The document discusses various endocrine emergencies including hypoglycemia, diabetic ketoacidosis, hyperosmolar hyperglycemic state, syndrome of inappropriate antidiuretic hormone secretion, myxedema, thyroid storm, and adrenocortical insufficiency. It covers the definitions, etiologies, pathophysiology, clinical manifestations, diagnostic evaluations, and management of each condition. Nursing responsibilities in assessment and treatment are also outlined.
2. HYPOGLYCEMI
A
Hypoglycemia relating to an abnormally low level of the
sugar glucose in the blood, usually a complication of diabetes,
in which body does not produce enough insulin to fully
metabolize glucose which known as hypoglycemia.
4. Due to etiological causes
Redundant counter-regulatory mechanisms
As glucose levels decline, major defenses
include
Decrease in insulin secretion
Increase in glucagon secretion
5. Increase in epinephrine secretion.
Increased cortisol and growth hormone secretion also
occur.
If these defenses fail, plasma glucose levels will
continue to fall.
Hypoglycemia
8. Moderate hypoglycemia
▶ CNS may include inability to concentrate
▶ Headache
▶ Lightheadedness
▶ Confusion
▶ Memory lapses
9. Moderate hypoglycemia
▶ Numbness of the lips and tongue
▶ Slurred speech, impaired coordination
▶ Emotional changes
▶ Irrational, double vision, and drowsiness.
10. ▶ CNS function is so impaired that the patient needs the assistance of
another person for treatment of hypoglycemia.
▶ Symptoms may include disoriented behavior, seizures, difficulty arousing
from sleep, or loss of consciousness
13. MANAGEMENT
NON PHARMACOLOGICALMANAGEMENT
Immediate treatment must be given when hypoglycemia occurs. The usual
recommendation is for 15 g of a fast-acting concentrated source of
carbohydrate such as the following, given orally:
Three or four commercially prepared glucose tablets
4 to 6 of fruit juice or regular soda
6 to 10 Life Savers or other hard candies
2 to 3 teaspoons of sugar or honey
14. ▶ It is not necessary to add sugar to juice, even if it is labeled as unsweetened juice: the
fruit sugar in juice contains enough carbohydrate to raise the blood glucose level.
▶ The blood glucose level should be retested in 15 minutes and retreated if it is less than 70
to 75 mg/dL .
15. ▶ If the symptoms persist more than 10 to 15 minutes after initial treatment, the treatment
is repeated even if blood glucose testing is not possible.
▶ Once the symptoms resolve, a snack containing protein and starch (eg, milk or cheese
and crackers) is recommended unless the patient plans to eat a regular meal or snack
within 30 to 60 minutes.
16. ▶ An injection of glucagon 1 mg can be administered either subcutaneously or
intramuscularly.
▶ Injectable glucagon is packaged as a powder in 1-mg vials and must be mixed with a diluent
before being injected.
17. ▶ After injection of glucagon, it may take up to 20 minutes for the patient to regain
consciousness.
▶ Assuring patency of the intravenous (IV) line used for injection of 50% dextrose is
essential because hypertonic solutions such as 50% dextrose are very irritating to the
vein.
19. DEFINITION
▶ DKA is caused by an absence or
markedly inadequate amount of
insulin. This deficit in available
insulin results in disorders in the
metabolism of carbohydrate,
protein, and fat.
25. COLLABORATIVE MANAGEMENT
Ensure patent airway.
Administer O2 via nasal cannula or non-rebreather mask.
Establish IV access with large-bore catheter.
Begin fluid resuscitation with 0.9% NaCl solution 1 L/hr
until BP stabilized and urine output 30-60 mL/hr.
Begin continuous regular insulin drip 0.1 U/kg/hr.
Administration of IV fluids
IV administration of short-acting insulin
26. ▶ Assessment of mental status
▶ Recording of intake and output
▶ Central venous pressure monitoring (if indicated)
▶ Assessment of blood glucose levels
▶ Assessment of blood and urine for ketones
▶ ECG monitoring
▶ Assessment of cardiovascular and respiratory status
▶ Correction of fluid loss with intravenous fluids.
27. MEDICAL MANAGEMENT
▶ Correction of hyperglycemia with insulin.
▶ Correction of electrolyte disturbances, particularly
potassium loss.
▶ Correction of acid-base balance.
▶ Treatment of concurrent infection, if present.
29. HYPEROSMOLARHYPERGLYCAEMI
C STATE
▶ Hyperosmolar hyperglycemic state (HHS), also known as non-ketotic
hyperglycemic hyperosmolar syndrome (NKHS), is characterized by
profound hyperglycemia (glucose >600 mg/dL), hyperosmolality and volume
depletion in the absence of significant ketoacidosis (pH >7.3 and HCO3 >15
mEq/L), and is a serious complication of diabetes.
31. CLI
NI
CALMANI
FESTATI
ON
▶ The clinical picture of HHNS is one of hypotension
▶ Visual deficits
▶ profound dehydration
▶ Tachycardia
▶ Variable neurologic signs
34. SIADH (syndrome of inappropriate secretion of antidiuretic
hormone)
Syndrome of inappropriate secretion of antidiuretic hormone
(develops when too much antidiuretic hormone (vasopressin) is
released by the pituitary gland under certain inappropriate conditions,
causing the body to retain fluid and lower the blood sodium level by
dilution.
35. ETI
OLOGY
▶ Medicines, such as certain type 2 diabetes drugs, seizure drugs,
antidepressants, heart and blood pressure drugs, cancer drugs,
anesthesia
▶ Surgery under general anesthesia
▶ Disorders of the brain, such as injury, infections, stroke
▶ Brain surgery in the region of the hypothalamus
▶ Lung disease, such as pneumonia, tuberculosis, cancer, chronic
infection.
36. ▶ OHP PATHO
Due to etiological causes
Increased antidiuretic hormone
Increased water reabsorption in renal
tubules
42. Management objectives in SIADH are:
▶ Looking for the cause if possible
▶ Measure the liquid electrolyte is not balanced
▶ Prevent complications
43. Medical management
▶ Hypertonic IV fluids to correct hyponatremia
▶ Sodium restriction
▶ Diuretics to correct low plasma osmolality
▶ Monitor urine electrolyte loss
▶ Replace electrolyte loss
44. ▶ Demeclocycline to facilitate free water clearance
▶ Conivaptan
▶ Tolvaptan
46. COMPLICATIONS
• Seizures
• Coma
• Permanent brain damage
• Hyperuricemia
• Fluid overload
• Decrease in chloride levels (plasma or serum)
47. • Decrease in osmolarity (plasma)
• Hypokalaemia
• Hypomagnesemia
• Increased levels of sodium (urine)
48. MYXEDEMA
▶ Hypothyroidism results from suboptimal levels of thyroid hormone. Thyroid
deficiency can affect all body functions and can range from mild, subclinical forms
to myxedema.Symptoms of hypethyroidism may later be followed by those of
hypothyroidism and myxedema.
49. ETIOLOGY
▶ Chronic lymphocytic thyroiditis (Hashimoto’s thyroiditis)
▶ Atrophy of thyroid gland with aging
▶ Therapy for hyperthyroidism
▶ Radioactive iodine (131I)
▶ Thyroidectomy
▶ Medications
50. ▶ Lithium
▶ Antithyroid medications
▶ Radiation to head and neck for treatment of head and neck cancers, lymphoma
▶ Infiltrative diseases of the thyroid (amyloidosis, scleroderma)
53. Since T3 is available for parenteral use, hence T3 (tri-idothyronine) 20µg IV as a
bolus is given.
A bolus dose of oral thyroxine (500µg) followed by 100µg twice or thrice is
administered, if parenteral preparation is not available.
Body temperature rises and patient regains consciousness within 48-72 hours at
which maintenance oral thyroxine may be started.
54.
55. THYROID STORM
▶ Thyroid storm is a form of severe
hyperthyroidism, usually of abrupt onset.
Untreated it is almost always fatal, but
with proper treatment the mortality rate
is reduced substantially. The patient with
thyroid storm or crisis is critically ill and
requires observation and aggressive and
supportive nursing care during and after
the acute stage of illness.
56. ETIOLOGY
▶ Graves’disease, an autoimmune disease that attacks the thyroid gland
▶ viral infections, other autoimmune conditions,
▶ overactive thyroid nodules
▶ tests that use iodine
▶ eating too many foods that contain iodine
▶ consuming large amounts of thyroid hormone
▶ certain tumors of the ovaries or testes
57. PATHOPHYSIOLOGY
▶ Due to etiological causes like Graves’ disease, consuming large amounts of thyroid
hormone
▶ Production of T4 binding inhibitors resulting in decreased binding affinity of T4 and
increase free T4 levels
▶ Rapid release of T4 into the circulation could binding capacity
▶ Development of tissue intolerance
▶ Homeostatic decompensation despite similar hormone levels.
▶ Role of adrenergic activation normal plasma levels of adrenaline noted.
▶ But T4 causes increased receptors in some tissues.
▶ Post receptor action to alter responsiveness to catecholamine
▶ Clinical features
58. CLINICAL MANIFESTATION
▶ High fever (hyperpyrexia) above 38.5°C (101.3°F)
▶ Extreme tachycardia
▶ Exaggerated symptoms of hyperthyroidism with disturbances of a major
system
▶ GI (weight loss, diarrhea,nausea and vomiting,abdominal pain)
▶ Cardiovascular (edema, chest pain, dyspnea, palpitations)
▶ Irregular heart rhythm,
▶ Heart failure
63. ADRENOCORTICAL INSUFFICIENCY
▶ DEFINITION
▶ Addison’s disease: chronic
adrenocortical insufficiency
secondary to destruction of
the adrenal glands adrenal
cortex function is inadequate
to meet the patient’s need for
cortical hormones.
64. ETIOLOGY
▶ Adrenocortical insufficiency (hypofunction of the adrenal cortex) may
be from a primary cause (Addison’s disease) secondary cause (lack of
pituitaryACTH secretion).
▶ All three classes of adrenal corticosteroids are reduced.
▶ ACTH deficiency may be caused by pituitary disease or suppression of
the hypothalamic-pituitary axis because of the administration of
exogenous corticosteroids.
▶ Autoimmune response.
65. CLINICAL MANIFESTATIONS
▶ progressive weakness, fatigue, weight loss, and anorexia as
primary features.
▶ bronze-colored skin hyperpigmentation.
▶ sun-exposed areas of the body; at pressure points; over joints;
and in the creases, especially palmar creases
▶ Other manifestations of adrenal insufficiency are orthostatic
hypotension, hyponatremia, salt craving, hyperkalemia, nausea
and vomiting, and diarrhea.
▶ Irritability and depression
66. History and physical examination
ACTH stimulation test.
Urine levels
ECG
CT scans and MRI
67. COLLABORATIVE MANAGEMENT
•Daily glucocorticoid (e.g., hydrocortisone) replacement (two thirds on awakening
in morning, one third in late afternoon)*
• Daily mineralocorticoid (fludrocortisone [Florinef]) in morning*
• Salt additives for excess heat or humidity
• Increased doses of cortisol for stress situations (e.g., surgery, hospitalization)
