wikidoc - Recent changes [en]

Deep vein thrombosis CT

2012-05-17T04:31:54Z

Template:Deep vein thrombosis

2012-05-17T04:20:28Z

Deep vein thrombosis venography

2012-05-17T04:16:45Z

Created page with "'''Editors-in-Chief:''' C. Michael Gibson, M.S., M.D. '''Associate Editor-In-Chief''': Ujjwal Rastogi, MBBS[mailto:urastogi@perfuse.org]; [[User:K..."

New page

'''Editors-in-Chief:''' [[C. Michael Gibson, M.S., M.D.]] '''Associate Editor-In-Chief''': [[User:Ujjwal Rastogi|Ujjwal Rastogi, MBBS]][mailto:urastogi@perfuse.org]; [[User:Kashish Goel|Kashish Goel, M.D.]]
{{Deep vein thrombosis}}
==Overview==
Venography is the "[[gold standard]]" to diagnose venous thrombosis, however it is not the preferred test in clinical settings. It includes injection of contrast into the dorsal foot vein and checking for a intraluminal filling defect that is present in more than one view. It has gone out of favor and is unsuitable for clinical practice because of the following reasons:

* Invasive procedure
* Expensive
* Not available widely
* Large intra-observer and inter-observer variation
* Side effects of [[contrast]] administration including severe allergy, nephrotoxicity, [[nausea]], [[dizziness]], etc
* Upto 20% tests are inadequate for assessment
* Post-venography [[DVT]] (0-2%)

==References==
{{reflist|2}}

[[Category:Hematology]]
[[Category:Pulmonology]]
[[Category:Cardiology]]
[[Category:Emergency medicine]]
[[Category:Mature chapter]]

{{WH}}
{{WS}}

Deep vein thrombosis

2012-05-17T04:05:30Z

Diagnosis

Deep vein thrombosis physical examination

2012-05-17T03:24:17Z

Deep vein thrombosis laboratory tests

2012-05-17T03:14:17Z

Neurocardiogenic syncope

2012-05-17T02:42:12Z

Diagnosis

Postural orthostatic tachycardia syndrome

2012-05-17T02:35:29Z

Template:Neurocardiogenic syncope

2012-05-17T02:24:18Z

Neurocardiogenic syncope

2012-05-17T02:22:01Z

Neurocardiogenic syncope pathophysiology

2012-05-17T02:14:44Z

Neurocardiogenic Syncope pacemaker therapy

2012-05-17T02:14:01Z

moved [[Neurocardiogenic Syncope pacemaker therapy]] to [[Neurocardiogenic syncope pacemaker therapy]]

Neurocardiogenic syncope medical treatment

2012-05-17T02:13:50Z

Neurocardiogenic Syncope medical treatment

2012-05-17T02:10:55Z

moved [[Neurocardiogenic Syncope medical treatment]] to [[Neurocardiogenic syncope medical treatment]]

Neurocardiogenic syncope physical examination

2012-05-17T02:10:35Z

Neurocardiogenic Syncope physical examination

2012-05-17T02:10:14Z

moved [[Neurocardiogenic Syncope physical examination]] to [[Neurocardiogenic syncope physical examination]]

Neurocardiogenic syncope symptoms

2012-05-17T02:09:58Z

Recovery Phase

Neurocardiogenic Syncope symptoms

2012-05-17T02:09:35Z

moved [[Neurocardiogenic Syncope symptoms]] to [[Neurocardiogenic syncope symptoms]]

Neurocardiogenic syncope differentiating from other diseases

2012-05-17T02:09:18Z

Neurocardiogenic Syncope differentiating from other diseases

2012-05-17T02:08:53Z

moved [[Neurocardiogenic Syncope differentiating from other diseases]] to [[Neurocardiogenic syncope differentiating from other diseases]]

Neurocardiogenic syncope epidemiology and demographics

2012-05-17T02:08:36Z

Neurocardiogenic Syncope epidemiology and demographics

2012-05-17T02:07:47Z

moved [[Neurocardiogenic Syncope epidemiology and demographics]] to [[Neurocardiogenic syncope epidemiology and demographics]]

Neurocardiogenic Syncope pathophysiology

2012-05-17T02:07:02Z

moved [[Neurocardiogenic Syncope pathophysiology]] to [[Neurocardiogenic syncope pathophysiology]]

Neurocardiogenic Syncope epidemiology and demographics

2012-05-17T00:37:00Z

Created page with "{{SI}} {{CMG}} ==Overview== Neurocardiogenic syncope is the most common cause of syncope in children and adults. ==Incidence== The prevalence is 22% in the general populatio..."

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{{SI}}
{{CMG}}

==Overview==
Neurocardiogenic syncope is the most common cause of syncope in children and adults.

==Incidence==
The prevalence is 22% in the general population. Approximately 50%-66% of syncope cases are classified as due to vasovagal syncope.

Neurally mediated syncope

2012-05-17T00:32:22Z

Created page with "{{SI}} {{CMG}} This form of syncope occurs in the context of severe throat or facial pain as occurs in glossopharyngeal neuralgia or trigeminal neuralgia. ==Referenc..."

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{{SI}}
{{CMG}}

This form of syncope occurs in the context of severe throat or facial pain as occurs in [[glossopharyngeal neuralgia]] or [[trigeminal neuralgia]].

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Neurocardiogenic Syncope differentiating from other diseases

2012-05-17T00:31:36Z

Overview

Mediastinal widening

2012-05-17T00:25:20Z

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#redirect:[[Widened mediastinum]]

Wide mediastinum

2012-05-17T00:25:00Z

Wide mediastinum

2012-05-17T00:24:40Z

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#redirect:[[Widened mediastinum]]

Neurocardiogenic Syncope pacemaker therapy

2012-05-17T00:22:37Z

Neurocardiogenic Syncope pacemaker therapy

2012-05-17T00:21:20Z

Created page with " ==ACC / AHA Guidelines- Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT) <ref name="Epstein"> Epstein AE, DiMarco JP, Elle..."

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==ACC / AHA Guidelines- Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT) <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>==
{{cquote|
===Class I===
1. Permanent [[pacemaker|pacing]] is indicated for recurrent [[syncope]] caused by spontaneously occurring [[carotid sinus]] stimulation and [[carotid sinus]] pressure that induces [[ventricular asystole]] of more than 3 seconds. ''(Level of Evidence: C)''

===Class IIa===
1. Permanent [[pacemaker|pacing]] is reasonable for [[syncope]] without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. ''(Level of Evidence: C)''

===Class IIb===
1. Permanent [[pacemaker|pacing]] may be considered for significantly symptomatic neurocardiogenic [[syncope]] associated with [[bradycardia]] documented spontaneously or at the time of tilt-table testing. ''(Level of Evidence: B)''

===Class III===
1. Permanent [[pacemaker|pacing]] is not indicated for a hypersensitive cardioinhibitory response to [[carotid sinus]] stimulation without symptoms or with vague symptoms. ''(Level of Evidence: C)''

2. Permanent [[pacemaker|pacing]] is not indicated for situational vasovagal [[syncope]] in which avoidance behavior is effective and preferred. ''(Level of Evidence: C)''}}

==Sources==
* The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>

Neurocardiogenic syncope

2012-05-17T00:21:08Z

Neurocardiogenic Syncope medical treatment

2012-05-17T00:20:31Z

Created page with "{{Neurocardiogenic syncope}} {{CMG}} ==Treatment== *Infrequent episodes of vasovagal syncope that are preceded by a warning prodrome probably do not require any interventio..."

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{{Neurocardiogenic syncope}}
{{CMG}}

==Treatment==

*Infrequent episodes of vasovagal syncope that are preceded by a warning prodrome probably do not require any intervention besides counseling and observation. Attention to hydration and salt intake may suffice.
*Beta blockers are preferred as initial treatment but have not been demonstrated as effective in a RCT. The [[Prevention of Syncope Trial]] showed that metoprolol was overall ineffective in preventing syncope.
*In patients with borderline low blood pressure who may be subject to symptomatic orthostasis, fludrocortisone, midodrine, and compression hose are often used initially.
**Midodrine (ProAmantine 2.5-10 TID), an alpha agonist has been shown to be effective in several randomized controlled clinical trials. Side effects include nausea and supine hypertension.
**Fludrocortisone 0.1 mg/ Day, a mineralocorticoid that promotes renal reabsorption of sodium to cause increased blood volume has been used in the treatment of vasodepressor syncope in both children and adults. Caution is needed in elderly patients because they poorly tolerate the drug and there is a risk of hypertension, cardiac failure, and edema.
*Scopolamine, an anticholinergic agent, has central nervous system depressant effects and has been used successfully in some patients with syncope
*Selective serotonin reuptake inhibitors (Paxil 20mg/ Day) selectively block serotonin, which has been shown to induce vagally mediated bradycardia and blood pressure lowering.
*Pyridostigmine (Mestinon 60mg po BID), an acetylcholinesterase inhibitor which increases acetylcholine levels at the autonomic ganglia. It prevents a drop in blood pressure without causing supine hypertension. Demonstrated to be effective in POTS and orthostatic Hypotension. Can be used in conjuction with Midrodrine.
*In regards to pacing, in the '''VPS II Study''', 100 patients whoo were > 19 years of age who had a history of recurrent vasovagal syncope with 6 episodes of syncope ever or 3 episodes in the past 2 years, and a positive result on the head-up tilt table test (TTT) with a heart rate × blood pressure product < 6000/min × mm Hg were randomized to receive dual chamber pacing with rate drop. The results demonstrated that fewer patients in the DDD group than the ODO group had syncope during follow-up, but the difference did not reach statistical significance. Compared with ODO, the relative risk reduction in time to syncope with DDD was 30% (95% CI −33% to 63%). The number of pacemaker complications was similar between the DDD and ODO groups (10 vs 9 complications).

Neurocardiogenic syncope

2012-05-17T00:20:15Z

Template:Neurocardiogenic syncope

2012-05-17T00:19:15Z

Neurocardiogenic Syncope physical examination

2012-05-17T00:16:50Z

Neurocardiogenic Syncope physical examination

2012-05-17T00:16:25Z

Created page with "==Overview== The physical examination is unremarkable in 50% of patients."

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==Overview==
The physical examination is unremarkable in 50% of patients.

Neurocardiogenic syncope

2012-05-17T00:15:59Z

Physical Examination

Micturation syncope

2012-05-17T00:15:31Z

Created page with "{{SI}} {{CMG}} ==Overview== Micturation syncope is defined as a syncopal episode of fainting spell in the setting of micturation or urination. ==References== {{Reflist|2}} ..."

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{{SI}}
{{CMG}}

==Overview==
Micturation syncope is defined as a syncopal episode of fainting spell in the setting of micturation or urination.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Defecation syncope

2012-05-17T00:14:46Z

Created page with "{{SI}} {{CMG}} ==Overview== Defecation syncope is defined as a syncopal episode of fainting spell in the setting of defecating (bowel movement). ==References== {{Reflist|2}}..."

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{{SI}}
{{CMG}}

==Overview==
Defecation syncope is defined as a syncopal episode of fainting spell in the setting of defecating (bowel movement).

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Cough syncope

2012-05-17T00:13:31Z

Created page with "{{SI}} {{CMG}} ==Overview== Cough syncope is defined as a syncopal episode of fainting spell in the setting of a coughing paroxysm. ==References== {{Reflist|2}} {{WH}} {{WS}}"

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{{SI}}
{{CMG}}

==Overview==
Cough syncope is defined as a syncopal episode of fainting spell in the setting of a coughing paroxysm.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Neurocardiogenic Syncope differentiating from other diseases

2012-05-17T00:10:32Z

Neurocardiogenic Syncope differentiating from other diseases

2012-05-17T00:10:10Z

Created page with "{{Neurocardiogenic Syncope}} {{CMG}} ==Overview== Neurocardiogenic syncope must be distinguished from situational syncope (cough syncope, defecation syncope, [[mictur..."

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{{Neurocardiogenic Syncope}}
{{CMG}}

==Overview==
Neurocardiogenic syncope must be distinguished from situational syncope ([[cough syncope]], [[defecation syncope]], [[micturation syncope]] and [[carotid sinus hypersensitivity]].

==Situational Syncope==
The syncope comes on after [[cough syncope|cough]], [[defecation syncope]], [[micturation syncope]]

Assessment of the symptoms and setting may yield clues as to the possible cause of the syncope. Syncope after cough, defecation, and micturition suggests situational syncope; syncope associated with throat or facial pain (glossopharyngeal or trigeminal neuralgia) is indicative of neurally mediated syncope with neuralgia; and syncope after pain, fear, or noxious stimuli suggests neurocardiogenic syncope.4 Carotid sinus syncope may occur with rotation or turning of the head or pressure on the carotid sinus (for example, carotid massage, shaving, tight collars or neckwear, or tumour compression).4

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 '''Editors-in-Chief:''' [[C. Michael Gibson, M.S., M.D.]]  '''Associate Editor-In-Chief''': [[User:Ujjwal Rastogi|Ujjwal Rastogi, MBBS]] [mailto:urastogi@perfuse.org]
 {{Deep vein thrombosis}}
 ==Overview==
-More than 90% of all Pulmonary Embolism arise from thrombi within the large deep veins of the legs, typically the popliteal vein and the larger veins above it. Since Pulmonary embolism and deep vein thrombosis are different spectrum of the same disease, CT venography of the pelvis and lower extremities is often incorporated into the CT angiography PE protocol to identify or exclude concurrent deep venous thrombosis. <ref name="pmid15051664">{{cite journal| author=Kanne JP, Lalani TA| title=Role of computed tomography and magnetic resonance imaging for deep venous thrombosis and pulmonary embolism. | journal=Circulation | year= 2004 | volume= 109 | issue= 12 Suppl 1 | pages= I15-21 | pmid=15051664 | doi=10.1161/01.CIR.0000122871.86662.72 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15051664  }} </ref>
+Venous thrombosis in the proximal deep veins is responsible for more than 90% of the [[pulmonary embolism]]s. Some of the investigators have suggested combined use of CT PE protocol and CT scan venography in cases of suspected [[DVT]] and [[PE]].<ref name="pmid15051664">{{cite journal| author=Kanne JP, Lalani TA| title=Role of computed tomography and magnetic resonance imaging for deep venous thrombosis and pulmonary embolism. | journal=Circulation | year= 2004 | volume= 109 | issue= 12 Suppl 1 | pages= I15-21 | pmid=15051664 | doi=10.1161/01.CIR.0000122871.86662.72 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15051664  }} </ref> However, it is not done routinely in clinical settings because of certain limitations:
-A study had showen that CTPA positively diagnosed acute PE, in 14% to 44% patient having non-diagnostic V/Q scan and with normal lower extremity ultrasound imaging. <ref name="pmid9356628">{{cite journal| author=Ferretti GR, Bosson JL, Buffaz PD, Ayanian D, Pison C, Blanc F et al.| title=Acute pulmonary embolism: role of helical CT in 164 patients with intermediate probability at ventilation-perfusion scintigraphy and normal results at duplex US of the legs. | journal=Radiology | year= 1997 | volume= 205 | issue= 2 | pages= 453-8 | pmid=9356628 | doi= | pmc= | url= }} </ref> Another randomized control trial involving seventy patients with clinically suspected pulmonary embolism, showed that, compared to sonography, CT venography in addition to CT pulmonary angiography is a relatively accurate method for evaluation of femoropopliteal venous thrombosis.<ref name="pmid11000152">{{cite journal| author=Garg K, Kemp JL, Wojcik D, Hoehn S, Johnston RJ, Macey LC et al.| title=Thromboembolic disease: comparison of combined CT pulmonary angiography and venography with bilateral leg sonography in 70 patients. | journal=AJR Am J Roentgenol | year= 2000 | volume= 175 | issue= 4 | pages= 997-1001 | pmid=11000152 | doi= | pmc= | url= }} </ref>
+==Uses==
 ==References==

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+[[Deep vein thrombosis laboratory tests|D-dimer]]
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-[[Deep vein thrombosis CT|CT]]
+[[Deep vein thrombosis venography|Venography]]
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+!
 [http://blogsearch.google.com/blogsearch?q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}&ie=UTF-8&oe=utf-8&rls=org.mozilla:en-US:official&client=firefox-a&um=1&sa=N&tab=wb Blogs on {{PAGENAME}}]</small>
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+!

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 ==Diagnosis==
-[[Deep vein thrombosis diagnosis algorithm|Diagnosis Approach]] | [[Pretest probability of DVT|Pretest probability]] | [[Deep vein thrombosis history and symptoms|History & Symptoms]] | [[Deep vein thrombosis physical examination|Physical Examination]] | [[Deep vein thrombosis laboratory tests|Lab Tests]] | [[Deep vein thrombosis ultrasound|Ultrasound]] | [[Deep vein thrombosis CT|CT]] | [[Deep vein thrombosis MRI|MRI]] | [[Deep vein thrombosis other imaging findings|Other Imaging Findings]]
+[[Deep vein thrombosis diagnosis algorithm|Diagnosis Approach]] | [[Pretest probability of DVT|Pretest probability]] | [[Deep vein thrombosis history and symptoms|History & Symptoms]] | [[Deep vein thrombosis physical examination|Physical Examination]] | [[Deep vein thrombosis laboratory tests|D-dimer]] | [[Deep vein thrombosis ultrasound| Ultrasound]] | [[Deep vein thrombosis venography| Venography]] | [[Deep vein thrombosis CT|CT scan venography]] | [[Deep vein thrombosis MRI|MRI]] | [[Deep vein thrombosis other imaging findings|Other Imaging Findings]]
 ==[[Deep vein thrombosis treatment|Treatment]]==

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 {{Deep vein thrombosis}}
 ==Overview==
-The actual physical signs of venous thrombosis can be quite unreliable. There may be pain and tenderness in the thigh along the course of the major veins
+Physical exam may be completely normal in patients with [[DVT]]. A high degree of suspicion is necessary for early identification of venous thrombosis, as sometimes these patients are admitted with a different complaint and a thorough physical exam gives a clue to the diagnosis.
-==Appearance of the Patient==
+==Vitals==
 ==Extremities==
-Physical examination may reveal
+The most significant part of physical exam in a patient with suspected [[DVT]] is measurement of the size of both legs at same point (usually measured vertically from the knee joint), to assess for difference. If a difference is detected and there is suspicion of DVT, further tests should be conducted. It may also reveal:
-*Palpable cord (reflecting a thrombosed vein)
+* Palpable cord (reflecting a thrombosed vein)
-*Calf or thigh pain
+* Calf or thigh pain
-*Unilateral edema or swelling with a difference in calf diameters, warmth, tenderness and erythema.
+* Unilateral edema or swelling with a difference in calf diameters, warmth, tenderness and erythema.
-*Superficial venous dilation.
+* Superficial venous dilation.
-−
-===Screening for malignancy===
-Venous thromboembolism may be the first manifestation of an underlying malignancy. However, a detailed and routine search for an occult malignancy is neither mandatory nor cost effective.<ref name="pmid16954002">{{cite journal| author=Oudega R, Moons KG, Karel Nieuwenhuis H, van Nierop FL, Hoes AW| title=Deep vein thrombosis in primary care: possible malignancy? | journal=Br J Gen Pract | year= 2006 | volume= 56 | issue= 530 | pages= 693-6 | pmid=16954002 | doi= | pmc=PMC1876636 | url= }} </ref>
-−
-The following test should be considered:
-'''In Females'''
+'''[[Homans test]]''' is mainly of historical perspective. It is said to positive when passive dorsiflexion of the ankle (knee in flexed position) elicits sharp pain in the calf. However, the test has very poor positive or negative predictive value. Previous studies have shown that Homans test was present  only in 30% of the patients with positive [[DVT]].
-*Pelvic examinations to rule out any mass/malignancy.
 ==References==
 {{reflist|2}}

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 * [[renal function]] and [[electrolyte]]s
 * [[prostate specific antigen]] measurement in men over the age of 50.
-==Test==
-*[[Homan's test]]: is said to be present when passive dorsiflexion of the ankle by the examiner elicits sharp pain in the calf.. A '''positive Homans''' sign does not positively diagnose DVT (poor positive predictive value), and a'''negative Homans''' sign does not rule out the DVT diagnosis (poor negative predictive value).
-*Pratt's sign: Squeezing of posterior calf elicits pain
-However, these [[medical sign]]s do not perform well and are not included in [[clinical prediction rule]]s that combine best findings in order to diagnose DVT.<ref name="pmid16403932">{{cite journal| author=Wells PS, Owen C, Doucette S, Fergusson D, Tran H| title=Does this patient have deep vein thrombosis? | journal=JAMA | year= 2006 |volume= 295 | issue= 2 | pages= 199-207 | pmid=16403932 | doi=10.1001/jama.295.2.199 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16403932  }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16813372 Review in: ACP J Club. 2006 Jul-Aug;145(1):24]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213132 Review in: Evid Based Med. 2006 Aug;11(4):119] </ref>
 ==References==

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 ==Diagnosis==
-[[Neurocardiogenic syncope symptoms|History & Symptoms]] | [[Neurocardiogenic syncope physical examination|Physical Examination]] | [[Neurocardiogenic syncope electrocardiogram|Electrocardiogram]] | [[Neurocardiogenic syncope chest x-ray|Chest X-Ray]] | [[Neurocardiogenic syncope echocardiography|Echocardiography]] | [[Neurocardiogenic syncope cardiac catheterization|Cardiac Catheterization]]
+[[Neurocardiogenic syncope symptoms|History & Symptoms]] | [[Neurocardiogenic syncope physical examination|Physical Examination]] | [[Neurocardiogenic syncope electrocardiogram|Electrocardiogram]] | [[Neurocardiogenic syncope chest x-ray|Chest X-Ray]] | [[Tilt table test]] | [[Neurocardiogenic syncope echocardiography|Echocardiography]] | [[Neurocardiogenic syncope cardiac catheterization|Cardiac Catheterization]]
 ==Treatment==
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 ====[[Neurocardiogenic syncope pacemaker therapy|Pacemaker Therapy]]====
 ==Additional Resources==

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 }}
 {{SI}}
-{{CMG}}
+{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}
-'''Associate Editor-In-Chief:''' {{CZ}}
+'''''Synonyms and Keywords:''''' postural tachycardia syndrome, POTS
-{{EH}}
+==Overview==
 '''Postural orthostatic tachycardia syndrome''' is a condition of [[dysautonomia]], and more specifically, [[orthostatic intolerance]], in which a change from the [[supine position]] to an upright position causes an abnormally large increase in heart rate, called [[tachycardia]].  This is often, but not always, accompanied by a fall in blood pressure. Patients with POTS have problems maintaining homeostasis when changing position, i.e. moving from one chair to another or reaching above their heads. Many patients also experience symptoms when stationary or even while lying down. Symptoms present in various degrees of severity depending on the patient. POTS is a serious, though non-life threatening, medical condition that can be severely disabling and debilitating. Many patients are unable to attend school or work, and especially severe cases can completely incapacitate the patient.
-'''Postural orthostatic tachycardia syndrome''' (often referred to as just '''postural tachycardia syndrome''' or '''POTS''') is a condition of [[dysautonomia]], and more specifically, [[orthostatic intolerance]], in which a change from the [[supine position]] to an upright position causes an abnormally large increase in heart rate, called [[tachycardia]].  This is often, but not always, accompanied by a fall in blood pressure. Patients with POTS have problems maintaining homeostasis when changing position, i.e. moving from one chair to another or reaching above their heads. Many patients also experience symptoms when stationary or even while lying down. Symptoms present in various degrees of severity depending on the patient. POTS is a serious, though non-life threatening, medical condition that can be severely disabling and debilitating. Many patients are unable to attend school or work, and especially severe cases can completely incapacitate the patient.
 ==History==
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 *Newton et al: Symptoms of autonomic dysfunction in chronic fatigue syndrome. QJM 2007 Aug;100(8):519-26 Epub 2007 Jul 7
-==External links==
+==Resources==
 *[http://www.ndrf.org National Dysautonomia Research Foundation (NDRF)]
 *[http://www.dynakids.org Dysautonomia Youth Network of America, Inc.]
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 {{Electrocardiography}}
 {{Circulatory system pathology}}
 [[Category:Cardiology]]

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+!
-[[Neurocardiogenic Syncope symptoms|History & Symptoms]]
+[[Neurocardiogenic syncope symptoms|History & Symptoms]]
 |-
+!
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+!
-[[Neurocardiogenic Syncope physical examination|Physical Examination]]
+[[Neurocardiogenic syncope physical examination|Physical Examination]]
 |-
+!
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+!
-[[Neurocardiogenic Syncope electrocardiogram|Electrocardiogram]]
+[[Neurocardiogenic syncope electrocardiogram|Electrocardiogram]]
 |-
+!
@@ Line 88: / Line 88: @@
 |- bgcolor="LightSkyBlue"
+!
-[[Neurocardiogenic Syncope chest x-ray|Chest X-Ray]]
+[[Neurocardiogenic syncope chest x-ray|Chest X-Ray]]
 |-
+!
@@ Line 94: / Line 94: @@
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+!
-[[Neurocardiogenic Syncope echocardiography|Echocardiography]]
+[[Neurocardiogenic syncope echocardiography|Echocardiography]]
 |-
+!
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 |- bgcolor="LightSkyBlue"
+!
-[[Neurocardiogenic Syncope cardiac catheterization|Cardiac Catheterization]]
+[[Neurocardiogenic syncope cardiac catheterization|Cardiac Catheterization]]
 |-
+!
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 |- bgcolor="PaleTurquoise"
+!
-:[[Neurocardiogenic Syncope medical treatment|Pharmacotherapy]]
+|- bgcolor="PaleTurquoise"
-:[[Neurocardiogenic Syncope pacemaker therapy|Pacemaker therapy]]
 |-
+!

@@ Line 1: / Line 1: @@
 {{Neurocardiogenic syncope}}
 {{CMG}}
-==References==
+==[[Neurocardiogenic syncope overview|Overview]]==
-{{reflist|2}}
 # Neurocardiogenic syncope. Carol Chen-Scarabelli, Tiziano M Scarabelli. BMJ 2004;329:336–41
 # Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al for the Task Force on Syncope, European Society of Cardiology.Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J 2001;22:1256-306.
@@ Line 9: / Line 32: @@
 # Connolly SJ, Sheldon R, Thorpe KE, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope: Second Vasovagal Pacemaker Study (VPS II): a randomized trial. JAMA. 2003;289:2224-9.
-{{SIB}}
+[[Category:Disease]]
-−
 [[Category:Cardiology]]
 {{WikiDoc Help Menu}}
 {{WikiDoc Sources}}

← Older revision		Revision as of 02:14, 17 May 2012
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	==Overview==		==Overview==
	[[Neurocardiogenic Syncope]] is defined as a syndrome in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral [[vasodilation]]. It is caused by an abnormal or exaggerated autonomic response to various stimuli which results from excessive autonomic reflex activity, which shows as abnormal vascular tone and heart rate. In contrast, [[Orthostatic Hypotension]] is a failure of the autonomic reflex response.		[[Neurocardiogenic Syncope]] is defined as a syndrome in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral [[vasodilation]]. It is caused by an abnormal or exaggerated autonomic response to various stimuli which results from excessive autonomic reflex activity, which shows as abnormal vascular tone and heart rate. In contrast, [[Orthostatic Hypotension]] is a failure of the autonomic reflex response.
		+
		+	==References==
		+	{{reflist\|2}}
		+
		+	[[Category:Cardiology]]
		+
		+	{{WH}}
		+	{{WS}}

← Older revision		Revision as of 02:10, 17 May 2012
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	==Overview==		==Overview==
	The physical examination is unremarkable in 50% of patients.		The physical examination is unremarkable in 50% of patients.
		+
		+	==References==
		+	{{reflist\|2}}
		+
		+	[[Category:Cardiology]]
		+
		+	{{WikiDoc Help Menu}}
		+	{{WikiDoc Sources}}

← Older revision		Revision as of 02:09, 17 May 2012
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	==Recovery Phase==		==Recovery Phase==
	* “Washed out” and [[tired feeling]]		* “Washed out” and [[tired feeling]]
		+
		+	==References==
		+	{{reflist\|2}}
		+
		+	[[Category:Cardiology]]
		+
		+	{{WikiDoc Help Menu}}
		+	{{WikiDoc Sources}}

@@ Line 1: / Line 1: @@
 {{Neurocardiogenic syncope}}
 {{CMG}}
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 ==Carotid Sinus Syncope==
 Carotid sinus syncope may occur with rotation or turning of the head or pressure on the carotid sinus (for example, carotid massage, shaving, tight collars or neckwear, or tumour compression).

@@ Line 1: / Line 1: @@
-{{SI}}
+{{Neurocardiogenic syncope}}
 {{CMG}}
@@ Line 7: / Line 7: @@
 ==Incidence==
 The prevalence is 22% in the general population. Approximately 50%-66% of syncope cases are classified as due to vasovagal syncope.

@@ Line 1: / Line 1: @@
 {{Neurocardiogenic syncope}}
 {{CMG}}
 ==Overview==
-Neurocardiogenic syncope must be distinguished from situational syncope ([[cough syncope]], [[defecation syncope]], [[micturation syncope]] and [[carotid sinus hypersensitivity]].
+Neurocardiogenic syncope must be distinguished from situational syncope ([[cough syncope]], [[defecation syncope]], [[micturation syncope]], [[neurally mediated syncope]] and [[carotid sinus hypersensitivity]].
 ==Situational Syncope==
-The syncope comes on after [[cough syncope|cough]], [[defecation syncope]], [[micturation syncope]]
+The syncope comes on after [[cough syncope|cough]], [[defecation syncope|defecation]], or [[micturation syncope|micturation]]
-Assessment of the symptoms and setting may yield clues as to the possible cause of the syncope. Syncope after cough, defecation, and micturition suggests situational syncope; syncope associated with throat or facial pain (glossopharyngeal or trigeminal neuralgia) is indicative of neurally mediated syncope with neuralgia; and syncope after pain, fear, or noxious stimuli suggests neurocardiogenic syncope.4 Carotid sinus syncope may occur with rotation or turning of the head or pressure on the carotid sinus (for example, carotid massage, shaving, tight collars or neckwear, or tumour compression).4
+==Neurally Mediated Syncope==

← Older revision		Revision as of 00:25, 17 May 2012
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−
−
	#redirect:[[Widened mediastinum]]		#redirect:[[Widened mediastinum]]

@@ Line 1: / Line 1: @@
 ==ACC / AHA Guidelines- Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT) <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>==
@@ Line 18: / Line 20: @@
 ==Sources==
 * The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>

@@ Line 112: / Line 112: @@
 |- bgcolor="PaleTurquoise"
+!
-Acute Neurocardiogenic Syncope:
 :[[Neurocardiogenic Syncope medical treatment|Pharmacotherapy]]
-:[[Neurocardiogenic Syncope surgical treatment|Surgery]]
+:[[Neurocardiogenic Syncope pacemaker therapy|Pacemaker therapy]]
-|-
-−
-−
-|- bgcolor="PaleTurquoise"
-−
-Chronic Neurocardiogenic Syncope:
-:[[Neurocardiogenic Syncope medical therapy|Pharmacotherapy]]
-:[[Neurocardiogenic Syncope surgery indications|Surgical indications]]
-:[[Neurocardiogenic Syncope surgical therapy|Surgical procedure]]
-|-
-−
-−
-|- bgcolor="PaleTurquoise"
-−
-[[Neurocardiogenic Syncope precautions|Precautions and Prophylaxis]]
-|-
-−
-−
-|- bgcolor="PaleTurquoise"
-−
-Special Scenarios:
-:[[Neurocardiogenic Syncope in pregnancy|Pregnancy]]
-:[[Neurocardiogenic Syncope in elderly|Elderly]]
-:[[Neurocardiogenic Syncope in young patients|Young Adults]]
-:[[Neurocardiogenic Syncope in renal disease|End-stage Renal Disease]]
 |-
+!

← Older revision		Revision as of 00:16, 17 May 2012
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		+	{{Neurocardiogenic syncope}}
		+	{{CMG}}
		+
	==Overview==		==Overview==
	The physical examination is unremarkable in 50% of patients.		The physical examination is unremarkable in 50% of patients.

← Older revision		Revision as of 00:15, 17 May 2012
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	{{CMG}}		{{CMG}}

−
−	~~===Physical Examination===~~
−	~~THe physical examination is unremarkable in 50% of patients.~~

	==Treatment==		==Treatment==

← Older revision		Revision as of 00:10, 17 May 2012
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−	{{Neurocardiogenic ~~Syncope~~}}	+	{{Neurocardiogenic syncope}}
	{{CMG}}		{{CMG}}