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?
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.
References:
A 73-year-old female with hypertension, hyperlipedemia, and atrial fibrillation on oral anticoagulation with coumadin sustained a mechanical fall backwards and hit the right posterior aspect of her head. Following the fall, there was no loss of consciousness. On initial arrival to the emergency department (ED), she was interactive, but over the course of 30 minutes, she had neurologic deterioration with loss of spontaneous movement on the left side and multiple episodes of emesis and was intubated for airway protection. A head CT was completed at that time and is shown below. Her labs are remarkable for an elevated international normalized ratio (INR) of 2.1, Cr 1.4.
Vitals are remarkable for blood pressure (BP) 126/88 mm Hg, pulse 80 but irregular.
What is the age of the hemorrhage that is present on the noncontrast head CT?
Correct Answer: A
The head CT demonstrates a large right-sided subdural hemorrhage. This blood collection accumulates in the space between the dura and arachnoid mater. This hemorrhage is not limited by the cranial sutures as is the case with an epidural hemorrhage. Subdural hemorrhages are seen in all ages, most commonly due to trauma. Subdural hemorrhages are typically formed from stretching and tearing of bridging critical veins as they cross the subdural space. In the hyperacute (first hour) phase, the hemorrhage typically will have a swirled appearance due to a mixture of clot, serum, and unclotted blood. An acute subdural hemorrhage is typically a homogenous hyperdense extra-axial collection and can have areas of unclotted blood causing mixed densities within the hemorrhage. A subacute subdural hemorhage (between day 3 and 21) will become isodense to the adjacent cortex. Lastly, a chronic subdural hemorrhage becomes hypodense and appears similar to cerebrospinal fluid (CSF) and can mimic subdural hygromas.
Although not pictured here, MRI imaging can be used to age hemorrhage.
A 45-year-old female was riding her bicycle when she was struck by a car. She suffered a severe TBI requiring intracranial pressure (ICP) monitoring and treatment of elevated ICP with hyperosmolar therapy. Patient’s neurological status remained poor despite aggressive medical treatment, and she was eventually discharged to a skilled nursing facility following placement of a tracheostomy and gastrostomy tube. Six weeks following her initial injury, she was able to spontaneously open her eyes, track family, move all her extremities spontaneously, and reach for objects but not following commands. She had no verbal output or attempts at verbalization. Amantadine was considered by the primary team.
Which of the below comments is correct?
Approximately 10% to 15% of patients with severe TBI are discharged from acute care in a vegetative state. Amantadine is a weak antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor, which increases dopamine release and blocks dopamine reuptake. The largest study of amantadine evaluated its use in the subacute setting (approximately 1- 2 months following TBI) and involved 184 patients. All patients were in a minimally conscious state or vegetative state. Of those that received amantadine, the initial dose was 100 mg twice a day and could be increased to 200 mg twice a day. Those that received the medication had a more rapid improvement in the behavioral domains examined and of those the most affected was object recognition with the least affected being verbal output. At the end of the 4-week study, there was a 2 week washout phase all patients had continued improvement, but those in the placebo group had more rapid recovery and improvement to the same functional outcome. There were no differences in the number of adverse events with the medication as compared to placebo, and specifically there were two patients in the treatment and four patients in the placebo group with seizures. Although postulated in the trial, there is an uncertain mechanism of action for amantadine’s activation in severe TBI. Studies have demonstrated increase in PET activity in the prefrontal cortex as well as increase in striatal D2 dopamine-receptor availability.
A 21-year-old male with no past medical history is brought in via emergency medical services (EMS) for evaluation of a gunshot wound to the head. Police and EMS were called, and he was found at the scene awake, interactive but confused. There appeared to be a left frontotemporal entry site without an exit site. His initial vital signs were heart rate 136, BP 95/54, and SpO2 98% on 2 L nasal cannula (NC). His initial examination demonstrated an uncomfortable young man oriented to person only, following simple commands with antigravity movements throughout his extremities with some decreased movement on the right homebody. A head CT was completed (see figures below).
Which of these statements is most correct regarding penetrating head trauma?
Correct Answer: D
Penetrating head trauma has limited data compared to nonpenetrating head trauma with much of the literature and treatment paradigms extrapolated from military interventions. The head CT in this case demonstrates a number of findings: retained bullet fragments in eloquent cortex, intraparenchymal bone fragments, crossing of the midline with involvement of the bilateral hemispheres, and small epidural and SAH. The prognosis from penetrating head trauma is worse than nonpenetrating head trauma. Initial evaluation of penetrating head trauma is similar to other trauma with evaluation of airway, breathing, and circulation (ABC), then a trauma assessment. There is need for careful evaluation of the entry and potential exit wound. Specific evaluation of any CSF leakage, brain parenchymal, and ongoing bleeding at these sites is crucial. A detailed neurologic examination should be completed as well. Following this neuroimaging will assist with determination of surgical planning if needed. Imaging can reveal intracranial fragments, missile tract and relationship to blood vessels, intracranial air, ventricular injury, basal ganglia and brain stem injury, basal cistern effacement, herniation, and mass effect. CT and CTA are the standard imaging modalities for penetrating brain imaging. There are high-risk vascular areas including near the Sylvian fissure, supraclinoid carotid artery, vertebrobasilar vessel, aversions signs, and major dural venous sinuses. Other common findings on imaging are the presence of blood product including within the subarachnoid space. This type of hemorrhage is due to vascular injury and although there is risk of cerebral vasospasm similar to the typical aneurysmal SAH. As is in this case, there are retained fragments, and this places the patient at higher risk for intracranial infection. There are varying treatment paradigms for prophylactic antibiotic use, but it is recommended. The common infections are skin flora including Staphylococcus aureus, but also gram-negative organisms can cause infection. Therefore, broad-spectrum antibiotic therapy with a cephalosporin, vancomycin, and aerobic coverage (metronidazole) is considered mainstay therapy, but the duration of therapy is quite variable from 7 to 14 days up to 6 weeks. Lastly, following penetrating head injury, it is common to have epilepsy. About 50% of penetrating TBI patients may develop epilepsy in during the 15 years post injury.
A 24-year-old male was a nonhelmeted motorcyclist hit by a car. EMS arrived to find him with labored breathing and intubated him. His GCS was 6 prior to intubation: eyes did not open, incomprehensible speech, and withdrawal of all extremities to painful stimulation. On presentation to the ED, he underwent a trauma evaluation and had nondisplaced parietal bone fracture, mastoid fracture, and multiple noncongruent rib fractures. His head CT demonstrated small bifrontal and temporal lobe intraparenchymal hemorrhages, a small amount of bilateral frontal SAH, and a 2 mm right frontal subdural hemorrhage. He was admitted to the neurologic intensive care unit (ICU) where a bolt was placed, which demonstrated a normal ICP. He continued in the same comatose state for 12 hours with a repeat head CT that was stable.
What is the next best test?
Nonconvulsive status epilepticus is a common (22%) finding in severe TBI. Those who have prolonged, unexplained depressed level of consciousness within the ICU should undergo prolonged EEG monitoring for evaluation of possible nonconvulsive seizures and status epilepticus. In comatose patients, it frequently takes 24 hours of monitoring to capture the first seizure. Further prolonged EEG monitoring can still capture further electrographic seizures; however, there are no recommendations regarding the length of EEG monitoring. Patient’s multicompartment contusions will make him at higher risk of seizures. The other answers may be appropriate in certain clinical settings but are not the best answers. GRE is a specific MRI sequence that evaluates for iron deposition and is related to the extent of diffuse axonal injury, which is overall helpful in guiding our outcome prognostication. Cerebral vasospasm can occur with traumatic SAH, within 48 hours of the initial head injury. The hyperacuity of the patient’s current presentation is likely to exclude vasospasm. There is no clear need to start hyperosmolar therapy; patient’s bolt shows normal ICPs and his repeat head CT that was stable.
Click to expand