Jump to content

Distributive shock: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
→‎Examples: Grammar change
bold rewrite
Line 1: Line 1:
'''Distributive shock''' is a [[Medicine|medical]] condition in which abnormal distribution of [[blood flow]] in the [[Microvessel|smallest blood vessels]] results in inadequate supply of blood to the body's [[Tissue (biology)|tissues]] and [[Organ (anatomy)|organs]].<ref name= "Kanaparthi 2013">{{citation |last1= Kanaparthi |first1= Lalit K. |last2= Klaus-Dieter |first2= Lessnau |first3= Ruben |last3= Peralta |editor1-first= Michael R. |editor1-last= Pinsky |title= Distributive Shock: Overview: Background |work= Medscape Reference |publisher= [[Medscape]] |date= 12 February 2013 |url= http://emedicine.medscape.com/article/168689 |registration= yes |accessdate= 2014-04-28 |postscript= . |ref= {{SfnRef|Kanaparthi et al.|2013}}}}</ref><ref name= "Elbers 2006">{{cite journal |first1= Paul W.G. |last1= Elbers |first2= Can |last2= Ince |title= Mechanisms of critical illness--classifying microcirculatory flow abnormalities in distributive shock |journal= [[Critical Care (journal)|Critical Care]] |date= 19 July 2006 |volume= 10 |issue= 4 |page= 221 |doi= 10.1186/cc4969 |pmid= 16879732 |pmc= 1750971 |url= http://ccforum.com/content/10/4/221 |ref= {{SfnRef|Elbers & Ince|2006}}}}</ref> It is one of four categories of '''[[Shock (circulatory)|shock]]''', a condition where there is not enough [[oxygen]] carrying blood to meet the [[Metabolism|metabolic]] needs of the [[Cell (biology)|cells]] which make up the body's tissues and organs.<ref name= "Elbers 2006"/> Distributive shock is different from the other three categories of shock in that it occurs even though the the [[Cardiac output|output of the heart]] is at or above a normal level.<ref name= "Elbers 2006"/> The most common cause is [[sepsis]] leading to type of distributive shock called [[septic shock]] a condition that can be fatal.<ref name= "Kanaparthi 2013"/>
'''Distributive shock''' is defined by hypotension and generalized tissular [[Hypoxia (medical)|hypoxia]]. This form of relative [[hypovolemia]] is the result of [[blood vessel]] [[vasodilation|dilation]].<ref name="urlShock: Heart and Blood Vessel Disorders: Merck Manual Home Edition">{{cite web |url=http://www.merck.com/mmhe/sec03/ch024/ch024a.html |title=Shock: Heart and Blood Vessel Disorders: Merck Manual Home Edition |work= |accessdate=}}</ref> [[Septic shock]] is the major cause,<ref name=Kumar>{{cite book |author=Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson |title=Robbins Basic Pathology: With STUDENT CONSULT Online Access |publisher=Saunders |location=Philadelphia |year= |pages= |chapter=Chapter 4 |edition=8th |isbn=1-4160-2973-7 |oclc= |doi=}}</ref> but there are other examples as well.


==Examples==
==Causes==
In addition to sepsis, distributive shock can be caused by [[systemic inflammatory response syndrome]] (SIRS) due to conditions other than [[infection]] such as [[pancreatitis]], burns or [[Injury|trauma]].{{sfn|Kanaparthi et al.|2013|loc= Overview: Etiology}} Other causes include, [[toxic shock syndrome]] (TSS), [[anaphylaxis]] (a sudden, severe allergic reaction), [[adrenal insufficiency]], reactions to [[Pharmaceutical drug|drugs]] or [[toxin]]s, [[Heavy metal (chemistry)|heavy metal]] poisoning, hepatic ([[liver]]) insufficiency and damage to the [[central nervous system]].{{sfn|Kanaparthi et al.|2013|loc= Overview: Etiology}} Causes of adrenal insufficiency leading to distributive shock include acute worsening of chronic adrenal insufficiency, destruction or removal of the adrenal glands, suppression of adrenal gland function due to exogenous steroids, hypopituitarism and metabolic failure of hormone production.{{sfn|Kanaparthi et al.|2013|loc= Overview: Etiology}}
Examples of this form of shock are:
*'''[[Septic shock]]''' - This is caused by an overwhelming infection leading to [[vasodilation]], such as by [[Gram negative]] bacteria i.e. ''[[Escherichia coli]]'' which releases an [[endotoxin]] which produces adverse biochemical, [[immunological]] and occasionally neural mechanisms which are harmful to the body. Although tissues are being hyperperfused due to the massive vasodilation, the hypotensive state of the individual, paired with the massive inflammation found in septic shock, causes a reduction in tissular oxygen extraction (tissular hypoxia). As a result [[SvO<sub>2</sub>]] levels are very high.


Septic shock is treated by [[antibiotics]], fluid replacement, and [[vasoconstrictor]]s.
*'''[[Anaphylactic shock]]''' - Caused by a severe [[anaphylaxis|anaphylactic reaction]] to an [[allergen]], [[antigen]], [[drug]] or foreign protein causing the release of [[histamine]] which causes widespread vasodilation. Leading to hypotension and increase capillary permeability.
*Acute '''[[adrenal insufficiency]]''' is frequently the result of discontinuing [[corticosteroid]] treatment without tapering the dosage.
*'''[[Neurogenic shock]]''' - Caused by any traumatic injuries with immense pain. [[Bradycardia]] may be present.


== References ==
==Pathophysiology==
The cause of inadequate tissue [[perfusion]] (blood delivery to tissues) in distributive shock is a lack of normal responsiveness of [[blood vessel]]s to [[Vasoconstriction|vasoconstrictive]] agents and direct [[vasodilation]].{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}}

There are four types of distributive shock. The most common, '''[[septic shock]]''', is caused by an infection, most frequently by [[bacteria]], but [[virus]]es, [[Fungus|fungi]] and [[parasite]]s have been implicated.{{sfn|Kanaparthi et al.|2013|loc= Overview: Etiology}} Infection sites most likely to lead to septic shock are chest, [[abdomen]] and [[Genitourinary system|genitourinary tract]].{{sfn|Kanaparthi et al.|2013|loc= Overview: Etiology}} In septic shock the blood flow in the microvasculature is abnormal with some [[Capillary|capillaries]] under perfused and others with normal to high blood flow.<ref name= "Ince 2005">{{cite journal |last= Ince |first= Can |date= 25 August 2005 |title= The microcirculation is the motor of sepsis |url= http://ccforum.com/content/9/S4/S13 |journal= [[Critical Care (journal)|Critical Care]] |volume= 4 |issue= Supp 4 |pages= S13-9 |doi= 10.1186/cc3753 |pmid= 16168069 |pmc= 3226164}}</ref> The [[Endothelium|endothelial]] cells lining the blood vessels become less responsive to vasocontrictive agents, lose their [[glycocalyx]] (normal coating) and negative [[ion]]ic charge, become leaky and cause extensive over-expression of [[nitric oxide]].<ref name= "Elbers 2006"/> The [[coagulation]] cascade is also disrupted.{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}} [[Tissue factor]] that iniates the clotting cascade is produced by activated [[monocyte]]s and the endothelial cells lining the blood vessels while [[antithrombin]] and [[fibrinolysis]] are impaired.{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}} [[Disseminated intravascular coagulation]] (DIC) can result from the [[thrombin]] produced in the [[Inflammation|inflammatory]] response.{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}} The ability of red blood cells to [[Erythrocyte deformability|change shape]] decreases and their tendency to [[Erythrocyte aggregation|clump together]] increases, inhibiting their flow through the microvasculature.<ref name= "Ince 2005"/>

In '''[[Anaphylaxis#Diagnosis|anaphylactic shock]]''' low blood pressure is related to decreased [[vascular resistance|systemic vascular resisitance]] (SVR) triggered primarily by a massive release of histamine by mast cells activated by by [[antigen]]-bound [[immunoglobulin E]] and also by increased production and release of [[prostaglandin]]s.{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}}

'''[[Neurogenic shock]]''' is caused by the loss of vascular [[Muscle tone|tone]] normally supported by the [[sympathetic nervous system]] due to injury to the central nervous system especially [[spinal cord injury]].{{sfn|Kanaparthi et al.|2013|loc= Overview: Pathophysiology}}<ref name= "Weaver 2012">{{cite book |last1= Weaver |first1= Lynne C. |last2= Fleming |first2= Jennifer C. |last3= Mathias |first3= Christopher J. |last4= Krassioukov |first4= Andrie V. |year= 2012 |chapter= Ch. 13: Disordered Cardiovascular Control After Spinal Cord Injury |title= Handbook of Clinical Neurology |volume= 109 |pages= 213-33 |doi= 10.1016/B978-0-444-52137-8.00013-9 |pmid= 23098715 |editor1-first= Joost |editor1-last= Verhaagen |editor2-first= John W. |editor2-last= McDonald |isbn= 9780444521378}}</ref>

Distributive shock associated with '''[[adrenal crisis]]''' results from inadequate steroid hormones.

==Forms==
Elbers and Ince have identified five classes of abnormal microcirculatory flow in distributive shock using side stream [[dark field microscopy]].
*Class I: all capillaries are stagnant when there is normal or sluggish venular flow.
*Class II: there are empty capillaries next to capillaries that have flowing red blood cells.
*Class III: there stagnant capillaries next to capillaries with normal blood flow.
*Class IV: hyperdynamic flow in capillaries adjacent to capillaries that are stagnant.
*Class V: widespread hyperdynamic flow in the microcirculatory system.<ref name= "Elbers 2006"/>

==Treatment==
The main goals of treatment in distributive shock are to reverse the underlying cause and achieive [[Hemodynamics|hemodynamic]] stabilization.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Approach Considerations}} Immediate treatement involves [[Fluid replacement|fluid resuscitation]] and the use of [[vasoactive]] drugs, both [[Vasoconstriction|vasopressors]] and [[inotrope]]s.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Resuscitation}} Hydrocortisone is used for patients whose hypotension does not respond to fluid resuscitation and vasopressors.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Corticosteroids}} Opening and keeping open the microcirculation is a consideration in the treatment of distributive shock, as a result limiting the use of vasopressors has been suggested.<ref name= "Elbers 2006"/> Control of inflammation, vascular function and coagulation to correct pathological differences in blood flow and microvascular shunting has been pointed to as a potentially important adjunct goal in the treatment of distributive shock.<ref name= "Elbers 2006"/>

Patients with septic shock are treated with [[antimicrobial]] drugs to treat the causative infection.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Antimicrobial Treatment}} Some sources of infection require surgical intervention including [[necrotizing fasciitis]], [[Ascending cholangitis|cholangitis]], [[abscess]], [[Mesenteric ischemia|intestinal ischemia]], or infected [[medical device]]s.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Surgical Control of Shock Sources}}

Anaphylactic shock is treated with [[epinephrine]].{{sfn|Kanaparthi et al.|2013|loc= Treatment: Treatment of Anaphylaxis}}

==Prognosis==
Septic shock is associated with significant mortality and is the leading non cardiac cause of death in [[intensive care unit]]s (ICU's).<ref name= "Kanaparthi 2013"/>

==Research Directions==
The choice of fluids for resuscitation remains an area of research, the [[Surviving Sepsis Campaign]] an international consortium of experts, did not find adequate evidence to support the superiority [[Volume expander#Crystalloids|crystalloid]] fluids versus [[Volume expander#Colloids|colloid]] fluids.{{sfn|Kanaparthi et al.|2013|loc= Treatment: Resuscitation}} Drugs such as, pyridoxalated hemoglobin polyoxyethylene, which scavenge nitric oxide from the blood have been investigated.<ref name= "Kinasewitz 2008">{{cite journal |last1= Kinasewitz |first1= Gary T. |last2= Privalle |first2= Christopher T. |last3= Imm |first3= Amy |last4= Steingrub |first4= Jay S. |last5= Malcynski |first5= John T. |last6= Balk |first6= Robert A. |last7= DeAngelo |first7= Joseph |displayauthors= 4 |date= July 2008 |title= Multicenter, randomized, placebo-controlled study of the nitric oxide scavenger pyridoxalated hemoglobin polyoxyethylene in distributive shock |journal= [[Critical Care Medicine]] |volume= 36 |issue= 7 |pages= 1999-2007 |doi= 10.1097/CCM.0b013e31817bfe84 |pmid= 18552688}}</ref> As well as methylene blue which may inhibit the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway which has been suggested to play a significant role in distributive shock.<ref name= "Jang 2013">{{cite journal |last1= Jang |first1= D.H. |last2= Nelson |first2= L.S. |last3= Hoffman |first3= R.S. |date= September 2013 |title= Methylene blue for distributive shock: A potential new use of an old antidote |journal= [[Journal of Medical Toxicology]] |volume= 9 |issue=3 |pages= 242-9 |pmid= 23580172 |pmc= 3770994 |doi= 10.1007/s13181-013-0298-7}}</ref>

==References==
{{reflist}}
{{reflist}}


Revision as of 02:35, 9 May 2014

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs.[1][2] It is one of four categories of shock, a condition where there is not enough oxygen carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs.[2] Distributive shock is different from the other three categories of shock in that it occurs even though the the output of the heart is at or above a normal level.[2] The most common cause is sepsis leading to type of distributive shock called septic shock a condition that can be fatal.[1]

Causes

In addition to sepsis, distributive shock can be caused by systemic inflammatory response syndrome (SIRS) due to conditions other than infection such as pancreatitis, burns or trauma.[3] Other causes include, toxic shock syndrome (TSS), anaphylaxis (a sudden, severe allergic reaction), adrenal insufficiency, reactions to drugs or toxins, heavy metal poisoning, hepatic (liver) insufficiency and damage to the central nervous system.[3] Causes of adrenal insufficiency leading to distributive shock include acute worsening of chronic adrenal insufficiency, destruction or removal of the adrenal glands, suppression of adrenal gland function due to exogenous steroids, hypopituitarism and metabolic failure of hormone production.[3]


Pathophysiology

The cause of inadequate tissue perfusion (blood delivery to tissues) in distributive shock is a lack of normal responsiveness of blood vessels to vasoconstrictive agents and direct vasodilation.[4]

There are four types of distributive shock. The most common, septic shock, is caused by an infection, most frequently by bacteria, but viruses, fungi and parasites have been implicated.[3] Infection sites most likely to lead to septic shock are chest, abdomen and genitourinary tract.[3] In septic shock the blood flow in the microvasculature is abnormal with some capillaries under perfused and others with normal to high blood flow.[5] The endothelial cells lining the blood vessels become less responsive to vasocontrictive agents, lose their glycocalyx (normal coating) and negative ionic charge, become leaky and cause extensive over-expression of nitric oxide.[2] The coagulation cascade is also disrupted.[4] Tissue factor that iniates the clotting cascade is produced by activated monocytes and the endothelial cells lining the blood vessels while antithrombin and fibrinolysis are impaired.[4] Disseminated intravascular coagulation (DIC) can result from the thrombin produced in the inflammatory response.[4] The ability of red blood cells to change shape decreases and their tendency to clump together increases, inhibiting their flow through the microvasculature.[5]

In anaphylactic shock low blood pressure is related to decreased systemic vascular resisitance (SVR) triggered primarily by a massive release of histamine by mast cells activated by by antigen-bound immunoglobulin E and also by increased production and release of prostaglandins.[4]

Neurogenic shock is caused by the loss of vascular tone normally supported by the sympathetic nervous system due to injury to the central nervous system especially spinal cord injury.[4][6]

Distributive shock associated with adrenal crisis results from inadequate steroid hormones.

Forms

Elbers and Ince have identified five classes of abnormal microcirculatory flow in distributive shock using side stream dark field microscopy.

  • Class I: all capillaries are stagnant when there is normal or sluggish venular flow.
  • Class II: there are empty capillaries next to capillaries that have flowing red blood cells.
  • Class III: there stagnant capillaries next to capillaries with normal blood flow.
  • Class IV: hyperdynamic flow in capillaries adjacent to capillaries that are stagnant.
  • Class V: widespread hyperdynamic flow in the microcirculatory system.[2]

Treatment

The main goals of treatment in distributive shock are to reverse the underlying cause and achieive hemodynamic stabilization.[7] Immediate treatement involves fluid resuscitation and the use of vasoactive drugs, both vasopressors and inotropes.[8] Hydrocortisone is used for patients whose hypotension does not respond to fluid resuscitation and vasopressors.[9] Opening and keeping open the microcirculation is a consideration in the treatment of distributive shock, as a result limiting the use of vasopressors has been suggested.[2] Control of inflammation, vascular function and coagulation to correct pathological differences in blood flow and microvascular shunting has been pointed to as a potentially important adjunct goal in the treatment of distributive shock.[2]

Patients with septic shock are treated with antimicrobial drugs to treat the causative infection.[10] Some sources of infection require surgical intervention including necrotizing fasciitis, cholangitis, abscess, intestinal ischemia, or infected medical devices.[11]

Anaphylactic shock is treated with epinephrine.[12]

Prognosis

Septic shock is associated with significant mortality and is the leading non cardiac cause of death in intensive care units (ICU's).[1]

Research Directions

The choice of fluids for resuscitation remains an area of research, the Surviving Sepsis Campaign an international consortium of experts, did not find adequate evidence to support the superiority crystalloid fluids versus colloid fluids.[8] Drugs such as, pyridoxalated hemoglobin polyoxyethylene, which scavenge nitric oxide from the blood have been investigated.[13] As well as methylene blue which may inhibit the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway which has been suggested to play a significant role in distributive shock.[14]

References

  1. ^ a b c Kanaparthi, Lalit K.; Klaus-Dieter, Lessnau; Peralta, Ruben (12 February 2013), Pinsky, Michael R. (ed.), "Distributive Shock: Overview: Background", Medscape Reference, Medscape, retrieved 2014-04-28. {{citation}}: Unknown parameter |registration= ignored (|url-access= suggested) (help)
  2. ^ a b c d e f g Elbers, Paul W.G.; Ince, Can (19 July 2006). "Mechanisms of critical illness--classifying microcirculatory flow abnormalities in distributive shock". Critical Care. 10 (4): 221. doi:10.1186/cc4969. PMC 1750971. PMID 16879732.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ a b c d e Kanaparthi et al. 2013, Overview: Etiology.
  4. ^ a b c d e f Kanaparthi et al. 2013, Overview: Pathophysiology.
  5. ^ a b Ince, Can (25 August 2005). "The microcirculation is the motor of sepsis". Critical Care. 4 (Supp 4): S13-9. doi:10.1186/cc3753. PMC 3226164. PMID 16168069.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ^ Weaver, Lynne C.; Fleming, Jennifer C.; Mathias, Christopher J.; Krassioukov, Andrie V. (2012). "Ch. 13: Disordered Cardiovascular Control After Spinal Cord Injury". In Verhaagen, Joost; McDonald, John W. (eds.). Handbook of Clinical Neurology. Vol. 109. pp. 213–33. doi:10.1016/B978-0-444-52137-8.00013-9. ISBN 9780444521378. PMID 23098715.
  7. ^ Kanaparthi et al. 2013, Treatment: Approach Considerations.
  8. ^ a b Kanaparthi et al. 2013, Treatment: Resuscitation.
  9. ^ Kanaparthi et al. 2013, Treatment: Corticosteroids.
  10. ^ Kanaparthi et al. 2013, Treatment: Antimicrobial Treatment.
  11. ^ Kanaparthi et al. 2013, Treatment: Surgical Control of Shock Sources.
  12. ^ Kanaparthi et al. 2013, Treatment: Treatment of Anaphylaxis.
  13. ^ Kinasewitz, Gary T.; Privalle, Christopher T.; Imm, Amy; Steingrub, Jay S.; Malcynski, John T.; Balk, Robert A.; DeAngelo, Joseph (July 2008). "Multicenter, randomized, placebo-controlled study of the nitric oxide scavenger pyridoxalated hemoglobin polyoxyethylene in distributive shock". Critical Care Medicine. 36 (7): 1999–2007. doi:10.1097/CCM.0b013e31817bfe84. PMID 18552688. {{cite journal}}: Unknown parameter |displayauthors= ignored (|display-authors= suggested) (help)
  14. ^ Jang, D.H.; Nelson, L.S.; Hoffman, R.S. (September 2013). "Methylene blue for distributive shock: A potential new use of an old antidote". Journal of Medical Toxicology. 9 (3): 242–9. doi:10.1007/s13181-013-0298-7. PMC 3770994. PMID 23580172.


Stub icon

This article about a disease, disorder, or medical condition is a stub. You can help Wikipedia by expanding it.

Retrieved from "https://en.wikipedia.org/w/index.php?title=Distributive_shock&oldid=607721592"