DIABETIC EMERGENCIES

Trevor Langhan MD

January 31st, 2008

University of Calgary

Objectives

Case based approach to important glucose related presentations

Mixed in with some physiology to understand treatment plans

Case 1

21 year old Japanese exchange student

In Canada past 6 months Felt sick for past 2 days and was not

eating Now billeting family says he is acting

confused

Case 1

In to ED via EMS Pt too drowsy to provide accurate

history Responds to pain Thin male, looks dehydrated PMHx: Type 1 DM since 6 yrs old Questions?

Case 1

Vitals: T – 38.2 HR – 130 BP – 100/60 RR – 28 Sats – 98%

Bedside tests: Chemstrip – “high”

Additional labs?

Case 1

Na+ 130 K+ 6.3 HCO 8 Cl 108 Cr 165 Glucose 38 What is his AG?

14 – is this right?

Na+ correction for increase Glucose

Multiple sources of information for formula….

Common: Increase Na+ 1.6 for every 5.6 mmol/L

glucose Easiest:

Increase Na+ 3 mmol/L for every 10 mmol/L of glucose

Na+ correction for increase Glucose

Hyperglycemia (and hyperlipidemia) leads to increase in osmolar funciton of blood

H20 is drawn from the cells into the vascular space

Dilutional hyponatremia For our guy his Na+ = 139 mmol/L

3 mmol increase Na+ / 10 mmol glucose

Case 1

With the new Na+ his AG is actually 23 So he has an anion gap metabolic

acidosis….

How are you going to get his acid/base status?

ABG vs. VBG…..

Ma OJ et al. Arterial Blood Gas Results Rarely Influence Emergency Physician Management of Patients with Suspected Diabectic Ketoacidosis. Acad Emerg Med. Aug 2003, 10:8.

Prospective observational study Inclusion: DKA pts VBG, ABG, chem 6

ABG result changed: Altered treatment in 7/200 (3.5%, 1.7-7.1% CI) dispostion in 2/200 cases (1%, 0.3-3.6% CI)

VBG pH correlated with ABG pH (r = 0.951)

Case 1

What is the source of his gap acidosis? Ketone production from fatty acid

breakdown

How are you going to prove that? Urine vs. blood….

Urine vs. blood Urine dip stick

Nitroprusside reaction Qualitatively assess for ketones

Only measures which ketone? Acetoacetate Does not measure B-Hydroxy Buterate

AA:BHB ratio is 1:3 (can be as high as 1:30)

So might have false –ve urine dip despite gross ketosis

Case 1

So you’ve proven he’s got an AGMA And shown where the acidosis is

coming from….

Dx: Diabetic ketoacidosis

DKA - Diagnosis

Clinical Dehydration High cap glucose Ketones in urine or plasma

Confirmed: Blood pH Serum Bicarb Serum Osmolality

DKA

Three main problems:1. Hyperglycemia

Osmotic diuresis Dehydration – can be profound 5-7 litre total fluid deficit

2. Loss of electrolytes K+, Na+, Mg+, PO4-

3. Acidosis Transcelluar shift of H+ and K+ Falsely normal K+ (or even high)

DKA - Treatment

Fluid rehydration Pts in hypovolemic shock need

assessment of ABCs Treat with boluses of 0.9% NS Avoid pressors – etiology of shock is

decreased intravascular volume Adults – 1-2 litres over 1 hour Subsequent fluid change to 0.45% NS

DKA- Treatment

Peds – 20 cc/kg bolus initially if shock Otherwise start with 10 cc/kg Goal to replace fluid deficit over 24-48

hours Dreaded risk of cerebral edema….

Multi-center, retrospective Included DKA pts with CE Matched for illness severity to DKA pts with

no CE Log regression Risk Factors:

High urea Use of Bicarb Low PCO2

Why do they get Cerebral Edema?

Marcin JP et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. Journal of Pediatrics. 141(6); Dec 2002.

3 variables were found to be associated with a poor outcome of children with DKA-related cerebral edema Elevated initial BUN concentration More profound neurologic depression at the time

of diagnosis of cerebral edema Intubation with associated hyperventilation to a

PCO2 level <22 mm Hg.

DKA - Treatment

Boluses of fluid to increase intravascular volume

What next?

Stop lipolysis and the production of ketone bodies His glucose is 38 mmol/L How do you want to treat him?

DKA - Treatment

IV regular insulin is the start No RCT to prove bolus vs. just starting an

infusion Current practice is to only start an infusion

at 0.1 unit/kg/hour No need to quickly drive glucose into the

cells Rehydration and osmotic diuresis will eliminate

most excess glucose

Umpierrez GE et al. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome. Am J Med Sci. 311(5); May 1996, pp 225-233.

Kitabchi et al. Compare ‘high dose’ to ‘low dose insulin’ in DKA treatment

RCT, prospective No difference in:

Rate of decline of blood glucose Rate of decline of ketone body concentration Time to resolve acidosis

High doses of insulin associated with: 25% increase in hypoglycemic events Greater hypokalemia

DKA - Treatment

Current standard has become ‘low dose’ insulin

Constant infusion at 0.1 units/kg

No current need to bolus administer insulin

DKA - Treatment

As glucose is trending down add a glucose containing solution to IV fluid

Glucose < 14 mmol/L Drop insulin infusion by 50% Add D5 to your ½ NS maintenance

Run at 200-400 cc/hr for first 12 hours

Loss of Electrolytes

Electrolyte Replacement

Loss of: Cl-, Na+, K+, PO4

Most NB to replace is K+ Myocardial cell membrane stability Risk of dysrhythmia, death

Electrolyte Replacement

DKA – K+ may be normal or elevated Acidosis may lead to ‘false normal’ K+

levels True body K+ much lower Treatment of DKA may lead to

lowering of K+ Insulin HCO3

Electrolyte Replacement

Hold insulin until you’ve checked the K+ Don’t give insulin if K+ < 3.3 mmol/L If K+ normal or high start rehydration

and insulin K+ < 5.0 mmol add 20-40 mmol/L of K+

to IV fluids Ensure Mg+ supplemented as well

DKA – Treatment summary

IV fluids – bolus ++ if shocky Check lytes

Replace K+ early Add to IV fluid as K+ < 5.0 mmol/L

Insulin infusion 0.1 units/kg/hr Look for inciting event…

Infection, MI, trauma, pancreatitis…

DKA - Treatment

Bicarb is rarely indicated Risk of hypokalemia No proven indications Guidelines suggest that if:

pH < 7.0 – after 1 hour of treatment Give one amp diluted in 200 cc over 1

hour

CASE 1-B

77 y F from nursing home Not eating or drinking lately Vague abdominal pain expressed to

care home staff yesterday Didn’t come down for lunch

CASE 1-B

EMS called when she was found in her room

HR 120 BP 90/50 RR 18 Sat 98% GCS 9 Glucose ‘high’

CASE 1-B

Labs: Na+ 144 mmol/L K+ 5.4 mmol/L Cl- 124 mmol/L HCO3 20 mmol/L Glucose 49 mmol/L Urea 15 mmol/L VBG 7.34 / 40 / 90 / 21

Hyperosmolarity

2 Na+ + gluc + urea = osmolarity

DKA osmo usually < 320 mmol/L

HHS > 320 mmol/L

Hyperglycemic Hyperosmolar State

Formerly known as HONK Pts can have ketosis so misleading name

Marked hyperglycemia and dehydration

Profound electrolyte losses Due to insulin resistance and excess

counter regulatory hormones

Hyperglycemic Hyperosmolar State

More likely to occur in older, obese pts More often Type 2 DM May develop over days – weeks Frequent in elderly:

free water deprived compromised renal fxn

Hyperglycemic Hyperosmolar State

Some insulin present so no ketone production

No subsequent acidosis (pH > 7.3)

Hyperglycemic Hyperosmolar State

LOOK for underlying cause Older more frail pts

IV fluids Insulin infusion Monitoring and correction of electrolytes K+ depleted but not as low as DKA

No acidosis, so no shift

Diagnosis - Laboratory

Complications of DKA and HHS

Cerebral Edema ARDS Hypoglycemia and Hypokalemia Thrombosis and PE

No RCT to tell us what to do Venous stasis, viscous blood, underlying

artherosclerosis – set up for clot Consider Heparin sc for DVT prophylaxis in high

risk patients

Prognosis - summary

DKA mortality 4-10% HHA mortality 10-50%

Not as different as I always thought: IV fluids Lower glucose with IV insulin infusion Anticipate and correct electrolyte abnormalities (K+

most NB in DKA) Add glucose to IV at gluc < 15 mmol/L Look for precipitant

CASE 2

3 month old boy with gastroenteritis To ED with parents lethargic Has not been eating well Clinically looks dry Glucose 1.6 mmol/L

Tx: 4 cc/kg D10W IV fluids, improved

CASE 3

25 y female Took her insulin 30 minutes ago to kill

self Seizure in waiting room Tx: IV glucose

1 amp D50W Additional amps as needed May require infusion of D10W

CASE 4

27 year old Type 1 DM Took insulin this am as usual Skipped breakfast, then vigorous

exercise Now confused, cant’ find keys EMS called

CASE 4

Initial glucose 2.2 mmol/L Vitals stable, GCS 13 Given IM glucagon and some oral CHO Now glucose is 6.6 mmol/L Feels well, A&O x 3 EMS patches to cancel transport

Alert, cooperative pts, responsible adults Tolerating oral CHO

Hypoglycemia - Summary

Bolus IV glucose D50W adults (1-3 amps) D25W peds (4 cc/kg) D10W neonate-2 years (4 cc/kg)

NO IV can give Glucagon IM 1-2 mg

Prolonged hypoglycemia after OD of insulin may need Dextrose infusion D10W

Treatment is eating CHO meals

CASE 5

55 year old male Type 2 DM Acting confused at home Wife called EMS Meds:

Metformin Altace Glyburide ASA

CASE 5

Given IM glucagon and some juice Alert and oriented 25 minutes after EMS patches to ED to cancel transport

Pancreatic Beta Cell

GLUCOSE

K+

Ca+

INSULIN

Sul-onlyurea

Oral Hypoglycemics

Variety of classes Long half lives Potentiate action of beta cells to

secrete insulin in setting of glucose Can have rebound hypoglycemia due

to our treatments

Prospective, DBRCT Included hypoglycemia, on sulfonylureas Standard tx: 1 amp D50 and oral CHO placebo or octreotide (75 mcg sc)

Oral hypoglycemics - summary

Tx acute hypoglycemia as expected Longer period of observation

Not just for ODs Can happen with therapeutic use and change in

drug clearance or increase in dose Need admission to hospital Octreotide 50 mcg SC q 6h if they have a

rebound event Treatment is eating CHO

Hypoglycemia

Check glucose as another vital sign Treat low glucose with boluses Oral feeding is most NB IM glucagon an option Octreotide for REBOUND event in oral

hypoglycemic ingestion

DM - Emergencies

HHS and DKA treatment is similar Avoid iatrogenic complications treat low glucose with bolus Monitor as appropriate

Questions?