Imaging features of hypoxic-ischemic encephalopathy in adults

Hypoxic-ischemic brain injury (HII) generally occurs in newborns due to their immature brain tissue and poor tolerance to ischemia. HII can also occur in adults, mainly due to cardiac arrest, suffocation, drowning, etc. So what are the characteristics of hypoxic-ischemic encephalopathy in adults?

Imaging characteristics

Plain CT scan of the brain revealed swelling of the brain parenchyma, shallowing and disappearance of the cerebral sulci, unclear boundaries between gray and white matter, and high-density cerebrospinal fluid cavity, similar to the signal of subarachnoid hemorrhage. The thalamus and cerebellum are relatively dense, and this "reversal" sign generally correlates with the severity of the injury and a poor prognosis. The signs on the MRI images confirmed the ischemic and hypoxic damage to the brain, with diffuse diffusion restriction and obvious high signal on T2 in the cerebral cortex and basal ganglia.

Differential diagnosis: hypoxic-ischemic brain injury; traumatic cerebral edema; toxic/metabolic lesions; posterior reversible encephalopathy; Creutzfeldt-Jakob disease; acute cerebral infarction.

Diagnosis: Hypoxic-ischemic brain injury (HII). The patient was confirmed to have attempted suicide by taking an overdose of drugs. When he was found, he had stopped breathing and cardiopulmonary resuscitation was performed.

Pathophysiology

Hypoxic-ischemic brain damage is caused by a series of causes that lead to reduced cerebral blood flow, such as cardiac arrest, cerebrovascular disease, suffocation, drowning, etc. The following factors will first lead to brain hypoxia and eventually cause cerebral ischemia: ① The body's breathing mode is converted from aerobic respiration to anaerobic respiration, and a large amount of lactic acid is generated and accumulated; ② Cerebral ischemia and hypoxia cause a decrease in the activity of sodium-potassium ATPase, a large amount of excitatory amino acids are released, and postsynaptic neurons are over-excited and damaged; ③ When energy is insufficient, nerve cells eventually undergo apoptosis.

The vulnerable areas of brain parenchyma damage are divided into: ① Mild to moderate: watershed infarction. ② Severe: Gray matter (reflecting the area with the highest concentration of glutamate receptors and the most sensitive to glutamate excitotoxicity), including the hippocampus, cerebellum, cerebral cortex, thalamus, and basal ganglia.

Age factors: Immature brain tissue is most sensitive to ischemia; middle-aged brain tissue is most tolerant to ischemia.

Imaging findings

CT manifestations: preferred for older children. Diffuse cerebral edema, smaller ventricles, decreased gray matter density, unclear gray-white matter boundaries, and decreased density of bilateral basal ganglia can be seen. Inversion sign and white cerebellar sign may be seen in adults and indicate a poor prognosis.

MR manifestations: DWI is the earliest imaging method to detect abnormalities. In the first 24 hours, DWI shows increased signal in the cerebellar hemispheres, basal ganglia, and cerebral cortex, and the thalamus, brainstem, or hippocampus may also be affected. At the end of the first week, DWI showed a false negative. Conventional T1/T2 sequences are normal or slightly abnormal in the early stage (within 24 hours). In subacute stage (2 days to 2 weeks), T2 images show increased signal and edema in the damaged gray matter, and on T1-weighted images, signal abnormalities may persist until the end of the second week. In the chronic stage, T2-weighted images show local low signal in the basal ganglia, and T1-weighted images show cortical necrosis, which appears as high signal.

Treatment: Supportive care; hypothermia; excitatory amino acid receptor antagonists; anticonvulsant drugs.

Clinical prognosis: About 75% of patients can fully or partially recover within 6 to 12 months; about 25% of patients have sequelae of neurological damage, such as epilepsy, dementia, etc.; a very small number of patients have worsening conditions, develop into a vegetative state, or die.