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
