EMERGENCIES IN DIABETES

Zulfachmi Wahab
Internist, FINASIM,IFO
 KOMPLIKASI KRONIK
Microvascular Macrovascular
Stroke
Diabetic
retinopathy 1.2- to 1.8-fold
increase in stroke3
Leading cause
of blindness
in working-age
adults1 Cardiovascular
disease
75% diabetic patients
Diabetic die from CV events4
nephropathy

Diabetic
Leading cause of neuropathy
end-stage renal disease2 Leading cause of
non-traumatic lower
Erectile Dysfunction extremity amputations5
The most secretive
Complication of DM
Diabetic Foot

SlideME,
Fong DS, et al. Diabetes Care 2003;e 26 (Suppl.1):S99–S102. 2Molitch
1 2 et al. Diabetes Care 2003; 26 (Suppl.1):S94–S98. 3Kannel WB, et al. Am
Heart J 1990; 120:672–676. Gray RP & Yudkin JS. Textbook of Diabetes 1997. 5Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl.1):S78–S79.
4
DISCUSSION

 HYPOGLYCEMIA
 HYPERGLYCEMIC HYPEROSMOLAR STATE
(HONK)
 DIABETIC KETOACIDOSIS (KAD)
 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
 Most common symptoms of Hypoglycemia
Sweating
Blurred vision
Weakness
Tremor
Slurred speech
Palpitations
Hunger
Circumoral paraesthesia
Vertigo
Headache
Cold feeling
Anxiety
Euphoria
Nausea
Difficulties in concentration

0 20 40 60 80 100
Patients (%)
 Severity of hypoglycaemia
• Mild hypoglycemia • Severe hypoglycemia
• Usually self-treated, as the
patient recognises the
signs and symptoms of
decreasing blood glucose
levels
• There is enough time to
take preventive action to
restore blood glucose levels
back to normal
• Signs usually include
confusion and loss of
cognitive ability
• Patients require help from
another person for
treatment
• Increased risk by
asymptomatic
hypoglycemic episodes
 Sequel of hypoglycaemia
• Mild symptomatic hypoglycaemia
• No direct serious clinical effects
• May impair subsequent hypoglycaemia awareness

• Severe hypoglycaemia associated with

• Stroke and transient ischaemic attacks
• Memory loss/cognitive impairment
• Myocardial infarction
• Injury (direct/indirect)
• Death

Turner et al. (UKPDS 33), 1998. The Lancet; 352: 837-853

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 ß-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, ß-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
 Adjusting Dosage after a Hypoglycemic Event

OAD: Depending on drug

If hypoglycemic events are

repeated, OAD and / or Insulin
dosages should be reduced
Insulin: Initially decrease
with 2 units / day
 DIABETIC KETOACIDOSIS

AND

HYPERGLYCEMIC HYPEROSMOLAR STATE

Pathophysiology of diabetic ketoacidosis (DKA) and
hyperglycemic hyperosmolar state (HHS)
 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
• Drowsiness
 Weight loss
 Clinical presentation

 Lost more than 5% body weight

 More than 35 breaths a minute
 Can’t 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