Anoxic brain injury

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Anoxic brain injury or post-cardiac arrest is defined as absence of pulses requiring chest compressions, regardless of location or presenting rhythm. Post-cardiac arrest syndrome is characterized by resumption of spontaneous systemic circulation after prolonged ischemia of whole body.^[1] Anoxic or hypoxic brain injury is often seen after cardiac arrest as part of the post-cardiac arrest syndrome. 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, mannitol, diuresis and hyperventilation have not been documented to meaningfully improve clinical outcomes.

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.

Persons with anoxic brain injury are at a high risk of death due to factors such as cardiac arrest, congestive heart failure, pneumonia, and sepsis. There are predictors of survival that have been studied. For example, persons with in-hospital cardiac arrest have a better chance of survival than out-of-hospital arrest, rapid defibrillation improves survival, and VT and VF have a better prognosis than asystole or PEA.

Physical examination involves a thorough neurologic evaluation, with a focus on the extent of involvement of the brainstem.

A number of laboratory tests are obtained in order to evaluate the underlying cause of the anoxic brain injury. Common laboratory tests include complete blood count, ABG, electrolytes, cardiac enzymes and serum lactate.

In the early hours and days after anoxic brain injury, there is often diffuse cerebral edema and blurring of the border between the grey and white matter. In some patients there may be discrete infarcts after a few days.

Most often the EEGs of patients in coma after cardiac arrest shows diffuse slowing of both the theta and delta waves, and periodic epileptiform firing. Severe slowing or a flat line appearance is associated with a poor prognosis.

Other pertinent diagnostic studies in anoxic brain injury, include evoked-response testing, and the steps in diagnosing brain death.

Medical therapy for anoxic brain injury, includes the use of therapeutic hypothermia. This has been associated with a reduction in ischemic brain injury, particularly in animal models. There are specific guidelines associated with the use of therapeutic hypothermia, as there can be significant complications and side effects from using this method of treatment.

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.

The underlying mechanism of post cardiac arrest syndrome is a combination of: ^{[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11]}

• Circulatory collapse
• Hyperglycemia
• Hypotension
• Infections
• Multiorgan failure
• Ongoing tissue hypoxia / ischemia
• Fever

• Circulatory collapse
• Dysrhythmias
• Hypotension
• Reduced cardiac output

• Brain death
• Cognitive dysfunction
• Coma
• Cortical stroke
• Myoclonus
• Persistent vegetative state
• Secondary parkinsonism
• Seizures
• Spinal stroke

• 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)

Template:WH Template:WS CME Category::Cardiology

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

Template:WH Template:WS CME Category::Cardiology

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

Template:WH Template:WS CME Category::Cardiology

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Persons with anoxic brain injury are at a high risk of death due to factors such as cardiac arrest, congestive heart failure, pneumonia, and sepsis. There are predictors of survival that have been studied. For example, persons with in-hospital cardiac arrest have a better chance of survival than out-of-hospital arrest, rapid defibrillation improves survival, and VT and VF have a better prognosis than asystole or PEA.

Patients with anoxic injury due to cardiac arrest are at 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.

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).

A major determining factor in survival is the initially documented electrocardiographic rhythm. Patients with ventricular fibrillation (VF) or ventricular 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 intervention with a defibrillator increases survival rates.^[1][2]

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.^[3]

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^[4]. 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.

• Patients who had the initial absence of pupillary light reflexes did not recover independent functioning (52 patients, 25% of patients)^[4].
• 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).^[4].
• 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 ^[5][6]. By 6 hours, all the patients who survived had the presence of three brainstem reflexes: pupillary light reflex, corneal reflex, and reflex eye movements.
• The absence of spontaneous limb movements and the absence of withdrawal to pain in the early hours is a poor prognostic sign.
• The presence of either decorticate or decerebrate posturing is a poor prognostic sign.
• Frequent myoclonic jerking is associated with a poor prognosis.
• The presence of seizures in the initial 24 hours is modestly associated with outcomes: 53% of patients who seize survive compared to 70% of those who do not seize during the first day^[7].

• Most patients who survive become alert by 24-48 hours. In one series, of those patients who were in a coma through day 2, only 2 of the 27 (7%) survived.^[8] In a second series, no patient who remained in a coma by the third day survived.^[9]
• 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. ^[4].
• 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.^[4].
• Seizures that occur after the initial 24 hours are associated with a poorer outcomes. In one study only 3 of 15 patients who seized recovered consciousness, and only one patient lived a year^[10]. The presence of status epilepticus at any time following cardiac arrest is associated with a very poor prognosis as all nine patients with status epilepticus died in one series.^[11]
• The absence of spontaneous eye opening and intermittent visual fixation by the end of the first day is associated with a poor prognosis. Although eye opening is necessary for a good outcomes, it alone is not sufficient, as many patients who have spontaneous eye opening still go on to have a poor prognosis. Roving eye movements in the absence of visual fixation is often indicative of extensive bilateral cerebral hemispheral damage and portends a poor prognosis. If the gaze is sustained in an upward direction, this carries a poor prognosis as well.^[12]

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 ^[13][14]. 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%.^[15]

Template:WH Template:WS CME Category::Cardiology