Anoxic brain injury pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
There are a variety of factors that contribute to anoxic brain injury. The primary mechanism for injury is a result of a lack of oxygen to the brain. | There are a variety of factors that contribute to anoxic brain injury. The primary mechanism for injury is a result of a lack of oxygen to the brain, therefore any condition which causes this, such as [[cardiac arrest]] or [[airway obstruction]], can cause anoxic brain injury. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 19:41, 11 February 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
There are a variety of factors that contribute to anoxic brain injury. The primary mechanism for injury is a result of a lack of oxygen to the brain, therefore any condition which causes this, such as cardiac arrest or airway obstruction, can cause anoxic brain injury.
Pathophysiology
The underlying mechanism of post cardiac arrest syndrome is a combination of: [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11]
Systemic Response to Ischemia and Reperfusion
Myocardial Dysfunction
Brain Injury
Effects of Persistent Precipitating Pathologies
- Cardiovascular disease (Acute coronary syndromes, cardiomyopathy)
- Chronic obstructive pulmonary disease
- Central nervous system diseases (e.g. cerebrovascular accident)
- Thromboembolic disorders (e.g. pulmonary emboli)
- Drug /substance overdose, poisoning
- Infections (sepsis, pneumonia)
- Volume loss (Hypovolemia: e.g. hemorrhage, dehydration)
References
- ↑ Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med. Sep 10 2001; 161(16): 2007-2012.
- ↑ van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. New England Journal of Medicine. Nov 8 2001;345(19): 1359-1367.
- ↑ Van den Berghe G, Wouters PJ, Bouillon R, et al. Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control. Crit Care Med. Feb 2003;31(2):359-366.
- ↑ Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862-871.
- ↑ Zandbergen EG, de Haan RJ, Stoutenbeek CP, et al. Systematic review of early prediction of poor outcome in anoxic-ischaemic coma. Lancet. Dec 5 1998; 352(9143): 1808-1812.
- ↑ Rello J. Risk factors for developing pneumonia within 48 hours of intubation. Am J Respir Crit Care Med. 1999;159:1742-1746.
- ↑ Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. New England Journal of Medicine. Jun 5 1997;336(23):1629-1633.
- ↑ Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease after cardiac arrest: a sepsis-like syndrome? Curr Opin Crit Care. Jun 2004;10(3):208-212.
- ↑ Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine. 2001;345(19):1368-1377.
- ↑ Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of hospital cardiac arrest with induced hypothermia. New England Journal of Medicine. Feb 21 2002;346(8):557-563.
- ↑ Hypothermia after Cardiac Arrest Study G. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. Erratum appears in N Engl J Med 2002 May 30;346(22):1756]. New England Journal of Medicine. Feb 21 2002;346(8):549-556.