Transcript Endocrine Emergencies

Project: Ghana Emergency Medicine Collaborative
Document Title: Endocrine Emergencies
Author(s): Danielle Dobrot, RN-BSN
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2
Endocrine
Emergencies
Danielle Dobrot, RN-BSN
3
Objectives
• Describe the assessment of the endocrine system.
• Discuss the neuroendocrinology of stress and critical illness
• Apply the above-mentioned knowledge when analyzing a case
scenario (paper based and real life scenarios).
• List the drugs used in your unit to manage the endocrine
emergencies.
• Delineate the nursing process in the management of a patient
with endocrine emergencies.
4
Endocrine System
Endocrine system is “a collection of glands that produce hormones that
regulate your body's growth, metabolism, and sexual development and
function” (AMA).
5
Endocrine Organs
These glands and organs include
pineal body, pituitary,
hypothalamus, thyroid gland,
parathyroid, thymus, pancreas, and
adrenal glands. Then there are the
gender specific endocrine organs
including either the testes or
ovaries.
https://www.biologycorner.com/anatomy/endocrine/no
tes_endocrine_system.html
6
What are hormones?
● Peptides, e.g. insulin
● Glycoproteins, e.g. thyroid-stimulating hormone
(TSH)
● Amines, e.g. noradrenaline (norepinephrine)
● Steroid hormones, e.g. cortisol
● Oestrogen
● Triiodothyronine
7
Assessment of Endocrine System
● Being able to diagnose an endocrine issue can be challenging due to the
varied and non-specific symptoms.
● An understanding of each organ is needed
● A full exam and history should be completed for an accurate assessment
● Thyroid gland - palpate for enlargement (goiter), thyroid bruit, or nodules
o Also assess pt for thyroid eye disease, digital acropachy, pretibial
myxoedema, cold peripheries, dry skin and hair, bradycardia and
delayed muscle relaxation when testing tendon reflexes
● Parathyroid glands - few physical signs notable
o Parathyroid glands produces parathyroid hormone which increases the
level of calcium in the bloodstream
o Pt may have corneal calcification, carpopedal spasms, or Trousseau’s
sign
o Typically short people with round faces if diagnosed with autosomal
dominant pseudohypoparathyroidism
8
Assessment of Endocrine System
● Pancreas - endocrine functions include the production of insulin,
glucagon, somatostatin, gastrin and vasoactive intestinal peptide.
● Pituitary - Two lobes
o The anterior pituitary secretes several hormones: adrenocorticotrophic
hormone (ACTH), prolactin, growth hormone (GH), TSH and gonadotrophins
(luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
o The posterior pituitary, actually an extension of the hypothalamus, secretes
vasopressin (antidiuretic hormone (ADH)) and oxytocin.
● Hypothalamus - links the nervous system to the endocrine system using
the pituitary gland
9
Assessment of the Endocrine System
● Thymus - actually is a more active participant in the immune system in
children with the creation of T cells; however it does produce hormones
that are involved in the maturation of T cells
● Adrenals - lie above the kidneys
o Adrenal medulla - participate in the sympathetic nervous system
secreting catecholamines
o Adrenal cortex - secretes cortisol, mineralocorticoids, and androgens
● Gonads - release estrogen, testosterone, hormones after gonadotropins
are released by the pituitary
o Look for c/o hirsutism, gynecomastia, reduced pubic hair, small
testis, and reduced sex drive in adults
10
Assessment of Endocrine System
Common clinical features in endocrine disease
Symptom, sign or problem
Differential diagnoses
● Weight gain
Hypothyroidism, polycystic ovary syndrome (PCOS), Cushing’s syndrome
● Weight loss
Hyperthyroidism, diabetes mellitus, adrenal insuffi ciency
● Short stature
Constitutional, non-endocrine systemic disease, e.g. coeliac disease, growth
hormone deficiency
● Delayed puberty
Constitutional, non-endocrine systemic disease, hypothyroidism, hypopituitarism,
primary gonadal failure
● Menstrual disturbance
PCOS, hyperprolactinaemia, thyroid dysfunction
● Diffuse neck swelling
Simple goitre, Graves ’ disease, Hashimoto’s thyroiditis
● Excessive thirst
Diabetes mellitus or insipidus, hyperparathyroidism, Conn’s syndrome
● Hirsutism
Idiopathic, PCOS, Cushing’s syndrome, congenital adrenal hyperplasia
● ‘Funny turns’
Hypoglycaemia, phaeochromocytoma, neuroendocrine tumour
● Sweating
Hyperthyroidism, hypogonadism, acromegaly, phaeochromocytoma
● Flushing
Hypogonadism (especially menopause), carcinoid syndrome
● Resistant hypertension
Conn’s syndrome, Cushing’s syndrome, phaeochromocytoma, acromegaly, renal artery
stenosis
● Erectile dysfunction
Primary or secondary hypogonadism, diabetes mellitus, non-endocrine systemic
disease
● Muscle weakness
Cushing’s syndrome, hyperthyroidism, hyperparathyroidism, osteomalacia
● Bone fragility and fractures
Cushing’s syndrome, hypogonadism, hyperthyroidism
● Altered facial appearance
Hypothyroidism, Cushing’s syndrome, acromegaly, PCOS
11
Stress
& Critical
Illness
●Effects
Stress can be of
defined
by an condition
or interaction that
threatens to disrupt
the body’s equilibrium.
● Critical illness- “best applied to a life-threatening condition that merits
intensive medical and/or surgical intervention” (Becker, 2077).
● Often when stress and therefore critical illness occurs the hypothalamus
connects the nervous system to the endocrine system through the pituitary
and therefore the endocrine system is part of maintaining homeostasis.
o “The hypothalamic-pituitary-adrenal (HPA) axis… comprises systems to
regulate sodium and water balance, steroid hormone production,
glucose metabolism, and thyroid function,” (Atkins, 21).
● Hypothalamus releases corticotropin-releasing factor (CRF) which stimulates
the pituitary to release adrenocorticotropin (ACTH) then stimulating the
adrenal cortex and adrenal medulla to release cortisol in response to stress,
which in turn increases release of epinephrine and norepinephrine.
12
Effects of Stress & Critical Illness
Fight or Flight Response
● Epinephrine and cortisol
then increase the
availability of glucose
and fatty acids to be
used by the nervous
system and the muscles,
respectively.
● These hormones are
released and play a role
in interacting with the
nervous system for fight
or flight response.
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/PNS.html
13
Effects of Stress & Critical Illness
● Unfortunately in chronic state of stress, these
elevated levels of hormones can begin to create
harmful effects and hinder some healing processess,
which can lead to several endocrine diseases as
discussed later.
● There are many other hormones that are also affected
by a stress, which can be studied further at the link
below.
o http://www.ncbi.nlm.nih.gov/pmc/articles/PMC30
79864/
14
Adrenal Crisis
• Adrenal cortex produces 3 hormones:
– Glucocorticoids (cortisol), mineralocoticoids
(aldosterone, 11-deoxycorticosterone), and
androgens (dehydroepiandrosterone).
• Cortisol & Aldosterone are most important
hormones affected
15
Adrenal Crisis
• Cortisol – this hormone is key to the use & balance of sugar &
stress in the body
– Enhances gluconeogensis, performs proteolysis, assists with insulin
secretion & sensitivity, has anti-inflammatory effects, helps with free-fluid
clearance, increases appetite and suppresses adrenocorticotropic hormone
(ACTH).
• Aldosterone – assists with the balance of salt & water in the body
– Targets the kidney in order to reabsorb sodium, secrete potassium and
hydrogen, and increase intravascular volume.
• Adrenal Crisis occurs when the adrenal gland does not release
enough of one or both of these hormones
16
Adrenal Crisis - Assessment
• Assess airway, breathing, circulation, and mental status initially
• Obtain a brief history to determine causation:
– Any prior steroid use? Especially high dose steroids taken that are stopped suddenly
can cause adrenal crisis.
– Haemophilus influenzae, staphylococcus aureus, streptococcus pneumonia, or fungal
infections can precipitate adrenal crises
– Severe physiologic stress like sepsis, trauma, burns, and surgery
– Anticoagulants
– AIDS
– Andrenocorticotropin therapy in known insufficiency patients
– Invasive or infiltrative disorders
– TB
– Newborns with complicated pregnancy or birth
17
Adrenal Crisis
• Signs & Symptoms:
–
–
–
–
–
–
–
Sudden onset of symptoms
Nausea, vomiting, abdominal or flank pain
Hyperthermia or hypothermia
Weakness
Fever
Confusion
Unexplained shock
18
Adrenal Crisis
• Treatment/ Interventions:
– Obtain labs:
• Serum chemistry (CMP), serum cortisol, ACTH test, CBC, thyroid, cultures
– Radiology:
• Chest xray, abdominal CT (to view adrenal glands)
– ECG (prolonged QT, inverted T waves)
– Glucocorticoids is the best & most definitive therapy
– Place IV and fluid replacement (some mixture of 5% or 10% dextrose &
saline mixture)
– Pressors to treat hypotension
– Determine precipitating factors
19
Adrenal Crisis
• Differential Nursing Diagnosis: Septic shock
• Evaluation:
– Possible admission to ICU for further fluid resuscitation and cardiac
monitoring
– Monitor serum electrolytes, magnesium, and glucose every 4-6 hours until
stable
– Resolve any precipitating factors
– Continue to monitor for complications such as: immunosuppression, HTN, salt
retention, hypokalemia, weight gain, delayed wound healing, hyperglycemia,
metabolic alkalosis
20
Diabetes and Diabetic Complications
• Diabetes Insipidus (DI)
• Diabetes Mellitus (DM)
– Two types of DM:
• Type 1
• Type 2
21
Diabetes Insipidus
• Diabetes Insipidus (DI) is “the passage of large volumes (>3
L/24h) of dilute urine (<300m Osm/kg).”
• Two types:
– Central DI is a decrease in antidiuretic hormone (ADH) causing
an inability to concentrate urine.
– Nephrogenic DI occurs because of an inability to respond to
ADH within the kidneys.
22
• Assessment:
DI
– Assess airway, breathing, and circulation
• Possible issues of circulation & hypotension due to decrease in circulating fluid
– History:
• Assess pt thirst & urinary frequency
• Ask if there is already a diagnosis of DI (central or nephrogenic)
• Central is common after injuries to pituitary and/ or hypothalamus
– Common symptoms associated with this type excessive fatigue, diminished libido or erectile
dysfunction, headache, dry skin, and hair loss
– Signs & Symptoms:
• Polyuria, polydipsia, and nocturia
• Outside of these S/S very few others seen
• Occasionally pt has enlarged bladder
23
DI
• Assessment:
– Work-up:
• Labs:
– 24-hour urine, I&O, electrolytes, glucose, urine specific gravity, plasma &
urinary osmolality, and plasma ADH level
• Water deprivation testing
– All water intake is held & urine osmolality & body weight are measured
hourly. When 2 osmolalities vary by less than 30 mOsm/kg or weight
decreases by 3% 5units of aqueous ADH or desmopressin are administered
together. The last urine specimen collected within 60min.
• Pituitary studies
– MRI
24
• Age-Specific Considerations:
DI
– S/S for infants: crying, irritability, growth retardation, hyperthermia, weight loss
– S/S for children: Enuresis, anorexia, linear growth defects, and fatigability
• Treatment/ Interventions:
– Make sure pt continues to take in enough fluid to replace loss (oral or IV fluids)
– When pt cannot take oral & hypernatremia develops give dextrose water that is
hyperosmolar
– Set IV fluids to infuse no faster that 500-750 mL/hr in order to prevent
hyperglycemia, volume overload, and rapid correction of hypernatremia
– Give desmopression in pt with central or gestational DI – synthetic ADH
– Synthetic vasopressin and the non-hormonal agent chlorpropamide can also be
used
– NSAIDs might be used as a last resort in nephrogenic DI
25
DI
• Evaluation/ Follow-up:
– Monitor I&O status and electrolytes
– Usually good prognosis
– Monitor for severe dehydration, hypernatremia, fever, cardiovascular
collapse, and death especially in children and older patients
– Perform teaching related to fluid balance especially when patients are
sick or exposed to excessive heat
26
Diabetes Mellitus
• Type 1 diabetes mellitus (DM) also known as juvenile diabetes
due to prevalence in children
–
An autoimmune endocrine disease where patients cannot produce insulin as
caused by destruction of beta cells in pancreas
• Type 2 DM is the most common type of DM
– Hyperglycemia due to a breakdown in the ability to utilize insulin or make
insulin
– Seen to develop at any age
27
DM
• Assessment:
– Assess airway, breathing, circulation, and neuro status especially with
complications of untreated DM (will be discussed later)
– History:
• Assess for the signs and symptoms of DM
• Ask if there is any family history of juvenile diabetes
• Ask about recent weight gain or weight loss
• Determine if the patient has been susceptible to infection especially urinary tract,
skin, and respiratory tract infections.
28
•
Assessment:
DM
– Signs and symptoms:
•
•
•
•
•
•
•
•
Hyperglycemia
Glycosuria
Polydipsia
Unexplained weight loss – with Type 1
Obesity specifically centrally – with Type 2
Nonspecific malaise
Symptoms of ketoacidosis
Hypertension
– Physical exam:
• With Type 1 there are no specific physical findings aside from dehydration and some
nutritional deficiencies
• Occasionally patient may have other endocrine autoimmune diseases
• With Type 2 and untreated DM patient may develop diabetic ulcers, dry skin, neuropathy, and
diabetic retinopathy
29
• Treatment/ Interventions:
DM
– Labs:
– Urinalysis – looking for ketones & glucose
– Blood glucose
» Random glucose >200 mg/dL
» Fasting glucose >120 mg/dL
– HgbA1c >6.5% indicative of positive diagnosis associated with increased blood glucose
– Presence of Islet cell antibodies (in Type 1) – although not needed for diagnosis
– Thyroid function – Children with Type 1 DM may have hidden thyroid disease and an
untreated thyroid disease can hinder diabetes management
– Fasting C-peptide can be indicative of Type 2 vs. Type 1 indicating some functioning beta
cells
– Lipid profiles – may be abnormal at diagnosis due to circulating triglycerides due to
gluconeogenesis
30
DM
• Treatment/ Interventions:
– Insulin therapy is only long-term treatment for diabetes
• Type 2 does not always need long-term insulin therapy and diet change should
be a first resort
• Oral Medications
– Can be used for treatment of Type 2 diabetes
– Glucagon and Metformin are common
– IV fluids can be utilized to initially lower hyperglycemia
31
DM
• Subcutaneous
– Rapid acting: onset of 15 min, peaks in 30-90 minutes, duration of 3-5 hours
» Lispro (Humalog)
» Aspart (Novolog)
– Short acting: onset 30-60 minutes, peaks in 2-4 hours, duration of 5-8 hours
» Regular insuling (Humalin R or Novolin R)
– Intermediate acting: onset 1-3 hours, peaks in 8 hours, duration of 12-16 hours
» NPH (Humilin N or Novolin N)
– Long acting: onset 1 hour, no peak, duration of 20 -26 hours
» Insulin determir (Levemir)
» Insulin glargine (Lantus)
– Pre-mixed insulin aspart protamine and insulin aspart: onset 5-15 minutes, peaks varies,
duration of 10-16 hours
» Novolog 70/30 mix
– Pre-mixed NPH and regular: onset 30-60 minutes, peaks varies, duration of 10-16 hours
» Humlin 70/30 or Novolin 70/30
32
DM
• Evaluation & Monitoring:
– Inpatient care is occasionally necessary for initial treatment
– Blood sugar should be maintained at 90-130 mg/dL
– Education is vital for patient & parents to properly care for
diabetes and perform insulin therapy
– Diet is important in the care of diabetic patients
• Current research supports a diet of:
– Carbohydrates - Should provide 50-55% of daily energy intake; no more than
10% of carbohydrates should be from sucrose or other refined carbohydrates
– Fat - Should provide 30-35% of daily energy intake
– Protein - Should provide 10-15% of daily energy intake
33
Diabetic Ketoacidosis and
Hyperosmolar Hyperglycemic State
• Diabetic Ketoacidosis (DKA): a serious diabetic complication
characterized by a triad of symptoms: hyperglycemia, anion
gap metabolic acidosis, and ketonemia.
– Serum glucose is often >500 mg/dL and <800 mg/dL
• Hyperosmolar hyperglycemic state (HHS) (nonketotic
hyperglycemia) occurs when serum glucose often exceeds
1000 mg/dL accompanied by neurologic abnormalities with
comas in 25-50% of the cases.
– Ketonemia is rare
34
DKA & HHS
• Pathophysiology:
– Without insulin the body begins to break down
fats for energy causing release of ketones.
– Ketones cause metabolic acidosis characteristic of
DKA
35
• Assessment:
– History:
DKA & HHS
• Recent infections
– Pneumonia or UTI often precipitate DKA or HHS
• Major illnesses
– Myocardial infarction, CVA, or pancreatitis
•
•
•
•
•
•
New onset type 1 diabetes often presents with DKA
Cocaine use
Eating disorders
Poor compliance with insulin regimen
Malfunction with continuous subcutaneous insulin infusion devices
Any drugs that affect carbohydrate metabolism
– These can include glucocorticoids, higher dose thiazide diuretics, sympathomimetic
agents, and second-generation antipsychotic agents
36
DKA
• Assessment:
– Assess airway, breathing, circulation, and neuro
– Signs/ Symptoms:
• DKA usually develops over a 24 hour period
–
–
–
–
–
–
Hyperventilation (Kussmaul respirations) and abdominal pain are common
Fruity odor due to exhaled acetone
Malaise, generalized weakness, and fatigability
Nausea & vomiting, decreased appetite, and anorexia
Rapid weight loss in patients newly diagnosed with type 1 diabetes
History of not taking insulin therapy or missed insulin injections due to vomiting or
psychological reasons
– Decreased perspiration
– Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may
occur when the condition is neglected or with severe dehydration/acidosis
37
HHS
• HHS develops over a couple of days with polyuria, polydipsia, and weight
loss
–
–
–
–
–
Neurological symptoms often leading to a coma are most common
Hyperglycemia
Hyperosmolarity
Dehydration
Focal or global neurologic deficits
»
»
»
»
»
»
»
Drowsiness or lethargy
Delirium
Coma
Focal or generalized seizures
Visual disturbances
Hemiparesis
Sensory deficits
38
DKA & HHS
• Treatment/ Interventions:
– Labs:
• Serum glucose, serum electrolytes, BUN, serum creatinine, CBC with diff, urinalysis, plasma
osmolality, serum ketones (if urine ketones are present), arterial blood gas
• Frequent blood sugar checks necessary, often performed hourly until stable
– ECG
– Place IV
• Give IV fluids to correct fluid loss & osmolality
– Give Insulin
• May initially be given IV
– Correct electrolytes especially potassium
– Correct acid-base balance
– Treat infection that may be present
39
DKA & HHS
• Age-related conditions:
– Higher mortality in elderly patients with DKA & HHS.
• Evaluation/ Monitoring:
– Usually ICU admission until patient has been stabilized
– Consult endocrinologist
– Educate patient on proper insulin therapy during illness & on frequent
blood sugar checks at home
40
Hypoglycemia
• A decrease in serum blood glucose to a level that
induces neurologic changes and sympathetic nervous
system stimulation
– <50 mg/dL
• Often cause by missing a meal while continuing to
take insulin or over-treating with insulin amount
41
Hypoglycemia
• Assessment:
– Assess airway, breathing, circulation, and neuro status
– History:
•
•
•
•
•
•
Ethanol intake & nutritional deficiency
Weight reduction
Nausea or vomiting
Last meal
Last dose of insulin
Increase of fatigue
42
Hypoglycemia
–
Signs/ Symptoms:
• Neurogenic (adrenergic):
– Sweating, shakiness, tachycardia, anxiety, and a sensation of hunger
• Neuroglycopenic symptoms:
– Weakness, tiredness, or dizziness; inappropriate behavior (sometimes
mistaken for inebriation), difficulty with concentration; confusion;
blurred vision; and, in extreme cases, coma and death
43
Hypoglycemia
• Treatment/ Intervention:
– Rapid diagnosis vital
• Obtain a blood sugar as soon as possible
– Treat immediately with either oral glucagon or IV dextrose, which ever
can be done more expediently
– Obtain vital signs
– Recheck glucose about 30 minutes after then hourly until patient is stable
– If patient can tolerate give food with a balance of carbs, proteins and fats
– Draw labs:
• Glucose & electrolyte level, CBC, and possibly liver function, serum insulin and
thyroid levels
– Search for underlying cause
44
Hypoglycemia
• Evaluation/ Monitoring:
–
–
–
Admit patient for monitoring if blood sugar cannot be
stabilized
If patient frequently suffers from hypoglycemia, apply diet
restrictions with frequent snacks
Educate on early recognition and treatment at home
45
Myxedema Coma
• “Uncommon but life-threatening form of untreated
hypothyroidism with physiological decompensation”
(Medscape).
• Happens in patients that have long-term, untreated
hypothyroidism
• Precipitated by climate-induced hypothermia, infection, or drug
therapy
• Myxedema Coma is decompensated hypothyroidism
46
Myxedema Coma
• Age-related considerations:
– Elderly woman, over the age of 60, are most susceptible
especially when at a state of stress and in the winter
•
Assessment:
– Assess airway, breathing, circulation
– Obtain history:
•
•
Determine if patient has increasing fatigue, weight gain, coldintolerance, constipation, hair & skin changes, and edema.
Ask for recent overmedication, stroke, congestive heart failure,
trauma, exposure to cold environmental temperatures, or
infection.
47
Myxedema Coma
• Assessment:
– Signs/ Symptoms:
•
•
•
Primary symptoms: altered mental status & hypothermia
Airway/ Breathing: Slow respiration rate, hypoventilation, congestion,
pleural effusions, consolidation
Circulation:
– Hypotension/ shock
– Soft or distant heart sounds, diminished apical impulse, bradycardia, enlarged
heart, pericardial effusion
•
Neurologic: Confusion, stupor, obtundation, coma, slow speech, seizures,
reflexes with slow relaxation phase
48
Myxedema Coma
• Assessment:
– Signs/ Symptoms (cont.):
• Periorbital, nonpitting edema; facial swelling or coarseness;
•
•
•
•
macroglossia; enlargement of tonsils, nasopharynx, and larynx; coarse
or thinning hair
Thyroid enlargement
Distended abdomen & bladder
Cold, nonpitting edema of the hands and feet
Cool, pale, dry, scaly, thickened skin; dry, brittle nails; ecchymoses and
purpura
49
Myxedema Coma
• Treatments/ Interventions:
– Labs:
•
•
•
•
•
•
•
Thyroid levels (free T4 & TSH)
Electrolytes & serum osmolality
Creatinine
Glucose
CBC with diff
Creatine kinase
ABG
– Chest x-ray - look for cardiomegaly, pericardial effusion, congestive
heart failure, and/or pleural effusion
– Mechanical ventilation is a priority if severe respiratory acidosis,
hypercapnia, or hypoxia
– Put patient on monitor - monitor for cardiac ischemia (especially after
medication administration)
50
Myxedema Coma
• Treatment/ Interventions:
– Place IV
• Begin thyroid replacement even if myxedema is only a possible
cause
– Give levothyroxine loading dose of 500-800 mcg then daily
IV dose 50-100 mcg
– Can give Liothyronine, synthetic form of T3
• Give steroid replacement after cortisol level is obtained
• Give IV fluids, either NS (if severely hyponatremia) or dextrose
5-10% mixed with either 0.45% NS or 0.9% NS, carefully since
most patients are fluid overloaded even though they are
hypotensive
51
Myxedema Coma
• Treatment/ Interventions:
– Monitor core temperature - passively rewarm patient with warm
blankets and warm room
– Treat any concurrent infections
52
Myxedema Coma
• Evaluation/ Monitoring:
– Admit patient to ICU for further monitoring
– Continue to monitor thyroid levels, which should begin declining in
24 hours and resolve in 7 days
– Start soft food when patient is extubated and has a return of bowel
sounds because of the decrease in GI motility
– Monitor for adrenal crisis, which is a common complication
– Watch for myocardial infarction since it can occur after IV hormone
replacement
– Begin physical therapy for recuperation
– Have patient follow-up with endocrinologist for hormone
replacement outpatient
53
Case Study
Derek, 10 year old male, is brought to the ER after his family notices he has been
increasingly fatigued and wetting the bed. As soon as he is brought in a blood sugar is
checked. The result is >500 mg/dL. You also obtain a urine sample, which is positive
for ketones and glucose. What is your priority intervention? What orders will you
expect from the doctor?
Jane, 72-year-old female, is found by her daughter only responding to painful stimuli and
brought to the ED. She has a glascow coma score (GCS) of 6. According to the
daughter, Jane had not been feeling well for about a week after getting over
pneumonia experiencing lethargy, decrease of appetite, and eye’s appear “a bit more
swollen.” Her oxygen saturation was 81 percent then she was being ventilated by bag
valve mask, stabilizing at 91 percent. Her vital signs HR 48, BP 94/56, Temp (oral) 29.4
C, and no palpable radial pulses. What is the priority intervention? What diagnosis
would you suspect? What interventions would you expect?
54
References
•
AMA. http://www.ama-assn.org//ama/pub/physician-resources/patient-education-materials/atlas-of-humanbody/endocrine-system.page
•
Atkins, J. Neuroendocrine physiology: Fundamentals and common syndromes.
•
Bevan, J. The endocrine system.
•
Mazurek, P. (2010, November 1). The "myx-up" of myxedema coma. Retrieved from http://www.ems1.com/air-medicaltransport/articles/903254-The-myx-up-of-Myxedema-Coma/
Stress. Retrieved from http://www.mhhe.com/biosci/ap/saladin/endocrine/reading4.mhtml
Types of insulin. Retrieved from http://diabetes.niddk.nih.gov/dm/pubs/medicines_ez/insert_C.aspx
Taylor, T. Endocrine system. Retrieved from http://www.innerbody.com/image/endoov.htm
http://www.medscape.com/
•
•
•
•
55