Complications

Rib fractures

Hemothorax

Hemopericardium

Hemoperitoneum

Solid organ injuries, e.g., liver

Skin burns

Complications of intubation

Ischemic cardiomyopathy

Acute kidney injury

Shock liver

Multiorgan dysfunction syndrome

Neurological dysfunction

Definition: global brain injury caused by complete cessation of blood flow during cardiac arrest

Epidemiology: most common cause of death in patients surviving cardiac arrest [31]

Pathophysiology: cardiac arrest → cessation of blood flow to the brain → anoxia → irreversible neuronal damage and death

Neurological deficits (determined by the severity of injury and the affected structures)

• Comatose state

• Absent or abnormal motor response (e.g., extensor posturing)

• Absent spontaneous eye movements

• Absent brainstem reflexes (e.g., pupillary light reflex, oculocephalic reflex)

Convulsions (e.g., status epilepticus)

Clinical features consistent with cardiac arrest

It is imperative to exclude other causes of coma (e.g., toxic and metabolic encephalopathies, shock).

Laboratory studies (e.g., CBC, serum electrolytes, toxicology screens)

Imaging

• CT brain

  • Usually normal within the first 2 days

  • Findings of anoxic injury: cerebral edema, inversion of gray-white matter density

• MRI brain: allows for early detection of brain injury

EEG

• Characteristic pattern: slowing of the EEG followed by delta activity and, eventually, EEG flattening

• Some EEG patterns are markers of a poor prognosis

Postresuscitation care (see above)

Avoid hyperthermia. [35][36]

Prevention of hyperglycemia

Complications

• Brain death

• Coma

• Persistent vegetative state

• Minimally conscious state

• Seizures

Prognosis

• The majority of cases have a poor prognosis, indicators of which include:

  • Increased duration of anoxia

  • Clinical markers

    • Absent brainstem reflexes (e.g., pupillary light reflex, corneal reflex)

    • Persistent dilated pupils

    • Absent or abnormal motor response

    • Myoclonic status epilepticus

  • Other specific markers

    • Laboratory studies: elevated serum level of neuron-specific enolase

    • EEG: nonreactive or presence of burst-suppression pattern (suggestive of myoclonic status epilepticus)