HANDOUTS FOR ACUTE BIOLOGIC CRISIS

Note: Please refer to your book. Read about all of these in your MS book.

Hepatic encephalopathy
 Frequent terminal complication in liver disease
 Diseased liver is unable to convert ammonia to urea
Causes:
 Cirrhosis
 GI hemorrhage
 Hyperbilirubinemia
 Transfusions
 Thiazide diuretics
 Uremia
 dehydration
Assessment Findings
 Early in the course of disease
 Changes in mental functioning(irritability)
 Insomnia
 Slowed affect
 Slow slurred speech
 Impaired judgement
 Slight tremor
 Babinski’s reflex
 Hyperactive reflexes
 Progressive disease
 Asterixis
 Disorientation
 Apraxia
 Tremors
 Fetor hepaticus
 Facial grimacing
 Late in disease:
 COMA, ABSENT REFLEXES

West Haven Criteria

 The severity of hepatic encephalopathy is graded with the West Haven Criteria; this is based on
the level of impairment of autonomy, changes in consciousness, intellectual function, behavior,
and the dependence on therapy.
 Grade 1 - Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired
performance of addition or subtraction
 Grade 2 - Lethargy or apathy; minimal disorientation for time or place; subtle personality
change; inappropriate behaviour
 Grade 3 - somnolence to semistupor, but responsive to verbal stimuli; confusion; gross
disorientation
 Grade 4 - coma(unresponsive to verbal or noxious stimuli)

Diagnostic tests
 Increased serum ammonia levels
 PT prolonged
 Hgb and hct decreased

Nursing Interventions
 Conduct ongoing neurologic assessment and report deteriorations
 Restrict protein in diet; provide carbohydrate intake and Vitamin K supplements
 Administer enemas, cathartics, intestinal antibiotics and lactulose as ordered
 Reduces ammonia level
 Protect client from injury: keep side rails up; provide eye care with use of artificial tears/eye
patch.
 Avoid administration of drugs detoxified in liver
 Maintain client on bed rest to decrease metabolic demands on liver.

Specific Disorders of the Thyroid Gland

SEVERE HYPOTHYROIDISM (MYXEDEMA)
DEFINITION
 Slowing of metabolic processes caused by hypofunction of the thyroid gland with decrease
thyroid hormone secretion
 Myxedema(adult); cretinism(children)
 A rare and life-threatening complication of hypothyroidism (low levels of thyroid hormones in
the bloodstream)

Incidence
 Occurs more often in women between age 30-60.
Causes:
 Primary
 Secondary
 Iatrogenic
 In severe or untreated cases
 Failure to take prescribe medications
 Infection
 Trauma
 Exposure to cold
 Use of sedatives, narcotics or anesthetics
Treatment
 Drug Therapy
 Levothyroxine(Synthroid)
 Thyroglobulin(Proloid)
 Dessicated Thyroid
 Liothyronine(Cytomel)

MC is an medical emergency!!
 IV thyroid hormones
 Correction of hypothermia
 Maintenance of Vital Functions
 Treatment of Precipitating Causes

Assessment Findings
 Fatigue; lethargy; slowed mental processes; dull look; slow, clumsy movements
 Anorexia, weight gain, constipation
 Intolerance to cold; dry scaly skin; dry, sparse hair; brittle nails
 Menstrual irregularities; generalized insterstitial nonpitting edema
 Bradycardia, cardiac complications(MI, CHF)
 Increased sensitivity to sedatives, narcotics and anesthetics
 Exaggeration of these findings in myexedema coma: weakness, lethargy, syncope, bradycardia,
hypotension, hypoventilation, subnormal body temperature
Diagnostics Tests
 Serum T3 and T4 level low
 Serum cholesterol elevated
 RAIU decreased
Nursing Interventions
 Monitor V/s, I&O daily weights; Observe for edema and signs of cardiovascular complications
 Administer thyroid hormone replacement therapy as ordered and monitor effects
 Observe for signs of thyrotoxicosis
 Increase dosage gradually, especially with cardiac complications
 Provide a comfortable, warm environment
 Provide a low- calorie diet
 Avoid use of sedatives; reduce the dose of any sedative, narcotic, or anesthetic agent by half or
as ordered.
 Institute measure to prevent skin breakdown
 Provide increased fluids or foods high in fiber to prevent constipation; admin. stool softeners as
ordered.
 Observe for signs of myexedema coma; provide appropriate nursing care.
 Admin medications as ordered
 Maintain vital functions; correct hypothermia, maintain adequate ventilation
 Provide client teaching and discharge planning concerning
 Thyroid hormone replacement
  Regular follow-up care
 Need for additional protection in cold weather
 Measures to prevent complication.

THYROID STORM
 Uncontrolled and potentially life threatening hyperthyroidism caused by sudden and excessive
release of thyroid hormone into the bloodstream.
Precipitating factors:
 Stress
 Infection
 Unprepared thyroid surgery

Assessment Findings
 Apprehension
 Restlessness
 Extremely high temperature
 Tachycardia
 Respiratory distress
 Delirium
 coma
Nursing Interventions
 Maintain a patent airway and adequate ventilation; administer oxygen as ordered
 Administer IV therapy as ordered.
 Administer medications as ordered: antithyroid drugs, corticosteroids, sedatives, cardiac drugs.
Management of thyroid storm
 Recognition of signs and symptoms: hyperthermia, tachycardia, confusion, vomiting,
hypotension, diaphoresis, irritability
 Reversal of thyrotoxicosis with antithyroid drugs
1. Propylthiouracil 300-600 mg by mouth immediately, followed by 150-300 mg by mouth every 6
hours; can be administered by nasogastric tube or as a rectal suppository if patient is unable to
take by mouth.
 2. Saturated solution of potassium iodide 2-5 drops every 8 hours or sodium iodide 0.5-1 g
intravenously every 8 hours
 3. β-Blockers to decrease effects on the cardiovascular system
  Supportive therapy
1. Fluids
2. Nutritional support
3. Oxygen
4. Antipyretics (possibly cooling blanket)
5. Correction of electrolyte imbalance
6. Glucocorticoids such as dexamethasone 2 mg every 6 hours for 4 doses.
7. Barbiturates if needed for sedation

ADDISONIAN CRISIS
 Severe exacerbation of Addison’s disease caused by acute adrenal insufficiency.

Adrenal Gland
 Normal Physiology
 The adrenal cortex produces 3 steroid hormones: glucocorticoids (cortisol),
mineralocorticoids (aldosterone, 11-deoxycorticosterone), and androgens
(dehydroepiandrosterone).
 The androgens are relatively unimportant in adults, and 11-deoxycorticosterone is a
fairly weak mineralocorticoid in comparison with aldosterone.
 The primary hormone of importance in acute adrenal crisis is cortisol; adrenal
aldosterone production is relatively minor.

 Cortisol
 enhances gluconeogenesis and provides substrate
 o through proteolysis, protein synthesis inhibition, fatty acid mobilization, and
enhanced hepatic amino acid uptake.
 indirectly induces insulin secretion
o to counterbalance hyperglycemia but also decreases insulin sensitivity.
 exercises a significant anti-inflammatory effect
o by stabilizing lysosomes, reducing leukocytic responses, and blocking cytokine
production.
 enhances appetite, and suppresses adrenocorticotropic hormone (ACTH) synthesis.
o
 Aldosterone
 released in response to angiotensin II stimulation via the renin-angiotensin-aldosterone
system, hyperkalemia, hyponatremia, and dopamine antagonists.
 Its effect on its primary target organ, the kidney, is to promote reabsorption of sodium
and secretion of potassium and hydrogen.

 Primary adrenocortical insufficiency

 occurs when the adrenal glands fail to release adequate amounts of these hormones to
meet physiologic needs, despite release of ACTH from the pituitary.
 Causes: Infiltrative or autoimmune disorders
adrenal exhaustion from severe chronic illness
 Secondary adrenocortical insufficiency
 Causes: exogenous steroids
- suppresses the hypothalamic-pituitary-adrenal (HPA) axis.
 Too rapid withdrawal of exogenous steroid
- precipitate adrenal crisis
 : sudden stress
- induce cortisol requirements in excess of the adrenal glands' ability to respond
immediately.
• Note:
• In acute illness, a normal cortisol level may actually reflect adrenal insufficiency
- the cortisol level should be quite elevated.

 Precipitating factors
 Strenous activity, infection, trauma, stress, failure to take prescribed medications.
 Iatrogenic: surgery on pituitary or adrenal glands, rapid withdrawal of exogenous
steroids in a client on long-term steroid therapy.
 Assessment:
 Severe generalized muscle weakness,
 severe hypotension,
 hypovolemia,
 shock(vascular collapse)
 Nursing Interventions
 Administer IV fluids(D5 saline) as ordered
o To treat vascular collapse
 Administer IV glucocorticoids(hydrocortisone (Solu-Cortef) and vasopressors as ordered
o If crisis precipitated by infection, administer antibiotics as ordered.
 Maintain strict bed rest and eliminate all forms of stressful stimuli.
 Monitor vital signs, I & O, daily weights
 Protect client from infection
 Provide client teaching and discharge planning.

DIABETIC KETOACIDOSIS

Metabolic Processes
 Three Metabolic processes are important in ensuring a supply of glucose for body fuel.
1) Glycolysis- the process through which glucose is broken down into water and carbon dioxide
with the release of energy
o
 2) Glycogenolysis- the breakdown of stored glycogen ( from the liver or skeletal muscles).
 This action is controlled by 2 hormones:
o epinephrine-breaks down glycogen in the muscle
o glucagon-breaks down glycogen in the liver. Glucose from here can be directly
released into the blood stream and used by the nervous system
 3) Gluconeogenesis-building of glucose from new sources.
  Hormones that stimulate gluconeogenesis
Glucagon
Glucocorticoid hormones
Thyroid hormones
 Process usually occurs in the liver

Normal Insulin Metabolism

 Counterregulatory hormones.
 They work to oppose the effects of insulin.
 These hormones work to increase blood glucose levels by stimulating glucose
production and output by the liver and decreasing the movt of glucose into the cells.
Glucagons
Epinephrine
Growth hormone
Cortisol

Hormonal Control of Metabolism

 Insulin
 A hormone secreted by the beta cells in the islet of Langerhans,
 Normally released in small increments when food is ingested.
 Controls blood glucose levels by regulating glucose production and storage
 Insulin is regulated by serum glucose levels.
 Rise in plasma insulin after a meal stimulates storage of glucose as glycogen in the liver
and muscle.
It also inhibits gluconeogenisis and enhances fat deposition (enhances fat to be
placed/stored in the adipose tissue) in the adipose tissue and increase protein
synthesis
 The fall in insulin levels during the night when not eating facilitates the release of the
stored glucose from the liver, protein from the muscles and fat, and that’s how it kind of
compensates for hypoglycemia
 Insulin and glucagon are hormones secreted by islet cells within the pancreas
 Insulin is normally secreted by the beta cells (a type of islet cells) of the pancreas
 Stimulus for insulin is high blood glucose levels

DEFINITION
 a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia,
dehydration, and acidosis-producing derangements in intermediary metabolism.
 defined clinically as an acute state of severe uncontrolled diabetes associated with ketoacidosis
 requires emergency treatment with insulin and intravenous fluids.
CAUSES:
 underlying infection
 disruption of insulin treatment
 and new onset of diabetes
ASSESSMENT
Common Laboratory Findings
 Blood glucose greater than 14mmol/L[250 mg/l
 Arterial pH less than 7.3
 Ketone urea
 Arterial bicarbonate less than 15
 Hyper magnesimia
 Hypokalemia
 Cardiac enzymes
 Pco2-35 - reflects respiratory compensation
NURSING DIAGNOSIS
1. Fluid Volume Deficit
related to:
osmotic diuresis due to hyperglycemia,
excessive discharge: diarrhea, vomiting; restriction intake due to nausea, mental mess.
2. Imbalanced Nutrition Less than body requirements
related to:
insufficiency of insulin,
decreased oral input,
hypermetabolism status.

3. Risk for Infection(sepsis)

related to:
increased levels of glucose,
decreased leukocyte function,
changes in the circulation.

4. Risk for Sensory-Perceptual Alterations

related to:
glucose / insulin and / or electrolytes.

5. Fatigue
related to:
decreased metabolic energy production,
insufficiency of insulin,
increasing energy demand: status hypermetabolic / infection.

6. Powerlessness
related to:
long-term illness,
dependence on others.

7. Knowledge Deficit: the disease, prognosis, and treatment

related to:
interpreting the error information,
do not know the source of information.

TREATMENT
 Fluid resuscitation
 Reversal of the acidosis and ketosis
 Reduction in the plasma glucose concentration to normal
 Replenishment of electrolyte and volume losses
 Identification the underlying cause
 The goal of treatment is to correct the high blood sugar level with insulin. Another goal is to
replace fluids lost through urination and vomiting.
 Insulin replacement
 Fluid and electrolyte replacement
 The cause of the condition (such as infection) should be found and treated
MEDICAL
 Regular and analog human insulins
 correction of hyperglycemia
 Rapid-acting insulins (eg, insulin aspart, insulin glulisine, insulin lispro)
 Medical
 Short-acting insulins (eg, regular insulin)
 Electrolyte supplements (eg, potassium chloride)
 Alkalinizing agents (eg, sodium bicarbonate)
NURSING MANAGEMENT
 Ongoing clinical assessment of the patient.
 involves regular (at least hourly) monitoring of vital signs and level of consciousness
during the acute phase
 Accurate monitoring of fluid balance: this includes accurate intake and output charts
 Prescribed fluids should be administered and patients monitored for signs of
complications related to fluid overload, dehydration and electrolyte imbalance.
 Insulin therapy administered as prescribed
 Monitoring of metabolic acidosis and electrolytes.
 Support early referral to the diabetes team
 Provide psychological support for patients
 Providing patient education including sick-day management and arranging follow-up support for
patients after discharge.
 Stabilize the patient’s airway, breathing, circulation
 Obtain 16 gauge iv line on both site and assess cardiac monitoring and pulse oximetry.
 Monitor serum glucose hourly and urine ketone
 Monitor basic electrolyte, osmolarity and venous pH every 4 hourly until pt is stable.
 Determine and treat any underlying causes of DKA eg;; pneumonia,UTI and MI.

FLUID REPLACEMENT[ADULT
 Give 0.9% NSS rapidly via No I8 gauge cannula if cardiac function is normal.
 Administer NSS/ hour 1 L, for 1st 3 hrs for those individuals who are in shock.
 Give 250-500ml /hr of NSS depending on hydration status until blood sugar is 14 mmol/L(250
mg/L]. blood sugar level<14 mmol/L 0.9%should be switched to D51/2NS or DNS at 125 to
250ml/hour.
 Assess blood pressure & heart rate frequently.
 Monitor intake and out put for signs of fluid overload.
 Monitor urine specific gravity to assess fluid changes
PATIENT EDUCATION
 Instruct to take insulin or oral diabetic agent as usual
 Check blood sugar and urine sugar every 4 hours
 Report elevated glucose and urine acetone to physician
 Usual meal plan cannot be followed substitute soft foods 6- 8 times /day
 If any symptoms like vomiting and diarrhea or fever consume liquid diet every half to one hour
to prevent dehydration and provide calories
 Inform physician about extreme fluid loss maybe dangerous.
 For type 1 diabetic, inability to retain oral fluid needs hospitallization to avoid DKA and possible
coma
 Hyperglycemia Hyperosmolar Nonketotic Syndrome (HHNS)
 Serious condition – Blood glucose 800-1000 mg/dl
 Ketosis usually minimal or absent
 Defect is usually lack of effective insulin (insulin resistance)
 Presistent hyperglycemia causes osmotic diuresis which results in losses of water and
electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid
space to the extracellular fluid space.
 With glycosurea and dehydration, hypernatremia and increased osmolarity occurs.
 Usually occurs in older adults