New York Methodist Hospital

About: New York Methodist Hospital is a healthcare organization based out in Brooklyn, New York, United States. It is known for research contribution in the topics: Myocardial infarction & Percutaneous coronary intervention. The organization has 948 authors who have published 936 publications receiving 29954 citations.

Small bowel ischemia following laparoscopic cholecystectomy.

Abstract: Background: Among a myriad of physiological adverse affects of pneumoperitoneum-associated intra-abdominal hypertension, compromise of the mesenteric circulation is well documented.

Relationship between B-type natriuretic peptide and adverse outcome in patients with clinical evidence of sepsis presenting to the emergency department.

Abstract: ACADEMIC EMERGENCY MEDICINE 2011; 18:219–222 © 2011 by the Society for Academic Emergency Medicine Abstract Objectives: Myocardial dysfunction is an important aspect of sepsis pathophysiology. B-type natriuretic peptide (BNP) is a neurohormone released from the ventricles in response to myocardial stretch and volume overload. The authors hypothesized that an elevated BNP in patients presenting to the emergency department (ED) with suspected sepsis are at increased risk for development of adverse events. Methods: This was a prospective, observational, multicenter cohort study in 10 EDs. Patients were eligible if they were older than 18 years, had two or more systemic inflammatory response syndrome (SIRS) criteria, and had suspected infection or a serum lactate level > 2.5 mmol/L. Patients were excluded if they were pregnant, had do-not-attempt-resuscitation status, sustained a cardiac arrest prior to hospital arrival, had known chronic renal insufficiency, or were on dialysis. BNP levels were obtained at arrival. The primary outcome was a composite of severe sepsis, septic shock within 72 hours, or in-hospital mortality. Results: There were 825 patients enrolled (mean ± standard deviation [SD] age = 53.5 ± 19.6 years; 51% were female and 37% were African American). The area under the curve (AUC) for BNP to predict the triple composite outcome was 0.69, and the optimal cut-point of BNP was 49 pg/mL. Patients with a BNP > 49 pg/mL had a greater mortality rate (11.6% vs. 2.1%; p = 0.0001), a greater risk of development of severe sepsis (67.7% vs. 36.8%; p = 0.0001) and septic shock (51.7% vs. 26.4%; p = 0.0001), and a higher rate of the triple composite outcome (69% vs. 37%; unadjusted odds ratio [OR] = 1.9, 95% confidence interval [CI] = 1.6 to 2.1; p < 0.001). The sensitivity was 63% (95% CI = 58% to 67%), specificity was 69% (95% CI = 65% to 73%), negative predictive value (NPV) was 63% (95% CI = 58% to 67%), and positive predictive value (PPV) was 69% (95% CI = 65% to 74%). In multivariate modeling, after adjusting for age, sex, heart rate, white blood cell count, and creatinine, an elevated BNP was associated with increased odds of having the composite outcome. The outcome was similar in the subset of patients who did not have severe sepsis or septic shock upon arrival. Conclusions: In patients who present to the ED with SIRS criteria and suspected infection, an elevated BNP is associated with a worse prognosis but has limited diagnostic utility.

The Disappearance of Cobalamin Absorption Testing: A Critical Diagnostic Loss

Abstract: An appreciation of the physiological peculiarities of cobalamin (vitamin B-12) is indispensable to understanding cobalamin deficiency. Almost alone among B vitamins, cobalamin deficiency is very often linked to failures of absorption (1,2). Adults rarely become symptomatic or anemic just because of poor dietary intake. One peculiarity is how tightly the complicated, high-affinity binding proteinand receptor-dependent absorptive process built around gastric intrinsic factor (IF), and around other binding proteins throughout the body, controls every aspect of cobalamin transport and transfer (2). The IF system assures both delivery from limited animal-derived dietary sources and reabsorption of biliary cobalamin, partially explaining the often muted clinical impact of poor intake. Yet the saturable system’s own somewhat limited capacity and subtly restrictive, even exclusionary features (perhaps meant to exclude nonfunctional cobalamin analogs) also create inefficiencies that are not always obvious. Barely .1 mg of cobalamin is made available from most meals no matter their cobalamin content, and then only if the IF-mediated process functions properly (2,3). The greatest weakness, however, also lies in the heavy dependence of absorption, and thus cobalamin status, on the IFbased system, whose sole back-up, a nonsaturable but dismally inefficient carrier-free diffusion, can transport only 1% of presented cobalamin. Should IF secretion be lost (‘‘pernicious anemia’’) or its delivery of cobalamin to IF receptors fail (intestinal malabsorption), it cannot be compensated dietarily except with cobalamin intake so massive as to be unavailable in nature. As much as 1000 mg would need to be ingested daily to compensate for the failure of both absorption and enterohepatic reabsorption by the IF system, but very few food items contain .1–2 mg/ 100 gm portion (3). The carrier-mediated and carrier-free absorption processes of most other B vitamins, such as folate, are more effective. An important saving grace derives from another peculiarity of cobalamin, its slow turnover. Except for rare defects of cellular utilization, whatever causes cobalamin deficiency in adults must persist for several years to deplete body stores (which exceed daily intake 1000-fold) to the point of clinical consequences. Many potential disturbances, whether malabsorptive or not, are too transitory to produce clinical cobalamin deficiency or often even subclinical deficiency, which consists of biochemical changes without apparent clinical consequences (2,4). Absorption testing Because a clinical diagnosis of cobalamin deficiency, with hematologic or neurologic changes, implies the presence of long-standing gastrointestinal disease until proven otherwise (1), absorption testing has always been an essential task for clinicians and investigators. The traditional Schilling test, designed in 1953, identifies malabsorption by the poor urinary excretion of an orally administered cobalamin dose. When repeated along with a dose of IF, the test also distinguishes between gastric and intestinal defects. If malabsorptive processes stay undiagnosed, management decisions and vitamin replacement strategies tend to be haphazard and incomplete (Table 1). In 1973, Doscherholmen and Swaim (5) expanded the scope of malabsorption to include food-cobalamin malabsorption (FCM), an inability to release food-bound cobalamin and make it available to gastric IF. FCM cannot be diagnosed with the Schilling test, whose radiolabeled test dose of free cobalamin bypasses the need to release food-bound cobalamin. Work from many laboratories in the 1980s and early 1990s established that FCM was associated with 30–50% of all low cobalamin levels, a frequency at least 10-fold that of the more clinically ominous malabsorption of free cobalamin that occurs when gastric IF secretion or its uptake by intestinal IF receptors fails (6). However, the individual impact of FCM on cobalamin status is typically milder and more delayed. That is because FCM affects only a preparatory step and thus compromises rather than abrogates the final IF-mediated steps of absorption (and presumably does not impair reabsorption of biliary cobalamin). Pernicious anemia, the absence of IF, was originally lethal and even now carries the risk of neurologic deterioration if not properly diagnosed and treated (2,3), whereas most persons with FCM have asymptomatic, subclinical cobalamin deficiency or sometimes no deficiency at all (6,7). Numerous studies explored absorption testing methods and the mechanisms of FCM, as reviewed elsewhere (6). It became evident that the mechanisms were more diverse than initially suspected, that FCM does not always require atrophic gastritis and achlorhydria, and that our understanding of FCM and its implications was incomplete (5–7). As one poorly understood example, the intriguing reversal of FCM after antibiotic treatment has been attributed separately to Helicobacter pylori and facultative anaerobes, although neither organism’s role was identified or directly proven (4,7–10). FCM testing never became clinically available and much work remains to be done (6,7). 1 Author disclosures: R. Carmel, no conflicts of interest. * To whom correspondence should be addressed. E-mail: rac9001@nyp.org.

Neuromotor Adverse Effects in 342 Youth During 12 Weeks of Naturalistic Treatment With 5 Second-Generation Antipsychotics

Abstract: Objective Second-generation antipsychotic (SGA) effects in youth were monitored to quantify extrapyramidal side effects (EPS) and to identify risk profiles for treatment-emergent EPS. Method Data were analyzed for the nonrandomized, prospective Second-generation Antipsychotic Treatment Indications, Effectiveness and Tolerability in Youth (SATIETY) inception cohort study. EPS were assessed at baseline and 4, 8, and 12 weeks after naturalistic SGA initiation for schizophrenia, mood, disruptive behavior, and autism spectrum disorders using the Simpson–Angus Scale (SAS), Barnes Akathisia Scale, Abnormal Involuntary Movement Scale (AIMS), and Treatment Emergent Side Effect Scale. Drug-induced parkinsonism was defined by incident mean SAS score >0.33, anticholinergic initiation, or increasing total SAS score ≥2 in patients with baseline EPS. Results In 342 youth aged 13.6 ± 3.5 years (male = 58.2%, antipsychotic-naive = 65.8%), 15.2% developed drug-induced parkinsonism. Raw SGA-grouped drug-induced parkinsonism rates were as follows: quetiapine = 1.5%, olanzapine = 13.8%, risperidone = 16.1%, ziprasidone = 20.0%, and aripiprazole = 27.3%. SGA type, dose, higher age, and lower baseline functioning were jointly associated with drug-induced parkinsonism ( R 2 = 0.18; p p = .0004). Treatment-emergent dyskinesia ranged from 4.5% (aripiprazole) to 15.5% (olanzapine). SGA type, younger age, white race/ethnicity, and baseline AIMS were jointly associated with treatment-emergent dyskinesia ( R 2 = 0.31; p Conclusion In youth, SGA-related EPS rates did not generally exceed those reported in adults, with particularly low rates with quetiapine and olanzapine.