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RUNNING HEAD: Room 587 — Adrenal insufficiency"
Care Plan Room 587: "
Adrenal Insufficiency"
Elizabeth K. Bennett"
Liberty University #
Room 587 — Adrenal insufficiency $$$$$$$$2
Patient Profile Worksheet (Profile Part I)
A. Personal Information
Room #: 278 Gender: Female Ethnicity: Caucasian Age if < 90: 53
Place of Residence: Bedford, VA MD: Dr. Kryzyzanowski
EmergencyContact: Spouse MaritalStatus: Married
Admitting Diagnosis: Primary adrenal insufficiency
Co-Morbidities: HTN, loss of bowel function,
Date of Admission: 1/23/2018 Date of Surgery: None Allergies: Zofran, Bactrim,
Doxycycline, Honeydew melon
Code Status: Full code Mental Status: Oriented x 4
B. Activity and Nutrition
Diet order: NPO Route/Rate: TPN Last Wt: 61.35kg
Level of Activity (bedrest, up ad lib, BRP, turning): Up ad lib
Level of self-care: Assist x1
C. Nursing Care:
Drainage devices (foley, NGT, JPs, T-tube, etc.): Foley catheter placed 1/26 d/t
neurogenic bladder; Epidural placed for PRN morphine administration; NG tube placed for low
intermittent gastric suction.
NGT Flushes: None
Wound care/Dressing (be specific): Occlusive dressing on central line.
IV access (peripheral, central, location, care): Dual lumen central line placed 1/24 in RIJ
for administration of midrip lipids.
IVF: Lipids @250 mL/24hr Saline Lock? No TPN? Ye s
Frequency of vital signs (including pulse oximetry): Q4H
Frequency of Glucometer: Q6H Supplemental oxygen: None OSA: None known
Falls Risk: Low risk
Precautions: Contact precautions: VRE
Room 587 — Adrenal insufficiency $$$$$$$$3
Most Recent Labs (include date of labs):
Common Hematology/Chemistries/RFTs
Other Pertinent Labs (make sure to document important trends):
Initial CBC values were slightly low, but have normalized as of 1/31. TCO2, Osmolality, and
Albumin are elevated at 30, 304, and 3.2, respectively. Glucose readings have been elevated, but
are currently normal and not a cause for a concern at this time.
Patient History Worksheet:
Chief Complaint: Nausea, vomiting, abdominal pain, lack of stool formation.
History of Present Illness (discuss clinical course from admission until current date): The
patient, a 53 year old Caucasian female, has a history of hospitalization for GI-related
complications. Following her last discharge on 11/10/2017 she was doing well, returning to her
occupation as a nurse practitioner and participating in a 10 mile foot race. Per the patient’s
report, the symptoms leading to her current hospitalization began on 1/14, when she awoke
feeling “sluggish.” She injected herself with Decadron, which was ineffective. She visited her
Lab
Normal range
Patient value
Date/time
Out of range?
WBC
4-10 x 10^9/L
7.5 x 10^9/L
1-31-2018 1017
WNL
Hb
13.5-17.5 g/dL
11.3 g/dL
1-31-2018 1017
Low
Hct
38.8-50%
34.3%
1-31-2018 1017
Low
Plts
50-400 x 10^9/L
203 x 10^9/L
1-31-2018 1017
WNL
Na+
135-145 mmol/L
142 mmol/L
2-01-2018 1106
WNL
K+
3.5-5 mmol/L
4.1 mmol/L
2-01-2018 1106
WNL
Cl-
95-105 mmol/L
106 mmol/L
2-01-2018 1106
WNL
HC03
18-22 mmol/L
20 mmol/L
2-01-2018 1106
WNL
BUN
8-21 mg/dL
17 mmol/L
2-01-2018 1106
WNL
Cr
0.6-1.2 mg/dL
0.7 mmol/L
2-01-2018 1106
WNL
Glucose
70-100mg/dL
96
2-01-2018 1106
WNL
Room 587 — Adrenal insufficiency $$$$$$$$4
primary care physician on 1/17, and tested positive for FluA at that time. She again visited her
PCP on 1/23 after noticing that she had not produced stool over the weekend. CBC/CMP labs
drawn at the office were normal, as were her vital signs. A chest x-ray, and KUB also came back
unremarkable and she returned to her home. The patient reports that her blood pressure fell
throughout the day as indicated by readings using her home device. After developing severe
nausea and vomiting and still not passing any stool, she decided to self-admit to LGH. Upon
arrival, the patient was weak and hypotensive, nearly passing out while awaiting a bed. Once
admitted her supine blood pressure was recorded as 90/50, and she was administered 4mg IM
Decatron and 25mg IM Phenergan for relief of nausea. Her vital signs have since stabilized and
she has been placed on gastric rest with TPN infusions through a central line placed on 1/26. Her
primary complaint at this time is pain, which she consistently reports to be in the range of 5-9. A
morphine epidural is in place and is employed frequently. The patient is alert and oriented, is
able to ambulate without difficulty.
Past Medical History: PMI of recurrent intestinal pseudo-obstruction status post ileostomy
takedown, adrenal insufficiency, hypertension, recurrent UTI’s.
Past Surgical History: Extensive abdominal surgeries including: total colectomy and ill
resction, TAH/BSO, appendectomy, cholecystectomy, hysterectomy.
Family History: CAD, Diabetes, HTN, Thyroid disorders
Tobacco: Patient denies Alcohol: Patient denies Illegal Drugs: Patient denies
Occupational Status: Nurse practitioner
Religious Preference: None listed
Cultural Support Needs: Patient is a physically active practicing NP. !
Room 587 — Adrenal insufficiency $$$$$$$$5
II. Medications
Student should also have medication cards or book available on clinical.
Include PRNs that have been administered with the last 24 hours.
Medication
Generic &
Trade
Rou
te
Dosag
e &
Frequ
ency
Category/
Mechanism of
Action
Side Effects
Use for
this
patient
Lovenox
(Enoxaparin)
SQ
40mg
daily
Subclass:
Anticoagulants
Mechanism of
Action
binds to
antithrombin
III and
accelerates
activity,
inhibiting
thrombin and
factor Xa
(low-
molecular
weight
heparin)
Serious Reactions
hemorrhage, major;
epidural/spinal
hematoma; prosthetic
heart valve
thrombosis; anemia;
thrombocytopenia;
thrombocytopenia w/
thrombosis;
thrombocytosis;
anaphylactoid rxn;
hypersensitivity rxn;
skin necrosis;
hyperkalemia;
hepatotoxicity;
Common Reactions
anemia; hemorrhage;
fever; peripheral
edema; local injection
site rxn; hematuria;
ALT, AST elevated;
nausea;
thrombocytopenia;
diarrhea; osteoporosis
(long-term use)
Preventio
n of
blood
clot
formation
Fat Emulsion
20%
IV
250ml
daily
Room 587 — Adrenal insufficiency $$$$$$$$6
Hydrocortiso
ne SOD
Succinate
IV
125mg
Q12H
Subclass:
Corticosteroids
, Systemic
Mechanism of
Action
exact
mechanism of
anti-
inflammatory
action
unknown;
inhibits
multiple
inflammatory
cytokines;
produces
multiple
glucocorticoid
and
mineralocortic
oid effects
Serious Reactions
anaphylaxis; adrenal
insufficiency; steroid
psychosis; steroid
myopathy; Cushing
syndrome; infection;
diabetes mellitus;
pseudotumor cerebri;
ICP incr.; seizures;
hypokalemic
alkalosis; HTN; CHF;
pancreatitis; GI
perforation; PUD;
exophthalmos;
osteonecrosis;
Charcot-like
arthropathy; tendon
rupture; osteoporosis
(long-term use);
glaucoma (long-term
use); cataracts (long-
term use);
immunosuppression
(long-term use);
Kaposi sarcoma (long-
term use); withdrawal
sx if abrupt D/C (high
dose or long-term use)
Common Reactions
Cushingoid
appearance; hirsutism;
weight gain;
erythema; abdominal
discomfort; appetite
changes; emotional
lability; rash/urticaria;
nausea/vomiting;
sodium and fluid
retention;
hypokalemia; BP
elevated; edema;
diaphoresis; muscle
atrophy; impaired
wound healing (long-
term use); skin
atrophy (long-term
use); petechiae/
ecchymosis; skin
pigmentation
abnormality; acne;
headache; dizziness/
vertigo; insomnia;
depression; anxiety;
glucose intolerance;
Cushing syndrome
(long-term use);
menstrual
irregularities; IOP
incr.; leukocytosis;
injection site rxn;
epidural lipomatosis;
central serous
chorioretinopathy
Reductio
n of
inflamma
tion
Room 587 — Adrenal insufficiency $$$$$$$$7
Ativan
(Lorazepam)
IM
25mg
at
bedtim
e
Subclass:
Insomnia;
Seizure
Disorders;
Benzodiazepin
es (BZDs) 2:
Intermediate-
acting;
Sedation
Mechanism of
Action
binds to
benzodiazepin
e receptors;
enhances
GABA effects
Serious Reactions
respiratory depression;
apnea; respiratory
failure; dependency,
abuse; seizures;
suicidality;
tachycardia;
hypotension; syncope;
blood dyscrasias;
jaundice; CNS
stimulation,
paradoxical; gangrene
(intra-arterial);
withdrawal sx if
abrupt D/C (long-term
use); cognitive deficits
(pts <3 yo, >3h or
repeat sedation use);
behavioral changes
(pts <3 yo, >3h or
repeat sedation use)
Common Reactions
sedation; dizziness;
asthenia; ataxia; local
injection site rxn;
respiratory depression;
hypoventilation (IV
use); hypotension;
fatigue; amnesia;
confusion;
disinhibition;
irritability; libido
changes; menstrual
irregularities;
diplopia; dysarthria;
appetite changes;
constipation;
incontinence; urinary
retention; dystonia;
ALT, AST elevated
Sleep aid
Room 587 — Adrenal insufficiency $$$$$$$$8
Morphine
IV
30mg
PRN:
2mg
loadin
g dose,
0.5mg
mainte
nance
Q0.5H
PRN
Subclass:
Opioids
Mechanism of
Action
binds to
various opioid
receptors,
producing
analgesia and
sedation
(opioid
agonist)
Serious Reactions
Respiratory
depression; apnea;
respiratory arrest;
cardiac arrest;
circulatory depression;
hypotension, severe;
shock; ICP incr.;
seizures; arrhythmias;
paralytic ileus; biliary
spasm;
hypersensitivity rxn;
anaphylaxis;
dependency, abuse;
adrenal insufficiency;
opioid-induced
androgen deficiency
(long-term use);
withdrawal sx if
abrupt D/C (prolonged
or long-term use)
Common Reactions
somnolence;
constipation; nausea/
vomiting; dizziness;
diaphoresis;
dysphoria; euphoria;
headache; edema;
abdominal pain;
pruritus; flushing;
xerostomia; asthenia;
paresthesia; urinary
retention; libido decr.;
miosis
Relief of
moderate
to severe
pain
Room 587 — Adrenal insufficiency $$$$$$$$9
Phenergan
IV
25mg
IV
PRN
Subclass:
Nausea/
Vomiting;
Antihistamines
, 1st generation
Mechanism of
Action
non-selectively
antagonizes
central and
peripheral
histamine H1
receptors;
possesses
anticholinergic
properties,
resulting in
antiemetic and
sedative
effects
(phenothiazine
)
Serious Reactions
extravasation/tissue
damage (IV use > IM
use); apnea;
respiratory depression;
seizures; leukopenia;
thrombocytopenia;
agranulocytosis;
hallucinations;
extrapyramidal sx;
cholestatic jaundice;
neuroleptic malignant
syndrome;
angioedema;
bradycardia;
tachycardia; heat
stroke
Common Reactions
drowsiness; sedation;
blurred vision;
dizziness; confusion;
disorientation;
extrapyramidal sx;
xerostomia;
photosensitivity;
dermatitis; rhinitis;
urinary retention
Relief of
nausea
Albuterol
Nebi
lizer
3ml
PRN
RTQ4
H
Subclass:
Beta-2
Agonists 1:
Short-acting
Inhaled
(SABAs)
Mechanism of
Action
selectively
stimulates
beta-2
adrenergic
receptors,
relaxing
airway smooth
muscle
Serious Reactions
bronchospasm,
paradoxical;
anaphylaxis;
hypersensitivity rxn;
HTN; hypotension;
angina; cardiac arrest;
arrhythmia;
hypokalemia;
hyperglycemia
Common Reactions
throat irritation; URI
sx; cough; bad taste;
tremor; dizziness;
nervousness; nausea/
vomiting; headache;
palpitations;
tachycardia; pain;
hyperlactatemia
Bronchod
ilator
Room 587 — Adrenal insufficiency $$$$$$$$10
V. Top Three Prioritized Medical and Nursing Diagnosis
1. Primary adrenal insufficiency: (actual) acute pain r/t GI disturbances AEB decreased
gastrointestinal motility, patient reports pain as being 5-9 on a 10 point scale, positional posturing to
relieve abdominal discomfort, and prescription of morphine epidural.
2. Primary adrenal insufficiency: (risk for) aspiration r/t GI disturbances AEB NG tube
placement, patient report of nausea, delayed gastric emptying, decreased gastrointestinal motility.
3. Primary adrenal insufficiency: (risk for) deficient fluid volume r/t increase in sodium and
water excretion with potassium retention typical of adrenal insufficiency AEB lowered sodium levels on
1/24/2018, hypotensive blood pressure of 90/50 on admission, GI disturbances, and patient reports feeling
“sluggish.”
Care Plan
Medical &
Nursing Dx
Nursing Outcomes
(NOC)
Nursing Interventions (NIC)
1. Primary
adrenal
insufficiency:
(actual) acute
pain r/t GI
disturbances AEB
decreased
gastrointestinal
motility, patient
reports pain as
being 5-9 on a 10
point scale,
positional
posturing to
relieve abdominal
discomfort, and
prescription of
morphine
epidural.
1A. During the nurse’s
8 hour shift, the
patient’s pain level will
be kept within
acceptable parameters
as set and expressed by
the patient using a
numeric scale.
1B. During the nurse’s
8 hour shift, the patient
will be encouraged to
ambulate as tolerated
for the purpose of
regaining and
maintaining her
ambulatory
independence and
encouraging bowel
stimulation.
1C. During the nurse’s
8 hour shift, the nurse
will seek to discover
the underling cause of
the patient’s pain, in
order to better treat and
repair the disorder.
1A-1. The nurse will administer pain medications as prescribed in
order to keep the patient’s pain level within acceptable parameters
as set and expressed by the patient using a numeric scale.
1A-2. The nurse will check with the patient often to ensure that the
patient is in a comfortable position, has enough pillows, etc. to help
the patient minimize her pain.
1A-3. The nurse will employ non-medical means of pain control
such as distraction, meditation, relaxation, etc. to help the patient
manage her pain.
1B-1. The nurse will consult with the patient at the beginning of her
shift to establish a schedule for the day that includes times to
ambulate.
1B-2. The nurse will gather the necessary help and/or supplies in
preparation to assist the patient in ambulation.
1B-3. The nurse will administer pain medicine as prescribed 30
minutes prior to ambulation to minimize the patient’s pain while
ambulating.
1C-1. The nurse will discuss with the patient possible causes of his
lower back pain.
1C-2. The nurse will educate the patient on safe ambulating
techniques, and ways in which to minimize one's chances of injury
in the home (i.e. reducing clutter, padding sharp corners/objects,
etc.) in order to reduce his risk of future injury.
1C-3. The nurse will inform the patient about possible treatment
options as recommended by the attending physician.
Room 587 — Adrenal insufficiency $$$$$$$$11
Pathophysiology"
$Mrs. S, a 53 year old Caucasian female, was admitted to Lynchburg General
Hospital on 1/23/2018 with severe nausea, vomiting, and hypotension secondary to
adrenal crisis and pseudo-obstruction of the small intestine. The following is a
discussion of the pathophysiology of her conditions, as well as the rational behind
current treatment strategies. "
$The patient has a history of hospitalization for GI-related complications and has
undergone extensive abdominal surgeries as a result, including total colectomy and
ileal resection, total abdominal hysterectomy with bilateral salpingo-oophorectomy
(TAH/BSO), appendectomy, and a cholecystectomy. The majority of her gastric issues
can be traced to a motor vehicle accident in which she sustained traumatic injury to
the pineal gland, permanently impairing adrenocorticotropin hormone (ATCH)
production and predisposing Mrs. S to inefficient stress-coping mechanisms and
adrenal crisis. ACTH is a steroid hormone released dinurally from the anterior pituitary
gland (Hannon, 2017). ACTH travels through the bloodstream and binds to a protein
complex of the seven-(pass)-trasmembrane domain receptor (7TM receptor) family
found on the plasma membrane of cells in the adrenal glands (Hyman, 2012). For the
purposes of this paper, these protein complexes will be referred to as G-protein
receptors (GPCR) because of the specific guanine nucleotide-binding proteins (G-
proteins) to which they are coupled. This coupling allows GPCR’s to use ACTH as a
catalyst for the activation of internal signal transduction pathways (Dores, 2018). G-
proteins are a family of proteins that act as molecular switches inside cells, functioning
in the transmission of signals from the outside of a cell to its interior. G-proteins are
part of a broader category of proteins known as GTP-ases, meaning they derive their
Room 587 — Adrenal insufficiency $$$$$$$$12
operating energy from the hydrolysis of GTP to GDP. When bound to GTP, extracellular
signals are transmitted to the interior of the cell, allowing the cell to respond to
extracellular stimuli. When bound to GDP, the G-proteins are “off” and no signals are
transmitted (Gupta, 2015). In the case of ACTH GCPR’s on the cells of the second layer
of the adrenal cortex, the signal transmitted by the binding of ATCH stimulates the cells
of the zona fasiculata to release of cortisol into the bloodstream (Hannon, 2017)."
$Because, in a well-functioning system, ATCH production has a direct linear
proportion to that of the release of its target hormones, a deficiency in ATCH is
functionally equivalent with insufficient levels of the hormone products whose release it
triggers (Dores, 2018). ATCH has minor influence over the production and release of
aldosterone; however, it is its main target, cortisol, that will be the focus of this
discussion. Cortisol essentially acs as a both a “housekeeping” and an “emergency
supply” hormone, having widespread systemic effects on the body. Cortisol affects
insulin metabolism, bone formation, immune function, electrolyte balance, gastric
activity and waste elimination, serving to repair and regulate these systems during
times of rest, as well as to assist epinephrine and norepinephrine in the allocation of
energy reserves to vital functions of the body during times of stress (DeGroot, 2006).
For the purposes of this paper, we will focus primarily on the immunological and gastric
effects of cortisol as they are most relevant to Mrs. S’s current disease processes."
$Cortisol affects bone formation by reducing calcium absorption in the intestine
and segregating absorbed calcium and potassium away from bone formation.
Prolonged elevation in cortisol levels can predispose an individual to osteoporosis as a
result of decreased bone formation and increased use of bone minerals to maintain
serum mineral levels (Hannon, 2013). Mrs. S’s serum calcium and potassium levels
were within normal limits at 9.4mg/dL and 4.1mg/dL, respectively. If this were not the
Room 587 — Adrenal insufficiency $$$$$$$$13
case, it may have indicated that her cortisol levels had been chronically imbalanced,
leading to a serum deficiency or elevation in these minerals (Gupta, 2015)."
$Cortisol works to increase blood glucose by stimulating hepatic glycogenesis
and preventing translocation of glucose transporters to the cell membrane in peripheral
cells. It acts primarily against GLUT4 receptors, which are found in striated muscle and
adipose tissues. In this sense, cortisol’s actions directly oppose insulin, which triggers
the sequestering of glucose into cells via GLUT4 and other glucose receptors (Kanzaki,
2006). However, cortisol acts in synergy with insulin in the hepatic system by increasing
glycogen synthesis in the liver. The permissive effect of cortisol on insulin action in liver
glycogenesis is observed in hepatocyte culture in the laboratory, but the exact
mechanism for this phenomenon is unknown (Hannon, 2017)."
$In the absence of cortisol, patients are ultimately at risk for hypoglycemia due to
the lack of inhibition of the effects of insulin. Any glucose in the bloodstream is quickly
absorbed into cells, and hepatic glucose stores are eventually depleted, putting the
patient in serious risk of hypoglycemic coma and death. This is, in fact, the primary
danger of adrenal crisis, and one of the first symptoms of insufficient cortisol levels.
Per the patient’s report, the symptoms leading to her current hospitalization began on
1/14/2018, when she awoke feeling “sluggish.” Lethargy is one of the first symptoms of
hypoglycemia, and is a typical marker of the beginning of Addisonian crisis (Misra,
2011). "
$ Cortisol also affects sodium and potassium levels by acting as a diuretic,
increasing the glomerular filtration rate and preventing sodium absorption in the distal
convoluted tubule. It promotes the simultaneous transport of sodium ions in and
potassium ions out of the body (Hannon, 2017). On admission, Mrs. S was dehydrated,
and hyponatremic (120mg/dL) which may have been a partial result of the uncontrolled
Room 587 — Adrenal insufficiency $$$$$$$$14
emesis in addition to lowered cortisol levels. Nausea and vomiting are typical
symptoms of adrenal crisis, due in part to rapidly diminishing glucose levels, and in
part to the unique effects of cortisol on the gastric system (Misra, 2011). "
$Mrs. S was given IV bolus fluids to normalize her hydration level, and her sodium
levels have since corrected to be within normal limits. Serum albumen levels can also
appear elevated secondary to increased fluid excretion when viewed as a ratio to total
fluid volume. The patient’s serum albumin was initially elevated at 304 mg/dL, but has
since corrected following fluid replacement and restoration of adequate nutrition.
Cortisol affects gastric secretion by stimulating cells of the gastric mucosa to produce
gastric acid. It is also believed that it stimulates contraction of the smooth muscle
lining the digestive tract. In the absence of cortisol, the patient is at risk for ineffective
digestion leading to nausea, vomiting, abdominal pain, ineffective stool clearance, and
hypoglycemia. Lower GI symptoms may vary, and range from severe diarrhea to
constipation (Schteingart, 2008). In Mrs. S’s case, stool formation was inhibited to the
point of pseudo-obstruction, the pathophysiology of which will be further discussed
below. "
$Imbalanced electrolyte levels, hyperemesis, inadequate absorption, and
hypoglycemia typical of adrenal crisis all contribute to make the patient hypotensive
(Hannon, 2017). Although her vital signs were normal at her visit to her PCP on the
morning of 1/23/2018, the patient reports that her blood pressure fell throughout the
day as indicated by readings using her home device. She self-administered an
intramuscular dose of Decadron (Dexamethasone), which did not relieve her
symptoms. After developing severe nausea and vomiting and still not passing any
stool, she decided to self-admit to LGH. Upon arrival, the patient was weak, faint, and
critically hypotensive. Her supine blood pressure was recorded as 60/40 on admission,
Room 587 — Adrenal insufficiency $$$$$$$$15
and she was administered 4mg IM Decatron and 25mg IM Phenergan for relief of
nausea. Phenergan (promethazine) has anti-histamine, sedative, and antiemetic
functions. Promethazine competes with histamine for H1 receptor on cells, blocking
the stimulatory action of histamine cells, preventing perpetuation of the inflammatory
response. Promethazine also blocks the action of acetylcholine, which may explain its
benefit in reducing the nausea (Gomella, 2008). Decadron (a glucocoirticoid) also has
anti-inflammatory properties. It works by reducing the expression of cytokines,
chemokines, adhesion molecules and other inflammatory proteins, as well as the
recruitment of inflammatory cells to sites of inflammation. Furthermore, glucocorticoids
promote the cell death of many inflammatory cells and this may further contribute to
reducing the inflammatory cell burden (Physicians desk reference, 2016). $"
!Cortisol’s effect on the immune system is complex and tightly regulated. In a
healthy system, stress naturally induces cortisol production, however, both a chronic
excess or deficiency in cortisol levels can have deleterious effects on immune function.
Hypocorticism results in hypertrophy of lymphoid tissue (ie, thymus, spleen, lymph
nodes) and hypercorticism leads to dimunition or total loss of these tissues (DeGroot,
2006). Glucocorticoids induce changes in sequesterization of the cells, or by
influencing the rate of formation or destruction of lymphoid cells. Acute effects of
glucocorticoid observed in lymphoid tissue can usually be traced to a sequesterization
action, while more gradual changes are often a result of cortisol-induced lysis of
immune cells (Dores, 2018).
!Studies have shown that high levels of perceived stress and increases in cortisol
have been found to lengthen wound-healing time due to cortisol’s role in increasing
inflammatory mediators (Hannon, 2017). Although inflammation is useful as a second
line defense in preventing the spread of infection, it can be deleterious in wound
Room 587 — Adrenal insufficiency $$$$$$$$16
healing and systemic response and recovery to pathogens. Additionally, high levels of
stress can cause systemic inflammation, weakening the body’s immune system and
predisposing it to infection by bacteria which would normally be easily fought off. Viral
infections are known to increase cortisol levels through activation of the HPA axis by
cytokines. Influenza, a common virus in the winter months, would stress the immune
system and may have placed a higher demand on Mrs. S’s body that what her cortisol
levels could contend with (Mims, 2013). "
$Another factor in known to contribute to the elevation of serum cortisol levels is
high intensity or prolonged aerobic exercise. Strenuous exertion transiently increases
cortisol levels to increase gluconeogenesis and maintain blood glucose (Misra, 2011).
While some exercise is beneficial, and in healthy systems cortisol declines to normal
levels after a neutral energy balance is restored (i.e. after eating or a period of rest),
Mrs. S would not have the adrenal reserves to cope with the level of strain incurred by
an activity such as a half marathon (Hannon, 2013). Her participation in the 10 mile
race may have predisposed her to infection with the influenza A virus. These two
factors together almost certainly pushed her system into adrenal crisis, and from there
pseudoobstruction of the small intestine.
$Pseudoobstruction of bowel occurs when the intestines behave as though there
were a mechanical obstruction, with no identifiable cause (Hannon, 2017). Due to the
nature of the malady, diagnosis is inferred by process of elimination rather than direct
identification. Diagnostic procedures typically include x-ray and fluid-imaging
techniques to screen for mechanical obstruction, in addition to identification of
possible precipitating factors such as prior abdominal trauma, endocrine imbalances
known to affect smooth muscle motility, or pharmacotherapy with GI-irritating drugs
(Wood, 2004). Mrs. S states that her GI symptoms probably began around 1/21. She
Room 587 — Adrenal insufficiency $$$$$$$$17
paid a second visit to her PCP on 1/23 after noticing that she had not produced stool
over the weekend. Complete blood count/ complete metabolic panel CBC/CMP labs
drawn at the office were found to be unremarkable, as were her vital signs. A chest x-
ray and KUB also came back unremarkable and she returned to her home."
$Although the exact cause of the correlation between adrenal insufficiency and
pseudo-obstruction remains unclear, it is believed that a sudden withdrawal of
glucocorticoid therapy or the introduction of stressful stimuli, such as infection or
surgery, may precipitate the condition (Kunjal, 2013). Just prior to the onset of her
bowel symptoms, Mrs. S was diagnosed with FluA on 1/17/2018. The influenza virus is
would have further weakened her already compromised immune system and is very
probably a major contributing factor to the onset of her adrenal crisis. It has further
been established that influenza is particularly damaging to the intestinal system,
particularly that of an individual in whom the intestinal health is already compromised
(Mims, 2013). Mrs. S’s long history of intestinal surgeries and chronic pseudo-
obstruction suggest that her digestive system was an easy target for the flu virus. "
$Another factor which may have contributed to weakening Mrs. S’s digestive
system may have been her high level of physical exertion just prior to the onset of her
GI symptoms. The patient reports that following her last discharge on 11/10/2017 she
was doing well, returning to her occupation as a nurse practitioner and participating in
a half marathon. Per the patient’s report, the symptoms leading to her current
hospitalization began on 1/14/2018, when she awoke feeling “sluggish.” During periods
of extended physical exertion, such as that undergone during a ten mile race, blood is
shunted away from organs involved in digestion and excretion and to the skeletal
muscles and brain (Hannon, 2017). Given the fragile state of her small intestine, it is
possible that the relative lack of blood flow may have disrupted the delicate
Room 587 — Adrenal insufficiency $$$$$$$$18
mechanisms by which the intestines regulate their contraction, and they were unable to
recover full functionality."
$Mrs. S’s vital signs have since stabilized, but she still suffers from extreme
nausea when not on high doses of phenergan. She has been placed on gastric rest
with low-intermittent suctioning of gastric secretions through a nasogastric tube which
remains in place around the clock. Nutrition is provided through TPN infusions
administered via a central line placed on 1/26. It is the hope of the physicians that by
allowing her GI tract to rest, it will eventually “re-set” and begin to function normally
again. Her bowel sounds are monitored closely to detect signs of returning function.
Mrs. S’s primary complaint at this time is pain, which she consistently reports to be in
the range of 5-9 on a 10 point scale. A continuous morphine infusion is in place and is
employed to the full extent of the prescription. The patient is alert and oriented, is able
to ambulate without difficulty. Primary nursing considerations at this time include pain
management, maintenance of independence, emotional support, and monitoring of
gastric motility. #
Room 587 — Adrenal insufficiency $$$$$$$$19
References"
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$Dores, R. M. (2018). ACTH, Melanocortin Receptors, MRAP Accessory Proteins.
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$Gomella, L. G. (2008). Clinicians pocket drug reference 2008. New York:
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$Gupta, P. K. (2015). Cell and molecular biology. S.I.: Rastogi Publications."
$Hannon, R. A., & Porth, C. (2017). Porth pathophysiology: concepts of altered
health states. Philadelphia: Wolters Kluwer."
$Hyman, P. E., & Thapar, N. (2012). Chronic Intestinal Pseudo-Obstruction. $$
Pediatric Neurogastroenterology, 257-270. doi:10.1007/978-1-60761-709-9_22"
$Kanzaki, M. (2006). Insulin Receptor Signals Regulating GLUT4 Translocation
and Actin Dynamics. Endocrine Journal, 53(3), 267-293. doi:10.1507/endocrj.kr-65"
$Kawanaka, K. (2006). Effects of exercise on muscle GLUT4. Trends In The
Sciences, 11(10), 42-46. doi:10.5363/tits.11.10_42"
$Kunjal, R. A., Ramadoo, R. R., Teelucksingh, S., & Naraynsingh, V. (2013).
Adrenal insufficiency and bowel obstruction: An overlooked association. Case Reports
in Clinical Medicine, 02(02), 111-114. doi:10.4236/crcm.2013.22029"
$Mims, C. A., & Goering, R. V. (2013). Mims medical microbiology. Philadelphia?:
Elsevier/Saunders."
$Misra, S. (2011). Chapter-11.3 Adrenal Insufficiency and Addisonian Crisis.
Approach to Pediatric Emergency, 262-264. doi:10.5005/jp/books/11218_7"
$Physicians desk reference. (2016). Montvale, NJ: PDR Network."
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$Schteingart, D. (2008). Measurement of Salivary Cortisol Concentration in the
Assessment of Adrenal Function in Critically Ill Subjects: A Surrogate Marker of the
Circulating Free Cortisol. Yearbook of Endocrinology, 2008, 259-260. doi:10.1016/
s0084-3741(08)79168-6"
$Wood, J. D. (2004). Intestinal Pseudoobstruction. Encyclopedia of
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