History Of Chronic Alcohol Abuse Research Articles

Mediastinitis and septic shock complicating spontaneous esophageal rupture “Boerhaave’s syndrome”: a case report

Boerhaave’s syndrome, also known as spontaneous esophageal rupture, is a rare but life-threatening condition characterized by a tear in the esophagus. It is most commonly caused by a sudden increase in intraesophageal pressure, often due to severe vomiting or retching.Early diagnosis of Boerhaave’s syndrome is crucial for improving patient outcomes. The classic triad of symptoms includes severe chest pain, vomiting, and subcutaneous emphysema (air under the skin). However, not all patients present with this triad, and the diagnosis can be challenging, especially in patients without the typical symptoms.In this case report, we present the clinical details of a 52-year-old male patient who presented to the emergency department (ED) with severe abdominal pain and vomiting for several days. The patient had a history of chronic alcohol abuse and a recent episode of vigorous vomiting.

Histopathological examination of characteristic brain MRI findings in acute hyperammonemic encephalopathy: A case report and review of the literature.

Acute hyperammonemic encephalopathy is associated with distinct brain MRI findings, namely, hyperintensity in T2-weighted sequences as well as restricted diffusion in diffusion-weighted imaging with accentuation in the insular cortex and cingulate gyrus. The pathophysiology and the histopathological correlates of these characteristic MRI findings are largely unknown. We present a 57-year-old male with a history of chronic alcohol abuse, liver cirrhosis and portal hypertension, and a clinical syndrome (variceal bleeding, depression of consciousness, seizures), elevated plasma ammonia levels, and characteristic brain MRI abnormalities suggestive of acute hyperammonemic encephalopathy. A postmortem histopathological examination revealed extensive hypoxic ischemic encephalopathy without evidence for metabolic encephalopathy. No episodes of prolonged cerebral hypoxemia were documented throughout the course of the disease. We conducted a review of the literature, which exhibited no reports of hyperammonemic encephalopathy in association with characteristic brain MRI findings and a consecutive histopathological examination. This is the first report of a patient with acute hyperammonemic encephalopathy together with characteristic brain MRI findings and a histopathological correlation. Although characteristic MRI findings of acute hyperammonemic encephalopathy were present, a histopathological examination revealed only hypoxic pathology without signs of metabolic encephalopathy.

Wernicke's Encephalopathy in Type 2 Achalasia: Case Report and Literature Review.

Achalasia is primarily a smooth muscle motility disorder of the esophagus driven by aberrant peristalsis and failure of sphincter relaxation. Notably, achalasia is a heterogeneous disease with primarily 3 possible pattern subtypes. According to the review of current cases and literature regarding achalasia, patients primarily present with dysphagia, usually to solids and, if progressed, to solids and liquids. Rarely, untreated achalasia may result in thiamine deficiency and present as Wernicke-Korsakoff syndrome (WKS). This acute neurologic condition primarily affects the central and peripheral nervous system and is known by the triad of ataxia, ophthalmoplegia, and confusion. Individuals who present with WKS typically have a notable history of chronic alcohol abuse with decreased thiamine intake and metabolism. Although less common, individuals with WKS may have a pertinent history of starvation, anorexia nervosa, and malnutrition. This case highlights a unique presentation of Wernicke's encephalopathy (WE) in a 30-year-old woman with severe type II achalasia complicated by a 60-pound weight loss in a span of 2 months. According to our literature review, there have only been 2 previously reported cases of severe achalasia leading to the development of WE. Considering the limited number of case reports available, WE must be in the differentials in patients with underlying achalasia, and our case report highlights this unusual presentation with corresponding brain imaging and manometry testing.

Histomorphological Changes in Pancreas and Liver among Chronic AlcoholicsAn Autopsy Study

Introduction: The clinical and pathological association between pancreatitis and alcohol abuse is well recognised, however the concurrence of prevalence of alcoholic related pancreatitis and liver disease is less well studied. Aim: To evaluate frequency of histomorphological changes in pancreas and liver among patients with history of alcohol abuse and observe the prevalence of coexistence between chronic pancreatitis and liver cirrhosis. Materials and Methods: This was observational cross-sectional study conducted in Department of Pathology at Lokmanya Tilak Municipal Medical College, Mumbai, Maharashtra, India, from July 2013 to July 2018. The study included 1917 autopsies and 107 cases with a documented history of chronic alcohol abuse. Haematoxylin and Eosin (H&E) staining was done on all sections and special stain like Masson’s trichrome was performed as per indication. Gross and microscopy were studied under variable defined parameters. Data was entered in Microsoft Excel sheets. Results: Histomorphologically, 12 cases (11.21%) were diagnosed as pancreatitis; 10 cases (9.34%) were of acute pancreatitis and two cases (1.86%) were of chronic pancreatitis. Total 21 cases were diagnosed as liver cirrhosis. The most dominant pattern of fibrosis seen in pancreatitis was perilobular and interlobular periductal fibrosis. The frequency of pancreatitis (14.28%) and pancreatic fibrosis (38.09%) was found to be more in cirrhotics. Chronic pancreatitis was commonly seen in cirrhotics than in non cirrhotics. Similarly, liver cirrhosis was more commonly observed in cases of chronic pancreatitis. Conclusion: The frequency of histomorphological changes seen in pancreas and liver was observed considerably among patients giving history of alcohol abuse. The prevalence of co-existence of chronic pancreatitis and liver cirrhosis was 50%.

Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori

Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

The Course of Cognitive Performance during Inpatient Treatment in Patients with Alcohol Use Disorder with No, Mild or Major Neurocognitive Disorders.

AimsIn patients with a history of chronic alcohol abuse, neurocognitive disorders (NCD) are not uncommon. The current study aimed to explore the course of cognitive performance, as measured by the Montreal Cognitive Assessment (MoCA), and everyday cognitive functioning, as measured by the Patient Competency Rating Scale (PCRS), in a large group of patients with alcohol use disorder (AUD) admitted to the Center of Excellence for Korsakov and Alcohol-related Cognitive Impairments.MethodsA multiple time-series design was used, in which the MoCA was administered at three time points of assessment, and the PCRS was completed by both the patient and a clinician at two time points, all during clinical treatment.ResultsA total of 524 patients were included, 71 of whom were diagnosed with AUD only, 284 with AUD and mild NCD (ARCI) and 169 with AUD, major NCD and fulfilling criteria for Korsakoff’s syndrome (KS).ConclusionsCognitive performance improved for all three groups during treatment, sustained abstinence and recovery from AUD. A low memory performance on the MoCA without improvement over time was predictive for KS, while improvement on this domain did not differentiate between AUD and ARCI. Changes in overall cognitive performance and orientation in patients with KS were positively related to changes in everyday cognitive functioning.

S3321 Recurrent Acute Pancreatitis Secondary to Pancreatic Divisum Anomaly

INTRODUCTION: Pancreatic divisum (PD) is a congenital malformation that occurs when the ventral and dorsal ducts of the pancreas fail to fuse. Inadequate drainage of pancreatic secretions from the minor papilla results in ductal distension and recurrent pancreatitis. We present a patient with PD who developed acute necrotizing pancreatitis (ANP) complicated by walled off pancreatic necrosis (WOPN). CASE DESCRIPTION/METHODS: 64-year-old female with history of chronic alcohol abuse and IBD presented with epigastric abdominal pain and emesis. Labs showed normal triglycerides, elevated lipase and amylase. Abdominal US ruled out gallstones. Abdominal CT showed pancreatic inflammation with several cystic-appearing fluid collections. She was treated conservatively. Repeat abdominal CT showed multiple increased peripancreatic fluid collections with mass effect on the stomach (Figure 1). Persistent abdominal pain led to ERCP which displayed complete PD and high-grade pancreatic duct fistula in the body and tail. Ventral and dorsal duct sphincterotomies were done with stent deployment in each duct. EUS revealed 3 peripancreatic fluid collections (consistent with WOPN); the largest was adjacent to the gastric antrum. Purulent drainage was noted after 3 cystogastrostomy incisions. Antibiotics were initiated. Patient eventually had recurrent pancreatitis, requiring repeat minor papilla sphincterotomy with dorsal pancreatic duct stent exchange. DISCUSSION: WOPN is a late complication of ANP, occurring more than 4 weeks after the initial attack. It can cause obstruction and fistula. Due to her PD anatomy, we suspect the patient had previous indolent acute pancreatitis episodes however they were falsely attributed to her IBD. Thus, delaying diagnosis of acute pancreatitis and leading to ANP and WOPN. The lifetime risk of pancreatitis in PD patients is similar to the general population. Consider PD in young, female patients in whom etiologies such as, gallstones and alcohol use, have been excluded. Alcohol abuse in context of her PD anatomy could have amplified our patient’s risk of acute pancreatitis. CT and MRI scans do not reliably detect PD thus ERCP remains the diagnostic test. Minor papilla sphincterotomy, papillary dilatation, stent insertion and pancreatic resection are treatment options. Since recurrent acute pancreatitis can lead to chronic pancreatitis, it is important to detect PD early. Follow up imaging in 3-6 months after pancreatitis resolution is vital, especially in patients with WOPN, to exclude neoplasm.Figure 1Figure 2.: Fig 1. and 2: CT abdomen and pelvis with contrast showing significantly compressed gastric lumen and multiloculated collections surrounding the pancreas, along the fundus of the stomach measuring 8 × 4.3 cm with mass effect, slightly inferiorly along the fundus and body measuring 7.7 × 4.2 cm, and along the antrum measuring 7.9 × 4.3 cm with surrounding fat stranding and mass effect.

Unusual subdural empyema in a homeless patient diagnosed by molecular approach: a case report

BackgroundWe report a case of subdural empyema in a homeless patient caused by Bartonella quintana. B. quintana is a facultative intracellular bacteria for which bacterial growth is fastidious. The molecular biology approach has been a real help in establishing the diagnosis.Case reportA 59-years old homeless patient, with a history of chronic alcohol abuse, was brought to the emergency department with a massive subdural empyema. Extensive microbiological evaluation didn’t reveal any pathogen in the pus collected before antibiotic treatment. B. quintana was detected in the pus from the empyema using a 16S rRNA-based PCR. Histology of intraoperative samples was consistent with the diagnosis and a serological assay was positive. The patient responded well to a treatment that included craniectomy with drainage of the loculated pus, total removal of the infected capsule and a combination of antibiotics.ConclusionThis unique case of B. quintana-related empyema illustrates the risk of secondary infection of subdural hematoma with B. quintana since such infections have recently reemerged, predominantly among the homeless populations. Patients with subdural empyema in at-risk populations should be systematically evaluated for B. quintana with an appropriate diagnostic approach involving molecular biology.

Peripheral polyneuropathy after acute methanol poisoning: Six-year prospective cohort study

BackgroundMethanol is a widely used industrial short-chain aliphatic alcohol with known neurotoxic properties. Mass poisoning outbreaks due to the consumption of methanol-adulterated alcoholic drinks present a challenge to healthcare providers due to the high mortality and serious central nervous system (CNS) damage in survivors. However, the impact of methanol exposure on the peripheral nervous system is unknown. ObjectivesTo investigate the role of acute methanol exposure in the development of peripheral polyneuropathy (PNP) during the years following discharge from the hospital. MethodsA total of 55 patients with confirmed methanol poisoning (mean age of 47.9 ± 3.6 years; 9 females) were examined 4 times within a 6-year prospective longitudinal cohort study. The program included neurological and electromyographic examinations, visual evoked potentials, ocular examinations with retinal nerve fibre layer thickness measurements, brain magnetic resonance imaging, and a series of biochemical and toxicological tests. ResultsPNP was observed in 20/55 (36 %) patients, which, in most of the cases, was mild axonal sensorimotor neuropathy. In 8/55 (15 %) patients, worsening of electromyographic findings was registered during the follow-up period, including 5 cases with newly diagnosed PNP and 3 cases of PNP progression. In one subject, complete reversal of PNP was registered after cessation of alcohol intake. The patients with PNP were significantly older (57.3 ± 5.3 versus 42.5 ± 3.9 years; p < 0.001), with higher blood glucose (5.93 ± 0.97 versus 4.81 ± 0.32 mmol/L; p = 0.035) and lower vitamin B1 (45.5 ± 7.4 versus 57.5 ± 5.2 ug/L; p = 0.015) concentrations. The number of chronic alcohol abusers was significantly higher in the PNP group (17/20 versus 20/35; p = 0.034). No associations between PNP prevalence/ dynamics and acute parameters of poisoning severity, arterial blood pH (7.26 ± 0.07 with PNP versus 7.18 ± 0.09 without PNP; p = 0.150), or serum methanol (1320.0 ± 700.0 with PNP versus 1430.0 ± 510.0 mg/L without PNP; p = 0.813) and ethanol (460.0 ± 560.0 with PNP versus 340.0 ± 230.0 mg/L without PNP; p = 0.675) concentrations at admission were found. No difference in the number of patients with visual (9/20 with PNP versus 12/35 patients without PNP; p = 0.431) and CNS sequelae (9/20 with PNP versus 15/35 patients without PNP; p = 0.877) of poisoning was present. DiscussionDespite the relatively high number of PNP cases, no association was found between the severity of acute methanol poisoning and the prevalence of PNP and its dynamics during six years of observation. We did not find an association between methanol-induced visual/ brain damage and the prevalence of PNP in survivors of poisoning. A high prevalence of PNP and its progression might be attributed to other causes, mainly a history of chronic alcohol abuse and insufficiently treated diabetes mellitus. Our results highlight the importance of complete cessation of alcohol consumption and better control of glycaemia in diabetic patients in the prevention and treatment of peripheral PNP.

Intubation in acute alcohol intoxications at the emergency department

BackgroundGuidelines recommend endotracheal intubation in trauma patients with a Glasgow coma scale (GCS) < 9 because of the loss of airway reflexes and consequential risk of airway obstruction. However, in patients with acute alcohol intoxication guidelines are not clear. Thus, we aimed to determine the proportional incidence of intubation in alcohol intoxication and compare the clinical characteristics of intubated and non-intubated patients, as well as reasons for intubation in all patients and in the subgroup of patients with reduced GCS (< 9) but without traumatic brain injury.MethodsWe performed a retrospective analysis of all consultations to an urban ED in Switzerland that presented with an acute alcohol intoxication between 1st June 2012 and 31th Mai 2017. Patient and emergency consultations’ characteristics, related injuries, intubation and reason for intubations were extracted. As a subgroup analysis, we analysed the patients with a GCS < 9 without a traumatic brain injury.ResultsOf 3003 consultations included from 01.06.2012 to 31.05.2017, 68 were intubated, leading to a proportional incidence of 2.3% intubations in alcohol-intoxication. Intubated patients had a lower blood alcohol concentration (1.3 g/kg [IQR 1.0–2.2] vs. 1.6 g/kg [IQR1.1–2.2], p = 0.034) and less often suffered from chronic alcohol abuse (1183 [39.4%] patients vs. 14 [20.6%], p = 0.001) than non-intubated patients. Patients with trauma were intubated more often (33 patients [48.5%] vs. 742 [25.3%], p < 0.001). In subgroup analysis, 110/145 patients (74.3%) were not intubated; again, more intubated patients had a history of trauma (9 patients [25.7%] vs. 10 [9.1%], p = 0.011).ConclusionsIntubation in alcohol-intoxicated patients is rare and, among intoxicated patients with GCS < 9, more than two thirds were not intubated in our study - without severe complications. Trauma in general, independent of the history of a traumatic brain injury, and a missing history of chronic alcohol abuse are associated with intubation, but not with blood alcohol concentration. Special caution is required for intoxicated patients with trauma or other additional intoxications or diseases.

Health-related quality of life determinants in survivors of a mass methanol poisoning outbreak: six-year prospective cohort study

Purpose: The effect of acute methanol poisoning on the follow-up quality of life of survivors in mass poisoning outbreaks is not known. The objective of this is to study the impact of visual and central nervous system (CNS) sequelae of methanol poisoning on long-term health-related quality of life (QoL) of survivors, its clinical determinants, and dynamics.Materials and methods: A total of 54 patients with confirmed methanol poisoning (mean age 46.7 ± 13.4 years, 9 females) were examined consequently three times within six-year prospective cohort study and compared to 23 controls with the history of chronic alcohol abuse. The following tests were performed: SF-36 QoL questionnaire, visual evoked potentials (VEP) of optic nerve, ocular examination with retinal nerve fiber layer (RNFL) thickness measurement, brain magnetic resonance imaging (MRI), and biochemical and toxicological tests.Results: Acute methanol poisoning led to significant decrease in physical component summary (PCS) compared to PCS of age-adjusted controls (mean score with SD 46.8 ± 11.0 versus 52.3 ± 9.4 points; p = .003). In 17/40 (42.5%) patients with three rounds of examination, signs of severe disability (≤30 points in at least one score) were present six years after discharge, with negative dynamics of PCS score during the observation period. The patients with abnormal RNFL thickness had lower PCS (mean difference 10.5 points; 95%CI 3.5–17.5, p = .004) and mental component summary score (9.5 points; 95%CI 1.9–17.1, p = .015) compared to the patients with normal RNFL. Signs of physical and mental adaptation to long-term visual sequelae were registered with gradual reduction of difference in most of physical and mental components scores compared to the patients with normal RNFL during six years of observation. Signs of hemorrhagic brain lesions were associated with permanent decrease of PCS score (mean difference 7.4 points; 95%CI 0.6–14.0; p = .033), bodily pain (8.7 points; 95%CI 1.6–17.6; p = .018), and social functioning (8.2 points; 95%CI 3.0–17.4; p = .005) six years after discharge. No effect of type of antidote (fomepizole versus ethanol) and extracorporeal enhanced elimination modality (intermittent hemodialysis versus continuous renal replacement therapy) applied in hospital on long-term QoL was found (all p > .05).Conclusion: Acute methanol poisoning was associated with a significant decrease of health-related quality of life of survivors persisting for at least six years after discharge. The more pronounced decrease in QoL scores was observed in the patients with hemorrhagic brain lesions and visual sequelae of poisoning with abnormal RNFL thickness.

Skate or die: Unusual circumstances surrounding a natural cause of death

In a forensic pathologist's mind, a suspicious death scene involving inflicted injuries and a weapon always raises three possible hypotheses regarding the manner of death—homicide, suicide, or accident; the latter is slightly less common. We present a case of a 43-year-old homeless man with a history of chronic alcohol abuse who was found dead in a skate park in Geneva. He was inflicted with a stab wound to his abdomen, with a knife found in situ. With the suspicion of homicide, a crime scene investigation team, including a forensic pathologist, was summoned to the scene. However, further examination of the body revealed a deep cut with hesitation marks on the left forearm. This discovery raised the hypothesis of a suicide. Here, we have described the investigations made by the police and forensic department, along with the circumstances and autopsy findings that determined the cause of death as an effect of a natural disease.

Alcoholic cerebellar degeneration: A case report

Introduction Alcohol-induced cerebellar degeneration is the commonest type of acquired toxic ataxia. The onset of the cerebellar symptoms usually occurs at middle age, with a significant history of chronic alcohol abuse. Permanent cerebellar deficits are observed among alcoholics, and they persist even with alcoholic abstinence. The cerebellum is the structure that controls the stability of the gaze, chronic cerebellar diseases and acute alcohol intoxication affect cerebellar function. Ataxia and nystagmus are neurological manifestations present in this disease. To verify vestibulocochlear disorders observed in a case of alcohol-induced cerebellar ataxia. Material and method It is a clinical case study of alcohol-induced cerebellar ataxia. The patient featured troubled walking (wide-based gait, preserved tactile sensitivity, hyperesthesia of the lower limbs, nystagmus, dysmetria, mild dysdiadochokinesia, numbness in the distal phalanges of the upper limbs, and uncoordinated movement). Results The patient evidenced bilateral hearing loss from the frequency of 3 kHz and absence of ipsilateral reflexes; magnetic resonance imaging (MRI) showed atrophy of the Cerebellar Vermis; scale for the assessment and rating of ataxia (SARA) scored 15; brainstem auditory evoked potential test (BAEP) evidenced diffused dysfunction of the auditory pathways; balance testing showed labyrinthine hypofunction with presence of bidirectional nystagmus, featuring central vestibular disorder and the falls efficacy scale (FES-1-Brazil) evidenced abnormalities. Conclusion The patient started treatment using B12 vitamin, thiamine, and physical therapy. Currently, despite reported balance improvement, he needs ambulation support. He features nystagmus, bilateral dysmetria, mild dysdiadochokinesia, continuous tinnitus in his left ear, blurred vision, and neck pain while moving it.

1848 Chronic Diarrhea Complicated by Hyponatremia as a First Clue to Establish the Diagnosis of Pellagra

INTRODUCTION: We report a case of middle age man with a history of chronic alcohol abuse, who presented with chronic diarrhea for a month resulted in moderate to severe hyponatremia and was diagnosed with a rare in Western World disease of Pellagra. CASE DESCRIPTION/METHODS: This is a relatively young man 49yo with long history of alcohol abuse, who presented with mainly GI symptoms of nausea, non bloody vomiting, watery diarrhea for a month, abdominal pain, and leg rash. Blood work was significant for hyponatremia (121), thrombocytopenia (133), and alcohol level of 87.5. The physical exam was significant for erythematous, dry rash with areas of desquamation on both legs, associated with pruritus and LLQ tenderness. He was evaluated by MICU team, treated for moderate to severe hyponatremia in ER with IV fluids and admitted to medical floor for chronic diarrhea and LE rash workup. Patient has been evaluated by dermatology and Pellagra with other nutritional deficiencies vs Tinea was suspected. He underwent a punch biopsy and started on niacin as well as urea 40% cream. Pathology was consistent with nutritional deficiencies (i.e. zinc, niacin). After careful compilation of all parts of history, physical exam, and pathology, patient was diagnosed with Pellagra and continued on niacin supplementation with resolution of diarrhea and improvement of skin appearance. DISCUSSION: Pellagra is a nutritional disorder that results from inadequate intake of niacin or its precursor, the essential amino acid tryptophan. Pellagra is a disease very nearly eradicated in US and Europe except sporadic cases in at-risk groups (chronic alcoholism, malnutrition, malabsorption. It is classically described by the 3 D’s “diarrhea, dermatitis, and dementia”. While the life threatening presentation of Pellagra is very uncommon nowadays, the most severe cases are usually presented as encephalopathy. In our case patient presented with chronic diarrhea, which caused almost life threatening hyponatremia. Diarrhea as the first presenting symptom along with characteristic rash and history of chronic alcohol leaded to diagnosis of Pellagra, the disease easily treated with prompt administration on niacin. Pellagra is mostly a clinical diagnosis and careful collection of all parts of history and physical exam required to early recognize the disease and initiate a niacin intake. Physicians should have a high index of suspicion in certain groups of patients to early diagnose and cure this potentially fatal but treatable disease.

2314 Pyogenic Liver Abscess in the Setting of Recent Polypectomy

INTRODUCTION: Pyogenic liver abscess (PLA) is a bacterial infection of the liver parenchyma with reported mortality of 6-14%. Early detection is vital to reduce overall morbidity and mortality. Due variability in clinical presentation, a high index of suspicion is necessary to avoid delay in diagnosis and treatment. Intra-abdominal infections such as diverticulitis or pathologic conditions of the biliary tract are the most common etiologies of PLA but micro-perforations in the setting of recent polypectomy leading to bacterial seeding through the portal circulation may account as an under-reported precipitant. CASE DESCRIPTION/METHODS: A 63-year-old male with history of chronic alcohol abuse who was admitted to the ICU on broad spectrum antibiotics after developing acute respiratory failure requiring mechanical ventilation and septic shock. The patient had several days of vague abdominal pain which led to acute worsening with encephalopathy. Initial evaluation in the ED revealed temperature of 106.2 and laboratory results revealed WBC 27.8, lactic acid of 3.6, procalcitonin level 52 ng/mL, alkaline phosphatase 131, AST 90, and ALT 65. CT of the abdomen and pelvis revealed multiloculated cystic mass in the dome of right liver measuring 8.6 cm × 8.1 cm x 7.2 cm. It was noted that patient had underwent a screening colonoscopy approximately three weeks prior to admission and multiple polyps were removed with a hot snare in the ascending, descending and sigmoid colon. Admission blood cultures revealed polymicrobial bacteremia and grew streptococcus and E. coli. Due to concern for underlying liver abscess from recent bacterial seeding from polypectomy, patient underwent IR guided drainage and placement of drain which relieved purulent fluid that cultures eventually became positive for Streptococcus intermedius. Despite appropriate antibiotic coverage, patient had persistent fevers and required transfer to hepatobiliary service for definitive surgical management. Patient underwent hepatic lobectomy and laparoscopic marsupialization of the liver abscess with dramatic improvement of fever curve and leukocytosis. DISCUSSION: PLA in the setting of recent colonoscopy is a known phenomenon, however the incidence is unclear. As colorectal cancer screening rates continue to increase in practice, awareness of the development of PLA in the setting of immunocompromised patients must be highlighted. Patient counseling on this potentially fatal complication should occur especially to immunocompromised patients.

Serum iron, Magnesium, Copper, and Manganese Levels in Alcoholism: A Systematic Review.

The aim of this paper was to review recent literature (from 2000 onwards) and summarize the newest findings on fluctuations in the concentration of some essential macro- and microelements in those patients with a history of chronic alcohol abuse. The focus was mainly on four elements which the authors found of particular interest: Iron, magnesium, copper, and manganese. After independently reviewing over 50 articles, the results were consistent with regard to iron and magnesium. On the other hand, data were limited, and in some cases contradictory, as far as copper and manganese were concerned. Iron overload and magnesium deficiency are two common results of an excessive and prolonged consumption of alcohol. An increase in the levels of iron can be seen both in the serum and within the cells, hepatocytes in particular. This is due to a number of factors: Increased ferritin levels, lower hepcidin levels, as well as some fluctuations in the concentration of the TfR receptor for transferrin, among others. Hypomagnesemia is universally observed among those suffering from alcoholism. Again, the causes for this are numerous and include malnutrition, drug abuse, respiratory alkalosis, and gastrointestinal problems, apart from the direct influence of excessive alcohol intake. Unfortunately, studies regarding the levels of both copper and manganese in the case of (alcoholic) liver disease are scarce and often contradictory. Still, the authors have attempted to summarize and give a thorough insight into the literature available, bearing in mind the difficulties involved in the studies. Frequent comorbidities and mutual relationships between the elements in question are just some of the complications in the study of this topic.

Porphyria cutanea tarda increases risk of hepatocellular carcinoma and premature death: a nationwide cohort study

BackgroundPorphyria cutanea tarda (PCT) is a skin disorder originating from a deficit of the liver enzyme uroporphyrinogen decarboxylase. PCT may be a risk factor for hepatocellular carcinoma (HCC) and other cancers, but the evidence is unclear. We aimed to investigate cancer and premature mortality risk in persons with PCT.MethodsThe cohort study consisted of all Norwegian residents from 18 years between 2000 and 2016 (n = 5.4 million). 612 persons with PCT, and all cancer diagnoses and causes of death were identified through record linkage between national registries. Hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) were adjusted for age, sex, education and calendar years. We additionally compared persons with PCT to persons with a history of chronic alcohol abuse (n = 30,468).ResultsPersons with PCT were more likely to be diagnosed with HCC [adjusted HR (aHR) = 19.7, CI = 8.8–44.0) and gallbladder and biliary tract cancer (aHR = 6.8, CI = 2.2–21.0) than the reference population. A moderate increased risk for HCC (aHR = 3.1, CI = 1.2–7.7) and gallbladder and biliary tract cancer (aHR = 4.0, CI = 1.1–14.4) remained when compared to persons with a history of chronic alcohol abuse. Additionally, compared to the reference population, persons with PCT had an increased risk of premature death (aHR = 1.5, CI = 1.2–1.7), due to the following causes of death: malignant neoplasms (aHR = 1.4, CI = 1.0–1.9), diseases of the liver (HR = 5.5, CI = 2.5–12.2), and drug and alcohol overdose (HR = 9.9, CI = 4.7–20.8).ConclusionsPersons with PCT had an increased risk of HCC and cancer of the gallbladder and biliary tract, as well as premature death. Although most of our findings can likely be explained by common lifestyle risk factors, something inherent in PCT may contribute to the development of HCC.

Development of permanent brain damage after subacute encephalopathy with seizures in alcoholics

PurposeTo describe additional cases of subacute encephalopathy with seizures in alcoholics (SESA) syndrome, and to question the clinical and radiological course. MethodsWe retrospectively analyzed the clinical characteristics, electroencephalography (EEG), MRI studies at the admission and over the following 6 months of 5 cases of SESA syndrome visited our neurology department between 2010 and 2016. ResultsFive middle-aged males with history of chronic alcohol abuse were admitted for confusion, neurological deficit and seizures. Four patients had recurrent partial seizures requiring 2 or more antiepileptic drugs. EEG showed interictal periodic lateralized discharges in 4 patients and focal rhythmic delta activities in 1. Initial MRI studies revealed unilateral hemispheric cortical–subcortical areas of increased T2/ FLAIR signal and restricted diffusion. Follow up examination after 6 months, revealed persistent focal neurological deficits in 3 patients. Follow-up cerebral MRI at 6 months showed a resolution of the hyperintense lesions, but developing focal atrophic changes in all patients. ConclusionSESA syndrome should be included among the alcohol-related encephalopathies as a particular pathophysiological entity. The possibility of permanent brain damage should encourage a better clinical awareness of this syndrome to establish prompt diagnosis, relevant investigation and appropriate treatment of recurrent seizures including, if necessary, intensive care unit treatment.

ACTINOMYCOSIS

SESSION TITLE: Chest Infections 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Actinomycosis is a rarely encountered infection and technically difficult to culture, hence may pose a challenge for the clinician. Awareness regarding this uncommon infection, when dealing with susceptible patients, can lead to early diagnosis and optimal treatment. CASE PRESENTATION: 37 M with history of chronic alcohol abuse, presented complaining of hemoptysis, SOB, subjective fever and generalized myalgias for 2 weeks. PE revealed tachypnea, fever and left lung crackles. Labs showed acute hypoxic respiratory failure and lactate elevation. CT revealed 9 x 6 cm inflammatory-appearing cavitary lung mass in the left lower lobe most likely representing a lung abscess, along with large left sided loculated pleural effusion. Patient was intubated and empiric antibiotic therapy was started.2 left CT were placed for loculated pleural effusion. Sputum and pleural fluid AFB were negative. Pleural fluid was exudative and revealed Gram positive cocci and Gram positive rods, with identification of sulfur granules which was highly suggestive of Actinomyces. Intrapleural fibrinolytic agents were given with optimal drainage of empyema. Patient was extubated and improved clinically DISCUSSION: Diagnosis of Pulmonary Actinomycosis, solely based on clinical presentation is not possible. Imaging studies commonly show air-space consolidation and/or cavitary or mass-like lesions. Parenchymal disease can also extend to pleural cavity and chest wall. BAL for culture is inappropriate since it may only represent colonization. Acceptable specimen include lung biopsy or pleural fluid. Gold-standard for diagnosing Actinomycosis is growth of the bacteria in culture, but is technically difficult and occurs only in a minority of cases. If the suspicion is high, the clinician should indicate this to the microbiologist to ensure appropriate processing specimen measures. Identification of sulfur granules from pleural fluid is strongly supportive of Actinomycosis and may be enough to lead the clinician into the diagnosis and appropriate management. Carbapenems or combination of a beta-lactam with beta-lactamase inhibitor in the setting of lung abscess, is a proper empiric approach.Therapy should be targeted once Actinomycosis has been diagnosed. Intravenous therapy should be given for 2 to 6 weeks, followed by oral route.Length of the oral antibiotic depends on clinical and radiological response. Resolution of radiographic findings may take several months, with 6 months to 1 yr. of oral antibiotics being recommended. CONCLUSIONS: Actinomycosis should be suspected in patients with history of aspiration or at risk for it and individuals with chronic alcohol abuse. A high clinical index of suspicion could lead to the proper usage of diagnostic tools and facilitate the rare growth of the causative pathogen in culture. Proper diagnosis should guide to targeted treatment and follow up, along with optimal duration of antibiotics. Reference #1: Choi J, Koh WJ, Kim TS, et al. Optimal duration of IV and oral antibiotics in the treatment of thoracic actinomycosis. Chest. 2005 Oct. 128(4):2211-7. Reference #2: De Montpreville VT, Nashashibi N, Dulmet EM. Actinomycosis and other bronchopulmonary infections with bacterial granules. Ann Diagn Pathol. 1999 Apr. 3(2):67-74. Reference #3: Kim TS, Han J, Koh WJ, et al. Thoracic Actinomycosis: CT Features with Histopathologic Correlation. AJR Am J Roentgenol. 2006 Jan. 186(1):225-31. DISCLOSURES: No relevant relationships by Jonathan Arnedo, source=Web Response No relevant relationships by Yesika Garcia, source=Web Response No relevant relationships by Seyedmohammad Pourshahid, source=Web Response No relevant relationships by Theo Trandafirescu, source=Web Response

Hemosuccus Pancreaticus: Side-Viewing Endoscopic Diagnosis of a Rare but Fatal Cause of Gastrointestinal Hemorrhage

Hemosuccus pancreaticus (HP) is an extremely rare disease that is usually defined as bleeding in the pancreatic duct. Although it is infrequent, HP can lead to massive gastrointestinal bleeding, which is potentially life threatening. 70-year-old male with a history of chronic alcohol abuse, chronic pancreatitis and UGIB presented with melena. Initial physical examination was unremarkable and vitals were stable. Laboratory studies were significant for hemoglobin of 8.7 g/dL. Endoscopy was insignificant. Patient had repeat episode of melena but repeat endoscopy was again insignificant for cause of bleed. After 3 days, LFT's increased: possibly from drug-induced liver injury or obstructing lesion. CT scan showed a large 4.2x2.9 cm pseudoaneurysm in the head of the pancreas possibly from gastroduodenal artery. Interventional radiology (IR) performed coil embolization, but follow-up ultrasound showed vascular mass enlarged to 5.6x5.8cm. Patient reported melena again and dark blood noted on rectal examination. CT angiography also could not identify the cause of his bleeding. The patient underwent repeat endoscopy with side-viewing scope, Blood extravasation was noted from the ampulla consistent with HP (Figure 1A,B,C). Patient continued to have intermittent bleeding requiring transfusions. After discussion with IR, decision was made to attempt repeat embolization, but the patient clinically worsened and passed away. Although HP is a rare cause of gastrointestinal hemorrhage, it is very important to include it in the differential in patients with history of chronic pancreatitis. HP frequently occurs as a complication of pancreatitis with rupture of a visceral artery aneurysm, but can be caused by trauma, neoplasms, or iatrogenic causes. [1,2] Although CT angiography is the gold standard, it can fail to diagnose HP. In terms of management, surgery or endovascular therapy by interventional radiology showed promising outcomes. [3] In this case, repeated attempt with endoscopy and CT angiography could not identify the HP lesion, which was subsequently successfully detected utilizing a side-viewing endoscope.1378_A.tif Figure 1: No Caption available.1378_B.tif Figure 2: No Caption available.1378_C.tif Figure 3: Repeat endoscopy using side-viewing endoscope showing blood extravasation from ampulla in the duodenum consistent with hemosuccus pancreaticus.