Treatment of Hyponatremia in Patients with Acute Neurological Injury.

BACKGROUND: Little data exist regarding the practice of sodium management in acute neurologically injured patients. This study describes the practice variations, thresholds for treatment, and effectiveness of treatment in this population. METHODS: This retrospective, multicenter, observational study identified 400 ICU patients, from 17 centers, admitted for ≥48 h with subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), intraparenchymal hemorrhage, or intracranial tumors between January 1, 2011 and July 31, 2012. Data collection included demographics, APACHE II, Glascow Coma Score (GCS), serum sodium (Na+), fluid rate and tonicity, use of sodium-altering therapies, intensive care unit (ICU) and hospital length of stay, and modified Rankin score upon discharge. Data were collected for the first 21 days of ICU admission or ICU discharge, whichever came first. Sodium trigger for treatment defined as the Na+ value prior to treatment with response defined as an increase of ≥4 mEq/L at 24 h. RESULTS: Sodium-altering therapy was initiated in 34 % (137/400) of patients with 23 % (32/137) having Na+ >135 mEq/L at time of treatment initiation. The most common indications for treatment were declining serum Na+ (68/116, 59 %) and cerebral edema with mental status changes (21/116, 18 %). Median Na+ treatment trigger was 133 mEq/L (IQR 129-139) with no difference between diagnoses. Incidence and treatment of hyponatremia was more common in SAH and TBI [SAH (49/106, 46 %), TBI (39/97, 40 %), ICH (27/102, 26 %), tumor (22/95, 23 %); p = 0.001]. The most common initial treatment was hypertonic saline (85/137, 62 %), followed by oral sodium chloride tablets (42/137, 31 %) and fluid restriction (15/137, 11 %). Among treated patients, 60 % had a response at 24 h. Treated patients had lower admission GCS (12 vs. 14, p = 0.02) and higher APACHE II scores (12 vs. 10, p = 0.001). There was no statistically significant difference in outcome when comparing treated and untreated patients. CONCLUSION: Sodium-altering therapy is commonly employed among neurologically injured patients. Hypertonic saline infusions were used first line in more than half of treated patients with the majority having a positive response at 24 h. Further studies are needed to evaluate the impact of various treatments on patient outcomes.

Risk factors and outcomes associated with vancomycin-resistant Enterococcus infections with reduced susceptibilities to linezolid.

A retrospective matched case-control study of hospitalized patients with vancomycin-resistant Enterococcus (VRE) infection with reduced susceptibility to linezolid was performed in order to identify risk factors for this infection and describe patient outcomes. Forty-eight linezolid nonsusceptible VRE cases were identified between January 1, 2000, and September 30, 2008, and compared to 96 controls with linezolid-susceptible VRE, matched based on culture date and anatomic site of infection. Demographic, clinical and microbiological data were collected. On univariable analysis, risk factors for reduced linezolid susceptibility included allogeneic hematopoietic stem cell transplant and/or solid organ transplant (odds ratio [OR]: 2.63; 95% confidence interval [CI]: 1.13-6.15; P = 0.025), receipt of immunosuppressive medications (OR: 2.39; 95% CI: 1.08-5.29; P = 0.032) including corticosteroids (OR: 2.40; 95% CI: 1.03-5.58; P = 0.042) and noncorticosteroid immunosuppressives (OR: 2.31; 95% CI: 1.00-5.30; P = 0.049), and receipt of linezolid within 1 year prior to infection (OR: 34.50, 95% CI: 4.60-259.02; P < 0.001). On multivariable analysis, only receipt of linezolid within 1 year remained an independent risk factor for reduced linezolid susceptibility (OR: 31.84; 95% CI: 4.20-241.39; P < 0.001), although most patients with VRE with reduced linezolid susceptibility had not received linezolid in the year prior. Reduced linezolid susceptibility did not impact patient outcomes including clinical or microbiological cure, hospital length of stay, or all-cause mortality.

Evaluation and management of shock States: hypovolemic, distributive, and cardiogenic shock.

Shock states have multiple etiologies, but all result in hypoperfusion to vital organs, which can lead to organ failure and death if not quickly and appropriately managed. Pharmacists should be familiar with cardiogenic, distributive, and hypovolemic shock and should be involved in providing safe and effective medical therapies. An accurate diagnosis is necessary to initiate appropriate lifesaving interventions and target therapeutic goals specific to the type of shock. Clinical signs and symptoms, as well as hemodynamic data, help with initial assessment and continued monitoring to provide adequate support for the patient. It is necessary to understand these hemodynamic parameters, medication mechanisms of action, and available mechanical support when developing a patient-specific treatment plan. Rapid therapeutic intervention has been proven to decrease morbidity and mortality and is crucial to providing the best patient outcomes. Pharmacists can provide their expertise in medication selection, titration, monitoring, and dose adjustment in these critically ill patients. This review will focus on parameters used to assess hemodynamic status, the major causes of shock, pathophysiologic factors that cause shock, and therapeutic interventions that should be employed to improve patient outcomes.