Distributive shock: Difference between revisions

| name = {{PAGENAME}}Distributive shock

'''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 |url-access=registration |accessdateaccess-date= 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 |ref= {{SfnRef|Elbers & Ince|2006}} |doi-access= free }}</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 [[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 a type of distributive shock called [[septic shock]], a condition that can be fatal.<ref name= "Kanaparthi 2013"/>

*[[Neurogenic shock]]: Decreased sympathetic stimulation leading to decreased vasalvessel tone.

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}}

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]] underperfused 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 |journal= [[Critical Care (journal)|Critical Care]] |volume= 4 |issue= Supp 4 |pages= S13-9 |doi= 10.1186/cc3753 |pmid= 16168069 |pmc= 3226164 |doi-access= free }}</ref> The [[Endothelium|endothelial]] cells lining the blood vessels become less responsive to vasocontrictivevasoconstrictive 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 initiates 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"/>

[[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. |title= Spinal Cord Injury |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 |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|series= Handbook of Clinical Neurology }}</ref> Rupture of a hollow organ, with subsequent evacuation of contents in the peritoneal cavity could also determine neurogenic shock, a subtype of distributive shock. This happens due to the widespread peritoneal irritation by the ruptured viscus contents, as in peptic ulcer perforation, with consequent strong vagal activation, and generalized, extensive peripheral vasodilation and bradycardia.<ref>{{cite journal | author = De-Giorgio F, Lodise M, Pascali VL, Spagnolo AG, d'Aloja E, Arena V. | year = 2015 | title = An Unusual Case Showing Fatal Rupture of a Gastric Ulcer or Gastromalacia? The Importance/Role of Histology for Differential Diagnosis. J| journal = Journal of Forensic Sci.Sciences 2015| volume = Jan;60( | issue = 1):240-2.| pages = 240–2 {{doi| doi = 10.1111/1556-4029.12665}}. {{PMID| pmid = 25388056 | s2cid = 1458157 }}</ref><ref>Civetta, Taylor, & Kirby's Critical Care, 4th Edition. Chapter 59 Neurogenic Shock. Lippincott Williams & Wilkins 2009</ref> Thus, in neurogenic shock, there is decreased systemic vascular resistance, CVP is typically decreased, CO decreased or normal, and PAOP decreased. <ref name="Elbers 2006" />

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

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 of [[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 |displayauthorsdisplay-authors= 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|s2cid= 30123186 }}</ref> Asas 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>