Management of acute subdural hematoma in a patient with portopulmonary hypertension on prostanoid therapy

BACKGROUND: Treprostinil is a prostacyclin analog used to treat portopulmonary hypertension (PPHTN) and is one of several drugs shown to increase survival, but results in platelet dysfunction. Little is known about the management of patients on treprostinil who present with an acute subdural hematoma (aSDH). We describe such a case and offer our recommendations on management based on our experience and review of the literature. CASE DESCRIPTION: A 63-year-old, right-handed female with a history of PPHTN presented with severe headache and was found to have a large left aSDH with midline shift on imaging. She was admitted to the neurosurgical intensive care unit (ICU) where she developed hemiparesis and subsequently underwent emergent decompression. Postoperatively she improved, but several hours after became obtunded and imaging showed reaccumulation of the aSDH, which required reoperation. At 6 months postoperatively she had only a mild hemiparesis and was being reconsidered for treprostinil therapy as a bridge to liver transplant. Only one paper in the literature thus far has reported a patient with an aSDH managed with treprostinil. The authors achieved adequate intraoperative hemostasis without the use of platelet transfusion and lack of complications intraoperatively. CONCLUSION: While concerns related to the risk of bleeding in surgery are valid, intraoperative hemostasis does not appear to be profoundly affected. Surgical intervention should not be delayed and prostanoid therapy discontinued, if possible, postoperatively. Patients should be placed in an intensive care setting with assistance from pulmonary specialists and close monitoring of neurological status and blood pressure

Comparison of 1 vs 2 Brain Death Examinations on Time to Death Pronouncement and Organ Donation: A 12-year Single Center Experience

OBJECTIVE: To fill the evidence gap on the value of a single (SBD) or dual brain death (DBD) exam by providing data on irreversibility of brain function, organ donation consent and transplantation. METHODS: 12-year tertiary hospital and organ procurement organization data on brain death (BD) were combined and outcomes, including consent rate for organ donation and organs recovered and transplanted after SBD and DBD were compared after multiple adjustments for co-variates. RESULTS: two-hundred sixty-six patients were declared BD, 122 after SBD and 144 after DBD. Time from event to BD declaration was longer by an average of 20.9 hours after DBD (p=0.003). Seventy-five (73%) families of patients with SBD and 86 (72%) with DBD consented for organ donation (p=0.79). The number of BD exams was not a predictor for consent. No patient regained brain function during the periods following BD. Patients with SBD were more likely to have at least one lung transplanted (p = 0.033). The number of organs transplanted was associated with the number of exams [beta coefficient, (95% CI) -0.5 (-0.97 to -0.02), p=0.044], along with age (for 5 year increase, -0.36 (-0.43 to -0.29), p\u3c0.001) and PaO2 level (for 10 mmHg increase, 0.026 (0.008 to 0.044), p=0.005) and decreased as the elapsed time to BD declaration increased (p=0.019). CONCLUSIONS: A single neurologic examination to determine brain death is sufficient in patients with non-anoxic catastrophic brain injuries. A second examination is without additional yield in this group and its delay reduces the number of organs transplanted

Microbleed Prevalence and Burden in Anticoagulant-Associated Intracerebral Bleed

Prior studies suggest an association between Vitamin K antagonists (VKA) and cerebral microbleeds (CMBs); less is known about nonvitamin K oral anticoagulants (NOACs). In this observational study we describe CMB profiles in a multicenter cohort of 89 anticoagulation-related intracerebral hemorrhage (ICH) patients. CMB prevalence was 51% (52% in VKA-ICH, 48% in NOAC-ICH). NOAC-ICH patients had lower median CMB count [2(IQR:1–3) vs. 7(4–11); P \u3c 0.001]; ≥5 CMBs were less prevalent in NOAC-ICH (4% vs. 31%, P = 0.006). This inverse association between NOAC exposure and high CMB count persisted in multivariable logistic regression models adjusting for potential confounders (OR 0.10, 95%CI: 0.01–0.83; P = 0.034)

Neuroimaging and clinical outcomes of oral anticoagulant-associated intracerebral hemorrhage

Objective Methods Whether intracerebral hemorrhage (ICH) associated with non-vitamin K antagonist oral anticoagulants (NOAC-ICH) has a better outcome compared to ICH associated with vitamin K antagonists (VKA-ICH) is uncertain. We performed a systematic review and individual patient data meta-analysis of cohort studies comparing clinical and radiological outcomes between NOAC-ICH and VKA-ICH patients. The primary outcome measure was 30-day all-cause mortality. All outcomes were assessed in multivariate regression analyses adjusted for age, sex, ICH location, and intraventricular hemorrhage extension. Results Interpretation We included 7 eligible studies comprising 219 NOAC-ICH and 831 VKA-ICH patients (mean age = 77 years, 52.5% females). The 30-day mortality was similar between NOAC-ICH and VKA-ICH (24.3% vs 26.5%; hazard ratio = 0.94, 95% confidence interval [CI] = 0.67-1.31). However, in multivariate analyses adjusting for potential confounders, NOAC-ICH was associated with lower admission National Institutes of Health Stroke Scale (NIHSS) score (linear regression coefficient = -2.83, 95% CI = -5.28 to -0.38), lower likelihood of severe stroke (NIHSS > 10 points) on admission (odds ratio [OR] = 0.50, 95% CI = 0.30-0.84), and smaller baseline hematoma volume (linear regression coefficient = -0.24, 95% CI = -0.47 to -0.16). The two groups did not differ in the likelihood of baseline hematoma volume <30cm(3) (OR = 1.14, 95% CI = 0.81-1.62), hematoma expansion (OR = 0.97, 95% CI = 0.63-1.48), in-hospital mortality (OR = 0.73, 95% CI = 0.49-1.11), functional status at discharge (common OR = 0.78, 95% CI = 0.57-1.07), or functional status at 3 months (common OR = 1.03, 95% CI = 0.75-1.43). Although functional outcome at discharge, 1 month, or 3 months was comparable after NOAC-ICH and VKA-ICH, patients with NOAC-ICH had smaller baseline hematoma volumes and less severe acute stroke syndromes. Ann Neurol 2018;84:702-712Peer reviewe

Antiepileptic Drugs in the Neurosurgical Intensive Care

The etiology of seizures in the Neurosurgical/Neurological Intensive Care Unit (NICU) can be categorized as emanating from either primary brain pathology, at either macro- or microscopic level, or from physiological derangements of critical care illness such as toxic or metabolic abnormalities. Particular etiologies at risk for seizures include ischemic or hemorrhagic stroke and traumatic brain injury. The use of prophylactic antiepileptic drug administration remains controversial in many situations, with most of the larger studies having used older antiepileptic drugs prophylactically. If seizures do occur, patients are typically treated with parenteral antiepileptic drugs. The duration of treatment is unknown in most situations, but it should be individualized depending on acute and monophasic injury versus chronic process. Late seizures, which occur after the first 2 weeks from the insult, have a more ominous risk for subsequent epilepsy and should be treated for extended periods of time or indefinitely. Electrolyte and glucose abnormalities and medications at high or low levels, when corrected, usually lead to seizure control. This review discusses the risk for seizures with commonly encountered types of brain injuries in the NICU and ends by examining the treatment algorithms for simple seizures and status epilepticus and the role newer antiepileptics may potentially play

Role of pial collateral flow in acute ischemic stroke outcomes.

Objective: In the patients with acute ischemic stroke (AIS) due to middle cerebral artery (MCA) occlusion who underwent endovascular treatment (ET), we explored the relationship between digital subtraction angiography (DSA) pial collateral status and clinical outcomes. Background: Collateral flow can influence the pace and extent of evolution to irreversible tissue damage and thus have a significant impact on the clinical outcome of patients with AIS. Design/Methods: We reviewed the data of all patients with acute MCA occlusion treated with ET within the past 5 years. Baseline DSA collaterals were classified as - no (0), poor (1), intermediate (2) and good (3). Clinical outcomes were assessed using the National Institute of Health Stroke Scale (NIHSS) at 24-48 hours and at the time of discharge. Multivariable regression analysis was done to evaluate association of DSA collateral score with the outcome. The regression model was adjusted for age, baseline NIHSS, infusion of intravenous (IV) thrombolytic (tPA) and symptom-onset to angiographic recanalization time. Results: 50 patients with the MCA occlusion were treated with ET and 25 (50%) patients received IV tPA prior to ET. Median baseline NIHSS score was 19.5. Median time from the onset to IV tPA was 122 minutes and from onset to angiographic recanalization was 277 minutes. Every 1-point increase in the DSA collateral score was associated with 4.5-point reduction in NIHSS at 24-48 hours and 4.9 point reduction in NIHSS at the time of discharge (standard error 1.4, p\u3c0.01 for both). Conclusions: In the patients with acute ischemic stroke due to MCA occlusion, better collaterals on the DSA are independently associated with improved neurological outcome at 24-48 hour after ET and at the time of discharge. This concept needs to be explored further in a larger dataset that will also include additional imaging parameters

Modern Approach to Brain Death

People die either when their heart and respiration stop or when their brain irreversibly stops functioning. This latter mode of death by neurologic criteria (also called brain death) emerged after the development of ventilators and intensive care units in the late 1950s and 1960s. Brain death is universally accepted as a modern entity, but the complex process for declaring a patient brain dead is not uniformly followed across country and state lines or even hospital policies, creating unacceptable variability and risks for falsely pronouncing a patient dead. If, however, the declaring physician has expertise and diligently follows the steps that have been published in guidelines, this risk is mitigated. In this article, the authors describe the steps for brain death declaration, discuss how to avoid pitfalls, and examine the modern controversies regarding this medical reality