Alcoholic Ketoacidosis
Alcoholic ketoacidosis is a common reason for admission of alcohol dependent persons in hospitals emergency rooms. The term refers to a metabolic acidosis syndrome caused by increased ketone levels in serum . Glucose concentration is usually normal or a little lower. In 1940, Drs Edward S. Dillon, W. Wallace, and Leon S. Smelo, first described alcoholic ketoacidosis as a distinct syndrome . They stated that "because of the many and complex factors, both physiologic and pathologic , which influence the acid-base balance of the body, a multitude of processes may bring about the state of acidosis as an end result." [1] In the 1971, David W. Jenkins and colleagues described cases of three nondiabetic 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. [2] Patients regularly report nausea , vomiting, and pain in abdomen which are the most commonly observed complaints. This syndrome is rapidly reversible and, if taken care of has a low mortality. Other patients present tachypnoea , tachycardia , and hypotension . [3] The main differences between patients with diabetic ketoacidosis is that patients with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis and marked ketonaemia. [4] However, there are cases where alcoholic ketoacidosis can cause death of the patient if not treated with administration of dextrose and saline solutions. [5] Dillon, E.; Dyer, W. Wallace; Smelo, L. S. (November 1940). "Ketone Acidosis in Nondiabetic Adults". Medical Clinics of North America. 24 (6): 18131822. doi : 10.1016/S0025-7125(16)36653-6 . Jenkins, David W.; Eckel, Robert E.; Craig, James W. Continue reading >>
Alcoholic Ketoacidosis As A Cause Of Death, Who Came First?
I read with interest the article ‘The Postmortem Diagnosis of Alcoholic Ketoacidosis’ by Palmiere and Augsburger (2014). However for the sake of truth I must protest against the statement on page 272: ‘The first report in the forensic field suggesting that ketoacidosis could be partially responsible for unexplained deaths in alcoholics dates back to 1993 and concerns a study performed by L.N. Denmark on 49 autopsy cases that included chronic alcohol-abuse related deaths’. Together with my co-authors I submitted an article that was acknowledged by Forensic Science International on 19 January 1993 and published in vol. 60 (Thomsen et al., 1993). In that article we described our results as ‘strongly indicative of ketoacidosis as the sole or contributing cause of death…’. We were convinced that we solved the riddle of ‘Fatty liver deaths’. L.N. Denmarks excellent work on beta-hydroxybutyrate was received at Forensic Science International, 4 April 1993 and published in vol. 62. It had been known for many years that alcoholics, who stop drinking after a binge, may be found dead shortly after. The only abnormality to be found is a fatty liver. There are no drugs to be detected and only insignificant levels of alcohol or none at all. There have been numerous speculations as to the cause and mechanism of death. Severe metabolic disturbances including high levels of free fatty acids do probably play a major role due to the effect on the Krebs Cycle. It has since our publications been confirmed that alcoholic ketoacidosis is the cause of death in a substantial number of alcohol abusers. A quantitative measurement of ketone bodies is now a routine analysis at the institutes of forensic medicine in Denmark. Denmark (1993) measured the levels of beta-hydroxybutyrate Continue reading >>
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 >>
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 >>
Alcoholic Ketoacidosis
Increased production of ketone bodies due to: Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake) Elevated ratio of NADH/NAD due to ethanol metabolism Increased free fatty acid production Elevated NADH/NAD ratio leads to the predominate production of β–hydroxybutyrate (BHB) over acetoacetate (AcAc) Dehydration Fever absent unless there is an underlying infection Tachycardia (common) due to: Dehydration with associated orthostatic changes Concurrent alcohol withdrawal Tachypnea: Common Deep, rapid, Kussmaul respirations frequently present Nausea and vomiting Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms): Usually diffuse with nonspecific tenderness Epigastric pain common Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon Mandates a search for an alternative, coexistent illness Decreased urinary output from hypovolemia Mental status: Minimally altered as a result of hypovolemia and possibly intoxication Altered mental status mandates a search for other associated conditions such as: Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage Hypoglycemia Alcohol withdrawal Encephalopathy Toxins Visual disturbances: Reports of isolated visual disturbances with AKA common History Chronic alcohol use: Recent binge Abrupt cessation Physical Exam Findings of dehydration most common May have ketotic odor Kussmaul respirations Palmar erythema (alcoholism) Lab Acid–base disturbance: Increased anion gap metabolic acidosis hallmark Mixed acid–base disturbance common: Respiratory alkalosis Metabolic alkalosis secondary to vomiting and dehydration Hyperchlorem Continue reading >>
Alcoholic Ketoacidosis
Workup When a chronic alcoholic presents with signs of AKA, the clinician should carefully evaluate the patient, obtain a history, perform a physical exam, and order the appropriate laboratory tests. Laboratory tests and results A comprehensive metabolic profile will allow the medical team to determine the overall clinical picture of the patient. This includes measurement of serum electrolytes, glucose, blood urea nitrogen (BUN), creatinine, lipase, amylase, and plasma osmolality. Also, urinalysis is helpful to detect ketones. Another useful tool is the blood alcohol level [8]. Finally, critically ill patients with positive ketones must have an analysis of their arterial blood gas (ABG) and serum lactate levels. With regards to expected findings, all patients demonstrate ketonuria and a majority display ketonemia. Also common are electrolyte imbalances such as hypokalemia, hyponatremia, hypophosphatemia, and hypomagnesemia. Additionally, the serum glucose may range from low to modest elevation while another abnormality is an increased osmolar gap (secondary to increased acetone and possibly ethanol). Most importantly, AKA is typically characterized by a high anion gap metabolic acidosis, which may be complicated by metabolic alkalosis secondary to concurrent vomiting. In cases where the pH is normal, the increased anion gap is an indicator of ketoacidosis. If there is a normal gap, this is the result of the excretion of ketoacid ions. Additionally, lactic acidosis is observed in more than 50% of cases due to hypoperfusion [9]. Differential diagnoses Differentials include diabetic ketoacidosis (DKA),however, the absence of hyperglycemia excludes this. Pancreatitis may also present similar to AKA and should be ruled out. If alcohol intoxication is not conclusive, serum me Continue reading >>
Homepage Of Awareness Of Sudden Death Syndrome In Alcoholism
Alcoholism is rampant in U.S. and world.People like you reading this page know someone who is alcoholic. They canbe your relatives, friends or co-workers. We are all familiar with thealcohol associated problems in our daily life. These include alcohol relatedsocial, occupational, or legal difficulties such as alcohol related blackouts,argument with friends/family, marital problems, poor job performance, decreasedlife quality and so on. Health professionals may be familiar with the definitionof alcohol abuse or alcohol dependence (as indicated in DSM-III), alcoholrelated health problems such as alcohol withdrawal, alcohol hepatitis,cirrhosis, GI bleeding, cardiomyopathy, and CNS complications (deliriumtremens, generalized seizures), etc. However, few people are aware of thesudden death syndrome associated with alcoholism. The sudden, unexpecteddeath associated with alcoholism is one of the most mystifying complicationsof the abuse of alcohol and it is an entity so poorly understood that itdoes not even bear a generally accepted label or name. In general, deathassociated with alcohol may be classified as following categories: 1. Acute alcoholism and acutealcohol poisoning 3. Increased susceptibilityto diseases and conditions of all manner 4. Aggravation of existingdiseases (hepatic or extra hepatic conditions) 5. Alcohol obscuring co-existingdisease or injury 6. Coincidental death (alcoholuse and death due to other causes) 7. Sudden, unexpected deathassociated with alcoholism Alcohol associated suddendeath syndrome is also termed as unexpected death associated with fattyliver syndrome. This death situation is one of the more frequent amongmedical examiner cases. Typically, the body was found alone at his residenceand the death could not be explained with apparent reasons Continue reading >>
Sudden Cardiac Arrest Induced By Hypoglycemia And Hypokalemia In A Chronic Alcoholic Patient
Sudden cardiac arrest induced by hypoglycemia and hypokalemia in a chronic alcoholic patient Chair and Department of Internal Medicine, Medical University, Lublin, Poland Student Scientifi c Society, Medical University, Lublin, Poland Chair and Department of Nephrology, Medical University, Lublin, Poland A 44-year-old alcoholic patient was admitted to the Cardiac Intensive Care Unit due to sudden cardiac arrest in the mechanism of asystole. Additional examinations revealed hypoglycemia 13 mg/dl and hypokalemia 3.27 mmol/l. Thanks to prompt resuscitation and intravenous infusion of 40% glucose and potassium, the condition of the patient improved. Based on the case reported, causes of sudden cardiac death in alcoholics are discussed. Department of Internal Medicine,Medical University, Staszica 16, 20-081 Lublin, Poland. Sovari A, Kocheril AG, Baas AS: Sudden Cardiac Death, at: http:// emedicine.medscape.com/article... . Brown TM, Harvey AM: Spontaneous hypoglycemia in smoke drinkers. JAMA 941, 117, 12-15. Robinson RT, Harris ND, Ireland RH, Lee S, Newman C, Heller SR: Mechanisms of abnormal cardiac repolarisation during insulin-induced hypoglycemia. Diabetes 2003, 52, 1469-1474. Gordon T, Kannel WB: Drinking habits and cardiovascular disease. The Framingham Study. Am Heart J 1983, 105, 667-673. Kupari M, Koskinen P: Alcohol, cardiac arrhythmias and sudden death. Novartis Found Symp 1998, 216, 68-79, discussion 79-85. Wannamethee G, Shaper AG: Alcohol and sudden cardiac death. Br Heart J, 1992, 68, 443448. Urbano-Marquez A, Estruch R, Navarro-Lopez F, Grau JM, Mont L, Rubin E: The eff ects of alcoholism on skeletal and cardiac muscles. N Engl J Med 1989, 320, 409415. Sieradzki J: Cukrzyca. Vol. 2. Via Medica, Gdask 2006, 646654. Garland PB, Newsholme EA, Randle PJ: Regula Continue reading >>
Alcoholic Ketoacidosis As The Cause Of Death: Thomsen And Co-workers Came First | Marc Augsburger - Academia.edu
Alcoholic Ketoacidosis as the cause of death: Thomsen and co-workers came first Alcohol and Alcoholism Vol. 49, No. 6, pp. 687688, 2014 LETTERS TO THE EDITOR Alcoholic Ketoacidosis as a Cause of Death, REFERENCES Who Came First? Denmark LN. (1993) The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. Jrgen L. Thomsen* Forensic Sci Int 62:22532. Palmiere C, Augsburger M. (2014) The postmortem diagnosis of Institute of Forensic Medicine, University of Southern Denmark, alcoholic ketoacidosis. Alcohol Alcohol 49:27181. Winslwparken 17B, DK-5000 Odense C, Denmark Thomsen JL, Theilade P, Felby S et al. (1993) Alcoholism and ketoacidosis. Forensic Sci Int 60:34. *Corresponding author. Tel.: +45-65503001; Fax: +45-65916227; E-mail: [email protected] doi: 10.1093/alcalc/agu059 Advance Access publication 21 September 2014I read with interest the article The Postmortem Diagnosis ofAlcoholic Ketoacidosis by Palmiere and Augsburger (2014). Alcoholic Ketoacidosis as the Cause of Death: However for the sake of truth I must protest against thestatement on page 272: The first report in the forensic field Thomsen and Co-workers Came Firstsuggesting that ketoacidosis could be partially responsible Cristian Palmiere* and Marc Augsburgerfor unexplained deaths in alcoholics dates back to 1993 andconcerns a study performed by L.N. Denmark on 49 autopsy University Centre of Legal Medicine, rue du Bugnon 21, 1011 Lausanne,cases that included chronic alcohol-abuse related deaths. Switzerland Together with my co-authors I submitted an article thatwas acknowledged by Forensic Science International on 19 *Corresponding author: University Center of Legal Medicine, Rue du Bugnon 21, 1011 Lausanne, Switzerland. Tel.: +41-021-314-49-61;January Continue reading >>
Sudden Unexpected Death In Alcohol Misusean Unrecognized Public Health Issue?
Int J Environ Res Public Health. 2009 Dec; 6(12): 30703081. Published online 2009 Dec 4. doi: 10.3390/ijerph6123070 Sudden Unexpected Death in Alcohol MisuseAn Unrecognized Public Health Issue? Alexa H. Templeton ,1,* Karen L.T. Carter ,1 Nick Sheron ,1,2 Patrick J. Gallagher ,3 and Clare Verrill 3 1 Liver Research Group, University of Southampton, Southampton General Hospital, Southampton University Hospitals NHS Trust, Tremona Road, Southampton, SO16 6YD, UK; E-Mails: ku.gro.srotcod@retracnerak (K.L.T.C.); [email protected] (N.S.) 2 Clinical Hepatology, Division of Infection, Inflammation and Immunity, University of Southampton Medical School, Southampton, SO16 6YD, UK 3 Department of Histopathology, Southampton University Hospitals NHS Trust, Southampton, UK; E-Mails: [email protected] (P.J.G.); moc.liamtoh@llirreveralc (C.V.) * Author to whom correspondence should be addressed; E-Mail: ku.oc.liamtoh@407ta ; Tel.: 07841427173; Fax: +44(0)23 8079 6603. Received 2009 Oct 29; Accepted 2009 Nov 29. Copyright 2009 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( ). This article has been cited by other articles in PMC. Sudden arrhythmic cardiac death can occur in chronic misusers of alcohol. The only findings at post mortem are fatty liver and a negative or low blood alcohol. This is an under-recognized entity. Coroners post mortems in a typical UK city were studied. Seven out of 1,292 (0.5%) post mortems were deemed to have died of alcohol associated arrhythmic death. Applying this study to the UK as a whole, alcohol related arrhythmic death or as we have termed it SUDAM (Sudden Unexpecte Continue reading >>
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 >>
Alcoholic Ketoacidosisunderrecognized Cause Of Metabolic Acidosis In The Elderly
Alcoholic KetoacidosisUnderrecognized Cause of Metabolic Acidosis in the Elderly The Substance Abuse & Mental Health Services Administration (SAMHSA) reported that substance abuse among adults age 60 years and older is a rapidly growing health problem. The report also stated that in 2000, 17% of Americans age 65 and older had problems with prescription drug and alcohol abuse.1 Most elderly people with alcohol abuse problems have a history of early-life alcohol abuse. However, a significant proportion start drinking later in life in response to traumatic life events such as the death of a loved one, loneliness, pain, insomnia, and retirement. This subset often experiences periods of binge drinking with little or no food intake. Alcoholic ketoacidosis (AKA) is an acute anion gap metabolic acidosis that typically occurs in people with a recent history of binge drinking and little or no nutritional intake. Some patients with AKA also have intractable vomiting and dehydration, and in these cases there is a concomitant metabolic alkalosis. An 86-year-old female, who had been a widow for the past 20 years, presented to the hospital with complaints of nausea, epigastric discomfort, and breathlessness for 2 days. She confessed to a history of alcohol abuse starting shortly after her husbands death and to regularly consuming a pint of hard liquor each day. She had been on an alcohol binge for 4-5 days without eating any food, but she had stopped consuming alcohol because of nausea for 2 days prior to presentation. Although the patient was depressed and admitted to suicidal ideation, she denied ingestion of antifreeze, methanol-containing solvents, rubbing alcohol, or salicylates. Physical examination was remarkable for only signs of dehydration and epigastric tenderness. Fundosc Continue reading >>
Alcoholic Ketoacidosis: Another Risk Of Chronic Alcohol Abuse
Alcoholic Ketoacidosis: Another Risk ofChronic Alcohol acts like poison within the human body. It enters the bloodstream and affects every part of the body, making the drinker vulnerable to serious health consequences. Chronic alcohol abuse exposes the central nervous, digestive, circulatory, immune, skeletal, and muscle systems to severe and long-lasting damage. Alcoholic ketoacidosis (AKA) is a disease that develops from drinking too much alcohol. Learn about this harmful condition and what you can do to prevent it. Alcoholic ketoacidosis occurs when there is an unhealthy buildup of ketones in the body. Ketones are a byproduct of the body burning fat instead of glucose for energy. Cells need glucose and insulin to function properly. The pancreas produces insulin, and glucose comes from the foods you eat. Consuming too much alcohol regularly, combined with a poor diet, can lead to the pancreas failing to produce insulin for a short time. This leads to your body burning fat for energy instead of using the glucose you consume. Without the production of insulin, ketones build up in the bloodstream, causing the life-threatening condition of AKA. Ketoacidosis occurs when the body digests something that gets turned into acid. Alcoholic ketoacidosis happens when excessive amounts of alcohol cause digestive problems. Failure to follow a holistic approach , such as eating a balanced diet, combined with excessive drinking and/or vomiting, leads to blood that is too acidic. Alcoholic ketoacidosis can be fatal, and requires treatment right away. Knowing how to identify AKA will help you recognize this condition in yourself or loved ones early on, giving you the best chance of recovery. This condition is treatable, but only with swift action to stop excessive alcohol consumption, Continue reading >>
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 >>
Characteristics Of Severe Alcoholic Ketoacidosis With A Reversible Visual Disturbance
No. Age Sex Alcohol intake Alcoho history Conscious Level Pupil diameter Light reflex Systolic BP unit year g/day year mm mmHg 1 66 Male ? 24 Alert 4 none 82 2 53 Male 100 20 Semicoma 6 none 90 3 63 Male ? ? Alert ? ? 90 4 44 Male 200 over 5 Alert 7 none 80 5 59 Male 170 40 Alert 4 sluggish 73 6 48 Male 180 over 8 Semicoma 7 none 87 7 61 Male ? ? Disoriented 5 ? 65 8 49 Male ? ? Alert ? ? 73 9 48 Female over 110 ? Disoriented ? sluggish 134 10 68 Male ? ? Disoriented 3.5 none 150 11 56 Male ? ? Disoriented 5 none 79 12 49 Female ? ? Alert 3 none 130 13 43 Male 180 over 10 Disoriented ? ? 80 14 57 Female ? ? Alert Dilated sluggish 120 No. pH PCO2 PO2 HCO3 Base excess Lactate Glucose Alcohol BHBA AAA Thiamine deficiency Require of_IC Arrest DH Outcome unit mmHg mmHg mmHg mg/dl mg/dl mmol/l mmol/l mg/dl μmol/l μmol/l 1 6.855 13.9 190.5 2.5 -31.4 ? 69 45.8 140 14 no yes no survival 2 6.497 51 ? 3.8 -29 ? ? 8 1190 332 no yes yes survival 3 6.612 14 ? 1.5 -28 ? ? not exam 6360 261 no yes yes survival 4 6.707 13.6 272.8 1.6 -30 ? 91 0 245 11 no yes yes death 5 6.748 13 134 1.7 -33 270 70 not exam 2160 220 no yes no survival 6 6.748 20.3 151 2.6 -33.9 297 85 27.4 ? ? not exam yes no survival 7 6.623 35.0 231 3.5 -34 ? ? ? 2960 460 no yes yes death 8 6.78 15.5 118 2.3 -31 ? ? ? ? ? no no no survival 9 6.64 8.3 159 ? -37.5 109 153 not exam 823 272 no yes yes survival 10 6.79 11.8 137.2 1.8 -33 ? 38 not exam 4825 210 not exam yes no survival 11 6.55 44.4 198 3.7 -29.4 ? 20 not exam not exam not exam not exam yes no survival 12 6.79 8 196 ? ? 90 ? 68 ? 8.82 no ? no survival Arrest No-Arrest p-value n=6 n=8 Age 52.0 + 3.4 56.5 + 2.7 n.s. Sex (Male/Female) 5/1 6/2 n.s. Consciousness (number of alert) 2 5 n.s. Systolic blood pressure (mmHg) 89.8 + 9.5 99.2 + 10.5 n.s. pH 6.637 + 0.0 Continue reading >>
