Case presenation

Dr.Suad Al-Abri

R4

At 10: 20 am

19 yrs old girl brought by family

H/o becoming unresponsive since 1 am

1 survey R2 2 survey R1 History R1

DD R3 Invex R4 RX R4

Dispostion

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

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

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

DD

Causes of AMS

TIPS OF AEIOU

T Trauma; temperature; tumors

I Infection

P Psychiatric; poisonings

S Shock; stroke; space-occupying lesions; subarachnoid hemorrhage

A Alcohol; abuse

E Epilepsy; electrolyte disorders; encephalopathy; endocrine

I Insulin; intussusception; intoxication

O Overdose; oxygen

U Uremia (and other metabolic causes)

CT brain

Generalized brain edema ,

No focal space occupying lesion

Reassessed at 13:00

Noticed to have active seizure tonic clonic convulsion with uprolling of eyes and making gargeling sounds

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

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

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

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

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

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

She was feeling better, responding

Neurological exam was normal

Discharged home with referral to psychiatric SQUH

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

Hypoglycemia

Symptomatic hypoglycemia 40-50 mg/dl (2.2-2.7 mmol)

S&S caused by excessive secretion of epineph and by CNS dysfunction

Hypoglycemia is the most common metabolic cause of seizures

New-onset seizure. Ann Emerg Med 1990;19:373-377.

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

Sulfonylureas (Oral Hypoglycemic drugs)

Tolbutamide Acetohexamide

Tolazamide

Chlorpropamide GlipizideGlyburide

(Glibenclamide)

Glimepiride

Short

acting

First generation

Intermediate

acting

Long

acting

Long

acting

Short

acting

Second generation

Mechanism of action

Sulfonylureas

Lower blood sugar by stimulating pancreatic islet cells and facilitating the release of preformed pancreatic insulin

Gen. Generic name Trade name

Time to peak (hr)

Duration of Action

(hr)

First Chlorpropamide

Diabinase 2-7 60

First Tolbutamide Orinase 3-4 6-12

Second Glipizide Glucatrol (XL)

1-3(6-12)

12-24(24)

Second Glyburide MicronaseDiaBeta

2-6 12-24

Third Glimepiride Amaryl 2-3 16-24

Sulfonylureas

Initial Managements

Sulfonylureas

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)

Sulfonylureas

3. Diazoxide

Direct inhibitor of insulin release Increases hepatic glucose output Effective in several case reports and chart review May cause hypotension, hypernatremia

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

Octreotide:

• Long-acting somatostatin analogue• suppresses hormone release

GH, gastrin, glucagon, and, most interestingly,

INSULIN

Sulfonylureas

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)