Jan 26th 2010 Case Presenation By Suad Al Abri

1. Case presenation
Dr.Suad Al-Abri
R4

2.  At 10: 20 am
 19 yrs old girl brought by family
 H/o becoming unresponsive since 1
am

3. History R1 1 survey R2 2 survey R1
DD R3 Invex R4 RX R4
Dispostion

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. 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. 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. DD

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.  A Alcohol; abuse
 E Epilepsy; electrolyte disorders;
encephalopathy; endocrine
 I Insulin; intussusception; intoxication
 O Overdose; oxygen
 U Uremia (and other metabolic causes)

17. CT brain
 Generalized brain edema ,
 No focal space occupying lesion

18.  Reassessed at 13:00
 Noticed to have active seizure tonic
clonic convulsion with uprolling of
eyes and making gargeling sounds

19. 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

20. 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

21. 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

22. 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

23. 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


24. 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

25.  She was feeling better, responding
 Neurological exam was normal
 Discharged home with referral to
psychiatric SQUH

26. 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

27. Hypoglycemia
 Symptomatic hypoglycemia 40-50
mg/dl (2.2-2.7 mmol)
 S&S caused by excessive secretion of
epineph and by CNS dysfunction

28.  Hypoglycemia is the most common
metabolic cause of seizures
 New-onset seizure. Ann Emerg Med
1990;19:373-377.

29.  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

30. 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

31. Sulfonylureas
Mechanism of action
Lower blood sugar by stimulating pancreatic
islet cells and facilitating the release of
preformed pancreatic insulin

32. 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

33. 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)

34. 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

35. Sulfonylureas
Octreotide:
• Long-acting somatostatin analogue
• suppresses hormone release
 GH, gastrin, glucagon, and, most interestingly,
INSULIN

36. 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)