Faculty Bibliography

BACKGROUND:Little data exists regarding reversal and resumption of antithrombotics following left ventricular assist device (LVAD)-associated intracranial hemorrhage (ICH). METHODS:Prospectively collected data of LVAD patients with ICH was reviewed. Coagulopathy reversal agents, antithrombotic regimens and thrombotic (venous thromboembolism, ischemic stroke, myocardial infarction) and hemorrhagic (recurrent ICH, gastrointestinal bleed, anemia requiring transfusion) complications were recorded. RESULTS:Of 405 patients, intracranial hemorrhage occurred in 39 (10%): 23 intracerebral hemorrhages, 10 subarachnoid hemorrhages, and 6 subdural hematomas. Of 27 patients who received antithrombotic reversal, 8 (30%) had inadequate coagulopathy reversal and 3 of these had hemorrhage expansion or died before repeat imaging. One (4%) had a thrombotic complication (deep vein thrombosis). Antithrombotic therapy was resumed in 17(100%) survivors in a median time 8 days for antiplatelet agents, and 14 days for warfarin. Recurrent intracranial hemorrhage occurred within a median of 7 days of antithrombotic resumption, while ischemic stroke occurred in a median of 428 days. Patients who resumed antiplatelets alone (N=4) had a trend toward more thrombotic events (1.37 vs. 0.14 events-per-patient-year [EPPY],P=0.08), including more fatal thrombotic events (0.34 EPPY vs. 0.08, P=0.89) compared to those resuming warfarin±antiplatelet (N=14). Non-fatal hemorrhage event rates were 0.34 EPPY in the warfarin±antiplatelet vs. 0 EPPY in the antiplatelet alone group (P=0.16). No fatal hemorrhagic events occurred. CONCLUSIONS:Reversal of anticoagulation appears safe following LVAD-associated intracranial hemorrhage, though inadequate reversal was common. Resumption of warfarin±antiplatelet was associated with fewer fatal and non-fatal thrombotic events compared to antiplatelets alone, though more non-fatal hemorrhage events occurred.

BACKGROUND:Infection has been associated with stroke in patients with left ventricular assist devices (LVAD); however, little data exist on the timing, type and mortality impact of infection-related stroke. METHODS:Prospectively collected data of HeartMate II (N = 332) and HeartWare (N = 70) LVAD patients from a single center were reviewed. Only strokes (ischemic or hemorrhagic) that occurred within 6 weeks following a LVAD infection were considered in analyses. The association between LVAD infections (wound, pump pocket, driveline and/or bloodstream infection [BSI]), specific pathogens and ischemic and hemorrhagic strokes was evaluated using multivariable logistic regression analysis. The impact of infection-related stroke on cumulative survival was assessed using Kaplan-Meier analysis. RESULTS:Of 402 patients, LVAD infection occurred in 158 (39%) including BSI in 107 (27%), driveline infection in 67 (17%), wound infection in 31 (8%) and pump pocket infection in 24 (6%). LVAD infection-related stroke occurred in 20/158 (13%) patients in a median of 4 days (0-36 days) from documented infection. In multivariable analysis, ischemic stroke was associated with wound infection (aOR 9.0, 95% CI 2.4-34.0, P = 0.001) and BSI (aOR 7.7, 95% CI 0.9-66.0, P = 0.064), and hemorrhagic stroke was associated with BSI in 100% of cases (P = 0.01). There was no association with driveline or pump pocket infection. The cumulative survival rate among patients with infection-related stroke was significantly lower compared to those with LVAD infection but no stroke (log-rank P < 0.001). There was a trend toward shorter stroke-free survival among patients with LVAD infection. CONCLUSIONS:LVAD infections, particularly BSI, are significantly associated with stroke, and infection-related stroke conferred significantly lower cumulative survival.

BACKGROUND AND PURPOSE/OBJECTIVE:Patients with intracerebral hemorrhage (ICH) frequently present with hypertension, but it is unclear if this is due to pre-existing hypertension (prHTN) or to the bleed itself or associated pain. We sought to assess the relationship between prHTN and admission systolic blood pressure (aBP) and bleed severity. METHODS:We retrospectively assessed the relationship between prHTN and aBP and NIHSS in patients with ICH at 3 institutions. RESULTS:Of 251 patients, 170 (68%) had prHTN based on history of hypertension/antihypertensive use. Median aBP was significantly higher in those with prHTN (155 mm Hg (IQR 135-181) versus 139 mm Hg (IQR 124-158), P < .001). Patients with left ventricular hypertrophy (LVH) on electrocardiogram (ECG) or transthoracic echocardiogram (TTE) had significantly higher aBP than those without LVH (median aBP 195 mm Hg (IQR 155-216) for patients with LVH on ECG versus 147 mm Hg (IQR 129-163) for patients with no LVH on ECG, P < .001; median aBP 181 mm Hg (IQR 153-214) for patients with LVH on TTE versus 152 mm Hg (IQR 137-169) for patients with no LVH on TTE, P = .01). prHTN was associated with a higher median NIHSS (11 (IQR 3-20) for patients with history of hypertension/antihypertensive use versus 6 (IQR 1-14) for patients without this history (P = .02); 9 (IQR 3-19) versus 5 (IQR 2-13) for patients with/without LVH on ECG (P = .085); and 10 (IQR 5-18) versus 5 (IQR 1-13) for patients with/without LVH on TTE (P = .046). CONCLUSIONS:Patients with ICH who have prHTN have higher aBP and NIHSS, suggesting that prHTN may worsen reactive hypertension in the setting of ICH.

Introduction Elevated body mass index (BMI) and obesity have been associated with decreased mortality rates in hospitalized cardiac patients, and improved 3-month functional outcomes in patients with intracerebral hemorrhage. The mechanism for this association in unknown and validation in larger cohorts is lacking. Methods Prospectively collected data from intracranial hemorrhage patients (SAH, ICH and SDH) from two institutions were retrospectively reviewed for the association of BMI (evaluated continuously and in quartiles defined as underweight BMI<18.5, normal weight BMI 18.5-24.9, overweight BMI 25-29.9 and obese BMI>30) and 12-month mRS (dichotomized as 0-3 versus 4-6). Multivariable, backward, step-wise logistic regression models were constructed to evaluate the impact of BMI on outcome adjusting for bleed type, age, APACHE-2 score, admission NIHSS, black race, sex, diabetes, hypertension, baseline mRS and comfort care status. Results A total of 711 patients (N=275 SAH, 188 SDH, 311 ICH) were enrolled between 7/2008-5/2016. The median BMI was 27 (range 13-67), 4% were underweight, 33% normal weight, 33% overweight and 30% obese. Factors associated with increased BMI included younger age, diabetes, ICH or SAH (compared to SDH), black race, and worse baseline mRS (all P<0.05). Sex, income strata, history of cancer, hypertension, coronary artery disease, tobacco use, admission NIHSS and comfort care status were not significantly associated with BMI. The odds ratios (OR) for 12-month mRS 0-3 increased progressively across BMI quartiles (underweight OR 0.4, normal weight OR 0.6, overweight OR 1.3 and obese OR 1.6; P<0.001; ROC 0.594). In multivariable analysis, after adjusting for other factors, each quartile increase of BMI lead to a nearly two-fold improved odds of favorable 12-month outcome (aOR 1.8, 95% CI 1.3-2.4, P<0.001). Conclusions In intracranial hemorrhage patients, increasing BMI and obesity were associated with improved 12-month functional outcomes independent of baseline mRS, bleed type, age, race, sex, diabetes, hypertension, comfort care or admission clinical status

OBJECTIVE:To determine the incidence and predictors of acute cerebral ischemia and neurologic deterioration in intracerebral hemorrhage (ICH) patients after an institutional protocol change in systolic blood pressure (SBP) target from <160 to <140 mm Hg. METHODS:We retrospectively compared persons admitted with primary ICH before and after a protocol change in SBP target from <160 to <140 mm Hg. The primary outcomes were presence of acute cerebral ischemia on MRI completed within 2 weeks of ICH and acute neurologic deterioration. RESULTS:= 0.022). A minimum SBP ≤120 mm Hg over 72 hours was associated with cerebral ischemia, while no patient with a minimum SBP ≥130 mm Hg had cerebral ischemia. Acute cerebral ischemia was significantly associated with worse discharge NIH Stroke Scale score, while SBP target was not. CONCLUSIONS:Intensive lowering of SBP <140 mm Hg in acute ICH, particularly allowing SBP <120 mm Hg, is associated with increased remote cerebral ischemic lesions and acute neurologic deterioration.

Burn specialists have long recognized the need for and have role modeled a comprehensive approach incorporating relief of distress as part of care during critical illness. More recently, palliative care specialists have become part of the healthcare team in many U.S. hospitals, especially larger academic institutions that are more likely to have designated burn centers. No current literature describes the intersection of palliative care and burn care or integration of primary and specialist palliative care in this unique context. This Perspective gives an overview of burn care; focuses on pain and other symptoms in burn intensive care unit settings; addresses special needs of critically ill burned patients, their families, and clinicians for high-quality palliative care; and highlights potential benefits of integrating primary and specialist palliative care in burn critical care. MEDLINE and the Cumulative Index to Nursing and Allied Health Literature were searched, and an e-mail survey was used to obtain information from U.S. Burn Fellowship Program directors about palliative medicine training. The Improving Palliative Care in the Intensive Care Unit Project Advisory Board synthesized published evidence with their own research and clinical experience in preparing this article. Mortality and severe morbidity for critically ill burned patients remains high. American Burn Association guidelines lay the foundation for a robust system of palliative care delivery, embedding palliative care principles and processes in intensive care by burn providers. Understanding basic burn care, challenges for symptom management and communication, and the culture of the particular burn unit, can optimize quality and integration of primary and specialist palliative care in this distinctive setting.

Introduction: The efficacy of MDCT-based-angiography in management of acute stroke and/or emergent-large-vessel-occlusion is well established. However, concern for contrast-induced nephropathy(CIN) especially in patients with major risk factors like Diabetes & Chronic kidney disease often delays rapid evaluation of ELVO patients. Many published studies report the overall incidence of CIN after administration of IV or IA iodinated contrast and highlight the direct correlation of dose on higher incidence of CIN. None, however, have examined impact of sequential IV-IA bolus for neuroangiographic evaluation on renal function in patients with DM and/or CKD. Methods: A retrospective study of our 2015-2017 stroke database of 168 patients was conducted to identify all patients with preexisting DM and/or CKD who developed CIN during their hospital course. We also reviewed the prevalence of dehydration (BUN/Cr <20), CHF and anemia (Hb <8 g/dL) for these patients on admission. Results: For all 168 patients; average IA, IV and cumulative IV-IA contrast (Omnipaque 350) doses within 24 hours were 89.9, 91.7 and 181.6 cc respectively. 68 patients had DM and/or CKD of which 3 developed CIN. Under the definition of >=25% increase in baseline Cr within 72-120 hours of receiving contrast, all 3 had CIN. However, under the definition of >=0.5 mg/dL increase in Cr within 72 hours, none had CIN. All 3 only had preexisting DM as risk factor and had age appropriate baseline Cr on admission. The baseline Cr for each of the 3 patients were 0.82, 1.17 & 0.47 mg/dL respectively while the elevated Cr were 1.03, 1.17 & 0.76 mg/dL respectively. All 3 returned to within baseline by discharge with no mortality or need for hemodialysis. Conclusions: There is low risk of developing CIN in high risk patients like CKD or DM following rapid sequential dual IV/IA contrast bolus in acute stroke patients and therefore should not delay rapid neuro-angiographic evaluation

Introduction: Adult onset focal dystonia often affects the upper extremities and cervical region but less often the lower extremities. Dystonia is the second most reported movement disorder post-stroke and often has a delayed presentation ranging from weeks to months. Most reports are in cases where there is permanent and substantial tissue injury. The clinical significance of Basal ganglia infarction or petechial hemorrhage following endovascular therapy for MCA occlusion is not well understood. The development of dystonia in the setting of a recanalized LMCA has never been reported before. Methods: A 39-year-old female presented with Left MCA occlusion. She had no other medical history except for an idiopathic left basal ganglia hemorrhagic stroke 6 months ago with residual mild forearm weakness. She underwent urgent mechanical thrombectomy with successful sequential recanalization of her inferior followed by superior division. The latter was complicated by a mild self-limiting subarachnoid hemorrhage in the left sylvian fissure. She had small petechial hemorrhages in the left basal ganglia on MRI. However, she recovered completely in 5 days and was discharged with a NIHSS of 1 (similar to baseline) as well as mRS of 2. Ten months later, she developed a painful, fixed right lower extremity dystonia where her ankle was inverted and plantarflexed with her toes curled. This was treated with multiple anticholinergic & GABAergic medications as well as Botox to only achieve partial success. Currently

OPINION STATEMENT: Anticoagulation is a vital therapy in a number of different disease processes, and is strongly recommended for the prevention of stroke in patients with atrial fibrillation and/or with mechanical prosthetic heart valves. Studies involving patients on oral anticoagulants (OACs) have revealed that ICH can occur eight times more frequently in this population, with an annual estimated incidence of 0.25 to 1.1%. The decision of whether and when to resume anticoagulation following intracranial hemorrhage is challenging and requires an assessment of associated risks and benefits. Clinical data, imaging, and risk factors for both ischemic and hemorrhagic complications may aid in decision-making. Baseline functional status, life expectancy, compliance with therapy, and family support also impact decision analyses. Currently available data suggest that anticoagulation could be safely restarted in select groups of OAC-ICH patients within 4 weeks of intracranial hemorrhage; however, high-quality randomized, clinical trials are needed.