36
to as fasting or postprandial hypoglycemia. Fasting hypoglycemia results from an
imbalance between glucose production and utilization. Postprandial hypoglycemia
is considered by hyperinsulinemia in the diet, often seen in patients undergoing
gastric surgery. Many conditions can trigger fasting hypoglycemia, but most common are severe enzyme deficiency, pancreatic tumors (e.g., insulinoma), severe
infections, liver disease, and drug overdose (e.g., insulin, sulfonylureas). Clinical
features are similar to those of diabetic hypoglycemia [72].
Signs and Symptoms
The clinical precipitations of hypoglycemia typically develop rapidly. Patients will
strive for the treatment of variety of signs and symptoms directly linked with the
release of endocrine stress hormones, including sweating, cold, pale, sticky skin,
tremors, and tachycardia. If you do not treat hypoglycemia, you may experience
mental status changes and generalized seizures. It is essential to check the blood
glucose of each active seizure patient to rule out hypoglycemia. Hypoglycemia
refers to a blood glucose level of <70 mg/dL, but the medical history of patient,
gender, age, and overall health may change the absolute level of signs and symptoms. Elder people having a complex medical history may experience severe hypoglycemia when glucose levels are >50 mg/dL (>2.8 mmol/L). However, young
adults may experience severe hypoglycemia, which is quite below 50 mg/dL
(<2.8 mmol/L). Many clinical signs of hypoglycemia occur by the production of
counter-regulatory hormones (such as epinephrine), secreting in response to
decrease glucose concentrations [73].
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is associated with a plasma glucose concentration
>350 mg/dL (>19.4 mmol/L), ketone production, serum bicarbonate levels
<15 mEq, and anion gap metabolic acidosis. DKA has a mortality rate of 9–14%. It
is an acute endocrine disorder where insulin insufficiency and elevated glucagon
levels together lead to hyperglycemia, volume depletion, and acidosis. This situation is usually associated with electrolyte imbalance. Certain metabolic stress factors (e.g., infection, trauma, myocardial infarction, and sometimes even pregnancy)
may cause DKA. A common trigger in these situations is usually the disruption of
insulin therapy in diabetic patients. Lack of insulin inhibits glucose from entering
the cell, so cells are unable to metabolize cellular functions due to lack of glucose
and switch to other sources of energy, such as fat. Consequently, glucose tends to
accumulate in the blood [74].
The flow of glucose into the renal tubules pulls water, potassium, magnesium,
sodium, and other ions into the urine, producing an important osmotic diuretic
effect. This diuretic effect, along with vomiting, can lead to electrolyte imbalance,
volume depletion, and subsequent shock. All such changes in permeability are the
A. Ahsan et al.
to as fasting or postprandial hypoglycemia. Fasting hypoglycemia results from an
imbalance between glucose production and utilization. Postprandial hypoglycemia
is considered by hyperinsulinemia in the diet, often seen in patients undergoing
gastric surgery. Many conditions can trigger fasting hypoglycemia, but most common are severe enzyme deficiency, pancreatic tumors (e.g., insulinoma), severe
infections, liver disease, and drug overdose (e.g., insulin, sulfonylureas). Clinical
features are similar to those of diabetic hypoglycemia [72].
Signs and Symptoms
The clinical precipitations of hypoglycemia typically develop rapidly. Patients will
strive for the treatment of variety of signs and symptoms directly linked with the
release of endocrine stress hormones, including sweating, cold, pale, sticky skin,
tremors, and tachycardia. If you do not treat hypoglycemia, you may experience
mental status changes and generalized seizures. It is essential to check the blood
glucose of each active seizure patient to rule out hypoglycemia. Hypoglycemia
refers to a blood glucose level of <70 mg/dL, but the medical history of patient,
gender, age, and overall health may change the absolute level of signs and symptoms. Elder people having a complex medical history may experience severe hypoglycemia when glucose levels are >50 mg/dL (>2.8 mmol/L). However, young
adults may experience severe hypoglycemia, which is quite below 50 mg/dL
(<2.8 mmol/L). Many clinical signs of hypoglycemia occur by the production of
counter-regulatory hormones (such as epinephrine), secreting in response to
decrease glucose concentrations [73].
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is associated with a plasma glucose concentration
>350 mg/dL (>19.4 mmol/L), ketone production, serum bicarbonate levels
<15 mEq, and anion gap metabolic acidosis. DKA has a mortality rate of 9–14%. It
is an acute endocrine disorder where insulin insufficiency and elevated glucagon
levels together lead to hyperglycemia, volume depletion, and acidosis. This situation is usually associated with electrolyte imbalance. Certain metabolic stress factors (e.g., infection, trauma, myocardial infarction, and sometimes even pregnancy)
may cause DKA. A common trigger in these situations is usually the disruption of
insulin therapy in diabetic patients. Lack of insulin inhibits glucose from entering
the cell, so cells are unable to metabolize cellular functions due to lack of glucose
and switch to other sources of energy, such as fat. Consequently, glucose tends to
accumulate in the blood [74].
The flow of glucose into the renal tubules pulls water, potassium, magnesium,
sodium, and other ions into the urine, producing an important osmotic diuretic
effect. This diuretic effect, along with vomiting, can lead to electrolyte imbalance,
volume depletion, and subsequent shock. All such changes in permeability are the
A. Ahsan et al.