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Search on : Insulin and Coma [Words]
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[PMID]: 29405355
[Au] Autor:Bensalah M; Donaldson M; Aribi Y; Iabassen M; Cherfi L; Nebbal M; Medjaher M; Haffaf E; Abdennebi B; Guenane K; Djermane A; Kemali Z; OuldKablia S
[Ad] Address:Endocrinology Unit, Central Hospital of Army, Algiers, Algeria.
[Ti] Title:Cortisol evaluation during the acute phase of traumatic brain injury-A prospective study.
[So] Source:Clin Endocrinol (Oxf);, 2018 Feb 05.
[Is] ISSN:1365-2265
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Biochemical diagnosis of adrenal insufficiency (AI) is difficult in the context of traumatic brain injury (TBI). AIM: To assess the frequency and predictive factors of AI in victims of TBI from Algiers. METHODS: Between November 2009 and December 2013, TBI victims had a single 8-9 am serum cortisol measurement during the acute postinjury period (0-7 days). AI was defined according to basal cortisol levels of 83, 276 and 414 nmol/L. Variables studied were TBI severity according to Glasgow coma scale, duration of intubation and coma, pupillary status, hypotension, anaemia, brain imaging findings, diabetes insipidus and medication. Insulin tolerance test was performed during the recovery phase, defining AI as peak cortisol <500 nmol/L. RESULTS: Cortisol samples were obtained at median 3 (1-7) days from 277 patients (257M: 20F) aged 32 (18-65) years. Acute AI frequency was 8 (2.8%), 20 (21%) and 35 (37%), respectively using the three cortisol cut-offs. Factors predicting AI were diastolic hypotension, sedative medication, diabetes insipidus, skull base fracture and intraparenchymal haematoma. Mortality was highest in patients with acute cortisol <276 nmol/L (44.6% with OR for death 1.64, 95% CI 0.92-3.0, P = .12). During the recovery phase, AI was present in 3 of 3, 12 of 24, 4 of 16 and 20 of 66 patients with week 1 cortisol <83, 83-276, 277-414 and >414 nmol/L. CONCLUSION: Hydrocortisone replacement is advised in TBI patients with morning cortisol <276 nmol/L or those <414 nmol/L with additional risk factors for AI. As acute and subsequent AI are poorly correlated, patients with moderate/severe TBI require adrenal re-evaluation during the recovery phase.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1111/cen.13562

  2 / 2538 MEDLINE  
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[PMID]: 29431405
[Au] Autor:Stoner GD
[Ad] Address:University of Illinois College of Medicine, Peoria, IL, USA.
[Ti] Title:Hyperosmolar Hyperglycemic State.
[So] Source:Am Fam Physician;96(11):729-736, 2017 Dec 01.
[Is] ISSN:1532-0650
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose and hyperosmolarity with little or no ketosis. Although there are multiple precipitating causes, underlying infections are the most common. Other causes include certain medications, nonadherence to therapy, undiagnosed diabetes mellitus, substance abuse, and coexisting disease. In children and adolescents, hyperosmolar hyperglycemic state is often present when type 2 diabetes is diagnosed. Physical findings include profound dehydration and neurologic symptoms ranging from lethargy to coma. Treatment begins with intensive monitoring of the patient and laboratory values, especially glucose, sodium, and potassium levels. Vigorous correction of dehydration is critical, requiring an average of 9 L of 0.9% saline over 48 hours in adults. After urine output is established, potassium replacement should begin. Once dehydration is partially corrected, adults should receive an initial bolus of 0.1 units of intravenous insulin per kg of body weight, followed by a continuous infusion of 0.1 units per kg per hour (or a continuous infusion of 0.14 units per kg per hour without an initial bolus) until the blood glucose level decreases below 300 mg per dL. In children and adolescents, dehydration should be corrected at a rate of no more than 3 mOsm per hour to avoid cerebral edema. Identification and treatment of underlying and precipitating causes are necessary.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180212
[Lr] Last revision date:180212
[St] Status:In-Data-Review

  3 / 2538 MEDLINE  
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[PMID]: 29376579
[Au] Autor:Ostojic S; Vukovic R; Milenkovic T; Mitrovic K; Djuric M; Nikolic L
[Ad] Address:Department of Neurology, Mother and Child Health Care Institute of Serbia "Dr Vukan Cupic", Belgrade, Serbia.
[Ti] Title:Alpha coma in an adolescent with diabetic ketoacidosis.
[So] Source:Turk J Pediatr;59(3):318-321, 2017.
[Is] ISSN:0041-4301
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:Ostojic S, Vukovic R, Milenkovic T, Mitrovic K, Djuric M, Nikolic L. Alpha coma in an adolescent with diabetic ketoacidosis. Turk J Pediatr 2017; 59: 318-321. This is the first report of alpha coma (AC) caused by brain edema in a patient with diabetic ketoacidosis (DKA). A previously healthy 15-year-old girl was admitted to the intensive care unit due to altered state of consciousness during the course of treatment for DKA. Patient was in a coma, intubated and had tachycardia with poor peripheral perfusion. Results of laboratory analyses indicated severe DKA and computed tomography scan indicated diffuse brain edema. The EEG pattern showed uniform alpha activity. Treatment with intravenous fluids, insulin and mannitol was started. Patient`s state of consciousness gradually improved and on the third day she was extubated. On the fifth day, her neurologic status and EEG findings were completely normal with no residual neurological deficits. In conclusion, although AC is associated with a high fatality rate, favorable outcome can be achieved with prompt recognition and treatment of cerebral edema in pediatric patients with DKA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180129
[Lr] Last revision date:180129
[St] Status:In-Data-Review

  4 / 2538 MEDLINE  
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[PMID]: 29258472
[Au] Autor:Bai K; Fu Y; Liu C; Xu F; Zhu M
[Ad] Address:Intensive Care Unit, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Children Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Labortory of Pediatrics, 136 Zh
[Ti] Title:Pediatric non-diabetic ketoacidosis: a case-series report.
[So] Source:BMC Pediatr;17(1):209, 2017 Dec 19.
[Is] ISSN:1471-2431
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: This study is to explore the clinical characteristics, laboratory diagnosis, and treatment outcomes in pediatric patients with non-diabetic ketoacidosis. METHODS: Retrospective patient chart review was performed between March 2009 to March 2015. Cases were included if they met the selection criteria for non-diabetic ketoacidosis, which were: 1) Age ≤ 18 years; 2) urine ketone positive ++ or >8.0 mmol/L; 3) blood ketone >3.1 mmol/L; 4) acidosis (pH < 7.3) and/or HCO < 15 mmol/L; 5) random blood glucose level < 11.1 mmol/L. Patients who met the criteria 1, 4, 5, plus either 2 or 3, were defined as non-diabetic ketoacidosis and were included in the report. RESULTS: Five patients with 7 episodes of non-diabetic ketoacidosis were identified. They all presented with dehydration, poor appetite, and Kussmaul breathing. Patients treated with insulin plus glucose supplementation had a quicker recovery from acidosis, in comparison to those treated with bicarbonate infusion and continuous renal replacement therapy. Two patients treated with bicarbonate infusion developed transient coma and seizures during the treatment. CONCLUSION: Despite normal or low blood glucose levels, patients with non-diabetic ketoacidosis should receive insulin administration with glucose supplementation to correct ketoacidosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171222
[Lr] Last revision date:171222
[St] Status:In-Process
[do] DOI:10.1186/s12887-017-0960-3

  5 / 2538 MEDLINE  
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[PMID]: 29180613
[Au] Autor:Lu Z; Liu J; He Q; Chakraborty A; Zhu T
[Ad] Address:Department of Endocrinology, General Hospital, Tianjin Medical University, Tianjin, China (mainland).
[Ti] Title:Analysis of Risk Factors for Hypoglycemic Coma in 194 Patients with Type 2 Diabetes.
[So] Source:Med Sci Monit;23:5662-5668, 2017 Nov 28.
[Is] ISSN:1643-3750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND The present study was conducted to analyze possible risk factors in patients with type 2 diabetes who are in hypoglycemic coma. MATERIAL AND METHODS A total of 194 patients with type 2 diabetic hypoglycemic coma who were admitted to our hospital between January 2010 and January 2016 were included. The patients were all in coma on admission, and their blood glucose levels were lower than 2.8 mmol/L. None of the patients had type I diabetes, specific types of diabetes, or gestational diabetes. Multiple linear regression analysis was used to determine possible factors associated with hypoglycemic coma. RESULTS Among the patients, 82 were male and 112 were female (mean age, 66.88±10.62 years). In addition, 72 patients lived in urban areas and 122 lived in rural areas. Occurrence of hypoglycemic coma was correlated with difference between urban and rural residence, glycosylated hemoglobin (HbA1c) level, combined hypertension, and combined neural complications. Self-purchased drugs resulted in significantly lower blood glucose level at the onset of hypoglycemic coma than insulin, secretagogue, or non-secretagogue drugs. Blood glucose level at onset was correlated with season. Patients living in rural areas or with combined macrovascular or microvascular complications had prolonged hospital stay and poor prognosis. CONCLUSIONS Our results demonstrate that rural residence, higher HbA1c level, combined hypertension, and combined neural complications increase the incidence of hypoglycemic coma. Use of self-purchased drugs and colder seasons may result in lower blood glucose levels in patients with hypoglycemic coma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171219
[Lr] Last revision date:171219
[St] Status:In-Process

  6 / 2538 MEDLINE  
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[PMID]: 29181767
[Au] Autor:Castrejón-Pérez RC; Aguilar-Salinas CA; Gutiérrez-Robledo LM; Cesari M; Pérez-Zepeda MU
[Ad] Address:Geriatric Epidemiology Research Department, National Institute of Geriatrics, Periférico Sur 2767, Colonia San Jerónimo Lídice, Delegación Magdalena Contreras, C.P. 10200, Mexico City, Mexico.
[Ti] Title:Frailty, diabetes, and the convergence of chronic disease in an age-related condition: a population-based nationwide cross-sectional analysis of the Mexican nutrition and health survey.
[So] Source:Aging Clin Exp Res;, 2017 Nov 27.
[Is] ISSN:1720-8319
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:AIMS: To describe the associations of frailty with diabetes mellitus and related conditions in older adults. METHODS: We conducted a cross-sectional analysis of a representative sample of older adults (n = 5379). We generated a 35-item frailty index (FI) and obtained information on diabetes and related conditions (peripheral neuropathy, lower limb amputation, diabetic coma, number of physician visits due to diabetes-related conditions, all-cause hospitalizations in the past year, years since diabetes diagnosis, and type of treatment). Logistic and Poisson regression models were used to determine the associations between frailty and diabetes and its complications. RESULTS: The mean age was 70.3 years (± 7.8); 54.7% were women. Those with an FI ≤ 0.082 composed the reference group. Multivariate analysis showed an OR of 2.32 (95% CI 1.93-2.73, p < 0.001) for the association between diabetes and frailty. People who were hospitalized for any cause during the previous year, those receiving both insulin and an oral compound to manage diabetes, and those with peripheral neuropathy showed ORs of 2.32 (95% CI 1.69-3.18, p < 0.001), 5.6 (95% CI 1.58-19.8, p = 0.008), and 2.02 (95% CI 1.42-2.86, p < 0.001), respectively, for being in the most frail group. CONCLUSIONS: People with diabetes have higher frailty scores. Furthermore, older adults with diabetes and higher burden of frailty have more diabetes-related complications.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171128
[Lr] Last revision date:171128
[St] Status:Publisher
[do] DOI:10.1007/s40520-017-0852-2

  7 / 2538 MEDLINE  
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[PMID]: 29118840
[Au] Autor:Hopkins LE; Sunkersing J; Jacques A
[Ad] Address:Intensive Care Unit, Royal Berkshire NHS Foundation Trust, Reading, UK.
[Ti] Title:Too many pills to swallow: A case of a mixed overdose.
[So] Source:J Intensive Care Soc;18(3):247-250, 2017 Aug.
[Is] ISSN:1751-1437
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Propranolol is a highly lipid-soluble beta-receptor antagonist. We describe a case of mixed overdose, including propranolol, amlodipine and olanzapine, resulting in severe resistant hypotension which was successfully treated. A 21-year-old student ingested 6.4 g of propranolol, 280 mg of amlodipine and 560 mg of olanzapine. The patient was brought to the emergency department and exhibited signs of severe systemic toxicity - profound hypotension and circulatory collapse, respiratory depression and coma. The patient had conventional therapy but failed to respond to this and was therefore commenced on IntraLipid infusion, high-dose insulin infusion and inotrope infusion. An endoscopy was performed in intensive care which revealed a large drug beozar - this was removed. We believe that this combination of infusions with early endoscopy could be beneficial in treating similar patients in the future and present the first case of a propranolol drug bezoar.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171112
[Lr] Last revision date:171112
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1177/1751143717693860

  8 / 2538 MEDLINE  
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[PMID]: 29047291
[Au] Autor:Languren G; Montiel T; Ramírez-Lugo L; Balderas I; Sánchez-Chávez G; Sotres-Bayón F; Bermúdez-Rattoni F; Massieu L
[Ad] Address:División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, Ciudad de México, México.
[Ti] Title:Recurrent moderate hypoglycemia exacerbates oxidative damage and neuronal death leading to cognitive dysfunction after the hypoglycemic coma.
[So] Source:J Cereb Blood Flow Metab;:271678X17733640, 2017 Jan 01.
[Is] ISSN:1559-7016
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Moderate recurrent hypoglycemia (RH) is frequent in Type 1 diabetes mellitus (TIDM) patients who are under intensive insulin therapy increasing the risk for severe hypoglycemia (SH). The consequences of RH are not well understood and its repercussions on neuronal damage and cognitive function after a subsequent episode of SH have been poorly investigated. In the current study, we have addressed this question and observed that previous RH during seven consecutive days exacerbated oxidative damage and neuronal death induced by a subsequent episode of SH accompanied by a short period of coma, in the parietal cortex, the striatum and mainly in the hippocampus. These changes correlated with a severe decrease in reduced glutathione content (GSH), and a significant spatial and contextual memory deficit. Administration of the antioxidant, N-acetyl-L-cysteine, (NAC) reduced neuronal death and prevented cognitive impairment. These results demonstrate that previous RH enhances brain vulnerability to acute hypoglycemia and suggests that this effect is mediated by the decline in the antioxidant defense and oxidative damage. The present results highlight the importance of an adequate control of moderate hypoglycemic episodes in TIDM.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171019
[Lr] Last revision date:171019
[St] Status:Publisher
[do] DOI:10.1177/0271678X17733640

  9 / 2538 MEDLINE  
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[PMID]: 28888993
[Au] Autor:Graveling AJ; Frier BM
[Ad] Address:JJR Macleod Centre for Diabetes & Endocrinology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB25 2ZP, UK. Electronic address: alex.graveling@nhs.net.
[Ti] Title:The risks of nocturnal hypoglycaemia in insulin-treated diabetes.
[So] Source:Diabetes Res Clin Pract;133:30-39, 2017 Nov.
[Is] ISSN:1872-8227
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Over half of all episodes of severe hypoglycaemia (requiring external help) occur during sleep, but nocturnal hypoglycaemia is often asymptomatic and unrecognised. The precise incidence of nocturnal hypoglycaemia is difficult to determine with no agreed definition, but continuous glucose monitoring has shown that it occurs frequently in people taking insulin. Attenuation of the counter-regulatory responses to hypoglycaemia during sleep may explain why some episodes are undetected and more prolonged, and modifies cardiovascular responses. The morbidity and mortality associated with nocturnal hypoglycaemia is probably much greater than realised, causing seizures, coma and cardiovascular events and affecting quality of life, mood and work performance the following day. It may induce impaired awareness of hypoglycaemia. Cardiac arrhythmias that occur during nocturnal hypoglycaemia include bradycardia and ectopics that may provoke dangerous arrhythmias. Treatment strategies are discussed that may help to minimise the frequency of nocturnal hypoglycaemia.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1709
[Cu] Class update date: 171110
[Lr] Last revision date:171110
[St] Status:In-Process

  10 / 2538 MEDLINE  
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[PMID]: 28849301
[Au] Autor:Kalscheuer H; Serfling G; Schmid S; Lehnert H
[Ad] Address:Medizinische Klinik I, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23562, Lübeck, Deutschland. hannes.kalscheuer@uksh.de.
[Ti] Title:Diabetologische Notfälle : Hypoglykämie, ketoazidotisches und hyperglykämisches Koma. [Diabetic emergencies : Hypoglycemia, ketoacidotic and hyperglycemic hyperosmolar nonketotic coma].
[So] Source:Internist (Berl);58(10):1020-1028, 2017 Oct.
[Is] ISSN:1432-1289
[Cp] Country of publication:Germany
[La] Language:ger
[Ab] Abstract:The diabetic emergencies diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS) and hypoglycemia represent severe and potentially life-threatening complications of diabetes mellitus that require prompt diagnostics and treatment. Absolute or relative insulin insufficiency is characteristic of DKA und HHS along with severe dehydration. They differ by the prevalence of ketone bodies and the severity of acidosis; however, the treatment regimens are similar. In contrast, hypoglycemia is the limiting factor for achieving ambitious glucose targets. This article decribes the clinical presentation, diagnostics and emergency management of these metabolic derangements.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Em] Entry month:1708
[Cu] Class update date: 171117
[Lr] Last revision date:171117
[St] Status:In-Process
[do] DOI:10.1007/s00108-017-0317-x


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