Critical Care Medicine-Neurologic Disorders>>>>>Neurotrauma
Question 1#

A 15-year-old boy was struck by a car traveling 35 miles per hour and was thrown 15 feet. He was unresponsive and posturing upon arrival. He was intubated without use of paralytic or anesthetic agents. His examination prior to intubation was Glascow Coma Scale (GCS) 3 with reactive pupils at 4 mm. Following intubation and trauma screen, he was taken to CT scan, which demonstrated diffuse subarachnoid hemorrhage (SAH) and diffuse cerebral edema. He was admitted to the neurocritical care unit for ongoing management. Ten days into his hospital course, he was noted to have events of tachycardia, extensor posturing, and tachypnea in the setting of being bathed.

Which of the following is true regarding his likely diagnosis?

a. Start antiepileptic medications to better control seizure activities
b. The most common cause of this disease is traumatic brain injury (TBI).
c. The pathophysiology of this disease results from basal ganglia or thalamic synchronous neuronal firing
d. The patient’s age is not associated with this disease process

Correct Answer is B


Correct Answer: B

Paroxysmal sympathetic hyperactivity (PSH) is a syndrome associated with multiple different brain injuries, including TBI, anoxic brain injury, stroke, and autoimmune encephalitis. The prevalence of PSH has been reported in between 7.5% and 33% of patients admitted to the ICU. Risk factors associated with the development of PSH following TBI are the severity of initial injury, younger age, and male gender. The pathophysiology of PSH nor anatomic etiology is fully understood, but there is a final common pathway of imbalance of adrenergic outflow. An excitatory-inhibitory ratio model which also describes spinal cord modulation via diencephalic centers and loss of these centers into the mesencephlaom results in loss of control of allodynic inhibition. The episodes typically consist of worsening mental status, increased heart rate, BP, respiratory rate, diaphoresis, and posturing, but all do not need to be present to make the diagnosis. There is limited evidence to pharmacologic treatment of PSH, and medications currently are targeted at managing the symptoms associated with PSH and include opiates, nonselective betablockers, dopamine agonists, alpha 2-agonists, GABAergic agents, benzodiazepines, and muscle relaxants. There can be delay in diagnosing PSH as this can appear similar to seizures, but given the hemodynamics and posturing part of the presentation, the more likely diagnosis is PSH. There is no clear clinical seizure activity, so there is no need to start seizure treatment at this point.


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