Timing of diffusion weighted imaging lesions in spontaneous intracerebral hemorrhage.

INTRODUCTION: Diffusion weighted imaging (DWI) lesions are common after spontaneous intracerebral hemorrhage (sICH). However, their timing relative to a patient's admission to the hospital is unknown. The purpose of this study is to estimate the timing of new DWI lesions after admission for acute sICH. MATERIAL AND METHODS: Select patients enrolled in a single center prospective study examining the prevalence DWI lesions in acute primary sICH received two MRI scans of the brain after admission. The presence of a new DWI lesion between MRI scans was defined as a new DWI event. A lognormal parametric model was used to estimate the median time (50% percentile) to develop a new DWI lesion. RESULTS: Among the 121 participants enrolled in the study, 63 (52%) had two brain MRIs. The median time from admission to 1st MRI was 1 day (IQR 1.2, range 0.1-8.4). The median time between the 2 MRI scans was 2.1 (IQR 2.9, range 0.02-17.4) days. 30.2% (n = 19) of participants developed a new DWI lesion between MRI scans. The estimated median time from 1st MRI to new DWI event was 6.3 days (95% CI, 4.1 to 9.6). DISCUSSION AND CONCLUSION: Accounting for time from admission to 1st MRI, we found that 50% of new DWI lesions occurred by 7.3 days after sICH admission. Pathophysiologic changes in sICH during this time frame need to be studied in order to elucidate a mechanism for DWI lesions.

Association of Longitudinal Glycemia with Diffusion Weighted Imaging Lesions in Spontaneous Intracerebral Hemorrhage.

OBJECTIVES: Higher glycemia on admission has been associated with diffusion weighted imaging (DWI) lesions in patients with spontaneous intracerebral hemorrhage (sICH). However, the influence of longitudinal glycemia after admission and during a patient's hospitalization on DWI lesions in sICH has not been studied. Our aim was to compare longitudinal glycemia in sICH patients with and without DWI lesions. MATERIAL AND METHODS: Glycemia measurements were abstracted on participants enrolled in a prospective observational study examining predictors for DWI lesions in sICH. Univariate analysis was used to compare mean longitudinal glycemia in sICH patients with and without DWI lesions. Logistical regression was used to determine whether mean longitudinal glycemia was predictive of DWI lesions. RESULTS: DWI lesions were found in 60 of the 121 (49.6%) participants. Mean time-to-MRI was 99.6 h (SD ± 89). During this time interval, 2,101 glucose measurements were analyzed with a median number of 7 (IQR 12, 1-261) measurements per patient. Mean longitudinal glycemia was higher in the DWI positive group compared to the DWI negative group until time-to-MRI (132 mg/dL vs 122 mg/dL, p = 0.03). Mean longitudinal glycemia was found to be predictive of DWI lesions (OR 1.02, 95% CI 1.005 to 1.035, p = 0.011). CONCLUSIONS: Mean longitudinal glycemia was higher in sICH patients with DWI lesions compared to those without DWI lesions. Future research into the association between higher glycemia and DWI lesions in sICH may provide insight into a pathophysiologic mechanism.

Hyponatremia in the Neurologically Ill Patient: A Review.

Hyponatremia is a well-known disorder commonly faced by clinicians managing neurologically ill patients. Neurological disorders are often associated with hyponatremia during their acute presentation and can be associated with specific neurologic etiologies and symptoms. Patients may present with hyponatremia with traumatic brain injury, develop hyponatremia subacutely following aneurysmal subarachnoid hemorrhage, or may manifest with seizures due to hyponatremia itself. Clinicians caring for the neurologically ill patient should be well versed in identifying these early signs, symptoms, and etiologies of hyponatremia. Early diagnosis and treatment can potentially avoid neurologic and systemic complications in these patients and improve outcomes. This review focuses on the causes and findings of hyponatremia in the neurologically ill patient and discusses the pathophysiology, diagnoses, and treatment strategies for commonly encountered etiologies.

Newer Immunotherapies for the Treatment of Acute Neuromuscular Disease in the Critical Care Unit.

OPINION STATEMENT: PURPOSE OF REVIEW: In this review, we discuss current treatment options for commonly encountered neuromuscular disorders in intensive care units. We will discuss epidemiology, pathophysiology, and acute and chronic treatment options for myasthenia gravis, Guillain-Barré syndrome, West Nile virus, Botulism, and amyotrophic lateral sclerosis. RECENT FINDINGS: Eculizumab is the newest immunomodulator therapy approved by the Food and Drug Administration in treatment of myasthenia gravis, shown to improve long-term functional outcomes. Edaravone is the newest therapy in management of amyotrophic lateral sclerosis, shown to slow functional deterioration. Efgartigimod showed great promise in a phase 2 safety and efficacy trial in the treatment of stable generalized myasthenia gravis. Eculizumab was found to be safe in a small phase 2 trial for use in Guillain-Barré syndrome. Currently, therapies such as plasma exchange, intravenous immunoglobulins, and steroids remain the mainstay of treatment in the ICU for many neuromuscular disorders. While there are some newer immunotherapies available, few have been studied in the acute setting. However, with the advent of new immunotherapies and biologics, changes in these approaches may be on the horizon.

Review of Critical Illness Myopathy and Neuropathy.

Critical illness myopathy (CIM) and neuropathy are underdiagnosed conditions within the intensive care setting and contribute to prolonged mechanical ventilation and ventilator wean failure and ultimately lead to significant morbidity and mortality. These conditions are often further subdivided into CIM, critical illness polyneuropathy (CIP), or the combination-critical illness polyneuromyopathy (CIPNM). In this review, we discuss the epidemiology and pathophysiology of CIM, CIP, and CIPNM, along with diagnostic considerations such as detailed clinical examination, electrophysiological studies, and histopathological review of muscle biopsy specimens. We also review current available treatments and prognosis. Increased awareness and early recognition of CIM, CIP, and CIPNM in the intensive care unit setting may lead to earlier treatments and rehabilitation, improving patient outcomes.

Morbidity and mortality rates associated with serial bleeding from the superficial temporal vein in mice.

The authors reviewed 3 years' worth of records of superficial temporal vein phlebotomies that had been carried out in Balb/c mice. Mice that had undergone the phlebotomies had a mortality rate of approximately 1% (4 deaths per 490 procedures). Although the mice were being used in a drug study, necropsy and blood assay results suggest that the four deaths were caused by failure to stop the bleeding after the phlebotomies. The authors offer suggestions for improving morbidity and mortality associated with temporal vein phlebotomy.

Effect of hyperglycemia on progressive paraparesis in a rat etastatic spinal tumor model.

OBJECT: Hyperglycemia has been shown to potentiate ischemic injury of the spinal cord by quenching vasodilators and potentiating tissue acidosis and free radical production. Steroid-induced hyperglycemia is a common event in the surgical management of metastatic epidural spinal cord compression (MESCC). The goal in this study was to determine whether experimentally induced hyperglycemia accelerates neurological decline in an established animal model of MESCC. METHODS: Sixteen Fischer 344 rats underwent a transabdominal approach for implantation of a CRL-1666 breast adenocarcinoma cell line within the vertebral body of L-6. After 72 hours of recovery from tumor implantation, the animals received intraperitoneal injections every 12 hours of either 2 g/kg dextrose in 5 ml 0.09% saline (hyperglycemia, 8 rats) or 5 ml 0.09% saline alone (normoglycemia, 8 rats). Weights were taken daily, and the hindlimb function was tested daily after tumor implantation by using the Basso-Beattie-Bresnahan (BBB) scale (score range 1-21). Animals were killed at time of paralysis (BBB Score < 7), and the volume of epidural tumor growth within the spinal canal was measured. To determine the degree of hyperglycemia induced by this dextrose regimen, a surrogate group of 10 Fischer 344 rats underwent intraperitoneal injections of 2 g/kg dextrose (5 rats) or 0.09% saline (5 rats) every 12 hours, and serum glucose levels were assessed 1, 3, 6, 8, 10, and 12 hours after injections for 24 hours. RESULTS: Dextrose versus saline injections resulted in elevated mean serum glucose at 3 (259 vs 103 microg/dl), 6 (219 vs 102 microg/dl), 8 (169 vs 102 microg/dl), and 10 hours (118 vs 99 microg/dl) after injection, returning to normal levels by 12 hours (96 vs 103 microg/dl) just prior to subsequent injection. All rats had normal hindlimb function for the first 8 days after tumor implantation. Hyperglycemic versus normoglycemic rats demonstrated a worsened median BBB score by postimplantation Day 9 (Score 20 vs 21, p = 0.023) through Day 16 (Score 8 vs 12, p = 0.047). Epidural tumor volume demonstrated a near-linear growth rate across both groups; however, hyperglycemic rats developed paralysis earlier (median 15.5 vs 17.5 days, p = 0.0035), with significantly less epidural tumor volume (2.75 +/- 0.38 cm(3) vs 4 +/- 0.41 cm(3), p < 0.001) at time of paralysis. CONCLUSIONS: In a rat model of metastatic epidural spinal cord compression, rats maintained in a hyperglycemic state experienced accelerated time to paralysis. Also, less epidural tumor volume was required to cause paralysis in hyperglycemic rats. These results suggest that hyperglycemic states may contribute to decreased spinal cord tolerance to compression resulting from MESCC. Clinical studies evaluating the effect of aggressive glucose control in patients with MESCC may be warranted.