Reperfusion injury natural history

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Editors-In-Chief: Anjan K. Chakrabarti, M.D. [1]; C. Michael Gibson, M.S., M.D. [2]; Dr. Shivam Singla M.D. [2] Associate Editors-In-Chief: Kashish Goel, M.D ;

Complications

Complications of IRI

Myocardial stunning: Delayed recovery, usually 2-3 days, of the viable myocardium after reperfusion is termed as "myocardial stunning". It is mainly due to the release of reactive oxygen species and intracellular calcium overload.

  • Myocardial infarction: Irreversible myocyte cell death secondary to reduced oxygen delivery for more than 20-30 minutes, will lead to infarction. Reperfusion helps prevent complete loss of the involved area, however oxidative stress due to this may prevent complete resolution.
  • Acute heart failure: Loss of myocardial contractility and systolic dysfunction associated with ischemia/reperfusion injury may lead to development of acute heart failure. Early reperfusion in the course of STEMI prevents myocardial necrosis and may lead to complete recovery of function.
  • Ventricular arrhythmias: Reperfusion of the blocked coronary artery can also precipitate arrhythmias ranging from ventricular premature beats to life-threatening ventricular fibrillation.

Prognosis

Prognosis in CNS patients

  • Those patients who are identified and treated early, the prognosis is better along with the decreased incidence of intracranial hemorrhage. Outcomes usually depends on timely recognition and prevention of precipitating factors. Hypertension management is most important before it can inflict damage in the form of edema or hemorrhage.

The prognosis following hemorrhagic transformation is poor. Mortality in such cases is 3663%, and 80% of survivors have significant morbidity.<ref Piepgras DG, Morgan MK, Sundt TM Jr, Yanagihara T, Mussman LM. Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg. 1988 Apr. 68(4):532-6.</ref>

Studies indicate that reperfusion injury is involved directly in the potentiation of stroke damage. Components of the inflammatory response, including cytokine release and leukocyte adhesion, appear to play key roles in these deleterious effects.

References