Case Presenation R 4 Suad Al Abri

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Jan 26th 2010
Case Presenation By Suad Al Abri

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Case Presenation R 4 Suad Al Abri

  1. 1. Case presenation Dr.Suad Al-Abri R4
  2. 2.  At 10: 20 am  19 yrs old girl brought by family  H/o becoming unresponsive since 1 am
  3. 3. History R1 1 survey R2 2 survey R1 DD R3 Invex R4 RX R4 Dispostion
  4. 4. Primary survery  A: patent  B :normal , spo: 98%, RR: 16  C: PR:68, BP:116/70  D: GCS? , pup: 2mm Reflow: 8.6  E: no signs of trauma, T: 36.5
  5. 5. History  S:?  A: Non  M : Non  P: Not known , h/o previous similar eposides 3 times , CT brain and EEG normal  L : ? She had her dinner  E : she was preparing her clothes and books for school , went to bathroom and came out and became unrespoinsive
  6. 6. Secondary Survey  HEENT: she is frothing saliva , no signs of trauma, no neck stiffness  Chest: clear  Cvs:s1,2, no murmur  p/a: soft  CNS: difficult to asses as the patient was not cooperative , keeping her eye closed and not responding to commands, moving all limbs  Reflexes are normal
  7. 7. DD
  8. 8. Causes of AMS  TIPS OF AEIOU  T Trauma; temperature; tumors  I Infection  P Psychiatric; poisonings  S Shock; stroke; space-occupying lesions; subarachnoid hemorrhage
  9. 9.  A Alcohol; abuse  E Epilepsy; electrolyte disorders; encephalopathy; endocrine  I Insulin; intussusception; intoxication  O Overdose; oxygen  U Uremia (and other metabolic causes)
  10. 10. CT brain  Generalized brain edema ,  No focal space occupying lesion
  11. 11.  Reassessed at 13:00  Noticed to have active seizure tonic clonic convulsion with uprolling of eyes and making gargeling sounds
  12. 12. What is next ?  Shifted to resus area  She was given midazolam 3 mg iv  Loaded with Na valporate of 1000 mg , her siezure activity decrease  Repeated vitals remain stable  Her reflow came as 1.5  Given 50 ml of 50% dextrose
  13. 13. In resus  She received octerotide 50 micro sc  Seen by consultant neurologist and registrar medical oncall  Blood sugar picked upto 9  Admitted to Medical ward HD
  14. 14. Lab investigation  CBC: hb : 14 , wbc : 8.4 , plt : 351  UE1: Na: 136 , k: 5.2 , CO2 : 23 , urea: 2.1 , creat : 57  LFT : bilirubin ; 18 , ALT : 52 , ALP: 54 , Alb: 44  Bone: Ca: 2.37 , phosp :1.12 , Mg: 1.03  Paracetomol level : neg  ASA : neg  Glucose : 0.5
  15. 15. Inpatients , D1  EEG was done and showed encephalopathy  Seen by consultant neurologist  She received ceftraixone 2 gm od and dexamethsone 8 mg stat and 4 mg 6 hrly  Kept on 10% dextrose  MRI brain
  16. 16. Inpatient , D2  She was still restless, not responding  She dropped her blood sugar to 1.9 at night and she received 50 ml of 50% dextrose  She was continue in 10% Dextrose 
  17. 17. Inpatient, D3  Patient became more awake and responsive  Her father , mother and grandmother are diabetic on OHD ( metformin and glipizide)  She admits taking > 10 tablets of her father medication
  18. 18.  She was feeling better, responding  Neurological exam was normal  Discharged home with referral to psychiatric SQUH
  19. 19. Learning points  When things goes wrong , start ABCD again  It is always organic , organic and then organic until proven otherwise  Bedside glucose stick are not always accurate , keep higher index of suspicion  When u r stuck , involve seniors
  20. 20. Hypoglycemia  Symptomatic hypoglycemia 40-50 mg/dl (2.2-2.7 mmol)  S&S caused by excessive secretion of epineph and by CNS dysfunction
  21. 21.  Hypoglycemia is the most common metabolic cause of seizures  New-onset seizure. Ann Emerg Med 1990;19:373-377.
  22. 22.  Glucometry is widely used to confirm or exclude hypoglycemia in patients with suggestive clinical findings. Nonglucose sugars may be detected by certain types of glucometers, causing false elevation of the glucometer analysis of the blood sugar. Since these other sugars are not functionally glucose and may even induce excess insulin release, clinical hypoglycemia may be missed. Journal of Medical Toxicology March 2009
  23. 23. Sulfonylureas (Oral Hypoglycemic drugs) First generation Second generation Short Intermediate Long Short Long acting acting acting acting acting Glyburide Tolbutamide Acetohexamide Chlorpropamide Glipizide (Glibenclamide Tolazamide Glimepiride
  24. 24. Sulfonylureas Mechanism of action Lower blood sugar by stimulating pancreatic islet cells and facilitating the release of preformed pancreatic insulin
  25. 25. Sulfonylureas Gen. Generic name Trade Time to Duration name peak of Action (hr) (hr) First Chlorpropamid Diabinase 2-7 60 e First Tolbutamide Orinase 3-4 6-12 Second Glipizide Glucatrol 1-3 12-24 (XL) (6-12) (24) Second Glyburide Micronase 2-6 12-24 DiaBeta Third Glimepiride Amaryl 2-3 16-24
  26. 26. Sulfonylureas Initial Managements 1. Dextrose  Initial management for all hypoglycemia BUT: Glucose itself stimulates release of insulin 1. Results in recurrent, rebound hypoglycemia. 2. Requires ICU monitoring, blood glucose measurements q 20-60 minutes 3. Duration of treatment can be very long (>2-4 days)
  27. 27. Sulfonylureas 2. Glucagon  Raises glucose levels by stimulating gycogenolysis.  Effective only if sufficient glycogen present, has no effects in starvation, chronic hypoglycemia  Since it stimulates Insulin secretion, it i contraindicated in Sulfonylurea O.D 3. Diazoxide  Direct inhibitor of insulin release  Increases hepatic glucose output  Effective in several case reports and chart review  May cause hypotension, hypernatremia
  28. 28. Sulfonylureas Octreotide: • Long-acting somatostatin analogue • suppresses hormone release  GH, gastrin, glucagon, and, most interestingly, INSULIN
  29. 29. Sulfonylureas Octreotide - How to give: • Can be given IV or SQ • Initial dose: 50 g q 6 hours (Infusion doses: 100 g /hr) • Pediatric dose: 1.0 g /kg (single case report) • End point: 24-48 hrs (remember: PO intake is the optimal glucose source)

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