Intracranial pressure following cardiopulmonary resuscitation

Abstract

Intracranial pressure (ICP) was measured in six patients following cardiopulmonary resuscitation (CPR). The causes of cardiac arrest were respiratory or circulatory problems and the primary intracranial pathology was not detected. The measurement of ICP started 3 to 10 h following CPR except one patient in whom it started on the day 7. Duration of ICP measurement ranged from 2 to 7 days. In five out of six patients, ICP persistently remained below 20 mmHg. In the remaining one patient, ICP elevation associated with seizure activity was observed and ICP ultimately increased to 57 mmHg. Among these, four patients died and two remained in a persistent vegetative state. These results suggest that ICP following CPR does not necessarily increase if the patient has no primary intracranial pathology or seizures.

Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)

“…Although transient brain oedema is observed early after ROSC, most commonly after asphyxial cardiac arrest, it is rarely associated with clinically relevant increases in ICP (Sakabe et al, 1987;Morimoto et al, 1993;Torbey et al, 2000;lida et al, 1997). In contrast, delayed brain oedema, occurring days to weeks after cardiac arrest, has been attributed to delayed hyperaemia; this is more likely the consequence rather than the cause of severe ischaemic neurodegeneration (Morimoto et al, 1993;Torbey et al, 2000;lida et al, 1997) No published prospective trials have examined the value of monitoring and managing ICP in post-cardiac arrest patients.…”

Management of Brain Injury After Resuscitation From Cardiac Arrest

“…Usually, ICP is not elevated after cardiac arrest [110], but high ICP can compromise cerebral blood flow, and cerebral herniation can cause structural brain damage and death. In comatose patients with evidence of increased ICP, such as clinical signs of herniation or cerebral edema on CT scan, ICP monitoring may be helpful to guide therapies for optimization of ICP and cerebral perfusion pressure [111].…”

Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest.

“…In indirect support of this assumption is the fact that the lower limit could be identified at a higher arterial pressure in 5 of the 13 patients. Conversely, there is no evidence of generally increased intracranial pressure shortly after resus- citation, 1,6,21,22 , whereas there is an increase in the number of patients with increased intracranial pressure in the days after resuscitation. 23 To conclude that the lower limit of autoregulation was identical in control subjects and patients, intracranial pressure should have been increased on average to 40 mm Hg, which seems unlikely.…”