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Case Study: Diabetic Ketoacidosis in Female Patient

A detailed medical case study of a female patient presenting with symptoms of nausea, weakness, and hyperglycemia leading to a diagnosis of diabetic ketoacidosis. Follow the treatment course and outcome in this informative report.

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Case Study: Diabetic Ketoacidosis in Female Patient

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  1. 病人姓名: 劉x玲 • 性別: 女 • 病歷號碼: U221424340 • 住院日期: 94.3.31

  2. Chief complaint • Nausea and vomitting for one day

  3. Present illness • She was 18 y/o female with previous healthy condition. She suffered form nausea and vomitting since one week ago. And generalized weakness was also found. Dyspnea and body weight loss of 8 kg in one month ago were noted. No palpitation or hand tremor was told. She went to Dr 李`s OPD for help. Thyrotoxicosis was suspected and T3/T4/TSH were measured on 3/29.

  4. Present illness • But nausea and generalized weakness were getting worse .So she was sent to our ER for help. At ER, generalized weakness and Kussmauel respiration were noted. Hyperglycemia(1036 mg/dL)with blood osmorlity 344 mOsm/Kg was found. Metabolic acidosis (anion gap >12) was also noted . Urine analysis also revealed ketone body(+++). Under impression of diabetic keto-acidosis ,she was admitted to our hospital for further treatment.

  5. Personal history • Social history: a student, no history of smoking, drinking, or betel nut chewing • Allergy history: No history of food or drua allergy • Family: Father has DM with OHA control for thirty years

  6. Review of system • General : weight loss(+), fatigue(+), weakness(+) appetite change(-), fever(-), chills(-), night sweats(-) • Skin: rashes(-), pruritus(-), bruising(-), dryness(-) itching(-), skin cancer or other lesions(-). • Head: trauma(-), headache(-), tenderness(-), dizziness(+),syncope(-)

  7. Review of system • Eyes: glasses(-), photophobia(-), blurring(-), diplopia(-),inflammation(-), discharge(-), dry eyes(-) excessive tearing(-), changes in visual field(-) history of cataracts or glaucoma(-) • Ears: tinnitus(-), pain(-), discharge(-), vertigo(-) history of ear infections(-), hearing impairment(-)

  8. Review of system • Nose: epistaxis(-), obstruction(-), polyps(-), sinus problems(-), sense of smell loss(-) • Mouth and Throat: bleeding gums(-), voice change(-), dysphagia(-),ulcerations or other lesions of tongue(-), gums(-),or buccal mucosa(-) • Respiratory: chest pain(-)wheezing(-), dyspnea(-), cough(-) hemoptysis(-), sputum(-), history of pneumonia(-) or TB(-)

  9. Review of system • Cardiovascular: dyspnea on exertion(-), chest pain(-), orthopnea(-), claudication(-), varicose vein(-), palpitation(-), peripheral edema(-), History of MI(-) or murmur(-), paroxysmal noctural dyspnea(-) (-) • Gastrointestinal: abdominal pain(-), heartburn(-), nausea(-), vomiting(-), hematemesis(-), diarrhea(-), indigestion(-),destension(-), constipation(-), melena(-), intolerace for greasy food(-), change in stool shapes and color(-)

  10. Review of system Musculoskeletal musculoskeletal trauma(-), arthralgia(-), arthritis(-), redness(-), tenderness(-), back pain(+), joint swelling(-), limitation of range of motion(-)

  11. Physical exam • Blood pressure 109/63 mmHg. BT: 37.3 degree Celcius. • Pulse rate 74/min, regular. • Respiration rate 18/min • Conciousness: dizziness (Glasgow scale: E4M6V5) • Skin: normal skin turgor, cold • Lymph node: negative. • Head: normal.

  12. Physical exam • Eyes: conjunctiva: pale, sclera: anicteric, • Jugular vein: no engorgement • Heart: RHB without murmur • Chest wall: symmetric • Lung: Breathing sound: clear. • Abdomen: flat, Soft, no tenderness • Bowel sound: normoactive

  13. Physical exam • Liver: not palpable • Spleen: not palpable. • Muscle power:normal • Coordination: normal. • Extremities: no pitting edema hand tremor(-)

  14. BCS data

  15. BCS data

  16. CBC and D/C data

  17. Urine exam

  18. Endocrine survy

  19. Active problems • Type 1 DM with Ketoacidosis and hyperosmolarity

  20. Treatment course • After admission,prompt intravenous fluid challenge and insulin injection were administerred. Her sugar was under control step by step. Jusonin had been infused due to diabetic ketoacidosis. She was transferred to ordinary ward on April 1st. Her insulin dosage escalated progressively due to poor control of serum sugar. Glucagon test was performed on April 8th to evaluate her islet cells reserved function. She was discharged with drug home on April 8th 2005.

  21. Novorapid 10 units tidac Lantus 10 units qhs Novorapid 15 units tidac RI 6uints tidac NPH 6 units qhs RI 8 units tidac NPH 8 units qhs Novorapid 12 units tidac Lantus 15 units qhs

  22. Glucagon test ( C-peptide level) C-peptide level 1.09 0.64 0.54 0.5 0.52 0.52 <0.5 <0.5 <0.5 打前1.5分 打時 5 6 10 20 40 60 時間

  23. Glucagon test ( Glucose level) 208 Sugar level 203 200 192 190 185 180 170 169 165 160 156 154 150 打前1.5分 打時 5 6 10 20 40 60 時間

  24. Journal of Clinical Endocrinology and Metabolism, Vol. 80, No. 21995 Modified Glucagon Test Allowing Simultaneous Estimation of Insulin Secretion and Insulin Sensitivity: Application to Obesity, Insulin-Dependent Diabetes Mellitus, and Noninsulin-Dependent Diabetes Mellitus

  25. Preface • The test is based on the ability of iv glucagon to stimulate insulin secretion and the efficiency of insulin to decrease the blood glucose levels previously raised by glucagon. • Indices of insulin secretion and insulin sensitivity have been compared in various populations: lean controls, nondiabetic obese subjects, IDDM patients, and NIDDM patients with or without weight excess.

  26. Materials and Methods • Subjects: • The following groups of individuals were examined: • 1) 11 lean [body mass index (BMI), <25 kg/m*] and healthy volunteers, • 2) 5 obese (BMI, >30 kg/m2 ,1 subjects with normal fasting blood glucose and normal to mildly impaired glucose tolerance • 3) 9 IDDM patients, • 4) 7 nonobese NIDDM patients, and • 5) 8 moderately obese (BMI, >25 kg/m2) NIDDM subjects.

  27. Materials and Methods • Diabetic patients with marked hyperglycemia were connected to glucose-controlled insulin infusion (GCII) system during the night preceding the study to control fasting blood glucose.

  28. Instrumentation • The glucose-controlled insulin infusion system used in this study was the Biostator (Miles Martin Laboratories, Eklhart, IN). This is a closed loop device that continuously samples blood for glucose analysis and infuses insulin to mimic insulin secretion.

  29. Test • glucagon (Nova-Nordisk, Copenhagen, Denmark) at a dose of 1 mg/m’ corporeal surface. • During the 20 min after glucagon injection, blood glucose levels were allowed to rise freely, i.e. blood glucose levels were continuously recorded by the Biostator, but insulin was not infused. • After that time, the Biostator was allowed to infuse insulin in a glucose-controlled basis (static and dynamic mode).

  30. Test • This insulin infusion was maintained for the next 30 min, and then the test was completed. • Two continuous blood collections were obtained: from O-20 min and from 20-50 min.

  31. Computations • Evaluation of the hepatic response. The hepatic ability to increase glucose output in response to glucagon was estimated as the rate of increase in blood glucose when this increase was linear, that is from l0-20 min of the test.

  32. Computations • Evaluation of the B-cell response. The C-peptide concentration was measured in plasma from both tubes of continuous blood collection (from O-20 min and from 20-50 min)

  33. Computations • Evaluation of the sensitivity to insulin. An index of insulin sensitivity was obtained by dividing the rate of decrease in blood glucose (when this decrease was linear, i.c. from 40-50 min) by the total amount of insulin entering the circulation (insulin secreted + insulin infused)

  34. Results • Maximum blood glucose levels (9.6 2 0.3 mmol/L) were attained in 16-38 min (mean, 30 2 1 min). • No significant differences were seen in the rising blood glucose profile of the different groups of subjects studied. • Most subjects exhibited a similar hepatic response to glucagon.

  35. Results • In the subsequent decline in blood glucose, both normal controls and IDDM patients showed faster decreases than obese or NIDDM subjects.

  36. Results • The rates of decrease in blood glucose concentration were significantly (P < 0.001) higher in normal controls (0.208 ± 0.018 mmol/L.min) and IDDM patients (0.155 ± 0.030 mmol/L.min) than in obese subjects (0.110 ± 0.015 mmol/L.min ) or NIDDM patients (0.094 ± 0.011 mmol/L.min).

  37. Results • the obese subjects showed a significantly greater endogenous insulin secretion • In the nonobese NIDDM group, the endogenous insulin secretion tended to be slightly lower than that in lean controls or overweight NIDDM patients

  38. Results • The index of sensitivity to insulin, calculated by dividing the rate of decrease in blood glucose in the last 10 min of the test by the total amount of insulin entering the circulation, is lower in obese subjects and even more decreased in NIDDM patients than in normal controls and IDDM patients (Table 4).

  39. Discussion • The estimate of insulin sensitivity was obtained by comparing the decline in blood glucose levels and the total amount of insulin entering the circulation. • As insulin secretion is markedly deficient in some diabetic patients, we used a glucose-controlled insulin infusion in the last 30 min of the test to induce a rapid decrease in blood glucose levels.

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