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Alcoholic Ketoacidosis Post Mortem

Alcoholic Ketoacidosis As A Cause Of Death In Forensic Cases

Alcoholic Ketoacidosis As A Cause Of Death In Forensic Cases

Volume 75, Issues 23 , 30 October 1995, Pages 163-171 Alcoholic ketoacidosis as a cause of death in forensic cases Author links open overlay panel Jrgen L.Thomsen Get rights and content Forensic pathologists are familiar with alcohol abusers, who are found dead and in whom the cause of death cannot be ascertained. In order to examine the possible role of ketoacidosis for the cause of death in this group of alcohol abusers, the concentrations of ketone bodies (acetone, acetoacetate, D--hydroxybutyrate) were determined in post mortem blood specimens. Determination of the ketone body concentrations were made by a coupled enzymatic head-space gas chromatographic method. The material consisted of blood specimens from 131 deceased persons and was divided into three groups: Group 1: controls, 79 cases of non alcohol abusers; group 2: 35 cases of alcohol abusers with known causes of death and group 3: 17 cases of alcohol abusers without ascertainable cause of death. The geometric means for the sum of the ketone body concentrations in blood were: controls, 109 mol/l; alcohol abusers with known causes of death, 152 mol/l; and alcohol abusers without known cause of death, 590 mol/l. The limit value between the controls and the group of alcoholics with unascertainable cause of death was by logistic regression found to be 531 mol/l (3431224 mol/l). The term ketoalcoholic death is, therefore, suggested, when the measured post mortem blood ketone body concentration in an alcoholic with otherwise unknown cause of death exceeds 531 mol/l. Continue reading >>

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Abstract Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Effect of Alcohols on Serum Osmolality and the Osmolal Gap The normal serum Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Go to: CHARACTERISATION In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Further case series by Levy et al, Cooperman et al, and Fulop et al were subsequently reported, with remarkably consistent features.3,4,5 All patients presented with a history of prolonged heavy alcohol misuse, preceding a bout of particularly excessive intake, which had been terminated several days earlier by nausea, severe vomiting, and abdominal pain. Clinical signs included tachypnoea, tachycardia, and hypotension. In 1974, Cooperman's series of seven ketoacidotic alcoholic patients all displayed diffuse epigastric tenderness on palpation.4 In contrast to patients with diabetic ketoacidosis, the patients were usually alert and lucid despite the severity of the acidosis and marked ketonaemia. When altered mental status occurred, this was clearly attributable to other causes. Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap. This acidosis appeared to result from the accumulation in plasma of lactate and ketone bodies including beta‐hydroxybutyrate (BOHB) and acetoacetate (AcAc).3 Cooperman et al found that near patient testing for ketone bodies using nitroprusside test (Acetest, Ketostix) produced a low to moderate result in th Continue reading >>

The Postmortem Diagnosis Of Alcoholic Ketoacidosis.

The Postmortem Diagnosis Of Alcoholic Ketoacidosis.

Alcohol Alcohol. 2014 May-Jun;49(3):271-81. doi: 10.1093/alcalc/agt177. Epub 2013 Dec 10. The postmortem diagnosis of alcoholic ketoacidosis. Corresponding author: University Center of Legal Medicine, Rue du Bugnon 21, 1011 Lausanne, Switzerland. [email protected] The aim of this article is to review the forensic literature covering the postmortem investigations that are associated with alcoholic ketoacidosis fatalities and report the results of our own analyses. Eight cases of suspected alcoholic ketoacidosis that had undergone medico-legal investigations in our facility from 2011 to 2013 were retrospectively selected. A series of laboratory parameters were measured in whole femoral blood, postmortem serum from femoral blood, urine and vitreous humor in order to obtain a more general overview on the biochemical and metabolic changes that occur during alcoholic ketoacidosis. Most of the tested parameters were chosen among those that had been described in clinical and forensic literature associated with alcoholic ketoacidosis and its complications. Ketone bodies and carbohydrate-deficient transferrin levels were increased in all cases. Biochemical markers of generalized inflammation, volume depletion and undernourishment showed higher levels. Adaptive endocrine reactions involving insulin, glucagon, cortisol and triiodothyronine were also observed. Metabolic and biochemical disturbances characterizing alcoholic ketoacidosis can be reliably identified in the postmortem setting. The correlation of medical history, autopsy findings and biochemical results proves therefore decisive in identifying pre-existing disorders, excluding alternative causes of death and diagnosing alcoholic ketoacidosis as the cause of death. Continue reading >>

Alcohol Abuse Killed Devon Woman Found Dead At Home By Husband, Coroner Concludes

Alcohol Abuse Killed Devon Woman Found Dead At Home By Husband, Coroner Concludes

Alcohol abuse killed Devon woman found dead at home by husband, coroner concludes She was found by her husband lying unresponsive on the floor in the hallway of her home Could not subscribe, try again laterInvalid Email A woman was found dead at her home by her husband after suffering from alcohol abuse, a coroner has said. Sharon Dorothy Humphreys was unemployed when she died age 57 at her home on Barnstaple Street, Bideford, on February 12, 2017. Evidence around the circumstances of her death was heard at an inquest at South Molton Town Hall. Dr Deborah Cook, forensic pathologist, conducted the post-mortem and gave a cause of death of alcoholic ketoacidosis, and acute hemorrhagic pancreatitis, which was contributory but did not cause her death. More ambulance staff hit out at South Western Ambulance Service after calls for boss to resign Dr Aaron Mills, from Wooda Surgery, Bideford, said the last time Mrs Humphreys mentioned alcohol consumption to a doctor she stated she was drinking about two to four times a month, having three to four drinks. He stated she also suffered from asthma and seizures, which were under investigation, but she had missed multiple neurology appointments. On February 12, Mrs Humphreys was found by her husband lying unresponsive on the floor in the hallway of her home. A neighbour called 999 for an ambulance. South Western Ambulance Service Trust were called at 10.46am on February 12, and arrived at 10.55am but resuscitation was withheld. Lesley Patrick, Property Management owner, said when he visited the house every two weeks there was evidence Mrs Humphreys was drinking vodka regularly up until she died. Coroner Dr Elizabeth Earland summarised the evidence and gave her conclusion. She said: It is clear she had a history of alcoholism and ass Continue reading >>

Postmortem Diagnosis Of Alcoholic Ketoacidosis | Alcohol And Alcoholism | Oxford Academic

Postmortem Diagnosis Of Alcoholic Ketoacidosis | Alcohol And Alcoholism | Oxford Academic

Aims: The aim of this article is to review the forensic literature covering the postmortem investigations that are associated with alcoholic ketoacidosis fatalities and report the results of our own analyses. Methods: Eight cases of suspected alcoholic ketoacidosis that had undergone medico-legal investigations in our facility from 2011 to 2013 were retrospectively selected. A series of laboratory parameters were measured in whole femoral blood, postmortem serum from femoral blood, urine and vitreous humor in order to obtain a more general overview on the biochemical and metabolic changes that occur during alcoholic ketoacidosis. Most of the tested parameters were chosen among those that had been described in clinical and forensic literature associated with alcoholic ketoacidosis and its complications. Results: Ketone bodies and carbohydrate-deficient transferrin levels were increased in all cases. Biochemical markers of generalized inflammation, volume depletion and undernourishment showed higher levels. Adaptive endocrine reactions involving insulin, glucagon, cortisol and triiodothyronine were also observed. Conclusions: Metabolic and biochemical disturbances characterizing alcoholic ketoacidosis can be reliably identified in the postmortem setting. The correlation of medical history, autopsy findings and biochemical results proves therefore decisive in identifying pre-existing disorders, excluding alternative causes of death and diagnosing alcoholic ketoacidosis as the cause of death. Alcoholic ketoacidosis: definition and clinical features The entity of alcoholic ketoacidosis, sometimes called alcoholic acidosis in the literature, was first described by Dillon et al. in 1940. In this report, the authors described a series of nine patients who had episodes of sever Continue reading >>

Alcoholic Ketoacidosis (aka)

Alcoholic Ketoacidosis (aka)

Alcoholic ketoacidosis (AKA) is a clinical syndrome seen mostly in chronic alcoholics and frequently seen in patients who binge drink. Typical patients are usually chronic drinkers who are unable to tolerate oral nutrition for a 1 to 3 day period. Patients often have a recent bout of heavy drinking before the period of relative starvation, with persistent vomiting and abdominal pain contributing to their inability to tolerate PO intake. The etiology of Alcoholic ketoacidosis stems from the patient's inability to ingest, absorb and utilize glucose from their diet. The vomiting and nausea prevent the patient from keeping foodstuffs in the GI tract that can cross over and provide nourishment. The alcohol further depressed gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient's ability to eat. The lack of nutrients other than alcohol causes the creation of ketones and an elevated gap ketoacidosis in the absence of diabetes. The prevalence correlates with the incidence of alcohol abuse in a community. No racial or sexual differences in incidence are noted. AKA can occur in adults of any age; it more often occurs persons aged 20-60 years who are chronic alcohol abusers. Rarely, AKA occurs after a binge in persons who are not chronic drinkers. Patients present in a dehydrated state after a bout of heavy drinking and then an ongoing lack of oral intake. This period of poor PO intake lasts from 1 to 3 days. The pathophysiology of AKA starts with low glycogen stores and a lack of oral food intake, which shifts the metabolism from Carbohydrates to fats and lipids. The decreased PO intake causes decreased insulin levels and an increase in counterregulatory hormones, Cortisol, Glucagon, and Epinephrine. Continue reading >>

Www.forensicmed.co.uk

Www.forensicmed.co.uk

patterns of electrolytes in post mortem analysis of vitreous humour (see Coe 1993) Dehydration pattern (e.g. salt consumption, water deprivation, and water loss in diabetes mellitus) Low salt/hypotonic pattern (e.g. cystic fibrosis, fluid loss from the gastrointestinal tract, fatty liver, cirrhosis, and polydipsia). (Expected vitreous electrolytes at post-mortem: sodium 140 – 145mmol/L (Coe 1993) or 150 – 155mmol/L (Dolinak 2005); chloride 115 – 125 mmol/L (Coe 1993); urea 10 – 15mg/dL (Coe 1993) or 25mg/dL (Dolinak 2005)). Madea and Musshoff (2007) highlighted problems with using vitreous humour for post-mortem biochemical analysis; the ante-mortem values for the deceased individual were not known, different analytical methods were used on vitreous humour than for serum, and the equilibration rates were unknown. The following notes regarding post-mortem biochemical analysis can be found in Coe (1993): Urea nitrogen – post-mortem serum levels are stable; average levels in those with no renal disease = 47.4mg/dL (16.9mmol/L), and in cases of sudden death = 13 – 15.5mg/dL (4.64 – 5.5mmol/L); vitreous humour levels apparently mirror serum levels; creatinine is stable and reflects serum levels Sodium – levels fall after death in serum, but are stable in vitreous humour in the early post-mortem period Chloride – serum levels fall after death, whilst vitreous humour levels fall slightly after death Potassium – very high in serum after death, but increases in the vitreous humour in a “linear fashion”, although the post-mortem level is affected by sampling and testing methods, body temperature, urea retention, and a more rapid increase after death in infants. The potassium level in vitreous humour is also erratic in those who died after chronic illness. Continue reading >>

Alcoholic Ketoacidosis Publications And Abstracts | Pubfacts.com

Alcoholic Ketoacidosis Publications And Abstracts | Pubfacts.com

Chem Biol Interact 2018 Jun 5;289:129-140. Epub 2018 May 5. Biological Sciences, Clemson University, Clemson, SC 29634, United States; Environmental Toxicology Program, Clemson University, Clemson, SC 29634, United States. Electronic address: Recent studies indicate a role for the constitutive androstane receptor (CAR), pregnane X-receptor (PXR), and hepatic xenobiotic detoxifying CYPs in fatty liver disease or obesity. Therefore, we examined whether Cyp3a-null mice show increased obesity and fatty liver disease following 8-weeks of exposure to a 60% high-fat diet (HFD). Surprisingly, HFD-fed Cyp3a-null females fed a HFD gained 50% less weight than wild-type (WT; B6) females fed a HFD. Read More Diabetes Metab 2018 Mar 21. Epub 2018 Mar 21. Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai key Laboratory of Diabetes Mellitus, 600, Yishan Road, 200233 Shanghai, China. Electronic address: Aim: As the prevalence and clinical characteristics of non-alcoholic fatty liver disease (NAFLD) are still unknown in ketosis-onset diabetes, the present study compared the characteristics of NAFLD in type 1 diabetes (T1D), ketosis-onset and non-ketotic type 2 diabetes (T2D) patients. Methods: This cross-sectional study was performed with newly diagnosed Chinese patients with diabetes, including 39 T1D, 165 ketosis-onset and 173 non-ketotic T2D, with 30 non-diabetics included as controls. NAFLD was determined by hepatic ultrasonography, then its clinical features were analyzed and its associated risk factors evaluated. Read More Department of Gastroenterology and Hepatology, NYP-Brooklyn Methodist Hospital, Brooklyn, NY 11215, United States. Glycogenic Continue reading >>

An Evaluation Of The Stability And Prevalence Of Alcohol And Related Biomarkers In Biological Matrices With Applications To The Interpretation Of Medico-legal Cases

An Evaluation Of The Stability And Prevalence Of Alcohol And Related Biomarkers In Biological Matrices With Applications To The Interpretation Of Medico-legal Cases

An evaluation of the stability and prevalence of alcohol and related biomarkers in biological matrices with applications to the interpretation of medico-legal cases Hassan, Huda Mustafa A. (2011)An evaluation of the stability and prevalence of alcohol and related biomarkers in biological matrices with applications to the interpretation of medico-legal cases. PhD thesis, University of Glasgow. Printed Thesis Information: Ethanol is a poison that adversely affects the health of individuals and is detrimental to society as a whole. Analysis of ethanol in biological matrices is the most frequent test carried out in forensic toxicology laboratories with application across a range of cases types including fatalities, road traffic accidents, criminal investigations and workplace drug testing.The interpretation of ethanol concentrations in post mortem samples can be challenging in relation to medico-legal investigations. The source of ethanol can be as a result of the ingestion of an alcoholic beverage or it may have been formed after death. The stability of alcohol is also adversely affected by the presence of bacteria, high temperatures and unsuitable storage containers.A robust and sensitive method was developed for the analysis of common volatiles such as ethanol, methanol, isopropanol, acetone and n-propanol using headspace gas chromatography coupled with a flame ionization detector (HS-GC-FID). The method was validated in accordance with ISO/IEC 17025, and was used to investigate the stability of volatiles in blood when stored under different conditions, and to investigate the prevalence of volatiles in different biological matrices collected post-mortem. Storage of blood samples in the freezer within sample vials containing preservative and antioxidant improved the stab Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [ 1 , 2 ] Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting. [ 3 , 4 , 5 ] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). [ 6 ] Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). The pathogenesis of AKA is complex. [ 7 ] Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not been fully elucidated. The following are the 3 main predisposing events: Delay and decrease in insulin secretion and excess glucagon secretion, induced by starvation and counter-regulatory hormones Elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) secondary to alcohol metabolism Volume depletion resulting from vomiting and poor oral intake of fluids During starvation there is decrease in insulin secretion and increases in production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth horm Continue reading >>

Vitreous Humor: A Short Review On Post-mortem Applications

Vitreous Humor: A Short Review On Post-mortem Applications

Received Date: September 01, 2014; Accepted Date: November 12, 2014; Published Date: November 15, 2014 Citation: Baniak N, Campos-Baniak G, Mulla A, Kalra J (2015) Vitreous Humor: A Short Review on Post-mortem Applications. J Clin Exp Pathol 5:199. doi: 10.4172/2161-0681.1000199 Copyright: 2015 Baniak N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Vitreous humor has been investigated since the 1960s, with many debates occurring over the years with regard to the usefulness of its specific applications. The composition of several electrolytes in post-mortem vitreous humour has been extensively studied. Using the fluid for determining the cause of death has also become commonplace, including testing glucose levels of diabetic related deaths, as well as alcohol and drug related fatalities. The debate regarding the composition between two eyes of the same individual has been an issue in the past, but has since been resolved. Vitreous humor; Post-mortem; Thanatochemistry Analysis of chemical changes within intraocular fluid , post-mortem, was introduced by Naumann [ 1 ] and has since generated great interest in the many applications of Vitreous Humor (VH) analysis [ 2 ]. VH is a colourless, jelly-like, hydrophilic gel within the vitreous body with approximately 45 mL in quantity [ 3 ]. It is composed of a complex network of cross-linked collagen fibers and hydrophilic glycosaminoglycan hyaluronan [ 4 ], which constitutes a hydrated gel containing few cells [ 5 , 6 ]. It contains 99% water and solids in the form of macromolecular and low molecular weight constituents, such as suga Continue reading >>

Alcoholic Ketoacidosis As A Cause Of Death In Forensic Cases

Alcoholic Ketoacidosis As A Cause Of Death In Forensic Cases

Alcoholic ketoacidosis as a cause of death in forensic cases PUBLISHED | 1995 in Forensic Science International [IF: 1.99] Abstract Forensic pathologists are familiar with alcohol abusers, who are found dead and in whom the cause of death cannot be ascertained. In order to examine the possible role of ketoacidosis for the cause of death in this group of alcohol abusers, the concentrations of ketone bodies (acetone, acetoacetate, D--hydroxybutyrate) were determined in post mortem blood specimens. Determination of the ketone body concentrations were made by a coupled enzymatic head-space gas chromatographic method. The material consisted of blood specimens from 131 deceased persons and was divided into three groups: Group 1: controls, 79 cases of non alcohol abusers; group 2: 35 cases of alcohol abusers with known causes of death and group 3: 17 cases of alcohol abusers without ascertainable cause of death. The geometric means for the sum of the ketone body concentrations in blood were: controls, 109 mol/l; alcohol abusers with known causes of death, 152 mol/l; and alcohol abusers without known cause of death, 590 mol/l. The limit value between the controls and the group of alcoholics with unascertainable cause of death was by logistic regression found to be 531 mol/l (3431224 mol/l). The term ketoalcoholic death is, therefore, suggested, when the measured post mortem blood ketone body concentration in an alcoholic with otherwise unknown cause of death exceeds 531 mol/l. Continue reading >>

Investigation Of Markers To Indicate And Distinguish Death Due To Alcoholic Ketoacidosis, Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State Using Post-mortem Samples.

Investigation Of Markers To Indicate And Distinguish Death Due To Alcoholic Ketoacidosis, Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State Using Post-mortem Samples.

Data from 191 post-mortem cases where post-mortem blood beta-hydroxybutyrate (HB) and acetone concentrations and vitreous humor glucose concentrations (where available) had been measured were retrospectively investigated to determine the markers required to identify and distinguish between Alcoholic Ketoacidosis (AKA), Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS). Blood HB concentrations above 250 g/mL were considered significant and it was shown to be the preferred marker of ketoacidosis. All cases with significant HB detected also had acetone present (greater than 2mg/dL) demonstrating that acetone can be used as a marker to identify ketoacidosis and can be used to indicate when HB measurement is necessary. Vitreous humor glucose concentrations above 6.9 mmol/L were considered high and indicative of hyperglycemia prior to death. Vitreous humor glucose concentrations can be used to distinguish between DKA and ketoacidosis from other causes and to identify deaths due to HHS. The data showed that ketoacidosis can occur without a history of alcoholism or diabetes. Many diabetics are undiagnosed for many years. Therefore, DKA or HHS should be considered in sudden or unexplained deaths and glucose should be routinely measured especially in cases with risk factors for diabetes including obesity, old age, a history of mental health problems or treatment with atypical antipsychotic drugs including clozapine, olanzapine, quetiapine and risperidone. Continue reading >>

Sudden Unexplained Death In Alcohol Misuse (sudam) Patients Have Different Characteristics To Those Who Died From Sudden Arrhythmic Death Syndrome (sads)

Sudden Unexplained Death In Alcohol Misuse (sudam) Patients Have Different Characteristics To Those Who Died From Sudden Arrhythmic Death Syndrome (sads)

, Volume 13, Issue3 , pp 278283 | Cite as Sudden unexplained death in alcohol misuse (SUDAM) patients have different characteristics to those who died from sudden arrhythmic death syndrome (SADS) There is growing awareness of sudden unexplained death in alcohol misuse (SUDAM) in which there is no obvious cause of death, no evidence of acute alcohol toxicity or alcoholic ketoacidosis, and the heart is morphologically normal. This study describes the characteristics of a cohort with SUDAM from a tertiary cardiovascular referral center and compares the findings with those of individuals who died from sudden arrhythmic death syndrome (SADS). Cases in this retrospective cross-sectional study were identified from a database of referrals to our center spanning approximately 40 years. Cases with recorded heavy use of alcohol and non-alcohol users were selected, then limited to those with SUDAM or SADS aged 16 to 64 years. 62 cases of SUDAM and 41 cases of SADS were identified. The SUDAM group were older than the SADS group; mean age 35.8 years and 27.7 years respectively (P=0.0002). There was also a higher incidence of significant psychiatric illness in SUDAM (19.7%) than SADS (2.4%) cases. Post mortem liver examination was more likely to reveal heavy livers in SUDAM than SADS (2196.1g and 1572.4g respectively; P=0.0033) and more fatty liver change (24.2% and 2.4%). SUDAM tends to occur in individuals who are older and have heavier livers than those with SADS. Psychiatric illness is also more common. SADS, unlike SUDAM, is often associated with heritable channelopathies that may affect surviving family members. Therefore, differentiating between SUDAM and SADS identifies families likely to benefit from screening for these mutations, thus preventing further sudden arrhythmic de Continue reading >>

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