Hyperglycemic

Hyperosmolar state

Definition:
progressive hyperglycaemia and
hyperosmolarity
typically found in a debilitated patient
with poorly controlled or undiagnosed
type II diabetes mellitus (DM),

AETIOLOGY
Any illness that predisposes to dehydration or
reduced insulin activity.
1. Infection
Infection is the major precipitating factor that increase
production of counter regulatory hormones as a
systemic response to infection. They induced insulin
resistance, decrease insulin production

2. Stroke
3. Intracranial hemorrhage
4. Silent myocardial infarction
5. Pulmonary embolism
Underlying renal dysfunction or congestive heart
failure (CHF).

 Drugs that raise serum glucose levels,

inhibit insulin, or cause dehydration:
Diuretics (thiazides)
Beta blockers
Antiepileptic (phenytoin)
Calcium channel blockers
Corticosteroids
Histamine-receptor blockers
(cimetidine)
Noncompliance with oral hypoglycaemic
or insulin therapy.

CLINICAL FEATURES
HISTORY (SYMPTOMS)

Occur in type 2 DM
Patient often elderly
Polydipsia
Polyuria
Weight loss
Impairment of consciousness
Visual changes or
disturbance
COMA (severe electrolyte
disturbances occur in
association with hypotension)

PHYSICAL EXAMINATION
(SIGNS)

Extreme dehydration
Fever
Tachycardia
Low systolic blood
pressure

Diagnostic features of HHS

Plasma glucose level of 600 mg/dL
or greater
Effective serum osmolality of 320
mOsm/kg or greater
Profound dehydration, up to an
average of 9 L
Serum pH greater than 7.30
Bicarbonate concentration greater
than 15 mEq/L
N o ketonuria and ketonemia
Some alteration in consciousness

INVESTIGATIONS
Investigation

Explainations

Plasma glucose

Hyperglycemia, >600mg/dL. (>35mmol/L)

Arterial/ venous blood gas

Absent acidosis, >pH 7.3, serum bicarbonate

>15mEq/L

Serum ketones

Small or absent

Urine ketones (dipstick)

Small or absent ketones

Osmolality

> 320 mosmol/kg.

2[Na+] + [urea] +[glucose] mmol/L

Electrolyte and calculated

anion gap

Hyponatremia (osmotic intracellular to

extracellular flux)
Hyperkalemia (extracellular shift caused by
insulin deficiency and hypertonicity)
Variable anion gap.

INVESTIGATIONS
Investigation

Explaination

Urea / creatinine ratio

Increase urea with ratio >30.

FBC with differential

Leukocytosis (due to stress,

dehydration)
Increase haematocrit level
(dehydration)

HBA1c

Suspect acute episode/poorly

controlled DM.

Bacterial C&S (urine, blood,

throat)

Sources of infection if suspected.

ECG

Essential because of electrolyte

imbalance can cause cardiac
arrhythmia

DKA VS HHS
DKA
Characteristic

Mortality rate
Population
affected
Time course
Clinical
manifestation

Hyperglycemia
Ketonacidosis
Dehydration
2- 5%
Mainly in type 1 DM

HHS

Hyperglycemia
Dehydration
Hyperosmolality
15- 20 %
Mainly in type 2 DM,
elderly
Rapidly (hours)
Slow (days, week)
Dry mouth, polydipsia, polyuria, polyphagia, dehydration,
dry skin, hypotension, weakness, mental confusion,
tachycardia, changes in level of consciousness,
Ketonacidosis, acetone breath
No ketosis, no breath
odor, respiration deep and rapid, odor, respiration rapid
nausea, vomiting.
and shallow, usually
mild nausea/ vomiting.

DKA VS HHS
Lab tests

DKA

HHS

Glucose

>250 mg/dL

>600 mg/dL

ketone

Strongly positive

Normal/ mild elevated

pH

<7.3

>7.3

Osmolarity

<350 mosm/L

>350 mosm/L

Sodium

Normal/ low

Normal/ elevated

Potassium

Normal/ low/ elevated

Low/ normal/ elevated

Bicarbonate

< 18mEq/L

>15 mEq/L

Ketone (plasma/ urine)

Moderate/ high

Normal/ mild

Complication

Vascular Complications
The severe dehydration of HHS leads to
hypotension and hyperviscosity of the blood,
Predispose patients to thromboembolic disease
of the coronary, cerebral, pulmonary, and
mesenteric beds.
Disseminated intravascular coagulation (DIC)
also may complicate HHS. Together, these
vascular syndromes account for much of the
morbidity and mortality in HHS.

Cerebral Edema
Occur from rapid lowering of glucose levels and rapid
drop in plasma osmolarity. Brain cells absorb water and
swell during rapid rehydration. Leading to uncal
herniation may be the cause of death in persons with
HHS.
However, death from cerebral edema due to HHS is rare,
presumably because the older population that it affects
has underlying cerebral atrophy.
Thus, even with the edema of rehydration, the
intracranial volume does not reach the critical level that
causes uncal herniation.

ARDS
Rapid correction of hyperglycemia and
hyperosmolarity gives rise to pulmonary edema
in much the same manner as it gives rise to
cerebral edema. To compensate for hypoxia
and mild acidosis, an increase in the minute
ventilation with tachypnea develops.
Continuing pulmonary disease may lead to
acute respiratory failure that necessitates full
respiratory support, including mechanical
ventilation.

MANAGEMENT
Consist of 3 main management:
1. Fluid therapy
2. Insulin therapy
3. Electrolyte replacement