Mortality in juvenile diabetes mellitus over 25 years.

Smith, CE; Hudson, F. P.

doi:10.1136/adc.51.4.297

Archives of Disease in Childhood

1976

DOI: 10.1136/adc.51.4.297

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Mortality in juvenile diabetes mellitus over 25 years.

CE Smith¹,

F. P. Hudson²

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1977

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Cited by 9 publications

(1 citation statement)

References 15 publications

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“…Diabetic ketoacidosis is the most common cause of death in children and teenagers with diabetes mellitus (Smith and Hudson 1976). A major contributor to this mortality is acute cerebral oedema, a recognised and dangerous complication of ketoacidosis (Rosenbloom et al 1981).…”

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Cerebral Oedema Complicating Diabetic Ketoacidosis

Greene

Jefferson

Baum

1990

Develop Med Child Neuro

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SUMMARY Four children presented with cerebral oedema secondary to diabetic ketoacidosis, each of whom had a different clinical picture and time of onset of neurological deterioration. No single factor emerged as the cause of the cerebral oedema, but disturbances in brain water balance appeared to be already operative at the time of presentation with ketoacidosis. Irregularities in treatment may exacerbate these disturbances, leading to frank cerebral oedema. Diagnosis of this dangerous complication of diabetic ketoacidosis depends on clinical awareness; the diagnosis may be confirmed by CT scan. Management remains empirical. RéSUMé Oedéme cérébral compliquant un diabéte acido‐cétosique Quatre enfants présentant un oedème cérébral secondaire à une acidocétose diabétique sont présentés, chacun d'entre eux differant par l'allure clinique et le moment du début de la détérioration neurologique. Aucun facteur unique n'est apparu comme la cause de l'oedéme cérébral mais les perturbations de la balance des liquides cérébraux apparaissaient déjá présentes au moment du tableau d'acidocétose. Des anomalies de traitements peuvent exagérer ces perturbations conduisant á un oedème cérébral franc. Le diagnostic de cette complication dangereuse de l'acidocétose dépend de l'alerte clinique; le diagnostic peut être confirmé par le scanner. Le traitement demeure empirique. ZUSAMMENFASSUNG Hirnödem als Komplikation bei diabetischer Ketoazidose Vier Kinder hatten nach einer diabetischen Ketoazidose ein Hirnödem, jedes zeigte andere klinische Symptome und wurde zu unterschiedlichen Zeitpunkten neurologisch auffällig. Kein einzelner Faktor erwies sich als Ursache für das Hirnödem, aber Störungen im Wasserhaushalt des Gehirns schienen schon zum Zeitpunkt der Ketoazidose wirksam zu sein. Unregelmäßigkeiten bei der Therapie können diese Störungen verstärken und so zum Hirnödem führen. Die Diagnose dieser gefährlichen Komplikation der diabetischen Ketoazidose hängt von der klinischen Aufmerksamkeit ab. Die Diagnose kann durch CT Untersuchungen bestätigt werden. Die Behandlung bleibt empirisch. RESUMEN Edema cerebral complicando una cetoacidosis diabética Cuatro niflos sufrieron un edema cerebral secundario a una cetoacidosis diabética, cada uno de los cuales tenía un cuadro clinico diferente, asi como un momento de inicio diferente en la deterioracion neurológica. No apareció ningúin factor único como causa del edema cerebral, pero las alteraciones en el equilibrio acuoso del cerebro estaban presentes en el momento de la aparición de la cetoacidosis. Las irregularidades en el tratamiento pueden exacerbar estas alteraciones, dando lugar a un franco edema cerebral. El diagnóstico de esta peligrosa complicacióin de la cetoacidosis diabética depende de la vigilancia clínica. El diagnóstico puede ser confirmado por una TAC. El tratamiento continúa siendo empirico.

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confidence: 99%

Cerebral Oedema Complicating Diabetic Ketoacidosis

Greene

Jefferson

Baum

1990

Develop Med Child Neuro

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Granulocyte chemotaxis in the canine trachea: Inhibition by lipid mediator antagonists and systemic inhibitors

Johnson

McNee

1991

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Inflammation of the airways contributes to the multicomponent disease known as asthma. The primary cells that infiltrate the airways in response to antigen exposure are PMNs and eosinophils, cells that can release cellular components, and damage the airways. We adapted a double-balloon endotracheal tube to study the cellular response to three de novo synthesized lipid mediators (LTB4, PAF-acether and 15 HETE) found in respiratory fluids following antigen exposure. In random repeat challenges in groups of 7 dogs using mongrel dogs at 240 min following exposure to 10(-6) M agonists, the PMN content of the perfused fluid was 870 +/- 240, 1632 +/- 883, 515 +/- 395, and 1575 +/- 214 cells/ml/5 high power fields for vehicle, LTB4, PAF, and 15 HETE respectively. Eosinophils that infiltrated the lumen at 240 min were 162 +/- 23, 608 +/- 287, 502 +/- 23, 115 +/- 14 cells/ml/5 HPF for vehicle, LTB4, PAF, and 15 HETE respectively. Thus LTB4 and PAF-acether significantly (p less than 0.05) increased eosinophils, and LTB4 and 15 HETE increased PMNs (p less than 0.05). After determining the agonist response for the 3 agonists we included 2 specific antagonists in the perfusate. The LTB4 antagonist U-75,302 10(-5) M, and the PAF antagonist L 652,731 10(-5) M in chambers containing LTB4 and PAF-acether respectively blocked significantly the influx of PMNs and eosinophils compared to vehicle (p less than 0.01). Methylprednisolone 5 mg/kg i.m.--18 hrs blocked eosinophilia to PAF and LTB4. Oral U-78,517F a Trolox amine lazaroid, active as an inhibitor of lipid peroxidation, 30 mg/kg--18 hrs significantly blocked eosinophilia to PAF-acether and LTB4 directed chemotaxis compared to vehicle (p less than 0.05) but not 15 HETE. Specificity was shown for each antagonist since the PAF and LTB4 antagonists did not block the opposite agonist. Use of this novel in vivo chemotaxis model allows the additional advantage of studying chemotaxis in living tissue.

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Serum thymic hormone thymulin activity is normal in children with asthma

Lurie¹,

Chaussain²,

Raynaud³

et al. 1989

Journal of Allergy and Clinical Immunology

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Mortality in juvenile diabetes mellitus over 25 years.

Cited by 9 publications

References 15 publications

Cerebral Oedema Complicating Diabetic Ketoacidosis

Cerebral Oedema Complicating Diabetic Ketoacidosis

Granulocyte chemotaxis in the canine trachea: Inhibition by lipid mediator antagonists and systemic inhibitors

Serum thymic hormone thymulin activity is normal in children with asthma

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