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Sulfonilurea Palpitation
Low intake
Pallor
Sweating Weakness
DEFINITION
The lower limit of the fasting plasma glucose concentration is
normally approximately 70 mg/dL (3.9 mmol/L). Glucose levels
<55 mg/dL (3.0 mmol/L) with symptoms that are relieved promptly
after the glucose level is raised document hypoglycemia.
Hypoglycemia is most convincingly documented by Whipple’s
triad:
(1) symptoms consistent with hypoglycaemia
(2) a
low plasma glucose concentration measured with a precise
method (not a glucose monitor), and
(3) relief
of those symptoms after the plasma glucose level is
raised.
ETIOLOGY
HYPOGLICEMIA IN DIABETES
Hypoglycemia is a fact of life for people with T1DM. An estimated 2–4% of people
with T1DM die as a result of hypoglycemia. Overall, hypoglycemia is less frequent in
T2DM.
Relative or absolute insulin excess occurs when
(1) insulin (or insulin secretagogue) doses are excessive, ill-timed, or of the wrong
type;
(2) the influx of exogenous glucose is reduced (e.g., during an overnight fast or
following missed meals or snacks);
(3) insulin-independent glucose utilization is increased (e.g., during exercise);
(4) sensitivity to insulin is increased (e.g., with improved glycemic control, in the
middle of the night, late after exercise, or with increased fitness or weight loss);
(5) endogenous glucose production is reduced (e.g., following alcohol ingestion);
(6) insulin clearance is reduced (e.g., in renal failure).
CLINICAL MANIFESTATION
Neuroglycopenic symptoms of hypoglycemia are the direct result
of central nervous system (CNS) glucose deprivation.They
include behavioral changes, confusion, fatigue, seizure, loss of
consciousness, and, if hypoglycaemia is severe and prolonged,
death.
Adrenergic symptoms such as palpitations, tremor, and anxiety
Cholinergic symptoms such as sweating, hunger, and
paresthesias
Common signs of hypoglycemia include diaphoresis and pallor.
Transient focal neurologic deficits occur occasionally. Permanent
neurologic deficits are rare
URGENT MANAGEMENT
Oral treatment with glucose tablets or glucose- containing fluids, candy,
or food is appropriate if the patient is able and willing to take these. A
reasonable initial dose is 20 g of glucose. If the patient is unable or
unwilling, because of neuroglycopenia, to take carbohydrates orally,
parenteral therapy is necessary. IV glucose (25 g) should be given and
followed by a glucose infusion guided by serial plasma glucose
measurements. If IV therapy is not practical, SC or IM glucagon (1.0 mg
in adults) can be used, particularly in patients with T1DM.
Because it acts by stimulating glycogenolysis, glucagon is ineffective in
glycogen-depleted individuals (e.g., those with alcohol-induced
hypoglycemia). It also stimulates insulin secretion and is therefore less
useful in T2DM.
These treatments raise plasma glucose concentrations only transiently,
and patients should therefore be urged to eat as soon as is practical to
replete glycogen stores.
ALGORITHM HYPOGLYCEMIA
Kussmaul
Inadequate Hyppotension
insulin
Vomit Keton urine
Infection
Coma Polyuria
Dehydration
PATHOGENESIS DKA AND HHS
CLINICAL MANIFESTATION DKA
CLINICAL MANIFESTATION HHS
MANIFESTATION OF
HYPERGLICEMIC HYPEROSMOLAR STATE
Altered mental states
(mental confusion, lethargy, coma)
Profound dehydration
Hypotension, tachycardia
Precipitating factor :
Infection, sepsis
Myocardial infarct, CVA
Debilitating condition (prior stroke/dementia)
Social situation
DIAGNOSTIC CRITERIA
MANAGEMENT ALGORITHM
TRANSITION TO
SUBCUTANEUS INSULIN