Porth's Essentials of Pathophysiology, 4e - page 830

812
U N I T 9
Endocrine System
administration of insulin and intravenous fluid and elec-
trolyte replacement solutions. Because insulin resistance
accompanies severe acidosis, low-dose insulin therapy is
used. An initial loading dose of short-acting (i.e., regu-
lar) or rapid-acting insulin often is given intravenously,
followed by continuous low-dose short-acting insulin
infusion. Frequent laboratory tests are used to moni-
tor blood glucose and serum electrolyte levels and to
guide fluid and electrolyte replacement. It is important
to replace fluid and electrolytes and correct pH while
bringing the blood glucose concentration to a normal
level. Too rapid a drop in blood glucose may cause hypo-
glycemia. A sudden change in the osmolality of extracel-
lular fluid can also occur when blood glucose levels are
lowered too rapidly, and this can cause cerebral edema.
Cerebral and other autoregulatory mechanisms may not
be as well developed in younger children, placing them
at particular risk for development of cerebral edema.
42
Serum potassium levels often fall as acidosis is corrected
and potassium moves from the extracellular into the
intracellular compartment. Thus, it may be necessary to
add potassium to the intravenous infusion. Identification
and treatment of the underlying cause, such as infection,
also are important.
Hyperglycemic Hyperosmolar State
The hyperglycemic hyperosmolar state (HHS) is char-
acterized by hyperglycemia (blood glucose >600 mg/dL
[33.3 mmol/L]), hyperosmolarity (plasma osmolarity
>320 mOsm/L) and dehydration, the absence of ketoaci-
dosis, and depression of the sensorium.
40
Hyperglycemic
hyperosmolar state may occur in various conditions,
including type 2 diabetes, acute pancreatitis, severe infec-
tion, myocardial infarction, and treatment with oral or
parenteral nutrition solutions. It is seen most frequently
in people with type 2 diabetes. A partial or relative insu-
lin deficiency may initiate the syndrome by reducing
glucose utilization while inducing a glucagon-stimulated
increase in hepatic glucose output. With massive glycos-
uria, obligatory water loss occurs. If the person is unable
to maintain adequate fluid intake because of associated
acute or chronic illness or has excessive fluid loss, dehy-
dration develops. As the plasma volume contracts, renal
insufficiency develops and the resultant limitation of
renal glucose losses leads to increasingly higher blood
glucose levels and an increase in severity of the hyper-
osmolar state.
In hyperosmolar states, the increased serum osmo-
larity has the effect of pulling water out of body cells,
including brain cells. The condition may be complicated
by thromboembolic events arising because of the high
serum osmolality. The most prominent manifestations
are weakness, dehydration, polyuria, neurologic signs
and symptoms, and excessive thirst. The neurologic
signs include hemiparesis, Babinski reflex, aphasia,
muscle fasciculations, hyperthermia, hemianopia, nys-
tagmus, visual hallucinations, seizures, and coma. The
onset of HHS often is insidious, and because it occurs
most frequently in older people, it may be mistaken for
a stroke.
The treatment of HHS requires judicious medical
observation and care as water moves back into brain
cells, posing a threat of cerebral edema. Extensive potas-
sium losses that also have occurred during the diuretic
phase of the disorder require correction. Because of the
problems encountered in the treatment and the serious
nature of the disease conditions that cause HHS, the
prognosis for this disorder is less favorable than that for
ketoacidosis.
Hypoglycemia
Hypoglycemia, or an insulin reaction, occurs from a rel-
ative excess of insulin in the blood and is characterized
by below-normal blood glucose levels.
43,44
It occurs most
commonly in people treated with insulin injections, but
prolonged hypoglycemia also can result from some oral
hypoglycemic agents (i.e., sulfonylurea). There are many
factors that can precipitate an insulin reaction in a per-
son with type 1 or type 2 diabetes, including error in
insulin dose, failure to eat, increased exercise, decreased
insulin need after removal of a stress situation, medi-
cation changes, and a change in insulin injection site.
Alcohol decreases liver gluconeogenesis, and people
with diabetes need to be cautioned about its potential
for causing hypoglycemia, especially if it is consumed in
large amounts or on an empty stomach.
Hypoglycemia usually has a rapid onset and progres-
sion of symptoms. The signs and symptoms of hypo-
glycemia can be divided into two categories: (1) those
caused by altered cerebral function and (2) those related
to activation of the autonomic nervous system. Because
the brain relies on blood glucose as its main energy
source, hypoglycemia produces behaviors related to
altered cerebral function. Headache, difficulty in prob-
lem solving, disturbed or altered behavior, coma, and
seizures may occur. At the onset of the hypoglycemic
episode, activation of the parasympathetic nervous sys-
tem often causes hunger. The initial parasympathetic
response is followed by activation of the sympathetic
nervous system; which causes anxiety, tachycardia,
sweating, and a cool and clammy skin due to constric-
tion of the skin vessels.
The signs and symptoms of hypoglycemia are highly
variable, especially in children and the elderly, and not
everyone manifests all or even most of the symptoms.
Elderly people may not display the typical autonomic
responses, but typically do display signs of altered cere-
bral function, including mental confusion. Also, some
medications, such as
β
-adrenergic blocking drugs,
interfere with the autonomic response normally seen
in hypoglycemia. Some people develop hypoglycemic
unawareness; that is, they do not report symptoms
when their blood glucose concentrations are less than
50 to 60 mg/dL (2.8 to 3.3 mmol/L). This occurs most
commonly in people who have a longer duration of dia-
betes and A1C levels within the normal range.
43
The most effective treatment of an insulin reaction
is the immediate administration of 15 g of glucose in
a concentrated carbohydrate source. According to the
so-called
rule of 15
, this 15 g of glucose can be repeated
1...,820,821,822,823,824,825,826,827,828,829 831,832,833,834,835,836,837,838,839,840,...1238
Powered by FlippingBook