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Case report n°1 Case report n°1 Metabolic disorder Metabolic disorder A&E meeting A&E meeting 22 february 2012 22 february 2012
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Case report n°1 Metabolic disorder

Mar 13, 2016

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rhea-tyson

Case report n°1 Metabolic disorder. A&E meeting 22 february 2012. Presentation of the case. Male Korean patient 39 years old, coming for confusion anorexia, hypothermia. Past history: HTN, diabetes (according his friend), depressive mood. Unknown treatment (Insuline?) - PowerPoint PPT Presentation
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Page 1: Case report n°1  Metabolic disorder

Case report n°1 Case report n°1 Metabolic disorderMetabolic disorder

A&E meeting A&E meeting 22 february 201222 february 2012

Page 2: Case report n°1  Metabolic disorder

Presentation of the casePresentation of the case

Male Korean patient 39 years old, coming for Male Korean patient 39 years old, coming for confusion anorexia, hypothermia. confusion anorexia, hypothermia. Past history: HTN, diabetes (according his Past history: HTN, diabetes (according his friend), depressive mood.friend), depressive mood.Unknown treatment (Insuline?)Unknown treatment (Insuline?)5 days ago, after drinking alcohol, he 5 days ago, after drinking alcohol, he presented abdominal pain & vomiting, after presented abdominal pain & vomiting, after that, he didn’t eat/drink much. that, he didn’t eat/drink much. Today, his girlfriend discovered him with Today, his girlfriend discovered him with confusion and major asthenia. confusion and major asthenia.

Page 3: Case report n°1  Metabolic disorder

Clinical examinationClinical examination

Shock statusShock status with blood pressure 80/50, with blood pressure 80/50, tachycardia 92/min , “marbrures”, tachycardia 92/min , “marbrures”, dehydration with “pli cutane”. dehydration with “pli cutane”.

CrCrackels in both lungsackels in both lungs, confusion , confusion syndrome with Glasgow score 14, no focal syndrome with Glasgow score 14, no focal neurodeficit.neurodeficit.

ECGECG

Page 4: Case report n°1  Metabolic disorder
Page 5: Case report n°1  Metabolic disorder

Electric sign of hyperkaliemiaElectric sign of hyperkaliemia

Page 6: Case report n°1  Metabolic disorder

AbdominalAbdominal CT scanner CT scannerMotif:Motif:

Pancréatite? Pancréatite? TechniqueTechnique:: Coupes axiales avant et après Injection de contraste des coupoles Coupes axiales avant et après Injection de contraste des coupoles

diaphragmatiques à la symphyse pubienne. Le patient ne peut bloquer sa respiration. diaphragmatiques à la symphyse pubienne. Le patient ne peut bloquer sa respiration. Résultat:Résultat:  

Aspect normal du parenchyme hépatique. Aspect normal du parenchyme hépatique. Vésicule et voies biliaires sans particularité. Vésicule et voies biliaires sans particularité. Aspect normal de la rate. Aspect normal de la rate. Aspect normal du pancréas sans syndrome de masse. Absence d'infiltration Aspect normal du pancréas sans syndrome de masse. Absence d'infiltration péripancréatique.péripancréatique.Aspect normal des surrénales et des deux reins. Aspect normal des surrénales et des deux reins. Pas d'épaississement pariétal intestinal. Pas d'épaississement pariétal intestinal. Absence d'épanchement péritonéal. Absence d'épanchement péritonéal. Aspect normal de l'aorte, absence d'adénopathies coelio-mésentériques ou rétro Aspect normal de l'aorte, absence d'adénopathies coelio-mésentériques ou rétro péritonéales. péritonéales. Absence de masse pelvienne.Absence de masse pelvienne.Pneumopathie basale bilatérale. Pneumopathie basale bilatérale. 

AU TOTAL:AU TOTAL:      Pneumopathie basale.Pneumopathie basale.

Page 7: Case report n°1  Metabolic disorder

Prescriptions in A&EPrescriptions in A&E

12h50: arrival in A&E, Immediate evaluation by A&E 12h50: arrival in A&E, Immediate evaluation by A&E nurse & Doctor , nurse & Doctor , Dextro HI + confusion Dextro HI + confusion && dehydration; dehydration; hypotensionhypotension13h0013h00 Start rehydration with Ringer 500ml rapid Start rehydration with Ringer 500ml rapid followed by NaCL 0.9% 500ml x 4 rapid then followed by NaCL 0.9% 500ml x 4 rapid then 50ml/h50ml/h13h0013h00 Start Insuline bolus 10UI Start Insuline bolus 10UI13h1513h15 Start Insulin IV continuous 10UI/h Start Insulin IV continuous 10UI/h14h17: Blood gas available 14h17: Blood gas available 15h15: blood test available (ionogram)15h15: blood test available (ionogram)15h3015h30 Ceftriaxon 1g Ceftriaxon 1g

Page 8: Case report n°1  Metabolic disorder

Biological resultsBiological results

Creat 179 micromole/lCreat 179 micromole/lNa 102 mmol/l & Cl 65mmol/lNa 102 mmol/l & Cl 65mmol/lK 7,2 mmol/lK 7,2 mmol/lCa 2,33mmol/lCa 2,33mmol/lAlcalin Reserve 3mmol/l Alcalin Reserve 3mmol/l Glycemy 16g/lGlycemy 16g/lUrine: Glucose ++++, Cetone ++Urine: Glucose ++++, Cetone ++

Page 9: Case report n°1  Metabolic disorder

Biologic results at 14h17 & 15h15Biologic results at 14h17 & 15h1514h1714h17:: pH 6.96 pH 6.96, , pCO2 6.9mmHgpCO2 6.9mmHg, pO2, pO2 132 132mmHg, mmHg, Bicar 1.6mmol/lBicar 1.6mmol/l (23-29), (23-29), CO2T 1.8mmol/lCO2T 1.8mmol/l (20-30); (20-30); Base Excess -29mmol/lBase Excess -29mmol/l, SaO2 95%, SaO2 95%

15H1515H15: Creat 179micmol, : Creat 179micmol, Na 102mmol/lNa 102mmol/l, , K K 7.2mmol/l7.2mmol/l, , Glycemie 16g/lGlycemie 16g/l (89mmol/l), (89mmol/l), RA 3mmol/lRA 3mmol/l

WBC 38600WBC 38600 (93%PN), Hb 15.1g, Pl 321.000 (93%PN), Hb 15.1g, Pl 321.000

CRP 1.5mg, CRP 1.5mg, Lipase 249Lipase 249 (N<60), ASAT 20, ALAT (N<60), ASAT 20, ALAT 25, 25, TP 58%TP 58%

Urine test: Urine test: Glucose ++++, Ketosis ++Glucose ++++, Ketosis ++

Page 10: Case report n°1  Metabolic disorder

Anion Gap calculationAnion Gap calculation

Anion Gap* = Na –(Cl + HCO3) Anion Gap* = Na –(Cl + HCO3) Anion Gap = Anion Gap = 35 mmol/l35 mmol/l (very increased) (very increased)

* Normal Anion Gap = 12 +/-2mmol/l

Page 11: Case report n°1  Metabolic disorder

Evolution of Evolution of acidosis & kaliemiaacidosis & kaliemia

13h 13h (H0)(H0) 16h (H3)16h (H3) 21h (H8)21h (H8)

PHPH 6.966.96 7.077.07 7.357.35

PCO2PCO2 6.9mmHg6.9mmHg 8.7mmHg8.7mmHg 28mmHg28mmHg

BicarBicar 1.6mmol/l1.6mmol/l 2.6mmol/l2.6mmol/l 15.5mmol/l15.5mmol/l

Base Base excessexcess -29mmol/l-29mmol/l -25.8mmol/l-25.8mmol/l -8.4mmol/l-8.4mmol/l

KK 7.2mmol/l7.2mmol/l ?? 3.2mmol/l3.2mmol/l

Page 12: Case report n°1  Metabolic disorder

A&E A&E DiabeticDiabetic

ketoacidosis ketoacidosis “DKA” “DKA”

protocolprotocol

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1) Rehydration1) Rehydration

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2) Insulino-therapy2) Insulino-therapy

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3) Potassium supplementation3) Potassium supplementation

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Interest of bicarbonates?Interest of bicarbonates?SFAR 2006: Complications metaboliques du diabeteSFAR 2006: Complications metaboliques du diabete: “L’acidose : “L’acidose metabolique severe a ete accusee de nombreuses dysfonctions d’organe, metabolique severe a ete accusee de nombreuses dysfonctions d’organe, notamment cardiaque. Un travail montre clairement qu’il n’existe pas de notamment cardiaque. Un travail montre clairement qu’il n’existe pas de dysfonction myocardique chez les patients presentant une acicocetose dysfonction myocardique chez les patients presentant une acicocetose diabetique (ACD). L’administration de bicarbonates n’a aucun effet diabetique (ACD). L’administration de bicarbonates n’a aucun effet benefique dans cette indication et n’est donc pas recommendee dans le benefique dans cette indication et n’est donc pas recommendee dans le traitenent de l’ACD.”traitenent de l’ACD.”

XIX conference de consensus en reanimation – medecine d’urgence XIX conference de consensus en reanimation – medecine d’urgence (juin 1999):(juin 1999): Les bicarbonates permettent de corriger le pH plasmatique Les bicarbonates permettent de corriger le pH plasmatique mais tendent a augmenter la PCO2 tissulaire et veineuse entrainant une mais tendent a augmenter la PCO2 tissulaire et veineuse entrainant une acidose intra-cellulaire paradoxale. L’alcalinisation relance la glycolyse et la acidose intra-cellulaire paradoxale. L’alcalinisation relance la glycolyse et la production de lactates et de corps cetoniques. Cet effet peut etre deletere production de lactates et de corps cetoniques. Cet effet peut etre deletere en cas d’acido-cetose ou d’acidose lactique. en cas d’acido-cetose ou d’acidose lactique.

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ControversiControversial use of al use of bicarbonates bicarbonates in DKA in DKA

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Problem of hyponatremiaProblem of hyponatremia

Hyponatremia is ususal in case of diabetic Hyponatremia is ususal in case of diabetic ketoacidosis. This is due to hyperglycemia. ketoacidosis. This is due to hyperglycemia. The real natremia can be calculated by the The real natremia can be calculated by the following formula:following formula:

NaNacc = Na = Namm + ((Glycemia + ((Glycemia g/lg/l – 1) x 1.6) – 1) x 1.6)

Do not try to correct this false hypoDo not try to correct this false hyponatremianatremia

Nac: Corrected Na (Real Na) Nam: Mesured Na (Lab. Result)

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CCalcul of the corrected Natremiaalcul of the corrected Natremia

NaNamm = 102mmol/l = 102mmol/l Glycemia = 16g/l Glycemia = 16g/lNaNacc = 102 + = 102 + ((16-1) x 1.6) = 102 + 24 = 126((16-1) x 1.6) = 102 + 24 = 126

Real Na = 126mmol/lReal Na = 126mmol/l

Always look at the glycemia when you see a Always look at the glycemia when you see a hyponatremia in diabetic patientshyponatremia in diabetic patients

Page 21: Case report n°1  Metabolic disorder

Conclusion Conclusion

Correction of hypovolemia and dehydration are the Correction of hypovolemia and dehydration are the 11stst therapeutic measures therapeutic measuresInsulinotherapy IV (0.1UI/Kg/h) has to be started Insulinotherapy IV (0.1UI/Kg/h) has to be started quicklyquicklyPotassium supplementation must be administrated Potassium supplementation must be administrated as soon as K < 5mmol/l as soon as K < 5mmol/l Hyponatremia is “normal” and doesn’t reflect the Hyponatremia is “normal” and doesn’t reflect the real natremia (correction according glycemia)real natremia (correction according glycemia)The place of bicarbonate in DKA is not clearly The place of bicarbonate in DKA is not clearly established. Most of guidelines recommend not to established. Most of guidelines recommend not to use it.use it.