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High doses of sedating drugs are often used to manage critically ill patients with alcohol withdrawal syndrome. To describe outcomes and risks for pneumonia and endotracheal intubation in patients with alcohol withdrawal syndrome treated with high-dose intravenous sedatives and deferred endotracheal intubation. Observational cohort study of consecutive patients treated in the intensive care unit (ICU) of a university-affiliated, community hospital for alcohol withdrawal syndrome, where patients were not routinely intubated to receive high-dose or continuously infused sedating medications. We studied 188 patients hospitalized with alcohol withdrawal syndrome from 2008 through 2012 at one medical center. The mean age (SD) of the subjects was 50.8 ± 9.0 years and their mean ICU admission APACHE (Acute Physiology and Chronic Health Evaluation) II score was 6.2 ± 3.4. Thirty subjects (16%) developed pneumonia, and 38 (20.2%) required intubation. All of the 188 patients received lorazepam (median total dose, 42.5 mg), and 170 of 188 received midazolam, all but 2 by continuous intravenous infusion (median total dose, 527 mg; all administered in ICU); 19 received propofol (median total dose, 6,000 mg); and 19 received dexmedetomidine (median total dose, 1,075 mg). Intubated patients received substantially more benzodiazepine (median total dose, 761 mg of lorazepam equivalent vs. 229 mg for subjects in the nonintubated group; P < 0.0001). Endotracheal intubation was associated with pneumonia and higher acuity of illness (APACHE II score, >10). Intubated patients had a longer duration of hospital stay (median, 15 d vs. 6 d; P ≤ 0.0001). One patient did not survive hospitalization. In this single-center, observational study, where endotracheal intubation was deferred until aspiration or cardiopulmonary decompensation, treatment of alcohol withdrawal syndrome with high-dose, continuously infused sedating medications was not associated with excess morbidity or mortality.

Both alcohol withdrawal syndrome (AWS) and benzodiazepines can cause delirium. Benzodiazepine-associated delirium can complicate AWS and prolong hospitalization. Benzodiazepine delirium can be diagnosed with flumazenil, a GABA-A receptor antagonist. By reversing the effects of benzodiazepines, flumazenil is theorized to exacerbate symptoms of AWS and precludes its use. For patients being treated for alcohol withdrawal, flumazenil can diagnose and treat benzodiazepine delirium without precipitating serious or life-threatening adverse events. Hospital admission records were retrospectively reviewed for patients with the diagnosis of AWS who received both benzodiazepines and flumazenil from December 2006 to June 2012 at a university-affiliated inpatient toxicology center. The day of last alcohol consumption was estimated from available blood alcohol content or subjective history. Corresponding benzodiazepine, flumazenil, and adjunctive sedative pharmacy records were reviewed, as were demographic, clinical course, and outcome data. Eighty-five patients were identified (average age 50.3 years). Alcohol concentrations were detectable for 42 patients with average 261 mg/dL (10–530 mg/dL). Eighty patients were treated with adjunctive agents for alcohol withdrawal including antipsychotics ( n  = 57), opioids ( n  = 27), clonidine ( n  = 35), and phenobarbital ( n  = 23). Average time of flumazenil administration was 4.7 days (1–11 days) after abstinence, and average dose was 0.5 mg (0.2–1 mg). At the time of flumazenil administration, delirium was described as hypoactive ( n  = 21), hyperactive ( n  = 15), mixed ( n  = 41), or not specified ( n  = 8). Response was not documented in 11 cases. Sixty-two (72.9 %) patients had significant objective improvement after receiving flumazenil. Fifty-six patients required more than one dose (average 5.6 doses). There were no major adverse events and minor adverse effects included transiently increased anxiety in two patients: 1 patient who received 0.5 mg on abstinence day 2 and another patient who received 0.2 mg flumazenil on abstinence day 11. This is the largest series diagnosing benzodiazepine delirium after AWS in patients receiving flumazenil. During the treatment of AWS, if delirium is present on day 5, a test dose of flumazenil may be considered to establish benzodiazepine delirium. With the limited data set often accompanying patients with AWS, flumazenil diagnosed benzodiazepine delirium during the treatment of AWS and improved impairments in cognition and behavior without serious or life-threatening adverse events in our patients.

Nelson comments on a study by Moore et al concerning the use of flumazenil to aid in alcohol withdrawal. In nearly three quarters of their patients, there was objective evidence of improvement, although it was only really prominent in over-sedated patients. Those patients with agitated delirium still responded however, which may be akin to reversal of the paradoxical release effects of benzodiazepines seen commonly in young and old patients.

A 57 year-old woman with no history of cardiac disease presented to the emergency department with confusion and seizures secondary to alcohol withdrawal. Elevated troponin levels and an electrocardiogram demonstrating global T-wave inversions prompted coronary angiography, which revealed coronary vessels free of significant disease. An echocardiogram showed both hypokinesis of the left-ventricular mid-segments with apical involvement and a hyperkinetic base consistent with tako-tsubo cardiomyopathy (TCM). Several clinical conditions have been reported as triggers of TCM. We report a case of TCM in a post-menopausal woman that was precipitated by alcohol withdrawal.

Upregulation of glutamatergic neurotransmission resulting from chronic ethanol intoxication may cause a hyperexcitable state during alcohol withdrawal, which may lead to seizures and delirium tremens. The aim of our study was to evaluate the association between a history of alcohol withdrawal-induced seizures and delirium tremens, and a functional polymorphism (Ser310Ala) of the GRIK3 gene coding for the glutamatergic kainate receptor subunit GlurR7 in a sample of well-characterized alcoholics compared to controls. In total, 233 patients meeting DSM-IV alcohol dependence criteria and 309 controls, all of German descent, were investigated. GRIK3 functional polymorphism was determined using PCR (polymerase chain reaction) of lymphocyte DNA. History of alcohol withdrawal-induced delirium tremens and seizures were obtained using the SSAGA (Semi-Structured Assessment for the Genetics of Alcoholism). Data were cross-checked with in-patients’ clinical files. While a significant relationship between history of delirium tremens and the Ser310 allele was detected, no significant results were obtained for alcohol withdrawal-related seizures. Although this result is suggestive for a significant role of this polymorphism in the pathogenesis of delirium tremens in alcohol-dependent individuals, further investigation and confirmation are warranted.

Animal and human studies have shown tolerance, consumption, relapse, and behavioral interactions between ethanol and nicotine, but little is understood about their interaction, especially as it relates to ethanol withdrawal in adulthood for subjects who have an adolescent history of using these drugs. This study investigated nicotine's influence on ethanol withdrawal seizures in two different age groups of male C3H mice. Adolescent and adult male C3H mice, beginning at postnatal day 28 or 70, respectively, were subjected to a 7-day chronic exposure to ethanol only, ethanol plus nicotine, nicotine only, or vehicle treatment. Six weeks later, all the groups were subjected to chronic exposure to ethanol vapors and the severity of their ethanol withdrawal seizures was assessed by handling-induced convulsions. An adolescent exposure to chronic nicotine resulted in an exacerbation of ethanol withdrawal seizures in adulthood. Given this, adolescence may contain a neurophysiological critical period that is sensitive to nicotine and which may result in an altered response to ethanol dependency in adulthood. These findings have serious implications for the long-term consequences following co-abuse of these drugs during adolescence.

In Germany, clomethiazole (CLO) and benzodiazepines are predominantly used as therapeutic agents in the treatment of the alcohol withdrawal syndrome (AWS). These agents have disadvantages such as sedation, risk of respiratory insufficiency, and cardiovascular complications as well as addictive potential. Alternatively, it could be demonstrated that both tiapride (TIA) and carbamazepine (CBZ) are efficient in the treatment of AWS with less toxicity. However, they seem to be less effective in AWS than CLO as single agents. But no systematic comparison of the combination of TIA and CBZ against an established therapeutic standard can be found in the literature. Therefore, we compared the combination of TIA and CBZ with CLO in two open exploratory studies with matched samples. Outcome parameters were heart rate, blood pressure, complications, withdrawal symptoms (CIWA-Ar scale), and general clinical state (CGI scale). A retrospective evaluation of medical records (30 TIA+CBZ, 30 CLO) was followed by an open prospective study (40 TIA+CBZ, 40 CLO). Both studies revealed similar efficacy in terms of psychopathologic and vegetative symptoms. Vegetative recovery seems to be faster with TIA+CBZ. Results of this exploratory study have to be confirmed by a controlled double-blind study with severity of AWS as an experimental factor.

It is well established that genetic factors play a major role in the development of alcoholism in both sexes. Several twin studies demonstrated a nearly equally high magnitude of genetic influence for men and women. However, the genetic sources of vulnerability are supposed to only partially overlap in men and women. Therefore, we evaluated the gender-specific effects of two single nucleotide polymorphisms affecting dopaminergic neurotransmission (dopamine D2 receptor: -141C Ins/Del polymorphism; Dopamine D3 receptor: Bal I) in our large sample of primary alcoholics. Only a gender-specific analysis of subgroups with a putatively high genetic load, e.g., family-history-positive or presence of severe withdrawal complications, revealed significant differences in allele-/genotype-frequency. Our results demonstrate that a varying sex distribution in the samples investigated might contribute to the heterogeneous results reported in association studies for candidate genes in alcoholism and, therefore, should be taken into account in future studies.

Alcohol abuse and alcohol dependence are common problems. It is estimated that more than 10 million Americans have problems with alcohol dependence that adversely affect their lives and the lives of their families. Many of these patients, if hospitalized, have the potential to experience symptoms of alcohol withdrawal. Major alcohol withdrawal symptoms may include seizures and the development of delirium tremens. Obtaining an alcohol consumption history is a critical component to identifying patients at risk and determining the appropriate treatment plan for potential alcohol withdrawal. A protocol was established for identifying and treating patients at risk for alcohol withdrawal. The initiation of the treatment protocol is history- and symptom-based; treatment is symptom-triggered on the basis of frequent objective assessments. The purpose of the protocol is to prevent and control withdrawal symptoms without heavily sedating or hindering a patients' neurological assessment.

Thrombocytopenia is a decrease in the platelet count below 150,000 in a microliter of blood, i.e., below the lower limit of the reference range, which is 150,000–400,000/μL. The phenomenon of thrombocytopenia related to heavy drinking began to arouse interest in the 1960s and 1970s. It was initially described in case reports and clinical studies on small groups. In the following years, the phenomenon itself and the significance of alcohol-induced thrombocytopenia was studied. Many methodological difficulties inhibiting objective conclusions from research were encountered. Model pathological mechanisms of alcohol thrombocytopenia and the effects of alcohol on the structure and function of platelets were described. Furthermore, the phenomenon of rapid normalization of the number of platelets in people who stopped drinking was described. Relationships between alcohol use, its intensity and occurrence, and intensity of thrombocytopenia have been demonstrated. Predictive platelet counts for alcohol withdrawal syndrome complications have been proven and calculated. The risk of occurrence of withdrawal seizures or delirium tremens in alcohol withdrawal syndrome increases significantly when the platelet count is less than 119,000/μL. The knowledge of the nature of the phenomenon of alcohol-induced thrombocytopenia in a clinical environment allows decisions that are more rational. The attention of clinicians should be drawn to the importance of results of blood tests routinely collected on admission. •Heavy drinking may cause thrombocytopenia.•Alcohol use may impact the shape and functions of platelets.•Low platelet counts may predict alcohol withdrawal complications.