HYPEROSMOLAR

HYPERGLYCEMIC STATE
(HHS)
M. Roshan Chandar
 DEFINITION
Hyperglycaemic hyperosmolar state (HHS) is a medical EMERGENCY that is a consequence
of PROLONGED RELATIVE INSULIN DEFICIENCY

Characterised by:
Hypovolaemia
Severe Hyperglycaemia : >30mmol/L (>540mg/dL)
Hyperosmolality: serum osmolality > 320 mOsmol/kg
Without:
Significant ketonaemia : <3 mmol/L OR
Acidosis:
pH > 7.3 | H+ <50 nmol/L | bicarbonate >15 mmol/L
 PATHOGENESIS
Seen most commonly in ELDERLY with TYPE 2 DIABETES MELLITUS
Triggered by Stress (Precipitating factors)
THREE MAJOR UNDERLYING CAUSES TO HHS
Relative Insulin deficiency - Uncontrolled Hyperglycaemia (2-3 week)
Counter regulatory hormones - Further causes Hyperglycaemia
Dehydration - Increases serum osmolality
 STRESS/ PRECIPITATING
FACTORS Relative insulin deficiency

+ SYMPATHETIC N.S

Too low to stimulate glucose

RELEASE OF COUNTER uptake in insulin-sensitive tissues
REGULATORY HORMONES
(EPI/NE/GLUCAGON)

Gluconeogenesis Glycogenolysis
Still sufficient to prevent lipolysis
and subsequent ketogenesis.
Uncontrolled Hyperglycaemia

Osmotic diuresis

Decreased
LOSS OF WATER AND ELECTROLYTES
Fluid Intake Hyperosmolarity
Fluid loss (10-22
Dehydration L)

Impaired renal function

 I
PRECIPITATING INADEQUATE INSULIN

FACTORS
THERAPY
INFECTIO Pneumonia, Cellulitis,
N UTI
INFLAMMATIO Pancreatitis,
N Cholecystitis
6 INTOXICATIO Alcohol,
Cocaine
N
I’s INFARCTIO
N
Acute MI,
Stroke
IATROGENI Corticosteroids Therapy,
C Surgery
 CLINICAL MANIFESTATIONS SKIN TURGOR
DRY MUCOUS
DUE TO DUE TO MEMBRANES
HYPEROSMOLARITY DEHYDRATION

DECREASED BLOOD
VOLUME

HYPOTENSIO ACTIVATE
Draws out H20 N BARORECEPTORS

DECREASED
ALTERED MENTAL STATUS RENAL INCREASED SNS
SEIZURES PERFUSION ACTIVITY
COMA
REFLEX DIAPHERESI
TACHYCARDIA S
 INVESTIGATIONS
Investigation Rationale

Blood glucose level To diagnose hyperglycemia and monitor treatment progress

Serum electrolytes (sodium, potassium, chloride) To assess electrolyte imbalances commonly seen in HHS

Serum osmolality To diagnose hyperosmolality and assess treatment progress

Arterial blood gas (ABG) To assess acid-base status and respiratory compensation in HHS

Complete blood count (CBC) To assess for infections, dehydration, and other complications

Renal function tests (BUN, creatinine) To assess kidney function and detect acute kidney injury

Liver function tests (AST, ALT, bilirubin) To assess liver function and detect any liver damage

Serum lactate To assess for lactic acidosis, a potential complication of HHS

Urinalysis To assess for glucose and ketones in the urine, which may indicate uncontrolled diabetes or HHS

Serum ketones To assess for ketosis and differentiate HHS from diabetic ketoacidosis

Electrocardiogram (ECG) To assess for cardiac complications associated with HHS, such as arrhythmias or ischemia

Imaging studies (CT scan, MRI) To assess for cerebral edema, a potential complication of HHS
 OTHER INVESTIGATIONS
Serum amylase and lipase To assess for pancreatitis, a potential complication of HHS

Coagulation studies (PT, PTT, INR) To assess for bleeding disorders or coagulopathies that may occur in severe cases of HHS

Blood culture To identify the presence of bacterial infections that may be contributing to HHS

Thyroid function tests (TSH, T4) To assess for underlying thyroid disorders that may contribute to HHS

Serum cortisol To assess for adrenal insufficiency, a potential cause of HHS

Serum magnesium To assess for magnesium deficiency, which may contribute to electrolyte imbalances and HHS

Serum phosphate To assess for phosphate depletion, which may occur in severe cases of HHS

Serum calcium To assess for hypocalcemia, which may occur in HHS and contribute to cardiac arrhythmias

Blood ammonia To assess for hepatic encephalopathy, a potential complication of HHS

Serum prolactin To assess for pituitary gland dysfunction, which may contribute to HHS
 MANAGEMENT OF PRECIPITATING
FACTORS
Inadequate insulin therapy
Initiate or adjust insulin therapy to achieve
glucose control
Monitor blood glucose levels frequently and
adjust insulin dose as needed.
Provide patient education on insulin use,
including proper administration and storage,
as well as recognition and management of
hypoglycemia.
Infection
Treat the underlying infection with
appropriate antibiotics or antivirals.
Monitor blood glucose levels frequently
and adjust insulin dose as needed.
Ensure adequate hydration to prevent
dehydration.
Monitor for signs and symptoms of sepsis
or other complications.
Intoxication
Provide supportive care, such as
intravenous fluids to correct fluid and
electrolyte imbalances and monitoring
for signs of dehydration or electrolyte
abnormalities.
Monitor blood glucose levels
frequently and adjust insulin therapy
as needed
Also manage withdrawal symptoms
 MANAGEMENT OF HHS
The aims are to:
Normalise osmolality and blood glucose
Replace fuid and electrolyte losses
Prevent complications such as:
Arterial or venous thrombosis (via subcutaneous thromboprophylaxis)
Foot ulceration (with careful protection of feet)
Cerebral oedema and central pontine myelinosis.
Co-morbidities also need to be taken into account:
Rapid fuid replacement may precipitate cardiac failure in patients with
coronary artery disease
Delirium commonly occurs in older patients.
MANAGEMENT - KEY POINTS
SLOWER APPROACH TO CORRECT ELECTROLYTE AND
METABOLITE ABNORMALITIES

No Immediate need to correct the Ketoacidosis - DKA

Rapid shift in serum osmolality should be avoided - Risk of Brain injury

0.9% Sodium Chloride solution is used - NS is avoided - Hypernatremia

Insulin is introduced - Rate of fall of glucose is plateaued

MANAGEMENT - FLUIDS AND
POTASSIUM
0-60 Mins
1 L 0.9% saline over 1 hour (more rapid if BP < 90 mmHg)

AFTER 1 Hour

Adjust rate of fluids - Hydration status and