Anoxic brain injury: Difference between revisions
| Line 28: | Line 28: | ||
The brainstem is more resistant to hypoperfusion that the cerebral cortex, and if the brainstem does not recover, the cerebral cortex is not likely to recover. The presence of brain stem reflexes is therefore critical to recovery. Preservation of brainstem function is indicated by the presence of blinking, coughing, gagging, sneezing, and yawning. | The brainstem is more resistant to hypoperfusion that the cerebral cortex, and if the brainstem does not recover, the cerebral cortex is not likely to recover. The presence of brain stem reflexes is therefore critical to recovery. Preservation of brainstem function is indicated by the presence of blinking, coughing, gagging, sneezing, and yawning. | ||
====Pupillary Size==== | |||
The presence of peristently dilated pupils is a poor prognostic sign <ref>Steen-Hansen JE, Hansen NN, Vaagenes P, Schreiner B: Pupil size and light reactivity during cardiopulmonary resuscitation. A clinical study. Crit Care Med 1988;16:69-70.</ref>. It should be noted that both [[catecholamines]] and [[atropine]], can affect pupillary size, and confound the assessment of pupillary size. | |||
==Incidence and Predictors of Entering Into a Vegetative State versus Making a Full Neurologic Recovery== | ==Incidence and Predictors of Entering Into a Vegetative State versus Making a Full Neurologic Recovery== | ||
Revision as of 17:51, 28 February 2011
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editors-In-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
Overview
Anoxic or hypoxic brain injury is often seen after cardiac arrest. Major efforts are underway to improve "The Chain of Survival" based upon early access to medical care, early defibrillation, early CPR and early hospital care. Therapeutic hypothermia may improve outcomes. Steroids, manitol, diuresis and hyperventilation have not been documented to meaningfully improve clinical outcomes.
Epidemiology
In a 1990s study from the UK, resuscitation for cardiac arrest was attempted in 10,081 patients. Of these only 1476 (14.6%) survived to be admitted to the hospital [1][2]. Of these small number of patients who survived to admission, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff). Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.
In a review of 68 studies through 1997, the incidence of survival to discharge was higher at 14% with a wide range of 0-28%.[3]
Predictors of Survival
Improved Prognosis with In-Hospital versus Out-of-Hospital Cardiac Arrest
Out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% survival at discharge) than in-hospital cardiac arrest (15% survival at discharge).
Improved Prognosis with VT/VF versus PEA or Asystole
A major determining factor in survival is the initially documented electrocardiographic rhythm. Patients with ventricular fibrilation (VF) or ventricual tachycardia (VT) (aka VT/VF) have a 10-15 fold greater chance of survival than patients with pulseless electrical activity (PEA) or asystole. VT and VF are responsive to defibrillation, whereas asystole and PEA are not.
Rapid Defibrillation is Associated with Imporved Survival
Rapid intervention with a defibrillator increases survival rates.[4][5]
Signs and Symptoms
Serial neurologic examinations are critical in the assessment of long term prognosis.
Assessment of the Brain Stem
The brainstem is more resistant to hypoperfusion that the cerebral cortex, and if the brainstem does not recover, the cerebral cortex is not likely to recover. The presence of brain stem reflexes is therefore critical to recovery. Preservation of brainstem function is indicated by the presence of blinking, coughing, gagging, sneezing, and yawning.
Pupillary Size
The presence of peristently dilated pupils is a poor prognostic sign [6]. It should be noted that both catecholamines and atropine, can affect pupillary size, and confound the assessment of pupillary size.
Incidence and Predictors of Entering Into a Vegetative State versus Making a Full Neurologic Recovery
Cardiac arrest is the third leading cause of coma. Approximately 80% of patients who suffered a cardiac arrest who survived to be admitted to the hospital will be in coma for varying lengths of time. Of these patients, approximately 40% will enter into a persistent vegetative state and 80% die within 1 year. In contrast, those rare patients who survive until discharge without significant neurological impairment can expect a fair to good quality of life.
The duration of hypoxia/ischemia determines the extent of neuronal injury i.e. in patients who suffer hypoxia for less than 5 minutes, are less likely to have permanent neurologic deficits, while with prolonged, global hypoxia, patients may develop myoclonus or a persistent vegetative state.[7]
The duration of coma is an important predictor of the recovery of neurologic function. In a 1979 study of 181 cardiac arrest patients who survived to hospital admission, 84% were comatose for more than 1 hour and 56% were comatose for more than 24 hours[8]. There was minimal neurologic deficit if coma lasted less than 24 hours. However, among the 85 patients who were comatose for more than 24 hours, only 7 of them were discharged alive. The severity of neurological impairment increased with increased duration of coma. Of the patients who were in coma for more than 7 days, none regained consciousness. It should be noted that 80 patients died in a coma.
A JAMA article in 1985 attempted to identify the multivariate predictors neurologic prognosis in 210 patients with coma due to cerebral hypoxia. A total of 13% of patients regained neurologic function and independent function at some time during the first year.
Initial Neurologic Findings:
- Patients who had the initial absence of pupillary light reflexes did not recover independent functioning (52 patients, 25% of patients)[8].
- In contrast, patients who had the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the presence of either extensor, flexor, or withdrawal responses to pain had a 41% chance of regaining independent function (of the 27 patients in this group, 11 (41%) regained independence).[8].
- In a study by Snyder et al, the absence of corneal or pupillary light reflexes at 3 hours after cardiac arrest was associated with death in all patients [9][10]. By 6 hours, all the patients who survived had the presence of three brainstem reflexes: pupillary light response, corneal reflex, and reflex eye movements.
24 Hour Neurologic Findings:
- Absent motor responses, the presence of posturing (extensor / flexor motor responses) and the lack of spontaneous eye movements that were either orienting or roving conjugate was associated with a lack of independent recovery in 92 of 93 patients. [8].
- In contrast, of the 30 patients who showed improvement in their eye-opening responses, obeyed commands or had withdraw to pain, 19 (63%) regained independent function.[8].
Imaging Findings
If there is irreversible bilateral medial tegmental brainstem injury, then patients do not survive.
Systematic Efforts to Improve Survival Following Cardiac Arrest: The Chain of Survival
Multiple organizations now promote the "Chain of Survival" as a way to maximise prognosis following cardiac arrest. The Chain of Survival is made up of 4 links:
- Early Access - Early identification of patients at risk of cardiac arrest early is an effective way of improving prognosis, as it is often possible to prevent the cardiac arrest. Similarly, if the arrest is witnessed there is a much greater chance of survival, as treatment can be innitiated immediately.
- Early CPR - Cardiopulmonary resuscitation (CPR) buys time by maintaining a limited circulation until it is possible to defibrillate the patient. Effective CPR may minimize the risk of cerebral hypoxia (which can lead to neurological impairment following restoration of circulation).
- Early defibrillation - The earlier defibrillation of VT/VF is performed, the better the prognosis. Untreated VF/VT often degenerates into asystole which is poorly responsive to defibrillation.
- Early hospital care - Many patients suffer recurrent cardiac arrest within the first 24 hours of admission, and outcomes are improved with inpatient care in a monitored setting that allows early defibrillation.
Causes of Death in Patients with Anoxic Brain Injury
Patients with anoxic injury due to cardiac arrest are due to a risk of death from a variety of causes including recurrent sudden cardiac death, congestive heart failure, pneumonia, sepsis from a variety of sources and pulmonary embolism.
References
- ↑ Lyon RM, Cobbe SM, Bradley JM, Grubb NR (2004). "Surviving out of hospital cardiac arrest at home: a postcode lottery?". Emerg Med J. 21 (5): 619–24. doi:10.1136/emj.2003.010363. PMC 1726412. PMID 15333549. Unknown parameter
|month=ignored (help) - ↑ Cobbe SM, Dalziel K, Ford I, Marsden AK (1996). "Survival of 1476 patients initially resuscitated from out of hospital cardiac arrest". BMJ. 312 (7047): 1633–7. PMC 2351362. PMID 8664715. Unknown parameter
|month=ignored (help) - ↑ Ballew KA (1997). "Cardiopulmonary resuscitation". BMJ. 314 (7092): 1462–5. PMC 2126720. PMID 9167565. Unknown parameter
|month=ignored (help) - ↑ Eisenberg MS, Mengert TJ (2001). "Cardiac resuscitation". N. Engl. J. Med. 344 (17): 1304–13. PMID 11320390. Unknown parameter
|month=ignored (help) - ↑ Bunch TJ, White RD, Gersh BJ; et al. (2003). "Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation". N. Engl. J. Med. 348 (26): 2626–33. doi:10.1056/NEJMoa023053. PMID 12826637. Unknown parameter
|month=ignored (help) - ↑ Steen-Hansen JE, Hansen NN, Vaagenes P, Schreiner B: Pupil size and light reactivity during cardiopulmonary resuscitation. A clinical study. Crit Care Med 1988;16:69-70.
- ↑ Mellion ML (2005). "Neurologic consequences of cardiac arrest and preventive strategies". Medicine and Health, Rhode Island. 88 (11): 382–5. PMID 16363390. Unknown parameter
|month=ignored (help) - ↑ 8.0 8.1 8.2 8.3 8.4 Thomassen A, Wernberg M (1979). "Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units". Acta Anaesthesiologica Scandinavica. 23 (2): 143–8. PMID 442945. Unknown parameter
|month=ignored (help) - ↑ Snyder BD, Loewenson RB, Gumnit RJ, et al: Neurologic prognosis after cardiopulmonary arrest: II. Level of consciousness. Neurology 1980;30:52-58.
- ↑ Snyder BD, Gumnit RJ, Leppik IE, et al: Neurologic prognosis after cardiopulmonary arrest: IV. Brainstem refl exes. Neurology 1981;31: 1092-1097