KASTURBA GANDHI NURSING COLLEGE

MEDICAL SURGICAL NURSING

SEMINAR
ON
ENDOCRINE
EMERGENCIES

SUBMITTED BY: SUBMITTED TO:

M . MALARMATHI , Mrs. PRAIMATHI . A,
MSC NURSING, TUTOR,
II YEAR, DEPT OF MSN,
KGNC. KGNC.

SUBMITTED ON:
 HYPOGLYCEMIA
DEFINITION
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.
ETIOLOGY

 Medications. Taking someone else's oral diabetes medication accidentally is a possible cause of

hypoglycemia.
 Excessive alcohol drinking. Drinking heavily without eating can block liver from releasing stored
glucose into bloodstream, causing hypoglycemia.
 Critical illnesses. Severe liver illnesses such as severe hepatitis or cirrhosis can cause hypoglycemia.
Kidney disorders, which can keep body from properly excreting medications, can affect glucose levels
due to a buildup of those medications.
 Long-term starvation, as can occur in the eating disorder anorexia nervosa, can result in too little of
substances body needs to create glucose.
 Insulin overproduction. A rare tumor of the pancreas (insulinoma) can cause to produce too much
insulin, resulting in hypoglycemia.
 Hormone deficiencies. Certain adrenal gland and pituitary tumor disorders can result in a deficiency of
key hormones that regulate glucose production. Children can have hypoglycemia if they have too little
growth hormone.

PATHOPHYSIOLOGY

Due to etiological causes

Redundant counter-regulatory mechanisms

As glucose levels decline, major defenses include

Decrease in insulin secretion

Increase in glucagon secretion

Increase in epinephrine secretion.

↓
 Increased cortisol and growth hormone secretion also occur.

If these defenses fail, plasma glucose levels will continue to fall. In type 1 and longstanding type 2 diabetes
these counter-regulatory responses to hypoglycemia are frequently impaired.

This increases the risk of hypoglycemia and also contributes to hypoglycemia unawareness.

CLINICAL MANIFESTATIONS
In mild hypoglycemia, as the blood glucose level falls, the sympathetic nervous system is stimulated,
resulting in a of epinephrine and norepinephrine.
 Sweating
 Tremor
 Tachycardia
 Palpitation, nervousness, and hunger.
In moderate hypoglycemia, the fall in blood glucose level deprives the brain cells of needed fuel for
functioning.
 CNS may include inability to concentrate
 Headache
 Lightheartedness
 Confusion
 Memory lapses
 Numbness of the lips and tongue
 Slurred speech, impaired coordination,
 Emotional changes
 Irrational or combative behavior, double vision, and drowsiness.
 Any combination of these symptoms (in addition to adrenergic symptoms) may occur with moderate
hypoglycemia.
In severe hypoglycemia,
 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
DIAGNOSTIC EVALUATION
- History collection
Family history DM, excessive alcohol drinking, reveals hypoglycemia
- Physical examination
Sweating ,Tremor, Tachycardia, abdominal pain,Palpitation, nervousness, and hunger, Confusion reveals
hypoglycemia
- Blood glucose level
In the hyperglycemic range (eg, in the 200s or greater) may feel hypoglycemic (adrenergic) symptoms when
their blood glucose quickly drops to 120 mg/dL (6.6 mmol/L) or less.
- The diagnosis can easily be confirmed using bedside glucose testing
MANAGEMENT
NON PHARMACOLOGIICAL MANAGEMENT
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 oz of fruit juice or regular soda
• 6 to 10 Life Savers or other hard candies
• 2 to 3 teaspoons of sugar or honey
 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.
 Adding table sugar to juice may cause a sharp increase in the blood glucose level, and the patient may
experience hyperglycemia for hours after treatment.
 The blood glucose level should be retested in 15 minutes and retreated if it is less than 70 to 75 mg/dL
(3.8 to 4 mmol/L).
 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.
PHARAMACOLOGICAL MANAGEMENT
 For patients who are unconscious and cannot swallow, an injection of glucagon 1 mg can be
administered either subcutaneously or intramuscularly.
 Glucagon is a hormone produced by the alpha cells of the pancreas that stimulates the liver to release
glucose (through the breakdown of glycogen, the stored glucose).
 Injectable glucagon is packaged as a powder in 1-mg vials and must be mixed with a diluent before
being injected.
 After injection of glucagon, it may take up to 20 minutes for the patient to regain consciousness.
 Patients who are unconscious or cannot swallow may be treated with 25 to 50 mL 50% dextrose in
water (D50W) administered intravenously.
 .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.
NURSING MANAGEMENT
 It is important for patients with diabetes, especially those receiving insulin, to learn that they must carry
some form of simple sugar with them at all times (ADA, Insulin Administration.
 If the patient has a hypoglycemic reaction and does not have any of the recommended emergency foods
available, any available food (preferably a carbohydrate food) should be eaten.
 Patients are advised to refrain from eating high-calorie, highfat dessert foods (eg, cookies, cakes,
doughnuts, ice cream) to treat hypoglycemia.
 The high fat content of these foods may slow the absorption of the glucose, and the hypoglycemic
symptoms may not resolve as quickly as they would with the intake of carbohydrates. The patient may
subsequently eat more of the foods when symptoms do not resolve rapidly.
 This in turn may cause very high blood glucose levels for several hours after the reaction and may also
contribute to weight gain.
 Patients who feel unduly restricted by their meal plan may view hypoglycemic episodes as a time to
reward themselves with desserts.
 It may be more prudent to teach these patients to incorporate occasional desserts into the meal plan.
This may make it easier for them to limit their treatment of hypoglycemic episodes to simple (low-
calorie) carbohydrates such as juice or glucose tablets.

DKA ( DIABETES KETOACIDOSIS)

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.
The three main
DKA are:
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis
ETIOLOGY
• Undiagnosed diabetes mellitus
• Inadequate treatment of existing diabetes mellitus
• Insulin not taken as prescribed
• Infection
• Change in diet, insulin, or exercise regimen

PATHOPHYSIOLOGY
CLINICAL FEATURES
R Dehydration occurs in DKA with manifestations of poor skin turgor, dry mucous membranes,
tachycardia, and orthostatic hypotension.
R Early symptoms may include lethargy and weakness.
R As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyes become soft
and sunken.
R Abdominal pain may be present and accompanied by anorexia, nausea, and vomiting.
R Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body’s attempt to reverse
metabolic acidosis through the exhalation of excess carbon dioxide. Acetone is noted on the breath as a
sweet, fruity odor. (of respiratory compensation of metabolic acidosis.)
R Laboratory findings include a blood glucose level greater than or equal to 250 mg/dL (13.9 mmol/L),
arterial blood pH less than 7.30, serum bicarbonate level less than 16 mEq/L (16 mmol/L), and moderate to
large ketones in the urine or serum.
DIAGNOSTIC EVALUATION:
- History Collection
Family history DM, abdominal pain may be nausea,vomiting reveals that DKA
- Physical examination:
Thirst, Abdominal pain ,Nausea and vomiting Gradually increasing restlessness, confusion, lethargy
Flushed, dry skin , Eyes appearing sunken Breath odor of ketones , Rapid, weak pulse Labored breathing
(Kussmaul respirations) Serum glucose >250 mg/dL (13.9 mmol/L) one of the test shows that DKA
-- Blood studies:
Including immediate blood glucose, complete blood count, pH, ketones, electrolytes, blood urea nitrogen,
arterial or venous blood gases
- Urinalysis, including specific gravity, glucose, acetone.
- Chest radiography:
To rule out pulmonary infection such as pneumonia.
- Head CT scanning:
To detect early cerebral edema; use low threshold with DKA and altered mental status.
- Head MRI:
To detect early cerebral edema (order only if altered consciousness is present.
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.
• Identify history of diabetes, time of last food, and time and amount of last insulin injection.
• Administration of IV fluids
• IV administration of short-acting insulin
• 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.
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.
CORRECTION OF FLUID LOSS
• It is a critical part of treating patients with DKA.
• Use of isotonic saline.
• 15-20mL/kg/hour for the first few hours.
• Recommended schedule:
• Administer 1-3 L during first hour.
• Administer 1 L during second hour.
• Administer 1 L during the following 2 hours.
• Administer 1 L every 4 hours, depending on the degree of dehydration and CVP.
• When patient becomes euvolemic, switch to 0.45% saline is recommended, particularly if hypernatremia
exists.
INSULIN THERAPY
• Insulin therapy to be initiated only if potassium levels are above 3.3 mEq/L.
• Intravenous regular insulin preferred.
• Initiated with IV bolus of regular insulin (0.1 units/kg) followed by continuous infusion of regular insulin
of 0.1 units/kg/hour.
• SC route may be taken in uncomplicated DKA (0.3 U/kg then 0.2 U/kg one hour later).
• When serum glucose reaches 200 mg/dl, reduce insulin infusion to 0.02-0.03 U/kg/hour and switch the IV
saline solution to dextrose in saline.
• Revert to SC insulin, after patient begins to eat (continue IV infusion simultaneously for 1 to 2 hours).
 POTASSIUM REPLACEMENT
• If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride is started with saline (20 to 40
mEq/hour).
• If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCl (20 to 30 mEq) is added to each liter
of IV replacement fluid and continued until the serum potassium concentration has increased to the 4.0 to
5.0 mEq/L range.
• If the serum potassium is initially greater than 5.3 mEq/L, then potassium replacement should be delayed.
 CORRECTION OF ACIDOSIS
• Bicarbonate therapy is a bone of contention among physicians and still remains a controversial subject, as
clear evidence of benefit is lacking.
• Bicarbonate therapy is only administered if the arterial pH is less than 6.9.
• 100 mEq of sodium bicarbonate in 400 mL sterile water is administered over two hours.
Repeat doses until pH rises above 7.0.
• Bicarbonate therapy has several potential harmful effects.
NURSING MANAGEMENT
• Monitor vital signs, level of consciousness, cardiac rhythm, O2 saturation, and urine output.
• Assess breath sounds for fluid overload.
• Monitor serum glucose and serum potassium.
• Administer potassium to correct hypokalemia.
• Administer sodium bicarbonate if severe acidosis (pH <7.0).
COMPLICATIONS
Myocardial Infarction
DVT
Acute gastric dilatation
Erosive gastritis
Late hypoglycemia
Respiratory distress
Infection (UTI)
Hypophosphatemia
CVA.
HYPEROSMOLAR HYPERGLYCAEMIC STATE 
Hyperosmolar hyperglycemic state (HHS), also known as non-ketotic hyperglycemic hyperosmolar
syndrome (NKHS), is characterized by profound hyperglycemia (glucose >600 mg/dL), hyperosmolality
(effective serum osmolality ≥320 mOsm/kg), and volume depletion in the absence of significant
ketoacidosis (pH >7.3 and HCO3 >15 mEq/L), and is a serious complication of diabetes.
ETIOLOGY
- Patient DM2 prone to develop it 
- Old age 
- No access to medical treatment 
- Acute infection, burns, and trauma 
- CVA, MI 
- Alcohol excess 
- Recurrent vomiting/diarrhea 
DRUGS: 
- Thiazide 
- Steroids 
- Atypical antipsychotic 
- Antiarrythmics 
- Antiepileptic 
- Antihypertensive
CLINICAL MANIFESTATIONS
 The clinical picture of HHNS is one of hypotension
 Visual deficits
 profound dehydration (dry mucous membranes, poor skin turgor),
 Tachycardia
 Variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis).
DIAGNOSTIC EVALUATION
 History collection
Focus on the signs and symptoms of prolonged hyperglycemia and on physical, social, and emotional factors
that may affect the patient’s ability to learn and perform diabetes self-care activities. The patient is asked to
describe symptoms that preceded the diagnosis of diabetes, such as polyuria, polydipsia, polyphagia, skin
dryness, blurred vision, weight loss, vaginal itching, and nonhealing ulcers. History shows that HHNS.

 Physical examination
Helps to reveals Postural hypotension accompanies the dehyDration.tachycardia,lteration of sensorium,
seizures, hemiparesis shows that HHNS
 Laboratory tests
 Including blood glucose, electrolytes, BUN, complete blood count, serum osmolality, and arterial blood
gas analysis.
 The blood glucose level is usually 600 to 1,200 mg/dL, and the osmolality exceeds 350 mOsm/kg.
Electrolyte and BUN levels are consistent with the clinical picture of severe dehydration.
 Mental status changes, focal neurologic deficits, and hallucinations are common secondary to the
cerebral dehydration that results from extreme hyperosmolality. Postural hypotension accompanies the
dehydration.
COLLABRATIVE MANAGEMENT
NON PHAMACOLOGICAL MANAGEMENT
 HHNS, close monitoring of volume and electrolyte status is important for prevention of fluid overload,
heart failure, and cardiac dysrhythmias.
 Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient’s sodium level and the
severity of volume depletion.
 Central venous or arterial pressure monitoring guides fluid replacement.
 Potassium is added to IV fluids when urinary output is adequate and is guided by continuous
electrocardiographic monitoring and frequent laboratory determinations of potassium.
 Extremely elevated blood glucose levels drop as the patient is rehydrated.
 Insulin plays a less important role in the treatment of HHNS because it is not needed for reversal of
acidosis, as in DKA.
PHARMACOLOGICAL MANAGEMENT
 Nonetheless, insulin is usually administered at a continuous low rate to treat hyperglycemia, and
replacement IV fluids with dextrose are administered (as in DKA) when the glucose level is decreased
to the range of 250 to 300 mg/dL .
 Other therapeutic modalities are determined by the underlying illness of the patient and the results of
continuing clinical and laboratory evaluation.
 Treatment is continued until metabolic abnormalities are corrected and neurologic symptoms clear. It
may take 3 to 5 days for neurologic symptoms to resolve; thus, treatment of HHNS usually continues
well beyond the time when metabolic abnormalities are resolved.
 After recovery from HHNS, many patients can control their diabetes with diet alone or with diet and
oral antidiabetic agents. Insulin may not be needed once the acute hyperglycemic complication is
resolved.

NURSING MANAGEMENT
 Nursing care of the patient with HHNS includes close monitoring of vital signs, fluid status, and
laboratory values. In addition, strategies are implemented to maintain safety and prevent injury
 related to changes in the patient’s sensorium secondary to HHNS.
 Fluid status and urine output are closely monitored because of the high risk for renal failure secondary
to severe dehydration.
 In addition, the nurse must direct nursing care to the condition that may have precipitated the onset of
HHNS.
 Because HHNS tends to occur in older patients, the physiologic changes that occur with aging make
careful assessment of cardiovascular, pulmonary, and renal function important throughout the acute and
recovery phases of HHNS.
SIADH (syndrome of inappropriate secretion antidiuretic hormone)
DEFINITION
Syndrome of inappropriate secretion antidiuretic hormone excess secretion of antidiuretic hormone from the
pituitary gland despite low serum osmolality level.
ETIOLOGY
 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.

PATHOPHYSIOLOGY
Due to etiological causes
↓
Increased antidiuretic hormone
↓
Increased water reabsorption in renal tubules
↓
Increased intravascular fluid volume
↓
Dilutional hyponatremia and decreased serum osmolality
↓
Clinical features

CLINICAL MANIFESTATION
• Gastro-intestinal- Anorexia, Nausea, vomiting
• Musculoskeletal- Muscle aches, Generalized muscle weakness
• Neuro-muscular- Myoclonus, Decreased reflexes, Ataxia, instability of gait and falls
• Pathological reflexes- Tremor, Asterixis
• Respiratory- Cheyne-Stokes respiration, respiratory insufficiency
• Neurological- Dysarthria, Lethargy, poor concentration, Confusion, Delirium, Seizures, Coma (from brain
swelling), Death.
DIAGNOSTIC FINDINGS
1. History collection
• Present health history-Chief complaints, onset, duration, acute or chronic, etc.
• Past health history- Any malignancy, surgery, HIV infection, pulmonary disease, etc.
• Medication history- Chemotherapy, anti-depressants, diuretics, etc.
• Family history of SIADH
2. Physical examination
- Anorexia, Nausea, Myoclonus, Decreased reflexes, Ataxia, Tremor, Asterixis, etc. Reveals that SIADH
3. Lab investigations-
The Schwartz and Bartter Clinical Criterion
• Serum sodium less than 135mEq/L
• Serum osmolality less than 275 mOsm/kg
• Urine sodium greater than 40 mEq/L (due to ADH-mediated free water absorption from renal collecting
tubules)
• Urine osmolality greater than 100 mOsm/kg
• Plasma uric acid <4 mg/dl.
• Blood urea nitrogen <10 mg/dl.
• The absence of clinical evidence of volume depletion - normal skin turgor, blood pressure within the
reference range
• The absence of other causes of hyponatremia - adrenal insufficiency, hypothyroidism, cardiac failure,
pituitary insufficiency, renal disease with salt wastage, hepatic disease, drugs that impair renal water
excretion.
• Correction of hyponatremia by fluid restriction
• Renal function tests and random blood sugar test should be done to check hyperglycemia and uremia as
these are the potential causes of pseudohyponatremia.

COLLABRATIVE MANAGEMENT
Principles of treatment of hyponatremia Treatment depends on
• Volume status
• Duration of hyponatremia (whether acute/<48 h or chronic >48 h))
• Presence or absence of symptoms
• Etiology of hyponatremia.
Management objectives in SIADH are:
•Looking for the cause if possible
•Measure the liquid electrolyte is not balanced
•Prevent complications
Medical management
• Hypertonic IV fluids to correct hyponatremia
• Diuretics to correct low plasma osmolality
• Monitor urine electrolyte loss
• Replace electrolyte loss
• Demeclocycline to facilitate free water clearance
• Conivaptan – an antagonist of both V1A and V2 vasopressin receptors
• Tolvaptan – an antagonist of the V2 vasopressin receptor
• Treat underlying cause
Mild asymptomatic hyponatremia (serum Na>125mEq/L)
• Fluid restriction is the 1st line treatment.
• It generally improves with correction of underlying cause and restriction of free fluid intake to 800-1000
ml/d.
• If no response, fluid intake can be restricted to 500-600 ml/d.
Mild symptomatic hyponatremia
• Fluid restriction.
• Loop diuretic- it interferes with the action of ADH in collecting tubules by inhibiting free water
reabsorption.
• The osmolality of infused saline must exceed the osmolality of patient’s urine.
Severe symptomatic hyponatremia (serum Na <125 mEq/L)
• Fluid restriction
• Hypertonic saline- infused via pump and urine osmolality can be followed to guide therapy.
• Hypertonic saline can be switched to isotonic saline when urine osmolality is <300 mOsm/L.
COMPLICATIONS
• Seizures
• Coma
• Permanent brain damage
• Hyperuricemia
• Fluid overload
• Decrease in chloride levels (plasma or serum)
• Decrease in osmolarity (plasma)
• Hypokalaemia
• Hypomagnesemia
• Increased levels of sodium (urine)
MYXEDEMA COMA
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.
ETIOLOGY
- Chronic lymphocytic thyroiditis (Hashimoto’s thyroiditis)
- Atrophy of thyroid gland with aging
- Therapy for hyperthyroidism
- Radioactive iodine (131I)
- Thyroidectomy
- Antithyroid medications
- Radiation to head and neck for treatment of head and neck cancers, lymphoma
- Infiltrative diseases of the thyroid (amyloidosis, scleroderma)
- Iodine deficiency and iodine excess.
CLINICAL FEATURES

R Myxedema coma describes the most extreme, severe stage of hypothyroidism, in which the patient is
hypothermic and unconscious.
R Myxedema coma may follow increasing lethargy, progressing to stupor and then coma.
R The patient’s respiratory drive is depressed, resulting in alveolar hypoventilation, progressive CO2
retention, narcosis, and coma.
R These symptoms, along with cardiovascular collapse and shock, require aggressive and intensive therapy
if the patient is to survive.
DIAGNOSTIC EVALUATION
History collection
Patient having history of hypothyrodism, radiation therapy helps to identify Myxedema.
Physcial examination
Unconscious, increasing lethargy, progressing to stupor and then coma, cardiovascular collapse and shock
helps to identify Myxedema.
Blood test 
With a high level of thyroid-stimulating hormone (TSH) may have hypothyroidism, as the body may
produce extra TSH to make up for the underactive thyroid. As a result, a doctor may measure how much
TSH a person’s pituitary gland produces.
Thyroxine or T4 test
Can also be taken to measure a person’s T4 level. Low levels of T4 are a good indicator of hypothyroidism,
especially if combined with high levels of TSH. Hypothyroidism, they will perform more tests to measure
thyroid function and to find an underlying cause.
If a doctor suspects myxedema coma, they will recommend that treatment begins immediately. The sooner a
person is treated, the more likely they are to recovery.
COLLABRATIVE MANAGEMENT
The primary objective in the management of hypothyroidism is to restore a normal metabolic state by
replacing the missing hormone.
 THYROXINE REPLACEMENT THERAPY:
 Since T3 is available for parenteral use, hence T3 (tri-idothyronine) 20µg IV as a bolus is given, then
repeated after 8 hours till there is clinical improvement.
 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.
 BODY TEMPERATURE: Raise the body temperature by warm blankets or external warming.
 CORTICOSTEROIDS:
 Myxedema coma and addison’s disease may be associated due to autoimmune process. If
both are present, then hydrocortisone 400 mg intramuscular is given after every 8 hours.
 The cortisol levels must be monitored.
 In combined deficiency of cortisol and thyroxine, cortisol must be replaced first followed by
thyroxine replacement.
 ANTIBIOTICS: In case of infections, antibiotics may be employed.
1. OXYGEN THERAPY:
If there is hypoxaemia or hypercarbia, O2 therapy may be started through endotracheal intubation
 along with assisted ventilation.
2. FLUIDS AND ELECTROLYTES:
Fluids (glucose, saline) should be adequately used for replacement and electrolytes are monitored.
NURSING MANAGEMENT:
1. Activity intolerance related to fatigue and depresses cognitive process
INTERVENTIONS:
 Promote independence in self care activities
 Space activities to promote rest and exercise as tolerated
 Assist with self-care activities when patient is fatigued.
 Provide stimulation through conversation and non stressful activities.
2. Risk for imbalanced body temperature
INTERVENTION:
 Providing extra layer of clothing or extra blanket
 Avoid and discourage the use of external heat sources
 Monitor patient’s body temperature
3. Constipation related to depresses gastrointestinal function
INTERVENTION:
 Encourage increased fluid intake
 Provide foods high in fibre
 Instruct patient about foods with high water content
 Monitor bowel function
 Encourage the patient to use laxatives and enemas.
THYROID STORM
Thyroid storm (thyrotoxic crisis) 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.
ETIOLOGY
→ Graves’ disease, an autoimmune disease that attacks the thyroid gland
→ viral infections, other autoimmune conditions, or the stress of childbirth, can all inflame the thyroid
→ 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
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 saturate 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

CLINICAL MANIFESTATIONS
Thyroid storm is characterized by:
• High fever (hyperpyrexia) above 38.5°C (101.3°F)
• Extreme tachycardia (more than 130 beats/min
• 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
• Altered neurologic or mental state, agitation which frequently appears as delirium psychosis, somnolence,
or coma.

DIAGNOSTIC EVALUATION
History collection
- Helps to identify any common symptoms of hyperthyroidism, such as high temperature, fast heart rate,
nausea and vomiting, or confusion diagnose thyroid storm.
Physical examination
- Helps to reveals that hyperpyrexia, weight loss, diarrhea,nausea and vomiting,abdominal pain, neurologic
or mental state helps identify the thyroid storm.
Blood tests
- As part of the evaluation to look for high levels of thyroid hormones (free T4 and free T3) in the blood.
Thyroid-stimulating hormone (TSH)
Test will show a low level of TSH and can also provide information about what is happening in the body.
Thyroid storm is a very dangerous condition. In many cases, waiting on blood test results may cost vital
moments when the doctor could be administering aggressive treatment.
MANAGEMENT:
The steps of treatment are:
 FLUIDS: Plenty of fluids and saline is given to correct dehyration and to raise blood pressure.
 ANTIBIOTICS: Broad spectrum antibiotics are given to treat infections.
 BETABLOCKERS:
 Propranolol (60 – 80 mg/8 hourly or 1 – 5 mg IV 6 hourly) is started to overcome
sympathetic stimulation. It may aggravate hypotension which can be treated.
 IODINE THERAPY:
 Lugol iodine is given 1 hour after the first dose of antithyroid to block the thyroid hormone
sysnthesis by wolfe-chaikoff effect.
 Sodium iopodate 500 - 1000µg/day or KI (potassium iodide) 5 drops 6 hourly orally will
restore thyroid hormone levels within 48-72 hours.
 It is a radioactive contrast material, is more effective than potassium iodate or lugol’s
solution.
 ANTITHYROID DRUGS:
 Since no injectable preparation available, hence, carbimazole 15 – 20 mg 8 hourly or
propylthiouracil 600 mg loading dose followed bby 200-300 mg 6 hourly is given orally as
treatment of choice.
 CORTICOSTERIODS:
 Corticosteriods (dexamethasone 2 mg IV 6 hourly) and dopamine infusion is started to
resusciate the shock.
 In addition, corticosteroids inhibit hormonal release, impair the peripheral conversion of T4
to T3.
 DIGITALIS:
It may be used if atrial fibrillation is present.
 MONITOR pulse, blood pressure, ECG, elctrolytes and hormone levels. After recovery, patient is put
only on regular antithyroid drugs.
NURSING MANAGEMENT:
 Monitor vitals, intake and output, neurological an cardiovascular status every hourly.
  Procure IV line for drugs and fluids.
 Give antithyroid medications as ordered.
 Lower the body temperature by cold baths, external cooling or by drug.
 Supportive oxygen therapy
Once crisis is controlled, the nursing care must continue to control hyperthyroidism.
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.
ETIOLOGY
 Adrenocortical insufficiency (hypofunction of the adrenal cortex) may be from a primary cause
(Addison’s disease) secondary cause (lack of pituitary ACTH secretion).
 All three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) 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.
CLINICAL MANIFESTATIONS
→ The manifestations have a slow (insidious) onset and include progressive weakness, fatigue, weight loss,
and anorexia as primary features.
→ Increased ACTH causes the striking feature of a bronze-colored skin hyperpigmentation.
→ It is seen primarily in sun-exposed areas of the body; at pressure points; over joints; and in the creases,
especially palmar creases
→ The changes in the skin are most likely due to increased secretion of β-lipotropin (which contains
melanocyte-stimulating hormone [MSH]).
→ This tropic hormone is increased because of decreased negative feedback and subsquent low
corticosteroid levels.
→ Other manifestations of adrenal insufficiency are orthostatic hypotension, hyponatremia, salt craving,
hyperkalemia, nausea and vomiting, and diarrhea.
→ Irritability and depression may also occur in primary adrenal hypofunction.
→ However, they usually do not have hyperpigmented skin because ACTH levels are low.

DIAGNOSTIC EVAUATION
History and physical examination
Progressive weakness, fatigue, weight loss, and anorexia as primary features, bronze-colored skin
hyperpigmentation Identify the adrenal insufficiency.
- ACTH stimulation test.
Adrenal insufficiency is characterized by depressed serum and urinary cortisol levels. ACTH levels are
increased in primary adrenal insufficiency and decreased in secondary disease. Primary adrenal
insufficiency is confirmed when cortisol levels fail to rise over basal levels with an ACTH stimulation test.
A positive response to ACTH stimulation test indicates a functioning adrenal gland and points to a probable
diagnosis of secondary adrenocortical insufficiency related to the pituitary gland.
Urine levels of free cortisol are low, as is the urine level of aldosterone.
Other abnormal laboratory findings in some cases include hyperkalemia, hypochloremia, hyponatremia,
hypoglycemia, anemia, and increased BUN levels.
ECG
May show low voltage and peaked T waves caused by hyperkalemia.
CT scans and MRI
May be used to identify causes other than autoimmune, including tumors, fungal infections, tuberculosis, or
adrenal calcification.
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)

- Treatment of adrenocortical insufficiency is focused on management of the underlying cause when

possible. The main stay of treatment for the adrenocortical insufficiency is hormone therapy.
- Hydrocortisone, the most commonly used form of hormone therapy, has both glucocorticoid and
mineralocorticoid properties.
- During stressful situations the glucocorticoid dosage is increased to prevent addisonian crisis.
- Mineralocorticoid replacement with fludrocortisone (Florinef) is administered daily.
- Increased salt needs to be added in the diet.
- Addisonian crisis is a life-threatening emergency requiring aggressive management.
- Treatment must be directed toward shock management and high-dose hydrocortisone replacement.
- Large volumes of 0.9% saline solution and 5% dextrose are administered to reverse hypotension and
electrolyte imbalances until BP returns to normal.
- Assess vital signs and signs of fluid volume deficit and electrolyte imbalance.
- Monitor trends in serum glucose, sodium, and potassium.
- Establish baseline data regarding mental status, vital signs, and weight. Obtain a complete medication
history to determine drugs that can potentially interact with corticosteroids.
- These drugs include oral hypoglycemics, cardiac glycosides, oral contraceptives, anticoagulants, and
NSAIDs.
- Note changes in BP, weight gain, weakness, or other manifestations of Cushing syndrome. In addition,
protect against exposure to infection and assist with daily hygiene. Protect the patient from noise, light, and
environmental temperature extremes.
- The patient cannot cope with these stresses because of the inability to produce corticosteroids.
NURSING MANAGEMENT
1. Names, dosages, and actions of drugs
2. Symptoms of overdosage and underdosage
3. Conditions requiring increased medication (e.g., trauma, infection, surgery, emotional crisis)
4. Course of action to take relative to changes in medication
• Increase in dose of corticosteroid
• Administration of large dose of corticosteroid intramuscularly, including demonstration and return
demonstration
• Consultation with health care provider
5. Prevention of infection and need for prompt and vigorous treatment of existing infections
6. Need for lifelong replacement therapy
7. Need for lifelong medical supervision
8. Need for medical identification device
9. Prevention of falls
10. Adverse effects of corticosteroid therapy and prevention
techniques
11. Special instruction for patients who are diabetics and management of blood glucose when taking
corticosteroids.

JOURNAL ABSTRACT
Endocrine emergencies
MW Savage1 et al
Diabetic and endocrine emergencies are traditionally treated by the acute medical admitting team or accident
and emergency department staff. Most will see diabetic emergencies on a regular basis, as they are common
and both type 1 and type 2 disease are increasing in prevalence. Diabetic emergencies are usually easily
treated and the patients discharged. However, it is vital not to become complacent as these disorders can
lead to death. It is particularly important to follow local guidance and to involve the diabetes team both
during and after each episode. Recently it has become clear that about 30% of patients admitted with acute
coronary syndrome (including infarction) have either diabetes or “stress hyperglycaemia”; evidence suggests
that these patients should be treated not only as a cardiac emergency but also as a diabetic one. Thus, every
patient with acute coronary syndrome or acute myocardial infarction needs diabetes to be excluded. The
other endocrine emergencies are less common, but in some ways more important simply because of their
rarity. A high level of suspicion is often required to make a diagnosis, although some, such as myxoedema
coma, are usually obvious. Treatment must be started before the diagnosis can be confirmed. Guidance on
making the diagnosis and initiating treatment should be made available on the local NHS intranet for non-
endocrinologists to access; and where possible expert advice made available by telephone. The basic
management steps in the common diabetic and endocrine emergencies are outlined; this is not a complete
list, but rather an insight for those involved in non-selected emergency admissions.
THEORY APPLICATTION

A. PHYSIOLOGIC FUNCTION:
 It involves the body’s basic needs and way to adapt.
 It includes a person’s patterns of oxygenation, nutrition, elimination, activity and rest,
 skin integrity, fluids and electrolytes, and neurologic and endocrine function.
B. SELF CONCEPT:
 Self concept refers to beliefs and feelings.
 Comprises the physical self(includes sensation and body image), and moral and
ethical self (includes self observation and evaluation)
C. ROLE FUNCTION:
 It involves behaviour based on a person’s positions in society.
 It can be classified as primary(age, sex) secondary(husband, wife) or
tertiary(temporary role of a coach)
D. INTERDEPENDENCE:
 Involves a person’s relationship with significant others and support systems.
 Meets a persons need for love and affection
 Strikes a balance between dependent behaviours(seeking help, attention and affection)
and independent behaviours (taking initiative and obtaining satisfaction from work.
E. COPING MECHANISMS:
 Cognator subsystem – A major coping process involving 4 cognitive-emotive
channels: perceptual and information processing, learning, judgement and emotions.
 Regulator subsystem – A basic type of adaptive process that responds automatically
through neural, chemical and endocrine coping channels.
BIBLIOGRAPHY

1. Teachers bibliography
1. Brunner & Suddarth’s, Textbook of medical surgical nursing, 11 th edition, volume II, Lippincott
Williams & William publication 2008, Pg.No:386 to 390
2. Lewis(2018) . Textbook of medical surgical nursing, Elsiever publication, Pg.no : 1141 to 1152
3. BT Basvanthappa, medical surgical nursing, 2nd edition, jaypee publication new Delhi, pg.no 436 to
443
4. Kathryn L. Mc Cance, a guide to physical assessment, 3 rd edition, New Delhi, Elsevier publication
2015, pg.no :82 to 89
5. BT Basvanthappa, medical surgical nursing, 2nd edition, Jaypee publication new Delhi, pg.no 436 to
443
6. Long & Phipps -Medical Surgical Nursing, (2017), Elseivier publication, New Delhi. 588-589.

2. Student’s bibliography
1. Lewis(2018) . Textbook of medical surgical nursing, Elsiever publication, Pg.no : 1141 to 1152
2. Brunner & Suddarth’s, (2008). Textbook of medical surgical nursing, 11 th edition, volume II,
Lippincott Williams & William publication, Pg.No:386 to 390