Author, Donkey, Bureaucrats, Administrators
53,803
edits
Changes
mLine 4:
Line 4: − + + Line 18:
Line 19: − + Line 33:
Line 34: − + + + + + + + + + + + + + + + + + + + + + + − * Post-mortem findings are non-specific. − * The lungs are wet and heavy, showing congestion and oedema. − ** The alveolar capillaries are distended with blood. − ** The alveoli are filled with haemorrhage and oedema fluid. − * A degree of atelectasis (collapse) also develops. − * In the intestine, the blood vessels are congested and there is patchy haemorrhage of the mucosa due to localised anoxia. − ** There is also a considerable amount of blood stained fluid within the lumen. − *** May be mistaken for inflammation. − * The kidneys cortex appears pale due to tubular necrosis, while the medulla is darkened by congestion. − ** Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium. − + + +
Reverted edits by Sdebrabernard (talk) to last revision by Bara
* Reflexes are subnormal.
* Reflexes are subnormal.
* Respiration is shallow.
* Respiration is shallow.
* There is a rapid thready pulse.
* There is a rapid thready pulse.
* Tissue perfusion is decreased.
==Causes of Shock==
==Causes of Shock==
===Endotoxaemia===
===Endotoxaemia===
Endotoxaemia can occur in severe infections by Gram negative bacteria. The toxins produced by the bacteria are thought to induce blood clotting in very small vessels, occluding blood flow and resulting in blood pools in the peripheral tissues. Endotoxaemia is a risk factor for the development of [[Disseminated Intravascular Coagulation|Disseminated Intravascular Coagulation]].
Endotoxaemia can occur in severe infections by Gram negative bacteria. The toxins produced by the bacteria are thought to induce blood clotting in very small vessels, occluding blood flow and resulting in blood pools in the peripheral tissues. Endotoxaemia is a risk factor for the development of [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]].
===Cardiac disruption===
===Cardiac disruption===
==Treatment of Shock==
==Treatment of Shock==
The aim of treatment is to recover full circulatory function and thus increase tissue perfusion to normal levels. The mainstay of treatment is [[Fluid Therapy|fluid therapy]] and drugs that can counteract the predisposing cause of the condition.
The aim of treatment is to recover full circulatory function and thus increase tissue perfusion to normal levels. The mainstay of treatment is [[Principles of Fluid Therapy|fluid therapy]] to increase circulatory volume and drug therapy as required to counteract the predisposing cause of the condition. Oxygen therapy will be required if signs of hypoxia are present.
Drug therapies may include antiprostaglandins, [[Antibiotics|antibiotics]], sympathomimetics, antiarrhythmics, vasodilators, bicarbonate and glucose, as indicated by the underlying cause and the diagnostic lab work. [[Steroids|Glucocorticosteriods]] are contra-indicated unless a specific deficiency is noted i.e [[Hypoadrenocorticism|hypoadrenocorticism]].
==Post-Mortem Findings==
==Post-Mortem Findings==
Post-mortem findings are non-specific for shock, and include:
* The lungs are wet and heavy, showing congestion and oedema. A degree of atelectasis (collapse) also develops. The alveolar capillaries are distended with blood and the alveoli are filled with haemorrhage and oedematous fluid.
* In the intestine, the blood vessels are congested and there is patchy haemorrhage of the mucosa due to localised anoxia. There is also a considerable amount of blood stained fluid within the lumen which can be mistaken for inflammation.
* The kidneys cortex appears pale due to tubular necrosis, while the medulla is darkened by congestion.
* Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium.
{{Learning
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093135269.pdf ''' Nursing management of the hypovolemic shock patient.''' Davis, H.; The North American Veterinary Conference, Gainesville, USA, Veterinary technicians. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 19-22]
}}
{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840760811_sample.pdf
|chaptername = Recognizing shock and its laboratory signs
|book = Equine Pediatric Medicine
|author = William Bernard, Bonnie S. Barr
|isbn =9781840760811
}}
[[Category:WikiBlood]][[Category:To Do - Blood]][[Category:To Do - Clinical]]
[[Category:WikiBlood]]
[[Category:Cardiovascular System - Pathology]]
[[Category:Cardiology Section]]