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Introduction Tranexamic Acid (TXA) is an intravenous antifibrinolytic agent that is used routinely for elective surgery. We report a case of inadvertent intrathecal injection of TXA resulting in refractory status epilepticus. Methods Case report. Results A 71-year-old healthy female admitted for bilateral total knee replacement was inadvertently administered 300mg of TXA intrathecally instead of bupivacaine. Soon after administration, she developed myoclonic jerking. When the error was identified, 15cc of CSF was removed. She was intubated, administered levetiracetam, started on a propofol infusion, and transferred to the neurointensive care unit (NICU). She developed persistent spontaneous and stimulus induced generalized myoclonus refractory to propofol. Midazolam infusion was added. NCHCT and CTA demonstrated pneumocephalus, but no acute arterial or venous thrombosis or stroke. vEEG revealed generalized nonconvulsive seizures occurring once per minute, not correlating with spinal myoclonus . Propofol and midazolam infusions were increased to 150 mcg/kg/min and 2.6 mg/kg/hr, respectively, to achieve burst suppression, and valproic acid was added. Over the following week, the drips were adjusted to suppress seizure activity. By hospital day 8, she was weaned off all infusions without recurrence of seizures. By hospital day 19, she was on levetiracetam monotherapy. She was discharged to rehab after a 22-day hospital course, and was discharged home 45 days after initial presentation. Residual deficits at the time of discharge included mild cognitive impairment and gait instability. She remains seizure-free since hospital day 45 on levetiracetam 500mg BID. Conclusions We report a case of refractory status epilepticus and spinal myoclonus after accidental intrathecal TXA administration. With aggressive management, the patient survived with mild residual deficits. The mechanism by which TXA causes status epilepticus and spinal myoclonus is hypothesized to be related to its inhibitory effects on GABA and glycine receptors, respectively

Management of patients with terminal brain disorders can be medically, socially, and ethically complex. Although a growing number of feasible treatment options may exist, there are times when further treatment can no longer meaningfully improve either quality or length of life. Clinicians and patients should discuss goals of care while patients are capable of making their own decisions. However, because such discussions can be challenging, they are often postponed. These discussions are then conducted with patients' health care proxies after patients lose the capacity to make their own decisions. Disagreements may arise when a patient's surrogate desires continued aggressive interventions that are either biologically futile (incapable of producing the intended physiologic result) or potentially inappropriate (potentially capable of producing the patient's intended effect but in conflict with the medical team's ethical principles). This article explores best practices in addressing these types of conflicts in the critical care unit, but these concepts also broadly apply to other sites of care.

BACKGROUND AND PURPOSE/OBJECTIVE:The relationship between in-hospital hyperglycemia and neurological outcome after intracerebral hemorrhage (ICH) is not well studied. METHODS:We analyzed the relationships between pre-hospital and hospital variables including highest in-hospital glucose (HIHGLC) and discharge Glasgow Coma Scale (GCS), discharge Modified Rankin Scale (MRS) and 3-month MRS using a single-institution cohort of ICH patients between 2013 and 2015. RESULTS:There were 106 patients in our sample. Mean HIHGLC was 154 ± 58mg/dL for patients with discharge GCS of 15 and 180 ± 57mg/dL for patients with GCS < 15; 146 ± 55mg/dL for patients with discharge MRS 0-3 and 175 ± 58mg/dL for patients with discharge MRS 4-6; and 149 ± 52mg/dL for patients with 3-month MRS of 0-3 and 166 ± 61mg/dL for patients with 3-month MRS of 4-6. On univariate analysis, discharge GCS was associated with HIHGLC (P = .01), age (P = .006), ICH volume (P = .008), and length of stay (LOS) (P = .01); discharge MRS was associated with HIHGLC (P < .001), age (P < .001), premorbid MRS (P = .046), ICH volume (P < .001), and LOS (P < .001); and 3-month MRS was associated with HIHGLC (P = .006), discharge MRS (P < .001), age (P = .001), sex (P = .002), ICH volume (P = .03), and length of stay (P = .004). On multivariate analysis, discharge GCS only had a significant relationship with ICH volume (odds ratio [OR] .949, .927-.971); discharge MRS had a significant relationship with age (OR 1.043, 1.009-1.079), premorbid MRS (OR 2.622, 1.144-6.011), and ICH volume (OR 1.047, 1.003-1.093); and 3-month MRS only had a significant relationship with age (OR 1.039, 1.010-1.069). CONCLUSIONS:The relationship between in-hospital hyperglycemia and neurological outcomes in ICH patients was meaningful on univariate, but not multivariate, analysis. Glucose control after ICH is important.