Anoxic brain injury pathophysiology

Revision as of 19:41, 11 February 2013 by Charmaine Patel (talk | contribs)
Jump to navigation Jump to search

Anoxic brain injury Microchapters

Home

Patient Information

Overview

Pathophysiology

Causes

Differentiating Anoxic brain injury from other Diseases

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Echocardiography or Ultrasound

Electroencephalogram

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Anoxic brain injury pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Anoxic brain injury pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Anoxic brain injury pathophysiology

CDC on Anoxic brain injury pathophysiology

Anoxic brain injury pathophysiology in the news

Blogs on Anoxic brain injury pathophysiology

Directions to Hospitals Treating Anoxic brain injury

Risk calculators and risk factors for Anoxic brain injury pathophysiology

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

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. Rello J. Risk factors for developing pneumonia within 48 hours of intubation. Am J Respir Crit Care Med. 1999;159:1742-1746.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.

Template:WH Template:WS