○ Predisposing Factors
The most common are genetic factors, sepsis,
Pulmonary Insufficiency:
ACUTE RESPIRATORY
DISTRESS SYNDROME
1. What makes the condition life threatening?
Acute Respiratory Distress Syndrome (ARDS) is
widely recognised as a severe form of acute
respiratory failure. Acute lung injury (ALI) and
○ Pathophysiology:
ARDS represent a spectrum of acute lung
inflammation and diffuse alveolocapillary injury.
ARDS is the most severe form and is defined as
● Acute onset of bilateral infiltrates on chest
radiograph not explained by cardiac
overload or fluid overload
● Low ratio of the partial pressure of arterial
oxygen to the fraction of inhaled oxygen
○ This clinical syndrome is characterized by a
severe inflammatory process causing diffuse
alveolar damage that results in sudden and
progressive pulmonary edema, increasing
bilateral infiltrates on chest x- ray, hypoxemia
unresponsive to oxygen supplementation
regardless of the amount of positive end-
expiratory pressure(PEEP), and the absence of
an elevated left atrial pressure
○ ARDS has been associated with a mortality rate
ranging from 26% to 58% depending on severity
of illness and comorbidities. The major cause of
death in ARDS is nonpulmonary multiple organ
dysfunction syndrome (MODS), often with
sepsis.
2. How does the progression of the etiologic
changes lead to a life threatening situation?
and multiple trauma (especially when
multiple transfusions are received); however,
there are many other causes, including
pneumonia, burns, aspiration,
cardiopulmonary bypass surgery,
pancreatitis, drug overdose, smoke or
noxious gas inhalation, oxygen toxicity,
radiation therapy, and disseminated
intravascular coagulation
Exudative (Inflammatory) Phase (Within
72 Hours).
⇢ The initial lung injury damages the
alveolocapillary membrane.
⇢ Lung injury activates neutrophils,
platelets, macrophages, lung epithelial
and endothelial cells, and uncontrolled
inflammation.
⇢ Inflammatory mediators include
complement, cytokines, arachidonic acid
metabolites, platelet-activating factor,
reactive oxygen species, and other
mediators (specifically tumor necrosis
factor [TNF], interleukin-1 [IL-1], and
IL-6).
⇢ Activated complement factors and
platelet aggregation result in
intravascular microthrombus formation
and further damage to lung capillaries.
⇢ In ARDS caused by sepsis, bacterial
toxins are recognized by the CD14
receptors on macrophage and lead to
chemotaxis of large numbers of
neutrophils to the lungs.
⇢ A cascade of inflammatory mediators is
released by the macrophages, including
TNF, IL-1, alpha and beta chemokines,
and other interleukins.
⇢ The role of neutrophils is central to the
development and progression of ARDS.
 Activated neutrophils release a battery of ⇢ Within 1 to 3 weeks after the initial lung
harmful inflammatory mediators, among injury, there is resolution of the
them proteolytic enzymes, oxygen free pulmonary edema and proliferation of
radicals (superoxide radicals, hydrogen type II pneumocytes, fibroblasts, and
peroxide, hydroxyl radicals), arachidonic myofibroblasts.
acid metabolites (prostaglandins, ⇢ The intra-alveolar hemorrhagic exudate
thromboxanes, leukotrienes), and platelet becomes a cellular granulation tissue
activating factor. These mediators cause appearing as hyaline membranes and
extensive damage to the alveolocapillary there is progressive hypoxemia.
membrane and greatly increase capillary
membrane permeability. Fibrotic Phase (14 to 21 Days).
⇢ Increased capillary permeability, a
⇢ About 2 to 3 weeks after the initial injury,
hallmark of ARDS, allows fluids,
remodeling and fibrosis occur.
proteins, and blood cells to leak from the
⇢ The fibrosis progressively obliterates the
capillary bed into the pulmonary
alveoli, respiratory bronchioles, and
interstitium and alveoli (hemorrhagic
interstitium, leading to a decrease in
exudate).
functional residual capacity (FRC) and
⇢ The resulting pulmonary edema and
continuing ˙ V/˙Q mismatch with severe
hemorrhage severely reduce lung
right-to-left shunt.
compliance and impair alveolar
⇢ The result of this overwhelming
ventilation.
inflammatory response by the lungs is
⇢ Mediators released by neutrophils, and to
acute respiratory failure.
a certain extent by macrophages, also
⇢ The same chemical mediators responsible
cause pulmonary vasoconstriction.
for the alveolocapillary damage of ARDS
⇢ Because vasoconstriction occurs more in
often cause inflammation, endothelial
some vascular beds than others, blood
damage, and capillary permeability
flow to selected areas of the lungs is
throughout the body, resulting in the
decreased, resulting in ˙ V/˙Q (ventilation
systemic inflammatory response
: perfusion ratio) mismatching.
syndrome (SIRS).
⇢ Pulmonary hypertension occurs early in
⇢ SIRS then leads to multiple organ
the course of the disease secondary to
dysfunction syndrome (MODS). In fact,
vasoconstriction.
death may not be caused by respiratory
⇢ Thrombi composed of aggregated
failure alone, but by MODS associated
neutrophils, macrophages, platelets, and with ARDS.
fibrin are formed.
⇢ Surfactant is inactivated, and its
production by type II alveolar cells is
impaired as alveoli and respiratory
bronchioles fill with fluid or collapse.
The lungs become less compliant, the
work of breathing increases, ventilation
of alveoli decreases, and hypercapnia
develops.

Proliferative Phase (4 to 21 Days).

 4. How are these signs and symptoms assessed?

ARDS diagnosis can be controversial and is of

exclusion -- there are no specific markers that
identify alveolar-capillary membrane damage

○ Includes excluding other causes of

respiratory failure; as such, ARDS have the
following confirmatory features
● Acute bilateral lung infiltrates
● PF ratio of less than 200 mmHg
● No evidence of heart failure or
volume overload
○ Chest x-ray

3. What clinical presentations or presenting

complaints are expected in clients with the ● Findings: diffuse bilateral infiltrates
condition? without cardiomegaly or pulmonary
vascular redistribution, also can be
Symptoms of ARDS depend on the cause and
seen as a “whiteout”
severity of the case, as well as pre-existing lung
● Explanation: Reflects
or heart conditions. Clinical presentations
noncardiogenic pulmonary edema
include:

○ Severe Dyspnea ○ Arterial blood gases

○ Labored and unusually rapid ● Findings: PaO2 < 80 mmHg;
breathing PaCO2 varies; SaO2 < 95%
○ Hypotension ● Explanation: Poor gas exchange
○ Confusion leads to hypoxemia, and as
○ Extreme Fatigue respiratory failure progresses, into
○ Rapid Heart Rate hypercapnia. When PaO2 is divided
○ Cyanosis (fingernails and lips) by the FiO2, result is 200 or less
○ Cough and chest pain (Normal value is at least 400
mmHg)
If ARDS is caused by severe infection (sepsis), ➤ PF ratio can identify acute
symptoms of sepsis may also be present such as hypoxemic respiratory failure
fever and hypotension. when supplemental oxygen has
 already been administered and
no room air ABG is available,
or pulse oximetry readings are
unreliable.
➤ PF ratio clarifies severity
⇢ Mild - 200-300 mmHg
⇢ Moderate - 100-200 mmHg
⇢ Severe - > 100 mmHg
● Also, hallmark of ARDS is
refractory hypoxemia to
supplemental oxygen
○ Physical examination
● Lung sounds may differ depending
5. What are the basic interventions for each
on ARDS stage
➤ Early stage - lungs have
decreased breath sounds
➤ Middle stage - basilar crackles
or coarse crackles
➤ Late stage - bronchial breath
sounds or no breath sounds
with little gas exchange
➤ When patient is intubated and
on mech ventilation - lungs
sound extremely congested,
with wheezes and coarse
crackles throughout
● Peripheral pulses are rapid and
sometimes thready
○ Differential diagnosis
● Since ARDS is a physiologic and
radiographic syndrome rather than a
specific disease, differential
diagnoses do not strictly apply.
● Other supporting tests include
pulmonary function tests, pulse
oximetry, and pulmonary capillary
wedge pressure, histologic studies,
and blood and urine cultures.
➤ PF tests show decreased FRC,
decreased lung volumes,
decreased lung compliance,
and a ventilation-perfusion
(VA/Q) mismatch with a large
right-to-left shunt
➤ Histologic studies found on
open lung biopsy reveal
atelectasis, hyaline
membranes, cellular debris,
and interstitial & alveolar
edema
➤ Blood and urine cultures will
help determine whether
infection is the etiology.
condition?
The five P’s of supportive therapy include
perfusion, positioning, protective lung
ventilation, protocol weaning, and preventing
complications.
a. Perfusion
- Increase the patient's fluid volume without
overloading him or her. Replace the fluids
that have leaked from the capillaries into the
alveolar spaces with crystalloids or colloids.
Blood transfusions can improve oxygen
delivery, but they can also trigger an
inflammatory response, increasing the risk of
infection and death.
- Measure blood pressure, respiratory
variations of pulmonary and systemic arterial
pulse pressure, central venous pressure, and
urine output to determine the patient's
volume status.
- Certain drugs can also help increase
perfusion. Inotropics such as dobutamine
(Dobutrex) can increase cardiac output to
boost oxygenation. Milrinone lactate
(Primacor), another inotropic, improves
perfusion by causing vasodilation in the
pulmonary bed.
b. Positioning
● Kinetic therapy (bilateral turning of a
patient 40 degrees or more per side) - This
 works in immobilized patients at angles of up
to 62 degrees. This therapy both prevents and
treats severe respiratory complications
associated with prolonged immobilization.
This prevents and treats pneumonia and
ARDS when started early.
● Continuous lateral rotational therapy
(bilateral turning of a patient no more than 40
degrees per side) - The patient must be
consistently turned to 40 degrees; otherwise,
the therapy has no effect on secretion
clearance, pneumonia risk, or length of ICU
stay.
● Prone positioning - The V/Q ratio improves
with prone positioning. With the patient
prone, most lung tissue in the posterior areas
moves toward the anterior, clearing the
airways of debris, decreasing atelectasis,
decreasing lung inflammation, and producing
more efficient oxygenation and perfusion.
- If you’re not using a device: Turn the
patient from the supine position
toward the ventilator, using the chest
and pelvic area to improve diaphragm
motion and lung mechanics. Place the
patient in a prone position, with
pillows or cushions supporting the
chest and pelvis and allowing the
abdomen to hang freely. Arrange the
arms in the swimmer's pose with one
at the side of the body and the other
extended above the head while the
patient is prone. To prevent
dislodgement, place all tubes and
drains at the head or foot of the bed.
To relieve pressure and prevent skin
breakdown, rotate the patient's head
from side to side. Also, every couple
of hours, reposition the patient and
assess the pressure points.
- Using positioning devices: The
Stryker frame maintains the prone
position by sandwiching the patient
between two boards. This device,
however, does not provide any
pressure relief or safety features. Both
the Triadyne Proning Accessory
Kit and the Vollman Proner make
positioning the patient easier and
more effective. The Triadyne Proning
Accessory Kit includes a positioning
sheet and position packs to assist
patients in the prone position. The
Vollman Proner positioning device is
a frame with padding over the
patient's forehead, chin, chest, and
pelvic areas, as well as straps to help
with positioning. The device is placed
on top of the patient, and the straps
are used to pull and roll the patient
into the prone position. The
RotoProne bed is an automated
system that combines Kinetic
Therapy with up to 62 degrees of
prone positioning. This device
enables a single nurse to change
positions and provide multiple
intervals of prone positioning
throughout the day.
- Prone positioning does have some
downsides, such as the possibility of
tube dislodgement, patient
desaturation, skin breakdown, and
facial edema. Most of these
complications, however, can be
avoided or treated with diligent
nursing care and awareness.
c. Protective Lung Ventilation
- Use mechanical ventilation to open collapsed
alveoli in the early stages of ARDS. The
primary goal of ventilation is to support
organ function by providing adequate
ventilation and oxygenation while reducing
the patient's work of breathing. However,
mechanical ventilation can harm the alveoli,
requiring protective lung ventilation.
- Current recommendations for protective lung
ventilation include:
○ limiting plateau pressures to less than
30 cm H2O
○ maintaining PEEP
○ reducing FiO2 to 50% to 60%, if
doing so doesn’t compromise PaO2
○ providing low VTs (6 ml/kg of ideal
body weight).
- At least every 4 hours and after any change in
PEEP or VT, check the patient for changes in
respiratory status, such as increased
respiratory rate, adventitious breath sounds,
 decreased oxygenation saturation, and
dyspnea.
d. Protocol Weaning
- Weaning strategies can help ARDS patients
live longer and healthier lives by reducing the
amount of time and money they spend in the
hospital.
- The general guideline is: the patient either
needs full ventilatory support or needs to be
weaned.
- The following are in accordance to the
evidence-based guidelines:
● Instead of synchronous intermittent
mechanical ventilation, use
spontaneous breathing trials.
● Not just for physicians, but the design
and the implemented protocols
should be appropriate for all qualified
healthcare providers
● Protocols should be tailored as a
guideline for patient care rather than
as hard rules.
● Protocols should be used to enhance
clinical judgement, not replace it.
● Use of sedation goals to cut down on
the time spent on mechanical
ventilation and the length of time
spent in the ICU.
e. Preventing Complications
- VILI, deep vein thrombosis (DVT), pressure
ulcers, reduced nutritional status, and
ventilator-associated pneumonia (VAP) are
the most prevalent complications.
Deep Vein Thrombosis
- DVT is an acute disorder in which the deep
veins become inflamed and thrombus forms,
which can lead to pulmonary embolism.
- Approximately 16% of patients on
mechanical ventilation develop DVT within
the first 5 days of their stay in the ICU.
- Therapy should begin on admission to
prevent DVT, and include range-of-motion
exercises, frequent position changes,
anticoagulant prophylaxis, and the use of
sequential compression devices and
thromboembolic stockings.
- The following interventions are used to treat
DVT:
● Application of warm, moist compress
● Elevation of the affected
leg/extremity.
● Administration of analgesics,
thrombolytics, and anticoagulants
Pressure Ulcer
- Pressure ulcers can form as a result of
inadequate tissue perfusion and restricted
movement.
- Relieving pressure with regular position
changes, restoring circulation with mobility,
and supporting enough nutrition are all
nursing strategies that may help to prevent
this problem.
- You can lessen the risk of pressure ulcers by
regularly checking your patient's skin,
offering thorough skin care, monitoring
nutrition status, and installing pressure-
relieving devices such as air mattresses.
Poor Nutrition
- Because ARDS patients' nutritional condition
is severely deteriorated, start nutritional
therapy as soon as possible—ideally within
24 hours of arrival.
- Enteral nutrition is the recommended route of
support since it involves fewer complications
than parenteral nutrition. Always seek the
advice of a nutritionist when caring for an
ARDS patient.
VAP
- Ventilator-associated pneumonia (VAP), a
nosocomial pneumonia that develops after 48
hours or more of mechanical ventilation,
affects up to 40% of ARDS patients.
- The majority of infections are caused by
bacteria being aspirated from the mouth and
gastrointestinal tract.
- The recovery of an ARDS patient is
complicated by this condition, which
 necessitates a lengthier period of mechanical
ventilation and a longer hospital stay.

Putting the 5 P’s into practice

- ARDS, its complications, and its therapy or
treatment all have a number of risks. By
implementing the five evidence-based P's,
you can safely avoid all of the risks while also
enhancing your patient's outcome and
shortening his stay in the ICU.
Cardiac Insufficiency (MI)
Group 2 (1:30-2 pm)

Link for PPT:

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Y0alvi2aum4w0dVGg&role=EDITOR&utm_content=DAErYgyXR5Y&utm_ca
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1. What makes the condition life threatening?

○ Myocardial infarction is a severe form of coronary heart disease. A myocardial
infarction (MI) occurs because of sustained ischemia, causing irreversible
myocardial cell death (necrosis). It occurs when myocardial tissue is abruptly
and severely deprived of oxygen. If the blood supply is disrupted for 15-20
minutes or more, the “starving” part of the heart dies since cardiac cells can
withstand ischemic conditions for approximately 20 minutes before cell death
begins. This site destruction (necrosis) of cardiac cells is called myocardial
infarction. Blood flow to the appropriate department of the cardiac muscle is
disrupted when atherosclerotic plaque, located in the lumen of one of the
walls of the heart, the load is destroyed and the damaged spot forms a blood
clot (thrombus), and the person feels unbearable pain behind the breastbone

○ Cardiac cells can withstand ischemic conditions for approximately 20 minutes

before cell death begins. The earliest tissue to become ischemic is the
subendocardium (the innermost layer of tissue in the cardiac muscle). If
ischemia persists, it takes approximately 4 to 6 hours for the entire thickness
of the heart muscle to become necrosed. If the thrombus is not completely
blocking the artery, the time to complete necrosis may be as long as 12 hours.

Heart attacks can cause damage to how the heart functions and complications which
may result include:

● Abnormal heart rhythms (arrhythmias). Electrical "short circuits" can develop,

resulting in abnormal heart rhythms, some of which can be serious, and may lead
to death.
● Heart failure. A heart attack might damage so much heart tissue that the
remaining heart muscle can't pump enough blood out of your heart. Heart failure
can be temporary, or it can be a chronic condition resulting from extensive and
permanent damage to your heart.
 ● Sudden cardiac arrest. Without warning, your heart stops due to an electrical
disturbance that causes an abnormal heart rhythm (arrhythmia). Heart attacks
increase the risk of sudden cardiac arrest, which can cause death without
immediate treatment
● All of these cases can be treated but, in some cases, the complications of a heart
attack can lead to death.

Other complications:

● Cardiogenic shock
● Rupture
● Aneurysm
● Tamponade
● Heart valve damage
● Mural thrombus
● Repeat Heart attack

2. How does the progression of the etiologic changes lead to a life threatening
situation?

○ Myocardial infarction (MI) usually results from an imbalance in oxygen

supply and demand, which is most often caused by plaque rupture with
thrombus formation in an epicardial coronary artery, resulting in an acute
reduction of blood supply to a portion of the myocardium.
○ Non-modifiable Risk Factors: Sex, Age, Family history
○ Modifiable Risk Factors: Smoking, Dyslipidemia, Diabetes mellitus,
Hypertension, Obesity, Sedentary lifestyle, Poor oral hygiene, Presence of
peripheral vascular disease, Elevated levels of homocysteine.
○ Pathophysiology:
1. Endothelial cell injury and inflammation
2. Plaque Formation
3. Plaque rupture and thrombogenesis
4. Reduce blood supply and increased oxygen demand
5. Myocardial ischemia
6. Myocardial cell necrosis
7. Acute myocardial infarction
 3. What clinical presentations or presenting complaints are expected in clients
with the condition?

Cardiovascular
● Chest pain or discomfort not relieved by rest or nitroglycerin; palpitations. Heart
sounds may include S3, S4, and new onset of a murmur.
● Increased jugular venous distention may be seen if the myocardial infarction (MI)
has caused heart failure.
● Blood pressure may be elevated because of sympathetic stimulation or
decreased because of decreased contractility, impending cardiogenic shock, or
medications.
● Irregular pulse may indicate atrial fibrillation.
● In addition to ST-segment and T-wave changes, the electrocardiogram may show
tachycardia, bradycardia, or other dysrhythmias.
Respiratory
● Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused
pulmonary congestion. Pulmonary edema may be present.
Gastrointestinal
● Nausea, indigestion, and vomiting.
Genitourinary
● Decreased urinary output may indicate cardiogenic shock.
Skin
● Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation
may indicate cardiogenic shock.
Neurologic
● Anxiety, restlessness, and lightheadedness may indicate increased sympathetic
stimulation or a decrease in contractility and cerebral oxygenation. The same
symptoms may also herald cardiogenic shock.
Psychological
● Fear with feeling of impending doom, or denial that anything is wrong.

4. How are these signs and symptoms assessed?

The diagnosis of MI are basically based on the presenting symptoms stated
above.
The different laboratory test is used to differentiate the location and type of MI.
● ECG (to check whether it is unstable angina, NSTEMI, or STEMI)
● ABG/PulseOx
● Troponin level I and T
● Coronary Angiography
 ● Total Creatine kinase level
● CK-MB isoenzyme
● Myoglobin
● White blood cell count
*Physical examination is always conducted, but the examination alone does not confirm
the diagnosis.

5. What are the basic interventions for the condition?

A. Relieve pain
a. Morphine IV
b. Oxygen
c. Nitroglycerine
d. Aspirin
e. Anticoagulants
f. Thrombolytics
B. Reduce Heart Workload
a. Rest (Bed rest)
b. Position (Semi Fowlers)
c. Bedside commode
d. Stool softener
C. Diet
a. Low in fat/cholesterol (<50g/day)
b.
c. High in fiber (>30g/day)
d. Small frequent feedings
e. Calories (800-1200/day)
f. Soft foods
g. Avoid fried foods
D. Health Teaching
a. BP control
b. Exercise eg. walking
c. Avoid smoking/alcohol
d. Reduce Stress

Drug Dosage Action Nursing Side effects:

responsibilities

Vasodilat 0.3 to 0.4 mg/ Arterial and ● Ensuring Hypotension

ors 0.3 to 0.6 mg venous administration Tachycardia
Nitroglycer vasodilator. It of a therapeutic Flushed skin
in increases dose: Headache
coronary blood Sublingual: 0.3 Confusion
flow by dilating to 0.4 mg q 3 to Ethanol
the coronary 5 min intoxication (if
arteries. (maximum dose high doses of
Reduces is three tablets nitro is given
systolic, in 15 minutes); due to diluent)
diastolic, and Intravenous:
mean BP and Start infusion at
has antianginal, 5 mcg/min and
anti-ischemic, titrate every 3
and to 5 minutes
antihypertensiv until the desired
e effects. When response is
administered achieved.
sublingually to a ● Ensuring use
patient with with extreme
angina, it caution in
usually results patients with
in a reduction in hypotension;
pain in 3 to 5 monitoring for
minutes unresponsivene
ss and cardiac
dysrhythmias.
● Monitor blood
pressure every
3 to 5 minutes if
on intravenous
dose to
maintain SBP >
to 90 mmHg.
● If the patient’s
blood pressure
does decrease,
lowering the
head of the
bed, increasing
the rate of IV
fluids, or
decreasing the
dose of
nitroglycerin
temporarily
should resolve
the problem.
● Assess patients
 for a headache
(50% of
patients
develop this
effect).

Morphine 2 to 10 mg IV Opioid ● Obtaining Respiratory

Sulfate in divided analgesic, is baseline depression
doses used when respiratory rate, Orthostatic
chest depth and hypotension
discomfort is rhythm, and Constipation
not relieved with size of pupils. Opioid overdose
nitroglycerin, ● Recording pain (Antidote:
when the level and Naloxone)
patient duration of
becomes analgesia.
agitated, or ● Continuing to
when he or she monitor for
is experiencing respiratory
the complication depression.
of pulmonary
congestion.
Morphine helps
to increase the
coronary blood
flow by dilating
arteries and
veins while it
controls severe
pain and
anxiety. It also
reduces
preload, which,
in effect,
decreases the
workload of the
myocardial
tissue

Antiarrhyt 5 mg followed Beta blockers ● Administering a Bradycardia

hmic by two block the therapeutic Hypotension
Beta additional cardiac effects dose once the Heart blocks
Blockers doses at of patient’s Bronchospasm
5-minute beta-adrenergic hemodynamic and
 intervals for a stimulation; as a condition has dyspnea may
total of 15 mg result, heart stabilized also occur as
rate, myocardial following an MI. may indications
irritability, and ● AHA of poor
force of recommends perfusion such
contraction an initial as syncope,
decrease. They intravenous confusion, or
have dose of 5 mg of dizziness
also been metoprolol Contraindicated
associated with followed by two to people with
a decrease in additional COPD and
platelet doses at asthma
aggregability. 5-minute
When intervals for a
administered total of 15 mg.
intravenously The patient is
the effects converted to
occur within 1 to oral dosing if IV
2 minutes is tolerated.
● Observing
monitor pattern,
heart rate,
respiration,
blood pressure,
and circulation
closely during
administration.
● Administration
is stopped if
bradycardia,
heart block, or
hypotension
develop.
● Monitoring for
signs and
symptoms of
heart failure.

Thrombol 0.9 mg/kg (not Disintegrates ● Administer Streptokinase

ytics to exceed 90 blood clot by immediately • Hemorrhage
Streptokin mg total activating the after the event (intracranial of
ase treatment fibrinolytic for better greatest
tPA dose) infused processes. outcome, concern) and
Tenectopla over 60 Dissolve preferably anemia
se minutes. existing within 3 to 6 • Hypotension
10% of the thrombi rather hours. and fever
 treatment dose than prevent ● Monitor intake • Allergic
should be them from and output and reactions-itching
administered occurring. hematocrit , urticaria,
as an initial Treatment of during headache,
bolus over 1 acute treatment. anaphylaxis
minute myocardial ● Monitor patient
infarction, for bleeding Activase (tPA)
pulmonary and and
embolism, anaphylactic tenectoplase
thrombotic reactions. • Risk of
strokes, and ● While receiving intracranial
deep vein the medication, hemorrhage is
thrombosis maintain patient higher.
on bed rest. • Does not
cause
hypotension.

Antiplatel 160 to It inhibits ● The patient Bleeding

et 325 mg platelet should chew GI discomfort
Aspirin aggregation, the dose in the Tinnitus
reducing the acute phase to
ability of blood increase
to clot. It is used absorption.appr
to prevent opriate dosage.
recurrence of ● Monitoring
MI, and platelet count,
administered prothrombin
after time and
thrombolytic international
therapy. ratio unit in
Giving aspirin patients with
as soon as concurrent
possible inhibits anticoagulant
platelet activity therapy.
and ● Using
interrupts enteric-coated
platelet tablets to
aggregation at reduce
the site of gastrointestinal
plaque rupture. disturbances.
PRESENTATION PPT:

● https://drive.google.com/file/d/1IhBdAtjo3loPGcI64vHHfcSfoQQ08l7k/view?usp=sharing

Group 3 (2-2:30 pm) - Vascular Insufficiency (Shock)

What is Shock?
Shock can best be defined as a condition in which wide- spread perfusion to the cells is inadequate to deliver
oxygen and nutrients to support vital organs and cellular function (VonRueden, Bolton & Vary, 2008).

1. What makes the condition life threatening?

- Shock is a life-threatening condition because the body is not getting enough blood flow to the
vital organs such as the brain, heart, and lungs. Lack of blood flow in the body means the cells
and organs do not get enough oxygen and nutrients to function properly. If the blood flow is not
restored, the person may die from complications due to lack of oxygen supply to major organs
(hypoxia).
- It is a life-threatening condition of circulatory failure and most commonly manifested as
hypotension (systolic blood pressure less than 90 mm Hg or Mean Arterial Pressure of less than
65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal
without timely management.

2. How does the progression of the etiologic changes lead to a life threatening situation?
Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or
inadequate oxygen utilization leading to cellular and tissue hypoxia. Because of the inadequate tissue
perfusion, not enough oxygen is delivered to the tissues that would eventually develop into ischemia.
When ischemia happens over a long period of time, the tissues would become necrotic and would
possibly lead to organ failure if left untreated. The progression of the etiologic changes leading to life
threatening situations can be separated into four stages: initial stage, compensatory stage, progressive
stage, and irreversible stage.

In the initial stage, cardiac output is low enough to cause the cells to experience hypoxia. The
cells will switch from aerobic to anaerobic metabolism. Anaerobic metabolism will create lactic acid,
which will accumulate in the blood and lead to lactic acidosis.
In the compensatory stage of shock, the body systems are coming to the rescue. Hence, they are
going to “try” to compensate by using the body’s natural built-in survival team: the hormonal, neural, and
biochemical processes in the body. This built-in system will try to fight the results of anaerobic
metabolism. In this stage, the BP remains within normal limits. Vasoconstriction, increased heart rate,
and increased contractility of the heart contribute to maintaining adequate cardiac output. This results
from stimulation of the sympathetic nervous system and subsequent release of catecholamines (e.g.,
epinephrine, norepinephrine). The body shunts blood from organs such as the skin, kidneys, and
gastrointestinal (GI) tract to the brain, heart, and lungs to ensure adequate blood supply to these vital
organs.

In the progressive stage of shock, the mechanisms that regulate BP can no longer compensate,
and the MAP falls below normal limits. Patients are clinically hypotensive; this is defined as a systolic BP
of less than 90 mm Hg or a decrease in systolic BP of 40 mm Hg from baseline. The patient is progressing
 to MODS (multiple organ dysfunction syndrome). The cells will start to swell (the ion pumps are failing)
and capillary permeability is increased.

The irreversible (or refractory) stage of shock represents the point along the shock continuum
at which organ damage is so severe that the patient does not respond to treatment and cannot survive.

It is a life-threatening condition of circulatory failure and most commonly manifested as

hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final
manifestation of a complex list of etiologies and could be fatal without timely management. There are
mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive.

1. Distributive Shock
Characterized by peripheral vasodilatation. Types of distributive shock include:
a. Septic Shock
Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated
host response to infection.
b. Anaphylactic Shock
A clinical syndrome of severe hypersensitivity reaction mediated by
immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory
distress due to bronchospasm. The immediate hypersensitivity reactions can
occur within seconds to minutes after the presentation of the inciting antigen.
c. Neurogenic Shock.
Can occur in the setting of trauma to the spinal cord or the brain. The underlying
mechanism is the disruption of the autonomic pathway resulting in decreased
vascular resistance and changes in vagal tone.
2. Hypovolemic Shock
Characterized by decreased intravascular volume and increased systemic venous
assistance (compensatory the mechanism to maintain perfusion in the early stages of
shock). In the later stages of shock due to progressive volume depletion, cardiac output
also decreases and manifests as hypotension. Hypovolemic shock divides into two broad
subtypes: hemorrhagic and nonhemorrhagic.
3. Cardiogenic Shock
Occurs when either systolic or diastolic dysfunction of the heart’s pumping action results
in reduced cardiac output (CO). Due to intracardiac causes leading to decreased cardiac
output and systemic hypoperfusion.
4. Obstructive Shock
Develops when a physical obstruction to blood flow occurs with a decreased CO. Mostly
due to extracardiac causes leading to a decrease in the left ventricular cardiac output
● Pulmonary vascular - due to impaired blood flow from the right heart to the left
heart.
● Mechanical - impaired filling of the right heart or due to decreased venous return
to the right heart due to extrinsic compression.

3. What clinical presentations or presenting complaints are expected in clients with the condition?
a. Cardiovascular changes - start with decreased mean arterial pressure (MAP) leading to
compensatory responses. Increased heart rate is the first sign of shock.
 i. Decreased cardiac output
ii. Increased pulse rate
iii. Thready pulse
iv. Decreased blood pressure
v. Narrowed pulse pressure
vi. Postural hypotension
vii. Low central venous pressure
viii. Flat neck and hand veins in dependent positions
ix. Slow capillary refill in nail beds
x. Diminished peripheral pulses
b. Respiratory changes - are an adaptive response to help maintain gas exchange when tissue
perfusion is decreased.
i. Increased respiratory rate
ii. Shallow depth of respirations
iii. Increased PaCO2
iv. Decreased PaO2
v. Cyanosis, especially around lips and nail beds
c. Gastrointestinal changes
i. Decreased motility
ii. Diminished or absent bowel sounds
iii. Nausea and vomiting
iv. Constipation
d. Neuromuscular changes
i. Early
1. Changes in mental status and behavior
2. Restlessness
3. Increased thirst
ii. Late
1. Decreased central nervous system activity (lethargy to coma)
2. Generalized muscle weakness
3. Diminished or absent deep tendon reflexes
4. Sluggish pupillary response to light
e. Kidney changes - occur with shock to compensate for decreased mean arterial pressure (MAP)
by saving body water through decreased filtration and increased water reabsorption.
i. Decreased urine output
ii. Increased specific gravity
iii. Sugar and acetone present in urine
f. Integumentary changes - occur because of reduced blood flow in the skin. An early
compensatory mechanism is skin blood vessel constriction, which reduces skin perfusion. This
allows more blood to perfuse the vital organs, which cannot tolerate low oxygen levels.
i. Cool to cold
ii. Pale to mottled to cyanotic
iii. Moist, clammy skin
iv. Mouth dry; pastelike coating present
 g. Hematologic changes - The combination of hypotension, sluggish blood flow, metabolic acidosis,
coagulation system imbalance, and generalized hypoxemia can interfere with normal hemostatic
mechanisms.
i. Bruises (ecchymoses)
ii. Bleeding (petechiae)

4. How are these signs and symptoms assessed?

- Although no single laboratory finding confirms or rules out shock, changes in laboratory data may
support the diagnosis. (Chart 39-2 lists laboratory changes occurring with hypovolemic shock.)
- A focused history should be obtained from the patient (if feasible) and/or patient's relatives. Also, a
review of the patient’s outpatient medical records (information regarding risk factors, medications, and
trend of baseline vital signs including blood pressure), as well as hospital medical records, could give
valuable clues regarding the patient's risk for shock and potential etiology. Clinical features and
symptoms can vary according to the type and stage of shock. The most common clinical features/labs
which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal
mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia
- Patients with hypovolemic shock can have general features as mentioned above as well as
evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have
sequelae of chronic liver disease (in case of variceal bleeding).
- Patients with septic shock may present with symptoms suggestive of the source of infection
(example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-
tissue infections), and cutaneous manifestations of infective endocarditis.
- Patients with anaphylactic shock can have hypotension, flushing, urticaria, tachypnea,
hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of
exposure to common allergens such as medications or food items the patient is allergic to or
insect stings.
- Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock
had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous
pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.
- Decreased tissue perfusion in shock leads to an elevation of lactate and a base deficit (the
amount needed to bring the pH back
to normal). These laboratory
changes may reflect an increase in
anaerobic metabolism.
Diagnostic studies include:
- 12-lead electrocardiogram, (ECG), continuous ECG monitoring (ECGs might show
evidence of acute coronary syndrome, arrhythmias, or provide diagnostic clues
suggestive of pericardial effusion or pulmonary embolism.), chest x-ray, continuous
pulse oximetry, and hemodynamic monitoring (e.g., arterial pressure, central
venous or PA pressure, ScvO2/SvO2).
- CT scans can also assist in unmasking the etiology of shock in appropriate clinical
scenarios
- Blood pressure measurement. People in shock have very low blood pressure.
- Electrocardiogram (ECG or EKG). This quick, noninvasive test records the
electrical activity of your heart using electrodes attached to your skin. If you have
damaged heart muscle or fluid buildup around your heart, the heart won't send
electrical signals normally.
- Chest X-ray. A chest X-ray shows the size and shape of your heart and whether
there's fluid in your lungs. To look for the source of infection such as pneumonia,
complications of shock such as ARDS, clinical findings supporting the diagnosis of
pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection.
- Blood tests. You'll have blood drawn to check for organ damage, infection and
heart attack. An arterial blood gas test might be done to measure oxygen in your
blood.
- Echocardiogram. Sound waves produce an image of your heart. This test can help
identify damage from a heart attack.
- Cardiac catheterization (angiogram). This test can reveal blocked or narrowed arteries. A
doctor inserts a long, thin tube (catheter) through an artery in your leg or wrist and guides
 it to your heart. Dye flows through the catheter, making your arteries more easily seen on
X-ray.

5. What are the basic interventions for each condition?

a. Support of the respiratory system with supplemental oxygen and/or mechanical
ventilation to provide optimal oxygenation
i. Ensuring that the patient has a patent airway.
ii. Supplemental oxygen and mechanical ventilation may be necessary to
maintain an arterial oxygen saturation of 90% or more (PaO2 greater than
60 mm Hg) to avoid hypoxemia
b. Fluid replacement to restore intravascular volume
i. The goal for fluid resuscitation is restoration of tissue perfusion.
 ii. Currently, isotonic crystalloids, such as normal saline, are used in the initial
resuscitation
1. crystalloids
2. colloids
3. blood components

c. Vasoactive medications to restore vasomotor tone and improve cardiac function

d. Nutritional support to address the metabolic requirements that are often

dramatically increased in shock
i. May require more than 3000 calories daily.
ii. Enteral/ Parenteral Feeding
1. Enteral nutrition should be started within the first 24 hours.
 2. Start the patient on a slow continuous drip of small amounts of
enteral feedings (e.g., 10 mL/hr).
iii. Weigh the patient daily on the same scale at the same time of day. If the
patient experiences a significant weight loss, rule out dehydration before
adding more calories.
Nursing Management/ Interventions:
● Focus your initial assessment on the ABCs: airway, breathing, and circulation.
● Obtain a brief history from the patient or significant other, including a description of the
events leading to the shock condition, time of onset and duration of symptoms, and a
health history
● Neurologic Status.
○ Assess the patient’s neurologic status, including orientation and level of
consciousness, at least every 1 to 2 hours.
● Cardiovascular Status.
○ Continuously assess heart rate and rhythm, BP, CVP, and PA pressures, including
CO, SVR, and SVV
○ Assess heart sounds for an S3 or S4 sound or new murmurs.
● Assess the patient’s response to fluid and medication administration as often as every 10
to 15 minutes.
● Respiratory Status.
○ Initially monitor the rate, depth, and rhythm of respirations as frequently as every
15 to 30 minutes.
○ Assess breath sounds every 1 to 2 hours and as needed.
○ Initial interpretation of ABGs is often your responsibility.
● Renal Status.
○ Initially, measure urine output every 1 to 2 hours to assess the adequacy of renal
perfusion.
● Body Temperature and Skin Changes.
○ Monitor temperature every 4 hours if normal.
○ Monitor the patient’s skin for signs of adequate perfusion. Changes in
temperature, pallor, flushing, cyanosis, diaphoresis, and piloerection may indicate
hypoperfusion.
● Gastrointestinal Status.
○ Auscultate bowel sounds at least every 4 hours, and monitor for abdominal
distention. If a nasogastric tube is present, measure drainage and check for occult
blood.
● Personal Hygiene.
○ Perform bathing and other nursing measures carefully because a patient in shock
is experiencing problems with oxygen delivery to tissues.
○ Turn the patient at least every 1 to 2 hours and maintain good body alignment to
help prevent pressure ulcers.
 ○ Use a pressure-relieving or pressure-reducing mattress or a specialty bed as
needed.
○ Perform passive range of motion three or four times a day to maintain joint
mobility.
○ Apply a water-soluble lubricant to the lips to prevent drying and cracking.
○ Brush the patient’s teeth or gums with a soft toothbrush every 12 hours, and swab
the lips and oral mucosa with a moisturizing solution every 2 to 4 hours.
● Emotional Support and Comfort.
○ Talk to the patient and encourage the caregiver to talk to the patient, even if the
patient is intubated, is sedated, or appears comatose.
○ Provide the patient with simple explanations of all procedures before you carry
them out, as well as information regarding the current plan of care.
○ Provide privacy as much as possible, but assure the patient and caregiver that
assistance is readily available should it be needed.
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem

NCM 71 LEC: Metabolic Insufficiency (DKA and HHS)

Diabetic Ketoacidosis (DKA)

1. What makes the condition life-threatening?

● Diabetic ketoacidosis (DKA) is a life-threatening problem that affects people with diabetes. It occurs when
the body starts breaking down fat at a rate that is much too fast. The liver processes the fat into a fuel called
ketones, which causes the blood to become acidic.
● The fat is broken down by the liver into a fuel called ketones. Ketones are normally produced by the liver
when the body breaks down fat after it has been a long time since your last meal. These ketones are
normally used by the muscles and the heart. When ketones are produced too quickly and build up in the
blood, they can be toxic by making the blood acidic. This condition is known as ketoacidosis.
● Health problems that may result from DKA include any of the following:
● Fluid buildup in the brain (cerebral edema)
○ as brain swelling. It's a life-threatening condition that causes fluid to develop in the brain.
This fluid increases the pressure inside of the skull — more commonly referred to as
intracranial pressure (ICP).
● Heart stops working (cardiac arrest)
● Kidney failure
○ DKA is associated with hyperglycemic crises and featured by metabolic acidosis, the
production of ketoacids, volume depletion, and electrolyte imbalance. Due to glucose-
induced osmotic polyuria and even emesis, volume depletion is a major cause of acute
kidney injury (AKI) in DKA patients [3].
2. How does the progression of the etiologic changes lead to a life-
threatening situation?
➔ Simplified pathophysiology:

Diabetes-related ketoacidosis (DKA) is caused by a profound

deficiency of insulin. It is characterized by hyperglycemia,
ketosis, acidosis, and dehydration
1. Precipitating factors: Type 1 or 2 DM, (mostly type 1); severe
stress, illness; infection; inadequate insulin dosage;
undiagnosed type 1 diabetes; lack of education, understanding,
or resources; and neglect.
2. Insulin deficiency: When the circulating supply of insulin is
insufficient, glucose cannot be properly used for energy.
3. Increased protein catabolism & lipolysis. The body
compensates by breaking down fat stores and amino acids as
secondary sources of fuel (Ketogenesis & Gluconeogenesis)
4. Ketoacidosis & Hyperglycemia. Wherein, apart from the
cardinal signs of DM, ketosis alters the pH balance, causing
metabolic acidosis and ketonuria along with glycosuria. All of
which may exacerbate volume depletion, further contributing to:
5. DIABETIC KETOACIDOSIS
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem
The patient may eventually become comatose due to dehydration, electrolyte imbalance and acidosis. If left untreated,
death is inevitable.

3. What clinical presentations or presenting complaints are expected in clients with the condition?

Dehydration occurs in DKA with manifestations of poor skin turgor, dry mucous membranes, tachycardia,
and orthostatic hypotension. Early symptoms may include lethargy and weakness. As the patient becomes severely
dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken. Abdominal pain may be present
and accompanied by anorexia, nausea, and vomiting. 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. 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.

4. How are these signs and symptoms assessed?

Blood tests are used to test for Diabetic Ketoacidosis, the following are measured to arrive at a definite diagnosis:

1. Blood Sugar Level

- If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level
will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar
level will continue to rise.
- The plasma glucose concentration required to diagnose for DKA is above 250 mg per dL (although
it is usually much higher) or 11 mmol/L and above

2. Ketone Level
- When your body breaks down fat and protein for energy, acids known as ketones enter your
bloodstream.
- Slightly increased risk for DKA- 0.6 to 1.5 mmol/L
- Increased risk for DKA- 1.6 to 2.9 mmol/L
- Very high risk for DKA- 3 mmol/L and above
- During a urine ketone test, a result of more than 2+ will indicate a high chance of DKA and you should
get medical help immediately

3. Blood Acidity
- If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the
normal function of organs throughout your body.
- The pH levels are less than 7.30, and the bicarbonate levels are 18 mEq per L or less

Other tests may be used to also identify underlying problems include:

- Blood electrolyte tests- During diabetic ketoacidosis, there may be rapid shifts in the plasma concentration
of potassium ions. Although diabetic ketoacidosis leads to a deficit in total-body stores of potassium ion, the
plasma concentration is usually normal or elevated, since the acidemia leads to the exit of potassium ions
from cells.
- Osmotic diuresis is associated with large losses of electrolytes in urine, so that patients with DKA typically
have a whole-body sodium and potassium deficit of 500-700 mmol and 200-300 mmol, respectively.
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem
- Urinalysis - Ketones can also enter the urine, so a doctor can use a urine test to detect DKA. People with
diabetes can do a urine test at home if they start to experience the signs and symptoms of DKA. According to
the American Diabetes Association, symptoms of DKA include: a “fruity” or acetone smell on the breath.

- Chest X-ray - Chest radiography helps rule out pulmonary infections, such as pneumonia

- ECG- Diabetic ketoacidosis (DKA) can cause changes in the electrocardiogram (ECG) in the form of transient
ST-segment depression, QT prolongation, changes in T-wave morphology and the appearance of U
wave, possibly due to changes in the serum potassium level.

Hyperosmolar Hyperglycemic State (HHS)

1. What makes the condition life-threatening?

● Hyperosmolar hyperglycemic syndrome (HHS) is a serious complication of diabetes mellitus. HHS occurs
when a person’s blood glucose (sugar) levels are too high for a long period, leading to severe dehydration
(extreme thirst) and confusion.
● People who develop HHS are often already ill.
● HHS is a very serious medical condition. If it is not treated, it can lead to:
○ Seizures.
○ Coma.
■ The serum osmolality is very high in HHS. Levels between 320 to 400mOsm/kg are very
common in HHS. Normal serum osmolarity is around 280 -290 mOsm/kg. Higher serum
osmolarity is associated with alteration in the level of consciousness and might eventually
lead to a coma
○ Swelling of the brain.
■ a rare, but frequently fatal, complication in HHS.
■ Cerebral edema occurs from rapid lowering of glucose levels and an ensuing rapid drop in
plasma osmolarity.
○ Organ failure.
■
○ Death.
■ Overall mortality for HHS is estimated at 5-20% and is usually due to the underlying
illness that caused the hyperglycemic crisis. Prognosis is worse for elderly patients and
patients in whom coma and hypotension are found

2. How does the progression of the etiologic changes lead to a life-threatening situation?
➔ Simplified pathophysiology:
Hyperglycemic hyperosmolar syndrome (HHS) is a life threatening emergency created by a relative insulin
deficiency and significant insulin resistance, resulting in severe hyperglycemia with profound osmotic
diuresis, leading to life-threatening
dehydration and hyperosmolality.
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem

1. State is triggered by physiologic stress such as

infections, cardiovascular diseases, inadequate diabetic
treatment, or drugs (e.g. steroids and diuretics). Stress
stimulates sympathetic nervous system which releases
epinephrine, norepinephrine, and glucagon.
2. These three hormones act on the liver, which
promotes gluconeogenesis, and glycogenolysis. Glucose level
increases.
3. Insulin level is too low to prevent hyperglycemia,
although high enough to prevent fat breakdown. Extreme
hyperglycemia occurs, which causes the blood to become
very concentrated, resulting in hyperosmolarity.
4. The hyperosmolarity of blood (that contains very
high levels of glucose) causes water to be pulled out from
the cells, and cells shrivel up and become dehydrated.
5. Kidneys can’t absorb all of the glucose, so it leaks to
the urine, which causes osmotic diuresis that pulls the
water as well as electrolytes out (Na+, K+, Cl-). This leads to
dehydration or hypovolemia, which, when left untreated,
can cause shock, coma, or even death.

3. What clinical presentations or presenting complaints are expected in clients with the condition?

Physical findings in patients with HHS include profound dehydration with poor skin turgor; dry buccal mucosa; soft,
sunken eyeballs; cool extremities; and a rapid, thready pulse. Adults often present with a low-grade fever. Children
may present with nonspecific symptoms such as headache, weakness, and vomiting with or without abdominal pain.
Abdominal distention may occur secondary to gastroparesis induced by hypertonicity. Abdominal distention that
persists after rehydration may have another underlying cause and requires further investigation.

Depending on effective serum osmolarity, mental status can range from complete lucidity to disorientation and
lethargy to coma. Coma often occurs once the serum osmolarity is greater than 340 mOsm per kg. Seizures occur in
up to 25% of patients and may be generalized, focal, myoclonic jerking, or movement induced. Hemiparesis may
occur but should resolve when the fluid deficit is corrected.
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem
4. How are these signs and symptoms assessed?

Blood tests are used to test for Hyperosmolar Hyperglycemic Syndrome, the following are measured to arrive at a
definite diagnosis:

1. Blood Sugar Level

- If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level
will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar
level will continue to rise.
- The plasma glucose concentration required to diagnose for HHS is above 600 mg per dL
- In the absence of ketoacidosis, an increased effective plasma osmolality of greater than 320
mOsm/kg is used to make a diagnosis for HHS

2. Ketone Level
- When your body breaks down fat and protein for energy, acids known as ketones enter your
bloodstream
- Low ketone levels will also help the physician in making a diagnosis for HHS
- The urine ketone concentration is usually less than 1.5 mmOl/L

3. Blood Acidity
- If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the
normal function of organs throughout your body.
- The pH levels are less than 7.30, and the bicarbonate levels are 20 mEq per L or less

5. What are the basic interventions for DKA and HHS?

Dehydration - 0.9% normal saline

Kill the sugar SLOWLY
- over 250 BS we give IV Regular Insulin only
- below 200 BS (or ketones resolve) = SQ Insulin + D5W
Add potassium (even if normal)
- during IV insulin

Hydration 0.9% normal saline

Stabilize the sugars
- IV Regular Insulin only
- IV drip ---> IV titration ---> SQ injection & IV ----> SQ only

● Immediate IV Insulin
● 0.9% or 0.45% NaCl for fluid replacement
● Dextrose
● Electrolyte replacement
 NCM 71 LEC Common Acutely Ill/Multi-Organ Problem
Monitoring

● Assess for signs of potassium imbalance

● Assess vital signs and mental status
● Closely monitor blood and urine tests for ketones.
● Monitor Intake and Output
● Cardiac and Respiratory monitoring
● Interpreting ABG results

BRIEF SUMMARY:
➔ Main difference between the two:
The main difference between HHS and DKA is that the patient with HHS usually has enough circulating
insulin so that ketoacidosis does not occur. Because HHS has fewer symptoms in the earlier stages, blood
glucose levels can climb quite high before the problem is recognized. The higher blood glucose levels
increase serum osmolality and cause more severe neurologic manifestations (i.e., somnolence, coma,
seizures, hemiparesis, and aphasia) (Lewis, 2019).
 NCM 71 LECTURE
RENAL INSUFFICIENCY (END-STAGE RENAL DISEASE) HANDOUT

Answer the following questions:

1. What makes the condition life threatening?
End-Stage Renal Disease (ESRD) or also called End-stage kidney disease (ESKD), is the fifth
and final stage of chronic kidney disease (CKD) progression. CKD is a progressive, irreversible
disorder where kidney function does not recover. When kidney function is too poor to sustain life, CKD
becomes end-stage kidney disease (ESKD). Terms used with kidney dysfunction include azotemia
(buildup of nitrogen-based wastes in the blood), uremia (azotemia with clinical symptoms, and uremic
syndrome. Commented [1]: IGNATCVICIUS

Going back, ESKD marks the point when kidney function drops to very low levels (below 10%
of their normal ability) which may mean they’re barely functioning or not functioning at all. The
glomerular filtration rate (GFR) of ESRD is <15 ml/min/1.73 m2. As renal function declines, the end
products of protein metabolism (normally excreted in urine) accumulate in the blood. Because of this,
Uremia develops and adversely affects every system in the body. The greater the buildup of waste
products, the more pronounced the symptoms are. The rate of decline in renal function and Commented [2]: Brunner and Suddarth
progression of ESRD is related to the underlying disorder, the disease also tends to progress more Commented [3]: THANK YOUU
rapidly in patients who excrete significant amounts of protein or have elevated blood pressure than in
those without these conditions. Commented [4]: Brunner and Suddarth

Kidney failure is life threatening, but dialysis or transplantation can relieve weakened kidneys. Commented [5]: THANK YOUU

This means the kidneys can’t:

● Filter blood to remove waste, extra water and acid.

● Help the body maintain a healthy balance of water, salt and minerals such as potassium, calcium
and magnesium.
● Make urine, or pee, so the body can remove waste.
● Make hormones to help control blood pressure, keep bones strong and create red blood cells to
prevent anemia.

Because the kidneys are highly adaptive, kidney disease is often not recognized until there has been
considerable loss of nephrons. Patients with CKD are often asymptomatic, resulting in CKD being
underdiagnosed and untreated.

2. How does the progression of the etiologic changes lead to a life threatening situation?
● The most common cause of sudden death in patients with ESRD is hyperkalemia, which often
follows missed dialysis or dietary indiscretion.
ETIOLOGICAL FACTORS
Category Diseases
Congenital/hereditary disorders Polycystic kidney disease, renal tubular acidosis

Connective tissue disorders Progressive systemic sclerosis, systemic lupus

erythematosus

Infections/inflammatory conditions Chronic pyelonephritis, glomerulonephritis, tuberculosis

Vascular disease Hypertension, renal nephrosclerosis, renal artery stenosis

Metabolic/endocrine diseases Diabetes mellitus, gout, amyloidosis, hyperparathyroidism

Obstructive diseases Renal calculi

Nephrotoxic conditions Medication therapy, drug overdose

  Stages of Chronic Kidney Disease
The kidneys lose function (fail) in an organized fashion involving five stages based on estimated
glomerular filtration rate (GFR).
Progression toward ESKD usually starts with a gradual decrease in GFR.
In this first stage, the person may have a normal GFR (greater than 90 mL/min) with normal kidney
function and no obvious kidney disease. However, there may be a reduced renal reserve in which
reduced kidney function occurs without buildup of wastes in the blood because the unaffected
nephrons overwork to compensate for the diseased nephrons. Although no manifestations of kidney
dysfunction are usually present at this stage, if the patient is stressed with infection, fluid overload,
pregnancy, or dehydration, kidney function at this stage can appear reduced.
In the next stage, mild CKD, GFR is reduced, ranging between 60 and 89mL/min. Kidney nephron
damage has occurred, and there may be slight elevations of metabolic wastes in the blood because
not enough healthy nephrons remain to compensate completely for the damaged nephrons. Levels of
blood urea nitrogen (BUN), serum creatinine, uric acid, and phosphorus are not sensitive enough to
define this stage, however, and reduced GFR is the best measure of CKD. Increased output of dilute
urine may occur at this stage of CKD and, if the problem is untreated at this stage, can cause severe
dehydration.
In moderate CKD, GFR reduction continues and ranges between 30 and 59 mL/min. Nephron
damage has continued, and the remaining nephrons cannot manage metabolic wastes, fluid balance,
and electrolyte balance. Restriction of fluids, proteins, and electrolytes is needed.
Over time, patients progress to severe CKD (the fourth stage) and end-stage kidney disease
(ESKD) (the fifth stage). Excessive amounts of urea and creatinine build up in the blood, and the
kidneys cannot maintain homeostasis. Severe fluid, electrolyte, and acid-base imbalances occur
(Pradeep & Verrelli, 2010). Without renal replacement therapy, fatal complications occur. Commented [6]: @francisuestolloso@su.edu.ph

3. What clinical presentations or presenting complaints are expected in clients with the
condition?

CLINICAL PRESENTATIONS/ PRESENTING COMPLAINTS

● Because virtually every body system is affected in ESRD, patients exhibit a number of signs
and symptoms (Broscious & Castagnola, 2006).
● The severity of these signs and symptoms depends in part on the degree of renal impairment,
other underlying conditions, and the patient’s age.
● Cardiovascular disease is the predominant cause of death in patients with ESRD (Burrows
& Muller, 2007).
● Peripheralneuropathy, a disorder of the peripheral nervous system, is present in some
patients.
● Patients complain of severe pain and discomfort.
● Restless leg syndrome and burning feet can occur in the early stage of uremic peripheral
neuropathy (Phillips & Ryr, 2005; Slack & Landis, 2006).
● The precise mechanisms for many of these systemic signs and symptoms have not been
identified.
● However, it is generally thought that the accumulation of uremic waste products is the
probable cause.
● ESRD - is characterized by two groups of clinical manifestations: deranged excretory and
regulatory mechanisms and a distinctive grouping of GI, CDV, Neuromuscular,
hematologic, integumentary, skeletal, and hormonal manifestations. The kidneys can no
longer maintain homeostasis
● The clinical manifestations of CRF are present throughout the body. No organ system is
spared. Renal alterations include the kidney’s inability to concentrate urine and regulate
electrolyte excretion.
○ Polyuria progresses to anuria, and the client loses normal diurnal patterns of voiding.
In addition, all normal functions of the kidney become curtailed and are eventually lost.
 4. How are these signs and symptoms assessed?

ASSESSMENT DEFINITION IMPLICATION

● Screening ● Includes weight, intake Increased incidence in hypertensive,

Indications and output balance, skin and diabetic patients, cardiovascular
turgor, presence of disease, aging population, history of
edema, vital signs, low birth weight, obesity, and a family
personal health history, history of kidney failure.
family's health history,
physical examination,
and neurological
examination

● Renal ultrasound, ● Provide data estimating Reduced renal cortical thickness <6
Renal Scan size, obstructions, mm, reduced renal length, increased
stones, cystic renal renal cortical echogenicity, poor
disease, mass lesions, visibility of the renal pyramids and the
 echogenicity, and renal sinus, marginal irregularities,
cortical thinning. papillary calcifications, and cysts.

● Urinalysis/ urine test ● Checks for presence of Persistent proteinuria is usually the
for albumin-to- protein albumin and first indication of kidney damage. A
creatinine ratio blood in urine. These value higher than 30 mg of albumin
substances indicate that per gram of creatinine is considered
the kidneys aren’t abnormal, while values greater than
processing waste 300mg/g are considered severely
properly. Urine impaired renal function.
albumin/creatinine ratio
provides an accurate
estimate of the protein
and albumin excretion
rate.

● BUN, Serum ● These tests check the The creatinine

creatinine, and renal function. The BUN clearance decreases, whereas the
creatinine clearance test measures the serum creatinine and BUN levels
levels amount of urea nitrogen increase.
in your blood. Testing
the rate of creatinine
clearance shows the
kidneys' ability to filter
the blood.

● Estimated ● Measures how much GFR of less than 15 mL/min

glomerular filtration blood the kidneys filter
rate (GFR) each minute, recorded
as milliliters per minute
(mL/min). As the GFR
declines, so does kidney
function.

● Complete blood ● Blood work will In ESRD, erythropoietin production

count (CBC) determine if there is decreases and
secondary anemia and profound anemia results, producing
will detect evidence of fatigue, angina, and shortness of
electrolyte breath.
derangement.

● Arterial Blood Gas ● A test that is performed Metabolic acidosis occurs in ESRD
Analysis to measure the pH and because the kidneys are unable to
the amount of oxygen, excrete increased loads of acid.
and carbon dioxide Decreased acid secretion results
present in a sample of from the inability of the kidney tubules
blood in order to detect to excrete ammonia and to reabsorb
an acid-base imbalance sodium bicarbonate. There is also
that could indicate decreased excretion of phosphates
kidney disorder. and other organic acids.
 ● Phosphorus test and ● Phosphorus tests are With a decrease in filtration through
calcium test most often ordered the glomerulus of the kidney, there is
along with other tests, an increase in the serum phosphate
such as those for level and a reciprocal decrease in the
calcium, parathyroid serum calcium level. This may also
hormone (PTH), and/or lead to bone changes and bone
vitamin D, to help disease as well as calcification of
diagnose and/or monitor major blood vessels in the body.
treatment of various
conditions that cause
calcium and phosphorus
imbalances.

● Renal biopsy ● Obtains renal tissue for Necessary if the etiology remains
examination to unclear
determine type of kidney
disease or to follow
progress of kidney
disease, how severe it
is, and the best
treatment for it. A renal
biopsy can also be used
to monitor the
effectiveness of kidney
treatments and see if
there are any
complications following
a kidney transplant.

5. What are the basic interventions for each condition?

CLINICAL BASIC INTERVENTION (Include Medications)

PRESENTATION/CONDITION

Hyperphosphatemia and ● Administer calcium and phosphorus binders as

Hypocalcemia ordered.

Ex. Calcium Carbonate (Os-Cal), Calcium Acetate

(PhosLo)

Because excess body stores of calcium leads to

calcification of the soft-tissue and vessel in chronic
kidney disease, the Kidney Disease Outcomes
Quality Initiative Guidelines suggest that doses
should not exceed 1500 mg/day of elemental calcium,
based on evidence that this promotes a positive
calcium balance. However, if calcium is high, or the
 calcium-phosphorus product exceeds 55mg/dL,
Sevelamer Hydrochloride (Renagel), a polymeric
phosphate binder, may be administered.
● Because phosphate elimination by the kidneys is
decreased as the kidneys deteriorate, limit phosphate
rich foods intake to around 1g/day. Foods that are
high in phosphate include meat and dairy products
(milk, ice cream, cheese, yogurt, pudding).

Hypertension and Cardiovascular
conditions
● Auscultate heart and lung sounds. Evaluate presence
of peripheral edema, vascular congestion and reports
of dyspnea. S3 and S4 heart sounds with muffled
tones, tachycardia, irregular heart rate, tachypnea,
dyspnea, crackles, wheezes,edema and jugular
distension suggest HF.

● Administer angiotensin - converting enzyme (ACE)

inhibitors and angiotensin receptor blockers (ARBs)
for blood pressure reduction.

Ex.
Captopril (Capoten), Clonidine
(Catapres),Hydralazine (Apresoline)

Losartan (Cozaar)
Olmesartan (Benicar)
Telmisartan (Micardis)

● Administer inotropic agents (Digoxin)

Strengthens the force of the heartbeat by increasing
the amount of calcium in the heart's cells. Calcium
stimulates the heart to contract.

● Dobutamine (Dobutrex)
Stimulates heart muscle and improves blood flow by
helping the heart pump better.

● Investigate reports of chest pain, noting location,

radiation, severity (0–10 scale), and whether or not it
is intensified by deep inspiration and supine position.
Although hypertension and chronic HF may cause MI,
patients with Renal Disease on dialysis develop
pericarditis, making them at risk of pericardial effusion
or tamponade.

Fluid Restriction

● Compare current weight gain with previously stated

weight to monitor fluid retention and evaluate degree
 of excess.

● Auscultate breath sounds for presence of crackles or

congestion.

● Monitor intake and output. Water and any other fluids

are not routinely restricted in patients with CKD stages
1 to 5 who are not receiving Hemodialysis (HD).
However, for those receiving HD, as their urine output
decreases, fluids are restricted.
● Teach patients to limit fluid intake so that weight gains
are no more than 1 to 3 kg between dialysis
(interdialytic weight gain).
● Check daily urine output for the recommended fluid
intake. To reduce fluid retention, diuretics
(Furosemide) are often administered as ordered.
Generally, 600 mL (according to insensible loss) plus
an amount equal to the previous day’s urine output is
allowed for a patient receiving HD.

● To reduce fluid retention, diuretics (Furosemide) are

often administered as ordered.

● Check food intake as foods that are liquid at room

temperature, such as ice and gelatin, are counted as
fluid intake.

● Space fluid allotment throughout the day so that the

patient does not become thirsty.

Sodium Restriction

● Recommended diets may vary from 2 to 4 g sodium

rich foods per day. These foods include cured meats,
cold cuts, soy sauce, pickled foods, canned soups,
and salad dressings.

Potassium Restriction

● Recommended diet includes potassium rich foods

restricted to 2-3 g per day. These foods include
potatoes, strawberries, bananas, spinach, avocados,
and oranges.

Anemia associated with ESRD ● Anemia does not cause kidney disease. Anemia is a
complication of CKD. Administer erythropoietin -
stimulating agents (recombinant human
erythropoietin). In ESRD, epoetin alfa is administered
 IV or subcutaneously 3 times a week in
ESRD. However, because it takes 2-6 weeks for the
hematocrit to increase, it is not indicated for patients
in need of immediate correction of severe anemia.
● Administer iron sucrose or ferric gluconate to build the
iron levels in your body, orally or intravenously as
ordered.

Convulsions ● To control seizures, administer IV diazepam (Valium)

or phenytoin.

● Raise side rails of the bed and add pads to protect the
patient.

Undergoing Dialysis ● A patient with increasing symptoms of kidney disease

is referred to a dialysis and transplantation center
early in the course of progressive kidney disease.
When the patient cannot maintain a reasonable
lifestyle with conservative treatment, this procedure is
usually initiated to help decrease the level of uremic
waste products in the blood and control electrolyte
balance.

● Patients with advanced CKD and ESRD who require

long-term or permanent renal replacement therapy
undergo Hemodialysis (HD).

● Patients with kidney disease who are unable or

unwilling to undergo hemodialysis or kidney
transplantation may opt for a peritoneal dialysis (PD).
This is usually indicated for older patients, with
diabetic or cardiovascular disease, and those at risk
for adverse effects of systemic heparin.
References:
 Benjamin, O., & Lappin, S.L. (2021, February 04). End-Stage Renal Disease. StatPearls.
Retrieved September 30, 2021 from https://www.ncbi.nlm.nih.gov/books/NBK499861/
 Black, J., Hawks, J., Keene, A. (2002). Medical-Surgical Nursing: clinical management for
positive outcomes 6TH ed. Saunders
 End stage renal disease (ESRD). Johns Hopkins Medicine. (n.d.). Retrieved October 1, 2021,
from https://www.hopkinsmedicine.org/health/conditions-and-diseases/end-stage-renal-
disease-esrd.
 Harding, M. M., Kwong, J., Roberts, D., Hagler, D., & Reinisch, C. (2020). Chapter 46: Acute
Kidney Injury and Chronic Kidney Disease. In Lewis’s Medical Surgical Nursing (11th ed.).
Elsevier Inc.
 Hinkle, J. L., & Cheever, K. H. (2018). Chapter 54: Management of Patients with Kidney
Disorders. In Brunner & Suddarth's Textbook of Medical-Surgical Nursing (14th ed., pp. 4172-
4207). Wolters Kluwer
 Ignatavicius, D. D., & Workman, M. L. (2013). Chapter 71: Care of Patients with Acute Kidney
Injury and Chronic Kidney Disease. In Medical-Surgical Nursing Patient-Centered Collaborative
Care (7th ed.). Elsevier Inc.
 Lab Tests Online. (2019, December 09). Blood Gases. Retrieved October 01, 2019 from
https://labtestsonline.org/tests/blood-gases
 Lab Tests Online. (2021, March 25). Phosphorus. Retrieved October 01, 2019 from
https://labtestsonline.org/tests/phosphorus
 Lewis, S.L., Dirksen, S.R., Heitkemper, & M.M., Bucher, L., (2013). Medical-Surgical Nursing:
Assessment and Management of Clinical Problems (9th ed.). Elsevier Health Sciences
 PHEOCHROMOCYTOMA HANDOUT
Aller | Baldado | Dagooc | Raging | Suminguit | Vera Cruz

I. What makes the condition life threatening?

Definition

Pheochromocytoma is a tumor that is usually benign and originates from the chromaffin cells of
the adrenal medulla that secretes excessive amounts of catecholamines. The release of these
neurotransmitters trigger the sympathetic nervous system.

Pheochromocytomas are rare endocrine tumors that can present insidiously and remain
undiagnosed until death or onset of clear manifestations of catecholamine excess. They are often referred
to as one of the ‘great mimics’ in medicine (Dar et al., 2012).

Pheochromocytoma Crisis

Pheochromocytoma multisystem crisis (PMC) is a feared and possibly fatal presentation of

pheochromocytoma. It can occur spontaneously or can be precipitated by triggers such as:
● Pressure on the tumor
● Massage
 ● Medications, especially anesthesia or beta-blockers
● Emotional stress
● Physical activity
● Childbirth
● Surgery
● Foods with a lot of the amino acid tyramine, such as red wine, chocolate, or cheese

If left untreated (such blood pressure elevations, etc. will cause:

Neurologic Manifestations: cerebrovascular accidents and seizures
Cardiac Manifestations: cardiomyopathy, myocarditis, myocardial ischemia and necrosis
secondary to coronary vasospasm, congestive heart failure, cardiac arrhythmias and cardiogenic
shock
Pulmonary Manifestations: pulmonary edema and acute respiratory distress syndrome
Gastrointestinal Manifestations: paralytic ileus and intestinal ischemia secondary to
vasoconstriction
Vascular Manifestations: peripheral thrombosis, embolism and vasospasm
Other Manifestations: acute liver failure, acute kidney injury, disseminated intravascular
coagulation, lactic acidosis, diabetic ketoacidosis and rhabdomyolysis

II. How does the progression of the etiologic changes lead to a life threatening situation?
➢ Although there is not much known about the condition, existing data have shown that
Pheochromocytoma may arise from familial disorders/pre-existing disorders or genetics.

➢ People who have certain rare inherited disorders (familial disorders) such as Multiple endocrine
neoplasia types A and B, Von Hippel-Lindau disease, Neurofibromatosis 1, and familial
pheochromocytoma have an increased risk of developing the condition. Likewise, approximately
25-35 percent of cases of pheochromocytomas may be from genetic disruptions or changes
(mutations) to certain genes.
➢ Various tumor suppressor proteins dysfunction and mutate (VHL, RET, SDH, and other similar
genes)
➢ Rapid increase of chromaffin cells in the medulla of the adrenal glands take place
➢ Formation of a benign tumor; Pheochromocytoma (detected through CT scan)
➢ Tumor triggers secretion of excessive amounts of catecholamine hormone (norepinephrine,
epinephrine)
➢ Episodic hyperactivity of the sympathetic nervous system; overstimulation of G protein-coupled
receptors
➢ Emergence of symptoms
○ Hyperglycemia, weight-loss, and fatigue - hyperstimulation of G protein-coupled
receptors result to enhanced lipolysis, glycogenolysis, gluconeogenesis causing increased
ability to mobilize glucose in the bloodstream
○ Diaphoresis (excessive sweating) - hyperactivity of the sympathetic nervous system
causes increased secretion from eccrine sweat glands
○ Panic, tremor, and anxiety - “fight or flight” response is activated due to overproduction
of catecholamines
○ Pallor - increased vasoconstriction of peripheral blood vessels by catecholamines
○ Hypertension - vasoconstriction of blood vessels raises blood flow resistance causing
higher blood pressure
○ Headache - high blood pressure activates neural pain receptors
○ Tachycardia, palpitations - increased production of catecholamines causes
hyperstimulation of adrenergic receptors of the cardiac myocytes resulting to increased
heart rate and myocardial contractility
➢ If left untreated, a pheochromocytoma can result in severe or life-threatening damage to other
body systems (Pheochromocytoma multisystem crisis) and may present with the following
complications:
○ Heart muscle disease (cardiomyopathy) - excessive catecholamine-induced stimulation
of cardiac myocytes leads to damage to the heart muscle.
○ Inflammation of the heart muscle (myocarditis) - catecholamine and their oxidation
products may have a toxic effect on the myocardium thus causing inflammation.
○ Cerebral hemorrhaging - may be due to the sudden fluctuations in the blood pressure.
○ Accumulation of fluid in the lungs (pulmonary edema) - may be due to
catecholamine-induced postcapillary venoconstriction resulting in a rise in
pulmonary-capillary hydrostatic pressure.
○ Severe cases might even lead to heart attack, stroke, and even death
III. What clinical presentations or presenting complaints are expected in clients
with the condition?

Clinical Manifestations

The nature and severity of symptoms of functioning tumors of the adrenal medulla depend on the
relative proportions of epinephrine and norepinephrine secretion. The typical triad of symptoms is
headache, diaphoresis, and palpitations in the patient with hypertension.

F - acial flushing, fluttering in chest

I - ncreasaed HR & BP (hypertension may be intermittent or persistent)
G - lucose, high (result from conversion of liver and muscle glycogen to glucose due to
epinephrine secretion; insulin may be required to maintain normal blood glucose levels)
H - eadaches (sudden & severe)
T- remors
F - requent sweating (↑ BMR, thermogenesis)
L - oss of weight
I - increased anxiety/fear
G - rowing tumor that cause abdominal pressure pain
H - eat intolerance
T - ired & weak

Pheochromocytoma Crisis
The clinical picture in the paroxysmal form of pheochromocytoma is usually characterized by
acute, unpredictable attacks lasting seconds or several hours. Symptoms usually begin abruptly, subside
slowly, and vary anywhere from several times a day to a couple of times a month. During these attacks,
the patient is
➔ Extremely anxious, tremulous, weak, profuse sweating
➔ Headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea
➔ Other symptoms: polyuria, nausea, vomiting, diarrhea, abdominal pain, and a feeling of
impending doom
➔ Palpitations and tachycardia
➔ Blood pressures (SBP: >180; DBP: >120)

IV. How are these signs and symptoms assessed?

Assessment
The patient often has intermittent episodes of hypertension or attacks that range from a few
minutes to several hours.
During these episodes the patient has:
● severe headaches
 ● Palpitations
● profuse diaphoresis
● Flushing
● Apprehension
● sense of impending doom.
● nausea and vomiting
● Pain in the chest or abdomen
● Increased abdominal pressure
● The patient may also report heat intolerance, weight loss, and tremors.

ACTION ALERT: Do not palpate the abdomen of a patient with pheochromocytoma, because
this action could stimulate a sudden release of catecholamines and trigger severe hypertension.
- vigorous abdominal palpation can provoke a hypertensive crisis.

Drugs such as:

- induce a hypertensive crisis in the patient with pheochromocytoma.
● tricyclic antidepressants
● Droperidol
● Glucagon
● Metoclopramide
● Phenothiazines
● naloxone

Foods or beverages:
● high in tyramine (e.g., aged cheese, red wine, smoke/dried meat, bananas, chocolate) also
induce hypertension.

❖ The most common diagnostic test is a 24-hour urine collection for vanillylmandelic
acid (VMA) (a product of catecholamine metabolism), metanephrine, and
catecholamines, all of which are elevated in the presence of a pheochromocytoma.
❖ MRI or CT scans can precisely locate tumors in the adrenal gland.
❖ After diagnosis, CT scans of the chest and abdomen may be used to locate any other
tumors.

Any patient with hypertension accompanied by symptoms of sympathoadrenal stimulation should

be referred to a health care provider for a definitive diagnosis.
➢ Assess the patient for the classic triad of symptoms of pheochromocytoma
■ severe pounding headache, tachycardia, and profuse sweating
○ Monitor the BP immediately if the patient is experiencing an “attack.”
○ Attempt to make the patient with pheochromocytoma as comfortable as possible.
○ BP fluctuations from catecholamine excesses tend to be severe and must be carefully
monitored.
○ Assess for Diabetes Mellitus and monitor for a blood glucose level.
○ Patients need rest, nourishing food, and emotional support during this period.
 ○ Emphasize the importance of follow-up and routine BP monitoring.
○ If metyrosine is being used, instruct the patient to rise slowly and hold onto a secure
object, since this drug can cause orthostatic hypotension.

How are pheochromocytomas diagnosed?

● Establishing the diagnosis of pheochromocytoma is dependent on the demonstration of
significant catecholamine excess.
● Levels of epinephrine (adrenaline), norepinephrine (noradrenaline), and their
metabolites (breakdown products of epinephrine and norepinephrine) can be
measured in either urine or blood. Catecholamine metabolites include
metanephrine, normetanephrine, dopamine, and vanillylmandelic acid (VMA).
Because catecholamine release varies throughout the day, the best method of diagnosing
pheochromocytomas is using a 24-hour urine collection. This involves obtaining a
special urine container, which has a small amount of preservative, from a medical
laboratory and filling it with one entire day's worth of urine. The test is somewhat
inconvenient but well worth the trouble due to its reliability and unrivaled specificity.
● Blood tests are available for metanephrine, normetanephrine, and chromogranin A. The
most commonly ordered blood test for pheochromocytoma is the plasma free
metanephrine test. Though more convenient to obtain than a 24-hour urine collection,
plasma free metanephrine testing is plagued by frequent false positive results. This test
creates a false alarm where the patient appears to have a pheochromocytoma, but in
reality s/he does not. False positive results like these are a frequent source of
confusion for both patients and physicians alike. For this reason, 24-hour urine
testing remains the gold standard.

V. What are the basic interventions for each condition?

Medical Intervention

- Adrenalectomy is surgery to remove one or both adrenal glands.

A. Bilateral adrenalectomy is a surgical procedure in which both of the adrenal glands are
removed in totality.
B. Unilateral Adrenalectomy remove one adrenal gland

Treatments for cancerous tumors and cancer that has spread in the body, related to a pheochromocytoma,
include:

- MIBG. This radiation therapy combines MIBG, a compound that attaches to adrenal tumors, with
a type of radioactive iodine. The treatment goal is to deliver radiation therapy to a specific site
and kill cancerous cells.

- Peptide receptor radionuclide therapy (PRRT). PRRT combines a drug that targets cancer cells
with a small amount of a radioactive substance. It allows radiation to be delivered directly to the
cancer cells. One PRRT drug, lutetium Lu 177 dotatate (Lutathera), is used to treat advanced
neuroendocrine tumors.

- Chemotherapy. Chemotherapy is the use of powerful drugs that kill fast-growing cancer cells.

- Radiation therapy. This may be used for symptomatic treatment of tumors that have spread to
the bone, for example, that are causing pain.
 - Adrenalectomy - The definitive treatment of pheochromocytoma is surgical removal of the
tumor, usually with adrenalectomy (removal of one or both adrenal glands). Surgery may be
performed using a laparoscopic approach or an open operation. The laparoscopic approach is the
preferred method for patients with solitary intra-adrenal pheochromocytomas less than 8 cm in
diameter without malignancy (Young et al., 2016). Bilateral adrenalectomy may be necessary if
tumors are present in both adrenal glands.

- Targeted cancer therapies. These medications hinder the function of naturally occurring
molecules that promote the growth and spread of cancerous cells.

Pharmacologic Therapy

The patient may be treated preoperatively on an inpatient or outpatient basis. Regardless of the
setting, monitoring of blood pressure and cardiac function is essential. The goals are to control
hypertension before and during surgery and volume expansion.

● Alpha-adrenergic blockers - Dibenzyline

○ Blocks norepinephrine from tightening the muscles in the walls of smaller arteries and
veins, reduces catecholamines which decreases blood pressure and prevents hypertensive
crisis
○ Watch out for REFLEX TACHYCARDIA - due to decreased blood pressure, the body
tried to compensate by increasing the heart rate
○ In tandem with beta-adrenergic blockers
○ Preoperatively, the patient may begin treatment with a low dose of an alpha-adrenergic
blocker 10 to 14 days or longer prior to surgery.
○ The dosage is increased every 2 to 3 days as needed to control blood pressure, with the
final dose usually ranging between 20 to 100 mg daily
○ Some practitioners may prefer the use of a selective alpha1-adrenergic blocker with fewer
side effects, such as prazosin (Minipress), terazosin (Hytrin), or doxazosin (Cardura),
when long-term therapy is indicated.
○ After administration of the alpha-blockers, the blood pressure should be monitored
closely. In an outpatient setting, the blood pressure should be taken twice daily in a sitting
and standing position.
○ Side/adverse effects: orthostatic hypotension, nasal stuffiness, increased fatigue, and
retrograde ejaculation in menPrecautions: Caution is advised when using this drug in the
elderly because they may be more sensitive to its effects, especially dizziness.

● Beta-adrenergic blockers - Propranolol

 ○ To prevent tachycardia
○ Only initiated once adequate alpha-adrenergic control has been achieved.
○ The dosage is adjusted according to the patient response and ability to tolerate the drug.
○ The dosage may be initiated in daily divided doses and on day 2 adjusted to a single
long-acting dose.
○ On subsequent days, the dose may be increased to control tachycardia as needed with a
target heart rate of 60 to 80 bpm.

● Calcium channel blockers - Nifedipine

○ Sometimes used as an alternative or supplement to preoperative alpha and beta blockers,
when blood pressure control is inadequate or the patient is unable to tolerate the side
effects.
○ For episodes of severe hypertension, nifedipine is a fast and effective treatment, because
the capsules can be pierced and chewed.

● Catecholamine Synthesis Inhibitors - Metyrosine

○ Additional medication that may be used preoperatively
○ Long-term use of metyrosine may result in many adverse effects, including sedation,
depression, diarrhea, anxiety, nightmares, dysuria, impotence, anemia, thrombocytopenia,
crystalluria, galactorrhea, drooling, speech impairment, tremors
○ If metyrosine is being used, instruct the patient to rise slowly and hold onto a secure
object since they might also experience orthostatic hypotension

Nursing Intervention:
1. Monitor the patient until stable with special attention given to ECG changes, arterial pressures,
fluid and electrolyte balance, and blood glucose levels.
2. Monitor VS especially heart rate and blood pressure
○ To watch out fo hypertensive crisis and tachycardia
3. Monitor hypertensive crisis.
○ It is when Systolic Blood Pressure is >180 or the Diastolic Blood Pressure is >120
○ May damage kidneys, eyes, brain and heart
4. Monitor chest pain, neuro status and EKG changes
○ Chest pain may indicate myocardial infarction
○ Patient may be at risk for stroke
5. Monitor for hyperglycemia
 ○ Caused by catecholamine excess since catecholamines have an inhibitory effect on
insulin secretion
6. Monitor IV access for signs of infection.
○ It is important for IV access to be free of infection, swelling, redness and pain since we
administer some of the medications here
7. Make the patient as comfortable as possible.
8. Provide a calm and cool environment.
9. Provide emotional support.
10. Encourage the patient to rest, hydrate and eat nourishing food. (High calorie diet, discourage
caffeine, energy drinks and smoking)
○ High calorie diet - px with pehochromocytoma burns a lot of calories
○ Caffeine, energy drinks and smoking constricts the blood vessels which increases blood
pressure
11. Emphasize the importance of follow-up and routine BP monitoring.
 References

Calgary Guide. (n.d.) Pheochromocytoma: Pathogenesis and Clinical Findings.

https://calgaryguide.ucalgary.ca/Pheochromocytoma:-Pathogenesis-and-Clinical-Findings/

Castelino, T., & Mitmaker, E. (2016, May 18). Pheochromocytoma Crisis.

https://www.intechopen.com/chapters/55596

Greenleaf, C. Griffin, L., Shake, J., & Orr, W. (2017, July). Hypertensive crisis secondary to
pheochromocytoma. Proceedings (Baylor University. Medical Center), 30(3), 314–315.
https://doi.org/10.1080/08998280.2017.11929629https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C5468026/

Hinkle, J. L., & Cheever, K. H. (2018). Brunner & Suddarth’s Textbook of Medical-Surgical Nursing
(14th ed.). Wolters Kluwer.

Ignatavicius, D. (2013). Medical-Surgical Nursing: Patient-centered collaborative care (7th ed.).

Saunders, an imprint of Elsevier Inc.

Lewis, S. L., Dirksen, S. R., Heitkemper, M. M., & Bucher, L. (2014). Medical-Surgical Nursing:
Assessment and Management of Clinical Problems (9th ed.). Mosby, an imprint of Elsevier Inc.

Martin, J. (2020, February 15). Pheochromocytoma.

https://www.webmd.com/cancer/what_is_pheochromocytoma

Mayo Clinic. (2020, March 3). Pheochromocytoma.

https://www.mayoclinic.org/diseases-conditions/pheochromocytoma/diagnosis-treatment/drc-203
55372

NORD - National Organization for Rare Disorders. (2018, July 18). Pheochromocytoma.
https://rarediseases.org/rare-diseases/pheochromocytoma/

Pheochromocytoma. (2020, February 12). National Cancer Institute.

https://www.cancer.gov/pediatric-adult-rare-tumor/rare-tumors/rare-endocrine-tumor/pheochromo
cytoma

Pheochromocytoma (Adrenal Medulla Tumor): Symptoms, Diagnosis & Treatment - Urology Care
Foundation. (2018). Urology Care Foundation.
https://www.urologyhealth.org/urology-a-z/p/pheochromocytoma-(adrenal-medulla-tumor)

Pheochromocytoma Symptoms, Treatment, Diagnosis & More. (2021, August 9). Pheo Para Alliance.
https://pheopara.org/education/pheochromocytoma
RegisteredNurseRN. (2016, November 23). Pheochromocytoma Symptoms, Nursing NCLEX Lecture,
Pathophysiology and Treatment | Endocrine.
https://www.youtube.com/watch?v=VTTge9OfGGw&t=139s
Stöppler, M. C. (2020, December 15). Pheochromocytoma Symptoms, Treatment, Diagnosis & Prognosis.
MedicineNet. https://www.medicinenet.com/pheochromocytoma/article.htm

UCLA HEALTH (n.d). Pheochromocytoma - Treatment and Diagnosis.

https://www.uclahealth.org/endocrine-center/pheochromocytoma-treatment-and-diagnosis
G7: Neonatal Alterations (Premature newborn)

OUTLINE (PPT AND REPORTERS)

I. INTRODUCTION: DEFINITION (Sophia)
II. PHYSICAL EXAMINATION / CLINICAL PRESENTATION(Jannen)
III. ETIOLOGIC CHANGES
A. Alteration in Respiratory and Cardiovascular Physiology (Sophia)
B. Alteration in Thermoregulation (Kersty)
C. Alteration in Neurologic Physiology (Jannen)
D. Alteration in Gastrointestinal Physiology (Sophia)
E. Alteration in Hepatic and Hematologic Physiology (Kersty)
IV. IMMEDIATE CARE (Jannen)

Care of the Preterm (Premature) Newborn

A. Definition: Infant born prior to the start of the 37th week of gestation
a. Very premature: Neonates born at less than 32 weeks gestation
b. Premature: Neonates born between 32 and 34 weeks gestation
c. Late premature: Neonates born between 34 and 37 weeks gestation

B. Etiologic Changes
a. Alteration in Respiratory and Cardiovascular Physiology
i. Risk for respiratory problems because the lungs are not fully mature and not fully ready to take over
the process of gas exchange until 37 to 38 weeks gestation.
ii. A preterm infant is unable to produce sufficient amounts of surfactant thereby increasing the
inspiratory pressure needed to expand each alveoli with air, thus causing alveoli collapse. This
progressive atelectasis leads to an inability to develop a functional residual capacity (FRC) and causes
an ineffective exchange of oxygen and carbon dioxide. As a result, the infant becomes hypoxic.
iii. The muscular coat of the pulmonary blood vessels is incompletely developed. Consequently, the
pulmonary arterioles do not constrict as well in response to decreased oxygen levels. This lowered
pulmonary vascular resistance leads to increased left-to-right shunting through the ductus arteriosus,
which increases the blood flow back into the lungs.
iv. Normally the ductus arteriosus responds to increasing oxygen and prostaglandin E levels by
vasoconstriction; in the preterm infant, who has higher susceptibility to hypoxia, the ductus arteriosus
may remain open. A patent ductus increases the blood volume to the lungs, causing pulmonary
congestion, increased respiratory effort, carbon dioxide retention, and bounding femoral pulses.
Complications:
● RDS (Respiratory distress syndrome) - leading cause of morbidity and mortality among preterm neonates. The
lungs lack surfactant, which prevents alveolar collapse at the end of respiration. It is a life-threatening lung disorder
that results from underdeveloped and small alveoli and insufficient levels of pulmonary surfactant. It affects 10% of
all premature infants, the majority of these born at less than 28 weeks’ gestation (Askin, 2010).
○ Clinical presentation
■ Respiratory distress shortly upon delivery
■ Tachypnea
■ Intercostal retractions; seesaw breathing patterns (on inspiration, the anterior chest wall retracts and
the abdomen protrudes; on expiration, the sternum rises)
■ Expiratory grunting
■ Nasal flaring
■ Increased O2 demand
■ Gray or dusky skin color
■ Breath sounds decreased, presence of rales ----> RDS progresses
■ Lethargic and hypotonic
■ Hypoxemia resulting to acidosis
G7: Neonatal Alterations (Premature newborn)
○ Assessment
■ X-ray exam shows a reticulogranular pattern of the peripheral lung fields and air bronchogram So
reticulogranular pattern has a ground glass appearance, uniformly distributed throughout both
lung fields is. characteristic of RDS. Because of surfactant deficiency, alveoli.
■ Arterial Blood Gas Analysis may show hypoxemia that responds to increased oxygen supplementation
and hypercapnia. Serial blood gases may show evidence of worsening respiratory and metabolic
acidosis, including lactic acidemia in infants with worsening RDS.
■ Echocardiography to rule out heart defects as the cause of newborn’s breathing problem.
■ Complete blood counts may show evidence of anemia and abnormal leukocyte counts, suggesting
infection.
■ Infant’s appearance, color, and breathing efforts. These can point to a baby's need for help with
breathing.

○ Interventions
a. Medical Management
■ Cardiac monitoring, O2 saturation, ABGs, continuous pulse oximetry
■ Administration of surfactant
■ Respiratory support: oxygen administration via O2 mask, CPAP or continuous positive airway
pressure therapy or continuous positive airway pressure therapy machine increases air pressure
in your throat so that your airway doesn't collapse when you breathe in., mechanical ventilation,
extracorporeal membrane oxygenation therapy
■ Antibiotics

b. Nursing Management
■ Provide respiratory support to maintain PO2 and pH levels
■ Maintain a patent airway.
■ Listen for equal breath sounds bilaterally, assess for equal chest rise, use commercial end tidal
CO2 detector.
■ Administer oxygen as ordered to maintain oxygen saturation within ordered parameters.
■ Hypoxemia and acidosis may further decrease surfactant production.
■ Short-term oxygen administration may be given using a mask or tubing.
■ Long-term oxygen administration may be given using a nasal cannula or oxygen hood.
■ Oxygen is humidified and warmed.
Minimize oxygen demand by maintaining a neutral thermal environment, clustering care to
decrease stress, and treating acidosis as clinically indicated and ordered.
■ Suction airway as needed for removal of secretions as neonates have a smaller airway diameter,
which increases the risk of obstruction. Suctioning may stimulate the vagus nerve, causing
bradycardia, hypoxemia, or bronchospasm.
■ Maintain a neutral thermal environment to decrease risk of cold stress.
■ Monitor intake and output and daily weight.
■ Promote rest by implementing calming measures or administering ordered sedation.

● Bronchopulmonary dysplasia (BPD) - caused by damage to the delicate tissue of the lungs; lungs may be
less compliant because of the damage caused by being a preterm neonate, infection, or mechanical ventilation and
secondary to fibrosis, atelectasis, increased pulmonary resistance, and overdistention of the lungs. Babies with
BPD have a higher risk of lung infections than other babies and BPD can lead to lung damage.
■ Chest retractions
■ Audible wheezing, rales, and ronchi
■ Hypoxia
■ Respiratory acidosis
■ Bronchospasm
■ Intolerance to fluids: edema, decreased urinary output, and weight gain
■ Difficulty weaning from ventilator or increased requirements for ventilator
G7: Neonatal Alterations (Premature newborn)

○ Assessment (add more)

■ Assess the need for additional oxygen and continue to show signs of respiratory problems after 28
days of age (or past 36 weeks postconceptional age).
■ Chest x-ray exam results exhibit cardiomegaly, lung hyperinflation, and infiltrates
■ Blood tests
■ Echocardiograms to rule out heart defects as the cause of your child’s breathing issues.

○ Interventions:
a. Medical Management:
■ Oxygen administration
■ Mechanical ventilation
■ Electrolytes, ABGs (may reveal acidosis, hypercarbia, and hypoxia (with increased oxygen
requirements).
■ Bronchodilators, corticosteroids, diuretics
■ Prophylaxis treatment (nutrition supplementation, fluid restriction, diuretics, oxygen
supplementation, Respiratory syncytial virus (RSV) monoclonal antibody (palivizumab)
■ Restrict fluid intake (provide maximum calories with minimal fluid)
■ Maintaining good nutrition

b. Nursing management:
■ Administer oxygen as ordered by the physician.
■ Perform chest physiotherapy
■ Administer medications
■ I&O monitoring
■ Regimen of support and time: time for the normal repair process within the lungs to improve
functioning and time for the infant to grow and thrive

● Patent ductus arteriosus (PDA) - occurs when the ductus arteriosus reopens after birth due to lowered oxygen
tension associated with respiratory impairment.
○ Clinical presentation
■ Heart murmur heard at the upper left sternal border (some neonates with PDA may not have an
audible murmur)
■ Active precordium
■ Widened pulse pressure with decreased diastolic blood pressure
■ Tachycardia and tachypnea
■ Recurrent apnea
■ Increased work of breathing and oxygen needs
■ Bounding pulses
■ Acidosis
■ Hypotension
○ Assessment
■ Presence of a patent ductus arteriosus is confirmed by echocardiogram
■ Chest x-ray exam may show increased pulmonary vasculature, pulmonary edema, and mild
enlargement of the heart (Sadwoski, 2010)
○ Interventions
a. Medical Management
■ Fluid regulation
■ Respiratory support (oxygen administration and mechanical ventilation)
■ Administration of indomethacin (Indocin) or NeoProfen to facilitate the closure and reduces the risk
for surgical intervention
- Indomethacin (dose: 0.2 mg/kg IV every 12 hours), a prostaglandin inhibitor
G7: Neonatal Alterations (Premature newborn)
■ Ibuprofen lysine (Neoprofen) is used to close the ductus; the three-dose course consists of one
dose of 10 mg/kg IV followed by two subsequent doses of 5 mg/kg IV at 24- and 48-hour intervals
after the initial dose. Common side effect: transient renal dysfunction, oliguria, platelet dysfunction,
and GI bleeding
■ Diuretics
■ Surgical ligation (if the neonate doesn’t respond to other therapies)

b. Nursing management
■ Administer oxygen as ordered.
■ Restrict fluids as per orders.
■ Administer medications as per orders.
■ Monitor intake and output for signs of fluid overload.
■ Prepare the neonate and family for surgery.

● Apnea - cessation of breathing for 20 seconds or longer or for less than 20 seconds when associated with cyanosis,
pallor, and bradycardia. The etiology of apnea is multifactorial but is thought to be primarily a result of neuronal
immaturity, a factor that contributes to the preterm infant’s irregular breathing patterns (central apnea).
○ Clinical presentation
■ Central, obstructive, or mixed
■ Onset is insidious, may occur during feeding, suctioning, or stooling or vagal stimulation: need
cardiorespiratory monitoring
■ Periodic breathing - defined as three or more periods of apnea >3 seconds within a 20-second
period of normal respirations
○ Assessment
■ Observe signs of cyanosis, decreased heart rate, low oxygen level
■ Physical exam
■ Blood oxygen levels
■ Blood tests to check for blood counts, blood sugar levels, and electrolyte levels. They also check
for signs of infection.
■ X-ray, ultrasound, or other imaging studies
■ Sleep studies
■ Lab tests for the fluid around the brain and spinal cord, urine, and stool for infection and other
problems
○ Interventions
a. Medical Management
■ Methylxanthines (Caffeine) - stimulates the respiratory center of the brain to increase minute
ventilation and to decrease the CNS threshold to carbon dioxide
■ CPAP
● Monitor for any nasal or musical injury

b. Nursing management
■ Adequate positioning (side-lying or prone position with the head of the bed elevated 30 degrees)
■ Oxygen
■ Ventilation PRN

b. Alteration in Thermoregulation
i. Two limiting factors in heat production, however, are the availability of glycogen in the liver and
the amount of brown fat available for heat production. Both of these limiting factors appear in the
third trimester.
ii. Five physiologic and anatomic factors increase heat loss in the preterm infant:
1. A preterm baby has a high ratio of body surface to body weight. This means that the
baby’s ability to produce heat (based on body weight) is much less than the potential for
losing heat (based on surface area).
G7: Neonatal Alterations (Premature newborn)
2. Preterm baby has very little subcutaneous fat, which is the human body’s insulation.
Heat is lost from the body as the blood vessels, which lie close to the skin surface in the
preterm infant, transport blood from the body core to the subcutaneous tissues.
3. Preterm baby has thinner, more permeable skin than the term infant. This increased
permeability contributes to a greater insensible water loss as well as heat loss.
4. The posture of the preterm baby influences heat loss. Flexion of the extremities
decreases the amount of surface area exposed to the environment. Extension of the
extremities in the hypotonic “frog” position increases the surface area exposed to the
environment and thus increases heat loss.
5. Preterm baby has a decreased ability to vasoconstrict superficial blood vessels and
conserve heat in the body core.

NOTES: Hypothermia occurs when the body's temperature falls below 35 °C. Hypothermia can occur in any
situation where the body is losing more heat to the environment than it is generating. Severe hypothermia is life-
threatening without prompt medical attention.

Early babies and those with low birth weight run a higher risk of hypothermia because of their large surface-area-
to-volume ratio. This refers to the fact that a baby is a tiny human — especially if they’re born early or with low
birth weight — which means they can’t hold as much heat inside their bodies as older children or adults.

Additional contributing factors are their:

lack of insulating body fat
still developing nervous system
inability to efficiently conduct heat

Complication:
● Hypothermia - neonates with temperatures below 36.5°C (97.7°F) are at risk for hypothermia.
○ Clinical presentation:
○ NEONATAL HYPOTHERMIA - PedsCases

■ pale, cool skin

■ sluggishness
■ poor feeding
■ weak cry
■ difficulty in breathing
■ Irritability
■ metabolic acidosis
■ Hypotonia
■ Bradycardia
■ hypoglycemia
■ Tachypnea, restlessness, shallow and irregular respirations
■ Respiratory distress, apnea, hypoxemia,
■ Transient hyperglycemia
■ Bleeding from the mouth, nose or needle punctures

○ Assessment:
■ Rectal temperature < 36.5 to 37.5° C

○ Interventions:
a. Medical Management
■ Warm the infant in a closed incubator, overhead radiant warmer or warm room
G7: Neonatal Alterations (Premature newborn)
■ Provide energy (calories) by oral, nasogastric tube or intravenous feeding. Energy can be given as
oral or nasogastric milk, or intravenous maintenance fluid containing 10% dextrose water (e.g.
Neonatalyte).
■ Oxygen administration - Provide oxygen. Although centrally pink, cold infants are often hypoxic.
Therefore, give 30% oxygen (FiO₂ 0.3) while the infant is being warmed. A normal oxygen
saturation in a cold infant does to exclude tissue hypoxia as oxygen is trapped in the red cells.
■ Give 4% sodium bicarbonate. Most hypothermic infants have a metabolic acidosis. If intravenous
fluid is given, add 10 ml 4% sodium bicarbonate to 100 ml of maintenance fluid (Neonatalyte).
Obtain a blood gas analysis if possible and half correct any base deficit.
■ Antibiotics. Give parenteral antibiotics if there are any signs of infection.

b. Nursing Management
■ Monitor and record the infant’s temperature, pulse, respiration, skin colour and blood glucose
concen-tration until they are normal and stable.
■ Encourage parent-infant skin-to-skin contact with a warm blanket over both the neonate and the
parent.
■ If the temperature remains below 36.5°C (97.7°F), place the neonate under a preheated warmer or
incubator. Unwrap the neonate so that the skin is exposed to the radiant heat. Attach the electronic
skin probe. The warmer is set at 1.5°C above the neonate’s temperature. Continue to adjust the
radiant temperature in relationship to the neonate’s temperature.
■ Monitor the blood glucose level as hypothermia can lead to hypoglycemia.
■ Notify the physician if the neonate’s temperature does not return to normal range.
■ Place cap on newborn’s head.

c. Alteration in Gastrointestinal Physiology: As a result of GI immaturity, the preterm newborn has the
following ingestion, digestion, and absorption problems:
i. Marked danger of aspiration and its associated complications due to the infant’s poorly developed
gag reflex, incompetent esophageal cardiac sphincter, and inadequate
suck/swallow/breathe reflex.
ii. Difficulty in meeting high caloric and fluid needs for growth due to small gastric capacity.
iii. Limited ability to convert certain essential amino acids to nonessential amino acids. These
amino acids, such as histidine, taurine, and cysteine, are essential to the preterm infant
iv. Feeding intolerance is extremely common because premature infants have a small stomach,
immature sucking and swallowing reflexes, and inadequate gastric and intestinal motility. These
factors hinder the ability to tolerate both oral and nasogastric feedings and create a risk of
aspiration.
Complication:
● Necrotizing enterocolitis (NEC) - a gastrointestinal disease that affects neonates; results in inflammation and
necrosis of the bowel, usually the proximal colon or terminal ileum (Bradshaw, 2010). Preterm neonates are
predisposed to NEC because of multiple factors, including:
- Altered blood flow regulation, particularly to the intestines
- Impaired gastrointestinal host defense when faced with stress/injury to the intestinal tissue
- Alterations in the inflammatory response (Caplan, 2011)

○ Clinical presentation: (add)

■ Abdominal distention
■ Decreased bowel sound
■ Poor feeding
■ Increased gastric residuals
■ Blood streak bile vomiting
■ Bloody or mucoid stools
G7: Neonatal Alterations (Premature newborn)
○ Assessment: (add)
■ Blood tests
■ Abdominal x-ray show gas or air bubbles in the wall of their intestines
■ Doctor may insert a needle into the belly to withdraw fluid to see whether there is a hole in the
intestine

○ Interventions:
a. Medical management
■ Nasogastric tube (gavage)
■ Oxygen
■ Starting antibiotic therapy
■ If the bowel perforates, peritoneal drainage or a laparotomy is done to help remove fecal secretions
from the abdomen.
■ Temporary colostomy may be performed to allow for bowel function.

b. Nursing management
■ Stop all regular feedings. Baby receives nutrients through an IV catheter
■ Check stools for blood
■ Provide oxygen or mechanically assisted breathing if abdominal swelling affects breathing
■ Handle the abdomen gently to lessen the possibility of bowel perforation.
■ Frequently measure the infant’s abdominal cavity to see if there’s swelling.

d. Alteration in Hepatic and Hematologic Physiology:

Immaturity of the preterm newborn’s liver predisposes the infant to several problems.
i. After birth, the glycogen stores in the liver are rapidly used for energy.
ii. Baby born preterm has decreased glycogen stores at birth and frequently experiences stress,
which rapidly uses up these limited stores. Therefore, the preterm newborn is at high risk for
hypoglycemia and its complications.
iii. Iron is stored in the last trimester of pregnancy, therefore a premature newborn is born with low
iron stores.
iv. Due to the relatively short half-life of the fetal hemoglobin molecule, bilirubin, the end product of its
breakdown, accumulates at a faster rate in the preterm infant. It is within the liver that the bilirubin
is bound to albumin and converted, or conjugated, to a more excretable form. However,
conjugation of bilirubin in the liver is impaired in the preterm infant. Thus bilirubin levels
increase more rapidly and to a higher level than in the full-term infant.

Complication:
● Hypoglycemia
- a serum glucose level of less than 45 mg/dL
- may develop because the fetus had to use stores of glycogen for nourishment in the last weeks of intrauterine life
○ Clinical presentation
■ Shakiness
■ Blue tint to skin and lips (cyanosis)
■ Apnea
■ Hypothermia
■ Floppy muscles (poor muscle tone)
■ Not interested in feeding
■ Lethargy
■ Seizures

○ Assessment
■ Physical examination
■ Serum glucose level
G7: Neonatal Alterations (Premature newborn)
■ Serum electrolyte
■ CBC to rule out sepsis & Polycythemia
■ Serum glucose test. It is a blood test that measures blood sugar in a newborn using a heel stick,
an easy and minimally invasive way to do blood work for newborns where blood is drawn from the
heel of the foot. If blood sugar is low, the healthcare provider will keep checking until it is at normal
levels for 12 to 24 hours. Sometimes, additional newborn testing is done to look for metabolic
disorders, conditions that affect the normal metabolic process and may cause low blood sugar.

○ Interventions
a. Medical Management
■ Dextrose gel 200 mg/kg massaged into the buccal mucosa
■ Intravenous glucose given as a bolus of 200 mg/kg (dextrose 10% at 2 mL/kg), followed by
continuous infusion of dextrose 10% at 5 to 8 mg/kg per minute (80 to 100 mL/kg per day) to
maintain blood glucose levels of 40 to 50 mg/dL
■ Corticosteroids or glucagon - Steroid medications can raise blood glucose levels by reducing the
action of insulin (causing insulin resistance) and making the liver release stored glucose into the
bloodstream.

b. Nursing Management
■ Encourage diabetic women to feed infants early with formula
■ Encourage mother to increase feeding frequency.
■ Maintain a neutral thermal environment.
■ Provide early enteral feeding, if appropriate, or perform IV infusion of D10W as ordered by the
physician.
■ Administer a continuous infusion of glucose as ordered by the physician.
■ Check blood glucose levels after treatment.

● Anemia
- Occurs due to low iron stores, vitamin E deficiency, inadequate production of erythropoietin (EPO), shortened RBC
life span, blood loss
- An exaggerated, pathologic response of a preterm infant
- Normocytic and normochromic anemia

○ Clinical presentation
■ Tachypnea and increased in apneic and bradycardic episodes
■ Pale skin
■ Sluggishness
■ Tachycardia
■ Low arterial blood pressure
■ Decreased hematocrit value
■ Metabolic acidosis - increased lactic acid secretions secondary to anaerobic metabolism

○ Assessment
■ Blood test, specifically hemoglobin, hematocrit level and a reticulocyte count, which gives an
indication of how fast RBCs are being produced and released from the bone marrow.
■

○ Interventions
a. Medical management
■ Iron, Vitamin E, folate/folic acid supplementation
■ Blood transfusion
■ Recombinant Erythropoietin - Recombinant erythropoietin drugs are known as erythropoietin-
stimulating agents (ESAs). These drugs are given by injection (shot) and work by stimulating the
G7: Neonatal Alterations (Premature newborn)
production of more red blood cells. These cells are then released from the bone marrow into the
bloodstream.
■ Enteral iron

b. Nursing management
■ Assist in blood transfusion.
■ Administer medications as ordered by the physician.
■

Note: Early clinical assessment of jaundice associated with indirect hyperbilirubinemia is more difficult in preterm newborns
because they lack subcutaneous fat.

● Jaundice
○ Clinical presentation
■ yellow discoloration of skin and eyes
■ listless, difficult to awaken
■ Poor feeding
■ high-pitched cries

NOTES:
Jaundice within the first 24 hours is pathological; usually related to problem of the liver
Jaundice occurring after 24 hours is referred to as physiological jaundice and is related to increased amount of
unconjugated bilirubin in the system

○ Assessment
■ Visual examination to look for signs of jaundice
■ Blood test
■ Gently pressing the infant’s forehead or nose (If the skin looks yellow where you pressed, it's likely
your baby has mild jaundice.)
■ Check the infant’'s urine and stool. The baby may have jaundice if their urine is yellow (a newborn
baby's urine should be colourless) or their stool is pale (it should be yellow or orange).
■ Transcutaneous bilirubinometer - measures the reflection of a special light shone through the skin.

○ Interventions
a. Medical
■ Phytotherapy - helps to convert the bilirubin in a baby’s body to a different type of bilirubin that is
more easily excreted in the baby’s stool
■ Phototherapy - treatment with a special type of light. used to treat newborn jaundice by lowering
the bilirubin levels in your baby's blood through a process called photo-oxidation.
■ Exchange transfusion / Complete blood transfusion - baby's blood will be removed through a thin
plastic tube placed in blood vessels in their umbilical cord, arms or legs. The blood is replaced with
blood from a suitable matching donor.
■ Phenobarbital - Medications are not usually administered in infants with physiologic neonatal
jaundice. However, in certain instances, phenobarbital, an inducer of hepatic bilirubin metabolism,
has been used to enhance bilirubin metabolism.

b. Nursing management
■ During treatment, remove the infant’s clothes (except for the diaper) because treatment is most
effective when there is a large amount of skin exposed to the light.
G7: Neonatal Alterations (Premature newborn)
■ During phototherapy, cover the baby’s eyes with eye-patches to prevent damage to the retina by
the bright lights; gonads should also be covered.
■ Monitor serum bilirubin at least every 12 hours.
■ Provide feedings every 2-3 hours for adequate hydration.
■ Assess jaundice using a transcutaneous meter or fingers to blanch the neonate’s skin on the
face, upper trunk, abdomen, thigh, and lower leg and feet.
■ Phototherapy is discontinued if two serum bilirubin values are <10mg/dl.

● Retinopathy of prematurity (ROP) - disease caused by abnormal growth of retinal blood vessels. Prematurity may
cause abnormal vessels to grow. Supplemental oxygen is also thought to contribute to this growth. If injury or
exposure to a stressor occurs, the normal vascularization of the retina may be interrupted. Vasoproliferation, an
abnormal growth of vasculature, occurs when tissue grows within the retina, or extends into the vitreous body.
Ultimately, abnormal vascularization and associated bleeding, and fluid leakage, cause scar tissue that pulls and
distorts the retina and displaces the macula (Phelps, 2011). It also causes retinal folds and can lead to retinal
detachment (Phelps, 2011).
○ Clinical presentation
■ Mild to severe vision problems
- severe: white pupils (leukocoria), abnormal eye movements (nystagmus), crossed eyes
(strabismus), severe nearsightedness (myopia)
■ Blindness

○ Assessment
■ Dilating eye drops to enlarge the pupil
■ Eyelid speculum - holds the eyelids open
■ Scleral depressor - helps move the eye into different positions so the entire retina can be
checked
■ Indirect ophthalmoscope - has a special lens that sends a bright light into the eye, enabling
the doctor to examine the retina

○ Interventions
a. Medical Management:
■ Laser photocoagulation - laser is used to coagulate the avascular periphery of the retina to prevent
vessel proliferation
■ Cryotherapy - a supercooled probe is used to prevent vessel proliferation by freezing the avascular
retina
■ Vitreoretinal surgery - to reattach the retina if the retina becomes detached
G7: Neonatal Alterations (Premature newborn)
■ Scleral buckling - involves placing a flexible band, usually made of silicone, around the
circumference of the eye. The band goes around the sclera, or the white of the eye, causing it to
push in, or "buckle." This, in turn, pushes the torn retina closer to the outer wall of the eye. This
surgery takes 1–2 hours.

b. Nursing Management:
■ Monitor baby’s oxygen saturation levels. Use oxygen blenders and oxygen calibrating systems to
ensure exact concentration of oxygen.
■ Avoid bright lights by keeping lighting in the nursery at a low level and by covering isolettes and
cribs with blankets.
■ Closely monitor the baby's breathing and heart rate during the surgery.
■ EBP: Retinopathy of prematurity is caused by high concentrations of oxygen therapy. Evidence
Based practice guidelines pertain to the management of supplemental oxygen, specifically lower
oxygen saturation ranges for premature infants. Oxygen saturation target ranges in the mid 80s to
lower-mid 90s are safe.
NOTES:
Research shows that limiting supplemental oxygen so oxygen saturation is less than 95 percent decreases ROP.
Maintaining oxygen saturation within limits is difficult with variable compliance.

e. Alteration in Neurologic Physiology

i. A common interruption of neurologic development with significant long-term sequelae in the
preterm infant is caused by intraventricular hemorrhage (IVH). It is the germinal matrix, the
immature cerebral vascular network, that is vulnerable to the stressors of birth asphyxia,
hypoxemia, fluctuations in blood pressure, and acidosis.

Complication:
● Intraventricular hemorrhage (IVH) - bleeding in or around the ventricles of the brain. It’s most common in neonates
born before 32 weeks’ gestation, especially those weighing less than 1500 g. Damage to brain function and long-
term effects vary.
○ Clinical presentation
■ Sudden drop in hemoglobin with severe onset of metabolic acidosis, a “waxy” color
■ Hypotension
■ Bradycardia
■ Oxygen desaturation
■ Hypotonia
■ Shock
■ Decreased hematocrit
■ Full and/or tense anterior fontanel
■ Hyperglycemia
■ Four grades of IVF:
● Grade I: Hemorrhage in germinal matrix
● Grade II: Intraventricular hemorrhage without ventricular dilatation
● Grade III: Intraventricular hemorrhage with ventricular dilatation; clots fill more than 50% of
the ventricle
● Grade IV: Extension of blood into cerebral tissue or parenchymal involvement
○ Assessment ADD
■ Most common site of hemorrhage is the periventricular subependymal germinal matrix in the lateral
ventricles of the brain, where there is a rich blood supply and the capillary walls are thin and fragile
■ Cranial Ultrasound
■ Physical examination

○ Interventions:
a. Medical Management
G7: Neonatal Alterations (Premature newborn)
■ Blood transfusion
■ Spinal tap
■ Surgery

b. Nursing Management
■ Monitor vital signs.
■ Reduce stress to neonate by maintaining a quiet and dark environment.
■ Administer fluid volume replacement slowly to minimize fluctuation in blood pressure.
■ EBP: Implementing midline or neutral head positioning at a 30-degree elevation in the head of bed
in infants less than 32 weeks’ gestation for the first 72 hours of life is recommended to reduce the
incidence of IVH.

C. Prematurity Clinical Presentation (Jannen)

a. History
In assessing prematurity, gestational age dating by using the mother's history can be unreliable because
of uncertainty of the dates. About 20% of women have an uncertain last menstrual period (LMP).
Gestational age assessment begins prenatally with obstetric ultrasonography in the first trimester.
Discovery of many fetal anomalies, unsuspected multiple gestation, location of the placenta, and an accurate dating
of the pregnancy are additional major benefits of early ultrasonography.

b. Physical Examination

Confirmation of gestational age in the newborn is based on physical and neurologic characteristics. In 1979,
the Dubowitz scoring system for determining gestational age based on neurologic and physical parameters was
revised to include 12 items. The Ballard Scoring System, revised again to include extremely low birth weight
(ELBW) infants, remains the main tool clinicians use after delivery to confirm gestational age by means of physical
examination.
The major parts of the anatomy for physical characteristic markers are ear cartilage, sole creases, breast
tissue, and genitalia.
G7: Neonatal Alterations (Premature newborn)
G7: Neonatal Alterations (Premature newborn)

FROM MCN BOOK (pages 713-716)

G7: Neonatal Alterations (Premature newborn)
G7: Neonatal Alterations (Premature newborn)

● What are the basic interventions for each condition?

Immediate care of the preterm infant (Jannen)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC521580/
G7: Neonatal Alterations (Premature newborn)

Figure 1: The “inverted triangle” shows how commonly certain interventions are needed

A. Assessment and Resuscitation

○ Preterm infants should be delivered into warm towels, dried, and transferred to a dedicated
neonatal resuscitation platform or trolley with an integral radiant heater.
○ Immediate occlusive wrapping in polythene may be at least as effective in reducing evaporative
heat loss, especially in extremely preterm infants.
○ Suctioning for 5 s-10 seconds to prevent stimulation of vagus nerve
B. Airway
○ To obtain a patent airway, the infant's head should be maintained in a neutral position and the chin
should be supported while applying gentle forward traction to the mandible (jaw thrust).
○ Careful suction under direct vision may be used to clear secretions that can obstruct the airway.
C. Breathing
○ The aim is to inflate the newborn's poorly compliant, fluid filled lungs to recruit (?) alveoli for gas
exchange.
○ About five initial “inflation” breaths of 2-3 seconds duration followed by ventilation at a rate
of around 40 breaths per minute using pressures of 20-25 cm H2O is appropriate while checking
for spontaneous respiration every 30 seconds.
○ Inflation breaths, and subsequent ventilation if spontaneous respiration is not established, can be
delivered via a facemask attached to a Y piece system with a blow-off valve or via a bag valve
mask.
○ A range of masks should be available to fit over the infant's mouth and nose (but not the orbital
margin).
D. Circulation
○ Chest compression is indicated if, despite adequate artificial ventilation, the infant's heart rate
remains < 60 beats per minute and is not improving.
○ Apply around 90 compressions per minute with lung reinflation after every three chest
compressions.
E. Drugs
○ If there is no improvement in clinical condition after adequate ventilation and chest compression,
then certain drugs may be useful in the acute resuscitation of preterm infants.
○ Persistent bradycardia may respond to adrenaline (epinephrine) and sometimes intravenous
sodium bicarbonate can be used to correct acidosis.
○ Dextrose may also be useful during prolonged resuscitation to correct hypoglycemia.
○ The use of intravenous fluids (normal saline, plasma, and blood) for volume expansion in
preterm infants should be limited to those infants known to have volume depletion—for example,
after antepartum hemorrhage.
G7: Neonatal Alterations (Premature newborn)

REFERENCES:

Necrotizing Entercolitis (NEC) Symptoms and Treatment. Children’s Hospital of Pittsburgh. (n.d.). Retrieved October 1 2021, from h ttps://www.chp.edu/our-services/transplant/intestine/education/intestine-disease-
states/necrotizing-entercolitis.

Ward, S. L., & Hisley, S. M. (2016). Maternal-Child Nursing Care with The Women’s Health Companion: Optimizing Outcomes for Mothers, Children, and Families. FA Davis.

Pillitteri, A. (2010). Maternal & Child Health Nursing: Care of the Childbearing & Childrearing Family 6th ed. Philadelphia. Lippincott William and Wilkins.

Abramowski A, Ward R, Hamdan AH. Neonatal Hypoglycemia. [Updated 2020 Sep 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK537105/

Apnea of Prematurity. Stanford Children's Health - Lucile Packard Children's Hospital Stanford. (n.d.). Retrieved October 2, 2021, from https://www.stanfordchildrens.org/en/topic/default?id=apnea-of-prematurity-90-P02922.

Dirnberger, D. R. (Ed.). (2018, October). Necrotizing Enterocolitis . KidsHealth. Retrieved October 2, 2021, from https://kidshealth.org/en/parents/nec.html.

Khazaeni, L. M. (2020, June). Retinopathy of prematurity . MSD Manual Professional Edition. Retrieved October 2, 2021, from https://www.msdmanuals.com/professional/pediatrics/eye-defects-and-conditions-in-
children/retinopathy-of-prematurity.

Mayo Foundation for Medical Education and Research. (2020, March 17). Infant jaundice. Mayo Clinic. Retrieved October 2, 2021, from https://www.mayoclinic.org/diseases-conditions/infant-jaundice/symptoms-causes/syc-
20373865.