EMERGENCIES IN DIABETES

Dr. Rusdiana, SpPD, M.Sc

DISCUSSION

HYPOGLYCEMIA
HYPERGLYCEMIC HYPEROSMOLAR
STATE
DIABETIC KETOACIDOSIS
 HYPOGLYCEMIA

Hypoglycemia is a blood glucose value of less

than 50 mg/dl
Clinically, it is defined by Whipple triad: low
plasma glucose level, symptoms consistent
with hypoglycemia, and resolution of
symptoms with correction of plasma glucose
Epidemiology

30% of type 1 or type 2 diabetic patients on

insulin therapy
10% of type 2 diabetic patients
Mortality rate 3-4% especially elderly taking
long acting oral hypoglycemic agents
 Symptoms
Adrenergic symptoms (catecholamine mediated):
diaphoresis, palpitations, pallor, tachycardia
apprehension, anxiety, sensation of hunger
headache, weakness, restlessness

Neuroglycopenic symptoms:
reduced intellectual capacity, irritability,
confusion, abnormal behavior,
convulsion, coma
Glucoregulatory factors

Blood-glucose-lowering Blood-glucose-raising
factor factors
Glucose-counterregulatory
factors

Glucagon in minutes
Epinephrine
Insulin
Growth hormone In hours
Cortisol
Physiologic response in hypoglycemia

Blood glucose 56-48 mg/dl

* adrenalin secretion
* diaphoresis, tremor
* reduced function of central nervous system
Blood glucose <48-36 mg/dl
* reduced consciousness
Blood glucose <36-18 mg/dl
* coma, convulsion
Blood glucose <18 mg/dl
* permanent brain damage
 Syndromes of compromised glucose
counterregulation in type 1 diabetes mellitus

Defective glucose counterregulation

Impaired awareness of hypoglycemia
Elevated glycemic threshold during intensive therapy
Elevated glycemic threshold following recent
hypoglycemia
Elevated glycemic threshold during -adrenergic
blockade

Autonomic failure

The syndromes may occur in advanced type 2 diabetes mellitus

(insulin-deficient)
Schematic diagram of the concept of hypoglycemia-
associated autonomic failure in T1DM

Insulin deficiency IDDM

No glucagon responses to decreased glucose levels

Epinephrine Imperfect insulin

responses responses

Episodes of hypoglycemia

Hypoglycemia-associated autonomic failure

@ symptomatic responses (awareness)

@ autonomic (including epinephrine) responses
Risk factors

Tight glycemic control

Age
Duration of diabetes
History of hypoglycemia
Sleeping
Alcoholism
Fasting
Increased insulin sensitivity: fitness, body weight
Clearance/metabolism of drugs: renal or hepatic
insufficiency
Mechanisms by which drugs increase the
hypoglycemic effect of sulfonilureas

Increase in half-life due to inhibition of metabolism or

excretion rate: ethanol, phenylbutazone, coumarin
anticoagulants, chloramphenicol, doxycycline,
sulfonamides, allopurinol
Competition for albumin-binding sites:
phenylbutazone, salicylates, sulfonamides
Inhibition of gluconeogenesis, increase in glucose
oxidation, or stimulation of insulin secretion: ethanol,
-adrenergic drugs, monoamine oxidase inhibitors,
tranylcypromine, t
Management of hypoglycemia

Mild hypoglycemia when self treatment with

oral carbohydrate suffices
Sever hypoglycemia when external help is
required to effect recovery
Management of hypoglycemia: Prevention

1. Early familiarization with the symptoms of

hypoglycemia
2. Do reviewing at intervals
3. Explain the relationship between insulin
administration, timing of meals, and exercise
4. Explain methods of self-treating hypoglycemia
5. Choose appropriate insulin regimens, dose schedules
with appropriate therapeutic goals
Management of hypoglycemia: Treatment

Mild hypoglycemia: oral glucose 15-20 g, wait 10-15 min

then check blood glucose. If glucose level does not
increase 18 mg/dl, give oral glucose again
Sever hypoglycemia: solution 50 ml of dextrose 50%
given intravenously, check blood glucose in 20 min. If
it is still hypoglycemia administrate once again
Glucagon 1.0 mg s.c/i.m/i.v. adverse effects include
nausea, vomiting, and headache. Contraindicated to
sulfonylureas-induced hypoglycemia. Ineffective in
patient who is anorectic, or with protracted
hypoglycemia
 DIABETIC KETOACIDOSIS

AND

HYPERGLYCEMIC HYPEROSMOLAR STATE

Pathophysiology of diabetic ketoacidosis (DKA) and
hyperglycemic hyperosmolar state (HHS)
laktic acid
 DKA
(DIABETIC KETOACIDOSIS)

Occurs when muscle cells become so starved for

energy that body takes emergency measures &
breaks down fat toxic acids as ketones
Most common type 1 DM insufficient insulin to
adjust raise of blood sugar
Cause by extreme stress or illness
Infection body produce adrenalin works
against insulin
Forget to take insulin
 Signs & symptoms of DKA

Deep, rapid breathing

Sweet, fruity smell on breath
Loss of appetite
Nausea
Fatigue
Vomiting
Weakness
Fever
Confusion
Stomach pain
Weight loss
Drowsiness
 Clinical presentation

Lost more than 5% body weight

More than 35 breaths a minute
Cant control blood sugar
Become confused
Nausea and vomiting
 What should you do?
Check ketones if feeling especially
stressed or blood sugar persistently above
240mg/dL
High ketones in blood ketones excreted
in urine.
High ketones in urine should be treated & n
hospitalized
DKA can lead into coma and possibly death.
 Treatment

Correcting lost fluids through i.v. line

Glucose infusion with insulin may stop
ketones production
Decrease blood sugar level gradually,
decreasing glucose rapidly may
produce brain swelling
 HHS (HYPERGLYCEMIC HYPEROSMOLAR STATE)

A high level of blood glucose may interfere blood

circulation (level >600 mg/dl)
Glucose uptake by the cells decreases, the glucose
passed from blood to urine draws tremendous
amounts of fluid from body and produces
dehydration
Common in type 2 DM, especially who does not
monitor blood sugar, and who does not know have
DM
Trigger factors: high-dose steroid, diuretics,
infection, illness, stress or drinking excessive alcohol
 HHS: signs & symptoms

Excessive thirst
Increased urination
Weakness
Leg cramps
Confusion
Rapid pulse
Convulsions
Coma
 What should you do?

Check blood glucose level (> 600mg/dL)

Emergency treatment can correct the
problem within hours
Give intravenous fluids to restore water to
the tissue
Short acting insulin to help cells can uptake
glucose
Without prompt treatment can be fatal