Paroxysmal sympathetic hyperactivity is a syndrome associated with brain trauma, stroke, encephalitis, and other forms of brain injury. It is characterized by uncontrolled episodes of unbalanced sympathetic surges causing hyperthermia, diaphoresis, tachycardia, hypertension, tachypnea, and dystonic posturing. Patients who develop paroxysmal sympathetic hyperactivity have worse neurologic outcomes, longer hospital stays, and more complications. Despite the clear negative impact on outcome, consensus regarding diagnostic criteria, risk factors, pathophysiology, and treatment approaches is lacking. Recently, the importance of consensus regarding diagnostic criteria has been emphasized, and new theories of pathophysiology have been proposed. Many treatment options are available, but only a few systemic studies of the efficacy of treatment algorithms exist. Treatments should focus on decreasing the frequency and intensity of episodes with regularly scheduled doses of medications, such as long-acting benzodiazepines, nonselective β-blockers, α2-agonists, morphine, baclofen, and gabapentin, usually in combination. Treatment of acute breakthrough episodes should focus on doses of as-needed morphine and short-acting benzodiazepines. A balance between control of symptoms without oversedation is the goal.
Utilizing an anti-Xa protocol to monitor heparin infusion showed favourable results compared with utilizing an aPTT protocol by maintaining values within the therapeutic goal range. The most common discordant pattern in our study was a disproportionate prolongation of aPTT to anti-Xa values. Patients with discordant values presenting with high aPTT to normal anti-Xa values may have an increased risk of bleeding complications.
Paroxysmal sympathetic hyperactivity (PSH) is a result of acute brain injury that has been well known for many decades. However, the evidence for management of PSH is almost entirely anecdotal in nature. We reviewed case reports or series of pharmacotherapy management of PSH. These studies mentioned treatment options, but few studies exist to guide treatment strategies. For many years, the syndrome was not clearly understood; therefore, the therapy has focused on control of symptoms. In 2014, a Steering Committee came together to develop a conceptual definition and produced a consensus set of diagnostic criteria. Although understanding the diagnostic criteria is very well needed in management of patients with PSH, pharmacologic management is also crucial. Data describing the drug choices, dosing, and duration of therapy are also sparse. Recognition of appropriate medications is important because PSH is associated with morbidity, longer hospitalization, delaying transfer to rehabilitation units, and increasing cost. In this review article, we discussed the common medications used in the treatment of PSH. Treatment should target symptom abortion, prevention of symptoms, and refractory treatment. Symptom-abortive medications are indicated to control discrete breakthrough episodes, using medications such as morphine and short-acting benzodiazepines. Other medications used for prevention of symptoms and refractory treatment include long-acting benzodiazepines, nonselective β-blockers, α2 agonists, opioids, and GABA agonists. The mechanisms by which these agents improve symptoms of PSH remain speculative. However, a combination of medications from different classes seems the most effective approach in managing PSH symptoms. There is wide variability in clinical practice with regard to drug choices, dosing, and duration of therapy. Future research needs to be conducted using the new PSH assessment measure to appropriately apply drug management.
Objective: This study investigated the percentage of patients who achieved hemostasis with 4-factor prothrombin complex concentrate (4-factor PCC) 35 U/kg. The primary end point was to determine the effect of 4-factor PCC 35 U/kg on bleeding progression, assessed using computed tomography. Methods: This was a retrospective, observational, single-center study conducted in patients with a major bleed admitted to a level 1 trauma center from May 1, 2013, to June 15, 2015, who received 4-factor PCC 35 U/kg for reversal of a direct factor Xa inhibitor taken prior to admission. Results: Thirty-three patients were included in the study, with 31 patients in the final analysis. The mean (standard deviation) age was 73 (14.8) years; 54.5% of patients were female. Of the 33 patients, 13 presented with a traumatic brain injury, 9 with an aneurysmal subarachnoid hemorrhage, 8 with an intracerebral hemorrhage, 1 with a gastrointestinal bleed, 1 with a hematoma with active extravasation, and 1 with an intra-abdominal bleed. The most frequently used direct factor Xa inhibitor was rivaroxaban (81.8%). Overall, 83.8% of patients achieved hemostasis with 4-factor PCC 35 U/kg. Progression of hemorrhage was observed in 4 patients on repeat computed tomography scan and 1 patient had continued surgical bleeding. No thromboembolic events were reported. Conclusions: Low-dose, 4-factor PCC 35 U/kg appeared to produce hemostasis in a majority of the patients. This may be an effective dosing regimen for anticoagulant reversal of factor Xa inhibitors in clinically bleeding patients.
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