Anoxia is defined by the total absence of oxygen to the tissues or a particular organ such as the brain. The term anoxic brain injury (ABI) is frequently used synonymously in the literature with terms hypoxic-ischemic , anoxic-ischemic , hypoxic , or cerebral anoxia .
One of the earliest documented cases of ABI was in 1945 with eight cases of poisoning from nitrous oxide anesthesia that resulted in persistent deficits in judgment, attention, and memory; loss of insight; apathy; indifference, and restlessness.
Etiology
The etiology of ABI can be related to any event that deprives the brain of sufficient oxygenation. In addition to cardiac arrest and respiratory failure, a variety of disorders such as carbon monoxide poisoning, asphyxiation because of hanging, near drowning, obstructive sleep apnea, complications from anesthesia, metabolic conditions, and pulmonary disease can be attributable causes.
Epidemiology
The majority of data for ABIs are in the setting of cardiac arrest. The majority of cardiac arrest events occur outside of the hospital in a private residence. The incidence of emergency medical services (EMS)-assessed cardiac arrest in the adult population is 347,322 per year, based on the most recent data by the American Heart Association (AHA).
Survival with good functional outcomes was present for a majority of these patients, as defined by independence with activities of daily living (ADLs) with possible residual deficits of hemiplegia, seizures, or memory impairment. There are also large regional variations in survival to hospital discharge and survival with functional recovery. However, as many as 18% of out of hospital cardiac arrest survivors have moderate to severe functional deficits at discharge. But, survival rates to hospital discharge after EMS-treated cardiac arrest increased from 10.2% in 2006 to 12.4% in 2015.
Pathophysiology
There are two primary mechanisms of injury with ABI: primary and secondary. During the primary injury, there is first ischemia and then subsequent reperfusion. During the process of the brain ischemia, there is anoxic depolarization, adenosine triphosphate (ATP) depletion, glutamate release, free radical formation, and nitric oxide production. The primary injury causes considerable neuronal damage, but the successive reperfusion accounts for substantial cerebral ischemia and cell death. Despite the return of spontaneous circulation during cardiac arrest, there is a brief period of hyperemia that is quickly replaced by a longer period of global and multifocal hypoperfusion known as the no reflow phenomenon .
Secondary injury occurs immediately after return of spontaneous circulation and is the result of the additive cerebral injury caused by an imbalance of postresuscitation cerebral oxygen delivery. Secondary injury consists of ongoing ischemia, autoregulatory failure, cerebral hypoperfusion, blood-brain barrier breakdown, seizures, oxidative injury, and hyperpyrexia.
There are specific areas of the brain that are more vulnerable to damage than others: the hippocampus (CA1 pyramidal neurons); Purkinje cells of the cerebellum; pyramidal neurons in layers three, five,and six of the neocortex; reticular neurons of the thalamus; neurons of the striatum; and vascular border zone areas.
Examination and prognosis
Initial evaluations begin with a thorough history regarding the onset of the injury, mechanism, duration of ischemia to reperfusion; medical history; family history; social history including illicit, prescription, and over the counter drug use; prior psychiatric history; functional history; educational history; and social support.
The clinical manifestations of ABIs are varied and complex. Neurologists are often asked to evaluate patients after cardiopulmonary resuscitation and to help provide prognostication. The clinical examination is focused on brainstem reflexes, the presence of generalized myoclonus, and motor responses to noxious stimuli. Additionally, it is important to assess for range of motion, skin breakdown, and muscle tone. In the acute care setting, physicians and families are interested in long term prognostication so that goals of care discussions can be established early.
There are many studies that summarize factors that are associated with poor outcomes. However, each study defines poor outcomes differently ( Table 55-1 ).
| Symptom | Time Frame |
|---|---|
| Anoxia duration | >8–10 min |
| Duration of cardiopulmonary resuscitation | >30 min |
| Myoclonic status epilepticus | Day 1 |
| Absent pupillary or corneal reflexes | Days 1–3 |
| Serum neuron-specific enolase (NSE) >33 μg/L | Days 1–3 for nontherapeutic hypothermia patients |
| Absent N20 responses on somatosensory evoked potentials (SSEP) bilaterally | Days 1–3 |
| Motor response extensor or none | Day 3 for nontherapeutic hypothermia patients; possibly longer for therapeutic hypothermia patients |
| Electroencephalogram (EEG) with nonreactive background | |
| EEG with burst suppression and generalized epileptiform activity | |
| Loss of gray-white matter differentiation on head computed tomography | |
| Widespread cortical restricted diffusion on brain magnetic resonance imaging |
In conscious patients, it is important to also assess for cognitive impairments. These cognitive impairments include:
- •
Attention
- •
Processing speed
- •
Memory impairments
- •
Executive dysfunction
- •
Language impairments
- •
Calculation impairments
- •
Apraxia
- •
Agnosia
- •
Visuospatial impairments
- •
Balint syndrome: simultagnosia, optic ataxia, ocular apraxia
- •
Anton syndrome: anosognosia for visual impairment
- •
Alterations in personality and behavior
- •
Affective dysregulation
Additionally, one should also assess for neurological impairments such as motor deficits, parkinsonism, dystonia, chorea, tremor, tics, athetosis, seizures, and myoclonic syndromes.
Clinical sequelae also include:
- •
Man-in-a-barrel syndrome: bilateral proximal upper limb paresis with preservation of lower limb function caused by injury between the anterior cerebral artery and middle cerebral artery watershed zone
- •
Paraparesis and quadriparesis in the upper and lower thoracic and lumbar regions of the spinal cord
- •
Cortical blindness and Balint syndrome are examples of disorders of sensory function
- •
Akinetic-rigid syndrome
- •
Amnestic syndrome caused by hippocampal damage
- •
Lance-Adams syndrome: significant action myoclonus associated with ataxia ,
Further evaluation by electroencephalogram (EEG) and somatosensory evoked potentials (SSEP) can also help with prognostication. Biochemical markers are also being used for prognosticating outcomes such as serum neuron-specific enolase (NSE) and serum S100. ,
Treatment
The acute period of ischemia is treated with high-quality cardiopulmonary resuscitation (CPR) with the goal of return of spontaneous circulation (ROSC). However, once ROSC has been achieved, it is imperative for postcardiac arrest care to help mitigate the subsequent ischemia-reperfusion injury to multiple organ systems.
The 2015 updated guidelines on postcardiac arrest care by the AHA identify and note several points:
- •
Identify acute ST elevation, and if present perform urgent coronary angiography with prompt recanalization of any infarct-related artery.
- •
Avoid and immediately correct hypotension (systolic blood pressure less than 90 mm Hg, mean arterial pressure less than 65 mm Hg).
- •
Targeted temperature management (TTM) for comatose adults is between 32° and 36°C for at least 24 hours.
- •
Actively prevent fever in comatose patient after TTM.
- •
EEG for diagnosis of seizure should monitored frequently or continuously in a comatose patient after ROSC.
- •
Maintain normocarbia levels and avoiding hypoxia.
- •
The target range for glucose control remains uncertain.
However, the 2017 guidelines from the American Academy of Neurology (AAN) found level A evidence for the use of TTM for patients with either pulseless ventricular tachycardia or ventricular fibrillation after an out-of-hospital cardiac arrest, to be 32° to 34°C for 24 hours.
Rehabilitation-specific treatment
Traumatic brain injury (TBI) and ABI rehabilitation outcomes in a retrospective study found similar functional independent measurement (FIM) scores on discharge between the two groups. However, older studies have shown the ABI group to have a higher discharge rate than skilled nursing facilities compared with TBI and slower recoveries.
Physiatrists are an essential part of the post-ABI team and are frequently consulted in the intensive care unit setting to determine the medical and physical readiness for inpatient rehabilitation.
Patients can present with disorders of consciousness (DOC), but other presentations can include cognitive deficits, behavioral changes, affective changes, visual difficulties, movement disorders, spasticity, and alterations in gait. Physiatrists can help differentiate DOC patients with metrics such as the JFK Coma Recovery Scale-Revised (CRS-R) and Individual Quantitative Behavioral Assessment (IQBA) with the help of an interdisciplinary team. Initially, pharmacologic interventions are focused on arousal and increasing participation. However, as the patient progresses, the pharmacological interventions also include treatment for agitation, attention, processing speed, memory deficits, sleep disturbances, depression, headaches, and spasticity.
Spasticity is defined as velocity-dependent increases in muscle tone resulting in resistance to muscle stretch. It is a part of the upper motor neuron syndrome. Determining when to treat spasticity requires knowledge of not only the advantages and disadvantages of treatment options but also defining and integrating goals of care from the patient, family members, and caretakers.
The treatment of spasticity helps with ambulation, transfers, muscle bulk maintenance, deep vein thrombosis prevention, improved range of motion, improved hygiene, and osteoporosis prevention.
There are conventional oral agents such as baclofen, tizanidine, dantrolene, diazepam, and clonazepam. However, there is limited evidence as to the effect they have on ABI patients. Additionally, the side effects of sedation frequently limit patients from reaching a therapeutic dose. Focal treatment can include the use of injectable intramuscular chemodenervation agents such as botulinum toxin, phenol, and alcohol. Injectable therapies are unique in that specific muscles can be targeted to help with function; whereas others can be left alone if the patient is using their spasticity functionally. However, when more diffuse spasticity is present, intrathecal baclofen pump therapy should be considered. Careful consideration of patient selection must be done as patients require regular medication refills and pump maintenance. Two small studies have been shown to be effective in decreasing spasticity objectively in the severe TBI population. ,
Review questions
- 1.
Which of these indicates a poor prognostic outcome for anoxic brain injury (ABI) patients?
- a.
Anoxic duration is greater than 5 minutes
- b.
Cardiopulmonary resuscitation (CPR) duration is greater than 20 minutes
- c.
Myoclonic status epilepticus
- d.
Electroencephalogram (EEG) with spindle pattern
- a.
- 2.
Which pattern on an EEG indicates a better prognostic outcome for ABI patients?
- a.
Burst suppression
- b.
Nonreactive background
- c.
Low amplitude delta activity
- d.
Spindle activity
- a.
- 3.
What type of lesion results in bilateral upper extremity paresis with preserved lower extremity function?
- a.
Infarction between the anterior cerebral artery (ACA) and middle cerebral artery (MCA)
- b.
Infarction between the ACA and internal carotid artery
- c.
Infarction between the MCA and posterior cerebral artery (PCA)
- d.
Infarction between PCA and basilar artery
- a.
Answers on page 402.
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- 4.
What are the rehabilitation outcomes for TBI patients versus ABI patients?
- a.
TBI patients have greater functional independent measurement (FIM) gains than ABI patients at discharge.
- b.
TBI patients have the same FIM gains as ABI patients at discharge.
- c.
TBI patients have less FIM gains than ABI patients at discharge.
- a.
- 5.
According to the American Academy of Neurology (AAN), what is the goal for targeted temperature management for comatose patients with ventricular tachycardia/ventricular fibrillation for improving functional neurological outcome and survival?
- a.
24° to 26°C
- b.
28° to 30°C
- c.
32° to 34°C
- d.
36° to 38°C
- a.
- 6.
Which of these is NOT a common etiology of anoxic brain injury?
- a.
Chronic obstructive pulmonary disease
- b.
Cardiac disease
- c.
Complications of anesthesia
- d.
Gastrointestinal disease
- a.
- 7.
Where is the most common location of out-of-hospital cardiac arrest occurring?
- a.
Skilled nursing facilities
- b.
Fast food restaurants
- c.
Private residence
- d.
Shopping centers
- a.
- 8.
Which of these is a mechanism of secondary injury?
- a.
Intracellular Na+ accumulation resulting in cytotoxic edema
- b.
Blood-brain barrier disruption
- c.
Mitochondrial dysfunction
- d.
Adenosine triphosphate production halts
- a.
- 9.
Which structure in the brain is most vulnerable to damage after prolonged ischemia?
- a.
Pyramidal neuron of the hippocampus
- b.
Cerebellar Purkinje cells
- c.
Basal ganglia
- d.
Vascular watershed zones
- a.
- 10.
What syndrome manifests as significant action myoclonus with associated ataxia?
- a.
Anton syndrome
- b.
Lance-Adams syndrome
- c.
Balint syndrome
- d.
Man-in-a-barrel syndrome
- a.
References
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