Risk factors for super-refractory and mortality in generalized convulsive status epilepticus: a 10-year retrospective cohort study.

Background: Generalized convulsive status epilepticus (GCSE) is one of the most challenging life-threatening neurological emergencies. If GCSE becomes super-refractory, it is associated with significant mortality. Although aggressive management of prolonged status epilepticus was conducted, the mortality has not decreased since the late 1990s. Objectives: The present study aimed to explore the risk factors for progression to super-refractory in patients with generalized convulsive status epilepticus (GCSE). Moreover, we illustrated the risk factors for mortality in GCSE patients. Design: An observational retrospective cohort study. Methods: We conducted a retrospective study of patients with GCSE admitted to our neurocritical unit, in Guangzhou, China, from October 2010 to February 2021. The data of sociodemographic information, etiology, laboratory results, treatment, and prognosis were collected and analyzed. Results: A total of 106 patients were enrolled; 51 (48%) of them developed super-refractory status epilepticus (SRSE). Multivariate logistic regression analysis demonstrated that patients with autoimmune encephalitis (p = 0.015) and intracranial infection (p = 0.019) are likely to progress to SRSE. The in-hospital mortality was 11.8% and 9.1% for patients in the SRSE and non-SRSE groups, respectively (p = 0.652). Multivariate logistic regression analysis showed that neutrophil-to-lymphocyte ratios (NLR) at admission were independently associated with in-hospital mortality. Up to 31.4% of SRSE patients and 29.1% of non-SRSE patients died within 6 months after discharge (p = 0.798). Multivariate logistic regression analysis showed that plasma exchange (PE) was a protective factor for 6-month mortality. A high NLR at discharge was a risk factor for 6-month mortality. Conclusion: In the current study, about 48% of GCSE patients progressed to SRSE. Regarding etiology, autoimmune encephalitis or intracranial infection was prone to SRSE. No significant differences were observed in the in-hospital and 6-month mortality between SRSE and non-SRSE groups. Multivariate logistic regression analysis showed that NLR at admission and discharge was an independent predictor of in-hospital and 6-month mortality, respectively. Moreover, PE significantly reduced the 6-month mortality.

Safety of Tigecycline in Patients on Antithrombotic Therapy: A Single-Center Retrospective Study.

INTRODUCTION: The aims of the study were to investigate the risk factors of tigecycline-induced hypofibrinogenemia and to evaluate the safety of tigecycline with concomitant antithrombotic drugs. METHODS: We performed a retrospective analysis of patients who received tigecycline for more than 3 days between January 2015 and June 2019. Clinical and laboratory data were collected including fibrinogen concertation, tigecycline dose, duration of treatment, disease severity, complete blood count, indicators of infection, liver and renal function. Risk factors of hypofibrinogenemia were analyzed by univariate and multivariate analysis. To evaluate the safety of tigecycline and concomitant antithrombotic drugs, bleeding events were assessed by comparing the decline in hemoglobin and the amount of red blood cell transfusion in patients with antithrombotic drugs and those without. RESULTS: This study included a total of 68 cases, 20 of which experienced hypofibrinogenemia while receiving tigecycline treatment. Duration of treatment, cefoperazone/sulbactam combination therapy, and fibrinogen levels prior to initiation of tigecycline were risk factors associated with tigecycline-induced hypofibrinogenemia. There were 26 recorded bleeding incidents, 25 of which happened before the start of tigecycline. Antithrombotic and non-antithrombotic patients did not differ in their hemoglobin decline or need for red blood cell transfusions while taking tigecycline. CONCLUSION: A longer treatment duration, cefoperazone/sulbactam combination therapy, and a lower level of fibrinogen before tigecycline were associated with an increased risk of tigecycline-induced hypofibrinogenemia. A combination of antithrombotic drugs and tigecycline did not aggravate the bleeding events during tigecycline treatment.

Subacute Balamuthia mandrillaris encephalitis in an immunocompetent patient diagnosed by next-generation sequencing.

Balamuthia mandrillaris is a free-living heterotrophic amoeba found in soil that causes a rare and usually fatal granulomatous amebic encephalitis. We report an immunocompetent patient infected with B. mandrillaris encephalitis diagnosed by next-generation sequencing (NGS). Clinical manifestations included sudden headache and epilepsy with disturbance of consciousness. The opening pressure of cerebrospinal fluid (CSF) was 220 mmH2O, with mildly elevated white blood cell numbers and elevated protein levels. Cranial magnetic resonance imaging revealed abnormal signals in the right frontal lobe, left parietal lobe, and left occipital lobe. CSF NGS detected B. mandrillaris. Albendazole and metronidazole combined with fluconazole were administered to the patient immediately, but his condition deteriorated and he eventually died. Encephalitis caused by B. mandrillaris is rare and has a high mortality rate. Clinical manifestations are complex and diverse, but early diagnosis is very important for successful treatment. This can be aided by the metagenomic NGS of CSF.

Could clinical nursing procedures lead to tracheal cuff pressure drop? A prospective observational study.

AIM: To evaluate the dynamic changes in tracheal cuff pressure before and after four clinical nursing procedures including sputum suction, oral care, atomisation inhalation, and turning over, and thus provide references for the adjustment time of cuff pressure in clinical practice. BACKGROUND: Cuff pressure must be kept within the range of 25-30 cmH2 O to ensure effective ventilation and prevent aspiration, while maintaining tracheal blood flow perfusion. DESIGN: A prospective observational study. METHODS: The cuff pressure of 56 intubated patients was adjusted to 28-30 cmH2 O. A cuff pressure monitor was used to continuously monitor cuff pressure changes before and after four clinical nursing procedures (sputum suction, oral care, atomisation inhalation, and turning over) and the cuff pressures at various time points were compared. The semi-quantitative cough strength score (SCSS) was used to evaluate cough strength during sputum suction and the effect of cough strength on cuff pressure during sputum suction. This study followed the STROBE checklist for cross-sectional studies. RESULTS: The cuff pressures during the four clinical nursing procedures of sputum suction, atomisation inhalation, turning over, and oral care, all temporarily increased (p < 0.001) and decreased to varying degrees 20 min later (p < 0.001). Among them, the cuff pressure rose the highest under a state of moderate or strong coughing during sputum suction (78.38 ± 12.13 cmH2 O) and dropped the most at 20 min after the procedure (21.71 ± 4.80 cmH2 O). CONCLUSIONS: The four clinical nursing procedures of sputum suction, atomisation inhalation, turning over, and oral care can all cause different degrees of cuff pressure drop. The decision on whether the cuff pressure needs to be corrected depends on the specific situation. RELEVANCE TO CLINICAL PRACTICE: During clinical practice, the cuff pressure can be individually corrected according to different clinical nursing procedures, which can increase the qualified rate of cuff pressure and reduce the workload of nurses.

The effect of different inflating volume on the measurement accuracy of the modified cuff pressure measurement method.

To evaluate the effect of different inflation volume on the measurement accuracy of the modified cuff pressure measurement method in different shapes of cuffs, so as to provide reference for the correct monitoring of cuff pressure in clinic. In vitro study: The traditional cuff pressure measurement method (the cuff pressure gauge before measurement shows 0 cm H2O) and the modified cuff pressure measurement method (the cuff pressure before measurement shows 25 cm H2O, 28 cm H2O, 30 cm H2O or 32 cm H2O) were used to measure cylindrical and tapered cuffs, and the effect of different inflation volume on cuff pressure was analyzed statistically. Clinical study: patients with the artificial airway established by orotracheal intubation or tracheotomy in Neuro-ICU were prospectively selected as subjects, and the measurement procedure was the same as in vitro study. In vitro study showed that the pressure loss values of cylindrical cuff and tapered cuff using the traditional cuff pressure measurement method were (3.75 ± 0.31) cm H2O and (4.92 ± 0.44) cm H2O, respectively, and clinical study showed that the pressure loss values were (5.07 ± 0.83) cm H2O and (5.17 ± 0.93) cm H2O, respectively. The actual measured values measured by the traditional cuff pressure measurement method of the two cuff shapes were compared with the corrected target value of 28 cm H2O, and the differences were statistically significant (P < 0.000). Both in vitro and clinical study had shown that all differences between the actual measured value and the corrected target value using the modified cuff pressure measurement method (measured with 25 cm H2O, 30 cm H2O, 32 cm H2O) were statistically significant (P < 0.000), and the range of overall differences was (0-1.23 ± 0.25) cm H2O. In vitro study had shown that the pressure variation coefficient (CV) of the tapered cuff was greater than that of the cylindrical cuff, and the difference was statistically significant (3.08 ± 0.25 VS 2.41 ± 0.21, P < 0.000). The traditional cuff pressure measurement method can directly lead to the cuff pressure drop, which is easy to cause the leakage of secretions on the cuffs and the misjudgment of the cuff pressure by medical personnel. However, the modified cuff pressure measurement method can effectively reduce cuff pressure loss, and taking the actual cuff pressure value as the inflation volume is the highest measurement accuracy.The tapered cuff is more susceptible to air volume, so it is necessary to pay attention to its measurement and correction in clinical practice.

Paroxysmal Sympathetic Hyperactivity in Severe Anti-N-Methyl-d-Aspartate Receptor Encephalitis: A Single Center Retrospective Observational Study.

Background: Paroxysmal sympathetic hyperactivity (PSH) is a disorder with excessive sympathetic activity commonly recognized in patients with acquired brain injury. Autonomic instability is frequent in anti-N-methyl-d-aspartate receptor encephalitis (anti-NMDARE). However, PSH in anti-NMDARE has gained little attention. Methods: We retrospectively reviewed 24 patients diagnosed with severe anti-NMDARE in the neuro-intensive care unit (NICU) between 2014 and 2019. Patients were assessed with the PSH assessment measure (PSH-AM) scale, and categorized into "PSH+" group and "PSH-" group. The clinical characteristics, hospital mortality, and functional outcome by modified Rankin Scale (mRS) score at six months after discharge were compared between the two groups. Among patients with PSH+, the clinical features and pharmacotherapy of PSH were summarized and compared. Results: Twenty-four patients were included in the study. Twelve of them (50%) were categorized as PSH+ based on PSH-AM scores. There were no significant differences in the demographic characteristic, GCS scores upon admission, incidence of status epilepticus, teratoma occurrence, hospital mortality, and 6-month mRS between PSH+ and PSH- groups. Patients with PSH+ had increased length of NICU stay, hospital stay and duration of mechanical ventilation. The most prominent clinical features of PSH in severe anti-NMDARE were tachycardia and hyperthermia, while posturing was the relatively mildest clinical feature. Propranolol and clonazepam were more commonly used than gabapentin in pharmacotherapy of PSH in severe anti-NMDARE. Conclusions: The incidence of PSH in severe anti-NMDARE patients was as high as 50%. Patients with PSH demonstrated prolonged NICU stay, hospital stay and increased duration of mechanical ventilation, while no effect on hospital mortality and functional outcome. Clinicians should be aware of the distinctive characteristics and treatment options of PSH in severe anti-NMDARE.

Cell permeable HMGB1-binding heptamer peptide ameliorates neurovascular complications associated with thrombolytic therapy in rats with transient ischemic stroke.

BACKGROUND: Blood-brain barrier (BBB) breakdown and inflammatory responses are the major causes of tissue-type plasminogen activator (tPA)-induced hemorrhagic transformation (HT), while high-mobility group box 1 (HMGB1) exacerbates inflammatory damage to BBB during the process of brain ischemia/reperfusion. This study aimed to investigate the change of HMGB1 after thrombolytic therapy and whether blocking HMGB1 could ameliorate the neurovasculature complications secondary to tPA treatment in stroke rats. METHODS: Sera from acute stroke patients and rats with thrombolytic therapy were collected to investigate HMGB1 secretion. Male Sprague-Dawley rats with 2 h or 4.5 h middle cerebral artery occlusion were continuously infused with tPA followed by administration of membrane permeable HMGB1-binding heptamer peptide (HBHP). The mortality rate, neurological score, HT, brain swelling, BBB permeability, and inflammatory factors were determined. RESULTS: The results revealed that HMGB1 levels were elevated in both stroke patients and rats after tPA treatment. Blocking HMGB1 signaling by HBHP in the rat model of 4.5 h brain ischemia significantly attenuated tPA-related complications, including mortality rate, the degree of hemorrhage, brain swelling, neurological deficits, BBB impairment, microglia activation, and the expressions of inflammatory cytokines. CONCLUSIONS: tPA treatment might induce HMGB1 secretion while blocking HMGB1 with HBHP could markedly reduce the risk of thrombolysis-associated brain hemorrhage and mortality through attenuating BBB damage and inflammatory reactions. These results indicate that HMGB1 may potentiate the risk of HT in tPA administration and that blocking HMGB1 signaling would be helpful in preventing complications brought by thrombolysis in ischemic stroke. TRIAL REGISTRATION: http://www.chictr.org.cn . Unique identifier: ChiCTR-OOC-16010052. Registered 30 November 2016.