Causes de décès en milieu de réanimation polyvalente au Centre Hospitalier Universitaire Analakininina, Madagascar / Causes of death in the intensive care unit Of the Analakininina teaching hospital, Madagascar

Background: Intensive Care Unit unit is taking care the serious patients whose vital prognosis is engaged. Death remains the main fear of those patients who are admitted to intensive care. The main objective of our study was to identify the causes of death in the intensive care unit at the Analakininina teaching hospital, Toamasina, madagascar. Methods: This was a descriptive, retrospective study carried out from January 1, 2019 to June 30, 2019. Results: We had identified 110 cases of death with a high male prevalence and a sex ratio of 1.75. The average age was 48.73 +/- 17.60 years. The main reason for admission was disturbance of consciousness in 63.64% of cases with 24.45% of severe coma. Regarding the causes of death, a total of 25 diagnosis were made. The shock states represented 30% of the causes of death of which 69% were septic, 18% cardiogenic and 15.15% hypovolemic. Next, stroke accounted for 28%, cerebral malaria 7.27% and diabetic coma accounted for 5.45% of causes of death. The average length of hospital stay was 1.91 days. Conclusion: Our study provides a better understanding of the causes of death of patients in the intensive care unit. These data can point towards initiatives to improve the quality of care

One hundred years ago: the dawning of the insulin era.

The dawn of the insulin era can be placed in 1921, when Banting and Best started their experiments which led, a year later, to the successful treatment of diabetes. They were preceded by the discoveries of the pancreatic cause of diabetes by Minkowski and von Mering in 1889 and of the islets by Paul Langerhans in 1869. The achievement of the first targeted treatment in medical history was a landmark of medical progress. However, it was accompanied by a mixture of human greatness and misery. Genius and recklessness, ambition and deception, camaraderie and rivalry, selflessness and pursuit of glory went along with superficial search of the existing literature, poor planning, faulty interpretation of results, failure to reproduce them, and misquoting of reports from other laboratories. Then as now, such faults surface whenever human nature aims to push forward the boundaries of knowledge and pose a real challenge in today's world, as the scientific method strives to keep healthy in the face of growing anti-scientific feelings.

Startling hyperglycaemia with transient beta cell stunning in a patient with type 2 diabetes.

A 59-year-old woman unaware of having diabetes was transferred due to coma. Upon discovery at home, her consciousness on the Glasgow Coma Scale was E1V2M4, BP 95/84 mmHg, body temperature 34.7°C. On arrival at ER, height was 1.63 m, weight 97 kg, plasma glucose (PG) 1,897 mg/dL, HbA1c 13.6%, osmolality 421 mosm/kg, arterial pH 7.185, lactate 6.34 mmol/L, ß-hydroxybutyrate 7.93 mmol/L. With saline and regular insulin infusion, PG was lowered to 1,440 mg/dL at 2 hours and then to 250 mg/dL by Day 3, and consciousness normalized by Day 5. On admission, serum immunoreactive insulin (IRI) was undetectable (<0.03 U/mL), C-peptide immunoreactivity (CPR) undetectable (<0.003 ng/mL), and anti-glutamic acid decarboxylase antibody negative. Following the above-described treatment, fasting PG was 186 mg/dL and CPR 1.94 ng/mL, respectively, on Day 14; 2-h post-breakfast PG 239 mg/dL and CPR 6.28 ng/mL, respectively, on Day 18. The patient discharged on Day 18 with 1,800 kcal diet, 32 U insulin glargine and 40 mg gliclazide. Fifteen months later at outpatient clinic, her HbA1c was 6.9% and 2-h post-breakfast PG 123 mg/dL and CPR 5.30 ng/dL with 750 mg metformin, 10 mg gliclazide and 18 U insulin glargine. Transient, but total cessation of insulin secretion was documented in a patient with type 2 diabetes under severe metabolic decompensation. Swift, sustained recovery of insulin release indicated that lack of insulin at the time of emergency was due to secretory failure, i.e., unresponsive exocytotic machinery or depletion of releasable insulin, rather than loss of beta cells.

Persistent Vegetative State after Diabetic Ketoacidosis Triggered by an Overdose of Psychotropic Agents.

A 28-year-old man with type 1 diabetes mellitus was admitted for shock and coma due to diabetic ketoacidosis. Despite aggressive treatment and management of the patient's underlying clinical issues, the patient remained in a comatose state. Further investigations revealed an excess consumption of psychotropic agents; however, there was no evidence of an insulin overdose. Physicians should be aware that, in patients who are highly dependent upon insulin, an overdose of psychotropic agents can lead to hypoxic-ischemic brain injury.

Short-term Effect of Ambient Air Pollution on Emergency Department Visits for Diabetic Coma in Seoul, Korea.

OBJECTIVES: A positive association between air pollution and both the incidence and prevalence of diabetes mellitus (DM) has been reported in some epidemiologic and animal studies, but little research has evaluated the relationship between air pollution and diabetic coma. Diabetic coma is an acute complication of DM caused by diabetic ketoacidosis or hyperosmolar hyperglycemic state, which is characterized by extreme hyperglycemia accompanied by coma. We conducted a time-series study with a generalized additive model using a distributed-lag non-linear model to assess the association between ambient air pollution (particulate matter less than 10 µm in aerodynamic diameter, nitrogen dioxide [NO2], sulfur dioxide, carbon monoxide, and ozone) and emergency department (ED) visits for DM with coma in Seoul, Korea from 2005 to 2009. METHODS: The ED data and medical records from the 3 years previous to each diabetic coma event were obtained from the Health Insurance Review and Assessment Service to examine the relationship with air pollutants. RESULTS: Overall, the adjusted relative risks (RRs) for an interquartile range (IQR) increment of NO2 was statistically significant at lag 1 (RR, 1.125; 95% confidence interval [CI], 1.039 to 1.219) in a single-lag model and both lag 0-1 (RR, 1.120; 95% CI, 1.028 to 1.219) and lag 0-3 (RR, 1.092; 95% CI, 1.005 to 1.186) in a cumulative-lag model. In a subgroup analysis, significant positive RRs were found for females for per-IQR increments of NO2 at cumulative lag 0-3 (RR, 1.149; 95% CI, 1.022 to 1.291). CONCLUSIONS: The results of our study suggest that ambient air pollution, specifically NO2, is associated with ED visits for diabetic coma.

Development and pharmacist-mediated use of tools for monitoring atypical antipsychotic-induced side effects related to blood glucose levels.

PURPOSE: Drug side effects often lead to serious outcomes. Administration of second-generation antipsychotics has resulted in diabetic ketoacidosis and diabetic coma leading to death. Therefore, pharmacists are required to collect information on clinical test values, determine the appropriate test timing, and coordinate with doctors for further clinical laboratory orders, all of which are labor-intensive and time-intensive tasks. In this study, we developed a side effect-monitoring tool and aimed to clarify the influence and efficiency of monitoring side effects by using the tool in patients taking atypical antipsychotics in whom it is necessary to check clinical test values such as blood sugar levels. METHODS: We extracted clinical test values for patients treated with second-generation antipsychotics from electronic medical records. The test values are automatically displayed in the side effect grade classification specified by CTCAE ver. 4.0. A database was constructed using scripts to provide alerts for the timing of clinical testing. The pharmacist used this tool to confirm clinical test values for patients taking medication and requested the physician to inspect orders based on the appropriate test timings. RESULTS: The management tool reduced the pharmacists' effort in collecting information on patients' prescription status and test values. It enabled patients to undergo tests at the appropriate time according to the progression of glucose metabolism and allowed for easy monitoring of side effects. CONCLUSIONS: The results suggested that regardless of pharmacists' experience or skill, the introduction of this tool enables centralization of side effect monitoring and can contribute to proper drug use.

Euglisemic diabetic ketoacidotic coma caused by dapagliflozin.

Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening acute complication of diabetes mellitus (DM). Sodium-glucose co-transporter-2(SGLT-2) inhibitors are new orally administered antihyperglycemic agents. These agents are related with rarely seen euglycemic diabetic ketoacidosis (eDKA) cases, which are difficult to diagnose in emergency department (ED) because of absence of an evident hyperglycemia and may result with potentially dangerous outcomes if missed. In this study, we present a clinical case of a patient, admitted to ED with altered mental status after SGLT2 inhibitor dapagliflozin administration.

1,5-Anhydro-d-glucitol in vitreous humor and cerebrospinal fluid - A helpful tool for identification of diabetes and diabetic coma post mortem.

Since there are no characteristic morphological findings post mortem diagnosis of diabetes mellitus and identification of diabetic coma need to be confirmed by suitable biomarkers. The postmortem identification of preexisting hyperglycemia or diabetic coma can be difficult if the matrices for the determination of the established biomarkers are not available or the obtained results are close to the established cut-off values. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for renal reabsorption. Therefore low serum concentrations of 1,5-AG, reflect hyperglycemic excursions over the prior 1-2 weeks in diabetic patients. To evaluate postmortem 1,5-AG concentrations in vitreous humor (VH) and cerebrospinal fluid (CSF), a liquid chromatographic mass spectrometric method for the quantification of 1,5-AG in VH and CSF was developed and validated according to international guidelines. In order to establish a cut-off for the identification of an ante mortem existing diabetes and the diagnosis of a diabetic coma in deceased the relationships between 1,5-AG concentrations in VH and CSF to other diabetes associated biochemical parameters of 47 non-diabetic, 86 diabetic and 9 cases of diabetic coma were examined. In 83 of these cases, both matrices could be obtained and analyzed. Comparisons of the respective HbA1c, Glucose in VH or Sum-formula of Traub to 1,5-AG concentrations in VH and CSF resulted in correlation coefficients R2≤0.2. For the application of 1,5-AG concentrations in VH against CSF, a linear regression gave a correlation coefficient of R2=0.955. Comparable linear correlations of 1,5-AG concentrations could be observed between VH and femoral venous blood (FVB) (R2=0.839) as well as between CSF and FVB (R2=0.756). Due to overlapping concentration ranges, the determination of a reliable cut-off for the differentiation of diabetic disease to diabetic coma cases was not possible. However, the 1,5-AG concentrations in VH and CSF in cases of deceased diabetics were significantly lower (p<0.05) than in non-diabetic deceased and therefore indicate a pre-existing diabetes or even a diabetic coma as the cause of death.

Evaluation of 1,5-anhydro-d-glucitol in clinical and forensic urine samples.

Because of the lack of characteristic morphological findings post mortem diagnosis of diabetes mellitus and identification of diabetic coma can be complicated. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for renal reabsorption. Therefore low serum concentrations of 1,5-AG, reflect hyperglycemic excursions over the prior 1-2 weeks in diabetic patients. Next to clinical applications determination of 1,5-AG can also be used in forensic analysis. To investigate the elimination of 1,5-AG, a liquid chromatographic-mass spectrometric method for the determination of 1,5-AG and creatinine in urine was developed and validated according to international guidelines. To evaluate ante mortem concentrations of 1,5-AG spot urine samples of 30 healthy subjects, 46 type 1 and 46 type 2 diabetic patients were analyzed. 1,5-AG urine concentrations of diabetic patients were significantly (p<0.001) lower (mean: 1.54µg/ml, n=92) compared to concentrations of healthy subjects (mean: 4.76µg/ml, n=30) which led to the idea that 1,5-AG urine concentrations post mortem might help in the interpretation of a diabetic coma post mortem. Urine of 47 deceased non-diabetics, 37 deceased diabetic and 9 cases of diabetic coma were measured. Comparison of blood and urine 1,5-AG concentrations in clinic samples (linear, R2=0.13) and forensic samples (linear, R2=0.02) showed no correlation. Urinary levels of 1,5-AG in deceased diabetic (mean 6.9µg/ml) and in non-diabetic patients (mean 6.3µg/ml) did not show a significant difference (p=0.752). However, urinary 1,5-AG concentrations in deceased due to diabetic coma (mean: 1.7µg/ml) were significantly lower than in non-diabetic (mean: 6.3µg/ml, p=0.039) and lower than in diabetic cases (mean: 4.7µg/ml, p=0.058). The determination of a reliable cut-off for the differentiation of diabetic to diabetic coma cases was not possible. Normalization of urinary 1,5-AG concentrations with the respective creatinine concentrations did not show any gain of information. In clinical (serum) and forensic blood samples a significant difference between all groups could be detected (p<0.05). Comparison of blood and urine 1,5-AG concentrations in clinical samples (linear, R2=0.13) and forensic samples (linear, R2=0.02) showed no correlation.

Short-term Effect of Ambient Air Pollution on Emergency Department Visits for Diabetic Coma in Seoul, Korea / 예방의학회지

OBJECTIVES: A positive association between air pollution and both the incidence and prevalence of diabetes mellitus (DM) has been reported in some epidemiologic and animal studies, but little research has evaluated the relationship between air pollution and diabetic coma. Diabetic coma is an acute complication of DM caused by diabetic ketoacidosis or hyperosmolar hyperglycemic state, which is characterized by extreme hyperglycemia accompanied by coma. We conducted a time-series study with a generalized additive model using a distributed-lag non-linear model to assess the association between ambient air pollution (particulate matter less than 10 μm in aerodynamic diameter, nitrogen dioxide [NO2], sulfur dioxide, carbon monoxide, and ozone) and emergency department (ED) visits for DM with coma in Seoul, Korea from 2005 to 2009. METHODS: The ED data and medical records from the 3 years previous to each diabetic coma event were obtained from the Health Insurance Review and Assessment Service to examine the relationship with air pollutants. RESULTS: Overall, the adjusted relative risks (RRs) for an interquartile range (IQR) increment of NO2 was statistically significant at lag 1 (RR, 1.125; 95% confidence interval [CI], 1.039 to 1.219) in a single-lag model and both lag 0-1 (RR, 1.120; 95% CI, 1.028 to 1.219) and lag 0-3 (RR, 1.092; 95% CI, 1.005 to 1.186) in a cumulative-lag model. In a subgroup analysis, significant positive RRs were found for females for per-IQR increments of NO2 at cumulative lag 0-3 (RR, 1.149; 95% CI, 1.022 to 1.291). CONCLUSIONS: The results of our study suggest that ambient air pollution, specifically NO2, is associated with ED visits for diabetic coma.

Esofagitis necrosante aguda asociada coma diabético hiperosmolar / Acute necrotising oesophagitis associated with hyperosmolar diabetic coma

No disponible

Estudio descriptivo de las complicaciones agudas diabéticas atendidas en un servicio de urgencias hospitalario / Acute diabetic complications attended in a hospital emergency department: a descriptive analysis

Objetivo. Conocer las complicaciones agudas diabéticas atendidas en un servicio de urgencias hospitalario (SUH). Metodología. Estudio descriptivo transversal retrospectivo, realizado en un SUH de un hospital universitario de tercer nivel asistencial de los pacientes diagnosticados de hiperglucemias e hipoglucemias durante el año 2012. Resultados. Se incluyeron 237 pacientes con una edad media de 61 (± 26) años. El 86,5% presentaba diabetes: el 74% tipo 2 y el 26% tipo 1. Las hiperglucemias supusieron un 72%. Las causas de descompensación más frecuentes fueron el mal control en los diabéticos tipo 1 (41,2%) y las infecciones en los diabéticos tipo 2 (51,5%). Las hipoglucemias supusieron el 28%, producidas principalmente por mal control metabólico (50%). La estancia media fue menor que en las hiperglucemias. Los pacientes diabéticos tipo 2 tuvieron más ingresos que los tipo 1. Conclusiones. Los diabéticos tipo 2 suponen una mayor frecuentación, mayor índice de ingresos y una estancia media mayor que los tipo 1 (AU)

Objective. To analyze the characteristics of acute diabetic complications attended in a hospital emergency department. Methods. Cross-sectional, descriptive, retrospective study of patients with hyper- and hypoglycemic emergencies attended in a tertiary-care university hospital emergency department. Results. We included 237 patients with a mean (SD) age of 61 (26) years. Diabetes had been diagnosed previously in 86.5% (type 2 in 74% and type 1 in 26%). Hyperglycemic emergencies were treated in 72%. The most frequent reasons for decompensation were poor control of type 1 diabetes (41.2%) and infections in type 2 diabetes (51.5%). Twenty-eight percent had low blood sugar levels caused by poor control of disease (50%). Patients with hypoglycemia had shorter mean stays. More admissions were made in type 2 diabetes than in type 1. Conclusions. Type 2 diabetes leads to more visits to the emergency department, more admissions, and a longer hospital stay than type 1 diabetes (AU)

Cognitive, neurophysiologic and metabolic sequelae of previous hypoglycemic coma revealed by hyperinsulinemic-hypoglycemic clamp in type 1 diabetic patients.

To examine the relationship between electroencephalographic (EEG) activity and hypoglycemia unawareness, we investigated early parameters of vigilance and awareness of various symptom categories in response to hypoglycemia in intensively treated type 1 diabetic (T1DM) patients with different degrees of hypoglycemia unawareness. Hypoglycemia was induced with a hyperinsulinemic-hypoglycemic clamp in six T1DM patients with a history of hypoglycemia unawareness previous severe hypoglycemic coma (SH) and in six T1DM patients without (C) history of hypoglycemia unawareness previous severe hypoglycemic coma. Cognitive function tests (four choice reaction time), counterregulatory responses (adrenaline), and symptomatic responses were evaluated at euglycemia (90 mg/dl) and during step-wise plasma glucose reduction (68, 58 and 49 mg/dl). EEG activity was recorded continuously throughout the study and analyzed by spectral analysis. Cognitive function deteriorated significantly at a glucose threshold of 55 ± 1 mg/dl in both groups (p = ns) during hypoglycemia, while the glucose threshold for autonomic symptoms was significantly lower in SH patients than in C patients (49 ± 1 vs. 54 ± 1 mg/dl, p < 0.05, respectively). In SH patients, eye-closed resting EEG showed a correlation between the mean dominance frequency and plasma glucose (r = 0.62, p < 0.001). Theta relative power increased during controlled hypoglycemia compared to euglycemia (21.6 ± 6 vs. 15.5 ± 3% Hz p < 0.05) and was higher than in the C group (21.6 ± 6 vs. 13.8 ± 3%, p < 0.03). The cognitive task beta activity was lower in the SH group than in the C group (14.8 ± 3 Hz, vs. 22.6 ± 4 vs. p < 0.03). Controlled hypoglycemia elicits cognitive dysfunction in both C and SH patients; however, significant EEG alterations during hypoglycemia were detected mainly in patients with a history of hypoglycemia unawareness and previous severe hypoglycemic coma. These data suggest that prior episodes of hypoglycemic coma modulate brain electric activity.

Glycated hemoglobin A1c as a risk factor for severe hypoglycemia in pediatric type 1 diabetes.

OBJECTIVE: To assess the risk of severe hypoglycemia related to glycated hemoglobin A1c (HbA1c) levels in a population-based cohort of pediatric type 1 diabetes patients during two time periods since 1995. METHODS: The association between HbA1c levels and severe hypoglycemia (defined as requiring assistance from another person) or hypoglycemic coma (loss of consciousness or seizures) was analyzed by multivariable regression analysis in children and adolescents with type 1 diabetes from the DPV Diabetes Prospective Follow-up in Germany and Austria in 1995-2003 (n = 15 221 patients) and 2004-2012 (n = 22 318 patients). RESULTS: Mean adjusted rates of severe hypoglycemia and hypoglycemic coma decreased from 19.18 [95% confidence interval (CI), 17.95-20.48] and 4.36 (3.93-4.83) per 100 patient-years in 1995-2003 to 15.01 (14.18-15.88) and 2.15 (1.94-2.39) in 2004-2012, respectively (p < 0.001). From the first to the second period, the relative risk (RR) for severe hypoglycemia and hypoglycemic coma per 1% lower HbA1c decreased from 1.22 (1.15-1.30) to 1.06 (1.01-1.12) and from 1.27 (1.15-1.40) to 1.04 (0.94-1.16), respectively. Risk of severe hypoglycemia and coma declined most in patients with HbA1c levels of 6-6.9% (RR 0.70 and 0.43, respectively) and with HbA1c of 7-7.9% (RR 0.63 and 0.38, respectively). Mean HbA1c levels fell from 8.4% in 1995-2003 to 8.2% in 2004-2012, while the use of insulin pumps, short- and long-acting insulin analogs, and glucose monitoring increased (p < 0.001). CONCLUSIONS: In contrast to 1995-2003, low HbA1c has become a minor risk factor for severe hypoglycemia and coma in pediatric patients with type 1 diabetes in the 2004-2012 period.

A nationwide population-based study on the risk of coma, ketoacidosis and hypoglycemia in patients with celiac disease and type 1 diabetes.

AIMS: Celiac disease (CD) may influence metabolic control in type 1 diabetes (T1D). This work examines whether CD in T1D influences hospital admissions due to coma, ketoacidosis and hypoglycemia. METHODS: In population-based cohort study, individuals with CD were identified using biopsy data (1969-2008) from Sweden's 28 pathology departments. T1D was defined as a recorded diagnosis of T1D at age ≤30 years in the Swedish National Patient Register between 1964 and 2009. In total, 906 individuals had both T1D and CD and were matched for sex, age and calendar period with 4303 reference individuals. Through stratified Cox regression analysis, we modeled CD as a time-dependent covariate and estimated the risk of future coma, ketoacidosis and hypoglycemia, defined by relevant international classification of disease codes among T1D patients with and without CD. RESULTS: During follow-up, patients with both T1D and CD had 49 hospital admissions with diabetic coma, 91 episodes of ketoacidosis and 25 hypoglycemic events. Among patients with T1D, CD did not influence the risk of coma (adjusted HR 0.97; 95 % CI 0.72-1.32), ketoacidosis (adjusted HR 1.08; 95 % CI 0.86-1.34), or hypoglycemia (adjusted HR 1.34; 95 % CI 0.87-2.05). The absolute risk of coma was 621/100,000 person-years in T1D and CD (637 in controls). Corresponding figures for ketoacidosis were 1175/100,000 person-years in T1D and CD (1092 in controls) and for hypoglycemia 316/100,000 person-years (236 in controls). HRs for metabolic emergencies in T1D were similar in the first 5 years after T1D diagnosis as thereafter. CONCLUSIONS: Having a diagnosis of CD is unlikely to influence the risk of coma, ketoacidosis and hypoglycemia in T1D patients.

Estimated life expectancy in a Scottish cohort with type 1 diabetes, 2008-2010.

IMPORTANCE: Type 1 diabetes has historically been associated with a significant reduction in life expectancy. Major advances in treatment of type 1 diabetes have occurred in the past 3 decades. Contemporary estimates of the effect of type 1 diabetes on life expectancy are needed. OBJECTIVE: To examine current life expectancy in people with and without type 1 diabetes in Scotland. We also examined whether any loss of life expectancy in patients with type 1 diabetes is confined to those who develop kidney disease. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort of all individuals alive in Scotland with type 1 diabetes who were aged 20 years or older from 2008 through 2010 and were in a nationwide register (n=24,691 contributing 67,712 person-years and 1043 deaths). MAIN OUTCOMES AND MEASURES: Differences in life expectancy between those with and those without type 1 diabetes and the percentage of the difference due to various causes. RESULTS: Life expectancy at an attained age of 20 years was an additional 46.2 years among men with type 1 diabetes and 57.3 years among men without it, an estimated loss in life expectancy with diabetes of 11.1 years (95% CI, 10.1-12.1). Life expectancy from age 20 years was an additional 48.1 years among women with type 1 diabetes and 61.0 years among women without it, an estimated loss with diabetes of 12.9 years (95% CI, 11.7-14.1). Even among those with type 1 diabetes with an estimated glomerular filtration rate of 90 mL/min/1.73 m2 or higher, life expectancy was reduced (49.0 years in men, 53.1 years in women) giving an estimated loss from age 20 years of 8.3 years (95% CI, 6.5-10.1) for men and 7.9 years (95% CI, 5.5-10.3) for women. Overall, the largest percentage of the estimated loss in life expectancy was related to ischemic heart disease (36% in men, 31% in women) but death from diabetic coma or ketoacidosis was associated with the largest percentage of the estimated loss occurring before age 50 years (29.4% in men, 21.7% in women). CONCLUSIONS AND RELEVANCE: Estimated life expectancy for patients with type 1 diabetes in Scotland based on data from 2008 through 2010 indicated an estimated loss of life expectancy at age 20 years of approximately 11 years for men and 13 years for women compared with the general population without type 1 diabetes.