Hypoxic Ischemic Brain Injury In Adults

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Hypoxic-ischemic encephalopathy, or HIE, is a brain injury caused by oxygen deprivation, or asphyxia. Also called perinatal encephalopathy can cause cerebral palsy. Background Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies, but the results were not definitive. To. Additional indications for TH after cardiac arrest remain controversial. Many clinicians treat hypoxic-ischemic encephalopathy due to pulseless electrical activity. Hyperbaric Oxygen Therapy Providers and Treatment Centers In The United States.

Temperature Modulation for Neuroprotection After Acute Brain Injury​A growing body of basic science as well as translational and human experimental data supports the concept that mild therapeutic hypothermia (TH) and therapeutic normothermia (TN) are beneficial for patients with acute neurologic injuries. At the cellular level, acute brain injury is characterized by an initial insult that is complicated by secondary biochemical and hemodynamic injuries. Events over hours to days lead to very different outcomes; injured cells may lyse, causing inflammation, releasing cytotoxic neurotransmitters, and perpetuating a cycle of injury. They may undergo apoptosis, or they may recover and return gradually to normal cellular function and activity. Aggressive clinical management during the early phases of injury can have a major impact on long- term neurologic outcomes.

Hypoxic Ischemic Brain Injury In Adults

CELL INJURY AND DEATH Ed Friedlander, M.D., Pathologist scalpel_blade@yahoo.com No texting or chat messages, please. Ordinary e-mails are welcome. Patients with acute hyperammonemic encephalopathy present with progressive drowsiness, seizures, and coma due to primary toxic effects of ammonia on the brain.

Pathophysiologic Response. The variable vulnerability of different regions of the brain to ischemia depends on intrinsic metabolic activity of specific subpopulations of neurons, the type and mechanism of injury, and anatomic differences in blood supply. In the setting of circulatory arrest, the medial temporal lobes, the caudate and putamen, and the Purkinje cells of the cerebellum are the first regions damaged. In low- flow states, neurons in a watershed distribution between large- vessel vascular territories are more likely to be injured. When ischemia is caused by the combination of high intracranial pressure (ICP) and low cerebral perfusion pressure, such as in global cerebral edema, an isolated pattern of cortical laminar necrosis may develop.

Finally, in traumatic brain injury (TBI), rotational points in the basal ganglia, midbrain and brainstem may develop ischemia and infarction due to disruption of the blood supply. Prolonged hypoperfusion due to any of these mechanisms may cause microvascular thrombosis, resulting in the “no- reflow” phenomenon and regional cellular necrosis, even if large vessel patency is restored. Brain temperature has direct effects on the speed of enzymatic reactions and cellular metabolism, and it is an important modulator of brain injury. Hypothermia reduces the metabolic demands (and therefore ischemia risk) of the injured brain, decreases cytotoxic neurotransmitter release and inflammation, and decreases ICP without affecting systemic blood pressure. This reduces secondary injury by multiple pathways.

Hypothermia also prevents the activation of apoptotic signaling pathways and stabilizes neuronal cell membranes. Conversely, fever activates inflammatory pathways, increases cellular metabolism, and is associated with more severe histological features of injury and worse long- term neurologic outcomes. Medical Assistance For Adults In Texas. Uses for Temperature Management. While moderate and deep hypothermia (below 3.

C) are associated with electrolyte  disturbances, cardiac electrical instability, coagulopathy, sepsis and circulatory collapse, mild TH (≥3. C) generally is tolerated well. Aside from asymptomatic bradycardia, TH is associated with a low incidence of bleeding, hypokalemia, hemodynamically significant arrhythmias and infection.(1,2)Development of pneumonia in mechanically ventilated patients with brain injury is common, and many clinicians offer preemptive antimicrobial prophylaxis.(3) Hypothermia is immunosuppressive, and the incidence of infectious complications rises steeply after two to three days of therapy. Similarly, shivering increases systemic and cerebral metabolic demands, and aggressive suppression of shivering may prevent exacerbation of ischemic brain injury.(4)Hypoxic- ischemic encephalopathy after cardiac arrest. Two randomized controlled trials confirm that 1. TH at 3. 2 to 3. 4ºC in encephalopathic adult survivors of cardiac arrest reduces mortality by 1.

Postimplementation reports have demonstrated that hypothermia can be initiated outside of the clinical trial environment with similar results.(7,8)Additional indications for TH after cardiac arrest remain controversial. Many clinicians treat hypoxic- ischemic encephalopathy due to pulseless electrical activity, asystole, hypoxemia or asphyxia, and in- hospital cardiac arrests. Although these patients suffer similar mechanisms of neuronal injury, fewer than 1.

Some clinicians worry that aggressive treatment of these patients may only increase the number of patients surviving with severe neurologic disabilities. It is our practice to perform TH on all encephalopathic cardiac arrest survivors unless severe shock is present or severe medical comorbidities exist. Neonatal post- anoxic encephalopathy. A meta- analysis of four randomized trials supports the routine administration of mild TH for newborns with asphyxial hypoxic- ischemic encephalopathy, also showing that one poor neurologic outcome or death is prevented for every six infants treated.(9) A randomized controlled trial involving 2. C for 7. 2 hours, followed by slow rewarming.(1.

Hepatic encephalopathy.