Neurohospitalist最新文献

Postpartum neuropathies are common, including femoral neuropathy, peroneal neuropathy, lumbosacral trunk plexopathy, and lateral femoral cutaneous neuropathy. Sciatic mononeuropathy in the peripartum period is rare. Postpartum sciatic neuropathy (PSN) in the setting of cesarean section has been reported before. We present a case series of 2 sciatic mononeuropathies after vaginal delivery. Case 1 is a 25-year-old woman who presented with a left foot drop after normal vaginal delivery after being in labor for 3 hours. Case 2 is a 24-year-old woman who presented with a right foot drop after normal vaginal delivery and being in labor for 31 hours. Both cases noted foot drops in the immediate postpartum period. Neurologic examinations revealed flail foot, 4/5 hamstring muscle strength on MRC scale and intact hip abduction. They had paresthesia on the posterolateral aspect of the leg, dorsal and plantar aspect of the foot with absent ankle reflex. MRI did not show evidence of spinal cord, nerve root or plexus involvement. Electrodiagnostic studies revealed evidence of sciatic mononeuropathy proximal to the short head of biceps femoris. They were discharged home with an ankle brace and therapy. At 3 months follow up, they had complete resolution of weakness. There have been a few reported cases of PSN secondary to cesarean section. Sciatic involvement after vaginal delivery is extremely rare. We report 2 cases of PSN after vaginal delivery to highlight that sciatic mononeuropathy can occur not only after cesarean section, but also after uncomplicated vaginal delivery and should raise awareness of this risk to clinicians.

Spinal dural tears are being increasingly recongnized to cause superficial siderosis and intracranial hypotension. We report a patient with chronic headache who was detected to have cerebellar superficial siderosis and subtle signs of intracranial hypotension on imaging. Spinal imaging showed an upper thoracic dural tear secondary to a paradiscal osteophyte. She improved significantly with surgical repair of the tear. We highlight the importance of recognizing superficial sideorsis in patients with chronic headache as it serves as a marker for dural tear and intracranial hypotension.

Background and purpose: Over-sedation may confound neurologic assessment in critically ill neurologic patients and prolong duration of mechanical ventilation (MV). Decreased sedative use may facilitate early functional independence when combined with early mobility. The objective of this study was to evaluate the impact of a stepwise, multidisciplinary analgesia-first sedation pathway and early mobility protocol on medication use and mobility in the neuroscience intensive care unit (ICU).

Methods: We performed a single-center prospective cohort study with adult patients admitted to a neuroscience ICU between March and June 2016-2018 who required MV for greater than 48 hours. Patients were included from three separate phases of the study: Phase I - historical controls (2016); Phase II - analgesia-first pathway (2017); Phase III - early mobility protocol (2018). Primary outcomes included propofol requirements during MV, total rehabilitation therapy provided, and functional mobility during ICU admission.

Results: 156 patients were included in the analysis. Decreasing propofol exposure was observed during Phase I, II, and III (median 2243.7 mg/day vs 2065.6 mg/day vs 1360.8 mg/day, respectively; P = .04 between Phase I and III). Early mobility was provided in 59.7%, 40%, and 81.6% of patients while admitted to the ICU in Phase I, II, and III, respectively (P < .01). An increased proportion of patients in Phase III were walking or ambulating at ICU discharge (26.7%; 8/30) compared to Phase I (7.9%, 3/38, P = .05).

Conclusions: An interdisciplinary approach with an analgesia-first sedation pathway with early mobility protocol was associated with less sedative use, increased rehabilitation therapy, and improved functional mobility status at ICU discharge.

Background: There have been limited reports about brain activity during cardiac arrest. Here we report 4 patients presenting with seizure who had cardiac arrest leading to their deaths while being on continuous video-EEG (cVEEG) monitoring and one-lead cardiac telemetry. Purpose: We illustrate characteristic stepwise EEG and EKG changes in these critically ill patients prior to their death. Research Design/Study Sample: All patients showed progressive broad spectrum of cardiac arrhythmias at or before the beginning of EEG suppression while there were no such changes seen in a control group of 4 randomly selected patients without cardiac arrest who had seizure on presentation and underwent cVEEG monitoring. Data Collection and Results: There was a progressive decline in EEG potentials associated with decreasing heart rate starting from the posterior region, more pronounced on the left, progressing to complete unilateral deactivation of the left fronto-central head regions while the right-sided networks became hyperactive before bilateral deactivation by the time of asystole. Conclusions: This case series provides a rare opportunity to compare EEG and EKG changes in patients who died while being on continuous EEG and EKG monitoring from hours to minutes prior to cardiac arrest and death.

Background and purpose: Medical-legal claims for malpractice relating to the use of alteplase for acute ischemic stroke (AIS) are usually for failure to treat rather than for complications. The advent of mechanical thrombectomy (MT) as a standard of AIS treatment has added a new dimension to the medical-legal landscape as there is a need for the delivery of a higher level of care creating the potential for delays and errors associated with such treatment. Information on causes of malpractice related to mechanical thrombectomy (MT) is currently lacking.

Methods: We conducted a systematic review of legal databases (Westlaw, LexisNexis, Google Scholar Case Law, and VerdictSearch) to identify medical malpractice cases with and without verdicts filed in the United States up to March 31, 2021 which pertained to performance or non-performance of MT for AIS. We collected various case characteristics, case outcomes, and root causes for malpractice claims.

Results: We found 25 cases, 16 of which alleged failure to treat with MT, 8 for harm due to delay in treatment and 1 case that alleged complications. Root causes included delay in vascular imaging, communication breakdowns, and transportation delays. Eight cases had an outcome in favor of the defendant, 9 in favor of the plaintiff, and 8 remained to be determined.

Conclusions: As with alteplase, malpractice allegations regarding MT for AIS are largely for failure to treat or delay in treatment as opposed to complications. Addressing root causes of diagnostic delay, communication breakdowns, and transportation delays may reduce subsequent malpractice risk.

Chimeric antigen receptor (CAR-T) cell therapy is highly effective against hematological cancers but is associated with immune mediated side effects, including neurotoxicity. The most commonly described presentations of immune cell mediated neurotoxicity syndrome (ICANS) include cortical symptoms and generally localize to the central nervous system. In this report, we present a patient with acute onset of bilateral facial nerve palsy following CAR-T cell therapy, followed by a complete clinical recovery. Aside from a temporary anisocoria, he had no other neurologic symptoms and no encephalopathy or seizures. MRI Brain was non-contributory and cerebrospinal fluid revealed a modest increase in lymphocytes without systemic leukocytosis and viral studies were all negative. He was diagnosed with bilateral facial nerve palsy secondary to CAR-T cell therapy and subsequently treated with a course of steroids. Several weeks after presentation he returned to his neurological baseline. The presentation of CAR-T cell mediated facial nerve palsy is both clinically and scientifically relevant for physicians, patients, and researchers.

Background: Laboratory monitoring is not recommended when subcutaneous unfractionated heparin (SQ-UFH) is administered at prophylactic doses. However, aPTT prolongation and associated hemorrhage has been reported in the neurocritically ill. At our institution, Neuroscience Intensive Care Unit (Neuro-ICU) patients with prolonged aPTT are further evaluated with a follow up aPTT and anti-factor Xa.

Purpose: The purpose of this study was to describe concordance between aPTT and anti-factor Xa in neurocritically ill patients receiving prophylactic SQ-UFH with evidence of aPTT prolongation.

Methods: A retrospective chart review of adult patients admitted to the Neuro-ICU from June 2017 to June 2019 was performed. Patients were included if they received SQ-UFH with aPTT levels and at least one anti-factor Xa level drawn within one hour of each other. Concordance between paired aPTT and anti-factor Xa was evaluated using Cohen's weighted kappa.

Results: Forty two patients with 56 paired aPTT and anti-factor Xa levels were included. The most prescribed SQ-UFH regimen was 5000 units every 8 hours (60.7%) and anti-factor Xa levels were drawn a median (IQR) of 5.7 (3.1-10.7) hours after the SQ-UFH dose. Only 16 (28.6%) pairs were in concordance. The analysis showed a weighted kappa of .09; 95% CI [-.05 to .22] indicating poor agreement.

Conclusions: In neurocritically ill patients receiving prophylactic SQ-UFH with aPTT prolongation, there was poor concordance between aPTT and anti-factor Xa. This suggests that aPTT prolongation may not be solely driven by heparin activity and further evaluation of mechanistic drivers for coagulopathy in this population is necessary.

Cancer and stroke comprise two of the most common causes of death worldwide. Despite a significantly increased risk of stroke among patients with cancer, most stroke trials have excluded patients with malignancy. There is thus limited evidence to help guide management decisions in this complex population. We present the case of a 78-year-old man with recurrent strokes - both ischemic and hemorrhagic - in the setting of newly-identified metastatic prostate cancer. An atypical cause of cancer-associated stroke is reviewed and the management is discussed.