Isolated unilateral hypoglossal nerve palsy due to vertebral artery dissection.

We report the case of a patient with unilateral tongue weakness secondary to an isolated lower motor neuron hypoglossal nerve palsy that was caused by a right vertebral artery dissection in the lower neck. The patient had a boggy tongue with a deviation to the right side but an otherwise normal neurological examination. Magnetic resonance angiography showed a narrow lumen of the right vertebral artery in the neck. After initially treating the patient with aspirin in the emergency room and later with warfarin for three months, there was complete recanalization of the right vertebral artery. Only one other case of vertebral artery dissection and twelfth nerve palsy has been reported before.

Red cell distribution width and all-cause mortality in critically ill patients.

OBJECTIVE: Red cell distribution width is a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown. The objective of this study was to investigate the association between red cell distribution width at the initiation of critical care and all cause mortality. DESIGN: Multicenter observational study. SETTING: Two tertiary academic hospitals in Boston, MA. PATIENTS: A total of 51,413 patients, aged ≥ 18 yrs, who received critical care between 1997 and 2007. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The exposure of interest was red cell distribution width as a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown and categorized a priori in quintiles as ≤ 13.3%, 13.3% to 14.0%, 14.0% to 14.7%, 14.7% to 15.8%, and >15.8%. Logistic regression examined death by days 30, 90, and 365 postcritical care initiation, inhospital mortality, and bloodstream infection. Adjusted odds ratios were estimated by multivariable logistic regression models. Adjustment included age, sex, race, Deyo-Charlson index, coronary artery bypass grafting, myocardial infarction, congestive heart failure, hematocrit, white blood cell count, mean corpuscular volume, blood urea nitrogen, red blood cell transfusion, sepsis, and creatinine. Red cell distribution width was a particularly strong predictor of all-cause mortality 30 days after critical care initiation with a significant risk gradient across red cell distribution width quintiles after multivariable adjustment: red cell distribution width 13.3% to 14.0% (odds ratio [OR], 1.19; 95% confidence interval [CI], 1.08-1.30; p <.001); red cell distribution width 14.0% to 14.7% (OR, 1.28; 95% CI, 1.16-1.42; p <.001); red cell distribution width 14.7% to 15.8% (OR, 1.69; 95% CI, 1.52-1.86; p <.001); red cell distribution width >15.8% (OR, 2.61; 95% CI, 2.37-2.86; p <.001), all relative to patients with red cell distribution width ≤ 13.3%. Similar significant robust associations postmultivariable adjustments are seen with death by days 90 and 365 postcritical care initiation as well as inhospital mortality. In a subanalysis of patients with blood cultures drawn (n = 18,525), red cell distribution width at critical care initiation was associated with the risk of bloodstream infection and remained significant after multivariable adjustment. The adjusted risk of bloodstream infection was 1.40- and 1.44-fold higher in patients with red cell distribution width values in the 14.7% to 15.8% and >15.8% quintiles, respectively, compared with those with red cell distribution width ≤ 13.3%. Estimating the receiver operating characteristic area under the curve shows that red cell distribution width has moderate discriminative power for 30-day mortality (area under the curve = 0.67). CONCLUSION: Red cell distribution width is a robust predictor of the risk of all-cause patient mortality and bloodstream infection in the critically ill. Red cell distribution width is commonly measured, inexpensive, and widely available and may reflect overall inflammation, oxidative stress, or arterial underfilling in the critically ill.

Association of low serum 25-hydroxyvitamin D levels and mortality in the critically ill.

OBJECTIVE: We hypothesized that deficiency in 25-hydroxyvitamin D before hospital admission would be associated with all-cause mortality in the critically ill. DESIGN: Multicenter observational study of patients treated in medical and surgical intensive care units. SETTING: A total of 209 medical and surgical intensive care beds in two teaching hospitals in Boston, MA. PATIENTS: A total of 2399 patients, age ≥ 18 yrs, in whom 25-hydroxyvitamin D was measured before hospitalization between 1998 and 2009. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Preadmission 25-hydroxyvitamin D was categorized as deficiency in 25-hydroxyvitamin D (≤ 15 ng/mL), insufficiency (16-29 ng/mL), and sufficiency (≥ 30 ng/mL). Logistic regression examined death by days 30, 90, and 365 post-intensive care unit admission, in-hospital mortality, and blood culture positivity. Adjusted odds ratios were estimated by multivariable logistic regression models. Preadmission 25-hydroxyvitamin D deficiency is predictive for short-term and long-term mortality. At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D deficiency have an odds ratio for mortality of 1.69 (95% confidence interval of 1.28-2.23, p < .0001) relative to patients with 25-hydroxyvitamin D sufficiency. 25-Hydroxyvitamin D deficiency remains a significant predictor of mortality at 30 days following intensive care unit admission following multivariable adjustment (adjusted odds ratio of 1.69, 95% confidence interval of 1.26-2.26, p < .0001). At 30 days following intensive care unit admission, patients with 25-hydroxyvitamin D insufficiency have an odds ratio of 1.32 (95% confidence interval of 1.02-1.72, p = .036) and an adjusted odds ratio of 1.36 (95% confidence interval of 1.03-1.79, p = .029) relative to patients with 25-hydroxyvitamin D sufficiency. Results were similar at 90 and 365 days following intensive care unit admission and for in-hospital mortality. In a subgroup analysis of patients who had blood cultures drawn (n = 1160), 25-hydroxyvitamin D deficiency was associated with increased risk of blood culture positivity. Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for blood culture positivity of 1.64 (95% confidence interval of 1.05-2.55, p = .03) relative to patients with 25-hydroxyvitamin D sufficiency, which remains significant following multivariable adjustment (odds ratio of 1.58, 95% confidence interval of 1.01-2.49, p = .048). CONCLUSION: Deficiency of 25-hydroxyvitamin D before hospital admission is a significant predictor of short- and long-term all-cause patient mortality and blood culture positivity in a critically ill patient population.

Elevation of blood urea nitrogen is predictive of long-term mortality in critically ill patients independent of "normal" creatinine.

OBJECTIVE: We hypothesized that elevated blood urea nitrogen can be associated with all-cause mortality independent of creatinine in a heterogeneous critically ill population. DESIGN: Multicenter observational study of patients treated in medical and surgical intensive care units. SETTING: Twenty intensive care units in two teaching hospitals in Boston, MA. PATIENTS: A total of 26,288 patients, age ≥ 18 yrs, hospitalized between 1997 and 2007 with creatinine of 0.80-1.30 mg/dL. INTERVENTIONS: None. MEASUREMENTS: Blood urea nitrogen at intensive care unit admission was categorized as 10-20, 20-40, and >40 mg/dL. Logistic regression examined death at days 30, 90, and 365 after intensive care unit admission as well as in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models. MAIN RESULTS: Blood urea nitrogen at intensive care unit admission was predictive for short- and long-term mortality independent of creatinine. Thirty days following intensive care unit admission, patients with blood urea nitrogen of >40 mg/dL had an odds ratio for mortality of 5.12 (95% confidence interval, 4.30-6.09; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Blood urea nitrogen remained a significant predictor of mortality at 30 days after intensive care unit admission following multivariable adjustment for confounders; patients with blood urea nitrogen of >40 mg/dL had an odds ratio for mortality of 2.78 (95% confidence interval, 2.27-3.39; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Thirty days following intensive care unit admission, patients with blood urea nitrogen of 20-40 mg/dL had an odds ratio of 2.15 (95% confidence interval, 1.98-2.33; <.0001) and a multivariable odds ratio of 1.53 (95% confidence interval, 1.40-1.68; p < .0001) relative to patients with blood urea nitrogen of 10-20 mg/dL. Results were similar at 90 and 365 days following intensive care unit admission as well as for in-hospital mortality. A subanalysis of patients with blood cultures (n = 7,482) demonstrated that blood urea nitrogen at intensive care unit admission was associated with the risk of blood culture positivity. CONCLUSION: Among critically ill patients with creatinine of 0.8-1.3 mg/dL, an elevated blood urea nitrogen was associated with increased mortality, independent of serum creatinine.

Facial paralysis: a critical review of accepted explanation.

Historically, paralysis of facial muscles has been divided into "upper motor neuron injury" and "lower motor neuron injury". Patients who experience a stroke in the cortex or internal capsule have UMN injury and cannot purse their lips or smile on command. They are, however, able to wrinkle their forehead, raise their eyebrows, and completely close their eyes. Patients with LMN injury, in addition to the aforementioned impairments cannot raise their eyebrows. The classical explanations for these clinical findings are that the upper facial muscles receive bilateral innervation from the cerebral cortex and the lower facial muscles receive only unilateral innervation from the contralateral cerebral cortex. However, a review of the basic science literature indicates that commonly accepted explanations and the pattern of cortical projections are not consistent with anatomical studies. Studies in monkeys demonstrate that both the upper facial nucleus and the lower facial nucleus receive bilateral cortical projections. As well, there is no direct anatomical evidence in human beings that the facial nucleus (upper or lower) receives any innervation from the cortex.