenic Crisis
**Respiratory failure is feared complication
**Much more common
**D/t med non-compliance, infection, surgery, tapering of immunosuppressants, meds
*Cholinergic Crisis
**Excessive anticholinesterase medication may cause weakness and cholinergic symptoms
**Rarely if ever seen w/ dose limitation of pyridostigmine to less than 120mg q3hr
**If on usual dose of meds assume exacerbation due to MG even w/ cholinergic side effects
*Edrophonium (Tensilon) test to distinguish the two is controversial
**Give 1-2 mg IV slow push. If any fasciculations, resp depression, or cholinergic symptoms within a few minutes, problem is likely cholinergic crisis (no more edrophonium). If no evidence of cholinergic excess, give total of 10 mg and observe improvement in case of myasthenic crisis.
**Side effects of Edrophonium: Arrhythmias, Hypotension, Bronchospasm
**Thus, need to be on a monitor, with atropine on hand
**Treatment: Atropine

==Treatment==
#Always evaluate tidal volume, FEV, negative inspiratory force (NIF), ability to handle secretions
#Meds
#*Pyridostigmine
#**If pt's usual dose has been missed the next dose is usually doubled
#**PO route: 60-90mg q4hr
#**IV route: 1/30th of the PO dose (2-3mg) by slow IV infusion
#*Neostigmine
#**0.5mg IV
#[[Intubation]]
#*If possible avoid depolarizing AND non-depolarizing agents
#**If pt requires paralysis use non-depolarizing agent at smaller dose
#**If must use depolarizing agents, will need higher doses
#Plasmapherisis
#IVIG

==See Also==
*[[Weakness]]

==References==
<references/>

[[Category:Neurology]]

User:Peterdmorris

2016-05-13T03:37:43Z

Peterdmorris:

#Name: Peter D Morris
#Medical school: St. Louis University
#Emergency Medicine Residency: MetroHealth/Case Western Reserve University/Cleveland Clinic Foundation
#Current employment: Clinical Instructor of Emergency Medicine, UT Southwestern Medical Center, Dallas TX

Myasthenia gravis

2016-05-13T03:36:42Z

Peterdmorris:

# Numbered list item
==Background==
*Autoantibody degradation, dysfunction, and blockade of acetylcholine receptor at the NMJ<ref>Medications and Myasthenia Gravis (A Reference for Health Care Professionals) [http://www.myasthenia.org/LinkClick.aspx?fileticket=JuFvZPPq2vg%3d PDF]</ref>
*Thymus is abnormal in 75% of pts
**Thymectomy resolves or improves symptoms in most pts, especially those with a thymoma
*No sensory, reflex, pupillary, or cerebellar deficits

==Clinical Features==
*Muscle weakness
**Proximal extremities
**Neck extensors
**Facial/bulbar muscles (dysphagia, dysarthria, dysphonia)
*Ocular weakness
**Ptosis
**[[Diplopia]]
**CN III, IV, or VI weakness

==Differential Diagnosis==

===Drug-induced myasthenia===
*[[Antibiotics]] ([[aminoglycosides]], [[fluroquinolones]], [[clindamycin]], [[metronidazole]], [[macrolides]])<ref>Sanders DB, Guptill JT. Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. Continuum. 2014 Oct;20(5)</ref>
*Steroids
*Anticonvulsants (phenytoin, barbiturates, lithium)
*Psychotropics (haloperidol)
*Beta-blockers / calcium-channel blockers
*Local anesthetics
*Narcotics
*Anticholinergics (diphenhydramine)
*NMJ blocking agents (roc, sux)

{{Weakness DDX}}

==Diagnosis==
*Symptoms worsen with repetitive use / as the day progresses<ref>Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e (2010), Chapter 167. Chronic Neurologic Disorders</ref>
**Ice Pack Test- should improve symptoms temporarily (usually ptosis; high specificity)
***Place ice-pack on eyes for 2 mins, if ptosis decreases by ≥2mm the test is positive

==Drugs that may unmask or worsen myasthenia gravis==
*Antibiotics (Aminoglycosides, Clinda, Fluoroquinolones, Vancomyacin)<ref> UpToDate Clinical manifestations of myasthenia gravis may 2016</ref>
*Cardiovasular drugs (Beta blockers, procainamide)
*Other (Botox, quinines, Magnesium)
===Drugs Usually well-tolerated in myasthenia gravis but occasionally associated with an exacerbation===
*Local anesthetics
*Antibiotics (Tetracycline/doxy, Macrolides, Flagyl, nitrofurantoin)
*Anticonvulsants (carbamazepine, ethosuximide, gabapentin, phenobarbital, phenytoin)
*Butyrophenones (haldol)
*Phenothiazines (chlorpromazine/prochlorpromazine)
*Calcium Channel Blockers
*Steroids
*Opthalmic drugs (betaxolol/timolol/proparacaine)
*Other (Iodinated contrast agent)

==Myasthenic Crisis versus Cholinergic Crisis==
*Myasthenic Crisis
**Respiratory failure is feared complication
**Much more common
**D/t med non-compliance, infection, surgery, tapering of immunosuppressants, meds
*Cholinergic Crisis
**Excessive anticholinesterase medication may cause weakness and cholinergic symptoms
**Rarely if ever seen w/ dose limitation of pyridostigmine to less than 120mg q3hr
**If on usual dose of meds assume exacerbation due to MG even w/ cholinergic side effects
*Edrophonium (Tensilon) test to distinguish the two is controversial
**Give 1-2 mg IV slow push. If any fasciculations, resp depression, or cholinergic symptoms within a few minutes, problem is likely cholinergic crisis (no more edrophonium). If no evidence of cholinergic excess, give total of 10 mg and observe improvement in case of myasthenic crisis.
**Side effects of Edrophonium: Arrhythmias, Hypotension, Bronchospasm
**Thus, need to be on a monitor, with atropine on hand
**Treatment: Atropine

==Treatment==
#Always evaluate tidal volume, FEV, negative inspiratory force (NIF), ability to handle secretions
#Meds
#*Pyridostigmine
#**If pt's usual dose has been missed the next dose is usually doubled
#**PO route: 60-90mg q4hr
#**IV route: 1/30th of the PO dose (2-3mg) by slow IV infusion
#*Neostigmine
#**0.5mg IV
#[[Intubation]]
#*If possible avoid depolarizing AND non-depolarizing agents
#**If pt requires paralysis use non-depolarizing agent at smaller dose
#**If must use depolarizing agents, will need higher doses
#Plasmapherisis
#IVIG

==See Also==
*[[Weakness]]

==References==
<references/>

[[Category:Neurology]]

Needed pages

2014-10-17T19:56:35Z

Peterdmorris: /* Suggestions (Add/Delete as made) */

==Suggestions (Add/Delete as made)==
*[[AVM]]
*[[TIPS]]
*[[Scleroderma]]
*[[Polyarteritis Nodosa]]
*[[Wegener's Granulomatosis]]
*[[Peritonitis]]
*[[Leprosy]]
*[[Giardia]]
*[[Chemical Weapons]]: [[Nerve Agents]] ([[Vx]], [[Sarin]], [[Sabin]]); [[Vesicants]] ([[Sulfur Mustard]], [[Lewisite]]); [[Urticants]] ([[phosgene]])
*[[Psittacosis]]
*[[Smallpox]]
*[[Lassa]]
* [[Marburg]]
*[[Q-fever]]
*[[Rift Valley Fever]]
*[[Fasciola hepatica]]
*[[Strongyloides stercoralis]]
*[[Ovarian cyst‏‎]]
*[[Mesenteric adenitis‎]]
*[[Lacosamide]]
*[[Lamotrigine]]
*[[Levetiracetam]]
*[[Phenytoin]]
*[[Wound care dressing basics]]
*[[Fosphenytoin]]
*[[Valproate]]
*[[Erythema Multiforme]]

==See Also==
*[[Special:WantedPages|Auto-generated Wanted Pages]]

[[Category:WikEM]]

Needed pages

2014-10-14T18:31:55Z

Peterdmorris: erythema multiforme

==Suggestions (Add/Delete as made)==
*[[AVM]]
*[[TIPS]]
*[[Scleroderma]]
*[[Polyarteritis Nodosa]]
*[[Wegener's Granulomatosis]]
*[[Peritonitis]]
*[[Leprosy]]
*[[Giardia]]
*[[Chemical Weapons]]: [[Nerve Agents]] ([[Vx]], [[Sarin]], [[Sabin]]); [[Vesicants]] ([[Sulfur Mustard]], [[Lewisite]]); [[Urticants]] ([[phosgene]])
*[[Psittacosis]]
*[[Smallpox]]
*[[Lassa]]
* [[Marburg]]
*[[Q-fever]]
*[[Rift Valley Fever]]
*[[Fasciola hepatica]]
*[[Strongyloides stercoralis]]
*[[Ovarian cyst‏‎]]
*[[Mesenteric adenitis‎]]
*[[Lacosamide]]
*[[Lamotrigine]]
*[[Levetiracetam]]
*[[Phenytoin]]
*[[Fosphenytoin]]
*[[Valproate]]
*[[Erythema Multiforme]]

==See Also==
*[[Special:WantedPages|Auto-generated Wanted Pages]]

[[Category:WikEM]]

Subarachnoid hemorrhage

2014-10-14T16:53:55Z

Peterdmorris: Ottawa SAH rules

== Background ==

=== Pearls ===

#Obtain GCS before intubation
#If intubate prevent HTN (rebleeding)
##Pretreatment
###Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
###Fentanyl 200mcg (sympatholytic)
##Sedation
###If pt has high BP - use propofol
###If pt has adequate BP - use etomidate
##Treat pain
###Prevents incr catacholamines / incr BP

=== Epidemiology ===

*Of All pts in ED who p/w HA:
**1% will have SAH
**10% will have SAH if c/o worst HA of life
**25% will have SAH if c/o worst HA of life + any neuro deficit

=== Risk Factors ===

#Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
#Hypertension
#Atherosclerosis
#Cigarette smoking
#Alcohol
#Age >50
#Cocaine use
#Estrogen deficiency

=== Etiology of Spontaneous SAH ===

#Ruptured aneurysm (85%)
#Nonaneurysmal (15%)
##Perimesencephalic hemorrhage (10%) - lower risk of complications
##Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis

== Clinical Features ==

#Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
##Sudden onset is more important finding than worst HA
#May be a/w syncope, seizure, nausea/vomiting, meningismus
##Meningismus may not develop until hrs after bleed (blood breakdown -> aseptic meningitis)
#Retinal hemorrhage
##May be the only clue in comatose patients
#Sentinel bleed/HA 6-20d before SAH (30-50% of pts)

== DDX ==

#Other intracranial hemorrhage
#Drug toxicity
#Ischemic stroke
#Meningitis
#Encephalitis
#Intracranial tumor
#Intracranial hypotension
#Metabolic derangements
#Venous thrombosis
#Primary headache syndromes (benign thunderclap headache, migraine, cluster headache)

== Diagnosis ==

#Ottawa SAH Rules
##Never has been externally and prospectively validated, authors caution implementation into routine use
##100% sensitive to rule out SAH (97.1%-100%)
##Can exclude SAH if all of the following are true
*Age < 40
*No Neck pain or stiffness
*No Witnessed LOC
*No onset during exertion
*No Thunderclap symptomatology (max intensity at honest)
*No limited neck flexion on physical exam

'''If concerned for SAH and CT normal strongly consider LP'''

#Non-Contrast Head CT
##Sensitivity
###Within 12hr of onset of symptoms: 98% Sn
###Within 24hr of onset of symptoms: 93% Sn
###Within 5d of onset of symptoms: 50% Sn
###Not as sensitive/specific for minor bleeds
##Findings
###SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
###SAH due to trauma - look at convexities of frontal and temporal cortices
#Lumbar Puncture
##Findings:
###Elevated RBC count that doesn't decrease from tube one to four
####Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
###Opening pressure >20 (60% of pts)
####Can help differentiate from a traumatic tap (opening pressure expected to be normal)
####Elevated opening pressure also seen in cerebral venous thrombosis, IIH
###Xanthrochromia
####May help differentiate between SAH and a traumatic tap
####Takes at least 2hr after bleed to develop (beware of false negative if measure early)
####Sn (93%) / Sp (95%) highest after 12hr
##If unable to obtain CSF consider CTA
###CTA also highly sensitive for predicting delayed cerebral ischemia

== Treatment ==
Physiologic derangements, such as hypoxemia, metabolic acidosis, hyperglycemia, BP instability, and fever, can worsen brain injury and has been independently associated with increased M&M, but no studies showing benefit of corrections.

{{AHA SAH BP Guidelines}}

#Avoid hypotension
##Maintain MAP >80
##Give IVF
##Give pressors if IVF ineffective
#Discontinue/reverse all anticoagulation
##Coumadin - (Prothrombin complex conc or FFP) + vit K
##Aspirin - DDAVP
##Plavix - Platelets
#Nimodipine
##Prevents vasospasm (a/w improved neuro outcomes and decreased cerebral infarction)
##Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome
##Keep an eye on BP for fluctuations
#Magneisum
##Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 2-2.5 mmol/L
#Seizure prophylaxis
##Controversial; 3 day course may be preferable
##Phenytoin, levetiracetam, carbamazepine and phenobarb. Phenytoin can be a/w worse neurologic & cognitive outcome
#Glucocorticoid therapy
##Controversial; evidence suggests is neither beneficial nor harmful
#Glycemic control
##Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
#Keep head of bed elevated
#Aneurysm Tx
##Surgical clipping and endovascular coiling are definitive tx
##Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid

== Complications ==

#Rebleeding
##Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
##Usually diagnosed by CT after acute deterioration in neuro status
##Only aneurysm treatment is effective in preventing rebleeding
#Vasospasm
##Leading cause of death and disability after rupture
##Typically begins no earlier than day three after hemorrhage
##Characterized by decline in neuro status
##Aggressive treatment can only be started after aneurysm has been treated
###Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
####Studies have not provided strong evidence of benefit Triple-H therapy
#Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
##Ischemia
###Elevated troponin (20-40% of cases)
###ST segment depression
##Rhythm disturbances
###Torsades, A-fib/flutter
##QT prolongation
##Deep, symmetric TWI
##Prominent U waves
#Hydrocephalus
##Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
#Hyponatremia
##Usually due to SIADH
###Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
##Rarely due to cerebral salt-wasting
###Volume depleted, so treat with isotonic saline

== Prognosis ==

=== Hunt and Hess ===
Subjective terminology, but good interobserver variability
*Grade 0: Unruptured aneurysm
*Grade 1: Asymptomatic or mild HA and slight nuchal rigidity
:Grade 1a: No acute meningeal/brain reaction, with fixed neurological def
*Grade 2: Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy
*Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
*Grade 4: Stupor or moderate to severe hemiparesis
*Grade 5: Coma or decerebrate rigidity

 

:Grade 1 or 2 have curable disease

:Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)

=== World Federation of Neurosurgical Societies (WFNS) ===
Objective terminology, and fair interobserver variability
*Grade 1: GCS of 15, no motor deficits
*Grade 2: GCS of 13 or 14, no motor deficits
*Grade 3: GCS of 13 or 14, with motor deficits
*Grade 4: GCS of 7–12, with or without motor deficits
*Grade 5: GCS of 3–6, with or without motor deficits

Other scales are also available, including the Ogilvy and Carter scale (comprehensive, yet complex), and the Fisher scale or Claassen grading system (vasospasm index risk).

Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.

== See Also ==
*[[Intracranial Hemorrhage (Main)]]
*[[Head Trauma]]

== Source ==
*EB Emergency Medicine, July 2009
*EMCrit Podcast 8
<references/>
*www.epmonthly.com/features/current-features/lp-for-subarachnoid-hemorrhage-the-700-club
*Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018

[[Category:Neuro]]

Subarachnoid hemorrhage

2014-10-14T16:51:57Z

Peterdmorris: /* Diagnosis */

== Background ==

=== Pearls ===

#Obtain GCS before intubation
#If intubate prevent HTN (rebleeding)
##Pretreatment
###Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
###Fentanyl 200mcg (sympatholytic)
##Sedation
###If pt has high BP - use propofol
###If pt has adequate BP - use etomidate
##Treat pain
###Prevents incr catacholamines / incr BP

=== Epidemiology ===

*Of All pts in ED who p/w HA:
**1% will have SAH
**10% will have SAH if c/o worst HA of life
**25% will have SAH if c/o worst HA of life + any neuro deficit

=== Risk Factors ===

#Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
#Hypertension
#Atherosclerosis
#Cigarette smoking
#Alcohol
#Age >50
#Cocaine use
#Estrogen deficiency

=== Etiology of Spontaneous SAH ===

#Ruptured aneurysm (85%)
#Nonaneurysmal (15%)
##Perimesencephalic hemorrhage (10%) - lower risk of complications
##Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis

== Clinical Features ==

#Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
##Sudden onset is more important finding than worst HA
#May be a/w syncope, seizure, nausea/vomiting, meningismus
##Meningismus may not develop until hrs after bleed (blood breakdown -> aseptic meningitis)
#Retinal hemorrhage
##May be the only clue in comatose patients
#Sentinel bleed/HA 6-20d before SAH (30-50% of pts)

== DDX ==

#Other intracranial hemorrhage
#Drug toxicity
#Ischemic stroke
#Meningitis
#Encephalitis
#Intracranial tumor
#Intracranial hypotension
#Metabolic derangements
#Venous thrombosis
#Primary headache syndromes (benign thunderclap headache, migraine, cluster headache)

== Diagnosis ==

#Ottawa SAH Rules
##Never has been externally and prospectively validated, authors caution implementation into routine use
##100% sensitive to rule out SAH (97.1%-100%)
###Can exclude SAH if all of the following are true
####Age < 40
####No Neck pain or stiffness
####No Witnessed LOC
####No onset during exertion
####No Thunderclap symptomatology (max intensity at honest)
####No limited neck flexion on physical exam

'''If concerned for SAH and CT normal strongly consider LP'''

#Non-Contrast Head CT
##Sensitivity
###Within 12hr of onset of symptoms: 98% Sn
###Within 24hr of onset of symptoms: 93% Sn
###Within 5d of onset of symptoms: 50% Sn
###Not as sensitive/specific for minor bleeds
##Findings
###SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
###SAH due to trauma - look at convexities of frontal and temporal cortices
#Lumbar Puncture
##Findings:
###Elevated RBC count that doesn't decrease from tube one to four
####Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
###Opening pressure >20 (60% of pts)
####Can help differentiate from a traumatic tap (opening pressure expected to be normal)
####Elevated opening pressure also seen in cerebral venous thrombosis, IIH
###Xanthrochromia
####May help differentiate between SAH and a traumatic tap
####Takes at least 2hr after bleed to develop (beware of false negative if measure early)
####Sn (93%) / Sp (95%) highest after 12hr
##If unable to obtain CSF consider CTA
###CTA also highly sensitive for predicting delayed cerebral ischemia

== Treatment ==
Physiologic derangements, such as hypoxemia, metabolic acidosis, hyperglycemia, BP instability, and fever, can worsen brain injury and has been independently associated with increased M&M, but no studies showing benefit of corrections.

{{AHA SAH BP Guidelines}}

#Avoid hypotension
##Maintain MAP >80
##Give IVF
##Give pressors if IVF ineffective
#Discontinue/reverse all anticoagulation
##Coumadin - (Prothrombin complex conc or FFP) + vit K
##Aspirin - DDAVP
##Plavix - Platelets
#Nimodipine
##Prevents vasospasm (a/w improved neuro outcomes and decreased cerebral infarction)
##Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome
##Keep an eye on BP for fluctuations
#Magneisum
##Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 2-2.5 mmol/L
#Seizure prophylaxis
##Controversial; 3 day course may be preferable
##Phenytoin, levetiracetam, carbamazepine and phenobarb. Phenytoin can be a/w worse neurologic & cognitive outcome
#Glucocorticoid therapy
##Controversial; evidence suggests is neither beneficial nor harmful
#Glycemic control
##Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
#Keep head of bed elevated
#Aneurysm Tx
##Surgical clipping and endovascular coiling are definitive tx
##Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid

== Complications ==

#Rebleeding
##Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
##Usually diagnosed by CT after acute deterioration in neuro status
##Only aneurysm treatment is effective in preventing rebleeding
#Vasospasm
##Leading cause of death and disability after rupture
##Typically begins no earlier than day three after hemorrhage
##Characterized by decline in neuro status
##Aggressive treatment can only be started after aneurysm has been treated
###Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
####Studies have not provided strong evidence of benefit Triple-H therapy
#Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
##Ischemia
###Elevated troponin (20-40% of cases)
###ST segment depression
##Rhythm disturbances
###Torsades, A-fib/flutter
##QT prolongation
##Deep, symmetric TWI
##Prominent U waves
#Hydrocephalus
##Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
#Hyponatremia
##Usually due to SIADH
###Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
##Rarely due to cerebral salt-wasting
###Volume depleted, so treat with isotonic saline

== Prognosis ==

=== Hunt and Hess ===
Subjective terminology, but good interobserver variability
*Grade 0: Unruptured aneurysm
*Grade 1: Asymptomatic or mild HA and slight nuchal rigidity
:Grade 1a: No acute meningeal/brain reaction, with fixed neurological def
*Grade 2: Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy
*Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
*Grade 4: Stupor or moderate to severe hemiparesis
*Grade 5: Coma or decerebrate rigidity

 

:Grade 1 or 2 have curable disease

:Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)

=== World Federation of Neurosurgical Societies (WFNS) ===
Objective terminology, and fair interobserver variability
*Grade 1: GCS of 15, no motor deficits
*Grade 2: GCS of 13 or 14, no motor deficits
*Grade 3: GCS of 13 or 14, with motor deficits
*Grade 4: GCS of 7–12, with or without motor deficits
*Grade 5: GCS of 3–6, with or without motor deficits

Other scales are also available, including the Ogilvy and Carter scale (comprehensive, yet complex), and the Fisher scale or Claassen grading system (vasospasm index risk).

Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.

== See Also ==
*[[Intracranial Hemorrhage (Main)]]
*[[Head Trauma]]

== Source ==
*EB Emergency Medicine, July 2009
*EMCrit Podcast 8
<references/>
*www.epmonthly.com/features/current-features/lp-for-subarachnoid-hemorrhage-the-700-club

[[Category:Neuro]]

Rhythm diagnosis in regular wide complex tachycardia

2014-07-10T16:48:29Z

Peterdmorris: monomoprhic VT clues

==Background==
*Ventricular Tachycardia vs. Supraventricular Tachycardia
**<big>'''Assume V-tach until proven otherwise'''</big>

== V-Tach vs. [[SVT]] ==

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| '''Factor''' 
| '''V Tach'''
| '''SVT w/ Aberrancy'''
|-
| Age
| >50
| <35
|-
| History
| MI, CHF, CABG, MVR
| MVR, WPW
|-
| Cannon A Waves
| Present
| Absent
|-
| Arterial Pulse
| Variation
| No variation
|-
| First heart sound
| Variable
| Not variable
|-
| Fusion Beats
| Present
| Absent
|-
| AV dissociation
| Present
| Absent
|-
| QRS
| >0.14sec
| <0.14sec
|-
| Axis
| Extreme LAD (< -30)
| Normal or slightly abnl
|-
| Vagal Maneuvers
| No response
| Slows or terminates
|-
|
QRS morphology

(RBBB-like pattern)

|
V1 - R or qR

V6 - rS

|
V1 - rsR'

V6 - R(slurredS)

|-
|
QRS morphology

(LBBB-like pattern)

|
V1 or V2 - Broad R wave (>40msec)

V6 - Any Q or QS

|
V1 - rS or QS

V6 - qRs

|}

== Algorithms ==

*Only for regular rhythms
*Only for treatment decision if pt is stable
*Assume V-tach until proven otherwise

=== Brugada Algorithm ===

#Absence of an RS complex in all precordial leads?
##If yes then VT
##If no then continue
#RS interval >100ms in any precordial lead? (onset of R wave to deepest part of S wave)
##If yes then VT
##If no then continue
#AV dissociation?
##If yes then VT
##If no then continue
#Morphology criteria for v-tach present in both V1-2 and V6?
##If yes then VT
##If no then possibly SVT w/ aberrant conduction

=== aVR Algorithm ===

*In lead aVR:

#Presence of an initial R wave?
##If yes then VT
##If no then continue
#Presence of an initial r or q wave >40ms
##If yes then VT
##If no then continue
#Presence of a notch on descending limb of a negative onset, predominantly negative QRS?
##If yes then VT
##If no then continue
#Ventricular activation-velocity ratio (Vi/Vt) ≤1?
##If yes then VT
##If no then SVT

=== Niemann Algorithm<ref>James Niemann MD FACEP is EM Faculty at Harbor-UCLA Medical Center and prominent resuscitation researcher</ref> ===

*Combination of the most specific aspects of the above two algorithms
Acronym: <big>CARMA</big> -> '''Concordance -> aVR ->Regular -> Morphology ->AV dissociation'''

#Presence of an initial '''R wave in aVR'''? <ref>Vereckei A et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachy- cardia. Heart Rhythm 2008; 5:89-98</ref><ref>Szelenyi Z, et al. Acad Emerg Med 2013;20:1121- 1130</ref>
##If yes then VT
##If no then continue
#Is there '''concordance''' (monophasic with same polarity) in all of the precordial leads? <ref>Brugada P et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649-1659</ref>
##If yes then VT
##If no then continue
#Is there evidence of '''AV dissociation'''?
##If yes then VT
##If no then continue
#Is the QRS '''morphology''' in V1 and V6 consistent with either '''LBBB''' or '''RBBB'''? <ref>Brugada, Circulation; Griffith MJ et al. Lancet 1994;343:386-388</ref><ref>Wellens HJJ et al. Am J Med 1978; 64:27-33</ref>
##If no then VT
##If yes then SVT with aberrancy

=== R-Wave Peak Time Method===
#In lead II, if the TIME in (ms) it takes the R wave to go from the isoelectric line to its peak voltage is greater than 50ms, it is VT
#Positive Likelihood ratio of 34.8

=== Lesser Known Criteria===

Monomorphic Ventricular tachycrdia 

1. Josephson's sign --- notching or slurring near the nadir of the S-wave 
2. Rsr' sign --- A taller left R wave in v1-v2 is very specific for VT, as opposed in a RBBB where the second/right R-wave (R') is taller 
3. "Northwest" axis deviation -- Negative QRS complex in I, AVF and Positive QRS in AVR

== See Also ==
*[[Tachycardia (Wide)]]
*[[SVT]]
*[[ACLS (Main)]]
*[[ACLS: Tachycardia]]
*[[PALS (Main)]]
*[[PALS: Tachycardia]]

== Source ==
*James Niemann MD. Harbor-UCLA Grand Rounds 2013
*Pava et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm. 2010 Jul;7(7):922-6

<references/>
[[Category:Cards]]

Rhythm diagnosis in regular wide complex tachycardia

2014-07-10T16:46:58Z

Peterdmorris: Monomorphic VT clues

==Background==
*Ventricular Tachycardia vs. Supraventricular Tachycardia
**<big>'''Assume V-tach until proven otherwise'''</big>

== V-Tach vs. [[SVT]] ==

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| '''Factor''' 
| '''V Tach'''
| '''SVT w/ Aberrancy'''
|-
| Age
| >50
| <35
|-
| History
| MI, CHF, CABG, MVR
| MVR, WPW
|-
| Cannon A Waves
| Present
| Absent
|-
| Arterial Pulse
| Variation
| No variation
|-
| First heart sound
| Variable
| Not variable
|-
| Fusion Beats
| Present
| Absent
|-
| AV dissociation
| Present
| Absent
|-
| QRS
| >0.14sec
| <0.14sec
|-
| Axis
| Extreme LAD (< -30)
| Normal or slightly abnl
|-
| Vagal Maneuvers
| No response
| Slows or terminates
|-
|
QRS morphology

(RBBB-like pattern)

|
V1 - R or qR

V6 - rS

|
V1 - rsR'

V6 - R(slurredS)

|-
|
QRS morphology

(LBBB-like pattern)

|
V1 or V2 - Broad R wave (>40msec)

V6 - Any Q or QS

|
V1 - rS or QS

V6 - qRs

|}

== Algorithms ==

*Only for regular rhythms
*Only for treatment decision if pt is stable
*Assume V-tach until proven otherwise

=== Brugada Algorithm ===

#Absence of an RS complex in all precordial leads?
##If yes then VT
##If no then continue
#RS interval >100ms in any precordial lead? (onset of R wave to deepest part of S wave)
##If yes then VT
##If no then continue
#AV dissociation?
##If yes then VT
##If no then continue
#Morphology criteria for v-tach present in both V1-2 and V6?
##If yes then VT
##If no then possibly SVT w/ aberrant conduction

=== aVR Algorithm ===

*In lead aVR:

#Presence of an initial R wave?
##If yes then VT
##If no then continue
#Presence of an initial r or q wave >40ms
##If yes then VT
##If no then continue
#Presence of a notch on descending limb of a negative onset, predominantly negative QRS?
##If yes then VT
##If no then continue
#Ventricular activation-velocity ratio (Vi/Vt) ≤1?
##If yes then VT
##If no then SVT

=== Niemann Algorithm<ref>James Niemann MD FACEP is EM Faculty at Harbor-UCLA Medical Center and prominent resuscitation researcher</ref> ===

*Combination of the most specific aspects of the above two algorithms
Acronym: <big>CARMA</big> -> '''Concordance -> aVR ->Regular -> Morphology ->AV dissociation'''

#Presence of an initial '''R wave in aVR'''? <ref>Vereckei A et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachy- cardia. Heart Rhythm 2008; 5:89-98</ref><ref>Szelenyi Z, et al. Acad Emerg Med 2013;20:1121- 1130</ref>
##If yes then VT
##If no then continue
#Is there '''concordance''' (monophasic with same polarity) in all of the precordial leads? <ref>Brugada P et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649-1659</ref>
##If yes then VT
##If no then continue
#Is there evidence of '''AV dissociation'''?
##If yes then VT
##If no then continue
#Is the QRS '''morphology''' in V1 and V6 consistent with either '''LBBB''' or '''RBBB'''? <ref>Brugada, Circulation; Griffith MJ et al. Lancet 1994;343:386-388</ref><ref>Wellens HJJ et al. Am J Med 1978; 64:27-33</ref>
##If no then VT
##If yes then SVT with aberrancy

=== R-Wave Peak Time Method===
#In lead II, if the TIME in (ms) it takes the R wave to go from the isoelectric line to its peak voltage is greater than 50ms, it is VT
#Positive Likelihood ratio of 34.8

=== Lesser Known Criteria===

Monomorphic Ventricular tachycrdia

1. Josephson's sign --- notching or slurring near the nadir of the S-wave
2. Rsr' sign --- A taller left R wave in v1-v2 is very specific for VT, as opposed in a RBBB where the second/right R-wave (R') is taller
3. "Northwest" axis deviation -- Negative QRS complex in I, AVF and Positive QRS in AVR

== See Also ==
*[[Tachycardia (Wide)]]
*[[SVT]]
*[[ACLS (Main)]]
*[[ACLS: Tachycardia]]
*[[PALS (Main)]]
*[[PALS: Tachycardia]]

== Source ==
*James Niemann MD. Harbor-UCLA Grand Rounds 2013
*Pava et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm. 2010 Jul;7(7):922-6

<references/>
[[Category:Cards]]

Rhythm diagnosis in regular wide complex tachycardia

2014-07-10T16:43:09Z

Peterdmorris: /* R-Wave Peak Time Method */

==Background==
*Ventricular Tachycardia vs. Supraventricular Tachycardia
**<big>'''Assume V-tach until proven otherwise'''</big>

== V-Tach vs. [[SVT]] ==

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| '''Factor''' 
| '''V Tach'''
| '''SVT w/ Aberrancy'''
|-
| Age
| >50
| <35
|-
| History
| MI, CHF, CABG, MVR
| MVR, WPW
|-
| Cannon A Waves
| Present
| Absent
|-
| Arterial Pulse
| Variation
| No variation
|-
| First heart sound
| Variable
| Not variable
|-
| Fusion Beats
| Present
| Absent
|-
| AV dissociation
| Present
| Absent
|-
| QRS
| >0.14sec
| <0.14sec
|-
| Axis
| Extreme LAD (< -30)
| Normal or slightly abnl
|-
| Vagal Maneuvers
| No response
| Slows or terminates
|-
|
QRS morphology

(RBBB-like pattern)

|
V1 - R or qR

V6 - rS

|
V1 - rsR'

V6 - R(slurredS)

|-
|
QRS morphology

(LBBB-like pattern)

|
V1 or V2 - Broad R wave (>40msec)

V6 - Any Q or QS

|
V1 - rS or QS

V6 - qRs

|}

== Algorithms ==

*Only for regular rhythms
*Only for treatment decision if pt is stable
*Assume V-tach until proven otherwise

=== Brugada Algorithm ===

#Absence of an RS complex in all precordial leads?
##If yes then VT
##If no then continue
#RS interval >100ms in any precordial lead? (onset of R wave to deepest part of S wave)
##If yes then VT
##If no then continue
#AV dissociation?
##If yes then VT
##If no then continue
#Morphology criteria for v-tach present in both V1-2 and V6?
##If yes then VT
##If no then possibly SVT w/ aberrant conduction

=== aVR Algorithm ===

*In lead aVR:

#Presence of an initial R wave?
##If yes then VT
##If no then continue
#Presence of an initial r or q wave >40ms
##If yes then VT
##If no then continue
#Presence of a notch on descending limb of a negative onset, predominantly negative QRS?
##If yes then VT
##If no then continue
#Ventricular activation-velocity ratio (Vi/Vt) ≤1?
##If yes then VT
##If no then SVT

=== Niemann Algorithm<ref>James Niemann MD FACEP is EM Faculty at Harbor-UCLA Medical Center and prominent resuscitation researcher</ref> ===

*Combination of the most specific aspects of the above two algorithms
Acronym: <big>CARMA</big> -> '''Concordance -> aVR ->Regular -> Morphology ->AV dissociation'''

#Presence of an initial '''R wave in aVR'''? <ref>Vereckei A et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachy- cardia. Heart Rhythm 2008; 5:89-98</ref><ref>Szelenyi Z, et al. Acad Emerg Med 2013;20:1121- 1130</ref>
##If yes then VT
##If no then continue
#Is there '''concordance''' (monophasic with same polarity) in all of the precordial leads? <ref>Brugada P et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649-1659</ref>
##If yes then VT
##If no then continue
#Is there evidence of '''AV dissociation'''?
##If yes then VT
##If no then continue
#Is the QRS '''morphology''' in V1 and V6 consistent with either '''LBBB''' or '''RBBB'''? <ref>Brugada, Circulation; Griffith MJ et al. Lancet 1994;343:386-388</ref><ref>Wellens HJJ et al. Am J Med 1978; 64:27-33</ref>
##If no then VT
##If yes then SVT with aberrancy

=== R-Wave Peak Time Method===
#In lead II, if the TIME in (ms) it takes the R wave to go from the isoelectric line to its peak voltage is greater than 50ms, it is VT
#Positive Likelihood ratio of 34.8

=== Lesser Known Criteria===

Josephson's sign --- notching or slurring near the nadir of the S-wave

Rsr' sign --- A taller left R wave in v1-v2 is very specific for VT, as opposed in a RBBB where the second/right R-wave (R') is taller

== See Also ==
*[[Tachycardia (Wide)]]
*[[SVT]]
*[[ACLS (Main)]]
*[[ACLS: Tachycardia]]
*[[PALS (Main)]]
*[[PALS: Tachycardia]]

== Source ==
*James Niemann MD. Harbor-UCLA Grand Rounds 2013
*Pava et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm. 2010 Jul;7(7):922-6

<references/>
[[Category:Cards]]

Cyanide toxicity

2014-05-25T20:39:00Z

Peterdmorris: lacatate is sensitive

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate (normal lactate highly suggests another diagnosis)
#VBG and ABG (narrowing of the venous-arterial PO2 gradient, causes venous hyperoxemia/increased redness -- as does CO poisoning)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)<ref>Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. Jun 2007;25(5):551-8.</ref><ref>Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. 2010;55(4):345-51. </ref>===
1st line therapy
====Mechanism of action====
Directly binds CN forming cyanocobalamin which is readily excreted in the urine
====Administration====
#Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
#Also give 25% Na thiosulfate 1.65ml/kg IV (12.5g max dose) over 10min; may repeat at 1/2 original dose if needed
====Adverse Effects====
#May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
#'''Interferes with colorimetric tests''' -- Pulse ox, Hemoglobin, Carboyxhemoglobin, methemeglobin, oxyhemoglobin, Serum Cr, AST/ALT, bilirubin, magnesium for 2-3 days<ref>Lee J, Mukai D, Kreuter K, et al. Potential interference by hydroxocobalamin on co-oximetry hemoglobin measurements during cyanide and smoke inhalation treatments. Ann Emerg Med. 2007;49(6):802-805.</ref>
;OBTAIN Co-ox and labs prior to Hydroxocobalamin administration

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable<ref>Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52.</ref>
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning since nitrate administration will severely decrease oxygen carrying capacity

====Mechanism of action====
#Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)

====Warnings====
#Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
#Induction of metHb further exacerbates O2 delivery
#Avoid nitrites in presence of severe hypotension if diagnosis is unclear

====Administration====
;Amyl nitrite
#Inhaled by pt (only use if unavailable to obtain IV)
#Hold under pt's nose for 30s of each minute, for 3 minutes
;Sodium nitrite
#10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
#Lack of measurable MetHb levels after administration confirms CN presence
#Monitor MetHb and keep level <30%
;Pediatric dosing is based on Hemoblogin (see Peds dosing below)
;25% Sodium thiosulfate
#1.65ml/kg IV (12.5g max dose) over 10min
#may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
<references/>
*Anseeuw K. et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. Feb 2013;20(1):2-9

[[Category:Tox]]

Cyanide toxicity

2014-05-25T19:09:12Z

Peterdmorris: venous changes

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient, causes venous hyperoxemia/increased redness -- as does CO poisoning)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)<ref>Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. Jun 2007;25(5):551-8.</ref><ref>Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. 2010;55(4):345-51. </ref>===
1st line therapy
====Mechanism of action====
Directly binds CN forming cyanocobalamin which is readily excreted in the urine
====Administration====
#Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
#Also give 25% Na thiosulfate 1.65ml/kg IV (12.5g max dose) over 10min; may repeat at 1/2 original dose if needed
====Adverse Effects====
#May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
#'''Interferes with colorimetric tests''' -- Pulse ox, Hemoglobin, Carboyxhemoglobin, methemeglobin, oxyhemoglobin, Serum Cr, AST/ALT, bilirubin, magnesium for 2-3 days<ref>Lee J, Mukai D, Kreuter K, et al. Potential interference by hydroxocobalamin on co-oximetry hemoglobin measurements during cyanide and smoke inhalation treatments. Ann Emerg Med. 2007;49(6):802-805.</ref>
;OBTAIN Co-ox and labs prior to Hydroxocobalamin administration

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable<ref>Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52.</ref>
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning since nitrate administration will severely decrease oxygen carrying capacity

====Mechanism of action====
#Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)

====Warnings====
#Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
#Induction of metHb further exacerbates O2 delivery
#Avoid nitrites in presence of severe hypotension if diagnosis is unclear

====Administration====
;Amyl nitrite
#Inhaled by pt (only use if unavailable to obtain IV)
#Hold under pt's nose for 30s of each minute, for 3 minutes
;Sodium nitrite
#10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
#Lack of measurable MetHb levels after administration confirms CN presence
#Monitor MetHb and keep level <30%
;Pediatric dosing is based on Hemoblogin (see Peds dosing below)
;25% Sodium thiosulfate
#1.65ml/kg IV (12.5g max dose) over 10min
#may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
<references/>
*Anseeuw K. et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. Feb 2013;20(1):2-9

[[Category:Tox]]

Cyanide toxicity

2014-05-25T19:06:13Z

Peterdmorris: VBG hyperoxemia

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient, causes venous hyperoxemia -- as does CO poisoning)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)<ref>Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. Jun 2007;25(5):551-8.</ref><ref>Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. 2010;55(4):345-51. </ref>===
1st line therapy
====Mechanism of action====
Directly binds CN forming cyanocobalamin which is readily excreted in the urine
====Administration====
#Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
#Also give 25% Na thiosulfate 1.65ml/kg IV (12.5g max dose) over 10min; may repeat at 1/2 original dose if needed
====Adverse Effects====
#May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
#'''Interferes with colorimetric tests''' -- Pulse ox, Hemoglobin, Carboyxhemoglobin, methemeglobin, oxyhemoglobin, Serum Cr, AST/ALT, bilirubin, magnesium for 2-3 days<ref>Lee J, Mukai D, Kreuter K, et al. Potential interference by hydroxocobalamin on co-oximetry hemoglobin measurements during cyanide and smoke inhalation treatments. Ann Emerg Med. 2007;49(6):802-805.</ref>
;OBTAIN Co-ox and labs prior to Hydroxocobalamin administration

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable<ref>Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52.</ref>
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning since nitrate administration will severely decrease oxygen carrying capacity

====Mechanism of action====
#Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)

====Warnings====
#Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
#Induction of metHb further exacerbates O2 delivery
#Avoid nitrites in presence of severe hypotension if diagnosis is unclear

====Administration====
;Amyl nitrite
#Inhaled by pt (only use if unavailable to obtain IV)
#Hold under pt's nose for 30s of each minute, for 3 minutes
;Sodium nitrite
#10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
#Lack of measurable MetHb levels after administration confirms CN presence
#Monitor MetHb and keep level <30%
;Pediatric dosing is based on Hemoblogin (see Peds dosing below)
;25% Sodium thiosulfate
#1.65ml/kg IV (12.5g max dose) over 10min
#may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
<references/>
*Anseeuw K. et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. Feb 2013;20(1):2-9

[[Category:Tox]]

Cyanide toxicity

2014-05-25T17:56:37Z

Peterdmorris: UTD changes

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)===
#1st line therapy
#Mechanism of action
##Directly binds CN forming cyanocobalamin which is readily excreted in the urine
#How to use:
##Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
##Also give 25% Na thiosulfate 12.5g (max dose) over 10min; may repeat at 1/2 original dose if needed
## 1.65ml/kg IV is the weight based dose
#Side effects
##May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
###Interferes w/ colorimetric tests -- Pulse ox, Hemoglobin, Carboyxhemoglobin, methemeglobin, oxyhemoglobin, Serum Cr, AST/ALT, bilirubin, magnesium for 2-3 days; Obtain Co-ox and labs prior to Hydroxocobalamin administration

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning
#Mechanism of action
##Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)
#Warnings
##Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
###Induction of metHb further exacerbates O2 delivery
##Avoid nitrites in presence of severe hypotension if diagnosis is unclear
#How to use:
##Amyl nitrite inhaled by pt (only use if unavailable to obtain IV)
###Hold under pt's nose for 30s of each minute, for 3 minutes
##Sodium nitrite 10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
###Lack of measurable MetHb levels after administration confirms CN presence
###Monitor MetHb and keep level <30%
###Peds requires dosing based on Hb (see Peds dosing below)
##Sodium thiosulfate 12.5g over 10min; may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
*Tintinalli
*UpToDate

[[Category:Tox]]

Cyanide toxicity

2014-05-25T17:52:30Z

Peterdmorris: /* Cyanokit (Hydroxocobalamin) */

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)===
#1st line therapy
#Mechanism of action
##Directly binds CN forming cyanocobalamin which is readily excreted in the urine
#How to use:
##Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
##Also give 25% Na thiosulfate 12.5g (max dose) over 10min; may repeat at 1/2 original dose if needed
## 1.65ml/kg IV is the weight based dose
#Side effects
##May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
###Interferes w/ co-oximetry measurements

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning
#Mechanism of action
##Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)
#Warnings
##Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
###Induction of metHb further exacerbates O2 delivery
##Avoid nitrites in presence of severe hypotension if diagnosis is unclear
#How to use:
##Amyl nitrite inhaled by pt (only use if unavailable to obtain IV)
###Hold under pt's nose for 30s of each minute, for 3 minutes
##Sodium nitrite 10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
###Lack of measurable MetHb levels after administration confirms CN presence
###Monitor MetHb and keep level <30%
###Peds requires dosing based on Hb (see Peds dosing below)
##Sodium thiosulfate 12.5g over 10min; may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
*Tintinalli
*UpToDate

[[Category:Tox]]

Cyanide toxicity

2014-05-25T17:48:07Z

Peterdmorris: /* Sodium Thiosulfate (Peds Dosing) */

==Background==
*Sources
**Burning of nitrogen-containing polymers (plastics, wool, silk)
**Prolonged use of nitroprusside
**Pits of peaches, pears, apricots, crab apples
*Pathophysiology
**Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
***Causes switch from aerobic to anaerobic metabolism despite adequate O2

==Clinical Features==
===Acute Intoxication===
*Affected by dose, route, formulation and exposure pattern
**Inhaled toxins more rapid than ingested
***Inhalation exposure may cause syncope and death after only a few breaths
*'''Early signs'''
**CNS stimulation (Headache, anxiety, confusion)
**Tachycardia, palpitations and hypertension
**Tachypnea
**Cherry-red color (rarely seen)
*'''Late signs'''
**Nausea, Vomiting
**Bradycardia, hypotension, arrhythmias, asystole
**Coma, Seizures (rare), Mydiriasis
**bradypnea and pulmonary edema (non-cardiogenic), apnea
**Renal Failure
**Hepatic Necrosis
**Cyanosis
**Rhabdo, bright red venules seen on fundoscopy

===Chronic===
*Retrobulbar Optic Atropy (proposed)
**Heavy smokers
*Ataxic peripheral neuropathy
*Konzo
**Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

==Diagnosis==
#Smell of bitter almonds (only 60-80% of population can detect this)
#Severe unexplained metabolic acidosis (lactic)
#PO2 of venous blood similar to arterial blood
#normal SpO2
#Cherry-red skin color is uncommon

==Work-Up==
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient)
#Co-oximetry
#Chemistry (anion gap acidosis)

==Treatment==
#Supportive care
##O2 100% NRB
##IVF and vasopressors for hypotension
##Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
#Antidote

===Cyanokit (Hydroxocobalamin)===
#1st line therapy
#Mechanism of action
##Directly binds CN forming cyanocobalamin which is readily excreted in the urine
#How to use:
##Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
##Also give Na thiosulfate 12.5g over 10min; may repeat at 1/2 original dose if needed
#Side effects
##May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
###Interferes w/ co-oximetry measurements

===Cyanide Antidote Package===
#2nd line therapy - use if Cyanokit unavailable
#Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning
#Mechanism of action
##Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
##Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)
#Warnings
##Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
###Induction of metHb further exacerbates O2 delivery
##Avoid nitrites in presence of severe hypotension if diagnosis is unclear
#How to use:
##Amyl nitrite inhaled by pt (only use if unavailable to obtain IV)
###Hold under pt's nose for 30s of each minute, for 3 minutes
##Sodium nitrite 10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
###Lack of measurable MetHb levels after administration confirms CN presence
###Monitor MetHb and keep level <30%
###Peds requires dosing based on Hb (see Peds dosing below)
##Sodium thiosulfate 12.5g over 10min; may repeat at 1/2 original dose if needed

===Sodium Nitrite (Peds Dosing)===
*Max dose should not exceed 10mL
*Do not give faster than 5mL/min (to avoid hypotension)
#Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
#Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
#Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
#Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
#Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
#Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
#Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
#Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

==Disposition==
#Admit all pts for obs

==See Also==
*[[Carbon Monoxide (CO)]]
*[[Hydrogen Sulfide]]
*[[Burns]]
*[[Acrylonitrile]]

==Source==
*Tintinalli
*UpToDate

[[Category:Tox]]

Retropharyngeal abscess

2013-12-16T16:29:39Z

Peterdmorris: references

==Background==
*Polymicrobial abscess in space between posterior pharyngeal wall and prevertebral fascia
*Adults: Due to direct extension of purulent debris from adjacent site (e.g. Ludwig angina)
**More likely to extend into the mediastinum
*Children: Due to suppurative changes within a lymph node (primary infection elsewhere in head or neck)

==Clinical Features==
*Sore throat (76%)
*Fever (65%)
*Torticollis (37%)
*Dysphagia (35%)
*Late symptoms:
**Stridor, respiratory distres, chest pain (mediastinitis)

==Diagnosis==
*CT neck w/ IV contrast
**Gold standard

*XR Soft tissue
** The prevertebral space should be less than 7mm at C2, 14mm at C6 in children regardless of the age
** The prevertebral space should be less than 22mm at C6 in adults
** If the prevertebral space should be less than one-half the width of the corresponding vertebral body
** If equivocal XR, order CT

==Treatment==
*Emergent ENT consult
**Most patients require I&D
*Secure airway
*Abx
**Clindamycin 600-900mg IV OR cefoxitin 2gm IV

==Disposition==
*Admit

==See Also==
#[[PTA]]
#[[Ludwig's Angina]]
#[[Pharyngitis]]

==Source==
*Tintinalli
*emedicine.com
*Emergency Medicine Oral Board Review Illustrated, Okuda

[[Category:Peds]]
[[Category:ID]]

Retropharyngeal abscess

2013-12-16T16:29:07Z

Peterdmorris: references

==Background==
*Polymicrobial abscess in space between posterior pharyngeal wall and prevertebral fascia
*Adults: Due to direct extension of purulent debris from adjacent site (e.g. Ludwig angina)
**More likely to extend into the mediastinum
*Children: Due to suppurative changes within a lymph node (primary infection elsewhere in head or neck)

==Clinical Features==
*Sore throat (76%)
*Fever (65%)
*Torticollis (37%)
*Dysphagia (35%)
*Late symptoms:
**Stridor, respiratory distres, chest pain (mediastinitis)

==Diagnosis==
*CT neck w/ IV contrast
**Gold standard

*XR Soft tissue
** The prevertebral space should be less than 7mm at C2, 14mm at C6 in children regardless of the age
** The prevertebral space should be less than 22mm at C6 in adults
** If the prevertebral space should be less than one-half the width of the corresponding vertebral body
** If equivocal XR, order CT

==Treatment==
*Emergent ENT consult
**Most patients require I&D
*Secure airway
*Abx
**Clindamycin 600-900mg IV OR cefoxitin 2gm IV

==Disposition==
*Admit

==See Also==
#[[PTA]]
#[[Ludwig's Angina]]
#[[Pharyngitis]]

==Source==
Tintinalli
emedicine.com
Emergency Medicine Oral Board Review Illustrated, Okuda

[[Category:Peds]]
[[Category:ID]]

Retropharyngeal abscess

2013-12-16T16:28:23Z

Peterdmorris: XR RPA

Henoch-Schonlein purpura

2013-12-10T21:56:26Z

Peterdmorris: added reference (rosen's already referenced)

==Background==
*Most common vasculitis in childhood
*Usually affects 2-11yr
*5% of cases are a/w intussusception (abd vasculitis)
*Renal involvement is feared complication
*95% recover completely after 3-4wk

==Diagnosis==
*Tetrad:
**Palpable purpura (extremities, buttock)
**Acute abdominal pain (diffuse, colicky)
***Develops after onset of rash
**Arthritis
***Migratory, usually involves knees/ankles
**Renal disease (50% of the time)
[[File:HSPVasc01.jpg|center|frame|500px|Palpable Purpura]]
*Rare manifestations
** Melena, hematemesis, hepatosplenomegaly
** Headache, seizures
** Fever
** Non-pitting edema of the extremities and face

==DDx==
#Meningococcemia
#Erythema nodosum
#Intussusception
#Rheumatic fever
#Polyarteritis nodosa
#SLE
#RA
#Drug reaction

==Work-Up==
#UA
##Hematuria, proteinuria
#Chemistry

==Treatment==
*Supportive
*NSAIDs for pain, may worsen renal disease or GI disease
*consider prednisone 1mg/kg/day for severe arthralgias

==Disposition==
*Outpt management for most w/ rheum f/u

==See Also==
[[Pediatric Rashes]]

==Source==
*Rosen's, Tintinalli
*Images provided by University of Iowa Dept. of Dermatology
*First Aid for the Emergency Medicine Boards
[[Category:Derm]]
[[Category:Peds]]

Henoch-Schonlein purpura

2013-12-10T21:54:58Z

Peterdmorris: added rare manifestations, treatment of arthraligias

Henoch-Schonlein purpura

2013-12-10T21:52:19Z

Peterdmorris: /* Diagnosis */

==Background==
*Most common vasculitis in childhood
*Usually affects 2-11yr
*5% of cases are a/w intussusception (abd vasculitis)
*Renal involvement is feared complication
*95% recover completely after 3-4wk

==Diagnosis==
*Tetrad:
**Palpable purpura (extremities, buttock)
**Acute abdominal pain (diffuse, colicky)
***Develops after onset of rash
**Arthritis
***Migratory, usually involves knees/ankles
**Renal disease (50% of the time)
[[File:HSPVasc01.jpg|center|frame|500px|Palpable Purpura]]
*Rare manifestations
** Melena, hematemesis, hepatosplenomegaly
** Headache, seizures
** Fever
** Non-pitting edema of the extremities and face

==DDx==
#Meningococcemia
#Erythema nodosum
#Intussusception
#Rheumatic fever
#Polyarteritis nodosa
#SLE
#RA
#Drug reaction

==Work-Up==
#UA
##Hematuria, proteinuria
#Chemistry

==Treatment==
*Supportive
*NSAIDs for pain

==Disposition==
*Outpt management for most w/ rheum f/u

==See Also==
[[Pediatric Rashes]]

==Source==
*Rosen's, Tintinalli
*Images provided by University of Iowa Dept. of Dermatology
[[Category:Derm]]
[[Category:Peds]]

Henoch-Schonlein purpura

2013-12-10T21:46:47Z

Peterdmorris: /* Diagnosis */

==Background==
*Most common vasculitis in childhood
*Usually affects 2-11yr
*5% of cases are a/w intussusception (abd vasculitis)
*Renal involvement is feared complication
*95% recover completely after 3-4wk

==Diagnosis==
*Tetrad:
**Palpable purpura (extremities, buttock)
**Acute abdominal pain (diffuse, colicky)
***Develops after onset of rash
**Arthritis
***Migratory, usually involves knees/ankles
**Renal disease (50%)
[[File:HSPVasc01.jpg|center|frame|500px|Palpable Purpura]]
*** Rare manifestations:
**** Melena, hematemesis, hepatosplenomegaly
**** Headache, seizures
**** Fever
**** Non-pitting edema of the extremities and face

==DDx==
#Meningococcemia
#Erythema nodosum
#Intussusception
#Rheumatic fever
#Polyarteritis nodosa
#SLE
#RA
#Drug reaction

==Work-Up==
#UA
##Hematuria, proteinuria
#Chemistry

==Treatment==
*Supportive
*NSAIDs for pain

==Disposition==
*Outpt management for most w/ rheum f/u

==See Also==
[[Pediatric Rashes]]

==Source==
*Rosen's, Tintinalli
*Images provided by University of Iowa Dept. of Dermatology
[[Category:Derm]]
[[Category:Peds]]

Monteggia fracture-dislocation

2013-11-10T21:50:28Z

Peterdmorris: added radial nerve injury features

==Background==
*Ulna fx (proximal third) + radial head dislocation
*Easy to overlook the radial head dislocation (will result in worse outcome)

==Clinical Features==
*Pain/swelling at elbow
*Radial head may be palpable in an anterolatera or posterolateral location
*May be associated with radial nerve injury (wrist drop, inability to extend the fingers et cetera)

==Management==
*Consult ortho in the ED; likely requires ORIF

==See Also==
[[Forearm Fracture]]

==Source==
*Tintinalli

[[Category:Ortho]]

Pulmonary embolism

2013-09-27T22:32:07Z

Peterdmorris: hedge

==Background==
*Suspect in pt w/ dyspnea, tachypnea, or pleuritic pain
*Only 40% of ambulatory ED pts w/ PE have concomitant DVT

==Types==
#Massive
##Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
##Pulselessness
##Persistent profound bradycardia (HR <40 with signs of shock)
#Submassive
##Sys BP >90 but with either RV dysfunction or myocardial necrosis
###RV dysfunction
####RV dilation or dysfunction on TTE
####RV dilation on CT
####Elevation of BNP (>90)
####ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI
###Myocardial necrosis: Troponin I >0.4

==Diagnosis==
===Wells Criteria===
#Symptoms of DVT - 3pts
#No alternative diagnosis better explains the illness - 3pts
#HR > 100 - 1.5 pts
#Immobilization within prior 4wks - 1.5pts
#Prior history of DVT or PE - 1.5pts
#Active malignancy - 1pt
#Hemoptysis - 1pt

'''Wells Score'''
#0-1 point: Low probability (3.4%)
#2-6 points: Moderate probability (27.8%)
#7-12 points: High probability (78.4%)

===Workup by Probability===
====Low Probability====
*If low prob and [[PERC Rule]] neg then d/c
*If low prob and [[PERC Rule]] pos then d-dimer

====Moderate Probability====
*Obtain d-dimer

====High Probability====
*Consider anticoagulation before imaging!
*CTPA if GFR >60
*V/Q if GFR <60

==Treatment==
===Anticoagulation===
*Indicated for all patients with confirmed PE or high clinical suspicion (don't wait for imaging)
*Treatment options:
**LMWH SC
***1st line for most hemodynamically stable pts
***contraindicated in renal failure
**UFH
***Consider in pts w/:
****Persistent hypotension
****Increased risk of bleeding
****Recent sx/trauma
****Renal failure (GFR <30)
****Morbid obesity or anasarca (poor sc absorption)
****Thrombolysis is being considered
***80 units/kg bolus; then 18 units/kg/hr
****Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control

===Thrombolysis===
====Indications====
#Pt w/ massive PE and acceptable risk of bleeding complications
#Pt w/ submassive PE w/ e/o adverse prognosis + low risk of bleeding complications
##Hemodynamic instability
##Worsening resp insufficiency
##Severe RV dysfunction
##Major myocardial necrosis

====Instructions====
#Review contraindications
#Discontinue heparin during infusion
#tPA 100mg over 2hr OR 0.6 mg/kg over 2min
#After infusion complete measure PTT
##Once value is <2x upper limit restart anticoagulation

====Absolute contraindications====
#Any prior intracranial hemorrhage,
#Known structural intracranial cerebrovascular disease (e.g. AVM)
#Known malignant intracranial neoplasm
#Ischemic stroke within 3mo
#Suspected aortic dissection
#Active bleeding or bleeding diathesis
#Recent surgery encroaching on the spinal canal or brain
#Recent closed-head or facial trauma w/ radiographic evidence of bony fx or brain injury

====Relative contraindications====
#Age >75 years
#Current use of anticoagulation
#Pregnancy
#Noncompressible vascular punctures
#Traumatic or prolonged CPR (>10min)
#Recent internal bleeding (within 2 to 4 weeks)
#History of chronic, severe, and poorly controlled hypertension
#Severe uncontrolled HTN on presentation (sys BP >180 or dia BP >110)
#Dementia
#Remote (>3 months) ischemic stroke
#Major surgery within 3 weeks

===IVC Filter===
*Indications
**anticoagulation contraindicated in pt with PE
**failure to attain adequate anticoagulation during treatment

==PE in Pregnancy==
*[[Heparin]] and [[Enoxaparin]] are safe (coumadin is not)
*Consider utz as initial test
*CT (with shield) vs. V/Q is roughly equilivalent radiation exposure
*D-Dimer MAY BE (no RCTs) used with following limits:
**1st trimester: <750 (+50% increase from normal lab threshold)
**2nd trimester: <1000 (+100% from normal)
**3rd trimester: <1250 (+150% from normal)

===Algorithm===
#Clinical features suggestive of PE
##Bilateral LE Ultrasound
###Positive-->LMWH
###Negative-->CTA

==Source==
#Circulation. 2011 Apr 26;123(16):1788-830
#Tintinalli
#UpToDate
#D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary embolism

2013-09-27T22:26:56Z

Peterdmorris: typo

==Background==
*Suspect in pt w/ dyspnea, tachypnea, or pleuritic pain
*Only 40% of ambulatory ED pts w/ PE have concomitant DVT

==Types==
#Massive
##Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
##Pulselessness
##Persistent profound bradycardia (HR <40 with signs of shock)
#Submassive
##Sys BP >90 but with either RV dysfunction or myocardial necrosis
###RV dysfunction
####RV dilation or dysfunction on TTE
####RV dilation on CT
####Elevation of BNP (>90)
####ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI
###Myocardial necrosis: Troponin I >0.4

==Diagnosis==
===Wells Criteria===
#Symptoms of DVT - 3pts
#No alternative diagnosis better explains the illness - 3pts
#HR > 100 - 1.5 pts
#Immobilization within prior 4wks - 1.5pts
#Prior history of DVT or PE - 1.5pts
#Active malignancy - 1pt
#Hemoptysis - 1pt

'''Wells Score'''
#0-1 point: Low probability (3.4%)
#2-6 points: Moderate probability (27.8%)
#7-12 points: High probability (78.4%)

===Workup by Probability===
====Low Probability====
*If low prob and [[PERC Rule]] neg then d/c
*If low prob and [[PERC Rule]] pos then d-dimer

====Moderate Probability====
*Obtain d-dimer

====High Probability====
*Consider anticoagulation before imaging!
*CTPA if GFR >60
*V/Q if GFR <60

==Treatment==
===Anticoagulation===
*Indicated for all patients with confirmed PE or high clinical suspicion (don't wait for imaging)
*Treatment options:
**LMWH SC
***1st line for most hemodynamically stable pts
***contraindicated in renal failure
**UFH
***Consider in pts w/:
****Persistent hypotension
****Increased risk of bleeding
****Recent sx/trauma
****Renal failure (GFR <30)
****Morbid obesity or anasarca (poor sc absorption)
****Thrombolysis is being considered
***80 units/kg bolus; then 18 units/kg/hr
****Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control

===Thrombolysis===
====Indications====
#Pt w/ massive PE and acceptable risk of bleeding complications
#Pt w/ submassive PE w/ e/o adverse prognosis + low risk of bleeding complications
##Hemodynamic instability
##Worsening resp insufficiency
##Severe RV dysfunction
##Major myocardial necrosis

====Instructions====
#Review contraindications
#Discontinue heparin during infusion
#tPA 100mg over 2hr OR 0.6 mg/kg over 2min
#After infusion complete measure PTT
##Once value is <2x upper limit restart anticoagulation

====Absolute contraindications====
#Any prior intracranial hemorrhage,
#Known structural intracranial cerebrovascular disease (e.g. AVM)
#Known malignant intracranial neoplasm
#Ischemic stroke within 3mo
#Suspected aortic dissection
#Active bleeding or bleeding diathesis
#Recent surgery encroaching on the spinal canal or brain
#Recent closed-head or facial trauma w/ radiographic evidence of bony fx or brain injury

====Relative contraindications====
#Age >75 years
#Current use of anticoagulation
#Pregnancy
#Noncompressible vascular punctures
#Traumatic or prolonged CPR (>10min)
#Recent internal bleeding (within 2 to 4 weeks)
#History of chronic, severe, and poorly controlled hypertension
#Severe uncontrolled HTN on presentation (sys BP >180 or dia BP >110)
#Dementia
#Remote (>3 months) ischemic stroke
#Major surgery within 3 weeks

===IVC Filter===
*Indications
**anticoagulation contraindicated in pt with PE
**failure to attain adequate anticoagulation during treatment

==PE in Pregnancy==
*[[Heparin]] and [[Enoxaparin]] are safe (coumadin is not)
*Consider utz as initial test
*CT (with shield) vs. V/Q is roughly equilivalent radiation exposure
*D-Dimer can MAY BE used with following limits:
**1st trimester: <750 (+50% increase from normal lab threshold)
**2nd trimester: <1000 (+100% from normal)
**3rd trimester: <1250 (+150% from normal)

===Algorithm===
#Clinical features suggestive of PE
##Bilateral LE Ultrasound
###Positive-->LMWH
###Negative-->CTA

==Source==
#Circulation. 2011 Apr 26;123(16):1788-830
#Tintinalli
#UpToDate
#D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary embolism

2013-09-27T20:33:55Z

Peterdmorris: stated claim is has not been prospectively studied, is not standard of care

==Background==
*Suspect in pt w/ dyspnea, tachypnea, or pleuritic pain
*Only 40% of ambulatory ED pts w/ PE have concomitant DVT

==Types==
#Massive
##Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
##Pulselessness
##Persistent profound bradycardia (HR <40 with signs of shock)
#Submassive
##Sys BP >90 but with either RV dysfunction or myocardial necrosis
###RV dysfunction
####RV dilation or dysfunction on TTE
####RV dilation on CT
####Elevation of BNP (>90)
####ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI
###Myocardial necrosis: Troponin I >0.4

==Diagnosis==
===Wells Criteria===
#Symptoms of DVT - 3pts
#No alternative diagnosis better explains the illness - 3pts
#HR > 100 - 1.5 pts
#Immobilization within prior 4wks - 1.5pts
#Prior history of DVT or PE - 1.5pts
#Active malignancy - 1pt
#Hemoptysis - 1pt

'''Wells Score'''
#0-1 point: Low probability (3.4%)
#2-6 points: Moderate probability (27.8%)
#7-12 points: High probability (78.4%)

===Workup by Probability===
====Low Probability====
*If low prob and [[PERC Rule]] neg then d/c
*If low prob and [[PERC Rule]] pos then d-dimer

====Moderate Probability====
*Obtain d-dimer

====High Probability====
*Consider anticoagulation before imaging!
*CTPA if GFR >60
*V/Q if GFR <60

==Treatment==
===Anticoagulation===
*Indicated for all patients with confirmed PE or high clinical suspicion (don't wait for imaging)
*Treatment options:
**LMWH SC
***1st line for most hemodynamically stable pts
***contraindicated in renal failure
**UFH
***Consider in pts w/:
****Persistent hypotension
****Increased risk of bleeding
****Recent sx/trauma
****Renal failure (GFR <30)
****Morbid obesity or anasarca (poor sc absorption)
****Thrombolysis is being considered
***80 units/kg bolus; then 18 units/kg/hr
****Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control

===Thrombolysis===
====Indications====
#Pt w/ massive PE and acceptable risk of bleeding complications
#Pt w/ submassive PE w/ e/o adverse prognosis + low risk of bleeding complications
##Hemodynamic instability
##Worsening resp insufficiency
##Severe RV dysfunction
##Major myocardial necrosis

====Instructions====
#Review contraindications
#Discontinue heparin during infusion
#tPA 100mg over 2hr OR 0.6 mg/kg over 2min
#After infusion complete measure PTT
##Once value is <2x upper limit restart anticoagulation

====Absolute contraindications====
#Any prior intracranial hemorrhage,
#Known structural intracranial cerebrovascular disease (e.g. AVM)
#Known malignant intracranial neoplasm
#Ischemic stroke within 3mo
#Suspected aortic dissection
#Active bleeding or bleeding diathesis
#Recent surgery encroaching on the spinal canal or brain
#Recent closed-head or facial trauma w/ radiographic evidence of bony fx or brain injury

====Relative contraindications====
#Age >75 years
#Current use of anticoagulation
#Pregnancy
#Noncompressible vascular punctures
#Traumatic or prolonged CPR (>10min)
#Recent internal bleeding (within 2 to 4 weeks)
#History of chronic, severe, and poorly controlled hypertension
#Severe uncontrolled HTN on presentation (sys BP >180 or dia BP >110)
#Dementia
#Remote (>3 months) ischemic stroke
#Major surgery within 3 weeks

===IVC Filter===
*Indications
**anticoagulation contraindicated in pt with PE
**failure to attain adequate anticoagulation during treatment

==PE in Pregnancy==
*[[Heparin]] and [[Enoxaparin]] are safe (coumadin is not)
*Consider utz as initial test
*CT (with shield) vs. V/Q is roughly equilivalent radiation exposure
*D-Dimer can MAYBE used with following limits:
**1st trimester: <750 (+50% increase from normal lab threshold)
**2nd trimester: <1000 (+100% from normal)
**3rd trimester: <1250 (+150% from normal)

===Algorithm===
#Clinical features suggestive of PE
##Bilateral LE Ultrasound
###Positive-->LMWH
###Negative-->CTA

==Source==
#Circulation. 2011 Apr 26;123(16):1788-830
#Tintinalli
#UpToDate
#D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary embolism

2013-09-27T20:32:51Z

Peterdmorris: ddimer in preg

==Background==
*Suspect in pt w/ dyspnea, tachypnea, or pleuritic pain
*Only 40% of ambulatory ED pts w/ PE have concomitant DVT

==Types==
#Massive
##Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
##Pulselessness
##Persistent profound bradycardia (HR <40 with signs of shock)
#Submassive
##Sys BP >90 but with either RV dysfunction or myocardial necrosis
###RV dysfunction
####RV dilation or dysfunction on TTE
####RV dilation on CT
####Elevation of BNP (>90)
####ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI
###Myocardial necrosis: Troponin I >0.4

==Diagnosis==
===Wells Criteria===
#Symptoms of DVT - 3pts
#No alternative diagnosis better explains the illness - 3pts
#HR > 100 - 1.5 pts
#Immobilization within prior 4wks - 1.5pts
#Prior history of DVT or PE - 1.5pts
#Active malignancy - 1pt
#Hemoptysis - 1pt

'''Wells Score'''
#0-1 point: Low probability (3.4%)
#2-6 points: Moderate probability (27.8%)
#7-12 points: High probability (78.4%)

===Workup by Probability===
====Low Probability====
*If low prob and [[PERC Rule]] neg then d/c
*If low prob and [[PERC Rule]] pos then d-dimer

====Moderate Probability====
*Obtain d-dimer

====High Probability====
*Consider anticoagulation before imaging!
*CTPA if GFR >60
*V/Q if GFR <60

==Treatment==
===Anticoagulation===
*Indicated for all patients with confirmed PE or high clinical suspicion (don't wait for imaging)
*Treatment options:
**LMWH SC
***1st line for most hemodynamically stable pts
***contraindicated in renal failure
**UFH
***Consider in pts w/:
****Persistent hypotension
****Increased risk of bleeding
****Recent sx/trauma
****Renal failure (GFR <30)
****Morbid obesity or anasarca (poor sc absorption)
****Thrombolysis is being considered
***80 units/kg bolus; then 18 units/kg/hr
****Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control

===Thrombolysis===
====Indications====
#Pt w/ massive PE and acceptable risk of bleeding complications
#Pt w/ submassive PE w/ e/o adverse prognosis + low risk of bleeding complications
##Hemodynamic instability
##Worsening resp insufficiency
##Severe RV dysfunction
##Major myocardial necrosis

====Instructions====
#Review contraindications
#Discontinue heparin during infusion
#tPA 100mg over 2hr OR 0.6 mg/kg over 2min
#After infusion complete measure PTT
##Once value is <2x upper limit restart anticoagulation

====Absolute contraindications====
#Any prior intracranial hemorrhage,
#Known structural intracranial cerebrovascular disease (e.g. AVM)
#Known malignant intracranial neoplasm
#Ischemic stroke within 3mo
#Suspected aortic dissection
#Active bleeding or bleeding diathesis
#Recent surgery encroaching on the spinal canal or brain
#Recent closed-head or facial trauma w/ radiographic evidence of bony fx or brain injury

====Relative contraindications====
#Age >75 years
#Current use of anticoagulation
#Pregnancy
#Noncompressible vascular punctures
#Traumatic or prolonged CPR (>10min)
#Recent internal bleeding (within 2 to 4 weeks)
#History of chronic, severe, and poorly controlled hypertension
#Severe uncontrolled HTN on presentation (sys BP >180 or dia BP >110)
#Dementia
#Remote (>3 months) ischemic stroke
#Major surgery within 3 weeks

===IVC Filter===
*Indications
**anticoagulation contraindicated in pt with PE
**failure to attain adequate anticoagulation during treatment

==PE in Pregnancy==
*[[Heparin]] and [[Enoxaparin]] are safe (coumadin is not)
*Consider utz as initial test
*CT (with shield) vs. V/Q is roughly equilivalent radiation exposure
*D-Dimer can still be used with following limits:
**1st trimester: <750 (+50% increase from normal lab threshold)
**2nd trimester: <1000 (+100% from normal)
**3rd trimester: <1250 (+150% from normal)

===Algorithm===
#Clinical features suggestive of PE
##Bilateral LE Ultrasound
###Positive-->LMWH
###Negative-->CTA

==Source==
#Circulation. 2011 Apr 26;123(16):1788-830
#Tintinalli
#UpToDate
#D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary embolism

2013-09-27T20:32:08Z

Peterdmorris: /* Source */

==Background==
*Suspect in pt w/ dyspnea, tachypnea, or pleuritic pain
*Only 40% of ambulatory ED pts w/ PE have concomitant DVT

==Types==
#Massive
##Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
##Pulselessness
##Persistent profound bradycardia (HR <40 with signs of shock)
#Submassive
##Sys BP >90 but with either RV dysfunction or myocardial necrosis
###RV dysfunction
####RV dilation or dysfunction on TTE
####RV dilation on CT
####Elevation of BNP (>90)
####ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI
###Myocardial necrosis: Troponin I >0.4

==Diagnosis==
===Wells Criteria===
#Symptoms of DVT - 3pts
#No alternative diagnosis better explains the illness - 3pts
#HR > 100 - 1.5 pts
#Immobilization within prior 4wks - 1.5pts
#Prior history of DVT or PE - 1.5pts
#Active malignancy - 1pt
#Hemoptysis - 1pt

'''Wells Score'''
#0-1 point: Low probability (3.4%)
#2-6 points: Moderate probability (27.8%)
#7-12 points: High probability (78.4%)

===Workup by Probability===
====Low Probability====
*If low prob and [[PERC Rule]] neg then d/c
*If low prob and [[PERC Rule]] pos then d-dimer

====Moderate Probability====
*Obtain d-dimer

====High Probability====
*Consider anticoagulation before imaging!
*CTPA if GFR >60
*V/Q if GFR <60

==Treatment==
===Anticoagulation===
*Indicated for all patients with confirmed PE or high clinical suspicion (don't wait for imaging)
*Treatment options:
**LMWH SC
***1st line for most hemodynamically stable pts
***contraindicated in renal failure
**UFH
***Consider in pts w/:
****Persistent hypotension
****Increased risk of bleeding
****Recent sx/trauma
****Renal failure (GFR <30)
****Morbid obesity or anasarca (poor sc absorption)
****Thrombolysis is being considered
***80 units/kg bolus; then 18 units/kg/hr
****Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control

===Thrombolysis===
====Indications====
#Pt w/ massive PE and acceptable risk of bleeding complications
#Pt w/ submassive PE w/ e/o adverse prognosis + low risk of bleeding complications
##Hemodynamic instability
##Worsening resp insufficiency
##Severe RV dysfunction
##Major myocardial necrosis

====Instructions====
#Review contraindications
#Discontinue heparin during infusion
#tPA 100mg over 2hr OR 0.6 mg/kg over 2min
#After infusion complete measure PTT
##Once value is <2x upper limit restart anticoagulation

====Absolute contraindications====
#Any prior intracranial hemorrhage,
#Known structural intracranial cerebrovascular disease (e.g. AVM)
#Known malignant intracranial neoplasm
#Ischemic stroke within 3mo
#Suspected aortic dissection
#Active bleeding or bleeding diathesis
#Recent surgery encroaching on the spinal canal or brain
#Recent closed-head or facial trauma w/ radiographic evidence of bony fx or brain injury

====Relative contraindications====
#Age >75 years
#Current use of anticoagulation
#Pregnancy
#Noncompressible vascular punctures
#Traumatic or prolonged CPR (>10min)
#Recent internal bleeding (within 2 to 4 weeks)
#History of chronic, severe, and poorly controlled hypertension
#Severe uncontrolled HTN on presentation (sys BP >180 or dia BP >110)
#Dementia
#Remote (>3 months) ischemic stroke
#Major surgery within 3 weeks

===IVC Filter===
*Indications
**anticoagulation contraindicated in pt with PE
**failure to attain adequate anticoagulation during treatment

==PE in Pregnancy==
*[[Heparin]] and [[Enoxaparin]] are safe (coumadin is not)
*Consider utz as initial test
*CT (with shield) vs. V/Q is roughly equilivalent radiation exposure
*D-Dimer can still be used with following limits:
**1st trimester: <750 (+50% increase from normal lab threshold)
**2nd trimester: <1000 (+100% from normal)
**3rd trimester: <1250 (+150% from normal)

===Algorithm===
#Clinical features suggestive of PE
##Bilateral LE Ultrasound
###Positive-->LMWH
###Negative-->CTA

==Source==
#Circulation. 2011 Apr 26;123(16):1788-830
#Tintinalli
#UpToDate
#D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829

[[Category:Cards]]
[[Category:Pulm]]

Needed pages

2013-09-25T20:03:53Z

Peterdmorris:

= Tinea Versicolor =

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare. Also known as Malassezia furfur

2. More common in areas of increased sebaceous glands

3. Equally common is light and dark skinned individuals, but more noticeable in the later

== DDx ==

1. Pityriasis Alba

2. Guttate Psoriasis

3. Seborrheic Dermatitis

4. Tinea Corporis

5. Vitiligo

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== See Also ==

http://www.wikem.org/wiki/Tinea

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T20:03:41Z

Peterdmorris:

= Tinea Versicolor

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare. Also known as Malassezia furfur

2. More common in areas of increased sebaceous glands

3. Equally common is light and dark skinned individuals, but more noticeable in the later

== DDx ==

1. Pityriasis Alba

2. Guttate Psoriasis

3. Seborrheic Dermatitis

4. Tinea Corporis

5. Vitiligo

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== See Also ==

http://www.wikem.org/wiki/Tinea

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T20:03:02Z

Peterdmorris: tv 1.0

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare. Also known as Malassezia furfur

2. More common in areas of increased sebaceous glands

3. Equally common is light and dark skinned individuals, but more noticeable in the later

== DDx ==

1. Pityriasis Alba

2. Guttate Psoriasis

3. Seborrheic Dermatitis

4. Tinea Corporis

5. Vitiligo

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== See Also ==

http://www.wikem.org/wiki/Tinea

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T20:00:04Z

Peterdmorris: tinea versicolor

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare. Also known as Malassezia furfur

2. More common in areas of increased sebaceous glands

3. Equally common is light and dark skinned individuals, but more noticeable in the later

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== See Also ==

http://www.wikem.org/wiki/Tinea

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:57:06Z

Peterdmorris: Tinea versicolor 1.0

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare. Also known as Malassezia furfur

2. More common in areas of increased sebaceous glands

3. Equally common is light and dark skinned individuals, but more noticeable in the later

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:54:49Z

Peterdmorris: tv

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)

2. More common in areas of increased sebaceous glands

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

== References ==

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:54:22Z

Peterdmorris: tv 1.0

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)

2. More common in areas of increased sebaceous glands

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

== Treatment ==

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

=== References ===

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:49:31Z

Peterdmorris: tv 1.0

<big>=== Tinea Versicolor ===</big>

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)

2. More common in areas of increased sebaceous glands

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

=== Treatment ===

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

=== References ===

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:47:39Z

Peterdmorris: /* Diagnosis */

=== Tinea Versicolor ===

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)

2. More common in areas of increased sebaceous glands

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp

2. KOH wet prep (Spaghetti and Meatballs appearance)

3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

=== Treatment ===

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)

2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy-of-use

3. Griseofulvin is not effective

=== References ===

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:47:08Z

Peterdmorris: /* Tinea Versicolor */

=== Tinea Versicolor ===

== History and Physical ==

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)

2. More common in areas of increased sebaceous glands

== Diagnosis ==

1. Some demonstrate coppery-orange fluoresence under Woods Lamp
2. KOH wet prep (Spaghetti and Meatballs appearance)
3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

=== Treatment ===

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)
2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy of use
3. Griseofulvin is not effective

=== References ===

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Needed pages

2013-09-25T19:45:48Z

Peterdmorris: Tinea Versicolor beta version 1.0

== Tinea Versicolor ==

-- History and Physical --

1. Hypopigmented or hyperpigmented lesions predominantly on the trunk caused by fungus Pityrosporum ovale (oval form) or obiculare (aka Malassezia furfur)
2. More common in areas of increased sebaceous glands

--- Diagnosis ---

1. Some demonstrate coppery-orange fluoresence under Woods Lamp
2. KOH wet prep (Spaghetti and Meatballs appearance)
3. Almost never cultured given difficult culture medium, benign course, and diagnostic KOH prep.

--- Treatment ---

1. First line topical treatment is ketoconazole (nightly application x 2 weeks) or selenium sulfide (10 minutes x bid)
2. Single dose 400mg ketoconazole PO or fluconazole 150-300mg PO per week x 2-4 weeks for more resistant cases or for easy of use
3. Griseofulvin is not effective

--- References ---

1. http://emedicine.medscape.com/article/1091575

[[Category:derm]]

Pediatric fever of uncertain source

2013-09-25T13:47:51Z

Peterdmorris: /* Source */

== From Tintinalli ==

- '''Management of patients who are well-appearing, vaccinated, and no clinical source of fever'''

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| Age Group
| Evaluation
| Treatment
|-
|
0-28d, ≥38C

SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

|
CBC, blood Cx

UA, Ucx

CSF cell count, GS, Cx

CXR (only if resp sx)

Stool testing (if diarrhea present)

|
Admit

Ampicillin 50mg/kg + (cefotaxime 50mg/kg or gentamicin 2.5mg/kg)

|-
|
29-56d, ≥ 38.2 (100.8) (Philadelphia Protocol)

 SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

 

| Same as for neonates
|
Discharge if:

1. WBC <15K but >5K and <20% bands

2. UA negative

Admit and perform LP if above are not met

Treat with CTX 50mg/kg (if CSF normal), 100mg/kg (if signs of meningitis)

|-
|
57d-6mo, ≥38

Non-UTI SBI incidence is estimated to be negligible

UTI is 3%–8% 

 

|
UA and Ucx alone

OR

treat 57-90d using Philadelphia Protocol

|
Discharge if negative

Treat UTI w/ cefixime 8mg/kg/d or cefpodoxime 10mg/kg/d divided into BID or cefdinir 14mg/kg/d x 7-10days as outpatient

Admit and tx with CTX if fail criteria for d/c

|-
|
57d-6mo, ≥39 (102.2)

SBI incidence is estimated <1%;

non-UTI SBI incidence is estimated to be negligible.

UTI is 3%–8%

|
UA and Ucx alone

OR

UA and Ucx + CBC + blood cx

|
:

Discharge if negative

Treat for UTI as above

If WBC>15K consider treatment with CTX 50 mg/kg IV/IM, and follow-up in 24hr

If WBC>20K consider CXR and CSF

|-
|
 6–36 mo

Non-UTI SBI incidence is <0.4% 

UTI in girls ≤8%

UTI in boys (<12 mo) ≤ 2%

Uncircumcised boys (1–2 y) remains 2%

|
UA and Ucx in:

(girls 6-24mo)

(circ 6-12mo)

(uncirc 6-24mo)

|
Discharge if negative

Treat for UTI as above as outpatient

|-
| >36mo
| No further w/u is routinely necessary
| 
|}

Note: Preemies - Count age by estimated postconception date (not by actual delivery date) for 1st 90d

== Harbor-UCLA Protocol ==
===Background===
*Medicine is an art as well as science, practice clinical judgment when using this guideline
*Preemies: Count age by estimated postconception date (not by actual delivery date) for 1st-90d
*If RSV+ or influenza+
**Low risk of bacterial illness
**Still some risk of concurrent UTI

=== 0-28dy ===

{| style="width: 497px; height: 45px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Child Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38'''
'''Toxic or Well'''

|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^
|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100-200 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| N/A
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs

=== 28dy-90dy ===

{| style="width: 491px; height: 505px" cellspacing="1" cellpadding="1" width="491" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38 + Toxic'''
|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^

|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| NA
|-
|
'''T>=38 + Well'''

'''(Option 1)'''

|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
#Ceftriaxone (50mg/kg IM/IV)
|
If W/U (+) admit

Outpatient^^^^

| If W/U negative, meets outpt
|-
|
'''T>=38 + Toxic'''

'''(Option 2)'''

|
#CBC
#Blood Cx
#UA, UCx
#CXR^

|
#None

For very well appearing 60-90 day olds (many would not use this option)

| Outpatient^^^^
|
|}

*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs
*^^^^Outpatient

=== 90dy-36mo ===

{| style="width: 497px; height: 124px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=39 + Toxic'''
|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
Ceftriaxone (50-100mg/kg)

OR

Cefotaxime (50-100mg/kg)

AND

Consider Vanco (15mg/kg)^^^^

| Admit
| N/A
|-
|
'''T>=39^^^^^ + Well + Prevnar^^'''

|
#UA, UCx^^^
#CXR^

|
If + W/U, oral abx

| Outpatient
|
|-
|
'''T>=39^^^^^ + Well + NO Prevnar^^'''

|
#UA, UCx^^^
#CBC
#CXR^

|
Ceftriaxone 50mg/kg if >15 WBC (also then consider BCx and LP)

| Outpatient
|
|-
| '''T>=38-38.9 + Well'''
|
None

Consider UA, CXR based on sx, etc

|
None

| Outpatient
| Return if worsening sx or fever persists >72hrs
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Prevnar = has 3 Prevnar or >=4 wks post 2nd Prevnar dose
*^^^Urine workup for:
**Circumcised males <6 months
**Uncircumcised males <12 months
**All females
*^^^^Vancomycin if evidence of bacterial meningitis on CSF
*^^^^^>=39.5 for 24-36mo

===Work-Up Results===
*WBC: 5-15, ANC <10k, <1,500 bands
*UA: (-)Gm Stain, (-) leuks, (-) nitrite, <5-10 wbc/hpf
*CSF: <8wbc, (-) Gm Stain
*When diarrhea present, <5 wbc

If low-risk criteria below not met, LP (if not done) and admit for inpt abx

===Petechia===
#CBC
#BCx
#Ceftriaxone
#LP depending on clinical

===Facts and Figures from ACEP's Clinical Policy on Pediatric Fevers===
7% of patients < 2 years old with fever have PNA, however the etiology (viral/bacterial) or even the presence of pneumonia has low inter-observer reliability even among pediatric radiologists

4% Prevalence of UTI with common other sources of fever (OM, viral URI, et cetera)

1.5-2% background prevalence of asymptomatic bacteruria in healthy afebrile controls

0.3% Rate of occult bactremia with healthy, well-appearing child who has a fever 2-24 months

0.3% of previously well children aged 3-36 months who have a fever without a source will develop significant sequelae, 0.03% will develop sepsis or meningitis

=== Concomitant RSV infection ===

In RSV+ (by PCR) neonates aged 0-28 days, 6.1% had UTIs and 3.7% were bactremic; there was no difference in rates of SBI between RSV+ and RSV- neonates in a large prospective multicenter study entailing 1,248 children

RSV+ infants aged 29-60 days, the SBI rate was 5.5%, all of which were UTIs

== See Also ==

*[[UTI (Peds)]]
*[[Sepsis (Peds)]]
*[[Meningitis (Peds)]]
*[[Febrile Seizure]]

== External Links ==

1.PEM ED Podcast and easy-to-follow diagnostic/treatment flow chart
http://www.pemed.org/blog/2011/10/9/fever-of-unknown-source-part-1.html

== Source ==
*Tintinalli
*Clinical Policy for Children Younger Than Three Years Presenting to the Emergency Department With Fever. Annuals of Emergency Medicine 2003 42. 530-545
*Risk of Serious Bacterial Infection in Young Febrile Infants With Respiratory Syncytial Virus Infections. Levine et all. PEDIATRICS Vol. 113 No. 6 June 1, 2004 pp. 1728 -1734

[[Category:Peds]]

Pediatric fever of uncertain source

2013-09-25T13:45:22Z

Peterdmorris: RSV+ infants

Pediatric fever of uncertain source

2013-09-25T13:44:38Z

Peterdmorris: /* Facts and Figures from ACEP's Clinical Policy on Pediatric Fevers */

== From Tintinalli ==

- '''Management of patients who are well-appearing, vaccinated, and no clinical source of fever'''

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| Age Group
| Evaluation
| Treatment
|-
|
0-28d, ≥38C

SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

|
CBC, blood Cx

UA, Ucx

CSF cell count, GS, Cx

CXR (only if resp sx)

Stool testing (if diarrhea present)

|
Admit

Ampicillin 50mg/kg + (cefotaxime 50mg/kg or gentamicin 2.5mg/kg)

|-
|
29-56d, ≥ 38.2 (100.8) (Philadelphia Protocol)

 SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

 

| Same as for neonates
|
Discharge if:

1. WBC <15K but >5K and <20% bands

2. UA negative

Admit and perform LP if above are not met

Treat with CTX 50mg/kg (if CSF normal), 100mg/kg (if signs of meningitis)

|-
|
57d-6mo, ≥38

Non-UTI SBI incidence is estimated to be negligible

UTI is 3%–8% 

 

|
UA and Ucx alone

OR

treat 57-90d using Philadelphia Protocol

|
Discharge if negative

Treat UTI w/ cefixime 8mg/kg/d or cefpodoxime 10mg/kg/d divided into BID or cefdinir 14mg/kg/d x 7-10days as outpatient

Admit and tx with CTX if fail criteria for d/c

|-
|
57d-6mo, ≥39 (102.2)

SBI incidence is estimated <1%;

non-UTI SBI incidence is estimated to be negligible.

UTI is 3%–8%

|
UA and Ucx alone

OR

UA and Ucx + CBC + blood cx

|
:

Discharge if negative

Treat for UTI as above

If WBC>15K consider treatment with CTX 50 mg/kg IV/IM, and follow-up in 24hr

If WBC>20K consider CXR and CSF

|-
|
 6–36 mo

Non-UTI SBI incidence is <0.4% 

UTI in girls ≤8%

UTI in boys (<12 mo) ≤ 2%

Uncircumcised boys (1–2 y) remains 2%

|
UA and Ucx in:

(girls 6-24mo)

(circ 6-12mo)

(uncirc 6-24mo)

|
Discharge if negative

Treat for UTI as above as outpatient

|-
| >36mo
| No further w/u is routinely necessary
| 
|}

Note: Preemies - Count age by estimated postconception date (not by actual delivery date) for 1st 90d

== Harbor-UCLA Protocol ==
===Background===
*Medicine is an art as well as science, practice clinical judgment when using this guideline
*Preemies: Count age by estimated postconception date (not by actual delivery date) for 1st-90d
*If RSV+ or influenza+
**Low risk of bacterial illness
**Still some risk of concurrent UTI

=== 0-28dy ===

{| style="width: 497px; height: 45px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Child Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38'''
'''Toxic or Well'''

|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^
|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100-200 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| N/A
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs

=== 28dy-90dy ===

{| style="width: 491px; height: 505px" cellspacing="1" cellpadding="1" width="491" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38 + Toxic'''
|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^

|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| NA
|-
|
'''T>=38 + Well'''

'''(Option 1)'''

|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
#Ceftriaxone (50mg/kg IM/IV)
|
If W/U (+) admit

Outpatient^^^^

| If W/U negative, meets outpt
|-
|
'''T>=38 + Toxic'''

'''(Option 2)'''

|
#CBC
#Blood Cx
#UA, UCx
#CXR^

|
#None

For very well appearing 60-90 day olds (many would not use this option)

| Outpatient^^^^
|
|}

*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs
*^^^^Outpatient

=== 90dy-36mo ===

{| style="width: 497px; height: 124px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=39 + Toxic'''
|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
Ceftriaxone (50-100mg/kg)

OR

Cefotaxime (50-100mg/kg)

AND

Consider Vanco (15mg/kg)^^^^

| Admit
| N/A
|-
|
'''T>=39^^^^^ + Well + Prevnar^^'''

|
#UA, UCx^^^
#CXR^

|
If + W/U, oral abx

| Outpatient
|
|-
|
'''T>=39^^^^^ + Well + NO Prevnar^^'''

|
#UA, UCx^^^
#CBC
#CXR^

|
Ceftriaxone 50mg/kg if >15 WBC (also then consider BCx and LP)

| Outpatient
|
|-
| '''T>=38-38.9 + Well'''
|
None

Consider UA, CXR based on sx, etc

|
None

| Outpatient
| Return if worsening sx or fever persists >72hrs
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Prevnar = has 3 Prevnar or >=4 wks post 2nd Prevnar dose
*^^^Urine workup for:
**Circumcised males <6 months
**Uncircumcised males <12 months
**All females
*^^^^Vancomycin if evidence of bacterial meningitis on CSF
*^^^^^>=39.5 for 24-36mo

===Work-Up Results===
*WBC: 5-15, ANC <10k, <1,500 bands
*UA: (-)Gm Stain, (-) leuks, (-) nitrite, <5-10 wbc/hpf
*CSF: <8wbc, (-) Gm Stain
*When diarrhea present, <5 wbc

If low-risk criteria below not met, LP (if not done) and admit for inpt abx

===Petechia===
#CBC
#BCx
#Ceftriaxone
#LP depending on clinical

===Facts and Figures from ACEP's Clinical Policy on Pediatric Fevers===
7% of patients < 2 years old with fever have PNA, however the etiology (viral/bacterial) or even the presence of pneumonia has low inter-observer reliability even among pediatric radiologists

4% Prevalence of UTI with common other sources of fever (OM, viral URI, et cetera)

1.5-2% background prevalence of asymptomatic bacteruria in healthy afebrile controls

0.3% Rate of occult bactremia with healthy, well-appearing child who has a fever 2-24 months

0.3% of previously well children aged 3-36 months who have a fever without a source will develop significant sequelae, 0.03% will develop sepsis or meningitis

=== Concomitant RSV infection ===

In RSV+ (by PCR) neonates aged 0-28 days, 6.1% had UTIs and 3.7% were bactremic; there was no difference in rates of SBI between RSV+ and RSV- neonates in a large prospective multicenter study entailing 1,248 children

RSV+ infants aged 29-60 days, the SBI rate was 5.5%, all of which were coming from UTIs

== See Also ==

*[[UTI (Peds)]]
*[[Sepsis (Peds)]]
*[[Meningitis (Peds)]]
*[[Febrile Seizure]]

== External Links ==

1.PEM ED Podcast and easy-to-follow diagnostic/treatment flow chart
http://www.pemed.org/blog/2011/10/9/fever-of-unknown-source-part-1.html

== Source ==
*Tintinalli
*Clinical Policy for Children Younger Than Three Years Presenting to the Emergency Department With Fever. Annuals of Emergency Medicine 2003 42. 530-545

[[Category:Peds]]

Sgarbossa's criteria

2013-09-25T13:17:27Z

Peterdmorris: emcrit

==Background==
*Assesses likelihood that pt w/ chest pain and baseline LBBB has myocardial damage (+CK-MB)
**Criteria also applies to LBBB due to paced rhythm
*Low Sn, High Sp
**Still consider PCI/t-PA for pts w/ LBBB and "good story" despite not meeting the criteria

==Criteria==
*ST elevation ≥1 mm in a lead with upward (concordant) QRS complex - 5 points
*ST depression ≥1 mm in lead V1, V2, or V3 - 3 points
*ST elevation ≥5 mm in a lead with downward (discordant) QRS complex - 2 points
*(See [[#Example | below]] for example of all 3 criteria)

*Smith's modification of the third rule of the Sgarbossa criteria to ST depression or elevation discordant with the QRS complex and with a magnitude of at least 25% of that of the QRS complex increases sensitivity from 52% to 91% at the expense of reducing specificity from 98% to 90%.

==Points==
*≥3 points = 98% probability of [[STEMI]]

==Example==
[[File:Sgarbossa.jpg]]

==See Also==
[[ST-Elevation Myocardial Infarction (STEMI)]]

==External Links==

1. http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/

2. http://emcrit.org/podcasts/left-bundle-branch-block/

==Source==
*Sgarbossa, American Heart Journal 2006
*Sgarbossa, NEJM, February, 1996

[[Category:Cards]]

Sgarbossa's criteria

2013-09-25T13:16:25Z

Peterdmorris: litfl

==Background==
*Assesses likelihood that pt w/ chest pain and baseline LBBB has myocardial damage (+CK-MB)
**Criteria also applies to LBBB due to paced rhythm
*Low Sn, High Sp
**Still consider PCI/t-PA for pts w/ LBBB and "good story" despite not meeting the criteria

==Criteria==
*ST elevation ≥1 mm in a lead with upward (concordant) QRS complex - 5 points
*ST depression ≥1 mm in lead V1, V2, or V3 - 3 points
*ST elevation ≥5 mm in a lead with downward (discordant) QRS complex - 2 points
*(See [[#Example | below]] for example of all 3 criteria)

*Smith's modification of the third rule of the Sgarbossa criteria to ST depression or elevation discordant with the QRS complex and with a magnitude of at least 25% of that of the QRS complex increases sensitivity from 52% to 91% at the expense of reducing specificity from 98% to 90%.

==Points==
*≥3 points = 98% probability of [[STEMI]]

==Example==
[[File:Sgarbossa.jpg]]

==See Also==
[[ST-Elevation Myocardial Infarction (STEMI)]]

==External Links==

1. http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/

==Source==
*Sgarbossa, American Heart Journal 2006
*Sgarbossa, NEJM, February, 1996

[[Category:Cards]]

Pediatric fever of uncertain source

2013-09-24T20:21:19Z

Peterdmorris:

== From Tintinalli ==

- '''Management of patients who are well-appearing, vaccinated, and no clinical source of fever'''

{| style="width: 500px" cellspacing="1" cellpadding="1" border="1"
|-
| Age Group
| Evaluation
| Treatment
|-
|
0-28d, ≥38C

SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

|
CBC, blood Cx

UA, Ucx

CSF cell count, GS, Cx

CXR (only if resp sx)

Stool testing (if diarrhea present)

|
Admit

Ampicillin 50mg/kg + (cefotaxime 50mg/kg or gentamicin 2.5mg/kg)

|-
|
29-56d, ≥ 38.2 (100.8) (Philadelphia Protocol)

 SBI incidence of ill appearing: 13%–21%

if not ill appearing: <5%

 

| Same as for neonates
|
Discharge if:

1. WBC <15K but >5K and <20% bands

2. UA negative

Admit and perform LP if above are not met

Treat with CTX 50mg/kg (if CSF normal), 100mg/kg (if signs of meningitis)

|-
|
57d-6mo, ≥38

Non-UTI SBI incidence is estimated to be negligible

UTI is 3%–8% 

 

|
UA and Ucx alone

OR

treat 57-90d using Philadelphia Protocol

|
Discharge if negative

Treat UTI w/ cefixime 8mg/kg/d or cefpodoxime 10mg/kg/d divided into BID or cefdinir 14mg/kg/d x 7-10days as outpatient

Admit and tx with CTX if fail criteria for d/c

|-
|
57d-6mo, ≥39 (102.2)

SBI incidence is estimated <1%;

non-UTI SBI incidence is estimated to be negligible.

UTI is 3%–8%

|
UA and Ucx alone

OR

UA and Ucx + CBC + blood cx

|
:

Discharge if negative

Treat for UTI as above

If WBC>15K consider treatment with CTX 50 mg/kg IV/IM, and follow-up in 24hr

If WBC>20K consider CXR and CSF

|-
|
 6–36 mo

Non-UTI SBI incidence is <0.4% 

UTI in girls ≤8%

UTI in boys (<12 mo) ≤ 2%

Uncircumcised boys (1–2 y) remains 2%

|
UA and Ucx in:

(girls 6-24mo)

(circ 6-12mo)

(uncirc 6-24mo)

|
Discharge if negative

Treat for UTI as above as outpatient

|-
| >36mo
| No further w/u is routinely necessary
| 
|}

Note: Preemies - Count age by estimated postconception date (not by actual delivery date) for 1st 90d

== Harbor-UCLA Protocol ==
===Background===
*Medicine is an art as well as science, practice clinical judgment when using this guideline
*Preemies: Count age by estimated postconception date (not by actual delivery date) for 1st-90d
*If RSV+ or influenza+
**Low risk of bacterial illness
**Still some risk of concurrent UTI

=== 0-28dy ===

{| style="width: 497px; height: 45px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Child Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38'''
'''Toxic or Well'''

|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^
|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100-200 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| N/A
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs

=== 28dy-90dy ===

{| style="width: 491px; height: 505px" cellspacing="1" cellpadding="1" width="491" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=38 + Toxic'''
|
#CBC
#Blood Cx
#UA, Ucx
#LP-CSF
#CXR^

|
#Cefotaxime^^ 50-100 mg/kg
#Ampicillin 100 mg/kg
#Acyclovir^^^ 20 mg/kg

| Admit
| NA
|-
|
'''T>=38 + Well'''

'''(Option 1)'''

|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
#Ceftriaxone (50mg/kg IM/IV)
|
If W/U (+) admit

Outpatient^^^^

| If W/U negative, meets outpt
|-
|
'''T>=38 + Toxic'''

'''(Option 2)'''

|
#CBC
#Blood Cx
#UA, UCx
#CXR^

|
#None

For very well appearing 60-90 day olds (many would not use this option)

| Outpatient^^^^
|
|}

*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Can use ceftriaxone 50-100 mg/kg, but concern for bilirubin displacement
*^^^Acyclovir if:
**HSV infection in baby or mother
**CSF pleocytoisis
**Concerning skin lesions
**Seizures
**Abnl LFTs
*^^^^Outpatient

=== 90dy-36mo ===

{| style="width: 497px; height: 124px" cellspacing="1" cellpadding="1" width="497" border="1"
|-
| '''Appearance'''
| '''Work Up'''
| '''Treatment'''
| '''Disposition'''
| '''Follow Up'''
|-
| '''T>=39 + Toxic'''
|
#CBC
#Blood Cx
#UA, UCx
#LP-CSF
#CXR^

|
Ceftriaxone (50-100mg/kg)

OR

Cefotaxime (50-100mg/kg)

AND

Consider Vanco (15mg/kg)^^^^

| Admit
| N/A
|-
|
'''T>=39^^^^^ + Well + Prevnar^^'''

|
#UA, UCx^^^
#CXR^

|
If + W/U, oral abx

| Outpatient
|
|-
|
'''T>=39^^^^^ + Well + NO Prevnar^^'''

|
#UA, UCx^^^
#CBC
#CXR^

|
Ceftriaxone 50mg/kg if >15 WBC (also then consider BCx and LP)

| Outpatient
|
|-
| '''T>=38-38.9 + Well'''
|
None

Consider UA, CXR based on sx, etc

|
None

| Outpatient
| Return if worsening sx or fever persists >72hrs
|}
*^CXR for (use clinical judgment):
**Resp symptoms
**Fever >48 hrs
**Tachypnea
**Decreased SaO2
*^^Prevnar = has 3 Prevnar or >=4 wks post 2nd Prevnar dose
*^^^Urine workup for:
**Circumcised males <6 months
**Uncircumcised males <12 months
**All females
*^^^^Vancomycin if evidence of bacterial meningitis on CSF
*^^^^^>=39.5 for 24-36mo

===Work-Up Results===
*WBC: 5-15, ANC <10k, <1,500 bands
*UA: (-)Gm Stain, (-) leuks, (-) nitrite, <5-10 wbc/hpf
*CSF: <8wbc, (-) Gm Stain
*When diarrhea present, <5 wbc

If low-risk criteria below not met, LP (if not done) and admit for inpt abx

===Petechia===
#CBC
#BCx
#Ceftriaxone
#LP depending on clinical

===Facts and Figures from ACEP's Clinical Policy on Pediatric Fevers===
7% of patients < 2 years old with fever have PNA, however the etiology (viral/bacterial) or even the presence of PNA has low inter-observer reliability among pediatric radiologists

4% Prevalence of UTI with common other sources of fever (OM, viral URI, et cetera)

1.5-2% background prevalence of asymptomatic bacteruria in healthy afebrile controls

0.3% Rate of occult bactremia with healthy, well-appearing child who has a fever 2-24 months

0.3% of previously well children aged 3-36 months who have a fever without a source will develop significant sequelae

0.03% will develop sepsis or meningitis

== See Also ==

*[[UTI (Peds)]]
*[[Sepsis (Peds)]]
*[[Meningitis (Peds)]]
*[[Febrile Seizure]]

== External Links ==

1.PEM ED Podcast and easy-to-follow diagnostic/treatment flow chart
http://www.pemed.org/blog/2011/10/9/fever-of-unknown-source-part-1.html

== Source ==
*Tintinalli
*Clinical Policy for Children Younger Than Three Years Presenting to the Emergency Department With Fever. Annuals of Emergency Medicine 2003 42. 530-545

[[Category:Peds]]